From: Subject: What if It's All Been a Big Fat Lie? (Sorry, you must use Internet Explorer to view the content correctly) Date: Tue, 9 Jul 2002 11:19:42 -0400 MIME-Version: 1.0 Content-Type: multipart/related; boundary="----=_NextPart_000_0000_01C2273A.858A3950"; type="text/html" X-MimeOLE: Produced By Microsoft MimeOLE V5.50.4910.0300 This is a multi-part message in MIME format. ------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.nytimes.com/2002/07/07/magazine/07FAT.html?pagewanted=print&position=top What if It's All Been a Big Fat = Lie?
=
July 7, 2002

What if It's All Been a Big Fat = Lie?

By GARY=20 TAUBES

3DIf the members of the American medical = establishment=20 were to have a collective=20 find-yourself-standing-naked-in-Times-Square-type nightmare, this = might be=20 it. They spend 30 years ridiculing Robert Atkins, author of the=20 phenomenally-best-selling ''Dr. Atkins' Diet Revolution'' and = ''Dr.=20 Atkins' New Diet Revolution,'' accusing the Manhattan doctor of = quackery=20 and fraud, only to discover that the unrepentant Atkins was right = all=20 along. Or maybe it's this: they find that their very own dietary=20 recommendations -- eat less fat and more carbohydrates -- are the = cause of=20 the rampaging epidemic of obesity in America. Or, just possibly = this: they=20 find out both of the above are true.

When Atkins first published his ''Diet Revolution'' in 1972, = Americans=20 were just coming to terms with the proposition that fat -- = particularly=20 the saturated fat of meat and dairy products -- was the primary=20 nutritional evil in the American diet. Atkins managed to sell = millions of=20 copies of a book promising that we would lose weight eating steak, = eggs=20 and butter to our heart's desire, because it was the = carbohydrates, the=20 pasta, rice, bagels and sugar, that caused obesity and even heart = disease.=20 Fat, he said, was harmless.

Atkins allowed his readers to eat ''truly luxurious foods = without=20 limit,'' as he put it, ''lobster with butter sauce, steak with = bearnaise=20 sauce . . . bacon cheeseburgers,'' but allowed no = starches or=20 refined carbohydrates, which means no sugars or anything made from = flour.=20 Atkins banned even fruit juices, and permitted only a modicum of=20 vegetables, although the latter were negotiable as the diet = progressed.=20

Atkins was by no means the first to get rich pushing a high-fat = diet=20 that restricted carbohydrates, but he popularized it to an extent = that the=20 American Medical Association considered it a potential threat to = our=20 health. The A.M.A. attacked Atkins's diet as a ''bizarre regimen'' = that=20 advocated ''an unlimited intake of saturated fats and = cholesterol-rich=20 foods,'' and Atkins even had to defend his diet in Congressional = hearings.=20

Thirty years later, America has become weirdly polarized on the = subject=20 of weight. On the one hand, we've been told with almost religious=20 certainty by everyone from the surgeon general on down, and we = have come=20 to believe with almost religious certainty, that obesity is caused = by the=20 excessive consumption of fat, and that if we eat less fat we will = lose=20 weight and live longer. On the other, we have the ever-resilient = message=20 of Atkins and decades' worth of best-selling diet books, including = ''The=20 Zone,'' ''Sugar Busters'' and ''Protein Power'' to name a few. All = push=20 some variation of what scientists would call the alternative = hypothesis:=20 it's not the fat that makes us fat, but the carbohydrates, and if = we eat=20 less carbohydrates we will lose weight and live longer.

The perversity of this alternative hypothesis is that it = identifies the=20 cause of obesity as precisely those refined carbohydrates at the = base of=20 the famous Food Guide Pyramid -- the pasta, rice and bread -- that = we are=20 told should be the staple of our healthy low-fat diet, and then on = the=20 sugar or corn syrup in the soft drinks, fruit juices and sports = drinks=20 that we have taken to consuming in quantity if for no other reason = than=20 that they are fat free and so appear intrinsically healthy. While = the=20 low-fat-is-good-health dogma represents reality as we have come to = know=20 it, and the government has spent hundreds of millions of dollars = in=20 research trying to prove its worth, the low-carbohydrate message = has been=20 relegated to the realm of unscientific fantasy.

Over the past five years, however, there has been a subtle = shift in the=20 scientific consensus. It used to be that even considering the = possibility=20 of the alternative hypothesis, let alone researching it, was = tantamount to=20 quackery by association. Now a small but growing minority of = establishment=20 researchers have come to take seriously what the low-carb-diet = doctors=20 have been saying all along. Walter Willett, chairman of the = department of=20 nutrition at the Harvard School of Public Health, may be the most = visible=20 proponent of testing this heretic hypothesis. Willett is the de = facto=20 spokesman of the longest-running, most comprehensive diet and = health=20 studies ever performed, which have already cost upward of $100 = million and=20 include data on nearly 300,000 individuals. Those data, says = Willett,=20 clearly contradict the low-fat-is-good-health message ''and the = idea that=20 all fat is bad for you; the exclusive focus on adverse effects of = fat may=20 have contributed to the obesity epidemic.''

These researchers point out that there are plenty of reasons to = suggest=20 that the low-fat-is-good-health hypothesis has now effectively = failed the=20 test of time. In particular, that we are in the midst of an = obesity=20 epidemic that started around the early 1980's, and that this was=20 coincident with the rise of the low-fat dogma. (Type 2 diabetes, = the most=20 common form of the disease, also rose significantly through this = period.)=20 They say that low-fat weight-loss diets have proved in clinical = trials and=20 real life to be dismal failures, and that on top of it all, the = percentage=20 of fat in the American diet has been decreasing for two decades. = Our=20 cholesterol levels have been declining, and we have been smoking = less, and=20 yet the incidence of heart disease has not declined as would be = expected.=20 ''That is very disconcerting,'' Willett says. ''It suggests that = something=20 else bad is happening.''

