bacon<\/em> cheeseburgers,” but allowed no\nstarches or refined carbohydrates, which means no sugars or anything made from\nflour. Atkins banned even fruit juices, and permitted only a modicum of\nvegetables, although the latter were negotiable as the diet progressed. <\/p>\n\n\n\nAtkins was by no means the first to get rich pushing a high-fat\ndiet that restricted carbohydrates, but he popularized it to an extent that the\nAmerican Medical Association considered it a potential threat to our health.\nThe A.M.A. attacked Atkins’s diet as a ”bizarre regimen” that advocated ”an\nunlimited intake of saturated fats and cholesterolrich foods,” and Atkins even\nhad to defend his diet in Congressional hearings.\n<\/p>\n\n\n\n
Thirty years later, America has become weirdly polarized on the\nsubject of weight. On the one hand, we’ve been told with almost religious\ncertainty by everyone from the surgeon general on down, and we have come to\nbelieve with almost religious certainty, that obesity is caused by the\nexcessive consumption of fat, and that if we eat less fat we will lose weight\nand live longer. On the other, we have the ever-resilient message of Atkins and\ndecades’ worth of best-selling diet books, including ”The Zone,” ”Sugar\nBusters” and ”Protein Power” to name a few. All push some variation of what\nscientists would call the alternative hypothesis: it’s not the fat that makes\nus fat, but the carbohydrates, and if we eat less carbohydrates we will lose\nweight and live longer. <\/p>\n\n\n\n
The perversity of this alternative hypothesis is that it\nidentifies the cause of obesity as precisely those refined carbohydrates at the\nbase of the famous Food Guide Pyramid — the pasta, rice and bread — that we\nare told should be the staple of our healthy low-fat diet, and then on the\nsugar or corn syrup in the soft drinks, fruit juices and sports drinks that we\nhave taken to consuming in quantity if for no other reason than that they are\nfat free and so appear intrinsically healthy. While the low-fat-is-good-health\ndogma represents reality as we have come to know it, and the government has\nspent hundreds of millions of dollars in research trying to prove its worth,\nthe low-carbohydrate message has been relegated to the realm of unscientific\nfantasy. <\/p>\n\n\n\n
Over the past five years, however, there has been a subtle shift\nin the scientific consensus. It used to be that even considering the\npossibility of the alternative hypothesis, let alone researching it, was\ntantamount to quackery by association. Now a small but growing minority of\nestablishment researchers have come to take seriously what the low-carb-diet\ndoctors have been saying all along. Walter Willett, chairman of the department\nof nutrition at the Harvard School of Public Health, may be the most visible\nproponent of testing this heretic hypothesis. Willett is the de facto spokesman\nof the longest-running, most comprehensive diet and health studies ever\nperformed, which have already cost upward of $100 million and include data on\nnearly 300,000 individuals. Those data, says Willett, clearly contradict the\nlow-fat-is-good-health message ”and the idea that all fat is bad for you; the\nexclusive focus on adverse effects of fat may have contributed to the obesity\nepidemic.” <\/p>\n\n\n\n
These researchers point out that there are plenty of reasons to\nsuggest that the low-fatis-good-health hypothesis has now effectively failed\nthe test of time. In particular, that we are in the midst of an obesity\nepidemic that started around the early 1980’s, and that this was coincident\nwith the rise of the low-fat dogma. (Type 2 diabetes, the most common form of\nthe disease, also rose significantly through this period.) They say that\nlow-fat weight-loss diets have proved in clinical trials and real life to be\ndismal failures, and that on top of it all, the percentage of fat in the\nAmerican diet has been decreasing for two decades. Our cholesterol levels have\nbeen declining, and we have been smoking less, and yet the incidence of heart\ndisease has not declined as would be expected. ”That is very disconcerting,”\nWillett says. ”It suggests that something else bad is happening.” <\/p>\n\n\n\n
The science behind the alternative hypothesis can be called\nEndocrinology 101, which is how it’s referred to by David Ludwig, a researcher\nat Harvard Medical School who runs the pediatric obesity clinic at Children’s\nHospital Boston, and who prescribes his own version of a\ncarbohydrate-restricted diet to his patients. Endocrinology 101 requires an\nunderstanding of how carbohydrates affect insulin and blood sugar and in turn\nfat metabolism and appetite. This is basic endocrinology, Ludwig says, which is\nthe study of hormones, and it is still considered radical because the low-fat\ndietary wisdom emerged in the 1960’s from researchers almost exclusively\nconcerned with the effect of fat on cholesterol and heart disease. At the time,\nEndocrinology 101 was still underdeveloped, and so it was ignored. Now that\nthis science is becoming clear, it has to fight a quarter century of anti-fat\nprejudice. <\/p>\n\n\n\n
The alternative hypothesis also comes with an implication that is\nworth considering for a moment, because it’s a whopper, and it may indeed be an\nobstacle to its acceptance. If the alternative hypothesis is right — still a\nbig ”if” — then it strongly suggests that the ongoing epidemic of obesity in\nAmerica and elsewhere is not, as we are constantly told, due simply to a\ncollective lack of will power and a failure to exercise. Rather it occurred, as\nAtkins has been saying (along with Barry Sears, author of ”The Zone”),\nbecause the public health authorities told us unwittingly, but with the best of\nintentions, to eat precisely those foods that would make us fat, and we did. We\nate more fat-free carbohydrates, which, in turn, made us hungrier and then\nheavier. Put simply, if the alternative hypothesis is right, then a low-fat\ndiet is not by definition a healthy diet. In practice, such a diet cannot help\nbeing high in carbohydrates, and that can lead to obesity, and perhaps even\nheart disease. ”For a large percentage of the population, perhaps 30 to 40\npercent, low-fat diets are counterproductive,” says Eleftheria MaratosFlier,\ndirector of obesity research at Harvard’s prestigious Joslin Diabetes Center.\n”They have the paradoxical effect of making people gain weight.” <\/p>\n\n\n\n
