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Health condition · Clinically reviewed

High cholesterol, lifestyle, statins - and the modern ladder that now reaches every target.

Cholesterol is quiet but consequential. A stepped medical approach - built on lifestyle and a well-chosen statin, with modern add-ons where needed - prevents heart attacks and strokes.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE NG181, ESC/EAS and JBS3 sources you can see at the end.

  • 03

    Current for 2026

    Reflects the modern UK ladder including bempedoic acid, PCSK9 inhibitors, inclisiran and icosapent ethyl.

Key facts

High cholesterol at a glance.

The essentials, in plain English - what it is, why it matters and how the modern UK ladder now looks.

  • What it is

    Hypercholesterolaemia and dyslipidaemia - raised LDL-C, non-HDL-C or triglycerides, or a low HDL-C, driving atherosclerotic cardiovascular disease.

  • Why it matters

    LDL-C is a causal driver of heart attacks and strokes. Lowering it lowers events - the effect is durable and dose-dependent.

  • Familial FH

    Familial hypercholesterolaemia is autosomal dominant, affects up to 1 in 250 people in the UK and remains widely underdiagnosed.

  • Assessment

    A lipid profile plus QRISK3 for primary prevention. Specialist genetic testing where FH is suspected.

  • Foundation therapy

    Lifestyle plus atorvastatin - 20 mg for primary prevention, 80 mg for secondary prevention where tolerated.

  • Modern add-ons

    Ezetimibe, bempedoic acid, PCSK9 inhibitors and inclisiran now let almost everyone reach LDL-C targets - even statin-intolerant patients.

Why this guide matters

A stepped plan, built on evidence.

Cardiovascular disease is preventable. Three points shape everything else on this page - and shape how UK lipid clinics now practise.

  • LDL-C is causal

    Lowering LDL-C lowers cardiovascular events. The relationship is dose-dependent and durable across decades of trial evidence.

  • Statins are the foundation

    Atorvastatin remains the most cost-effective, best-evidenced first step. Modern UK practice uses 20 mg for primary prevention and 80 mg for secondary prevention where tolerated.

  • Modern add-ons close the gap

    Ezetimibe, bempedoic acid, PCSK9 inhibitors, inclisiran and icosapent ethyl now reach almost every target, even in statin-intolerant patients.

How the diagnosis is made

From a blood test to a clear plan.

The steps a UK GP, cardiologist or lipid specialist will normally follow, in order - so you know what to expect and why.

  1. 01

    Assessing

    History and family history

    A structured look at cardiovascular history, family events under 60 and features suggestive of FH such as tendon xanthomata or a very high LDL-C.

  2. 02

    Assessing

    Full lipid profile

    Total cholesterol, LDL-C, HDL-C, triglycerides, non-HDL-C and, where available, apolipoprotein B. Fasting or non-fasting is acceptable in current UK practice.

  3. 03

    Assessing

    Rule out secondary causes

    Thyroid function, HbA1c, renal function, liver function and urinary protein - to catch hypothyroidism, diabetes, nephrotic syndrome, cholestasis and chronic kidney disease.

  4. 04

    Confirming

    QRISK3 for primary prevention

    A ten-year cardiovascular risk score guides whether a statin is offered. Anyone with a QRISK3 of 10% or more is normally treated.

  5. 05

    Confirming

    FH assessment

    Simon Broome or Dutch Lipid Clinic criteria identify probable FH. Confirmed cases are referred for specialist commissioned genetic testing for LDLR, APOB and PCSK9 mutations.

  6. 06

    Preparing

    Cardiovascular workup where needed

    For high-risk patients or established disease - coronary CT angiography, echocardiogram or specialist review to define the ceiling of LDL-C target.

  7. 07

    Preparing

    Cascade screening

    Where FH is confirmed, first-degree relatives are offered specialist commissioned cascade testing. Early detection prevents premature cardiovascular events.

Typical timeline: a first blood test to a settled treatment plan in weeks, not months.

Symptoms

What high cholesterol actually looks like.

Usually nothing - which is why it is picked up on blood tests. The visible signs, when they occur, matter.

  • Usually silent

    High cholesterol itself causes no symptoms - it is picked up on blood tests or after a cardiovascular event.

  • Tendon xanthomata

    Firm, painless nodules on the Achilles or extensor tendons of the hands - highly suggestive of familial hypercholesterolaemia.

