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Old Mon, Jun-30-03, 10:45
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gotbeer gotbeer is offline
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Default "Cracking The Fat Riddle"

Cracking The Fat Riddle

Should you count calories or carbs? Is dietary fat your biggest enemy? The latest research may surprise you


Time Europe Posted Sunday, June 29, 2003; 14:08BST

link to article

link to older thread on an earlier article by this same author

Until he hit his fifties, Martin Andrew ran 16 km every evening, played cricket every week and maintained a steady weight of 81 kg. Then the buildings-conservation officer from Haddenham, England, hurt his back, stopped running and found his cricket trousers no longer fit. After five years of feeling fed up with his double chin and the extra 12 kg he had put on — and frustrated that low-calorie diets just left him hungry and no slimmer — he went on the Atkins diet, the famous weight-loss program that seems to defy nutritional wisdom. Most health experts advise you to favor carbohydrates, found in everything from fruits to grains, while going easy on the protein and fat. On the Atkins diet, you are allowed to eat all the protein- and fat-drenched meat and butter you want but must cut out cereal and bread. Andrew is happy to stick with a regime "that allows me to eat strawberries and cream." And he's even happier that after just two months on the diet, he's lost nearly 13 kg. He's even playing cricket again. "It's a very easy diet to follow because it is so obvious what you shouldn't be eating," he says. "But it's slightly surprising how many carbohydrates there are in things. You can eat your entire daily ration in one apple."

Dr. Robert Atkins, who died in April from head injuries sustained during a fall, first formulated his weight-loss plan 30 years ago. It slips in and out of favor every few years, persistently bucking the skepticism of mainstream nutritionists. Could it really be, as Atkins argued, that low-fat diets, which are typically high in carbohydrates, are bad and that low-carbohydrate diets, which often contain considerable fat, are good? Is it really O.K., as Atkins advocated, to slather mayonnaise all over salmon and tuna and douse asparagus and lobster with butter while friends look on in envy? Shades of the 1973 movie Sleeper, in which Woody Allen plays a 20th century Rip Van Winkle who awakens after a couple hundred years to a world in which fatty delights like steak and cream pies are deemed beneficial to your health.

Alas, Sleeper was and is a fantasy. The indictment of excessive amounts of saturated fat — the kind found in steaks and butter — as a major contributor to heart disease and stroke has not changed and seems unlikely to do so. A formidable lineup of experts holds to the low-fat approach, none more tenaciously than Dr. Dean Ornish, whose regimen prescribes no more than 10% of daily calories from fat. But there are hints now that Atkins may have struck a vein of truth. Two studies reported in the New England Journal of Medicine in May showed that people on the Atkins diet lost more weight than others on conventional diets — without suffering any damaging nutritional deficiencies. One study, by the University of Pennsylvania's Weight and Eating Disorders Program, took 63 men and women in their forties with an average weight of 97 kg and put half on the Atkins diet and the rest on a low-calorie regime. After three months, the Atkins group had lost an average 6.6 kg against the others' 2.6 kg. The other study, by the Philadelphia Veterans Administration Center, put 132 obese men and women — over 127 kg — on either low-carb or low-fat diets and found that the low-carb group lost around twice as much as the low-fat group. What was perhaps more interesting — even baffling — was that the group on the Atkins low-carb diet showed lower levels of the blood lipids that contribute to arterial disease.

Of course, the mere suggestion that the Atkins diet and others like it are worthy of scientific attention still makes many experts bristle. Yet it is also clear that the low-fat paradigm has developed some cracks in its faηade. It turns out that not all fats are bad for you. Those found in fish, nuts and certain vegetables may actually increase your chances of living a good long life. By the same token, not all diets that are low in fat are necessarily healthy — as anyone who has ever truly considered the difference between a low-fat banana cream pie and a banana could tell you. About one thing, however, there is no dispute. The developed world is clearly in a state of nutritional crisis and in need of radical remedies.

The statistics are sobering. After 30 years of seemingly solid advice aimed at lowering dietary fat, Europeans have grown collectively fatter than ever. Today more than 50% of adults in the European Union are classified as overweight or obese. So many children have become heavy that pediatricians are now facing an epidemic of Type 2 diabetes and hypertension — diseases that are closely associated with being overweight and were unheard of among youngsters just a generation ago. (See following story.) On one level, there is no mystery about why we as a society are fat: because we consume too many calories and expend too few. Though it is true that the proportion of fat in our diet has fallen from 40% in 1990 to roughly 36.5% today, the calories available in the food we consume have gone up, from 3,187 calories per capita per day in the 1970s to 3,400 in the 1990s, according to the U.S. Department of Agriculture (USDA). Even the traditionally slender French are succumbing to the trend. A recent study by the French National Institute of Medical Research found that the proportion of obese people rose from 9.6% in 2000 to 11.3% in 2003.

