How the Sugar Industry Stole Half a Century of Nutrition Science

The article reveals how the American Sugar Research Foundation secretly funded Harvard scientists in the 1960s to downplay the health risks of sugar and shift the blame onto fat in a landmark NEJM paper. This influence shaped nutritional guidelines for half a century, drove the low-fat, high-carbohydrate diet, and contributed to the epidemics of obesity, type 2 diabetes, and fatty liver disease. British scientist John Yudkin, who had correctly identified sugar as a risk factor back in the 1950s, was marginalized for his conclusions and only rehabilitated posthumously.

In 1967, the prestigious New England Journal of Medicine published a two-part review article, "Dietary Fats, Carbohydrates and Atherosclerotic Disease." Its authors — Robert McGandy, D. Mark Hegsted, and Fredrick Stare of the Department of Nutrition at the Harvard School of Public Health — reached an unequivocal conclusion: to prevent heart disease, one must reduce dietary cholesterol and replace saturated fats with unsaturated ones. As for sugar, they declared that the evidence of its harmfulness was weak and inconclusive.

The article helped set the direction of dietary recommendations in the United States and worldwide for decades to come. Few suspected at the time that behind its creation stood precisely the industry whose product it was meant to protect.

When the Great Western Sugar Company, one of the largest American sugar-refining companies, ceased operations in the 1980s, its records made their way into the archives of Colorado universities. There, in 2009, they were encountered by Cristin Kearns, a dental surgeon who had decided to trace how the sugar industry influenced scientific research. In the archives of Colorado State University and other libraries, she gradually assembled hundreds of pages of internal documents. Together with colleagues, she ultimately analyzed more than 340 documents totaling 1,582 pages — correspondence, internal reports, and minutes from meetings of the Sugar Research Foundation (SRF), the trade association of the American sugar industry.

In September 2016, Kearns, together with Laura A. Schmidt and Stanton Glantz of the University of California San Francisco, published a historical analysis of these documents in JAMA Internal Medicine. The conclusion was devastating: the SRF had funded and actively steered the creation of that groundbreaking NEJM article — and this fact had never been disclosed anywhere.

Why does this matter? Because this single article helped steer nutrition science, public health policy, and the eating habits of billions of people down a path that proved to be mistaken. And because it happened at a time when another scientist had been right — and paid for it with his career.

The story begins in the 1950s, when the United States was facing an epidemic of heart disease among men of working age. Scientists looked to diet for the cause, and two camps gradually crystallized.

Ancel Keys, an American physiologist from the University of Minnesota, was convinced that the culprits were saturated fats and cholesterol. He was influential, persuasive, and aggressive in promoting his conclusions. In 1961 he made the cover of TIME magazine. His Seven Countries Study became one of the most influential epidemiological projects of the 20th century — despite later criticism that he had selected his data selectively.

On the other side of the Atlantic stood John Yudkin, a British physiologist and founder of the Department of Nutrition at Queen Elizabeth College in London. On the basis of his own epidemiological data, Yudkin argued that the correlation between food consumption and heart disease was stronger for sugar than for fats. As early as 1957 he had published data suggesting a stronger link between sucrose consumption and coronary mortality than between fat consumption and coronary mortality.

Keys responded with personal attacks. He labeled Yudkin's work unscientific and his conclusions absurd. Yudkin's book "Pure, White and Deadly" (1972), in which he systematically dissected the dangers of sugar, came under attack from the sugar industry, processed-food manufacturers — and from Keys himself.

But Keys did not win by the force of his arguments alone. He won also because he had an invisible ally.

In 1965, the SRF observed a sharp rise in media attention to the health risks of sucrose. It responded offensively: it approved Project 226 — a commission for a review article that was to summarize the existing scientific literature on sugar and heart disease. The authors were scientists from Harvard's Department of Nutrition, led by Fredrick Stare.

