Does fat make you fat? The story of a misconception

You are standing in front of the chilled shelf. On the left the low fat yoghurt, 0.1 percent, in friendly white. On the right the Greek one, 10 percent, in the heavy pot. And somewhere inside you sits a sentence you have never checked, because everyone says it.

Fat makes you fat.

Maybe you avoided butter for years and wondered why nothing was moving. And maybe at some point you heard that it is all the other way round: the fat is not to blame, the bread is.

Both sentences are too simple for the body you have. The first can be traced historically in detail, and it does not hold. The second is popular, but the strictest experiments do not support it. I will show you both. Including where the result does not suit me.

1. The sentence that was never tested that way

Ask yourself something different for a moment. Not whether fat makes you fat. But: how do you know that?

Most people cannot answer it. The sentence is simply there. Yet it is the translation of an entirely different question. In the 1950s the topic was not weight, it was heart attacks. The physiologist Ancel Keys from Minnesota suspected the fats in food. Out of that came the Seven Countries Study.

I do not want to belittle Keys. His team documented cleanly that this was about country averages. His colleague Henry Blackburn openly placed the study thirty years later as a hypothesis generator, not as proof.

The problem arose later. In the public translation, a heart hypothesis about saturated fatty acids became a rule about body fat. Two different questions, pushed into one sentence.

In 1977 a committee of the US Senate recommended less fat, in 1983 the United Kingdom followed. Zoë Harcombe later asked the most obvious question: which randomised trials were on the table at the time?

The work is contested: few trials, mostly secondary prevention. The same group followed up in 2016 with 62,421 people and the same pattern. Christopher Ramsden recovered the lost raw data of the Minnesota Coronary Experiment for this question. That, however, is a question of fat quality and belongs in the article on the cholesterol myth.

The fat debate on a timeline

And now you know why this sentence sounds so self evident, although it answers a question that was never asked.

2. Who paid the bill in 1967

There is one point in this story where I pause every time. Not because it is scandalous. Because it happened so undramatically. In 2016 three researchers from San Francisco published an analysis of internal documents of the Sugar Research Foundation, the research foundation of the American sugar industry.

The same group reconstructed Project 259 in 2017, an experiment in germ free rats funded by the foundation. Under a sugar rich diet an enzyme rose there that had previously been linked to bladder cancer. The project ended without publication. Animal data are not transferable. What is remarkable is how it was handled.

And now you know why the suspicion against sugar needed decades to be heard.

3. Putting it to the test: almost 49,000 women

At this point you are probably expecting the next sentence. The one that is everywhere: that the low fat recommendation made us fat.

I cannot write it. Because at some point somebody went and looked.

The same randomisation was analysed for heart and circulation over 8.1 years. For coronary heart disease the hazard ratio was 0.97, for stroke 1.02. Eight years of eating low fat, with a level of support that nobody gets in everyday life. And the curve does not move.

The highest level of evidence says the same. A Cochrane review by Lee Hooper analysed 32 randomised trials with around 54,000 people, all without an intention to lose weight. Result: minus 1.5 kg, stable over the years. In the cohort studies, mostly no link at all was found between fat intake and later body fat. Hooper L et al. Cochrane Database Syst Rev. 2015;(8):CD011834. PMID: 26250104 [Systematic Review]

And now you know why I become cautious when a single lever is meant to explain a whole era.

4. Low fat versus low carb: the duel without a winner

If you want to lose weight today, you apparently have to pick a camp. Team butter or team oats. The question has long since become a question of identity.

Luckily, somebody let both camps compete directly against each other.

DIETFITS does not stand alone. In POUNDS Lost, 811 people on four different diets all landed between minus 2.9 and minus 3.4 kg after two years. The strongest predictor was a different one and rather disarming: 0.2 kg per group session attended. Not the macro split. Attendance.

The two meta-analyses are the most honest summary of this debate. I describe ketogenic nutrition as a form of therapy separately in the article on ketogenic diets and mental illness.