Scientists are still arguing about fat, despite a century of\nresearch, because the regulation of appetite and weight in the human body\nhappens to be almost inconceivably complex, and the experimental tools we have\nto study it are still remarkably inadequate. This combination leaves\nresearchers in an awkward position. To study the entire physiological system\ninvolves feeding real food to real human subjects for months or years on end,\nwhich is prohibitively expensive, ethically questionable (if you’re trying to\nmeasure the effects of foods that might cause heart disease) and virtually\nimpossible to do in any kind of rigorously controlled scientific manner. But if\nresearchers seek to study something less costly and more controllable, they end\nup studying experimental situations so oversimplified that their results may\nhave nothing to do with reality. This then leads to a research literature so\nvast that it’s possible to find at least some published research to support\nvirtually any theory. The result is a balkanized community — ”splintered,\nvery opinionated and in many instances, intransigent,” says Kurt Isselbacher,\na former chairman of the Food and Nutrition Board of the National Academy of\nScience — in which researchers seem easily convinced that their preconceived\nnotions are correct and thoroughly uninterested in testing any other hypotheses\nbut their own. <\/p>\n\n\n\n
What’s more, the number of misconceptions propagated about the\nmost basic research can be staggering. Researchers will be suitably scientific\ndescribing the limitations of their own experiments, and then will cite\nsomething as gospel truth because they read it in a magazine. The classic\nexample is the statement heard repeatedly that 95 percent of all dieters never\nlose weight, and 95 percent of those who do will not keep it off. This will be\ncorrectly attributed to the University of Pennsylvania psychiatrist Albert\nStunkard, but it will go unmentioned that this statement is based on 100\npatients who passed through Stunkard’s obesity clinic during the Eisenhower\nadministration. <\/p>\n\n\n\n
With these caveats, one of the few reasonably reliable facts\nabout the obesity epidemic is that it started around the early 1980’s.\nAccording to Katherine Flegal, an epidemiologist at the National Center for\nHealth Statistics, the percentage of obese Americans stayed relatively constant\nthrough the 1960’s and 1970’s at 13 percent to 14 percent and then shot up by 8\npercentage points in the 1980’s. By the end of that decade, nearly one in four\nAmericans was obese. That steep rise, which is consistent through all segments\nof American society and which continued unabated through the 1990’s, is the\nsingular feature of the epidemic. Any theory that tries to explain obesity in\nAmerica has to account for that. Meanwhile, overweight children nearly tripled\nin number. And for the first time, physicians began diagnosing Type 2 diabetes\nin adolescents. Type 2 diabetes often accompanies obesity. It used to be called\nadultonset diabetes and now, for the obvious reason, is not. <\/p>\n\n\n\n
So how did this happen? The orthodox and ubiquitous explanation\nis that we live in what Kelly Brownell, a Yale psychologist, has called a\n”toxic food environment” of cheap fatty food, large portions, pervasive food\nadvertising and sedentary lives. By this theory, we are at the Pavlovian mercy\nof the food industry, which spends nearly $10 billion a year advertising\nunwholesome junk food and fast food. And because these foods, especially fast\nfood, are so filled with fat, they are both irresistible and uniquely\nfattening. On top of this, so the theory goes, our modern society has\nsuccessfully eliminated physical activity from our daily lives. We no longer\nexercise or walk up stairs, nor do our children bike to school or play outside,\nbecause they would prefer to play video games and watch television. And because\nsome of us are obviously predisposed to gain weight while others are not, this\nexplanation also has a genetic component — the thrifty gene. It suggests that\nstoring extra calories as fat was an evolutionary advantage to our Paleolithic\nancestors, who had to survive frequent famine. We then inherited these\n”thrifty” genes, despite their liability in today’s toxic environment. <\/p>\n\n\n\n
This theory makes perfect sense and plays to our puritanical\nprejudice that fat, fast food and television are innately damaging to our\nhumanity. But there are two catches. First, to buy this logic is to accept that\nthe copious negative reinforcement that accompanies obesity — both socially\nand physically — is easily overcome by the constant bombardment of food\nadvertising and the lure of a supersize bargain meal. And second, as Flegal\npoints out, little data exist to support any of this. Certainly none of it\nexplains what changed so significantly to start the epidemic. Fast-food\nconsumption, for example, continued to grow steadily through the 70’s and 80’s,\nbut it did not take a sudden leap, as obesity did. <\/p>\n\n\n\n
As far as exercise and physical activity go, there are no\nreliable data before the mid80’s, according to William Dietz, who runs the\ndivision of nutrition and physical activity at the Centers for Disease Control;\nthe 1990’s data show obesity rates continuing to climb, while exercise activity\nremained unchanged. This suggests the two have little in common. Dietz also\nacknowledged that a culture of physical exercise began in the United States in\nthe 70’s — the ”leisure exercise mania,” as Robert Levy, director of the <\/p>\n\n\n\n
