Clinical and well-replicated disease SNPs.

The most common genotype. Average late-onset Alzheimer and lipid risk — not ε4, not ε2.

ε4 (rs429358 C) is the well-known Alzheimer and CHD risk allele. ε2 (rs7412 T) is associated with lower Alzheimer risk and a different lipid pattern. This genome is ε3/ε3. That is not protective like ε2, and it is not the elevated-risk ε4 genotype. Microarray cannot see rare APOE coding changes or APP/PSEN mutations.

The most common Mendelian Parkinson variant on consumer chips is absent.

G2019S is the A allele. G/G is wild-type. GBA risk alleles were not confidently called. TREM2 R47H (rs75932628) was a no-call. Microarray is a screen, not a Parkinson panel.

One copy of the 9p21 risk haplotype. Small, well-replicated increase in coronary disease risk independent of lipids.

9p21 is the original common CAD locus. It acts through vascular cell-cycle genes, not LDL. Heterozygotes have a modest increase (on the order of 15–25% relative). LPA SNPs that tag high lipoprotein(a) (rs10455872, rs3798220) were both non-risk here, which is favorable, but those two SNPs do not fully determine Lp(a). Standard prevention still dominates.

Once-in-a-lifetime Lp(a) plus a standard lipid panel is a reasonable conversation with a clinician. Blood pressure, not smoking, and fitness matter more than this SNP.

The promoter risk C allele is absent.

−786C is associated with lower endothelial nitric-oxide synthase transcription in some studies. T/T is the common non-risk promoter. The Glu298Asp SNP was not called on this extract.

The two SNPs that tag many high lipoprotein(a) haplotypes in Europeans are both non-risk.

Lp(a) is still best measured once directly. KIV-2 repeat number, the real driver, is not on this chip. A non-risk tag genotype makes very high Lp(a) less likely, not impossible.

The protective loss-of-function R46L allele is absent — the common background.

R46L (T) lowers LDL and coronary risk. G/G is the typical non-carrier state. SORT1 rs646776 is T/T (not the LDL-lowering C). None of this replaces a lipid panel.

Heterozygous for the T allele. Modest but well-replicated increase in type 2 diabetes risk.

TCF7L2 rs7903146-T is the largest-effect common variant for T2D in European-ancestry GWAS (roughly 1.4× per T allele). It affects incretin signaling and insulin secretion, not just BMI. Combined here with one FTO risk haplotype, the genetic nudge is real but still smaller than body weight, fitness, and diet. Lifestyle change has repeatedly been shown to blunt this risk.

Worth a baseline fasting glucose or HbA1c with a clinician. Resistance training and fiber-rich meals pay extra dividends with this genotype.

Heterozygous at the well-known FTO obesity locus, including the IRX3/ARID5B-disrupting rs1421085 C allele.

This haplotype slightly increases appetite and adiposity on a Western diet. Effect sizes are a few kilograms on average, not destiny. The same locus has been associated with higher protein-intake preference and a better response to structured exercise in some trials. It does not override calories or muscle mass.

Prioritize protein and resistance training. The genotype is a reason to be deliberate, not fatalistic.

The common gout / high-uric-acid allele is absent.

Q141K (T) reduces urate excretion. G/G is wild-type. Diet and thiazides still move uric acid.

One copy of the MUC5B promoter variant. Raises idiopathic pulmonary fibrosis risk, still a rare disease.

The T allele is the strongest common genetic risk factor for IPF (roughly 4–8× in heterozygotes). Lifetime risk remains on the order of about 1% in carriers versus ~0.2% in non-carriers — most people with this genotype never get IPF. Carriers who do develop IPF tend to have better survival than non-carriers. Smoking, agricultural dust, and reflux amplify risk. This is a reason to take unexplained chronic dry cough or breathlessness seriously, not a diagnosis.

Do not smoke. Avoid concentrated organic/agricultural dust. Treat reflux. Stay current on influenza, COVID, and pneumococcal vaccines. See a clinician for unexplained dry cough lasting weeks.

The two common alpha-1 antitrypsin deficiency alleles are absent.

Pi*Z (rs28929474 T) and Pi*S (rs17580 A) cause the vast majority of clinically relevant A1AT deficiency. Both are wild-type here. This does not replace serum A1AT testing if there is early emphysema or unexplained liver disease.

The main inherited clotting variant is absent.

rs6025 T is Factor V Leiden. C/C is wild-type. Prothrombin G20210A (rs1799963) was not on this extract. Factor XIII V34L is C/C (Val/Val, the common non-Leu genotype).

One H63D allele. Alone this rarely causes iron overload. C282Y (the main hemochromatosis variant) is absent.

C282Y homozygotes and C282Y/H63D compound heterozygotes account for most hereditary hemochromatosis. Simple H63D heterozygotes have at most a trivial ferritin shift. TMPRSS6 rs855791 is A/A, a genotype associated with slightly lower iron and hemoglobin — a push in the opposite direction. Net: no classic genetic hemochromatosis, and iron could even run a bit low if diet is poor.

A one-time ferritin / transferrin-saturation check is inexpensive peace of mind if never measured. Do not donate blood aggressively or take iron supplements without a lab.

The main celiac-risk HLA tags are all non-risk. Genetic celiac risk is low.

Almost all celiac disease requires DQ2.5, DQ8, or (less often) DQ2.2. Absence of these tags makes celiac disease unlikely as a genetic predisposition. It does not make it impossible — rare haplotypes exist — and it does not speak to non-celiac gluten sensitivity, which is not HLA-tied.

The strongest common multiple-sclerosis HLA risk allele is present once.

rs3135388 A tags HLA-DRB1*15:01 / DQ6. Heterozygotes have a few-fold higher MS risk than non-carriers; absolute risk remains low (MS is still uncommon). This is information, not a forecast. Vitamin D sufficiency and not smoking are the controllable factors most often discussed with this haplotype.

Protective IL23R R381Q is present. ATG16L1 T300A is homozygous (Crohn risk). Common NOD2 R702W is absent.

IL23R R381Q is one of the stronger protective alleles against Crohn’s. ATG16L1 T300A (G) impairs autophagy and is a common Crohn risk allele — GG is the risk homozygote, but effect size is modest. NOD2 R702W is wild-type. Net genetic IBD load is not high. Family history and smoking matter more.

The main genetic fatty-liver risk allele is absent.

I148M (G) raises NAFLD / NASH risk, especially with adiposity and alcohol. C/C is the lower-risk genotype. Alcohol and weight still dominate liver fat. PEMT TT (above) is the more relevant liver-nutrition finding here.

Neither CFH Y402H nor ARMS2 A69S risk alleles are present.

These two loci explain a large fraction of age-related macular degeneration heritability. Non-risk at both is favorable. Smoking and UV still matter. This is not a substitute for dilated-eye exams after midlife.

The Nordic familial-prostate variant is absent.

G84E is a moderate-penetrance prostate-cancer allele in Northern European men. C/C is wild-type. MSMB rs10993994 is C/T (one common GWAS risk allele) — tiny effect.

Y179C and G396D, the two European MUTYH polyposis alleles, are absent.

Biallelic MUTYH causes MAP (colonic polyposis). Carrier screening on a microarray is incomplete. These two common European alleles are wild-type.