The science behind the alternative hypothesis can be called=20 Endocrinology 101, which is how it's referred to by David Ludwig, = a=20 researcher at Harvard Medical School who runs the pediatric = obesity clinic=20 at Children's Hospital Boston, and who prescribes his own version = of a=20 carbohydrate-restricted diet to his patients. Endocrinology 101 = requires=20 an understanding of how carbohydrates affect insulin and blood = sugar and=20 in turn fat metabolism and appetite. This is basic endocrinology, = Ludwig=20 says, which is the study of hormones, and it is still considered = radical=20 because the low-fat dietary wisdom emerged in the 1960's from = researchers=20 almost exclusively concerned with the effect of fat on cholesterol = and=20 heart disease. At the time, Endocrinology 101 was still = underdeveloped,=20 and so it was ignored. Now that this science is becoming clear, it = has to=20 fight a quarter century of anti-fat prejudice.

The alternative hypothesis also comes with an implication that = is worth=20 considering for a moment, because it's a whopper, and it may = indeed be an=20 obstacle to its acceptance. If the alternative hypothesis is right = --=20 still a big ''if'' -- then it strongly suggests that the ongoing = epidemic=20 of obesity in America and elsewhere is not, as we are constantly = told, due=20 simply to a collective lack of will power and a failure to = exercise.=20 Rather it occurred, as Atkins has been saying (along with Barry = Sears,=20 author of ''The Zone''), because the public health authorities = told us=20 unwittingly, but with the best of intentions, to eat precisely = those foods=20 that would make us fat, and we did. We ate more fat-free = carbohydrates,=20 which, in turn, made us hungrier and then heavier. Put simply, if = the=20 alternative hypothesis is right, then a low-fat diet is not by = definition=20 a healthy diet. In practice, such a diet cannot help being high in = carbohydrates, and that can lead to obesity, and perhaps even = heart=20 disease. ''For a large percentage of the population, perhaps 30 to = 40=20 percent, low-fat diets are counterproductive,'' says Eleftheria=20 Maratos-Flier, director of obesity research at Harvard's = prestigious=20 Joslin Diabetes Center. ''They have the paradoxical effect of = making=20 people gain weight.''

3DScientists are still arguing about fat, despite a = century of=20 research, because the regulation of appetite and weight in the = human body=20 happens to be almost inconceivably complex, and the experimental = tools we=20 have to study it are still remarkably inadequate. This combination = leaves=20 researchers in an awkward position. To study the entire = physiological=20 system involves feeding real food to real human subjects for = months or=20 years on end, which is prohibitively expensive, ethically = questionable (if=20 you're trying to measure the effects of foods that might cause = heart=20 disease) and virtually impossible to do in any kind of rigorously=20 controlled scientific manner. But if researchers seek to study = something=20 less costly and more controllable, they end up studying = experimental=20 situations so oversimplified that their results may have nothing = to do=20 with reality. This then leads to a research literature so vast = that it's=20 possible to find at least some published research to support = virtually any=20 theory. The result is a balkanized community -- ''splintered, very = opinionated and in many instances, intransigent,'' says Kurt = Isselbacher,=20 a former chairman of the Food and Nutrition Board of the National = Academy=20 of Science -- in which researchers seem easily convinced that = their=20 preconceived notions are correct and thoroughly uninterested in = testing=20 any other hypotheses but their own.

What's more, the number of misconceptions propagated about the = most=20 basic research can be staggering. Researchers will be suitably = scientific=20 describing the limitations of their own experiments, and then will = cite=20 something as gospel truth because they read it in a magazine. The = classic=20 example is the statement heard repeatedly that 95 percent of all = dieters=20 never lose weight, and 95 percent of those who do will not keep it = off.=20 This will be correctly attributed to the University of = Pennsylvania=20 psychiatrist Albert Stunkard, but it will go unmentioned that this = statement is based on 100 patients who passed through Stunkard's = obesity=20 clinic during the Eisenhower administration.

With these caveats, one of the few reasonably reliable facts = about the=20 obesity epidemic is that it started around the early 1980's. = According to=20 Katherine Flegal, an epidemiologist at the National Center for = Health=20 Statistics, the percentage of obese Americans stayed relatively = constant=20 through the 1960's and 1970's at 13 percent to 14 percent and then = shot up=20 by 8 percentage points in the 1980's. By the end of that decade, = nearly=20 one in four Americans was obese. That steep rise, which is = consistent=20 through all segments of American society and which continued = unabated=20 through the 1990's, is the singular feature of the epidemic. Any = theory=20 that tries to explain obesity in America has to account for that.=20 Meanwhile, overweight children nearly tripled in number. And for = the first=20 time, physicians began diagnosing Type 2 diabetes in adolescents. = Type 2=20 diabetes often accompanies obesity. It used to be called = adult-onset=20 diabetes and now, for the obvious reason, is not.

So how did this happen? The orthodox and ubiquitous explanation = is that=20 we live in what Kelly Brownell, a Yale psychologist, has called a = ''toxic=20 food environment'' of cheap fatty food, large portions, pervasive = food=20 advertising and sedentary lives. By this theory, we are at the = Pavlovian=20 mercy of the food industry, which spends nearly $10 billion a year = advertising unwholesome junk food and fast food. And because these = foods,=20 especially fast food, are so filled with fat, they are both = irresistible=20 and uniquely fattening. On top of this, so the theory goes, our = modern=20 society has successfully eliminated physical activity from our = daily=20 lives. We no longer exercise or walk up stairs, nor do our = children bike=20 to school or play outside, because they would prefer to play video = games=20 and watch television. And because some of us are obviously = predisposed to=20 gain weight while others are not, this explanation also has a = genetic=20 component -- the thrifty gene. It suggests that storing extra = calories as=20 fat was an evolutionary advantage to our Paleolithic ancestors, = who had to=20 survive frequent famine. We then inherited these ''thrifty'' = genes,=20 despite their liability in today's toxic environment.

