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Is Sugar Toxic?

By Gary Taubes

• April 13, 2011

On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.

Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.

The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”

It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”

If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.

The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.

This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?

It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.

If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat , appeared in this magazine —– and I have come to conclusions similar to Lustig’s.

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A . report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.

Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.

In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.

European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.

By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”

What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.

Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.

You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.

Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.

When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.

This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”

That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.

Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.

This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”

In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?

Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.

At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.

Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.

So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.

One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?

One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.

This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that .

One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.

The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.

In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.

Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”

So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.

Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.

But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.

“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”

Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.

Gary Taubes ([email protected]) is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.” Editor: Vera Titunik ([email protected]).

A Guide to Sugar and Other Sweeteners

One of the best things you can do for your health is to cut back on foods with added sugar . Here’s how to get started .

A W.H.O. agency  has classified aspartame as a possible carcinogen . If the announcement has you worried, consider these alternatives to diet soda .

A narrative that sugar feeds cancer has been making the rounds for decades. But while a healthy diet is important, you can’t “starve a tumor.”

Sugar alcohols are in many sugar-free foods. What are they, and are they better than regular sugar ?

Many parents blame sugar for their children’s hyperactive behavior . But the myth has been debunked .

Are artificial sweeteners a healthy alternative to sugar? The W.H.O. warned against using them , saying that long-term use could pose health risks.

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One Man Against Sugar

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In December of 2006, Robert Lustig ’77 was sifting through journal articles on liver disease in preparation for a talk on obesity for an environmental-health symposium when he was struck by a realization about sugar. Little did he realize that his simple insight would change the course of his career—and quite possibly change the way all of us eat.

Lustig, an endocrinologist and professor of pediatrics at the University of California, San Francisco, was already an authority on childhood obesity and director of the university’s weight assessment program for kids and teens, but he wasn’t yet the famous antisugar crusader he is today. He hadn’t yet been featured in the New York Times Magazine or appeared on 60 Minutes . He hadn’t published his popular book, Fat Chance , or exchanged barbs with Stephen Colbert on The Colbert Report .

And so when asked to discuss why so many of us were becoming obese and sick, he didn’t yet have a good answer. He understood that the hormone insulin plays a role in obesity. The children with brain tumors whom he’d cared for at St. Jude Children’s Research Hospital in Memphis often suffered from hypothalamic damage, either from the cancer itself or from the treatment, and many of them became obese. Following up on suspicions posited in the 1970s by other researchers, Lustig had shown in 1999 that those obese patients had increased activity of the vagus nerve, which in turn led to greater insulin secretion. When he administered an insulin-­suppressive agent, they lost weight and became more active.

Although Lustig understood that elevated insulin levels were linked to obesity, he hadn’t focused on the relationship between insulin and sugar. Like most other medical professionals at the time, he thought all calories were essentially alike in their ability to make us fat. The problem with sugar, this line of thinking goes, is that it provides only empty calories, negligible in nutritional value.

And yet as Lustig began to look more closely at the literature on sugar in preparation for the symposium, a different picture emerged. Table sugar, or sucrose, is made up of equal parts glucose and fructose, but it was the molecule of fructose that grabbed his attention. Fructose didn’t seem to act at all like most substances we consume. Rather, Lustig realized, it behaved like one particular substance: alcohol.

In some ways, the connection between alcohol and fructose was obvious enough. After all, fermentation can turn both glucose and fructose into alcohol. But while glucose is metabolized by every cell in the body, fructose—like alcohol—is primarily metabolized in the liver, where some of it is converted into fat through a process known as de novo lipogenesis. Consume enough fructose and you could very well end up not only increasing the fat in your blood but also fattening your liver, just as you might by drinking too much alcohol. In fact, that’s exactly what happens in rodents. “I started to research the sugar literature, and it was almost like a one-to-one match,” Lustig says of the similarities between the metabolism of fructose and alcohol. This led him to his controversial conclusion: consumed chronically in large amounts—that is, the way most of us consume it—sugar is poison.

Scientists are still unraveling the biological mechanism at work and sorting out exactly how much fructose might be too much in humans. What’s clear is that fructose and glucose are metabolized very differently, and that unlike glucose, which is the body’s main source of energy, fructose isn’t biologically necessary. Although humans have always consumed carbohydrates, which we convert into glucose, essentially all the fructose we ate before the rise of the worldwide sugar industry 500 years ago came from the small amount in fruits and honey. (The natural fructose in fruit isn’t thought to be a health concern because the fruit’s fiber and cellular structure slow down the rate at which it hits the liver.)

Glucose, too, can be dangerous in excess, Lustig acknowledges. The glucose from our meals that doesn’t end up being used for fuel or stored in the form of glycogen can also end up as liver fat. And whether it’s being driven by fructose or glucose, this accumulation of liver fat appears to be the first step toward insulin resistance and increased insulin levels—the same phenomenon that was making Lustig’s young cancer patients obese. Worse yet, insulin resistance is believed to contribute to a cascade of other metabolic disorders that result in type 2 diabetes, heart disease, and even many cancers. Either way, sugar looked like a villain.

Lustig feared that he would be booed off the stage when he delivered this news to the environmental-health scientists. After all, he was doing much more than telling them that their favorite foods could be toxic. He was also challenging the medical establishment’s most basic dietary advice. For decades Americans had been warned by doctors, scientists, and government agencies that eating too much fat, particularly saturated fat, would clog their arteries and shorten their lives. Now one of the nation’s experts on childhood obesity was declaring that maybe everyone had been focusing on the wrong target. Or, as Lustig would later declare, “It ain’t the fat, people.”

Lustig set out to learn as much as he could on the subject. And the more he learned, the worse the picture looked. Each day, Americans were consuming a startling 22 teaspoons of “added” sugar—that is, sugar beyond the naturally occurring fructose in fruit or lactose in dairy products. Lustig believes that amount far exceeds what our livers can handle. The safe upper limit, both he and the American Heart Association believe, is four teaspoons of added sugar per day for children, six for women, and nine for men (nine teaspoons—or 36 grams—is about what you’ll find in a typical 12-ounce can of soda). More troubling yet, sugar is no longer something manufacturers add only to sweets. Today, it’s almost impossible to avoid. “Of the 600,000 items in the American grocery store, 77 percent of them have added sugar,” Lustig says. “You can’t even reduce your consumption when you’re trying to.”

Although Lustig quickly made an impression in public-health circles, it wasn’t until July 2009, when University of California Television posted one of his lectures on YouTube, that he reached a mainstream audience. The lecture, called “ Sugar: The Bitter Truth ,” is an hour and a half long and packed with scientific data on fructose metabolism. In other words, it isn’t exactly the type of video that has “Internet sensation” written all over it. And yet, it has been viewed more than four million times.

Why did a long scientific lecture go viral? It turns out that Lustig, who has authored more than 100 research articles and is the former chairman of the Obesity Task Force of the Pediatric Endocrine Society, is also a veteran performer.

In “Sugar: The Bitter Truth,” his talents for public speaking are on full display. Between the graphs and the dense scientific explanations, he peppers the talk with personal anecdotes about his childhood, long dramatic pauses, provocative statements (he calls fructose “alcohol without the buzz”), and plenty of tantalizing, if unproven, claims—he not only suggests that Coke includes lots of salt to make us thirstier (and extra sugar to cover the taste of all that salt) but dubs this supposed scheme “the Coca-Cola conspiracy.”

“Lustig deservedly gets attention for his ideas, not least because he’s fun,” says Marion Nestle, a New York University nutritionist and the author of the book Food Politics . “He is a master of exaggeration and hyperbole, but underneath all that, he really knows what he’s talking about and cares deeply about keeping kids healthy.”

Lustig, who lives with his wife and two daughters in San Francisco, can trace his foundations in science to his undergraduate days at MIT. He credits 20.30, Sanford A. Miller’s course in nutritional biochemistry, with spurring his curiosity about diet and nutrition. (Miller would later serve as director of the FDA’s Center for Food Safety and Applied Nutrition.) But Lustig’s MIT experience also contributed to his ability to engage an audience. In the three years he spent at the Institute, he managed to be involved in 14 plays, acting in most of them. “It taught me how to get on stage and how not to be scared,” he says.

If Lustig’s gift for public speaking has earned him a lot of online fans, some of his fellow researchers seem less enthused by what they see as his willingness to make bold claims that aren’t substantiated by the scientific literature. Critics point out that the strongest evidence against fructose comes from animal studies, which can’t tell us very much about our own metabolism. Other studies that point to the hazards of sugar, if not fructose specifically, generally are not controlled experiments but merely associations observed between the foods consumed in certain countries (or by specific groups of people) and the health problems those people later develop. Even though such studies may receive a lot of media attention, they can’t conclusively show that sugar is driving the disease process. And while small clinical trials with human subjects have pointed to the dangers of fructose—one 2009 study found that a single week of fructose overfeeding could increase triglycerides (associated with cardiovascular disease) and decrease insulin sensitivity—the large, randomly controlled trials that might provide a more definitive answer would be extremely difficult to carry out.

