John Yudkin and Sugar: Early Insights into Metabolism and Cardiovascular Risks

# HE ACCUSED SUGAR 50 YEARS AGO
## Did Professor John Yudkin understand something nutrition would only rediscover decades later?

**by Laurent Glatz – for Athletic Carnivore**

Long before the modern debates about insulin, fructose, metabolic fatty liver, or triglycerides, a British professor was already asking a troubling question:

**what if part of the cardiovascular problem attributed to fats actually came from sugar?**

This researcher was **John Yudkin**.

And contrary to the sometimes simplistic image given today, Yudkin was not just "the man who said sugar was bad." His work was far more biologically interesting.

He focused on **sucrose**, table sugar, seeking to understand why its consumption could alter triglycerides, insulin, weight, and even the behavior of blood platelets.

In other words, he was no longer just looking at what a person ate.

He was looking at **what their metabolism did with what they ate**.

WHO WAS JOHN YUDKIN?

Born in 1910, John Yudkin was simultaneously a **physiologist, biochemist, physician, and nutrition researcher**. He studied physiology and biochemistry, earned a doctorate and a medical degree, before working in nutritional research. ([history.rcp.ac.uk](https://history.rcp.ac.uk/inspiring-physicians/john-yudkin))

In 1945, he took the chair of physiology at **Queen Elizabeth College in London**.

Then something quite remarkable happened.

At a time when academic nutrition was still an emerging discipline, Yudkin helped establish in 1954 the first British university courses specifically dedicated to nutrition. He became the UK’s first professor of nutrition. ([history.rcp.ac.uk](https://history.rcp.ac.uk/inspiring-physicians/john-yudkin))

So he was not an outsider observing nutrition.

**He was literally helping build the discipline.**

And from the 1950s and 1960s, two topics gradually dominated his work: obesity and the metabolic consequences of high sugar consumption. ([kcl.ac.uk](https://www.kcl.ac.uk/archive/publications/comment-archive/pdfs/2003/comment-145.pdf))

WHAT YUDKIN REALLY SAID

The debate of that era is often oversimplified:

**Ancel Keys blamed fat. John Yudkin blamed sugar.**

Historically, this is convenient.

Biologically, it’s far too simplistic.

Yudkin was not merely saying:

**"Eat sugar and your arteries clog."**

He was trying to show that sucrose could trigger a series of **intermediate metabolic changes** potentially important in cardiovascular diseases.

That’s a very different story.

In 1964, he already published in *The Lancet* an article titled *Dietary Fat and Dietary Sugar in Relation to Ischaemic Heart-Disease and Diabetes*. That same year, he published with John Roddy a study specifically on sucrose consumption levels in patients with occlusive atherosclerotic disease. ([pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/14149218/?utm_source=chatgpt.com))

But what happened a few years later deserves particular attention.

IN 1969, YUDKIN MADE A SURPRISINGLY MODERN OBSERVATION

Yudkin and Stephen Szanto studied **19 apparently healthy men**.

They subjected them to successive 14-day periods of low and high sucrose consumption.

Then they measured several parameters.

Cholesterol?

No significant change.

Blood phospholipids?

No significant change.

Glucose tolerance?

No significant change.

But **triglycerides increased significantly in all 19 participants** when sucrose intake rose. ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC2466139/?page=0))

This is already extremely interesting.

Because it means lipid metabolism can be strongly altered without immediately seeing a dramatic change in cholesterol or even blood sugar.

But Yudkin discovered something even more intriguing.

In **6 of the 19 men**, the high-sucrose diet also caused a marked increase in insulin.

And these same six individuals also showed more weight gain and a significant increase in platelet adhesiveness. ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC2466139/?page=0))

When participants returned to their usual diet, these changes almost completely disappeared within two weeks.

Yudkin then formulated a particularly interesting hypothesis:

**the sugar problem might not be the same for everyone.**

He even proposed that **sucrose-induced hyperinsulinemia** might be more relevant to understanding coronary risk than changes in blood lipids alone. ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC2466139/?page=0&utm_source=chatgpt.com))

This was **1969**.

The modern concept of metabolic syndrome was not yet structured as it is today.

Insulin resistance had not yet taken the central place it would decades later.

Yet Yudkin was already simultaneously looking at:

**sugar → insulin → triglycerides → weight gain → platelets → individual metabolic terrain.**

This is what makes his work remarkable.

WHY CAN SUGAR INCREASE TRIGLYCERIDES?

