Cholesterol Explained — LDL, HDL, and Heart Risk

Cholesterol has the worst public-relations profile in biology. Most people know it as the stuff that clogs arteries, yet every cell in your body needs it, your sex hormones are built from it, and your nervous system relies on it. The real story is about where cholesterol travels and where it ends up, not simply how much of it exists. This article explains what cholesterol is, how LDL and HDL differ, how plaques form, and what large trials show about the drugs that lower it.

Educational content, not medical advice. Talk to your doctor before changing any medication, treatment, or routine. This article describes research and general guidance, and every person's risk is different.

Key takeaways

• Cholesterol is a necessary molecule. The trouble comes from LDL (low-density lipoprotein) particles that lodge in artery walls, not from cholesterol as such.
• Genetic studies and randomized trials agree that lowering LDL lowers cardiovascular risk, by about 22% per 1 mmol/L (roughly 39 mg/dL) in statin trials.
• Different drugs lower LDL by very different amounts, and the benefit tracks the amount of LDL lowered over time.
• HDL ("good" cholesterol) is a marker of risk, but drugs that raise it have not shown a reliable benefit.

What cholesterol actually is

Cholesterol is a waxy molecule from a family called sterols. It has three jobs that nothing else can do.

• Cell membranes. Cholesterol sits between the fatty molecules that form the membrane around every cell. It helps keep that membrane firm enough to hold its shape and fluid enough to work.
• Steroid hormones. Testosterone, estrogen, progesterone, cortisol, and aldosterone are all made from cholesterol (how sex hormones work).
• Vitamin D and bile acids. Ultraviolet light converts a cholesterol precursor in skin into vitamin D, and the liver turns cholesterol into bile acids that help digest fat.

Without it, cells could not hold together and hormone production would stop. The body treats cholesterol as valuable and manages it carefully. Much of the cholesterol in the body is made by the body itself, mainly in the liver, and the liver adjusts its output when more arrives from food (what the liver does).

That regulation is why dietary cholesterol is a weaker lever than many people expect. MedlinePlus lists saturated fat and dietary cholesterol among the dietary factors that raise LDL, along with excess weight, physical inactivity, smoking, age, genetics, certain medicines, and conditions such as diabetes and chronic kidney disease. People differ in how much their blood levels respond to what they eat, which is why advice to one patient does not always fit another.

Lipoproteins: the delivery trucks

Cholesterol is a fat, and blood is mostly water. A fat cannot travel through blood on its own any more than a stick of butter can dissolve in a river. The body solves this by packaging cholesterol and other fats into particles called lipoproteins, which have a fatty core and a shell of protein and phospholipid that lets them mix with water.

Think of lipoproteins as delivery trucks and cholesterol as the cargo. The truck type matters more than the cargo, because the same cargo delivered to the wrong address causes damage.

Particle	Main job	Why it matters
Chylomicrons	Carry fat absorbed from the gut	Present after meals, cleared quickly
VLDL (very low-density lipoprotein)	Carry fat and cholesterol from the liver to tissues	Becomes LDL after it unloads fat
LDL (low-density lipoprotein)	Deliver cholesterol to tissues	The particle that can lodge in artery walls
HDL (high-density lipoprotein)	Carry cholesterol back to the liver	A marker of lower risk, not a proven protector
Lp(a) (lipoprotein little a)	An LDL-like particle with an added protein	Largely inherited; an independent risk factor

The labels "good" and "bad" are shorthand. MedlinePlus describes LDL as the "bad" cholesterol because high levels lead to cholesterol buildup in the arteries, and HDL as the "good" kind because it carries cholesterol back to the liver for removal. A cholesterol panel measures the cholesterol carried by each particle type, not the particles themselves, which is a detail that comes up again below.

How the liver controls LDL: receptors and PCSK9

LDL in the blood is cleared mainly by LDL receptors, proteins on the surface of liver cells that grab LDL particles and pull them in. The more receptors a liver cell has, the more LDL it removes. This receptor system was worked out by the physician-scientists Michael Brown and Joseph Goldstein, and it explains why one inherited condition causes such extreme cholesterol levels.

That condition is familial hypercholesterolemia (FH). According to MedlinePlus Genetics it affects about 1 in 200 to 1 in 250 people in most countries. The most common cause is a variant in the LDLR gene that reduces the number of LDL receptors or impairs their function, and less common causes involve APOB, LDLRAP1, and PCSK9. People with FH have very high cholesterol from birth and a high risk of coronary artery disease at a young age.