Luc Tappy, a researcher at the University of Lausanne in Switzerland and a leading authority on fructose metabolism, isn’t yet convinced about the dangers of fructose. In a 2012 paper, he wrote that for humans, “there is no solid evidence that fructose, when consumed in moderate amounts, has deleterious effects.” Though Tappy doesn’t question the honesty of Lustig’s intentions, he says he should not be relied upon as a scientific expert on the topic: “He certainly does not provide a balanced view of things.”

But if Tappy has doubts about Lustig’s presentation of the science, he also thinks he has played a key role in bringing the sugar debate to the public. “At some stage, you have to take decisions without knowing everything, because it would take forever to collect all relevant scientific data,” he says.

Lustig refutes the idea that he’s more provocateur than scientist. He says he wouldn’t be sticking his neck out if he didn’t believe that the science supported his claims. “The science is there,” he insists. He recently coauthored both The Fat Chance Cookbook and a study in the journal PLOS One that shows a strong link between the amount of sugar in a country’s food supply and the prevalence of diabetes in that country. And last year he earned a master of studies in law from the UC Hastings College of the Law in order to better understand how to influence public policy. His ultimate goal is to see fructose removed from the FDA’s list of foods that are “generally recognized as safe.” He points to the recent announcement that the FDA plans to take trans fats off the list—a change that came after 25 years of scientific debate—as evidence that such change is possible.

Lustig may not have to wait a quarter of a century to see some of the steps he seeks. In February the FDA proposed major changes to nutrition labels on food packages. One of those changes: a new line that would highlight added sugars.

“I can’t take credit, and they most certainly won’t bestow it,” Lustig says. “But it does validate the work I’ve been doing.”

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The sugar conspiracy

In 1972, a British scientist sounded the alarm that sugar – and not fat – was the greatest danger to our health. But his findings were ridiculed and his reputation ruined. How did the world’s top nutrition scientists get it so wrong for so long?

R obert Lustig is a paediatric endocrinologist at the University of California who specialises in the treatment of childhood obesity. A 90-minute talk he gave in 2009, titled Sugar: The Bitter Truth, has now been viewed more than six million times on YouTube. In it, Lustig argues forcefully that fructose, a form of sugar ubiquitous in modern diets, is a “poison” culpable for America’s obesity epidemic.

A year or so before the video was posted, Lustig gave a similar talk to a conference of biochemists in Adelaide, Australia. Afterwards, a scientist in the audience approached him. Surely, the man said, you’ve read Yudkin. Lustig shook his head. John Yudkin, said the scientist, was a British professor of nutrition who had sounded the alarm on sugar back in 1972, in a book called Pure, White, and Deadly.

“If only a small fraction of what we know about the effects of sugar were to be revealed in relation to any other material used as a food additive,” wrote Yudkin, “that material would promptly be banned.” The book did well, but Yudkin paid a high price for it. Prominent nutritionists combined with the food industry to destroy his reputation, and his career never recovered. He died, in 1995, a disappointed, largely forgotten man.

Perhaps the Australian scientist intended a friendly warning. Lustig was certainly putting his academic reputation at risk when he embarked on a high-profile campaign against sugar. But, unlike Yudkin, Lustig is backed by a prevailing wind. We read almost every week of new research into the deleterious effects of sugar on our bodies. In the US, the latest edition of the government’s official dietary guidelines includes a cap on sugar consumption. In the UK, the chancellor George Osborne has announced a new tax on sugary drinks. Sugar has become dietary enemy number one.

This represents a dramatic shift in priority. For at least the last three decades, the dietary arch-villain has been saturated fat. When Yudkin was conducting his research into the effects of sugar, in the 1960s, a new nutritional orthodoxy was in the process of asserting itself. Its central tenet was that a healthy diet is a low-fat diet. Yudkin led a diminishing band of dissenters who believed that sugar, not fat, was the more likely cause of maladies such as obesity, heart disease and diabetes. But by the time he wrote his book, the commanding heights of the field had been seized by proponents of the fat hypothesis. Yudkin found himself fighting a rearguard action, and he was defeated.

Not just defeated, in fact, but buried. When Lustig returned to California, he searched for Pure, White and Deadly in bookstores and online, to no avail. Eventually, he tracked down a copy after submitting a request to his university library. On reading Yudkin’s introduction, he felt a shock of recognition.

“Holy crap,” Lustig thought. “This guy got there 35 years before me.”

I n 1980, after long consultation with some of America’s most senior nutrition scientists, the US government issued its first Dietary Guidelines. The guidelines shaped the diets of hundreds of millions of people. Doctors base their advice on them, food companies develop products to comply with them. Their influence extends beyond the US. In 1983, the UK government issued advice that closely followed the American example.

The most prominent recommendation of both governments was to cut back on saturated fats and cholesterol (this was the first time that the public had been advised to eat less of something, rather than enough of everything). Consumers dutifully obeyed. We replaced steak and sausages with pasta and rice, butter with margarine and vegetable oils, eggs with muesli, and milk with low-fat milk or orange juice. But instead of becoming healthier, we grew fatter and sicker.

Look at a graph of postwar obesity rates and it becomes clear that something changed after 1980. In the US, the line rises very gradually until, in the early 1980s, it takes off like an aeroplane. Just 12% of Americans were obese in 1950, 15% in 1980, 35% by 2000. In the UK, the line is flat for decades until the mid-1980s, at which point it also turns towards the sky. Only 6% of Britons were obese in 1980. In the next 20 years that figure more than trebled. Today, two thirds of Britons are either obese or overweight, making this the fattest country in the EU. Type 2 diabetes, closely related to obesity, has risen in tandem in both countries.

At best, we can conclude that the official guidelines did not achieve their objective; at worst, they led to a decades-long health catastrophe. Naturally, then, a search for culprits has ensued. Scientists are conventionally apolitical figures, but these days, nutrition researchers write editorials and books that resemble liberal activist tracts, fizzing with righteous denunciations of “big sugar” and fast food. Nobody could have predicted, it is said, how the food manufacturers would respond to the injunction against fat – selling us low-fat yoghurts bulked up with sugar, and cakes infused with liver-corroding transfats.

Nutrition scientists are angry with the press for distorting their findings, politicians for failing to heed them, and the rest of us for overeating and under-exercising. In short, everyone – business, media, politicians, consumers – is to blame. Everyone, that is, except scientists.

But it was not impossible to foresee that the vilification of fat might be an error. Energy from food comes to us in three forms: fat, carbohydrate, and protein. Since the proportion of energy we get from protein tends to stay stable, whatever our diet, a low-fat diet effectively means a high-carbohydrate diet. The most versatile and palatable carbohydrate is sugar, which John Yudkin had already circled in red. In 1974, the UK medical journal, the Lancet, sounded a warning about the possible consequences of recommending reductions in dietary fat: “The cure should not be worse than the disease.”

Still, it would be reasonable to assume that Yudkin lost this argument simply because, by 1980, more evidence had accumulated against fat than against sugar.

After all, that’s how science works, isn’t it?

I f, as seems increasingly likely, the nutritional advice on which we have relied for 40 years was profoundly flawed, this is not a mistake that can be laid at the door of corporate ogres. Nor can it be passed off as innocuous scientific error. What happened to John Yudkin belies that interpretation. It suggests instead that this is something the scientists did to themselves – and, consequently, to us.

We tend to think of heretics as contrarians, individuals with a compulsion to flout conventional wisdom. But sometimes a heretic is simply a mainstream thinker who stays facing the same way while everyone around him turns 180 degrees. When, in 1957, John Yudkin first floated his hypothesis that sugar was a hazard to public health, it was taken seriously, as was its proponent. By the time Yudkin retired, 14 years later, both theory and author had been marginalised and derided. Only now is Yudkin’s work being returned, posthumously, to the scientific mainstream.

These sharp fluctuations in Yudkin’s stock have had little to do with the scientific method, and a lot to do with the unscientific way in which the field of nutrition has conducted itself over the years. This story, which has begun to emerge in the past decade, has been brought to public attention largely by sceptical outsiders rather than eminent nutritionists. In her painstakingly researched book, The Big Fat Surprise, the journalist Nina Teicholz traces the history of the proposition that saturated fats cause heart disease, and reveals the remarkable extent to which its progress from controversial theory to accepted truth was driven, not by new evidence, but by the influence of a few powerful personalities, one in particular.

Teicholz’s book also describes how an establishment of senior nutrition scientists, at once insecure about its medical authority and vigilant for threats to it, consistently exaggerated the case for low-fat diets, while turning its guns on those who offered evidence or argument to the contrary. John Yudkin was only its first and most eminent victim.

Today, as nutritionists struggle to comprehend a health disaster they did not predict and may have precipitated, the field is undergoing a painful period of re-evaluation. It is edging away from prohibitions on cholesterol and fat, and hardening its warnings on sugar, without going so far as to perform a reverse turn. But its senior members still retain a collective instinct to malign those who challenge its tattered conventional wisdom too loudly, as Teicholz is now discovering.

T o understand how we arrived at this point, we need to go back almost to the beginning of modern nutrition science. On 23 September, 1955, US President Dwight Eisenhower suffered a heart attack. Rather than pretend it hadn’t happened, Eisenhower insisted on making details of his illness public. The next day, his chief physician, Dr Paul Dudley White, gave a press conference at which he instructed Americans on how to avoid heart disease: stop smoking, and cut down on fat and cholesterol. In a follow-up article, White cited the research of a nutritionist at the University of Minnesota, Ancel Keys.

