Fats and cholesterol: what has really changed

Daniel Platteau

In short: cholesterol is not a poison; it is an essential molecule that the body makes itself. The danger comes from the particles that carry it, above all LDL: the more of them there are and the longer they are around, the more the arteries clog up. This link is proven (genetics, clinical trials). On the plate, replacing part of the saturated fat (butter, fatty meat, biscuits) with unsaturated fat (olive or rapeseed oil, nuts, fish) cuts cardiovascular events by about 17%. The "new paradigms" are real but more modest than what you read: the food matters more than the isolated molecule, and the aim is lower levels, earlier. What to do? Have your cholesterol measured, and your Lp(a) at least once, then discuss it with your doctor in the light of your overall risk, not a single number.

Updated on 28 October 2026.

In January 2026, the new US dietary guidelines put butter and beef tallow on the list of "healthy fats". In September, a drug that slashed a genetic form of cholesterol, Lp(a), by up to 80% failed to reduce heart attacks. At the same time, a cholesterol-lowering pill and a new family of drugs were reaching the market. No wonder people no longer know what to believe. Here is where things stand, from the simplest to the most technical.

Fats: what are we talking about?

Dietary fats (or lipids) are mostly fatty acids, chains of carbon atoms. Their shape changes everything:

Type	Where is it found?	Effect on LDL	Level of evidence
Saturated	butter, cream, cheese, fatty meat, cured meats, coconut and palm oil, biscuits, pastries	raises it	controlled trials: solid
Monounsaturated (omega-9)	olive oil, rapeseed oil, avocado, almonds, hazelnuts	neutral or slight decrease	solid
Polyunsaturated omega-6	sunflower, corn and soybean oils, walnuts, seeds	lowers it	solid
Polyunsaturated omega-3	rapeseed, walnuts, flax (ALA); oily fish (EPA, DHA)	little effect on LDL, lower triglycerides	solid
Industrial trans	old hard margarines, partially hydrogenated oils	raises it and lowers HDL	solid: the worst

A saturated fatty acid has no double bond: it is straight, and fats rich in it are solid at room temperature (butter, lard). An unsaturated fatty acid has one or more double bonds that bend it: oils stay liquid. "Omega-3" and "omega-6" simply indicate the position of the first double bond.

Trans fats are mainly produced when an oil is hardened by partial hydrogenation. They are the most harmful. Since 2 April 2021, the European Union has limited industrial trans fats to 2 grams per 100 grams of fat in food sold to consumers (Regulation 2019/649). A little remains, naturally, in the milk and meat of ruminants.

For additives in ready meals, see our article on food additives.

Cholesterol: a friend with a transport problem

Cholesterol is a special, essential fat: it is part of the membrane of every cell and is used to make sex hormones, cortisol, vitamin D and bile. The liver produces most of it; the cholesterol on your plate (eggs, offal, shellfish) plays only a secondary role in most people. That is why EFSA has not set a reference value for dietary cholesterol, and why an egg a day is no longer demonised (read our article on eggs).

The problem lies elsewhere. Cholesterol does not mix with blood: it travels in "lorries", the lipoproteins.

LDL (low-density lipoproteins): they deliver cholesterol to the tissues. In excess, they cross the artery wall and get stuck there. This is the "bad cholesterol".
HDL (high-density): they bring cholesterol back to the liver. The "good cholesterol", but we will see that the label is misleading.
Triglycerides: another form of blood fat, which rises with sugar, alcohol, excess weight and diabetes.
ApoB: a protein present on every particle capable of clogging the arteries (LDL, VLDL remnants, Lp(a)). Measuring it amounts to counting the lorries rather than weighing their load.
Lp(a) (lipoprotein "little a"): an LDL with an extra protein attached. Its level is more than 90% set by genes and barely changes with diet. About one person in five has a high Lp(a).

Where is the real danger?

LDL particles that get stuck in the artery wall trigger local inflammation and, over the years, form an atheromatous plaque. The day a plaque cracks, a clot can block the artery: heart attack or stroke.

