People call cholesterol the “silent killer”. A disorder of fat metabolism shows up, for a very long time, only in blood tests. It doesn’t hurt, it doesn’t limit you, and often it stays that way right up to the moment of catastrophe – a heart attack or a stroke.

Correia and co-authors (2021) put it plainly: the disease runs without symptoms until the cardiovascular event itself.

The mysterious numbers

In a lipid panel we look at four main numbers. Low-density lipoprotein cholesterol, LDL, is the “bad cholesterol”: its excess is what starts the inflammation in the vessel wall that later grows into an atherosclerotic plaque. Triglycerides, TG, are the transport form of fat, and they react very sensitively to what you eat, especially sugar and alcohol. High-density lipoprotein, HDL, is the conditionally “good cholesterol”. And there is lipoprotein (a), Lp(a), which is set by your genes and hardly depends on lifestyle at all.

Where a lipid disorder comes from

Not every hyperlipidemia depends on what you eat.

Familial hypercholesterolemia occurs in one person out of 250. That is not rare, that is one person in an average office. In these people the gene for the LDL receptor, or the APOB protein, or PCSK9 is broken, and the liver physically cannot clear cholesterol from the blood. No diet will help here. Their LDL is above 190 mg/dL from childhood, early heart attacks run in their families, and here, with all my love for drug-free treatment, there is nothing for me to do. Pharmacological intervention in familial hyperlipidemia is necessary, and fairly early. If someone in your family had an early heart attack or stroke (early means a heart attack or stroke in a man before 55 or a woman before 65), you need to get a lipid panel done and be followed by a doctor.

Acquired dyslipidemia is more common. Brandts and co-authors (2026) call it diabetic dyslipidemia, although the name is not quite accurate: acquired dyslipidemia is not always accompanied by diabetes. But it is characterised by visceral fat around the belly, insulin resistance and, as a result, high triglycerides, small dense LDL particles, which are the ones mostly building plaques on vessel walls, and low HDL.

The 2026 ACC/AHA guideline (Blumenthal et al.) also lists among the causes of acquired dyslipidemia: hypothyroidism, kidney disease, certain medications (glucocorticoids, thiazide diuretics, estrogens, atypical antipsychotics), pregnancy and the menopausal transition.

Let’s stop here for a minute and sort out what cholesterol actually is and why we need it. Cholesterol is not a poison, it is building material. The membranes of every cell in the body are made of it, the liver makes bile acids from it, without which fat cannot be digested, and sex hormones, cortisol and vitamin D are synthesised from it. The body takes it so seriously that it doesn’t trust food: roughly three quarters of your cholesterol is made by the body itself, mostly in the liver, and only about a quarter comes from what you eat. Which is why, by the way, a cholesterol-free diet on its own does not solve much: the liver simply increases its own production.

Cholesterol leaves the body by one route: the liver turns it into bile, bile goes into the gut, part is reabsorbed and part leaves the body. Soluble fibre and plant sterols work exactly here, they interfere with reabsorption.

Triglycerides are built differently. They are storage fat, three fatty acids on a glycerol backbone. Part comes from dietary fat, but a large part the liver assembles itself from excess carbohydrates and alcohol. An extra bun and an extra glass turn into triglycerides within hours. Physical activity burns them first: a working muscle switches on the enzyme lipoprotein lipase, which pulls triglycerides out of the blood as fuel. That is why movement lowers TG so noticeably and affects LDL so modestly.

Where is the line between what is necessary and what is pathology? It lies not in the substance itself but in the amount and the packaging. Cholesterol travels in the blood inside lipoproteins, and the danger is not cholesterol as such but an excess of LDL particles that get stuck in the vessel wall. The generally accepted thresholds are: LDL preferably below 100 mg/dL, triglycerides below 150 mg/dL, HDL above 40 mg/dL in men and 50 in women. LDL of 190 mg/dL and above is what the 2026 ACC/AHA guideline calls severe hypercholesterolemia. But the same LDL of 130 in a twenty-year-old athlete and in a sixty-year-old smoker with diabetes means a completely different risk, and that is exactly why decisions are made not on a number but on the whole picture.

What to pay attention to

When changes show up in a lipid panel, it is very important to see the full picture:

• Family history
• Chronic diseases
• Long-term medications
• The calendar of women’s cycles
• Eating habits
• Routine physical activity

The window of opportunity in treatment

As I said, in hereditary dyslipidemia drug therapy is necessary. But it is important to remember that the same person can have both the hereditary and the acquired form.

Acquired dyslipidemia calls for a more thoughtful attitude than simply taking the pills a doctor prescribed.

