Cholesterol and heart disease — the big questions answered

In the UK, a healthy total cholesterol is generally below 5 mmol/L, with non-HDL cholesterol below 4 mmol/L and LDL ("bad") cholesterol below 3 mmol/L. These are population targets — your personal target depends on overall cardiovascular risk.

For patients who have already had a heart attack, stroke or stent, the targets are much tighter: LDL below 1.8 mmol/L (and ideally below 1.4 mmol/L under European guidelines), with the principle that "lower is better" within safe limits. There is no recognised lower threshold below which LDL becomes harmful.

Whether you need a statin depends on your 10-year cardiovascular risk, calculated using the QRISK3 calculator from age, sex, blood pressure, smoking status, family history, cholesterol levels and other factors. NICE recommends offering a statin to anyone with a 10-year risk of 10% or more, and to all patients with existing cardiovascular disease, diabetes, chronic kidney disease or familial hypercholesterolaemia.

Statins are among the most extensively studied drugs in medicine. In high-risk patients they reduce the risk of heart attack and stroke by around 25% per mmol/L drop in LDL. If you are genuinely uncertain about starting, a coronary calcium score can refine the decision — a score of zero argues against starting, a score over 100 argues firmly for it.

The most commonly reported statin side effect is muscle aches, but high-quality blinded trials show the rate of muscle symptoms on statins is barely different from placebo — the "nocebo effect" (expecting side effects produces them) is powerful here. Fewer than 1% of people have genuine statin myopathy.

Other side effects include a small increase in the risk of developing type 2 diabetes (around 1 extra case per 200 person-years on treatment) and rare cases of liver enzyme elevation. Serious side effects are uncommon, and the benefit for high-risk patients vastly outweighs the risks. Most "side effects" attributed to statins resolve on switching to a different statin or reducing the dose.

Yes — lifestyle changes can lower LDL by 10–20% in many people. The strongest dietary lever is replacing saturated fat (butter, fatty meat, full-fat dairy, coconut oil) with unsaturated fat (olive oil, nuts, seeds, avocado, oily fish), plus eating more soluble fibre from oats, pulses, fruit and vegetables.

Weight loss, regular exercise, plant sterol-enriched foods and reducing alcohol all help further. Whether lifestyle alone is enough depends on your starting numbers and overall risk. For patients with markedly raised LDL or established heart disease, lifestyle should complement — not replace — medication.

LDL (low-density lipoprotein) carries cholesterol to the artery wall and is the main driver of atherosclerosis — the "bad" cholesterol. HDL (high-density lipoprotein) transports cholesterol away from the artery wall and is associated with lower risk, though raising HDL with drugs has not been shown to reduce events.

Lp(a) (lipoprotein little a) is a genetic form of cholesterol entirely independent of diet and lifestyle. Around 1 in 5 people has elevated Lp(a), and it is a strong independent risk factor for early heart attacks, strokes and aortic valve disease. Total cholesterol is the sum of these fractions, but LDL and Lp(a) are the most actionable numbers for predicting future events.

Yes — current European guidelines recommend measuring Lp(a) at least once in every adult's lifetime, because the result has lifelong implications and you only need to know once. UK NICE guidance is more selective, recommending it where there is premature cardiovascular disease, familial hypercholesterolaemia, recurrent events despite treatment, or a strong family history.

A high Lp(a) — above approximately 75 nmol/L or 30 mg/dL — doesn't currently have a specific licensed treatment, but it changes how aggressively other risk factors should be managed. New Lp(a)-lowering drugs are in late-stage clinical trials and may become available within the next few years.

A genuinely good diet can lower LDL by 10–20% — meaningful but not unlimited. The Mediterranean and DASH diets have the strongest evidence base, with reductions in cardiovascular events of around 30% in trials. The single largest dietary lever is swapping saturated fat for unsaturated fat, not cutting fat overall.

Soluble fibre (oats, beans, lentils, apples), nuts (around 30 g a day) and plant sterols all contribute additional reductions. Ultra-processed foods, sugary drinks and excess alcohol push cholesterol in the wrong direction. Diet matters — but expecting it alone to fix markedly elevated LDL or established coronary disease is unrealistic.

UK practice uses the QRISK3 calculator to estimate your 10-year risk of a heart attack or stroke, taking into account age, sex, ethnicity, postcode-based deprivation, smoking, diabetes, family history, blood pressure (and its variability), cholesterol levels, BMI, and several specific conditions including chronic kidney disease, atrial fibrillation, rheumatoid arthritis, severe mental illness and erectile dysfunction.

A risk above 10% is the threshold for considering a statin under NICE guidance. For patients in the "decision-uncertain" zone — typically 7.5–15% — a coronary calcium score can refine the estimate substantially in either direction, and is often the most useful single investigation.

QRISK3 is the best general-population risk calculator in the UK, but no calculator is perfect for individuals. It works well in average-risk middle-aged adults of British background, and less well in young adults, the very elderly, certain ethnic groups, and people with strong family histories not fully captured in the tool.

In practice, QRISK is best treated as a starting point. For patients in the decision-uncertain zone, additional information — calcium score, Lp(a), detailed family history, lifetime risk projection — refines the picture. The point of risk assessment is to make better treatment decisions, not to chase a number.

Yes — regular aerobic exercise typically raises HDL by 5–10% and modestly lowers triglycerides. The effect on LDL is smaller (around 5%) unless combined with weight loss, in which case LDL can fall more substantially.

But the cardiovascular benefit of exercise far exceeds its cholesterol effect. Regular physical activity reduces the risk of heart attack and stroke by around 25–35% — comparable to a statin in many patients — through improved endothelial function, blood pressure, insulin sensitivity, weight, mood and inflammation. Aim for 150 minutes a week of moderate-intensity activity plus two sessions of resistance work.

The evidence on eggs has shifted substantially. Up to one egg a day is not associated with increased cardiovascular risk in most healthy adults, despite the dietary cholesterol content, because saturated fat — not dietary cholesterol — is the main driver of blood LDL.

The exception is people with familial hypercholesterolaemia, established coronary disease or diabetes, in whom limiting dietary cholesterol may add a small additional benefit. For most people, an egg-rich breakfast is a far better choice than a sugary or ultra-processed alternative.

For most people without known cardiovascular disease, daily aspirin is no longer recommended. The bleeding risk — gastrointestinal and intracranial — outweighs the small reduction in cardiovascular events for primary prevention. This represents a clear shift in guidance over the last decade.

The picture is different for secondary prevention — anyone who has had a heart attack, stroke or stent benefits clearly from aspirin (or another antiplatelet), and the treatment balance firmly favours continuing it. If you are currently on aspirin without a clear secondary prevention indication, discuss with your doctor whether to continue.