This theory makes perfect sense and plays to our puritanical = prejudice=20 that fat, fast food and television are innately damaging to our = humanity.=20 But there are two catches. First, to buy this logic is to accept = that the=20 copious negative reinforcement that accompanies obesity -- both = socially=20 and physically -- is easily overcome by the constant bombardment = of food=20 advertising and the lure of a supersize bargain meal. And second, = as=20 Flegal points out, little data exist to support any of this. = Certainly=20 none of it explains what changed so significantly to start the = epidemic.=20 Fast-food consumption, for example, continued to grow steadily = through the=20 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=20 before the mid-80's, according to William Dietz, who runs the = division of=20 nutrition and physical activity at the Centers for Disease = Control; the=20 1990's data show obesity rates continuing to climb, while exercise = activity remained unchanged. This suggests the two have little in = common.=20 Dietz also acknowledged that a culture of physical exercise began = in the=20 United States in the 70's -- the ''leisure exercise mania,'' as = Robert=20 Levy, director of the National Heart, Lung and Blood Institute, = described=20 it in 1981 -- and has continued through the present day.

As for the thrifty gene, it provides the kind of evolutionary = rationale=20 for human behavior that scientists find comforting but that simply = cannot=20 be tested. In other words, if we were living through an anorexia = epidemic,=20 the experts would be discussing the equally untestable = ''spendthrift=20 gene'' theory, touting evolutionary advantages of losing weight=20 effortlessly. An overweight homo erectus, they'd say, would have = been easy=20 prey for predators.

It is also undeniable, note students of Endocrinology 101, that = mankind=20 never evolved to eat a diet high in starches or sugars. ''Grain = products=20 and concentrated sugars were essentially absent from human = nutrition until=20 the invention of agriculture,'' Ludwig says, ''which was only = 10,000 years=20 ago.'' This is discussed frequently in the anthropology texts but = is=20 mostly absent from the obesity literature, with the prominent = exception of=20 the low-carbohydrate-diet books.

What's forgotten in the current controversy is that the low-fat = dogma=20 itself is only about 25 years old. Until the late 70's, the = accepted=20 wisdom was that fat and protein protected against overeating by = making you=20 sated, and that carbohydrates made you fat. In ''The Physiology of = Taste,'' for instance, an 1825 discourse considered among the most = famous=20 books ever written about food, the French gastronome Jean Anthelme = Brillat-Savarin says that he could easily identify the causes of = obesity=20 after 30 years of listening to one ''stout party'' after another=20 proclaiming the joys of bread, rice and (from a ''particularly = stout=20 party'') potatoes. Brillat-Savarin described the roots of obesity = as a=20 natural predisposition conjuncted with the ''floury and feculent=20 substances which man makes the prime ingredients of his daily=20 nourishment.'' He added that the effects of this fecula -- i.e.,=20 ''potatoes, grain or any kind of flour'' -- were seen sooner when = sugar=20 was added to the diet.

This is what my mother taught me 40 years ago, backed up by the = vague=20 observation that Italians tended toward corpulence because they = ate so=20 much pasta. This observation was actually documented by Ancel = Keys, a=20 University of Minnesota physician who noted that fats ''have good = staying=20 power,'' by which he meant they are slow to be digested and so = lead to=20 satiation, and that Italians were among the heaviest populations = he had=20 studied. According to Keys, the Neapolitans, for instance, ate = only a=20 little lean meat once or twice a week, but ate bread and pasta = every day=20 for lunch and dinner. ''There was no evidence of nutritional = deficiency,''=20 he wrote, ''but the working-class women were fat.''

By the 70's, you could still find articles in the journals = describing=20 high rates of obesity in Africa and the Caribbean where diets = contained=20 almost exclusively carbohydrates. The common thinking, wrote a = former=20 director of the Nutrition Division of the United Nations, was that = the=20 ideal diet, one that prevented obesity, snacking and excessive = sugar=20 consumption, was a diet ''with plenty of eggs, beef, mutton, = chicken,=20 butter and well-cooked vegetables.'' This was the identical = prescription=20 Brillat-Savarin put forth in 1825.

It was Ancel Keys, paradoxically, who introduced the=20 low-fat-is-good-health dogma in the 50's with his theory that = dietary fat=20 raises cholesterol levels and gives you heart disease. Over the = next two=20 decades, however, the scientific evidence supporting this theory = remained=20 stubbornly ambiguous. The case was eventually settled not by new = science=20 but by politics. It began in January 1977, when a Senate committee = led by=20 George McGovern published its ''Dietary Goals for the United = States,''=20 advising that Americans significantly curb their fat intake to = abate an=20 epidemic of ''killer diseases'' supposedly sweeping the country. = It peaked=20 in late 1984, when the National Institutes of Health officially=20 recommended that all Americans over the age of 2 eat less fat. By = that=20 time, fat had become ''this greasy killer'' in the memorable words = of the=20 Center for Science in the Public Interest, and the model American=20 breakfast of eggs and bacon was well on its way to becoming a bowl = of=20 Special K with low-fat milk, a glass of orange juice and toast, = hold the=20 butter -- a dubious feast of refined carbohydrates.

