What if it isn't black or white? What if it's grey? What if "no no, don't eat fat" and "no no, don't eat carbohydrates" are too polarized?
What we've learned also includes the fact that some fats not only don't contribute to coronary artery disease, but may actually fight cholesterol and plaque - monounsaturated fats like olive oil, canola oil, foods like avocado and nuts. And not all carbos are alike. And none of these "diet warriors" seem to be addressing the quantity of food, the role of exercise on metabolism, etc. Plus, they are gauging their diet's "success" by how much people lose - not whether they keep it off. Sounds like kids arguing "did so", "did not", "oh yeah?" <sigh> -Ben > http://www.nytimes.com/2002/07/07/magazine/07FAT.html?ex=1027152773&ei=1&en= > 26e1f71eb4478e2a > > What if It's All Been a Big Fat Lie? > > July 7, 2002 > By GARY TAUBES > > If the members of the American medical establishment were > to have a collective > find-yourself-standing-naked-in-Times-Square-type > nightmare, this might be it. They spend 30 years ridiculing > Robert Atkins, author of the phenomenally-best-selling > ''Dr. Atkins' Diet Revolution'' and ''Dr. Atkins' New Diet > Revolution,'' accusing the Manhattan doctor of quackery and > fraud, only to discover that the unrepentant Atkins was > right all along. Or maybe it's this: they find that their > very own dietary recommendations -- eat less fat and more > carbohydrates -- are the cause of the rampaging epidemic of > obesity in America. Or, just possibly this: they find out > both of the above are true. > > When Atkins first published his ''Diet Revolution'' in > 1972, Americans were just coming to terms with the > proposition that fat -- particularly the saturated fat of > meat and dairy products -- was the primary nutritional evil > in the American diet. Atkins managed to sell millions of > copies of a book promising that we would lose weight eating > steak, eggs and butter to our heart's desire, because it > was the carbohydrates, the pasta, rice, bagels and sugar, > that caused obesity and even heart disease. Fat, he said, > was harmless. > > Atkins allowed his readers to eat ''truly luxurious foods > without limit,'' as he put it, ''lobster with butter sauce, > steak with bearnaise sauce . . . bacon cheeseburgers,'' but > allowed no starches or refined carbohydrates, which means > no sugars or anything made from flour. Atkins banned even > fruit juices, and permitted only a modicum of vegetables, > although the latter were negotiable as the diet progressed. > > > Atkins was by no means the first to get rich pushing a > high-fat diet that restricted carbohydrates, but he > popularized it to an extent that the American Medical > Association considered it a potential threat to our health. > The A.M.A. attacked Atkins's diet as a ''bizarre regimen'' > that advocated ''an unlimited intake of saturated fats and > cholesterol-rich foods,'' and Atkins even had to defend his > diet in Congressional hearings. > > Thirty years later, America has become weirdly polarized on > the subject of weight. On the one hand, we've been told > with almost religious certainty by everyone from the > surgeon general on down, and we have come to believe with > almost religious certainty, that obesity is caused by the > excessive consumption of fat, and that if we eat less fat > we will lose weight and live longer. On the other, we have > the ever-resilient message of Atkins and decades' worth of > best-selling diet books, including ''The Zone,'' ''Sugar > Busters'' and ''Protein Power'' to name a few. All push > some variation of what scientists would call the > alternative hypothesis: it's not the fat that makes us fat, > but the carbohydrates, and if we eat less carbohydrates we > will lose weight and live longer. > > The perversity of this alternative hypothesis is that it > identifies the cause of obesity as precisely those refined > carbohydrates at the base of the famous Food Guide Pyramid > -- the pasta, rice and bread -- that we are told should be > the staple of our healthy low-fat diet, and then on the > sugar or corn syrup in the soft drinks, fruit juices and > sports drinks that we have taken to consuming in quantity > if for no other reason than that they are fat free and so > appear intrinsically healthy. While the > low-fat-is-good-health dogma represents reality as we have > come to know it, and the government has spent hundreds of > millions of dollars in research trying to prove its worth, > the low-carbohydrate message has been relegated to the > realm of unscientific fantasy. > > Over the past five years, however, there has been a subtle > shift in the scientific consensus. It used to be that even > considering the possibility of the alternative hypothesis, > let alone researching