  • Xanthelasma

    Yellowish plaques on the eyelids - a soft sign that can occur with or without raised cholesterol, worth a lipid profile.

  • Corneal arcus under 45

    A pale ring around the cornea in a younger adult - another feature that raises the suspicion of FH.

  • Premature vascular disease

    Angina, heart attack, stroke or peripheral arterial disease in the patient or a close relative under 60.

  • Very high triglycerides

    Marked hypertriglyceridaemia can cause eruptive xanthomata, abdominal pain and, at extreme levels, pancreatitis.

  • Metabolic clustering

    Central obesity, raised blood pressure, low HDL-C and glucose intolerance often travel together and share the same lifestyle levers.

  • Red flag - young cardiovascular event

    A heart attack or stroke under 55 in men or under 60 in women should prompt an FH assessment and genetic referral.

Treatment

How high cholesterol is treated in the UK.

Lifestyle first, atorvastatin next, then a modern ladder of ezetimibe, bempedoic acid, PCSK9 inhibitors, inclisiran and, for triglycerides, icosapent ethyl.

  • Lifestyle foundation

    A Mediterranean or plant-forward pattern, less saturated and trans fat, more fibre, regular exercise, healthy weight, no smoking and moderate alcohol. Small, steady changes compound over years.

  • Atorvastatin

    20 mg for primary prevention, 80 mg for secondary prevention where tolerated. The best-evidenced LDL-C lowering drug in UK practice and the cornerstone of NICE NG181.

  • Ezetimibe

    Added when LDL-C targets are not met on a statin, or used alone in statin intolerance. Reduces LDL-C by a further 15 to 20 percent.

  • Bempedoic acid

    An oral ATP-citrate lyase inhibitor - useful when statins are not tolerated or LDL-C remains high on a statin plus ezetimibe. NICE approved since 2021 - see the bempedoic acid clinic.

  • PCSK9 inhibitors

    Alirocumab and evolocumab - subcutaneous every two to four weeks. Specialist commissioned for familial hypercholesterolaemia and high-risk patients on maximal oral therapy - see the PCSK9 inhibitor clinic.

  • Inclisiran

    A twice-yearly siRNA that silences PCSK9 - practice-changing for adherence. NICE approved since 2021 and specialist commissioned - see the inclisiran clinic.

  • Icosapent ethyl (Vazkepa)

    Purified EPA for residual cardiovascular risk with raised triglycerides on a statin. NICE approved in 2022 - see the icosapent ethyl clinic.

  • Advanced FH therapies

    Lomitapide, apoB antisense, evinacumab (an ANGPTL3 inhibitor) and LDL apheresis - specialist commissioned options for homozygous or severe familial hypercholesterolaemia.

Specialist commissioned

Advanced pathways for severe and familial disease.

Homozygous familial hypercholesterolaemia and severe refractory disease may need lomitapide, apoB antisense therapy, evinacumab (Evkeeza, an ANGPTL3 inhibitor) or LDL apheresis. These are specialist commissioned services delivered through designated UK lipid centres and paired with genetic counselling and cascade screening.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and specialist society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP, cardiologist or lipid specialist knows your history and can tell you which parts apply to you. If in doubt, get seen.

  • NICE. Cardiovascular disease: risk assessment and reduction, including lipid modification (NG181).

  • NICE. Familial hypercholesterolaemia: identification and management (CG71).

  • ESC/EAS. Guidelines for the management of dyslipidaemias.

  • Joint British Societies. JBS3 consensus recommendations on the prevention of cardiovascular disease.

  • MHRA. Advice on statin safety and monitoring.

Red flags

When high cholesterol needs urgent attention.

Most dyslipidaemia is managed in primary care. These are the situations that need specialist input - and, sometimes, urgently.

  • Cardiovascular event under 55 or 60

    A heart attack, stroke or acute coronary syndrome in a younger adult should trigger an FH assessment and specialist lipid referral.

  • Tendon xanthomata

    These are near-specific for familial hypercholesterolaemia and warrant genetic testing and cascade screening of first-degree relatives.

  • LDL-C above 4.9 mmol/L in adults

    A very high untreated LDL-C, especially with a family history, should prompt formal FH criteria assessment and specialist referral.

  • Triglycerides above 10 mmol/L

    Severe hypertriglyceridaemia carries a risk of acute pancreatitis and needs urgent specialist input alongside dietary and pharmacological control.