Heart disease, which had been a relative rarity in the 1920s, was now felling middle-aged men at a frightening rate, and Americans were casting around for cause and cure. Ancel Keys provided an answer: the “diet-heart hypothesis” (for simplicity’s sake, I am calling it the “fat hypothesis”). This is the idea, now familiar, that an excess of saturated fats in the diet, from red meat, cheese, butter, and eggs, raises cholesterol, which congeals on the inside of coronary arteries, causing them to harden and narrow, until the flow of blood is staunched and the heart seizes up.

Ancel Keys was brilliant, charismatic, and combative. A friendly colleague at the University of Minnesota described him as, “direct to the point of bluntness, critical to the point of skewering”; others were less charitable. He exuded conviction at a time when confidence was most welcome. The president, the physician and the scientist formed a reassuring chain of male authority, and the notion that fatty foods were unhealthy started to take hold with doctors, and the public. (Eisenhower himself cut saturated fats and cholesterol from his diet altogether, right up until his death, in 1969, from heart disease.)

Many scientists, especially British ones, remained sceptical. The most prominent doubter was John Yudkin, then the UK’s leading nutritionist. When Yudkin looked at the data on heart disease, he was struck by its correlation with the consumption of sugar, not fat. He carried out a series of laboratory experiments on animals and humans, and observed, as others had before him, that sugar is processed in the liver, where it turns to fat, before entering the bloodstream.

He noted, too, that while humans have always been carnivorous, carbohydrates only became a major component of their diet 10,000 years ago, with the advent of mass agriculture. Sugar – a pure carbohydrate, with all fibre and nutrition stripped out – has been part of western diets for just 300 years; in evolutionary terms, it is as if we have, just this second, taken our first dose of it. Saturated fats, by contrast, are so intimately bound up with our evolution that they are abundantly present in breast milk. To Yudkin’s thinking, it seemed more likely to be the recent innovation, rather than the prehistoric staple, making us sick.

John Yudkin was born in 1910, in the East End of London. His parents were Russian Jews who settled in England after fleeing the pogroms of 1905. Yudkin’s father died when he was six, and his mother brought up her five sons in poverty. By way of a scholarship to a local grammar school in Hackney, Yudkin made it to Cambridge. He studied biochemistry and physiology, before taking up medicine. After serving in the Royal Army Medical Corps during the second world war, Yudkin was made a professor at Queen Elizabeth College in London, where he built a department of nutrition science with an international reputation.

Ancel Keys was intensely aware that Yudkin’s sugar hypothesis posed an alternative to his own. If Yudkin published a paper, Keys would excoriate it, and him. He called Yudkin’s theory “a mountain of nonsense”, and accused him of issuing “propaganda” for the meat and dairy industries. “Yudkin and his commercial backers are not deterred by the facts,” he said. “They continue to sing the same discredited tune.” Yudkin never responded in kind. He was a mild-mannered man, unskilled in the art of political combat.

That made him vulnerable to attack, and not just from Keys. The British Sugar Bureau dismissed Yudkin’s claims about sugar as “emotional assertions”; the World Sugar Research Organisation called his book “science fiction”. In his prose, Yudkin is fastidiously precise and undemonstrative, as he was in person. Only occasionally does he hint at how it must have felt to have his life’s work besmirched, as when he asks the reader, “Can you wonder that one sometimes becomes quite despondent about whether it is worthwhile trying to do scientific research in matters of health?”

Throughout the 1960s, Keys accumulated institutional power. He secured places for himself and his allies on the boards of the most influential bodies in American healthcare, including the American Heart Association and the National Institutes of Health . From these strongholds, they directed funds to like-minded researchers, and issued authoritative advice to the nation. “People should know the facts,” Keys told Time magazine. “Then if they want to eat themselves to death, let them.”

This apparent certainty was unwarranted: even some supporters of the fat hypothesis admitted that the evidence for it was still inconclusive. But Keys held a trump card. From 1958 to 1964, he and his fellow researchers gathered data on the diets, lifestyles and health of 12,770 middle-aged men, in Italy, Greece, Yugoslavia, Finland, Netherlands, Japan and the United States. The Seven Countries Study was finally published as a 211-page monograph in 1970. It showed a correlation between intake of saturated fats and deaths from heart disease, just as Keys had predicted. The scientific debate swung decisively behind the fat hypothesis.

Keys was the original big data guy (a contemporary remarked: “Every time you question this man Keys, he says, ‘I’ve got 5,000 cases. How many do you have?’). Despite its monumental stature, however, the Seven Countries Study, which was the basis for a cascade of subsequent papers by its original authors, was a rickety construction. There was no objective basis for the countries chosen by Keys, and it is hard to avoid the conclusion that he picked only those he suspected would support his hypothesis. After all, it is quite something to choose seven nations in Europe and leave out France and what was then West Germany, but then, Keys already knew that the French and Germans had relatively low rates of heart disease, despite living on a diet rich in saturated fats.

The study’s biggest limitation was inherent to its method. Epidemiological research involves the collection of data on people’s behaviour and health, and a search for patterns. Originally developed to study infection, Keys and his successors adapted it to the study of chronic diseases, which, unlike most infections, take decades to develop, and are entangled with hundreds of dietary and lifestyle factors, effectively impossible to separate.

To reliably identify causes, as opposed to correlations, a higher standard of evidence is required: the controlled trial. In its simplest form: recruit a group of subjects, and assign half of them a diet for, say, 15 years. At the end of the trial, assess the health of those in the intervention group, versus the control group. This method is also problematic: it is virtually impossible to closely supervise the diets of large groups of people. But a properly conducted trial is the only way to conclude with any confidence that X is responsible for Y.

Although Keys had shown a correlation between heart disease and saturated fat, he had not excluded the possibility that heart disease was being caused by something else. Years later, the Seven Countries study’s lead Italian researcher, Alessandro Menotti, went back to the data, and found that the food that correlated most closely with deaths from heart disease was not saturated fat, but sugar.

By then it was too late. The Seven Countries study had become canonical, and the fat hypothesis was enshrined in official advice. The congressional committee responsible for the original Dietary Guidelines was chaired by Senator George McGovern. It took most of its evidence from America’s nutritional elite: men from a handful of prestigious universities, most of whom knew or worked with each other, all of whom agreed that fat was the problem – an assumption that McGovern and his fellow senators never seriously questioned. Only occasionally were they asked to reconsider. In 1973, John Yudkin was called from London to testify before the committee, and presented his alternative theory of heart disease.

A bemused McGovern asked Yudkin if he was really suggesting that a high fat intake was not a problem, and that cholesterol presented no danger.

“I believe both those things,” replied Yudkin.

“That is exactly the opposite of what my doctor told me,” said McGovern.

I n a 2015 paper titled Does Science Advance One Funeral at a Time?, a team of scholars at the National Bureau of Economic Research sought an empirical basis for a remark made by the physicist Max Planck: “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”

The researchers identified more than 12,000 “elite” scientists from different fields. The criteria for elite status included funding, number of publications, and whether they were members of the National Academies of Science or the Institute of Medicine. Searching obituaries, the team found 452 who had died before retirement. They then looked to see what happened to the fields from which these celebrated scientists had unexpectedly departed, by analysing publishing patterns.

What they found confirmed the truth of Planck’s maxim. Junior researchers who had worked closely with the elite scientists, authoring papers with them, published less. At the same time, there was a marked increase in papers by newcomers to the field, who were less likely to cite the work of the deceased eminence. The articles by these newcomers were substantive and influential, attracting a high number of citations. They moved the whole field along.

A scientist is part of what the Polish philosopher of science Ludwik Fleck called a “thought collective”: a group of people exchanging ideas in a mutually comprehensible idiom. The group, suggested Fleck, inevitably develops a mind of its own, as the individuals in it converge on a way of communicating, thinking and feeling.

This makes scientific inquiry prone to the eternal rules of human social life: deference to the charismatic, herding towards majority opinion, punishment for deviance, and intense discomfort with admitting to error. Of course, such tendencies are precisely what the scientific method was invented to correct for, and over the long run, it does a good job of it. In the long run, however, we’re all dead, quite possibly sooner than we would be if we hadn’t been following a diet based on poor advice.

I n a series of densely argued articles and books, including Why We Get Fat (2010), the science writer Gary Taubes has assembled a critique of contemporary nutrition science, powerful enough to compel the field to listen. One of his contributions has been to uncover a body of research conducted by German and Austrian scientists before the second world war, which had been overlooked by the Americans who reinvented the field in the 1950s. The Europeans were practising physicians and experts in the metabolic system. The Americans were more likely to be epidemiologists, labouring in relative ignorance of biochemistry and endocrinology (the study of hormones). This led to some of the foundational mistakes of modern nutrition.

The rise and slow fall of cholesterol’s infamy is a case in point. After it was discovered inside the arteries of men who had suffered heart attacks, public health officials, advised by scientists, put eggs, whose yolks are rich in cholesterol, on the danger list. But it is a biological error to confuse what a person puts in their mouth with what it becomes after it is swallowed. The human body, far from being a passive vessel for whatever we choose to fill it with, is a busy chemical plant, transforming and redistributing the energy it receives. Its governing principle is homeostasis, or the maintenance of energy equilibrium (when exercise heats us up, sweat cools us down). Cholesterol, present in all of our cells, is created by the liver. Biochemists had long known that the more cholesterol you eat, the less your liver produces.

