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 . 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 . Suggesting that sugar might kill us is what zealots do. 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. 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. And I also have a disclaimer to acknowledge. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. This is a critical point, particularly because high- fructose corn syrup has indeed become . In the early 1. 98. It was also cheaper than sugar, which didn. 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. 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 5. It was first marketed in the late 1. 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 2. 01. 0 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. 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 . Refined sugar and H. F. C. S. It allows everyone to assign blame for obesity and, by extension, diabetes . 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 . The calories are the same, but the metabolic consequences are quite different. The fructose component of sugar and H. F. C. S. 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 . 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. 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. Watch 'The Skinny on Obesity' with Dr. Lustig: http:// Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology, explores the damage caused by sugary foods. WebMD experts and contributors provide answers to your health questions. How Many Grams Of Sugar Should A Diabetic Have 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 2. 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 . There was enough ambiguity, they concluded, that they couldn. Referring back to the 2. Explore traits, the characteristics that make us unique. We are pleased to offer you a partial preview of our new Tour of Basic Genetics. More chapters will be available soon. But we wanted to make the new chapters.Institute of Medicine report released last fall reiterated, . To be precise, the F. D. A. 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. This is 2. 00 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. By the early 2. 00. U. S. D. A., we had increased our consumption to more than 9. That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it. In 1. 98. 0, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn. By the early 2. 00. Americans was obese, and 1. This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. In 1. 92. 4, 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 1. Civil War years, and that deaths increased as much as fourfold in some U. S. This coincided, he noted, with an equally significant increase in sugar consumption . 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. 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 1. 96. 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 1. John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called . 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. Few in the medical community took Yudkin. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. Brody wrote in The Times in 1. 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. Photo. Credit. Kenji Aoki for The New York Times In 1. 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. In 1. 97. 1, Keys published an article attacking Yudkin and describing his evidence against sugar as . And anybody else who said something bad about sucrose, they? 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 7. 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. 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 . 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 . 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 . But having chronically elevated insulin levels has harmful effects of its own . A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the . 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 5. 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 ?
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