The archival documents uncovered by Kearns show how the project unfolded. The SRF paid the Harvard scientists a total of $6,500 in then-current dollars — roughly $48,900 in 2016 terms. John Hickson, vice president of the SRF, specified in correspondence that the organization was "particularly interested" in evaluating studies focused on sucrose. One of the Harvard scientists replied that he was "well aware" of this and would cover it as best he could.

The project took longer than planned — for in the meantime, further studies kept appearing that suggested a link between sugar and heart disease. When the article was finally completed, Hickson, according to the archival documents, wrote to the authors that the result was exactly what they had had in mind, and that he looked forward to its publication.

The review article applied a double standard. Studies suggesting that sugar was harmful were dismissed on grounds of methodological shortcomings. Studies blaming fats — with similar or greater methodological problems — passed without objection. The article concluded that there was "no doubt" that the only dietary intervention necessary to prevent heart disease was the reduction of cholesterol and saturated fats.

The industry funding was not disclosed.

The consequences reached far beyond a single journal article. D. Mark Hegsted, co-author of the sugar-industry-funded review article, became the first head of the newly established Office of Nutrition at the U.S. Department of Agriculture (USDA). In this role he oversaw the creation of the first official Dietary Guidelines for Americans, issued in 1980.

Even earlier, in 1977, the Senate Select Committee on Nutrition, chaired by Senator George McGovern, issued "Dietary Goals for the United States" — a document that recommended Americans increase carbohydrates to 55–60% of daily energy intake and reduce fat intake. The text of the dietary goals was written by Nick Mottern, a journalist specializing in labor-related topics, with no scientific training in nutrition, who, according to available sources, relied almost exclusively on input from Mark Hegsted.

The recommendation that Americans eat less fat and more carbohydrates became official policy. The food industry responded predictably: it flooded the market with low-fat products in which the missing fat was replaced by sugar. Low-fat yogurts, granola, "healthy" bars, and whole-grain cereals — products promoted as the healthy choice — typically contained 50–75% of their energy from carbohydrates, often including large amounts of added sugar.

What exactly did the studies the SRF wanted to suppress show? And what has research shown since then?

The key lies in the biochemistry of fructose. Sucrose — ordinary table sugar — is broken down in the body into two components: glucose and fructose, each roughly half. And it is fructose that is metabolically problematic — not because it is sweet, but because of how the body processes it.

Glucose, once absorbed, is distributed throughout the entire body. The brain, muscles, adipose tissue — all cells can use it as fuel. The process is regulated by insulin, which acts as a gatekeeper: it controls how much glucose goes where, and signals satiety to the body through the hormone leptin.

Fructose takes a different route. Via the portal vein it heads almost exclusively to the liver, where it is immediately captured and processed. Unlike glucose, its metabolism proceeds without insulin and without energetic feedback — the liver processes it regardless of whether it is replete with energy or not. It is a fuel that bypasses all the brakes.

In the liver, fructose stimulates the formation of new fat molecules (de novo lipogenesis). It activates the transcription factors SREBP-1c and ChREBP, which act as switches for triglyceride production. The result is that fat accumulates in the liver — a condition we now know as metabolic dysfunction-associated steatotic liver disease (MASLD), formerly designated nonalcoholic fatty liver disease (NAFLD).

And there is one more problem: fructose practically fails to activate leptin, the satiety hormone. After consuming sucrose or fructose-rich foods, the brain therefore does not receive the "enough" signal — and the person keeps eating.

Modern research confirms what Yudkin argued in the 1970s — and adds new findings.

MASLD has become the most widespread chronic liver disease in the world. According to current meta-analyses, it affects an estimated 30–32% of the adult population worldwide, and its prevalence keeps rising — from roughly 25% in studies from 2005 to nearly 38% in studies after 2016. Among children and adolescents the situation is alarming: MASLD is today the most common chronic liver disease in pediatrics. Clinical studies show that fructose intake is significantly higher in patients with MASLD than in control groups without fatty liver.