National Heart, Lung and Blood Institute, described it in 1981 —\nand has continued through the present day.\n<\/p>\n\n\n\n
As for the thrifty gene, it provides the kind of evolutionary\nrationale for human behavior that scientists find comforting but that simply\ncannot be tested. In other words, if we were living through an anorexia\nepidemic, the experts would be discussing the equally untestable ”spendthrift\ngene” theory, touting evolutionary advantages of losing weight effortlessly.\nAn overweight homo erectus, they’d say, would have been easy prey for\npredators. <\/p>\n\n\n\n
It is also undeniable, note students of Endocrinology 101, that\nmankind never evolved to eat a diet high in starches or sugars. ”Grain\nproducts and concentrated sugars were essentially absent from human nutrition\nuntil the invention of agriculture,” Ludwig says, ”which was only 10,000\nyears ago.” This is discussed frequently in the anthropology texts but is\nmostly absent from the obesity literature, with the prominent exception of the\nlow-carbohydrate-diet books. <\/p>\n\n\n\n
What’s forgotten in the current controversy is that the low-fat\ndogma itself is only about 25 years old. Until the late 70’s, the accepted\nwisdom was that fat and protein protected against overeating by making you\nsated, and that carbohydrates made you fat. In ”The Physiology of Taste,” for\ninstance, an 1825 discourse considered among the most famous books ever written\nabout food, the French gastronome Jean Anthelme BrillatSavarin says that he\ncould easily identify the causes of obesity after 30 years of listening to one\n”stout party” after another proclaiming the joys of bread, rice and (from a\n”particularly stout party”) potatoes. Brillat-Savarin described the roots of\nobesity as a natural predisposition conjuncted with the ”floury and feculent\nsubstances which man makes the prime ingredients of his daily nourishment.” He\nadded that the effects of this fecula — i.e., ”potatoes, grain or any kind of\nflour” — were seen sooner when sugar was added to the diet. <\/p>\n\n\n\n
This is what my mother taught me 40 years ago, backed up by the\nvague observation that Italians tended toward corpulence because they ate so\nmuch pasta. This observation was actually documented by Ancel Keys, a\nUniversity of Minnesota physician who noted that fats ”have good staying power,”\nby which he meant they are slow to be digested and so lead to satiation, and\nthat Italians were among the heaviest populations he had studied. According to\nKeys, the Neapolitans, for instance, ate only a little lean meat once or twice\na week, but ate bread and pasta every day for lunch and dinner. ”There was no\nevidence of nutritional deficiency,” he wrote, ”but the workingclass women\nwere fat.” <\/p>\n\n\n\n
By the 70’s, you could still find articles in the journals\ndescribing high rates of obesity in Africa and the Caribbean where diets\ncontained almost exclusively carbohydrates. The common thinking, wrote a former\ndirector of the Nutrition Division of the United Nations, was that the ideal\ndiet, one that prevented obesity, snacking and excessive sugar consumption, was\na diet ”with plenty of eggs, beef, mutton, chicken, butter and wellcooked\nvegetables.” This was the identical prescription Brillat-Savarin put forth in\n1825. <\/p>\n\n\n\n
It was Ancel Keys, paradoxically, who introduced the\nlow-fat-is-good-health dogma in the 50’s with his theory that dietary fat\nraises cholesterol levels and gives you heart disease. Over the next two\ndecades, however, the scientific evidence supporting this theory remained\nstubbornly ambiguous. The case was eventually settled not by new science but by\npolitics. It began in January 1977, when a Senate committee led by George\nMcGovern published its ”Dietary Goals for the United States,” advising that\nAmericans significantly curb their fat intake to abate an epidemic of ”killer\ndiseases” supposedly sweeping the country. It peaked in late 1984, when the\nNational Institutes of Health officially recommended that all Americans over\nthe age of 2 eat less fat. By that time, fat had become ”this greasy killer”\nin the memorable words of the Center for Science in the Public Interest, and\nthe model American breakfast of eggs and bacon was well on its way to becoming\na bowl of Special K with low-fat milk, a glass of orange juice and toast, hold\nthe butter — a dubious feast of refined carbohydrates. <\/p>\n\n\n\n
In the intervening years, the N.I.H. spent several hundred\nmillion dollars trying to demonstrate a connection between eating fat and\ngetting heart disease and, despite what we might think, it failed. Five major\nstudies revealed no such link. A sixth, however, costing well over $100 million\nalone, concluded that reducing cholesterol by drug therapy could prevent heart\ndisease. The N.I.H. administrators then made a leap of faith. Basil Rifkind,\nwho oversaw the relevant trials for the N.I.H., described their logic this way:\nthey had failed to demonstrate at great expense that eating less fat had any\nhealth benefits. But if a cholesterol-lowering drug could prevent heart\nattacks, then a low-fat, cholesterol-lowering diet should do the same. ”It’s\nan imperfect world,” Rifkind told me. ”The data that would be definitive is\nungettable, so you do your best with what is available.” <\/p>\n\n\n\n
Some of the best scientists disagreed with this low-fat logic,\nsuggesting that good science was incompatible with such leaps of faith, but\nthey were effectively ignored. Pete Ahrens, whose Rockefeller University\nlaboratory had done the seminal research on cholesterol metabolism, testified\nto McGovern’s committee that everyone responds differently to low-fat diets. It\nwas not a scientific matter who might benefit and who might be harmed, he said,\nbut ”a betting matter.” Phil Handler, then president of the National Academy\nof Sciences, testified in Congress to the same effect in 1980. ”What right,”\nHandler asked, ”has the federal government to propose that the American people\nconduct a vast nutritional experiment, with themselves as subjects, on the\nstrength of so very little evidence that it will do them any good?” <\/p>\n\n\n\n