In the intervening years, the N.I.H. spent several hundred = million=20 dollars trying to demonstrate a connection between eating fat and = getting=20 heart disease and, despite what we might think, it failed. Five = major=20 studies revealed no such link. A sixth, however, costing well over = $100=20 million alone, concluded that reducing cholesterol by drug therapy = could=20 prevent heart disease. The N.I.H. administrators then made a leap = of=20 faith. Basil Rifkind, who oversaw the relevant trials for the = N.I.H.,=20 described their logic this way: they had failed to demonstrate at = great=20 expense that eating less fat had any health benefits. But if a=20 cholesterol-lowering drug could prevent heart attacks, then a = low-fat,=20 cholesterol-lowering diet should do the same. ''It's an imperfect = world,''=20 Rifkind told me. ''The data that would be definitive is = ungettable, so you=20 do your best with what is available.''

Some of the best scientists disagreed with this low-fat logic,=20 suggesting that good science was incompatible with such leaps of = faith,=20 but they were effectively ignored. Pete Ahrens, whose Rockefeller=20 University laboratory had done the seminal research on cholesterol = metabolism, testified to McGovern's committee that everyone = responds=20 differently to low-fat diets. It was not a scientific matter who = might=20 benefit and who might be harmed, he said, but ''a betting = matter.'' Phil=20 Handler, then president of the National Academy of Sciences, = testified in=20 Congress to the same effect in 1980. ''What right,'' Handler = asked, ''has=20 the federal government to propose that the American people conduct = a vast=20 nutritional experiment, with themselves as subjects, on the = strength of so=20 very little evidence that it will do them any good?''

Nonetheless, once the N.I.H. signed off on the low-fat = doctrine,=20 societal forces took over. The food industry quickly began = producing=20 thousands of reduced-fat food products to meet the new = recommendations.=20 Fat was removed from foods like cookies, chips and yogurt. The = problem=20 was, it had to be replaced with something as tasty and pleasurable = to the=20 palate, which meant some form of sugar, often high-fructose corn = syrup.=20 Meanwhile, an entire industry emerged to create fat substitutes, = of which=20 Procter & Gamble's olestra was first. And because these = reduced-fat=20 meats, cheeses, snacks and cookies had to compete with a few = hundred=20 thousand other food products marketed in America, the industry = dedicated=20 considerable advertising effort to reinforcing the = less-fat-is-good-health=20 message. Helping the cause was what Walter Willett calls the = ''huge=20 forces'' of dietitians, health organizations, consumer groups, = health=20 reporters and even cookbook writers, all well-intended = missionaries of=20 healthful eating.

3DFew experts now deny that the low-fat message is = radically=20 oversimplified. If nothing else, it effectively ignores the fact = that=20 unsaturated fats, like olive oil, are relatively good for you: = they tend=20 to elevate your good cholesterol, high-density lipoprotein = (H.D.L.), and=20 lower your bad cholesterol, low-density lipoprotein (L.D.L.), at = least in=20 comparison to the effect of carbohydrates. While higher L.D.L. = raises your=20 heart-disease risk, higher H.D.L. reduces it.

What this means is that even saturated fats -- a k a, the bad = fats --=20 are not nearly as deleterious as you would think. True, they will = elevate=20 your bad cholesterol, but they will also elevate your good = cholesterol. In=20 other words, it's a virtual wash. As Willett explained to me, you = will=20 gain little to no health benefit by giving up milk, butter and = cheese and=20 eating bagels instead.

But it gets even weirder than that. Foods considered more or = less=20 deadly under the low-fat dogma turn out to be comparatively benign = if you=20 actually look at their fat content. More than two-thirds of the = fat in a=20 porterhouse steak, for instance, will definitively improve your=20 cholesterol profile (at least in comparison with the baked potato = next to=20 it); it's true that the remainder will raise your L.D.L., the bad = stuff,=20 but it will also boost your H.D.L. The same is true for lard. If = you work=20 out the numbers, you come to the surreal conclusion that you can = eat lard=20 straight from the can and conceivably reduce your risk of heart = disease.=20

The crucial example of how the low-fat recommendations were=20 oversimplified is shown by the impact -- potentially lethal, in = fact -- of=20 low-fat diets on triglycerides, which are the component molecules = of fat.=20 By the late 60's, researchers had shown that high triglyceride = levels were=20 at least as common in heart-disease patients as high L.D.L. = cholesterol,=20 and that eating a low-fat, high-carbohydrate diet would, for many = people,=20 raise their triglyceride levels, lower their H.D.L. levels and = accentuate=20 what Gerry Reaven, an endocrinologist at Stanford University, = called=20 Syndrome X. This is a cluster of conditions that can lead to heart = disease=20 and Type 2 diabetes.

It took Reaven a decade to convince his peers that Syndrome X = was a=20 legitimate health concern, in part because to accept its reality = is to=20 accept that low-fat diets will increase the risk of heart disease = in a=20 third of the population. ''Sometimes we wish it would go away = because=20 nobody knows how to deal with it,'' said Robert Silverman, an = N.I.H.=20 researcher, at a 1987 N.I.H. conference. ''High protein levels can = be bad=20 for the kidneys. High fat is bad for your heart. Now Reaven is = saying not=20 to eat high carbohydrates. We have to eat something.''

Surely, everyone involved in drafting the various dietary = guidelines=20 wanted Americans simply to eat less junk food, however you define = it, and=20 eat more the way they do in Berkeley, Calif. But we didn't go = along.=20 Instead we ate more starches and refined carbohydrates, because = calorie=20 for calorie, these are the cheapest nutrients for the food = industry to=20 produce, and they can be sold at the highest profit. It's also = what we=20 like to eat. Rare is the person under the age of 50 who doesn't = prefer a=20 cookie or heavily sweetened yogurt to a head of broccoli.