PCSK9 is a protein that tags LDL receptors for destruction. Block PCSK9 and receptors survive longer and recycle back to the cell surface, so the liver clears more LDL. This one mechanism explains two modern drug classes, the PCSK9 antibodies and the RNA-based drug inclisiran, covered below.

How plaques form

Heart attacks and most strokes begin with atherosclerosis, a process that unfolds over decades (the biology of atherosclerosis). The usual sequence is:

1. LDL particles enter the artery wall. They cross the thin layer of cells lining the artery and become trapped in the tissue beneath it. The more LDL in the blood, and the longer the exposure, the more particles are retained.
2. Trapped LDL is chemically modified. Oxidation and other changes make the particles inflammatory.
3. Immune cells respond. White blood cells called macrophages engulf the modified LDL and swell into foam cells, which gather into fatty streaks.
4. A plaque forms. Foam cells, cholesterol, smooth muscle cells, and fibrous tissue build a bulge that may narrow the artery.
5. The plaque can rupture. A thin fibrous cap can tear, exposing the contents to the blood, which clots on contact. A clot that blocks a coronary artery causes a heart attack, and one that blocks an artery in the brain causes an ischemic stroke.

A point that surprises many people is that the plaques that rupture are not always the most narrowing ones. A moderately sized plaque with a thin cap can be more dangerous than a larger, stable one. That is one reason risk is estimated from blood measurements and other factors rather than from how narrow an artery looks on a scan. For the heart itself, see how the heart works.

Is LDL really the cause? The evidence

"Bad" cholesterol is a strong claim, and the evidence for it is unusually thorough. In 2017, the European Atherosclerosis Society published a consensus statement in the European Heart Journal concluding that evidence from genetic, epidemiologic, and trial studies "unequivocally establishes that LDL causes ASCVD" (atherosclerotic cardiovascular disease). It rests on three kinds of evidence working together (EAS consensus statement, European Heart Journal 2017).

Genetics. People are born with random variations in genes that affect LDL. This natural experiment is called Mendelian randomization. Variants in more than 50 genes that lower LDL are associated with a proportionally lower risk of coronary heart disease, in a log-linear, dose-dependent relationship. Variants in HMGCR (the statin target), NPC1L1 (the ezetimibe target), and PCSK9 had similar effects per unit of LDL lowering. A meta-analysis of over 300,000 participants and 80,000 cases found the effect was largely independent of how LDL was lowered.

Trials. In 26 statin trials with almost 170,000 people, each 1 mmol/L reduction in LDL cholesterol was associated with a 22% proportional reduction in major cardiovascular events over a median of five years. Other approaches fit the same line. The IMPROVE-IT trial of ezetimibe, with a 0.40 mmol/L reduction, showed a 6.5% reduction in events, and the SHARP trial, with 0.85 mmol/L, showed 17%. FOURIER, with 1.4 mmol/L, showed 20%.

Exposure over time. The statement estimated that the relative risk falls by about 10% in the first year of lower LDL, about 16% after two years, and about 20% after three, then roughly 1.5% more per additional year. Five years of lowering gives about 20% to 25% per mmol/L, and forty years gives about 50% to 55%. In plain terms, a lifetime of slightly lower LDL, as in people who inherit a LDL-lowering variant, protects much more than a few years of treatment late in life.

Correlation is not causation, and this is the kind of case where the distinction can be settled. Randomized trials remove the usual confounders, and genetic variants are assigned at conception, before diet or lifestyle can interfere (correlation versus causation).

The statin story

The first statin came from a fungus. A historical review by Akira Endo, the Japanese biochemist who began the search at the company Sankyo, describes nearly a century of work linking blood cholesterol, atherosclerosis, and coronary heart disease before statins were developed (Endo, Proceedings of the Japan Academy 2010). Merck's lovastatin reached the market in 1987 as Mevacor. In the Scandinavian Simvastatin Survival Study, reported in The Lancet in 1994, 4,444 patients with heart disease and high cholesterol took simvastatin or placebo. Simvastatin lowered LDL cholesterol by about 35%, and the relative risk of coronary death was 0.58, a 42% reduction.