  • Statin intolerance claims

    Never simply stop lifelong therapy. Confirm true intolerance with a structured re-challenge, then move to ezetimibe, bempedoic acid or PCSK9 pathways.

  • Rhabdomyolysis symptoms

    Severe muscle pain, weakness or dark urine on a statin needs same-day assessment with creatine kinase and renal function.

  • Pregnancy planning

    Statins are avoided in pregnancy - a specialist plan for pause and restart, and for lipid control during and after pregnancy, is essential in FH.

  • Homozygous FH features

    Very high LDL-C from childhood, extensive xanthomata and early vascular disease need specialist commissioned advanced therapies without delay.

  • Secondary cause missed

    Untreated hypothyroidism, nephrotic syndrome or cholestasis can look like primary dyslipidaemia - treat the cause first.

Living with it

A treatable condition, with a clear ladder.

Four things that make the biggest difference year on year - a Mediterranean pattern, regular movement, honest adherence to therapy and, where relevant, family screening.

A quiet reminder

Consistency beats intensity, every time.

Small, steady habits kept up for decades do more than a heroic month that does not last.

  1. 01 Diet

    Eat like the Mediterranean

    Olive oil, oily fish, nuts, legumes, vegetables and whole grains - a pattern with the strongest evidence for cardiovascular protection.

  2. 02 Move

    Aim for 150 minutes a week

    Brisk walking, cycling or swimming - moderate activity lifts HDL-C, lowers triglycerides and helps weight, sleep and mood.

  3. 03 Adhere

    Take the statin every day

    Effects are cumulative. Missed doses add up - a simple reminder and a fixed daily slot make the biggest difference.

  4. 04 Family

    Screen your relatives

    If FH is confirmed, first-degree relatives deserve testing. Early treatment in childhood can prevent premature heart disease entirely.

Frequently asked

Everything we get asked about high cholesterol.

Quick answers on statins, familial hypercholesterolaemia, PCSK9 inhibitors, inclisiran and triglycerides.

  • What is high cholesterol?

    It is a group of blood-lipid abnormalities - typically a raised LDL-C or non-HDL-C, high triglycerides, or a low HDL-C - that drives atherosclerosis and cardiovascular events. In UK practice it covers polygenic hypercholesterolaemia, familial combined dyslipidaemia, familial hypercholesterolaemia and secondary causes such as hypothyroidism, diabetes, chronic kidney disease and nephrotic syndrome.

  • How is familial hypercholesterolaemia different?

    Familial hypercholesterolaemia is an autosomal dominant condition caused by mutations in LDLR, APOB or PCSK9. It affects up to 1 in 250 people in the UK, is widely underdiagnosed and produces very high LDL-C from birth. Untreated, it causes heart attacks decades earlier than average. Cascade screening of relatives and early statin therapy are life-changing - see our guide on familial hypercholesterolaemia.

  • Do I really need a statin?

    If your ten-year cardiovascular risk on QRISK3 is 10 percent or more, or you have established heart disease, diabetes with risk factors, chronic kidney disease or FH, current UK guidance recommends a statin. Atorvastatin 20 mg is the primary-prevention dose and 80 mg the secondary-prevention dose where tolerated. Benefits are large and side effects, in properly diagnosed intolerance, are uncommon.

  • What if I cannot tolerate statins?

    True intolerance is less common than it feels. A structured re-challenge, a different statin or a lower dose helps many people. Where intolerance is genuine, ezetimibe, bempedoic acid, PCSK9 inhibitors and inclisiran can all lower LDL-C effectively and are used routinely in specialist lipid clinics.

  • What are PCSK9 inhibitors and inclisiran?

    PCSK9 inhibitors (alirocumab and evolocumab) are subcutaneous antibodies given every two to four weeks that dramatically lower LDL-C. Inclisiran is a small interfering RNA (siRNA) that silences PCSK9 in the liver and is given twice a year after loading. Both are NICE approved and specialist commissioned - see the PCSK9 inhibitor clinic and inclisiran clinic pages.

  • What about high triglycerides?

    Lifestyle, alcohol reduction, weight and glycaemic control come first. Fibrates and omega-3 preparations have a role. Icosapent ethyl (Vazkepa), a purified EPA, is NICE approved for people with raised triglycerides and cardiovascular risk despite a statin - see the icosapent ethyl clinic. Triglycerides above 10 mmol/L need urgent specialist review because of pancreatitis risk.

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