Unsurprisingly, then, repeated attempts to prove a correlation between dietary cholesterol and blood cholesterol failed. For the vast majority of people, eating two or three, or 25 eggs a day, does not significantly raise cholesterol levels. One of the most nutrient-dense, versatile and delicious foods we have was needlessly stigmatised. The health authorities have spent the last few years slowly backing away from this mistake, presumably in the hope that if no sudden movements are made, nobody will notice. In a sense, they have succeeded: a survey carried out in 2014 by Credit Suisse found that 54% of US doctors believe that dietary cholesterol raises blood cholesterol.

To his credit, Ancel Keys realised early on that dietary cholesterol was not a problem. But in order to sustain his assertion that cholesterol causes heart attacks, he needed to identify an agent that raises its levels in the blood – he landed on saturated fats. In the 30 years after Eisenhower’s heart attack, trial after trial failed to conclusively bear out the association he claimed to have identified in the Seven Countries study.

The nutritional establishment wasn’t greatly discomfited by the absence of definitive proof, but by 1993 it found that it couldn’t evade another criticism: while a low-fat diet had been recommended to women, it had never been tested on them (a fact that is astonishing only if you are not a nutrition scientist). The National Heart, Lung and Blood Institute decided to go all in, commissioning the largest controlled trial of diets ever undertaken. As well as addressing the other half of the population, the Women’s Health Initiative was expected to obliterate any lingering doubts about the ill-effects of fat.

It did nothing of the sort. At the end of the trial, it was found that women on the low-fat diet were no less likely than the control group to contract cancer or heart disease. This caused much consternation. The study’s principal researcher, unwilling to accept the implications of his own findings, remarked: “We are scratching our heads over some of these results.” A consensus quickly formed that the study – meticulously planned, lavishly funded, overseen by impressively credentialed researchers – must have been so flawed as to be meaningless. The field moved on, or rather did not.

In 2008, researchers from Oxford University undertook a Europe-wide study of the causes of heart disease. Its data shows an inverse correlation between saturated fat and heart disease, across the continent. France, the country with the highest intake of saturated fat, has the lowest rate of heart disease; Ukraine, the country with the lowest intake of saturated fat, has the highest. When the British obesity researcher Zoë Harcombe performed an analysis of the data on cholesterol levels for 192 countries around the world, she found that lower cholesterol correlated with higher rates of death from heart disease.

In the last 10 years, a theory that had somehow held up unsupported for nearly half a century has been rejected by several comprehensive evidence reviews, even as it staggers on, zombie-like, in our dietary guidelines and medical advice.

The UN’s Food and Agriculture Organisation, in a 2008 analysis of all studies of the low-fat diet, found “no probable or convincing evidence” that a high level of dietary fat causes heart disease or cancer. Another landmark review, published in 2010, in the American Society for Nutrition, and authored by, among others, Ronald Krauss, a highly respected researcher and physician at the University of California, stated “there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD [coronary heart disease and cardiovascular disease]”.

Many nutritionists refused to accept these conclusions. The journal that published Krauss’s review, wary of outrage among its readers, prefaced it with a rebuttal by a former right-hand man of Ancel Keys, which implied that since Krauss’s findings contradicted every national and international dietary recommendation, they must be flawed. The circular logic is symptomatic of a field with an unusually high propensity for ignoring evidence that does not fit its conventional wisdom.

Gary Taubes is a physicist by background. “In physics,” he told me, “You look for the anomalous result. Then you have something to explain. In nutrition, the game is to confirm what you and your predecessors have always believed.” As one nutritionist explained to Nina Teicholz, with delicate understatement: “Scientists believe that saturated fat is bad for you, and there is a good deal of reluctance toward accepting evidence to the contrary.”

W hen obesity started to become recognised as a problem in western societies, it too was blamed on saturated fats. It was not difficult to persuade the public that if we eat fat, we will be fat (this is a trick of the language: we call an overweight person “fat”; we don’t describe a person with a muscular body as “proteiny”). The scientific rationale was also pleasingly simple: a gramme of fat has twice as many calories as a gramme of protein or carbohydrate, and we can all grasp the idea that if a person takes in more calories than she expends in physical activity, the surplus ends up as fat.

Simple does not mean right, of course. It’s difficult to square this theory with the dramatic rise in obesity since 1980, or with much other evidence. In America, average calorific intake increased by just a sixth over that period. In the UK, it actually fell. There has been no commensurate decline in physical activity, in either country – in the UK, exercise levels have increased over the last 20 years. Obesity is a problem in some of the poorest parts of the world, even among communities in which food is scarce. Controlled trials have repeatedly failed to show that people lose weight on low-fat or low-calorie diets, over the long-term.

Those prewar European researchers would have regarded the idea that obesity results from “excess calories” as laughably simplistic. Biochemists and endocrinologists are more likely to think of obesity as a hormonal disorder, triggered by the kinds of foods we started eating a lot more of when we cut back on fat: easily digestible starches and sugars. In his new book, Always Hungry, David Ludwig , an endocrinologist and professor of pediatrics at Harvard Medical School, calls this the “Insulin-Carbohydrate” model of obesity. According to this model, an excess of refined carbohydrates interferes with the self-balancing equilibrium of the metabolic system.

Far from being an inert dumping ground for excess calories, fat tissue operates as a reserve energy supply for the body. Its calories are called upon when glucose is running low – that is, between meals, or during fasts and famines. Fat takes instruction from insulin, the hormone responsible for regulating blood sugar. Refined carbohydrates break down at speed into glucose in the blood, prompting the pancreas to produce insulin. When insulin levels rise, fat tissue gets a signal to suck energy out of the blood, and to stop releasing it. So when insulin stays high for unnaturally long, a person gains weight, gets hungrier, and feels fatigued. Then we blame them for it. But, as Gary Taubes puts it, obese people are not fat because they are overeating and sedentary – they are overeating and sedentary because they are fat, or getting fatter.

Ludwig makes clear, as Taubes does, that this is not a new theory – John Yudkin would have recognised it – but an old one that has been galvanised by new evidence. What he does not mention is the role that supporters of the fat hypothesis have played, historically, in demolishing the credibility of those who proposed it.

I n 1972, the same year Yudkin published Pure, White and Deadly, a Cornell-trained cardiologist called Robert Atkins published Dr Atkins’ Diet Revolution. Their arguments shared a premise – that carbohydrates are more dangerous to our health than fat – though they differed in particulars. Yudkin focused on the evils of one carbohydrate in particular, and didn’t explicitly recommend a high-fat diet. Atkins argued that a high-fat, low-carbohydrate diet was the only viable route to weight loss.

Perhaps the most important difference between the two books was tone. Yudkin’s was cool, polite and reasonable, which reflected his temperament, and the fact that he saw himself as a scientist first and a clinician second. Atkins, resolutely a practitioner rather than an academic, was unbound by gentlemanly conventions. He declared himself furious that he had been “duped” by medical scientists. Unsurprisingly, this attack enraged the nutritional establishment, which hit back hard. Atkins was labelled a fraud, and his diet a “fad”. It was a successful campaign: even today, Atkins’s name brings with it the odour of quackery.

A “fad” implies something new-fangled. But low-carbohydrate, high-fat diets had been popular for well over a century before Atkins, and were, until the 1960s, a method of weight loss endorsed by mainstream science. By the start of the 1970s, that had changed. Researchers interested in the effects of sugar and complex carbohydrates on obesity only had to look at what had happened to the most senior nutritionist in the UK to see that pursuing such a line of inquiry was a terrible career move.

John Yudkin’s scientific reputation had been all but sunk. He found himself uninvited from international conferences on nutrition. Research journals refused his papers. He was talked about by fellow scientists as an eccentric, a lone obsessive. Eventually, he became a scare story. Sheldon Reiser, one of the few researchers to continue working on the effects of refined carbohydrates and sugar through the 1970s, told Gary Taubes in 2011: “Yudkin was so discredited. He was ridiculed in a way. And anybody else who said something bad about sucrose [sugar], they’d say, ‘He’s just like Yudkin.’”

If Yudkin was ridiculed, Atkins was a hate figure. Only in the last few years has it become acceptable to study the effects of Atkins-type diets. In 2014, in a trial funded by the US National Institutes of Health, 150 men and women were assigned a diet for one year which limited either the amount of fat or carbs they could eat, but not the calories. By the end of the year, the people on the low carbohydrate, high fat diet had lost about 8lb more on average than the low-fat group. They were also more likely to lose weight from fat tissue; the low-fat group lost some weight too, but it came from the muscles. The NIH study is the latest of more than 50 similar studies, which together suggest that low-carbohydrate diets are better than low-fat diets for achieving weight loss and controlling type 2 diabetes. As a body of evidence, it is far from conclusive, but it is as consistent as any in the literature.

The 2015 edition of the US Dietary Guidelines (they are revised every five years) makes no reference to any of this new research, because the scientists who advised the committee – the most eminent and well-connected nutritionists in the country – neglected to include a discussion of it in their report. It is a gaping omission, inexplicable in scientific terms, but entirely explicable in terms of the politics of nutrition science. If you are seeking to protect your authority, why draw attention to evidence that seems to contradict the assertions on which that authority is founded? Allow a thread like that to be pulled, and a great unravelling might begin.