Nonetheless, once the N.I.H. signed off on the low-fat doctrine,\nsocietal forces took over. The food industry quickly began producing thousands\nof reduced-fat food products to meet the new recommendations. Fat was removed\nfrom foods like cookies, chips and yogurt. The problem was, it had to be\nreplaced with something as tasty and pleasurable to the palate, which meant\nsome form of sugar, often high-fructose corn syrup. Meanwhile, an entire\nindustry emerged to create fat substitutes, of which Procter & Gamble’s\nolestra was first. And because these reduced-fat meats, cheeses, snacks and\ncookies had to compete with a few hundred thousand other food products marketed\nin America, the industry dedicated considerable advertising effort to\nreinforcing the lessfat-is-good-health message. Helping the cause was what\nWalter Willett calls the ”huge forces” of dietitians, health organizations,\nconsumer groups, health reporters and even cookbook writers, all well-intended\nmissionaries of healthful eating.\n<\/p>\n\n\n\n
Few experts now deny that the low-fat message is radically\noversimplified. If nothing else, it effectively ignores the fact that\nunsaturated fats, like olive oil, are relatively good for you: they tend to\nelevate your good cholesterol, high-density lipoprotein (H.D.L.), and lower\nyour bad cholesterol, low-density lipoprotein (L.D.L.), at least in comparison\nto the effect of carbohydrates. While higher L.D.L. raises your heart-disease\nrisk, higher H.D.L. <\/p>\n\n\n\n
reduces it. <\/p>\n\n\n\n
What this means is that even saturated fats — a k a, the bad\nfats — are not nearly as deleterious as you would think. True, they will\nelevate your bad cholesterol, but they will also elevate your good cholesterol.\nIn other words, it’s a virtual wash. As Willett explained to me, you will gain\nlittle to no health benefit by giving up milk, butter and cheese and eating\nbagels instead. <\/p>\n\n\n\n
But it gets even weirder than that. Foods considered more or less\ndeadly under the lowfat dogma turn out to be comparatively benign if you\nactually look at their fat content. More than two-thirds of the fat in a\nporterhouse steak, for instance, will definitively improve your cholesterol\nprofile (at least in comparison with the baked potato next to it); it’s true\nthat the remainder will raise your L.D.L., the bad stuff, but it will also\nboost your H.D.L. The same is true for lard. If you work out the numbers, you\ncome to the surreal conclusion that you can eat lard straight from the can and\nconceivably reduce your risk of heart disease.\n<\/p>\n\n\n\n
The crucial example of how the low-fat recommendations were\noversimplified is shown by the impact — potentially lethal, in fact — of\nlow-fat diets on triglycerides, which are the component molecules of fat. By\nthe late 60’s, researchers had shown that high triglyceride levels were at\nleast as common in heart-disease patients as high L.D.L. cholesterol, and that\neating a low-fat, high-carbohydrate diet would, for many people, raise their\ntriglyceride levels, lower their H.D.L. levels and accentuate what Gerry\nReaven, an endocrinologist at Stanford University, called Syndrome X. This is a\ncluster of conditions that can lead to heart disease and Type 2 diabetes. <\/p>\n\n\n\n
It took Reaven a decade to convince his peers that Syndrome X was\na legitimate health concern, in part because to accept its reality is to accept\nthat low-fat diets will increase the risk of heart disease in a third of the\npopulation. ”Sometimes we wish it would go away because nobody knows how to\ndeal with it,” said Robert Silverman, an N.I.H. researcher, at a 1987 N.I.H.\nconference. ”High protein levels can be bad for the kidneys. High fat is bad\nfor your heart. Now Reaven is saying not to eat high carbohydrates. We have to\neat something.” <\/p>\n\n\n\n
Surely, everyone involved in drafting the various dietary\nguidelines wanted Americans simply to eat less junk food, however you define\nit, and eat more the way they do in Berkeley, Calif. But we didn’t go along.\nInstead we ate more starches and refined carbohydrates, because calorie for\ncalorie, these are the cheapest nutrients for the food industry to produce, and\nthey can be sold at the highest profit. It’s also what we like to eat. Rare is\nthe person under the age of 50 who doesn’t prefer a cookie or heavily sweetened\nyogurt to a head of broccoli.\n<\/p>\n\n\n\n
”All reformers would do well to be conscious of the law of\nunintended consequences,” says Alan Stone, who was staff director for\nMcGovern’s Senate committee. Stone told me he had an inkling about how the food\nindustry would respond to the new dietary goals back when the hearings were\nfirst held. An economist pulled him aside, he said, and gave him a lesson on\nmarket disincentives to healthy eating: ”He said if you create a new market\nwith a brand-new manufactured food, give it a brand-new fancy name, put a big\nadvertising budget behind it, you can have a market all to yourself and force\nyour competitors to catch up. You can’t do that with fruits and vegetables.\nIt’s harder to differentiate an apple from an apple.” <\/p>\n\n\n\n
Nutrition researchers also played a role by trying to feed\nscience into the idea that carbohydrates are the ideal nutrient. It had been\nknown, for almost a century, and considered mostly irrelevant to the etiology\nof obesity, that fat has nine calories per gram compared with four for\ncarbohydrates and protein. Now it became the fail-safe position of the low-fat\nrecommendations: reduce the densest source of calories in the diet and you will\nlose weight. Then in 1982, J.P. Flatt, a University of Massachusetts\nbiochemist, published his research demonstrating that, in any normal diet, it\nis extremely rare for the human body to convert carbohydrates into body fat.\nThis was then misinterpreted by the media and quite a few scientists to mean\nthat eating carbohydrates, even to excess, could not make you fat — which is\nnot the case, Flatt says. But the misinterpretation developed a vigorous life\nof its own because it resonated with the notion that fat makes you fat and\ncarbohydrates are harmless. <\/p>\n\n\n\n