Statins block HMG-CoA reductase, the enzyme that limits the speed of cholesterol production in the liver. When a liver cell makes less cholesterol, it builds more LDL receptors, and those receptors pull more LDL out of the blood. This is why a drug that acts on the liver's own factory lowers the cholesterol in the bloodstream.

Do statins work equally in women and men?

A 2015 analysis in The Lancet by the Cholesterol Treatment Trialists' Collaboration pooled individual data from 174,149 participants in 27 randomized trials, of whom 27% were women. The analysis weighted outcomes per 1 mmol/L of LDL lowered. For each 1 mmol/L of LDL lowered, the rate ratio for major vascular events was 0.84 in women and 0.78 in men, and for all-cause mortality it was 0.91 in women and 0.90 in men. The authors saw no adverse effect on cancer incidence or non-cardiovascular mortality (CTT Collaboration, The Lancet 2015).

How common are statin muscle symptoms?

Muscle pain is the side effect patients ask about most. A 2022 individual-participant meta-analysis in The Lancet pooled 19 placebo-controlled trials with 123,940 participants. Muscle pain or weakness was reported by 27.1% of people assigned to a statin and 26.6% of those assigned to placebo (rate ratio 1.03). In the first year, statins raised reports by about 7%, an absolute excess of about 11 events per 1,000 person-years, and after the first year there was no significant excess. The authors concluded that over 90% of muscle symptom reports in statin-treated participants were not due to the drug, describing the excess as a small number of mostly mild cases.

This is a population result, not a verdict on any one person. A patient who has muscle symptoms on a statin may still be the exception, and clinicians have options such as a different statin, a different dose, or a different drug class. The result does show why symptoms that arise by chance, or because a patient expects them, are common in open-label use (how expectation shapes symptoms).

Beyond statins: the other lipid drugs

Statins are the foundation, but they are not the only option. The table summarizes what the main classes do, with the strongest figures from the trials above.

Drug class	How it works	Evidence on LDL and outcomes
Statins	Block cholesterol production in the liver	22% fewer major events per 1 mmol/L of LDL lowered (26 trials, almost 170,000 people)
Ezetimibe	Blocks absorption of cholesterol in the intestine	IMPROVE-IT: 0.40 mmol/L reduction, 6.5% fewer events; SHARP: 0.85 mmol/L, 17%
PCSK9 antibodies (evolocumab, alirocumab)	Stop PCSK9 from destroying LDL receptors	FOURIER: LDL fell 59% from median 92 to 30 mg/dL; events down (HR 0.85)
Bempedoic acid	Blocks ATP-citrate lyase, a step before HMG-CoA reductase	CLEAR Outcomes: 21.1 percentage points greater LDL lowering; major events down (HR 0.87)
Inclisiran	siRNA that reduces PCSK9 production	LDL down 40% to 51% in phase 3 trials; outcome effect not yet determined

PCSK9 antibodies: the FOURIER trial

The FOURIER trial, published in the New England Journal of Medicine in 2017, enrolled 27,564 patients with atherosclerotic cardiovascular disease and an LDL of 70 mg/dL or more despite statin therapy. Patients received the antibody evolocumab or placebo by injection. Over a median follow-up of 2.2 years, LDL fell by 59% compared with placebo, from a median of 92 mg/dL to 30 mg/dL. The primary composite endpoint occurred in 9.8% of the evolocumab group and 11.3% of the placebo group (hazard ratio 0.85), and the key secondary endpoint of cardiovascular death, heart attack, or stroke occurred in 5.9% and 7.4% (hazard ratio 0.80). Results were consistent in patients with the lowest starting LDL, and there were no significant differences in new-onset diabetes or neurocognitive events (FOURIER, NEJM 2017).

Bempedoic acid: the CLEAR Outcomes trial

Many people who stop statins do so because of muscle symptoms. The CLEAR Outcomes trial, published in 2023, tested bempedoic acid in 13,970 statin-intolerant patients who had or were at high risk for cardiovascular disease. At six months, LDL was 29.2 mg/dL lower than with placebo, a 21.1 percentage-point greater reduction. Over a median of 40.6 months, the primary composite endpoint occurred in 11.7% of the bempedoic acid group compared with 13.3% of the placebo group (hazard ratio 0.87). Heart attacks fell more (hazard ratio 0.77), though there were no significant differences in cardiovascular death or all-cause death. Gout (3.1% versus 2.1%) and gallstones (2.2% versus 1.2%) were more common with bempedoic acid (CLEAR Outcomes, NEJM 2023).