''All reformers would do well to be conscious of the law of = unintended=20 consequences,'' says Alan Stone, who was staff director for = McGovern's=20 Senate committee. Stone told me he had an inkling about how the = food=20 industry would respond to the new dietary goals back when the = hearings=20 were first held. An economist pulled him aside, he said, and gave = him a=20 lesson on market disincentives to healthy eating: ''He said if you = create=20 a new market with a brand-new manufactured food, give it a = brand-new fancy=20 name, put a big advertising budget behind it, you can have a = market all to=20 yourself and force your competitors to catch up. You can't do that = with=20 fruits and vegetables. It's harder to differentiate an apple from = an=20 apple.''

Nutrition researchers also played a role by trying to feed = science into=20 the idea that carbohydrates are the ideal nutrient. It had been = known, for=20 almost a century, and considered mostly irrelevant to the etiology = of=20 obesity, that fat has nine calories per gram compared with four = for=20 carbohydrates and protein. Now it became the fail-safe position of = the=20 low-fat recommendations: reduce the densest source of calories in = the diet=20 and you will lose weight. Then in 1982, J.P. Flatt, a University = of=20 Massachusetts biochemist, published his research demonstrating = that, in=20 any normal diet, it is extremely rare for the human body to = convert=20 carbohydrates into body fat. This was then misinterpreted by the = media and=20 quite a few scientists to mean that eating carbohydrates, even to = excess,=20 could not make you fat -- which is not the case, Flatt says. But = the=20 misinterpretation developed a vigorous life of its own because it=20 resonated with the notion that fat makes you fat and carbohydrates = are=20 harmless.

As a result, the major trends in American diets since the late = 70's,=20 according to the U.S.D.A. agricultural economist Judith Putnam, = have been=20 a decrease in the percentage of fat calories and a ''greatly = increased=20 consumption of carbohydrates.'' To be precise, annual grain = consumption=20 has increased almost 60 pounds per person, and caloric sweeteners=20 (primarily high-fructose corn syrup) by 30 pounds. At the same = time, we=20 suddenly began consuming more total calories: now up to 400 more = each day=20 since the government started recommending low-fat diets.

If these trends are correct, then the obesity epidemic can = certainly be=20 explained by Americans' eating more calories than ever -- excess = calories,=20 after all, are what causes us to gain weight -- and, specifically, = more=20 carbohydrates. The question is why?

The answer provided by Endocrinology 101 is that we are simply = hungrier=20 than we were in the 70's, and the reason is physiological more = than=20 psychological. In this case, the salient factor -- ignored in the = pursuit=20 of fat and its effect on cholesterol -- is how carbohydrates = affect blood=20 sugar and insulin. In fact, these were obvious culprits all along, = which=20 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=20 you eat carbohydrates, they will be broken down into their = component sugar=20 molecules and transported into the bloodstream. Your pancreas then = secretes insulin, which shunts the blood sugar into muscles and = the liver=20 as fuel for the next few hours. This is why carbohydrates have a=20 significant impact on insulin and fat does not. And because = juvenile=20 diabetes is caused by a lack of insulin, physicians believed since = the=20 20's that the only evil with insulin is not having enough.

But insulin also regulates fat metabolism. We cannot store body = fat=20 without it. Think of insulin as a switch. When it's on, in the few = hours=20 after eating, you burn carbohydrates for energy and store excess = calories=20 as fat. When it's off, after the insulin has been depleted, you = burn fat=20 as fuel. So when insulin levels are low, you will burn your own = fat, but=20 not when they're high.

This is where it gets unavoidably complicated. The fatter you = are, the=20 more insulin your pancreas will pump out per meal, and the more = likely=20 you'll develop what's called ''insulin resistance,'' which is the=20 underlying cause of Syndrome X. In effect, your cells become = insensitive=20 to the action of insulin, and so you need ever greater amounts to = keep=20 your blood sugar in check. So as you gain weight, insulin makes it = easier=20 to store fat and harder to lose it. But the insulin resistance in = turn may=20 make it harder to store fat -- your weight is being kept in check, = as it=20 should be. But now the insulin resistance might prompt your = pancreas to=20 produce even more insulin, potentially starting a vicious cycle. = Which=20 comes first -- the obesity, the elevated insulin, known as=20 hyperinsulinemia, or the insulin resistance -- is a = chicken-and-egg=20 problem that hasn't been resolved. One endocrinologist described = this to=20 me as ''the Nobel-prize winning question.''

Insulin also profoundly affects hunger, although to what end is = another=20 point of controversy. On the one hand, insulin can indirectly = cause hunger=20 by lowering your blood sugar, but how low does blood sugar have to = drop=20 before hunger kicks in? That's unresolved. Meanwhile, insulin = works in the=20 brain to suppress hunger. The theory, as explained to me by = Michael=20 Schwartz, an endocrinologist at the University of Washington, is = that=20 insulin's ability to inhibit appetite would normally counteract = its=20 propensity to generate body fat. In other words, as you gained = weight,=20 your body would generate more insulin after every meal, and that = in turn=20 would suppress your appetite; you'd eat less and lose the weight. =

Schwartz, however, can imagine a simple mechanism that would = throw this=20 ''homeostatic'' system off balance: if your brain were to lose its = sensitivity to insulin, just as your fat and muscles do when they = are=20 flooded with it. Now the higher insulin production that comes with = getting=20 fatter would no longer compensate by suppressing your appetite, = because=20 your brain would no longer register the rise in insulin. The end = result=20 would be a physiologic state in which obesity is almost = preordained, and=20 one in which the carbohydrate-insulin connection could play a = major role.=20 Schwartz says he believes this could indeed be happening, but = research=20 hasn't progressed far enough to prove it. ''It is just a = hypothesis,'' he=20 says. ''It still needs to be sorted out.''