it, was tantamount to quackery by > association. Now a small but growing minority of > establishment researchers have come to take seriously what > the low-carb-diet doctors have been saying all along. > Walter Willett, chairman of the department of nutrition at > the Harvard School of Public Health, may be the most > visible proponent of testing this heretic hypothesis. > Willett is the de facto spokesman of the longest-running, > most comprehensive diet and health studies ever performed, > which have already cost upward of $100 million and include > data on nearly 300,000 individuals. Those data, says > Willett, clearly contradict the low-fat-is-good-health > message ''and the idea that all fat is bad for you; the > exclusive focus on adverse effects of fat may have > contributed to the obesity epidemic.'' > > These researchers point out that there are plenty of > reasons to suggest that the low-fat-is-good-health > hypothesis has now effectively failed the test of time. In > particular, that we are in the midst of an obesity epidemic > that started around the early 1980's, and that this was > coincident with the rise of the low-fat dogma. (Type 2 > diabetes, the most common form of the disease, also rose > significantly through this period.) They say that low-fat > weight-loss diets have proved in clinical trials and real > life to be dismal failures, and that on top of it all, the > percentage of fat in the American diet has been decreasing > for two decades. Our cholesterol levels have been > declining, and we have been smoking less, and yet the > incidence of heart disease has not declined as would be > expected. ''That is very disconcerting,'' Willett says. > ''It suggests that something else bad is happening.'' > > The science behind the alternative hypothesis can be called > Endocrinology 101, which is how it's referred to by David > Ludwig, a researcher at Harvard Medical School who runs the > pediatric obesity clinic at Children's Hospital Boston, and > who prescribes his own version of a carbohydrate-restricted > diet to his patients. Endocrinology 101 requires an > understanding of how carbohydrates affect insulin and blood > sugar and in turn fat metabolism and appetite. This is > basic endocrinology, Ludwig says, which is the study of > hormones, and it is still considered radical because the > low-fat dietary wisdom emerged in the 1960's from > researchers almost exclusively concerned with the effect of > fat on cholesterol and heart disease. At the time, > Endocrinology 101 was still underdeveloped, and so it was > ignored. Now that this science is becoming clear, it has to > fight a quarter century of anti-fat prejudice. > > The alternative hypothesis also comes with an implication > that is worth considering for a moment, because it's a > whopper, and it may indeed be an obstacle to its > acceptance. If the alternative hypothesis is right -- still > a big ''if'' -- then it strongly suggests that the ongoing > epidemic of obesity in America and elsewhere is not, as we > are constantly told, due simply to a collective lack of > will power and a failure to exercise. Rather it occurred, > as Atkins has been saying (along with Barry Sears, author > of ''The Zone''), because the public health authorities > told us unwittingly, but with the best of intentions, to > eat precisely those foods that would make us fat, and we > did. We ate more fat-free carbohydrates, which, in turn, > made us hungrier and then heavier. Put simply, if the > alternative hypothesis is right, then a low-fat diet is not > by definition a healthy diet. In practice, such a diet > cannot help being high in carbohydrates, and that can lead > to obesity, and perhaps even heart disease. ''For a large > percentage of the population, perhaps 30 to 40 percent, > low-fat diets are counterproductive,'' says Eleftheria > Maratos-Flier, director of obesity research at Harvard's > prestigious Joslin Diabetes Center. ''They have the > paradoxical effect of making people gain weight.'' > > Scientists are still arguing about fat, despite a century > of research, because the regulation of appetite and weight > in the human body happens to be almost inconceivably > complex, and the experimental tools we have to study it are > still remarkably inadequate. This combination leaves > researchers in an awkward position. To study the entire > physiological system involves feeding real food to real > human subjects for months or years on end, which is > prohibitively expensive, ethically questionable (if you're > trying to measure the effects of foods that might cause > heart disease) and virtually impossible to do in any kind > of rigorously controlled scientific manner. But if > researchers seek to study something less costly and more > controllable, they end