Detected format: VCF Parsed 618,400 SNPs from file ======================================================================== GENETIC REPORT ======================================================================== Input format : VCF SNPs in file : 618,400 Matched SNPs : 453 of 541 in knowledge base Total findings: 896 (one SNP can cover multiple traits) ──────────────────────────────────────────────────────────────────────── APPEARANCE & BEAUTY ──────────────────────────────────────────────────────────────────────── [Eyes] • Brown eye tendency (HERC2/OCA2) rsid : rs12913832 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23548203/ https://pubmed.ncbi.nlm.nih.gov/20585627/ https://pubmed.ncbi.nlm.nih.gov/20463881/ Interpretation: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the brown eye tendency range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 2.84 per copy. • Eye lightness (SLC45A2) rsid : rs16891982 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33692100/ https://pubmed.ncbi.nlm.nih.gov/30664655/ Interpretation: Both copies at this position carry the G variant — a G/G genotype. People with G/G tend to sit toward the higher end of the eye lightness range, with each G copy contributing a small upward shift. Per-copy effect size: β ≈ 0.65 per copy. • Brown eye tendency (HERC2/OCA2) ⚠ CAUTIOUS rsid : rs1129038 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33692100/ Interpretation: Both copies at this position carry the T variant — a T/T genotype, with no copies of the C variant present. People with T/T tend to sit toward the lower end of the brown eye tendency range; the C variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.98 per copy. • Eye color (OCA2) ⚠ CAUTIOUS rsid : rs4778138 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36672889/ Interpretation: Both copies at this position carry the A variant — a A/A genotype, with no copies of the G variant present. People with A/A tend to sit toward the lower end of the eye color range; the G variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.55 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Eye lightness (IRF4) [rs12203592]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the eye lightness range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.21 per copy. Eye lightness (SLC24A5) [rs1426654]: You inherited one A variant and one G variant — a heterozygous A/G genotype, one allele from each parent. This places you between the darker G/G and the lighter A/A genotypes for eye lightness. Per-copy effect size: beta about 0.68 per A copy. Uveal melanoma risk (HERC2) [rs1129038]: Both copies at this position carry the T risk variant — a T/T genotype, the highest-risk combination at this site. Risk for uveal melanoma is elevated above the C/C baseline, with each T copy contributing OR ≈ 1.79 per copy. Eye lightness (TYR) [rs1393350]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the eye lightness range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.28 per copy. Eye color – blue/green shift (OCA2) [rs1800407]: You have the C/C genotype at rs1800407, so you don't carry the T variant that shifts eye color toward green/hazel. Your eye color is determined mainly by other pigmentation genes. This is purely cosmetic. Eye and hair color (HERC2) [rs916977]: No notable finding at this locus. [Hair] • Hair lightness (HERC2) rsid : rs12913832 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30664655/ https://pubmed.ncbi.nlm.nih.gov/29662168/ https://pubmed.ncbi.nlm.nih.gov/26926045/ Interpretation: Both copies at this position carry the G variant — a G/G genotype. People with G/G tend to sit toward the higher end of the hair lightness range, with each G copy contributing a small upward shift. Per-copy effect size: β ≈ 1.61 per copy. • Hair lightness (SLC45A2) rsid : rs16891982 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30664655/ https://pubmed.ncbi.nlm.nih.gov/29662168/ https://pubmed.ncbi.nlm.nih.gov/20585627/ Interpretation: Both copies at this position carry the G variant — a G/G genotype (the European light-pigment form). People with G/G tend to sit toward the higher (lighter) end of the hair-lightness range. Per-copy effect size: OR ≈ 4.92 per copy of G. • Hair lightness (TYR rs1042602) rsid : rs1042602 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30664655/ https://pubmed.ncbi.nlm.nih.gov/30531825/ https://pubmed.ncbi.nlm.nih.gov/29662168/ Interpretation: You inherited one A variant and one C variant — a heterozygous C/A genotype, one allele from each parent. This places you in the middle of the hair lightness range, between the lower-end C/C and the higher-end A/A genotypes. Per-copy effect size: OR ≈ 1.32 per copy. • Eye colour (HERC2/OCA2) rsid : rs1129038 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34737440/ https://pubmed.ncbi.nlm.nih.gov/30531825/ Interpretation: You have the T/T genotype at HERC2 — two copies of the blue-eye-associated allele, the strongest single genetic predictor of blue eyes. Normal cosmetic variation, not a health risk. • Male pattern baldness (alopecia) ⚠ CAUTIOUS rsid : rs12558842 Your geno : CA Evidence : GWAS (binary) Source : https://www.ebi.ac.uk/gwas/variants/rs12558842 Interpretation: You have the C/A genotype — one copy of the A allele linked to higher risk of male-pattern hair loss (alopecia) and one copy of the protective C allele. This puts you at somewhat elevated risk relative to C/C. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Male/female pattern baldness risk rsid : rs12565727 Your geno : GG Evidence : GWAS (binary) Source : https://www.ebi.ac.uk/gwas/variants/rs12565727 Interpretation: You have the G/G genotype, with two copies of the protective G variant at this marker. This means you have a lower genetic risk for male/female pattern baldness. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Blond hair (KITLG) rsid : rs12821256 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34737440/ https://pubmed.ncbi.nlm.nih.gov/17952075/ Interpretation: You inherited one T variant and one C variant — a heterozygous T/C genotype, one allele from each parent. This places you in the middle of the blond hair range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: OR ≈ 2.32 per copy. • Lighter hair & eye color (SLC24A4) ⚠ CAUTIOUS rsid : rs12896399 Your geno : GT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23548203/ https://pubmed.ncbi.nlm.nih.gov/20585627/ https://pubmed.ncbi.nlm.nih.gov/18483556/ Interpretation: You inherited one T variant and one G reference — a heterozygous G/T genotype, one allele from each parent. This places you in the middle of the pigmentation range at this SNP, between G/G (less likely blonder/bluer) and T/T (more likely blonder/bluer). Per-copy effect size for the T allele: OR ≈ 2.56. • Male pattern baldness (androgenetic alopecia) rsid : rs2180439 Your geno : CC Evidence : GWAS (binary) Source : https://www.ebi.ac.uk/gwas/variants/rs2180439 Interpretation: You have the C/C genotype at this chromosome 20p11 baldness locus, meaning you carry no copies of the T allele that the largest study links to male-pattern baldness. This places you at lower genetic risk of androgenetic alopecia from this particular variant. Note that this is an autosomal (chromosome 20) locus, not an X-chromosome one, and baldness is highly polygenic, so many other genes and hormonal factors matter more. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Hair color (OCA2) ⚠ CAUTIOUS rsid : rs4778138 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36672889/ Interpretation: Both copies at this position carry the A variant — a A/A genotype, with no copies of the G variant present. People with A/A tend to sit toward the lower end of the hair color range; the G variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 1.13 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Male pattern baldness (androgenetic alopecia) rsid : rs6945541 Your geno : CT Evidence : GWAS (binary) Source : https://www.ebi.ac.uk/gwas/variants/rs6945541 Interpretation: You have the C/T genotype, carrying one copy of the C risk variant associated with androgenetic alopecia. This is linked to a moderately elevated risk of male pattern baldness. • Male-pattern baldness (androgenetic alopecia) ⚠ CAUTIOUS rsid : rs5934505 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/29146897/ https://pubmed.ncbi.nlm.nih.gov/28196072/ Interpretation: You have the T/T genotype at this position. The effect of this X-chromosome variant on male-pattern baldness is unresolved (published studies disagree on the risk allele), so no good/bad signal is shown. • Alopecia areata risk (CTLA4) ⚠ CAUTIOUS rsid : rs231775 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25608926/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for alopecia areata is elevated above the A/A baseline, with each G copy contributing OR ≈ 1.4 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Hair lightness (IRF4) [rs12203592]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the higher (lighter, more blond) end of the hair-lightness range; the T variant, which shifts hair toward darker/brown, is absent here. Per-copy effect size: β ≈ 0.35 per copy. Red hair (MC1R R151C) [rs1805007]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the red hair range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 2.34 per copy. Red hair & fair skin (MC1R R160W) [rs1805008]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the red hair & fair skin range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.77 per copy. Red hair (MC1R) [rs11547464]: You have the G/G genotype at MC1R — no copy of the R142H red-hair (A) allele here. G/G is associated with the lower end of the red-hair spectrum at this variant, though red hair depends on your other MC1R alleles too. Normal cosmetic variation. Male pattern baldness (20p11) [rs1160312]: No notable finding at this locus. Red/blonde hair tendency (MC1R region) [rs12931267]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the G variant present. People with C/C tend to sit toward the lower end of the red/blonde hair tendency range; the G variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.56 per copy. Hair lightness (TYR rs1393350) [rs1393350]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the hair lightness range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.16 per copy. Hair lightness (OCA2) [rs1800407]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the hair lightness range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.4 per copy. Red hair & fair skin (MC1R) [rs1805005]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the T variant present. People with G/G tend to sit toward the lower end of the red hair & fair skin range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.31 per copy. Red hair & fair skin (MC1R) [rs1805006]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the A variant present. People with C/C tend to sit toward the lower end of the red hair & fair skin range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.82 per copy. Red hair, freckles & fair skin (MC1R R163Q) [rs1805009]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the C variant present. People with G/G tend to sit toward the lower end of the red hair, freckles & fair skin range; the C variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.49 per copy. Freckling & sun sensitivity (20q11) [rs4911414]: No notable finding at this locus. Red/blonde hair tendency (ASIP) [rs6059655]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the red/blonde hair tendency range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.35 per copy. Male/female pattern baldness (androgenetic alopecia) [rs9287638]: You have the C/C genotype and do not carry the variant in this region that is linked to a higher risk of pattern hair loss. [Pigmentation] • Skin lightness & sun sensitivity (SLC45A2) rsid : rs16891982 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25963972/ https://pubmed.ncbi.nlm.nih.gov/31315583/ https://pubmed.ncbi.nlm.nih.gov/33600456/ Interpretation: Both copies at this position carry the G variant — a G/G genotype. People with G/G tend to sit toward the higher end of the skin lightness & sun sensitivity range, with each G copy contributing a small upward shift. Per-copy effect size: β ≈ 2.85 per copy. • Freckles, hair color & sun sensitivity (near MC1R) ⚠ CAUTIOUS rsid : rs1015362 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18488028/ Interpretation: Both copies at this position carry the C variant — a C/C genotype, with no copies of the G variant present. People with C/C tend to sit toward the lower end of the freckles, hair color & sun sensitivity range; the G variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.95 per copy. • Skin pigmentation / skin colour (TYR) rsid : rs1042602 Your geno : CA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39024449/ Interpretation: You have the C/A genotype at TYR — one lighter-pigment (A) allele and one darker (C). This places you in the middle of the pigmentation range at this gene. Normal cosmetic variation, not a health risk. • Vitiligo risk (TYR) ⚠ CAUTIOUS rsid : rs1393350 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20410501/ Interpretation: Both copies at this position carry the G variant — a G/G genotype, the highest-vitiligo-risk combination at this site. Vitiligo risk is elevated above the A/A baseline, with each G copy contributing about OR 1.53 per copy. Note: G is the vitiligo-risk allele even though A is the risk allele for melanoma at the same site. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Freckling tendency (BNC2) rsid : rs2153271 Your geno : CC Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs2153271 Interpretation: You have the C/C genotype at this BNC2 marker. The C allele is associated with fewer freckles, so you carry the lower-freckling version of this variant. Freckling is a normal cosmetic trait that also depends on sun exposure. • Skin pigmentation (OCA2) ⚠ CAUTIOUS rsid : rs4778138 Your geno : AA Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs4778138 Interpretation: You have the A/A genotype at rs4778138 in OCA2. You don't carry the G allele at this pigmentation marker. This variant nudges skin and pigmentation traits within the normal range as part of the larger OCA2/HERC2 region; on its own its effect is small. • Vitiligo risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/27723757/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for vitiligo is modestly higher than for people with the G/G baseline — about OR ≈ 1.38 per copy of the A variant. • Vitiligo risk (PTPN22) ⚠ CAUTIOUS rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39024449/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for vitiligo is modestly higher than for people with the C/C baseline — about β ≈ 0.41 per copy of the A variant. — Also checked, no unusual variants — Skin pigmentation (SLC24A5) [rs1426654]: You inherited one G variant and one A variant — a heterozygous A/G genotype, one allele from each parent. This places you in the middle of the skin pigmentation range, between the lower-end A/A and the higher-end G/G genotypes. Per-copy effect size: β ≈ 0.4 per copy. Freckles (MC1R region) [rs12931267]: You have the C/C genotype, so you don't carry the freckle-associated G allele at this MC1R-region marker. Your tendency to develop freckles from this variant is typical. Red hair & freckling tendency (MC1R) [rs2228479]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the red hair & freckling tendency range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 1.55 per copy. Freckling tendency [rs4911414]: No notable finding at this locus. [Skin] • Skin pigmentation & sun sensitivity (HERC2) rsid : rs12913832 Your geno : GG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31315583/ https://pubmed.ncbi.nlm.nih.gov/30664655/ Interpretation: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the skin pigmentation & sun sensitivity range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.21 per copy. • Skin lightness (TYR rs1042602) rsid : rs1042602 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/31315583/ https://pubmed.ncbi.nlm.nih.gov/30664655/ https://pubmed.ncbi.nlm.nih.gov/17999355/ Interpretation: You inherited one C variant and one A variant — a heterozygous C/A genotype, one allele from each parent. This places you in the middle of the skin pigmentation range, between the darker C/C and the lighter A/A genotypes. • Freckles (TYR) rsid : rs1042602 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17952075/ Interpretation: You inherited one C variant and one A variant — a heterozygous C/A genotype, one allele from each parent. This places you in the middle of the freckles range, between the lower-end A/A and the higher-end C/C genotypes. Per-copy effect size: OR ≈ 1.32 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Skin lightness & sun sensitivity (TYR rs1126809) rsid : rs1126809 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30664655/ https://pubmed.ncbi.nlm.nih.gov/23548203/ Interpretation: You inherited one A variant and one G variant — a heterozygous G/A genotype, one allele from each parent. This places you in the middle of the skin lightness & sun sensitivity range, between the lower-end G/G and the higher-end A/A genotypes. Per-copy effect size: β ≈ 0.16 per copy. • Melanoma risk (TYR) rsid : rs1126809 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39141363/ https://pubmed.ncbi.nlm.nih.gov/32887889/ https://pubmed.ncbi.nlm.nih.gov/32341527/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for melanoma is modestly higher than for people with the G/G baseline — about OR ≈ 1.2 per copy of the A variant. • Non-melanoma skin cancer risk (TYR) rsid : rs1126809 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33549134/ https://pubmed.ncbi.nlm.nih.gov/32041948/ https://pubmed.ncbi.nlm.nih.gov/31174203/ Interpretation: You inherited one A allele and one G allele — a heterozygous G/A genotype, one allele from each parent. The A allele carries a weak population-level association with slightly higher odds of non-melanoma skin cancer (about OR ≈ 1.13 per copy). The effect is small and, on its own, does not meaningfully predict your individual outcome. • Basal cell carcinoma risk (BNC2) ⚠ CAUTIOUS rsid : rs2153271 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36496446/ https://pubmed.ncbi.nlm.nih.gov/33549134/ Interpretation: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T allele present. Each T copy carries a weak population-level association with slightly higher odds of basal cell carcinoma (about +0.08 per copy, study scale), so C/C sits at the lower end of this association. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Acne susceptibility ⚠ CAUTIOUS rsid : rs7531806 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/24399259/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the higher-risk genotype at this single position. Risk for acne susceptibility is elevated above the G/G baseline, with each A copy contributing OR ≈ 1.22 per copy — but the effect is small and on its own does not meaningfully predict your outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atopic eczema risk (IL13) rsid : rs20541 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/37794016/ https://pubmed.ncbi.nlm.nih.gov/31361310/ Interpretation: You have the G/G genotype at IL13 — two copies of the G allele, which carries a small population-level association with lower atopic eczema. This is a weak effect and not individually predictive. • Psoriasis risk (IL13) rsid : rs20541 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19169254/ https://pubmed.ncbi.nlm.nih.gov/26626624/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the higher-risk genotype at this single position. Risk for psoriasis is elevated above the A/A baseline, with each G copy contributing OR ≈ 1.24 per copy. The per-copy effect is small and on its own does not meaningfully predict your outcome. — Also checked, no unusual variants — Freckles (IRF4) [rs12203592]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the freckles range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.46 per copy. Basal cell carcinoma risk (IRF4) [rs12203592]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for basal cell carcinoma sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.41 per copy. Cutaneous squamous cell carcinoma risk (IRF4) [rs12203592]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for cutaneous squamous cell carcinoma sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.6 per copy. Freckles (MC1R R151C) [rs1805007]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the freckles range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 4.37 per copy. Vitiligo risk (HERC2) [rs1129038]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C risk variant present. Your genetic risk for vitiligo sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by OR ≈ 1.22 per copy. Basal cell carcinoma risk (MC1R region) [rs12931267]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the G risk variant present. Your genetic risk for basal cell carcinoma sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.33 per copy. Skin pigmentation & sun sensitivity (OCA2) [rs1800407]: Both copies at this position carry the C variant — a C/C genotype. People with C/C tend to sit toward the higher end of the skin pigmentation & sun sensitivity range, with each C copy contributing a small upward shift. Per-copy effect size: β ≈ 0.23 per copy. Acne susceptibility [rs38055]: No notable finding at this locus. Fair skin, freckling & sun sensitivity (ASIP) [rs6059655]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the fair skin, freckling & sun sensitivity range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.33 per copy. Atopic eczema risk (IL13) [rs1295686]: You have the C/C genotype — two copies of the lower-risk C allele, with no copies of the eczema-raising T allele, giving the lowest genetic risk of atopic eczema at this IL13 variant. Psoriasis risk (IL13) [rs1295686]: Both copies at this position carry the C allele — a C/C genotype, the higher-risk combination at this site for psoriasis (each C copy contributing about β≈0.12). Evidence here is limited (a single record). Psoriasis risk (IL23R) [rs2201841]: No notable finding at this locus. [Sun sensitivity] • Melanoma & skin cancer risk (HERC2 pigmentation) ⚠ CAUTIOUS rsid : rs12913832 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/40495383/ https://pubmed.ncbi.nlm.nih.gov/34290314/ https://pubmed.ncbi.nlm.nih.gov/32341527/ Interpretation: Both copies at this position carry the G variant — a G/G genotype (the blue-eye / light-pigment form). The associated melanoma & skin cancer effect (OR ≈ 1.13 per copy) is real at the population level but small per person, so it is shown as informational rather than a personal risk flag. General sun protection benefits everyone with lighter pigmentation. • Skin cancer & sun damage risk (SLC24A5) ⚠ CAUTIOUS rsid : rs1426654 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34570997/ https://pubmed.ncbi.nlm.nih.gov/30895295/ https://pubmed.ncbi.nlm.nih.gov/30664655/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for skin cancer & sun damage is modestly higher than for people with the G/G baseline — about β ≈ 0.45 per copy of the A variant. • Melanoma & skin cancer risk (SLC45A2) rsid : rs16891982 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34813871/ https://pubmed.ncbi.nlm.nih.gov/28212542/ https://pubmed.ncbi.nlm.nih.gov/32341527/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for melanoma & skin cancer is elevated above the C/C baseline, with each G copy contributing OR ≈ 1.5 per copy. • Melanoma risk (OCA2) ⚠ CAUTIOUS rsid : rs4778138 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/28212542/ https://pubmed.ncbi.nlm.nih.gov/32041948/ https://pubmed.ncbi.nlm.nih.gov/26237428/ Interpretation: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G allele. The A allele shows a weak population-level association with higher odds of melanoma (about OR 1.19 per copy). On its own this does not meaningfully predict your individual melanoma risk; sun exposure and skin type matter far more. — Also checked, no unusual variants — Sun sensitivity & tanning response (IRF4) [rs12203592]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to tan more readily and burn less; the T variant (which shifts toward higher sun sensitivity / lower tanning) is absent here. Per-copy effect size: β ≈ 0.55 (standardized study scale). Fair skin & sun sensitivity (MC1R R151C) [rs1805007]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the fair skin & sun sensitivity range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 2.94 per copy. Melanoma & skin cancer risk (MC1R R151C) [rs1805007]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for melanoma & skin cancer sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.34 per copy. Melanoma & skin cancer risk (MC1R R160W) [rs1805008]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for melanoma & skin cancer sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.37 per copy. Sun sensitivity & sunburn risk (MC1R region) [rs12931267]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the G allele present. Each G copy is associated with a modestly lower sun-sensitivity / ease-of-sunburn measurement (about −0.44 per copy, study scale), so C/C sits toward the more sun-sensitive end of this association. This describes how easily skin burns — a reminder to be sun-smart, not a disease. Melanoma risk (TYR) [rs1393350]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with slightly higher odds of melanoma (about OR ≈ 1.17 per copy), so G/G sits at the lower end of this weak, population-level association. Skin sensitivity to sun (TYR) [rs1393350]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for skin sensitivity to sun sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.26 per copy. Melanoma & skin cancer risk (OCA2) [rs1800407]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T allele present. Each T copy is associated with slightly higher odds of melanoma & skin cancer (about OR ≈ 1.10 per copy), so C/C sits at the lower end of this weak, population-level association. Melanoma risk (MC1R) [rs1805009]: You have the G/G genotype and carry no copies of the C melanoma-risk allele at this MC1R marker — average-to-lower genetic risk at this position. Melanoma risk from MC1R variants is amplified by sun/UV exposure. Skin sensitivity to sun [rs4911414]: No notable finding at this locus. Melanoma & skin cancer risk (ASIP region) [rs6059655]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for melanoma & skin cancer sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.26 per copy. ──────────────────────────────────────────────────────────────────────── BRAIN, MOOD & BEHAVIOR ──────────────────────────────────────────────────────────────────────── [addiction] • Heroin dependence risk (DRD2) ⚠ CAUTIOUS rsid : rs12364283 Your geno : AA Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/1165389/ https://pubmed.ncbi.nlm.nih.gov/31025317/ Summary : rs12364283 is a functional promoter/enhancer variant about 2 kb upstream of DRD2 (dopamine D2 receptor); the minor G allele increases DRD2 expression. In a Pakistani case-control study the G allele was associated with roughly twice the odds of heroin dependence (about OR 2 per copy). This is a behavioral-susceptibility association from limited, mostly single-population data — it is a tendency, not a diagnosis, and only matters in the context of opioid exposure. Note: this is one of 2 correlated variants in/near DRD2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the A/A genotype, you carry the lower-risk version at this DRD2 variant and have a somewhat lower estimated risk of heroin/opioid dependence than people who carry one or two G copies. Risk of dependence is driven mostly by exposure and life circumstances; this variant is only a small genetic nudge. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cocaine dependence risk (CHRNA5) ⚠ CAUTIOUS rsid : rs16969968 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/32152934/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs16969968 is the CHRNA5 D398N coding variant. Unusually, the same minor A allele that raises nicotine-dependence risk is PROTECTIVE for cocaine dependence: in two independent samples of European descent each A copy lowered the odds of cocaine dependence by about a third (OR ~0.67 per allele). So at this variant the reference G allele is the higher-risk allele for cocaine dependence. This is a behavioral-susceptibility tendency, relevant only with cocaine exposure. Note: this is one of 3 correlated variants in/near CHRNA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: If you use cocaine and have the G/G genotype, you carry two copies of the higher-risk allele for cocaine dependence and may be at modestly increased risk compared with people who carry the protective A allele. This is a tendency, not destiny — exposure and personal factors dominate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid dependence risk (OPRM1) ⚠ CAUTIOUS rsid : rs510769 Your geno : CC Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/33589790/ https://pubmed.ncbi.nlm.nih.gov/24086514/ Summary : This variant is in OPRM1, the mu-opioid receptor gene. In curated association data, the T allele (the minor, alternate form here) has been weakly linked to higher odds of opioid-use disorder, the C allele to lower odds. As with the related heroin-dependence finding, the association is modest, comes largely from combined multi-variant analyses, and is far outweighed by personal and environmental factors. It is a small statistical tendency, not a diagnosis or a strong risk marker. No reliable single odds ratio is reported. Note: this is one of 4 correlated variants in/near OPRM1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: You have the C/C genotype — two copies of the lower-risk form. You carry none of the alleles weakly associated with opioid dependence here. This variant is at most a minor factor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid & heroin dependence risk (OPRM1) rsid : rs9479757 Your geno : GG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/829214/ https://pubmed.ncbi.nlm.nih.gov/11933204/ https://pubmed.ncbi.nlm.nih.gov/25122903/ https://pubmed.ncbi.nlm.nih.gov/24086514/ Summary : rs9479757 is a variant in OPRM1, the gene for the mu-opioid receptor that opioid drugs and heroin act on. The G (reference) allele is the risk allele: it strengthens binding of a splicing protein (hnRNPH) and shifts how the receptor is made, and people with the G/G genotype have been linked to more severe heroin dependence, while the less common A allele appears protective and is associated with milder dependence. Because the catalog's risk allele (G) is the reference base, having no A copies (G/G) carries the higher risk and carrying A copies lowers it. The A allele is uncommon (around 9% of alleles), and this only describes risk among people exposed to opioids. Note: this is one of 4 correlated variants in/near OPRM1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: You have the G/G genotype — two copies of the higher-risk G allele at OPRM1. If you are exposed to opioids or heroin, this genotype has been associated with a higher chance of more severe dependence compared with people who carry an A allele. It says nothing about you unless you actually use opioids, and many other factors affect dependence risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Opioid & substance use disorder susceptibility (OPRM1 A118G) [rs1799971]: Both copies here carry the A allele — an A/A genotype, with no copies of the G allele. The G allele shows only a weak population-level association with lower opioid / substance-use-disorder susceptibility (about OR ≈ 0.89 per G copy), so relative to G-carriers the A/A genotype carries a small, weak population-level signal — on its own it does not meaningfully predict your individual outcome. [Anxiety-related traits] • Caffeine-induced anxiety (ADORA2A) rsid : rs5751876 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18305461/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs5751876 sits in ADORA2A, the gene for the adenosine A2A receptor — the same receptor caffeine blocks to make you feel alert. The T allele (the reference allele here) is linked to feeling more anxious or jittery after caffeine. In small experimental studies, people with the T/T genotype reported clearly more anxiety after a moderate caffeine dose (around 150 mg, roughly 1-2 cups of coffee), while C-allele carriers (T/C and C/C) reported little or no anxiety increase. The effect is strongest in people who do not normally drink much caffeine. Effect sizes are not precisely quantified and studies are small, so treat this as a tendency, not a certainty. It only matters if you consume caffeine. Note: this is one of 3 correlated variants in/near ADORA2A reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the T/C genotype, which means you may be less likely to experience caffeine-induced anxiety compared to people with the T/T genotype. Other genetic and clinical factors can also influence your response to caffeine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Caffeine-induced anxiety (ADORA2A) rsid : rs3761422 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20520601/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant in the ADORA2A adenosine-receptor gene affects how anxious caffeine makes you feel. The T allele (the reference form here) is the one linked to a stronger anxiety response to caffeine; the C allele is linked to a calmer response. In a controlled caffeine-challenge study, people with two T copies reported the largest jump in anxiety after caffeine. The effect is about sensitivity to caffeine, not a disease, and only matters if you actually consume caffeine. No numeric effect size is reported for anxiety in the source data. Note: this is one of 3 correlated variants in/near ADORA2A reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the T/C genotype (one T, one C). If you consume caffeine, your anxiety response is likely intermediate — somewhere between the more-sensitive T/T type and the calmer C/C type. If you do not use caffeine, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cocaine dependence risk (CHRNA5) rsid : rs588765 Your geno : TT Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/32152934/ Summary : rs588765 is in the CHRNA5 nicotine-receptor gene cluster, a region best known for nicotine dependence but also studied in other addictions. REF=T, ALT=C. A case-control study in crack-cocaine users (PMID 32152934) found that people homozygous for the major C allele (C/C) had a nominally higher chance of cocaine/crack addiction (P=0.036). This is a single-study, weak, borderline-significant finding — not an established risk factor — so it should be read as a faint statistical hint, not a meaningful personal risk. It applies to people who use cocaine; it does not by itself cause anyone to use the drug. Note: this is one of 3 correlated variants in/near CHRNA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the T/T genotype (two T alleles). In the one small study of crack-cocaine users, the elevated-risk pattern was tied to the C/C genotype, so T/T was not the higher-risk group. The evidence is weak and from a single sample, so this carries little practical meaning for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cocaine addiction risk (CHRNA5) rsid : rs684513 Your geno : CC Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/20485328/ Summary : This is a common variant in the CHRNA5 nicotinic-receptor gene cluster (forward-strand REF C, ALT G), which tags the CHRNA5 substance-dependence signal. Notably, the direction is the opposite of the nicotine finding: in studies (PharmGKB level 3; Sherva 2010 OR about 1.43 in one sample), the G allele was associated with a higher risk of cocaine dependence, while the C allele — the nicotine-risk allele — was protective for cocaine. This well-documented flip means the same gene pushes the two addictions in opposite directions. It is a modest tendency from a marker variant, not a certainty, and only matters for people who use cocaine. Note: this is one of 3 correlated variants in/near CHRNA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the C/C genotype. If you use cocaine, you may be somewhat less likely to develop cocaine dependence than people with the G/G genotype (the same C allele is linked to higher nicotine-dependence risk — the directions differ by substance). If you do not use cocaine, this has no effect on you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. [Cognitive performance] • Antipsychotic response in schizophrenia (BDNF) rsid : rs11030104 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/36137488/ https://pubmed.ncbi.nlm.nih.gov/23433505/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs11030104 is a variant in BDNF, the brain-derived neurotrophic factor gene, in tight linkage with the well-known BDNF Val66Met variant. In schizophrenia, the G (alternate, minor) allele is associated with greater resistance to antipsychotic treatment: in one study each G copy raised the odds of treatment resistance (overall odds ratio about 2.6 for the variant), with G/G carriers far more likely to need clozapine. People with the common A/A genotype tended to respond best. This comes from a single pharmacogenomic study (PharmGKB level 3), so it is a tendency rather than a firm rule, and it only matters if you are being treated with antipsychotics. Interpretation: If you have schizophrenia and take antipsychotics, the A/A genotype (the common type) is associated with the best chance of responding to antipsychotic treatment — that is, the least treatment resistance — compared with people carrying the G allele. Many other genetic and clinical factors also affect how well antipsychotics work for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Schizophrenia risk (NT5C2) ⚠ CAUTIOUS rsid : rs11191580 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23453885/ https://pubmed.ncbi.nlm.nih.gov/22688191/ https://pubmed.ncbi.nlm.nih.gov/21926974/ Interpretation: Both copies at this position carry the T risk variant — a T/T genotype, the higher-risk genotype at this single position. Risk for schizophrenia is elevated above the C/C baseline, with each T copy contributing OR ≈ 1.2 per copy — but the effect is small and on its own does not meaningfully predict your outcome. — Also checked, no unusual variants — Alzheimer's disease risk (TOMM40/APOE region) [rs2075650]: You have the A/A genotype at rs2075650, carrying no copies of the G marker allele. At this TOMM40/APOE-region marker your associated Alzheimer's odds sit toward the lower end — but this SNP only tags the APOE ε4 risk haplotype, it does not confirm your ε-status. Your true APOE ε-genotype requires rs429358 and rs7412 together. Alzheimer's risk is probabilistic and shaped by age, lifestyle and many genes. Memory performance & cognitive decline (APOE region) [rs769449]: Both copies at this position carry the protective G variant — a G/G genotype, the strongest protective combination at this site. Each G copy adds benefit toward memory performance & cognitive decline (β ≈ 0.03 per copy) compared to the A/A baseline. [Depression-related traits] • Citalopram response in depression (TPH2) rsid : rs4570625 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23510446/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant sits just upstream of TPH2, the gene for the brain enzyme that makes serotonin, and has been studied for how people with depression respond to the antidepressant citalopram. The evidence is modest and not fully consistent, but PharmGKB curates it (level 3) with the G/G genotype (the reference form here) linked to a weaker antidepressant response to citalopram compared with people carrying the A allele. Many other genetic and clinical factors also shape antidepressant response, so this is a tendency, not a prediction. It only matters if you take citalopram or a similar SSRI. Interpretation: You have the G/G genotype. If you have depression and take citalopram, you may respond somewhat less well on average than people carrying an A allele — but response varies widely and depends on many factors. If you don't take citalopram or a similar SSRI, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antidepressant response in depression (FKBP5) ⚠ CAUTIOUS rsid : rs3800373 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20709156/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a variant in FKBP5, a gene that regulates the body's stress-hormone (cortisol) feedback system (here REF=C, ALT=A). Several pharmacogenetic studies have linked it to how well antidepressants work, with the C allele generally tied to a somewhat better chance of symptom improvement. The findings are inconsistent — some studies report the opposite or no effect — so this is a weak, contradictory signal, not an established predictor. No effect-size number is reported. It does not tell you your risk of depression itself, only a possible tendency in drug response. Note: this is one of 2 correlated variants in/near FKBP5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have depression and take antidepressants with the A/A genotype, some studies suggest you may be a bit less likely to improve than people carrying a C, but other studies disagree. Many other factors shape antidepressant response, so do not change treatment based on this alone. Warnings : - Based on limited evidence — informational, not a strong personal prediction. [Sleep] • Caffeine-induced insomnia (CYP1A2) rsid : rs762551 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/29668752/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs762551 (CYP1A2*1F, -163C>A) controls how fast your liver breaks down caffeine. REF=C is the slow allele and ALT=A is the fast one. Slow metabolizers (C/C, and C carriers generally) keep caffeine in the bloodstream longer, so caffeine — especially late in the day — is more likely to disturb their sleep, whereas fast metabolizers (A/A) clear it quickly and tend to be less affected. Sleep also depends on dose, timing, and many other personal factors. Interpretation: You have the A/A genotype, the fast caffeine-metabolizer type. You clear caffeine quickly, so you are generally less likely to have caffeine-induced insomnia than slow metabolizers (C carriers). Large or late doses can still affect anyone's sleep. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sleep apnea risk (FTO) ⚠ CAUTIOUS rsid : rs1421085 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39024449/ Interpretation: You inherited one C variant and one T allele — a heterozygous T/C genotype. The C allele carries a weak association with sleep apnea (about β≈0.09 per copy) — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Chronotype (morning vs. evening preference) ⚠ CAUTIOUS rsid : rs12140153 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30696823/ https://pubmed.ncbi.nlm.nih.gov/27992416/ Interpretation: Both copies at this position carry the G variant — a G/G genotype. People with G/G tend to sit toward the higher end of the chronotype range, with each G copy contributing a small upward shift. Per-copy effect size: OR ≈ 1.06 per copy. • Restless legs syndrome risk (BTBD9) rsid : rs3923809 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35489115/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for restless legs syndrome is elevated above the G/G baseline, with each A copy contributing OR ≈ 1.55 per copy. • Restless legs syndrome risk (PTPRD) rsid : rs4626664 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18660810/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for restless legs syndrome is modestly higher than for people with the G/G baseline — about OR ≈ 1.44 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Restless legs syndrome risk ⚠ CAUTIOUS rsid : rs9357271 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21779176/ Interpretation: Both copies at this position carry the T risk variant — a T/T genotype, the highest-risk combination at this site. Risk for restless legs syndrome is elevated above the A/A baseline, with each T copy contributing OR ≈ 1.47 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Restless legs syndrome risk [rs1026732]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for restless legs syndrome sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.42 per copy. Restless legs syndrome risk [rs1975197]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for restless legs syndrome sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.31 per copy. Restless legs syndrome risk (MEIS1) [rs2300478]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the G risk variant present. Your genetic risk for restless legs syndrome sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.68 per copy. Restless legs syndrome risk [rs6747972]: No notable finding at this locus. Insomnia risk (VEGFA) [rs833061]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T allele. The T allele carries a very small association with insomnia (β ≈ 0.008 per copy), so C/C sits at the low end of this tiny range. Informational, not a concern. ──────────────────────────────────────────────────────────────────────── HEART & CARDIOVASCULAR HEALTH ──────────────────────────────────────────────────────────────────────── [Blood pressure] • Blood pressure (HFE) rsid : rs1799945 Your geno : CG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/27618447/ https://pubmed.ncbi.nlm.nih.gov/27841878/ https://pubmed.ncbi.nlm.nih.gov/21909115/ Interpretation: You inherited one G risk variant and one C baseline variant — a heterozygous C/G genotype, one allele from each parent. Risk for blood pressure is modestly higher than for people with the C/C baseline — about β ≈ 0.35 per copy of the G variant. • Blood pressure & hypertension (CDKAL1) ⚠ CAUTIOUS rsid : rs10946398 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/33230300/ Interpretation: Both copies at this position carry the A allele — an A/A genotype, with no copies of the C variant. Relative to C-carriers this sits at the lower end for blood pressure, but the per-allele effect is small. • Blood pressure (NT5C2 region) rsid : rs11191580 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/38459180/ https://pubmed.ncbi.nlm.nih.gov/38689001/ https://pubmed.ncbi.nlm.nih.gov/30487518/ Interpretation: Both copies at this position carry the T allele — a T/T genotype. The T allele is associated with modestly higher blood pressure (about +0.4 mmHg per copy in the largest study), so a T/T reading sits slightly toward the higher-BP end of this single-marker range. This is a measurement nudge, not a diagnosis; less than 1 mmHg from one common variant is dwarfed by everyday factors like salt, weight, activity and the rest of your genome. • Blood pressure (PTPRD region) ⚠ CAUTIOUS rsid : rs4626664 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/33230300/ Interpretation: You inherited one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a slightly higher blood-pressure measurement (about +0.12 mmHg per copy on the study scale). This is a weak population-level association; on its own it does not meaningfully predict your individual blood pressure. • Antihypertensive drug response & resistant hypertension (NOS3) rsid : rs2070744 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/14016/ https://pubmed.ncbi.nlm.nih.gov/19650939/ Summary : This is the well-known NOS3 -786T>C promoter variant, in the gene for the enzyme (eNOS) that makes nitric oxide to relax blood vessels. The C allele lowers eNOS production. Studies link the C/C genotype to harder-to-control (resistant) hypertension, yet other studies found C carriers respond better to the ACE-inhibitor enalapril — so the direction of the effect changes depending on the drug and outcome. Because the evidence points different ways, this is informational only: an association exists, but no reliable per-genotype prediction can be made. Interpretation: The C/C genotype at NOS3 -786 has been associated with reduced eNOS promoter activity and, in some cohorts, with harder-to-treat (resistant) hypertension — but other studies linked the C allele to better response to the drug enalapril. Because findings conflict across drugs and outcomes, no reliable personal prediction can be made; this is informational only and any treatment choices are made by your doctor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - conflicting_evidence_direction • Enalapril blood pressure response (NOS3) rsid : rs2070744 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/14016/ https://pubmed.ncbi.nlm.nih.gov/22706620/ Summary : rs2070744 sits in the promoter of NOS3, the gene for the enzyme that makes nitric oxide (which relaxes blood vessels). In a study of people with high blood pressure, carriers of the C allele at this position had a greater drop in blood pressure on enalapril than people with two G copies. The evidence is limited (a single small pharmacogenetic study, PharmGKB level 3), so this is a weak tendency, not a firm rule, and it only matters if you are actually taking enalapril. Interpretation: If you have the C/C genotype and hypertension, you may have a greater reduction in blood pressure when treated with enalapril compared to people with the G/G genotype. Other genetic and clinical factors can also influence blood pressure reduction on enalapril. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Enalapril response in hypertension (VEGFA) rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26002049/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 (VEGF -2578 C>A) is in the promoter of VEGFA. In people with high blood pressure, carriers of the A allele (A/A and A/C) tended to have a better blood-pressure response to enalapril than those with two C copies. The evidence is limited (single study, PharmGKB level 3) and only relevant if you take enalapril. Interpretation: If you have hypertension and the A/A genotype, you may have an improved response to enalapril compared to people with the C/C genotype. Other clinical and genetic factors may also influence response to enalapril in hypertension. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Coronary artery disease risk (CNNM2/10q24) rsid : rs12413409 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21378990/ Interpretation: Both copies at this position carry the G allele — a G/G genotype. At the population level the G allele carries a weak association with coronary artery disease at this 10q24 locus (about OR ≈ 1.12 per copy); on its own it does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Intracranial (brain) aneurysm risk (CNNM2) ⚠ CAUTIOUS rsid : rs12413409 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20364137/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the higher-risk genotype at this single position. Risk for intracranial (brain) aneurysm is elevated above the A/A baseline, with each G copy contributing OR ≈ 1.29 per copy — but the effect is small and on its own does not meaningfully predict your outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Irbesartan blood pressure response (APOB) ⚠ CAUTIOUS rsid : rs1367117 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15453913/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is an APOB variant best known for raising LDL ('bad') cholesterol (the A allele increases LDL). A single small pharmacogenetic study also linked it to how well the blood-pressure drug irbesartan lowers blood pressure, with G/G carriers tending to respond better than A/A carriers. The drug-response evidence is limited (one study), so treat it as preliminary; your doctor judges how well a medicine is working. Interpretation: If you have the A/A genotype and take irbesartan, the same small study suggests you may be somewhat less likely to respond than G carriers. This is preliminary, single-study evidence; other genetic and clinical factors also matter, and it only applies if you take irbesartan. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Candesartan blood-pressure response (SH2B3) rsid : rs3184504 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31327267/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs3184504 is the R262W missense variant in SH2B3 (LNK), a top genetic signal for blood pressure: its T allele (reference base) raises blood pressure, the C allele (alternate base) is the lower-pressure version. A single low-level (level 3) pharmacogenetic study linked this site to how much blood pressure falls on the angiotensin-receptor blocker candesartan, with the lower-pressure C/C genotype tending to respond differently from T-carriers. The drug-response evidence is weak and single-study with no effect size, so this is only a tentative, drug-specific signal — your overall blood-pressure risk from this variant is covered by the separate coronary/blood-pressure entry. Interpretation: If you take candesartan and have the C/C genotype, you carry the lower-baseline-blood-pressure version of SH2B3; one small study suggests your response to candesartan may differ from T-carriers. The evidence is weak and not a basis for a treatment decision by itself; this only matters while on the drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Irbesartan blood pressure response (AGT) ⚠ CAUTIOUS rsid : rs4762 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/11910301/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the AGT Thr174Met variant in angiotensinogen, an early step in the blood-pressure-controlling renin–angiotensin system. A small pharmacogenetic study looked at how the genotype relates to blood-pressure response to the drug irbesartan, but the findings were inconsistent and the effect allele could not be reliably pinned down. So this is informational only: an association has been reported, but no dependable per-genotype prediction can be made. Interpretation: If you have the G/G genotype (Thr174) and take irbesartan, one small study suggested a possibly different blood-pressure response than G/A carriers, but the findings were inconsistent. No reliable personal prediction can be made; this is informational only and applies only while you take irbesartan. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Thiazide diuretic response in hypertension (ADD1) ⚠ CAUTIOUS rsid : rs4961 Your geno : GT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12623934/ https://pubmed.ncbi.nlm.nih.gov/14553962/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4961 is the Gly460Trp variant in ADD1 (alpha-adducin), a protein that helps the kidney handle sodium. The minor T allele (the alternate base, the 'Trp/W460' form) is linked to salt-sensitive high blood pressure, and carriers of this allele tend to lower their blood pressure more when treated with thiazide diuretics such as hydrochlorothiazide. The supporting evidence is a low-level (level 3) PharmGKB efficacy annotation drawn from many small studies with mixed results and no pooled effect size, so this is a modest, drug-specific signal. It only matters if you take a thiazide diuretic. Interpretation: If you take a thiazide diuretic and have the G/T genotype, you carry one T (Trp460) copy, which several studies link to a somewhat greater blood-pressure reduction on thiazides. The evidence is mixed across studies, so treat this as a modest signal, relevant only while on the drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Diuretic therapy & myocardial infarction risk (ADD1) ⚠ CAUTIOUS rsid : rs4961 Your geno : GT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/11926892/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4961 is the Gly460Trp variant in ADD1 (alpha-adducin), which affects kidney sodium handling and salt-sensitive blood pressure. In pharmacogenetic studies, the minor T allele (the alternate base, 'Trp/W460') has been studied for how diuretic treatment interacts with heart-attack (myocardial infarction) risk: some data suggest T-allele carriers on diuretics may have a different — in some reports lower — risk of myocardial infarction than non-carriers. The evidence is a low-level (level 3) annotation with no pooled effect size and is not fully consistent, so this is a weak, treatment-specific signal that only applies if you take a diuretic. Interpretation: If you take a diuretic and have the G/T genotype, you carry one T (Trp460) copy; limited data suggest diuretic therapy may interact with heart-attack risk differently in carriers, but the evidence is weak and inconsistent. This only matters if you are on a diuretic. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atenolol blood pressure response (AGT) rsid : rs5051 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/14700505/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs5051 is a promoter variant of AGT (angiotensinogen), the starting protein of the blood-pressure-regulating renin–angiotensin system; the A allele (the alternate base, the '-6A' form) increases AGT production. A low-level (level 3) pharmacogenetic study linked this site to how much blood pressure falls on the beta-blocker atenolol: people with the C/C genotype showed a smaller drop in systolic blood pressure on atenolol than A-allele carriers, with no significant difference in diastolic pressure. The evidence is single-study with no pooled effect size, so this is a weak, drug-specific signal that only matters if you take atenolol. Interpretation: If you have the C/C genotype and hypertension, you may have a smaller decrease in systolic blood pressure when treated with atenolol compared to people with the C/A or A/A genotype. No significant change in diastolic blood pressure was seen between genotypes. Other genetic and clinical factors can also influence the change in systolic blood pressure. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Benazepril / imidapril blood pressure response (AGT) rsid : rs5051 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25143324/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs5051 is a promoter variant of AGT (angiotensinogen), the first protein in the renin–angiotensin blood-pressure pathway; the A allele (the alternate base, '-6A') increases AGT production. A low-level (level 3) pharmacogenetic study linked this site to blood-pressure response to the ACE inhibitors benazepril and imidapril: people with the C/C genotype tended to respond better (a larger blood-pressure fall) than A-allele carriers. The evidence is single-study with no pooled effect size, so this is a weak, drug-specific signal that only matters if you take one of these ACE inhibitors. Interpretation: If you have the C/C genotype and hypertension, you may have a better response to treatment with benazepril or imidapril compared to people with the C/A or A/A genotype. Other genetic and clinical factors can also influence your response to benazepril or imidapril. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atenolol – blood pressure response (LDLR) rsid : rs688 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15453913/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take atenolol (a beta-blocker) for high blood pressure. People carrying the C allele of this LDLR variant tended to get more lowering of systolic (top-number) blood pressure on atenolol, while people with two T alleles tended to respond less. This describes how well the drug works for you, not a disease risk, and the evidence is limited (PharmGKB level 3, small study), so treat it as a tendency. Interpretation: If you have the C/T genotype, you may have more effective lowering of systolic blood pressure on atenolol compared to people with the T/T genotype. Other genetic and clinical factors may also influence your response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Systolic blood pressure ⚠ CAUTIOUS rsid : rs12478601 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/33230300/ Interpretation: You have one C and one T allele — a heterozygous C/T genotype, one from each parent. The T allele is associated with a modestly lower systolic blood pressure at the population level (about β ≈ 0.16 per copy, study scale). This is a measurement-level association, not a disease prediction. — Also checked, no unusual variants — Blood pressure (MTHFR) [rs1801133]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with a modestly higher blood-pressure measurement (about +0.36 per copy, study scale), so G/G sits at the lower end of this weak, population-level association. Blood pressure / hypertension risk (ALDH2) [rs671]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with a slightly lower blood-pressure measurement (about −0.06 per copy, study scale), so G/G sits at the higher end of this weak, population-level association. The effect is small and, on its own, does not meaningfully predict your blood pressure. Coffee and heart attack risk (CYP1A2) [rs762551]: You have the A/A genotype, the fast caffeine-metabolizer type. In coffee drinkers, A/A people did not show the increased heart-attack risk seen in slow metabolizers (C carriers). This is reassuring only in the context of caffeine intake; your overall heart risk still depends on many other genetic and lifestyle factors. Systolic blood pressure (CYP11B2) [rs1799998]: Both copies carry the G allele — a G/G genotype. At this CYP11B2 marker each G copy is associated with a slightly lower systolic blood-pressure measurement (about beta ≈ 0.02 per copy on the study scale). This is a very small measurement nudge, not a disease risk. Blood pressure (AGT M235T) [rs699]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the blood-pressure-raising G allele. Your genetic tendency for measured blood pressure sits at the lower end of this very small range; each G copy nudges it up by only β ≈ 0.02 on the study scale. ACE (angiotensin-converting enzyme) activity [rs4343]: With the G/A genotype, you have intermediate serum ACE activity — one G and one A copy. Abdominal aortic & intracranial aneurysm risk (9p21) [rs10757278]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the C risk variant present. Your genetic risk for abdominal aortic & intracranial aneurysm sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by β ≈ 0.13 per copy. Blood pressure / hypertension risk (10q24) [rs12413409]: With the G/G genotype you carry two copies of the G allele. At this 10q24 (CYP17A1–CNNM2) locus the G allele carries a weak population-level association with higher blood pressure / hypertension; on its own it does not meaningfully predict your individual blood pressure, which a cuff reading captures directly. Blood pressure & hypertension risk (SH2B3) [rs3184504]: Both copies at this position carry the C allele — a C/C genotype, with no T copies. Blood pressure tends to sit at the lower end relative to T-carriers; each T copy would nudge the measurement up by about β ≈ 0.03 on the study scale. This is a measurement-level association, not a disease prediction. Coronary artery disease risk (SH2B3) [rs3184504]: With the C/C genotype you carry two copies of the lower-risk version of SH2B3, associated with the lowest blood pressure and coronary-artery-disease contribution among the three genotypes at this site. This is a small protective nudge, not a guarantee. Blood pressure & hypertension risk (NPR3) [rs3918226]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for blood pressure & hypertension sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by β ≈ 0.55 per copy. Coronary artery disease risk (NPR3) [rs3918226]: Both copies at this position carry the C allele — a C/C genotype, with no T copies. This is the slightly more favourable version relative to T-carriers; each T copy is associated with about OR ≈ 1.12 higher coronary artery disease risk — a weak population-level association that, on its own, does not meaningfully predict your individual outcome. Brain (intracranial) aneurysm risk [rs4977574]: Both copies at this position carry the A allele — an A/A genotype, with no G copies. This is the slightly more favourable version relative to G-carriers; each G copy is associated with about OR ≈ 1.19 higher intracranial (brain) aneurysm risk — a weak population-level association that, on its own, does not meaningfully predict your individual outcome. Abdominal aortic aneurysm risk (9p21) [rs4977574]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for abdominal aortic aneurysm sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by β ≈ 0.17 per copy. Blood pressure (TERT) [rs10069690]: You have the C/C genotype — two copies of the C allele and no copies of the T allele. At a population level this is associated with the lower end of this marker's small blood-pressure shift (each T copy adds about β ≈ 0.01 on the study scale). Blood pressure is a measurement, not a diagnosis. [Cardiac rhythm] • QT interval length (NOS1AP) rsid : rs10494366 Your geno : GT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/16648850/ https://pubmed.ncbi.nlm.nih.gov/34616002/ Interpretation: You inherited one G allele and one T allele — a heterozygous G/T genotype. This places you in the middle of the QT-length range at this NOS1AP SNP, between the longer-QT G/G and the shorter-QT T/T. QT length is a biomarker, not a diagnosis. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Aortic valve stenosis risk (IL6) [rs1800797]: You have the G/G genotype — two copies of the G allele and no copies of the A allele. At a population level this is the lower-association version of this marker (each A copy carries about OR ≈ 1.14). The effect is weak and not individually predictive. [Cholesterol] • Statin response (APOE) rsid : rs7412 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16103896/ https://pubmed.ncbi.nlm.nih.gov/30363031/ Summary : rs7412 is one of the two SNPs that define APOE type; the T allele (ALT) is the ε2-defining allele. People who carry the T (ε2) allele tend to get a somewhat larger drop in LDL ('bad') cholesterol from statins such as atorvastatin than people with the common C/C (ε3/ε4) genotype. For example, one stroke-patient study saw the biggest LDL reductions in ε2 carriers. The effect is modest and not consistent across every study, and statins lower cholesterol effectively across all APOE types — so this nudges the expected response rather than deciding whether a statin will work. It is only relevant if you take a statin. Interpretation: You have the C/C genotype at rs7412 in APOE, which means you may have a decreased response to atorvastatin compared to people with the C/T or T/T genotype. Keep in mind that other genetic and clinical factors can also influence how you respond to atorvastatin treatment. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Triglyceride levels (FADS1) rsid : rs174546 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ https://pubmed.ncbi.nlm.nih.gov/20686565/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. The T allele is associated with higher triglycerides (about +0.07 SD per copy) but also with lower LDL and total cholesterol at this pleiotropic FADS1 locus. The triglyceride shift is small, so we treat it as neutral. • LDL cholesterol (FADS1) rsid : rs174547 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31566214/ https://pubmed.ncbi.nlm.nih.gov/29615537/ https://pubmed.ncbi.nlm.nih.gov/19060906/ Interpretation: Both copies at this position carry the C variant — a C/C genotype. The C allele is associated with lower LDL/non-HDL cholesterol (about −0.04 SD per copy) but with higher triglycerides at this pleiotropic FADS1 locus. The shift is small, so neutral. • LDL & total cholesterol (FADS1) ⚠ CAUTIOUS rsid : rs174550 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39414775/ Interpretation: Both copies carry the C allele — a C/C genotype. At this FADS1 marker each C copy is associated with a modestly lower LDL / total-cholesterol measurement (about beta ≈ 0.06 per copy on the study scale). This is a measurement nudge, not a disease risk. • LDL & total cholesterol (FADS1/FADS2) rsid : rs174583 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/29507422/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. The T allele is associated with lower LDL/total cholesterol (about −0.07 SD per copy), so T/T sits at the lower-cholesterol end at this site. The effect is small, so neutral. • HDL ("good") cholesterol level (LIPC) rsid : rs1800588 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/40841581/ https://pubmed.ncbi.nlm.nih.gov/33339817/ Interpretation: You inherited one protective T variant and one C variant — a heterozygous C/T genotype, one allele from each parent. You get partial protective benefit for hdl ("good") cholesterol level relative to the C/C baseline — about β ≈ 0.12 per copy of the T variant. • Statins – HDL cholesterol response (LIPC) rsid : rs1800588 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16103896/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800588 is the LIPC -514C>T variant in the hepatic lipase gene (REF=C, ALT=T). The T allele lowers hepatic lipase activity, which is linked to modestly higher HDL ('good') cholesterol (a strong GWAS signal, beta around 0.07–0.14). In statin studies, T-allele carriers showed a larger rise in HDL on treatment (about +7% on pravastatin) while C/C carriers had almost no HDL change, so the variant chiefly affects how much your HDL improves on a statin. Effect sizes are small and HDL is only one piece of overall lipid health. Interpretation: You have the C/T genotype, carrying one T allele that lowers hepatic lipase activity and is linked to somewhat higher HDL. If you take a statin, you may see a modestly greater rise in HDL than C/C individuals. The effect is small and one of many factors in your lipid profile. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Triglyceride levels (LPL S447X) rsid : rs328 Your geno : CG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32150548/ https://pubmed.ncbi.nlm.nih.gov/35945198/ https://pubmed.ncbi.nlm.nih.gov/22171074/ Interpretation: You inherited one G variant and one C variant — a heterozygous C/G genotype, one allele from each parent. The single G copy (the LPL S447X form) modestly lowers your triglycerides relative to C/C — a small favourable shift (β ≈ 0.19 per copy). • HDL ('good') cholesterol level (CETP) rsid : rs3764261 Your geno : CA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/33499410/ https://pubmed.ncbi.nlm.nih.gov/31211820/ https://pubmed.ncbi.nlm.nih.gov/30911093/ Interpretation: You inherited one protective A variant and one C variant — a heterozygous C/A genotype, one allele from each parent. You get partial protective benefit for hdl ('good') cholesterol level relative to the C/C baseline — about β ≈ 0.23 per copy of the A variant. • HDL cholesterol level (CETP) rsid : rs5882 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/35945198/ Interpretation: You inherited one G (Val) variant and one A (Ile) variant — a heterozygous G/A genotype, one allele from each parent. The single G copy is associated with modestly higher HDL than A/A (β ≈ 0.09 per copy) — a small favourable nudge. • HDL cholesterol level (CETP) rsid : rs708272 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39091897/ Interpretation: You inherited one protective A variant and one G variant — a heterozygous G/A genotype, one allele from each parent. You get partial protective benefit for hdl cholesterol level relative to the G/G baseline — about β ≈ 0.07 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Total and LDL cholesterol (FGF21 region) ⚠ CAUTIOUS rsid : rs838145 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/41044249/ https://pubmed.ncbi.nlm.nih.gov/34594039/ Interpretation: Both copies at this position carry the A allele — an A/A genotype. The A allele is associated with marginally lower measured total/LDL cholesterol (about β ≈ 0.02 per copy on the study scale) — a small, favourable nudge in a routine blood measurement relative to G-carriers. • Body mass index / obesity (FTO) ⚠ CAUTIOUS rsid : rs1121980 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/28334899/ https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You have the G/A genotype — one A weight-raising copy and one G copy. This is linked to a modestly higher body mass index than G/G (about +0.07 per copy on the study scale). The effect is real but modest and is reduced by an active lifestyle. • Statin response (PCSK9 loss-of-function) ⚠ CAUTIOUS rsid : rs11591147 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31969989/ https://pubmed.ncbi.nlm.nih.gov/22331829/ https://pubmed.ncbi.nlm.nih.gov/26902539/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each T allele is associated with lower Statin response (PCSK9 loss-of-function) (−0.372 per copy, study scale). The underlying association is well-replicated (4 publications), but there is no clinical pharmacogenetic guideline to act on it. Interpretation: Both copies at this position carry the G variant — a G/G genotype. People with G/G tend to sit toward the higher end of the statin response range, with each G copy contributing a small upward shift. Per-copy effect size: β ≈ 0.37 per copy. • Triglycerides & LDL cholesterol (GCKR) ⚠ CAUTIOUS rsid : rs1260326 Your geno : CC Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs1260326 Interpretation: You have the C/C genotype at GCKR, associated with lower triglyceride levels (and, via the same variant, higher fasting glucose). • LDL & total cholesterol levels (LDLR) ⚠ CAUTIOUS rsid : rs2228671 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31217584/ Interpretation: You inherited one T allele and one C reference allele — a heterozygous C/T genotype at LDLR rs2228671. The T allele lowers LDL-C by ≈0.19 mmol/L per copy and is associated with reduced coronary-artery-disease risk (per-allele OR≈0.82–0.83). One T copy gives you a modest favourable shift versus C/C. • LDL & total cholesterol (CELSR2/SORT1) rsid : rs646776 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30911093/ https://pubmed.ncbi.nlm.nih.gov/38116116/ Interpretation: Both copies here carry the T allele — a T/T genotype. On average this is associated with a modestly higher LDL/total-cholesterol measurement than C/C (about β ≈ 0.17 per T copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual cholesterol. • Coronary artery disease & heart attack risk (CELSR2/SORT1) rsid : rs646776 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21239051/ https://pubmed.ncbi.nlm.nih.gov/19198609/ Interpretation: Both copies here carry the T allele — a T/T genotype. On average this is associated with slightly higher odds of coronary artery disease than C/C (about OR ≈ 1.17 per T copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • LDL cholesterol & coronary artery disease risk (LDLR) rsid : rs6511720 Your geno : GT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31393916/ https://pubmed.ncbi.nlm.nih.gov/29212778/ Interpretation: You carry one G allele and one T allele — a heterozygous G/T genotype, one from each parent. The T allele is associated with a slightly lower LDL-cholesterol measurement (about β ≈ 0.23 per T copy on the study scale), so G/T sits between the two homozygous groups. This is a weak population-level association and does not on its own meaningfully predict your individual LDL. • LDL cholesterol & apolipoprotein B levels (APOB) rsid : rs693 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/41044249/ https://pubmed.ncbi.nlm.nih.gov/35213538/ Interpretation: Both copies here carry the A allele — an A/A genotype. On average this is associated with a slightly higher LDL / apoB measurement than G/G (about β ≈ 0.06 per A copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual LDL or apoB. • Triglyceride & HDL cholesterol levels (GCKR) rsid : rs780094 Your geno : CC Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs780094 Interpretation: You have the C/C genotype — two copies of the C allele. On average this is linked to lower fasting triglycerides, a lower triglyceride-to-HDL ratio and lower C-reactive protein, but slightly higher fasting blood glucose. It is a metabolic trade-off rather than a clearly favourable or unfavourable result. • Atorvastatin response (CYP3A4 *1G) ⚠ CAUTIOUS rsid : rs2242480 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18528690/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. CYP3A4 rs2242480 (the *1G allele, now PharmVar *36). In people with high cholesterol on atorvastatin, carrying the T allele (*1G) was associated with a BETTER cholesterol-lowering response, while C/C was associated with a weaker response. This is a single low-level association (PharmGKB level 3 Efficacy), so it is a weak tendency rather than a basis for changing treatment. Interpretation: If you have the C/C genotype and hyperlipidemia, you may have a reduced response to atorvastatin treatment (a lower reduction in total cholesterol) compared to people with the C/T or T/T genotype. Other genetic and clinical factors may also influence your response to atorvastatin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Statin response & residual CAD risk (LPA) rsid : rs10455872 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23903772/ https://pubmed.ncbi.nlm.nih.gov/22331829/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each G allele is associated with higher Statin response & residual CAD risk (LPA) (+4.8 per copy, study scale). The underlying association is well-replicated (5 publications), but there is no clinical pharmacogenetic guideline to act on it. Interpretation: If you have the A/A genotype, you may have an increased response to rosuvastatin compared to people with the A/G or G/G genotype. Other genetic and clinical factors may also affect your response to rosuvastatin. • Coronary artery disease & heart attack risk (PCSK9) rsid : rs11206510 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19198609/ Interpretation: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T allele. The C allele is the lower-odds allele here (OR ≈ 0.93 per copy), so C/C sits at the favourable end of this small range. Informational, not a concern. • LDL cholesterol level (PCSK9) ⚠ CAUTIOUS rsid : rs11206510 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/18193043/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. The C allele is associated with a modestly lower LDL cholesterol measurement (about −0.06 per copy on the study scale), so C/C sits at the lower end of this measurement range. This is informational, not a concern. • Coronary artery disease risk (9p21) rsid : rs1333049 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/29212778/ https://pubmed.ncbi.nlm.nih.gov/22144573/ Interpretation: Both copies at this position carry the G allele — a G/G genotype, with no copies of the C allele. At this well-studied 9p21 locus the C allele carries a weak per-copy association with coronary artery disease (about OR ≈ 1.17 per copy), so being G/G removes even that small statistical nudge. • LDL & total cholesterol (APOB) rsid : rs1367117 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: Both copies at this position carry the A allele — an A/A genotype. At the population level the A allele is associated with modestly higher average LDL & total cholesterol than the G allele (about β ≈ 0.09 per copy on the study's scale). This is a measurement-level association, not a disease prediction — it nudges an average lipid reading, and a blood test reflects your real LDL. • Coronary artery disease risk (PPAP2B/PLPP3) rsid : rs17114036 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21378990/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the higher-risk genotype at this single position. Risk for coronary artery disease is elevated above the G/G baseline, with each A copy contributing β ≈ 0.13 per copy — but the effect is small and on its own does not meaningfully predict your cardiovascular outcome. • Coronary artery disease risk (MIA3) rsid : rs17465637 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/29212778/ https://pubmed.ncbi.nlm.nih.gov/19198609/ Interpretation: Both copies are the C allele — a C/C genotype. The C allele shows a weak association with coronary artery disease (OR ≈ 1.14 per copy), so C/C sits at the upper end of this small signal. The per-copy effect is modest and, on its own, does not meaningfully predict your individual outcome — standard cardiovascular risk factors matter much more. • HDL ("good") cholesterol level (CETP) rsid : rs2070895 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39414775/ Interpretation: You inherited one protective A variant and one G variant — a heterozygous G/A genotype, one allele from each parent. You get partial protective benefit for hdl ("good") cholesterol level relative to the G/G baseline — about β ≈ 0.15 per copy of the A variant. • Total cholesterol level (CETP) rsid : rs2070895 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39414775/ Interpretation: You carry one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a slightly higher total cholesterol reading on average (β ≈ 0.06 per copy). This is a weak population-level association and, on its own, does not meaningfully predict your individual cholesterol level — a lipid panel is the real measure. • Triglyceride levels (CETP) ⚠ CAUTIOUS rsid : rs2070895 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/38116116/ Interpretation: You carry one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a slightly higher triglyceride reading on average (β ≈ 0.06 per copy). This is a weak population-level association and, on its own, does not meaningfully predict your individual triglyceride level — a lipid panel is the real measure. • Triglyceride levels (APOA5) rsid : rs2266788 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/21386085/ Interpretation: Both copies are the A allele — an A/A genotype. The A allele is associated with a lower triglyceride reading (β ≈ 0.28 per copy), so A/A sits at the lower end for this measurement. This is an average shift across people; a lipid panel confirms your actual number. • HDL ('good') cholesterol (APOA5) rsid : rs2266788 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/21386085/ Interpretation: Both copies at this position carry the protective A variant — a A/A genotype, the strongest protective combination at this site. Each A copy adds benefit toward hdl ('good') cholesterol (β ≈ 0.12 per copy) compared to the G/G baseline. • LDL & total cholesterol (APOA5) rsid : rs2266788 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/29507422/ Interpretation: Both copies are the A allele — an A/A genotype. The A allele is weakly associated with a slightly lower LDL/total cholesterol reading (β ≈ 0.11 per copy), so A/A sits at the lower end of this small average shift. The per-copy effect is tiny and, on its own, does not meaningfully predict your individual cholesterol level. • Coronary artery disease risk (MRAS) ⚠ CAUTIOUS rsid : rs2306374 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21378990/ Interpretation: With the T/C genotype, you carry one copy of the C allele, associated with a modestly increased risk of coronary artery disease (~12% per allele). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • LDL & total cholesterol (PCSK9) rsid : rs2479409 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ https://pubmed.ncbi.nlm.nih.gov/29748315/ Interpretation: Both copies are the A allele — an A/A genotype. The A allele is weakly associated with a slightly lower LDL/total cholesterol reading (β ≈ 0.05 per copy), so A/A sits at the lower end of this small average shift. The per-copy effect is tiny and, on its own, does not meaningfully predict your individual cholesterol level. • Triglyceride levels (APOA5 region) rsid : rs2954029 Your geno : AT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/38116116/ https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You inherited one A allele and one T allele — a heterozygous A/T genotype, one from each parent. Triglyceride levels tend to run slightly higher than for people with the T/T type — about β ≈ 0.09 per A copy on the study scale. This is a small measurement-level shift, not a disease prediction. • LDL & total cholesterol levels (APOA5 region) rsid : rs2954029 Your geno : AT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You inherited one A allele and one T allele — a heterozygous A/T genotype, one from each parent. LDL and total cholesterol tend to run slightly higher than for people with the T/T type — about β ≈ 0.06 per A copy on the study scale. This is a small measurement-level shift, not a disease prediction. • HDL ('good') cholesterol levels (APOA5 region) rsid : rs2954029 Your geno : AT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You inherited one protective T variant and one A variant — a heterozygous A/T genotype, one allele from each parent. You get partial protective benefit for hdl ('good') cholesterol levels relative to the A/A baseline — about β ≈ 0.04 per copy of the T variant. • Coronary artery disease risk (APOA5 region) rsid : rs2954029 Your geno : AT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/29212778/ Interpretation: You inherited one A allele and one T allele — a heterozygous A/T genotype, one from each parent. Any difference in coronary artery disease risk versus T/T is very small (about OR ≈ 1.04 per A copy) — a weak population-level association that does not meaningfully predict your individual outcome. • HDL cholesterol level (LIPG) rsid : rs4939883 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19060906/ https://pubmed.ncbi.nlm.nih.gov/19060911/ Interpretation: Both copies at this position carry the protective C variant — a C/C genotype, the strongest protective combination at this site. Each C copy adds benefit toward hdl cholesterol level (β ≈ 0.1 per copy) compared to the T/T baseline. • Total and LDL cholesterol levels (LIPG) rsid : rs4939883 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19060911/ https://pubmed.ncbi.nlm.nih.gov/19936222/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with modestly higher total and LDL cholesterol than the T/T type, with each C copy adding about β ≈ 0.04 on the study scale. This is a small measurement-level nudge, not a disease prediction. • LDL cholesterol level (PSRC1/CELSR2 region) rsid : rs4970834 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32203549/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with modestly higher LDL cholesterol than the T/T type, with each C copy adding about β ≈ 0.11 on the study scale. This is a measurement-level nudge, not a disease prediction. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • LDL & total cholesterol (ABO) rsid : rs579459 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30926973/ https://pubmed.ncbi.nlm.nih.gov/26582766/ Interpretation: Both copies at this position carry the T allele — a T/T genotype. T/T is associated with a modestly lower LDL & total cholesterol measurement than C/C (about −0.085 per copy, study scale). This is a measurement-level association, not a disease prediction. • Coronary artery disease & heart attack risk rsid : rs583104 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38297123/ Interpretation: Both copies at this position carry the T risk variant — a T/T genotype, the higher-risk genotype at this single position. Risk for coronary artery disease & heart attack is elevated above the G/G baseline, with each T copy contributing β ≈ 0.12 per copy. The per-copy effect is small and on its own does not meaningfully predict your outcome. • LDL cholesterol & coronary artery disease risk (ABCG5/ABCG8) ⚠ CAUTIOUS rsid : rs6544713 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36474045/ https://pubmed.ncbi.nlm.nih.gov/30926973/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly lower LDL cholesterol measurement than T/T (about −0.0492 per copy, study scale). This is mainly a measurement-level association, not a disease prediction. • LDL & total cholesterol levels rsid : rs660240 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/38116116/ https://pubmed.ncbi.nlm.nih.gov/40841581/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly higher LDL & total cholesterol measurement than T/T (about +0.22 per copy, study scale). This is a measurement-level association, not a disease prediction. • Lovastatin – cholesterol-lowering response (LDLR) rsid : rs688 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16103896/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take lovastatin (a statin) for high cholesterol. In one large statin study, the T allele of this LDLR variant was linked to a greater drop in total cholesterol on lovastatin. The pattern was not a simple step-by-step one: people with two T alleles had the biggest response and people with one of each (C and T) had the smallest, with two-C people in between. This describes how well the drug lowers your cholesterol, not a disease risk, and the evidence is limited (PharmGKB level 3), so treat it as a tendency. Interpretation: If you have the C/T genotype, you may have a smaller decrease in total cholesterol when treated with lovastatin compared to people with the C/C or T/T genotype. Other genetic and clinical factors may also influence total cholesterol levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Triglycerides & VLDL (APOA1/APOA5 cluster) rsid : rs964184 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/23505323/ https://pubmed.ncbi.nlm.nih.gov/27005778/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly lower triglycerides & VLDL measurement than G/G (about −0.21 per copy, study scale). This is a measurement-level association, not a disease prediction. • HDL ('good') cholesterol level (APOA1/APOA5) rsid : rs964184 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32203549/ Interpretation: Both copies at this position carry the protective C variant — a C/C genotype, the strongest protective combination at this site. Each C copy adds benefit toward hdl ('good') cholesterol level (β ≈ 0.09 per copy) compared to the G/G baseline. • Coronary artery disease risk (MRAS) rsid : rs9818870 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19198612/ Interpretation: You inherited one T variant and one C variant — a heterozygous C/T genotype, one allele from each parent. The T allele is linked to slightly higher odds of coronary artery disease (about OR ≈ 1.11 per copy), but the per-allele effect is small and on its own does not meaningfully shift your risk. • Rosuvastatin – cardiovascular outcome (CRP) ⚠ CAUTIOUS rsid : rs1205 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21094359/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1205 is in the CRP gene (C-reactive protein, an inflammation marker). In a small pharmacogenetic study (PharmGKB level 3 Efficacy, limited evidence), carriers of the T allele (C/T or T/T) tended to have better cardiovascular outcomes on rosuvastatin than people with the C/C genotype. The effect is modest, unquantified, and one of many factors that affect heart-disease risk; separately, the T allele is robustly linked to lower LDL cholesterol and lower CRP at the population level. Note: this is one of 2 correlated variants in/near CRP reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the C/C genotype and coronary disease, you may have poorer cardiovascular outcomes when treated with rosuvastatin compared to people with the C/T or T/T genotype. Other genetic and clinical factors may also influence cardiovascular outcomes. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rosuvastatin – cardiovascular outcomes (CRP/APOE region) rsid : rs2808630 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21094359/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2808630 sits near the CRP gene (which controls C-reactive protein, an inflammation marker). In the JUPITER statin trial, this variant was linked to C-reactive protein levels, and a pharmacogenetic analysis reported that carriers of the C allele tended to have better cardiovascular outcomes on rosuvastatin than people with the T/T genotype. This is a single, limited-evidence association (PharmGKB level 3) and the effect was not quantified, so treat it as a weak hint, not a reason to choose or avoid the drug. Note: this is one of 2 correlated variants in/near CRP reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take rosuvastatin and have the C/T genotype, you carry one C allele and may have somewhat better cardiovascular outcomes than people with the T/T genotype. This is based on a single trial analysis and is uncertain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — LDL & total cholesterol (HFE) [rs1800562]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the cholesterol-lowering A variant present. People with G/G tend to sit toward the higher end of the LDL & total cholesterol range. Per-copy effect size: β ≈ 0.06 per copy. Coronary artery disease / myocardial infarction risk (ALDH2) [rs671]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for coronary artery disease / myocardial infarction sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.54 per copy. LDL cholesterol level (APOE) [rs7412]: You have the C/C genotype at rs7412 — no APOE ε2 (T) copy here. C/C is associated with higher LDL cholesterol than T-carriers (each T copy lowers LDL by roughly 0.4–0.5 SD). Higher LDL is a cardiovascular risk factor, so this is the less favourable genotype at this site, though your overall risk depends on rs429358 and lifestyle. Coronary artery disease risk (APOE) [rs7412]: You have the C/C genotype at rs7412, so you do not carry the APOE ε2 allele at this position. Your coronary-artery-disease risk from APOE depends mainly on your other APOE variant (rs429358), which determines whether you carry ε3 or the higher-risk ε4. HDL cholesterol (FADS1) [rs174550]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the higher-HDL T variant. You miss the small upward shift in HDL that T-carriers get here. Each T copy would shift HDL by about +0.04 SD. HDL cholesterol level (APOA2) [rs5082]: You inherited one G variant and one A variant — a heterozygous G/A genotype, one allele from each parent. The single G copy is associated with modestly higher HDL than A/A (β ≈ 0.02 per copy) — a small favourable nudge, most relevant on a high-saturated-fat diet. Triglyceride levels (APOA5) [rs662799]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the triglyceride-raising G allele. Your genetic tendency for measured triglycerides sits at the lower end of the range — a favourable position relative to G-carriers. Coronary artery disease risk (APOA5) [rs662799]: Both copies at this position carry the A allele — an A/A genotype. The A allele is weakly associated with slightly lower coronary-artery-disease odds (about OR ≈ 0.93). The effect per copy is very small — a weak population-level association that, on its own, does not meaningfully predict your individual outcome. Lower LDL cholesterol & coronary artery disease risk (PCSK9) [rs11591147]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the protective T variant present. You miss the small LDL-lowering, CAD-protective benefit that T-carriers get at this site. Triglyceride/HDL ratio (LPL) [rs268]: Both copies at this position carry the A variant — an A/A genotype, with no copies of the G (N291S) variant present. People with A/A tend to sit toward the lower (more favourable) end of the triglyceride/HDL ratio range. Per-copy effect size: β ≈ 0.3 per copy. HDL ('good') cholesterol level (IRS1) [rs2943641]: You have the T/C genotype — one protective T allele and one C allele. You get part of the favourable HDL effect relative to C/C (the T allele is associated with higher HDL and lower triglycerides; about +0.016 per T copy on the study scale). LDL cholesterol level (SORT1) [rs629301]: Both copies here carry the T allele — a T/T genotype. On average this is associated with a modestly higher LDL-cholesterol measurement than G/G (about β ≈ 6.03 per T copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual LDL. Coronary artery disease risk (SORT1) [rs629301]: Both copies at this position carry the T risk variant — a T/T genotype, the higher-risk genotype at this single position. Risk for coronary artery disease is elevated above the G/G baseline, with each T copy contributing β ≈ 0.11 per copy — but the effect is small and on its own does not meaningfully predict your outcome. Aortic stenosis risk (LDLR) [rs6511720]: You carry one G allele and one T allele — a heterozygous G/T genotype, one from each parent. The T allele is associated with slightly lower odds of aortic stenosis, so G/T sits between the two homozygous groups (about OR ≈ 1.12 per G copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. Coronary artery disease & heart attack risk (LPA / Lp(a)) [rs10455872]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for coronary artery disease & heart attack risk (lpa / lp(a)) sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.31 per copy. Aortic valve stenosis risk (LPA / Lp(a)) [rs10455872]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for aortic valve stenosis risk (lpa / lp(a)) sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.45 per copy. LDL & total cholesterol level (LPA) [rs10455872]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G allele. The G allele is the one tied to a modestly higher LDL & total cholesterol reading (about +0.08 per copy on the study scale), so A/A sits at the lower end of this measurement range. Informational, not a concern. Coronary artery disease & heart attack risk (9p21) [rs10757278]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the C risk variant present. Your genetic risk for coronary artery disease & heart attack sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by OR ≈ 1.28 per copy. Coronary artery disease & heart attack risk (LDLR region) [rs1122608]: You inherited one G allele and one T allele — a heterozygous G/T genotype, one from each parent. The single G copy is associated with modestly higher coronary-artery-disease & heart-attack odds than T/T (about OR ≈ 1.14 per copy of G). On its own this does not meaningfully predict your individual outcome. LDL & total cholesterol levels (LDLR region) [rs1122608]: You inherited one G allele and one T allele — a heterozygous G/T genotype, one from each parent. At the population level, each G copy is associated with a slightly higher average LDL & total cholesterol than the T/T pattern (about β ≈ 2.71 per copy on the study's scale). This is a small measurement nudge, not a disease-risk prediction; a lipid panel reflects your real values. HDL cholesterol level (APOC3 loss-of-function) [rs116843064]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A (APOC3 loss-of-function) variant present. People with G/G tend to sit toward the lower end of the HDL cholesterol range. Per-copy effect size: β ≈ 0.22 per copy. Lower coronary artery disease risk (APOC3) [rs116843064]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the protective A variant present. You miss the small CAD-protective benefit that A-carriers get at this site. LDL & total cholesterol (HNF1A) [rs1169288]: Both copies at this position carry the A allele — an A/A genotype. At the population level, the A allele is associated with slightly lower average LDL & total cholesterol than the C allele. This is a measurement-level association, not a disease prediction, and on its own it does not determine your actual cholesterol — a blood test does. Coronary artery disease & heart attack risk (HNF1A) [rs1169288]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the C allele. The C allele shows only a weak population-level association with coronary artery disease at this site (about OR ≈ 1.05 per copy), so being A/A removes even that small statistical nudge. LDL cholesterol level (SORT1) [rs12740374]: Both copies at this position carry the G allele — a G/G genotype. At the population level the G allele is associated with modestly higher average LDL cholesterol than the T allele (about β ≈ 0.24 per copy on the study's scale). This is a measurement-level association, not a disease prediction — it nudges an average lipid reading, and a blood test reflects your real LDL. Coronary artery disease & heart attack risk (SORT1) [rs12740374]: Both copies at this position carry the G allele — a G/G genotype. At the population level the G allele carries a weak association with coronary artery disease at the SORT1 locus (about OR ≈ 1.1 per G copy); on its own it does not meaningfully predict your individual outcome. LDL cholesterol (APOE region) [rs157580]: You carry one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a slightly higher LDL reading on average (β ≈ 0.04 per copy). This is a weak population-level association and, on its own, does not meaningfully predict your individual LDL level; a blood lipid panel is what tells you your actual number. HDL ('good') cholesterol levels (CETP) [rs1800777]: Both copies at this position carry the protective G variant — a G/G genotype, the strongest protective combination at this site. Each G copy adds benefit toward hdl ('good') cholesterol levels (β ≈ 0.38 per copy) compared to the A/A baseline. HDL ('good') cholesterol level (HNF4A) [rs1800961]: Both copies at this position carry the protective C variant — a C/C genotype, the strongest protective combination at this site. Each C copy adds benefit toward hdl ('good') cholesterol level (β ≈ 0.01 per copy) compared to the T/T baseline. Total and LDL cholesterol (HNF4A) [rs1800961]: Both copies at this position are the C allele — a C/C genotype, with no T alleles. The T allele is the one weakly linked to a lower total/LDL cholesterol reading, so on average C/C sits at the upper end for this measurement. The per-copy shift is small (β ≈ 0.06) and, on its own, does not meaningfully predict your actual cholesterol level — a lipid panel is the real measure. Triglyceride & cholesterol levels (APOA5) [rs3135506]: Both copies at this position carry the G allele — a G/G genotype, with no C copies. Triglyceride and cholesterol levels tend to sit at the lower end relative to C-carriers; each C copy would nudge the measurement up by about β ≈ 0.25 on the study scale. This is a measurement-level association, not a disease prediction. Lipoprotein(a) & coronary artery disease (LPA) [rs41272114]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the protective T variant present. You miss the small lipoprotein(a)-lowering, CAD-protective benefit that T-carriers get at this site. LDL cholesterol & coronary artery disease risk (SORT1) [rs4299376]: Both copies at this position carry the T allele — a T/T genotype, with no G copies. This is the slightly more favourable version relative to G-carriers, associated with somewhat lower LDL cholesterol; each G copy would nudge LDL and coronary artery disease risk up by about OR ≈ 1.06 — a weak population-level association, not a meaningful predictor of your individual outcome. Triglycerides & HDL cholesterol (APOC1/APOE region) [rs439401]: You inherited one C variant and one T variant — a heterozygous T/C genotype, one allele from each parent. This places you in the middle of the triglycerides & hdl cholesterol range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: β ≈ 0.24 per copy. Coronary artery disease risk (9p21) [rs4977574]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for coronary artery disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.2 per copy. Triglyceride & lipid levels (APOC3) [rs5128]: No notable finding at this locus. Coronary artery disease risk (ABO) [rs579459]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the C allele present. Each C copy is associated with slightly higher odds of coronary artery disease (about OR ≈ 1.1 per copy), so T/T sits at the lower end of this weak, population-level association. Triglyceride levels & hypertriglyceridemia (APOA5) [rs651821]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the triglyceride-raising C allele. Your triglyceride measurement and odds of hypertriglyceridemia sit at the lower, favourable end at this site. HDL ('good') cholesterol (APOA5) [rs651821]: Both copies at this position carry the T variant — a T/T genotype. Each T copy raises HDL ('good') cholesterol, so T/T sits toward the higher (more favourable) end of the HDL range. Per-copy effect size: β ≈ 0.17 per copy. Coronary artery disease risk (WDR12) [rs6725887]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the C allele present. Each C copy is associated with slightly higher odds of coronary artery disease (about OR ≈ 1.15 per copy), so T/T sits at the lower end of this weak, population-level association. HDL ('good') cholesterol level (APOB) [rs676210]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the HDL-raising A variant present. You miss the modest HDL benefit that A-carriers get at this site — about β ≈ 0.06 lower per missing A copy relative to A-carriers. Triglyceride levels (APOB) [rs676210]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with a modestly lower triglyceride measurement (about −0.136 per copy, study scale), so G/G sits at the higher end of this measurement-level association. Total cholesterol level (APOB) [rs679899]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with a modestly lower total cholesterol measurement (about −0.0375 per copy, study scale), so G/G sits at the higher end of this measurement-level association. LDL & total cholesterol levels (LDLR) [rs688]: You inherited one T allele and one C allele — a heterozygous C/T genotype, one allele from each parent. The T allele is associated with a modestly higher LDL & total cholesterol measurement (about +0.057 per copy, study scale). This is a measurement nudge, not a disease prediction. LDL & total cholesterol (APOE region) [rs769449]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. This is the genotype associated with the lowest measured LDL & total cholesterol at this position. Each A copy is associated with higher measured cholesterol (about β ≈ 0.25 per copy, study scale). LDL ('bad') cholesterol level (APOA1/APOA5) [rs964184]: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly lower LDL ('bad') cholesterol measurement than G/G (about −0.0574 per copy, study scale). This is a measurement-level association, not a disease prediction. Coronary artery disease risk (APOA1/APOA5 cluster) [rs964184]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the G allele present. Each G copy is associated with slightly higher odds of coronary artery disease (about OR ≈ 1.06 per copy), so C/C sits at the lower end of this weak, population-level association. [Thrombosis / clotting] • Warfarin dose requirement (STX4) rsid : rs10871454 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18535201/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This common variant sits in the STX4 gene region (near genes involved in blood clotting). The T allele has been linked in genome-wide studies to needing a somewhat LOWER weekly maintenance dose of warfarin to reach the same anticoagulation. The C allele is the normal-dose-associated (reference) version. The effect is small compared with the major warfarin genes (VKORC1 and CYP2C9) and is a population-average tendency, not a personal dose. Warfarin is always dosed and checked by INR blood test, so this only nudges expectations and only matters if you take warfarin. Interpretation: You have the T/T genotype — two copies of the lower-dose-associated allele. If you take warfarin, population data suggest a modestly lower weekly maintenance dose on average; this is a minor nudge on top of the main warfarin genes, and your dose is still guided by INR. Only relevant while taking warfarin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin dose sensitivity (VKORC1) rsid : rs2359612 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31869433/ Summary : VKORC1 rs2359612. VKORC1 is the protein warfarin blocks to thin the blood. This SNP tags the well-known VKORC1 -1639 haplotype that lowers VKORC1 production. The A allele marks the warfarin-sensitive (low-expression) haplotype: A-carriers need LESS warfarin, while G/G people need MORE. This is a strong, well-replicated association (PharmGKB/CPIC level 1B), but warfarin is always dosed to INR, not genotype alone. Note: this is one of 6 correlated variants in/near VKORC1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the A/A genotype at rs2359612. If you take warfarin, you are likely warfarin-sensitive and tend to need a LOWER dose than average, because this genotype tags reduced VKORC1 production. Your actual dose is still set by INR blood tests. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin & acenocoumarol dose sensitivity (VKORC1) rsid : rs2884737 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18030307/ https://pubmed.ncbi.nlm.nih.gov/25519826/ Summary : This variant sits in VKORC1, the gene for the enzyme that warfarin and related coumarin blood-thinners block. rs2884737 tags the warfarin-sensitive VKORC1 haplotype (it travels together with the well-known dose-lowering −1639A promoter variant). The C allele marks the sensitive haplotype: people who carry it tend to need a lower coumarin dose to reach the same blood-thinning effect, while the A allele marks the higher-dose haplotype. VKORC1 is the single strongest genetic predictor of warfarin dose. This changes the dose you need, not whether the drug works — and it matters only while you are on a coumarin anticoagulant. Source data does not give a per-allele dose number for this specific marker. Note: this is one of 6 correlated variants in/near VKORC1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the C/C genotype — two copies of the warfarin-sensitive VKORC1 haplotype marker. If you take warfarin or acenocoumarol, you would, on average, need a lower dose than A-allele carriers, and standard starting doses may over-thin your blood. Your doctor should set and closely monitor your dose. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aspirin responsiveness (ITGB3) ⚠ CAUTIOUS rsid : rs5918 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16581111/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the platelet ITGB3 PlA1/PlA2 variant. The C allele (PlA2) has been linked to a reduced response to aspirin in some studies — meaning aspirin may dampen platelet activity less effectively — but the evidence is contradictory and far from settled. It only matters if you take aspirin as an antiplatelet medicine, and no firm per-genotype prediction should be drawn. Interpretation: If you have the T/C genotype and take aspirin, some studies suggest a somewhat reduced aspirin response compared with T/T, but the evidence conflicts. No firm personal prediction can be made; this matters only if you take aspirin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Clopidogrel antiplatelet response (ITGB3) ⚠ CAUTIOUS rsid : rs5918 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19106083/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the platelet ITGB3 PlA1/PlA2 variant. Some studies reported that T/T carriers get a stronger antiplatelet effect from a clopidogrel loading dose than C carriers, while other studies found no link at all. Evidence is limited and mixed, so it is informational only and matters only if you take clopidogrel. Interpretation: If you have the T/C genotype and take clopidogrel, some studies suggest a somewhat weaker antiplatelet effect than T/T, but others found no association. No firm personal prediction can be made; this matters only if you take clopidogrel. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Factor VII levels & clotting tendency (F7) rsid : rs6046 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/35870639/ https://pubmed.ncbi.nlm.nih.gov/35552711/ Interpretation: You inherited one G variant and one A variant — a heterozygous G/A genotype, one allele from each parent. This places you in the middle of the factor vii levels & clotting tendency range, between the lower-end A/A and the higher-end G/G genotypes. Per-copy effect size: β ≈ 1.08 per copy. — Also checked, no unusual variants — Prothrombin thrombophilia (Factor II G20210A) [rs1799963]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for prothrombin thrombophilia sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.95 per copy. Factor V Leiden – venous thrombosis risk [rs6025]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for factor v leiden – venous thrombosis sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 2.93 per copy. Abdominal aortic aneurysm risk (9p21) [rs2383207]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for abdominal aortic aneurysm sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.27 per copy. Venous thromboembolism risk (Factor V) [rs4524]: No notable finding at this locus. Venous thromboembolism risk [rs4970834]: Both copies at this position carry the C allele — a C/C genotype, with no T copies. This is the slightly more favourable version relative to T-carriers; each T copy is associated with a small increase in venous thromboembolism risk (about β ≈ 0.05 on the study scale) — a weak population-level association, based on limited evidence, that does not meaningfully predict your individual outcome. Venous thromboembolism risk (ABO) [rs579459]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C risk variant present. Your genetic risk for venous thromboembolism sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by OR ≈ 1.36 per copy. Factor XIII activity & clotting (F13A1 Val34Leu) [rs5985]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the A variant present. People with C/C tend to sit toward the lower end of the factor xiii activity & clotting range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 1.08 per copy. ──────────────────────────────────────────────────────────────────────── CLINICAL RISKS ──────────────────────────────────────────────────────────────────────── [Autoimmune / inflammatory] • Skin pigmentation / skin colour (TYR) rsid : rs1042602 Your geno : CA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39024449/ Interpretation: You have the C/A genotype at TYR — one lighter-pigment (A) allele and one darker (C). This places you in the middle of the pigmentation range at this gene. Normal cosmetic variation, not a health risk. • Vitiligo risk (TYR) ⚠ CAUTIOUS rsid : rs1393350 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20410501/ Interpretation: Both copies at this position carry the G variant — a G/G genotype, the highest-vitiligo-risk combination at this site. Vitiligo risk is elevated above the A/A baseline, with each G copy contributing about OR 1.53 per copy. Note: G is the vitiligo-risk allele even though A is the risk allele for melanoma at the same site. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Asthma risk (HLA-DQ) rsid : rs9272346 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/32296059/ https://pubmed.ncbi.nlm.nih.gov/29273806/ https://pubmed.ncbi.nlm.nih.gov/23181788/ Interpretation: You have the A/A genotype — two copies of the A asthma-associated tag allele. The per-copy effect on asthma odds is small (about OR 1.16), so even A/A reflects only a weak population-level association that does not on its own meaningfully predict your individual outcome. This is a tag SNP for the HLA-DQ region (a surrogate, not direct HLA typing). • Type 1 diabetes risk (HLA-DQ) rsid : rs9273363 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/40465716/ https://pubmed.ncbi.nlm.nih.gov/30659077/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for type 1 diabetes is elevated above the C/C baseline, with each A copy contributing OR ≈ 5.48 per copy. • Rheumatoid arthritis risk (FADS gene cluster) ⚠ CAUTIOUS rsid : rs968567 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30423114/ https://pubmed.ncbi.nlm.nih.gov/24390342/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. The C allele is weakly associated with slightly higher rheumatoid-arthritis odds (about OR ≈ 1.12 per copy), so C/C sits at the upper end of this small range. This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Metabolic syndrome risk (GCKR) rsid : rs780094 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30382898/ https://pubmed.ncbi.nlm.nih.gov/29632305/ https://pubmed.ncbi.nlm.nih.gov/22399527/ Interpretation: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for metabolic syndrome sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by β ≈ 0.13 per copy. • Psoriasis risk (HLA-C region) ⚠ CAUTIOUS rsid : rs2395029 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18369459/ Interpretation: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the G risk variant present. Your genetic risk for psoriasis sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 4.1 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Crohn's disease risk (HLA-C) ⚠ CAUTIOUS rsid : rs9264942 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/26192919/ https://pubmed.ncbi.nlm.nih.gov/23128233/ Interpretation: You inherited one C variant and one T variant — a heterozygous T/C genotype. The C variant is associated with a slightly higher Crohn's-disease risk (about 15% per copy), but this per-allele effect is small enough that it does not meaningfully shift your personal risk. • Autoimmune disease risk (PTPN22 R620W) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30572963/ Interpretation: You have the A/G genotype — one copy of the PTPN22 620W (A) risk allele, which modestly raises overall risk for autoimmune conditions. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rheumatoid arthritis risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36333501/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for rheumatoid arthritis is modestly higher than for people with the G/G baseline — about OR ≈ 1.72 per copy of the A variant. • Type 1 diabetes risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39749473/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for type 1 diabetes is modestly higher than for people with the G/G baseline — about β ≈ 0.43 per copy of the A variant. • Lupus (SLE) risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36750564/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for lupus (sle) is modestly higher than for people with the G/G baseline — about OR ≈ 1.35 per copy of the A variant. • Hypothyroidism & autoimmune thyroid disease (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36093044/ https://pubmed.ncbi.nlm.nih.gov/22922229/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for hypothyroidism & autoimmune thyroid disease is modestly higher than for people with the G/G baseline — about β ≈ 0.33 per copy of the A variant. • Vitiligo risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/27723757/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for vitiligo is modestly higher than for people with the G/G baseline — about OR ≈ 1.38 per copy of the A variant. • Crohn's disease risk (PTPN22) ⚠ CAUTIOUS rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/26192919/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for crohn's disease is modestly higher than for people with the A/A baseline — about OR ≈ 1.26 per copy of the G variant. • Type 1 diabetes risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18978792/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for type 1 diabetes is modestly higher than for people with the C/C baseline — about OR ≈ 1.82 per copy of the A variant. • Rheumatoid arthritis risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33310728/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for rheumatoid arthritis is modestly higher than for people with the C/C baseline — about OR ≈ 1.41 per copy of the A variant. • Systemic lupus erythematosus risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/28714469/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for systemic lupus erythematosus is modestly higher than for people with the C/C baseline — about OR ≈ 1.39 per copy of the A variant. • Juvenile idiopathic arthritis risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33106285/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for juvenile idiopathic arthritis is modestly higher than for people with the C/C baseline — about OR ≈ 1.59 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Inflammatory myositis risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30573655/ Interpretation: You have the C/A genotype — one copy of the PTPN22 risk variant, linked to a modestly higher risk of autoimmune myositis. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Crohn's disease risk (IL23R region) ⚠ CAUTIOUS rsid : rs1004819 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17804789/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous G/A genotype. Risk for Crohn's disease is modestly higher than for people with the G/G baseline — about OR ≈ 1.38 per copy of the A variant. • Multiple sclerosis risk (IL2RA) ⚠ CAUTIOUS rsid : rs12722489 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17660530/ Interpretation: You inherited one C risk variant and one T baseline variant — a heterozygous C/T genotype, one allele from each parent. Risk for multiple sclerosis is modestly higher than for people with the T/T baseline — about OR ≈ 1.23 per copy of the C variant. • Crohn's disease risk (IL2RA region) ⚠ CAUTIOUS rsid : rs12722489 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/37156999/ Interpretation: You have one C and one T allele — a heterozygous C/T genotype, one from each parent. The C allele carries a weak population-level association with Crohn's disease (about OR ≈ 1.11 per copy); on its own it does not meaningfully predict your individual outcome. • Asthma risk (IL33 region) rsid : rs1342326 Your geno : AC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20860503/ https://pubmed.ncbi.nlm.nih.gov/33328473/ Interpretation: You inherited one C risk variant and one A baseline variant — a heterozygous A/C genotype, one allele from each parent. Risk for asthma is modestly higher than for people with the A/A baseline — about OR ≈ 1.2 per copy of the C variant. • Asthma & allergic disease risk (TSLP) rsid : rs1837253 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36777996/ https://pubmed.ncbi.nlm.nih.gov/30929738/ https://pubmed.ncbi.nlm.nih.gov/29083406/ Interpretation: You have the C/C genotype — two copies of the C allele, which carries a small population-level association with asthma & allergic disease (about OR ≈ 1.07 per C copy). This is a weak association and on its own does not meaningfully predict your individual outcome. • Psoriasis risk (IL13) rsid : rs20541 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19169254/ https://pubmed.ncbi.nlm.nih.gov/26626624/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the higher-risk genotype at this single position. Risk for psoriasis is elevated above the A/A baseline, with each G copy contributing OR ≈ 1.24 per copy. The per-copy effect is small and on its own does not meaningfully predict your outcome. • Psoriasis risk (IL23R/STAT2 region) rsid : rs2066808 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25574825/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for psoriasis is elevated above the C/C baseline, with each A copy contributing OR ≈ 1.48 per copy. • Allergic disease & hay fever risk (IL6R) ⚠ CAUTIOUS rsid : rs2228145 Your geno : AC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/31361310/ https://pubmed.ncbi.nlm.nih.gov/29083406/ Interpretation: You have a heterozygous A/C genotype — one A and one C allele, one from each parent. The C allele carries a very small population-level association with allergic disease & hay fever (about OR ≈ 1.04 per copy); on its own this very weak association does not meaningfully predict your individual outcome. • Crohn's disease risk (ATG16L1) rsid : rs2241880 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17435756/ Interpretation: You carry one G risk variant (the ATG16L1 T300A / Ala300 change) and one A baseline variant — a heterozygous A/G genotype. Your risk for Crohn's disease is modestly higher than for people with the A/A genotype, about OR ≈ 1.32 per copy of the G variant. This is a common variant — most people carry at least one G copy. • Childhood-onset asthma risk (GSDMB) rsid : rs2305480 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35126453/ https://pubmed.ncbi.nlm.nih.gov/24241537/ Interpretation: You have the G/G genotype — two copies of the G allele, which carries a modest population-level association with childhood-onset asthma (about OR ≈ 1.18 per G copy). This is a weak-to-modest association and on its own does not meaningfully predict your individual outcome. • Asthma risk (IL18R1/IL1RL1) ⚠ CAUTIOUS rsid : rs3771166 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20860503/ Interpretation: You have the G/G genotype — two copies of the G allele, which carries a small population-level association with asthma (about OR ≈ 1.15 per G copy). This is a weak association and on its own does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Multiple sclerosis risk (IL7R) rsid : rs6897932 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21833088/ Interpretation: You have the C/C genotype — two copies of the C allele, which carries a small population-level association with multiple sclerosis (about OR ≈ 1.11 per C copy). This is a weak association and on its own does not meaningfully predict your individual outcome. • Systemic lupus erythematosus risk (IL7R) ⚠ CAUTIOUS rsid : rs6897932 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36750564/ Interpretation: You have the C/C genotype — two copies of the C allele at this IL7R site. At a population level the C allele carries a small association with systemic lupus erythematosus (about β ≈ 0.07 per copy on the study scale). This is a weak association and on its own does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Childhood-onset asthma risk (17q21 / GSDMB) rsid : rs7216389 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35126453/ Interpretation: Both copies at this position carry the T risk variant — a T/T genotype, the highest-risk combination at this site. Risk for childhood-onset asthma is elevated above the C/C baseline, with each T copy contributing OR ≈ 1.45 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Inflammatory bowel disease & Crohn's risk (STAT3) rsid : rs744166 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18587394/ Interpretation: You have the A/A genotype — two copies of the A allele, which carries a small population-level association with inflammatory bowel disease & Crohn's (about OR ≈ 1.18 per A copy). This is a weak association and on its own does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rheumatoid arthritis risk (HLA region) rsid : rs9268839 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30423114/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for rheumatoid arthritis is modestly higher than for people with the A/A baseline — about OR ≈ 1.35 per copy of the G variant. • Sjögren's syndrome risk (HLA region) rsid : rs9271588 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/24097066/ Interpretation: You have the T/C genotype — one copy of the T risk allele, with modestly increased odds of Sjögren's syndrome compared with people who carry two C alleles (about OR 1.75 per copy of T). • IgA nephropathy risk (HLA region) rsid : rs9275224 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25305756/ Interpretation: You have the A/G genotype — one copy of the G risk allele, linked to a modestly higher chance of IgA nephropathy (roughly OR 1.36 per copy). The absolute risk stays low for most people. • Lupus (SLE) risk ⚠ CAUTIOUS rsid : rs1317082 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33272962/ Interpretation: Both copies at this position carry the A variant — a A/A genotype. The A allele carries a weak association with slightly higher lupus (SLE) odds (about OR ≈ 1.1 per copy). This is a small population-level signal and does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Celiac disease risk (HLA-DQ2.5 tag) [rs2187668]: No notable finding at this locus. Systemic lupus erythematosus (SLE) risk (HLA-DR3/DQ2.5 tag) [rs2187668]: No notable finding at this locus. Membranous glomerulonephritis (kidney autoimmune) risk [rs2187668]: No notable finding at this locus. Celiac disease risk (HLA-DQ2.5 tag SNP) [rs2187668]: No notable finding at this locus. ANCA-associated vasculitis risk (HLA-DQ) [rs7454108]: Both copies at this position carry the T variant — a T/T genotype, with no copies of the C variant linked to higher MPO-ANCA vasculitis risk. You sit at the lower-risk end at this site relative to C-carriers. ANCA vasculitis is rare overall, and this is a tag-SNP estimate, not HLA typing. Asthma risk (HLA region) [rs7775228]: Both copies at this position carry the T allele — a T/T genotype. The T allele is weakly associated with slightly higher asthma odds (about OR ≈ 1.17 per copy), so T/T sits at the upper end of this small range. This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. Type 1 diabetes risk (HLA-DQ) [rs9272346]: You have the A/A genotype — no copies of the high-risk G allele. Your HLA-DQ-tagged genetic risk for type 1 diabetes sits at the lower end, a favourable position relative to G-carriers. This is a tag SNP for the HLA-DQ region (a surrogate, not direct HLA typing). Abdominal obesity & metabolic syndrome risk [rs10913469]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the C allele. Your genetic tendency for abdominal obesity / metabolic syndrome sits at the lower end of this small range (each C copy would add only about OR ≈ 1.1) — a weak population-level association that does not, on its own, meaningfully predict your individual outcome. COPD risk (CHRNA5) [rs16969968]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The A allele shows only a weak population-level association with COPD (about OR ≈ 1.11 per copy), and this association is driven largely by smoking. With no A copies, this genotype adds no signal from this site. COPD risk [rs8034191]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C risk variant present. Your genetic risk for copd sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by OR ≈ 1.4 per copy. Crohn's disease risk (TNF) [rs361525]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele. The A allele is the one weakly associated with slightly higher Crohn's disease odds at this locus. With no A copies, this is the lower-association genotype here, though the difference is small at the population level. Multiple sclerosis risk (HLA-DRA) [rs3135388]: No notable finding at this locus. Rheumatoid arthritis & autoimmune risk (SH2B3) [rs3184504]: Both copies at this position carry the C allele — a C/C genotype, with no T copies. This is the slightly more favourable version relative to T-carriers, but the per-copy effect is small (about OR ≈ 1.08) — a weak population-level association, not a meaningful predictor of your individual outcome. Rheumatoid arthritis risk (CTLA4) [rs3087243]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The G allele shows only a weak population-level association with rheumatoid arthritis (about OR ≈ 1.15 per copy); on its own it does not meaningfully predict your individual outcome. Type 1 diabetes risk (CTLA4) [rs3087243]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The G allele shows only a weak population-level association with type 1 diabetes (about OR ≈ 1.16 per copy); on its own it does not meaningfully predict your individual outcome. Systemic lupus erythematosus risk (CTLA4) [rs3087243]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The G allele shows only a weak population-level association with systemic lupus erythematosus (about OR ≈ 1.12 per copy); on its own it does not meaningfully predict your individual outcome. Hypothyroidism risk (FOXE1) [rs965513]: No notable finding at this locus. Multiple sclerosis risk [rs1026916]: Both copies carry the G allele — a G/G genotype, with no copies of the A allele that is associated with slightly higher multiple-sclerosis odds. Your genetic contribution from this single common variant is at the lower, baseline end, though the per-allele effect is small either way. Inflammatory bowel disease risk (JAK2 region) [rs10758669]: Both copies carry the A allele — an A/A genotype, with no copies of the C allele. The C allele (absent here) carries only a weak population-level association with inflammatory bowel disease (about OR ≈ 1.18 per copy), so this genotype sits at the lower-association end — a small effect either way that on its own does not meaningfully predict your individual outcome. Crohn's disease risk [rs11175593]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.54 per copy. Crohn's disease & IBD risk (IL23R) [rs11209026]: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for crohn's disease & ibd is elevated above the A/A baseline, with each G copy contributing OR ≈ 3.04 per copy. Ankylosing spondylitis risk (IL23R) [rs11209026]: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for ankylosing spondylitis is elevated above the A/A baseline, with each G copy contributing OR ≈ 1.65 per copy. Systemic lupus erythematosus (SLE) risk [rs1128334]: No notable finding at this locus. Atopic eczema risk (IL13) [rs1295686]: You have the C/C genotype — two copies of the lower-risk C allele, with no copies of the eczema-raising T allele, giving the lowest genetic risk of atopic eczema at this IL13 variant. Psoriasis risk (IL13) [rs1295686]: Both copies at this position carry the C allele — a C/C genotype, the higher-risk combination at this site for psoriasis (each C copy contributing about β≈0.12). Evidence here is limited (a single record). Childhood-onset asthma risk (IL13) [rs1295686]: Both copies carry the C allele — a C/C genotype, with no copies of the T allele. The T allele (absent here) carries only a weak population-level association with childhood-onset asthma (about OR ≈ 1.15 per copy), so this genotype sits at the lower-association end — a small effect either way that on its own does not meaningfully predict your individual outcome. Crohn's disease risk (NOD2) [rs17221417]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the G risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.29 per copy. Crohn's disease risk (chromosome 5p13) [rs17234657]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the G risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.54 per copy. Asthma & allergic disease risk (IL13) [rs20541]: You have the G/G genotype — two copies of the G allele and no copies of the A allele. At a population level this is the lower-association version of this marker (each A copy carries about OR ≈ 1.12). The effect is weak and not individually predictive. Crohn's disease risk (NOD2) [rs2066844]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 2.16 per copy. Childhood-onset asthma risk [rs2066844]: You have the C/C genotype — two copies of the C allele and no copies of the T allele. At a population level this is the lower-association version of this marker (each T copy carries about OR ≈ 1.09). The effect is weak and not individually predictive. Crohn's disease risk (NOD2) [rs2066845]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the C risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by β ≈ 0.91 per copy. Crohn's disease risk (NOD2) [rs2076756]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.66 per copy. Multiple sclerosis risk (IL2RA) [rs2104286]: No notable finding at this locus. Ulcerative colitis risk (IL23R) [rs2201841]: No notable finding at this locus. Psoriasis risk (IL23R) [rs2201841]: No notable finding at this locus. Rheumatoid arthritis risk (IL6R) [rs2228145]: You have a heterozygous A/C genotype — one A and one C allele, one from each parent. The A allele carries a small population-level association with rheumatoid arthritis (about OR ≈ 1.07 per copy); on its own this weak association does not meaningfully predict your individual outcome. Ulcerative colitis risk (ORMDL3/GSDMB) [rs2305480]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for ulcerative colitis sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.25 per copy. Multiple sclerosis risk (HLA-DRB1 region) [rs3129889]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for multiple sclerosis sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 2.97 per copy. Systemic lupus erythematosus (SLE) risk [rs3131379]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for systemic lupus erythematosus (sle) sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 2.36 per copy. Primary biliary cholangitis risk (IL7R) [rs6897932]: Both copies here carry the C baseline variant for this trait — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for primary biliary cholangitis sits at the lower end of the spectrum, a favourable position relative to T-carriers. Each T copy would raise PBC risk by OR ≈ 1.52 per copy. Multiple sclerosis risk (STAT3) [rs744166]: You have the A/A genotype — two copies of the A allele and no copies of the C allele. At a population level this is the lower-association version of this marker (each C copy carries about OR ≈ 1.15). The effect is weak and not individually predictive. Lupus (SLE) risk (STAT4) [rs7574865]: No notable finding at this locus. Rheumatoid arthritis risk (STAT4) [rs7574865]: No notable finding at this locus. Systemic sclerosis risk (STAT4) [rs7574865]: No notable finding at this locus. Asthma & allergic disease risk (IL13) [rs848]: You have the C/C genotype — two copies of the C allele and no copies of the A allele. At a population level this is the lower-association version of this marker (each A copy carries about β ≈ 0.10 on the study scale). The effect is weak and not individually predictive. Multiple sclerosis risk (HLA-DRB1) [rs9271366]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for multiple sclerosis sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 2.62 per copy. Crohn's disease risk (HLA region) [rs9271366]: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for crohn's disease is elevated above the G/G baseline, with each A copy contributing OR ≈ 1.66 per copy. Ulcerative colitis risk (HLA region) [rs9271366]: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for ulcerative colitis is elevated above the G/G baseline, with each A copy contributing OR ≈ 1.63 per copy. Systemic lupus erythematosus risk (HLA region) [rs9271366]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for systemic lupus erythematosus sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.26 per copy. [Cancer-related risk markers] • Melanoma & skin cancer risk (HERC2 pigmentation) ⚠ CAUTIOUS rsid : rs12913832 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/40495383/ https://pubmed.ncbi.nlm.nih.gov/34290314/ https://pubmed.ncbi.nlm.nih.gov/32341527/ Interpretation: Both copies at this position carry the G variant — a G/G genotype (the blue-eye / light-pigment form). The associated melanoma & skin cancer effect (OR ≈ 1.13 per copy) is real at the population level but small per person, so it is shown as informational rather than a personal risk flag. General sun protection benefits everyone with lighter pigmentation. • Skin cancer & sun damage risk (SLC24A5) ⚠ CAUTIOUS rsid : rs1426654 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34570997/ https://pubmed.ncbi.nlm.nih.gov/30895295/ https://pubmed.ncbi.nlm.nih.gov/30664655/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for skin cancer & sun damage is modestly higher than for people with the G/G baseline — about β ≈ 0.45 per copy of the A variant. • Melanoma & skin cancer risk (SLC45A2) rsid : rs16891982 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34813871/ https://pubmed.ncbi.nlm.nih.gov/28212542/ https://pubmed.ncbi.nlm.nih.gov/32341527/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for melanoma & skin cancer is elevated above the C/C baseline, with each G copy contributing OR ≈ 1.5 per copy. • Melanoma risk (TYR) rsid : rs1126809 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39141363/ https://pubmed.ncbi.nlm.nih.gov/32887889/ https://pubmed.ncbi.nlm.nih.gov/32341527/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for melanoma is modestly higher than for people with the G/G baseline — about OR ≈ 1.2 per copy of the A variant. • Non-melanoma skin cancer risk (TYR) rsid : rs1126809 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33549134/ https://pubmed.ncbi.nlm.nih.gov/32041948/ https://pubmed.ncbi.nlm.nih.gov/31174203/ Interpretation: You inherited one A allele and one G allele — a heterozygous G/A genotype, one allele from each parent. The A allele carries a weak population-level association with slightly higher odds of non-melanoma skin cancer (about OR ≈ 1.13 per copy). The effect is small and, on its own, does not meaningfully predict your individual outcome. • Basal cell carcinoma risk (BNC2) ⚠ CAUTIOUS rsid : rs2153271 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36496446/ https://pubmed.ncbi.nlm.nih.gov/33549134/ Interpretation: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T allele present. Each T copy carries a weak population-level association with slightly higher odds of basal cell carcinoma (about +0.08 per copy, study scale), so C/C sits at the lower end of this association. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Melanoma risk (OCA2) ⚠ CAUTIOUS rsid : rs4778138 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/28212542/ https://pubmed.ncbi.nlm.nih.gov/32041948/ https://pubmed.ncbi.nlm.nih.gov/26237428/ Interpretation: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G allele. The A allele shows a weak population-level association with higher odds of melanoma (about OR 1.19 per copy). On its own this does not meaningfully predict your individual melanoma risk; sun exposure and skin type matter far more. • Colorectal cancer risk (FADS1) ⚠ CAUTIOUS rsid : rs174537 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36539618/ https://pubmed.ncbi.nlm.nih.gov/30529582/ https://pubmed.ncbi.nlm.nih.gov/29471430/ Interpretation: Both copies carry the T allele — a T/T genotype, with no copies of the G allele. T is the lower-risk allele at this site. The per-allele effect here is small, so this marker on its own does not meaningfully predict your individual colorectal-cancer risk. • Breast cancer risk (FTO) rsid : rs17817449 Your geno : TG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/29059683/ https://pubmed.ncbi.nlm.nih.gov/25751625/ https://pubmed.ncbi.nlm.nih.gov/27117709/ Interpretation: You have the T/G genotype — one T allele and one G allele. At this FTO marker the T allele carries a slightly higher breast cancer association (about OR ≈ 1.06 per T copy). The per-allele effect is small — well below the threshold for a meaningful personal risk signal — so on its own it does not meaningfully predict your individual outcome. (Applies to people who can develop breast cancer.) • Lung cancer risk (CHRNA3/CHRNA5 region) ⚠ CAUTIOUS rsid : rs1051730 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19836008/ Interpretation: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for lung cancer sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.31 per copy. • Colorectal cancer risk (TGFB1) ⚠ CAUTIOUS rsid : rs1800469 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36539618/ Interpretation: You inherited one G allele and one A allele — a heterozygous A/G genotype, one from each parent. The G allele has a weak association with colorectal-cancer odds (about OR ≈ 1.09 per copy). On its own this does not meaningfully predict your individual outcome. • Bevacizumab-based chemotherapy response in colorectal cancer (VEGFA) rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20125120/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 (VEGF -2578 C>A) is in the promoter of VEGFA, the growth factor that bevacizumab is designed to block. In colorectal-cancer patients on bevacizumab-based chemotherapy, two C copies tended to track with a better response, while the A allele tracked with a weaker response. The evidence is limited (PharmGKB level 3) and only relevant in the context of this chemotherapy. Interpretation: If you have colorectal cancer and the A/A genotype, you may have a weaker response to bevacizumab-based chemotherapy (bevacizumab with capecitabine, fluorouracil, irinotecan, leucovorin or oxaliplatin) than people carrying a C copy. The evidence is limited, and tumour biology and other clinical factors influence response far more — treatment choices are made by your oncologist. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Docetaxel response in breast cancer (VEGFA) ⚠ CAUTIOUS rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24061601/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 sits in the promoter of VEGFA, the gene for vascular endothelial growth factor A, which tumours use to grow blood vessels. The A allele (the reference base) has been linked, in small pharmacogenetic studies, to a better/longer response to chemotherapy that interferes with tumour blood supply, while the C allele tends to track with shorter benefit. The evidence here is limited (low-level PharmGKB efficacy annotation, few studies, no pooled effect size), so this is a weak, drug-specific signal — not a firm predictor. It tells you nothing outside the context of this chemotherapy. Interpretation: If you have the A/A genotype and are treated with docetaxel for breast cancer, some studies suggest you may have a somewhat longer time before the cancer progresses than people with the C/C genotype. This is a weak signal from a few small studies; many other genetic and clinical factors matter more, and it is only relevant while on this drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anastrozole response in HR+ breast cancer (CYP19A1) rsid : rs727479 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27747906/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs727479 sits in CYP19A1, the gene for aromatase — the enzyme anastrozole blocks. The C allele is linked to higher estrogen (estradiol/estrone) levels, and a small pharmacogenetic study (PharmGKB level 3, limited evidence) reported that the C/C genotype was associated with a higher chance of breast cancer recurrence on anastrozole than the A/A genotype. The effect is modest, unquantified, and based on few patients; it is one of many factors that influence outcome. Interpretation: If you are a postmenopausal woman with HR+ breast cancer and the C/A genotype, you may have an increased likelihood of breast cancer recurrence when treated with anastrozole compared to women with the A/A genotype. Other clinical and genetic factors may also influence the likelihood of recurrence on anastrozole. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Papillary thyroid cancer risk (NKX2-1 region) ⚠ CAUTIOUS rsid : rs944289 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19198613/ Interpretation: You inherited one T risk variant and one C baseline variant — a heterozygous C/T genotype, one allele from each parent. Risk for papillary thyroid cancer is modestly higher than for people with the C/C baseline — about OR ≈ 1.37 per copy of the T variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Colorectal cancer risk (TERC region) ⚠ CAUTIOUS rsid : rs10936599 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36539618/ Interpretation: Both copies at this position carry the C variant — a C/C genotype. The C allele carries a weak association with slightly higher colorectal-cancer odds (about OR ≈ 1.06 per copy). This is a small population-level signal and does not meaningfully predict your individual outcome. • Prostate cancer risk (TERT) rsid : rs2242652 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/37945903/ https://pubmed.ncbi.nlm.nih.gov/38632662/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for prostate cancer is elevated above the A/A baseline, with each G copy contributing β ≈ 0.16 per copy. • Bladder cancer risk (TERT) rsid : rs2242652 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/37210288/ Interpretation: Both copies at this position carry the G variant — a G/G genotype. The G allele carries a modest association with higher bladder-cancer odds (about OR ≈ 1.18 per copy). This is a weak-to-modest population-level signal and, on its own, does not meaningfully predict your individual outcome. • Colorectal cancer risk (TERT) rsid : rs2735940 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36539618/ https://pubmed.ncbi.nlm.nih.gov/30510241/ Interpretation: You inherited one G allele and one A allele — a heterozygous A/G genotype, one allele from each parent. Each G copy is linked to slightly higher colorectal-cancer odds (about OR ≈ 1.08 per copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Lung cancer risk (TERT) rsid : rs2736100 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/27501781/ https://pubmed.ncbi.nlm.nih.gov/21725308/ Interpretation: You inherited one C risk variant and one A baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for lung cancer is modestly higher than for people with the A/A baseline — about OR ≈ 1.42 per copy of the C variant. • Glioma and brain tumor risk (TERT) rsid : rs2736100 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19578367/ https://pubmed.ncbi.nlm.nih.gov/32386320/ Interpretation: You inherited one C risk variant and one A baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for glioma and brain tumor is modestly higher than for people with the A/A baseline — about OR ≈ 1.27 per copy of the C variant. • Testicular germ cell tumor risk (TERT) rsid : rs2736100 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/28604728/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for testicular germ cell tumor is modestly higher than for people with the C/C baseline — about OR ≈ 1.28 per copy of the A variant. — Also checked, no unusual variants — Basal cell carcinoma risk (IRF4) [rs12203592]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for basal cell carcinoma sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.41 per copy. Cutaneous squamous cell carcinoma risk (IRF4) [rs12203592]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for cutaneous squamous cell carcinoma sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.6 per copy. Melanoma & skin cancer risk (MC1R R151C) [rs1805007]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for melanoma & skin cancer sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.34 per copy. Melanoma & skin cancer risk (MC1R R160W) [rs1805008]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for melanoma & skin cancer sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.37 per copy. Uveal melanoma risk (HERC2) [rs1129038]: Both copies at this position carry the T risk variant — a T/T genotype, the highest-risk combination at this site. Risk for uveal melanoma is elevated above the C/C baseline, with each T copy contributing OR ≈ 1.79 per copy. Basal cell carcinoma risk (MC1R region) [rs12931267]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the G risk variant present. Your genetic risk for basal cell carcinoma sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.33 per copy. Melanoma risk (TYR) [rs1393350]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with slightly higher odds of melanoma (about OR ≈ 1.17 per copy), so G/G sits at the lower end of this weak, population-level association. Melanoma & skin cancer risk (OCA2) [rs1800407]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T allele present. Each T copy is associated with slightly higher odds of melanoma & skin cancer (about OR ≈ 1.10 per copy), so C/C sits at the lower end of this weak, population-level association. Melanoma risk (MC1R) [rs1805009]: You have the G/G genotype and carry no copies of the C melanoma-risk allele at this MC1R marker — average-to-lower genetic risk at this position. Melanoma risk from MC1R variants is amplified by sun/UV exposure. Melanoma & skin cancer risk (ASIP region) [rs6059655]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for melanoma & skin cancer sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.26 per copy. Lung cancer risk in smokers (CHRNA5) [rs16969968]: You have the G/G genotype — no copies of the A risk allele at this CHRNA5 marker. Among people who smoke, your lung-cancer risk from this variant sits at the lower end; in never-smokers this variant carries minimal risk. Lung cancer risk (CHRNA3/5 region) [rs8034191]: You have the T/T genotype at this CHRNA3/5 site — no copy of the C risk allele here, so you carry the baseline genetic risk of lung cancer at this well-studied locus. Smoking is still by far the largest driver of lung-cancer risk regardless of this genotype. Thyroid cancer risk [rs116909374]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for thyroid cancer sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.81 per copy. Thyroid cancer risk (FOXE1) [rs965513]: No notable finding at this locus. Breast cancer risk (TERT region) [rs10069690]: You have the C/C genotype — no copies of the T allele, so this TERT marker sits at the lower-association end for breast cancer. Glioma and brain tumor risk (TERT) [rs10069690]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for glioma and brain tumor sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.45 per copy. Ovarian cancer risk (TERT) [rs10069690]: You have the C/C genotype — no copies of the T allele, so this TERT marker sits at the lower-association end for ovarian cancer. Thyroid cancer risk (TERT) [rs10069690]: You have the C/C genotype — two copies of the C allele and no copies of the T allele. At a population level this is the lower-association version of this marker for thyroid cancer (each T copy carries about OR ≈ 1.2). The effect is modest and not individually predictive. Multiple myeloma risk [rs10936599]: Both copies here carry the C reference allele. rs10936599 sits in a telomere-length / cancer-associated region, but the effect allele and direction for multiple myeloma could not be confidently resolved for this entry, so no personal up-or-down signal is asserted. Informational only. Uterine fibroids risk (TERT) [rs2242652]: You have the G/G genotype — two G alleles, with average genetic risk for uterine fibroids at this variant. Glioma risk (TERT) [rs2853676]: No notable finding at this locus. Lung cancer risk (TERT) [rs2853677]: You inherited one G risk variant and one A baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for lung cancer is modestly higher than for people with the A/A baseline — about OR ≈ 1.28 per copy of the G variant. Clonal hematopoiesis & myeloproliferative disorder risk (TERT) [rs2853677]: You inherited one G risk variant and one A baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for clonal hematopoiesis & myeloproliferative disorder is modestly higher than for people with the A/A baseline — about OR ≈ 1.32 per copy of the G variant. Clonal hematopoiesis risk (TERT) [rs7705526]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the A risk variant present. Your genetic risk for clonal hematopoiesis sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.37 per copy. Lung cancer risk (TERT) [rs7705526]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the A risk variant present. Your genetic risk for lung cancer sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.23 per copy. Ovarian cancer risk (TERT) [rs7705526]: You have the C/C genotype — no copies of the A risk allele, so your ovarian-cancer risk from this TERT variant is at the baseline end. [Hereditary disease risk] • HFE H63D variant (iron metabolism) rsid : rs1799945 Your geno : CG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/10/ https://pubmed.ncbi.nlm.nih.gov/28334935/ https://pubmed.ncbi.nlm.nih.gov/21208937/ Summary : rs1799945 is the HFE H63D variant (the G allele). On its own, H63D is a low-penetrance variant and is usually clinically insignificant — most carriers, including people with two H63D copies, never develop iron overload. Clinically meaningful hereditary haemochromatosis is rare unless H63D is paired with the HFE C282Y variant (rs1800562) as a compound heterozygote, or two C282Y copies are present. If you have symptoms or a reason to check, ferritin and transferrin saturation are the simple blood tests to look at — but only if clinically indicated. Interpretation: You carry one H63D (G) variant and one C allele — a C/G genotype. This makes you a single-copy H63D carrier, which on its own is usually clinically insignificant. Iron overload is rare unless H63D is paired with the HFE C282Y variant (rs1800562). No action is needed for this result alone; ferritin and transferrin saturation are worth checking only if clinically indicated. • Gilbert's syndrome / elevated bilirubin (UGT1A1) rsid : rs6742078 Your geno : GT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/23371916/ https://pubmed.ncbi.nlm.nih.gov/19414484/ Interpretation: You inherited one T variant and one G variant — a heterozygous G/T genotype. The T variant is associated with somewhat higher serum bilirubin (the Gilbert's-syndrome pattern). Mildly raised unconjugated bilirubin in this range is benign — not a disease risk — so this is an informational tendency, not a concern. • Gilbert's syndrome / elevated bilirubin (UGT1A1) rsid : rs887829 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38826804/ https://pubmed.ncbi.nlm.nih.gov/36580335/ https://pubmed.ncbi.nlm.nih.gov/35050183/ Interpretation: You inherited one T variant and one C variant — a heterozygous C/T genotype. The T variant is associated with somewhat higher serum bilirubin (the Gilbert's-syndrome pattern). Mildly raised unconjugated bilirubin is benign, so this is an informational tendency rather than a concern. — Also checked, no unusual variants — Prothrombin thrombophilia (Factor II G20210A) [rs1799963]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for prothrombin thrombophilia sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.95 per copy. Hereditary hemochromatosis risk (HFE C282Y) [rs1800562]: You have the G/G genotype at HFE C282Y — two copies of the wild-type G allele. This is the typical, non-risk genotype for hereditary hemochromatosis. Factor V Leiden – venous thrombosis risk [rs6025]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for factor v leiden – venous thrombosis sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 2.93 per copy. Bilirubin levels / Gilbert's syndrome tendency (UGT1A1) [rs4148323]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the bilirubin levels / gilbert's syndrome tendency range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.3 per copy. ──────────────────────────────────────────────────────────────────────── FITNESS & RECOVERY ──────────────────────────────────────────────────────────────────────── [Aerobic capacity] — Checked, no unusual variants found — Lung function (FEV1/FVC, CHRNA3) [rs1051730]: Both copies at this position carry the protective G variant — a G/G genotype, the strongest protective combination at this site. Each G copy adds benefit toward lung function (β ≈ 0.08 per copy) compared to the A/A baseline. [Injury risk] • Knee osteoarthritis risk (GDF5) ⚠ CAUTIOUS rsid : rs143383 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30374069/ Interpretation: You inherited one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele has a weak association with knee-osteoarthritis odds (about OR ≈ 1.04 per copy). On its own this does not meaningfully predict your individual outcome. • Knee osteoarthritis risk (GDF5) rsid : rs143384 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34450027/ Interpretation: You inherited one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele has a weak association with knee-osteoarthritis odds (about OR ≈ 1.07 per copy). On its own this does not meaningfully predict your individual outcome. • Developmental dysplasia of the hip (GDF5) ⚠ CAUTIOUS rsid : rs143384 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30273415/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for developmental dysplasia of the hip is modestly higher than for people with the G/G baseline — about OR ≈ 1.39 per copy of the A variant. — Also checked, no unusual variants — Hip & general osteoarthritis risk [rs11177]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele. The A allele carries a weak association with higher hip & general osteoarthritis odds (OR ≈ 1.09 per copy), so G/G sits at the lower end of this small range. Informational, not a concern. [Muscle fiber composition] — Checked, no unusual variants found — Sprint-power muscle tendency (ACTN3) [rs1815739]: You inherited one C variant and one T variant — a heterozygous C/T genotype, one allele from each parent. This places you in the middle of the sprint-power muscle tendency range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: β ≈ 0.17 per copy. Grip strength & lean mass (GDF5) [rs143384]: You inherited one G variant and one A variant — a heterozygous G/A genotype. The G allele nudges grip strength and lean mass slightly upward (the favourable direction) relative to A/A; a small but positive contribution. ──────────────────────────────────────────────────────────────────────── HORMONES & REPRODUCTIVE HEALTH ──────────────────────────────────────────────────────────────────────── [Pregnancy-related risks] • Caffeine and miscarriage risk in pregnancy (CYP1A2) rsid : rs762551 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15849225/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs762551 (CYP1A2*1F, -163C>A) sets how fast you clear caffeine: REF=C is slow, ALT=A is fast. During pregnancy caffeine clearance slows further for everyone, and slow metabolizers (C carriers) accumulate the most caffeine, raising fetal caffeine exposure. Some studies link this combination to a higher chance of miscarriage in women who consume caffeine, though the pregnancy data are mixed. The risk is driven by caffeine intake, so limiting caffeine removes the variant's relevance; it applies to women only. Interpretation: If you are pregnant and have the A/A genotype, you are a fast caffeine metabolizer and clear caffeine more quickly, so the slow-metabolizer accumulation effect doesn't apply to you. High caffeine intake is still discouraged in pregnancy for other reasons; follow your doctor's guidance. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin in pregnancy – craniofacial abnormality risk (EPHX1) ⚠ CAUTIOUS rsid : rs1051740 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19952982/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1051740 is a coding variant in EPHX1, which makes microsomal epoxide hydrolase — the enzyme that clears toxic breakdown products of phenytoin. The T allele (T/T and T/C genotypes) is the lower-activity form, so toxic phenytoin metabolites are cleared more slowly. A pharmacogenetic study (PharmGKB, level 3, toxicity) reported that when phenytoin is taken in early pregnancy, T-allele carriers have a higher chance of the baby developing craniofacial abnormalities than C/C carriers. The evidence is limited and no numeric effect size is given. This applies only to pregnancy with phenytoin exposure; the C/C genotype clears the metabolites faster and carries lower risk. Note: this is one of 2 correlated variants in/near EPHX1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the T/C genotype and use phenytoin during the first trimester of pregnancy, you may be more likely to have a child with a craniofacial abnormality compared to people with the C/C genotype. Other genetic and clinical factors may also influence your risk of toxicity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin in pregnancy – craniofacial abnormality risk (EPHX1) ⚠ CAUTIOUS rsid : rs2234922 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19952982/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. EPHX1 rs2234922 (His139Arg). EPHX1 helps detoxify reactive breakdown products of phenytoin. In one study, mothers carrying the G allele who took phenytoin in the first trimester had a higher risk of having a baby with a craniofacial abnormality than A/A mothers, who had a lower (but not zero) risk. This is a single low-level study (PharmGKB level 3 Toxicity) and applies only to phenytoin use in early pregnancy. Note: this is one of 2 correlated variants in/near EPHX1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the A/G genotype and are exposed to phenytoin during the first trimester of pregnancy, you may have an increased risk for having a child with a craniofacial abnormality compared to people with the A/A genotype. Other genetic and clinical factors may also influence your risk for toxicity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Birth weight & size rsid : rs1042725 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31681408/ Interpretation: You inherited one C variant and one T variant — a heterozygous C/T genotype, one allele from each parent. This places you in the middle of the birth weight & size range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: β ≈ 0.05 per copy. • Gestational diabetes risk (MTNR1B) ⚠ CAUTIOUS rsid : rs10830962 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/22233651/ Interpretation: If you have the C/C genotype, you carry no copies of the higher-glucose G allele at this MTNR1B position, so on this variant your gestational-diabetes risk is at the lower, baseline level. Many other genes, body weight, and lifestyle also affect pregnancy glucose, and routine antenatal screening still applies. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Gestational diabetes risk (MTNR1B) [rs10830963]: Both copies here carry the C variant — a C/C genotype, with no copies of the G risk variant. If you become pregnant, your genetic risk for gestational diabetes sits at the lower end of the spectrum, a favourable position relative to G-carriers. Outside of pregnancy this variant carries no gestational-diabetes signal. Each G copy would raise risk by OR ≈ 1.41 per copy. [Sex hormones] • Oral contraceptives & blood clot risk (F2) rsid : rs1799963 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12069454/ https://pubmed.ncbi.nlm.nih.gov/16769590/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799963 is the F2 (prothrombin) G20210A variant; the A allele raises the tendency to form blood clots. In people using systemic hormonal contraceptives, carrying an A allele has been linked to a higher risk of venous thrombosis (e.g. deep vein thrombosis). This is a PharmGKB level-2B drug-conditional signal with no CPIC dosing guideline, and it only matters if you use hormonal contraceptives. Interpretation: If you have the G/G genotype and are taking oral contraceptives (OCs), you may have a decreased risk for deep vein thrombosis (DVT) compared to people with the A/A or A/G genotypes, or compared to those not taking oral contraceptives. However, conflicting evidence has been reported, and other genetic and clinical factors may also influence your DVT risk on oral contraceptives. • Hormonal contraceptives – thrombosis risk (Factor V Leiden) rsid : rs6025 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15946211/ Summary : Each T allele is associated with higher Hormonal contraceptives – thrombosis risk (Factor V Leiden) (+0.148 per copy, study scale). Moderate evidence, 2 publications. Interpretation: You have the C/C genotype at rs6025, meaning you carry normal Factor V (no Factor V Leiden). Compared to people with the C/T or T/T genotype, you may have a decreased risk of thrombosis when taking oral contraceptives, though conflicting evidence has been reported. Both Factor V Leiden and oral contraceptives independently raise thrombosis risk and can have a cumulative effect together, and other genetic and clinical factors may also influence your overall risk. • Age at natural menopause rsid : rs1046089 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/22267201/ Interpretation: You have the G/A genotype at rs1046089. This is a known menopause-timing locus, but the two strongest studies disagree on the direction of the A allele's effect, so no reliable earlier-or-later tendency can be assigned from your genotype. • Age at natural menopause (BRSK1) ⚠ CAUTIOUS rsid : rs1172822 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19448621/ Interpretation: You inherited one C variant and one T variant — a heterozygous C/T genotype, one allele from each parent. This places you in the middle of the age at natural menopause range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: β ≈ 0.49 per copy. • Polycystic ovary syndrome (PCOS) risk rsid : rs12478601 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21151128/ Interpretation: You inherited one C risk variant and one T baseline variant — a heterozygous C/T genotype, one allele from each parent. Risk for polycystic ovary syndrome (pcos) is modestly higher than for people with the T/T baseline — about OR ≈ 1.39 per copy of the C variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Polycystic ovary syndrome (PCOS) risk ⚠ CAUTIOUS rsid : rs13405728 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21151128/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for polycystic ovary syndrome (pcos) is elevated above the C/C baseline, with each A copy contributing OR ≈ 1.35 per copy. • Polycystic ovary syndrome (PCOS) risk (DENND1A) rsid : rs2479106 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21151128/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for polycystic ovary syndrome (pcos) is modestly higher than for people with the A/A baseline — about OR ≈ 1.35 per copy of the G variant. • Age at menopause (UIMC1) rsid : rs365132 Your geno : GG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/26414677/ Interpretation: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the age at menopause range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.39 per copy. • Testosterone levels ⚠ CAUTIOUS rsid : rs5934505 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34337532/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. The T allele is the one tied to higher odds of low testosterone, so T/T sits toward the lower-testosterone end of the range. This is a neutral tendency, not a diagnosis. Per-copy effect size: OR ≈ 1.57 per T copy for low testosterone. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Polycystic ovary syndrome (PCOS) risk ⚠ CAUTIOUS rsid : rs705702 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/22885925/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for polycystic ovary syndrome (pcos) is modestly higher than for people with the A/A baseline — about OR ≈ 1.27 per copy of the G variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Estrogen levels (CYP19A1 / aromatase) rsid : rs727479 Your geno : CA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/29325096/ Interpretation: You inherited one A variant and one C variant — a heterozygous C/A genotype, one allele from each parent. This places you in the middle of the estrogen levels range, between the lower-end C/C and the higher-end A/A genotypes. Per-copy effect size: β ≈ 1.39 per copy. • Uterine fibroid risk (TERT) ⚠ CAUTIOUS rsid : rs10069690 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/40050615/ https://pubmed.ncbi.nlm.nih.gov/35803233/ Interpretation: You have the C/C genotype — two copies of the C allele and no copies of the T allele. At a population level this is the lower-association version of this marker (each T copy carries about OR ≈ 1.12). The effect is weak and not individually predictive. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Heavy menstrual bleeding (menorrhagia) – reduced risk [rs6025]: You have the C/C genotype — no Factor V Leiden copy. Your likelihood of heavy menstrual bleeding from this variant is typical (neither lowered nor raised), and you do not carry the Factor V Leiden clotting-risk allele here. Polycystic ovary syndrome (PCOS) risk [rs10818854]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for polycystic ovary syndrome (pcos) sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.51 per copy. Age at menopause [rs10852344]: Both copies at this position carry the C variant — a C/C genotype. People with C/C tend to sit toward the higher end of the age at menopause range, with each C copy contributing a small upward shift. Per-copy effect size: β ≈ 0.16 per copy. Age at menopause [rs11668344]: You inherited one A variant and one G variant — a heterozygous A/G genotype, one allele from each parent. This places you in the middle of the age-at-menopause range, between the lower-end G/G and the higher-end A/A genotypes. Per-copy effect size: β ≈ 0.43 per copy. Later age at menopause (MCM8) [rs16991615]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the protective A variant present. You miss the small protective benefit that A-carriers get at this site for later age at menopause. Each A copy would shift the effect by β ≈ 0.93 per copy. Uterine fibroid (leiomyoma) risk [rs16991615]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The A allele shows only a weak population-level association with uterine fibroid (leiomyoma) (about OR ≈ 1.14 per copy), so with no A copies this genotype sits at the lower-association end — on its own it does not meaningfully predict your individual outcome. Higher anti-Müllerian hormone & ovarian reserve (MCM8) [rs16991615]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the AMH-raising A variant. You sit at the lower-AMH / lower-ovarian-reserve end at this site relative to A-carriers. Per-copy effect size: β ≈ 0.16 per copy of A. Polycystic ovary syndrome (PCOS) risk (FSHR) [rs2268361]: No notable finding at this locus. Testosterone & SHBG levels (SHBG gene) [rs6258]: Both copies here carry the C reference allele — a C/C genotype, the most common genotype at this site. rs6258 is associated with SHBG and testosterone levels, but the effect-allele direction for this entry could not be confidently resolved, so no up-or-down personal signal is asserted. Informational only. Testosterone levels (SHBG locus) [rs727428]: You inherited one C variant and one T variant — a heterozygous T/C genotype, one allele from each parent. This places you in the middle of the testosterone levels range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: β ≈ 0.03 per copy. Uterine fibroids risk (TERT) [rs2242652]: You have the G/G genotype — two G alleles, with average genetic risk for uterine fibroids at this variant. Uterine fibroids (leiomyoma) risk [rs2853676]: No notable finding at this locus. [Thyroid function] • Hypothyroidism risk (MC4R region) ⚠ CAUTIOUS rsid : rs571312 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/41644669/ Interpretation: You have the C/A genotype — one copy of the A allele. One study reported a small increase in hypothyroidism risk per A copy (about β ≈ 0.03), but the evidence is single-source and probably tied to body-weight effects of this MC4R-region haplotype rather than direct thyroid biology. • Levothyroxine response & thyroid hormone conversion (DIO2) ⚠ CAUTIOUS rsid : rs225014 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24910925/ https://pubmed.ncbi.nlm.nih.gov/30367059/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each C allele is associated with lower Levothyroxine response & thyroid hormone conversion (DIO2) (−0.047 per copy, study scale). Limited evidence, 1 record. Interpretation: TT genotype — see evidence summary; per-genotype effect not quantified in source data. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Hypothyroidism & autoimmune thyroid disease (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36093044/ https://pubmed.ncbi.nlm.nih.gov/22922229/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for hypothyroidism & autoimmune thyroid disease is modestly higher than for people with the G/G baseline — about β ≈ 0.33 per copy of the A variant. • Hashimoto's thyroiditis & hypothyroidism risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/41644669/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for hashimoto's thyroiditis & hypothyroidism is modestly higher than for people with the C/C baseline — about OR ≈ 1.36 per copy of the A variant. • Thyroid hormone levels (TSH) ⚠ CAUTIOUS rsid : rs753760 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/23408906/ Interpretation: Both copies at this position carry the C variant — a C/C genotype. People with C/C tend to sit toward the higher end of the thyroid hormone levels range, with each C copy contributing a small upward shift. Per-copy effect size: β ≈ 0.13 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Autoimmune thyroid disease & Graves' disease (CTLA4) rsid : rs231775 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/32581359/ https://pubmed.ncbi.nlm.nih.gov/41644669/ Interpretation: You have the G/G genotype — two copies of the G allele, which carries a modest population-level association with autoimmune thyroid / Graves' disease (about OR ≈ 1.17 per G copy). This is a weak-to-modest association and on its own does not meaningfully predict your individual outcome. — Also checked, no unusual variants — Nodular goiter risk [rs116909374]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for nodular goiter sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by β ≈ 0.35 per copy. Thyroid function — TSH & hypothyroidism [rs116909374]: Both copies here carry the C allele — a C/C genotype, with no copies of the T allele. At the population level the C allele is associated with a modestly higher TSH measurement, and on the hypothyroidism liability scale C is the higher-liability allele (about β ≈ 0.16 per copy). This is a measurement/liability-level association, not a diagnosis. Note FOXE1 pleiotropy: the same T allele (absent here) runs the opposite way for thyroid cancer and nodular goiter. Thyroid hormone conversion & levothyroxine response (DIO1) [rs2235544]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the A variant present. People with C/C tend to sit toward the lower end of the thyroid hormone conversion & levothyroxine response range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.15 per copy. Autoimmune thyroid disease (hypothyroidism, Graves', Hashimoto's) [rs3087243]: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for autoimmune thyroid disease is elevated above the A/A baseline, with each G copy contributing β ≈ 0.24 per copy. Hypothyroidism risk (FOXE1) [rs965513]: No notable finding at this locus. Hypothyroidism risk (STAT4) [rs7574865]: No notable finding at this locus. ──────────────────────────────────────────────────────────────────────── IMMUNE & INFLAMMATORY ──────────────────────────────────────────────────────────────────────── [Autoimmune disease risk] • Skin pigmentation / skin colour (TYR) rsid : rs1042602 Your geno : CA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39024449/ Interpretation: You have the C/A genotype at TYR — one lighter-pigment (A) allele and one darker (C). This places you in the middle of the pigmentation range at this gene. Normal cosmetic variation, not a health risk. • Asthma risk (HLA-DQ) rsid : rs9272346 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/32296059/ https://pubmed.ncbi.nlm.nih.gov/29273806/ https://pubmed.ncbi.nlm.nih.gov/23181788/ Interpretation: You have the A/A genotype — two copies of the A asthma-associated tag allele. The per-copy effect on asthma odds is small (about OR 1.16), so even A/A reflects only a weak population-level association that does not on its own meaningfully predict your individual outcome. This is a tag SNP for the HLA-DQ region (a surrogate, not direct HLA typing). • Type 1 diabetes risk (HLA-DQ) rsid : rs9273363 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/40465716/ https://pubmed.ncbi.nlm.nih.gov/30659077/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for type 1 diabetes is elevated above the C/C baseline, with each A copy contributing OR ≈ 5.48 per copy. • Rheumatoid arthritis risk (FADS gene cluster) ⚠ CAUTIOUS rsid : rs968567 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30423114/ https://pubmed.ncbi.nlm.nih.gov/24390342/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. The C allele is weakly associated with slightly higher rheumatoid-arthritis odds (about OR ≈ 1.12 per copy), so C/C sits at the upper end of this small range. This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Psoriasis risk (HLA-C region) ⚠ CAUTIOUS rsid : rs2395029 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18369459/ Interpretation: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the G risk variant present. Your genetic risk for psoriasis sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 4.1 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Crohn's disease risk (HLA-C) ⚠ CAUTIOUS rsid : rs9264942 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/26192919/ https://pubmed.ncbi.nlm.nih.gov/23128233/ Interpretation: You inherited one C variant and one T variant — a heterozygous T/C genotype. The C variant is associated with a slightly higher Crohn's-disease risk (about 15% per copy), but this per-allele effect is small enough that it does not meaningfully shift your personal risk. • Autoimmune disease risk (PTPN22 R620W) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30572963/ Interpretation: You have the A/G genotype — one copy of the PTPN22 620W (A) risk allele, which modestly raises overall risk for autoimmune conditions. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rheumatoid arthritis risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36333501/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for rheumatoid arthritis is modestly higher than for people with the G/G baseline — about OR ≈ 1.72 per copy of the A variant. • Lupus (SLE) risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36750564/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for lupus (sle) is modestly higher than for people with the G/G baseline — about OR ≈ 1.35 per copy of the A variant. • Crohn's disease risk (PTPN22) ⚠ CAUTIOUS rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/26192919/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for crohn's disease is modestly higher than for people with the A/A baseline — about OR ≈ 1.26 per copy of the G variant. • Type 1 diabetes risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18978792/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for type 1 diabetes is modestly higher than for people with the C/C baseline — about OR ≈ 1.82 per copy of the A variant. • Rheumatoid arthritis risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33310728/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for rheumatoid arthritis is modestly higher than for people with the C/C baseline — about OR ≈ 1.41 per copy of the A variant. • Hashimoto's thyroiditis & hypothyroidism risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/41644669/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for hashimoto's thyroiditis & hypothyroidism is modestly higher than for people with the C/C baseline — about OR ≈ 1.36 per copy of the A variant. • Systemic lupus erythematosus risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/28714469/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for systemic lupus erythematosus is modestly higher than for people with the C/C baseline — about OR ≈ 1.39 per copy of the A variant. • Juvenile idiopathic arthritis risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33106285/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for juvenile idiopathic arthritis is modestly higher than for people with the C/C baseline — about OR ≈ 1.59 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Inflammatory myositis risk (PTPN22) rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30573655/ Interpretation: You have the C/A genotype — one copy of the PTPN22 risk variant, linked to a modestly higher risk of autoimmune myositis. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Vitiligo risk (PTPN22) ⚠ CAUTIOUS rsid : rs6679677 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39024449/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for vitiligo is modestly higher than for people with the C/C baseline — about β ≈ 0.41 per copy of the A variant. • Crohn's disease risk (IL23R region) ⚠ CAUTIOUS rsid : rs1004819 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17804789/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous G/A genotype. Risk for Crohn's disease is modestly higher than for people with the G/G baseline — about OR ≈ 1.38 per copy of the A variant. • Multiple sclerosis risk (IL2RA) ⚠ CAUTIOUS rsid : rs12722489 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17660530/ Interpretation: You inherited one C risk variant and one T baseline variant — a heterozygous C/T genotype, one allele from each parent. Risk for multiple sclerosis is modestly higher than for people with the T/T baseline — about OR ≈ 1.23 per copy of the C variant. • Crohn's disease risk (IL2RA region) ⚠ CAUTIOUS rsid : rs12722489 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/37156999/ Interpretation: You have one C and one T allele — a heterozygous C/T genotype, one from each parent. The C allele carries a weak population-level association with Crohn's disease (about OR ≈ 1.11 per copy); on its own it does not meaningfully predict your individual outcome. • Psoriasis risk (IL23R/STAT2 region) rsid : rs2066808 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25574825/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for psoriasis is elevated above the C/C baseline, with each A copy contributing OR ≈ 1.48 per copy. • Crohn's disease risk (ATG16L1) rsid : rs2241880 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17435756/ Interpretation: You carry one G risk variant (the ATG16L1 T300A / Ala300 change) and one A baseline variant — a heterozygous A/G genotype. Your risk for Crohn's disease is modestly higher than for people with the A/A genotype, about OR ≈ 1.32 per copy of the G variant. This is a common variant — most people carry at least one G copy. • Childhood-onset asthma risk (GSDMB) rsid : rs2305480 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35126453/ https://pubmed.ncbi.nlm.nih.gov/24241537/ Interpretation: You have the G/G genotype — two copies of the G allele, which carries a modest population-level association with childhood-onset asthma (about OR ≈ 1.18 per G copy). This is a weak-to-modest association and on its own does not meaningfully predict your individual outcome. • Autoimmune thyroid disease & Graves' disease (CTLA4) rsid : rs231775 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/32581359/ https://pubmed.ncbi.nlm.nih.gov/41644669/ Interpretation: You have the G/G genotype — two copies of the G allele, which carries a modest population-level association with autoimmune thyroid / Graves' disease (about OR ≈ 1.17 per G copy). This is a weak-to-modest association and on its own does not meaningfully predict your individual outcome. • Alopecia areata risk (CTLA4) ⚠ CAUTIOUS rsid : rs231775 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25608926/ Interpretation: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for alopecia areata is elevated above the A/A baseline, with each G copy contributing OR ≈ 1.4 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Asthma risk (IL18R1/IL1RL1) ⚠ CAUTIOUS rsid : rs3771166 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20860503/ Interpretation: You have the G/G genotype — two copies of the G allele, which carries a small population-level association with asthma (about OR ≈ 1.15 per G copy). This is a weak association and on its own does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Multiple sclerosis risk (IL7R) rsid : rs6897932 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21833088/ Interpretation: You have the C/C genotype — two copies of the C allele, which carries a small population-level association with multiple sclerosis (about OR ≈ 1.11 per C copy). This is a weak association and on its own does not meaningfully predict your individual outcome. • Systemic lupus erythematosus risk (IL7R) ⚠ CAUTIOUS rsid : rs6897932 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36750564/ Interpretation: You have the C/C genotype — two copies of the C allele at this IL7R site. At a population level the C allele carries a small association with systemic lupus erythematosus (about β ≈ 0.07 per copy on the study scale). This is a weak association and on its own does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Childhood-onset asthma risk (17q21 / GSDMB) rsid : rs7216389 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35126453/ Interpretation: Both copies at this position carry the T risk variant — a T/T genotype, the highest-risk combination at this site. Risk for childhood-onset asthma is elevated above the C/C baseline, with each T copy contributing OR ≈ 1.45 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Inflammatory bowel disease & Crohn's risk (STAT3) rsid : rs744166 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/18587394/ Interpretation: You have the A/A genotype — two copies of the A allele, which carries a small population-level association with inflammatory bowel disease & Crohn's (about OR ≈ 1.18 per A copy). This is a weak association and on its own does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rheumatoid arthritis risk (HLA region) rsid : rs9268839 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30423114/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for rheumatoid arthritis is modestly higher than for people with the A/A baseline — about OR ≈ 1.35 per copy of the G variant. • Sjögren's syndrome risk (HLA region) rsid : rs9271588 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/24097066/ Interpretation: You have the T/C genotype — one copy of the T risk allele, with modestly increased odds of Sjögren's syndrome compared with people who carry two C alleles (about OR 1.75 per copy of T). • Hydrolysed wheat protein allergy susceptibility (HLA region) ⚠ CAUTIOUS rsid : rs9271588 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/31301374/ Interpretation: You have the T/C genotype — one copy of the C susceptibility allele, linked in an HLA study to roughly doubled odds (about OR 2.3 per copy) of allergy to hydrolysed wheat protein. This is a tendency tied to that specific exposure, not a diagnosis; many carriers never develop a wheat allergy. • IgA nephropathy risk (HLA region) rsid : rs9275224 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25305756/ Interpretation: You have the A/G genotype — one copy of the G risk allele, linked to a modestly higher chance of IgA nephropathy (roughly OR 1.36 per copy). The absolute risk stays low for most people. • Lupus (SLE) risk ⚠ CAUTIOUS rsid : rs1317082 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33272962/ Interpretation: Both copies at this position carry the A variant — a A/A genotype. The A allele carries a weak association with slightly higher lupus (SLE) odds (about OR ≈ 1.1 per copy). This is a small population-level signal and does not meaningfully predict your individual outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Interstitial lung disease / pulmonary fibrosis risk (TERT) ⚠ CAUTIOUS rsid : rs2736100 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23583980/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous C/A genotype, one allele from each parent. Risk for interstitial lung disease / pulmonary fibrosis is modestly higher than for people with the C/C baseline — about OR ≈ 1.37 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Vitiligo risk (HERC2) [rs1129038]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C risk variant present. Your genetic risk for vitiligo sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by OR ≈ 1.22 per copy. Celiac disease risk (HLA-DQ2.5 tag) [rs2187668]: No notable finding at this locus. Systemic lupus erythematosus (SLE) risk (HLA-DR3/DQ2.5 tag) [rs2187668]: No notable finding at this locus. Membranous glomerulonephritis (kidney autoimmune) risk [rs2187668]: No notable finding at this locus. ANCA-associated vasculitis risk (HLA-DQ) [rs7454108]: Both copies at this position carry the T variant — a T/T genotype, with no copies of the C variant linked to higher MPO-ANCA vasculitis risk. You sit at the lower-risk end at this site relative to C-carriers. ANCA vasculitis is rare overall, and this is a tag-SNP estimate, not HLA typing. Asthma risk (HLA region) [rs7775228]: Both copies at this position carry the T allele — a T/T genotype. The T allele is weakly associated with slightly higher asthma odds (about OR ≈ 1.17 per copy), so T/T sits at the upper end of this small range. This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. Type 1 diabetes risk (HLA-DQ) [rs9272346]: You have the A/A genotype — no copies of the high-risk G allele. Your HLA-DQ-tagged genetic risk for type 1 diabetes sits at the lower end, a favourable position relative to G-carriers. This is a tag SNP for the HLA-DQ region (a surrogate, not direct HLA typing). Crohn's disease risk (TNF) [rs361525]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele. The A allele is the one weakly associated with slightly higher Crohn's disease odds at this locus. With no A copies, this is the lower-association genotype here, though the difference is small at the population level. Multiple sclerosis risk (HLA-DRA) [rs3135388]: No notable finding at this locus. Rheumatoid arthritis & autoimmune risk (SH2B3) [rs3184504]: Both copies at this position carry the C allele — a C/C genotype, with no T copies. This is the slightly more favourable version relative to T-carriers, but the per-copy effect is small (about OR ≈ 1.08) — a weak population-level association, not a meaningful predictor of your individual outcome. Rheumatoid arthritis risk (CTLA4) [rs3087243]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The G allele shows only a weak population-level association with rheumatoid arthritis (about OR ≈ 1.15 per copy); on its own it does not meaningfully predict your individual outcome. Autoimmune thyroid disease (hypothyroidism, Graves', Hashimoto's) [rs3087243]: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for autoimmune thyroid disease is elevated above the A/A baseline, with each G copy contributing β ≈ 0.24 per copy. Type 1 diabetes risk (CTLA4) [rs3087243]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The G allele shows only a weak population-level association with type 1 diabetes (about OR ≈ 1.16 per copy); on its own it does not meaningfully predict your individual outcome. Systemic lupus erythematosus risk (CTLA4) [rs3087243]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The G allele shows only a weak population-level association with systemic lupus erythematosus (about OR ≈ 1.12 per copy); on its own it does not meaningfully predict your individual outcome. Multiple sclerosis risk [rs1026916]: Both copies carry the G allele — a G/G genotype, with no copies of the A allele that is associated with slightly higher multiple-sclerosis odds. Your genetic contribution from this single common variant is at the lower, baseline end, though the per-allele effect is small either way. Inflammatory bowel disease risk (JAK2 region) [rs10758669]: Both copies carry the A allele — an A/A genotype, with no copies of the C allele. The C allele (absent here) carries only a weak population-level association with inflammatory bowel disease (about OR ≈ 1.18 per copy), so this genotype sits at the lower-association end — a small effect either way that on its own does not meaningfully predict your individual outcome. Crohn's disease risk [rs11175593]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.54 per copy. Crohn's disease & IBD risk (IL23R) [rs11209026]: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for crohn's disease & ibd is elevated above the A/A baseline, with each G copy contributing OR ≈ 3.04 per copy. Ankylosing spondylitis risk (IL23R) [rs11209026]: Both copies at this position carry the G risk variant — a G/G genotype, the highest-risk combination at this site. Risk for ankylosing spondylitis is elevated above the A/A baseline, with each G copy contributing OR ≈ 1.65 per copy. Systemic lupus erythematosus (SLE) risk [rs1128334]: No notable finding at this locus. Crohn's disease risk (NOD2) [rs17221417]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the G risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.29 per copy. Crohn's disease risk (chromosome 5p13) [rs17234657]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the G risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.54 per copy. Asthma & allergic disease risk (IL13) [rs20541]: You have the G/G genotype — two copies of the G allele and no copies of the A allele. At a population level this is the lower-association version of this marker (each A copy carries about OR ≈ 1.12). The effect is weak and not individually predictive. Crohn's disease risk (NOD2) [rs2066844]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 2.16 per copy. Crohn's disease risk (NOD2) [rs2066845]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the C risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by β ≈ 0.91 per copy. Crohn's disease risk (NOD2) [rs2076756]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for crohn's disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.66 per copy. Multiple sclerosis risk (IL2RA) [rs2104286]: No notable finding at this locus. Ulcerative colitis risk (IL23R) [rs2201841]: No notable finding at this locus. Psoriasis risk (IL23R) [rs2201841]: No notable finding at this locus. Rheumatoid arthritis risk (IL6R) [rs2228145]: You have a heterozygous A/C genotype — one A and one C allele, one from each parent. The A allele carries a small population-level association with rheumatoid arthritis (about OR ≈ 1.07 per copy); on its own this weak association does not meaningfully predict your individual outcome. Ulcerative colitis risk (ORMDL3/GSDMB) [rs2305480]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for ulcerative colitis sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.25 per copy. Multiple sclerosis risk (HLA-DRB1 region) [rs3129889]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for multiple sclerosis sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 2.97 per copy. Systemic lupus erythematosus (SLE) risk [rs3131379]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for systemic lupus erythematosus (sle) sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 2.36 per copy. Primary biliary cholangitis risk (IL7R) [rs6897932]: Both copies here carry the C baseline variant for this trait — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for primary biliary cholangitis sits at the lower end of the spectrum, a favourable position relative to T-carriers. Each T copy would raise PBC risk by OR ≈ 1.52 per copy. Multiple sclerosis risk (STAT3) [rs744166]: You have the A/A genotype — two copies of the A allele and no copies of the C allele. At a population level this is the lower-association version of this marker (each C copy carries about OR ≈ 1.15). The effect is weak and not individually predictive. Lupus (SLE) risk (STAT4) [rs7574865]: No notable finding at this locus. Rheumatoid arthritis risk (STAT4) [rs7574865]: No notable finding at this locus. Systemic sclerosis risk (STAT4) [rs7574865]: No notable finding at this locus. Hypothyroidism risk (STAT4) [rs7574865]: No notable finding at this locus. Asthma & allergic disease risk (IL13) [rs848]: You have the C/C genotype — two copies of the C allele and no copies of the A allele. At a population level this is the lower-association version of this marker (each A copy carries about β ≈ 0.10 on the study scale). The effect is weak and not individually predictive. Multiple sclerosis risk (HLA-DRB1) [rs9271366]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for multiple sclerosis sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 2.62 per copy. Crohn's disease risk (HLA region) [rs9271366]: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for crohn's disease is elevated above the G/G baseline, with each A copy contributing OR ≈ 1.66 per copy. Ulcerative colitis risk (HLA region) [rs9271366]: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for ulcerative colitis is elevated above the G/G baseline, with each A copy contributing OR ≈ 1.63 per copy. Systemic lupus erythematosus risk (HLA region) [rs9271366]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for systemic lupus erythematosus sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.26 per copy. [Infection susceptibility] • HIV-1 viral load control (HLA-C) rsid : rs9264942 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21051598/ https://pubmed.ncbi.nlm.nih.gov/20041166/ Interpretation: You inherited one C variant and one T variant — a heterozygous T/C genotype, one allele from each parent. This places you in the middle of the hiv-1 viral load control range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: OR ≈ 2.9 per copy. • Hepatitis B vaccine response (IL4R) ⚠ CAUTIOUS rsid : rs1805015 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21111021/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1805015 is a coding variant (Ser503Pro) in IL4R, the interleukin-4 receptor gene that helps regulate antibody production. A small immunogenetics study (PharmGKB level 3 Efficacy, limited evidence) linked the T allele to a weaker (non-immune) antibody response after the hepatitis B vaccine, while the C allele was associated with a stronger response. The effect is modest, unquantified, and one of several factors (age, sex, body weight) that determine whether the vaccine produces protective antibodies. Interpretation: If you have the T/T genotype, you may be at increased risk of non-immune response to the hepatitis B vaccine compared to people with the C/C genotype. Other genetic and clinical factors may also influence the risk of non-immune response to the hepatitis B vaccine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Hepatitis B vaccine response (IL13) [rs1295686]: No notable finding at this locus. HIV-1 viral-load control (HLA-B region) [rs2523608]: You have the A/A genotype — no copies of the control-associated G allele, so the favourable HIV-1 viral-load-control signal at this HLA-B-region locus is absent. This concerns post-infection control, not risk of acquiring HIV. [Inflammation] • Asthma risk (IL33 region) rsid : rs1342326 Your geno : AC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20860503/ https://pubmed.ncbi.nlm.nih.gov/33328473/ Interpretation: You inherited one C risk variant and one A baseline variant — a heterozygous A/C genotype, one allele from each parent. Risk for asthma is modestly higher than for people with the A/A baseline — about OR ≈ 1.2 per copy of the C variant. • Asthma & allergic disease risk (TSLP) rsid : rs1837253 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/36777996/ https://pubmed.ncbi.nlm.nih.gov/30929738/ https://pubmed.ncbi.nlm.nih.gov/29083406/ Interpretation: You have the C/C genotype — two copies of the C allele, which carries a small population-level association with asthma & allergic disease (about OR ≈ 1.07 per C copy). This is a weak association and on its own does not meaningfully predict your individual outcome. • Nasal polyps & chronic rhinosinusitis (TSLP) rsid : rs1837253 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30643255/ https://pubmed.ncbi.nlm.nih.gov/36653354/ Interpretation: Both copies at this position carry the C risk variant — a C/C genotype, the highest-risk combination at this site. Risk for nasal polyps & chronic rhinosinusitis is elevated above the T/T baseline, with each C copy contributing OR ≈ 1.11 per copy. • Eosinophil count (TSLP) ⚠ CAUTIOUS rsid : rs1837253 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32888494/ Interpretation: Both copies at this position carry the C variant — a C/C genotype. People with C/C tend to sit toward the higher end of the eosinophil count range, with each C copy contributing a small upward shift. Per-copy effect size: β ≈ 0.02 per copy. • Atopic eczema risk (IL13) rsid : rs20541 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/37794016/ https://pubmed.ncbi.nlm.nih.gov/31361310/ Interpretation: You have the G/G genotype at IL13 — two copies of the G allele, which carries a small population-level association with lower atopic eczema. This is a weak effect and not individually predictive. • Allergic disease & hay fever risk (IL6R) ⚠ CAUTIOUS rsid : rs2228145 Your geno : AC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/31361310/ https://pubmed.ncbi.nlm.nih.gov/29083406/ Interpretation: You have a heterozygous A/C genotype — one A and one C allele, one from each parent. The C allele carries a very small population-level association with allergic disease & hay fever (about OR ≈ 1.04 per copy); on its own this very weak association does not meaningfully predict your individual outcome. • Aspirin-induced asthma sensitivity (IL4) ⚠ CAUTIOUS rsid : rs2243250 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20921925/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a gene-environment / drug-response marker, relevant only if you have asthma and are exposed to aspirin (or related NSAIDs). It is the IL4 promoter variant -589C>T (rs2243250). The C allele has been linked, in a dose-dependent way, to a stronger aspirin-induced drop in lung function (FEV1) after an aspirin challenge - so C/C carriers showed the largest decline and T/T the smallest. A laboratory study supports a mechanism: aspirin boosts IL4 gene activity more strongly with the C allele. Evidence is limited (PharmGKB level 3). This is a sensitivity tendency, not a diagnosis. Interpretation: You have the C/T genotype of the IL4 promoter variant. If you have asthma, you may have a somewhat greater aspirin-induced drop in lung function (FEV1) after taking aspirin compared with people who have two T alleles, but less than C/C carriers - the effect tracks with the number of C alleles. Other genetic and clinical factors also affect how you respond to aspirin. If you have asthma, check with your doctor before using aspirin or NSAIDs. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Celiac disease risk (HLA-DQ2.5 tag SNP) [rs2187668]: No notable finding at this locus. C-reactive protein / inflammation marker (HNF4A) [rs1800961]: Both copies at this position are the C allele — a C/C genotype, with no T alleles. The T allele is the one weakly linked to a lower CRP reading, so on average C/C sits at the upper end for this inflammation measurement. The per-copy shift is small (β ≈ 0.10) and, on its own, does not meaningfully predict your actual CRP level — a blood test is the real measure. Atopic eczema risk (IL13) [rs1295686]: You have the C/C genotype — two copies of the lower-risk C allele, with no copies of the eczema-raising T allele, giving the lowest genetic risk of atopic eczema at this IL13 variant. Psoriasis risk (IL13) [rs1295686]: Both copies at this position carry the C allele — a C/C genotype, the higher-risk combination at this site for psoriasis (each C copy contributing about β≈0.12). Evidence here is limited (a single record). Childhood-onset asthma risk (IL13) [rs1295686]: Both copies carry the C allele — a C/C genotype, with no copies of the T allele. The T allele (absent here) carries only a weak population-level association with childhood-onset asthma (about OR ≈ 1.15 per copy), so this genotype sits at the lower-association end — a small effect either way that on its own does not meaningfully predict your individual outcome. Childhood-onset asthma risk [rs2066844]: You have the C/C genotype — two copies of the C allele and no copies of the T allele. At a population level this is the lower-association version of this marker (each T copy carries about OR ≈ 1.09). The effect is weak and not individually predictive. ──────────────────────────────────────────────────────────────────────── LONGEVITY & AGING ──────────────────────────────────────────────────────────────────────── [Alzheimer's risk] • Alzheimer's disease risk (APOE region) ⚠ CAUTIOUS rsid : rs157580 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30617256/ https://pubmed.ncbi.nlm.nih.gov/29777097/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for alzheimer's disease is modestly higher than for people with the G/G baseline — about β ≈ 0.4 per copy of the A variant. • Alzheimer's disease risk (SLC24A4) ⚠ CAUTIOUS rsid : rs10498633 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/24162737/ Interpretation: You have the G/G genotype — two copies of the G allele at this SLC24A4 site. At a population level each G copy carries a small association with Alzheimer's (about OR ≈ 1.10 per copy); this is a weak effect and on its own does not meaningfully shift your overall outlook. • Alzheimer's disease risk (SORL1) ⚠ CAUTIOUS rsid : rs11218343 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35379992/ https://pubmed.ncbi.nlm.nih.gov/34493870/ https://pubmed.ncbi.nlm.nih.gov/29777097/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. The T allele carries a modest association with higher Alzheimer's odds (about OR ≈ 1.18 per copy). This is a weak-to-modest population-level signal and, on its own, does not meaningfully predict your individual outcome. • Alzheimer's disease risk (NME8 region) ⚠ CAUTIOUS rsid : rs2718058 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/24162737/ Interpretation: You have the A/A genotype — two copies of the A risk variant near NME8. Each A copy is linked to a slightly higher Alzheimer's risk (about OR 1.08 per copy), a small per-copy effect on its own. • Alzheimer's disease risk (ABCA7) ⚠ CAUTIOUS rsid : rs3764650 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21460840/ https://pubmed.ncbi.nlm.nih.gov/39046104/ Interpretation: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the G risk variant present. Your genetic risk for Alzheimer's disease at this ABCA7 marker sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.23 per copy. • Alzheimer's disease risk (BIN1) ⚠ CAUTIOUS rsid : rs6733839 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35379992/ https://pubmed.ncbi.nlm.nih.gov/29777097/ https://pubmed.ncbi.nlm.nih.gov/35729600/ Interpretation: You inherited one T allele and one C allele — a heterozygous C/T genotype, one allele from each parent. Each T copy is linked to modestly higher Alzheimer's odds (about OR ≈ 1.15–1.17 per copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Alzheimer's disease risk (MAPT region) ⚠ CAUTIOUS rsid : rs7274581 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/24162737/ Interpretation: Both copies at this position carry the T allele — a T/T genotype. Each T copy is linked to slightly higher Alzheimer's odds (about OR ≈ 1.14 per copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Alzheimer's disease risk (BIN1) rsid : rs744373 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21460840/ https://pubmed.ncbi.nlm.nih.gov/39046104/ https://pubmed.ncbi.nlm.nih.gov/36066633/ Interpretation: You inherited one G allele and one A allele — a heterozygous A/G genotype, one allele from each parent. Each G copy is linked to modestly higher Alzheimer's odds (about OR ≈ 1.18 per copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. — Also checked, no unusual variants — Alzheimer's disease risk (APOE ε2) [rs7412]: You have the C/C genotype at rs7412, so you do not carry the ε2-defining T allele at this position. Your APOE-related Alzheimer's risk cannot be determined from rs7412 alone — it depends on your rs429358 genotype too, which together with rs7412 sets whether you carry ε3 or the higher-risk ε4. Alzheimer's disease risk (TOMM40/APOE region) [rs2075650]: You have the A/A genotype at rs2075650, carrying no copies of the G marker allele. At this TOMM40/APOE-region marker your associated Alzheimer's odds sit toward the lower end — but this SNP only tags the APOE ε4 risk haplotype, it does not confirm your ε-status. Your true APOE ε-genotype requires rs429358 and rs7412 together. Alzheimer's risk is probabilistic and shaped by age, lifestyle and many genes. Alzheimer's disease risk (APOE region) [rs769449]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant. The A allele here is a marker correlated with the APOE ε4 Alzheimer's-risk haplotype, so G/G sits toward the lower end of the risk this marker tracks — a relatively favourable position. This marker does not determine your APOE ε-status (that needs rs429358 + rs7412 together) and is not a diagnosis. Each A copy is associated with about β ≈ 0.09 higher per copy. Alzheimer's disease risk (CELF1) [rs10838725]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C variant. At this single CELF1 marker your position sits at the lower end of a very narrow range (each C copy is associated with only OR ≈ 1.08). The effect is small, so this tells you little on its own. Alzheimer's disease risk (CLU) [rs11136000]: You inherited one C risk variant and one T protective variant — a heterozygous T/C genotype, one allele from each parent. Risk for Alzheimer's disease is modestly higher than for people with the T/T genotype — about OR ≈ 1.22 per copy of the C variant. Alzheimer's disease risk (EPHA1) [rs11771145]: Both copies at this position carry the G variant — a G/G genotype. The G allele carries a weak association with slightly higher Alzheimer's odds (about OR ≈ 1.06 per copy). This is a small population-level signal that, on its own, does not meaningfully predict your individual outcome. Alzheimer's disease risk (ZCWPW1) [rs1476679]: No notable finding at this locus. Alzheimer's disease risk (FERMT2) [rs17125944]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C variant. At this single FERMT2 marker your position sits at the lower end of a narrow range; the per-allele effect is modest (OR ≈ 1.14), so this tells you little on its own. Alzheimer's disease risk (MEF2C) [rs190982]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A variant. At this single MEF2C marker your position sits at the lower end of a very narrow range; the per-allele effect is small (OR ≈ 1.08), so this tells you little on its own. Alzheimer's disease risk (INPP5D) [rs35349669]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for alzheimer's disease sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.08 per copy. Alzheimer's disease risk (CR1) [rs3818361]: No notable finding at this locus. Alzheimer's disease risk (PICALM) [rs3851179]: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C risk variant present. Your genetic risk for alzheimer's disease sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by OR ≈ 1.11 per copy. Alzheimer's disease risk (CLU) [rs9331896]: No notable finding at this locus. Alzheimer's disease risk (MS4A6A) [rs983392]: You inherited one A variant and one G variant — a heterozygous A/G genotype, one allele from each parent. The G allele is associated with slightly lower Alzheimer's odds and A with slightly higher (OR≈1.11 per A copy), so your risk sits close to the population average. [Biological aging] • Bone mineral density & osteoporosis risk ⚠ CAUTIOUS rsid : rs9533090 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/22504420/ Interpretation: You inherited one T risk variant and one C baseline variant — a heterozygous C/T genotype, one allele from each parent. Bone mineral density is modestly lower (osteoporosis risk modestly higher) than for people with the C/C baseline — about β ≈ 0.12 per copy of the T variant. • Bone mineral density & osteoporosis risk rsid : rs9594738 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/29304378/ https://pubmed.ncbi.nlm.nih.gov/30598549/ https://pubmed.ncbi.nlm.nih.gov/31015401/ Interpretation: You inherited one T allele and one C allele — a heterozygous C/T genotype, one from each parent. The T allele is associated with modestly lower bone mineral density (about β ≈ 0.06 per copy on the study scale), which corresponds to a slightly higher osteoporosis risk than C/C. This is a measurement-level association, not an individual diagnosis. • Bone mineral density (ESR1) ⚠ CAUTIOUS rsid : rs2234693 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30048462/ Interpretation: Both copies at this position carry the T variant — a T/T genotype, with no copies of the protective C variant present. You miss the small protective benefit that C-carriers get at this site for bone mineral density. Each C copy would shift the effect by β ≈ 0.01 per copy. • Age-related macular degeneration risk (CFH) rsid : rs1061147 Your geno : AC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23326517/ Interpretation: You inherited one A risk variant and one C baseline variant — a heterozygous A/C genotype, one allele from each parent. Risk for age-related macular degeneration is modestly higher than for people with the C/C baseline — about OR ≈ 1.4 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Age-related macular degeneration risk (CFH) ⚠ CAUTIOUS rsid : rs1329428 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20861866/ https://pubmed.ncbi.nlm.nih.gov/37079300/ Interpretation: You inherited one C risk variant and one T lower-risk variant — a heterozygous C/T genotype, one allele from each parent. Risk for age-related macular degeneration is higher than for people with the T/T genotype, but below that of C/C homozygotes. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Age-related macular degeneration risk (CFH) ⚠ CAUTIOUS rsid : rs1410996 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20385826/ Interpretation: You have the G/A genotype — one copy of the A allele in a CFH region strongly tied to higher age-related macular degeneration risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Age-related macular degeneration risk (C3) rsid : rs2230199 Your geno : GC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/26691988/ https://pubmed.ncbi.nlm.nih.gov/22705344/ Interpretation: You inherited one C risk variant and one G baseline variant — a heterozygous G/C genotype, one allele from each parent. Risk for age-related macular degeneration is modestly higher than for people with the G/G baseline — about OR ≈ 1.42 per copy of the C variant. • Age-related macular degeneration risk (ARMS2/HTRA1) rsid : rs3793917 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20385819/ Interpretation: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the G risk variant present. Your genetic risk for age-related macular degeneration at this ARMS2/HTRA1 marker sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 3.4 per copy. • Age-related macular degeneration risk (CFH) ⚠ CAUTIOUS rsid : rs380390 Your geno : GC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/15761122/ Interpretation: You inherited one C risk variant and one G baseline variant — a heterozygous G/C genotype, one allele from each parent. Risk for age-related macular degeneration is higher than for people with the G/G baseline (reported OR ≈ 4.6 for heterozygotes in the discovery study, with a wide confidence interval). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Age-related macular degeneration risk (C2/CFB region) rsid : rs429608 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23455636/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for age-related macular degeneration is modestly higher than for people with the A/A baseline — about OR ≈ 1.74 per copy of the G variant. • Age-related macular degeneration risk (CFB/C2 region) rsid : rs547154 Your geno : GT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/32843070/ Interpretation: You inherited one G risk variant and one T baseline variant — a heterozygous G/T genotype, one allele from each parent. Risk for age-related macular degeneration is modestly higher than for people with the T/T baseline — about OR ≈ 1.24 per copy of the G variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Age-related macular degeneration risk (CFB) ⚠ CAUTIOUS rsid : rs641153 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21665990/ https://pubmed.ncbi.nlm.nih.gov/22705344/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for age-related macular degeneration is modestly higher than for people with the A/A baseline — about OR ≈ 1.85 per copy of the G variant. • Age-related macular degeneration risk (CFH) rsid : rs800292 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/32277175/ https://pubmed.ncbi.nlm.nih.gov/37696869/ Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for age-related macular degeneration is modestly higher than for people with the A/A baseline — about OR ≈ 2.08 per copy of the G variant. • Age-related macular degeneration risk (C2) ⚠ CAUTIOUS rsid : rs9332739 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21665990/ https://pubmed.ncbi.nlm.nih.gov/22705344/ Interpretation: Both copies at this position carry the G variant — a G/G genotype, with no copies of the protective C variant present. You do not carry the C2 E318D protective allele, so your risk for age-related macular degeneration at this marker is at the typical baseline rather than reduced. • Telomere length (OBFC1) rsid : rs9420907 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/35530816/ Interpretation: Both copies at this position carry the A variant — an A/A genotype, associated with shorter telomeres at this site. Neutral measurement, not a health benefit or risk on its own. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Age-related macular degeneration risk (HERC2) [rs1129038]: Both copies at this position carry the T risk variant — a T/T genotype, the higher-risk genotype at this single position. Risk for age-related macular degeneration is elevated above the C/C baseline, with each T copy contributing β ≈ 0.13 per copy — but the effect is small and on its own does not meaningfully predict your outcome. Bone density & fracture risk (LRP5) [rs3736228]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic bone-mineral-density profile sits at the favourable end — a lower fracture-risk position relative to T-carriers. Parental longevity (APOE region) [rs769449]: Both copies at this position carry the G variant — a G/G genotype, the most favourable combination for parental longevity at this site, with no copies of the e4-tagging A variant. Each G copy is associated with about beta 0.06 higher longevity score per copy. Later age at menopause (MCM8) [rs16991615]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the protective A variant present. You miss the small protective benefit that A-carriers get at this site for later age at menopause. Each A copy would shift the effect by β ≈ 0.93 per copy. Age-related macular degeneration risk (ARMS2) [rs10490924]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the T risk variant present. Your genetic risk for age-related macular degeneration sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by OR ≈ 1.75 per copy. Age-related macular degeneration risk (HTRA1) [rs11200638]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the A risk variant present. Your genetic risk for age-related macular degeneration sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.6 per copy. Telomere length (TERC) [rs1317082]: You have the A/A genotype at this TERC variant, associated with slightly shorter telomere length. This is a neutral measurement, not a good or bad health signal. Telomere length (TERT) [rs2736100]: You inherited one C variant and one A variant — a heterozygous C/A genotype. This places you between the longer-telomere C/C and the shorter-telomere A/A genotypes (about beta 0.08 per C copy). Informational only. Telomere length (TERT) [rs2853677]: You inherited one G variant and one A variant — a heterozygous G/A genotype. This places you between the longer-telomere G/G and the shorter-telomere A/A genotypes (about beta 0.06 per G copy). Informational only. Clonal hematopoiesis & myeloproliferative disorder risk (TERT) [rs2853677]: You inherited one G risk variant and one A baseline variant — a heterozygous G/A genotype, one allele from each parent. Risk for clonal hematopoiesis & myeloproliferative disorder is modestly higher than for people with the A/A baseline — about OR ≈ 1.32 per copy of the G variant. Telomere length (TERT) [rs7705526]: Both copies at this position carry the C variant — a C/C genotype, associated with shorter telomeres at this site (each A copy would add about beta 0.07). Neutral measurement, not a health benefit or risk on its own. Clonal hematopoiesis risk (TERT) [rs7705526]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the A risk variant present. Your genetic risk for clonal hematopoiesis sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.37 per copy. [Cognitive aging] — Checked, no unusual variants found — Memory performance & cognitive decline (APOE region) [rs769449]: Both copies at this position carry the protective G variant — a G/G genotype, the strongest protective combination at this site. Each G copy adds benefit toward memory performance & cognitive decline (β ≈ 0.03 per copy) compared to the A/A baseline. Lewy body dementia risk (APOE region) [rs769449]: You have the G/G genotype — no copies of the A allele, so no extra Lewy body dementia risk from this APOE-region marker. This reflects average background risk; age and other genes still apply. This marker does not determine your APOE ε-status, which requires rs429358 + rs7412 together. ──────────────────────────────────────────────────────────────────────── METABOLISM & WEIGHT ──────────────────────────────────────────────────────────────────────── [Blood sugar] • Fasting blood sugar & type 2 diabetes risk (GCK) rsid : rs4607517 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/25631608/ https://pubmed.ncbi.nlm.nih.gov/20081858/ https://pubmed.ncbi.nlm.nih.gov/28869590/ Interpretation: You inherited one A variant and one G reference — a heterozygous G/A genotype, one from each parent. The A allele is associated with slightly higher fasting blood sugar (β ≈ 0.06 per copy, study scale). This is a weak population-level association and, on its own, does not meaningfully predict your individual blood sugar. — Also checked, no unusual variants — Lower HbA1c independent of blood sugar (HFE) [rs1800562]: Both copies at this position carry the G reference variant — a G/G genotype, with no copies of the HbA1c-lowering A variant. Your HbA1c (independent of blood sugar) is expected to sit at the higher end of the range for this site — you do not carry the A allele that modestly reduces HbA1c. Per-copy effect: each A allele would lower HbA1c by β ≈ −0.11 (study scale). Fasting blood glucose (FADS1) [rs174550]: You have the C/C genotype at FADS1, associated with slightly lower fasting blood glucose on average (a small effect). Blood sugar (HbA1c) levels [rs10150332]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the HbA1c-associated C allele. Your genetic tendency for measured HbA1c sits at the lower end of this very small range; each C copy nudges it up by only about β ≈ 0.02 on the study scale. Fasting blood glucose & HbA1c (MTNR1B) [rs10830963]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the glucose-raising G allele. Your genetic tendency for measured fasting glucose and HbA1c sits at the lower end of the range; each G copy would nudge it up by about OR ≈ 1.33 per copy. Gout risk (GCKR) [rs1260326]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T variant. Relative to T-carriers this is a favourable position for gout, though the per-allele effect is small. Gout & high uric acid risk (ABCG2) [rs2231142]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copy of the reduced-function T variant. Your gout and high-uric-acid risk from this gene sits at the lower end of the spectrum, a favourable position relative to T-carriers. Each T copy raises gout odds by roughly OR ≈ 1.75 per copy. Kidney stones / nephrolithiasis risk (ABCG2) [rs2231142]: You have the G/G genotype — two copies of the normal-function ABCG2 allele, with no copy of the reduced-function T variant. Your ABCG2 uric-acid transporter works at full strength, so this variant does not add to your urate, gout, or kidney-stone risk. Other genes, diet, and hydration still matter. [BMI / body weight] • BMI & obesity risk (MC4R) rsid : rs17782313 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19151714/ https://pubmed.ncbi.nlm.nih.gov/19079261/ https://pubmed.ncbi.nlm.nih.gov/18454148/ Interpretation: You inherited one C risk variant and one T baseline variant — a heterozygous T/C genotype, one allele from each parent. Risk for bmi & obesity is modestly higher than for people with the T/T baseline — about OR ≈ 1.26 per copy of the C variant. • Body mass index (PPARG Pro12Ala) ⚠ CAUTIOUS rsid : rs1801282 Your geno : CG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36581621/ https://pubmed.ncbi.nlm.nih.gov/29273807/ https://pubmed.ncbi.nlm.nih.gov/30108127/ Interpretation: You inherited one G allele and one C allele — a heterozygous C/G genotype, one allele from each parent. The G allele is associated with a very slightly higher BMI measurement (about +0.02 per copy, study scale). The effect is tiny and, on its own, does not meaningfully predict your BMI. • Body weight & BMI (FTO) rsid : rs9939609 Your geno : TA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31513605/ https://pubmed.ncbi.nlm.nih.gov/19079261/ https://pubmed.ncbi.nlm.nih.gov/17434869/ Interpretation: You inherited one A allele and one T allele — a heterozygous T/A genotype, one allele from each parent. The A allele is associated with a modestly higher body-weight / BMI measurement (about +0.33 per copy, study scale). The effect is small per person and strongly modified by lifestyle, so on its own it does not meaningfully predict your weight. • Body mass index (MTCH2) ⚠ CAUTIOUS rsid : rs10838738 Your geno : AG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19079261/ Interpretation: You inherited one G allele and one A allele — a heterozygous A/G genotype, one allele from each parent. Measured BMI tends to sit marginally above the A/A group — about β ≈ 0.07 per copy of the G allele. This is a tiny nudge in a measurement, easily outweighed by diet and activity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Body weight & BMI (FTO) rsid : rs1121980 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30239722/ https://pubmed.ncbi.nlm.nih.gov/18454148/ Interpretation: You inherited one A variant and one G allele — a heterozygous G/A genotype. The A allele is associated with a modestly higher body weight and BMI (about β≈0.07 per copy) — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Waist-to-hip ratio & central fat (FTO) rsid : rs1121980 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/25673412/ Interpretation: You inherited one A variant and one G allele — a heterozygous G/A genotype. The A allele is associated with a modestly higher waist-to-hip ratio (about β≈0.05 per copy) — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • BMI & body weight (MC4R region) rsid : rs12970134 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19079260/ https://pubmed.ncbi.nlm.nih.gov/18454146/ Interpretation: You have the G/A genotype — one A weight-raising copy and one G copy. This is linked to a modestly higher body mass index and weight than G/G (about +0.3 kg/m2 per A copy). • Higher BMI & obesity risk (FTO) rsid : rs1421085 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/34836030/ https://pubmed.ncbi.nlm.nih.gov/40216759/ https://pubmed.ncbi.nlm.nih.gov/29381148/ Interpretation: You inherited one C variant and one T allele — a heterozygous T/C genotype. The C allele is associated with a modestly higher BMI (about OR≈1.18 per copy) — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Body weight & obesity risk (FTO) rsid : rs1558902 Your geno : TA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23563607/ https://pubmed.ncbi.nlm.nih.gov/21544081/ https://pubmed.ncbi.nlm.nih.gov/25673413/ Interpretation: You have the T/A genotype — one A allele and one T allele. The A allele is associated with a modestly higher body weight / BMI (about OR ≈ 1.14 per copy). This is a measurement nudge and a weak population-level association; on its own it does not meaningfully predict your individual weight, which depends heavily on diet, activity and many other genes. • Body weight & obesity risk (FTO) ⚠ CAUTIOUS rsid : rs17817449 Your geno : TG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/33045005/ https://pubmed.ncbi.nlm.nih.gov/21552555/ Interpretation: You have the T/G genotype — one G allele and one T allele. The G allele is associated with a slightly higher body weight / BMI (β ≈ 0.07 per copy on the study scale). This is a measurement nudge and a weak population-level association; on its own it does not meaningfully predict your individual weight. • Body weight & BMI (MAP2K5) rsid : rs2241423 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/20935630/ Interpretation: You have the A/A genotype — two copies of the BMI-lowering A allele. The A allele is associated with a slightly lower body weight / BMI (β ≈ 0.03 per copy on the study scale). Even with two copies this is a weak population-level association; on its own it does not meaningfully predict your individual weight. • Body weight & BMI (NEGR1) rsid : rs2815752 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/20935630/ https://pubmed.ncbi.nlm.nih.gov/19079261/ Interpretation: You have the A/A genotype — two copies of the A allele. The A allele is associated with a modestly higher body weight / BMI (β ≈ 0.13 per copy on the study scale). Even with two copies this is a weak population-level association; on its own it does not meaningfully predict your individual weight, which depends far more on diet and activity. • Body weight & BMI (KCTD15) ⚠ CAUTIOUS rsid : rs29941 Your geno : GG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19079260/ https://pubmed.ncbi.nlm.nih.gov/28892062/ https://pubmed.ncbi.nlm.nih.gov/25673413/ Interpretation: Both copies at this position carry the G variant — a G/G genotype. People with G/G sit at the slightly higher end of the BMI range for this SNP, but the per-allele effect is very small (β ≈ 0.015 per copy, standardized units) and not individually meaningful. • Higher BMI tendency (FTO) rsid : rs3751812 Your geno : GT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/28448500/ Interpretation: You inherited one T variant and one G reference — a heterozygous G/T genotype. The T allele is associated with a modestly higher BMI (β ≈ 0.08 per copy, study scale). This is a weak population-level association and, on its own, does not meaningfully predict your individual weight. • Body weight & BMI (MTCH2) rsid : rs3817334 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/25673413/ https://pubmed.ncbi.nlm.nih.gov/20935630/ Interpretation: You inherited one T variant and one C reference — a heterozygous C/T genotype, one from each parent. The T allele is associated with a slightly higher BMI (β ≈ 0.03 per copy, study scale) — too small to be a meaningful personal signal on its own. • Body weight & BMI (MC4R region) rsid : rs6567160 Your geno : TC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36581621/ https://pubmed.ncbi.nlm.nih.gov/29381148/ https://pubmed.ncbi.nlm.nih.gov/31504550/ Interpretation: You carry one C allele and one T allele — a heterozygous T/C genotype, one from each parent. On average this is associated with a slightly higher BMI/body-weight measurement than T/T (about β ≈ 0.03 per C copy on the study scale). This is a weak population-level association and does not on its own meaningfully predict your individual weight. • Body weight & BMI (near ADCY3) rsid : rs713586 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/28892062/ https://pubmed.ncbi.nlm.nih.gov/20935630/ Interpretation: Both copies here carry the C allele — a C/C genotype. On average this is associated with a slightly higher BMI/body-weight measurement than T/T (about β ≈ 0.03 per C copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual weight. • Body weight & obesity risk (FAIM2) rsid : rs7138803 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/33045005/ https://pubmed.ncbi.nlm.nih.gov/26604143/ https://pubmed.ncbi.nlm.nih.gov/19079260/ Interpretation: Both copies here carry the A allele — an A/A genotype. On average this is associated with a slightly higher body-weight / BMI measurement than G/G (about OR ≈ 1.13 per A copy). The per-copy effect is small — a weak population-level signal, not a prediction of your individual weight. • Higher BMI & body weight (near TMEM18) rsid : rs7561317 Your geno : AG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19079260/ Interpretation: You inherited one G variant and one A baseline variant — a heterozygous A/G genotype. Your tendency toward higher BMI and body weight is modestly above the A/A baseline — on the order of +0.5 kg/m2 BMI per G copy in real-world terms. • Body weight & BMI (ETV5/SFRS10 region) rsid : rs7647305 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19079260/ Interpretation: Both copies here carry the C allele — a C/C genotype. On average this is associated with a slightly higher BMI/body-weight measurement than T/T (about β ≈ 0.04 per C copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual weight. • Body weight & BMI (FTO) rsid : rs8050136 Your geno : CA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19079260/ https://pubmed.ncbi.nlm.nih.gov/24348519/ Interpretation: You inherited one A variant and one C baseline variant — a heterozygous C/A genotype. Your tendency toward higher BMI and body weight is modestly above the C/C baseline — about +0.08 kg/m2 BMI per A copy on the study scale (~+0.4 kg/m2 in real-world terms). Diet and activity matter more than this single marker. • Body weight & obesity tendency (TFAP2B) rsid : rs987237 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23563607/ https://pubmed.ncbi.nlm.nih.gov/20935630/ https://pubmed.ncbi.nlm.nih.gov/26604143/ Interpretation: You have one G and one A allele — a heterozygous A/G genotype, one from each parent. The G allele is associated with a modestly higher body weight / BMI at the population level (about OR ≈ 1.2 per copy). This is a measurement-level association, not a disease prediction, and lifestyle matters more than the genotype. • Body weight & BMI tendency (FTO) rsid : rs9930506 Your geno : AG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/40465716/ https://pubmed.ncbi.nlm.nih.gov/17658951/ Interpretation: You have one G and one A allele — a heterozygous A/G genotype, one from each parent. The G allele is associated with a modestly higher body weight / BMI at the population level (about β ≈ 0.12 per copy). This is a measurement-level association, not a disease prediction. • Body weight & obesity tendency (FTO region) rsid : rs9941349 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19553259/ Interpretation: You have one T and one C allele — a heterozygous C/T genotype, one from each parent. The T allele is associated with a higher body weight / BMI at the population level (about OR ≈ 1.48 per copy). This is a measurement-level association, not a disease prediction, and lifestyle matters too. • Body weight & obesity tendency (BDNF) ⚠ CAUTIOUS rsid : rs6265 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/28892062/ https://pubmed.ncbi.nlm.nih.gov/19079260/ Interpretation: Both copies here carry the C allele — a C/C genotype, with no copies of the T allele. The T allele is weakly associated with a slightly lower body weight / BMI at the population level (about β ≈ 0.04 per copy), so relative to T-carriers this genotype sits marginally higher. The effect is tiny and on its own does not meaningfully predict your individual weight; it is a measurement nudge, not a disease. • Body weight & BMI (BDNF) rsid : rs11030104 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/26961502/ https://pubmed.ncbi.nlm.nih.gov/25673413/ https://pubmed.ncbi.nlm.nih.gov/24861553/ Interpretation: Both copies at this position carry the A allele — an A/A genotype. The A allele is associated with a modestly higher BMI (about +0.04 units per copy on the study scale), so an A/A reading sits slightly toward the higher-BMI end of this single-marker range. This is a measurement nudge, not a disease finding; one common variant has only a tiny effect on your actual body weight, which is shaped far more by overall genetics, diet and activity. • Adult height (HMGA2) rsid : rs1042725 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/18391950/ Interpretation: You have one C and one T allele (C/T) — an intermediate effect, with adult height nudged toward the middle relative to C/C and T/T. As always, this single variant contributes only a tiny amount to your overall height. • Body weight & BMI (TMEM18 region) rsid : rs12140153 Your geno : GG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36581621/ Interpretation: Both copies at this position carry the G allele — a G/G genotype. The G allele is associated with a modestly higher BMI (about +0.04 units per copy on the study scale), so a G/G reading sits slightly toward the higher-BMI end of this single-marker range. This is a measurement nudge, not a disease finding; one common variant has only a tiny effect on your actual body weight, which is shaped far more by overall genetics, diet and activity. • Adult height (GDF5) rsid : rs143384 Your geno : AG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36224396/ Interpretation: You inherited one G variant and one A variant — a heterozygous G/A genotype, placing you in the middle of the adult-height range between the shorter A/A and taller G/G (per-copy beta ≈ 0.08 SD). A tiny contribution to overall height. — Also checked, no unusual variants — Body weight & BMI (NRXN3) [rs10146997]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G allele. At this NRXN3 marker A tracks with the slightly lower end of the BMI measurement. Each G copy is associated with a modestly higher BMI (about beta ≈ 0.03 on the study scale) — a measurement nudge, not a disease risk. Higher BMI & body weight (NRXN3) [rs10150332]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the BMI-associated C allele. Your genetic tendency for measured BMI sits at the lower end of this very small range; each C copy nudges it up by only about β ≈ 0.03 on the study scale. Body weight & BMI (SH2B1 region) [rs10913469]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the BMI-associated C allele. Your genetic tendency for measured body weight and BMI sits at the lower end of this very small range; each C copy nudges it up by only about β ≈ 0.05 on the study scale. Abdominal obesity & metabolic syndrome risk [rs10913469]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the C allele. Your genetic tendency for abdominal obesity / metabolic syndrome sits at the lower end of this small range (each C copy would add only about OR ≈ 1.1) — a weak population-level association that does not, on its own, meaningfully predict your individual outcome. Higher BMI & obesity risk (GNPDA2) [rs10938397]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G variant. Relative to G-carriers, this sits at the lower end for BMI, but the per-allele effect is small. Body weight & obesity tendency (LRRN6C/NTRK2 region) [rs10968576]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G variant. Relative to G-carriers this sits at the lower end for body weight, but the per-allele effect is small. Body weight & obesity risk (BMI) [rs2112347]: You have the T/G genotype — one G allele and one T allele. The G allele is associated with a slightly lower body weight / BMI (β ≈ 0.03 per copy on the study scale). This is a measurement nudge and a weak population-level association; on its own it does not meaningfully predict your individual weight. Body weight & BMI (MC4R variant) [rs2229616]: You have the C/C genotype — no copies of the BMI-lowering T allele. At this MC4R marker your body-weight association sits slightly above T-carriers. The per-allele T effect is small (β ≈ 0.09 on the study scale), so this single marker does not meaningfully predict your individual weight on its own. Body weight & BMI (TMEM18) [rs2867125]: You have the T/C genotype — one C allele and one T allele. The C allele is associated with a modestly higher body weight / BMI (β ≈ 0.07 per copy on the study scale). This is a measurement nudge and a weak population-level association; on its own it does not meaningfully predict your individual weight. Higher BMI & body fat tendency (SEC16B) [rs543874]: Both copies at this position carry the A reference allele — an A/A genotype, with no copies of the G variant. The G allele is associated with a slightly higher BMI / body fat on average; you carry none, so this SNP sits at the lower end of its small range for you. Per-copy effect: β ≈ 0.03 (study scale). Body weight & BMI (MC4R region) [rs571312]: You inherited one A variant and one C reference — a heterozygous C/A genotype, one from each parent. The A allele is associated with a slightly higher BMI (β ≈ 0.06 per copy, study scale) — too small to be a meaningful personal signal on its own. Waist-to-hip ratio (body fat distribution) [rs727428]: You have one C and one T allele — a heterozygous T/C genotype, one from each parent. The C allele is weakly associated with a slightly lower waist-to-hip ratio at the population level (about β ≈ 0.01 per copy, study scale). This is a very small measurement-level association, not a disease prediction, and on its own it does not meaningfully predict your individual body-fat distribution. [Type 2 diabetes predisposition] • Type 2 diabetes risk (PPARG Pro12Ala) rsid : rs1801282 Your geno : CG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17463248/ https://pubmed.ncbi.nlm.nih.gov/17463249/ https://pubmed.ncbi.nlm.nih.gov/17463246/ Interpretation: You inherited one C allele and one G allele — a heterozygous C/G genotype, one allele from each parent. The C allele carries a weak population-level association with slightly higher odds of type 2 diabetes (about OR ≈ 1.16 per copy). The effect is small and, on its own, does not meaningfully predict your individual outcome. • Type 2 diabetes risk (TCF7L2) rsid : rs7903146 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38374256/ https://pubmed.ncbi.nlm.nih.gov/39379762/ https://pubmed.ncbi.nlm.nih.gov/32541925/ Interpretation: You inherited one T risk variant and one C baseline variant — a heterozygous C/T genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the C/C baseline — about OR ≈ 1.58 per copy of the T variant. • Type 2 diabetes risk (FTO) rsid : rs9939609 Your geno : TA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/22693455/ https://pubmed.ncbi.nlm.nih.gov/17554300/ Interpretation: You inherited one A risk variant and one T baseline variant — a heterozygous T/A genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the T/T baseline — about OR ≈ 1.25 per copy of the A variant. • Type 1 diabetes risk (HLA-DQ) rsid : rs9273363 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/40465716/ https://pubmed.ncbi.nlm.nih.gov/30659077/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the highest-risk combination at this site. Risk for type 1 diabetes is elevated above the C/C baseline, with each A copy contributing OR ≈ 5.48 per copy. • Type 2 diabetes risk (CDKN2A/2B) rsid : rs10811661 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39379762/ https://pubmed.ncbi.nlm.nih.gov/35956399/ https://pubmed.ncbi.nlm.nih.gov/35551307/ Interpretation: Both copies at this position carry the T allele — a T/T genotype. The T allele is weakly associated with slightly higher type-2-diabetes odds (about OR ≈ 1.17 per copy), so T/T sits at the upper end of this small range. This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Type 2 diabetes & blood sugar (FTO) rsid : rs1121980 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/40436827/ Interpretation: You inherited one A variant and one G allele — a heterozygous G/A genotype. The A allele is associated with slightly higher blood sugar (about β≈0.02 per copy) — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Type 2 diabetes risk (GCKR) ⚠ CAUTIOUS rsid : rs1260326 Your geno : CC Evidence : GWAS (binary) Source : https://www.ebi.ac.uk/gwas/variants/rs1260326 Interpretation: You have the C/C genotype at GCKR, carrying two copies of the C allele linked to a small increase in type 2 diabetes risk — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Type 2 diabetes risk (MC4R region) rsid : rs12970134 Your geno : GA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/22885922/ https://pubmed.ncbi.nlm.nih.gov/24509480/ Interpretation: You inherited one A variant and one G allele — a heterozygous G/A genotype. The A allele carries a weak association with type 2 diabetes (about OR≈1.08 per copy) — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Type 2 diabetes risk (FTO) rsid : rs1421085 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30297969/ https://pubmed.ncbi.nlm.nih.gov/30718926/ https://pubmed.ncbi.nlm.nih.gov/26818947/ Interpretation: You inherited one C variant and one T allele — a heterozygous T/C genotype. The C allele carries a weak association with type 2 diabetes (about OR≈1.14 per copy) — a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Type 2 diabetes risk (IGF2BP2) rsid : rs1470579 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23945395/ https://pubmed.ncbi.nlm.nih.gov/20581827/ https://pubmed.ncbi.nlm.nih.gov/20523342/ Interpretation: You have the C/C genotype — two copies of the C allele. The C allele is linked to modestly higher odds of type 2 diabetes (about OR ≈ 1.18 per copy, so roughly OR ≈ 1.4 for two copies). This remains a weak population-level association; on its own it does not meaningfully predict your individual outcome, and lifestyle and other genes matter far more. • Type 2 diabetes risk (FTO) rsid : rs1558902 Your geno : TA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38374256/ Interpretation: You inherited one A risk variant and one T baseline variant — a heterozygous T/A genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the T/T baseline — about β ≈ 0.13 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fasting glucose & type 2 diabetes risk (GCK/MTNR1B region) rsid : rs2191349 Your geno : GT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25631608/ https://pubmed.ncbi.nlm.nih.gov/20081858/ https://pubmed.ncbi.nlm.nih.gov/32541925/ Interpretation: You have the G/T genotype — one T allele and one G allele. The T allele is associated with a modestly higher fasting glucose level (β ≈ 0.07 per copy on the study scale). This is a measurement nudge and a weak population-level association; on its own it does not meaningfully predict your individual glucose or diabetes outcome. • Type 2 diabetes risk (KCNQ1) rsid : rs2237892 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19401414/ https://pubmed.ncbi.nlm.nih.gov/18711367/ https://pubmed.ncbi.nlm.nih.gov/21573907/ Interpretation: You have the C/C genotype — no copies of the protective T allele. At this KCNQ1 marker your type 2 diabetes association sits slightly above T-carriers. The per-allele effect is small (β ≈ 0.1 on the study scale), so this single marker does not meaningfully predict your individual outcome on its own. • Type 2 diabetes risk (KCNQ1) rsid : rs2237895 Your geno : AC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30297969/ https://pubmed.ncbi.nlm.nih.gov/20174558/ Interpretation: You inherited one C risk variant and one A baseline variant — a heterozygous A/C genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the A/A baseline — about OR ≈ 1.25 per copy of the C variant. • Type 2 diabetes risk (KCNQ1) rsid : rs2237897 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38685053/ https://pubmed.ncbi.nlm.nih.gov/38374256/ https://pubmed.ncbi.nlm.nih.gov/35551307/ Interpretation: Both copies at this position carry the C risk variant — a C/C genotype, the higher-risk genotype at this single position. Risk for type 2 diabetes is elevated above the T/T baseline, with each C copy contributing OR ≈ 1.22 per copy — but the effect is small and on its own does not meaningfully predict your diabetes outcome. • Type 2 diabetes risk (CDKN2A/B) rsid : rs2383208 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/23209189/ https://pubmed.ncbi.nlm.nih.gov/22961080/ https://pubmed.ncbi.nlm.nih.gov/19401414/ Interpretation: Both copies at this position carry the A risk variant — a A/A genotype, the higher-risk genotype at this single position. Risk for type 2 diabetes is elevated above the G/G baseline, with each A copy contributing OR ≈ 1.22 per copy — but the effect is small and on its own does not meaningfully predict your diabetes outcome. • Type 2 diabetes & insulin resistance risk (IRS1) ⚠ CAUTIOUS rsid : rs2943641 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/32042192/ https://pubmed.ncbi.nlm.nih.gov/31178129/ Interpretation: You have the T/C genotype — one C allele and one T allele. The C allele is associated with a slightly higher type 2 diabetes / insulin-resistance signal (β ≈ 0.06 per copy on the study scale). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Type 2 diabetes risk (IGF2BP2) ⚠ CAUTIOUS rsid : rs4402960 Your geno : TT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17463249/ https://pubmed.ncbi.nlm.nih.gov/17463248/ https://pubmed.ncbi.nlm.nih.gov/17463246/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. Two copies put you at the higher end of this SNP's modest range (OR ≈ 1.16 per copy), but this is a weak population-level association that, on its own, does not meaningfully predict your individual outcome. • Type 2 diabetes risk (TCF7L2) rsid : rs4506565 Your geno : AT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/25631608/ https://pubmed.ncbi.nlm.nih.gov/20081858/ https://pubmed.ncbi.nlm.nih.gov/17554300/ Interpretation: You inherited one T risk variant and one A baseline variant — a heterozygous A/T genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the A/A baseline — about OR ≈ 1.36 per copy of the T variant. • Type 2 diabetes risk (KCNJ11) rsid : rs5215 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/22885922/ https://pubmed.ncbi.nlm.nih.gov/17463249/ https://pubmed.ncbi.nlm.nih.gov/18372903/ Interpretation: You inherited one C allele and one T allele — a heterozygous C/T genotype, one from each parent. The C allele carries a slightly higher type 2 diabetes association than the T allele (β ≈ 0.06 per copy, study scale). This is a weak population-level association and, on its own, does not meaningfully predict your individual outcome. • Type 2 diabetes risk (KCNJ11) ⚠ CAUTIOUS rsid : rs5219 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17463248/ https://pubmed.ncbi.nlm.nih.gov/17463246/ https://pubmed.ncbi.nlm.nih.gov/19056611/ Interpretation: You inherited one T allele and one C allele — a heterozygous T/C genotype, one from each parent. The T allele carries a very small higher type 2 diabetes association than the C allele (OR ≈ 1.04 per copy) — a weak population-level association that, on its own, does not meaningfully predict your individual outcome. • Type 2 diabetes risk (MC4R region) rsid : rs6567160 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/35551307/ https://pubmed.ncbi.nlm.nih.gov/32541925/ Interpretation: You carry one C allele and one T allele — a heterozygous T/C genotype, one from each parent. On average this is associated with slightly higher odds of type 2 diabetes than T/T (about OR ≈ 1.07 per C copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. • Type 2 diabetes risk (CDKAL1) ⚠ CAUTIOUS rsid : rs7754840 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17463248/ https://pubmed.ncbi.nlm.nih.gov/17463246/ https://pubmed.ncbi.nlm.nih.gov/22961080/ Interpretation: Both copies here carry the G allele — a G/G genotype, with no copies of the C allele. On average, people with G/G sit slightly lower on this population-level association for type 2 diabetes than C-carriers (about OR ≈ 1.18 per C copy). • Type 2 diabetes risk (GCKR) rsid : rs780094 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39379762/ https://pubmed.ncbi.nlm.nih.gov/30054458/ https://pubmed.ncbi.nlm.nih.gov/22885922/ Interpretation: Both copies carry the C allele — a C/C genotype. Each C copy is weakly associated with type 2 diabetes at the population level (about OR ≈ 1.06 per copy), a small effect that on its own does not meaningfully predict your individual outcome. Note GCKR is pleiotropic: this same allele is associated with lower triglycerides and CRP, so it is favourable on the lipid side. • Type 2 diabetes risk (TCF7L2) rsid : rs7901695 Your geno : TC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30718926/ https://pubmed.ncbi.nlm.nih.gov/21347282/ https://pubmed.ncbi.nlm.nih.gov/17463249/ Interpretation: You inherited one C risk variant and one T baseline variant — a heterozygous T/C genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the T/T baseline — about OR ≈ 1.36 per copy of the C variant. • Type 2 diabetes risk (FTO) rsid : rs8050136 Your geno : CA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/17463248/ https://pubmed.ncbi.nlm.nih.gov/17463249/ https://pubmed.ncbi.nlm.nih.gov/18372903/ Interpretation: You have one A and one C allele — a heterozygous C/A genotype, one from each parent. The A allele carries a weak population-level association with type 2 diabetes (about OR ≈ 1.16 per copy); on its own it does not meaningfully predict your individual outcome. FTO acts largely through body weight, so lifestyle matters more than the genotype here. • Type 2 diabetes risk (HMGA2) ⚠ CAUTIOUS rsid : rs1042725 Your geno : CT Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30297969/ Interpretation: You inherited one T allele and one C allele — a heterozygous C/T genotype, one from each parent. The T allele carries a weak population-level association with slightly higher type 2 diabetes odds (~5% per copy); a single copy does not meaningfully shift your personal risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Gestational diabetes risk (MTNR1B) ⚠ CAUTIOUS rsid : rs10830962 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/22233651/ Interpretation: If you have the C/C genotype, you carry no copies of the higher-glucose G allele at this MTNR1B position, so on this variant your gestational-diabetes risk is at the lower, baseline level. Many other genes, body weight, and lifestyle also affect pregnancy glucose, and routine antenatal screening still applies. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Type 2 diabetes predisposition ⚠ CAUTIOUS rsid : rs12140153 Your geno : GG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38374256/ Interpretation: Both copies at this position carry the G allele — a G/G genotype. The G allele shows a weak population-level association with slightly higher type 2 diabetes odds (about 7% per copy, OR≈1.07). On its own this small per-allele effect does not meaningfully predict your individual outcome. • Fasting glucose & type 2 diabetes risk (MTNR1B) ⚠ CAUTIOUS rsid : rs1387153 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/19060909/ https://pubmed.ncbi.nlm.nih.gov/20581827/ https://pubmed.ncbi.nlm.nih.gov/20858683/ Interpretation: Both copies at this position carry the C allele — a C/C genotype, with no copies of the T allele. The T allele is associated with modestly higher fasting glucose and a weak population-level association with slightly higher type 2 diabetes odds (about 9% per copy, OR≈1.09). With no T copies, this sits at the lower-glucose end of this range, though the per-allele difference is small. • Type 1 diabetes risk (PTPN22) rsid : rs2476601 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/39749473/ Interpretation: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for type 1 diabetes is modestly higher than for people with the G/G baseline — about β ≈ 0.43 per copy of the A variant. • Type 2 diabetes risk (DENND1A) ⚠ CAUTIOUS rsid : rs2479106 Your geno : AG Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38374256/ Interpretation: You have the A/G genotype — one copy of the variant linked to a small increase in type 2 diabetes risk. — Also checked, no unusual variants — Type 2 diabetes risk (SLC30A8) [rs13266634]: You inherited one C allele and one T allele — a heterozygous C/T genotype, one allele from each parent. The C allele carries a weak population-level association with slightly higher odds of type 2 diabetes (about OR ≈ 1.14 per copy). The effect is small and, on its own, does not meaningfully predict your individual outcome. Type 2 diabetes risk (NRXN3) [rs10146997]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G allele. The G allele shows a weak population-level association with type 2 diabetes (about OR 1.07 per copy), so this marker on its own does not meaningfully predict your individual diabetes risk. Type 2 diabetes risk (TCF7L2) [rs12255372]: You have the G/G genotype at this TCF7L2 variant — no copies of the T risk allele. This is the lower-risk version at this SNP; it does not add genetic risk of type 2 diabetes. Type 2 diabetes risk (LPL) [rs328]: You inherited one C variant and one G variant — a heterozygous C/G genotype, one allele from each parent. The C allele carries a slightly higher type 2 diabetes risk, but the per-copy effect is very small (OR ≈ 1.05) and not individually meaningful. Type 2 diabetes risk (HLA-DQ region) [rs7454108]: Both copies at this position carry the T variant — a T/T genotype, with no copies of the C variant that tags the HLA-DQ8 haplotype. The single study linking C to type-2-diabetes risk reports only a small per-copy effect (OR ≈ 1.14), so this site is not a meaningful individual signal. This is a tag-SNP estimate, not HLA typing. Type 2 diabetes risk (MTNR1B) [rs10830963]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the G risk variant present. Your genetic risk for type 2 diabetes sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by OR ≈ 1.41 per copy. Gestational diabetes risk (MTNR1B) [rs10830963]: Both copies here carry the C variant — a C/C genotype, with no copies of the G risk variant. If you become pregnant, your genetic risk for gestational diabetes sits at the lower end of the spectrum, a favourable position relative to G-carriers. Outside of pregnancy this variant carries no gestational-diabetes signal. Each G copy would raise risk by OR ≈ 1.41 per copy. Type 2 diabetes predisposition (GNPDA2) [rs10938397]: You have the A/A genotype and do not carry the GNPDA2 variant linked to higher type 2 diabetes risk. Type 2 diabetes risk (CDKAL1) [rs10946398]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the C variant. Relative to C-carriers this is a favourable position, though the per-allele effect is small. Type 2 diabetes risk (SLC30A8) [rs11558471]: You inherited one A risk variant and one G baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the G/G baseline — about OR ≈ 1.25 per copy of the A variant. Type 2 diabetes risk (TMEM18) [rs2867125]: You have the T/C genotype — one C allele and one T allele. The C allele is linked to slightly higher odds of type 2 diabetes (about OR ≈ 1.06 per copy). This is a weak population-level association; on its own it does not meaningfully predict your individual outcome. Type 2 diabetes risk (SLC30A8) [rs3802177]: You inherited one G allele and one A allele — a heterozygous G/A genotype, one from each parent. The G allele carries a slightly higher type 2 diabetes association than the A allele (β ≈ 0.07 per copy, study scale). This is a weak population-level association and, on its own, does not meaningfully predict your individual outcome. Type 2 diabetes risk (SEC16B, weight-mediated) [rs543874]: Both copies at this position carry the A reference allele — an A/A genotype, with no copies of the G variant. The G allele shows a small association with higher type 2 diabetes odds (largely via body weight); you carry none, so you sit at the lower end of this SNP's small range. Per-copy effect: β ≈ 0.05 (study scale). Type 2 diabetes risk (CDKAL1) [rs7756992]: Both copies here carry the A allele — an A/A genotype, with no copies of the G allele. On average, people with A/A sit slightly lower on this population-level association for type 2 diabetes than G-carriers (about OR ≈ 1.11 per G copy). Fasting blood glucose & type 2 diabetes risk (MTNR1B) [rs10830962]: Both copies at this position carry the C allele — a C/C genotype, with no copies of the glucose-raising G allele. Your genetic contribution to fasting glucose at this MTNR1B SNP sits at the lower end — a favourable position relative to G-carriers. Type 2 diabetes risk (HNF1A) [rs1169288]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the C allele. The C allele shows only a weak population-level association with type 2 diabetes at this site (about OR ≈ 1.04 per copy), so being A/A removes even that small statistical nudge. Type 2 diabetes risk (HNF4A) [rs1800961]: Both copies at this position are the C allele — a C/C genotype, with no copies of the T allele. The T allele carries a weak association with type 2 diabetes, so C/C sits at the lower end of this small signal. The per-copy effect is modest (OR ≈ 1.16) and does not, by itself, predict your individual outcome. Type 2 diabetes risk (SHBG pathway) [rs727428]: You inherited one T risk variant and one C baseline variant — a heterozygous T/C genotype, one allele from each parent. Risk for type 2 diabetes is modestly higher than for people with the C/C baseline — about β ≈ 0.02 per copy of the T variant. [Lipids & cholesterol] • Fenofibrate response in hypertriglyceridemia (APOE) rsid : rs7412 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12042669/ Summary : rs7412 is one of the two SNPs that define APOE type; the T allele (ALT) is the ε2-defining allele. In people with high triglycerides treated with fenofibrate, ε2 (T-allele) carriers have been reported to get a larger triglyceride drop than people with the common C/C genotype — in one study triglyceride reductions were about 53% for ε2 versus roughly 33-36% for other types. ε2 carriers also tend to start with higher triglycerides. Findings are not unanimous (a larger study found no APOE effect), so this is a tendency rather than a rule, and fenofibrate lowers triglycerides across APOE types. It is only relevant if you take fenofibrate. Interpretation: If you have the C/C genotype and hypertriglyceridemia, you may have a decreased response to fenofibrate compared to people with the C/T or T/T genotype (carriers of E2 or E2/E2). Other genetic and clinical factors can also influence how you respond to fenofibrate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Triglyceride levels (FADS1) rsid : rs174546 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ https://pubmed.ncbi.nlm.nih.gov/20686565/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. The T allele is associated with higher triglycerides (about +0.07 SD per copy) but also with lower LDL and total cholesterol at this pleiotropic FADS1 locus. The triglyceride shift is small, so we treat it as neutral. • LDL cholesterol (FADS1) rsid : rs174547 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31566214/ https://pubmed.ncbi.nlm.nih.gov/29615537/ https://pubmed.ncbi.nlm.nih.gov/19060906/ Interpretation: Both copies at this position carry the C variant — a C/C genotype. The C allele is associated with lower LDL/non-HDL cholesterol (about −0.04 SD per copy) but with higher triglycerides at this pleiotropic FADS1 locus. The shift is small, so neutral. • Omega-6 fatty acid metabolism (FADS1) rsid : rs174547 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/26584805/ https://pubmed.ncbi.nlm.nih.gov/24823311/ Interpretation: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the omega-6 fatty acid metabolism range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 1.69 per copy. • Omega-3/Omega-6 fatty acid metabolism (FADS1) rsid : rs174550 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24823311/ Interpretation: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the omega-3/omega-6 fatty acid metabolism range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.05 per copy. • LDL & total cholesterol (FADS1) ⚠ CAUTIOUS rsid : rs174550 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39414775/ Interpretation: Both copies carry the C allele — a C/C genotype. At this FADS1 marker each C copy is associated with a modestly lower LDL / total-cholesterol measurement (about beta ≈ 0.06 per copy on the study scale). This is a measurement nudge, not a disease risk. • Triglyceride levels (FADS1) rsid : rs174550 Your geno : CC Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs174550 Interpretation: You have the C/C genotype at FADS1 — no copies of the triglyceride-lowering T allele, so C/C sits toward the higher end of the triglyceride range. • LDL & total cholesterol (FADS1/FADS2) rsid : rs174583 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/29507422/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. The T allele is associated with lower LDL/total cholesterol (about −0.07 SD per copy), so T/T sits at the lower-cholesterol end at this site. The effect is small, so neutral. • Omega-3 fatty acid levels (FADS1/FADS2) rsid : rs174583 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/25646338/ https://pubmed.ncbi.nlm.nih.gov/35120996/ https://pubmed.ncbi.nlm.nih.gov/35050183/ Interpretation: Both copies at this position carry the T variant — a T/T genotype, with no copies of the omega-3-preserving C variant. The T allele is associated with lower long-chain omega-3, so you miss the small upward shift C-carriers get. Each C copy would shift omega-3 by about +0.08 SD. • HDL ("good") cholesterol level (LIPC) rsid : rs1800588 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/40841581/ https://pubmed.ncbi.nlm.nih.gov/33339817/ Interpretation: You inherited one protective T variant and one C variant — a heterozygous C/T genotype, one allele from each parent. You get partial protective benefit for hdl ("good") cholesterol level relative to the C/C baseline — about β ≈ 0.12 per copy of the T variant. • Triglyceride levels (LPL S447X) rsid : rs328 Your geno : CG Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32150548/ https://pubmed.ncbi.nlm.nih.gov/35945198/ https://pubmed.ncbi.nlm.nih.gov/22171074/ Interpretation: You inherited one G variant and one C variant — a heterozygous C/G genotype, one allele from each parent. The single G copy (the LPL S447X form) modestly lowers your triglycerides relative to C/C — a small favourable shift (β ≈ 0.19 per copy). • HDL ('good') cholesterol level (CETP) rsid : rs3764261 Your geno : CA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/33499410/ https://pubmed.ncbi.nlm.nih.gov/31211820/ https://pubmed.ncbi.nlm.nih.gov/30911093/ Interpretation: You inherited one protective A variant and one C variant — a heterozygous C/A genotype, one allele from each parent. You get partial protective benefit for hdl ('good') cholesterol level relative to the C/C baseline — about β ≈ 0.23 per copy of the A variant. • HDL cholesterol level (CETP) rsid : rs5882 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/35945198/ Interpretation: You inherited one G (Val) variant and one A (Ile) variant — a heterozygous G/A genotype, one allele from each parent. The single G copy is associated with modestly higher HDL than A/A (β ≈ 0.09 per copy) — a small favourable nudge. • Metabolic syndrome risk (APOA5) ⚠ CAUTIOUS rsid : rs662799 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/38201907/ https://pubmed.ncbi.nlm.nih.gov/31910446/ https://pubmed.ncbi.nlm.nih.gov/29212154/ Interpretation: Both copies at this position carry the A variant — an A/A genotype (the −1131T form at both copies), with no copies of the G (−1131C) risk allele. Your APOA5-related triglyceride and metabolic-syndrome risk sits at the lower end at this site — a favourable position relative to G-carriers. • HDL cholesterol level (CETP) rsid : rs708272 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39091897/ Interpretation: You inherited one protective A variant and one G variant — a heterozygous G/A genotype, one allele from each parent. You get partial protective benefit for hdl cholesterol level relative to the G/G baseline — about β ≈ 0.07 per copy of the A variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Total and LDL cholesterol (FGF21 region) ⚠ CAUTIOUS rsid : rs838145 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/41044249/ https://pubmed.ncbi.nlm.nih.gov/34594039/ Interpretation: Both copies at this position carry the A allele — an A/A genotype. The A allele is associated with marginally lower measured total/LDL cholesterol (about β ≈ 0.02 per copy on the study scale) — a small, favourable nudge in a routine blood measurement relative to G-carriers. • Body mass index / obesity (FTO) ⚠ CAUTIOUS rsid : rs1121980 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/28334899/ https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You have the G/A genotype — one A weight-raising copy and one G copy. This is linked to a modestly higher body mass index than G/G (about +0.07 per copy on the study scale). The effect is real but modest and is reduced by an active lifestyle. • Triglycerides & LDL cholesterol (GCKR) ⚠ CAUTIOUS rsid : rs1260326 Your geno : CC Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs1260326 Interpretation: You have the C/C genotype at GCKR, associated with lower triglyceride levels (and, via the same variant, higher fasting glucose). • LDL & total cholesterol levels (LDLR) ⚠ CAUTIOUS rsid : rs2228671 Your geno : CT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31217584/ Interpretation: You inherited one T allele and one C reference allele — a heterozygous C/T genotype at LDLR rs2228671. The T allele lowers LDL-C by ≈0.19 mmol/L per copy and is associated with reduced coronary-artery-disease risk (per-allele OR≈0.82–0.83). One T copy gives you a modest favourable shift versus C/C. • LDL & total cholesterol (CELSR2/SORT1) rsid : rs646776 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30911093/ https://pubmed.ncbi.nlm.nih.gov/38116116/ Interpretation: Both copies here carry the T allele — a T/T genotype. On average this is associated with a modestly higher LDL/total-cholesterol measurement than C/C (about β ≈ 0.17 per T copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual cholesterol. • LDL cholesterol & coronary artery disease risk (LDLR) rsid : rs6511720 Your geno : GT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31393916/ https://pubmed.ncbi.nlm.nih.gov/29212778/ Interpretation: You carry one G allele and one T allele — a heterozygous G/T genotype, one from each parent. The T allele is associated with a slightly lower LDL-cholesterol measurement (about β ≈ 0.23 per T copy on the study scale), so G/T sits between the two homozygous groups. This is a weak population-level association and does not on its own meaningfully predict your individual LDL. • LDL cholesterol & apolipoprotein B levels (APOB) rsid : rs693 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/41044249/ https://pubmed.ncbi.nlm.nih.gov/35213538/ Interpretation: Both copies here carry the A allele — an A/A genotype. On average this is associated with a slightly higher LDL / apoB measurement than G/G (about β ≈ 0.06 per A copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual LDL or apoB. • Triglyceride & HDL cholesterol levels (GCKR) rsid : rs780094 Your geno : CC Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs780094 Interpretation: You have the C/C genotype — two copies of the C allele. On average this is linked to lower fasting triglycerides, a lower triglyceride-to-HDL ratio and lower C-reactive protein, but slightly higher fasting blood glucose. It is a metabolic trade-off rather than a clearly favourable or unfavourable result. • Metabolic syndrome risk (GCKR) rsid : rs780094 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/30382898/ https://pubmed.ncbi.nlm.nih.gov/29632305/ https://pubmed.ncbi.nlm.nih.gov/22399527/ Interpretation: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the T risk variant present. Your genetic risk for metabolic syndrome sits at the lower end of the spectrum — a favourable position relative to T-carriers. Each T copy would raise risk by β ≈ 0.13 per copy. • Gilbert's syndrome / elevated bilirubin (UGT1A1) rsid : rs6742078 Your geno : GT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/23371916/ https://pubmed.ncbi.nlm.nih.gov/19414484/ Interpretation: You inherited one T variant and one G variant — a heterozygous G/T genotype. The T variant is associated with somewhat higher serum bilirubin (the Gilbert's-syndrome pattern). Mildly raised unconjugated bilirubin in this range is benign — not a disease risk — so this is an informational tendency, not a concern. • Fenofibrate response in diabetes (PPARA) rsid : rs4253778 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15608561/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4253778 sits in PPARA — and fenofibrate works precisely by activating the PPAR-alpha protein this gene makes. In people with type 2 diabetes, those with two G copies were more likely to be strong responders (greater than 30% triglyceride reduction) to fenofibrate, while C-allele carriers responded less. The evidence is limited (single study, PharmGKB level 3) and only matters if you take fenofibrate. Interpretation: If you have the G/G genotype and diabetes, you may be more likely to respond to fenofibrate treatment compared to people with the G/C or C/C genotype. Other genetic and clinical factors may also influence response to fenofibrate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • LDL cholesterol level (PCSK9) ⚠ CAUTIOUS rsid : rs11206510 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/18193043/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. The C allele is associated with a modestly lower LDL cholesterol measurement (about −0.06 per copy on the study scale), so C/C sits at the lower end of this measurement range. This is informational, not a concern. • LDL & total cholesterol (APOB) rsid : rs1367117 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: Both copies at this position carry the A allele — an A/A genotype. At the population level the A allele is associated with modestly higher average LDL & total cholesterol than the G allele (about β ≈ 0.09 per copy on the study's scale). This is a measurement-level association, not a disease prediction — it nudges an average lipid reading, and a blood test reflects your real LDL. • Statin (cholesterol-lowering drug) use likelihood (APOB) ⚠ CAUTIOUS rsid : rs1367117 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/31015401/ Interpretation: With the A/A genotype you carry two LDL-raising A copies, giving the largest cholesterol-raising effect from this site and the highest likelihood, among the three genotypes, of being prescribed a statin. This is a probability shift, not a certainty — many people with A/A have normal cholesterol. • HDL ("good") cholesterol level (CETP) rsid : rs2070895 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39414775/ Interpretation: You inherited one protective A variant and one G variant — a heterozygous G/A genotype, one allele from each parent. You get partial protective benefit for hdl ("good") cholesterol level relative to the G/G baseline — about β ≈ 0.15 per copy of the A variant. • Total cholesterol level (CETP) rsid : rs2070895 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/39414775/ Interpretation: You carry one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a slightly higher total cholesterol reading on average (β ≈ 0.06 per copy). This is a weak population-level association and, on its own, does not meaningfully predict your individual cholesterol level — a lipid panel is the real measure. • Triglyceride levels (CETP) ⚠ CAUTIOUS rsid : rs2070895 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/38116116/ Interpretation: You carry one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a slightly higher triglyceride reading on average (β ≈ 0.06 per copy). This is a weak population-level association and, on its own, does not meaningfully predict your individual triglyceride level — a lipid panel is the real measure. • Triglyceride levels (APOA5) rsid : rs2266788 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/21386085/ Interpretation: Both copies are the A allele — an A/A genotype. The A allele is associated with a lower triglyceride reading (β ≈ 0.28 per copy), so A/A sits at the lower end for this measurement. This is an average shift across people; a lipid panel confirms your actual number. • HDL ('good') cholesterol (APOA5) rsid : rs2266788 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/21386085/ Interpretation: Both copies at this position carry the protective A variant — a A/A genotype, the strongest protective combination at this site. Each A copy adds benefit toward hdl ('good') cholesterol (β ≈ 0.12 per copy) compared to the G/G baseline. • LDL & total cholesterol (APOA5) rsid : rs2266788 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/29507422/ Interpretation: Both copies are the A allele — an A/A genotype. The A allele is weakly associated with a slightly lower LDL/total cholesterol reading (β ≈ 0.11 per copy), so A/A sits at the lower end of this small average shift. The per-copy effect is tiny and, on its own, does not meaningfully predict your individual cholesterol level. • Metabolic syndrome risk (APOA5) ⚠ CAUTIOUS rsid : rs2266788 Your geno : AA Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/21386085/ Interpretation: Both copies at this position carry the A baseline variant — an A/A genotype, with no copies of the G risk variant present. Your genetic tendency for metabolic syndrome sits at the lower end — a favourable position relative to G-carriers (A also lowers triglycerides and raises HDL). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • LDL & total cholesterol (PCSK9) rsid : rs2479409 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ https://pubmed.ncbi.nlm.nih.gov/29748315/ Interpretation: Both copies are the A allele — an A/A genotype. The A allele is weakly associated with a slightly lower LDL/total cholesterol reading (β ≈ 0.05 per copy), so A/A sits at the lower end of this small average shift. The per-copy effect is tiny and, on its own, does not meaningfully predict your individual cholesterol level. • Triglyceride levels (APOA5 region) rsid : rs2954029 Your geno : AT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/38116116/ https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You inherited one A allele and one T allele — a heterozygous A/T genotype, one from each parent. Triglyceride levels tend to run slightly higher than for people with the T/T type — about β ≈ 0.09 per A copy on the study scale. This is a small measurement-level shift, not a disease prediction. • LDL & total cholesterol levels (APOA5 region) rsid : rs2954029 Your geno : AT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You inherited one A allele and one T allele — a heterozygous A/T genotype, one from each parent. LDL and total cholesterol tend to run slightly higher than for people with the T/T type — about β ≈ 0.06 per A copy on the study scale. This is a small measurement-level shift, not a disease prediction. • HDL ('good') cholesterol levels (APOA5 region) rsid : rs2954029 Your geno : AT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/24097068/ Interpretation: You inherited one protective T variant and one A variant — a heterozygous A/T genotype, one allele from each parent. You get partial protective benefit for hdl ('good') cholesterol levels relative to the A/A baseline — about β ≈ 0.04 per copy of the T variant. • Fenofibrate response in high triglycerides (APOA5) rsid : rs3135506 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/17431185/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs3135506 is the S19W missense variant in APOA5 (apolipoprotein A-V), a gene that helps clear triglyceride-rich particles from blood. The minor C allele (the alternate base, the '19W' form) raises baseline triglycerides. In pharmacogenetic studies, carriers of this C allele tend to start with higher triglycerides and to show a larger drop in triglycerides when treated with the fibrate drug fenofibrate. The supporting evidence is a low-level (level 3) PharmGKB annotation with no pooled effect size, so this is a modest, drug-specific signal. It only matters if you take fenofibrate. Note: this is one of 2 correlated variants in/near APOA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: With the G/G genotype you carry the common version of APOA5 at this site, associated with typical baseline triglycerides. If you take fenofibrate, your triglyceride response is expected to be in the usual range; this variant gives no special signal for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • HDL cholesterol level (LIPG) rsid : rs4939883 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19060906/ https://pubmed.ncbi.nlm.nih.gov/19060911/ Interpretation: Both copies at this position carry the protective C variant — a C/C genotype, the strongest protective combination at this site. Each C copy adds benefit toward hdl cholesterol level (β ≈ 0.1 per copy) compared to the T/T baseline. • Total and LDL cholesterol levels (LIPG) rsid : rs4939883 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/19060911/ https://pubmed.ncbi.nlm.nih.gov/19936222/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with modestly higher total and LDL cholesterol than the T/T type, with each C copy adding about β ≈ 0.04 on the study scale. This is a small measurement-level nudge, not a disease prediction. • LDL cholesterol level (PSRC1/CELSR2 region) rsid : rs4970834 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32203549/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with modestly higher LDL cholesterol than the T/T type, with each C copy adding about β ≈ 0.11 on the study scale. This is a measurement-level nudge, not a disease prediction. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • LDL & total cholesterol (ABO) rsid : rs579459 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30926973/ https://pubmed.ncbi.nlm.nih.gov/26582766/ Interpretation: Both copies at this position carry the T allele — a T/T genotype. T/T is associated with a modestly lower LDL & total cholesterol measurement than C/C (about −0.085 per copy, study scale). This is a measurement-level association, not a disease prediction. • LDL cholesterol & coronary artery disease risk (ABCG5/ABCG8) ⚠ CAUTIOUS rsid : rs6544713 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/36474045/ https://pubmed.ncbi.nlm.nih.gov/30926973/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly lower LDL cholesterol measurement than T/T (about −0.0492 per copy, study scale). This is mainly a measurement-level association, not a disease prediction. • LDL & total cholesterol levels rsid : rs660240 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/38116116/ https://pubmed.ncbi.nlm.nih.gov/40841581/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly higher LDL & total cholesterol measurement than T/T (about +0.22 per copy, study scale). This is a measurement-level association, not a disease prediction. • Fenofibrate – triglyceride-lowering response (APOB) rsid : rs676210 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20724655/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take fenofibrate to lower triglycerides. In the GOLDN fenofibrate trial, each A allele of this APOB variant (Pro2739Leu; the literature calls it the minor 'T' allele on the gene's coding strand, which equals A on the dbSNP forward strand) was linked to a larger drop in triglycerides during fenofibrate treatment, in a dose-dependent way. People with two G alleles tended to have the smallest triglyceride response. This is about how well the drug works for you, not a disease risk; evidence is modest, so treat it as a tendency. Interpretation: If you have the G/G genotype and hypertriglyceridemia, you may have smaller decreases in triglyceride levels when treated with fenofibrate compared to people with the A/A genotype. Other genetic and clinical factors may also influence your response to fenofibrate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Triglycerides & VLDL (APOA1/APOA5 cluster) rsid : rs964184 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/23505323/ https://pubmed.ncbi.nlm.nih.gov/27005778/ Interpretation: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly lower triglycerides & VLDL measurement than G/G (about −0.21 per copy, study scale). This is a measurement-level association, not a disease prediction. • HDL ('good') cholesterol level (APOA1/APOA5) rsid : rs964184 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32203549/ Interpretation: Both copies at this position carry the protective C variant — a C/C genotype, the strongest protective combination at this site. Each C copy adds benefit toward hdl ('good') cholesterol level (β ≈ 0.09 per copy) compared to the G/G baseline. • Fenofibrate response in hypertriglyceridemia (APOA5) rsid : rs964184 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23119086/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each C allele reduces odds of Fenofibrate response in hypertriglyceridemia (APOA5) by ~49% (OR≈0.51). The underlying association is well-replicated (3 publications), but there is no clinical pharmacogenetic guideline to act on it. Note: this is one of 2 correlated variants in/near APOA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the C/C genotype and hypertriglyceridemia, you may have a decreased response when treated with fenofibrate compared to people with the G/G genotype. Other genetic and clinical factors may also influence your response to fenofibrate. — Also checked, no unusual variants — LDL & total cholesterol (HFE) [rs1800562]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the cholesterol-lowering A variant present. People with G/G tend to sit toward the higher end of the LDL & total cholesterol range. Per-copy effect size: β ≈ 0.06 per copy. HDL ('good') cholesterol level (ALDH2) [rs671]: You have the G/G genotype at ALDH2, which is associated with typical HDL ('good') cholesterol levels at this gene. LDL cholesterol level (APOE) [rs7412]: You have the C/C genotype at rs7412 — no APOE ε2 (T) copy here. C/C is associated with higher LDL cholesterol than T-carriers (each T copy lowers LDL by roughly 0.4–0.5 SD). Higher LDL is a cardiovascular risk factor, so this is the less favourable genotype at this site, though your overall risk depends on rs429358 and lifestyle. HDL cholesterol (FADS1) [rs174550]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the higher-HDL T variant. You miss the small upward shift in HDL that T-carriers get here. Each T copy would shift HDL by about +0.04 SD. HDL cholesterol level (APOA2) [rs5082]: You inherited one G variant and one A variant — a heterozygous G/A genotype, one allele from each parent. The single G copy is associated with modestly higher HDL than A/A (β ≈ 0.02 per copy) — a small favourable nudge, most relevant on a high-saturated-fat diet. Total and triglyceride cholesterol levels (APOA2) [rs5082]: You inherited one G allele and one A allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a modestly lower triglyceride / total-cholesterol measurement (about beta ≈ 0.03 per copy on the study scale). This is a small measurement nudge, not a disease prediction. Triglyceride levels (APOA5) [rs662799]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the triglyceride-raising G allele. Your genetic tendency for measured triglycerides sits at the lower end of the range — a favourable position relative to G-carriers. Lower LDL cholesterol & coronary artery disease risk (PCSK9) [rs11591147]: Both copies at this position carry the G baseline variant — a G/G genotype, with no copies of the protective T variant present. You miss the small LDL-lowering, CAD-protective benefit that T-carriers get at this site. Triglyceride/HDL ratio (LPL) [rs268]: Both copies at this position carry the A variant — an A/A genotype, with no copies of the G (N291S) variant present. People with A/A tend to sit toward the lower (more favourable) end of the triglyceride/HDL ratio range. Per-copy effect size: β ≈ 0.3 per copy. Fatty liver disease risk (LPL) [rs268]: Both copies at this position carry the A baseline variant — a A/A genotype, with no copies of the G risk variant present. Your genetic risk for fatty liver disease sits at the lower end of the spectrum — a favourable position relative to G-carriers. Each G copy would raise risk by β ≈ 0.25 per copy. HDL ('good') cholesterol level (IRS1) [rs2943641]: You have the T/C genotype — one protective T allele and one C allele. You get part of the favourable HDL effect relative to C/C (the T allele is associated with higher HDL and lower triglycerides; about +0.016 per T copy on the study scale). LDL cholesterol level (SORT1) [rs629301]: Both copies here carry the T allele — a T/T genotype. On average this is associated with a modestly higher LDL-cholesterol measurement than G/G (about β ≈ 6.03 per T copy on the study scale). The per-copy effect is small — a weak population-level signal, not a prediction of your individual LDL. LDL & total cholesterol level (LPA) [rs10455872]: Both copies at this position carry the A allele — an A/A genotype, with no copies of the G allele. The G allele is the one tied to a modestly higher LDL & total cholesterol reading (about +0.08 per copy on the study scale), so A/A sits at the lower end of this measurement range. Informational, not a concern. LDL & total cholesterol levels (LDLR region) [rs1122608]: You inherited one G allele and one T allele — a heterozygous G/T genotype, one from each parent. At the population level, each G copy is associated with a slightly higher average LDL & total cholesterol than the T/T pattern (about β ≈ 2.71 per copy on the study's scale). This is a small measurement nudge, not a disease-risk prediction; a lipid panel reflects your real values. HDL cholesterol level (APOC3 loss-of-function) [rs116843064]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A (APOC3 loss-of-function) variant present. People with G/G tend to sit toward the lower end of the HDL cholesterol range. Per-copy effect size: β ≈ 0.22 per copy. LDL & total cholesterol (HNF1A) [rs1169288]: Both copies at this position carry the A allele — an A/A genotype. At the population level, the A allele is associated with slightly lower average LDL & total cholesterol than the C allele. This is a measurement-level association, not a disease prediction, and on its own it does not determine your actual cholesterol — a blood test does. LDL cholesterol level (SORT1) [rs12740374]: Both copies at this position carry the G allele — a G/G genotype. At the population level the G allele is associated with modestly higher average LDL cholesterol than the T allele (about β ≈ 0.24 per copy on the study's scale). This is a measurement-level association, not a disease prediction — it nudges an average lipid reading, and a blood test reflects your real LDL. LDL cholesterol (APOE region) [rs157580]: You carry one A allele and one G allele — a heterozygous G/A genotype, one from each parent. The A allele is associated with a slightly higher LDL reading on average (β ≈ 0.04 per copy). This is a weak population-level association and, on its own, does not meaningfully predict your individual LDL level; a blood lipid panel is what tells you your actual number. HDL ('good') cholesterol levels (CETP) [rs1800777]: Both copies at this position carry the protective G variant — a G/G genotype, the strongest protective combination at this site. Each G copy adds benefit toward hdl ('good') cholesterol levels (β ≈ 0.38 per copy) compared to the A/A baseline. HDL ('good') cholesterol level (HNF4A) [rs1800961]: Both copies at this position carry the protective C variant — a C/C genotype, the strongest protective combination at this site. Each C copy adds benefit toward hdl ('good') cholesterol level (β ≈ 0.01 per copy) compared to the T/T baseline. Total and LDL cholesterol (HNF4A) [rs1800961]: Both copies at this position are the C allele — a C/C genotype, with no T alleles. The T allele is the one weakly linked to a lower total/LDL cholesterol reading, so on average C/C sits at the upper end for this measurement. The per-copy shift is small (β ≈ 0.06) and, on its own, does not meaningfully predict your actual cholesterol level — a lipid panel is the real measure. Triglyceride & cholesterol levels (APOA5) [rs3135506]: Both copies at this position carry the G allele — a G/G genotype, with no C copies. Triglyceride and cholesterol levels tend to sit at the lower end relative to C-carriers; each C copy would nudge the measurement up by about β ≈ 0.25 on the study scale. This is a measurement-level association, not a disease prediction. Lipoprotein(a) & coronary artery disease (LPA) [rs41272114]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the protective T variant present. You miss the small lipoprotein(a)-lowering, CAD-protective benefit that T-carriers get at this site. LDL cholesterol & coronary artery disease risk (SORT1) [rs4299376]: Both copies at this position carry the T allele — a T/T genotype, with no G copies. This is the slightly more favourable version relative to G-carriers, associated with somewhat lower LDL cholesterol; each G copy would nudge LDL and coronary artery disease risk up by about OR ≈ 1.06 — a weak population-level association, not a meaningful predictor of your individual outcome. Triglycerides & HDL cholesterol (APOC1/APOE region) [rs439401]: You inherited one C variant and one T variant — a heterozygous T/C genotype, one allele from each parent. This places you in the middle of the triglycerides & hdl cholesterol range, between the lower-end T/T and the higher-end C/C genotypes. Per-copy effect size: β ≈ 0.24 per copy. Triglyceride & lipid levels (APOC3) [rs5128]: No notable finding at this locus. Ritonavir – triglyceride elevation risk (APOC3) [rs5128]: No notable finding at this locus. Triglyceride levels & hypertriglyceridemia (APOA5) [rs651821]: Both copies at this position carry the T allele — a T/T genotype, with no copies of the triglyceride-raising C allele. Your triglyceride measurement and odds of hypertriglyceridemia sit at the lower, favourable end at this site. HDL ('good') cholesterol (APOA5) [rs651821]: Both copies at this position carry the T variant — a T/T genotype. Each T copy raises HDL ('good') cholesterol, so T/T sits toward the higher (more favourable) end of the HDL range. Per-copy effect size: β ≈ 0.17 per copy. Metabolic syndrome risk (APOA5) [rs651821]: Both copies at this position carry the T variant — a T/T genotype, with no copies of the metabolic-syndrome-risk C variant. Your risk at this site sits at the lower, favourable end. HDL ('good') cholesterol level (APOB) [rs676210]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the HDL-raising A variant present. You miss the modest HDL benefit that A-carriers get at this site — about β ≈ 0.06 lower per missing A copy relative to A-carriers. Triglyceride levels (APOB) [rs676210]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with a modestly lower triglyceride measurement (about −0.136 per copy, study scale), so G/G sits at the higher end of this measurement-level association. Total cholesterol level (APOB) [rs679899]: Both copies at this position carry the G allele — a G/G genotype, with no copies of the A allele present. Each A copy is associated with a modestly lower total cholesterol measurement (about −0.0375 per copy, study scale), so G/G sits at the higher end of this measurement-level association. LDL & total cholesterol levels (LDLR) [rs688]: You inherited one T allele and one C allele — a heterozygous C/T genotype, one allele from each parent. The T allele is associated with a modestly higher LDL & total cholesterol measurement (about +0.057 per copy, study scale). This is a measurement nudge, not a disease prediction. LDL & total cholesterol (APOE region) [rs769449]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. This is the genotype associated with the lowest measured LDL & total cholesterol at this position. Each A copy is associated with higher measured cholesterol (about β ≈ 0.25 per copy, study scale). LDL ('bad') cholesterol level (APOA1/APOA5) [rs964184]: Both copies at this position carry the C allele — a C/C genotype. C/C is associated with a modestly lower LDL ('bad') cholesterol measurement than G/G (about −0.0574 per copy, study scale). This is a measurement-level association, not a disease prediction. ──────────────────────────────────────────────────────────────────────── NUTRITION & NUTRIENTS ──────────────────────────────────────────────────────────────────────── [Folate / methylation] • Folate supplementation response in depression treatment (MTHFR A1298C) ⚠ CAUTIOUS rsid : rs1801131 Your geno : TG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31058543/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801131 is the MTHFR A1298C variant; the G allele (1298C) modestly lowers MTHFR enzyme activity, which can reduce how efficiently the body converts folate into its active form. In the context of depression treatment, carriers of the G (lower-activity) allele may respond better to added folate supplements (such as l-methylfolate) than people with the normal T/T genotype. The evidence is limited (PharmGKB level-3 efficacy annotation, no effect size), so this is a tendency, not a strong rule, and only relevant if folate is part of your depression treatment. Interpretation: You have the T/G genotype, and you may show an improved response to pharmacotherapy for depression when given folate supplements. Keep in mind that other genetic and clinical factors can also influence how you respond to folate supplementation. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — MTHFR folate metabolism & homocysteine [rs1801133]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the mthfr folate metabolism & homocysteine range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.3 per copy. [Iron / ferritin] • HFE H63D variant (iron metabolism) rsid : rs1799945 Your geno : CG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/10/ https://pubmed.ncbi.nlm.nih.gov/28334935/ https://pubmed.ncbi.nlm.nih.gov/21208937/ Summary : rs1799945 is the HFE H63D variant (the G allele). On its own, H63D is a low-penetrance variant and is usually clinically insignificant — most carriers, including people with two H63D copies, never develop iron overload. Clinically meaningful hereditary haemochromatosis is rare unless H63D is paired with the HFE C282Y variant (rs1800562) as a compound heterozygote, or two C282Y copies are present. If you have symptoms or a reason to check, ferritin and transferrin saturation are the simple blood tests to look at — but only if clinically indicated. Interpretation: You carry one H63D (G) variant and one C allele — a C/G genotype. This makes you a single-copy H63D carrier, which on its own is usually clinically insignificant. Iron overload is rare unless H63D is paired with the HFE C282Y variant (rs1800562). No action is needed for this result alone; ferritin and transferrin saturation are worth checking only if clinically indicated. • Serum iron & transferrin levels (TF gene) rsid : rs3811647 Your geno : GA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/21483845/ https://pubmed.ncbi.nlm.nih.gov/21208937/ https://pubmed.ncbi.nlm.nih.gov/19084217/ Interpretation: You inherited one A variant and one G variant — a heterozygous G/A genotype, one allele from each parent. This places you in the middle of the serum iron & transferrin levels range, between the lower-end G/G and the higher-end A/A genotypes. Per-copy effect size: β ≈ 0.36 per copy. • Iron levels (TMPRSS6) rsid : rs4820268 Your geno : GG Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs4820268 Interpretation: You have the G/G genotype at TMPRSS6. You carry no copies of the A allele linked to higher iron, so you tend toward the lower end of the serum iron range associated with this variant. Iron status is also strongly shaped by diet, blood loss, and other genes. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Iron levels & transferrin saturation (TMPRSS6) rsid : rs855791 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/33536631/ https://pubmed.ncbi.nlm.nih.gov/25352340/ https://pubmed.ncbi.nlm.nih.gov/38789058/ Interpretation: Both copies at this position carry the A variant — a A/A genotype, with no copies of the G variant present. People with A/A tend to sit toward the lower end of the iron levels & transferrin saturation range; the G variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.16 per copy. — Also checked, no unusual variants — Hereditary hemochromatosis risk (HFE C282Y) [rs1800562]: You have the G/G genotype at HFE C282Y — two copies of the wild-type G allele. This is the typical, non-risk genotype for hereditary hemochromatosis. Iron levels & ferritin (HFE) [rs1800562]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the iron-raising A variant present. People with G/G tend to sit toward the lower end of the iron levels & ferritin range. Per-copy effect size: β ≈ 0.35 per copy. Hemoglobin & red blood cell indices (HFE) [rs1800562]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the hemoglobin & red blood cell indices range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.04 per copy. Iron deficiency anemia – slightly reduced risk [rs6025]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the protective T variant present. You miss the small protective benefit that T-carriers get at this site for iron deficiency anemia – slightly reduced. Each T copy would shift the effect by β ≈ 0.15 per copy. Iron levels & red blood cell traits (TMPRSS6) [rs7385804]: Both copies at this position carry the C variant — a C/C genotype, with no copies of the A variant present. People with C/C tend to sit toward the lower end of the iron levels & red blood cell traits range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.05 per copy. Iron levels (TF / transferrin) [rs8177240]: No notable finding at this locus. [Lactose] • Lactose tolerance (LCT) rsid : rs4988235 Your geno : GG Evidence : GWAS (quantitative) Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/7685/ Interpretation: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the lactose tolerance range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.88 per copy. [taste] • Bitter taste perception (TAS2R38) rsid : rs10246939 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/30223776/ https://pubmed.ncbi.nlm.nih.gov/23966204/ Interpretation: You have the T/T genotype at this single TAS2R38 position. This is one of three positions in the PAV/AVI bitter-taste haplotype; T tends to occur in the less-tasting (AVI) haplotype, but your actual taster status cannot be read from this SNP alone — it depends on the full TAS2R38 haplotype (all three positions together). This is a normal taste variation, not a health concern. • Bitter taste perception (TAS2R38) rsid : rs1726866 Your geno : AA Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/31005965/ https://pubmed.ncbi.nlm.nih.gov/30223776/ Interpretation: You have the A/A genotype at this single TAS2R38 position. The A (Val262) allele tends to occur in the AVI haplotype, but a single SNP does not determine taster status — that depends on the full TAS2R38 haplotype (all three positions together). This is a normal taste variation, not a health concern. • Bitter taste perception (TAS2R38) ⚠ CAUTIOUS rsid : rs713598 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/20675712/ Interpretation: You have the C/C genotype at this single TAS2R38 position. The C (Pro49) allele tends to occur in the more-tasting (PAV) haplotype, but this is just one of three positions — your taster status cannot be read from this SNP alone and requires all three TAS2R38 positions together. This is a normal taste difference, not a health concern. • Carbohydrate & sugar (sweet) preference (FGF21) rsid : rs838145 Your geno : AA Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs838145 Interpretation: You have the A/A genotype — two copies of the allele linked to a weaker preference for sweet foods and a lower share of carbohydrate/sugar in the diet, with relatively more fat and protein. The effect is small; your actual diet still depends mostly on habits and what's available. [Vitamins & micronutrients] • Vitamin B12 levels ⚠ CAUTIOUS rsid : rs526934 Your geno : AA Evidence : GWAS (quantitative) Source : https://www.ebi.ac.uk/gwas/variants/rs526934 Interpretation: You have the A/A genotype. Weak evidence links the A allele to slightly higher circulating B12, but the supporting data are limited and partly conflicting, so this is a research-grade signal rather than a firm finding. Your actual level still depends mostly on what you eat. • Vitamin E levels with supplementation (CYP4F2) ⚠ CAUTIOUS rsid : rs2108622 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22437554/ https://pubmed.ncbi.nlm.nih.gov/17341693/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each T allele (CYP4F2 V433M) is associated with HIGHER vitamin E levels with supplementation (about +0.04 per copy, study scale). The T variant reduces CYP4F2 tocopherol-degrading activity, so less vitamin E is broken down and plasma levels rise. This is a quantitative tendency. Interpretation: You inherited one C variant and one T variant — a heterozygous C/T genotype. The T (V433M) allele partially reduces CYP4F2's ability to break down vitamin E, so this places you in the middle of the vitamin E range, between the lower-end C/C and the higher-end T/T genotypes. Per-copy effect size: beta ~ 0.04. — Also checked, no unusual variants — Vitamin D levels (CYP2R1) [rs10741657]: No notable finding at this locus. Vitamin D levels (GC / DBP) [rs2282679]: Both copies at this position carry the T variant — a T/T genotype, the combination linked to the highest vitamin D levels at this site. You sit furthest from the low-vitamin-D (deficiency) end relative to G-carriers. The effect is modest (β ≈ 0.38 per copy); your actual level still depends mainly on sun and diet. Vitamin B12 levels (FUT2) [rs492602]: You inherited one protective G variant and one A variant — a heterozygous A/G genotype, one allele from each parent. You get partial protective benefit for vitamin b12 levels relative to the A/A baseline — about β ≈ 0.09 per copy of the G variant. Vitamin D levels (GC / vitamin D-binding protein) [rs7041]: You inherited one protective C variant and one A variant — a heterozygous A/C genotype, one allele from each parent. You get partial protective benefit for vitamin d levels relative to the A/A baseline — about β ≈ 5.3 per copy of the C variant. ──────────────────────────────────────────────────────────────────────── PHARMACOGENETICS ──────────────────────────────────────────────────────────────────────── [Antidepressant response] • Folate supplementation response in depression treatment (MTHFR A1298C) ⚠ CAUTIOUS rsid : rs1801131 Your geno : TG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31058543/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801131 is the MTHFR A1298C variant; the G allele (1298C) modestly lowers MTHFR enzyme activity, which can reduce how efficiently the body converts folate into its active form. In the context of depression treatment, carriers of the G (lower-activity) allele may respond better to added folate supplements (such as l-methylfolate) than people with the normal T/T genotype. The evidence is limited (PharmGKB level-3 efficacy annotation, no effect size), so this is a tendency, not a strong rule, and only relevant if folate is part of your depression treatment. Interpretation: You have the T/G genotype, and you may show an improved response to pharmacotherapy for depression when given folate supplements. Keep in mind that other genetic and clinical factors can also influence how you respond to folate supplementation. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Amitriptyline / tricyclic antidepressants – CYP2C19 metabolism rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16044105/ Summary : rs4244285 is the CYP2C19*2 variant; the minor A allele makes a non-working CYP2C19 enzyme. Tricyclic antidepressants such as amitriptyline are broken down partly by CYP2C19 (which converts the parent drug to its active metabolite) and partly by CYP2D6. People who carry the A allele clear the parent drug more slowly, shifting the balance of parent drug versus metabolite and raising overall exposure, which can increase side effects. Guidelines (CPIC) consider both CYP2C19 and CYP2D6: poor metabolizers may need a lower dose or an alternative. The A allele is the slow (loss-of-function) allele; G is normal-function. CYP2D6 status (not covered here) is also important. Interpretation: If you take a tricyclic antidepressant and have the G/G genotype (CYP2C19 *1/*1), your CYP2C19 works normally and converts the drug at a typical rate. A standard dose is usually appropriate as far as CYP2C19 is concerned, though your CYP2D6 status (a separate gene not covered here) also affects tricyclic dosing. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Venlafaxine (Effexor) – response in depression (CYP2C19) rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23799451/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4244285 is the CYP2C19*2 variant; the minor A allele makes a non-working CYP2C19 enzyme. For venlafaxine the link to CYP2C19 is weak: venlafaxine is metabolised mainly by CYP2D6, not CYP2C19. A single small study reported that CYP2C19 *1/*2 carriers had more agitation/dysphoria than *1/*1 patients, but this has not been replicated and is not part of any dosing guideline. The A allele is the loss-of-function allele; G is normal-function. CYP2D6 status is the more meaningful variable for venlafaxine — treat this CYP2C19 finding as exploratory. Interpretation: If you have the G/G genotype (CYP2C19 *1/*1 at this site) and are treated with venlafaxine for depression, a single small study reported lower rates of agitation and dysphoria compared to G/A carriers. Note: venlafaxine is primarily metabolized by CYP2D6, not CYP2C19, so this CYP2C19*2 finding has limited clinical actionability. No CPIC guideline supports CYP2C19-based venlafaxine dose modification. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Citalopram response in depression (TPH2) rsid : rs4570625 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23510446/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant sits just upstream of TPH2, the gene for the brain enzyme that makes serotonin, and has been studied for how people with depression respond to the antidepressant citalopram. The evidence is modest and not fully consistent, but PharmGKB curates it (level 3) with the G/G genotype (the reference form here) linked to a weaker antidepressant response to citalopram compared with people carrying the A allele. Many other genetic and clinical factors also shape antidepressant response, so this is a tendency, not a prediction. It only matters if you take citalopram or a similar SSRI. Interpretation: You have the G/G genotype. If you have depression and take citalopram, you may respond somewhat less well on average than people carrying an A allele — but response varies widely and depends on many factors. If you don't take citalopram or a similar SSRI, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antidepressant response (COMT Val158Met) ⚠ CAUTIOUS rsid : rs4680 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22417933/ https://pubmed.ncbi.nlm.nih.gov/18989660/ https://pubmed.ncbi.nlm.nih.gov/20619611/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the COMT Val158Met variant (G = Valine, fast enzyme; A = Methionine, slow enzyme), which changes how quickly the brain clears dopamine and noradrenaline. It has been studied for whether it predicts antidepressant response, but the results are genuinely inconsistent: some studies favour the Met (A) allele for better response, others favour Val (G), and a meta-analysis found no reliable overall effect. Because the direction is not established, this is informational only — it should not be used to choose or avoid an antidepressant. It only relates to people taking antidepressants. Interpretation: You have the G/A (Val/Met) genotype. If you take antidepressants, this variant does not reliably predict your response — the evidence is mixed and inconclusive. If you don't take antidepressants, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antidepressant response – SSRIs (BDNF) rsid : rs6265 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20016225/ https://pubmed.ncbi.nlm.nih.gov/23619509/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6265 is the well-known BDNF Val66Met variant, which changes the brain growth factor BDNF. REF=C (Val), ALT=T (Met). It has been studied a lot as a predictor of how well SSRI antidepressants work. A meta-analysis (PMID 23733030) found that people with the heterozygous Val/Met (C/T) genotype tended to respond and remit slightly better on SSRIs than those with two identical alleles (C/C or T/T), an effect strongest in Asian populations (OR about 1.5). Overall this is a weak, modest effect and no single gene reliably predicts antidepressant success, so it is best treated as informational, not as a reason to choose or avoid an SSRI. Interpretation: You have the C/C (Val/Val) genotype. If you take an SSRI antidepressant, studies suggest people with two matching alleles like this may respond very slightly less well on average than heterozygotes, but the effect is small and inconsistent. Most people with this genotype still respond normally to SSRIs; how a given medicine works for you is decided in practice by trying it. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aripiprazole response in schizophrenia (DRD2) rsid : rs6277 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18926547/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6277 is the DRD2 C957T variant. On the forward strand REF=G (957C) and ALT=A (957T). A study of schizophrenia treated with aripiprazole (PMID 18926547) found that people with the 957T/957T genotype (A/A on this strand) responded better, especially for excitement symptoms, while 957C/957C (G/G) responded more poorly. This is a single study in 128 patients, so it is preliminary. Treatment response depends on many factors, so this is informational and only relevant if you take aripiprazole. Interpretation: If you have schizophrenia and the G/G genotype, one study found you may respond somewhat less well to aripiprazole (particularly for excitement symptoms) than people with the A/A genotype. The evidence is from a single small study, so it does not mean aripiprazole will not work for you — response is judged by how you actually do on the medicine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • SSRI antidepressant response (HTR1A) ⚠ CAUTIOUS rsid : rs6295 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19590397/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6295 is the well-studied HTR1A C(-1019)G promoter variant (the alternate allele is G, not A). The G allele has been associated in some studies with a poorer response to SSRIs and other antidepressants — G/G carriers tended to respond less well — but a meta-analysis found no overall association, so the evidence is weak and inconsistent. This only matters if you are taking an antidepressant. Interpretation: You have the C/C genotype at rs6295 (HTR1A). If you take an SSRI antidepressant, some studies suggest C/C carriers may respond somewhat better than G-allele carriers, but a meta-analysis found no overall effect, so this is uncertain. It is only relevant while taking an antidepressant. Many other genetic and clinical factors affect medication response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluoxetine response in major depression (HTR1A) ⚠ CAUTIOUS rsid : rs6295 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19590397/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6295 is the HTR1A C(-1019)G promoter variant (the alternate allele is G, not A). In major depression, the G allele has been weakly associated with a poorer response to fluoxetine in some studies, while others and a meta-analysis found no clear effect. This only matters if you are taking fluoxetine. Interpretation: You have the C/C genotype at rs6295 (HTR1A). If you take fluoxetine for depression, some studies suggest C/C carriers may respond somewhat better than G-allele carriers, but the evidence is weak and inconsistent. It is only relevant while taking fluoxetine. Many other genetic and clinical factors affect medication response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Milnacipran response in depression (HTR1A) ⚠ CAUTIOUS rsid : rs6295 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18484082/ https://pubmed.ncbi.nlm.nih.gov/25710119/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6295 is the HTR1A C(-1019)G promoter variant (the alternate allele is G, not A). Some studies link HTR1A genotype to milnacipran response in depression, with C/C carriers reported to respond better in some reports, but results conflict. This only matters if you are taking milnacipran. Interpretation: You have the C/C genotype at rs6295 (HTR1A). Some studies suggest C/C carriers may respond somewhat better to milnacipran for depression, but results conflict. It is only relevant while taking milnacipran. Many other genetic and clinical factors affect medication response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotic response in schizophrenia (BDNF) rsid : rs11030104 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/36137488/ https://pubmed.ncbi.nlm.nih.gov/23433505/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs11030104 is a variant in BDNF, the brain-derived neurotrophic factor gene, in tight linkage with the well-known BDNF Val66Met variant. In schizophrenia, the G (alternate, minor) allele is associated with greater resistance to antipsychotic treatment: in one study each G copy raised the odds of treatment resistance (overall odds ratio about 2.6 for the variant), with G/G carriers far more likely to need clozapine. People with the common A/A genotype tended to respond best. This comes from a single pharmacogenomic study (PharmGKB level 3), so it is a tendency rather than a firm rule, and it only matters if you are being treated with antipsychotics. Interpretation: If you have schizophrenia and take antipsychotics, the A/A genotype (the common type) is associated with the best chance of responding to antipsychotic treatment — that is, the least treatment resistance — compared with people carrying the G allele. Many other genetic and clinical factors also affect how well antipsychotics work for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Risperidone response in schizophrenia (COMT) rsid : rs165599 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19451915/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs165599 is a variant in COMT, the gene for the enzyme that clears dopamine in the brain. In a study of people with schizophrenia treated with risperidone, the G (reference) allele was associated with more symptom improvement, so people with the G/G genotype tended to respond better than A-allele carriers. This comes from a single pharmacogenomic study (PharmGKB level 3) and is therefore a tendency rather than a firm rule; it only matters if you are actually being treated with risperidone. (Note: for bupropion in smoking cessation the opposite allele is favourable — drug-response effects of this variant differ by drug.) Note: this is one of 3 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: If you have schizophrenia and take risperidone, the G/A genotype (one A allele) was associated with somewhat less symptom improvement than the G/G genotype. This is a weak, single-study tendency; other factors also shape your response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antidepressant response (TPH1) ⚠ CAUTIOUS rsid : rs1800532 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19590397/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800532 is a variant in TPH1, the gene for tryptophan hydroxylase 1, an enzyme in the pathway that makes serotonin. In people with major depression, the G (reference) allele has been linked to a better chance of responding to SSRI antidepressants, particularly citalopram, so people with the G/G genotype tended to respond better than A-allele carriers in some studies. The evidence is mixed (several studies found no association) and is rated PharmGKB level 3-4, so this is a weak tendency rather than a predictor, and it only matters while you are taking antidepressant medication. Note that some sources report this variant on the opposite strand (G/T), where their T = our A. Interpretation: If you take antidepressants such as citalopram, the G/G genotype was associated in some studies with a better chance of responding compared with people carrying the A allele, though other studies found no difference. This is a weak tendency; many other clinical and genetic factors influence your response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antidepressant response in depression (FKBP5) ⚠ CAUTIOUS rsid : rs3800373 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20709156/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a variant in FKBP5, a gene that regulates the body's stress-hormone (cortisol) feedback system (here REF=C, ALT=A). Several pharmacogenetic studies have linked it to how well antidepressants work, with the C allele generally tied to a somewhat better chance of symptom improvement. The findings are inconsistent — some studies report the opposite or no effect — so this is a weak, contradictory signal, not an established predictor. No effect-size number is reported. It does not tell you your risk of depression itself, only a possible tendency in drug response. Note: this is one of 2 correlated variants in/near FKBP5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have depression and take antidepressants with the A/A genotype, some studies suggest you may be a bit less likely to improve than people carrying a C, but other studies disagree. Many other factors shape antidepressant response, so do not change treatment based on this alone. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Risperidone response in schizophrenia (COMT) ⚠ CAUTIOUS rsid : rs4633 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22935916/ https://pubmed.ncbi.nlm.nih.gov/28696411/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a variant in COMT, an enzyme that breaks down dopamine in the brain (here REF=C, ALT=T). Pharmacogenetic studies (PMIDs 22935916, 28696411) tentatively linked the C/C genotype to a better response to the antipsychotic risperidone in schizophrenia, but the signal was weak: it lost statistical significance after correction in one study and was not found in another. This is therefore a very uncertain tendency, not an established predictor, with no effect-size number. Note: this is one of 3 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: If you have schizophrenia and take risperidone with the C/T genotype, your expected response leans toward the poorer-responding group relative to C/C, but this is a very weak and unreplicated signal, not a reliable prediction. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Quetiapine response in schizophrenia (COMT) rsid : rs6269 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26282453/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6269 tags a COMT haplotype affecting dopamine breakdown in the brain. A PharmGKB pharmacogenetic annotation (level 3) in people with schizophrenia reports that G/G carriers tended to respond better to quetiapine, while A/A carriers responded less well. This is a single, modest study with no numeric effect size, and it is relevant only to people taking quetiapine for schizophrenia. Note: this is one of 2 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the A/G genotype and schizophrenia, you may have a poorer response to treatment with quetiapine compared to people with the G/G genotype, or a better response compared to people with the A/A genotype. Other genetic and clinical factors may also influence your response to quetiapine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Citalopram/escitalopram response in depression (BDNF) ⚠ CAUTIOUS rsid : rs7103411 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19236730/ https://pubmed.ncbi.nlm.nih.gov/29748862/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs7103411 is an intron variant in the BDNF gene, which makes a growth factor important for nerve signalling and mood. Pharmacogenetic studies (PharmGKB, level 4) reported that, among people with major depression, those with the C/C genotype tended to respond better to citalopram or escitalopram, while T/T carriers tended to respond less well. The evidence is weak (small studies, no numeric effect size, and results are not consistent across all reports), so this is a tendency rather than a firm prediction, and only relevant if you take one of these antidepressants. Interpretation: If you have the T/T genotype and major depressive disorder, you may have a poorer response when treated with citalopram compared to people with the C/C genotype. Other genetic and clinical factors may also influence your response to citalopram. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antidepressant response (HTR2A) ⚠ CAUTIOUS rsid : rs7997012 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/33097827/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs7997012 is an intron variant in HTR2A, the gene for a serotonin receptor that several antidepressants act on. Pharmacogenetic studies (PharmGKB, level 3) have linked it to how well people respond to antidepressants, but the direction is not consistent: several studies report the G allele (A/G and G/G genotypes) with better response, while others report the A allele with better response. Because the evidence is mixed and no numeric effect size is established, this is at most a weak tendency and only relevant if you are taking an antidepressant. Interpretation: If you take antidepressants and have the G/G genotype at rs7997012, your response may differ slightly from A/A carriers. Several studies have linked the G allele to a somewhat better antidepressant response, but other studies point the opposite way, so the evidence is too inconsistent to rely on. Many other factors influence your response — discuss any medication decisions with your prescriber. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Citalopram response in depression (HTR2A) ⚠ CAUTIOUS rsid : rs7997012 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24192302/ https://pubmed.ncbi.nlm.nih.gov/16642436/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs7997012 is an intron variant in HTR2A, the gene for a serotonin receptor targeted by SSRIs. In the influential STAR*D depression trial and related studies (PharmGKB, level 3), the A allele was associated with a better response to citalopram, while G/G carriers tended to respond less well. The effect is modest and no numeric effect size is established, so this is a tendency only, relevant when citalopram is being used. Interpretation: If you take citalopram for depression and have the G/G genotype at rs7997012, you carry no copies of the A allele that some studies associated with a better citalopram response, so you may respond somewhat less well than A-allele carriers. This is a weak tendency, not a prediction — many other factors matter, so discuss treatment with your prescriber. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluoxetine response in depression (HTR2A) ⚠ CAUTIOUS rsid : rs7997012 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24192302/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs7997012 is an intron variant in HTR2A, the gene for a serotonin receptor that SSRIs act on. A pharmacogenetic annotation for fluoxetine (PharmGKB, level 4) linked the G/G genotype to a better response to fluoxetine. The evidence is limited (a single study, no numeric effect size), so treat this as a weak tendency that is only relevant if you take fluoxetine. Interpretation: If you take fluoxetine for depression and have the G/G genotype at rs7997012, you carry two copies of the allele that one study linked to a somewhat better fluoxetine response. This comes from limited evidence and is a weak tendency, not a guarantee — many other factors matter, so discuss treatment with your prescriber. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Antidepressant response & suicidal ideation risk (FKBP5) [rs1360780]: No notable finding at this locus. Clozapine response in schizophrenia (FKBP5) [rs1360780]: No notable finding at this locus. Antidepressant response (FKBP5) [rs4713916]: No notable finding at this locus. Fluoxetine response in mood disorders (FKBP5) [rs4713916]: No notable finding at this locus. Mirtazapine response in mood disorders (FKBP5) [rs4713916]: No notable finding at this locus. [Drug metabolism] • CYP2C19 *17 — ultra-rapid drug metabolism (clopidogrel, PPIs, SSRIs) rsid : rs12248560 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20531370/ Summary : rs12248560 marks the CYP2C19 *17 allele. The T allele speeds up the CYP2C19 liver enzyme, so carriers break down certain drugs faster than average ("ultra-rapid metabolizers"). The C allele is the normal-function version. This only matters if you take a drug that CYP2C19 handles. Faster metabolism can mean clopidogrel works better (it is activated by this enzyme) but acid-blocking PPIs and some antidepressants may be cleared too quickly to reach their usual effect. No effect size is established for the speed-up itself; this is a metabolizer-status marker, not a disease risk. Interpretation: You have the C/T genotype (CYP2C19 *1/*17), one fast-function copy. If you take a CYP2C19-processed drug (e.g. clopidogrel, a PPI, or an SSRI), you may clear it somewhat faster than average. Whether that helps or hinders depends on the specific drug — discuss with your doctor if relevant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Busulfan metabolism (CYP2C19 *17) ⚠ CAUTIOUS rsid : rs12248560 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24192117/ https://pubmed.ncbi.nlm.nih.gov/24165757/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs12248560 is the CYP2C19 *17 fast-metabolizer marker. Because CYP2C19 contributes to clearing busulfan, fast-function (T) carriers may metabolize it faster than people with the normal-function C/C genotype. The evidence is weak and conflicting (a single PharmGKB level-3 pharmacokinetic study), and it describes only how the drug is processed in the body, not transplant outcomes. It only matters if you are treated with busulfan. Interpretation: You have the C/T genotype (CYP2C19 *1/*17), which means that if you undergo transplantation you may have increased metabolism of busulfan compared to people with the C/C (*1/*1) genotype. However, conflicting evidence has been reported, and other genetic and clinical factors may also influence how you metabolize busulfan. This annotation only covers the pharmacokinetic relationship between rs12248560 and busulfan and does not include evidence about clinical outcomes. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Alcohol dependence risk (ADH1B) rsid : rs1229984 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/18182/ https://pubmed.ncbi.nlm.nih.gov/35094024/ https://pubmed.ncbi.nlm.nih.gov/32451486/ https://pubmed.ncbi.nlm.nih.gov/37282553/ Summary : Each C allele raises odds of alcohol dependence (~3x per copy, meta-analysis OR ~2.9-6.6) by removing the fast-metaboliser flushing response carried by T (His48 / ADH1B*2). C/C carriers have slower Arg48 ethanol oxidation with no aversive acetaldehyde build-up; the T allele is the well-established protective fast-metaboliser variant. Strong evidence, 23+ publications. Note: this is one of 3 correlated variants in/near ADH1B reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the C/C genotype — two copies of the slower-metabolizing ADH1B (Arg48) form. Without the fast His48 (T) allele, acetaldehyde does not build up rapidly, so drinking is not self-limited by flushing or aversion. Compared with carriers of the T allele this genotype gives no protective effect from fast ADH1B, and is associated with higher odds of alcohol dependence than T-carriers. Many other genetic and lifestyle factors also influence alcohol use. • Thiopurines (azathioprine, mercaptopurine) – metabolism & toxicity (TPMT*3A/3B) rsid : rs1800460 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/8644731/ https://pubmed.ncbi.nlm.nih.gov/39011784/ https://pubmed.ncbi.nlm.nih.gov/35431360/ Summary : rs1800460 is one of the two changes that define the low-activity TPMT *3A/*3B alleles. The T (variant) allele lowers TPMT enzyme activity — in lab studies it gave about 4-fold less TPMT protein and roughly 9-fold less enzyme activity than the normal C allele. TPMT clears thiopurine drugs (azathioprine, mercaptopurine), so lower activity means the drug builds up and the risk of bone-marrow toxicity rises. One variant copy (C/T) means moderately reduced activity; two copies (T/T) means very low activity and a high toxicity risk needing dose reduction. This only matters if you take a thiopurine. Interpretation: You have the C/C genotype — normal-function TPMT at this position. If you take a thiopurine (azathioprine or mercaptopurine), you are expected to metabolize it normally and follow standard dosing. This is the reassuring genotype for TPMT activity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atorvastatin exposure (SLCO1B1) rsid : rs4149056 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/32128760/ https://pubmed.ncbi.nlm.nih.gov/38493369/ Summary : Each C allele is associated with higher Atorvastatin exposure (SLCO1B1) (+0.38 per copy, study scale). Moderate evidence, 5 records. Interpretation: You have the C/T genotype, which means you may have increased exposure to atorvastatin compared to people with the T/T genotype. Other genetic and clinical factors can also influence your atorvastatin exposure. This annotation only covers the pharmacokinetic relationship between rs4149056 and atorvastatin and does not include evidence about clinical outcomes. • Irinotecan / SN-38 exposure (SLCO1B1) rsid : rs4149056 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18221820/ https://pubmed.ncbi.nlm.nih.gov/19390945/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. SLCO1B1 makes OATP1B1, a liver transporter that helps clear SN-38, the active and toxic breakdown product of the chemotherapy drug irinotecan. The minor C allele (the *5/*15 variant, c.521T>C) lowers transporter activity, so SN-38 is cleared more slowly and builds up to higher blood levels (higher exposure / AUC). Carriers of C therefore tend to have greater SN-38 exposure and a higher risk of irinotecan side effects such as low white-cell counts (neutropenia) and diarrhoea. People without the C allele clear SN-38 faster and reach lower levels. Interpretation: If you are treated with irinotecan and have the T/C genotype (one reduced-function C allele), your liver clears SN-38 somewhat more slowly than T/T, so SN-38 builds up to higher blood levels (higher exposure / AUC). This can mean a somewhat higher risk of side effects like neutropenia or diarrhoea. Other factors (such as UGT1A1) also matter — discuss monitoring with your oncologist. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Clopidogrel (Plavix) – reduced activation (CYP2C19*2) rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21972404/ https://pubmed.ncbi.nlm.nih.gov/21527445/ Summary : rs4244285 is the CYP2C19*2 variant. The minor A allele creates a faulty splice site that produces a non-working CYP2C19 enzyme. Clopidogrel is a 'prodrug' — it must be switched on by CYP2C19 to thin the blood. People who carry the A allele activate clopidogrel less, so they get less of its anti-clotting effect and have a higher risk of clots (heart attack, stent blockage, stroke). This is one of the best-established pharmacogenetic findings; guidelines (CPIC) recommend an alternative antiplatelet drug for poor metabolizers. The A allele is the loss-of-function allele; G is the normal-function allele. Interpretation: If you take clopidogrel and have the G/G genotype (CYP2C19 *1/*1), you have two normal-function copies and activate clopidogrel normally — a typical (normal-metabolizer) response. This variant gives no reason to change clopidogrel for you, though other CYP2C19 variants not covered here can still matter. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Proton pump inhibitors & SSRIs – CYP2C19 metabolism (*2 variant) rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21192344/ Summary : rs4244285 is the CYP2C19*2 variant; the minor A allele makes a non-working CYP2C19 enzyme. Unlike clopidogrel, proton pump inhibitors (PPIs) and several SSRIs (citalopram, escitalopram, sertraline) are these drugs' active forms that CYP2C19 breaks down. People who carry the A allele clear these drugs more slowly, so blood levels run higher. For PPIs that can mean stronger acid suppression and better ulcer/H. pylori treatment; for SSRIs it can mean higher exposure and a greater chance of dose-related side effects, so a lower starting dose is sometimes advised. The A allele is the slow (loss-of-function) allele; G is normal-function. Interpretation: If you take a PPI or a CYP2C19-metabolised SSRI and have the G/G genotype (CYP2C19 *1/*1), you break these drugs down at a normal rate (normal metabolizer). Expect typical drug levels and a typical response; this variant gives no reason to change your dose. Note that some people carry rapid-metabolizer variants (not covered here) that can lower PPI levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Voriconazole – CYP2C19 metabolism rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/35081606/ Summary : rs4244285 is the CYP2C19*2 variant; the minor A allele makes a non-working CYP2C19 enzyme. Voriconazole, an antifungal, is broken down mainly by CYP2C19. People who carry the A allele clear voriconazole more slowly, so blood levels run higher — poor metabolizers can reach roughly 3-fold higher trough levels than normal metabolizers, raising the risk of side effects (including liver and visual effects). Guidelines (CPIC) suggest poor metabolizers may need a lower dose or an alternative antifungal, with drug-level monitoring. The A allele is the slow (loss-of-function) allele; G is normal-function. Interpretation: If you take voriconazole and have the G/G genotype (CYP2C19 *1/*1), you break it down at a normal rate (normal metabolizer) and tend to reach typical blood levels — a standard dose is usually appropriate, with routine monitoring. (Separate rapid-metabolizer variants, not covered here, can lower levels and risk under-treatment.) Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin – CYP2C19 metabolism rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16815679/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4244285 is the CYP2C19*2 variant; the minor A allele makes a non-working CYP2C19 enzyme. Phenytoin is broken down mainly by a different enzyme, CYP2C9; CYP2C19 plays only a minor, back-up role that becomes more relevant at higher phenytoin doses. People who carry the A allele may clear phenytoin slightly more slowly, but CYP2C9 (not covered here) and VKORC-independent factors are the main genetic drivers of phenytoin levels and toxicity. The A allele is the loss-of-function allele; G is normal-function. Treat the CYP2C19 contribution as secondary. Interpretation: If you take phenytoin and have the G/G genotype (CYP2C19 *1/*1), your CYP2C19 works normally. Because phenytoin is cleared mainly by CYP2C9, this CYP2C19 result has little impact on your phenytoin levels on its own. Your CYP2C9 status (a separate gene not covered here) is the more important genetic factor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin – CYP2C19 effect on dosing ⚠ CAUTIOUS rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22549502/ https://pubmed.ncbi.nlm.nih.gov/36222113/ https://pubmed.ncbi.nlm.nih.gov/25126975/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4244285 is the CYP2C19*2 variant; the minor A allele makes a non-working CYP2C19 enzyme. Warfarin dosing is driven mainly by two other genes, CYP2C9 and VKORC1 — CYP2C19 is not a major warfarin-metabolising enzyme. Reports linking CYP2C19*2 to warfarin dose are inconsistent and any effect is small, so this variant is not used in standard warfarin dosing. The A allele is the loss-of-function allele; G is normal-function. For warfarin, your CYP2C9 and VKORC1 results (not covered here) are what matter. Interpretation: If you take warfarin and have the G/G genotype (CYP2C19 *1/*1), this variant has essentially no established effect on your warfarin dose. Warfarin response is driven by CYP2C9 and VKORC1 (separate genes not covered here) plus diet and other medicines — those are what guide dosing and INR monitoring. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Clopidogrel – reduced activation (CYP2C19 *3) ⚠ CAUTIOUS rsid : rs4986893 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25060201/ https://pubmed.ncbi.nlm.nih.gov/22462746/ https://pubmed.ncbi.nlm.nih.gov/39300676/ Summary : rs4986893 is the CYP2C19 *3 variant. Clopidogrel (Plavix) is an inactive 'prodrug' that the CYP2C19 enzyme must switch on in the body. The A allele produces a non-working enzyme, so each A copy lowers your ability to activate clopidogrel, leaving less of the active drug and weaker platelet (clot) inhibition. People who carry A alleles (intermediate or poor metabolizers) get less protection from clopidogrel and have a higher risk of clots and cardiovascular events; guidelines (CPIC) suggest an alternative antiplatelet drug such as prasugrel or ticagrelor for them. *3 is one of the two main loss-of-function alleles and is most common in East Asian populations. Relevant only if you take clopidogrel. Interpretation: You have the G/G genotype at rs4986893 (no CYP2C19 *3 loss-of-function copy here). If you take clopidogrel, your CYP2C19 enzyme can activate it normally through this variant, so you are expected to get the usual blood-thinning benefit. Other CYP2C19 variants (such as *2) and clinical factors can still affect your response, so this is not the whole picture. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Acetaldehyde accumulation from alcohol (ALDH2) rsid : rs671 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31002879/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs671 is the ALDH2 *2 variant. The enzyme ALDH2 normally breaks down acetaldehyde, the toxic intermediate your body makes when it processes alcohol. The A allele (ALT) makes a much less active enzyme, so after drinking, A-allele carriers clear acetaldehyde slowly and it builds up — driving the classic 'Asian flush' (red face, warmth, fast heartbeat, nausea). Even one A copy strongly reduces enzyme activity (heterozygotes can show several-fold higher acetaldehyde than people with two G alleles), and two A copies nearly abolish it. This describes the pharmacokinetic relationship only; it applies if you drink alcohol. Higher acetaldehyde is also a recognised carcinogen exposure, which is why ALDH2-deficient drinkers face elevated risk of certain cancers. Interpretation: You have the G/G genotype at rs671, which may mean lower concentrations of acetaldehyde — a metabolite of ethanol — compared to people with the G/A genotype. This reflects only the pharmacokinetic relationship between rs671 and acetaldehyde and does not cover clinical outcomes. Other genetic and clinical factors can also influence your acetaldehyde levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Naltrexone response for alcoholism (ALDH2) rsid : rs671 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/34680127/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs671 is the ALDH2*2 variant (A allele = inactive enzyme, the 'alcohol flush' allele common in East Asian populations). One small pharmacogenetic study suggested ALDH2 genotype may influence how well naltrexone works for alcohol use disorder, but reports disagree on which genotype responds better, so the direction is unresolved. This is preliminary and should not guide treatment. Interpretation: You have the G/G genotype (two fully active ALDH2 copies). A single small study looked at whether ALDH2 genotype predicts naltrexone response in alcohol use disorder, but the evidence is limited and reports disagree on which genotype does better, so no reliable per-genotype effect can be stated. Many other factors influence how well naltrexone works. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - Direction unresolved — single study, conflicting evidence on which genotype responds better. • Statin response (APOE) rsid : rs7412 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16103896/ https://pubmed.ncbi.nlm.nih.gov/30363031/ Summary : rs7412 is one of the two SNPs that define APOE type; the T allele (ALT) is the ε2-defining allele. People who carry the T (ε2) allele tend to get a somewhat larger drop in LDL ('bad') cholesterol from statins such as atorvastatin than people with the common C/C (ε3/ε4) genotype. For example, one stroke-patient study saw the biggest LDL reductions in ε2 carriers. The effect is modest and not consistent across every study, and statins lower cholesterol effectively across all APOE types — so this nudges the expected response rather than deciding whether a statin will work. It is only relevant if you take a statin. Interpretation: You have the C/C genotype at rs7412 in APOE, which means you may have a decreased response to atorvastatin compared to people with the C/T or T/T genotype. Keep in mind that other genetic and clinical factors can also influence how you respond to atorvastatin treatment. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fenofibrate response in hypertriglyceridemia (APOE) rsid : rs7412 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12042669/ Summary : rs7412 is one of the two SNPs that define APOE type; the T allele (ALT) is the ε2-defining allele. In people with high triglycerides treated with fenofibrate, ε2 (T-allele) carriers have been reported to get a larger triglyceride drop than people with the common C/C genotype — in one study triglyceride reductions were about 53% for ε2 versus roughly 33-36% for other types. ε2 carriers also tend to start with higher triglycerides. Findings are not unanimous (a larger study found no APOE effect), so this is a tendency rather than a rule, and fenofibrate lowers triglycerides across APOE types. It is only relevant if you take fenofibrate. Interpretation: If you have the C/C genotype and hypertriglyceridemia, you may have a decreased response to fenofibrate compared to people with the C/T or T/T genotype (carriers of E2 or E2/E2). Other genetic and clinical factors can also influence how you respond to fenofibrate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Salmeterol & beta-2 agonists – asthma response (ADRB2) rsid : rs1042713 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16772309/ https://pubmed.ncbi.nlm.nih.gov/19932356/ https://pubmed.ncbi.nlm.nih.gov/19800676/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1042713 is the ADRB2 Arg16Gly variant in the beta-2 receptor that asthma reliever/controller inhalers act on. REF=G is the Gly16 allele, ALT=A is the Arg16 allele. In studies of asthma response to salmeterol and other beta-2 agonists, Gly16 (G) carriers often responded better while Arg16 (A/A) was sometimes linked to a poorer response or more exacerbations with regular use — but the evidence is genuinely conflicting and not all studies agree. This only matters if you use these inhalers; treatment decisions rest with your doctor. Interpretation: You have the G/A genotype in ADRB2. If you take salmeterol-type inhalers, your response is generally reported as intermediate to good, similar to G/G in many studies, but the evidence is mixed. Relevant only while on these medications. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methotrexate – response & toxicity in rheumatoid arthritis (SLC19A1) rsid : rs1051266 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19827168/ https://pubmed.ncbi.nlm.nih.gov/33794950/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1051266 is the G80A variant in SLC19A1 (RFC1), the transporter that carries folate and the drug methotrexate into cells. REF=T and ALT=C here. Because the transporter helps methotrexate get into cells, this variant has been studied for how well methotrexate works and how likely it is to cause side effects in rheumatoid arthritis (PharmGKB level 2A for efficacy). However, study results point in different directions and no single allele is a reliable predictor; it is one of many factors. This is meaningful only if you take methotrexate. Interpretation: You have the T/C genotype at rs1051266. If you take methotrexate, you carry one of each allele at this folate/methotrexate transporter variant. Studies disagree on what this means for drug response or side effects, so it isn't a reliable individual predictor. This matters only while on methotrexate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Statins – HDL cholesterol response (LIPC) rsid : rs1800588 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16103896/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800588 is the LIPC -514C>T variant in the hepatic lipase gene (REF=C, ALT=T). The T allele lowers hepatic lipase activity, which is linked to modestly higher HDL ('good') cholesterol (a strong GWAS signal, beta around 0.07–0.14). In statin studies, T-allele carriers showed a larger rise in HDL on treatment (about +7% on pravastatin) while C/C carriers had almost no HDL change, so the variant chiefly affects how much your HDL improves on a statin. Effect sizes are small and HDL is only one piece of overall lipid health. Interpretation: You have the C/T genotype, carrying one T allele that lowers hepatic lipase activity and is linked to somewhat higher HDL. If you take a statin, you may see a modestly greater rise in HDL than C/C individuals. The effect is small and one of many factors in your lipid profile. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Statins – response (CELSR2) rsid : rs646776 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31969989/ https://pubmed.ncbi.nlm.nih.gov/20339536/ https://pubmed.ncbi.nlm.nih.gov/25350695/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each T allele is associated with higher Statins – response (CELSR2) (+0.02 per copy, study scale). Interpretation: Both copies at this position carry the T variant — a T/T genotype. People with T/T tend to sit toward the higher end of the statins – response range, with each T copy contributing a small upward shift. Per-copy effect size: β ≈ 0.02 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Thiopurine drugs (azathioprine, mercaptopurine, thioguanine) – metabolism & toxicity (TPMT*3C) rsid : rs1142345 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25624441/ https://pubmed.ncbi.nlm.nih.gov/27564568/ Summary : Each C allele (TPMT*3C, rs1142345) increases thiopurine toxicity risk (azathioprine, mercaptopurine, thioguanine) by causing reduced TPMT enzyme activity (+7.69 per copy, study scale). CPIC guideline-level evidence: heterozygotes (T/C) require ~30-80% dose reduction and homozygotes (C/C) require ~10x dose reduction or alternative therapy to avoid severe myelosuppression. Limited primary record but strong CPIC consensus. Interpretation: Both copies at this position carry the T baseline variant — a T/T genotype, with no copies of the C risk variant present. Your genetic risk for thiopurine drugs (azathioprine, mercaptopurine, thioguanine) – metabolism & toxicity sits at the lower end of the spectrum — a favourable position relative to C-carriers. Each C copy would raise risk by β ≈ 7.69 per copy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Thiopurine drugs (azathioprine, mercaptopurine) – TPMT metabolism & toxicity risk rsid : rs1800462 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/29683944/ https://pubmed.ncbi.nlm.nih.gov/35431360/ Summary : rs1800462 defines the TPMT*2 variant in the TPMT gene, which makes the enzyme that clears thiopurine drugs (azathioprine, mercaptopurine, thioguanine). The G allele (TPMT*2) is the reduced-function version: it lowers TPMT enzyme activity, so the drug and its toxic metabolites build up and the risk of dangerous bone-marrow suppression goes up. The normal-function allele is C. One G copy gives intermediate activity (often needs a moderate dose reduction); two G copies give very low activity (needs a large dose reduction or an alternative drug). This only matters if you actually take a thiopurine — CPIC guideline-level evidence. Interpretation: You have the C/C genotype — two normal-function TPMT copies, with no copy of the reduced-function G (TPMT*2) variant. If you take a thiopurine drug, you are expected to clear it normally and can usually receive a standard dose. This marker raises no thiopurine-toxicity concern for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine replacement therapy response (CHRNA3) rsid : rs1051730 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25891233/ https://pubmed.ncbi.nlm.nih.gov/23249876/ https://pubmed.ncbi.nlm.nih.gov/29621993/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each A allele is associated with higher Nicotine replacement therapy response (CHRNA3) (+0.1 per copy, study scale). Interpretation: If you have the G/G genotype, you may be more likely to adhere to nicotine replacement therapy (NRT) and to consume more NRT at 7 days post-quit attempt compared with people who carry the A/A or A/G genotype. Other genetic or clinical factors can also affect your adherence to and consumption of NRT. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Smoking cessation drug response (bupropion, varenicline, NRT) rsid : rs16969968 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24733007/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each A allele is associated with higher Smoking cessation drug response (bupropion, varenicline, NRT) (+0.23 per copy, study scale). Limited evidence, 1 record. Interpretation: If you have the G/G genotype at rs16969968, you may have a decreased — but not absent — risk of nicotine dependence when exposed to nicotine compared with people who carry the A/G or A/A genotype. Conflicting evidence has been reported, and some findings are based on haplotype studies with rs680244 or rs680244, rs569207, rs578776, and rs1051730. Other genetic and clinical factors can also influence the risk of nicotine dependence. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Isoniazid + phenytoin – toxicity risk (NAT2) rsid : rs1799930 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27488001/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799930 (590G>A) defines the NAT2*6 slow-acetylator allele in the NAT2 drug-metabolizing gene. The A allele lowers NAT2 acetylation capacity. When isoniazid and phenytoin are taken together, slow acetylators clear isoniazid poorly; the build-up of isoniazid blocks phenytoin breakdown, raising the risk of phenytoin toxicity. Evidence is limited (PharmGKB level 3) and no effect size is reported, so this is a tendency relevant only on this drug combination. Note: this is one of 3 correlated variants in/near NAT2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: If you take isoniazid with phenytoin and have the G/A genotype, you carry one slow-acetylator (A) copy and may have an increased risk of phenytoin toxicity from this interaction compared with G/G. Other NAT2 variants and clinical factors also affect your overall acetylator status and risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Isoniazid & TB drugs – NAT2 slow acetylator status rsid : rs1799931 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27488001/ https://pubmed.ncbi.nlm.nih.gov/41037485/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799931 (857G>A) defines the NAT2*7 slow-acetylator allele in the NAT2 drug-metabolizing gene. The A allele markedly reduces NAT2 acetylation activity, so it contributes to a 'slow acetylator' status. Slow acetylators clear isoniazid and related TB drugs more slowly and have a higher risk of drug-induced liver injury (slow acetylators overall ~3x the odds of isoniazid hepatotoxicity). NAT2 acetylator status depends on the full NAT2 genotype, not this SNP alone. Interpretation: If you take isoniazid or other NAT2-metabolized TB drugs and have the G/G genotype at this position, you do not carry the NAT2*7 slow-acetylator allele here, so this variant does not push you toward slow acetylation or higher TB-drug liver toxicity. Your overall acetylator status still depends on other NAT2 variants. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methadone dosing in heroin dependence (DRD2) rsid : rs1799978 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21902500/ https://pubmed.ncbi.nlm.nih.gov/26437921/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. DRD2 -241A>G (rs1799978) sits in the promoter region of the dopamine D2 receptor gene and can influence how much receptor is made. On the forward strand REF=T (the -241A allele) and ALT=C (the -241G allele), and the C/-241G allele is linked to higher DRD2 expression. Small studies have explored whether this variant affects methadone dose requirements in people treated for heroin dependence, but the evidence is preliminary and the direction is not firmly established. This is low-confidence pharmacogenetic information that only applies during methadone treatment. Note: this is one of 4 correlated variants in/near DRD2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: You have the T/T genotype (two reference T alleles, i.e. the -241A/A form). If you are on methadone maintenance, current evidence does not reliably predict your dose needs from this genotype — the studies are small and preliminary. Methadone dose is set by your clinical response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bupropion for smoking cessation – response (ANKK1/DRD2 Taq1A) ⚠ CAUTIOUS rsid : rs1800497 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15492764/ https://pubmed.ncbi.nlm.nih.gov/17654295/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Taq1A (rs1800497) lies in the ANKK1 gene next to DRD2 and tags the dopamine D2 receptor system. REF=G, ALT=A; the A allele is the historical 'A1' allele, associated with fewer striatal D2 receptors. In pooled smoking-cessation trials, people with the G/G genotype (A2/A2) responded better to bupropion — they were more likely to stay quit — while carriers of one or two A alleles (A1) showed little benefit from bupropion over placebo. The effect is real but modest and not fully consistent, and it only applies if bupropion is used. Interpretation: You have the G/A genotype (one G, one A; A1 carrier). If you take bupropion to quit smoking, studies suggest you may get less added benefit from bupropion than people with G/G, though findings are not fully consistent. Bupropion can still help; this is one input your doctor can weigh. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Isoniazid & anti-TB drugs – NAT2 slow acetylator status rsid : rs1801280 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27488001/ https://pubmed.ncbi.nlm.nih.gov/18421452/ https://pubmed.ncbi.nlm.nih.gov/29036176/ Summary : rs1801280 is the NAT2*5 variant (a 341T>C / Ile114Thr change) in the N-acetyltransferase 2 gene. The C (alternate) allele reduces NAT2 enzyme activity; people who carry two slow-acetylator alleles are "slow acetylators" who clear NAT2-metabolized drugs — most notably the TB drug isoniazid — more slowly. Slower clearance means the drug and its by-products build up, which raises the chance of side effects such as liver injury. This describes your metabolizer tendency rather than a yes/no disease risk; the strongest effect is seen in people carrying two slow alleles, and it only matters when you actually take one of these medicines. Interpretation: You have the T/T genotype at this NAT2 position — no copy of the slow-acetylator C allele here. On its own this site points toward faster (normal) acetylation. If you take isoniazid or related anti-TB drugs, this allele alone does not push you toward the slow-clearance, higher-side-effect group, but your full NAT2 status depends on other NAT2 variants too. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Naltrexone response in alcoholism (ADH1B) rsid : rs2066702 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/34680127/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each A allele is associated with lower Naltrexone response in alcoholism (ADH1B) (−0.202 per copy, study scale). Limited evidence, 1 record. Interpretation: If you have alcoholism and the G/G genotype at rs2066702, you may have an increased response to naltrexone compared with people who have the A/A or G/A genotypes. Other genetic and clinical factors also influence response to naltrexone. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Allopurinol response & dosing (ABCG2) rsid : rs2231142 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/29341237/ https://pubmed.ncbi.nlm.nih.gov/29342288/ Summary : Each T allele is associated with higher Allopurinol response & dosing (ABCG2) (+0.293 per copy, study scale). Moderate evidence, 2 publications. Interpretation: Both copies at this position carry the G variant — a G/G genotype, with no copies of the T variant present. People with G/G tend to sit toward the lower end of the allopurinol response & dosing range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.29 per copy. • Apixaban – drug levels (ABCG2) ⚠ CAUTIOUS rsid : rs2231142 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/28678049/ https://pubmed.ncbi.nlm.nih.gov/36186466/ https://pubmed.ncbi.nlm.nih.gov/29457840/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2231142 is the ABCG2 Q141K variant. The T (alternate) allele lowers the activity of the ABCG2 transporter, which helps move apixaban out of the body. With weaker transport, T carriers can reach somewhat higher apixaban blood levels for the same dose. Higher levels could mean slightly more anticoagulant effect (and a small theoretical increase in bleeding tendency), though apixaban is also handled by other pathways, so the effect is modest. This is an informational tendency about drug levels, not a fixed risk, and it only matters if you take apixaban. Interpretation: You have the G/G genotype — full-function ABCG2 transporter. If you take apixaban, you clear it normally and this variant does not push your drug levels up. Standard dosing considerations apply. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid pain medications – response & side effects (COMT Val158Met) rsid : rs4680 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/30704436/ https://pubmed.ncbi.nlm.nih.gov/19094200/ https://pubmed.ncbi.nlm.nih.gov/23773341/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the well-known COMT Val158Met variant. The G allele (reference) codes Valine = a fast dopamine-clearing enzyme; the A allele codes Methionine = a slow enzyme (about 3–4x less activity). For opioid painkillers, carriers of the A (Met) allele tend to need somewhat lower opioid doses to control pain — their mu-opioid receptors respond more, so the same dose goes further — while G/G (Val/Val) carriers often need somewhat more. The effect is modest and one of many factors in pain control. It only matters if you take opioids; no single odds ratio applies across studies. Note: this is one of 4 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: You have the G/A (Val/Met) genotype — intermediate enzyme activity. If you take opioids, your dose needs are likely in between the G/G and A/A groups. If you don't take opioids, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine replacement therapy response (CHRNA5) rsid : rs588765 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23249876/ https://pubmed.ncbi.nlm.nih.gov/26010901/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs588765 sits in the CHRNA5 nicotine-receptor gene cluster on chromosome 15, a region strongly tied to how heavily people smoke and how dependent they become. REF=T, ALT=C; the T allele is linked to higher CHRNA5 activity and somewhat heavier baseline smoking. Researchers hoped this marker would also predict who quits more easily on nicotine replacement or varenicline, but the best clinical-trial data (PMID 26010901) found no significant difference in quit success between genotypes for any treatment. So on current evidence this variant does not reliably tell you whether nicotine replacement or varenicline will work for you. It is informational only, with no good/bad signal. Interpretation: You have the T/T genotype (two T alleles) in this nicotine-receptor gene. If you smoke and try to quit, current studies do not show that this genotype changes how well nicotine patches/gum or varenicline work for you — quit success looks similar across genotypes. The T allele is associated with somewhat heavier smoking generally, but that does not reliably predict your response to stop-smoking medicines. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methadone response (DRD2) ⚠ CAUTIOUS rsid : rs6277 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18687376/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6277 is the DRD2 C957T variant. On the forward strand REF=G (957C) and ALT=A (957T). In methadone maintenance for opioid dependence, a study (PMID 18687376) found that 957C/957C carriers — the G/G genotype on this strand — were more often non-responders (about 2.4x the odds) and had a shorter period of clean urine tests, meaning the A allele (957T) is linked to better methadone response. The evidence is modest and methadone outcomes depend on many factors, so this is informational and only relevant if you are on methadone. Note: this is one of 4 correlated variants in/near DRD2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: If you have the G/G genotype and are on methadone, one study found people with this genotype were more likely to respond poorly to methadone maintenance than people with the A/A genotype. The effect is modest and methadone success depends heavily on dose, support and other factors, so this is background information rather than a prediction. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Clozapine response in schizophrenia (HTR1A) ⚠ CAUTIOUS rsid : rs6295 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25560469/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6295 is the HTR1A C(-1019)G promoter variant (the alternate allele is G, not A). Limited pharmacogenetic evidence has linked HTR1A genotype to clozapine response in schizophrenia, but findings are inconsistent and the direction is not firmly established. This only matters if you are taking clozapine. Interpretation: You have the C/C genotype at rs6295 (HTR1A). HTR1A genotype has been weakly linked to clozapine response in schizophrenia, but the evidence is limited and inconsistent, so no reliable per-genotype effect can be stated. It is only relevant while taking clozapine. Many other genetic and clinical factors affect medication response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Lurasidone response in schizophrenia (HTR1A) ⚠ CAUTIOUS rsid : rs6295 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31636356/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6295 is the HTR1A C(-1019)G promoter variant (the alternate allele is G, not A). A single small study (European ancestry) linked HTR1A genotype to lurasidone response in schizophrenia, with C/C carriers reported to respond better, but this is preliminary and not replicated. This only matters if you are taking lurasidone. Interpretation: You have the C/C genotype at rs6295 (HTR1A). One small study in people of European ancestry suggested C/C carriers may respond better to lurasidone, but this is preliminary and unreplicated. It is only relevant while taking lurasidone. Many other genetic and clinical factors affect medication response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bupropion response for smoking cessation (COMT) rsid : rs165599 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16876132/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs165599 is a variant in COMT, the gene for the enzyme that breaks down dopamine and related brain chemicals. In a study of smokers trying to quit with bupropion, carriers of the A (alternate) allele had a better chance of staying abstinent on bupropion, while people with the common G/G genotype tended to respond less well. This comes from a single pharmacogenomic study (PharmGKB level 3), so it is a tendency rather than a firm rule, and it only matters if you are actually using bupropion to quit smoking. Interpretation: If you are using bupropion to quit smoking, the G/A genotype (one A allele) was associated with a better chance of responding than the G/G genotype, though you can still relapse based on genotype alone. Other genetic and clinical factors also influence quitting success. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid response & side effects (COMT) rsid : rs4633 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24533707/ https://pubmed.ncbi.nlm.nih.gov/31745220/ https://pubmed.ncbi.nlm.nih.gov/27061230/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a variant in COMT, an enzyme that breaks down dopamine and related signalling chemicals and influences pain processing (here REF=C, ALT=T). A pharmacogenetic study (PMID 31745220) linked the C/T (heterozygous) genotype to a higher chance of dizziness in people on long-term opioids, compared with either homozygous genotype. The signal is a single level-3 toxicity finding with no effect-size number, so treat it as a weak heads-up about a possible side effect, relevant only while you are taking opioids. Note: this is one of 4 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: If you take long-term opioids and have the C/T genotype, one study suggests you may be a bit more likely to experience dizziness than people with either C/C or T/T. This is a weak single-study signal, not a certainty; tell your care team if dizziness occurs. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Quetiapine response in schizophrenia (COMT) rsid : rs4818 Your geno : CG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/28696411/ https://pubmed.ncbi.nlm.nih.gov/26282453/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a variant in COMT, an enzyme that breaks down dopamine in the brain (here REF=C, ALT=G). A pharmacogenetic study (PMID 26282453) linked the C/C genotype to a poorer response to the antipsychotic quetiapine in schizophrenia, with G/G responding better. The evidence is limited (a single level-3 finding, no effect-size number), so this is a weak tendency, not an established predictor of how quetiapine will work for you. Note: this is one of 2 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have schizophrenia and take quetiapine with the C/G genotype, your expected response is intermediate — likely better than C/C but not as good as G/G. The evidence is limited, so treat this as a weak hint. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Risperidone response in schizophrenia (COMT) ⚠ CAUTIOUS rsid : rs4818 Your geno : CG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/28696411/ https://pubmed.ncbi.nlm.nih.gov/26282453/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a variant in COMT, an enzyme that breaks down dopamine in the brain (here REF=C, ALT=G). A pharmacogenetic study (PMID 28696411) tentatively linked the C/C genotype to a poorer response to the antipsychotic risperidone in schizophrenia, with G-allele carriers responding better. The signal was weak and lost statistical significance after correction for multiple testing, and no effect-size number is given — so treat it as a very uncertain tendency, not an established predictor. Note: this is one of 3 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: If you have schizophrenia and take risperidone with the C/G genotype, you may respond somewhat better than people with C/C, based on a weak, unconfirmed signal. Do not rely on this alone; many other factors shape response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin dose requirement (STX4) rsid : rs10871454 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18535201/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This common variant sits in the STX4 gene region (near genes involved in blood clotting). The T allele has been linked in genome-wide studies to needing a somewhat LOWER weekly maintenance dose of warfarin to reach the same anticoagulation. The C allele is the normal-dose-associated (reference) version. The effect is small compared with the major warfarin genes (VKORC1 and CYP2C9) and is a population-average tendency, not a personal dose. Warfarin is always dosed and checked by INR blood test, so this only nudges expectations and only matters if you take warfarin. Interpretation: You have the T/T genotype — two copies of the lower-dose-associated allele. If you take warfarin, population data suggest a modestly lower weekly maintenance dose on average; this is a minor nudge on top of the main warfarin genes, and your dose is still guided by INR. Only relevant while taking warfarin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cisplatin chemotherapy response (GSTP1) ⚠ CAUTIOUS rsid : rs1138272 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22188361/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1138272 (GSTP1 Ala114Val on the protein; forward-strand C>G is Ala114Gly) sits in the glutathione S-transferase pi gene, which helps detoxify platinum chemotherapy drugs such as cisplatin. Some studies report that carriers of the variant (G) allele have longer survival on platinum-based chemotherapy, but the evidence is mixed and conflicting. This only matters during cisplatin treatment. Interpretation: You have the C/C genotype at rs1138272 (GSTP1) — the common form of this glutathione S-transferase. GSTP1 helps detoxify platinum chemotherapy, and some studies link the variant (G) allele rather than C/C to longer survival on cisplatin, but the evidence is mixed and conflicting. This is only relevant during cisplatin treatment. Many other genetic and clinical factors affect chemotherapy outcomes. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - Conflicting evidence for cisplatin survival association. • Thiotepa clearance (GSTP1) ⚠ CAUTIOUS rsid : rs1138272 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19076156/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1138272 (GSTP1, forward-strand C>G = Ala114Gly) sits in the glutathione S-transferase pi gene, which metabolises the chemotherapy drug thiotepa. A pharmacokinetic annotation reports that the common C/C form is associated with slower (decreased) thiotepa clearance than the variant G/G form. This is a drug-handling difference, not a disease risk, and only matters during thiotepa treatment. Interpretation: You have the C/C genotype at rs1138272 (GSTP1). If you receive thiotepa, the C/C form is associated with slower (decreased) clearance of the drug compared with the variant G/G form, meaning it may stay in the body a little longer. This is a drug-handling difference, not a disease risk, and only matters during thiotepa treatment. Many other clinical factors also affect clearance. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Thiopurines (mercaptopurine/azathioprine) – toxicity risk (NUDT15) rsid : rs116855232 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25624441/ https://pubmed.ncbi.nlm.nih.gov/30728528/ https://pubmed.ncbi.nlm.nih.gov/29923122/ Summary : NUDT15 c.415C>T (T allele = *3) is a loss-of-function variant that increases thiopurine toxicity (+11 per copy on study scale). CPIC Level A: *3/*3 (poor metabolizer) requires 50-65% dose reduction or alternative non-thiopurine drug. Limited evidence, 1 record. Interpretation: If you have the C/C genotype at rs116855232, you may tolerate an increased dose of mercaptopurine compared to people with the C/T or T/T genotype. Other genetic and clinical factors may also influence mercaptopurine dose. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tacrolimus dosing after transplant (CYP3A5) rsid : rs15524 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21047202/ https://pubmed.ncbi.nlm.nih.gov/39539273/ https://pubmed.ncbi.nlm.nih.gov/41057866/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs15524 is in the CYP3A5 gene and is in strong linkage with the CYP3A5*3 non-expresser allele (rs776746), which determines whether the CYP3A5 enzyme is active. CYP3A5 status strongly affects tacrolimus metabolism: non-expressers clear the drug slowly and reach higher blood levels per dose, while expressers need higher doses. rs15524 tags this difference, but reports disagree on which rs15524 allele aligns with non-expresser status, so no confident per-genotype direction is given here — CYP3A5*3 (rs776746) genotyping is the definitive test. Note: this is one of 3 correlated variants in/near CYP3A5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the A/A genotype at rs15524 (CYP3A5). This variant tracks with CYP3A5 enzyme activity, which strongly affects tacrolimus dosing after transplant, but reports disagree on which rs15524 allele matches the non-expresser (slow-metaboliser) state, so no reliable per-genotype direction can be stated from this marker alone. This is only relevant if you take tacrolimus; CYP3A5*3 (rs776746) testing is the definitive guide for dosing. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - Tag SNP for CYP3A5*3 — direction of the A/G allele relative to non-expresser status is not consistently reported; rs776746 genotyping is definitive. • Carbamazepine metabolism (CYP3A5) ⚠ CAUTIOUS rsid : rs15524 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26421491/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs15524 is in the CYP3A5 gene and is in strong linkage with the CYP3A5*3 non-expresser allele, which determines CYP3A5 enzyme activity. A single pharmacokinetic annotation links rs15524 genotype to carbamazepine concentrations (mainly when carbamazepine is combined with phenytoin or phenobarbital), but the evidence is limited and the direction relative to the A/G alleles is not firmly established. This only matters if you take carbamazepine. Interpretation: You have the A/A genotype at rs15524 (CYP3A5). This variant tracks with CYP3A5 enzyme activity, which can affect carbamazepine handling, but the evidence is limited (and mainly seen when carbamazepine is combined with phenytoin or phenobarbital), so no reliable per-genotype direction can be stated. This is only relevant if you take carbamazepine. Many other clinical factors also affect drug levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - Tag SNP for CYP3A5*3; carbamazepine PK association from a single level-3 annotation. • Acenocoumarol & phenprocoumon dose requirement (CYP4F2) rsid : rs2108622 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22486182/ https://pubmed.ncbi.nlm.nih.gov/21110013/ https://pubmed.ncbi.nlm.nih.gov/19578179/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. CYP4F2 rs2108622 (V433M). The T allele lowers CYP4F2 activity, the enzyme that clears vitamin K; with less vitamin K cleared, T-carriers tend to need a slightly HIGHER maintenance dose of vitamin K antagonists such as acenocoumarol and phenprocoumon. The effect is small and works the same way as for warfarin; dose is always set by INR monitoring, not by genotype alone. Interpretation: You have one T and one C allele (C/T). If you take acenocoumarol or phenprocoumon, you may need a slightly higher maintenance dose than C/C, because one reduced-activity T copy leaves a little more vitamin K in circulation. The effect is small and your dose is still guided by INR monitoring. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Carbamazepine dosing (EPHX1) ⚠ CAUTIOUS rsid : rs2234922 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23252947/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. EPHX1 rs2234922 (His139Arg). EPHX1 makes microsomal epoxide hydrolase, an enzyme that helps break down carbamazepine. The G allele (His139Arg) is the higher-activity form; people carrying G have tended to need a somewhat higher carbamazepine dose, while A/A people may need a lower dose. Evidence is modest (PharmGKB level 3) and one study disagreed, so this is a weak tendency, not a rule — dose is set by blood levels and seizure control. Interpretation: If you have the A/G genotype, you may require an increased dose of carbamazepine compared to people with the A/A genotype, although this is contradicted in one study. Other genetic and clinical factors may also influence your carbamazepine dose. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Docetaxel clearance (EPHX1) ⚠ CAUTIOUS rsid : rs2234922 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20157331/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. EPHX1 rs2234922 (His139Arg). In a single study, the A/A genotype was linked to faster clearance of the chemotherapy drug docetaxel, while carrying the G allele was linked to slower clearance. This rests on one small pharmacokinetic study (PharmGKB level 3), so it is a weak, preliminary signal rather than an established effect. Interpretation: If you have the A/G genotype, you may have decreased clearance of docetaxel compared to people with the A/A genotype. Other genetic and clinical factors may also influence docetaxel clearance. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tacrolimus dosing (CYP3A4 *1G) rsid : rs2242480 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22108237/ https://pubmed.ncbi.nlm.nih.gov/24189425/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. CYP3A4 rs2242480 (the *1G allele, now PharmVar *36). The T allele (*1G) is associated with increased CYP3A4 enzyme activity, which speeds up tacrolimus metabolism; T-carriers tend to clear tacrolimus faster and may need a higher dose to reach target blood levels, while C/C people metabolise it more slowly. Evidence is graded PharmGKB level 2A but is partly conflicting. Tacrolimus is always dosed to blood levels, so genotype is supportive context only. Interpretation: If you have the C/C genotype, you may have decreased metabolism of tacrolimus compared to people with the C/T or T/T genotype. However, conflicting evidence has been reported. This annotation only covers the pharmacokinetic relationship between rs2242480 and tacrolimus and does not include evidence about clinical outcomes. Other genetic and clinical factors may also influence tacrolimus metabolism. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fentanyl dose requirement (CYP3A4 *1G) rsid : rs2242480 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21513075/ https://pubmed.ncbi.nlm.nih.gov/30381583/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. CYP3A4 rs2242480 (the *1G allele, now PharmVar *36). CYP3A4 breaks down fentanyl. The T allele (*1G) speeds up this metabolism, so T/T people tend to clear fentanyl faster and have needed a LOWER dose for postoperative pain, whereas C/C (and to a lesser extent C/T) people have tended to need a higher dose. This is a PharmGKB level-2A association; fentanyl is always titrated to your actual pain and breathing. Interpretation: If you have the C/C genotype, you may require an increased dose of fentanyl to manage postoperative pain compared to people with the T/T genotype. Other genetic and clinical factors may also affect fentanyl dosage requirements. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atorvastatin response (CYP3A4 *1G) ⚠ CAUTIOUS rsid : rs2242480 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18528690/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. CYP3A4 rs2242480 (the *1G allele, now PharmVar *36). In people with high cholesterol on atorvastatin, carrying the T allele (*1G) was associated with a BETTER cholesterol-lowering response, while C/C was associated with a weaker response. This is a single low-level association (PharmGKB level 3 Efficacy), so it is a weak tendency rather than a basis for changing treatment. Interpretation: If you have the C/C genotype and hyperlipidemia, you may have a reduced response to atorvastatin treatment (a lower reduction in total cholesterol) compared to people with the C/T or T/T genotype. Other genetic and clinical factors may also influence your response to atorvastatin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin dose sensitivity (VKORC1) rsid : rs2359612 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31869433/ Summary : VKORC1 rs2359612. VKORC1 is the protein warfarin blocks to thin the blood. This SNP tags the well-known VKORC1 -1639 haplotype that lowers VKORC1 production. The A allele marks the warfarin-sensitive (low-expression) haplotype: A-carriers need LESS warfarin, while G/G people need MORE. This is a strong, well-replicated association (PharmGKB/CPIC level 1B), but warfarin is always dosed to INR, not genotype alone. Note: this is one of 6 correlated variants in/near VKORC1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the A/A genotype at rs2359612. If you take warfarin, you are likely warfarin-sensitive and tend to need a LOWER dose than average, because this genotype tags reduced VKORC1 production. Your actual dose is still set by INR blood tests. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • CYP3A4 *1B variant – altered drug metabolism rsid : rs2740574 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19802823/ https://pubmed.ncbi.nlm.nih.gov/15707415/ https://pubmed.ncbi.nlm.nih.gov/27574448/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. CYP3A4 rs2740574 marks the CYP3A4 *1B allele (a change in the gene's promoter region). CYP3A4 is a major drug-metabolising enzyme. Despite many studies, the *1B variant has little or no clearly proven effect on enzyme activity and is generally classified as a normal-function allele; reported drug associations are inconsistent. So this is mainly informational: it does not reliably predict how you handle CYP3A4 medications. Note its frequency also varies a lot by ancestry. Interpretation: You have the T/T genotype — two copies of the *1B variant. Even so, *1B is generally regarded as a normal-function allele with no reliably proven effect on CYP3A4 drug metabolism, so this is informational; any medication dosing is guided by your clinical response, not this variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin sensitivity & dosing (CYP2C9) rsid : rs28371686 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27121899/ https://pubmed.ncbi.nlm.nih.gov/28685643/ https://pubmed.ncbi.nlm.nih.gov/35108398/ Summary : CYP2C9 rs28371686 is the *5 allele (D360E). CYP2C9 is the main enzyme that clears warfarin. The G allele (*5) reduces CYP2C9 activity, so warfarin is broken down more slowly; G-carriers are warfarin-sensitive and tend to need a LOWER dose to avoid over-thinning and bleeding, while C/C people have normal clearance. *5 is most common in people of African ancestry. This is a recognised reduced-function allele (PharmGKB/CPIC); warfarin is always dosed to INR. Note: this is one of 4 correlated variants in/near CYP2C9 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: You have the C/C genotype, with no copies of the *5 (G) variant. Your CYP2C9 enzyme works at normal activity, so if you take warfarin you do not expect extra sensitivity from this variant. Your dose is still set by INR blood tests. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin metabolism (CYP2C9) rsid : rs28371686 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16220110/ Summary : This is the CYP2C9*5 variant (Asp360Glu) in the liver enzyme CYP2C9, which clears phenytoin, warfarin and several NSAIDs. The G allele (the *5 allele) is a reduced-function form — it slows the enzyme — while the reference C allele works normally. Each G copy lowers how fast these drugs are broken down, so they can build up to higher levels at a standard dose. The *5 allele is uncommon overall and most frequent in people of African ancestry. Effect sizes are not quantified in the source data; this is a function category, not a measured number. Note: this is one of 2 correlated variants in/near CYP2C9 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the C/C genotype — two normal-function copies of CYP2C9. If you take phenytoin, warfarin or similar CYP2C9-cleared drugs, you metabolise them at the usual rate and have no extra sensitivity from this variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • CYP2D6 drug metabolism (tamoxifen, propafenone, antidepressants) rsid : rs28371725 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/33043448/ https://pubmed.ncbi.nlm.nih.gov/18024866/ Summary : This is the CYP2D6*41 marker (the 2988G>A intron variant) in CYP2D6, a liver enzyme that activates or clears about a quarter of common medications. The T allele (the *41 allele on the reported strand) is a reduced-function form: it shifts more of the gene's message to a non-working spliced version, leaving less active enzyme. The reference C allele works normally. Each T copy modestly lowers CYP2D6 activity, nudging a person toward the 'intermediate metaboliser' range. It does not fully switch the enzyme off. The *41 allele is common, especially in people of Middle Eastern and South Asian ancestry. Source data gives no effect-size number; this is a function category. Interpretation: You have the C/C genotype — two normal-function copies at this CYP2D6 marker. If you take a CYP2D6 drug (such as tamoxifen, propafenone or many antidepressants), this variant adds no reduction in how you process it. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin & acenocoumarol dose sensitivity (VKORC1) rsid : rs2884737 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18030307/ https://pubmed.ncbi.nlm.nih.gov/25519826/ Summary : This variant sits in VKORC1, the gene for the enzyme that warfarin and related coumarin blood-thinners block. rs2884737 tags the warfarin-sensitive VKORC1 haplotype (it travels together with the well-known dose-lowering −1639A promoter variant). The C allele marks the sensitive haplotype: people who carry it tend to need a lower coumarin dose to reach the same blood-thinning effect, while the A allele marks the higher-dose haplotype. VKORC1 is the single strongest genetic predictor of warfarin dose. This changes the dose you need, not whether the drug works — and it matters only while you are on a coumarin anticoagulant. Source data does not give a per-allele dose number for this specific marker. Note: this is one of 6 correlated variants in/near VKORC1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the C/C genotype — two copies of the warfarin-sensitive VKORC1 haplotype marker. If you take warfarin or acenocoumarol, you would, on average, need a lower dose than A-allele carriers, and standard starting doses may over-thin your blood. Your doctor should set and closely monitor your dose. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Irinotecan / SN-38 metabolism (UGT1A9) ⚠ CAUTIOUS rsid : rs35350960 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12181437/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant (UGT1A1 P229Q, the *27 allele) changes one amino acid in a UGT glucuronidation enzyme that helps clear SN-38, the active, toxic metabolite of the chemotherapy drug irinotecan. The A allele makes a less active enzyme, so SN-38 is broken down more slowly. This only matters if you are treated with irinotecan, where reduced clearance can raise the risk of side effects such as diarrhoea and low white-cell counts. Evidence is limited; oncology teams consider UGT1A1 status when dosing. Interpretation: If you have the C/C genotype, you carry the normal-function form of this enzyme and break SN-38 (the active metabolite of irinotecan) down at the usual rate. This only matters if you are treated with irinotecan; other genetic and clinical factors also affect SN-38 clearance. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • CYP3A4 *22 – slower metabolism of many drugs rsid : rs35599367 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23327575/ https://pubmed.ncbi.nlm.nih.gov/22388796/ https://pubmed.ncbi.nlm.nih.gov/23665933/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. The A allele tags CYP3A4*22, a reduced-function version of the CYP3A4 enzyme that clears many medicines (for example tacrolimus, cyclosporine, statins, and some blood-pressure and cancer drugs). People carrying A copies tend to break these drugs down more slowly, so the same dose can build up to higher levels. This only matters if you are taking a drug that CYP3A4 handles — your doctor may use it to guide dosing. Interpretation: If you have the G/G genotype, you carry two fully active copies of CYP3A4 (no *22). You metabolise CYP3A4-handled drugs (such as cyclosporine, tacrolimus, or some statins) at the usual rate, so standard dosing is typically expected. This only applies if you take such a drug; other genetic and clinical factors also influence drug levels. • Simvastatin & atorvastatin – stronger LDL reduction (CYP3A4*22) rsid : rs35599367 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25274942/ https://pubmed.ncbi.nlm.nih.gov/20386561/ https://pubmed.ncbi.nlm.nih.gov/21946898/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the CYP3A4*22 variant in CYP3A4, the body's busiest drug-clearing enzyme. The A allele (the *22 allele on the reported strand) lowers CYP3A4 activity, so drugs the enzyme breaks down are cleared more slowly and reach higher levels. For statins cleared by CYP3A4 (simvastatin, atorvastatin, lovastatin), more drug in the blood usually means a stronger LDL-cholesterol drop at the same dose — but also a somewhat higher chance of statin side effects such as muscle aches. The reference G allele gives normal CYP3A4 activity. The *22 allele is uncommon. Some studies disagree on the size of the statin benefit, so evidence is moderate; source data gives no single effect-size number for the statin response. Interpretation: You have the G/G genotype — normal CYP3A4 activity. If you take simvastatin or atorvastatin, you clear it at the usual rate and get the standard LDL-lowering for your dose; this variant adds no extra effect. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tacrolimus dosing (CYP3A4*22) rsid : rs35599367 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/40604035/ https://pubmed.ncbi.nlm.nih.gov/36246675/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each A allele is associated with higher Tacrolimus dosing (CYP3A4*22) (+0.3 per copy, study scale). Moderate evidence, 2 publications. Interpretation: GG genotype — see evidence summary; per-genotype effect not quantified in source data. • Irinotecan – metabolism & toxicity (UGT1A1) ⚠ CAUTIOUS rsid : rs4124874 Your geno : TG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19390945/ https://pubmed.ncbi.nlm.nih.gov/15007088/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4124874 tags UGT1A1*60 (c.-3279T>G, plus strand T>G) in the UGT1A1 promoter. The G allele lowers UGT1A1 enzyme levels. UGT1A1 inactivates SN-38, the active and toxic form of the chemotherapy drug irinotecan, so lower UGT1A1 can mean slower clearance of SN-38 and a higher chance of irinotecan side effects such as low neutrophils and diarrhoea. The evidence here is modest (PharmGKB level 4) and *60 is usually considered alongside the stronger *28/*6 variants. It is only relevant if you receive irinotecan. Interpretation: You have the T/G genotype — one copy of the lower-expression UGT1A1 (*60) allele. If you are treated with irinotecan, you may clear SN-38 (its active toxic form) slightly more slowly than people with T/T, with a modestly higher chance of side effects. The effect is small on its own; tell your oncologist about your full UGT1A1 status. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Carvedilol – metabolism (UGT1A1) rsid : rs4148323 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16849011/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4148323 is UGT1A1*6 (c.211G>A, p.Gly71Arg; plus strand G>A). The A allele reduces UGT1A1 activity. UGT1A1 glucuronidates carvedilol (a beta-blocker for heart failure and angina), making it water-soluble for elimination. The A allele is therefore associated with reduced glucuronidation of carvedilol. This is a pharmacokinetic observation (how the body processes the drug) from limited evidence (PharmGKB level 3); it has not been tied to a specific clinical outcome, so there is no good/bad signal. It is only relevant if you take carvedilol. Interpretation: You have the G/G (UGT1A1 *1/*1) genotype — normal UGT1A1 activity. If you take carvedilol, you glucuronidate (process) it normally at this site, more efficiently than people with the A/A genotype. This is a metabolism observation only, with no established change to how well the drug works or its safety. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Letermovir – exposure (UGT1A1) rsid : rs4148323 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31022310/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4148323 is UGT1A1*6 (c.211G>A, p.Gly71Arg; plus strand G>A). The A allele reduces UGT1A1 activity, one of the enzymes that clears letermovir (an antiviral used to prevent CMV infection after a stem-cell transplant). The A allele is therefore associated with higher letermovir exposure (a higher AUC, meaning more drug stays in the blood). This is a pharmacokinetic observation from limited evidence (PharmGKB level 3) and has not been tied to a specific clinical benefit or harm, so there is no good/bad signal. It is only relevant if you take letermovir. Interpretation: You have the G/G genotype — normal UGT1A1 activity. If you take letermovir, your drug exposure (AUC) at this site is lower than in people carrying the A allele. This is a drug-level observation only, with no established clinical good or bad effect. