Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Know Your LDL Number: LDL cholesterol causes no symptoms, so the only way to know where you stand is a lipid panel, an ordinary blood test usually included in general health checks. A number you actually know is what makes dietary and activity changes measurable. American Heart Association
Optimize Dietary Fats: Replace saturated fats (red meat, full-fat dairy, tropical oils) with monounsaturated (olive oil, avocado, nuts) and polyunsaturated (fish, flaxseed) fats, and avoid trans fats. Adding soluble fiber (oats, beans, psyllium) and plant stanols/sterols further reduces LDL. The NHLBI Therapeutic Lifestyle Changes (TLC) diet sets out this approach in detail. NHLBI, NIH
Exercise Regularly: The direct LDL-lowering effect of aerobic exercise is modest - pooled studies show LDL drops of roughly 3-7% - but exercise also raises HDL, lowers triglycerides, and provides independent cardiovascular protection. Combining regular activity with dietary change works better than either alone. PMC (Sports Medicine review)
Know That Very High LDL Can Be Monogenic: Familial hypercholesterolemia is a single-gene condition affecting about 1 in 250 people, and it is widely underdiagnosed. Very high LDL, or a family history of heart disease at a young age, is the pattern that raises the question. A polygenic score cannot diagnose it: FH is confirmed by clinical criteria and gene testing, so it is a conversation to have with a clinician. MedlinePlus Genetics (NIH)
How much of this is genetic?
Genetics explains 50% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Zhang et al. 2018, Front Endocrinol
Background and further reading
LDL cholesterol is the main carrier of cholesterol in the bloodstream and a causal driver of atherosclerosis - the buildup of fatty plaques in artery walls. Unlike many risk factors where causality is debated, the case that LDL causes atherosclerotic cardiovascular disease is unusually strong: it rests on consistent evidence from prospective cohorts, Mendelian randomization (which uses genetic variants to test lifelong exposure), and randomized trials, together spanning more than two million participants [1].
Genetic Basis: Twin and family studies estimate the heritability of LDL cholesterol at roughly 40-60%, and some report higher figures. The strongest signals involve LDLR (the LDL receptor), PCSK9 (which controls how quickly LDL receptors are degraded), APOB (apolipoprotein B, the structural protein of the LDL particle), and HMGCR (HMG-CoA reductase, the enzyme statins inhibit). The largest multi-ancestry genome-wide study of blood lipids, in about 1.65 million people, mapped 923 loci associated with lipid levels, underscoring how polygenic LDL is [3]. People who inherit loss-of-function variants in PCSK9 have lifelong low LDL and substantially reduced coronary heart disease, which helped establish the drug target and supports the 'lower is better' principle [4]. This common-variant, polygenic architecture is distinct from familial hypercholesterolemia (FH) - a monogenic condition, usually from a single pathogenic variant in LDLR, APOB, or PCSK9 - which affects roughly 1 in 250 people and causes severely elevated LDL from birth. A polygenic score does not diagnose FH, which is identified through clinical criteria and gene-specific testing.
Modifiable Factors: Saturated fat and dietary cholesterol are the main dietary drivers of LDL, though individual response varies, reflecting genetic differences in cholesterol absorption and synthesis. Replacing saturated fat with unsaturated fat, adding soluble fiber (oats, legumes, psyllium), reaching and keeping a healthy weight, and exercising regularly all help lower LDL [5]. For many people these changes are not enough on their own, and statins are the first-line drugs - they lower LDL and reduce cardiovascular events in proportion to how much they lower it [2]. Because lowering LDL reduces atherosclerotic risk, treatment decisions weigh a person's LDL against their overall cardiovascular risk rather than the number alone.
The published research behind your score, and the variants it draws on.
65 published scores from 14 studies
The LDL cholesterol score combines 65 polygenic scores drawn from 14 published studies.
These traits are influenced by some of the same genes and variants as this one
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com