up studying experimental situations > so oversimplified that their results may have nothing to do > with reality. This then leads to a research literature so > vast that it's possible to find at least some published > research to support virtually any theory. The result is a > balkanized community -- ''splintered, very opinionated and > in many instances, intransigent,'' says Kurt Isselbacher, a > former chairman of the Food and Nutrition Board of the > National Academy of Science -- in which researchers seem > easily convinced that their preconceived notions are > correct and thoroughly uninterested in testing any other > hypotheses but their own. > > What's more, the number of misconceptions propagated about > the most basic research can be staggering. Researchers will > be suitably scientific describing the limitations of their > own experiments, and then will cite something as gospel > truth because they read it in a magazine. The classic > example is the statement heard repeatedly that 95 percent > of all dieters never lose weight, and 95 percent of those > who do will not keep it off. This will be correctly > attributed to the University of Pennsylvania psychiatrist > Albert Stunkard, but it will go unmentioned that this > statement is based on 100 patients who passed through > Stunkard's obesity clinic during the Eisenhower > administration. > > With these caveats, one of the few reasonably reliable > facts about the obesity epidemic is that it started around > the early 1980's. According to Katherine Flegal, an > epidemiologist at the National Center for Health > Statistics, the percentage of obese Americans stayed > relatively constant through the 1960's and 1970's at 13 > percent to 14 percent and then shot up by 8 percentage > points in the 1980's. By the end of that decade, nearly one > in four Americans was obese. That steep rise, which is > consistent through all segments of American society and > which continued unabated through the 1990's, is the > singular feature of the epidemic. Any theory that tries to > explain obesity in America has to account for that. > Meanwhile, overweight children nearly tripled in number. > And for the first time, physicians began diagnosing Type 2 > diabetes in adolescents. Type 2 diabetes often accompanies > obesity. It used to be called adult-onset diabetes and now, > for the obvious reason, is not. > > So how did this happen? The orthodox and ubiquitous > explanation is that we live in what Kelly Brownell, a Yale > psychologist, has called a ''toxic food environment'' of > cheap fatty food, large portions, pervasive food > advertising and sedentary lives. By this theory, we are at > the Pavlovian mercy of the food industry, which spends > nearly $10 billion a year advertising unwholesome junk food > and fast food. And because these foods, especially fast > food, are so filled with fat, they are both irresistible > and uniquely fattening. On top of this, so the theory goes, > our modern society has successfully eliminated physical > activity from our daily lives. We no longer exercise or > walk up stairs, nor do our children bike to school or play > outside, because they would prefer to play video games and > watch television. And because some of us are obviously > predisposed to gain weight while others are not, this > explanation also has a genetic component -- the thrifty > gene. It suggests that storing extra calories as fat was an > evolutionary advantage to our Paleolithic ancestors, who > had to survive frequent famine. We then inherited these > ''thrifty'' genes, despite their liability in today's toxic > environment. > > This theory makes perfect sense and plays to our > puritanical prejudice that fat, fast food and television > are innately damaging to our humanity. But there are two > catches. First, to buy this logic is to accept that the > copious negative reinforcement that accompanies obesity -- > both socially and physically -- is easily overcome by the > constant bombardment of food advertising and the lure of a > supersize bargain meal. And second, as Flegal points out, > little data exist to support any of this. Certainly none of > it explains what changed so significantly to start the > epidemic. Fast-food consumption, for example, continued to > grow steadily through the 70's and 80's, but it did not > take a sudden leap, as obesity did. > > As far as exercise and physical activity go, there are no > reliable data before the mid-80's, according to William > Dietz, who runs the division of nutrition and physical > activity at the Centers for Disease Control; the 1990's > data show obesity rates continuing to climb, while exercise > activity remained unchanged. This suggests the two have > little in common. Dietz also acknowledged that a culture of > physical