The guidelines of all major societies, the American one of 2026 (ACC/AHA, Blumenthal et al.), the endocrine one (Newman et al., 2020), the European practical recommendations (Siegel et al., 2026), call lifestyle change the first line of therapy. Not a “useful addition” to drug therapy, but precisely the first line.

In people who respond to diet, triglycerides fall by more than 70% from changing eating habits alone. Losing 5-10% of body weight lowers them by 20-30%; about 4 mg/dL for every kilogram lost. To achieve that you need to cut out added sugar, white flour and alcohol.

With LDL it is a little more complicated. The meta-analysis of 148 randomised trials that the guideline relies on shows a less impressive change in the lab numbers: LDL falls by 7 mg/dL from physical activity, HDL rises by 2 mg/dL and triglycerides fall by 8 mg/dL.

But the clinical picture changes noticeably. The PREDIMED trial (Estruch et al., 2018) shows the following. 7,447 people aged 55-80 at high cardiovascular risk but without heart disease at enrollment were randomly split into three groups. Two received a Mediterranean diet, one with added extra-virgin olive oil (about 50 mL a day), the other with nuts (30 g a day); the third, control, group got standard advice to cut down on fat. The trial was stopped early, after 4.8 years: in both Mediterranean groups there were about 30% fewer heart attacks, strokes and cardiac deaths than in the control group.

What exactly should change on the plate? The general principle is called a plant-based dietary pattern: the basis of the diet is vegetables, legumes, whole grains, nuts, olive oil and fish, while red and processed meat, sweets and white flour move to the margins. Three well-studied styles fit this principle: the Mediterranean diet (the only one with a proven reduction in heart attacks in a randomised trial, PREDIMED), DASH, designed to lower blood pressure, and vegetarian. Sugar and refined carbohydrates need to go first: it is they, not fat, that drive triglycerides up. Alcohol is unhelpful in any dyslipidemia, and with high triglycerides it is absolutely contraindicated, because it turns into triglycerides directly. If there is excess weight, the goal is minus 5% of the starting weight: that alone is enough for triglycerides to fall by 20-30%.

• Saturated fat (fatty meat, butter, cheese, coconut and palm oil): no more than 5-6% of daily calories (Endocrine Society, Newman et al., 2020). At 2,000 kcal a day that is 11-13 g, roughly one serving of fatty cheese. This is the main dietary lever for LDL.
• Trans fats (margarines, industrial baked goods, fast food): zero. They raise LDL and lower HDL at the same time.
• Added sugar: no more than 10% of calories, better below 5% (WHO, 2015). At 2,000 kcal that is 25-50 g, and one can of sugary soda already holds about 35 g. This is the main dietary lever for triglycerides.
• Fibre: 25-30 g a day, of which 5-10 g soluble (oats, barley, legumes, psyllium, apples). Soluble fibre binds bile acids in the gut and lowers LDL by about 4-5%.
• Nuts: 30 g a day, unsalted and unsweetened, as in PREDIMED.
• Extra-virgin olive oil instead of butter: in PREDIMED that was about 50 mL a day.
• Omega-3 (EPA and DHA): from oily fish twice a week, and in prescription doses of 2-4 g a day they lower triglycerides by 20-30%.
• Alcohol: with triglycerides above 500 mg/dL, complete abstinence.

Physical activity: at least 150 minutes of moderate aerobic exercise a week or 75-150 minutes of vigorous exercise (aerobic exercise is any movement in which large muscles work rhythmically and without stopping: brisk walking, swimming, cycling, dancing. The easiest way to check intensity is the talk test: at moderate intensity you can talk but not sing, at vigorous intensity you can say a few words and then have to catch your breath. By heart rate, moderate is about 50-70% of maximum and vigorous 70-85%, where the maximum is roughly 220 minus your age), plus strength training twice a week (strength training is exercise against resistance, where a muscle works against a load: your own body weight, dumbbells, a resistance band, a machine; squats, push-ups and climbing stairs with effort also count). One more very important recommendation is to stop smoking. One year after the last cigarette the excess risk of coronary heart disease is halved, and after 15 years it equals the risk of someone who never smoked (WHO, 2020; US Surgeon General’s report, 1990).

Treatment through lifestyle change, as we said, is the first line in acquired dyslipidemia. In the hereditary form, and in cases where lifestyle change alone turns out to be insufficient, drug therapy is added.

Cholesterol-regulating drugs, and statins above all, have grown a huge crop of myths. Like any pill, they have side effects, but let’s look at the numbers rather than at internet comments.