As a result, the major trends in American diets since the late\n70’s, according to the U.S.D.A. agricultural economist Judith Putnam, have been\na decrease in the percentage of fat calories and a ”greatly increased\nconsumption of carbohydrates.” To be precise, annual grain consumption has\nincreased almost 60 pounds per person, and caloric sweeteners (primarily high-fructose\ncorn syrup) by 30 pounds. At the same time, we suddenly began consuming more\ntotal calories: now up to 400 more each day since the government started\nrecommending low-fat diets. <\/p>\n\n\n\n
If these trends are correct, then the obesity epidemic can\ncertainly be explained by Americans’ eating more calories than ever — excess\ncalories, after all, are what causes us to gain weight — and, specifically,\nmore carbohydrates. The question is why?\n<\/p>\n\n\n\n
The answer provided by Endocrinology 101 is that we are simply\nhungrier than we were in the 70’s, and the reason is physiological more than\npsychological. In this case, the salient factor — ignored in the pursuit of\nfat and its effect on cholesterol — is how carbohydrates affect blood sugar\nand insulin. In fact, these were obvious culprits all along, which is why\nAtkins and the low-carb-diet doctors pounced on them early. <\/p>\n\n\n\n
The primary role of insulin is to regulate blood-sugar levels.\nAfter you eat carbohydrates, they will be broken down into their component\nsugar molecules and transported into the bloodstream. Your pancreas then\nsecretes insulin, which shunts the blood sugar into muscles and the liver as\nfuel for the next few hours. This is why carbohydrates have a significant\nimpact on insulin and fat does not. And because juvenile diabetes is caused by\na lack of insulin, physicians believed since the 20’s that the only evil with\ninsulin is not having enough.\n<\/p>\n\n\n\n
But insulin also regulates fat metabolism. We cannot store body\nfat without it. Think of insulin as a switch. When it’s on, in the few hours\nafter eating, you burn carbohydrates for energy and store excess calories as\nfat. When it’s off, after the insulin has been depleted, you burn fat as fuel.\nSo when insulin levels are low, you will burn your own fat, but not when they’re\nhigh. <\/p>\n\n\n\n
This is where it gets unavoidably complicated. The fatter you\nare, the more insulin your pancreas will pump out per meal, and the more likely\nyou’ll develop what’s called ”insulin resistance,” which is the underlying\ncause of Syndrome X. In effect, your cells become insensitive to the action of\ninsulin, and so you need ever greater amounts to keep your blood sugar in\ncheck. So as you gain weight, insulin makes it easier to store fat and harder\nto lose it. But the insulin resistance in turn may make it harder to store fat\n— your weight is being kept in check, as it should be. But now the insulin\nresistance might prompt your pancreas to produce even more insulin, potentially\nstarting a vicious cycle. Which comes first — the obesity, the elevated\ninsulin, known as hyperinsulinemia, or the insulin resistance — is a\nchicken-and-egg problem that hasn’t been resolved. One endocrinologist\ndescribed this to me as ”the Nobel-prize winning question.” <\/p>\n\n\n\n
Insulin also profoundly affects hunger, although to what end is\nanother point of controversy. On the one hand, insulin can indirectly cause\nhunger by lowering your blood sugar, but how low does blood sugar have to drop\nbefore hunger kicks in? That’s unresolved. Meanwhile, insulin works in the\nbrain to suppress hunger. The theory, as explained to me by Michael Schwartz,\nan endocrinologist at the University of Washington, is that insulin’s ability\nto inhibit appetite would normally counteract its propensity to generate body\nfat. In other words, as you gained weight, your body would generate more\ninsulin after every meal, and that in turn would suppress your appetite; you’d\neat less and lose the weight.\n<\/p>\n\n\n\n
Schwartz, however, can imagine a simple mechanism that would\nthrow this <\/p>\n\n\n\n
”homeostatic” system off balance: if your brain were to lose\nits sensitivity to insulin, just as your fat and muscles do when they are\nflooded with it. Now the higher insulin production that comes with getting\nfatter would no longer compensate by suppressing your appetite, because your\nbrain would no longer register the rise in insulin. The end result would be a\nphysiologic state in which obesity is almost preordained, and one in which the\ncarbohydrate-insulin connection could play a major role. Schwartz says he\nbelieves this could indeed be happening, but research hasn’t progressed far\nenough to prove it. ”It is just a hypothesis,” he says. ”It still needs to\nbe sorted out.” <\/p>\n\n\n\n
David Ludwig, the Harvard endocrinologist, says that it’s the\ndirect effect of insulin on blood sugar that does the trick. He notes that when\ndiabetics get too much insulin, their blood sugar drops and they get ravenously\nhungry. They gain weight because they eat more, and the insulin promotes fat\ndeposition. The same happens with lab animals. This, he says, is effectively\nwhat happens when we eat carbohydrates — in particular sugar and starches like\npotatoes and rice, or anything made from flour, like a slice of white bread.\nThese are known in the jargon as high-glycemic-index carbohydrates, which means\nthey are absorbed quickly into the blood. As a result, they cause a spike of\nblood sugar and a surge of insulin within minutes. The resulting rush of\ninsulin stores the blood sugar away and a few hours later, your blood sugar is\nlower than it was before you ate. As Ludwig explains, your body effectively\nthinks it has run out of fuel, but the insulin is still high enough to prevent\nyou from burning your own fat. The result is hunger and a craving for more\ncarbohydrates. It’s another vicious circle, and another situation ripe for\nobesity. <\/p>\n\n\n\n