It may already have done. Last December, the scientists responsible for the report received a humiliating rebuke from Congress, which passed a measure proposing a review of the way the advice informing the guidelines is compiled. It referred to “questions … about the scientific integrity of the process”. The scientists reacted angrily, accusing the politicians of being in thrall to the meat and dairy industries (given how many of the scientists depend on research funding from food and pharmaceutical companies, this might be characterised as audacious).

Some scientists agree with the politicians. David McCarron, a research associate at the Department of Nutrition at the University of California-Davis, told the Washington Post : “There’s a lot of stuff in the guidelines that was right 40 years ago but that has been disproved. Unfortunately, sometimes, the scientific community doesn’t like to backtrack.” Steven Nissen, chairman of cardiovascular medicine at the Cleveland Clinic, was blunter, calling the new guidelines “an evidence-free zone”.

The congressional review has come about partly because of Nina Teicholz. Since her book was published, in 2014, Teicholz has become an advocate for better dietary guidelines. She is on the board of the Nutrition Coalition, a body funded by the philanthropists John and Laura Arnold, the stated purpose of which is to help ensure that nutrition policy is grounded in good science.

In September last year she wrote an article for the BMJ (formerly the British Medical Journal), which makes the case for the inadequacy of the scientific advice that underpins the Dietary Guidelines. The response of the nutrition establishment was ferocious: 173 scientists – some of whom were on the advisory panel, and many of whose work had been critiqued in Teicholz’s book – signed a letter to the BMJ, demanding it retract the piece.

Publishing a rejoinder to an article is one thing; requesting its erasure is another, conventionally reserved for cases involving fraudulent data. As a consultant oncologist for the NHS, Santhanam Sundar, pointed out in a response to the letter on the BMJ website: “Scientific discussion helps to advance science. Calls for retraction, particularly from those in eminent positions, are unscientific and frankly disturbing.”

The letter lists “11 errors”, which on close reading turn out to range from the trivial to the entirely specious. I spoke to several of the scientists who signed the letter. They were happy to condemn the article in general terms, but when I asked them to name just one of the supposed errors in it, not one of them was able to. One admitted he had not read it. Another told me she had signed the letter because the BMJ should not have published an article that was not peer reviewed (it was peer reviewed). Meir Stampfer, a Harvard epidemiologist, asserted that Teicholz’s work is “riddled with errors”, while declining to discuss them with me.

Reticent as they were to discuss the substance of the piece, the scientists were noticeably keener to comment on its author. I was frequently and insistently reminded that Teicholz is a journalist, and not a scientist, and that she had a book to sell, as if this settled the argument. David Katz, of Yale, one of the members of the advisory panel, and an indefatigable defender of the orthodoxies, told me that Teicholz’s work “reeks of conflict of interest” without specifying what those conflicts were. (Dr Katz is the author of four diet books.)

Dr Katz does not pretend that his field has been right on everything – he admitted to changing his own mind, for example, on dietary cholesterol. But he returned again and again to the subject of Teicholz’s character. “Nina is shockingly unprofessional … I have been in rooms filled with the who’s who of nutrition and I have never seen such unanimous revulsion as when Miss Teicholz’s name comes up. She is an animal unlike anything I’ve ever seen before.” Despite requests, he cited no examples of her unprofessional behaviour. (The vitriol poured over Teicholz is rarely dispensed to Gary Taubes, though they make fundamentally similar arguments.)

In March this year, Teicholz was invited to participate in a panel discussion on nutrition science at the National Food Policy conference, in Washington DC, only to be promptly disinvited, after her fellow panelists made it clear that they would not share a platform with her. The organisers replaced her with the CEO of the Alliance for Potato Research and Education.

O ne of the scientists who called for the retraction of Nina Teicholz’s BMJ article, who requested that our conversation be off the record, complained that the rise of social media has created a “problem of authority” for nutrition science. “Any voice, however mad, can gain ground,” he told me.

It is a familiar complaint. By opening the gates of publishing to all, the internet has flattened hierarchies everywhere they exist. We no longer live in a world in which elites of accredited experts are able to dominate conversations about complex or contested matters. Politicians cannot rely on the aura of office to persuade, newspapers struggle to assert the superior integrity of their stories. It is not clear that this change is, overall, a boon for the public realm. But in areas where experts have a track record of getting it wrong, it is hard to see how it could be worse. If ever there was a case that an information democracy, even a very messy one, is preferable to an information oligarchy, then the history of nutrition advice is it.

In the past, we only had two sources of nutritional authority: our doctor and government officials. It was a system that worked well as long as the doctors and officials were informed by good science. But what happens if that cannot be relied on?

The nutritional establishment has proved itself, over the years, skilled at ad hominem takedowns, but it is harder for them to do to Robert Lustig or Nina Teicholz what they once did to John Yudkin. Harder, too, to deflect or smother the charge that the promotion of low-fat diets was a 40-year fad, with disastrous outcomes, conceived of, authorised, and policed by nutritionists.

Professor John Yudkin retired from his post at Queen Elizabeth College in 1971, to write Pure, White and Deadly. The college reneged on a promise to allow him to continue to use its research facilities. It had hired a fully committed supporter of the fat hypothesis to replace him, and it was no longer deemed politic to have a prominent opponent of it on the premises. The man who had built the college’s nutrition department from scratch was forced to ask a solicitor to intervene. Eventually, a small room in a separate building was found for Yudkin.

When I asked Lustig why he was the first researcher in years to focus on the dangers of sugar, he answered: “John Yudkin. They took him down so severely – so severely – that nobody wanted to attempt it on their own.”

Ian Leslie, the author of Curious: the Desire to Know and Why Your Future Depends On It, is a regular contributor to the Long Read. Twitter: @mrianleslie

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The Bitter Truth About Sugar by Robert Lustig (Full Transcript)

• December 6, 2013 9:17 am November 20, 2023 7:30 am
• by Pangambam S

Robert H. Lustig, a Professor of Clinical Pediatrics at University of California, San Francisco (UCSF), here details and explores the real truths about sugar that you perhaps never heard about much before. We thought it might be useful for our readers. So we decided to do a full transcript on his about 90-minute YouTube video called “Sugar: The Bitter Truth”. Hope you find it useful and informative. Please use the “The Bitter Truth About Sugar” slides below while reading this transcript…

The Bitter Truth About Sugar by Robert Lustig Slides  (PDF)

TRANSCRIPT: 

Introduction

I’m going to tell you tonight a story and this story dates that about 30 years. This story has a little bit of something for everybody. It has a little bit of biochemistry, a little bit of clinical research, a little bit of public health, a little bit of politics, a little bit of racial innuendo. The only thing it’s missing is sex. But well, we can see what we can do about that too.

By the end of the story, I hope I will have debunked the last 30 years of nutrition information in America. And I would very much appreciate if at the end of the talk you would tell me whether or not I was successful or not.

Atkins versus Japanese diet

Okay. So in order to get you in the mood as it were, let’s start with a little quiz. What do the Atkins diet and the Japanese diet have in common? Anybody? Well you have the answers right – yes, never mind, that’s right. You have the answer right there.

So the Atkins diet of course is all fat, no carb. The Japanese diet is all carb, no fat. They both work. So what do they share in common? They both eliminate the sugar fructose. With that, think about what it means to be on a diet and what macro-nutrients you are eating and which ones you’re not. And then we’ll go from there and I’ll try to explain how this all works.

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The New York Times

Well | learning to cut the sugar.

Learning to Cut the Sugar

Dr. Robert Lustig became widely known as “the anti-sugar guy” after a lecture of his called “Sugar: The Bitter Truth” was posted on YouTube and gained widespread attention. In his talk, Dr. Lustig explains why all calories are not created equal , and why he believes those from sugar in particular are driving an epidemic of obesity and chronic disease.

But Dr. Lustig, a pediatric endocrinologist who runs a weight management clinic for children and families at the University of California, San Francisco, says that “anti-processed food guy” would be a more appropriate nickname, since sugar — while his biggest concern — is just one of a number of ills he sees in the modern American diet. I recently sat down with Dr. Lustig to talk about his newest book, “The Fat Chance Cookbook,” which he wrote with his friend Cindy Gershen, a chef, as a follow-up to his 2012 bestseller “Fat Chance.” Every recipe was vetted by students at Mount Diablo High School in Concord, Calif., where Ms. Gershen teaches healthy cooking.

To find out more about how children (and their parents) can learn to eat better, why sugar is not banned from his cookbook and why polenta patties are, hands down, Dr. Lustig’s favorite recipe in the book, read our edited conversation.

Your lecture on sugar spread quickly and was viewed by millions of people. Were you surprised?

It blows my mind. I didn’t think anyone was going to watch it. I didn’t even know it was being taped. If I had, I would’ve worn a better tie.

A lot of studies lately have extolled the health benefits of the Mediterranean diet. Do you favor one diet or cuisine over another?

I don’t have any money on any specific cuisine or diet. I think they could all work, and they all did work at one time. But now they don’t because they’re processed.