Inclisiran: silencing the message

Inclisiran is a small interfering RNA (siRNA), a short strand of genetic material that tells liver cells to degrade the messenger RNA that carries the instructions for making PCSK9. With less PCSK9, more LDL receptors survive. According to the FDA, it is given with diet and maximally tolerated statin therapy to adults with heterozygous familial hypercholesterolemia or established cardiovascular disease who need more LDL lowering. Dosing is an initial injection, a second at three months, and then one every six months. In the three phase 3 trials (3,457 adults in total), LDL fell by 51%, 46%, and 40% compared with increases of 1%, 4%, and 8% on placebo. The FDA notes that its effect on cardiovascular morbidity and mortality has not been determined (FDA, Leqvio).

That last point is a useful reminder of how evidence matures. Lowering LDL is a surrogate marker, meaning a measurement that stands in for the outcome that matters. The link between LDL and events is strong enough that regulators approve LDL-lowering drugs on it, but a trial that counts heart attacks is still the stronger proof.

What a cholesterol test shows

A standard lipid panel reports several numbers. MedlinePlus lists adult LDL categories (in mg/dL) as below 100 optimal, 100 to 129 near or above optimal, 130 to 159 borderline high, 160 to 189 high, and 190 and above very high. It notes that people with coronary artery disease or high risk may have different targets set by their provider. The Centers for Disease Control and Prevention, citing the 2018 AHA/ACC guideline, gives optimal values of at least 40 mg/dL of HDL for men and at least 50 mg/dL for women, triglycerides below 150 mg/dL, and total cholesterol above 200 mg/dL as possibly high.

Marker	What it measures	Reference point (adults)
Total cholesterol	Cholesterol in all particles	Above 200 mg/dL may be high (CDC)
LDL-C	Cholesterol carried in LDL	Below 100 mg/dL optimal (MedlinePlus)
HDL-C	Cholesterol carried in HDL	At least 40 (men) or 50 (women) mg/dL (CDC)
Triglycerides	Fat carried mainly in VLDL and chylomicrons	Below 150 mg/dL (CDC)
ApoB	Number of LDL-type particles	Counts particles directly; no single cutoff given here
Lp(a)	Inherited particle level	About 20% of people exceed 50 mg/dL

Two of these deserve extra attention. ApoB is a protein found on each LDL-type particle, so counting it counts the particles instead of the cargo. The EAS consensus notes that LDL cholesterol can diverge from particle number in metabolic syndrome, diabetes, and high triglycerides, and in those cases apoB or particle measurements may better reflect risk. Lp(a) is mostly set by genes. Roughly 20% of people are estimated to have levels above 50 mg/dL. A 2022 European Atherosclerosis Society statement found a causal, continuous link between Lp(a) and cardiovascular outcomes, noted that it is a risk factor even when LDL is very low, and recommended measuring it at least once in adults. The statement notes that without Lp(a)-specific therapies, early intensive management of other risk factors is recommended, and that trials of Lp(a)-lowering treatments are still needed to confirm clinical benefit (EAS Lp(a) consensus, European Heart Journal 2022).

How often to test depends on age and risk. MedlinePlus gives a general schedule: children have a first test at ages 9 to 11 and then every five years, adults 20 and older every five years, men 45 to 65 and women 55 to 65 every one to two years, and adults over 65 yearly. More frequent testing may be needed with heart disease, diabetes, or a family history of high cholesterol. The CDC reports that about two-thirds of adults had their cholesterol checked in the previous five years.

How common is the problem?

The CDC reports that in 2017 to 2020, about 10% of US adults aged 20 and older had total cholesterol of 240 mg/dL or more, and about 86 million had total cholesterol above 200 mg/dL. Of adults who could benefit from cholesterol medicine, 54.5% (about 47 million people) were taking it (CDC cholesterol facts). Separately, the National Center for Health Statistics reported that 13.8% of US adults had low HDL (under 40 mg/dL) in August 2021 to August 2023 (NCHS Data Brief 515).

The numbers show two things. Elevated cholesterol is common, and a large minority of people who might benefit from treatment are not receiving it. The latter is partly a problem of awareness, because high cholesterol causes no symptoms until a cardiovascular event occurs.