But there is a deeper question — one that has plagued anyone who has ever struggled to take off more than a few pounds. And that is: How do some folks manage to live in the same "toxic environment" and never gain weight? The quest to answer this double-sided question is in its earliest stages. Already, however, a series of fascinating insights into the biology of obesity has emerged. Behind our broadening behinds and widening waistlines, scientists say, lies a complex array of genes that, directly and indirectly, links our gut to our brain.

These genes, honed by millions of years of evolution, appear to have betrayed many of us in the 21st century world. Scientists have long suspected that human beings come into the world equipped with dozens, perhaps hundreds, of genes and associated hormones that regulate what scientists call the energy-balance equation. On one side of the equation are the calories we consume; on the other side are the calories we burn — through physical activity as well as whatever is needed just to keep the body in good working order. Anything left over gets converted to body fat. With the notable exception of insulin, which helps the body process sugars from carbohydrates, the identity of most of the major players in this biochemical balancing act could for years only be guessed at.

Scientists thought they had a major breakthrough in 1995, when Jeffrey Friedman, a molecular geneticist at Rockefeller University, stunned the scientific world by announcing that he and his colleagues had discovered a hormone, called leptin, that caused fat to melt away, at least in laboratory mice. Genetically engineered mice that lacked the gene for making this hormone developed ravenous appetites and became grossly obese. When these same mice were injected with the missing hormone they shrugged off one-third of the weight they had gained.

Although leptin has since been dismissed as an obesity treatment — the vast majority of obese people turn out to have normal leptin levels — its discovery touched off a scientific gold rush that has yet to abate. Competing research teams in the U.S. and Europe have so far identified at least half a dozen other compounds that have surprising power to regulate appetite. Researchers at London's Imperial College of Medicine showed last year that one of those hormones, dubbed PYY3-36, which is released in the small intestine after a meal, actually promotes a sense of fullness. Each of these compounds is slightly different, and scientists are just beginning to figure out how they all work together. What is clear is that all of them are important nodes along an elaborate network of interconnecting pathways that feed into, and out of, the hypothalamus, a brain structure that is the control center for weight regulation. The body produces hormones that activate the hypothalamus. The neurons in the hypothalamus send new messages back to the body. And just like subliminal messages spliced into a filmstrip, these signals powerfully affect our behavior even when we are not aware of them.

Thus, while we read the paper or carry on a conversation, the hypothalamus — activated by leptin or some other compound — orders cells and tissues to ratchet up energy expenditure. The body responds by idly fidgeting to raise metabolic rates, or by increasing blood flow to the outer layers of the skin in an effort to dissipate heat. In this way, we carry out a process known as thermogenesis, which is the body's way of burning excess calories. Intriguingly, some people seem to be more efficient at thermogenesis than others. Researchers led by Dr. Bradford Lowell at Beth Israel Deaconess Medical Center in Boston last year pinpointed three genes that may account for at least some of that variation. Mice that lack the genes, they reported in the journal Science, grow grossly obese when fed a high-calorie diet enriched with fat and sucrose.

By contrast, normal mice fed the same diet gain very modest amounts of weight. The fact that up to 70% of obesity has genetic roots does not explain the larger mystery. If obesity is so bad for us — and there is no question it is — then why are so many people susceptible to layering on excess fat? The answer may well lie in what is referred to as the Thrifty Gene Hypothesis, which supposes that obesity genes have been maintained in the human population because they conferred an appreciable survival advantage in consuming and storing more calories than they expend. In this fashion, the body creates a reservoir of fat that comes in handy when food grows scarce. It's easy to imagine that repeated famines over the course of human development practically forced the biological system for regulating weight to skew strongly toward resisting weight loss rather than protecting against weight gain.

In principle, at least, no one should ever become obese. That's because the genetic system for regulating weight would seem to be exquisitely tuned. Researchers calculate that a man who keeps his weight stable at 80 kg will take in 1 million calories a year on average and will also expend 1 million calories. "Think about it," says Dr. Michael Schwartz, head of clinical nutrition at the University of Washington in Seattle. "How do you match a million with a million? It doesn't happen just by chance." Leptin, which exercises an influence on appetite and thermogenesis, is thought to be key to maintaining this balance. For as we layer on fat, we pump out more leptin, which signals the hypothalamus that it's time to accelerate energy output and brake caloric intake. The problem is, people who gain weight have now been shown to develop a remarkable resistance to leptin's power. The fatter they get, and the more leptin they make, the more impervious the hypothalamus becomes.