exercise began in the United States in the 70's -- > the ''leisure exercise mania,'' as Robert Levy, director of > the National Heart, Lung and Blood Institute, described it > in 1981 -- and has continued through the present day. > > As for the thrifty gene, it provides the kind of > evolutionary rationale for human behavior that scientists > find comforting but that simply cannot be tested. In other > words, if we were living through an anorexia epidemic, the > experts would be discussing the equally untestable > ''spendthrift gene'' theory, touting evolutionary > advantages of losing weight effortlessly. An overweight > homo erectus, they'd say, would have been easy prey for > predators. > > It is also undeniable, note students of Endocrinology 101, > that mankind never evolved to eat a diet high in starches > or sugars. ''Grain products and concentrated sugars were > essentially absent from human nutrition until the invention > of agriculture,'' Ludwig says, ''which was only 10,000 > years ago.'' This is discussed frequently in the > anthropology texts but is mostly absent from the obesity > literature, with the prominent exception of the > low-carbohydrate-diet books. > > What's forgotten in the current controversy is that the > low-fat dogma itself is only about 25 years old. Until the > late 70's, the accepted wisdom was that fat and protein > protected against overeating by making you sated, and that > carbohydrates made you fat. In ''The Physiology of Taste,'' > for instance, an 1825 discourse considered among the most > famous books ever written about food, the French gastronome > Jean Anthelme Brillat-Savarin says that he could easily > identify the causes of obesity after 30 years of listening > to one ''stout party'' after another proclaiming the joys > of bread, rice and (from a ''particularly stout party'') > potatoes. Brillat-Savarin described the roots of obesity as > a natural predisposition conjuncted with the ''floury and > feculent substances which man makes the prime ingredients > of his daily nourishment.'' He added that the effects of > this fecula -- i.e., ''potatoes, grain or any kind of > flour'' -- were seen sooner when sugar was added to the > diet. > > This is what my mother taught me 40 years ago, backed up by > the vague observation that Italians tended toward > corpulence because they ate so much pasta. This observation > was actually documented by Ancel Keys, a University of > Minnesota physician who noted that fats ''have good staying > power,'' by which he meant they are slow to be digested and > so lead to satiation, and that Italians were among the > heaviest populations he had studied. According to Keys, the > Neapolitans, for instance, ate only a little lean meat once > or twice a week, but ate bread and pasta every day for > lunch and dinner. ''There was no evidence of nutritional > deficiency,'' he wrote, ''but the working-class women were > fat.'' > > By the 70's, you could still find articles in the journals > describing high rates of obesity in Africa and the > Caribbean where diets contained almost exclusively > carbohydrates. The common thinking, wrote a former director > of the Nutrition Division of the United Nations, was that > the ideal diet, one that prevented obesity, snacking and > excessive sugar consumption, was a diet ''with plenty of > eggs, beef, mutton, chicken, butter and well-cooked > vegetables.'' This was the identical prescription > Brillat-Savarin put forth in 1825. > > It was Ancel Keys, paradoxically, who introduced the > low-fat-is-good-health dogma in the 50's with his theory > that dietary fat raises cholesterol levels and gives you > heart disease. Over the next two decades, however, the > scientific evidence supporting this theory remained > stubbornly ambiguous. The case was eventually settled not > by new science but by politics. It began in January 1977, > when a Senate committee led by George McGovern published > its ''Dietary Goals for the United States,'' advising that > Americans significantly curb their fat intake to abate an > epidemic of ''killer diseases'' supposedly sweeping the > country. It peaked in late 1984, when the National > Institutes of Health officially recommended that all > Americans over the age of 2 eat less fat. By that time, fat > had become ''this greasy killer'' in the memorable words of > the Center for Science in the Public Interest, and the > model American breakfast of eggs and bacon was well on its > way to becoming a bowl of Special K with low-fat milk, a > glass of orange juice and toast, hold the butter -- a > dubious feast of refined carbohydrates. > > In the intervening years, the N.I.H. spent several hundred > million dollars trying to demonstrate a connection between > eating fat and getting heart disease