A 2017 study found that merely nine days of restricted sugar intake in obese children — while keeping total caloric intake the same — led to reductions in liver fat, visceral fat, and de novo lipogenesis, and to an improvement in insulin kinetics.

In 2025, a study published in Nature Communications brought a further finding: in a mouse model with complete hepatic insulin resistance, fructose caused fatty liver even without the classic lipogenic pathway — through the secretion of follistatin from the liver, which induced insulin resistance in adipose tissue. If this mechanism is confirmed in humans as well, it would mean that there are more avenues of harm than previously thought.

Paradoxically, it turns out that it is precisely the low-fat, high-carbohydrate diet — the one recommended by the official guidelines — that worsens key cardiovascular indicators. It raises triglycerides, lowers "good" HDL cholesterol, and shifts LDL particles toward smaller, denser forms (the so-called phenotype B), which in epidemiological studies are associated with a markedly higher risk of heart attack. A meta-analysis of 38 randomized trials with 1,785 participants showed, conversely, that carbohydrate restriction leads to an enlargement of LDL particles and a shift toward the safer phenotype A.

It would be convenient to tell the story in black and white: sugar is evil, fat is innocent, the industry is the villain. The reality, however, is more nuanced.

First, Keys was not wrong about everything. Industrial trans fats — hydrogenated vegetable oils, whose consumption rose sharply in the 1960s — are demonstrably harmful. Keys's data partly reflected precisely their influence, even though he did not distinguish them from saturated fats.

Second, obesity is multifactorial. A sedentary lifestyle, growing portion sizes, industrially processed foods, stress — all of these play a role. Sugar is not the sole culprit; it is one of the culprits whose share of the problem was systematically downplayed.

Third, meta-analyses comparing high-fructose corn syrup (HFCS) with sucrose often find no significant differences in metabolic effects. HFCS-55 contains 55% fructose compared with 50% in sucrose — the difference is negligible. Sucrose is rapidly broken down in the gut into free glucose and fructose. The problem, then, is not the specific type of sugar, but the total amount of fructose in the diet.

And fourth, whole fruit — although it contains fructose — does not pose a comparable risk. The fiber in fruit slows absorption, and consumption of whole fruit is consistently associated in epidemiological studies with positive health outcomes. The problem is isolated and liquid fructose: sweetened beverages, fruit juices, industrial syrups.

Moreover, the debate over saturated fats is not fully settled. The American Heart Association still recommends limiting them, although a number of more recent review studies have found no statistically significant association between saturated fats and cardiovascular mortality.

In 1995, John Yudkin died — without rehabilitation, without recognition. He spent his final years in seclusion, pushed aside by a scientific community that had accepted Keys's hypothesis as dogma.

In 2009, Robert Lustig, a pediatric endocrinologist at UCSF, recorded a ninety-minute lecture, "Sugar: The Bitter Truth." The video went viral and remains to this day one of the most-watched scientific lectures on YouTube. In it, Lustig explained in detail precisely those mechanisms that Yudkin had described forty years earlier.

In 2012, a new edition of "Pure, White and Deadly" appeared with a foreword by Lustig, who emphasized how far ahead of his time Yudkin had been.

And in 2016, Cristin Kearns opened the dusty archival boxes in the Colorado libraries and found the answer to the question of why no one had listened to Yudkin.

That two-part article in the New England Journal of Medicine from 1967 — the one of which its commissioner wrote that it was "exactly what we had in mind" — did not stand at the beginning of research. It stood at the beginning of fifty years of mistaken dietary recommendations, an epidemic of obesity, type 2 diabetes, and fatty liver in children.

Yudkin was right. It just took fifty years before we believed him.

Sources

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The concept, structure, and editorial line of the article are the work of the author, who prepared the content sketch, established the key theses, and directed the entire creative process. Generative AI (Claude, Anthropic) was used as a technical tool for research, fact-checking, and fleshing out the author's draft.

The author edited the outputs continuously, verified the key findings, and approved the final wording. No part of the text was published without human review. All factual data were verified against the publicly available sources cited in the text.

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