Relative versus absolute benefit: why treatment advice differs by person

A 22% reduction sounds the same for everyone, but its meaning depends on where a person starts. This is the difference between relative and absolute risk, and it explains why guidelines recommend more intensive treatment for people at higher baseline risk.

Take a purely illustrative example, with invented numbers. If a person has a 10% chance of a major cardiovascular event over the next decade and treatment cuts relative risk by 22%, the absolute risk falls by 2.2 percentage points, from 10% to 7.8%. For a person with a 2% chance, the same 22% cut lowers it by 0.44 points. The relative effect is the same, but the number of people who need treatment to prevent one event is very different, and so is the weighing of benefit against cost, inconvenience, and side effects.

The FOURIER trial shows the same pattern with real data. The hazard ratio of 0.85 sounds modest, and the absolute difference in the primary endpoint was 1.5 percentage points (9.8% versus 11.3%) over a median of 2.2 years. The trial enrolled people who already had cardiovascular disease and whose baseline risk was high, so the absolute benefit would be smaller in people at lower risk over a similar period. Duration matters too. The EAS consensus estimate that benefit grows from about 20% to 25% per mmol/L after five years to about 50% to 55% after forty years suggests that a short trial understates what a lifetime of lower LDL does.

Units add a layer of confusion. Laboratories in the United States report cholesterol in milligrams per deciliter (mg/dL), while most of the world and many trial reports use millimoles per liter (mmol/L). As a rough conversion, 1 mmol/L of LDL cholesterol is about 39 mg/dL, which is consistent with FOURIER's own figures, where a median LDL of 92 mg/dL is given as 2.4 mmol/L. When a statement says "22% per mmol/L," it means about 22% per 39 mg/dL of LDL lowered.

Several things follow from this arithmetic:

• Intensity of treatment is matched to risk, not just to a cholesterol number, which is why two people with the same LDL can receive different advice.
• Starting early matters for people who inherit high LDL, because years of exposure accumulate. This is the logic behind testing children with a family history.
• A drug's LDL effect can be compared with another's using the same yardstick. A treatment that lowers LDL by 1.4 mmol/L, as evolocumab did in FOURIER, is expected to deliver more than one that lowers it by 0.4 mmol/L, as ezetimibe did in IMPROVE-IT, which matches the 20% versus 6.5% reductions in events.

None of this replaces a personal risk assessment. Doctors combine cholesterol with blood pressure, age, diabetes, smoking, and family history, and each of those shifts the baseline that the percentages apply to.

Does HDL really protect you?

HDL is associated with lower risk, and it is easy to conclude that raising it must help. The drug trials say otherwise. The CETP inhibitors, a drug class that raises HDL and lowers LDL, produced a mixed record. The EAS consensus notes that evacetrapib lowered LDL cholesterol but did not reduce events. The REVEAL trial of anacetrapib, published in 2017, enrolled 30,449 adults with atherosclerotic vascular disease who were already on intensive atorvastatin. HDL was 43 mg/dL higher with anacetrapib (a 104% relative difference), and non-HDL cholesterol was 17 mg/dL lower. Over a median 4.1 years, the primary outcome occurred in 10.8% of the anacetrapib group and 11.8% of the placebo group (rate ratio 0.91) (REVEAL, NEJM 2017).

Because the drug changed both HDL and non-HDL cholesterol, the trial cannot say which change produced the modest benefit. What the pooled evidence does show is that a simple "raise the good cholesterol" strategy has not been established as a way to prevent heart attacks. Many researchers now think HDL partly reflects overall metabolic health and that the quality of HDL particles may matter more than their number (how obesity and metabolic syndrome shift lipids).

Lifestyle: what moves the numbers

Lifestyle changes are the foundation of prevention for everyone, and they interact with drugs rather than replace them. The factors MedlinePlus lists as raising LDL point to the main levers: diet high in saturated fat, excess weight, physical inactivity, and smoking, which lowers HDL and so reduces the removal of LDL from arteries. Which diet changes matter most is a topic of ongoing research (how fats and other nutrients are handled), and exercise has broad benefits for the heart and metabolism beyond cholesterol (the science of exercise).