David Ludwig, the Harvard endocrinologist, says that it's the = direct=20 effect of insulin on blood sugar that does the trick. He notes = that when=20 diabetics get too much insulin, their blood sugar drops and they = get=20 ravenously hungry. They gain weight because they eat more, and the = insulin=20 promotes fat deposition. The same happens with lab animals. This, = he says,=20 is effectively what happens when we eat carbohydrates -- in = particular=20 sugar and starches like potatoes and rice, or anything made from = flour,=20 like a slice of white bread. These are known in the jargon as=20 high-glycemic-index carbohydrates, which means they are absorbed = quickly=20 into the blood. As a result, they cause a spike of blood sugar and = a surge=20 of insulin within minutes. The resulting rush of insulin stores = the blood=20 sugar away and a few hours later, your blood sugar is lower than = it was=20 before you ate. As Ludwig explains, your body effectively thinks = it has=20 run out of fuel, but the insulin is still high enough to prevent = you from=20 burning your own fat. The result is hunger and a craving for more=20 carbohydrates. It's another vicious circle, and another situation = ripe for=20 obesity.

The glycemic-index concept and the idea that starches can be = absorbed=20 into the blood even faster than sugar emerged in the late 70's, = but again=20 had no influence on public health recommendations, because of the=20 attendant controversies. To wit: if you bought the glycemic-index = concept,=20 then you had to accept that the starches we were supposed to be = eating 6=20 to 11 times a day were, once swallowed, physiologically = indistinguishable=20 from sugars. This made them seem considerably less than wholesome. = Rather=20 than accept this possibility, the policy makers simply allowed = sugar and=20 corn syrup to elude the vilification that befell dietary fat. = After all,=20 they are fat-free.

Sugar and corn syrup from soft drinks, juices and the copious = teas and=20 sports drinks now supply more than 10 percent of our total = calories; the=20 80's saw the introduction of Big Gulps and 32-ounce cups of Coca-Cola, blasted through with = sugar, but=20 100 percent fat free. When it comes to insulin and blood sugar, = these soft=20 drinks and fruit juices -- what the scientists call ''wet = carbohydrates''=20 -- might indeed be worst of all. (Diet soda accounts for less than = a=20 quarter of the soda market.)

The gist of the glycemic-index idea is that the longer it takes = the=20 carbohydrates to be digested, the lesser the impact on blood sugar = and=20 insulin and the healthier the food. Those foods with the highest = rating on=20 the glycemic index are some simple sugars, starches and anything = made from=20 flour. Green vegetables, beans and whole grains cause a much = slower rise=20 in blood sugar because they have fiber, a nondigestible = carbohydrate,=20 which slows down digestion and lowers the glycemic index. Protein = and fat=20 serve the same purpose, which implies that eating fat can be = beneficial, a=20 notion that is still unacceptable. And the glycemic-index concept = implies=20 that a primary cause of Syndrome X, heart disease, Type 2 diabetes = and=20 obesity is the long-term damage caused by the repeated surges of = insulin=20 that come from eating starches and refined carbohydrates. This = suggests a=20 kind of unified field theory for these chronic diseases, but not = one that=20 coexists easily with the low-fat doctrine.

At Ludwig's pediatric obesity clinic, he has been prescribing=20 low-glycemic-index diets to children and adolescents for five = years now.=20 He does not recommend the Atkins diet because he says he believes = such a=20 very low carbohydrate approach is unnecessarily restrictive; = instead, he=20 tells his patients to effectively replace refined carbohydrates = and=20 starches with vegetables, legumes and fruit. This makes a=20 low-glycemic-index diet consistent with dietary common sense, = albeit in a=20 higher-fat kind of way. His clinic now has a nine-month waiting = list. Only=20 recently has Ludwig managed to convince the N.I.H. that such diets = are=20 worthy of study. His first three grant proposals were summarily = rejected,=20 which may explain why much of the relevant research has been done = in=20 Canada and in Australia. In April, however, Ludwig received $1.2 = million=20 from the N.I.H. to test his low-glycemic-index diet against a = traditional=20 low-fat-low-calorie regime. That might help resolve some of the=20 controversy over the role of insulin in obesity, although the = redoubtable=20 Robert Atkins might get there first.

3DThe 71-year-old Atkins, a graduate of Cornell medical = school,=20 says he first tried a very low carbohydrate diet in 1963 after = reading=20 about one in the Journal of the American Medical Association. He = lost=20 weight effortlessly, had his epiphany and turned a fledgling = Manhattan=20 cardiology practice into a thriving obesity clinic. He then = alienated the=20 entire medical community by telling his readers to eat as much fat = and=20 protein as they wanted, as long as they ate little to no = carbohydrates.=20 They would lose weight, he said, because they would keep their = insulin=20 down; they wouldn't be hungry; and they would have less resistance = to=20 burning their own fat. Atkins also noted that starches and sugar = were=20 harmful in any event because they raised triglyceride levels and = that this=20 was a greater risk factor for heart disease than cholesterol.

Atkins's diet is both the ultimate manifestation of the = alternative=20 hypothesis as well as the battleground on which the=20 fat-versus-carbohydrates controversy is likely to be fought = scientifically=20 over the next few years. After insisting Atkins was a quack for = three=20 decades, obesity experts are now finding it difficult to ignore = the=20 copious anecdotal evidence that his diet does just what he has = claimed.=20 Take Albert Stunkard, for instance. Stunkard has been trying to = treat=20 obesity for half a century, but he told me he had his epiphany = about=20 Atkins and maybe about obesity as well just recently when he = discovered=20 that the chief of radiology in his hospital had lost 60 pounds on = Atkins's=20 diet. ''Well, apparently all the young guys in the hospital are = doing=20 it,'' he said. ''So we decided to do a study.'' When I asked = Stunkard if=20 he or any of his colleagues considered testing Atkins's diet 30 = years ago,=20 he said they hadn't because they thought Atkins was ''a jerk'' who = was=20 just out to make money: this ''turned people off, and so nobody = took him=20 seriously enough to do what we're finally doing.''

