Health condition · Clinically reviewed
High cholesterol, beyond the total number.
The lipid panel that matters — LDL, non-HDL, ApoB and Lp(a) — and the modern medication ladder that goes beyond statins.
Why trust this guide
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Clinically reviewed
Written by our editorial team and reviewed by a registered UK clinician before publication.
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Sourced, not summarised
Every claim is checked against NICE, HEART UK or a peer-reviewed source you can see at the end.
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Updated for 2026
Reflects the modern lipid panel — ApoB, Lp(a) and the full medication ladder beyond statins.
Key facts
High cholesterol at a glance.
The essentials, in plain English — what the modern lipid panel measures, why ApoB and Lp(a) matter, and how far treatment has moved beyond statins.
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What it is
Dyslipidaemia — a pattern of blood lipids that raises long-term cardiovascular risk.
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The primary targets
LDL and non-HDL cholesterol are the numbers most treatment decisions are built around.
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The best single marker
ApoB is emerging as the most accurate single measure of atherogenic particle number.
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Lp(a)
A once-in-a-lifetime, genetically fixed lipoprotein — a strong independent CV risk factor.
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How common is FH
Familial hypercholesterolaemia affects around 1 in 250 people — most remain undiagnosed.
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The modern ladder
Statins, ezetimibe, bempedoic acid, PCSK9 inhibitors and inclisiran — several rungs beyond statins alone.
Why this guide matters
The total number is not the whole story.
Total cholesterol on its own tells you very little. The pattern beneath it — LDL, non-HDL, ApoB and Lp(a) — is what actually shapes lifetime cardiovascular risk.
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LDL and non-HDL drive risk
These are the atherogenic fractions — the ones that build up in artery walls over decades.
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ApoB counts the particles
One ApoB measurement captures the true number of harmful particles, especially when triglycerides are high.
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Lp(a) is inherited and lifelong
A single check identifies a hidden, genetic risk factor that will not change with diet or exercise.
How the diagnosis is made
From first lipid panel to a clear plan.
The steps a UK GP or lipid clinic will normally follow, in order — so you know what to expect and why.
Phase 1 · Measuring
Baseline panel and risk assessment
Phase 2 · Investigating
Lp(a), family history and FH screening
Phase 3 · Managing
Optimisation and specialist referral
- 01
Measuring
Baseline lipid panel
Total cholesterol, LDL, HDL, non-HDL and triglycerides — the starting picture.
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Measuring
Non-fasting acceptable per NICE
You no longer need to fast for a routine lipid panel — non-fasting samples are validated for risk assessment.
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Measuring
QRISK3 cardiovascular risk assessment
A 10-year risk score that combines age, blood pressure, lipids and other factors to guide treatment.
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Investigating
Lp(a) once in a lifetime
Lipoprotein(a) is genetically fixed. A single measurement identifies a hidden inherited risk factor.
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Investigating
Family history for FH
Early heart attack in a first-degree relative under 60 is a red flag for familial hypercholesterolaemia.
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Managing
Cardiovascular risk factors optimised
Blood pressure, HbA1c, weight, smoking and activity — all reviewed alongside the lipids.
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Managing
Cardiology or lipid clinic referral
For suspected FH, statin intolerance or when specialist agents (PCSK9, inclisiran) are being considered.
Typical timeline: 2–6 weeks from first panel to a settled plan.
Symptoms and situations
When high cholesterol matters most.
Cholesterol itself is silent — but certain situations sharpen the priority to test, treat and escalate.
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Asymptomatic (screening)
High cholesterol has no symptoms of its own — it is picked up on a routine lipid panel or CV risk check.
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Family history of early MI
A parent or sibling with a heart attack under 60 is one of the strongest reasons to check lipids early.
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Pre-diabetes with dyslipidaemia
Raised triglycerides and low HDL alongside a rising HbA1c is a classic metabolic pattern.
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Very high LDL (>5 mmol/L)
An LDL above 5 mmol/L without treatment should always prompt consideration of familial hypercholesterolaemia.
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Statin intolerance
Muscle symptoms that limit statin use — a common reason for referral and for alternative therapies.
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Recurrent CV events
A second heart attack or stroke despite treatment prompts a step up the medication ladder.
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Raised Lp(a)
A single high Lp(a) result reframes lifetime risk and often lowers the threshold for other treatments.
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When to seek urgent care
Chest pain with an LDL above 7 mmol/L or visible tendon xanthomas — arrange urgent lipid-clinic referral.
Treatment
The modern medication ladder.
Lifestyle first, then a stepped medication ladder — statins, ezetimibe, bempedoic acid, PCSK9 inhibitors and inclisiran, alone or in combination.
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Dietary and lifestyle change
Reduced saturated fat, more soluble fibre, oily fish, weight loss and regular activity — the foundation for every plan.
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Statin (atorvastatin, rosuvastatin)
First-line pharmacological therapy. Typically lowers LDL by 30–55% depending on dose and choice.