The glycemic-index concept and the idea that starches can be\nabsorbed into the blood even faster than sugar emerged in the late 70’s, but\nagain had no influence on public health recommendations, because of the\nattendant controversies. To wit: if you bought the glycemic-index concept, then\nyou had to accept that the starches we were supposed to be eating 6 to 11 times\na day were, once swallowed, physiologically indistinguishable from sugars. This\nmade them seem considerably less than wholesome. Rather than accept this\npossibility, the policy makers simply allowed sugar and corn syrup to elude the\nvilification that befell dietary fat. After all, they are fat-free. <\/p>\n\n\n\n
Sugar and corn syrup from soft drinks, juices and the copious\nteas and sports drinks now supply more than 10 percent of our total calories;\nthe 80’s saw the introduction of Big Gulps and 32-ounce cups of Coca-Cola ,\nblasted through with sugar, but 100 percent fat free. When it comes to insulin and\nblood sugar, these soft drinks and fruit juices — what the scientists call\n”wet carbohydrates” — might indeed be worst of all. (Diet soda accounts for\nless than a quarter of the soda market.)\n<\/p>\n\n\n\n
The gist of the glycemic-index idea is that the longer it takes\nthe carbohydrates to be digested, the lesser the impact on blood sugar and\ninsulin and the healthier the food. Those foods with the highest rating on the\nglycemic index are some simple sugars, starches and anything made from flour.\nGreen vegetables, beans and whole grains cause a much slower rise in blood\nsugar because they have fiber, a nondigestible carbohydrate, which slows down\ndigestion and lowers the glycemic index. Protein and fat serve the same\npurpose, which implies that eating fat can be beneficial, a notion that is\nstill unacceptable. And the glycemic-index concept implies that a primary cause\nof Syndrome X, heart disease, Type 2 diabetes and obesity is the long-term\ndamage caused by the repeated surges of insulin that come from eating starches\nand refined carbohydrates. This suggests a kind of unified field theory for\nthese chronic diseases, but not one that coexists easily with the low-fat\ndoctrine. <\/p>\n\n\n\n
At Ludwig’s pediatric obesity clinic, he has been prescribing\nlow-glycemic-index diets to children and adolescents for five years now. He\ndoes not recommend the Atkins diet because he says he believes such a very low\ncarbohydrate approach is unnecessarily restrictive; instead, he tells his\npatients to effectively replace refined carbohydrates and starches with\nvegetables, legumes and fruit. This makes a low-glycemic-index diet consistent\nwith dietary common sense, albeit in a higher-fat kind of way. His clinic now\nhas a nine-month waiting list. Only recently has Ludwig managed to convince the\nN.I.H. <\/p>\n\n\n\n
that such diets are worthy of study. His first three grant\nproposals were summarily rejected, which may explain why much of the relevant\nresearch has been done in Canada and in Australia. In April, however, Ludwig\nreceived $1.2 million from the N.I.H. to test his low-glycemic-index diet\nagainst a traditional low-fat-low-calorie regime. That might help resolve some\nof the controversy over the role of insulin in obesity, although the\nredoubtable Robert Atkins might get there first.\n<\/p>\n\n\n\n
The 71-year-old Atkins, a graduate of Cornell medical school,\nsays he first tried a very low carbohydrate diet in 1963 after reading about\none in the Journal of the American Medical Association. He lost weight\neffortlessly, had his epiphany and turned a fledgling Manhattan cardiology\npractice into a thriving obesity clinic. He then alienated the entire medical\ncommunity by telling his readers to eat as much fat and protein as they wanted,\nas long as they ate little to no carbohydrates. They would lose weight, he\nsaid, because they would keep their insulin down; they wouldn’t be hungry; and\nthey would have less resistance to burning their own fat. Atkins also noted\nthat starches and sugar were harmful in any event because they raised\ntriglyceride levels and that this was a greater risk factor for heart disease\nthan cholesterol. <\/p>\n\n\n\n
Atkins’s diet is both the ultimate manifestation of the\nalternative hypothesis as well as the battleground on which the\nfat-versus-carbohydrates controversy is likely to be fought scientifically over\nthe next few years. After insisting Atkins was a quack for three decades,\nobesity experts are now finding it difficult to ignore the copious anecdotal\nevidence that his diet does just what he has claimed. Take Albert Stunkard, for\ninstance. <\/p>\n\n\n\n
Stunkard has been trying to treat obesity for half a century, but\nhe told me he had his epiphany about Atkins and maybe about obesity as well\njust recently when he discovered that the chief of radiology in his hospital\nhad lost 60 pounds on Atkins’s diet. ”Well, apparently all the young guys in\nthe hospital are doing it,” he said. ”So we decided to do a study.” When I\nasked Stunkard if he or any of his colleagues considered testing Atkins’s diet\n30 years ago, he said they hadn’t because they thought Atkins was ”a jerk”\nwho was just out to make money: this ”turned people off, and so nobody took\nhim seriously enough to do what we’re finally doing.” <\/p>\n\n\n\n
In fact, when the American Medical Association released its\nscathing critique of Atkins’s diet in March 1973, it acknowledged that the diet\nprobably worked, but expressed little interest in why. Through the 60’s, this\nhad been a subject of considerable research, with the conclusion that\nAtkins-like diets were low-calorie diets in disguise; that when you cut out\npasta, bread and potatoes, you’ll have a hard time eating enough meat,\nvegetables and cheese to replace the calories.\n<\/p>\n\n\n\n