In fact, when the American Medical Association released its = scathing=20 critique of Atkins's diet in March 1973, it acknowledged that the = diet=20 probably worked, but expressed little interest in why. Through the = 60's,=20 this had been a subject of considerable research, with the = conclusion that=20 Atkins-like diets were low-calorie diets in disguise; that when = you cut=20 out pasta, bread and potatoes, you'll have a hard time eating = enough meat,=20 vegetables and cheese to replace the calories.

That, however, raised the question of why such a low-calorie = regimen=20 would also suppress hunger, which Atkins insisted was the = signature=20 characteristic of the diet. One possibility was Endocrinology 101: = that=20 fat and protein make you sated and, lacking carbohydrates and the = ensuing=20 swings of blood sugar and insulin, you stay sated. The other = possibility=20 arose from the fact that Atkins's diet is ''ketogenic.'' This = means that=20 insulin falls so low that you enter a state called ketosis, which = is what=20 happens during fasting and starvation. Your muscles and tissues = burn body=20 fat for energy, as does your brain in the form of fat molecules = produced=20 by the liver called ketones. Atkins saw ketosis as the obvious way = to=20 kick-start weight loss. He also liked to say that ketosis was so=20 energizing that it was better than sex, which set him up for some=20 ridicule. An inevitable criticism of Atkins's diet has been that = ketosis=20 is dangerous and to be avoided at all costs.

When I interviewed ketosis experts, however, they universally = sided=20 with Atkins, and suggested that maybe the medical community and = the media=20 confuse ketosis with ketoacidosis, a variant of ketosis that = occurs in=20 untreated diabetics and can be fatal. ''Doctors are scared of = ketosis,''=20 says Richard Veech, an N.I.H. researcher who studied medicine at = Harvard=20 and then got his doctorate at Oxford University with the Nobel = Laureate=20 Hans Krebs. ''They're always worried about diabetic ketoacidosis. = But=20 ketosis is a normal physiologic state. I would argue it is the = normal=20 state of man. It's not normal to have McDonald's and a delicatessen around every = corner. It's=20 normal to starve.''

Simply put, ketosis is evolution's answer to the thrifty gene. = We may=20 have evolved to efficiently store fat for times of famine, says = Veech, but=20 we also evolved ketosis to efficiently live off that fat when = necessary.=20 Rather than being poison, which is how the press often refers to = ketones,=20 they make the body run more efficiently and provide a backup fuel = source=20 for the brain. Veech calls ketones ''magic'' and has shown that = both the=20 heart and brain run 25 percent more efficiently on ketones than on = blood=20 sugar.

The bottom line is that for the better part of 30 years Atkins = insisted=20 his diet worked and was safe, Americans apparently tried it by the = tens of=20 millions, while nutritionists, physicians, public- health = authorities and=20 anyone concerned with heart disease insisted it could kill them, = and=20 expressed little or no desire to find out who was right. During = that=20 period, only two groups of U.S. researchers tested the diet, or at = least=20 published their results. In the early 70's, J.P. Flatt and = Harvard's=20 George Blackburn pioneered the ''protein-sparing modified fast'' = to treat=20 postsurgical patients, and they tested it on obese volunteers. = Blackburn,=20 who later became president of the American Society of Clinical = Nutrition,=20 describes his regime as ''an Atkins diet without excess fat'' and = says he=20 had to give it a fancy name or nobody would take him seriously. = The diet=20 was ''lean meat, fish and fowl'' supplemented by vitamins and = minerals.=20 ''People loved it,'' Blackburn recalls. ''Great weight loss. We = couldn't=20 run them off with a baseball bat.'' Blackburn successfully treated = hundreds of obese patients over the next decade and published a = series of=20 papers that were ignored. When obese New Englanders turned to=20 appetite-control drugs in the mid-80's, he says, he let it drop. = He then=20 applied to the N.I.H. for a grant to do a clinical trial of = popular diets=20 but was rejected.

The second trial, published in September 1980, was done at the = George=20 Washington University Medical Center. Two dozen obese volunteers = agreed to=20 follow Atkins's diet for eight weeks and lost an average of 17 = pounds=20 each, with no apparent ill effects, although their L.D.L. = cholesterol did=20 go up. The researchers, led by John LaRosa, now president of the = State=20 University of New York Downstate Medical Center in Brooklyn, = concluded=20 that the 17-pound weight loss in eight weeks would likely have = happened=20 with any diet under ''the novelty of trying something under = experimental=20 conditions'' and never pursued it further.

Now researchers have finally decided that Atkins's diet and = other=20 low-carb diets have to be tested, and are doing so against = traditional=20 low-calorie-low-fat diets as recommended by the American Heart=20 Association. To explain their motivation, they inevitably tell one = of two=20 stories: some, like Stunkard, told me that someone they knew -- a = patient,=20 a friend, a fellow physician -- lost considerable weight on = Atkins's diet=20 and, despite all their preconceptions to the contrary, kept it = off. Others=20 say they were frustrated with their inability to help their obese=20 patients, looked into the low-carb diets and decided that = Endocrinology=20 101 was compelling. ''As a trained physician, I was trained to = mock=20 anything like the Atkins diet,'' says Linda Stern, an internist at = the=20 Philadelphia Veterans Administration Hospital, ''but I put myself = on the=20 diet. I did great. And I thought maybe this is something I can = offer my=20 patients.''

