Every finding, in the open.

Risk alleles at both of the two strongest LPA loci have been detected.

You have DNA changes at both of the two strongest spots in the LPA gene that drive high Lp(a) levels.

Two independent strong predictors of elevated lipoprotein(a) are both present. Together they predict markedly elevated Lp(a) and a substantially increased lifetime risk of coronary artery disease and aortic valve calcification. A clinical Lp(a) blood test is strongly advised — the actual circulating value matters.

Together these strongly predict very high levels of a heart-disease- linked blood particle called Lp(a). That means a meaningfully raised lifetime risk of heart artery disease and stiffening of the aortic valve. It's worth asking your GP for an actual Lp(a) blood test — the real number in your blood matters most.

APOE ε4/ε4 combined with the 9p21 coronary artery disease risk allele.

You have two copies of the higher-risk APOE ε4 version plus a DNA change in a region called 9p21 that's linked to heart artery disease.

Two independent cardiovascular risk signals stacked. APOE ε4 homozygosity raises both Alzheimer's and cardiovascular risk; the 9p21 locus adds an independent CAD risk increment. Together these support paying particular attention to blood pressure, lipid management, and lifestyle.

You have two separate genetic nudges towards heart artery disease, working through different biology. Together they make blood pressure control, cholesterol management, and lifestyle choices unusually worthwhile for you.

Both the PNPLA3 I148M fatty-liver variant and the ALDH2 deficient variant detected.

You have DNA changes in both PNPLA3 (a fatty-liver gene) and ALDH2 (the "Asian flush" gene).

In East Asian populations, carrying both PNPLA3 I148M and ALDH2 deficient alleles is associated with a substantially higher risk of alcohol-related liver disease in regular and heavy drinkers than carrying either variant alone — the PNPLA3 variant amplifies liver-fat accumulation while the ALDH2 variant means acetaldehyde builds up in the liver after drinking. Crucially, this risk is conditional on continued alcohol intake. For people who don't drink, this combination carries little additional clinical meaning beyond the PNPLA3 NAFLD signal.

For East Asian people who drink regularly or heavily, having both of these DNA changes is linked to a substantially higher risk of alcohol-related liver damage than having just one of them. The PNPLA3 change makes liver cells store fat more easily; the ALDH2 change means toxic by-products of alcohol pile up in the liver after a drink. The two together cost the liver much more per drink. The crucial point: this risk depends on actually drinking. For people in this group who don't drink, the combination is mostly just the PNPLA3 fatty-liver signal — no extra penalty.

Both Factor V Leiden and Prothrombin G20210A variants detected.

You have DNA changes in both of the two most common inherited clotting variants.

Carrying both variants substantially raises the lifetime risk of venous thromboembolism compared with carrying either alone. Risk modifies clinical decisions around surgery, pregnancy, and contraception.

Having both variants substantially raises your lifetime risk of a dangerous blood clot — much more than having either one alone. It's worth flagging to clinicians around surgery, pregnancy, and birth control choices.

One copy of HFE C282Y and one copy of HFE H63D detected (compound heterozygous).

You have one copy of each of the two main HFE iron-overload DNA changes — one C282Y and one H63D.

The C282Y/H63D compound heterozygous state carries a small but real risk of iron overload, particularly in combination with metabolic factors (fatty liver, alcohol use). Most compound heterozygotes never develop clinically significant iron overload, but a periodic iron-studies blood panel is reasonable.

Having one of each carries a small but real risk that your body will store too much iron over time, especially if you also have fatty liver or drink heavily. Most people with this combination never develop a real iron problem, but it's worth checking your iron levels with a blood test from time to time.

A CYP2C9 reduced-function allele combined with the VKORC1 high-sensitivity allele.

You have a slow version of one gene that clears the blood thinner warfarin, plus a version of another that makes warfarin extra-effective.

The two strongest pharmacogenetic predictors of warfarin dose are stacked here. If warfarin is ever prescribed, lower starting doses are essential to avoid over-anticoagulation. CPIC guidelines provide specific dose algorithms; please mention both findings to any prescribing clinician.

Together, these two DNA changes mean you would react strongly to even small doses of the blood thinner warfarin. If you're ever prescribed it, the starting dose needs to be lower than usual to avoid bleeding. Please mention both of these to any doctor planning to prescribe warfarin.