Eventually the hypothalamus interprets the elevated level of leptin as normal — and forever after misreads the drops in leptin caused by weight loss as a starvation signal. This phenomenon provides a biochemical explanation for why so many of those who lose weight end up putting it back on. Our bodies, backed by millions of years of evolution, fight us at every turn. So what causes leptin resistance? The answer may turn out to be exceedingly complicated. Not only do the other hormones of the digestive system play a role, but also researchers are learning that they must account for the influence of such mood-altering neurotransmitters as dopamine and serotonin, as well as the stress hormones adrenaline and cortisol. And then there are melanocortins, brain chemicals whose power to affect weight loss and gain is just now coming into focus. Genes, of course, do not make us fat. They merely set up a susceptibility to gaining weight under certain conditions — and without question, those conditions are now ubiquitous. With fast-food outlets lining our streets and time- and labor-saving gadgetry proliferating, the energy balance is increasingly tipped in favor of fatness. We expend less than a calorie every time we change channels using the remote control. If we'd only get up and go over to the TV, we'd use three. Using a car wash consumes 18 calories, while washing and waxing the car yourself consumes 300. "It is the minimal amount of energy you need to get through daily life in a European city that has made a huge impact," says Dr. Simon Coppack, who runs an obesity clinic at St Bartholomew's and Royal London Medical School.

Since they're having trouble changing our sedentary lifestyles, health professionals are focusing on making us at least eat more healthily. The British Medical Association is discussing levying a fat tax on high-fat foods like cakes, biscuits and processed meals. In another attack on unhealthy eating, a group of lawyers in Boston — led by tobacco-litigation veteran John Banzhaf — recently met to discuss ways of suing the fast food industry. Banzhaf has written to the bosses of McDonald's, Burger King, Wendy's, KFC, Taco Bell and Pizza Hut warning of growing evidence to suggest that fast food "can act on the brain in the same ways as alcohol or heroin." He intends to demand that they put up signs to that effect in their restaurants.

Why, then, do we like these foods so much? For answers, researchers are once again turning to laboratory animals, which exhibit many of the same dietary proclivities we do. Rats, for example, will labor mightily to obtain a sugar pellet even after they have dined on rat chow and aren't particularly hungry. The reason, thinks Allen Levine, director of the University of Minnesota's obesity center, has a lot to do with sugar's impact on mood-enhancing circuits in the brain. Sugar gives rats — and by extension humans — a buzz.

There is also reason to think that our penchant for making unhealthy choices may be enhanced by the abundance of particular foods. Consider the results of an experiment recently conducted at Philadelphia's Monell Chemical Senses Center. Rats given one cup each of fat, protein and carbohydrates were found to make balanced diet choices, eating a tad more protein than carbohydrates and a tad more carbohydrates than fats. But rats presented with more cups of fat and carbohydrates than protein dramatically increased their consumption of the former while sharply curtailing their intake of the latter — to the point, in some cases, that the rats became protein deficient. Why would rats do this? Perhaps because their brains are hard-wired to take advantage of sudden windfalls of food, and in the wild, of course, such windfalls do not occur every day.

They do, however, in restaurants. Soft drinks are now delivered in one-liter cups, observes Judith Stern, vice president of the American Obesity Association. The venerable Joy of Cooking has capitulated to the trend; the same recipes that used to provide meals for six now feed only four. And even in Paris, home of cuisine minceur, super-size pains au chocolat are now available from the patisserie. So cheap are carbohydrates and fats that making extra-large sizes costs the food industry next to nothing.

One of the reasons that fast foods are so attractive is their high fat content. Fat is energy dense, with twice as many calories per gram as carbohydrates or protein. "We are pretty much programmed to go for energy- dense foods," says Dr. Hannah Theobald of the British Nutrition Foundation. "So fat's attractive. It makes flavors melt in the mouth." The trouble is, those energy-dense foods pile on the pounds. "It's very easy to eat a little bit more at each meal," says Dr. John Wilding, a consultant physician who runs an obesity clinic in Liverpool. "An extra 100 calories a day and you will be 7 kg heavier at the end of the year."