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methotrexate clearance & GI toxicity (SLCO1B1) ⚠ CAUTIOUS rsid : rs4149081 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23233662/ https://pubmed.ncbi.nlm.nih.gov/19901119/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4149081 A allele is associated with decreased methotrexate clearance (higher systemic exposure) vs the G allele, which may translate to greater GI-toxicity exposure. Evidence is limited and conflicting (PharmGKB level 3). Annotation covers pharmacokinetics only. Note: this is one of 2 correlated variants in/near SLCO1B1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the G/A genotype at rs4149081, you may have increased clearance of methotrexate compared to people with the A/A genotype, but decreased clearance compared to people with the G/G genotype. However, conflicting evidence has been reported. This annotation only covers the pharmacokinetic relationship between rs4149081 and methotrexate and does not include evidence about clinical outcomes. Other genetic and clinical factors may also influence methotrexate clearance. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rosuvastatin response (SLCO1B1) ⚠ CAUTIOUS rsid : rs4149081 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22668755/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4149081 is an intronic SLCO1B1 variant (plus strand G>A); it is not the well-known c.521T>C myopathy variant. SLCO1B1 is a liver transporter that takes statins up into the liver. In one small study (PharmGKB level 3, PMID 22668755), the A allele was associated with a somewhat greater LDL-cholesterol-lowering response to rosuvastatin, while the G allele was linked to a weaker response. The evidence is limited and not used clinically to choose or dose rosuvastatin. It is only potentially relevant if you take rosuvastatin. Note: this is one of 2 correlated variants in/near SLCO1B1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the G/A genotype at rs4149081. If you take rosuvastatin and have coronary disease, your response may be intermediate — a little stronger than people with G/G and a little weaker than those with A/A. The evidence is limited and not used to guide dosing. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Simvastatin LDL-lowering response (SLCO1B1) ⚠ CAUTIOUS rsid : rs4149081 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22668755/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4149081 is an intronic SLCO1B1 variant (plus strand G>A); it is not the well-known c.521T>C myopathy variant. SLCO1B1 is a liver transporter that takes statins up into the liver. In one small study (PharmGKB level 3, PMID 22668755), the A allele was associated with a greater LDL-cholesterol reduction on simvastatin, and the G allele with less LDL lowering. The evidence is limited and is not used clinically to choose or dose simvastatin. It is only potentially relevant if you take simvastatin. Interpretation: You have the G/A genotype. If you take simvastatin and have coronary disease, you may have a somewhat greater LDL-cholesterol reduction than people with G/G. The evidence is limited and is not used to guide dosing. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tacrolimus dose requirements (CYP3A5) rsid : rs4646450 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/36248867/ https://pubmed.ncbi.nlm.nih.gov/29454235/ https://pubmed.ncbi.nlm.nih.gov/29318894/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4646450 is an intronic variant in the CYP3A5 region (plus strand G>A) that tracks with CYP3A5 expression. CYP3A5 is a liver/gut enzyme that breaks down tacrolimus, an anti-rejection drug used after organ transplant. The A allele is associated with the active, expressing form of CYP3A5: people with A copies metabolise tacrolimus faster, giving lower blood levels for a given dose, so they typically need a higher dose. People with G/G tend to have higher blood levels per dose. This is established transplant pharmacogenetics (PharmGKB level 3); it guides starting dose only if you take tacrolimus. Note: this is one of 3 correlated variants in/near CYP3A5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the G/G genotype. If you take tacrolimus after a transplant (your own or your donor's genotype can matter), you tend to have higher dose-adjusted blood levels than people carrying the A allele — meaning you usually need a lower dose to reach the target level. Your transplant team adjusts dosing using blood-level monitoring. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluoropyrimidine chemotherapy toxicity (DPYD) rsid : rs55886062 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24923815/ https://pubmed.ncbi.nlm.nih.gov/23588312/ Summary : This is the DPYD*13 variant (c.1679T>G), reported here on the plus strand as A>C. The C allele is classified by CPIC and the Dutch guideline (DPWG) as a no-function / fully dysfunctional allele: it lowers the activity of DPD, the enzyme that breaks down fluoropyrimidine chemotherapy (fluorouracil/5-FU, capecitabine, tegafur). People carrying it clear these drugs more slowly, so standard doses build up and can cause severe — occasionally life-threatening — toxicity (low blood counts, mouth sores, diarrhea). This matters only during fluoropyrimidine treatment; it says nothing about your everyday health. No odds ratio is given in the source — the effect is described as a function category, not a number. Note: this is one of 6 correlated variants in/near DPYD reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the A/A genotype — you do not carry the DPYD*13 (C) no-function allele at this position. If you are ever treated with fluorouracil (5-FU), capecitabine, or tegafur, this particular variant does not raise your toxicity risk. (Other DPYD variants and clinical factors can still matter, so this is not a green light by itself.) Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluoropyrimidine chemotherapy toxicity (DPYD) rsid : rs67376798 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23930673/ https://pubmed.ncbi.nlm.nih.gov/31486738/ Summary : This is the DPYD c.2846A>T variant (D949V), reported here on the plus strand with A as the variant allele. CPIC and the Dutch guideline (DPWG) classify the A allele as a decreased-function allele: it partly lowers the activity of DPD, the enzyme that breaks down fluoropyrimidine chemotherapy (fluorouracil/5-FU, capecitabine, tegafur). Carriers clear these drugs more slowly and have an increased risk of severe toxicity (low blood counts, mouth sores, diarrhea); guidelines recommend a dose reduction. This matters only during fluoropyrimidine treatment. No odds ratio is given in the source — the effect is described as a function category, not a number. Note: this is one of 6 correlated variants in/near DPYD reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the T/T genotype — you do not carry the decreased-function (A) allele at this DPYD position. If you are ever treated with fluorouracil (5-FU), capecitabine, or tegafur, this particular variant does not raise your toxicity risk (other DPYD variants and clinical factors can still apply). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rosuvastatin – blood levels & side effect risk (SLCO1B1) ⚠ CAUTIOUS rsid : rs71581941 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/41082948/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs71581941 (c.1738C>T) is a rare loss-of-function variant in SLCO1B1, the gene for the liver transporter OATP1B1 that pulls statins and bilirubin out of the bloodstream into the liver. The T allele disrupts this transporter; in its homozygous form it causes Rotor syndrome (a benign cause of high bilirubin), and GWAS confirms the T allele raises blood bilirubin — a direct readout of reduced transporter activity. Because OATP1B1 normally clears statins, carriers can have higher statin blood levels and therefore a higher risk of muscle-related side effects (aches, weakness, rarely myopathy), most relevant for rosuvastatin and simvastatin. Evidence specific to this rare variant for statins is limited (mechanistic plus a single PharmGKB rosuvastatin annotation), so treat this as a plausible flag, not a firm number. It matters only if you take a statin. Note: this is one of 2 correlated variants in/near SLCO1B1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the C/C genotype — you do not carry the loss-of-function (T) allele at this position. Your OATP1B1 transporter works normally here, so this variant does not raise your statin side-effect risk or your bilirubin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluorouracil & capecitabine toxicity (DPYD HapB3) rsid : rs75017182 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23736036/ https://pubmed.ncbi.nlm.nih.gov/31745289/ Summary : rs75017182 (c.1129-5923C>G) is the causal splicing variant of DPYD haplotype B3 (HapB3). The C allele creates aberrant splicing that introduces a premature stop, lowering activity of DPD — the enzyme that breaks down fluoropyrimidine chemotherapy (fluorouracil/5-FU, capecitabine) — to roughly half of normal. Carriers clear these drugs more slowly and have a moderately increased risk of toxicity (low blood counts, mouth sores, diarrhea, hand-foot syndrome). CPIC and the Dutch guideline (DPWG) recommend a modest dose reduction for carriers. This matters only during fluoropyrimidine treatment. The effect is given as a function category (~50% activity), not an odds ratio. Note: this is one of 6 correlated variants in/near DPYD reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the G/G genotype — you do not carry the HapB3 reduced-function (C) allele at this position. If you are ever treated with fluorouracil (5-FU) or capecitabine, this variant does not raise your toxicity risk (other DPYD variants and clinical factors can still apply). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tacrolimus metabolism (CYP3A5) rsid : rs776746 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22108237/ https://pubmed.ncbi.nlm.nih.gov/29393157/ https://pubmed.ncbi.nlm.nih.gov/33755393/ Summary : At CYP3A5 rs776746 (c.6986A>G), the T allele on this strand is the functional CYP3A5*1 'expresser' allele associated with HIGHER tacrolimus metabolism; the C allele is the non-functional *3 'non-expresser' allele associated with LOWER metabolism. Drug-response only — relevant if you are prescribed tacrolimus. Note: this is one of 3 correlated variants in/near CYP3A5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: Both copies at this position carry the C allele — a C/C genotype, corresponding to CYP3A5*3/*3, the non-functional 'non-expresser' form. The C (*3) allele creates a cryptic splice site that abolishes functional CYP3A5, so non-expressers have the LOWEST tacrolimus metabolism, higher trough levels, and typically need LOWER doses. This matters only if you are prescribed tacrolimus. • Statin response – atorvastatin (CYP3A5) rsid : rs776746 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18727922/ https://pubmed.ncbi.nlm.nih.gov/16103896/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs776746 defines the CYP3A5*3 allele. On the plus strand the C allele is *3 (non-functional, 'non-expresser') and the T allele is *1 (functional, 'expresser'). CYP3A5 is one of the enzymes that can metabolize atorvastatin. People who carry the functional T (*1) allele are 'expressers' and may metabolize atorvastatin somewhat faster, while C/C (*3/*3) non-expressers may clear it a little slower. In practice CYP3A5 plays only a minor role for atorvastatin (the closely related CYP3A4 dominates), so the clinical effect on statin response is small and the evidence is limited. This gene matters far more for drugs like tacrolimus. Treat this as informational; it should not change how you take atorvastatin without your doctor's input. Interpretation: You have the C/C genotype — two non-functional CYP3A5*3 alleles (a 'non-expresser', the most common type in many populations). If you take atorvastatin, you rely on other enzymes (mainly CYP3A4) to clear it; any difference in your atorvastatin response from this gene alone is expected to be small. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Deferasirox – response & drug levels (UGT1A1) rsid : rs887829 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25348619/ https://pubmed.ncbi.nlm.nih.gov/30651574/ https://pubmed.ncbi.nlm.nih.gov/28346059/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant is in the promoter of UGT1A1, the enzyme that helps clear several drugs and bilirubin; the T allele lowers UGT1A1 activity. Deferasirox is partly cleared by UGT1A1, so UGT1A1 genotype has been linked to differences in deferasirox blood levels and response in people treated for iron overload (e.g. beta-thalassemia). The reported studies are small and not fully consistent about the size or direction of the effect, so this is best read as a tendency rather than a firm rule. The C (reference) allele gives normal activity. It only matters while you are on deferasirox. Interpretation: You have one C and one T allele (C/T) — somewhat reduced UGT1A1 activity. If you take deferasirox, your drug levels or response may differ modestly from average, but the evidence is limited and mixed. Your team monitors iron levels and tolerability directly. No relevance unless you take deferasirox. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin – dose requirement (UGT1A1) ⚠ CAUTIOUS rsid : rs887829 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26223945/ https://pubmed.ncbi.nlm.nih.gov/28550460/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant is in the promoter of UGT1A1, where the T allele lowers UGT1A1 activity. A few small pharmacogenetic studies have linked UGT1A1 genotype to slightly different warfarin dose requirements, but UGT1A1 is a minor player in warfarin handling (the main genes are VKORC1 and CYP2C9), and the reported effect is weak and inconsistent. So this is at best a small tendency, not a dosing rule. The C (reference) allele is the normal-activity version. It only matters while you are on warfarin, and your dose is set by INR blood tests. Interpretation: You have one C and one T allele (C/T). If you take warfarin, any influence of this UGT1A1 variant on your dose is expected to be small and is not consistently shown across studies. Your dose is set by INR monitoring, not by this gene. No relevance unless you take warfarin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin & vitamin K antagonist dose sensitivity (VKORC1) rsid : rs9934438 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31114289/ https://pubmed.ncbi.nlm.nih.gov/22920394/ https://pubmed.ncbi.nlm.nih.gov/16201835/ Summary : Each A allele is associated with lower Warfarin & vitamin K antagonist dose sensitivity (VKORC1) (−0.16 per copy, study scale). Moderate evidence, 2 publications. Note: this is one of 6 correlated variants in/near VKORC1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: If you have the rs9934438 A/A genotype, you may require a lower dose of warfarin compared to people with the G/A or G/G genotype. However, conflicting evidence has been reported, and other genetic and clinical factors may also influence warfarin dose requirements. • Axitinib/sorafenib efficacy in renal cell carcinoma (HIF1A) rsid : rs11549465 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25816720/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant changes one amino acid in HIF1A (P582S), a master regulator of how cells respond to low oxygen and drive tumour blood-vessel growth — the same pathway that axitinib and sorafenib (anti-angiogenic kidney-cancer drugs) act on. One pharmacogenetic study suggested that HIF1A genotype tracks with how long renal-cell-carcinoma patients stay progression-free on these drugs, with the common C/C version linked to longer progression-free survival than carriers of the T variant. The evidence is preliminary (a single study, PharmGKB level 3), so this is a weak signal, not a treatment rule. The T allele is the less common variant (~10%). Interpretation: You have the C/C genotype (the common version of HIF1A at this position). If you are treated with axitinib or sorafenib for renal cell carcinoma, one small study links this genotype to somewhat longer progression-free survival than T-carriers — but this is a weak, single-study finding and many other factors drive the response. This has no relevance unless you are on these drugs. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methotrexate response in rheumatoid arthritis (AMPD1) rsid : rs17602729 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20386493/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant introduces a premature stop codon in AMPD1 (Q12X), switching off one copy of the muscle AMP-deaminase enzyme; the A allele is the loss-of-function version. Reduced AMPD1 activity raises adenosine, which is part of how methotrexate calms inflammation, so some studies linked the A allele to a better methotrexate response in rheumatoid arthritis (and some reported more adenosine-related side effects). However, the finding has been contradicted by other studies, so it is an inconsistent, modest signal rather than a reliable predictor. The G (reference) allele is the normal, full-function version. It only matters while you take methotrexate. Interpretation: You have one G and one A allele (G/A) — one loss-of-function AMPD1 copy. If you take methotrexate for rheumatoid arthritis, some studies link A-carriers to a better response (and possibly more adenosine-related side effects), but the evidence is mixed and not confirmed. Your rheumatologist judges response clinically. This has no effect when you are not on the drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Growth hormone (somatropin) dosing (COL1A1) rsid : rs1800012 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22026923/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800012 is the COL1A1 Sp1 binding-site variant (forward REF=C, ALT=A). In a study of growth-hormone-deficient patients, the COL1A1 genotype interacted with a separate growth hormone receptor (GHR exon-3 deletion) variant to influence the somatropin dose needed for a given response. The evidence is from a single small study (PharmGKB level 3 Dosage), and the C/A heterozygous group was not analysed, so any dosing signal is preliminary and not a basis for changing treatment on its own. Interpretation: You have the C/C genotype. If you are treated with somatropin for growth hormone deficiency, one small study suggested C/C patients who also carry the full-length GHR gene may need a somewhat higher somatropin dose than A/A patients who carry the GHR exon-3 deletion. This is preliminary (level 3) and depends on the separate GHR variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sorafenib response in hepatocellular carcinoma (VEGFA) rsid : rs2010963 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24510746/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2010963 is the VEGFA promoter variant -634G/C (forward REF=C, ALT=G), affecting VEGF-A production. In patients on sorafenib for hepatocellular carcinoma (liver cancer), the C allele was associated with longer progression-free and overall survival, while G/G was associated with poorer outcomes. The evidence is from limited studies (PharmGKB level 3 Efficacy), so it is a tentative signal rather than an established predictor. Interpretation: You have the G/G genotype. If you are treated with sorafenib for liver cancer, some studies link G/G to shorter progression-free and overall survival than C-allele carriers — but the evidence is limited and inconsistent (level 3) and does not reliably predict your outcome. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Capecitabine/oxaliplatin (XELOX) response in colorectal cancer (VEGFA) rsid : rs2010963 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20125120/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2010963 is the VEGFA promoter variant -634G/C (forward REF=C, ALT=G), affecting VEGF-A production. In colorectal cancer patients on the capecitabine + oxaliplatin (XELOX) regimen, one study reported that heterozygous C/G patients responded less well than the C/C and G/G homozygous groups (a non-linear pattern). This rests on a single small study (PharmGKB level 3 Efficacy), so the finding is preliminary. Interpretation: You have the G/G genotype. If you are treated with XELOX for colorectal cancer, one study found G/G patients responded somewhat better than C/G heterozygotes — but this rests on a single small study (level 3) and your response depends mainly on clinical factors. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cyclophosphamide response in prostate cancer (VEGFA) ⚠ CAUTIOUS rsid : rs2010963 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23860526/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2010963 is the VEGFA promoter variant -634G/C (forward REF=C, ALT=G), affecting VEGF-A production. In men with advanced prostate cancer on metronomic cyclophosphamide-based chemotherapy, one study linked the C/C genotype to shorter progression-free survival and G-allele carriers to longer progression-free survival. The evidence is from a single small study (PharmGKB level 3 Efficacy), so it is preliminary. Interpretation: You have the G/G genotype. If you are treated with cyclophosphamide for advanced prostate cancer, one small study linked G-allele carriers to longer progression-free survival than C/C — but the evidence is from a single level-3 study and other factors matter far more. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bevacizumab (Avastin) response in cancer (VEGFA) ⚠ CAUTIOUS rsid : rs3025039 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27139155/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs3025039 (often called VEGF +936 C>T) sits in the VEGFA gene, which makes the growth factor that bevacizumab blocks to starve tumours of blood supply. In breast-cancer patients treated with bevacizumab plus chemotherapy, those with two T copies tended to have shorter survival than people carrying the C allele. The evidence is limited and not yet confirmed for routine use (PharmGKB level 3), and it applies only in the context of bevacizumab treatment. Interpretation: If you have the C/C genotype and breast cancer, you may have better overall survival times when treated with bevacizumab (in combination with chemotherapy) compared to people with the T/T genotype. Other genetic and clinical factors may also influence response to bevacizumab. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Statin response & residual CAD risk (LPA) rsid : rs10455872 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23903772/ https://pubmed.ncbi.nlm.nih.gov/22331829/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each G allele is associated with higher Statin response & residual CAD risk (LPA) (+4.8 per copy, study scale). The underlying association is well-replicated (5 publications), but there is no clinical pharmacogenetic guideline to act on it. Interpretation: If you have the A/A genotype, you may have an increased response to rosuvastatin compared to people with the A/G or G/G genotype. Other genetic and clinical factors may also affect your response to rosuvastatin. • Irbesartan blood pressure response (APOB) ⚠ CAUTIOUS rsid : rs1367117 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15453913/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is an APOB variant best known for raising LDL ('bad') cholesterol (the A allele increases LDL). A single small pharmacogenetic study also linked it to how well the blood-pressure drug irbesartan lowers blood pressure, with G/G carriers tending to respond better than A/A carriers. The drug-response evidence is limited (one study), so treat it as preliminary; your doctor judges how well a medicine is working. Interpretation: If you have the A/A genotype and take irbesartan, the same small study suggests you may be somewhat less likely to respond than G carriers. This is preliminary, single-study evidence; other genetic and clinical factors also matter, and it only applies if you take irbesartan. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fenofibrate response in high triglycerides (APOA5) rsid : rs3135506 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/17431185/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs3135506 is the S19W missense variant in APOA5 (apolipoprotein A-V), a gene that helps clear triglyceride-rich particles from blood. The minor C allele (the alternate base, the '19W' form) raises baseline triglycerides. In pharmacogenetic studies, carriers of this C allele tend to start with higher triglycerides and to show a larger drop in triglycerides when treated with the fibrate drug fenofibrate. The supporting evidence is a low-level (level 3) PharmGKB annotation with no pooled effect size, so this is a modest, drug-specific signal. It only matters if you take fenofibrate. Note: this is one of 2 correlated variants in/near APOA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: With the G/G genotype you carry the common version of APOA5 at this site, associated with typical baseline triglycerides. If you take fenofibrate, your triglyceride response is expected to be in the usual range; this variant gives no special signal for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Candesartan blood-pressure response (SH2B3) rsid : rs3184504 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31327267/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs3184504 is the R262W missense variant in SH2B3 (LNK), a top genetic signal for blood pressure: its T allele (reference base) raises blood pressure, the C allele (alternate base) is the lower-pressure version. A single low-level (level 3) pharmacogenetic study linked this site to how much blood pressure falls on the angiotensin-receptor blocker candesartan, with the lower-pressure C/C genotype tending to respond differently from T-carriers. The drug-response evidence is weak and single-study with no effect size, so this is only a tentative, drug-specific signal — your overall blood-pressure risk from this variant is covered by the separate coronary/blood-pressure entry. Interpretation: If you take candesartan and have the C/C genotype, you carry the lower-baseline-blood-pressure version of SH2B3; one small study suggests your response to candesartan may differ from T-carriers. The evidence is weak and not a basis for a treatment decision by itself; this only matters while on the drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fenofibrate – triglyceride-lowering response (APOB) rsid : rs676210 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20724655/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take fenofibrate to lower triglycerides. In the GOLDN fenofibrate trial, each A allele of this APOB variant (Pro2739Leu; the literature calls it the minor 'T' allele on the gene's coding strand, which equals A on the dbSNP forward strand) was linked to a larger drop in triglycerides during fenofibrate treatment, in a dose-dependent way. People with two G alleles tended to have the smallest triglyceride response. This is about how well the drug works for you, not a disease risk; evidence is modest, so treat it as a tendency. Interpretation: If you have the G/G genotype and hypertriglyceridemia, you may have smaller decreases in triglyceride levels when treated with fenofibrate compared to people with the A/A genotype. Other genetic and clinical factors may also influence your response to fenofibrate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atenolol – blood pressure response (LDLR) rsid : rs688 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15453913/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take atenolol (a beta-blocker) for high blood pressure. People carrying the C allele of this LDLR variant tended to get more lowering of systolic (top-number) blood pressure on atenolol, while people with two T alleles tended to respond less. This describes how well the drug works for you, not a disease risk, and the evidence is limited (PharmGKB level 3, small study), so treat it as a tendency. Interpretation: If you have the C/T genotype, you may have more effective lowering of systolic blood pressure on atenolol compared to people with the T/T genotype. Other genetic and clinical factors may also influence your response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Lovastatin – cholesterol-lowering response (LDLR) rsid : rs688 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16103896/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take lovastatin (a statin) for high cholesterol. In one large statin study, the T allele of this LDLR variant was linked to a greater drop in total cholesterol on lovastatin. The pattern was not a simple step-by-step one: people with two T alleles had the biggest response and people with one of each (C and T) had the smallest, with two-C people in between. This describes how well the drug lowers your cholesterol, not a disease risk, and the evidence is limited (PharmGKB level 3), so treat it as a tendency. Interpretation: If you have the C/T genotype, you may have a smaller decrease in total cholesterol when treated with lovastatin compared to people with the C/C or T/T genotype. Other genetic and clinical factors may also influence total cholesterol levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fenofibrate response in hypertriglyceridemia (APOA5) rsid : rs964184 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23119086/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each C allele reduces odds of Fenofibrate response in hypertriglyceridemia (APOA5) by ~49% (OR≈0.51). The underlying association is well-replicated (3 publications), but there is no clinical pharmacogenetic guideline to act on it. Note: this is one of 2 correlated variants in/near APOA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the C/C genotype and hypertriglyceridemia, you may have a decreased response when treated with fenofibrate compared to people with the G/G genotype. Other genetic and clinical factors may also influence your response to fenofibrate. • Letrozole – lipid response in breast cancer (CYP19A1) rsid : rs10046 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26463708/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only for post-menopausal women with breast cancer taking letrozole (an aromatase inhibitor). It affects how your blood fats shift on letrozole. The A allele of this CYP19A1 variant was linked to a more favourable lipid response - lower triglycerides and higher 'good' HDL cholesterol - while the G allele tracked with the opposite (higher triglycerides, lower HDL). Because the two fats move in opposite directions, there is no simple 'good' or 'bad' label; this is informational. Evidence is limited (PharmGKB level 3). Note: this is one of 4 correlated variants in/near CYP19A1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: If you are a post-menopausal woman with the G/A genotype and breast cancer and you are taking letrozole, you may have decreased triglycerides and increased HDL cholesterol compared to women with the G/G genotype, and increased triglycerides and decreased HDL cholesterol compared to women with the A/A genotype. Other clinical and genetic factors may also influence these levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Leflunomide response in rheumatoid arthritis (ESR1) rsid : rs2234693 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21174621/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, studied in women, relevant only if you take leflunomide for rheumatoid arthritis. The T allele of this ESR1 (oestrogen receptor) variant was linked to a better response to leflunomide, while the C allele tracked with a poorer response. This describes how well the drug may work for you, not a disease risk; evidence is limited (PharmGKB level 3) and was seen in female patients. Note: this is one of 2 correlated variants in/near ESR1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you are female with the T/T genotype and rheumatoid arthritis, you may have a better response to leflunomide compared to women with the C/C genotype. Other genetic and clinical factors may also influence response to leflunomide. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Levothyroxine response & thyroid hormone conversion (DIO2) ⚠ CAUTIOUS rsid : rs225014 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24910925/ https://pubmed.ncbi.nlm.nih.gov/30367059/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each C allele is associated with lower Levothyroxine response & thyroid hormone conversion (DIO2) (−0.047 per copy, study scale). Limited evidence, 1 record. Interpretation: TT genotype — see evidence summary; per-genotype effect not quantified in source data. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • TNF-alpha inhibitor response in rheumatoid arthritis (PTPN22) rsid : rs2476601 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25834819/ https://pubmed.ncbi.nlm.nih.gov/23007924/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This PTPN22 variant (R620W) is a well-known autoimmune-risk marker, but as a predictor of whether TNF-alpha inhibitors (such as adalimumab, etanercept, infliximab) will work in rheumatoid arthritis it has NOT panned out. A large pooled analysis found the A allele was not associated with response to TNF-inhibitors compared with the G allele, and other studies agree it does not reliably predict anti-TNF response. So this entry records a studied-but-unconfirmed link, not a usable prediction of how the drugs will work for you. Interpretation: You have the A/G genotype of PTPN22. If you take a TNF-alpha inhibitor (such as adalimumab, etanercept, or infliximab) for rheumatoid arthritis, current evidence does not show that this genotype reliably predicts whether the drug will work for you - large studies found no clear link. Your response is better judged by your rheumatologist using disease activity over time. Warnings : - Evidence does not support this variant as a predictor of TNF-inhibitor response; included for completeness only. • Tamoxifen response in breast cancer (CYP19A1) ⚠ CAUTIOUS rsid : rs4646 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25793413/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4646 is a variant in CYP19A1, the aromatase gene. In premenopausal women with breast cancer treated with tamoxifen, the A/A genotype was associated with longer disease-free survival, while the C/C genotype tended to do worse; carrying the A (minor) allele was linked to better outcomes. The relationship can flip with menopausal status, the supporting studies are small (low pharmacogenetic level), and it is relevant only if you take tamoxifen. Interpretation: If you are a premenopausal woman taking tamoxifen for breast cancer and have the C/C genotype, you may tend toward shorter disease-free survival than women carrying the A allele. The evidence is limited and can differ by menopausal status, and many other factors drive cancer outcomes. It is relevant only while you take tamoxifen. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anastrozole response in HR+ breast cancer (CYP19A1) rsid : rs727479 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27747906/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs727479 sits in CYP19A1, the gene for aromatase — the enzyme anastrozole blocks. The C allele is linked to higher estrogen (estradiol/estrone) levels, and a small pharmacogenetic study (PharmGKB level 3, limited evidence) reported that the C/C genotype was associated with a higher chance of breast cancer recurrence on anastrozole than the A/A genotype. The effect is modest, unquantified, and based on few patients; it is one of many factors that influence outcome. Interpretation: If you are a postmenopausal woman with HR+ breast cancer and the C/A genotype, you may have an increased likelihood of breast cancer recurrence when treated with anastrozole compared to women with the A/A genotype. Other clinical and genetic factors may also influence the likelihood of recurrence on anastrozole. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Letrozole – triglyceride response in breast cancer (CYP19A1) ⚠ CAUTIOUS rsid : rs749292 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26463708/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs749292 is in CYP19A1, the aromatase gene targeted by letrozole. In a small pharmacogenetic study (PharmGKB level 3, limited evidence), the G/G genotype was associated with higher plasma triglycerides during letrozole treatment (alone or with a statin) than the A/A genotype, with the G/A genotype intermediate. The effect is modest, unquantified, and one of many factors affecting blood lipids. Note: this is one of 4 correlated variants in/near CYP19A1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: If you are a post-menopausal woman with the G/A genotype and breast cancer and you are taking letrozole, alone or with a statin, you may have decreased plasma triglycerides compared to women with the G/G genotype and increased triglycerides compared to women with the A/A genotype. Other clinical and genetic factors may also influence triglyceride levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Hepatitis C treatment response – interferons & ribavirin (IL18) ⚠ CAUTIOUS rsid : rs1946518 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19455410/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1946518 is a promoter variant in IL18 (the -607C>A variant; on our strand REF=T corresponds to the -607A allele and ALT=G to the -607C allele). In a pharmacogenetic study of chronic hepatitis C (PharmGKB level 3 Efficacy, limited evidence), the -607A allele (T/T on our strand) was associated with a better response to interferon-plus-ribavirin therapy, while the G allele was linked to a poorer response. The effect is modest, unquantified, and one of many factors (notably IFNL3/IL28B genotype) that determine treatment success. Interpretation: If you have the T/T genotype and chronic hepatitis C, you may have a better response to treatment with interferons and ribavirin compared to people with the G/G genotype. Other genetic and clinical factors may also influence response to interferon and ribavirin therapy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tacrolimus metabolism after transplantation (IL18) ⚠ CAUTIOUS rsid : rs1946518 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25487141/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1946518 is a promoter variant in IL18 (the -607C>A variant; on our strand REF=T corresponds to the -607A allele and ALT=G to the -607C allele). In pharmacogenetic studies of transplant patients (PharmGKB level 3 Metabolism/PK, limited evidence), the G-carrier genotypes (G/G and T/G) were associated with slower tacrolimus metabolism and therefore higher drug exposure, while T/T was linked to faster metabolism and lower exposure. The effect is modest, unquantified, and tacrolimus is always dosed by measured blood levels, so this is informational only. Interpretation: If you have the T/T genotype and have had a kidney or lung transplant, you may experience increased metabolism of tacrolimus, resulting in decreased exposure, compared to people with the G/G or T/G genotype. Other genetic and clinical factors may also influence tacrolimus metabolism. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tacrolimus response after kidney transplant (NOD2) rsid : rs2066844 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23175667/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2066844 is a coding variant in NOD2 (the gene more famously linked to Crohn's disease). A small pharmacogenetic study reported that, among kidney-transplant recipients on tacrolimus, the common C/C genotype was linked to a somewhat longer post-transplant hospital stay than people carrying the T allele. This is a single, low-level association (PharmGKB level 3) and the effect size was not quantified, so treat it as a weak hint, not a firm prediction. Interpretation: If you take tacrolimus after a kidney transplant and have the C/C genotype, you may have a somewhat longer post-transplant hospital stay than people who carry a T allele. This is based on a single small study, and many other genetic and clinical factors influence recovery, so the effect is uncertain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Tocilizumab & sarilumab response (IL6R) ⚠ CAUTIOUS rsid : rs2228145 Your geno : AC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24978393/ https://pubmed.ncbi.nlm.nih.gov/38001504/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2228145 (A>C, Asp358Ala) sits in IL6R, the receptor that drugs like tocilizumab and sarilumab block. The C allele raises the amount of soluble IL-6 receptor in the blood (well-replicated in protein-level GWAS). Small pharmacogenetic studies have linked the A allele to the response phenotype for these drugs, but the per-genotype effect on whether the drug works is not quantified and evidence is limited (PharmGKB level 3). Treat this as a weak hint, not a reliable predictor of response. Interpretation: If you take tocilizumab or sarilumab and have the A/C genotype, you carry one copy of each allele and likely fall between the two homozygous groups. Any effect on drug response is small and not quantified, so this is uncertain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rosuvastatin – cardiovascular outcomes (CRP/APOE region) rsid : rs2808630 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21094359/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2808630 sits near the CRP gene (which controls C-reactive protein, an inflammation marker). In the JUPITER statin trial, this variant was linked to C-reactive protein levels, and a pharmacogenetic analysis reported that carriers of the C allele tended to have better cardiovascular outcomes on rosuvastatin than people with the T/T genotype. This is a single, limited-evidence association (PharmGKB level 3) and the effect was not quantified, so treat it as a weak hint, not a reason to choose or avoid the drug. Note: this is one of 2 correlated variants in/near CRP reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take rosuvastatin and have the C/T genotype, you carry one C allele and may have somewhat better cardiovascular outcomes than people with the T/T genotype. This is based on a single trial analysis and is uncertain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bevacizumab response in macular degeneration (ARMS2) rsid : rs10490924 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22594510/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each T allele raises odds of Bevacizumab response in macular degeneration (ARMS2) by ~75% (OR≈1.75). The underlying association is well-replicated (12 publications), but there is no clinical pharmacogenetic guideline to act on it. Interpretation: Both copies at this position carry the G variant — a G/G genotype, with no copies of the T variant present. People with G/G tend to sit toward the lower end of the bevacizumab response in macular degeneration range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: OR ≈ 1.75 per copy. • Bevacizumab (Avastin) response in macular degeneration (CFH) rsid : rs800292 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22594510/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the CFH I62V variant (rs800292) in complement factor H, part of the immune complement system that drives age-related macular degeneration (AMD). The reference allele G is the AMD-risk version; the alternate allele A is the non-risk version. Several studies of people treated with bevacizumab (Avastin) for wet AMD found that those carrying more A alleles tended to gain more vision (in one study visual-acuity improvement rose stepwise from G/G to G/A to A/A). So the A allele is loosely associated with a better bevacizumab response and the risk-allele G with a poorer one. The evidence is modest and inconsistent across populations, so it is not used to decide treatment. Interpretation: If you have age-related macular degeneration and are treated with bevacizumab (Avastin), the G/A genotype (one risk allele, one A allele) is associated with an intermediate response — typically better than G/G and not as good as A/A in the studies that looked at this. The genetic effect is small and uncertain. If you are not taking bevacizumab, this has no effect on you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Amisulpride response in schizophrenia (DRD2) [rs1079597]: No notable finding at this locus. Naltrexone response in alcohol dependence (DBH) [rs1611115]: No notable finding at this locus. Levodopa response in cocaine-related disorders (DBH) [rs1611115]: No notable finding at this locus. Methadone dose requirement in heroin dependence (DRD2) [rs6275]: No notable finding at this locus. Rizatriptan response for migraine (DRD2) [rs6275]: No notable finding at this locus. Pravastatin – cholesterol-lowering response (ACE) [rs4341]: No notable finding at this locus. Olanzapine exposure (APOC3) [rs5128]: No notable finding at this locus. Methotrexate response in psoriasis (FOXP3) [rs3761548]: No notable finding at this locus. Etanercept response in rheumatoid arthritis (STAT4) [rs7574865]: No notable finding at this locus. [Drug sensitivity] • Phenazepam response (CYP2C19 *17) rsid : rs12248560 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/30325732/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs12248560 marks the CYP2C19 *17 allele, where the T allele speeds up the CYP2C19 liver enzyme. CYP2C19 helps clear the benzodiazepine phenazepam, so fast-metabolizer (T) carriers may break it down quicker and feel less of an effect at a given dose. The evidence here is from a single low-level (PharmGKB level 3) study in people with alcoholism, so the link is weak. It only matters if you actually take phenazepam. Interpretation: If you have the C/T genotype (*1/*17) and alcoholism, you may have an increased response to phenazepam compared to people with the T/T (*17/*17) genotype. Other genetic and clinical factors can also influence your response to phenazepam. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid sensitivity / analgesic response (MC1R) ⚠ CAUTIOUS rsid : rs1805008 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24086514/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1805008 is one of the MC1R variants behind red hair and fair, sun-sensitive skin. The minor T allele changes one amino acid (R160W) and lowers MC1R activity. Small studies link MC1R loss-of-function variants to altered pain processing — people with these variants (often red-haired) tend to show a stronger response to some opioid painkillers and may need different doses of anaesthetics. The evidence is limited and the exact direction of the opioid effect is not firmly established, so this is exploratory, not a dosing rule. No professional guideline currently recommends changing opioid dosing based on this single variant. Interpretation: You have the C/C genotype (the common form of MC1R at this position). Your MC1R activity is not reduced by this variant, so the red-hair-associated changes in pain and opioid response described in small studies are unlikely to apply to you. If you take opioid painkillers, expect a typical response; this variant gives no reason to change your dose. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Calcium supplementation – bone fracture risk (VDR) rsid : rs731236 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15861036/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs731236 is the VDR TaqI variant (vitamin D receptor gene). One small pharmacogenetic study suggested that VDR genotype may influence how well calcium therapy protects against vertebral fractures, but it did not clearly establish which genotype does better with calcium alone, and PharmGKB records conflicting directions across related drugs. Treat this as preliminary — it should not guide whether you take calcium. Interpretation: You have the A/A genotype at this VDR (TaqI) position. A single small study found that VDR genotype affected vertebral-fracture rates during calcium therapy, but it did not clearly establish a per-genotype direction for calcium alone, so no reliable effect can be stated here. Bone health depends on many factors including vitamin D status, diet, and activity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - Direction unresolved — single small study; per-genotype effect of calcium not clearly quantified. • Statin response (PCSK9 loss-of-function) ⚠ CAUTIOUS rsid : rs11591147 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31969989/ https://pubmed.ncbi.nlm.nih.gov/22331829/ https://pubmed.ncbi.nlm.nih.gov/26902539/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each T allele is associated with lower Statin response (PCSK9 loss-of-function) (−0.372 per copy, study scale). The underlying association is well-replicated (4 publications), but there is no clinical pharmacogenetic guideline to act on it. Interpretation: Both copies at this position carry the G variant — a G/G genotype. People with G/G tend to sit toward the higher end of the statin response range, with each G copy contributing a small upward shift. Per-copy effect size: β ≈ 0.37 per copy. • Amphetamine response & impulsivity (DRD2) ⚠ CAUTIOUS rsid : rs12364283 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19968402/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs12364283 is a DRD2 promoter/enhancer variant; the minor G allele increases DRD2 (dopamine D2 receptor) expression. In a small experimental study of healthy volunteers given d-amphetamine, G-allele carriers showed worse behavioral inhibition — a longer stop reaction time, i.e. greater impulsivity — while non-carriers improved. Evidence is limited (one small pharmacological challenge study; PharmGKB level 3) and no clinical effect size is reported, so treat this as an exploratory tendency. Interpretation: If you take amphetamine and have the A/A genotype, you may show better behavioral inhibition (a shorter stop reaction time, i.e. less impulsivity) than people who carry the G allele. Evidence is limited and exploratory; many other factors influence impulsivity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid response & side effects (OPRM1 A118G) rsid : rs1799971 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/34871222/ https://pubmed.ncbi.nlm.nih.gov/31806881/ https://pubmed.ncbi.nlm.nih.gov/31246565/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. OPRM1 A118G (Asn40Asp) changes the mu-opioid receptor, the main target of opioid painkillers. REF=A, ALT=G; the G allele removes a sugar-attachment site on the receptor and is the variant studied in pharmacogenetics. Across post-surgical, cancer and obstetric studies, carriers of the G allele tend to get less pain relief from a given dose of opioid and therefore need somewhat higher doses than people with two A alleles. The effect is modest and varies by opioid and population; it is not a fixed dose ratio. This matters only when opioids are actually used. Interpretation: You have the A/A genotype (two reference A alleles). If you take opioid painkillers, this is the most common, baseline response — you are likely to get the expected pain relief from a standard dose. Many other factors (pain type, weight, other medicines) also affect how opioids work for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Naltrexone response in alcohol use disorder (OPRM1) rsid : rs1799971 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31160146/ https://pubmed.ncbi.nlm.nih.gov/31961981/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. OPRM1 A118G (REF=A, ALT=G) sits in the mu-opioid receptor that naltrexone blocks. Some studies and meta-analyses suggest that people who carry at least one G allele have a better response to naltrexone for alcohol use disorder (for example, fewer heavy-drinking days) than people with two A alleles, while showing no such difference on placebo. However, the finding has failed to replicate in several large trials, so the evidence is genuinely mixed and not strong enough to choose treatment by genotype alone. It is relevant only while taking naltrexone. Interpretation: You have the A/A genotype (two reference A alleles). If you take naltrexone for alcohol use disorder, some studies found people with A/A respond a bit less well than G-allele carriers, but other large trials found no difference. Naltrexone can still work for A/A; genotype is not a reliable predictor on its own. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine replacement therapy response (OPRM1) rsid : rs1799971 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15007373/ https://pubmed.ncbi.nlm.nih.gov/16960700/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. OPRM1 A118G (REF=A, ALT=G) affects the mu-opioid receptor, part of the brain's reward pathway involved in nicotine reinforcement. A few studies have looked at whether this variant predicts who succeeds with nicotine replacement therapy when quitting smoking. Results are weak and inconsistent: some report that G-allele carriers do slightly better or worse, but no reliable, replicated direction has been established. This is low-confidence pharmacogenetic information and only relevant while using NRT. Interpretation: You have the A/A genotype (two reference A alleles). If you use nicotine replacement therapy to quit smoking, current evidence does not reliably predict your chance of success from this genotype — studies disagree on the direction. NRT can work regardless of genotype. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • General anesthesia recovery time (OPRM1) rsid : rs1799971 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/30136624/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. OPRM1 A118G (REF=A, ALT=G) changes the mu-opioid receptor that opioid anaesthetic drugs (such as fentanyl, remifentanil and sufentanil) act on. Because G-allele carriers tend to be less sensitive to opioids, some studies link the G allele to needing more opioid during surgery and to a faster apparent recovery from opioid effects, while A/A people are more sensitive and may take longer to clear opioid sedation. The effect is small and study-dependent and is one of many factors an anaesthetist already accounts for. Interpretation: You have the A/A genotype (two reference A alleles). If you have opioid-based anaesthesia, you are more sensitive to opioids and may take somewhat longer to recover from their sedating effect than G-allele carriers. This is modest and managed routinely by your anaesthetist. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Olanzapine response in schizophrenia (DRD2) rsid : rs1799978 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16513877/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. DRD2 -241A>G (rs1799978) is a promoter variant of the dopamine D2 receptor gene, which antipsychotics like olanzapine act on. On the forward strand REF=T is the -241A allele and ALT=C is the -241G allele, linked to higher DRD2 expression. A small number of studies have examined whether this variant predicts how well people with schizophrenia respond to olanzapine, but the evidence is limited and no firm direction has been established. This is low-confidence pharmacogenetic information relevant only during olanzapine treatment. Note: this is one of 2 correlated variants in/near DRD2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the T/T genotype (two reference T alleles, the -241A/A form). If you take olanzapine for schizophrenia, current evidence does not reliably predict your response from this genotype. Response is judged clinically over time. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine replacement therapy – smoking cessation response (ANKK1/DRD2 Taq1A) ⚠ CAUTIOUS rsid : rs1800497 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15077009/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Taq1A (rs1800497) in ANKK1 tags the dopamine D2 receptor system; REF=G, ALT=A, with the A allele (the 'A1' allele) linked to fewer striatal D2 receptors. Researchers have asked whether this variant predicts who succeeds with nicotine replacement therapy when quitting smoking. The findings are inconsistent: an early study suggested A-allele carriers did better on NRT, but later and larger trials did not confirm a reliable association. This is low-confidence pharmacogenetic information that only applies while using NRT. Interpretation: You have the G/A genotype (one G, one A; A1 carrier). If you use nicotine replacement therapy, an early study suggested A-allele carriers may quit slightly more often on NRT, but this has not held up in larger trials. Treat it as uncertain background information, not a predictor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aripiprazole response in schizophrenia (ANKK1/DRD2 Taq1A) ⚠ CAUTIOUS rsid : rs1800497 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18926547/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Taq1A (rs1800497) in ANKK1 tags the dopamine D2 receptor system that aripiprazole acts on. REF=G, ALT=A; the A allele (the 'A1' allele) is linked to fewer striatal D2 receptors. A small number of studies have explored whether this variant predicts symptom improvement (measured on the PANSS scale) in people with schizophrenia treated with aripiprazole, with some suggesting A-allele carriers respond better. The evidence is limited and not firmly established, so this is low-confidence pharmacogenetic information relevant only during aripiprazole treatment. Interpretation: You have the G/A genotype (one G, one A; A1 carrier). If you take aripiprazole for schizophrenia, carrying an A allele has been linked in some small studies to a somewhat better symptom response, but this is not firmly established. Treat it as background information for your psychiatrist. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Disulfiram response in cocaine dependence (ANKK1/DRD2 Taq1A) ⚠ CAUTIOUS rsid : rs1800497 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23635803/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Taq1A (rs1800497) in ANKK1 tags the dopamine D2 receptor system. REF=G, ALT=A; the A allele (the 'A1' allele) is associated with fewer striatal D2 receptors. A small body of research has looked at whether this variant predicts response to disulfiram when used to treat cocaine dependence, with some studies suggesting A-allele carriers respond better. The evidence is limited and preliminary, so this is low-confidence pharmacogenetic information that only applies if disulfiram is used. Interpretation: You have the G/A genotype (one G, one A; A1 carrier). If you take disulfiram for cocaine dependence, carrying an A allele has been linked in small studies to a somewhat better response, but this is not firmly established. Treat it as background information for your doctor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid dependence risk (OPRM1) ⚠ CAUTIOUS rsid : rs510769 Your geno : CC Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/33589790/ https://pubmed.ncbi.nlm.nih.gov/24086514/ Summary : This variant is in OPRM1, the mu-opioid receptor gene. In curated association data, the T allele (the minor, alternate form here) has been weakly linked to higher odds of opioid-use disorder, the C allele to lower odds. As with the related heroin-dependence finding, the association is modest, comes largely from combined multi-variant analyses, and is far outweighed by personal and environmental factors. It is a small statistical tendency, not a diagnosis or a strong risk marker. No reliable single odds ratio is reported. Note: this is one of 4 correlated variants in/near OPRM1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: You have the C/C genotype — two copies of the lower-risk form. You carry none of the alleles weakly associated with opioid dependence here. This variant is at most a minor factor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Amphetamine response – stimulation & euphoria (OPRM1) ⚠ CAUTIOUS rsid : rs510769 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21029375/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This OPRM1 (mu-opioid receptor) variant has been linked to how stimulating and euphoric amphetamine feels, because the opioid-reward system contributes to stimulant effects. In a single small human study, the C allele (the reference form here) was associated with feeling more euphoric, energetic and stimulated after a dose of amphetamine, while the T/T group felt these effects least. This describes a subjective response, not a disease, and is low-confidence single-study evidence. It only applies if you are exposed to amphetamine. Interpretation: You have the C/C genotype. If you take amphetamine, you are in the group reported to feel the most stimulation and euphoria from it — based on one small study. If you are not exposed to amphetamine, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotic response & weight gain in schizophrenia (BDNF) rsid : rs6265 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23433505/ https://pubmed.ncbi.nlm.nih.gov/16633140/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6265 is the BDNF Val66Met variant, which alters the brain growth factor BDNF. REF=C (Val), ALT=T (Met). In schizophrenia treated with antipsychotics, some studies link the Met (T) allele to poorer treatment response — for example one study found Met carriers were about twice as likely to be treatment-resistant (OR around 2). The evidence is mixed and modest, and findings on antipsychotic-related weight gain are inconsistent. No firm dose or drug-choice rule comes from this variant, so it is informational and matters only while you are actually on antipsychotic treatment. Interpretation: You have the C/C (Val/Val) genotype. If you take antipsychotics for schizophrenia, this is the more common genotype and is not the one linked to poorer response in the studies — carrying the Met (T) allele was the pattern tied to harder-to-treat illness, which does not apply to you here. Treatment response still depends mostly on the specific drug and your individual course. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Naltrexone response in alcohol use disorder (ADH1C) rsid : rs698 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/34680127/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs698 is the ADH1C Ile350Val variant. It distinguishes the faster-metabolizing ADH1C*1 (gamma-1 / isoleucine) form of the alcohol-dehydrogenase enzyme from the slower ADH1C*2 (gamma-2 / valine) form, which changes how quickly your body turns alcohol into acetaldehyde. In one small 12-week clinical trial (PharmGKB level 3 evidence), people carrying the faster-metabolizing ADH1C*1 genotype reported fewer drinking days on naltrexone, suggesting a possibly better treatment response. This is a single, limited study with no numerical effect size, and the exact letter-to-genotype mapping is reported inconsistently across sources, so treat it as a weak tendency rather than an established rule. It only matters if you are actually being treated with naltrexone for alcohol use disorder. Interpretation: You have the T/T genotype at this ADH1C position. If you are taking naltrexone to cut down on drinking, your alcohol-metabolizer genotype here is one factor that has been weakly linked to how well naltrexone works, but the evidence is from a single small trial and cannot tell you a firm direction for your genotype. Many other factors shape how well naltrexone helps you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cisplatin/cyclophosphamide response in ovarian cancer (ADH1C) rsid : rs698 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24533712/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs698 is the ADH1C Ile350Val variant, which marks the faster (ADH1C*1) versus slower (ADH1C*2) form of the alcohol-dehydrogenase enzyme. Separately from its role in alcohol metabolism, one study in women treated for ovarian cancer linked rs698 genotype to treatment outcome with the chemotherapy drugs cisplatin and cyclophosphamide, with the heterozygous (C/T) genotype noted as the effect group. This is a single, limited study (PharmGKB level 3 Efficacy) with no numerical effect size, so it is a possible tendency rather than an established predictor, and it applies only if you are actually receiving these chemotherapy drugs. Interpretation: You have the T/T genotype at this ADH1C position. If you are being treated with cisplatin or cyclophosphamide for ovarian cancer, this variant has been weakly linked to chemotherapy outcome in a single small study; on its own it does not give you a reliable prediction. Many other factors determine how you respond to chemotherapy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid & heroin dependence risk (OPRM1) rsid : rs9479757 Your geno : GG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/829214/ https://pubmed.ncbi.nlm.nih.gov/11933204/ https://pubmed.ncbi.nlm.nih.gov/25122903/ https://pubmed.ncbi.nlm.nih.gov/24086514/ Summary : rs9479757 is a variant in OPRM1, the gene for the mu-opioid receptor that opioid drugs and heroin act on. The G (reference) allele is the risk allele: it strengthens binding of a splicing protein (hnRNPH) and shifts how the receptor is made, and people with the G/G genotype have been linked to more severe heroin dependence, while the less common A allele appears protective and is associated with milder dependence. Because the catalog's risk allele (G) is the reference base, having no A copies (G/G) carries the higher risk and carrying A copies lowers it. The A allele is uncommon (around 9% of alleles), and this only describes risk among people exposed to opioids. Note: this is one of 4 correlated variants in/near OPRM1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: You have the G/G genotype — two copies of the higher-risk G allele at OPRM1. If you are exposed to opioids or heroin, this genotype has been associated with a higher chance of more severe dependence compared with people who carry an A allele. It says nothing about you unless you actually use opioids, and many other factors affect dependence risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Lithium response in bipolar disorder (TPH1) ⚠ CAUTIOUS rsid : rs1800532 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21047205/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800532 is a variant in TPH1, the gene for an enzyme in the serotonin-making pathway. In one study of people with bipolar disorder treated with lithium, the G (reference) allele was associated with a better chance of responding to lithium, so people with the G/G genotype tended to respond better than those with the A/A genotype. This comes from a single small pharmacogenomic study (PharmGKB level 3), so it is a weak tendency rather than an established predictor, and it only matters if you are actually taking lithium. Note that some sources report this variant on the opposite strand (G/T), where their T = our A. Interpretation: If you have bipolar disorder and take lithium, the G/G genotype was associated in a single study with a better chance of responding to lithium than the A/A genotype. This is a weak, single-study tendency; many other clinical and genetic factors affect how well lithium works for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid requirement after surgery (COMT) rsid : rs4818 Your geno : CG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24533707/ https://pubmed.ncbi.nlm.nih.gov/25185591/ https://pubmed.ncbi.nlm.nih.gov/27061230/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a variant in COMT, an enzyme that breaks down dopamine and shapes how the body processes pain (here REF=C, ALT=G). A pharmacogenetic study (PMID 25185591) linked the C/C genotype to a lower need for additional opioid pain medication after surgery (adenotonsillectomy) compared with G-allele carriers. The evidence is limited and the effect-size number is not reported, so this is a weak tendency about post-surgery pain-medication needs, relevant only if you receive opioids. Note: this is one of 4 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: If you receive opioids after surgery and have the C/G genotype, you may be somewhat more likely to need additional opioid pain relief than people with C/C, based on limited evidence. This is a weak tendency; your actual pain and response guide treatment. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid analgesic response (COMT) rsid : rs6269 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24533707/ https://pubmed.ncbi.nlm.nih.gov/31806881/ https://pubmed.ncbi.nlm.nih.gov/19094200/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6269 is one of the COMT gene markers that tag a haplotype influencing how the body processes pain signals and dopamine. In a study of children having tonsil/adenoid surgery (PharmGKB clinical annotation, level 3), carriers of the G allele (the A/G and G/G genotypes) were reported to need postoperative opioid intervention somewhat more often than people with the A/A genotype. The evidence is modest (single small study, no effect-size given) and applies only in the context of opioid pain treatment. It does not predict pain or addiction in people who are not taking opioids. Note: this is one of 4 correlated variants in/near COMT reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: If you have the A/G genotype, you may be more likely to require postoperative intervention with opioids after adenotonsillectomy compared with people who have the A/A genotype. Other genetic and clinical factors also influence the need for pain management. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Morphine analgesic response (COMT) rsid : rs6269 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31806881/ https://pubmed.ncbi.nlm.nih.gov/19094200/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6269 tags a COMT haplotype that affects pain processing and the dopamine system. PharmGKB pharmacogenetic annotations (level 3) report that carriers of the G allele (A/G and G/G genotypes) tend to have a stronger pain-relieving response to morphine than people with the A/A genotype, so they may achieve adequate pain control at lower doses. The signal is modest and the source gives no numeric effect size. It is meaningful only when morphine is actually being used; it says nothing about pain or drug response otherwise. Interpretation: If you have the A/G genotype at rs6269, you may have an increased analgesic response to morphine compared to people with the A/A genotype. Other genetic and clinical factors may also influence your response to morphine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Butorphanol analgesic response (COMT) rsid : rs6269 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31806881/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6269 tags a COMT haplotype involved in pain processing. A PharmGKB pharmacogenetic annotation (level 3) reports that for butorphanol the pattern runs the opposite way to morphine: people with the A/A genotype tend to get more pain relief from butorphanol, while G/G carriers get less. The evidence is limited (single study, no numeric effect size) and applies only when butorphanol is being used. Interpretation: If you have the A/G genotype at rs6269, you may have an increased analgesic response to butorphanol compared to people with the G/G genotype. Other genetic and clinical factors may also influence your response to butorphanol. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid use disorder risk (CYP3A5) ⚠ CAUTIOUS rsid : rs15524 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/36744646/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs15524 is in the CYP3A5/ZSCAN25 region and tags CYP3A5 enzyme activity. A single pharmacogenetic annotation links rs15524 genotype to opioid use disorder, but the evidence is limited and the direction relative to the A/G alleles is not firmly established, so no confident per-genotype direction is given. This only matters with opioid exposure. Note: this is one of 2 correlated variants in/near CYP3A5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the A/A genotype at rs15524 (CYP3A5/ZSCAN25 region). A single study linked this variant to opioid use disorder, but the evidence is limited and the direction is not firmly established, so no reliable per-genotype effect can be stated. This is only relevant with opioid exposure. Many other genetic and clinical factors affect opioid use. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - Direction unresolved: single level-3 annotation for the opioid-use-disorder association. • Abacavir hypersensitivity risk (HLA-B*57:01 tag) rsid : rs2395029 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/32173028/ Summary : rs2395029 (in HCP5, next to HLA-B) is a tag SNP for the HLA-B*57:01 immune type. People with HLA-B*57:01 are at high risk of a serious allergic (hypersensitivity) reaction to the HIV drug abacavir, so guidelines say not to give abacavir to them. The G allele tags HLA-B*57:01 (near-perfect in European populations, less reliable in African and Asian populations). Because this is a surrogate marker and not direct HLA typing, a positive G result must be confirmed with an HLA-B*57:01 test before any treatment decision. Interpretation: You have the T/T genotype, with no copies of the G tag allele. This predicts you most likely do NOT carry HLA-B*57:01, so your risk of an abacavir hypersensitivity reaction is low. This is a tag-SNP prediction, not a direct HLA test; clinicians still confirm with HLA-B*57:01 typing before prescribing abacavir. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluorouracil (5-FU) – toxicity risk (DPYD HapB3) rsid : rs56038477 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/100100/ https://pubmed.ncbi.nlm.nih.gov/19530960/ Summary : This variant (c.1236G>A, plus strand C>T) tags DPYD haplotype B3 (HapB3). The T allele marks the reduced-function HapB3 haplotype, which is in tight linkage with a splicing variant (rs75017182) that lowers DPD enzyme activity to roughly half of normal. DPD breaks down fluorouracil (5-FU), so carriers clear it more slowly and have a moderately increased risk of toxicity (low blood counts, mouth sores, diarrhea). The effect is milder than the full no-function DPYD variants. CPIC and the Dutch guideline (DPWG) recommend a modest dose reduction for carriers. This matters only during 5-FU treatment. No odds ratio is reported — the effect is given as a function category (~50% activity). Note: this is one of 6 correlated variants in/near DPYD reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the C/C genotype — you do not carry the DPYD HapB3 (T) reduced-function marker. If you are ever treated with fluorouracil (5-FU), this variant does not raise your toxicity risk (other DPYD variants and clinical factors can still apply). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluorouracil / capecitabine toxicity risk (DPYD) rsid : rs72549310 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24648345/ Summary : rs72549310 is a rare variant in DPYD, the gene for the enzyme (DPD) that breaks down fluoropyrimidine chemotherapy (fluorouracil/5-FU, capecitabine). ClinVar classifies the A allele as Pathogenic/Likely pathogenic for dihydropyrimidine dehydrogenase deficiency, meaning it reduces or abolishes DPD activity. Carriers clear these drugs more slowly and can have severely increased toxicity (low blood counts, mouth sores, diarrhea) at standard doses; a dose reduction or alternative is advised. This matters only during fluoropyrimidine treatment. The variant is rare and the supporting drug-response data are limited (a single PharmGKB row plus the ClinVar deficiency classification), so no quantitative risk number is given. Note: this is one of 6 correlated variants in/near DPYD reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the G/G genotype — you do not carry the pathogenic (A) allele at this DPYD position. If you are ever treated with fluorouracil (5-FU) or capecitabine, this particular variant does not raise your toxicity risk (other DPYD variants and clinical factors can still apply). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anti-VEGF therapy response in macular degeneration (VEGFA) rsid : rs2010963 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23953100/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2010963 is the VEGFA promoter variant -634G/C (+405 G/C; forward REF=C, ALT=G), which influences how much VEGF-A — the protein that drives abnormal blood-vessel growth in the eye — is made. In choroidal neovascularization (the abnormal vessels behind wet macular degeneration), some studies link the C/C genotype to a poorer response to anti-VEGF injections and G-allele carriers to a better response, but the evidence is limited and inconsistent (PharmGKB level 3 Efficacy). Note: this is one of 2 correlated variants in/near VEGFA reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the G/G genotype. If you receive anti-VEGF eye injections for wet macular degeneration, some studies link G-allele carriers to a somewhat better response than C/C — but the evidence is limited and inconsistent (level 3), so it is only a tentative signal. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antihypertensive drug response & resistant hypertension (NOS3) rsid : rs2070744 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/14016/ https://pubmed.ncbi.nlm.nih.gov/19650939/ Summary : This is the well-known NOS3 -786T>C promoter variant, in the gene for the enzyme (eNOS) that makes nitric oxide to relax blood vessels. The C allele lowers eNOS production. Studies link the C/C genotype to harder-to-control (resistant) hypertension, yet other studies found C carriers respond better to the ACE-inhibitor enalapril — so the direction of the effect changes depending on the drug and outcome. Because the evidence points different ways, this is informational only: an association exists, but no reliable per-genotype prediction can be made. Interpretation: The C/C genotype at NOS3 -786 has been associated with reduced eNOS promoter activity and, in some cohorts, with harder-to-treat (resistant) hypertension — but other studies linked the C allele to better response to the drug enalapril. Because findings conflict across drugs and outcomes, no reliable personal prediction can be made; this is informational only and any treatment choices are made by your doctor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - conflicting_evidence_direction • Enalapril blood pressure response (NOS3) rsid : rs2070744 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/14016/ https://pubmed.ncbi.nlm.nih.gov/22706620/ Summary : rs2070744 sits in the promoter of NOS3, the gene for the enzyme that makes nitric oxide (which relaxes blood vessels). In a study of people with high blood pressure, carriers of the C allele at this position had a greater drop in blood pressure on enalapril than people with two G copies. The evidence is limited (a single small pharmacogenetic study, PharmGKB level 3), so this is a weak tendency, not a firm rule, and it only matters if you are actually taking enalapril. Interpretation: If you have the C/C genotype and hypertension, you may have a greater reduction in blood pressure when treated with enalapril compared to people with the G/G genotype. Other genetic and clinical factors can also influence blood pressure reduction on enalapril. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sildenafil response in erectile dysfunction (NOS3) rsid : rs2070744 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/14016/ https://pubmed.ncbi.nlm.nih.gov/22064666/ Summary : rs2070744 is in the promoter of NOS3, the gene for the enzyme that makes nitric oxide — the signal that drives an erection. In men treated with sildenafil after prostate surgery, those carrying the C allele responded better than men with two G copies. The evidence is limited (one small study, PharmGKB level 3), so treat this as a weak tendency, relevant only if you actually take sildenafil. Interpretation: If you are a man with post-operative erectile dysfunction and the C/C genotype, you may have an increased response to sildenafil compared to people with the G/G genotype. Other genetic or clinical factors can also influence your response to sildenafil. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Beta blockers – outcome after coronary syndrome (PPARA) rsid : rs4253778 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18855529/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4253778 is in PPARA, a gene involved in how heart muscle uses energy and responds to adrenaline. In one study of people on beta blockers after acute coronary syndrome, those with two G copies had fewer heart-related rehospitalisations, while carriers of the C allele had a roughly threefold higher rehospitalisation rate. The evidence is limited (single study, PharmGKB level 3), so this is a weak signal, relevant only if you take beta blockers. Interpretation: If you have the G/G genotype and acute coronary artery syndrome and are treated with beta blockers, you may have a decreased, but not absent, chance of rehospitalization compared to people with the G/C or C/C genotype. Other genetic and clinical factors may also influence your risk for rehospitalization. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fenofibrate response in diabetes (PPARA) rsid : rs4253778 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15608561/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4253778 sits in PPARA — and fenofibrate works precisely by activating the PPAR-alpha protein this gene makes. In people with type 2 diabetes, those with two G copies were more likely to be strong responders (greater than 30% triglyceride reduction) to fenofibrate, while C-allele carriers responded less. The evidence is limited (single study, PharmGKB level 3) and only matters if you take fenofibrate. Interpretation: If you have the G/G genotype and diabetes, you may be more likely to respond to fenofibrate treatment compared to people with the G/C or C/C genotype. Other genetic and clinical factors may also influence response to fenofibrate. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sildenafil (Viagra) – erectile response (ACE) rsid : rs4343 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12837457/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4343 in the ACE gene tracks the ACE insertion/deletion variant, where the A allele marks the lower-activity 'insertion' form and G marks the higher-activity 'deletion' form. In men with erectile dysfunction, those with the lower-ACE-activity genotype (A allele) were more likely to have a positive response to sildenafil, while higher-ACE (G/G) men responded less well. The evidence is limited (single study, PharmGKB level 3) and only relevant if you take sildenafil. Interpretation: If you have the G/A genotype and erectile dysfunction and are treated with sildenafil, you may have a decreased chance of positive erectile response compared to people with the A/A genotype. Other genetic and clinical factors may also influence your response to sildenafil. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Spironolactone response in heart failure (ACE) rsid : rs4343 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15121491/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4343 in the ACE gene tracks the ACE insertion/deletion variant; the G allele marks the higher-activity 'deletion' (D) form and A marks the 'insertion' (I) form. In people with chronic heart failure, those who were NOT G/G (i.e. carried at least one A) showed real improvement on spironolactone — better pumping fraction and smaller heart volumes — while G/G (DD-equivalent) patients improved less. The evidence is limited (single study, PharmGKB level 3) and only relevant if you take spironolactone. Interpretation: If you have the G/A genotype, you may have improvement in left ventricular ejection fraction and in end-systolic and end-diastolic volume when treated with spironolactone for chronic heart failure compared to people with the G/G genotype. Other genetic and clinical factors may also influence your response. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sildenafil response in erectile dysfunction (VEGFA) rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23007311/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 (often called VEGF -2578 C>A) is in the promoter of VEGFA, the gene for the growth factor behind blood-vessel formation in erectile tissue. In men with non-surgical erectile dysfunction, the A allele (A/A and A/C) was linked to poorer response to sildenafil, while two C copies tended to respond better. The evidence is limited (single study, PharmGKB level 3) and only relevant if you take sildenafil. Interpretation: If you have the A/A genotype, you may have a decreased response to sildenafil for erectile dysfunction compared to people with the C/C genotype. Other genetic and clinical factors may also influence the response to sildenafil. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Enalapril response in hypertension (VEGFA) rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26002049/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 (VEGF -2578 C>A) is in the promoter of VEGFA. In people with high blood pressure, carriers of the A allele (A/A and A/C) tended to have a better blood-pressure response to enalapril than those with two C copies. The evidence is limited (single study, PharmGKB level 3) and only relevant if you take enalapril. Interpretation: If you have hypertension and the A/A genotype, you may have an improved response to enalapril compared to people with the C/C genotype. Other clinical and genetic factors may also influence response to enalapril in hypertension. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bevacizumab-based chemotherapy response in colorectal cancer (VEGFA) rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20125120/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 (VEGF -2578 C>A) is in the promoter of VEGFA, the growth factor that bevacizumab is designed to block. In colorectal-cancer patients on bevacizumab-based chemotherapy, two C copies tended to track with a better response, while the A allele tracked with a weaker response. The evidence is limited (PharmGKB level 3) and only relevant in the context of this chemotherapy. Interpretation: If you have colorectal cancer and the A/A genotype, you may have a weaker response to bevacizumab-based chemotherapy (bevacizumab with capecitabine, fluorouracil, irinotecan, leucovorin or oxaliplatin) than people carrying a C copy. The evidence is limited, and tumour biology and other clinical factors influence response far more — treatment choices are made by your oncologist. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Ranibizumab response in macular degeneration (VEGFA) ⚠ CAUTIOUS rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22840423/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 (VEGF -2578 C>A) is in the promoter of VEGFA, the growth factor that ranibizumab blocks in wet age-related macular degeneration. Some studies linked the C allele to an earlier treatment response and the A/A genotype to a weaker early response, but other studies found no association — so the signal is inconsistent. The evidence is weak (PharmGKB level 4) and only relevant if you receive ranibizumab. Note: this is one of 2 correlated variants in/near VEGFA reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the A/A genotype and macular degeneration and are treated with ranibizumab, you may have a lack of early response to treatment compared to people with the A/C or C/C genotype. No association with response was found in other studies, and other genetic and clinical factors may also influence your response to ranibizumab treatment. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Docetaxel response in breast cancer (VEGFA) ⚠ CAUTIOUS rsid : rs699947 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24061601/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs699947 sits in the promoter of VEGFA, the gene for vascular endothelial growth factor A, which tumours use to grow blood vessels. The A allele (the reference base) has been linked, in small pharmacogenetic studies, to a better/longer response to chemotherapy that interferes with tumour blood supply, while the C allele tends to track with shorter benefit. The evidence here is limited (low-level PharmGKB efficacy annotation, few studies, no pooled effect size), so this is a weak, drug-specific signal — not a firm predictor. It tells you nothing outside the context of this chemotherapy. Interpretation: If you have the A/A genotype and are treated with docetaxel for breast cancer, some studies suggest you may have a somewhat longer time before the cancer progresses than people with the C/C genotype. This is a weak signal from a few small studies; many other genetic and clinical factors matter more, and it is only relevant while on this drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Irbesartan blood pressure response (AGT) ⚠ CAUTIOUS rsid : rs4762 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/11910301/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the AGT Thr174Met variant in angiotensinogen, an early step in the blood-pressure-controlling renin–angiotensin system. A small pharmacogenetic study looked at how the genotype relates to blood-pressure response to the drug irbesartan, but the findings were inconsistent and the effect allele could not be reliably pinned down. So this is informational only: an association has been reported, but no dependable per-genotype prediction can be made. Interpretation: If you have the G/G genotype (Thr174) and take irbesartan, one small study suggested a possibly different blood-pressure response than G/A carriers, but the findings were inconsistent. No reliable personal prediction can be made; this is informational only and applies only while you take irbesartan. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Thiazide diuretic response in hypertension (ADD1) ⚠ CAUTIOUS rsid : rs4961 Your geno : GT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12623934/ https://pubmed.ncbi.nlm.nih.gov/14553962/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4961 is the Gly460Trp variant in ADD1 (alpha-adducin), a protein that helps the kidney handle sodium. The minor T allele (the alternate base, the 'Trp/W460' form) is linked to salt-sensitive high blood pressure, and carriers of this allele tend to lower their blood pressure more when treated with thiazide diuretics such as hydrochlorothiazide. The supporting evidence is a low-level (level 3) PharmGKB efficacy annotation drawn from many small studies with mixed results and no pooled effect size, so this is a modest, drug-specific signal. It only matters if you take a thiazide diuretic. Interpretation: If you take a thiazide diuretic and have the G/T genotype, you carry one T (Trp460) copy, which several studies link to a somewhat greater blood-pressure reduction on thiazides. The evidence is mixed across studies, so treat this as a modest signal, relevant only while on the drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Loop diuretic response – bumetanide, furosemide, torasemide (ADD1) ⚠ CAUTIOUS rsid : rs4961 Your geno : GT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20877298/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4961 is the Gly460Trp variant in ADD1 (alpha-adducin), which influences how the kidney handles sodium. The minor T allele (the alternate base, the 'Trp/W460' form) is associated with salt-sensitive high blood pressure, and a low-level (level 3) PharmGKB annotation links it to the response to loop diuretics (furosemide, bumetanide, torasemide), with T-allele carriers tending toward a different diuretic effect. The evidence is limited, single-annotation and has no pooled effect size, so this is a weak, drug-specific signal that only matters if you take a loop diuretic. Interpretation: If you take a loop diuretic and have the G/T genotype, you carry one T (Trp460) copy, which limited data link to an altered diuretic response. The evidence is weak, so treat this as a minor signal relevant only while on the drug. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Diuretic therapy & myocardial infarction risk (ADD1) ⚠ CAUTIOUS rsid : rs4961 Your geno : GT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/11926892/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4961 is the Gly460Trp variant in ADD1 (alpha-adducin), which affects kidney sodium handling and salt-sensitive blood pressure. In pharmacogenetic studies, the minor T allele (the alternate base, 'Trp/W460') has been studied for how diuretic treatment interacts with heart-attack (myocardial infarction) risk: some data suggest T-allele carriers on diuretics may have a different — in some reports lower — risk of myocardial infarction than non-carriers. The evidence is a low-level (level 3) annotation with no pooled effect size and is not fully consistent, so this is a weak, treatment-specific signal that only applies if you take a diuretic. Interpretation: If you take a diuretic and have the G/T genotype, you carry one T (Trp460) copy; limited data suggest diuretic therapy may interact with heart-attack risk differently in carriers, but the evidence is weak and inconsistent. This only matters if you are on a diuretic. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atenolol blood pressure response (AGT) rsid : rs5051 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/14700505/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs5051 is a promoter variant of AGT (angiotensinogen), the starting protein of the blood-pressure-regulating renin–angiotensin system; the A allele (the alternate base, the '-6A' form) increases AGT production. A low-level (level 3) pharmacogenetic study linked this site to how much blood pressure falls on the beta-blocker atenolol: people with the C/C genotype showed a smaller drop in systolic blood pressure on atenolol than A-allele carriers, with no significant difference in diastolic pressure. The evidence is single-study with no pooled effect size, so this is a weak, drug-specific signal that only matters if you take atenolol. Interpretation: If you have the C/C genotype and hypertension, you may have a smaller decrease in systolic blood pressure when treated with atenolol compared to people with the C/A or A/A genotype. No significant change in diastolic blood pressure was seen between genotypes. Other genetic and clinical factors can also influence the change in systolic blood pressure. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Benazepril / imidapril blood pressure response (AGT) rsid : rs5051 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25143324/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs5051 is a promoter variant of AGT (angiotensinogen), the first protein in the renin–angiotensin blood-pressure pathway; the A allele (the alternate base, '-6A') increases AGT production. A low-level (level 3) pharmacogenetic study linked this site to blood-pressure response to the ACE inhibitors benazepril and imidapril: people with the C/C genotype tended to respond better (a larger blood-pressure fall) than A-allele carriers. The evidence is single-study with no pooled effect size, so this is a weak, drug-specific signal that only matters if you take one of these ACE inhibitors. Interpretation: If you have the C/C genotype and hypertension, you may have a better response to treatment with benazepril or imidapril compared to people with the C/A or A/A genotype. Other genetic and clinical factors can also influence your response to benazepril or imidapril. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aspirin responsiveness (ITGB3) ⚠ CAUTIOUS rsid : rs5918 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16581111/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the platelet ITGB3 PlA1/PlA2 variant. The C allele (PlA2) has been linked to a reduced response to aspirin in some studies — meaning aspirin may dampen platelet activity less effectively — but the evidence is contradictory and far from settled. It only matters if you take aspirin as an antiplatelet medicine, and no firm per-genotype prediction should be drawn. Interpretation: If you have the T/C genotype and take aspirin, some studies suggest a somewhat reduced aspirin response compared with T/T, but the evidence conflicts. No firm personal prediction can be made; this matters only if you take aspirin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Clopidogrel antiplatelet response (ITGB3) ⚠ CAUTIOUS rsid : rs5918 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19106083/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the platelet ITGB3 PlA1/PlA2 variant. Some studies reported that T/T carriers get a stronger antiplatelet effect from a clopidogrel loading dose than C carriers, while other studies found no link at all. Evidence is limited and mixed, so it is informational only and matters only if you take clopidogrel. Interpretation: If you have the T/C genotype and take clopidogrel, some studies suggest a somewhat weaker antiplatelet effect than T/T, but others found no association. No firm personal prediction can be made; this matters only if you take clopidogrel. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aspirin – effect on Factor XIII activation (F13A1) rsid : rs5985 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12515735/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the Factor XIII Val34Leu variant (F13A1), a clotting-factor gene. The A allele (Leu34) makes a faster-activating clotting factor, and in a study of young men aspirin slowed Factor XIII activation more in Leu34 carriers than in non-carriers. The relevance is specific to aspirin's effect on clotting and was studied in males; it is informational, not a treatment instruction. Interpretation: If you are male and have the C/C genotype (Val34/Val34) and take aspirin, studies suggest aspirin slows your Factor XIII activation comparatively less than in A (Leu34) carriers. This is informational only and was studied in men; other genetic and clinical factors also matter. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Photodynamic therapy response in choroidal neovascularization (F13A1) rsid : rs5985 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26307969/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, not a disease risk. It only matters if you are being treated with photodynamic therapy (PDT, a light-activated drug treatment) for choroidal neovascularization or wet age-related macular degeneration. The A allele (Leu34 form of the clotting factor F13A1, the reverse-strand equivalent of the literature's 185T) has been linked to a weaker, slower response: A-allele carriers tended to need more PDT sessions and lost more vision over 2 years, while people with two C alleles (the wild-type form) responded better. Evidence is limited (PharmGKB level 3, a single retrospective study), so this is a tendency, not a firm prediction. Interpretation: If you have choroidal neovascularization and the C/C genotype, you may have an increased response to photodynamic therapy compared to people with the A/A or C/A genotype. Other factors may affect response to photodynamic therapy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methamphetamine-induced psychosis risk (ESR1) rsid : rs2234693 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19386276/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a gene-environment marker tied to methamphetamine use - it only matters for people who use methamphetamine. The C allele of this ESR1 (oestrogen receptor) variant has been linked, in people addicted to methamphetamine, to a higher chance of methamphetamine-induced psychosis; the C/C genotype carried the highest risk, while T-allele carriers had lower risk. Evidence is limited (PharmGKB level 3). This is not a disease you have and has no relevance unless methamphetamine is used. Interpretation: If you have the T/T genotype and are addicted to methamphetamines, you may have a decreased risk of methamphetamine-induced psychosis compared to people with the C/C genotype. Other genetic and clinical factors may also influence this risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Leflunomide response in rheumatoid arthritis (ESR1) ⚠ CAUTIOUS rsid : rs9340799 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21174621/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs9340799 (the ESR1 'XbaI' variant in the estrogen-receptor-alpha gene) has been studied for leflunomide response in rheumatoid arthritis. In a small pharmacogenetic study (PharmGKB level 3 Efficacy, limited evidence), the A/A genotype was associated with a greater response to leflunomide than the G/G genotype. The effect is modest, unquantified, and a related ESR1 variant (rs2234693) also contributes. Note: this is one of 2 correlated variants in/near ESR1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the A/A genotype, you may experience a greater response to leflunomide compared to people with the G/G genotype. Other genetic and clinical factors may also influence response to leflunomide, particularly rs2234693. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Hormone replacement therapy – bone density response (ESR1) ⚠ CAUTIOUS rsid : rs9340799 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/9860300/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs9340799 (the ESR1 'XbaI' variant in the estrogen-receptor-alpha gene) influences how bone responds to hormone replacement therapy. In a small pharmacogenetic study (PharmGKB level 3 Efficacy, limited evidence), the A/A genotype was associated with smaller gains in spine bone mineral density on conjugated-estrogen/medroxyprogesterone therapy than the G/G genotype. The effect is modest, unquantified, and one of many factors affecting bone density. Interpretation: If you have the A/A genotype, you may experience either smaller increases in spine bone mineral density when treated with conjugated estrogens and medroxyprogesterone, or larger decreases in spine bone mineral density when untreated, compared to people with the G/G genotype. Other genetic and clinical factors may also influence spine bone mineral density. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Adalimumab (Humira) response in IBD (CRP) rsid : rs1130864 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27096233/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1130864 is in the CRP gene (C-reactive protein, a marker of inflammation). In a small pharmacogenetic study (PharmGKB level 3 Efficacy, limited evidence), carriers of the A allele (G/A or A/A) showed a better response to adalimumab in inflammatory bowel disease than people with the G/G genotype. The effect is modest, unquantified, and one of many factors that influence whether the drug works for you. Interpretation: If you have the G/A genotype and inflammatory bowel disease, you may have an increased response to adalimumab compared to people with the G/G genotype. Other factors may affect response to adalimumab. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rosuvastatin – cardiovascular outcome (CRP) ⚠ CAUTIOUS rsid : rs1205 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21094359/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1205 is in the CRP gene (C-reactive protein, an inflammation marker). In a small pharmacogenetic study (PharmGKB level 3 Efficacy, limited evidence), carriers of the T allele (C/T or T/T) tended to have better cardiovascular outcomes on rosuvastatin than people with the C/C genotype. The effect is modest, unquantified, and one of many factors that affect heart-disease risk; separately, the T allele is robustly linked to lower LDL cholesterol and lower CRP at the population level. Note: this is one of 2 correlated variants in/near CRP reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the C/C genotype and coronary disease, you may have poorer cardiovascular outcomes when treated with rosuvastatin compared to people with the C/T or T/T genotype. Other genetic and clinical factors may also influence cardiovascular outcomes. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Hepatitis B vaccine response (IL4R) ⚠ CAUTIOUS rsid : rs1805015 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21111021/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1805015 is a coding variant (Ser503Pro) in IL4R, the interleukin-4 receptor gene that helps regulate antibody production. A small immunogenetics study (PharmGKB level 3 Efficacy, limited evidence) linked the T allele to a weaker (non-immune) antibody response after the hepatitis B vaccine, while the C allele was associated with a stronger response. The effect is modest, unquantified, and one of several factors (age, sex, body weight) that determine whether the vaccine produces protective antibodies. Interpretation: If you have the T/T genotype, you may be at increased risk of non-immune response to the hepatitis B vaccine compared to people with the C/C genotype. Other genetic and clinical factors may also influence the risk of non-immune response to the hepatitis B vaccine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aspirin-induced asthma sensitivity (IL4) ⚠ CAUTIOUS rsid : rs2243250 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20921925/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a gene-environment / drug-response marker, relevant only if you have asthma and are exposed to aspirin (or related NSAIDs). It is the IL4 promoter variant -589C>T (rs2243250). The C allele has been linked, in a dose-dependent way, to a stronger aspirin-induced drop in lung function (FEV1) after an aspirin challenge - so C/C carriers showed the largest decline and T/T the smallest. A laboratory study supports a mechanism: aspirin boosts IL4 gene activity more strongly with the C allele. Evidence is limited (PharmGKB level 3). This is a sensitivity tendency, not a diagnosis. Interpretation: You have the C/T genotype of the IL4 promoter variant. If you have asthma, you may have a somewhat greater aspirin-induced drop in lung function (FEV1) after taking aspirin compared with people who have two T alleles, but less than C/C carriers - the effect tracks with the number of C alleles. Other genetic and clinical factors also affect how you respond to aspirin. If you have asthma, check with your doctor before using aspirin or NSAIDs. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anti-TNF therapy response in IBD (IL17A) rsid : rs2275913 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24776844/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2275913 (G>A) lies in the promoter of IL17A, a gene that drives gut inflammation. In a study of inflammatory bowel disease (mainly ulcerative colitis), carriers of the A allele tended to respond less well to anti-TNF therapy, while the G/G genotype was linked to a better response. This is a single, limited-evidence association (PharmGKB level 3) and the effect was not quantified, so treat it as a weak hint rather than a firm predictor. Interpretation: If you have inflammatory bowel disease and take an anti-TNF drug, having the G/A genotype (one A allele) was linked to a somewhat poorer response than the G/G genotype. This is based on limited evidence and is uncertain; other factors matter too. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Postoperative opioid dose requirement (IL17A) rsid : rs2275913 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/30106258/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2275913 (G>A) is a promoter variant in IL17A. In a study of patients after surgery, opioid requirements rose with each copy of the A allele: A/A carriers needed the most opioid to control pain and G/G carriers the least, in a clear dose-dependent pattern. This is a single, limited-evidence association (PharmGKB level 3), so treat it as a weak hint rather than a basis for dosing. Interpretation: If you receive opioid painkillers and have the G/A genotype (one A allele), you may need an intermediate dose — more than people with G/G but less than those with A/A. This is based on a single study and is uncertain; clinical factors matter more. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Inhaled corticosteroid response in asthma (GLCCI1) ⚠ CAUTIOUS rsid : rs37973 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21991891/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs37973 sits near GLCCI1, a gene involved in the body's response to glucocorticoids (steroids). The G allele lowers GLCCI1 expression, and in asthma trials people with two G copies improved their lung function on inhaled steroids only about one-third as much as those with the A/A genotype. So G/G is linked to a poorer response and A/A to the best response, in a dose-dependent way. Evidence is replicated but modest in size (PharmGKB level 3), so it is a hint rather than a rule. Interpretation: If you have asthma and use an inhaled corticosteroid and have the G/A genotype, your response is likely intermediate — between G/G and A/A — matching the intermediate GLCCI1 expression of this genotype. Other genetic and clinical factors also affect how well steroids work for you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bevacizumab / ranibizumab response in macular degeneration (HTRA1) ⚠ CAUTIOUS rsid : rs11200638 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22594510/ https://pubmed.ncbi.nlm.nih.gov/23337555/ https://pubmed.ncbi.nlm.nih.gov/23559864/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you are treated with anti-VEGF eye injections (bevacizumab or ranibizumab) for wet age-related macular degeneration. The evidence here is weak and conflicting (PharmGKB level 4 - the overall evidence does NOT support a real association). Some bevacizumab studies suggested the G/G genotype of this HTRA1 variant improved vision more than A/A, but analyses combining bevacizumab and ranibizumab, and ranibizumab-alone studies, found no link with visual outcome. So this should not be read as a reliable predictor of how the injections will work for you. Interpretation: If you have the G/G genotype and age-related macular degeneration, you may have better improvement in visual acuity when treated with bevacizumab compared to people with the A/A genotype. Studies assessing bevacizumab and ranibizumab in a combined analysis, and studies assessing ranibizumab alone, have found no association with visual acuity response. Other genetic and clinical factors may also influence response to bevacizumab. Warnings : - PharmGKB level 4: overall evidence does not support an association between this variant and anti-VEGF treatment response. — Also checked, no unusual variants — Lithium response in bipolar disorder (DRD1) [rs4532]: No notable finding at this locus. Hepatitis B vaccine response (IL13) [rs1295686]: No notable finding at this locus. [Medication side effects] • Antipsychotic-induced weight gain (MC4R) rsid : rs17782313 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23277235/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs17782313 sits near the MC4R gene, which helps regulate appetite. The C allele is a well-established obesity-risk allele that raises average body weight. In people taking antipsychotics, C carriers tend to gain more weight on treatment than T/T individuals. This entry is the drug-specific angle: it is relevant if you take an antipsychotic. No reliable effect-size number is established for the antipsychotic-specific weight gain (PharmGKB level-3 toxicity annotations, no effect size in source); the direction (C = more weight gain) is consistent and well replicated for BMI generally. Note: this is one of 2 correlated variants in/near MC4R reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the C/T genotype at rs17782313, which means you may have an increased likelihood of weight gain when treated with antipsychotics, compared to people with the T/T genotype. Other genetic and clinical factors can also influence weight gain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Oral contraceptives & blood clot risk (F2) rsid : rs1799963 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/12069454/ https://pubmed.ncbi.nlm.nih.gov/16769590/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799963 is the F2 (prothrombin) G20210A variant; the A allele raises the tendency to form blood clots. In people using systemic hormonal contraceptives, carrying an A allele has been linked to a higher risk of venous thrombosis (e.g. deep vein thrombosis). This is a PharmGKB level-2B drug-conditional signal with no CPIC dosing guideline, and it only matters if you use hormonal contraceptives. Interpretation: If you have the G/G genotype and are taking oral contraceptives (OCs), you may have a decreased risk for deep vein thrombosis (DVT) compared to people with the A/A or A/G genotypes, or compared to those not taking oral contraceptives. However, conflicting evidence has been reported, and other genetic and clinical factors may also influence your DVT risk on oral contraceptives. • Cisplatin – hearing loss risk (TPMT) rsid : rs1800460 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23588304/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800460 is the reduced-function TPMT *3B variant (T allele lowers TPMT enzyme activity). Some early studies linked the T allele to a higher risk of cisplatin-induced hearing loss (ototoxicity) in children, which led to it being included on some chemotherapy labels. However, multiple later studies found no association, so the link is uncertain and disputed. It is only potentially relevant during cisplatin treatment, and other factors (age, dose, kidney function) matter more. Interpretation: If you have the C/C genotype and are a child with cancer being treated with cisplatin, you may have a decreased, but not absent, risk of hearing loss compared to children with the C/T or T/T genotype. That said, multiple studies have found no association between this SNP and cisplatin-induced ototoxicity, and other genetic and clinical factors can also influence your risk of hearing loss with cisplatin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Weight gain on clozapine/olanzapine (MTHFR A1298C) ⚠ CAUTIOUS rsid : rs1801131 Your geno : TG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24725652/ https://pubmed.ncbi.nlm.nih.gov/37924126/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801131 is the MTHFR A1298C variant; the G allele (1298C) lowers MTHFR enzyme activity. In people taking the antipsychotics clozapine or olanzapine, the lower-activity G/G genotype has been linked to greater weight gain, while T/G carriers gained less than G/G. The evidence is from a single low-level (PharmGKB level-3) study in people with schizophrenia or schizoaffective disorder and has no effect-size number, so treat it as a weak tendency. It only matters if you take clozapine or olanzapine. Interpretation: You have the T/G genotype (one lower-activity copy). If you take clozapine or olanzapine for schizophrenia or schizoaffective disorder, you may gain somewhat less weight than people with the G/G genotype. Other genetic and clinical factors also influence weight gain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methotrexate response & toxicity (MTHFR) rsid : rs1801133 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25007187/ https://pubmed.ncbi.nlm.nih.gov/11710708/ https://pubmed.ncbi.nlm.nih.gov/24637499/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801133 is the MTHFR C677T variant; the A allele (677T) makes the MTHFR enzyme less stable and lowers its activity. Because methotrexate works through the folate pathway that MTHFR sits in, the A (lower-activity) allele has been linked in some studies to a higher chance of methotrexate side effects, with the A/A genotype most affected and G/G least. The evidence is conflicting, and the Dutch pharmacogenetics group (DPWG) rated this gene-drug pair 'no recommendation' (not clinically actionable). It only matters if you take methotrexate. Interpretation: If you have the G/G genotype and arthritis, you may have a decreased risk of toxicity when treated with methotrexate compared to people with the A/A genotype. However, the evidence is conflicting, and other genetic and clinical factors can also influence methotrexate toxicity. DPWG has assigned this drug-variant pair a "no recommendation" rating, as it was determined to be not clinically actionable. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluorouracil / capecitabine toxicity (MTHFR) rsid : rs1801133 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26014925/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801133 is the MTHFR C677T variant; the A allele (677T) lowers MTHFR enzyme activity. In colorectal-cancer patients on fluoropyrimidine chemotherapy (fluorouracil/capecitabine, e.g. FOLFOX), some studies link the lower-activity A allele to a slightly different treatment response, but the evidence is limited and conflicting, with no effect-size number. No CPIC guideline supports adjusting fluoropyrimidine dose based on MTHFR — the DPYD gene is the clinically important one. Only relevant if you are on these drugs. Interpretation: If you have the G/G genotype and are treated with FOLFOX (fluorouracil/leucovorin/oxaliplatin) for colorectal neoplasms, you may have a slightly decreased treatment response compared to A/A or G/A carriers. Evidence is limited and conflicting; no CPIC guideline supports MTHFR-based dose modification for fluoropyrimidines. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Platinum chemotherapy toxicity (MTHFR) rsid : rs1801133 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19159907/ https://pubmed.ncbi.nlm.nih.gov/29662106/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801133 is the MTHFR C677T variant; the A allele (677T) lowers MTHFR enzyme activity. In people on platinum-based chemotherapy, the A/A (lowest-activity) genotype has been associated in some studies with a higher risk of drug toxicity than the G/G or G/A genotypes. The evidence is limited and no effect-size number is established, so this is a weak signal. It only matters if you receive platinum chemotherapy. Interpretation: You have the G/G genotype, which may give you a decreased risk of drug toxicity when treated with platinum chemotherapy compared to people with the A/A genotype. Keep in mind that other genetic and clinical factors can also influence your risk of toxicity from platinum-based chemotherapy. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotic-induced metabolic syndrome risk (MTHFR) rsid : rs1801133 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/17976958/ https://pubmed.ncbi.nlm.nih.gov/24725652/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801133 is the MTHFR C677T variant; the A allele (677T) lowers MTHFR enzyme activity. In people taking antipsychotics, the lower-activity A allele has been linked to a higher risk of metabolic syndrome (a cluster of weight gain, high blood sugar, high blood pressure and abnormal cholesterol), with the A/A genotype most affected and G/G least. The evidence is observational with no effect-size number, so treat it as a tendency. It only matters if you take antipsychotics. Interpretation: You have the G/G genotype, which means you may have a decreased risk for metabolic syndrome when treated with antipsychotics compared to people with the A/A or A/G genotype. You can still be at risk for adverse events when taking antipsychotics, and other genetic and clinical factors may also influence your overall risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Olanzapine-induced weight gain (PPARG) rsid : rs1801282 Your geno : CG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19622037/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801282 is the PPARG Pro12Ala variant. The common C allele codes proline (Pro12); the rarer G allele codes alanine (Ala12), which is generally associated with better insulin sensitivity and lower type-2-diabetes risk. In people taking olanzapine, carriers of the G (Ala12) allele have been reported to gain more weight than C/C individuals — the opposite of its protective metabolic effect in the general population. The evidence is from a small low-level study (no G/G patients were available), so it is weak. It only matters if you take olanzapine. Interpretation: You have the C/G genotype (Pro12/Ala12). If you take olanzapine for schizophrenia, you may experience greater weight gain than people with the C/C genotype. Other genetic and clinical factors also affect weight gain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Statins – myopathy risk (SLCO1B1) rsid : rs4149056 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/29242847/ https://pubmed.ncbi.nlm.nih.gov/30595243/ https://pubmed.ncbi.nlm.nih.gov/23942138/ Summary : Each C allele is associated with higher Statins – myopathy risk (SLCO1B1) (+0.38 per copy, study scale). Moderate evidence, 5 records. Note: this is one of 2 correlated variants in/near SLCO1B1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the C/T genotype at rs4149056, which may give you an increased risk of myopathy when treated with atorvastatin compared to people with the T/T genotype. However, conflicting evidence has been reported, and other genetic and clinical factors may also influence your risk of developing myopathy on atorvastatin. • Methotrexate clearance & toxicity (SLCO1B1) rsid : rs4149056 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23233662/ https://pubmed.ncbi.nlm.nih.gov/24386571/ https://pubmed.ncbi.nlm.nih.gov/29683944/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. SLCO1B1 makes OATP1B1, a liver transporter that clears methotrexate (and mercaptopurine) from the blood. The minor C allele (the *5/*15 variant, c.521T>C) lowers transporter activity, so the liver takes up these drugs more slowly. Carriers of C clear methotrexate more slowly, reach higher drug levels, and have a higher chance of side effects, so they may need lower doses or closer monitoring; people without the C allele clear it faster. This is a recognised pharmacogenetic effect, mainly studied in children treated with high-dose methotrexate. Note: this is one of 2 correlated variants in/near SLCO1B1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the T/C genotype and Precursor Cell Lymphoblastic Leukemia-Lymphoma, you may need a decreased dose of mercaptopurine or methotrexate compared to children with the T/T genotype. Other clinical and genetic factors can also influence the appropriate dose in children with this condition. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cyclophosphamide chemotherapy – outcomes & neutropenia risk (CYP2C19) rsid : rs4244285 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/29507678/ https://pubmed.ncbi.nlm.nih.gov/26456622/ https://pubmed.ncbi.nlm.nih.gov/20179710/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4244285 is the CYP2C19*2 variant; the minor A allele makes a non-working CYP2C19 enzyme. Cyclophosphamide is a prodrug that CYP2C19 helps switch on into its active, cancer-killing form. People who carry the A allele activate cyclophosphamide less, and studies (mainly in breast cancer treated with cyclophosphamide-based regimens) show a trend toward poorer outcomes for A/A carriers compared with G/G. The evidence is a trend rather than firm, and the effect can be masked after several chemotherapy cycles. The A allele is the loss-of-function allele; G is the normal-function allele. Interpretation: You have the G/G genotype at CYP2C19. If you have breast cancer and are treated with cyclophosphamide and doxorubicin, you may have a decreased risk of a poorer outcome compared to people with the A/A genotype. Keep in mind that other genetic and clinical factors can also influence your response to treatment. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin – DRESS hypersensitivity risk (CYP2C19 *3) rsid : rs4986893 Your geno : GG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/16899/ https://pubmed.ncbi.nlm.nih.gov/28391407/ Summary : rs4986893 is the CYP2C19 *3 variant: the A allele makes a non-working (loss-of-function) version of the CYP2C19 enzyme, which helps clear phenytoin. Carrying the A allele has been reported as a risk factor for phenytoin-induced DRESS (drug reaction with eosinophilia and systemic symptoms), a serious delayed skin-and-organ hypersensitivity reaction — likely because slower phenytoin clearance raises drug exposure. Reported odds ratios for poor-metabolizer CYP2C19 status and phenytoin hypersensitivity are sizeable (around 6-7 in some studies), but evidence is limited and DRESS is rare. This does not affect Stevens-Johnson syndrome risk, which tracks a different (CYP2C9) variant. Relevant only if you take phenytoin. Interpretation: You have the G/G genotype. If you are treated with phenytoin, you may have a decreased likelihood of developing drug reaction with eosinophilia and systemic symptoms (DRESS) compared to people with the G/A or A/A genotypes. There is no association with Stevens-Johnson syndrome (SJS), and other clinical and genetic factors may also influence your DRESS risk on phenytoin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anti-tuberculosis drugs – skin rash risk (CYP2C19 *3) rsid : rs4986893 Your geno : GG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/16899/ https://pubmed.ncbi.nlm.nih.gov/30458875/ Summary : rs4986893 is the CYP2C19*3 loss-of-function variant (A allele = no enzyme activity). In a single study of anti-tuberculosis treatment, carrying this reduced-function A allele was linked to a LOWER chance of a drug-induced skin rash (maculopapular exanthema), not a higher one. Evidence is limited (one small study) and the direction is not fully settled, so treat this as preliminary. Interpretation: You have the G/G genotype (normal-function CYP2C19 at this position). In one small study of anti-tuberculosis treatment, people without the reduced-function A allele appeared somewhat more likely to develop a drug-related skin rash (maculopapular exanthema) than A-allele carriers, but this finding comes from a single study and is not established. Many other genetic and clinical factors also affect rash risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. - Direction based on a single small study; not established. • Hormonal contraceptives – thrombosis risk (Factor V Leiden) rsid : rs6025 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15946211/ Summary : Each T allele is associated with higher Hormonal contraceptives – thrombosis risk (Factor V Leiden) (+0.148 per copy, study scale). Moderate evidence, 2 publications. Interpretation: You have the C/C genotype at rs6025, meaning you carry normal Factor V (no Factor V Leiden). Compared to people with the C/T or T/T genotype, you may have a decreased risk of thrombosis when taking oral contraceptives, though conflicting evidence has been reported. Both Factor V Leiden and oral contraceptives independently raise thrombosis risk and can have a cumulative effect together, and other genetic and clinical factors may also influence your overall risk. • Ritonavir-related triglyceride elevation risk (APOE) rsid : rs7412 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15809899/ Summary : This variant is associated with higher Ritonavir-related triglyceride elevation risk (APOE) (+0.184 per copy, study scale). Moderate evidence, 3 records. Note: this is one of 2 correlated variants in/near APOE reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the C/C genotype and HIV infection and are treated with antiretroviral regimens containing ritonavir, you may have a decreased risk of hypertriglyceridemia compared to people with the T/T genotype. Other genetic and clinical factors can also influence your triglyceride levels. • Antipsychotics – QT interval effect (CYP1A2) rsid : rs762551 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/17611010/ https://pubmed.ncbi.nlm.nih.gov/16490169/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs762551 (CYP1A2*1F, -163C>A) sets your caffeine/drug-metabolizing CYP1A2 speed: REF=C is slow, ALT=A is fast. In people taking antipsychotics at higher doses (chlorpromazine-equivalent above ~300 mg) for schizophrenia, carriers of the slow C allele (C/C and C/A) tended to have a longer QTc interval on the ECG than fast metabolizers (A/A) — a marker linked to heart-rhythm risk. This is only meaningful while on antipsychotic treatment and is one of many factors a prescriber weighs. Interpretation: You have the A/A genotype, the fast CYP1A2 type. On higher-dose antipsychotics, A/A individuals tended to have a shorter QT interval than C-allele carriers. This is reassuring only in the context of antipsychotic treatment; QT risk still depends on the specific drug, dose, and other factors. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aspirin hypersensitivity in asthma (PPARG) rsid : rs3856806 Your geno : CT Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/8139/ https://pubmed.ncbi.nlm.nih.gov/20224667/ Summary : rs3856806 is a PPARG variant (His449His, +82466C>T). In a Korean study of asthmatic patients, the T allele was associated with a higher risk of aspirin hypersensitivity (aspirin-exacerbated respiratory disease), with a large reported odds ratio (~4). Evidence is limited to a single population, so the size of the effect is uncertain, but the direction (T → more reactive) is consistent within that study. Interpretation: You have the C/T genotype, carrying one copy of the T allele linked to aspirin hypersensitivity in asthma. Your risk is intermediate based on a single study. If you have asthma, do not self-test aspirin tolerance; discuss NSAID use with your doctor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotic-induced weight gain (MC4R) rsid : rs489693 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22566560/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant sits near MC4R, a gene central to appetite control. In people taking antipsychotic medication, the A allele is linked to more weight gain, and the effect is mainly seen in people who carry two copies (A/A) — they gained roughly 2–3 times more weight than C/C carriers in several studies. People with one or no A copy (C/A or C/C) are closer to baseline. Evidence is moderate and somewhat conflicting; this is one of many factors that affect weight on these drugs. Note: this is one of 2 correlated variants in/near MC4R reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take antipsychotic medication and have the C/A genotype (one A copy), your risk of weight gain is close to that of C/C — the extra weight-gain signal at this variant shows up mainly in people with two A copies. Without antipsychotic treatment, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aripiprazole – weight gain risk (MC4R) rsid : rs489693 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22566560/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs489693 lies near the MC4R gene, which helps regulate appetite. The A allele is associated with more weight gain on second-generation antipsychotics: in pooled studies, people with two copies (A/A) gained roughly twice as much weight as C/C carriers in the first weeks of treatment. Aripiprazole tends to cause less weight gain than other antipsychotics, but the same genetic pattern applies if it occurs. Interpretation: You have the C/A genotype, carrying one copy of the A allele linked to antipsychotic-related weight gain. Your tendency to gain weight on aripiprazole is intermediate — between C/C and A/A carriers. Other genetic and lifestyle factors also influence weight change on this medication. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Risperidone – weight gain risk (MC4R) rsid : rs489693 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22566560/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant near MC4R, a key appetite gene, is linked to side effects of risperidone such as weight gain and raised blood triglycerides. The A allele is the risk form, and the effect is seen mainly in people who carry two copies (A/A); people with one or no A copy (C/A or C/C) are closer to baseline. Evidence is moderate and somewhat conflicting, and many other factors also influence side effects on risperidone. Interpretation: If you take risperidone and have the C/A genotype (one A copy), your risk of weight gain and high triglycerides is close to C/C — the added risk at this variant shows up mainly in people with two A copies. If you do not take risperidone, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Paliperidone – weight gain risk (MC4R) rsid : rs489693 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23920449/ https://pubmed.ncbi.nlm.nih.gov/22566560/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant near MC4R, a key appetite gene, is linked to weight gain on paliperidone. The A allele is the risk form, with the strongest effect in people carrying two copies (A/A); people with one or no A copy (C/A or C/C) are closer to baseline. The evidence is limited (a single-study, level-3 efficacy/toxicity annotation), and many other factors also affect weight on paliperidone. Interpretation: If you take paliperidone and have the C/A genotype (one A copy), your weight-gain risk is close to C/C — the added risk at this variant shows up mainly in people with two A copies. If you do not take paliperidone, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Haloperidol – weight gain & high triglycerides (MC4R) rsid : rs489693 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22566560/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant near MC4R, a key appetite gene, is linked to side effects of haloperidol such as weight gain and raised blood triglycerides. The A allele is the risk form, with the main effect in people carrying two copies (A/A); people with one or no A copy (C/A or C/C) are closer to baseline. Evidence is limited (level-3 annotation), and many other factors also influence side effects. Interpretation: If you take haloperidol and have the C/A genotype (one A copy), your risk is close to C/C — the added risk at this variant shows up mainly in people with two A copies. If you do not take haloperidol, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Amisulpride – weight gain & high triglycerides (MC4R) rsid : rs489693 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22566560/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant near MC4R, a key appetite gene, is linked to side effects of amisulpride such as weight gain and raised blood triglycerides. The A allele is the risk form, with the main effect in people carrying two copies (A/A); people with one or no A copy (C/A or C/C) are closer to baseline. Evidence is limited (level-3 annotation), and many other factors also influence side effects. Interpretation: If you take amisulpride and have the C/A genotype (one A copy), your risk is close to C/C — the added risk at this variant shows up mainly in people with two A copies. If you do not take amisulpride, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Quetiapine – high triglycerides risk (MC4R) rsid : rs489693 Your geno : CA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22566560/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant near MC4R, a key appetite gene, is linked to side effects of quetiapine such as raised blood triglycerides and weight gain. The A allele is the risk form, with the main effect in people carrying two copies (A/A); people with one or no A copy (C/A or C/C) are closer to baseline. Evidence is limited (level-3 annotation), and many other factors also influence these side effects. Interpretation: If you take quetiapine and have the C/A genotype (one A copy), your risk is close to C/C — the added risk at this variant shows up mainly in people with two A copies. If you do not take quetiapine, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Olanzapine – weight gain risk (ADRB3) rsid : rs4994 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19193342/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the Trp64Arg variant in ADRB3, the beta-3 adrenergic receptor gene involved in fat breakdown and energy use. The Arg64 form (the C allele on this strand) has long been linked to greater weight gain, and pharmacogenetic data suggest people carrying two copies (C/C) may gain more weight on olanzapine than people with the A/A (Trp64) form. Evidence is limited (a single-study, level-3 annotation) and many other factors also affect weight on olanzapine. Interpretation: If you take olanzapine and have the A/A genotype (two Trp64 copies), you tend toward a lower — though not absent — risk of weight gain compared with C/C carriers. If you do not take olanzapine, this finding does not apply to you, and weight gain still depends on many other factors. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid painkillers – substance-use risk (CHRNA3) ⚠ CAUTIOUS rsid : rs1051730 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20725741/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1051730 sits in the CHRNA3 nicotinic-receptor gene cluster (CHRNA5-A3-B4). Its strongest, most-replicated effect is on smoking: the A allele (the variant here, the classic 'T' allele on the other strand) is linked to smoking more cigarettes per day, stronger nicotine dependence and higher lung-cancer risk. A separate, much weaker pharmacogenetic annotation links this locus to opioid (opium-alkaloid) painkiller substance-use risk: the A/A genotype was associated with greater severity of substance-related disorders than G carriers. That opioid association is single-source, low-evidence and should be read as a tentative signal, not a firm risk. Interpretation: You have the G/G genotype at this CHRNA3 marker — the lower-risk version. If you are prescribed opioid painkillers, limited evidence suggests a lower tendency toward severe substance-use problems than A/A carriers. (At this same locus, G/G also tracks with lighter smoking and lower lung-cancer risk if you smoke.) Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid addiction risk during chronic pain treatment (CHRNA5) rsid : rs16969968 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20725741/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs16969968 is a coding change (D398N) in CHRNA5, a nicotinic acetylcholine receptor subunit gene. The same minor A allele that raises nicotine-dependence risk has been linked, in PharmGKB level-3 evidence, to greater risk of opioid addiction when opioids are used for chronic pain. Evidence is limited and no effect size is reported, so treat this as a weak tendency relevant only if you take opioids. Interpretation: If you are treated with opioids for chronic pain and have the G/G genotype, you carry the lower-risk version at this CHRNA5 variant and may have a somewhat lower risk of opioid addiction than people carrying the A allele. Evidence is limited; addiction risk is driven mostly by dose, duration and personal factors. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sulfamethoxazole/trimethoprim – adverse event risk (NAT2) rsid : rs1799930 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22850190/ https://pubmed.ncbi.nlm.nih.gov/9923584/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799930 (590G>A) is the NAT2*6 slow-acetylator allele; the A allele lowers NAT2 acetylation activity. Slow acetylators clear sulfamethoxazole more slowly and have been reported to have more adverse events on sulfamethoxazole/trimethoprim (co-trimoxazole). Evidence is limited and somewhat conflicting (PharmGKB level 3) with no effect size reported, so treat this as a weak, drug-specific tendency. Note: this is one of 2 correlated variants in/near NAT2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take sulfamethoxazole/trimethoprim and have the G/A genotype, you carry one slow-acetylator (A) copy and may have a somewhat increased risk of adverse events compared with G/G. Your overall acetylator status also depends on other NAT2 variants. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sulfamethoxazole/trimethoprim – hypersensitivity risk (NAT2) rsid : rs1799931 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22850190/ https://pubmed.ncbi.nlm.nih.gov/9923584/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799931 (857G>A) is the NAT2*7 slow-acetylator allele; the A allele lowers NAT2 acetylation activity. Because slow acetylation shifts sulfamethoxazole toward reactive metabolites, slow acetylators have been reported to have more adverse events and hypersensitivity reactions to sulfamethoxazole/trimethoprim. Evidence is limited and somewhat conflicting (PharmGKB level 3) with no effect size reported. Note: this is one of 2 correlated variants in/near NAT2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take sulfamethoxazole/trimethoprim and have the G/G genotype, you do not carry the NAT2*7 slow-acetylator allele here and may have a lower risk of sulfa hypersensitivity/adverse events from this variant than A-allele carriers. Evidence is limited; other NAT2 variants and clinical factors also matter. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Docetaxel & thalidomide – toxicity risk (NAT2) rsid : rs1799931 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20038957/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799931 (857G>A) is the NAT2*7 slow-acetylator allele. In a study of men with prostate cancer treated with docetaxel plus thalidomide, the reference G allele (faster acetylation) was associated with greater treatment toxicity, while the A allele was associated with less toxicity. Evidence is limited (PharmGKB level 3, single study) and no effect size is reported, so treat this as a weak, drug-specific tendency. Interpretation: If you are treated with docetaxel and thalidomide and have the G/G genotype, you carry two copies of the allele linked to greater toxicity from this combination, so you may be at higher risk of side effects than A-allele carriers. Evidence is limited; your oncologist weighs many factors. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Risperidone-induced hyperprolactinemia risk (DRD2) rsid : rs1799978 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19339912/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. DRD2 -241A>G (rs1799978) is a promoter variant of the dopamine D2 receptor gene. Risperidone blocks D2 receptors, which can raise the hormone prolactin (hyperprolactinemia). On the forward strand REF=T is the -241A allele and ALT=C is the -241G allele; the -241G (C) allele is associated with higher DRD2 expression and has been linked in some studies to a greater rise in prolactin on risperidone. The evidence is modest, so this is a tentative risk signal that only applies while taking risperidone and can be checked directly with a blood test. Interpretation: You have the T/T genotype (two reference T alleles, the -241A/A form). If you take risperidone, this genotype is not the one most linked to higher prolactin; some studies even report better tolerability for -241A/A. Prolactin can still rise for other reasons, so your prescriber may monitor it regardless. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cisplatin/cyclophosphamide – anemia risk (NAT2) rsid : rs1801280 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24533712/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801280 is the NAT2*5 slow-acetylator variant (341T>C). In one study of ovarian-cancer patients treated with cisplatin and cyclophosphamide, carrying the slow-acetylator C (alternate) allele was linked to a higher chance of treatment-related anemia (effect allele reported as C/C and C/T). The evidence is limited (single study, no numerical effect size reported), so this is a possible tendency rather than an established risk, and it only applies if you actually receive these chemotherapy drugs. Interpretation: You have the T/T genotype — no copy of the slow-acetylator C allele at this site. If you receive cisplatin or cyclophosphamide chemotherapy, this allele does not place you in the higher anemia-risk group reported in the study. Many other factors affect chemotherapy side effects. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin + isoniazid – toxicity risk (NAT2) rsid : rs1801280 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27488001/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1801280 is the NAT2*5 slow-acetylator variant (341T>C). Slow acetylators (carriers of the C / alternate allele) break isoniazid down more slowly. Because isoniazid can block the enzyme that clears phenytoin, slow acetylators on isoniazid can accumulate higher phenytoin levels, raising the risk of phenytoin toxicity when the two drugs are taken together. This is a drug-interaction tendency reported from a case/clinical report (no numerical effect size), and it only matters if you take both medicines. Note: this is one of 3 correlated variants in/near NAT2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the T/T genotype — no copy of the slow-acetylator C allele at this site, pointing toward normal acetylation. If you ever take isoniazid with phenytoin, this allele does not place you in the slow-clearance group most prone to the phenytoin build-up; other NAT2 variants still contribute to your overall status. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid dependence risk (CNR1) ⚠ CAUTIOUS rsid : rs2023239 Your geno : TT Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/33589790/ Summary : rs2023239 is in CNR1, the gene for the cannabinoid (CB1) receptor. The C (alternate) allele has been linked to higher CB1 receptor activity in the brain, greater drug-related reward, and increased susceptibility to substance dependence (including opioids and polysubstance use). So the C allele is the higher-risk allele and the T (reference) allele is lower-risk. The associations come from modest behavioral-genetics studies (no numerical effect size given), so this is a tendency, not a diagnosis, and it is most meaningful in the context of opioid exposure. Interpretation: You have the T/T genotype — no copy of the higher-risk C allele. If you are exposed to opioids, this type is associated with a comparatively lower genetic tendency toward opioid dependence than C carriers. Dependence risk is shaped by many genetic, psychological and environmental factors, so this is only one small piece. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Rosuvastatin – exposure & myopathy risk (ABCG2) rsid : rs2231142 Your geno : GG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/30389/ https://pubmed.ncbi.nlm.nih.gov/29950617/ Summary : rs2231142 is the ABCG2 Q141K variant. The T (alternate) allele lowers the activity of the ABCG2 transporter, which normally pumps rosuvastatin out of cells and into bile and urine. With weaker transport, T carriers reach higher blood levels of rosuvastatin for the same dose — meaning more cholesterol-lowering but also a greater chance of dose-related side effects such as muscle symptoms (myopathy). Many studies report this for rosuvastatin (effect seen in G/T and T/T carriers). Guidelines often suggest a lower maximum rosuvastatin dose for T/T individuals. This only matters if you take rosuvastatin. Interpretation: You have the G/G genotype — full-function ABCG2 transporter. If you take rosuvastatin, you clear it normally and have no extra genetic tendency toward high drug levels or muscle side effects from this variant. Standard dosing applies. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atorvastatin – toxicity risk (ABCG2) ⚠ CAUTIOUS rsid : rs2231142 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/28940218/ https://pubmed.ncbi.nlm.nih.gov/19474787/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2231142 is the ABCG2 Q141K variant. The T (alternate) allele lowers ABCG2 transporter function. ABCG2 helps clear atorvastatin, so T carriers tend to reach higher atorvastatin blood levels for a given dose, which can mean slightly more cholesterol-lowering but also a higher chance of dose-related side effects such as muscle symptoms. The effect on atorvastatin is smaller and less consistent than for rosuvastatin (atorvastatin relies more on other pathways), so this is a modest tendency. It only matters if you take atorvastatin. Interpretation: You have the G/G genotype — full-function ABCG2 transporter. If you take atorvastatin, you clear it normally and this variant adds no extra genetic tendency toward high drug levels or side effects. Standard dosing applies. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methotrexate – adverse event risk in rheumatoid arthritis (ADORA2A) ⚠ CAUTIOUS rsid : rs2236624 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/32448869/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2236624 is in ADORA2A, the gene for the adenosine A2A receptor. Methotrexate works partly by boosting adenosine signaling, so variation in this receptor has been studied for links to methotrexate side effects in rheumatoid arthritis. In our source data the T (reference) allele is the one tied to adverse events, with T-carriers reported at higher risk of methotrexate side effects in some studies. However, the evidence is genuinely conflicting — other studies found the opposite, or no effect — so the direction is not settled. No numerical effect size is available. This only matters if you take methotrexate. Note: this is one of 3 correlated variants in/near ADORA2A reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: If you have rheumatoid arthritis and the T/C genotype at rs2236624, you may have an increased risk of an adverse event when treated with methotrexate compared with people who have the C/C genotype, or a decreased — but not absent — risk compared with people who have the T/T genotype. Conflicting evidence has been reported. Other genetic and clinical factors also influence adverse event risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotics – weight gain risk (FAAH) rsid : rs324420 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20631561/ https://pubmed.ncbi.nlm.nih.gov/27741037/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs324420 (also called C385A or Pro129Thr) is a missense variant in the FAAH gene, which makes the enzyme that breaks down the body's own cannabis-like signalling molecules (endocannabinoids). REF=C, ALT=A; the A allele lowers FAAH activity. In studies of people on antipsychotics, carrying the A allele was associated with a greater chance of clinically meaningful weight gain (more than 7% of body weight), while C/C carriers had a lower chance - though one risperidone study found the opposite. Evidence is PharmGKB level 3 with no effect size, so this is a tendency, not a firm prediction. Interpretation: If you have a psychotic disorder and the C/C genotype, you may have a decreased likelihood of weight gain greater than 7% of baseline body weight when treated with aripiprazole, clozapine, haloperidol, olanzapine, quetiapine, or risperidone compared with people who have the A/A or C/A genotypes. This is contradicted in one study with risperidone. Other genetic and clinical factors also influence risk of treatment-induced weight gain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Morphine – side effect risk (FAAH) rsid : rs324420 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/34871222/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs324420 (C385A, Pro129Thr) is a missense variant in FAAH, the enzyme that clears the body's own cannabis-like molecules; the endocannabinoid system interacts with opioid pain signalling. REF=C, ALT=A; the A allele lowers FAAH activity. In studies of patients given morphine, carrying the A allele was associated with a higher risk of morphine-related side effects (such as nausea, drowsiness, constipation), while the C/C genotype was associated with a lower risk - though some studies disagree. Evidence is PharmGKB level 3 with no effect size, so this is a tendency, not a firm prediction. Interpretation: If you have the C/C genotype at rs324420, you may have a decreased risk of adverse events when treated with morphine compared with people who have the A/A or C/A genotypes. Conflicting evidence has been reported. Other genetic and clinical factors also influence risk of morphine-related adverse events. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methotrexate side effects in rheumatoid arthritis (ADORA2A) rsid : rs3761422 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18539621/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This ADORA2A variant has been linked to how well people tolerate methotrexate, a drug used for rheumatoid arthritis. Methotrexate works partly by releasing adenosine, which acts on the ADORA2A receptor. In a rheumatoid-arthritis cohort, the T allele (the reference form here) was associated with more side effects, mainly gastrointestinal ones; carrying two T copies raised the odds of GI adverse events several-fold (roughly OR 2.9–5.9 across related loci). The C allele was the better-tolerated form. This only matters if you take methotrexate. Note: this is one of 3 correlated variants in/near ADORA2A reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the T/C genotype (one T, one C). If you take methotrexate, your likelihood of side effects is intermediate — between the higher-risk T/T type and the better-tolerated C/C type. If you don't take methotrexate, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotics – blood pressure & metabolic side effects (COMT Val158Met) rsid : rs4680 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25048416/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the COMT Val158Met variant (G = Valine, fast enzyme; A = Methionine, slow enzyme), which influences dopamine and noradrenaline breakdown. In studies of people on antipsychotics, the A (Met) allele — lower enzyme activity — has been linked to a tendency toward higher blood pressure and more metabolic side effects, while the G/G (Val/Val) group tended to fare better on these measures. The findings are mixed across studies, so treat this as a weak tendency, not a firm prediction. It only matters while you are taking an antipsychotic; no reliable single effect size is reported. Interpretation: You have the G/A (Val/Met) genotype. If you take antipsychotics, your tendency toward blood-pressure and metabolic side effects is likely intermediate. If you don't take antipsychotics, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotics – tardive dyskinesia risk (COMT Val158Met) rsid : rs4680 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18180754/ https://pubmed.ncbi.nlm.nih.gov/25048416/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the COMT Val158Met variant (G = Valine, fast enzyme; A = Methionine, slow enzyme). Tardive dyskinesia is an involuntary-movement side effect that can develop with long-term antipsychotic use. Some meta-analyses link the G/G (Val/Val) genotype — high enzyme activity — to a higher risk of tardive dyskinesia, with Met (A) carriers somewhat protected (around OR 0.6–0.7 for Met carriers vs Val/Val). The evidence is inconsistent across populations, so this is a weak tendency. It only matters if you take antipsychotics. Interpretation: You have the G/A (Val/Met) genotype. If you take antipsychotics, your tardive-dyskinesia risk is likely lower than G/G carriers (Met carriers showed roughly OR 0.6–0.7 in some analyses). If you don't take antipsychotics, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Analgesic withdrawal headache risk (COMT Val158Met) rsid : rs4680 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25096645/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the COMT Val158Met variant (G = Valine, fast enzyme; A = Methionine, slow enzyme). It has been linked to the likelihood of a withdrawal (rebound) headache when stopping regular pain medication. In the curated evidence, the G allele (Val, fast enzyme) is associated with a greater chance of withdrawal headache, while the A/A (Met/Met) group is less prone. This is a tendency and applies only if you actually use and then discontinue analgesics; no numeric effect size is given in the source. Interpretation: You have the G/A (Val/Met) genotype. If you regularly take pain medications and then stop, you carry one copy of the higher-likelihood G allele, so your chance of a withdrawal headache is somewhat raised compared with A/A carriers. If you don't use such medications, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluoxetine side effects in depression (BDNF) ⚠ CAUTIOUS rsid : rs6265 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20016225/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6265 is the BDNF Val66Met variant. REF=C (Val), ALT=T (Met). A study of fluoxetine in major depression (PMID 20016225) reported that carriers of the Met (T) allele had a LOWER chance of certain side effects, specifically insomnia and reduced sexual desire, compared with people who had two Val (C) alleles. In other words, the Val (C) allele was linked to more of these side effects. The finding is from a single study and modest, so it is a soft tendency rather than a reliable predictor, and only matters if you actually take fluoxetine. Interpretation: You have the C/C (Val/Val) genotype. If you take fluoxetine, one study linked this genotype to a somewhat higher chance of side effects such as insomnia and lowered sexual desire compared with people who carry the Met (T) allele. The effect is modest and from a single study — many people with this genotype tolerate fluoxetine well, and side effects are managed by your prescriber if they occur. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Analgesic withdrawal headache risk (BDNF) ⚠ CAUTIOUS rsid : rs6265 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25096645/ https://pubmed.ncbi.nlm.nih.gov/38126330/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6265 is the BDNF Val66Met variant. REF=C (Val), ALT=T (Met). It has been studied as one of several genes that might influence headache when people withdraw from frequent painkiller use (such as during treatment of medication-overuse headache). The supporting evidence is a single PharmGKB level-3 annotation (PMID 25096645) where the T allele was the recorded effect allele, but the study's reported findings centred mostly on a different gene, so the BDNF direction here is not well established. Treat this as a weak, exploratory association that only matters if you are stopping regular painkiller use. Interpretation: You have the C/C (Val/Val) genotype. If you regularly use painkillers and then stop them, there is only weak, exploratory evidence linking this gene to withdrawal headache, and the direction for your genotype is not clearly established. Headache when stopping overused painkillers is common in everyone and is managed clinically, regardless of this variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotic-induced weight gain (clozapine/olanzapine, DRD2) rsid : rs6277 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20714340/ https://pubmed.ncbi.nlm.nih.gov/33378980/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6277 is the DRD2 C957T variant, which affects how much dopamine D2 receptor the gene makes. On the forward strand REF=G (the 957C wild-type) and ALT=A (the 957T variant). PharmGKB curation (PMID 20714340) links the 957C allele — the G allele on this strand — to a greater risk of weight gain on clozapine or olanzapine, two antipsychotics known for causing weight gain. So G/G people are at higher risk and A/A people at somewhat lower (but not zero) risk. Weight gain has many causes, so this is one contributing factor and only matters if you take these drugs. Interpretation: If you have the G/G genotype, you may have an increased risk of weight gain when treated with clozapine or olanzapine compared with people who have the A/A genotype. Many factors drive antipsychotic weight gain (diet, activity, the drug itself), so this is one contributor; monitoring weight and metabolic health during treatment is the practical step. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Citalopram – agitation risk in anxiety/depression (HTR1B) ⚠ CAUTIOUS rsid : rs6296 Your geno : GG Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/27324805/ Summary : This is a common synonymous variant in the HTR1B serotonin-receptor gene (forward-strand REF C, ALT G). In one study of people with anxiety disorders or major depression (PharmGKB level 3), the C/C genotype was associated with a higher risk of becoming agitated on citalopram, while carrying the G allele was linked to lower agitation risk. The effect size was not quantified and this rests on a single study, so it is a weak, drug-specific signal. Interpretation: You have the G/G genotype. If you take citalopram, the available data suggest a lower chance of agitation than people with the C/C genotype. If you do not take citalopram, this does not apply to you, and other factors also affect agitation. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • SSRI antidepressants – side effect risk (HTR2A) rsid : rs6311 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/33731884/ https://pubmed.ncbi.nlm.nih.gov/33097827/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the HTR2A serotonin-receptor promoter polymorphism -1438G/A, here recorded on the forward strand as REF C / ALT T (the literature 'G' = forward C, literature 'A' = forward T). rs6311 sits in strong linkage with rs6313 nearby. Some studies link the C allele (literature G) to a higher chance of certain SSRI side effects such as nausea or other discontinuation-related symptoms, but results are inconsistent and a CPIC review found the evidence insufficient to guide dosing. Treat this as a weak, drug-specific signal, not a prediction. Interpretation: You have the T/T genotype. If you take an SSRI, the limited data suggest a lower chance of the side effects linked to the C allele. If you do not take an SSRI, this does not apply to you, and many other factors affect side effects. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotics – tardive dyskinesia risk (HTR2A) rsid : rs6311 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/17688403/ https://pubmed.ncbi.nlm.nih.gov/37509727/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the HTR2A serotonin-receptor promoter polymorphism -1438G/A, recorded on the forward strand as REF C / ALT T (literature 'G' = forward C, literature 'A' = forward T). In small studies (PharmGKB level 3), the T allele (literature A) was associated with a higher risk of tardive dyskinesia — involuntary movements that can develop with long-term antipsychotic use. The effect size was not quantified and evidence is limited, so this is a weak, drug-specific signal. Interpretation: You have the T/T genotype. If you take antipsychotics, small studies suggest a higher risk of tardive dyskinesia than people with the C/C genotype. If you do not take antipsychotics, this does not apply to you, and many other factors affect this risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antidepressant side effect risk (HTR2A) rsid : rs6313 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/33097827/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the HTR2A synonymous variant 102T>C (rs6313), recorded on the forward strand as REF G / ALT A (forward G corresponds to coding C; forward A to coding T). It sits in strong linkage with rs6311. Some studies link carrying the A allele (coding T) to a higher chance of antidepressant adverse events, while the G allele has been linked to better response and fewer side effects — but findings conflict and a CPIC review found the evidence insufficient to guide dosing. Treat this as a weak, drug-specific signal. Interpretation: You have the A/A genotype. If you take an antidepressant, some studies link this genotype to a modestly higher chance of certain side effects than G/G, but the evidence is mixed. If you do not take an antidepressant, this does not apply to you, and many other factors affect side effects. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Citalopram – sexual dysfunction & palpitations risk (HTR2A) rsid : rs6313 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31792367/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the HTR2A synonymous variant 102T>C (rs6313), recorded on the forward strand as REF G / ALT A (forward G corresponds to coding C; forward A to coding T). In studies of major depression (PharmGKB level 3), the A allele (coding T) was associated with a higher chance of sexual dysfunction on citalopram, while the G allele was linked to more heart palpitations and less sexual dysfunction; no clear link to gastrointestinal side effects was seen. Effect sizes were not quantified and evidence is limited, so this is a weak, drug-specific signal. Interpretation: You have the A/A genotype. If you take citalopram, studies suggest you may be more likely to develop sexual dysfunction and less likely to notice palpitations than people carrying a G allele. No link to stomach/gut side effects was found. If you do not take citalopram, this does not apply to you, and other factors also affect side effects. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Efavirenz – sadness/mood side effect (HTR2A) rsid : rs6313 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23859571/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the HTR2A synonymous variant 102T>C (rs6313), recorded on the forward strand as REF G / ALT A (forward G corresponds to coding C; forward A to coding T). In one study of people taking efavirenz for HIV (PharmGKB level 3), the G/G genotype was associated with a higher risk of sadness as a side effect, while carrying the A allele was linked to lower risk. The effect size was not quantified and this rests on a single study, so it is a weak, drug-specific signal. Interpretation: You have the A/A genotype. If you take efavirenz, one study suggested a lower chance of sadness as a side effect than people with the G/G genotype. If you do not take efavirenz, this does not apply to you, and many other factors affect mood. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotic-induced weight gain (IL1B) rsid : rs1143634 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25560300/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1143634 is a variant in IL1B, the gene for the inflammatory signalling protein interleukin-1 beta. In people taking antipsychotics, the G (reference) allele has been linked to greater antipsychotic-induced weight gain: in a study of European patients, carrying the G allele was significantly associated with more weight gain (the strongest single IL-1 beta finding, p about 0.001). The less common A (alternate) allele is associated with less weight gain. This is a single-study pharmacogenomic tendency (PharmGKB level 3), so it is not a certainty, and it only applies while you are taking antipsychotic medication. Note: this is one of 2 correlated variants in/near IL1B reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take antipsychotics, the G/A genotype (one G allele) is associated with somewhat greater weight gain than the A/A genotype, but less than G/G. This is a weak, single-study tendency; many other factors influence weight change on antipsychotic medication. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Antipsychotic-induced weight gain (IL1B) rsid : rs16944 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25560300/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs16944 is a variant in the promoter region of IL1B, the gene for the inflammatory protein interleukin-1 beta. In people taking antipsychotics, the heterozygous A/G genotype was specifically associated with greater antipsychotic-induced weight gain in studies of both European and African-American patients, while the two homozygous genotypes (A/A and G/G) were associated with less. This unusual heterozygote pattern means the effect does not simply scale with the number of G alleles. The finding comes from a single pharmacogenomic study (PharmGKB level 3), so it is a tendency rather than a certainty, and it only applies while you are taking antipsychotic medication. Note: this is one of 2 correlated variants in/near IL1B reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take antipsychotics, the A/G genotype was the one specifically linked to greater antipsychotic-induced weight gain compared with both A/A and G/G. This heterozygote effect is from a single study and does not scale with the number of G alleles; many other factors also affect weight on antipsychotics. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Lithium – sleep disturbance risk (CLOCK) rsid : rs1801260 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/21781277/ https://pubmed.ncbi.nlm.nih.gov/21047205/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is the well-studied 3111T>C variant in the CLOCK gene, which helps run the body's circadian (day–night) clock (here recorded as REF=A, ALT=C on the forward strand). The clock-disrupting allele has been linked to more evening activity, later sleep onset and less sleep, and to a higher chance of insomnia and sleep disturbances in people with bipolar disorder. The genotype recorded here as C/C corresponds to two copies of that clock-disrupting allele. Lithium treatment tends to narrow these genotype differences over time. No precise effect-size number is reported; treat this as a direction-of-tendency signal, relevant only during lithium treatment. Interpretation: If you take lithium for bipolar disorder and have the A/A genotype, you carry none of the clock-disrupting allele, so you are at lower (though not zero) risk of lithium-associated sleep disturbances than people with the C/C genotype. Other genetic, circadian and clinical factors also affect your sleep on lithium. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Olanzapine side-effect risk (HTR2A) ⚠ CAUTIOUS rsid : rs7997012 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19636338/ https://pubmed.ncbi.nlm.nih.gov/33378980/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs7997012 is an intron variant in HTR2A, the gene for a serotonin receptor that olanzapine blocks. A pharmacogenetic annotation (PharmGKB, level 3, toxicity) linked the G allele to a higher chance of side effects from olanzapine. The evidence is limited and no numeric effect size is given, so this is a tendency only, relevant when olanzapine is being used. Interpretation: If you take olanzapine and have the G/G genotype at rs7997012, you carry two copies of the G allele linked to a higher chance of olanzapine side effects, so you may be somewhat more prone to them than A/A carriers. This is a weak tendency from limited evidence, not a prediction — discuss any concerns with your prescriber. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin in pregnancy – craniofacial abnormality risk (EPHX1) ⚠ CAUTIOUS rsid : rs1051740 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19952982/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1051740 is a coding variant in EPHX1, which makes microsomal epoxide hydrolase — the enzyme that clears toxic breakdown products of phenytoin. The T allele (T/T and T/C genotypes) is the lower-activity form, so toxic phenytoin metabolites are cleared more slowly. A pharmacogenetic study (PharmGKB, level 3, toxicity) reported that when phenytoin is taken in early pregnancy, T-allele carriers have a higher chance of the baby developing craniofacial abnormalities than C/C carriers. The evidence is limited and no numeric effect size is given. This applies only to pregnancy with phenytoin exposure; the C/C genotype clears the metabolites faster and carries lower risk. Note: this is one of 2 correlated variants in/near EPHX1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the T/C genotype and use phenytoin during the first trimester of pregnancy, you may be more likely to have a child with a craniofacial abnormality compared to people with the C/C genotype. Other genetic and clinical factors may also influence your risk of toxicity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Irinotecan – neutropenia risk (UGT1A) rsid : rs11563250 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25778466/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs11563250 lies in the UGT1A gene region (UGT1A1 3'-flanking), which controls how the body clears the chemotherapy drug irinotecan. The variant (G) allele is consistently associated with a LOWER risk of severe irinotecan-induced neutropenia (low white-blood-cell counts) — a pooled odds ratio of about 0.31 — and slightly lower bilirubin, suggesting better drug clearance. This only matters during irinotecan treatment. Interpretation: You have the A/A genotype at rs11563250 (UGT1A region). If you receive irinotecan, A/A carriers have a higher risk of severe neutropenia (low white-blood-cell counts) than people carrying the G allele. This is only relevant during irinotecan treatment, and other factors (such as the UGT1A1*28 variant rs8175347) also affect this risk. Discuss dosing with your oncologist. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anthracycline chemotherapy – cardiotoxicity risk (UGT1A6) ⚠ CAUTIOUS rsid : rs17863783 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23441093/ https://pubmed.ncbi.nlm.nih.gov/26968791/ https://pubmed.ncbi.nlm.nih.gov/21900104/ https://pubmed.ncbi.nlm.nih.gov/36728273/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs17863783 is a UGT1A6 variant (part of the UGT1A6*4 group) that lowers the activity of an enzyme that helps clear anthracycline chemotherapy drugs. The alternate T allele has been linked, across several paediatric cancer cohorts, to a higher risk of anthracycline-induced cardiotoxicity (heart-muscle damage), with a reported odds ratio around 8 in a replication cohort — a strong signal, though from relatively small studies and mainly in children. The likely mechanism is reduced glucuronidation, letting toxic anthracycline metabolites build up. This only matters if you are actually treated with an anthracycline. Interpretation: If you have the G/G genotype and receive anthracycline chemotherapy, you carry the lower-risk (reference) form at this position — you are not flagged by this particular variant for extra cardiotoxicity risk. Your overall risk still depends on the cumulative dose and other factors, and your oncology team monitors your heart during treatment. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anti-tuberculosis drugs – liver toxicity risk (NAT2) rsid : rs1799929 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/11595069/ https://pubmed.ncbi.nlm.nih.gov/24465778/ https://pubmed.ncbi.nlm.nih.gov/39954223/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799929 (NAT2 c.481C>T) is one of the variants that mark the NAT2 'slow acetylator' pattern — slower processing of isoniazid and related anti-tuberculosis drugs. The alternate T allele is associated with slower acetylation, which lets isoniazid and its by-products build up and raises the risk of drug-induced liver injury (hepatotoxicity) during TB treatment. The effect is real and replicated across populations (the T allele carries roughly a 1.3-fold higher risk in pooled analyses), but acetylator status depends on the full NAT2 haplotype, so this single SNP is one part of the picture. Only relevant during anti-TB treatment, when liver function is monitored. Interpretation: If you have the C/C genotype and tuberculosis (TB), you may have a decreased risk for hepatotoxicity when treated with anti-TB drugs compared to people with the C/T or T/T genotype. This SNP is present in a variety of NAT2 alleles resulting in different NAT2 acetylator phenotypes, and is the signature SNP of NAT2*11. Other genetic and clinical factors may also influence hepatotoxicity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Isoniazid–phenytoin interaction & phenytoin toxicity (NAT2) rsid : rs1799929 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27488001/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1799929 (NAT2 c.481C>T) marks slower NAT2 acetylation. This matters for a specific drug interaction: in slow acetylators, isoniazid (a TB drug) is cleared more slowly and more strongly blocks the enzyme that breaks down phenytoin, so phenytoin can build up to toxic levels when the two drugs are taken together. The alternate T allele is associated with the slow-acetylator pattern and a higher risk of phenytoin toxicity in this combination. The evidence is limited (PharmGKB level 3) and only applies when both drugs are used at once, with phenytoin levels monitored. Note: this is one of 3 correlated variants in/near NAT2 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: If you have the C/C genotype and are receiving concomitant phenytoin and isoniazid, you may be at a decreased risk of phenytoin toxicity from the isoniazid-phenytoin interaction compared to people with the C/T or T/T genotypes. Other genetic and clinical factors may also affect your risk of developing phenytoin toxicity when treated with both isoniazid and phenytoin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Phenytoin in pregnancy – craniofacial abnormality risk (EPHX1) ⚠ CAUTIOUS rsid : rs2234922 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19952982/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. EPHX1 rs2234922 (His139Arg). EPHX1 helps detoxify reactive breakdown products of phenytoin. In one study, mothers carrying the G allele who took phenytoin in the first trimester had a higher risk of having a baby with a craniofacial abnormality than A/A mothers, who had a lower (but not zero) risk. This is a single low-level study (PharmGKB level 3 Toxicity) and applies only to phenytoin use in early pregnancy. Note: this is one of 2 correlated variants in/near EPHX1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the A/G genotype and are exposed to phenytoin during the first trimester of pregnancy, you may have an increased risk for having a child with a craniofacial abnormality compared to people with the A/A genotype. Other genetic and clinical factors may also influence your risk for toxicity. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Fluoropyrimidine chemotherapy toxicity (DPYD) rsid : rs3918290 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/2429124/ https://pubmed.ncbi.nlm.nih.gov/20819423/ https://pubmed.ncbi.nlm.nih.gov/31745289/ Summary : rs3918290 is DPYD*2A, a splice-site variant (also written c.1905+1G>A / IVS14+1G>A) on the plus strand as C>T. The T allele produces a non-functional DPD enzyme, which the body needs to break down fluoropyrimidine chemotherapy drugs (5-fluorouracil, capecitabine, tegafur). One T copy roughly halves DPD activity; two T copies cause near-complete deficiency. Lower DPD activity lets these drugs build up and can cause severe, occasionally life-threatening toxicity (low blood counts, mouth sores, diarrhoea). This is clinical-grade evidence (CPIC/DPWG level 1A) and guidelines recommend dose reduction or avoidance in carriers. It only matters if you are given one of these drugs. Note: this is one of 6 correlated variants in/near DPYD reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 6 independent confirmations. Interpretation: You have the C/C genotype — two working copies of DPYD at this position (a DPD normal metaboliser at this variant). If you are ever treated with a fluoropyrimidine chemotherapy drug (5-fluorouracil, capecitabine or tegafur), this variant does not raise your toxicity risk; standard dosing applies. Other DPYD variants not covered here can still affect tolerance. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Deferasirox – risk of adverse reactions (UGT1A1) rsid : rs4124874 Your geno : TG Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/12288/ https://pubmed.ncbi.nlm.nih.gov/26403473/ Summary : rs4124874 tags UGT1A1*60 (c.-3279T>G, plus strand T>G) in the UGT1A1 promoter region. The G allele is associated with lower UGT1A1 enzyme levels, and UGT1A1 helps clear several drugs and bilirubin. One small pharmacogenetic study (PharmGKB level 3, PMID 26403473) linked this variant to the risk of adverse reactions on deferasirox, an iron-chelation drug. The evidence is limited and the exact size of the effect is not established. It is only potentially relevant if you take deferasirox. Interpretation: You have the T/G genotype — one copy of the lower-expression UGT1A1 (*60) allele. If you take deferasirox, you may have a modestly different chance of adverse reactions than people with T/T, but the evidence is limited (a single small study) and other factors matter more. Discuss any side effects with your doctor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Irinotecan – toxicity risk (UGT1A1) rsid : rs4148323 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/28367249/ https://pubmed.ncbi.nlm.nih.gov/28502040/ https://pubmed.ncbi.nlm.nih.gov/24897286/ Summary : rs4148323 is UGT1A1*6 (c.211G>A, p.Gly71Arg; plus strand G>A). The A allele reduces UGT1A1 enzyme activity and is common in East Asian populations. UGT1A1 inactivates SN-38, the active and toxic form of the chemotherapy drug irinotecan, so the A allele can slow SN-38 clearance and raise the risk of irinotecan side effects such as low neutrophils and diarrhoea (one study reported the A/A or A/G genotypes carrying an OR around 2.8 for hyperbilirubinaemia, reflecting the same reduced-activity mechanism). The effect is dose-dependent on the number of A copies. It only matters if you receive irinotecan. Interpretation: You have the G/G genotype — the normal-activity UGT1A1 (*1/*1) form at this position. If you are treated with irinotecan, this variant does not raise your toxicity risk, and you clear SN-38 (its active toxic form) normally at this site. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atazanavir – hyperbilirubinemia risk (UGT1A1) rsid : rs4148323 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25151207/ Summary : rs4148323 is UGT1A1*6 (c.211G>A, p.Gly71Arg; plus strand G>A). The A allele reduces UGT1A1 activity, the enzyme that clears bilirubin. Atazanavir (an HIV protease inhibitor) also blocks UGT1A1, so people carrying the A allele are more prone to raised bilirubin (hyperbilirubinaemia) and visible jaundice on atazanavir. This is usually a cosmetic, reversible side effect (yellowing of skin or eyes), not liver damage, but it can prompt a change of medicine. The effect grows with the number of A copies and is only relevant if you take atazanavir. Note: this is one of 2 correlated variants in/near UGT1A1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the G/G genotype — the normal-activity UGT1A1 (*1/*1) form. If you take atazanavir, your baseline genetic risk of raised bilirubin and jaundice from the drug is lower at this site, though atazanavir can still raise bilirubin in some people. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Indinavir – hyperbilirubinemia risk (UGT1A1) rsid : rs4148323 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16609363/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4148323 is UGT1A1*6 (c.211G>A, p.Gly71Arg; plus strand G>A). The A allele reduces UGT1A1 activity, the enzyme that clears bilirubin. Indinavir (an older HIV protease inhibitor) also inhibits UGT1A1, so A-allele carriers are more prone to raised bilirubin (hyperbilirubinaemia) and jaundice while on it. In the supporting study no A/A individuals were observed, but A/G carriers had higher hyperbilirubinaemia risk than G/G. This raised bilirubin is usually cosmetic and reversible. It only matters if you take indinavir. Interpretation: You have the G/G genotype — the normal-activity UGT1A1 (*1/*1) form. If you take indinavir, your genetic risk of raised bilirubin and jaundice from the drug is lower at this site, compared with people carrying the A allele. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Statins – myopathy risk & metabolism (SLCO1B1) ⚠ CAUTIOUS rsid : rs4363657 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25992810/ https://pubmed.ncbi.nlm.nih.gov/18650507/ https://pubmed.ncbi.nlm.nih.gov/37098851/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each C allele is associated with higher Statins – myopathy risk & metabolism (SLCO1B1) (+0.3 per copy, study scale). Note: this is one of 2 correlated variants in/near SLCO1B1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You inherited one C risk variant and one T baseline variant — a heterozygous T/C genotype, one allele from each parent. Risk for statins – myopathy risk & metabolism is modestly higher than for people with the T/T baseline — about β ≈ 0.3 per copy of the C variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Opioid use disorder risk (CYP3A5) ⚠ CAUTIOUS rsid : rs776746 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/36744646/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs776746 defines the CYP3A5*3 allele; on the plus strand the C allele is *3 (non-functional, 'non-expresser') and the T allele is *1 (functional). CYP3A5 helps metabolize several opioids, including fentanyl. Some studies report that the non-functional C (*3) allele — especially in C/C non-expressers — is associated with higher fentanyl blood levels and with modestly increased odds of opioid use disorder and opioid overdose, plausibly because slower opioid clearance raises exposure. The evidence is limited (a small number of association studies, modest sample sizes, not yet a guideline-grade finding), so this is a tentative tendency rather than an established risk. It is most relevant in the context of opioid exposure and does not predict that anyone will develop a disorder. Note: this is one of 2 correlated variants in/near CYP3A5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the C/C genotype — two non-functional CYP3A5*3 alleles ('non-expresser'). Some studies link this genotype to higher fentanyl exposure and modestly increased odds of opioid use disorder and overdose, likely from slower opioid clearance. The evidence is limited and this is a tendency, not a certainty — but it is worth being aware of if opioids are ever prescribed to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Atazanavir – jaundice & hyperbilirubinemia risk (UGT1A1) rsid : rs887829 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/24557078/ https://pubmed.ncbi.nlm.nih.gov/26180834/ Summary : This variant is in the promoter of UGT1A1, the liver enzyme that clears bilirubin (the yellow breakdown product of red blood cells) and is a strong marker for reduced UGT1A1 activity (it tags the same low-activity gene version as Gilbert syndrome). The T allele lowers UGT1A1 activity, so each T copy raises baseline bilirubin (GWAS shows a clear, large per-allele increase in bilirubin levels). Atazanavir further blocks UGT1A1, so people with the lower-activity T allele are much more likely to develop visible jaundice or yellowing of the eyes (benign hyperbilirubinemia) on atazanavir. The C (reference) allele gives normal activity. This is cosmetic and reversible, not liver damage — but it can prompt people to stop a working HIV drug, which is why it is worth knowing. Note: this is one of 2 correlated variants in/near UGT1A1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have one C and one T allele (C/T) — modestly reduced UGT1A1 activity and a slightly higher baseline bilirubin. If you take atazanavir, you have an intermediate, somewhat increased chance of visible jaundice compared with C/C. This is benign (cosmetic) hyperbilirubinemia, not liver injury. No drug relevance unless you take atazanavir or a similar UGT1A1-blocking medicine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Risperidone – hyperprolactinemia risk (UGT1A1) rsid : rs887829 Your geno : CT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/29955115/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant is in the promoter of UGT1A1, an enzyme involved in clearing risperidone and its active metabolite; the T allele lowers UGT1A1 activity. A single pharmacogenetic study linked carrying the T allele to a higher chance of elevated prolactin (hyperprolactinemia — a hormonal side effect that can cause breast changes, milk production or menstrual changes) during risperidone treatment. This rests on limited evidence (one small study, PharmGKB level 3), so treat it as a possible tendency, not a certainty. The C (reference) allele is the normal-activity version. It only matters while you take risperidone. Note: this is one of 2 correlated variants in/near UGT1A1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have one C and one T allele (C/T). If you take risperidone, you may have a somewhat higher chance of elevated prolactin than people with C/C, based on limited evidence. Tell your doctor if you notice related symptoms. No relevance unless you take risperidone. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Regadenoson side effects & blood pressure response (AMPD1) rsid : rs17602729 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26554440/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant introduces a premature stop codon in AMPD1 (Q12X); the A allele is the loss-of-function version, which raises adenosine levels because less of it is recycled. Regadenoson works by activating adenosine receptors during cardiac stress tests, so people carrying the A allele have been reported to have a stronger response — a greater rise in systolic blood pressure and more side effects — than people with two normal copies. This comes from one pharmacogenetic study (PharmGKB level 3), so it is a limited signal. The G (reference) allele is the normal, full-function version. It only matters during a regadenoson stress test. Interpretation: You have one G and one A allele (G/A) — one loss-of-function AMPD1 copy. If you are given regadenoson, you may have a greater rise in systolic blood pressure and more side effects than people with G/G, based on a single study. Your care team monitors you during the test. This has no effect otherwise. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Valproic acid – bone density risk (COL1A1) rsid : rs1800012 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26727275/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800012 is the COL1A1 Sp1 binding-site variant (often written G/T or +1245 G/T; the minor 's' allele corresponds to forward-strand ALT=A). The 's' (A) allele weakens a regulatory site in the collagen type-I gene and is associated with lower bone mineral density. In people with epilepsy taking valproic acid, carriers of the A ('s') allele had significantly lower lumbar and femoral bone density than C/C ('SS') homozygotes, suggesting the variant amplifies valproate's known bone-thinning effect. Interpretation: You have the C/C genotype (the 'SS' form), associated with relatively preserved bone density. If you take valproic acid, you are at the more favourable end for valproate-related bone loss compared with A-allele carriers — though valproate can still affect bone, and other factors matter. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aspirin – risk of aspirin-intolerant chronic urticaria (TGFB1) rsid : rs1800469 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19138248/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1800469 is the TGFB1 promoter variant -509C>T (forward REF=A, ALT=G; the -509T allele corresponds to forward-strand REF=A). It changes how much TGF-β1, an immune-regulating protein, is produced. In a Korean study, the A (-509T) allele was associated with a higher chance of developing aspirin-intolerant chronic urticaria — long-lasting hives triggered or worsened by aspirin. The evidence is from a single population study (PharmGKB level 3), so the effect is suggestive rather than firmly established. Interpretation: You have the A/G genotype, carrying one copy of the -509T (A) allele linked to aspirin-intolerant chronic urticaria. If you take aspirin, your genetic contribution to this reaction is intermediate in the available study; this is a weak (level-3) signal, not a prediction that you will react. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Irinotecan – diarrhea risk in colorectal cancer (TGFB1) rsid : rs1800469 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27160286/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each G allele raises odds of Irinotecan – diarrhea risk in colorectal cancer (TGFB1) by ~9% (OR≈1.09). The underlying association is well-replicated (4 publications), but there is no clinical pharmacogenetic guideline to act on it. Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for irinotecan – diarrhea risk in colorectal cancer is modestly higher than for people with the A/A baseline — about OR ≈ 1.09 per copy of the G variant. • Sorafenib – hand-foot syndrome risk (VEGFA) rsid : rs2010963 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26830973/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs2010963 is the VEGFA promoter variant -634G/C (forward REF=C, ALT=G), which affects VEGF-A production. In patients on sorafenib for renal cell carcinoma, the G allele was associated with a higher risk of hand-foot syndrome — painful redness, swelling and peeling of the palms and soles — while C/C carried lower risk. The evidence comes from limited studies (PharmGKB level 3 Toxicity), so the size of the effect is uncertain. Interpretation: You have the G/G genotype, two copies of the allele linked to the highest risk of sorafenib-related hand-foot syndrome. If you are treated with sorafenib, you may be more prone to sore, peeling palms and soles; report skin symptoms early to your oncologist. Evidence is limited (level 3). Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Sunitinib – hypertension risk (VEGFA) rsid : rs833061 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/22948895/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs833061 is a promoter variant in VEGFA (vascular endothelial growth factor A). It has been studied as a marker of how likely sunitinib — a drug that blocks VEGF signalling — is to raise blood pressure, a common side effect of this drug class. The evidence is conflicting and limited to a low-level (level 3 Toxicity) PharmGKB annotation: some studies link the C allele (the reference base) to higher risk of treatment-induced hypertension, others implicate the T allele, so a reliable risk direction cannot be assigned. No effect size is established. This variant only matters if you take sunitinib or a related VEGF inhibitor. Interpretation: If you take sunitinib and have the C/C genotype, some studies have linked this to a higher chance of developing high blood pressure as a side effect, but the evidence is conflicting and weak. If you are on this drug, your blood pressure should be monitored regardless of genotype. This variant has no effect if you are not taking sunitinib or a similar VEGF inhibitor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin bleeding risk after heart valve replacement (APOB) ⚠ CAUTIOUS rsid : rs1367117 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31186542/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This APOB variant (best known for raising LDL cholesterol) was also examined in one study of people on warfarin after heart-valve replacement. In that single report, the G/G genotype was linked to a higher chance of bleeding even at on-target INR, while A/A carriers had a lower bleeding risk. The evidence is limited to one study, so treat it as preliminary; warfarin care is guided by INR monitoring. Note: this is one of 2 correlated variants in/near APOB reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the A/A genotype on warfarin after heart-valve replacement, the single available study suggested a lower bleeding risk at therapeutic INR than G carriers. This is preliminary, single-study evidence; INR monitoring and other clinical factors remain the main determinants, and it only applies while you take warfarin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Warfarin – bleeding risk after heart valve replacement (APOB) ⚠ CAUTIOUS rsid : rs679899 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31186542/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs679899 is a variant in the APOB gene. In people on warfarin after a mechanical heart-valve replacement, an APOB study linked certain genotypes to a higher chance of minor bleeding even while the blood-thinning level (INR) was in the target range. The evidence is a single small pharmacogenetic study (low level), the effect size is not established for this exact variant, and it is not a concern unless you take warfarin. Note: this is one of 2 correlated variants in/near APOB reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you take warfarin after a heart-valve replacement and have the G/G genotype, you may have a somewhat higher chance of minor bleeding even at a therapeutic INR compared with the A/A genotype. This comes from a single small study, the effect is not quantified, and your INR control, dose and other medicines matter far more. It is relevant only while you are on warfarin. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Anastrozole – joint pain risk (CYP19A1) rsid : rs1008805 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/27747906/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1008805 is a variant in CYP19A1, the gene for aromatase — the enzyme that aromatase-inhibitor drugs like anastrozole block. In postmenopausal women with hormone-receptor-positive breast cancer taking anastrozole, the G/G genotype was strongly linked to LESS joint pain (arthralgia), while the A allele carried higher odds of this side effect (the G/G genotype had about a 76% lower odds of arthralgia, OR≈0.24). It tells you nothing about how well the cancer treatment works, and is relevant only if you take anastrozole. Interpretation: If you are a postmenopausal woman taking anastrozole for breast cancer and have the G/A genotype, you may be more likely to develop drug-related joint pain than women with the G/G genotype. This concerns a side effect only, and it matters only while you take anastrozole. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aromatase inhibitors (anastrozole/letrozole) – joint & muscle pain risk (ESR1) rsid : rs2234693 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23894347/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take an aromatase inhibitor (anastrozole or letrozole), usually for breast cancer. The C allele of this ESR1 (oestrogen receptor) variant has been linked to a higher chance of aromatase-inhibitor-related joint and muscle pain, while the T allele tracks with lower risk. This is a possible side-effect tendency, not a disease you have; evidence is limited (PharmGKB level 3). Knowing it does not change whether the drug treats your cancer. Note: this is one of 2 correlated variants in/near ESR1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have cancer and the T/T genotype, you may have a decreased risk of musculoskeletal pain on anastrozole or letrozole compared to people with the C/C genotype. Other genetic and clinical factors may also influence this risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • TNF-alpha inhibitors – paradoxical psoriasis risk (CTLA4) rsid : rs3087243 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26194362/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This is a drug-response (pharmacogenetic) marker, relevant only if you take a TNF-alpha inhibitor (such as adalimumab, etanercept, infliximab). The A allele of this CTLA4 variant (CT60) has been linked to a higher chance of 'paradoxical' psoriasis - a psoriasis-like skin reaction that can appear during TNF-inhibitor treatment - with the A/A genotype carrying the highest risk and G-allele carriers lower risk. This is a possible side-effect tendency, not a disease you have; evidence is limited (PharmGKB level 3). Interpretation: If you have psoriasis and the G/G genotype, you may have a decreased risk of paradoxical psoriasiform reactions on TNF-inhibitors compared to people with the A/A genotype. Other genetic and clinical factors may also influence this risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Letrozole and HDL cholesterol (CYP19A1) ⚠ CAUTIOUS rsid : rs4646 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26463708/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs4646 is a variant in CYP19A1 (the aromatase gene). In postmenopausal breast-cancer patients taking letrozole, this variant was linked to how 'good' HDL cholesterol changes on treatment: the A/A genotype was associated with lower HDL and the C/C genotype with higher HDL. This is a side-marker about a lipid level, not about how well the cancer treatment works; the evidence is a single low-level pharmacogenetic study and it is relevant only if you take letrozole. Note: this is one of 4 correlated variants in/near CYP19A1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 4 independent confirmations. Interpretation: If you are a postmenopausal woman taking letrozole for breast cancer (with or without a statin) and have the C/C genotype, you may tend toward higher 'good' HDL cholesterol than women carrying the A allele. This concerns a lipid level, not treatment effectiveness, the evidence is limited, and it is relevant only while you take letrozole. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Aromatase inhibitors (anastrozole/letrozole) – joint pain risk (ESR1) rsid : rs9340799 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23894347/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs9340799 (the ESR1 'XbaI' variant in the estrogen-receptor-alpha gene) has been linked to musculoskeletal side effects of aromatase inhibitors. In a small pharmacogenetic study (PharmGKB level 3 Toxicity, limited evidence), the A/A genotype was associated with a higher risk of joint and muscle pain on anastrozole or letrozole than the G/G genotype. The effect is modest, unquantified, and one of several factors that influence whether these aches develop. Note: this is one of 2 correlated variants in/near ESR1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have cancer and the A/A genotype, you may experience an increased risk of musculoskeletal pain on anastrozole or letrozole compared to people with the G/G genotype. Other genetic and clinical factors may influence this risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • TNF-inhibitor paradoxical psoriasis risk (IL23R) rsid : rs11209026 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/26194362/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant raises odds of TNF-inhibitor paradoxical psoriasis risk (IL23R) by ~49% (OR≈1.49). Limited evidence, 1 record. Interpretation: If you have psoriasis and the G/G genotype, you may have a decreased risk of paradoxical psoriasiform reactions on TNF-inhibitors compared to people with the G/A genotype. Other genetic and clinical factors may also influence this risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • NSAID hypersensitivity risk (CTLA4) rsid : rs231775 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/28750137/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs231775 (A>G, Thr17Ala) is in CTLA4, an immune 'brake' gene. In a study of cross-reactive NSAID hypersensitivity, the A allele was the risk allele and the G allele was protective (G carriers were less common among affected patients). So the A/A genotype carries the highest reported risk of NSAID hypersensitivity and G/G the lowest. This is a single, limited-evidence association, so treat it as a weak hint. Interpretation: If you take NSAIDs and have the G/G genotype, you may have a somewhat lower risk of NSAID hypersensitivity than people carrying the A allele. This is based on a single small study and is uncertain. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cyclosporine – gingival overgrowth risk (CTLA4) rsid : rs231775 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18021981/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs231775 (A>G, Thr17Ala) is in the immune-regulating gene CTLA4. In transplant patients on cyclosporine, the A allele has been linked to a higher risk of gingival overgrowth (swelling/enlargement of the gums, a known cyclosporine side effect), so A/A carries the most reported risk and G/G the least. This is a single, limited-evidence association (PharmGKB level 3), so treat it as a weak hint. Interpretation: If you take cyclosporine and have the G/G genotype, you may have a lower risk of gum overgrowth than people carrying the A allele. This is based on a single small study and is uncertain; other factors and dental care also matter. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Allopurinol – severe skin reaction risk (SJS/TEN) rsid : rs9469003 Your geno : TC Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/21801394/ Summary : Each C allele raises odds of Allopurinol – severe skin reaction risk (SJS/TEN) by ~73% (OR≈1.73). Limited evidence, 1 record. Interpretation: If you have the T/C genotype, you may have an increased risk of severe cutaneous adverse reactions such as Stevens-Johnson syndrome or toxic epidermal necrolysis when treated with allopurinol compared to people with the T/T genotype, or a decreased — but not absent — risk compared to people with the C/C genotype. Other genetic and clinical factors may also influence your risk of allopurinol-induced adverse reactions. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Chemotherapy (cyclophosphamide/doxorubicin/fluorouracil) leukopenia risk (CYP2C19) [rs12248560]: You have the C/T genotype. If you have breast cancer, you may have a decreased risk for leukopenia when treated with cyclophosphamide, doxorubicin, and fluorouracil (FAC) compared to people with the C/C genotype. Other genetic and clinical factors can also influence your risk for leukopenia on FAC chemotherapy. Risperidone – weight gain risk (CNR1) [rs1049353]: No notable finding at this locus. Prochlorperazine – nausea risk (DRD2) [rs1079597]: No notable finding at this locus. Headache risk during analgesic withdrawal (DBH) [rs1611115]: No notable finding at this locus. Olanzapine-induced prolactin elevation (DRD2) [rs6275]: No notable finding at this locus. Analgesic-withdrawal headache risk (DRD2) [rs6275]: No notable finding at this locus. ADHD stimulants – side effect severity (DRD1) [rs4532]: No notable finding at this locus. Thiazide diuretics – diabetes risk (ACE) [rs4341]: No notable finding at this locus. Ritonavir – triglyceride elevation risk (APOC3) [rs5128]: No notable finding at this locus. Letrozole – triglyceride response in breast cancer (CYP19A1) [rs700518]: No notable finding at this locus. Tacrolimus – acute renal toxicity risk (FOXP3) [rs3761548]: No notable finding at this locus. ──────────────────────────────────────────────────────────────────────── STIMULANTS & ADDICTIONS ──────────────────────────────────────────────────────────────────────── [Alcohol] • Alcohol consumption & dependence (ADH1B) rsid : rs1229984 Your geno : CC Evidence : GWAS (binary) Source : https://pubmed.ncbi.nlm.nih.gov/28485404/ https://pubmed.ncbi.nlm.nih.gov/31998841/ https://pubmed.ncbi.nlm.nih.gov/30643258/ Interpretation: Both copies at this position carry the C variant — a C/C genotype (Arg48, slower-metabolising). This is the higher end for alcohol consumption and dependence; without the fast-metaboliser flushing response, drinking tends not to be self-limited. Per-copy effect size: OR ≈ 1.77 per copy of C. • Alcohol dependence risk (ADH1B) rsid : rs1229984 Your geno : CC Evidence : Clinical / PharmGKB Source : https://www.ncbi.nlm.nih.gov/clinvar/variation/18182/ https://pubmed.ncbi.nlm.nih.gov/35094024/ https://pubmed.ncbi.nlm.nih.gov/32451486/ https://pubmed.ncbi.nlm.nih.gov/37282553/ Summary : Each C allele raises odds of alcohol dependence (~3x per copy, meta-analysis OR ~2.9-6.6) by removing the fast-metaboliser flushing response carried by T (His48 / ADH1B*2). C/C carriers have slower Arg48 ethanol oxidation with no aversive acetaldehyde build-up; the T allele is the well-established protective fast-metaboliser variant. Strong evidence, 23+ publications. Note: this is one of 3 correlated variants in/near ADH1B reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the C/C genotype — two copies of the slower-metabolizing ADH1B (Arg48) form. Without the fast His48 (T) allele, acetaldehyde does not build up rapidly, so drinking is not self-limited by flushing or aversion. Compared with carriers of the T allele this genotype gives no protective effect from fast ADH1B, and is associated with higher odds of alcohol dependence than T-carriers. Many other genetic and lifestyle factors also influence alcohol use. • Alcohol dependence risk (ALDH2) rsid : rs671 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16679777/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs671 is the ALDH2 *2 variant, common in East Asian populations. The A allele (ALT) makes a much less active version of the enzyme that clears acetaldehyde, the toxic by-product of alcohol. Because A-allele carriers build up acetaldehyde and get unpleasant flushing, nausea and a racing heart from even small amounts of alcohol, they tend to drink less and are strongly protected against alcohol dependence. So at the trait level, each A allele lowers the risk of alcoholism, and the G/G genotype (active enzyme, no flushing brake) carries the highest dependence risk. Reported associations are very strong (e.g. odds ratios of several-fold for drinking behaviour). This only applies if you drink alcohol. Interpretation: You have the G/G genotype at rs671 in ALDH2, which may put you at an increased risk of developing alcoholism compared to people with the A/A or A/G genotypes. Other genetic and clinical factors also influence your overall risk. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Acetaldehyde accumulation from alcohol (ALDH2) rsid : rs671 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31002879/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs671 is the ALDH2 *2 variant. The enzyme ALDH2 normally breaks down acetaldehyde, the toxic intermediate your body makes when it processes alcohol. The A allele (ALT) makes a much less active enzyme, so after drinking, A-allele carriers clear acetaldehyde slowly and it builds up — driving the classic 'Asian flush' (red face, warmth, fast heartbeat, nausea). Even one A copy strongly reduces enzyme activity (heterozygotes can show several-fold higher acetaldehyde than people with two G alleles), and two A copies nearly abolish it. This describes the pharmacokinetic relationship only; it applies if you drink alcohol. Higher acetaldehyde is also a recognised carcinogen exposure, which is why ALDH2-deficient drinkers face elevated risk of certain cancers. Interpretation: You have the G/G genotype at rs671, which may mean lower concentrations of acetaldehyde — a metabolite of ethanol — compared to people with the G/A genotype. This reflects only the pharmacokinetic relationship between rs671 and acetaldehyde and does not cover clinical outcomes. Other genetic and clinical factors can also influence your acetaldehyde levels. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Alcohol use disorder risk (FUT2) ⚠ CAUTIOUS rsid : rs492602 Your geno : AG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/30336701/ https://pubmed.ncbi.nlm.nih.gov/32451486/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each G allele is associated with higher Alcohol use disorder risk (FUT2) (+5.57 per copy, study scale). Interpretation: You inherited one G risk variant and one A baseline variant — a heterozygous A/G genotype, one allele from each parent. Risk for alcohol use disorder is modestly higher than for people with the A/A baseline — about β ≈ 5.57 per copy of the G variant. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Alcoholism risk (CHRNA3) ⚠ CAUTIOUS rsid : rs1051730 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/19132693/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs1051730 sits in the CHRNA3 nicotinic-receptor gene cluster, whose strongest and most-replicated effect is on smoking: the A allele is tied to heavier smoking, nicotine dependence and lung-cancer risk. A much weaker, single pharmacogenetic annotation links the locus to alcoholism risk via ethanol response — pointing to the G allele as the higher-alcoholism-risk version (G/G higher, A/A lower). This alcohol association is low-evidence and direction-uncertain, so it should be treated as a tentative signal rather than a real personal risk, and only matters if you drink. Note: this is one of 2 correlated variants in/near CHRNA3 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the G/G genotype at this CHRNA3 marker. A single low-evidence annotation links this version to a somewhat higher tendency toward alcoholism if you drink, compared with A/A — but this is weak and uncertain. If you do not drink alcohol, it does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Naltrexone response in alcohol use disorder (OPRM1) rsid : rs1799971 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/31160146/ https://pubmed.ncbi.nlm.nih.gov/31961981/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. OPRM1 A118G (REF=A, ALT=G) sits in the mu-opioid receptor that naltrexone blocks. Some studies and meta-analyses suggest that people who carry at least one G allele have a better response to naltrexone for alcohol use disorder (for example, fewer heavy-drinking days) than people with two A alleles, while showing no such difference on placebo. However, the finding has failed to replicate in several large trials, so the evidence is genuinely mixed and not strong enough to choose treatment by genotype alone. It is relevant only while taking naltrexone. Interpretation: You have the A/A genotype (two reference A alleles). If you take naltrexone for alcohol use disorder, some studies found people with A/A respond a bit less well than G-allele carriers, but other large trials found no difference. Naltrexone can still work for A/A; genotype is not a reliable predictor on its own. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Naltrexone response in alcoholism (ADH1B) rsid : rs2066702 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/34680127/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each A allele is associated with lower Naltrexone response in alcoholism (ADH1B) (−0.202 per copy, study scale). Limited evidence, 1 record. Interpretation: If you have alcoholism and the G/G genotype at rs2066702, you may have an increased response to naltrexone compared with people who have the A/A or G/A genotypes. Other genetic and clinical factors also influence response to naltrexone. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Alcoholism risk (CHRNA3) rsid : rs578776 Your geno : GA Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/20485328/ Summary : This CHRNA3 nicotinic-receptor variant also shows a weak association with alcohol dependence, in the same direction as its nicotine effect. The G allele (the reference, major form here) is the risk version and the A allele is protective: in a multi-substance study, rs578776 showed a protective association with alcohol dependence (OR about 0.78 for the protective allele). The effect on alcohol is smaller and less consistent than for nicotine, so treat it as a minor tendency, and it only matters if you drink. Note: this is one of 2 correlated variants in/near CHRNA3 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the G/A genotype (one G, one A). If you drink alcohol, your tendency is intermediate — one protective A copy slightly lowers the risk compared with G/G. If you do not drink, this has no effect on you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Naltrexone response in alcohol use disorder (ADH1C) rsid : rs698 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/34680127/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs698 is the ADH1C Ile350Val variant. It distinguishes the faster-metabolizing ADH1C*1 (gamma-1 / isoleucine) form of the alcohol-dehydrogenase enzyme from the slower ADH1C*2 (gamma-2 / valine) form, which changes how quickly your body turns alcohol into acetaldehyde. In one small 12-week clinical trial (PharmGKB level 3 evidence), people carrying the faster-metabolizing ADH1C*1 genotype reported fewer drinking days on naltrexone, suggesting a possibly better treatment response. This is a single, limited study with no numerical effect size, and the exact letter-to-genotype mapping is reported inconsistently across sources, so treat it as a weak tendency rather than an established rule. It only matters if you are actually being treated with naltrexone for alcohol use disorder. Interpretation: You have the T/T genotype at this ADH1C position. If you are taking naltrexone to cut down on drinking, your alcohol-metabolizer genotype here is one factor that has been weakly linked to how well naltrexone works, but the evidence is from a single small trial and cannot tell you a firm direction for your genotype. Many other factors shape how well naltrexone helps you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Alcohol flush reaction (ALDH2) [rs671]: Both copies at this position carry the G variant — a G/G genotype, with no copies of the A variant present. People with G/G tend to sit toward the lower end of the alcohol flush reaction range; the A variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 1.39 per copy. Naltrexone response in alcohol dependence (DBH) [rs1611115]: No notable finding at this locus. Alcohol dependence risk (ADH1B) [rs1789891]: Both copies at this position carry the C baseline variant — a C/C genotype, with no copies of the A risk variant present. Your genetic risk for alcohol dependence sits at the lower end of the spectrum — a favourable position relative to A-carriers. Each A copy would raise risk by OR ≈ 1.47 per copy. Alcohol dependence risk (ADH1B) [rs2066702]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. The A allele shows only a weak population-level association with lower alcohol-dependence risk (about OR ≈ 0.84 per A copy), so relative to A-carriers the G/G genotype carries a small, weak population-level signal that on its own does not meaningfully predict your individual outcome. Like other ADH1B effects, this is most relevant for people who drink. [Caffeine] • Caffeine-induced anxiety (ADORA2A) rsid : rs5751876 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18305461/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs5751876 sits in ADORA2A, the gene for the adenosine A2A receptor — the same receptor caffeine blocks to make you feel alert. The T allele (the reference allele here) is linked to feeling more anxious or jittery after caffeine. In small experimental studies, people with the T/T genotype reported clearly more anxiety after a moderate caffeine dose (around 150 mg, roughly 1-2 cups of coffee), while C-allele carriers (T/C and C/C) reported little or no anxiety increase. The effect is strongest in people who do not normally drink much caffeine. Effect sizes are not precisely quantified and studies are small, so treat this as a tendency, not a certainty. It only matters if you consume caffeine. Note: this is one of 3 correlated variants in/near ADORA2A reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the T/C genotype, which means you may be less likely to experience caffeine-induced anxiety compared to people with the T/T genotype. Other genetic and clinical factors can also influence your response to caffeine. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Caffeine metabolism (CYP1A2) rsid : rs762551 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/17370067/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs762551 marks the CYP1A2 *1F variant, in the gene for the main liver enzyme that breaks down caffeine. The A allele (ALT) is the 'fast' allele: more A copies mean you clear caffeine more quickly. People with A/A are fast metabolizers (caffeine wears off sooner), C/C are slow metabolizers (caffeine lingers, effects feel stronger and last longer), and C/A is in between. This affects how long coffee keeps you alert or disrupts sleep. Some studies link the slow (C-carrier) pattern to a higher heart-attack risk from heavy coffee intake, but findings are mixed and the effect on day-to-day caffeine feel is the most reliable part. It only matters if you consume caffeine. Interpretation: You have the A/A genotype, which makes you a fast caffeine metabolizer through CYP1A2. Your body breaks down caffeine quickly, so coffee's effects tend to wear off sooner. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Caffeine-induced insomnia (CYP1A2) rsid : rs762551 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/29668752/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs762551 (CYP1A2*1F, -163C>A) controls how fast your liver breaks down caffeine. REF=C is the slow allele and ALT=A is the fast one. Slow metabolizers (C/C, and C carriers generally) keep caffeine in the bloodstream longer, so caffeine — especially late in the day — is more likely to disturb their sleep, whereas fast metabolizers (A/A) clear it quickly and tend to be less affected. Sleep also depends on dose, timing, and many other personal factors. Interpretation: You have the A/A genotype, the fast caffeine-metabolizer type. You clear caffeine quickly, so you are generally less likely to have caffeine-induced insomnia than slow metabolizers (C carriers). Large or late doses can still affect anyone's sleep. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Caffeine and miscarriage risk in pregnancy (CYP1A2) rsid : rs762551 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15849225/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs762551 (CYP1A2*1F, -163C>A) sets how fast you clear caffeine: REF=C is slow, ALT=A is fast. During pregnancy caffeine clearance slows further for everyone, and slow metabolizers (C carriers) accumulate the most caffeine, raising fetal caffeine exposure. Some studies link this combination to a higher chance of miscarriage in women who consume caffeine, though the pregnancy data are mixed. The risk is driven by caffeine intake, so limiting caffeine removes the variant's relevance; it applies to women only. Interpretation: If you are pregnant and have the A/A genotype, you are a fast caffeine metabolizer and clear caffeine more quickly, so the slow-metabolizer accumulation effect doesn't apply to you. High caffeine intake is still discouraged in pregnancy for other reasons; follow your doctor's guidance. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Coffee & tea consumption (CYP1A1/CYP1A2) rsid : rs2472297 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/32193382/ https://pubmed.ncbi.nlm.nih.gov/35653391/ https://pubmed.ncbi.nlm.nih.gov/21357676/ Interpretation: Both copies at this position carry the C variant — a C/C genotype, with no copies of the T variant present. People with C/C tend to sit toward the lower end of the coffee & tea consumption range; the T variant (which would shift the trait upward) is absent here. Per-copy effect size: β ≈ 0.04 per copy. • Coffee consumption (AHR) rsid : rs4410790 Your geno : CC Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/29367735/ https://pubmed.ncbi.nlm.nih.gov/25288136/ Interpretation: Both copies at this position carry the C variant — a C/C genotype. People with C/C tend to sit toward the higher end of the coffee consumption range, with each C copy contributing a small upward shift. Per-copy effect size: β ≈ 0.04 per copy. • Coffee consumption (CYP1A1/CYP1A2 region) ⚠ CAUTIOUS rsid : rs6968865 Your geno : TT Evidence : GWAS (quantitative) Source : https://pubmed.ncbi.nlm.nih.gov/21357676/ Interpretation: Both copies at this position carry the T variant — a T/T genotype. People with T/T tend to sit toward the higher end of the coffee consumption range, with each T copy contributing a small upward shift. Per-copy effect size: β ≈ 0.26 per copy. • Caffeine-induced anxiety (ADORA2A) rsid : rs3761422 Your geno : TC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/20520601/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. This variant in the ADORA2A adenosine-receptor gene affects how anxious caffeine makes you feel. The T allele (the reference form here) is the one linked to a stronger anxiety response to caffeine; the C allele is linked to a calmer response. In a controlled caffeine-challenge study, people with two T copies reported the largest jump in anxiety after caffeine. The effect is about sensitivity to caffeine, not a disease, and only matters if you actually consume caffeine. No numeric effect size is reported for anxiety in the source data. Note: this is one of 3 correlated variants in/near ADORA2A reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the T/C genotype (one T, one C). If you consume caffeine, your anxiety response is likely intermediate — somewhere between the more-sensitive T/T type and the calmer C/C type. If you do not use caffeine, this does not apply to you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Coffee and heart attack risk (CYP1A2) [rs762551]: You have the A/A genotype, the fast caffeine-metabolizer type. In coffee drinkers, A/A people did not show the increased heart-attack risk seen in slow metabolizers (C carriers). This is reassuring only in the context of caffeine intake; your overall heart risk still depends on many other genetic and lifestyle factors. [Nicotine] • Nicotine replacement therapy response (CHRNA3) rsid : rs1051730 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/25891233/ https://pubmed.ncbi.nlm.nih.gov/23249876/ https://pubmed.ncbi.nlm.nih.gov/29621993/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Each A allele is associated with higher Nicotine replacement therapy response (CHRNA3) (+0.1 per copy, study scale). Interpretation: If you have the G/G genotype, you may be more likely to adhere to nicotine replacement therapy (NRT) and to consume more NRT at 7 days post-quit attempt compared with people who carry the A/A or A/G genotype. Other genetic or clinical factors can also affect your adherence to and consumption of NRT. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine replacement therapy response (OPRM1) rsid : rs1799971 Your geno : AA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15007373/ https://pubmed.ncbi.nlm.nih.gov/16960700/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. OPRM1 A118G (REF=A, ALT=G) affects the mu-opioid receptor, part of the brain's reward pathway involved in nicotine reinforcement. A few studies have looked at whether this variant predicts who succeeds with nicotine replacement therapy when quitting smoking. Results are weak and inconsistent: some report that G-allele carriers do slightly better or worse, but no reliable, replicated direction has been established. This is low-confidence pharmacogenetic information and only relevant while using NRT. Interpretation: You have the A/A genotype (two reference A alleles). If you use nicotine replacement therapy to quit smoking, current evidence does not reliably predict your chance of success from this genotype — studies disagree on the direction. NRT can work regardless of genotype. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bupropion for smoking cessation – response (ANKK1/DRD2 Taq1A) ⚠ CAUTIOUS rsid : rs1800497 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15492764/ https://pubmed.ncbi.nlm.nih.gov/17654295/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Taq1A (rs1800497) lies in the ANKK1 gene next to DRD2 and tags the dopamine D2 receptor system. REF=G, ALT=A; the A allele is the historical 'A1' allele, associated with fewer striatal D2 receptors. In pooled smoking-cessation trials, people with the G/G genotype (A2/A2) responded better to bupropion — they were more likely to stay quit — while carriers of one or two A alleles (A1) showed little benefit from bupropion over placebo. The effect is real but modest and not fully consistent, and it only applies if bupropion is used. Interpretation: You have the G/A genotype (one G, one A; A1 carrier). If you take bupropion to quit smoking, studies suggest you may get less added benefit from bupropion than people with G/G, though findings are not fully consistent. Bupropion can still help; this is one input your doctor can weigh. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine replacement therapy – smoking cessation response (ANKK1/DRD2 Taq1A) ⚠ CAUTIOUS rsid : rs1800497 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/15077009/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. Taq1A (rs1800497) in ANKK1 tags the dopamine D2 receptor system; REF=G, ALT=A, with the A allele (the 'A1' allele) linked to fewer striatal D2 receptors. Researchers have asked whether this variant predicts who succeeds with nicotine replacement therapy when quitting smoking. The findings are inconsistent: an early study suggested A-allele carriers did better on NRT, but later and larger trials did not confirm a reliable association. This is low-confidence pharmacogenetic information that only applies while using NRT. Interpretation: You have the G/A genotype (one G, one A; A1 carrier). If you use nicotine replacement therapy, an early study suggested A-allele carriers may quit slightly more often on NRT, but this has not held up in larger trials. Treat it as uncertain background information, not a predictor. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Cannabis (THC) dependence susceptibility (FAAH) rsid : rs324420 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/17290447/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs324420 (C385A, Pro129Thr) is a missense variant in FAAH, the enzyme that clears the body's own cannabis-like molecules (endocannabinoids). REF=C, ALT=A; the A allele lowers FAAH activity and raises endocannabinoid tone. In a study of cannabis users, the C/C genotype was associated with a higher likelihood of becoming THC-dependent, while the A/A genotype was associated with a lower likelihood. The literature is mixed (some studies link the A allele instead to problem drug/alcohol use), and there is no effect size in the source (PharmGKB level 3), so treat this as a weak tendency only relevant if you use cannabis. Interpretation: If you have the C/C genotype, you may be more likely to be tetrahydrocannabinol (THC) dependent compared with people who have the A/A genotype. Other genetic and clinical factors also influence THC dependence. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Methamphetamine dependence risk (FAAH) rsid : rs324420 Your geno : CC Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23556448/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs324420 (C385A, Pro129Thr) is a missense variant in FAAH, the enzyme that breaks down the body's own cannabis-like molecules. REF=C, ALT=A; the A allele lowers FAAH activity. In a study (in men) of methamphetamine users, carrying the A allele was associated with a higher risk of methamphetamine dependence, while the C/C genotype was associated with a lower risk; the variant was not linked to meth-induced psychosis or panic disorder. Evidence is PharmGKB level 3 with no effect size, so this is a tendency, not a firm prediction, and only applies to people who use methamphetamine. Interpretation: If you have the C/C genotype, you may have a decreased risk for methamphetamine dependence compared with men who have the A/A genotype. Genotype was not associated with risk of methamphetamine-induced psychosis or panic disorder. Other genetic and clinical factors also influence methamphetamine dependence and methamphetamine-induced side effects. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine dependence risk (CHRNA3) rsid : rs578776 Your geno : GA Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/20886544/ https://pubmed.ncbi.nlm.nih.gov/18618000/ Summary : This variant is in CHRNA3, part of the nicotinic-receptor gene cluster strongly tied to smoking behaviour. The G allele (the reference, major form here) is the risk version, associated with greater nicotine dependence; the A allele (minor, ~29%) is protective. Smokers with two A copies showed a strong protective effect against developing nicotine dependence (around OR 0.27 in one study, i.e. ~70% lower odds versus G/G). It describes how hooked someone tends to get once they smoke, so it only matters for people who use tobacco — it does not make anyone start smoking. Note: this is one of 3 correlated variants in/near CHRNA3 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 3 independent confirmations. Interpretation: You have the G/A genotype (one G, one A). If you smoke, your tendency toward nicotine dependence is intermediate — the single A copy gives partial protection compared with G/G. If you have never used tobacco, this has no effect on you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Smoking cessation after lung cancer diagnosis (CHRNA3/CHRNA5) ⚠ CAUTIOUS rsid : rs578776 Your geno : GA Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/20886544/ https://pubmed.ncbi.nlm.nih.gov/31402126/ https://pubmed.ncbi.nlm.nih.gov/18618000/ Summary : This variant lies in the CHRNA3/CHRNA5 nicotinic-receptor cluster, where the G allele (the reference form here) is part of the haplotype tied to heavier smoking and stronger nicotine dependence, and the A allele is the protective form. Stronger nicotine dependence tends to make quitting harder, including after a lung-cancer diagnosis, so the G allele has been studied as a marker of difficulty stopping smoking. The direct evidence on cessation specifically is limited and the per-genotype effect is not quantified in the source, so this is informational. It only applies to people who smoke or have smoked. Interpretation: You have the G/A genotype (one G, one A). If you smoke, your nicotine dependence — and so the difficulty of quitting — is likely intermediate between the G/G and A/A groups. If you have never smoked, this has no effect on you. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine replacement therapy response (CHRNA5) rsid : rs588765 Your geno : TT Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/23249876/ https://pubmed.ncbi.nlm.nih.gov/26010901/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs588765 sits in the CHRNA5 nicotine-receptor gene cluster on chromosome 15, a region strongly tied to how heavily people smoke and how dependent they become. REF=T, ALT=C; the T allele is linked to higher CHRNA5 activity and somewhat heavier baseline smoking. Researchers hoped this marker would also predict who quits more easily on nicotine replacement or varenicline, but the best clinical-trial data (PMID 26010901) found no significant difference in quit success between genotypes for any treatment. So on current evidence this variant does not reliably tell you whether nicotine replacement or varenicline will work for you. It is informational only, with no good/bad signal. Interpretation: You have the T/T genotype (two T alleles) in this nicotine-receptor gene. If you smoke and try to quit, current studies do not show that this genotype changes how well nicotine patches/gum or varenicline work for you — quit success looks similar across genotypes. The T allele is associated with somewhat heavier smoking generally, but that does not reliably predict your response to stop-smoking medicines. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine response & reward sensitivity (DRD2) rsid : rs6277 Your geno : GG Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/18690117/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs6277 is the DRD2 C957T variant. On the forward strand REF=G (957C) and ALT=A (957T). A study of initial nicotine response (PMID 18690117) found that men with the 957T/957T genotype (A/A on this strand) had a stronger subjective response to nicotine — greater 'feel' effects and reward — than men with the 957C (G) allele. The effect was seen in men but not women and the study is described as preliminary. This describes how strongly nicotine is experienced, not a disease, and is informational, relevant only to people who use nicotine. Interpretation: If you are male and have the G/G genotype, one study found you may have a weaker subjective response to nicotine (reward, mood and 'feel' effects) than men with the A/A genotype. This describes how nicotine feels, not a health risk, and the finding was not seen in women. The evidence is preliminary. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine / tobacco use disorder risk (CHRNA5) rsid : rs684513 Your geno : CC Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/20886544/ Summary : This is a common variant in the CHRNA5 nicotinic-receptor gene cluster (forward-strand REF C, ALT G), which tags the well-studied CHRNA5 nicotine-dependence signal. In studies of tobacco users (PharmGKB level 3), the C allele was associated with a higher likelihood of nicotine/tobacco use disorder, and the G allele with lower likelihood. The effect size was not quantified here and the variant is a marker (in linkage) rather than the proven causal change, so it is a modest tendency, not a certainty — and it only matters for people who use tobacco. Note: this is one of 2 correlated variants in/near CHRNA5 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: You have the C/C genotype. If you smoke or use tobacco, you may be somewhat more likely to develop nicotine dependence than people with the G/G genotype. If you have never used tobacco, this has no effect on you — and not starting removes the risk entirely. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Bupropion response for smoking cessation (COMT) rsid : rs165599 Your geno : GA Evidence : Pharmacogenomics Source : https://pubmed.ncbi.nlm.nih.gov/16876132/ Summary : Research-stage pharmacogenetic signal — not clinically actionable on its own. rs165599 is a variant in COMT, the gene for the enzyme that breaks down dopamine and related brain chemicals. In a study of smokers trying to quit with bupropion, carriers of the A (alternate) allele had a better chance of staying abstinent on bupropion, while people with the common G/G genotype tended to respond less well. This comes from a single pharmacogenomic study (PharmGKB level 3), so it is a tendency rather than a firm rule, and it only matters if you are actually using bupropion to quit smoking. Interpretation: If you are using bupropion to quit smoking, the G/A genotype (one A allele) was associated with a better chance of responding than the G/G genotype, though you can still relapse based on genotype alone. Other genetic and clinical factors also influence quitting success. Warnings : - Based on limited evidence — informational, not a strong personal prediction. • Nicotine dependence risk (DRD1) ⚠ CAUTIOUS rsid : rs686 Your geno : GA Evidence : Clinical / PharmGKB Source : https://pubmed.ncbi.nlm.nih.gov/18092181/ Summary : rs686 sits in the 3' untranslated region of the DRD1 gene, which makes the dopamine D1 receptor (part of the brain's reward system). A pharmacogenetic study (PharmGKB, level 3, Tobacco Use Disorder) reported that the A allele is associated with a higher chance of becoming dependent on nicotine, while the G allele is associated with lower risk. The effect is modest and no numeric effect size is given. This matters only for people who use nicotine; it is one of many genetic and environmental factors that influence whether dependence develops. Note: this is one of 2 correlated variants in/near DRD1 reported for this trait. Neighbouring variants at one locus are usually inherited together (linkage disequilibrium), so treat them as largely a single shared signal — not 2 independent confirmations. Interpretation: If you have the G/A genotype, you may be at increased risk for nicotine dependence compared to people with the G/G genotype, or at decreased risk compared to people with the A/A genotype. Other genetic and clinical factors may also influence your risk of nicotine dependence. Warnings : - Based on limited evidence — informational, not a strong personal prediction. — Also checked, no unusual variants — Nicotine dependence & cigarettes per day (CHRNA3) [rs1051730]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. Among people who smoke, each A copy is associated with a modestly higher number of cigarettes per day (about +0.8 per copy, study scale); with no A copies this measurement sits at the lower end. This describes smoking intensity once a person smokes, not whether they start, and it is a measurement nudge rather than a disease. Nicotine dependence & heavier smoking (CHRNA5) [rs16969968]: Both copies here carry the G allele — a G/G genotype, with no copies of the A allele. Among people who smoke, each A copy is associated with a modestly higher nicotine-dependence / smoking-intensity measurement (about +0.23 per copy, study scale); with no A copies this sits at the lower end. This is a measurement nudge among smokers, not a disease. Nicotine dependence & smoking addiction (CHRNA3) [rs3743078]: No notable finding at this locus. Nicotine dependence & cigarettes per day [rs8034191]: Both copies here carry the T allele — a T/T genotype, with no copies of the C allele. Among people who smoke, each C copy is weakly associated with a slightly higher number of cigarettes per day (about +0.06 per copy, study scale); with no C copies this sits at the lower end. The effect is small and on its own does not meaningfully predict your individual behavior; it is a measurement nudge among smokers, not a disease. Nicotine dependence risk (DRD1) [rs4532]: No notable finding at this locus. ======================================================================== DISCLAIMER: This report is for research and educational use only. It is not a substitute for professional medical advice. ========================================================================