Here is something I tell almost every patient I discuss cholesterol with: total cholesterol is almost meaningless as a standalone number.
A total cholesterol of 6.5 in a 35-year-old woman with no other risk factors is a very different clinical picture from the same number in a 58-year-old man with diabetes, hypertension, and a family history of early heart disease. The first may never need medication. The second needs to be on a statin immediately.
Yet the conversation about cholesterol tends to collapse into a single number, a recommendation to cut out butter and eggs, and a repeat blood test in three months - sometimes without ever discussing what the cholesterol is actually doing to this specific person's cardiovascular risk, or whether treatment is genuinely indicated.
This guide gives you the actual picture.
Understanding the lipid profile
When your GP gives you a cholesterol result, ideally they give you a full fasting lipid profile - not just total cholesterol.
Total cholesterol: All types of cholesterol combined. Moderately useful but inadequate in isolation. Target: below 5.0 mmol/L for most adults; below 4.0 mmol/L for high-risk patients.
LDL cholesterol (Low Density Lipoprotein): The main driver of cardiovascular risk. LDL particles deposit in artery walls, triggering inflammation and the formation of atherosclerotic plaques. Lower is better. Target: below 3.0 mmol/L for most people; below 1.8 mmol/L for people with established cardiovascular disease.
HDL cholesterol (High Density Lipoprotein): The protective form. HDL particles remove cholesterol from artery walls and transport it to the liver for disposal. Higher is better. Target: above 1.0 mmol/L in men, above 1.2 mmol/L in women.
Triglycerides: Blood fats affected primarily by diet (refined carbohydrates, sugar, alcohol) and by metabolic factors including insulin resistance and diabetes. Target: below 1.7 mmol/L fasting. Significantly elevated triglycerides (above 10 mmol/L) independently increase the risk of pancreatitis.
Non-HDL cholesterol: Total cholesterol minus HDL. Captures all atherogenic lipoproteins. Target: below 4.0 mmol/L for most people. Increasingly used as a better summary measure than LDL alone.
Total:HDL ratio: A combined risk marker. Target: below 4.0. A ratio above 6.0 indicates significantly elevated risk.
What actually causes high cholesterol
This is where most patient information goes wrong. People are told cholesterol is about diet. In reality:
Genetics contribute 75-80% of your blood cholesterol level. The liver produces most of your cholesterol independently of what you eat. This is why dietary changes alone typically reduce LDL by only 5-15%. It is also why some people eat extremely healthy diets and still have high LDL.
Familial Hypercholesterolaemia (FH): A genetic condition affecting approximately 1 in 250 people in the UK (about 260,000 people, though only a minority are diagnosed). Caused by a mutation in the LDL receptor gene that prevents the liver from clearing LDL from the blood. People with FH have very high LDL from birth - often above 5.0 mmol/L - regardless of diet. They have significantly elevated cardiovascular risk from early adulthood and require treatment with high-dose statins or, if inadequately controlled, with PCSK9 inhibitors.
FH is suspected when: LDL above 4.9 mmol/L (in adults), family history of early heart disease (men below 55, women below 65), or xanthelasmas or tendon xanthomata on examination. If suspected, the Simon Broome criteria can be used to estimate probability.
Diet: Saturated fat in the diet (from red meat, dairy, tropical oils) raises LDL. Trans fats (found in some processed foods) both raise LDL and lower HDL - the worst lipid combination. Dietary cholesterol itself (previously demonised) has less effect on blood cholesterol than previously thought - eggs are largely rehabilitated.
Secondary causes: Hypothyroidism, type 2 diabetes, kidney disease, liver disease, and certain medications (steroids, thiazide diuretics at high doses, some antipsychotics) raise cholesterol. Always exclude these before concluding that primary hyperlipidaemia is the diagnosis.
QRISK3 - your actual cardiovascular risk
The UK now uses QRISK3 to calculate an individual's 10-year risk of a cardiovascular event (heart attack or stroke). It incorporates age, sex, ethnicity, total:HDL ratio, systolic blood pressure, smoking status, diabetes, family history of cardiovascular disease, deprivation index, and several other factors.
NICE recommends offering statin treatment when QRISK3 is 10% or above. Your cholesterol number alone does not determine whether you need treatment. Your overall risk profile does. A QRISK3 score is more clinically meaningful than a cholesterol level in isolation.
Case study: Emmanuel's apparently worrying result
Emmanuel, 44, a teacher from Ghana based in Manchester, was told at a health check that his total cholesterol was 6.8 and was advised to cut out fatty foods and reduce his red meat intake. He did this meticulously for eight months. His total cholesterol fell to 6.4.
His GP expressed disappointment at the modest response. Emmanuel was frustrated and confused.
When I reviewed his full lipid profile: LDL 4.2, but HDL 1.9 (excellent), total:HDL ratio 3.6 (well within normal), triglycerides 0.8 (very low). His QRISK3 at 44 with no other risk factors: 4.3% - low risk.
His total cholesterol number was misleading in isolation. His actual cardiovascular risk was not elevated. His HDL was so high that it was pulling his total cholesterol up, but protectively. He had spent eight months restricting his diet unnecessarily.
This is why total cholesterol alone tells you almost nothing.
Statins - the honest picture
Statins are among the most studied medications in medical history, with robust evidence across tens of millions of patient-years of follow-up. For people with elevated cardiovascular risk, they significantly reduce the risk of heart attack, stroke, and cardiovascular death.
They are also among the most frequently refused and discontinued medications I encounter in practice - largely driven by internet misinformation.
What statins do: Inhibit HMG-CoA reductase, the enzyme the liver uses to produce cholesterol. The liver responds by upregulating LDL receptors, pulling more LDL out of the circulation. Most statins reduce LDL by 30-50% at standard doses. High-intensity statins (atorvastatin 40-80mg, rosuvastatin 20-40mg) reduce LDL by 50% or more.
Side effects - the honest picture: Muscle aches (myalgia): The most commonly reported side effect. Occurs in approximately 5-10% of patients in real-world practice. Severe muscle damage (rhabdomyolysis) is rare (approximately 1 in 10,000). The nocebo effect - experiencing side effects because you expect them after reading about them - is well documented with statins. Blinded studies show that patients report muscle aches at the same rate on placebo as on statin when they do not know which they are taking.
Liver effects: Mild, clinically insignificant transaminase elevations occur occasionally. Severe liver toxicity is extremely rare.
Diabetes risk: A small increase in the risk of type 2 diabetes, particularly in people already at high metabolic risk. This risk is outweighed by cardiovascular benefit in most patients at the risk levels for which statins are recommended.
If you are having side effects: Do not simply stop without discussing with your GP. Many side effects resolve with a different statin at a lower dose. Switching from simvastatin to rosuvastatin, or to a statin taken on alternate days, resolves myalgia in many people. There are now also non-statin options (ezetimibe, inclisiran, evolocumab) for people who cannot tolerate statins.
Sources: NICE Clinical Guideline CG181 - Cardiovascular Disease: Risk Assessment and Reduction (2014, updated 2023); Collins R et al, The Lancet 2016 (Cholesterol Treatment Trialists - statin safety and efficacy); Khera AV et al, NEJM 2016 (PCSK9 inhibitors); Benn M et al, European Heart Journal 2012 (familial hypercholesterolaemia); QRISK3 algorithm - Hippisley-Cox J et al, BMJ 2017.