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Ezetimibe (add-on)
Reduces cholesterol absorption in the gut. Adds a further 15–20% LDL reduction on top of a statin.
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Bempedoic acid
An oral option for statin-intolerant patients, or as add-on when LDL remains above target.
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PCSK9 inhibitor (evolocumab, alirocumab)
A fortnightly injection that can cut LDL by a further 50–60% on top of statin plus ezetimibe.
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Inclisiran (twice-yearly injection)
A small interfering RNA therapy given every six months after loading — a powerful, low-frequency option.
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Lipoprotein apheresis (very high risk)
Reserved for severe FH or very high Lp(a) with progressive disease despite maximal therapy.
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Familial hypercholesterolaemia genetics
Genetic testing and cascade screening of relatives when FH is suspected clinically.
What this guide is based on
The sources behind every number 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 or lipid specialist knows your history and can tell you which parts apply to you.
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National Institute for Health and Care Excellence (NICE). Cardiovascular disease: risk assessment and reduction, including lipid modification (NG238).
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HEART UK — The Cholesterol Charity. Clinical guidance and patient information.
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European Society of Cardiology / EAS. Guidelines for the management of dyslipidaemias.
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British Heart Foundation. High cholesterol: patient information.
Red flags
When high cholesterol needs urgent attention.
Most of the time, cholesterol is a slow-burn risk factor. These are the situations that should prompt a faster response — often referral to a lipid clinic or cardiology.
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Chest pain with FH
Any suspected cardiac chest pain in someone with familial hypercholesterolaemia is a same-day concern.
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Tendon xanthomas
Firm lumps over the Achilles or knuckle tendons are near-diagnostic of FH — urgent lipid-clinic referral.
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Corneal arcus in a young adult
A white or grey ring around the cornea under age 45 raises suspicion of severe familial dyslipidaemia.
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LDL >5 mmol/L untreated
An untreated LDL above 5 mmol/L should always trigger FH assessment and cascade screening of relatives.
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Very high Lp(a) with family history
A very high Lp(a) alongside early CV disease in the family markedly raises lifetime risk.
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Post-MI dyslipidaemia
After a heart attack, LDL targets are lower and the medication ladder is escalated quickly.
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Statin-associated muscle symptoms
Severe or persistent muscle pain, dark urine or weakness on a statin needs prompt review and CK testing.
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Fatty liver with dyslipidaemia
Non-alcoholic fatty liver disease alongside a metabolic lipid pattern warrants coordinated review.
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Pregnancy planning on a statin
Statins should usually be stopped before conception — plan ahead with your GP or lipid specialist.
Living with it
A long-term condition, but a very manageable one.
Four things that make the biggest difference day to day — habits, monitoring, medication and reviews.
A quiet reminder
Consistency beats intensity, every time.
Small, steady changes — kept up for months — do more than a heroic week that does not last.
- 01 Daily habits
Small changes, real reductions
Cutting saturated fat, adding oily fish and moving more can lower LDL meaningfully before any tablet is added.
- 02 Monitoring
Trust the trend, not one panel
A single lipid panel is a snapshot — repeated measurements over months show the real direction of travel.
- 03 Medication
Timing and side effects
Statins are usually taken in the evening. Most side effects settle — talk to your GP before stopping.
- 04 Reviews
Annual review as a minimum
A yearly lipid and cardiovascular risk review, more often if you are not yet at your LDL target.
Frequently asked
Everything we get asked about high cholesterol.
Quick answers on LDL vs non-HDL, ApoB, Lp(a), familial hypercholesterolaemia and the modern medication ladder.
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What is the difference between LDL and non-HDL cholesterol?
LDL is the classic "bad" cholesterol. Non-HDL is total cholesterol minus HDL, and captures all the atherogenic particles in one number — which is why NICE now uses non-HDL as a primary target.
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Why is ApoB considered a better marker?
ApoB measures the number of atherogenic particles directly, rather than the cholesterol carried inside them. In people with diabetes, metabolic syndrome or high triglycerides, ApoB reflects true risk more accurately than LDL alone.
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What is Lp(a) and why is it measured only once?
Lipoprotein(a) is a genetically inherited lipoprotein that is largely fixed for life. A single measurement identifies whether you carry this inherited risk factor — repeated testing is not usually needed.
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What is familial hypercholesterolaemia (FH)?
An inherited condition affecting about 1 in 250 people that causes very high LDL from birth and greatly raises the risk of early heart disease. Most people with FH are undiagnosed.
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Are statins the only treatment?
No. Ezetimibe, bempedoic acid, PCSK9 inhibitors (evolocumab, alirocumab) and inclisiran all sit on the modern ladder — used alone or in combination when statins are not enough or not tolerated.
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When should I be referred to a lipid clinic?
Suspected familial hypercholesterolaemia, statin intolerance, very high LDL or Lp(a), or when specialist injectable therapies are being considered.
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