Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Cut Back Or Stop Alcohol: Alcohol is one of the few clearly established and partly reversible causes of heart muscle disease. Chronic heavy intake causes myocyte loss, interstitial fibrosis and ventricular dilation, and the conventional diagnostic threshold for alcoholic cardiomyopathy is over 80 g a day for at least five years, although reviewers call that cut-off arbitrary and describe structural change at lower intakes. In European series applying that threshold, alcohol accounted for roughly 23% to 47% of cases previously labelled idiopathic dilated cardiomyopathy. The same review reports that people who stopped drinking had better ejection fraction trajectories and better transplant-free survival at seven years, 45% versus 27% for those who kept drinking. World Journal of Cardiology (PMC)
Manage Body Weight: Excess weight raises the workload on an already abnormal heart muscle, and it appears to shape the course of hypertrophic cardiomyopathy rather than simply accompany it. In the Sarcomeric Human Cardiomyopathy Registry of 3,282 patients followed for a median of 6.8 years, obesity was associated with a higher risk of the overall composite outcome (hazard ratio 1.63) and of the heart failure composite (hazard ratio 1.89), and with more obstructive physiology, 32.4% versus 20.9% in normal-weight patients. Obesity was also linked to more atrial fibrillation, but not to life-threatening ventricular arrhythmias. These are observational associations, so they do not prove that losing weight changes the course of the disease. JAMA Cardiology (PMC)
Stay Physically Active: Vigorous exercise was long discouraged in hypertrophic cardiomyopathy on the assumption that it triggered fatal arrhythmias. LIVE-HCM, a prospective observational study of 1,660 people aged 8 to 60, most with diagnosed hypertrophic cardiomyopathy and about 8% carrying a sarcomeric variant without the phenotype, followed for a median 38 months, found the composite rate of death, cardiac arrest, arrhythmic syncope or appropriate defibrillator shock was 4.7% among vigorous exercisers and 4.6% among those exercising moderately or not at all. The authors stress the design was observational, that most participants were cared for at high-volume centers and the findings may not extrapolate beyond them, and that exercise intensity for anyone with a diagnosed cardiomyopathy belongs in an individualised conversation with a cardiologist rather than a blanket rule. General national activity guidance for adults is about 150 minutes of moderate activity a week. JAMA Cardiology (PMC)
Avoid Anabolic Steroid Use: Anabolic-androgenic steroids are a documented cause of acquired heart muscle disease, acting through androgen receptor overactivation, oxidative stress and adverse remodelling. In the HAARLEM study, 31 amateur strength athletes had echocardiograms before a steroid cycle, in its final week and again about eight months after stopping: across a median 16 weeks, left ventricular mass rose by 28.3 g, three-dimensional ejection fraction fell by 4.9 percentage points and diastolic filling worsened. Higher average weekly doses were correlated with the increases in left ventricular mass and wall thickness, though not with the ejection fraction or diastolic changes. All measured parameters had returned to baseline by the eight-month follow-up, so at least the short-term changes appear reversible on discontinuation. Frontiers in Reproductive Health (PMC)
Know What Lifestyle Cannot Prevent: Much of cardiomyopathy is driven by inherited changes in the genes that build heart muscle, and no diet, supplement or training program has been shown to stop those forms from developing. Inherited risk is also less deterministic than it is often presented: a cross-sectional analysis of unselected adults estimated that by late adulthood roughly 22.5% of people carrying a pathogenic hypertrophic cardiomyopathy variant and about 35.0% of those carrying a pathogenic dilated cardiomyopathy variant had developed the condition, far below the figures reported from families identified through an affected relative. The honest role of behavior here is to avoid stacking acquired injury on top, not to remove the underlying risk. A family history of heart failure, an implanted defibrillator or sudden death at a young age, and symptoms such as fainting during exertion or breathlessness on mild effort, are worth raising with a clinician. American Journal of Human Genetics (PMC)
How much of this is genetic?
Genetics explains 30% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Estimate for the common-variant (polygenic) component, consistent with SNP-based heritability of roughly 30 percent reported for dilated and hypertrophic cardiomyopathy; note that familial cardiomyopathies are frequently caused by rare high-penetrance single-gene mutations that are not captured by this score.
Background and further reading
Cardiomyopathy refers to a group of diseases in which the heart muscle (myocardium) becomes structurally or functionally abnormal, making it harder for the heart to pump blood efficiently. The major subtypes are hypertrophic cardiomyopathy (HCM), in which the muscle thickens; dilated cardiomyopathy (DCM), in which the chambers enlarge and weaken; and arrhythmogenic cardiomyopathy (ACM/ARVC), in which muscle is replaced by fibrous and fatty tissue. Many people have no symptoms, while others experience breathlessness, palpitations, fatigue, chest discomfort, or fainting. Cardiomyopathies are an important cause of heart failure and are among the leading identifiable causes of sudden cardiac death in young people and athletes.
Genetic Basis: Cardiomyopathy has a strong hereditary component, and its genetic architecture spans a spectrum. In familial disease, single high-impact (monogenic) variants can be the primary cause: HCM is most often driven by sarcomere genes such as MYBPC3 and MYH7, DCM by truncating variants in titin (TTN) and by LMNA, and arrhythmogenic forms by desmosomal genes such as PKP2 and DSP. Beyond these rare high-penetrance mutations, common variants of small individual effect across the genome also shape susceptibility and how strongly the disease is expressed. Genome-wide association studies have highlighted loci including BAG3, HSPB7, FLNC, and TTN. This score reflects that common-variant polygenic background rather than the rare monogenic mutations, so it is not a test for inherited familial cardiomyopathy.
Non-Genetic Factors: Not all cardiomyopathy is inherited. Acquired causes and contributing factors include long-standing high blood pressure, coronary artery disease, viral infection of the heart muscle (myocarditis), heavy alcohol use, certain chemotherapy drugs, thyroid disease, iron overload, and the physiological changes of late pregnancy (peripartum cardiomyopathy). The same environmental factors that support general cardiovascular health, such as controlling blood pressure, avoiding excessive alcohol, staying physically active, and managing diabetes, also help protect the heart muscle. Because familial cardiomyopathy can run in families, a personal or family history of unexplained heart failure, fainting, or sudden death at a young age is more informative than a common-variant polygenic score.
The published research behind your score, and the variants it draws on.
11 published scores from 4 studies
The cardiomyopathy score combines 11 polygenic scores drawn from 4 published studies.
These traits are influenced by some of the same genes and variants as this one
Heart Failure: A syndrome in which the heart cannot pump enough blood to meet the body's needs.
Content updated August 2026.
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