That LDL is a cause, and not a mere bystander, is no longer debated by scientific societies. The European Atherosclerosis Society established it in 2017 by bringing together three types of evidence: genetic studies (people born with low LDL have far fewer heart attacks), observational studies and drug trials. In those trials, every 1 mmol/L (about 39 mg/dL) reduction in LDL on a statin cuts major cardiovascular events by about 22%.

Two important nuances:

Duration is what counts. A moderately high LDL for 40 years can damage the arteries as much as, or more than, a very high LDL for a few years. Hence the new idea of acting earlier.
Cholesterol is not the only factor. Smoking, diabetes, high blood pressure, abdominal fat and a sedentary lifestyle weigh as much or more. European doctors therefore reason in terms of overall risk (the SCORE2 calculator, and SCORE2-OP after 70), not an isolated number.

Saturated fat: guilty or acquitted?

This is the heart of the controversy. The story begins with the American physiologist Ancel Keys.

The Seven Countries Study was observational: it showed an association between saturated fat and heart disease, not proof. We also know that in 1967, the US sugar industry funded Harvard researchers for a review, published in the New England Journal of Medicine, that played down the role of sugar and blamed fat (documents published in 2016 in JAMA Internal Medicine). These two facts feed the idea that "it was all wrong". That is not what more recent studies show.

What the trials say. The 2020 Cochrane review (15 trials, more than 56,000 participants) concludes that cutting saturated fat for at least two years reduces cardiovascular events (heart attacks, strokes, etc.) by about 17%, with a moderate level of evidence. The effect on mortality is small or nil. And the benefit depends on the replacement: it appears when saturated fat is replaced with polyunsaturated fat or with good-quality carbohydrates. Replacing butter with white bread and sugar does nothing.

What the authorities recommend. The WHO (July 2023) advises limiting saturated fat to 10% of calories and trans fat to 1%, replacing them with unsaturated fats or fibre-rich carbohydrates. EFSA asks for them to be kept "as low as possible" within a balanced diet.

How are Belgians doing? According to Sciensano's food consumption survey (2022-2023), saturated fat accounts on average for 14% of calories, and 92% of the population exceeds 10%. It comes mainly from dairy products (29%), meat (19%), fats and oils (14%) and cakes and biscuits (14%).

The real change: the food rather than the molecule

The paradigm that is really shifting is that of the food matrix. Not all foods rich in saturated fat are equal. In observational studies, cheese and yoghurt are not associated with more heart disease, whereas processed meat clearly is. A 2020 review in the Journal of the American College of Cardiology (Astrup and colleagues) therefore proposes food-based recommendations rather than a numerical ceiling. Its authors, some of whom have links with the dairy industry, do not claim that butter protects the heart.

In short: saturated fat is not a poison, but eating less of it, in favour of unsaturated fat, remains useful. What has changed is that we look at the whole food.

Butter, tallow and seed oils: the new fat war

On social media, the trend is reversed: butter and tallow are supposedly "natural", while seed oils (sunflower, rapeseed, soybean, corn) are said to be toxic and inflammatory. The American MAHA movement ("Make America Healthy Again"), led by Health Secretary Robert F. Kennedy Jr., has made it a crusade.

The 2025-2030 US dietary guidelines, published on 7 January 2026, bear its mark: they list butter and beef tallow among acceptable cooking fats, alongside olive oil, and favour full-fat dairy. Yet they keep the 10% limit for saturated fat, which is hard to reconcile with that advice. The American Heart Association reiterated that butter, lard and tallow should be limited.

What does science say about seed oils?

Their main fatty acid, linoleic acid (omega-6), lowers LDL. Part of the effect in the Cochrane review rests on it.
The idea that it fuels inflammation comes mainly from animal studies and biochemical reasoning. In humans, an analysis presented in 2025 on nearly 1,900 people found the opposite: the more linoleic acid in the blood, the lower the inflammation markers. It is a cross-sectional study (a snapshot at one point in time), to be confirmed by trials.
Rapeseed oil, widely used in Belgium, provides both omega-6 and omega-3. Olive oil has the PREDIMED trial on its side: in Spain, a Mediterranean diet enriched with extra virgin olive oil or nuts reduced cardiovascular events by about 30% in people at risk (trial republished in 2018 after its methods were corrected).

