Action plan

What this genome is asking you to do.

Ranked by whether a result can change a decision this year. Common SNPs are not diagnoses. The items below are the ones with a guideline, a lab, or a clearly better habit.

This week

No lab required.

  1. 01

    Put SLCO1B1 on the medication list

    If a clinician ever starts a statin, this genome is a SLCO1B1*5 heterozygote. Simvastatin at high dose is the one to avoid. Atorvastatin, rosuvastatin, or pravastatin are the usual work-arounds. This is a CPIC-backed interaction, not a wellness guess.

    SLCO1B1 rs4149056 C/T

  2. 02

    Treat the lungs as non-renewable

    One MUC5B promoter T allele raises idiopathic pulmonary fibrosis risk. The disease is still uncommon. The useful moves are boring and high-leverage: do not smoke, do not vape, avoid concentrated farm or compost dust, treat chronic reflux, and do not ignore a dry cough that lasts weeks.

    MUC5B rs35705950 G/T

  3. 03

    Eat choline on purpose

    PEMT 175M/M means the liver makes phosphatidylcholine poorly. Two eggs most days covers a large share of the AI. Liver, meat, soy lecithin, or a choline bitartrate / CDP-choline supplement are backups if the diet is plant-forward.

    PEMT rs7946 T/T

With a clinician

Small, high-yield blood work.

  1. 01

    Get a small, high-yield lab set once

    Ask a clinician for: fasting lipids + Lp(a) once, HbA1c or fasting glucose, ferritin + transferrin saturation, 25-OH vitamin D, and (optional) homocysteine with B12 and folate. None of these genotypes diagnose a disease. They tell you which numbers are worth knowing.

    TCF7L2, FTO, 9p21, H63D, methylation stack

How to live it

Training, food, lungs, UV.

  1. 01

    Train like a power genotype that must stay insulin-sensitive

    ACTN3 RR responds well to heavy resistance and sprints. TCF7L2 and FTO make muscle and fiber unusually valuable for glucose control. A practical split: 3 lifting sessions + 1–2 short intervals + daily walking. That pattern matches this genome better than long slow cardio alone.

    ACTN3 RR + TCF7L2 CT + FTO het

  2. 02

    Do the unsexy coronary work

    9p21 is lipid-independent. Blood pressure, not smoking, sleep, and cardiorespiratory fitness move this risk more than any supplement. Know the numbers: BP, ApoB or LDL, and that once-only Lp(a).

    9p21 heterozygous

  3. 03

    Coffee is genetically in-bounds

    CYP1A2 *1F/*1F clears caffeine quickly. The slow-metabolizer coffee–MI story does not apply. Stop caffeine 8 hours before bed anyway if sleep is the goal. Lactase persistence means dairy in the coffee is fine.

    CYP1A2 AA + LCT persistent

  4. 04

    Get EPA/DHA from fish or algae

    Intermediate FADS conversion plus a PEMT-limited phospholipid pathway is a quiet argument for actual long-chain omega-3s rather than flax-only.

    FADS het + PEMT TT

  5. 05

    Light-European skin, blue-eye UV budget

    SLC24A5, SLC45A2, and HERC2 G/G describe a low-melanin iris and skin. Use sunscreen on long exposure. The vitamin D SNPs are favorable, so deficiency is more about indoor life than genes.

    Pigmentation cluster

When you are ready

PGx card, counseling, deeper DNA.

  1. 01

    Carry a one-line pharmacogenetic card

    CYP2C19 normal. CYP2C9 normal. VKORC1 higher-dose haplotype. SLCO1B1 intermediate (avoid high-dose simvastatin). TPMT/DPYD common alleles normal. HLA-B*5701 tag negative. CYP2D6 possibly *3 carrier — confirm before tamoxifen or codeine if those drugs appear.

    CPIC-relevant star alleles on the chip

  2. 02

    This chip is not a cancer panel

    Common BRCA, Lynch, and familial-hypercholesterolemia variants are mostly absent from 23andMe v5, and indel encodings are easy to misread. If a parent or sibling had early breast, ovarian, colorectal, or very high LDL, see a genetic counselor. Do not treat a quiet microarray as a negative clinical test.

    Assay limits, not a genotype

  3. 03

    Optional: deepen the haplogroups

    Y is R1a-L260 (West Slavic). mtDNA is J1c. A Big Y or full mitochondrial sequence will split those into modern subclades and match living testers. Autosomal AIMs already say Northwest/Central European — an imputation-based ancestry tool (e.g. a research PCA) would add percentages, not a new story.

    R1a-L260 + J1c + European AIMs