That, however, raised the question of why such a low-calorie\nregimen would also suppress hunger, which Atkins insisted was the signature characteristic\nof the diet. One possibility was Endocrinology 101: that fat and protein make\nyou sated and, lacking carbohydrates and the ensuing swings of blood sugar and\ninsulin, you stay sated. The other possibility arose from the fact that\nAtkins’s diet is ”ketogenic.” This means that insulin falls so low that you\nenter a state called ketosis, which is what happens during fasting and\nstarvation. Your muscles and tissues burn body fat for energy, as does your\nbrain in the form of fat molecules produced by the liver called ketones. Atkins\nsaw ketosis as the obvious way to kick-start weight loss. He also liked to say\nthat ketosis was so energizing that it was better than sex, which set him up\nfor some ridicule. An inevitable criticism of Atkins’s diet has been that\nketosis is dangerous and to be avoided at all costs. <\/p>\n\n\n\n
When I interviewed ketosis experts, however, they universally\nsided with Atkins, and suggested that maybe the medical community and the media\nconfuse ketosis with ketoacidosis, a variant of ketosis that occurs in\nuntreated diabetics and can be fatal. ”Doctors are scared of ketosis,” says\nRichard Veech, an N.I.H. researcher who studied medicine at Harvard and then\ngot his doctorate at Oxford University with the Nobel Laureate Hans Krebs. ”They’re\nalways worried about diabetic ketoacidosis. But ketosis is a normal physiologic\nstate. I would argue it is the normal state of man. It’s not normal to have\nMcDonald’s and a delicatessen around every corner. It’s normal to starve.” <\/p>\n\n\n\n
Simply put, ketosis is evolution’s answer to the thrifty gene. We\nmay have evolved to efficiently store fat for times of famine, says Veech, but\nwe also evolved ketosis to efficiently live off that fat when necessary. Rather\nthan being poison, which is how the press often refers to ketones, they make\nthe body run more efficiently and provide a backup fuel source for the brain.\nVeech calls ketones ”magic” and has shown that both the heart and brain run\n25 percent more efficiently on ketones than on blood sugar. <\/p>\n\n\n\n
The bottom line is that for the better part of 30 years Atkins\ninsisted his diet worked and was safe, Americans apparently tried it by the\ntens of millions, while nutritionists, physicians, public- health authorities\nand anyone concerned with heart disease insisted it could kill them, and\nexpressed little or no desire to find out who was right. During that period,\nonly two groups of U.S. researchers tested the diet, or at least published\ntheir results. In the early 70’s, J.P. Flatt and Harvard’s George Blackburn pioneered\nthe ”protein-sparing modified fast” to treat postsurgical patients, and they\ntested it on obese volunteers. Blackburn, who later became president of the\nAmerican Society of Clinical Nutrition, describes his regime as ”an Atkins\ndiet without excess fat” and says he had to give it a fancy name or nobody\nwould take him seriously. The diet was ”lean meat, fish and fowl”\nsupplemented by vitamins and minerals. ”People loved it,” Blackburn recalls.\n”Great weight loss. We couldn’t run them off with a baseball bat.” Blackburn\nsuccessfully treated hundreds of obese patients over the next decade and\npublished a series of papers that were ignored. When obese New Englanders\nturned to appetitecontrol drugs in the mid-80’s, he says, he let it drop. He\nthen applied to the N.I.H. for a grant to do a clinical trial of popular diets\nbut was rejected. <\/p>\n\n\n\n
The second trial, published in September 1980, was done at the\nGeorge Washington University Medical Center. Two dozen obese volunteers agreed\nto follow Atkins’s diet for eight weeks and lost an average of 17 pounds each,\nwith no apparent ill effects, although their L.D.L. cholesterol did go up. The\nresearchers, led by John LaRosa, now president of the State University of New\nYork Downstate Medical Center in Brooklyn, concluded that the 17-pound weight\nloss in eight weeks would likely have happened with any diet under ”the\nnovelty of trying something under experimental conditions” and never pursued\nit further. <\/p>\n\n\n\n
Now researchers have finally decided that Atkins’s diet and other\nlow-carb diets have to be tested, and are doing so against traditional\nlow-calorie-low-fat diets as recommended by the American Heart Association. To\nexplain their motivation, they inevitably tell one of two stories: some, like\nStunkard, told me that someone they knew — a patient, a friend, a fellow\nphysician — lost considerable weight on Atkins’s diet and, despite all their\npreconceptions to the contrary, kept it off. Others say they were frustrated\nwith their inability to help their obese patients, looked into the low-carb\ndiets and decided that Endocrinology 101 was compelling. ”As a trained\nphysician, I was trained to mock anything like the Atkins diet,” says Linda\nStern, an internist at the Philadelphia Veterans Administration Hospital, ”but\nI put myself on the diet. I did great. And I thought maybe this is something I\ncan offer my patients.” <\/p>\n\n\n\n
None of these studies have been financed by the N.I.H., and none\nhave yet been published. But the results have been reported at conferences —\nby researchers at Schneider Children’s Hospital on Long Island, Duke University\nand the University of Cincinnati, and by Stern’s group at the Philadelphia V.A.\nHospital. And then there’s the study Stunkard had mentioned, led by Gary Foster\nat the University of Pennsylvania, Sam Klein, director of the Center for Human\nNutrition at Washington University in St. <\/p>\n\n\n\n
Louis, and Jim Hill, who runs the University of Colorado Center\nfor Human Nutrition in Denver. The results of all five of these studies are\nremarkably consistent. Subjects on some form of the Atkins diet — whether\noverweight adolescents on the diet for 12 weeks as at Schneider, or obese\nadults averaging 295 pounds on the diet for six months, as at the Philadelphia\nV.A. — lost twice the weight as the subjects on the low-fat, low-calorie\ndiets. <\/p>\n\n\n\n