The real problem with seed oils is how industry uses them: repeated frying, crisps, ultra-processed meals. The oil gets blamed for what belongs to the food.

True or false: common beliefs

Claim	Verdict	What the studies show
"Dietary cholesterol (eggs) raises blood cholesterol"	Mostly false	modest effect in most people; saturated fat weighs more
"HDL protects: the higher the better"	False	drugs that raise HDL did not reduce heart attacks; a very high HDL is not protective
"Saturated fat is innocent"	False	replacing it with unsaturated fat reduces cardiovascular events (Cochrane, moderate)
"Seed oils are toxic"	False	they lower LDL; human studies do not show more inflammation
"Cholesterol is hereditary, diet can do nothing"	Half true	Lp(a) and familial hypercholesterolaemia are genetic; ordinary LDL responds to diet (10 to 15%)
"Statins do more harm than good"	False	in blinded trials, most muscle pain is not caused by the statin
"Low cholesterol makes you live longer"	Not proven on its own	lowering LDL reduces heart attacks and strokes; the effect on lifespan depends on baseline risk

Does this concern me?

A lipid profile (blood test) gives total cholesterol, LDL, HDL and triglycerides. Interpretation depends on your risk, which the doctor assesses using age, smoking, blood pressure, diabetes, kidneys and family history.

Situation	LDL target (European guidelines)
Low risk	below 116 mg/dL (3.0 mmol/L)
Moderate risk	below 100 mg/dL (2.6 mmol/L)
High risk	below 70 mg/dL (1.8 mmol/L) and a reduction of at least 50%
Very high risk (heart attack, stroke, diabetes with organ damage…)	below 55 mg/dL (1.4 mmol/L) and a reduction of at least 50%

Some signs that warrant talking about it without delay:

a close relative (man before 55, woman before 60) who had a heart attack or stroke;
an LDL above 190 mg/dL, which may point to familial hypercholesterolaemia (about one person in 300, often undiagnosed);
diabetes, kidney disease, pre-eclampsia or early menopause in your history.

Lp(a), at least once in your life. The European (2025 update) and American (March 2026) guidelines recommend measuring it once in adulthood. Above 50 mg/dL (about 105 nmol/L), risk is increased; a patient at moderate risk then moves into the high-risk category. Since Lp(a) does not change, one measurement is enough.

Medicines: what works

Diet lowers LDL by around 10 to 15%. When risk is high, that is not enough.

Medicine	How it works	LDL reduction	Evidence on heart attacks and strokes
Statins (atorvastatin, rosuvastatin…)	slow the liver's production of cholesterol	30 to over 50%	yes, dozens of trials
Ezetimibe	reduces intestinal absorption	about 20%	yes (added to a statin)
Bempedoic acid	slows production, without acting in muscle	about 20%	yes (CLEAR Outcomes trial, 2023)
Anti-PCSK9 antibodies (evolocumab, alirocumab), injection every 2 to 4 weeks	increase the receptors that capture LDL	about 60%	yes
Inclisiran, injection twice a year	same target, by "switching off" PCSK9 in the liver	about 50%	trials ongoing

Statins and muscles. This is the most frequent complaint. An analysis of 23 large double-blind trials (155,000 patients, 2022) shows that muscle pain is almost as common on placebo as on a statin: the statin accounts for only about one case in fifteen in the first year. The "nocebo" effect (you expect a side effect, so you feel it) is therefore significant. Genuine serious muscle damage exists but is rare. If a statin bothers you, changing the drug or the dose often solves the problem.

In Belgium, statins and ezetimibe are common and inexpensive; anti-PCSK9 injections are reimbursed only under conditions, for well-defined patients.