Here modern biology allows us to go much further than Yudkin.

Table sugar, **sucrose**, consists of two molecules linked together:

**one glucose molecule + one fructose molecule.**

Once digested, sucrose is split in two.

Glucose and fructose then follow different metabolic pathways.

Fructose enters intestinal cells via a transporter called **GLUT5**. A significant portion can be metabolized directly by the intestine.

But when fructose intake is high, more reaches the portal circulation and thus the **liver**. ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC11257042/?utm_source=chatgpt.com))

And here the mechanism becomes particularly interesting.

Inside the hepatocyte, the liver cell, fructose can be rapidly phosphorylated by an enzyme called **ketohexokinase**, or KHK.

Fructose then becomes **fructose-1-phosphate**.

Why is this important?

Because this pathway quickly provides three-carbon molecules that feed several metabolic routes.

Some can be used to make glucose.

Some provide glycerol.

Some produce acetyl-CoA.

And acetyl-CoA is precisely a building block for synthesizing **fatty acids**.

In other words:

**under certain conditions, sugar can be converted into fat in the liver.**

This process is called **de novo lipogenesis**.

YUDKIN HAD ALREADY TOUCHED ON THIS MECHANISM

In 1972, Yudkin’s team published a particularly interesting experiment in rats.

The researchers compared the effect of different carbohydrates on the activity of **fatty acid synthetase**, the enzyme complex responsible for fatty acid synthesis.

When animals received sucrose instead of starch, the activity of this fat-synthesizing machinery increased in the liver.

And this increase appeared rapidly: **within 18 hours after introducing sucrose**. ([pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/4643329/?utm_source=chatgpt.com))

At the time, obviously, Yudkin did not have the full molecular mapping we have today.

But he was already experimentally observing something fundamental:

**two carbohydrate sources do not necessarily produce the exact same metabolic response.**

Fifty years later, we have much more sophisticated methods to directly measure liver fat production.

And the results are very interesting.

A MODERN STUDY CONFIRMS PART OF THE MECHANISM

In 2021, a randomized trial involving **94 healthy men** compared for seven weeks drinks containing glucose, fructose, or sucrose.

Groups consuming fructose or sucrose showed about **twice the fractional hepatic synthesis of new fatty acids** compared to the control group.

This phenomenon was not significantly observed with glucose alone. ([pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/33684506/?utm_source=chatgpt.com))

This is a crucial detail.

Saying:

**"all carbohydrates end up as glucose"**

is biologically far too simplistic.

Glucose and fructose share some pathways, but their metabolic handling is not identical.

And the liver is particularly central when a significant fructose load arrives regularly.

SO WHY DO TRIGLYCERIDES RISE?

Imagine the liver as a factory.

When energy arrives in amounts matching needs, it can be used or stored.

When substrates arrive in excess, the factory can start producing more fatty acids.

These fatty acids are combined with glycerol to produce **triglycerides**.

The liver can then package them into particles called **VLDL** and send them into the bloodstream.

This is one reason why a sugar-rich diet can, under certain conditions, be accompanied by increased triglycerides.

And this is exactly the parameter that changed in **the 19 men studied by Yudkin in 1969**. ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC2466139/?page=0&utm_source=chatgpt.com))

However, a crucial nuance must be added.

Modern data show that fructose’s effect becomes particularly evident when it contributes to an **energy surplus**.

In a meta-analysis of controlled feeding trials, isocaloric replacement of other carbohydrates with fructose did not significantly alter triglycerides. However, when fructose was added to the diet creating a caloric surplus, triglycerides increased. ([pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/26358358/?utm_source=chatgpt.com))

So no:

**a single fructose molecule is not magically converted into fat the moment it hits your intestine.**

Quantity, food form, frequency, physical activity, and especially energy balance matter.

But the opposite is also false:

**sugar is not metabolically neutral just because it has calories like any other.**

AND INSULIN? THIS MAY BE WHERE YUDKIN WAS MOST AHEAD OF HIS TIME

Yudkin was not only interested in triglycerides.

He noticed that some of his subjects developed a much stronger insulin response under high sucrose consumption.

He then developed the idea that some individuals might be **more susceptible than others** to the metabolic consequences of high sugar intake. ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC2466139/?page=0&utm_source=chatgpt.com))

A second study on men with peripheral vascular disease showed their sucrose consumption correlated with insulin levels and platelet adhesiveness. This association was not found in men without vascular disease or predisposing factors like hypertension. ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC2466141/?page=-1&utm_source=chatgpt.com))

Yudkin was beginning to think in terms of **metabolic terrain**.