In all five studies, cholesterol levels improved similarly with\nboth diets, but triglyceride levels were considerably lower with the Atkins\ndiet. Though researchers are hesitant to agree with this, it does suggest that\nheart-disease risk could actually be reduced when fat is added back into the\ndiet and starches and refined carbohydrates are removed. ”I think when this\nstuff gets to be recognized,” Stunkard says, ”it’s going to really shake up a\nlot of thinking about obesity and metabolism.”\n<\/p>\n\n\n\n
All of this could be settled sooner rather than later, and with\nit, perhaps, we might have some long-awaited answers as to why we grow fat and\nwhether it is indeed preordained by societal forces or by our choice of foods.\nFor the first time, the N.I.H. is now actually financing comparative studies of\npopular diets. Foster, Klein and Hill, for instance, have now received more\nthan $2.5 million from N.I.H. to do a five-year trial of the Atkins diet with\n360 obese individuals. At Harvard, Willett, Blackburn and Penelope Greene have\nmoney, albeit from Atkins’s nonprofit foundation, to do a comparative trial as\nwell. <\/p>\n\n\n\n
Should these clinical trials also find for Atkins and his\nhigh-fat, low-carbohydrate diet, then the public-health authorities may indeed\nhave a problem on their hands. Once they took their leap of faith and settled\non the low-fat dietary dogma 25 years ago, they left little room for\ncontradictory evidence or a change of opinion, should such a change be\nnecessary to keep up with the science. In this light Sam Klein’s experience is\nnoteworthy. Klein is president-elect of the North American Association for the\nStudy of Obesity, which suggests that he is a highly respected member of his\ncommunity. And yet, he described his recent experience discussing the Atkins\ndiet at medical conferences as a learning experience. ”I have been\nimpressed,” he said, ”with the anger of academicians in the audience. Their\nresponse is ‘How dare you even present data on the Atkins diet!’ ” <\/p>\n\n\n\n
This hostility stems primarily from their anxiety that Americans,\ngiven a glimmer of hope about their weight, will rush off en masse to try a\ndiet that simply seems intuitively dangerous and on which there is still no\nlong-term data on whether it works and whether it is safe. It’s a justifiable\nfear. In the course of my research, I have spent my mornings at my local diner,\nstaring down at a plate of scrambled eggs and sausage, convinced that somehow,\nsome way, they must be working to clog my arteries and do me in. <\/p>\n\n\n\n
After 20 years steeped in a low-fat paradigm, I find it hard to\nsee the nutritional world any other way. I have learned that low-fat diets fail\nin clinical trials and in real life, and they certainly have failed in my life.\nI have read the papers suggesting that 20 years of low-fat recommendations have\nnot managed to lower the incidence of heart disease in this country, and may\nhave led instead to the steep increase in obesity and Type 2 diabetes. I have\ninterviewed researchers whose computer models have calculated that cutting back\non the saturated fats in my diet to the levels recommended by the American\nHeart Association would not add more than a few months to my life, if that. I\nhave even lost considerable weight with relative ease by giving up carbohydrates\non my test diet, and yet I can look down at my eggs and sausage and still\nimagine the imminent onset of heart disease and obesity, the latter assuredly\nto be caused by some bizarre rebound phenomena the likes of which science has\nnot yet begun to describe. The fact that Atkins himself has had heart trouble\nrecently does not ease my anxiety, despite his assurance that it is not\ndiet-related. <\/p>\n\n\n\n
This is the state of mind I imagine that mainstream\nnutritionists, researchers and physicians must inevitably take to the\nfat-versus-carbohydrate controversy. They may come around, but the evidence\nwill have to be exceptionally compelling. Although this kind of conversion may\nbe happening at the moment to John Farquhar, who is a professor of health\nresearch and policy at Stanford University and has worked in this field for\nmore than 40 years. When I interviewed Farquhar in April, he explained why\nlow-fat diets might lead to weight gain and low-carbohydrate diets might lead\nto weight loss, but he made me promise not to say he believed they did. He\nattributed the cause of the obesity epidemic to the ”force-feeding of a\nnation.” Three weeks later, after reading an article on Endocrinology 101 by\nDavid Ludwig in the Journal of the American Medical Association, he sent me an\ne-mail message asking the not-entirely-rhetorical question, ”Can we get the\nlow-fat proponents to apologize?”\nGary Taubes is a correspondent for the journal\nScience and author of ”Bad Science: The Short Life and Weird Times of Cold\nFusion.”<\/em> <\/em><\/p>\n","protected":false},"excerpt":{"rendered":"\u00a0July 7, 2002, Sunday \u00a0\u00a0The New York Times Courtesy of \u00a0Gary Taubes \u00a0 If the members of the American medical establishment were to have a collective findyourself-standing-naked-in-Times-Square-type nightmare, this might […]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":743,"menu_order":0,"comment_status":"open","ping_status":"closed","template":"","meta":{"advanced_seo_description":"","jetpack_seo_html_title":"","jetpack_seo_noindex":false,"jetpack_seo_schema_type":"","footnotes":""},"class_list":["post-513","page","type-page","status-publish","hentry"],"jetpack_sharing_enabled":true,"jetpack_likes_enabled":true,"jetpack-related-posts":[{"id":515,"url":"https:\/\/eqht.net\/?page_id=515","url_meta":{"origin":513,"position":0},"title":"Goitrogenic and Estrogenic Activity of Soy Isoflavones","author":"Info@EQHT.net","date":"2025-09-11","format":false,"excerpt":"Endocrine Disruptors Daniel R. 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