High cholesterol in the young: prevention, diagnosis and when to see a doctor

Young people rarely have a lipid panel done, and those who do often do not know how to interpret the result. Meanwhile, early detection of raised LDL gives decades for prevention. The editorial team explains when and which tests are worth taking, what can be changed through diet and training, and in which situations a doctor is indispensable.
When and for whom to check cholesterol
The ESC/EAS guidelines recommend assessing the lipid profile in adults as part of cardiovascular risk screening, and in the presence of a family history of early cardiovascular events or a suspicion of familial hypercholesterolaemia — as early as possible, including in childhood. Many experts consider it advisable for everyone to have at least one test in young adulthood.
It is especially important to check lipids if parents or siblings were diagnosed with high cholesterol, if a first-degree relative had a heart attack or stroke at a young age (in men before 55, in women before 60), or if there are xanthomas on the tendons.
For athletes, additional reasons are the use of hormonal drugs (especially anabolic steroids), prolonged extreme diets, isotretinoin for the treatment of acne, and signs of hypothyroidism. In these situations lipid monitoring should be regular.
The EAS consensus advises determining lipoprotein(a) at least once in life in every adult. Since its level is genetic and stable, one measurement is usually enough to understand whether a person belongs to a higher-risk group.
- Family history of early heart attacks, strokes or high cholesterol.
- Xanthomas, corneal arcus at a young age.
- Use of anabolic steroids or other hormones.
- Intake of isotretinoin, glucocorticoids.
- Obesity, raised blood pressure, disorders of carbohydrate metabolism.
Which indicators are part of a lipid panel
A standard lipid panel includes total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides. LDL is often calculated by a formula rather than measured directly; with very high triglycerides the calculation becomes inaccurate, and then other indicators are more useful.
Non-HDL cholesterol (total cholesterol minus HDL) reflects all atherogenic particles and does not require fasting. Apolipoprotein B (apoB) shows the number of atherogenic particles and in some situations, for example with raised triglycerides or obesity, reflects risk more accurately.
It is not obligatory to take the test on an empty stomach: modern guidelines allow a non-fasting lipid panel for most cases. However, with high triglycerides the test is better repeated fasting. Also, the test should not be taken against the background of an acute infection or right after extreme exertion.
For people who use hormonal drugs, the result reflects the state “on the drugs”. To assess one’s own profile, the test must be repeated some time after stopping, which a doctor should determine.
| Indicator | What it reflects | Comment |
|---|---|---|
| LDL-C | The main atherogenic fraction | The main target of treatment |
| HDL-C | “Reverse transport” of cholesterol | Drops sharply on AAS |
| Triglycerides | TG-rich lipoproteins | Depend on food, alcohol |
| Non-HDL-C | All atherogenic particles | Does not require fasting |
| apoB | Number of atherogenic particles | Refines risk |
| Lp(a) | Genetic risk factor | Enough to measure once |

Diagnosis of familial hypercholesterolaemia
If LDL is very high, the doctor assesses the likelihood of familial hypercholesterolaemia. For this, the Dutch Lipid Clinic Network criteria are common in Europe; they take into account the LDL level, family history, personal history of early cardiovascular events and physical signs. The point total determines whether the diagnosis is “possible”, “probable” or “definite”.
Genetic testing confirms the diagnosis and, importantly, makes it possible to carry out cascade screening of relatives. If a mutation is found in a person, their parents, siblings and children can undergo targeted examination. This approach is considered one of the most effective ways of detecting FH.
The doctor also rules out secondary causes: determines TSH (hypothyroidism), indicators of liver and kidney function, glucose, and if necessary protein in the urine. Secondary dyslipidaemia may be combined with a hereditary one.
In athletes it is important to separate the effects of pharmacology and heredity. If a person uses anabolic steroids, low HDL and high LDL may be a consequence of the drugs; to diagnose FH, tests outside their influence and a careful family history are needed.
Prevention: nutrition, training, pharmacological hygiene
Dietary measures with a proven effect on LDL are reducing saturated fats and replacing them with unsaturated ones (oils, nuts, fish), limiting trans fats, and adequate dietary fibre, especially soluble fibre (oats, legumes). Plant sterols in fortified products are also useful, although their effect is moderate.
For strength athletes it is often enough to review protein sources: replace some of the fatty meat with fish, poultry, legumes and low-fat dairy. Whey-based protein supplements do not significantly affect lipids and can help reduce the share of fatty foods.
Regular aerobic training raises HDL and improves particle composition; combining aerobic and strength work gives the best overall effect on metabolic health. Quitting smoking and limiting alcohol are important components of prevention.
Pharmacological hygiene means giving up anabolic steroids and other hormones without medical indication. No supplements “protect lipids” against the background of steroids enough to neutralise the risks. People with familial hypercholesterolaemia who also use AAS combine two powerful risk factors.
When to see a doctor and how it is treated
You should see a doctor (a therapist, cardiologist or lipidologist) if LDL significantly exceeds reference values, if Lp(a) is high, if there were early heart attacks in the family, or if changes persist despite dietary correction. A very high LDL at a young age is a direct reason for a consultation.
Emergency attention is required for symptoms that may indicate ischaemia: pain or pressure in the chest during exertion, shortness of breath disproportionate to the effort, fainting. In young people with FH a heart attack may occur much earlier than in the general population.
The basis of drug treatment is statins; if necessary, ezetimibe is added, and in severe cases — PCSK9 inhibitors. These drugs are prescribed by a doctor taking risk into account, and for people with FH treatment is usually started early. Statins are not on WADA’s Prohibited List.
Athletes sometimes fear the muscular side effects of statins. True statin myopathy occurs less often than is said, and most complaints can be resolved by changing the drug or dose under a doctor’s supervision. Stopping treatment on your own with FH is dangerous.
Editorial conclusions
Early determination of the lipid profile and Lp(a) is a simple step that makes it possible to detect hereditary disorders long before the first complications.
A modern lipid panel does not necessarily require fasting, and apoB and non-HDL cholesterol help to refine risk. Results against the background of hormonal drugs must be interpreted taking this effect into account.
A diet with less saturated fat, regular training and giving up AAS are the basis of prevention, but with familial hypercholesterolaemia drug treatment is usually unavoidable.
We also recommend reading our materials on the causes of high cholesterol in young athletes, on the effect of anabolic steroids on the heart and on interpreting a biochemical blood test.
References
- Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111–188.
- Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol. Circulation. 2019;139(25):e1082–e1143.
- Nordestgaard BG, Chapman MJ, Humphries SE, et al. Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease. Eur Heart J. 2013;34(45):3478–3490.
- Wiegman A, Gidding SS, Watts GF, et al. Familial hypercholesterolaemia in children and adolescents: gaining decades of life by optimizing detection and treatment. Eur Heart J. 2015;36(36):2425–2437.
- Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43(39):3925–3946.
- Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
Andriy Melnyk
A strength-sports coach and author of programs for beginner and intermediate levels. Writes about training planning.