The size of an effect depends on the person's starting point and genetics. For someone with familial hypercholesterolemia, lifestyle alone will rarely bring LDL into a safe range, and that is not a failing of discipline. It reflects how strongly a missing receptor controls the system.

Misconceptions

"I eat no cholesterol, so my levels should be low." Much of the body's cholesterol is made internally, and genetics, weight, and other conditions all influence LDL, so food is only one input.

"Cholesterol is a poison." It is an essential molecule. The risk comes from too much LDL over too many years, which allows particles to be trapped in artery walls.

"HDL above a certain number means I am safe." HDL is a marker, not a shield. Drugs that raise it have not reliably prevented events.

"Normal cholesterol means no heart disease risk." Lp(a), blood pressure, diabetes, smoking, inflammation, and family history all contribute, and the EAS consensus notes LDL-C can understate risk when particle number is high.

"Statins are dangerous." Like any drug, they have side effects, but in large pooled trials the excess of muscle symptoms was small and limited mainly to the first year. Anyone worried about side effects should discuss them with a clinician rather than stopping on their own.

FAQ

Q: Are eggs bad for cholesterol? A: The answer varies by person. Dietary cholesterol can raise LDL in some people and has little effect in others, and saturated fat and overall dietary pattern also matter. People with familial hypercholesterolemia, diabetes, or existing heart disease should ask their clinician for individual guidance.

Q: Why is LDL called "bad" if I need cholesterol to live? A: Because LDL particles can lodge in artery walls and start plaque formation. The cholesterol is not harmful in itself, since the body needs it. The harm comes from too much of it carried in LDL over a long time. HDL carries cholesterol back to the liver for removal.

Q: Do statins have serious side effects? A: Most people tolerate them. In a 2022 analysis of 19 placebo-controlled trials with 123,940 participants, muscle symptoms were reported by 27.1% on statins and 26.6% on placebo, and there was no significant excess after the first year. Rare serious effects exist and are listed on drug labels.

Q: Can you have heart disease with normal cholesterol? A: Yes. Lp(a), blood pressure, diabetes, smoking, inflammation, and genetics all contribute. The EAS consensus notes that LDL cholesterol can diverge from particle number in metabolic syndrome, diabetes, and high triglycerides, so apoB can sometimes reveal risk that LDL-C misses.

Q: Does raising HDL protect the heart? A: Not reliably. Evacetrapib raised HDL and lowered LDL without reducing events, and in the REVEAL trial the 9% reduction occurred alongside a drop in non-HDL cholesterol, so the effect cannot be attributed to HDL.

Q: How often should cholesterol be tested? A: MedlinePlus gives a general schedule of every five years for adults 20 and older, every one to two years for men 45 to 65 and women 55 to 65, and yearly after 65, with more frequent testing if you have heart disease, diabetes, or a family history. A clinician can tailor this to individual risk.

Q: Should I get Lp(a) measured? A: The European Atherosclerosis Society recommends measuring it at least once in adults. Roughly 20% of people are estimated to have levels above 50 mg/dL, and because it is mainly inherited, one measurement is usually informative. With no Lp(a)-specific therapy yet available, the result mainly guides how intensively to manage other risk factors.

The takeaway

The cleanest way to think about cholesterol is as a dose over time. The molecule is essential, but LDL particles that spend decades at high concentration in the blood are retained in artery walls, and that retention builds plaque. The evidence for that chain is unusually strong, with genetics and randomized trials pointing to the same conclusion, and it explains why drugs as different as statins, PCSK9 antibodies, and bempedoic acid all work in proportion to how much LDL they remove. It also explains what does not follow: raising HDL has not reliably protected anyone, and a normal panel does not rule out risk from Lp(a) or particle number. The practical message is to know your numbers, know your family history, and discuss them with a clinician who can weigh them together.

Sources

• European Atherosclerosis Society consensus statement on LDL and ASCVD, European Heart Journal, 2017
• CDC, cholesterol facts and statistics
• MedlinePlus, LDL: the "bad" cholesterol
• FDA, Leqvio (inclisiran) approval
• Evolocumab (FOURIER), NEJM 2017; Bempedoic acid (CLEAR Outcomes), NEJM 2023; Anacetrapib (REVEAL), NEJM 2017; Cholesterol Treatment Trialists' Collaboration, The Lancet 2015 and 2022; Scandinavian Simvastatin Survival Study, The Lancet 1994

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