and, despite what we > might think, it failed. Five major studies revealed no such > link. A sixth, however, costing well over $100 million > alone, concluded that reducing cholesterol by drug therapy > could prevent heart disease. The N.I.H. administrators then > made a leap of faith. Basil Rifkind, who oversaw the > relevant trials for the N.I.H., described their logic this > way: they had failed to demonstrate at great expense that > eating less fat had any health benefits. But if a > cholesterol-lowering drug could prevent heart attacks, then > a low-fat, cholesterol-lowering diet should do the same. > ''It's an imperfect world,'' Rifkind told me. ''The data > that would be definitive is ungettable, so you do your best > with what is available.'' > > Some of the best scientists disagreed with this low-fat > logic, suggesting that good science was incompatible with > such leaps of faith, but they were effectively ignored. > Pete Ahrens, whose Rockefeller University laboratory had > done the seminal research on cholesterol metabolism, > testified to McGovern's committee that everyone responds > differently to low-fat diets. It was not a scientific > matter who might benefit and who might be harmed, he said, > but ''a betting matter.'' Phil Handler, then president of > the National Academy of Sciences, testified in Congress to > the same effect in 1980. ''What right,'' Handler asked, > ''has the federal government to propose that the American > people conduct a vast nutritional experiment, with > themselves as subjects, on the strength of so very little > evidence that it will do them any good?'' > > Nonetheless, once the N.I.H. signed off on the low-fat > doctrine, societal forces took over. The food industry > quickly began producing thousands of reduced-fat food > products to meet the new recommendations. Fat was removed > from foods like cookies, chips and yogurt. The problem was, > it had to be replaced with something as tasty and > pleasurable to the palate, which meant some form of sugar, > often high-fructose corn syrup. Meanwhile, an entire > industry emerged to create fat substitutes, of which > Procter & Gamble's olestra was first. And because these > reduced-fat meats, cheeses, snacks and cookies had to > compete with a few hundred thousand other food products > marketed in America, the industry dedicated considerable > advertising effort to reinforcing the > less-fat-is-good-health message. Helping the cause was what > Walter Willett calls the ''huge forces'' of dietitians, > health organizations, consumer groups, health reporters and > even cookbook writers, all well-intended missionaries of > healthful eating. > > Few experts now deny that the low-fat message is radically > oversimplified. If nothing else, it effectively ignores the > fact that unsaturated fats, like olive oil, are relatively > good for you: they tend to elevate your good cholesterol, > high-density lipoprotein (H.D.L.), and lower your bad > cholesterol, low-density lipoprotein (L.D.L.), at least in > comparison to the effect of carbohydrates. While higher > L.D.L. raises your heart-disease risk, higher H.D.L. > reduces it. > > What this means is that even saturated fats -- a k a, the > bad fats -- are not nearly as deleterious as you would > think. True, they will elevate your bad cholesterol, but > they will also elevate your good cholesterol. In other > words, it's a virtual wash. As Willett explained to me, you > will gain little to no health benefit by giving up milk, > butter and cheese and eating bagels instead. > > But it gets even weirder than that. Foods considered more > or less deadly under the low-fat dogma turn out to be > comparatively benign if you actually look at their fat > content. More than two-thirds of the fat in a porterhouse > steak, for instance, will definitively improve your > cholesterol profile (at least in comparison with the baked > potato next to it); it's true that the remainder will raise > your L.D.L., the bad stuff, but it will also boost your > H.D.L. The same is true for lard. If you work out the > numbers, you come to the surreal conclusion that you can > eat lard straight from the can and conceivably reduce your > risk of heart disease. > > The crucial example of how the low-fat recommendations were > oversimplified is shown by the impact -- potentially > lethal, in fact -- of low-fat diets on triglycerides, which > are the component molecules of fat. By the late 60's, > researchers had shown that high triglyceride levels were at > least as common in heart-disease patients as high L.D.L. > cholesterol, and that eating a low-fat, high-carbohydrate > diet would, for many people, raise their triglyceride > levels, lower their H.D.L. levels and accentuate what Gerry > Reaven, an endocrinologist at Stanford