And now you know why both camps can point to their studies and both still overstate the case.

5. What happens in the lab when nobody can cheat

All the studies so far have the same problem. People do not eat what is written on the sheet.

There is one place where that does not happen: the metabolic ward. People live there, every meal is weighed, energy expenditure is measured in a chamber. The metabolism researcher Kevin Hall has run several experiments there. I write the results down as they are. Partly because they contradict my own leaning.

The authors name the limits themselves: six days, 19 people, isocaloric. In 2016 the same group tested a ketogenic diet in 17 men. Energy expenditure rose by 57 to 151 kcal per day, yet the loss of body fat slowed down.

The 26 kilocalories come from an analysis by Kevin Hall and Juen Guo across 32 feeding studies. Why a calorie in the body is still not the same as a calorie is described in the article on the calorie in metabolism. Even the animal data sit crosswise: in a study in mice, of all things a higher fat share went along with more intake and more body fat. That is not transferable to you.

And now you know why I cannot write the sentence "carbohydrates are more likely to make you fat" in that blanket form, even though it feels good.

6. Where the carbohydrate insulin model stays strong

And yet. In my consultations there regularly sits someone for whom less bread and less sweet food changed everything. Not three kilos, considerably more. That cannot be explained with averages.

The explanation for it is called the carbohydrate insulin model, from David Ludwig and Cara Ebbeling. Carbohydrates with a high glycaemic load drive blood sugar up, the pancreas answers with insulin, and insulin is a storage signal. According to this model it can direct energy into the fat cells. The rest of the body might then lack it, so hunger arises and expenditure falls.

What I find remarkable is that the authors name the weakness themselves: the feeding studies so far were not strict enough to test the model. This honesty is stronger than any outside criticism. Ludwig DS, Ebbeling CB. JAMA Intern Med. 2018;178(8):1098-1103. PMID: 29971406 [Mechanism Review]

The interesting part is not the whether. It is the for whom.

Even sharper is the finding by Marc-André Cornier. He divided 21 women with obesity by their fasting insulin. The insulin sensitive ones lost 13.5 percent on a carbohydrate rich diet, the insulin resistant ones the other way round 13.4 percent on the lower carbohydrate one. Same diet, opposite result, in 21 participants. Please keep both in mind. More on this in the article on insulin resistance and weight loss.

More robust is the analysis by Mads Hjorth across three randomised trials. In one of them, people in the prediabetic range regained 5.83 kg more on a high glycaemic load, people with normal values only 1.44 kg. In a study of 164 adults after weight loss, energy expenditure in the top insulin third was 308 kcal per day higher. Ghrelin and leptin were lower, more on that in the article on leptin and insulin.

A third lens comes on top. In an Israeli investigation, 800 people wore a glucose sensor for a week, and 46,898 meals were recorded. The responses to identical meals differed considerably. More on this in 14 days of glucose sensor.

And now you know why two people with the same breakfast can tell two different stories without either of them lying.

7. Why nuts and crisps put the question differently

Nuts are about half fat. Potato crisps are starch and fat. By macronutrient logic both would have to pull in the same direction. They do the opposite.

Dariush Mozaffarian analysed three US cohorts with 120,877 initially lean people over up to 20 years. Per additional daily serving and four year period, converted from pounds: potato crisps plus 0.77 kg, sugary drinks plus 0.45 kg, nuts minus 0.26 kg, yoghurt minus 0.37 kg. The most fat rich food on the list sits right at the bottom for weight gain. Mozaffarian D et al. N Engl J Med. 2011;364(25):2392-2404. PMID: 21696306 [Cohort, n=120,877]

These are observational data, not causes. But there is an experiment on exactly this question.

Why this is so hangs on chewing time, fibre structure and satiety signals, in detail in the article on unprocessed food and satiety. Twelve experts around Arne Astrup formulated the core sentence in 2020: the health effect of a food cannot be derived from a single nutrient group. What that means for fat quality is described in the articles on omega-3 and the calorie myth.

