High cholesterol: causes, blood tests and treatment

What is being measured, and why it matters

Cholesterol is carried in the blood by particles, and the particles behave differently. Low-density lipoprotein, reported as LDL cholesterol, deposits in artery walls and drives the process that ends in a heart attack or a stroke. High-density lipoprotein, reported as HDL, behaves in the opposite direction. Triglycerides are a separate fat that rises with alcohol, with sugar and with untreated diabetes.

A lipid profile usually reports total cholesterol, LDL, HDL and triglycerides, and often non-HDL cholesterol, which is total minus HDL and is a convenient single figure. Some laboratories report apolipoprotein B or lipoprotein(a); those are useful in particular situations rather than routinely.

What is done about a result depends on the rest of your risk: age, sex, blood pressure, smoking, diabetes, family history, kidney function and whether you have already had a cardiovascular event. Two people with an identical LDL can properly be given different advice, which is why there is no single target that fits everyone and why we do not print one here.

Why there are no symptoms

Cholesterol does not hurt. It does not cause tiredness, headaches or any of the things people attribute to it, and you cannot feel whether your level is high or low. The first symptom, in the unlucky, is the event the treatment was meant to prevent.

There are rare exceptions that are worth recognising, because they point to a strongly inherited form: fatty deposits in the tendons, particularly over the knuckles or the back of the heel, yellowish patches around the eyelids, or a pale ring at the edge of the cornea in a younger person.

Because it is silent, the only way to know is to be tested, and the reason to be tested is risk rather than symptoms: a family history of early heart disease, a parent with very high cholesterol, diabetes, high blood pressure, smoking, or simply reaching the age at which a check is offered.

The blood test in practice

A lipid profile is a simple blood test. Fasting is no longer required for most purposes, though a laboratory or a doctor may ask for it if triglycerides are the question. Take the result as a whole rather than fixing on total cholesterol, which can be misleading in either direction.

Results move with circumstances. Acute illness, a recent infection, pregnancy, marked weight change and some medicines all shift the figures, and a value measured in the weeks after a heart attack is not a baseline. That is why a doctor may repeat the test before acting on it.

Keep the printed report, with the date and the laboratory's reference ranges. Comparing your own sequence of results is far more informative than comparing one of them with a figure someone quoted you, and the report is also what any doctor needs in order to continue or adjust a treatment.

What raises cholesterol

Diet contributes, mostly through saturated fat rather than through dietary cholesterol itself, and the effect varies between people. Excess weight, inactivity, alcohol and smoking all push the profile in the wrong direction, smoking mainly by lowering HDL and damaging artery walls.

Several medical conditions raise it: an underactive thyroid, type 2 diabetes, kidney disease and liver disease among them. Some medicines do too, including steroids and certain treatments used in other conditions. This is why a raised result usually prompts a doctor to check a few other things rather than to reach straight for a tablet.

Then there is inheritance, which is the part most often missed. Familial hypercholesterolaemia is a genetic condition that produces a markedly raised LDL from childhood and a high risk of early heart disease. It runs in families in a clear pattern, and it needs specialist assessment and family testing rather than ordinary management, so a very high level or a family history of heart attacks in the forties or fifties should be mentioned explicitly to a doctor.

Diet, activity and what they can realistically achieve

Changes that have good evidence behind them are: less saturated fat, replaced by unsaturated fats rather than by refined carbohydrate; more soluble fibre from oats, pulses, fruit and vegetables; oily fish; nuts; less alcohol; and regular physical activity. A Mediterranean pattern of eating, which is close to what is traditional in Malta before the additions, is the pattern with the strongest evidence for cardiovascular outcomes.

Losing excess weight improves triglycerides markedly and LDL modestly. Activity does more for HDL and triglycerides than for LDL, and it improves cardiovascular risk through routes that a lipid panel does not show at all, so its value is not captured by the numbers.

Two honest limits. Diet and activity shift LDL by a proportion, not by a factor, so someone with a strongly inherited level will not reach a sensible figure by diet alone, and being told to try harder is not useful advice. And plant sterol spreads and supplements have a small measurable effect on LDL but no demonstrated effect on heart attacks and strokes, which is the outcome that matters.

None of this is a reason to skip the changes: they work alongside treatment, not instead of it.

Statins and the other medicines

Statins reduce the liver's production of cholesterol and are the best-studied medicines in this field, with clear evidence for fewer heart attacks and strokes in people at raised risk. Several are authorised in Malta, and our pages on /medicines/lipitor/ for atorvastatin and /medicines/simvastatin/ for simvastatin describe them in more detail. Which one, and at what strength, is chosen against your risk, your other medicines and your kidney and liver function.

Muscle symptoms are the side effect people ask about most. Aches do occur, they are usually mild and reversible, and in blinded trials they occur nearly as often on placebo, which does not make them imaginary but does mean the statin is not always the cause. The sensible response is not to stop silently but to tell a doctor, because a change of statin, a lower strength or an alternate-day regimen often solves it. Severe, widespread muscle pain with weakness and dark urine is different and needs urgent attention.

Where a statin is not enough or not tolerated, other options exist: ezetimibe, which reduces absorption, and injected treatments used in higher-risk or inherited cases. Fibrates and high-dose omega-3 preparations are used mainly for very high triglycerides.

Grapefruit juice interacts with some statins but not others, and several antibiotics and antifungals do too, so mention the statin whenever another medicine is started. Our category page /heart-and-cholesterol/ sets out how the groups compare.

Monitoring, and what to do if you stopped taking it

After starting or changing a statin, the lipid profile is repeated to see the effect, and liver tests are checked at intervals a doctor decides. Once things are stable, monitoring is less frequent, but it does not disappear: blood pressure, weight, glucose and smoking status all belong in the same review.

A large proportion of people stop taking a statin within a year or two, usually without telling anyone, and often after reading something alarming. If that is you, the useful step is to say so plainly at the next opportunity. The conversation is about what to try next, not about being told off, and the alternatives above exist precisely for this situation.

If you have had a heart attack, a stroke or a stent, the arithmetic of stopping is different and considerably less forgiving than in primary prevention. That is a decision to make with a doctor who has your history, not one to make from a website.

Keep a note of the substance, the strength, your last lipid result and its date. Those four items are what any doctor needs to continue the treatment.