Muscle pain, the most common reason people stop a statin. In 2022 the Cholesterol Treatment Trialists’ Collaboration published in the Lancet an analysis of 23 randomised double-blind trials, almost 155,000 people. Muscle symptoms were reported by 27.1% of those taking a statin and 26.6% of those taking placebo. In other words, of 15 people whose muscles hurt on a statin, in 14 the pain has nothing to do with the statin. The small real excess falls in the first year of treatment; after that there is no difference from placebo. Serious muscle injury with a rise in enzymes occurs in fewer than 1 in 10,000 people a year, rhabdomyolysis in about 2 in 100,000.

Diabetes. The meta-analysis by Sattar and co-authors (Lancet, 2010), 13 trials, more than 91,000 people: over four years diabetes developed in 4.9% of those taking a statin and 4.5% of those not taking one. One additional case per 255 people taking a statin for four years, and mostly in those already on the threshold of diabetes. The 2026 ACC/AHA guideline states plainly that this is no reason to refuse a statin: the benefit for the heart outweighs it.

Liver. In stable chronic liver disease, including fatty liver, statins are not contraindicated. They are contraindicated in acute liver failure, decompensated cirrhosis and during breastfeeding.

Intolerance. Roughly one patient in ten cannot tolerate the maximum statin dose, and it is exactly for such cases that drugs of other classes exist, more on them below.

But I believe that fearing statins more than a heart attack is a mistake. In each specific case the balance between the risks has to be found.

The decision to treat is made not on numerical changes in the tests but on overall risk: age, blood pressure, diabetes, smoking, events that have already happened. The PREVENT calculator. This is the American Heart Association’s 2023 calculator: from age, sex, total cholesterol and HDL, blood pressure, body mass index, kidney function and smoking it estimates the risk of a cardiovascular event over the next 10 and 30 years. It is designed for people aged 30-79 who have not yet had a heart attack, stroke or heart failure. I have built a version of it from the published equations, and it is right here in this article: age, sex, height and weight, two numbers from your lipid panel, blood pressure, kidney function and four checkboxes. You get your 10-year risk, and up to age 60 your 30-year risk as well, and you see it not only as a number but as a hundred people with your figures, among whom those who will have an event are marked. Nothing is sent anywhere, everything is calculated in your browser.

You can fill in the calculator yourself, but what to do with the result should be decided together with your doctor: family history, lipoprotein (a) and vascular imaging are not in the formula. Statins (in Israel: Lipitor, Litorva, Torid, Crestor, Simovil and their generics) remain the second line after lifestyle change. If they do not help enough or are not tolerated, ezetimibe, PCSK9 inhibitors, bempedoic acid and inclisiran are added (in Israel: Ezetrol, Repatha and Praluent, Nilemdo, Leqvio). These are well-studied drugs, and each of them has been shown to reduce not only the numbers but clinical outcomes.

The pill does not solve the problem

Everything written above you most likely knew before, and there are plenty of sources where this information is given in no less, and often more, professional language.

Yet I am writing this article anyway. Why?

Because it is endlessly important to me to get one main idea across to you: a statin lowers LDL. And that’s it!

It does not remove visceral fat. It does not fix insulin resistance. It does not lower triglycerides. It does not remove the inflammation that lives in fat tissue.

That is, the causes of the dyslipidemia remain.

With triglycerides the picture is no rosier: fibrates, which lower them, add no extra heart protection when given on top of a statin.

The 2026 ACC/AHA guideline puts it this way: lifestyle is the basis of therapy, not an alternative.

Lifestyle change and medication are not an “either-or” choice, they are two independent treatment methods that must be combined.

Separately I want to remind you that people with hereditary dyslipidemia also, most of the time, carry the risk factors for the acquired form, and the statement I often hear from patients, “My cholesterol is hereditary, I don’t need a diet”, is a delusion, and a very dangerous one.

The ostrich strategy

One can, of course, decide that numbers are only numbers, and if a person feels well, nothing needs to be done. But the treachery of dyslipidemia is precisely that clinically it is not felt at all until the moment a plaque blocks most of the vessel or ruptures, and a clot forms at the rupture, threatening a heart attack or a stroke. Untreated familial hypercholesterolemia leads to a heart attack as early as forty or fifty. Triglycerides above 1,000 mg/dL lead to severe pancreatitis. Untreated acquired dyslipidemia almost always comes together with other vascular risk factors and turns into “Russian roulette”, where a vascular catastrophe is only a matter of time.

Conclusion

So here is our version of “running away from a heart attack”:

This article is educational and does not replace a consultation with your doctor.