Pioppi, Italy, is where the Mediterranean diet was centered. Did they have pasta? No. It was meat and vegetables, and some red wine and olive oil. The bottom line is every country has its cuisine, and every cuisine works for that country. But there’s one thing that doesn’t work for any country: processed food. And any country that adopts processed food, which is now everywhere, is getting sick. This is why I want to be known as the anti-processed food guy, not the anti-sugar guy.

What are your thoughts on diets that focus on calories?

I’m not against reducing calories. But if that’s all you’re doing, it can’t work. It depends what those calories are. Everything that comes in a 100-calorie container, half of it is sugar, whether it’s yogurt, or cookies, or whatever. If a calorie is a calorie, then it should work. But it doesn’t, because a calorie is not a calorie. And this is the thing that we have to get past. That’s why I wrote the cookbook. Because the question is, once you realize that all calories are not the same, what do you do?

You treat many obese children in your clinic. Do you ever end up treating parents as well?

Almost always, we see an obese kid come in with an obese parent. And when the kid loses weight, the parent loses weight, because the parent actually changed what’s going on in the home. They made the home safe for the kid and safe for themselves as well. But if the parent is hooked on sugar and they won’t get it out of the house, then the kid can’t get better. If a parent says, ‘Oh, it’s my kid’s problem, but I’m going to eat the cookies,’ then nobody gets better. We see a lot of that.

How do you change behavior?

We do one thing at our clinic that nobody else does, and it’s the key to our success. We do something called “the teaching breakfast.” Every kid comes in fasting because we’re drawing blood. So they’re all hungry. They go to the teaching breakfast with their parents – it’s six families all at a communal table – and our dietitian spends an hour with them. The dietitian narrates exactly what’s on the table and teaches the parent and the kid at the same time.

We make sure four things happen. No. 1, we show the parent the kid will eat the food. No. 2, we show the parent that they will eat the food. No. 3, we show the parent that other kids will eat the food, because they have other kids at home and they have to be able to buy stuff that they know other kids will eat. And No. 4, we show them the grocery bill, so they see that they can afford the food. If you don’t do all four of those, they won’t change.

What are the foods you put on the table?

We tell them that they can make things like steel cut oats and eggs. And on the table we’ll have whole grain muffins, whole grain breads, cheeses. And we have plain yogurt with real fruit mixed in, not the standard American flavored yogurt, which is super high in sugar. And we say, ‘Look, breakfast is not the time for your sugar fix. The more sugar you eat at breakfast, the more trouble you’re going to be in.’ Sugar is the one thing you need to get out of your breakfast.

So these foods on the table are not what these children are used to eating?

If you get your breakfast through the national school breakfast program, which 25 percent of school kids do, guess what you’re getting: a bowl of Fruit Loops and an eight-ounce glass of orange juice. That’s 11 teaspoons of added sugar. This is what we have to fix. But it costs money to fix, and no one wants to do that. So as a country we’re spending it on the tail end, on diabetes, heart disease and everything else.

A lot of the recipes in your book use fruit to add sweet flavors. Was this a way to limit refined sugar?

Exactly. People always say to me, “What about fruit? It has sugar.” But I have nothing against fruit, because it comes with its inherent fiber, and fiber mitigates the negative effects. The way God made it, however much sugar is in a piece of fruit, there’s an equal amount of fiber to offset it.

There’s only one notable exception: grapes. Grapes are just little bags of sugar. They don’t have enough fiber for the amount of sugar that’s in them. But I have nothing against real food, and that includes real fruit. Eat all the fruit you want. It’s only when you turn it into juice that I have a problem with it, because then it loses its fiber.

You have two children at home. Do you let them eat sweets?

So, first of all, my wife is Norwegian. She bakes for therapy. When she’s mad at me, she bakes. That’s how she gets her aggression out. But she only bakes once a week, and the kids only get fresh cookies. We never buy store-bought. Ever. And when my wife bakes five-dozen cookies, she gives them out to the rest of the block. We keep about a dozen cookies for ourselves and for the kids.

My wife has learned by experimenting that she can take any cookie recipe, any cake recipe, and reduce the amount of sugar by one third, and it actually tastes better, and it doesn’t ruin the texture. If you go down by a half, then it does. But if you go down by a third, the cookies still come out just as good. And you can taste the chocolate, the nuts, the oatmeal, the macadamia – whatever is in it. So it’s actually better, and the kids get it as a treat. On weekdays, when they want something sweet, it’s fruit. On the weekends, they’re allowed cookies. So we’re not militant. We’re toeing the line.

What is your favorite recipe in the new book, and why?

Polenta patties with sautéed greens, poached eggs, Roma tomatoes and basil salsa. Hands down winner. It’s vegetables for breakfast. Even though it has carbohydrate, it’s unrefined. It’s high in fiber and micronutrients. It’s the highest quality protein: eggs. And it’s just downright amazing.

Here’s the recipe.

“The Fat Chance Cookbook” Polenta Patties With Sauteed Greens, Poached Eggs, Roma Tomatoes and Basil Salsa

Polenta is corn, but coarse and unrefined. Team it with some vegetables and you can get children to eat veggies for breakfast.

INGREDIENTS 1 batch polenta (see below) 2 tablespoons olive oil 6 cups greens: spinach, chard or kale, rinsed 6 eggs 1 teaspoon distilled white vinegar 1/2 cup Roma Tomato Basil Salsa (see below)

FOR THE POLENTA: 1 cup corn grits or cornmeal 4 cups water Salt to taste

Bring water and salt to a boil in a large pot over high heat. Once the liquid is boiling, slowly add the grits or cornmeal, stirring constantly with a whisk to keep lumps from forming. When the grain is mixed smoothly into the liquid, reduce the heat to low and simmer gently for 30 minutes until very thick. Stir occasionally to keep the polenta from sticking. Allow to cool in an oiled 8-inch square pan or loaf pan.

FOR THE SALSA: 1 pound Roma tomatoes, diced into 1/4-inch pieces 1 tablespoon garlic, peeled and minced 1/2 cup chopped fresh basil 1/2 cup extra-virgin olive oil 1/4 cup balsamic vinegar 1 tablespoon cracked black pepper 1 teaspoon salt

Mix the tomatoes, garlic, basil, oil, balsamic vinegar, pepper and salt together in a bowl. The salsa is best when used immediately. Yield: 2 cups.

PREPARATION:

1. Remove the polenta from the pan and divide into six servings.

2. Heat 1 tablespoon olive oil in a large pan over medium-high heat. Add the polenta slices and fry until golden brown on both sides, about 3 minutes per side. Transfer the polenta slices to a plate and keep warm.

3. Add the remaining 1 tablespoon of oil to the pan and sauté the greens until wilted and tender.

4. Heat 2 inches of water just to a boil in a separate medium-size frying pan, add the white vinegar, then reduce the heat to low. Crack the eggs into the water and poach them until desired doneness, 2 to 3 minutes for soft yolks. Using a slotted spoon, remove the eggs from the water, being careful not to break the yolks. Transfer the eggs to a plate.

5. Place a polenta patty on each of six plates. Top each patty with greens and a poached egg. Pour salsa over all. Or, place all the polenta slices on a platter, top with greens, poached eggs and salsa.

Yield: 6 servings

Nutritional information per serving: 450 calories; 18 grams fat; 3.5 grams saturated fat; 165 milligrams cholesterol; 61 grams carbohydrates; 3 grams dietary fiber; 330 milligrams sodium

Reprinted by arrangement with Hudson Street Press, a member of Penguin Group (USA) LLC, a Penguin Random House Company, from “The Fat Chance Cookbook” by Dr. Robert Lustig. Copyright 2013 by Dr. Robert Lustig.

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• worldfoodpolicy@duke.edu

E205: Here’s what sugar and zero-calorie sweeteners do to your body

The leading voices in food.

Hosted by: Kelly Brownell (Duke) May 17, 2023

Today we speak with an expert on sugar and things meant to replace it. The stakes are high. Very high. Sugar consumption in the population is astronomical and so is the use of sugar replacements. Knowing the impacts of both could help experts provide dietary guidance and help consumers make decisions. Dr. Robert Lustig is Professor Emeritus of Pediatrics in the Division of Endocrinology at the University of California, San Francisco. He specializes on the regulation of energy balance by the central nervous system; body weight regulation, appetite, metabolism, and is very well known for his work on sugar and their substitutes and on policies aimed at improving the diet of the population. A YouTube video on the effects of consuming sugar called “Sugar: The Bitter Truth,” has now been viewed 24 million times.

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Tags: Addiction & Food | Diet & Nutrition | Food Industry Behavior & Marketing | Food Safety & Food Defense | Microbiome | Zero Calorie Sweeteners |

Robert H. Lustig, M.D., M.S.L. is Emeritus Professor of Pediatrics in the Division of Endocrinology, and Member of the Institute for Health Policy Studies at UCSF. Dr. Lustig is a neuroendocrinologist, with expertise in metabolism, obesity, and nutrition. He is one of the leaders of the current “anti-sugar” movement that is changing the food industry. He has dedicated his retirement from clinical medicine to help to fix the food supply any way he can, to reduce human suffering and to salvage the environment. Dr. Lustig graduated from MIT in 1976, and received his M.D. from Cornell University Medical College in 1980. He also received his Masters of Studies in Law (MSL) degree at University of California, Hastings College of the Law in 2013. He is the author of the popular books Fat Chance (2012), The Hacking of the American Mind (2017), and Metabolical: The Lure and the Lies of Processed Food, Nutrition, and Modern Medicine (2021). He is the Chief Science Officer of the non-profit Eat REAL, he is on the Advisory Boards of the UC Davis Innovation Institute for Food and Health, the Center for Humane Technology, Simplex Health, Levels Health, and ReadOut Health, and he is the Chief Medical Officer of BioLumen Technologies, Foogal, Perfact, and Kalin Health.