University, called > Syndrome X. This is a cluster of conditions that can lead > to heart disease and Type 2 diabetes. > > It took Reaven a decade to convince his peers that Syndrome > X was a legitimate health concern, in part because to > accept its reality is to accept that low-fat diets will > increase the risk of heart disease in a third of the > population. ''Sometimes we wish it would go away because > nobody knows how to deal with it,'' said Robert Silverman, > an N.I.H. researcher, at a 1987 N.I.H. conference. ''High > protein levels can be bad for the kidneys. High fat is bad > for your heart. Now Reaven is saying not to eat high > carbohydrates. We have to eat something.'' > > Surely, everyone involved in drafting the various dietary > guidelines wanted Americans simply to eat less junk food, > however you define it, and eat more the way they do in > Berkeley, Calif. But we didn't go along. Instead we ate > more starches and refined carbohydrates, because calorie > for calorie, these are the cheapest nutrients for the food > industry to produce, and they can be sold at the highest > profit. It's also what we like to eat. Rare is the person > under the age of 50 who doesn't prefer a cookie or heavily > sweetened yogurt to a head of broccoli. > > ''All reformers would do well to be conscious of the law of > unintended consequences,'' says Alan Stone, who was staff > director for McGovern's Senate committee. Stone told me he > had an inkling about how the food industry would respond to > the new dietary goals back when the hearings were first > held. An economist pulled him aside, he said, and gave him > a lesson on market disincentives to healthy eating: ''He > said if you create a new market with a brand-new > manufactured food, give it a brand-new fancy name, put a > big advertising budget behind it, you can have a market all > to yourself and force your competitors to catch up. You > can't do that with fruits and vegetables. It's harder to > differentiate an apple from an apple.'' > > Nutrition researchers also played a role by trying to feed > science into the idea that carbohydrates are the ideal > nutrient. It had been known, for almost a century, and > considered mostly irrelevant to the etiology of obesity, > that fat has nine calories per gram compared with four for > carbohydrates and protein. Now it became the fail-safe > position of the low-fat recommendations: reduce the densest > source of calories in the diet and you will lose weight. > Then in 1982, J.P. Flatt, a University of Massachusetts > biochemist, published his research demonstrating that, in > any normal diet, it is extremely rare for the human body to > convert carbohydrates into body fat. This was then > misinterpreted by the media and quite a few scientists to > mean that eating carbohydrates, even to excess, could not > make you fat -- which is not the case, Flatt says. But the > misinterpretation developed a vigorous life of its own > because it resonated with the notion that fat makes you fat > and carbohydrates are harmless. > > As a result, the major trends in American diets since the > late 70's, according to the U.S.D.A. agricultural economist > Judith Putnam, have been a decrease in the percentage of > fat calories and a ''greatly increased consumption of > carbohydrates.'' To be precise, annual grain consumption > has increased almost 60 pounds per person, and caloric > sweeteners (primarily high-fructose corn syrup) by 30 > pounds. At the same time, we suddenly began consuming more > total calories: now up to 400 more each day since the > government started recommending low-fat diets. > > If these trends are correct, then the obesity epidemic can > certainly be explained by Americans' eating more calories > than ever -- excess calories, after all, are what causes us > to gain weight -- and, specifically, more carbohydrates. > The question is why? > > The answer provided by Endocrinology 101 is that we are > simply hungrier than we were in the 70's, and the reason is > physiological more than psychological. In this case, the > salient factor -- ignored in the pursuit of fat and its > effect on cholesterol -- is how carbohydrates affect blood > sugar and insulin. In fact, these were obvious culprits all > along, which is why Atkins and the low-carb-diet doctors > pounced on them early. > > The primary role of insulin is to regulate blood-sugar > levels. After you eat carbohydrates, they will be broken > down into their component sugar molecules and transported > into the bloodstream. Your pancreas then secretes insulin, > which shunts the blood sugar into muscles and the liver as > fuel for the next few hours. This is why carbohydrates have > a significant impact on insulin and fat does not. And > because juvenile diabetes is caused