Feature Public Health

Sugar and the heart: old ideas revisited

BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.e7800 (Published 15 January 2013) Cite this as: BMJ 2013;346:e7800
  1. Geoff Watts, freelance journalist, BMJ
  1. 1London, UK
  1. geoff{at}scileg.freeserve.co.uk

Forty years after he first put them forward, John Yudkin’s warnings on sugar are finally being recognised. Geoff Watts reports

“Diets high in added sugar raise heart disease risk”; “One soft drink a day raises heart attack danger”; “Added sugars increase heart disease risk.” Few things are more prey to fad and fashion than alleged dietary influences on health. So the word “sugar” in headlines where, for 30 years, we’ve been accustomed to expect the word “fat” may be little more than a caprice. Alternatively it may indicate a more substantial change. Which is perhaps why Penguin Books is reissuing Pure, White and Deadly, John Yudkin’s valiant, 40 year old attempt to warn us against our lust for sucrose.1

Born in 1910, Yudkin studied physiology and biochemistry at Cambridge University, embarked on a career in microbiology, but then switched to medicine and nutrition. In 1945 he was appointed professor of physiology at Queen Elizabeth College, London, and set about creating a department with an international reputation in nutrition. He died in July 1995.

His book Pure, White and Deadly is about the uses of sugar, who consumes it, in what amounts, and how it’s handled by the body. But most of all it’s about what he saw as sugar’s deleterious effects on health. As he points out, carbohydrates have always been part of our diet and, until 50 years ago, the general view was that the form in which you consumed them was neither here nor there. But the more he thought and read, the more doubtful he became—about this, and also about the role of fat in heart disease.

Back in 1957, commenting that much had been said on the role of diet in coronary thrombosis, he wrote: “In particular, many believe that the disease is related to the amount of dietary fat, or of a particular sort of fat. In support of these beliefs, we are presented with evidence of an epidemiological nature . . . From time to time, however, it becomes evident that some of the epidemiological data do not fit . . . As more and more of these awkward facts turn up, one begins to have the uneasy feeling that both the proponents and opponents of a dietary hypothesis are quoting only those data which support their view.”2

One of the earliest exponents of the hypothesis that fat is the principal culprit was the American biologist Ancel Keys. Following epidemiological work that began in the 1950s and led eventually to the Seven Countries Study,3 Keys suggested that a diet high in animal fats led to heart disease while one low in animal fat—a Mediterranean diet—offered protection against it. Although considerably refined since then, it’s this view that remains broadly prevalent.

In 1957 Yudkin tried his own hand at analysing the available statistics on heart disease and diet. He found a “moderate but my no means excellent relationship between fat consumption and coronary mortality.” Moreover he noted that the relationship with sugar consumption was actually closer. Typically, he also pointed to an even better one between coronary mortality and the possession of radio and television sets. “He could be a bit of a tease,” says Tom Sanders of King’s College London, the man who now occupies what was Yudkin’s chair in nutrition and dietetics.

From reading and thinking Yudkin moved to experiments: “not always very well organised,” according to Sanders. But his findings, initially on animals and later on humans, reinforced a growing conviction that fat was not the only or even the main culprit. By the time he published the second (1986) edition of Pure, White and Deadly he was even more certain that sugar was the guilty substance. In his first chapter he wrote, “If only a small fraction of what we already know about the effects of sugar were to be revealed in relation to any other material used as a food additive, that material would promptly be banned.”

Industry dismissal

The sugar industry responded to Yudkin and his views with a mixture of public rebuttal and private subversion. Jobs and research grants that might predictably have come Yudkin’s way did not always materialise. He comments in the second edition of the book that while the sugar industry’s product is pure and white it would be difficult to use these adjectives to describe the behaviour of some of its supporters. And in the end, thinks Yudkin’s son Michael, sometime professor of biochemistry at Oxford, the focus on fat rather than sugar as the prime culprit had as much—or more—to do with commercial pressures as with science. In the final chapter of the second edition of his book Yudkin itemises some of the responses of the industry to his views. These include the abrupt cancellation of conferences suspected of promulgating anti-sugar findings; attacks on Pure, White and Deadly as a work of fiction; and the application of pressure to other food industries that were drawing attention to the harmful effects of sugar. This all left the field clear for fat to assume the role of chief culprit.

Sanders dismisses any suggestion that Yudkin was devastated by the unenthusiastic reception for his ideas. “He had a sense of proportion,” says Sanders, adding that he wasn’t a “conviction scientist” like Denis Burkitt or Hugh Trowell, the pair who campaigned so vigorously in favour of dietary fibre. However, Michael Yudkin says that his father did feel a sense of personal disappointment. “He was disappointed not so much for himself as for the implications for public health. Public health was something he’d worked on since he was a young man.”