Same food.

Same sugar.

Different response.

This is an extremely current idea.

WHY WAS HE INTERESTED IN PLATELETS?

Platelets are tiny blood components involved in clotting.

When you cut yourself, they become sticky, aggregate, and help form the plug that stops bleeding.

This is essential for survival.

But in an artery already affected by atherosclerosis, platelet activation can also contribute to forming a **thrombus**, the clot that can abruptly block blood flow.

Yudkin wondered if an environment combining hyperinsulinemia, lipid changes, and increased platelet adhesiveness could contribute to an unfavorable cardiovascular terrain.

The hypothesis was intelligent.

However, it was not proof that sugar directly causes heart attacks.

And this distinction is essential.

DID YUDKIN THEN "HAVE IT RIGHT" AGAINST FAT?

Presenting it that way would fall into exactly the trap to avoid.

Cardiovascular disease does not have **a single dietary switch**.

Yudkin did not prove sucrose was the sole cause of atherosclerosis.

And current data do not justify replacing:

**"fat clogs arteries"**

with:

**"sugar clogs arteries."**

That would simply swap one slogan for another.

Atherosclerosis involves ApoB-containing lipoproteins, vascular inflammation, blood pressure, smoking, diabetes, genetics, and many metabolic factors.

Similarly, modern data on sugar reveal a more complex reality than "sugar = disease." A large *BMJ* review published in 2023 found many unfavorable associations between high sugar intake, especially from **sugary drinks**, and various metabolic or cardiovascular outcomes, but the quality of evidence varies widely by outcome. ([bmj.com](https://www.bmj.com/content/381/bmj-2022-071609?utm_source=chatgpt.com))

What Yudkin probably understood very early was more subtle:

**refined sugar, especially when consumed regularly and in large amounts, can profoundly alter the metabolic environment without necessarily causing immediate blood sugar spikes.**

That is the truly interesting part.

YOU CAN HAVE "NORMAL" BLOOD SUGAR AND ALREADY HAVE A DIFFERENT METABOLIC RESPONSE

Back to his 1969 experiment.

This is probably one of the most important points in the entire article.

High sucrose consumption did not significantly worsen glucose tolerance.

Yet:

**triglycerides rose in all participants, and insulin rose sharply in some.** ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC2466139/?page=0))

In other words, if you look only at glucose, you risk missing part of the picture.

The pancreas can increase insulin production to keep glucose within an apparently reassuring range.

It’s like perfectly maintaining a pool’s water level by running the pump twice as fast.

If you look only at the water height, everything seems normal.

But you haven’t looked at **the effort required to maintain that normality**.

That’s precisely why an isolated blood sugar measurement never tells the whole metabolic story.

AND THIS IS WHERE THE LINK WITH THE CARNIVORE DIET BECOMES INTERESTING

When someone switches from a diet rich in sweets, bread, cereals, desserts, sodas, or ultra-processed foods to a carnivore diet, they almost mechanically eliminate **sucrose and the vast majority of added sugars**.

They simultaneously change:

the carbohydrate load,

the insulin response,

the amount of fructose reaching the liver,

the energy density of ultra-processed foods,

the satiety,

the frequency of meals,

and often spontaneous energy intake.

If their triglycerides drop, their hunger decreases, or their waist circumference shrinks, simply saying:

**"it’s thanks to the meat"**

would be scientifically as poor as saying:

**"it was all because of fat."**

The real question is:

**what mechanism changed in that person?**

This is exactly where Yudkin remains relevant more than fifty years after his work.

He was no longer just looking at the food.

He was beginning to look at **the biological response to the food**.

And above all, he observed something we still often forget:

**two people exposed to the same sugar may not produce the same metabolic response.**

At this stage, the useful question is not whether "sugar is toxic" or "all carbs are bad."

The question becomes much more precise:

**what happens to the carbohydrates you consume, and what do your insulin, triglycerides, blood sugar, waist circumference, hunger, and energy levels collectively tell you?**

That’s exactly the difference between applying a nutritional slogan and truly understanding your terrain.

**Understand my metabolic terrain**

#JohnYudkin #Sugar #Sucrose #Fructose #Insulin #Triglycerides #InsulinResistance #Metabolism #MetabolicHealth #LowCarb #Carnivore #ScientificNutrition