by a lack of insulin, > physicians believed since the 20's that the only evil with > insulin is not having enough. > > But insulin also regulates fat metabolism. We cannot store > body fat without it. Think of insulin as a switch. When > it's on, in the few hours after eating, you burn > carbohydrates for energy and store excess calories as fat. > When it's off, after the insulin has been depleted, you > burn fat as fuel. So when insulin levels are low, you will > burn your own fat, but not when they're high. > > This is where it gets unavoidably complicated. The fatter > you are, the more insulin your pancreas will pump out per > meal, and the more likely you'll develop what's called > ''insulin resistance,'' which is the underlying cause of > Syndrome X. In effect, your cells become insensitive to the > action of insulin, and so you need ever greater amounts to > keep your blood sugar in check. So as you gain weight, > insulin makes it easier to store fat and harder to lose it. > But the insulin resistance in turn may make it harder to > store fat -- your weight is being kept in check, as it > should be. But now the insulin resistance might prompt your > pancreas to produce even more insulin, potentially starting > a vicious cycle. Which comes first -- the obesity, the > elevated insulin, known as hyperinsulinemia, or the insulin > resistance -- is a chicken-and-egg problem that hasn't been > resolved. One endocrinologist described this to me as ''the > Nobel-prize winning question.'' > > Insulin also profoundly affects hunger, although to what > end is another point of controversy. On the one hand, > insulin can indirectly cause hunger by lowering your blood > sugar, but how low does blood sugar have to drop before > hunger kicks in? That's unresolved. Meanwhile, insulin > works in the brain to suppress hunger. The theory, as > explained to me by Michael Schwartz, an endocrinologist at > the University of Washington, is that insulin's ability to > inhibit appetite would normally counteract its propensity > to generate body fat. In other words, as you gained weight, > your body would generate more insulin after every meal, and > that in turn would suppress your appetite; you'd eat less > and lose the weight. > > Schwartz, however, can imagine a simple mechanism that > would throw this ''homeostatic'' system off balance: if > your brain were to lose its sensitivity to insulin, just as > your fat and muscles do when they are flooded with it. Now > the higher insulin production that comes with getting > fatter would no longer compensate by suppressing your > appetite, because your brain would no longer register the > rise in insulin. The end result would be a physiologic > state in which obesity is almost preordained, and one in > which the carbohydrate-insulin connection could play a > major role. Schwartz says he believes this could indeed be > happening, but research hasn't progressed far enough to > prove it. ''It is just a hypothesis,'' he says. ''It still > needs to be sorted out.'' > > David Ludwig, the Harvard endocrinologist, says that it's > the direct effect of insulin on blood sugar that does the > trick. He notes that when diabetics get too much insulin, > their blood sugar drops and they get ravenously hungry. > They gain weight because they eat more, and the insulin > promotes fat deposition. The same happens with lab animals. > This, he says, is effectively what happens when we eat > carbohydrates -- in particular sugar and starches like > potatoes and rice, or anything made from flour, like a > slice of white bread. These are known in the jargon as > high-glycemic-index carbohydrates, which means they are > absorbed quickly into the blood. As a result, they cause a > spike of blood sugar and a surge of insulin within minutes. > The resulting rush of insulin stores the blood sugar away > and a few hours later, your blood sugar is lower than it > was before you ate. As Ludwig explains, your body > effectively thinks it has run out of fuel, but the insulin > is still high enough to prevent you from burning your own > fat. The result is hunger and a craving for more > carbohydrates. It's another vicious circle, and another > situation ripe for obesity. > > The glycemic-index concept and the idea that starches can > be absorbed into the blood even faster than sugar emerged > in the late 70's, but again had no influence on public > health recommendations, because of the attendant <<<Additional text truncated.>>> ______________________________________________________________________ Structure your ColdFusion code with Fusebox. Get the official book at http://www.fusionauthority.com/bkinfo.cfm Archives: http://www.mail-archive.com/[email protected]/ Unsubscribe: http://www.houseoffusion.com/index.cfm?sidebar=lists