Medical interest in the sugar hypothesis faded. The only lively discussion focused on its generally accepted role in dental caries. The book went out of print—but in Britain at least never entirely out of mind, partly on account of its clever title. The phrase “pure, white, and deadly” is memorable for the way in which the upbeat confidence of the first two adjectives is so swiftly contradicted by the damning verdict of the third.

New evidence

In recent years, and slowly, the sugar hypothesis has been making a comeback, driven in part by the emerging perception of heart disease as a consequence of what’s now described as the metabolic syndrome: obesity, dyslipidaemia, raised blood pressure, and insulin resistance. Although there is still no consensus about the causes of the syndrome, an excess of fat in the liver—a response to dietary sugar—is one of the acknowledged possibilities.4 5 Fructose, found in large quantities in nearly all added sugars, is known to increase lipogenesis in the liver and the synthesis of hepatic triglyceride.

Endocrinologist Robert Lustig, professor of paediatrics in the University of California at San Francisco, has contributed an enthusiastic introduction to the reissue of Yudkin’s book. He does not deny that fats—trans fats and omega-6 fatty acids in particular—have a role in the genesis of heart disease, but he does think sugar has been neglected until recently.

“There’s been a lot of research that’s come out lately showing that fructose, because of the way it’s metabolised, is different from glucose,” he says. “It contributes specifically to the emergence of the metabolic syndrome.” This, more than anything else, is what has started the ball rolling once again in a sweet direction. Fructose does things that other carbohydrates don’t, Lustig adds. “Because it’s metabolised in the liver it gets converted to liver fat, and this causes insulin resistance, which drives the metabolic syndrome.”

In the US, in parallel with awareness of the food industry’s increasing use of high fructose corn syrup, more researchers do seem to be giving sugars serious consideration. Last year a group at Emory University, Atlanta, found a statistically significant correlation between dietary added sugars and blood lipid levels in adults.6 More recently a New England Journal of Medicine editorial commenting on dietary fructose and the development of insulin resistance said: “An emerging association between the increased consumption of sugar-sweetened beverages and chronic diseases such as type 2 diabetes, hypertension, and coronary heart disease is a major concern.”7

In similar vein, a prospective cohort study of more than 40 000 men by Lawrence de Koning and colleagues at Harvard School of Public Health has shown that consuming sugar sweetened drinks is associated with an increased risk of coronary heart disease, while consuming artificially sweetened drinks is not.8 As Yudkin recalled in Pure, White and Deadly, as a child when he was thirsty he had a glass of water. “Nowadays when children are thirsty,” he went on, “it seems almost obligatory that they quench their thirst with some sugar-laden cola or other drink. And this is true for adults too.” Three decades later, he would have argued, we are witnessing the consequence.

Not surprisingly, the sugar lobby maintains its opposition to Yudkin’s views. In an email to the BMJ Dr Richard Cottrell, director of the World Sugar Research Organisation (WSRO), dismissed his theories as “based on flawed experiments in rats, whose metabolism of carbohydrate differs from that in humans.” Invited to comment on the de Koning study he said it will not “lead to any revision of the WSRO position statement, since the nature of this study is inherently unable to attribute causality to any associations observed. In addition, the relative risks quoted in this study are below the threshold for credibility normally set by epidemiologists for this kind of study.”

Since 1986 when Yudkin revised his book, much has been learnt about the metabolism of the carbohydrates, and its consequences. But the bones of the “new” view of sugar are already there. As Yudkin writes on page 105, “If the cells have become insensitive to insulin, the pancreas produces more and more insulin in order to counteract the insensitivity.” He also writes extensively of the links between heart disease, diabetes, obesity, and high blood pressure. The metabolic syndrome is there in all but name.

Where this debate on the role of sugar will lead is hard to predict. Michael Yudkin draws an analogy with smoking. “As time went on the denials that smoking tobacco had adverse effects became less and less tenable . . . I think we’re seeing the beginning of a similar shift in public opinion.”

Right now, beyond reiterating sugar’s obvious importance as a source of calories, even the British Heart Foundation feels that present uncertainties prevent it taking a position on other effects it might have. But Lustig remains confident that things will continue to move in his (and Yudkin’s) direction. We have causation as well as correlation, he says. “These shifts occur slowly. I think we’re in the middle of a shift. We will see where it goes.”


Cite this as: BMJ 2013;346:e7800


  • doi:10.1136/bmj.e8612
  • doi:10.1136/bmj.e8077
  • doi:10.1136/bmj.e7492
  • Competing interests: The author has completed the ICMJE unified disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declares no support from any organisation for the submitted work; no financial relationships with any organisation that might have an interest in the submitted work in the previous three years; and no other relationships or activities that could appear to have influenced the submitted work.

  • Provenance and peer review: Commissioned; not externally peer reviewed.