Interview Summary

URL for “ The Bitter Truth ” video.

Let’s start out with this – so the big hope is that sugar replacements, artificial sweeteners, non-nutritive sweeteners, all known as different things, replace sugar and that people can enjoy sweet taste without the calories. But, of course, the picture is way more complicated. Being an endocrinologist, you are in a good position to explain what happens when the sweeteners enter the body. I’d like to get to that in just a moment, but let’s lead off with another question. Why is it so important for people to consume less sugar?

First, let’s talk about what sugar is. The food industry tells you that sugar is just empty calories. I wish that were true. If that were true, then you could basically spend your discretionary calories on sugar with no problem. But it’s not true. There are two molecules in dietary sugar: the sucrose or the high fructose corn syrup or honey maple syrup agave. They are all basically the same. One molecule of something called glucose, one molecule of something called fructose. Glucose is the energy of life. Glucose is metabolizable by every cell on the planet. Glucose is so important that if you don’t consume it, your body makes it. The liver will take fats and turn it into glucose. It will take amino acids and turn it into glucose process called gluconeogenesis. Glucose actually makes your cells work better. It makes your mitochondria function better, the mitochondria being the little energy burning factories inside each of your cells. Glucose, for lack of a better word, we can call good. Fructose, on the other hand, it is completely different, is metabolized completely differently inside the body and inside the liver. What fructose does is it inhibits mitochondrial function. It actually inhibits three separate enzymes necessary for mitochondria to do their job. So, fructose inhibits energy generation. Now, the food industry will tell you fructose is four calories per gram. Fructose is ready energy. That is why they put high fructose corn syrup in the sports drinks, for example. Well, turns out, that fructose may be ready energy for a bomb calorimeter, but it is not ready energy for your mitochondria. You don’t burn in a bomb calorimeter (a laboratory instrument), you burn via your mitochondria. It turns out, mitochondria are actually poisoned by fructose. So in fact, fructose is a chronic, dose-dependent mitochondrial toxin and this is why we have to eat less of it. But the problem is the food industry keeps putting it in anyway despite the fact that it is killing us.

How much more of it are people consuming than what you might suggest?

The American Heart Association years ago came up with a upper limit per day of about 25 grams, which would be about six teaspoons per day. I was actually part of that group that came up with that and I stick to it because that’s what the data show. We are currently consuming 94 grams. We are consuming almost quadruple the amount that is the upper limit. Now, the notion that something could have empty calories but still be bad for you is not a crazy one. We have two things in our diet that we know are calories but are clearly toxic to us. One is alcohol. Alcohol, seven calories per gram, but alcohol is a poison. And then also trans fats. Trans fats are nine calories per gram, but trans fats are a poison. So just because something has calories doesn’t have anything to do with its metabolic impact.

Where are people getting all the sugar from? I’m assuming it’s not from their sugar bowl.

Exactly. It is not the sugar they add. It is the sugar the food industry adds. Now, where is it? Well, the obvious source is soft drinks. That’s number one by far and away. I mean soft drinks are basically, you know, the devil incarnate. Several municipalities have actually figured that out, and it’s one of the reasons we have soda taxes because it’s actually directed at the problem. A lot of it is in other things that we identify as sweet: candy, cakes, ice cream. A lot of it is in other things like breakfast, cereal, yogurt, even cured meats. It is in a whole host of other things. When you add it all up, 65% of the sugar you consume is in ultra-processed foods. It is not in regular food. It is not in sugar you added to your own food. It is in ultra-processed foods. An ultra-processed food is the vehicle by which the payload, that is that fructose, is doing its damage.

Thanks for that background. We’re really here to talk about the artificial sweeteners but it is irresistible talking to you about sugar in general because you described the whole picture in such a compelling way. So thank you for that. So, onto the artificial sweeteners. What are the main ones in the food supply ?

Well, there are a whole bunch. The most common ones that the food industry uses the most, obviously aspartame, which is Equal. And also sucralose, which is Splenda. But there are others now out on the market: Neotame, there’s Acesulfame-K, there’s monk fruit, there’s Stevia, and all the Steviol glycoside derivatives. There’s now Allulose, and there’s Tagatose. There’s a whole host of different sweeteners that are considered “non-nutritive” meaning they don’t have calories.

These things show up in ways that people don’t necessarily recognize. I mean Diet Coke, Diet Pepsi, those sort of things, it’s obvious they’re artificially sweetened. But these things are showing up in a lot of places, aren’t they?

Indeed. The food industry now understands that sugar is a problem and people have been calling for less sugar but what they’re not calling for is less sweet. And so the industry has a job. It has to deal with that dichotomy.

I know understanding their impacts is complicated by the fact that there are a lot of these things and they’re all chemically different from one another. I’m imagining they have different metabolic effects. What happens when these things get into the body?

Right, and that is the issue. It has nothing to do with calories. People think calories are the issue. This has nothing to do with calories. That’s one of the reasons, Kelly, that I’m committed to one concept: kill the calorie. Kill the calorie as a unit of measure. It was never appropriate. It was actually subterfuge, and it was actually promoted and promulgated by the food industry because if it is about calories, they can assuage their culpability for what they’ve done to our food supply. This has nothing to do with calories. This has to do with metabolic health.

Now, the World Economic Forum just published a white paper called the, “True Purpose of Nutrition,” and it comes down to two words: metabolic health. That is what is going on inside the cell and that’s where the artificial sweeteners do their damage, inside the cell. That’s what we have to talk about. There are several places in the body where artificial sweeteners can do damage that have absolutely nothing to do with calories. The first, you put something sweet on your tongue. Message goes tongue to brain, “Sugar’s coming.” Brain sends a message to the pancreas, “Sugar’s coming, release the insulin.” Then the sugar never comes because it was a diet sweetener. What does the pancreas do? It turns out it releases the insulin anyway even though it had no calories, even though it wasn’t sugar, just because of the sweet taste. So this is known as the cephalic phase of insulin secretion. That insulin is driving energy storage into fat, number one, and it’s also driving cell proliferation in your coronary arteries, cell proliferation in your breast tissue, in other words, cardiovascular disease and cancer and ultimately leading to burnout of your pancreas, and now you’ve got diabetes too. Even though these artificial sweeteners have no calories, they still generate an insulin response, which is still problematic from a metabolic standpoint.

So because of the sweet taste and the body’s response to that, I’m assuming what you’re saying would be true to all of sweeteners?

Exactly. All of them do that. The next step is the artificial sweetener goes down your gullet, goes into your intestine, and the intestine has these bacteria in it called the microbiome. Most people have now heard of that. Different bacteria lead to different effects in the intestine. But think of your intestine – I mean it’s a sewer. It has a whole lot of S-H-you-know-what in there. The goal of the intestine is to keep the S-H-you-know-what IN the lumen of the intestine and not allow it into the bloodstream. It uses three barriers. It has a physical barrier called the mucin layer. It has a biochemical barrier known as tight junctions or zonulins. It also has an immunological barrier called Th17 cells. Those three barriers have to work right to keep the junk out of your bloodstream because if the junk gets into your bloodstream, you now have systemic inflammation, which drives insulin resistance and drives chronic metabolic disease as well. So keeping your intestine in tiptop shape is really important. Well, it turns out those diet sweeteners alter the microbiome. Some of those bacteria like those sweeteners and utilize them to make toxic byproducts, which damage the mucin layer, damage that biochemical tight junction barrier and allow for things to seep through. This is a process called leaky gut. For reasons that are still unclear, sugar tends to deplete those Th17 cells, rendering the immunologic barrier devoid of function. The sum total of which means all the you-know-what in your intestine ends up in your bloodstream, goes to your liver, generates insulin resistance, and you are off to the chronic metabolic disease races as well, from diet sweeteners having nothing to do with calories.

What an amazing picture your painting of these things.

We’ve got one more mechanism. At the fat cell, now this I really don’t understand and it’s early data but seems to be consistent. Turns out adipocytes, fat cells, have receptors for diet sweeteners. Don’t ask me why. I don’t know why. But it turns out, diet sweeteners can act like insulin right at the fat cell to increase energy deposition into the fat cell. Growing those fat cells all by themselves, due to the diet sweetener rather than due to insulin. Now how dumb is that? As a result, there are a lot of different ways diet sweeteners might end up causing problems as well, having nothing to do with calories, having nothing to do with fructose. There was a paper that came out in the European Journal of Clinical Nutrition. It was a meta-analysis of sugar and also of diet sweeteners in terms of diabetes and heart disease. What I can say in one sentence to sum up what this paper showed is that the toxicity of one Coca-Cola equals the toxicity of two diet Coca-Colas. Half as bad. That doesn’t mean good. It means half as bad.