For the carbohydrate side there is a similarly clear answer. Andrew Reynolds analysed 185 prospective and 58 clinical studies. At a high fibre intake, total mortality was 15 to 30 percent lower, with the greatest benefit at 25 to 29 grams per day.

That leaves PURE, on almost every German page the star witness against carbohydrates: 135,335 people, 18 countries, in the highest carbohydrate fifth 28 percent higher total mortality. Three things are rarely mentioned alongside. The endpoint was mortality, not weight. For cardiovascular disease no increased risk was found. And the top fifth was above 70 percent of energy, from a rice and wheat dominated diet in poor countries.

And now you know why the debate of fat versus carbohydrate ends at the checkout, but not in your body.

8. Why this debate is so charged

If you read the comments under a nutrition video, you may be surprised by the tone. Hardly any medical topic generates so much anger. There are four reasons for that, and none has anything to do with biochemistry.

First: it is about identity. What you eat hangs on family, origin, morality and often on shame. If someone attacks your way of eating, that can feel to your nervous system like an attack on you.

Second: there was a genuine breach of trust. The documents from 1967 are real. Anyone who has lived through that often mistrusts the next recommendation faster. Understandable, and quickly a blanket judgement.

Third: both camps have genuine data. Kevin Hall measures carefully. David Ludwig measures carefully. Their results do not fit together. Then it is often not the argument that decides, but belonging.

Fourth: the effects are small, the stories big. One kilo of difference after a year does not carry a book title. "The secret fattener on your plate" does. Attention rewards clarity. The body is not clear cut.

That understanding is possible is shown by a paper from 2018. David Ludwig, Walter Willett, Jeff Volek and Marian Neuhouser wrote together in Science, with positions ranging from plant focused to ketogenic. They agreed on one point: the premise that a high fat intake causes excess weight and heart disease no longer holds.

And now you know why in the next argument you should look not for the loudest answer, but for the question behind it.

9. And what does that mean for your plate?

You want to know what you will do differently tomorrow morning. I deliberately give you no macro split, because the data do not support one. What they do support are four questions.

How processed is it? The best documented lever in this text. 508 kilocalories a day, with identical macronutrients. No comparison of fat and carbohydrate reaches that order of magnitude.

How much fibre and whole grain is in it? Across 185 prospective studies the most robust quality marker for carbohydrates, clearly more robust than the glycaemic index.

What is your own glucose and insulin situation? This is where the paths part. If your fasting glucose is in the prediabetic range or your fasting insulin is high, carbohydrate quality may count for more in your case. No certainty, but an assumption that can be measured. Practical routes are described in avoiding blood sugar spikes.

What can you keep up for twelve months? In POUNDS Lost, attendance at the sessions predicted success better than any macro split. A way of eating that you hate after six weeks loses in the end against one you like. More on this in the article on the calorie deficit.

From the perspective of clinical psychoneuroimmunology a fifth level comes on top. Your blood sugar also hangs on cortisol, so on stress and sleep. Inflammatory messengers can disturb insulin signalling inside the cell. And your gut flora can help decide how much of a meal arrives in you.

What I see, and what I do not know

What I observe regularly in my consultations: people with high fasting insulin who respond strongly to fewer refined carbohydrates. People in whom the afternoon slump changes after switching to unprocessed food. And people for whom neither does much, because the driver lies in sleep, in stress or in a silent inflammation.

What I do not know: whether the insulin response is a reliable signpost. The largest study says no, several smaller ones say yes.

If while reading you noticed that you do not know your own values at all, that can be talked through calmly. An appointment can be booked below this article.

And now you know why I do not write a number onto your plate, but hand you four questions instead.

Frequently asked questions

This question in a wider context

The macronutrient debate is only one door. Behind it lie the questions that usually decide more for your weight: how your hunger is regulated, how strong your silent inflammatory load is, how your blood sugar reacts in everyday life and what happens when you build in eating breaks.