What's new in 2025-2026

An anti-PCSK9 that works before the first heart attack. The VESALIUS-CV trial (12,257 high-risk patients with no prior heart attack or stroke, followed for 4.6 years) showed in November 2025 that evolocumab reduces the risk of coronary death, heart attack or ischaemic stroke by 25% (6.2% versus 8.0%). It is the first evidence of its kind in so-called "primary" prevention.

The first anti-PCSK9 pill. The US FDA approved enlicitide (Lipfendra, Merck) in July 2026, a once-daily tablet that lowers LDL by about 56% more than placebo. The trial that will show whether it reduces heart attacks (more than 14,500 participants) is still awaited. To our knowledge, it is not authorised in Europe to date.

A new class in Europe. On 21 September 2026, the European Commission authorised obicetrapib (Ubeslo, and Evlarco in combination with ezetimibe), a CETP inhibitor. This family had suffered resounding failures, including torcetrapib, which increased mortality. Obicetrapib lowers LDL by about a third and Lp(a) by about a third as well. The trial meant to prove a reduction in heart attacks (PREVAIL, more than 9,000 patients) has not yet reported.

The Lp(a) cold shower. On 4 September 2026, Novartis announced that pelacarsen, a monthly injection that slashes Lp(a), did not reduce cardiovascular events in the Lp(a)HORIZON trial (8,323 patients with existing heart disease). The full results have not yet been published. Should we conclude that Lp(a) is not dangerous? Not yet: the patients were already very well treated (average LDL around 66 mg/dL), the trial may have been too short or too ambitious, and the genetic evidence remains very strong. Other molecules are in trials: olpasiran (Amgen, results expected in 2028) and lepodisiran (Lilly, 2029).

General practitioner Brad Stanfield analyses this failure in a clear video:

Statins after 75: stop? A French trial published in August 2026 in The Lancet Healthy Longevity followed for three years just over 1,000 people aged around 80, without cardiovascular disease, who were taking a statin for prevention. Stopping did not increase mortality (7.2% versus 7.9%). But the trial recruited fewer patients than planned, and heart attacks were slightly more frequent among those who had stopped (2.1% versus 1.4%). It opens the door to case-by-case decisions, not to stopping across the board, and never without talking to your doctor. After a heart attack or stroke, the question does not arise: you continue.

Lower, earlier. The US guidelines of March 2026 align with the European ones on targets (below 55 mg/dL for very high-risk patients) and stress early screening in young adults with very high LDL or a family history.

Food supplements: caution

Plant sterols and stanols (enriched spreads, yoghurts): 1.5 to 3 g a day lower LDL by 7 to 12.5% in two to three weeks (claim authorised by the EU). No trial has shown a reduction in heart attacks. Useful as an add-on; the label advises against them for pregnant or breastfeeding women and children under 5.
Oat and barley beta-glucans: at least 3 g a day lower LDL slightly (EFSA claim); the content varies a lot between oat flakes and portions.
Omega-3 capsules: they lower triglycerides but have not reduced cardiovascular events in most trials. They increase the risk of atrial fibrillation (a heart rhythm disorder), especially above 1 g a day. A high-dose prescription form (icosapent ethyl) is reserved for certain high-risk patients. Eating oily fish once or twice a week remains the basic advice.

The 2025 European guidelines are clear: supplements and vitamins are not recommended to lower LDL or cardiovascular risk.

In practice

On the plate:

cook with olive or rapeseed oil; keep butter for flavour, not as your basic fat;
a handful of walnuts, almonds or hazelnuts a day;
oily fish (sardines, mackerel, salmon, herring) once or twice a week;
pulses, oat flakes, vegetables, fruit: their fibre traps some of the cholesterol;
limit cured meats, pastries, biscuits and ultra-processed meals (see also our article on sugar);
cheese and yoghurt: not forbidden, in reasonable amounts.

The rest matters just as much: stop smoking, move for 150 minutes a week, keep an eye on your blood pressure and waist size.

When to see a doctor:

for a first lipid profile if you have never had one, and for a one-time Lp(a) test;
if a relative had a heart event at a young age;
if a statin bothers you: do not stop it on your own; another molecule or another dose often exists.

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