Adults are free agents. They can overeat and gain weight if they want to. But perhaps what is most disturbing about their overeating is that they are unwittingly, and in myriad ways, passing on that tendency to children. It's not just that children pick up their parents' bad habits. There is growing evidence that what you eat early in life can permanently boost your body's desire for food. A 2001 study by German pediatrics professor Berthold Koletzko found that breast-feeding children for at least six months gave them a 40% lower risk of becoming obese in later life. "Infants fed formula are more likely to become obese," he says. "The higher protein content compared with breast milk could be a causal factor."

If we were to start from scratch, how would we design a diet to keep our weight under control? For starters, we could concentrate on diets geared for life rather than quick and easy weight loss. Over the years, we pick up a lot of bad eating habits, and it's tough to break them. "If you asked someone to get up and go to bed two hours earlier every day, they would have to completely change their lifestyles," says Coppack. "There's a lot of habit to break. You have to get them to pay attention to even the simple things, like the way they put food onto the plate." Second, we could stop paying such close attention to every jot and tittle in the diet debate. It will take decades for researchers to unravel all the reasons we eat what we do, and why we like to eat so much of it. But a few insights are emerging that should point us in the right direction, as long as we don't turn them into inviolable dietary laws. Not all carbohydrates seem to have been created equal. So-called simple carbohydrates, those found in white bread and cake, are so quickly digested by the body that they trigger a very rapid rise in the levels of glucose in the blood. The pancreas releases a massive amount of insulin to mop up the excess. Soon enough, however, blood- glucose levels plummet to the point where our brains may feel woozy, we become excessively hungry and are driven to eat again. Complex carbohydrates, on the other hand, particularly those rich in fiber, do not elicit the same kind of spike-and-crash response. Avoiding simple carbohydrates is part of the approach advocated by French diet guru Michel Montignac. The best-selling author of I Eat Therefore I Lose Weight concentrates not on the calorie content of food but its glycemic index. Researchers refer to the amount of glucose a single serving of a particular food releases in the bloodstream as its glycemic index. And there is growing evidence that we can manipulate it somewhat to control our hunger. Broccoli and peanuts, for example, have a low glycemic index, while instant rice and baked potatoes have an extremely high one. "The problem of calories is not quantitative," Montignac says, "but qualitative. It depends on the actual chemical composition of the food."

Dairy products and milk — which has been increasingly replaced by soft drinks in the diets of both children and adults — are also fast emerging as dietary "goods," despite the fact that a 0.35-L glass of skim milk has almost as many calories as a 0.35-L can of Coke. The reason may have to do with calcium, says Michael Zemel, professor of nutrition at the University of Tennessee. In the absence of calcium, levels of the hormone calcitriol increase. Among other things, calcitriol shuts off the mechanisms that break down fat and activates those that make it. Fats, too, are gaining new respect. Olives, nuts, avocados and other foods that are rich in mono- and polyunsaturated fat belong in our diets, many nutritionists believe. Not only do these good fats help lower the level of ldl, or bad, cholesterol, but they are also essential for the absorption of fat-soluble vitamins like E. So what's to be done? Crash diets are no good. Germans have long retreated to clinics for a "cure" that limits them to between 600 and 1,000 calories a day. A study found that during the fast people lost an average of 6.9 kg, but a year later weighed 0.9 kg more than they had done before the cure. At obesity clinics like the one run by Wilding, nutritionists recommend reducing fat intake from 40% to 30% of total calories, increasing mono-unsaturated fats like olive oil, and ensuring that a majority of carbohydrates come from fiber-rich sources like pulses, oats and rye bread. And we must get moving to use up more of those calories.

The question is whether the addition of new concepts like glycemic index can restore sanity to a collective eating binge that has spiraled out of control. And if not, then what can? An appetite suppressant that makes people eat less but has no side effects? A thermogenesis pill that one can take after overindulging in ice cream? Perhaps the future will bring better medications, at least for people who are morbidly obese. But for the broader population, the remedy must be sought elsewhere. And as we can't change the genes we are born with, we are left with one alternative — to change the environment that our genes have proved so ill equipped to handle. We, the species that invented barbecuing, domesticated corn and wheat and created foie gras and French fries, have powered through a series of food revolutions, says Oxford University historian Felipe Fernαndez-Armesto in his book, Food: a History. The purpose of the next revolution, he predicts, will be to undo the excesses of the last.

With reporting by David Bjerklie and Sora Song/New York, Dan Cray/Los Angeles, Alexandra Hartman/Paris, Elisabeth Kauffman/Nashville, Kate Noble/London, Ursula Sautter/Bonn and Steve Zwick/Cologne
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