compound matches

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 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.

One copy each of MTHFR C677T and A1298C detected (compound heterozygous).

You have one copy each of the two most-talked-about MTHFR DNA changes — one C677T and one A1298C.

Despite a great deal of online attention, mainstream medical genetics organisations do not recommend acting on this finding. The compound state reduces enzyme activity somewhat below either single variant, but most people with adequate folate intake have no clinical impact.

Despite a lot of online attention, the main medical genetics organisations don't recommend changing anything based on this finding. The combination slightly lowers an enzyme's activity, but for most people with a normal folate intake there's no real-world effect.

Both the ALDH2 deficient variant and the ADH1B fast variant detected.

You have DNA changes in both of the genes that handle alcohol, hitting the classic "Asian flush" combination.

A combination strongly associated with the "Asian flush" reaction to alcohol. ADH1B fast metabolism produces acetaldehyde quickly; ALDH2 deficiency means it can't be cleared fast enough. The result is flushing, nausea, and a substantially increased risk of upper aerodigestive cancers with continued alcohol exposure.

This combination causes the well-known "Asian flush" reaction. Your body turns alcohol into a toxic by-product faster than usual, then struggles to clear it away — leaving you flushed and queasy. If you drink heavily over time, the build-up substantially raises the risk of cancers of the throat, mouth, and oesophagus.

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.

An APOL1 high-risk genotype — two risk alleles in some combination.

You have two copies of a higher-risk APOL1 version (in some combination of the G1 and G2 forms).

Two APOL1 risk alleles substantially increase the lifetime risk of focal segmental glomerulosclerosis, hypertension-attributed chronic kidney disease, and HIV-associated nephropathy. Most carriers still do not develop kidney disease, but blood pressure control and regular kidney function checks are particularly important.

Having two copies substantially raises your lifetime risk of several kinds of kidney disease. Most people with this combination still don't develop kidney problems, but controlling blood pressure and having your kidney function checked regularly are particularly worthwhile.