Boy, I mean, any one of the three major pathways to harm would be of concern. If you add them all together, it is a pretty striking picture, isn’t it? I imagine, even if somebody knew about this, they might say, well, you know, I’m willing to accept those risks. I mean, even though you are making them sound substantial, but I’m willing to accept those risks if these products help me control my weight. Do they?

Well, they don’t. That’s part of the problem. There is not one study, not one study in the entire world’s literature, that shows that switching from sugared beverages to diet beverages actually controls weight. The reason is because even though the diet sweeteners don’t release as much insulin now, when you drink the diet sweetener, the pancreas releases it later. That’s actually been shown in several studies now. You get a delayed insulin response, so that the 24-hour insulin burden is the same whether you consume the sugar or the diet sweetener.

Let’s talk about safety for a minute. What about sort of the typical toxicology concerns that people have had for years about these substances, irrespective of what they’re doing to the pancreas and to the other, the microbiome, et cetera? What about the just kind of pure safety of them?

Right, so the one that has generated the most heat, not too much light, unfortunately, is aspartame, NutraSweet. It turns out that aspartame has a very long and checkered history. Did you know that aspartame was made by Searle, G.D. Searle? And, do you know who the CEO of G.D. Searle was at the time that aspartame was approved by the FDA?

His name was Donald Rumsfeld.

An interesting character in history.

Indeed, wouldn’t you think? It turns out that G.D. Searle actually buried most of the toxicology of aspartame in order to get it approved. It is a long complicated and involved story, which we don’t have time for. I’m not even privy to most of the details on that. The bottom line was it ultimately did get approved despite the fact that there was a significant amount of concern about toxicology of this compound. Those questions still remain today. That is one. Another one that is a big issue is sucralose. Sucralose is also called Splenda. Sucralose is a chlorinated poly-fructose and it’s extremely sweet, no question about that. It seems to have some GI side effects that a lot of people don’t like. It also has now been associated with cancer. And most recently, the one that’s gotten the most attention and almost assuredly, Kelly, the reason you called me is the paper that came out about three weeks ago in science about erythritol. So erythritol is a sugar alcohol, and now the meta-analysis of erythritol consumption suggests that it may in fact contribute to heart disease. Now, is that true? Meta-analysis are complicated. People think meta-analysis are the piece de resistance, the highest bar of medical information and analysis. I have four words for meta-analysis: garbage in, garbage out. Meta-analyses are only as good as the studies that they base the data on. If those studies were done by the food industry, which almost all of these are, because that’s who stands to benefit from them. These are almost never NIH studies. These are almost always food industry studies, as you know, the odds are 7.61 times more likely to find in favor of the compound of interest. So all of these are, shall we say, biased. All of these are tainted, and meta-analyses are basically a conglomeration of tainted studies. So what do you expect the result to be?

Thanks for that background. I’m imagining also regarding toxicology and safety, that some of the newer sweeteners like Splenda for example, sucralose, there hasn’t been enough years of use to pick up long-term chronic effects.

Well certainly, if you’re using cardiovascular or cancer events, you’re absolutely right. A lot of these events, you know, take a long time to manifest themselves. Sometimes, a generation or even two generations for that matter, especially for heart disease and cancer. The 15-year-old is drinking 10 diet sodas. When do you expect the heart attack to show up? You know, it’s complicated.

So we use biomarkers to try to answer these questions, but then the biomarker has to actually be a good proxy for those events and often they’re not. Let me give you an example, LDL. Everybody thought LDL was the bad guy. Turns out triglycerides are the way worse guy. LDL has a hazard risk ratio for heart disease of 1.3. Triglycerides have a hazard risk ratio of 1.8. Triglycerides are 50% more important in determining heart disease than LDL is, but we use LDL as the biomarker because it’s more stable. So you have to use the right biomarker and you have to interpret it properly and it actually has to mean something and it has to change relatively acutely. All of which are problematic for all of these biomarkers. It’s hard. It’s hard to do these kinds of analyses. Having said that, my group, a scientific advisory team that I convened to help an offshore ultra-processed food company improve the health of their products. We’ve published this just last month in Frontiers in Nutrition. The company is called Kuwaiti Danish Dairy Company, or KDD. The title of the paper is, “ The Metabolic Matrix: Re-Engineering Ultra-processed Foods to Protect the Liver, Feed the Gut, and Support the Brain .” We did a deep dive on diet sweeteners. We looked at all of these diet sweeteners and their proxies, all the biomarkers. The one that actually popped out that looked to be the most beneficial, at least acutely, is a new one that we’re actually kind of interested in and is picking up speed and it’s called allulose. Allulose currently is 12 times the cost of sugar, but that’s coming down. It turns out allulose lowers LDL and raises HDL. So it may have a better cardiovascular profile, but again, all the caveats that we mentioned before.

That’s very interesting. So given your interest in pediatrics, what about children using these sweeteners?

I am totally against children using sugar because they get fatty liver disease and Type 2 diabetes, and I am totally against them using diet sweeteners because, number one, we don’t know what they’re going to do. Number two, they don’t actually lead to weight loss. That data we do have. So as far as I’m concerned, we really only have one option and that is de-sweeten our lives. We have to de-sweeten the food.

Perfect lead in to the next question I was going to ask. So do you think it is possible for people to become accustomed to less sweetness? I mean, let’s say the food industry is required to gradually reduce sugar and sweetness from the sweeteners. What do you think would happen?

Absolutely. It is not only possible, it is eminently doable. And I know why and we have the data for why that is. So there is a very smart lady, neuroscientist at the University of Michigan by the name of Monica Dus, who has done all this work in fruit flies of all places. She has shown the desensitization of the tongue to sugar has to do with changes in receptors and changes in specific substrates in the taste buds of the tongue. When you stop the sugar availability, it takes three weeks for those receptors to increase and repopulate, and for those problematic substrates to go away. You can actually retrain your tongue in three weeks to be much more sensitive to the sugar that is in the food naturally. After a three-week abstinence period or a reduction or a weaning period, a blueberry will taste like a sugar bomb in your mouth. So we know this can happen and we actually have proven this for salt previously. The UK, as you know Kelly, back in 2003, the Blair government convened all the food industry concerns in Great Britain. So Marks & Spencer, and Weight Rose, and Tesco, et cetera, all around the big table, didn’t let media in, and basically said to every single food industry concerned in Great Britain, “Look, we have a hypertension and stroke problem and it’s because of the salt content of the food and we are going to play referee here in the government. And each of you is going to reduce the salt content of your food by 10% per year over a three-year period so that you’ll reduce your salt by 30% at the end of this and everyone’s going to play together, so that there’s no competitive disadvantage and most importantly, we’re not going to tell anybody.” That’s what they did. Sure enough, in 2011, a paper appeared in Burge Medical Journal, demonstrating a 40% reduction in hypertension and stroke because of the public health effort that the Blair government made in terms of reducing the amount of salt in processed food. We can do the same with sugar today.

The salt example is a good one because I think many people have sort of experienced this in their day-to-day lives, even in the United States, where industry hasn’t done exactly what’s happening in Britain. People have tried to reduce salt in their diet, add less salt, and buy products with less salt. And then sometimes they’ll go back and consume something that they had before and find it extremely salty, even unpleasantly salty. It’s interesting to hear on the sugar front that that same experience might be possible and that there’s a biological reason for it. It is not just that you psychologically get accustomed to different levels of sugar, in this case, but there’s a biological change occurring that might help keep that going.

Absolutely. You can change people’s behavior by changing their biochemistry. This is how I got into this field by using a drug that suppressed insulin and getting kids who were 400 pounds due to their brain tumor to actually lose weight and start exercising because we got their insulin down. You can fix the biochemistry and the behavior will follow suit. The food industry could do that and we wouldn’t even notice.

So I’m guessing I know the answer to this question before I even ask it, but let’s go ahead. Would you suggest the food industry be mandated to make gradual reductions in sugar, just like you mentioned with salt in the UK?

Absolutely, I’m working toward that. The only thing that I say is we should not tell anybody.

So it would be sort of a stealth move then. You would not necessarily have to make a big deal of it to the public, because they might assume there’s going to be a change in the desirability and the pleasure of the products when that’s not necessarily the case.

As soon as you do something to their food, someone’s going to scream, “Nanny state!” This is not nanny state. Ultimately, this is a public health problem. We have to deal with it with a public health solution. You know, that means changing things. If the amount of sugar in our food supply went down, say by 3% every six months down, so that we were able to cut our sugar consumption by 25%, which would be the same basically as what a tax would do. We would save so many billions of dollars in healthcare costs, and we would increase productivity so much. We actually published a paper, a microsimulation analysis in BMJ years ago where we quantified the savings to government, to insurers, to the public. If we actually got sugar down and, you know, actually listened to what the USDA told us, it would be amazing. There is data, there’s a pathway forward, there’s precedent for doing it. I absolutely think that is where we need to go.

Rob, you’re making me feel very smart at the moment, because I figured this was going to be a podcast filled with information and helpful bits of knowledge and it sure was. I’m really grateful that you were able to join us and the topic couldn’t be more important. Thank you again for being with us.

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Sugar: The Bitter Truth

7/27/2009; 89 minutes.

Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology, explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin. Recorded on 05/26/2009. (#16717)

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