None of these studies have been financed by the N.I.H., and = none have=20 yet been published. But the results have been reported at = conferences --=20 by researchers at Schneider Children's Hospital on Long Island, = Duke=20 University and the University of Cincinnati, and by Stern's group = at the=20 Philadelphia V.A. Hospital. And then there's the study Stunkard = had=20 mentioned, led by Gary Foster at the University of Pennsylvania, = Sam=20 Klein, director of the Center for Human Nutrition at Washington = University=20 in St. Louis, and Jim Hill, who runs the University of Colorado = Center for=20 Human Nutrition in Denver. The results of all five of these = studies are=20 remarkably consistent. Subjects on some form of the Atkins diet -- = whether=20 overweight adolescents on the diet for 12 weeks as at Schneider, = or obese=20 adults averaging 295 pounds on the diet for six months, as at the=20 Philadelphia V.A. -- lost twice the weight as the subjects on the = low-fat,=20 low-calorie diets.

In all five studies, cholesterol levels improved similarly with = both=20 diets, but triglyceride levels were considerably lower with the = Atkins=20 diet. Though researchers are hesitant to agree with this, it does = suggest=20 that heart-disease risk could actually be reduced when fat is = added back=20 into the diet and starches and refined carbohydrates are removed. = ''I=20 think when this stuff gets to be recognized,'' Stunkard says, = ''it's going=20 to really shake up a lot of thinking about obesity and = metabolism.''

All of this could be settled sooner rather than later, and with = it,=20 perhaps, we might have some long-awaited answers as to why we grow = fat and=20 whether it is indeed preordained by societal forces or by our = choice of=20 foods. For the first time, the N.I.H. is now actually financing=20 comparative studies of popular diets. Foster, Klein and Hill, for=20 instance, have now received more than $2.5 million from N.I.H. to = do a=20 five-year trial of the Atkins diet with 360 obese individuals. At = Harvard,=20 Willett, Blackburn and Penelope Greene have money, albeit from = Atkins's=20 nonprofit foundation, to do a comparative trial as well.

Should these clinical trials also find for Atkins and his = high-fat,=20 low-carbohydrate diet, then the public-health authorities may = indeed have=20 a problem on their hands. Once they took their leap of faith and = settled=20 on the low-fat dietary dogma 25 years ago, they left little room = for=20 contradictory evidence or a change of opinion, should such a = change be=20 necessary to keep up with the science. In this light Sam Klein's=20 experience is noteworthy. Klein is president-elect of the North = American=20 Association for the Study of Obesity, which suggests that he is a = highly=20 respected member of his community. And yet, he described his = recent=20 experience discussing the Atkins diet at medical conferences as a = learning=20 experience. ''I have been impressed,'' he said, ''with the anger = of=20 academicians in the audience. Their response is 'How dare you even = present=20 data on the Atkins diet!' ''

This hostility stems primarily from their anxiety that = Americans, given=20 a glimmer of hope about their weight, will rush off en masse to = try a diet=20 that simply seems intuitively dangerous and on which there is = still no=20 long-term data on whether it works and whether it is safe. It's a=20 justifiable fear. In the course of my research, I have spent my = mornings=20 at my local diner, staring down at a plate of scrambled eggs and = sausage,=20 convinced that somehow, some way, they must be working to clog my = arteries=20 and do me in.

After 20 years steeped in a low-fat paradigm, I find it hard to = see the=20 nutritional world any other way. I have learned that low-fat diets = fail in=20 clinical trials and in real life, and they certainly have failed = in my=20 life. I have read the papers suggesting that 20 years of low-fat=20 recommendations have not managed to lower the incidence of heart = disease=20 in this country, and may have led instead to the steep increase in = obesity=20 and Type 2 diabetes. I have interviewed researchers whose computer = models=20 have calculated that cutting back on the saturated fats in my diet = to the=20 levels recommended by the American Heart Association would not add = more=20 than a few months to my life, if that. I have even lost = considerable=20 weight with relative ease by giving up carbohydrates on my test = diet, and=20 yet I can look down at my eggs and sausage and still imagine the = imminent=20 onset of heart disease and obesity, the latter assuredly to be = caused by=20 some bizarre rebound phenomena the likes of which science has not = yet=20 begun to describe. The fact that Atkins himself has had heart = trouble=20 recently does not ease my anxiety, despite his assurance that it = is not=20 diet-related.

This is the state of mind I imagine that mainstream = nutritionists,=20 researchers and physicians must inevitably take to the=20 fat-versus-carbohydrate controversy. They may come around, but the = evidence will have to be exceptionally compelling. Although this = kind of=20 conversion may be happening at the moment to John Farquhar, who is = a=20 professor of health research and policy at Stanford University and = has=20 worked in this field for more than 40 years. When I interviewed = Farquhar=20 in April, he explained why low-fat diets might lead to weight gain = and=20 low-carbohydrate diets might lead to weight loss, but he made me = promise=20 not to say he believed they did. He attributed the cause of the = obesity=20 epidemic to the ''force-feeding of a nation.'' Three weeks later, = after=20 reading an article on Endocrinology 101 by David Ludwig in the = Journal of=20 the American Medical Association, he sent me an e-mail message = asking the=20 not-entirely-rhetorical question, ''Can we get the low-fat = proponents to=20 apologize?''

Gary Taubes is a correspondent for the journal Science and = author of=20 ''Bad Science: The Short Life and Weird Times of Cold = Fusion.''


Copy= right=20 2002 The New York Times Company | Per= missions | Privac= y=20 Policy
=20
------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: image/gif Content-Transfer-Encoding: base64 Content-Location: http://graphics.nytimes.com/images/misc/printlogo.gif R0lGODlhxwAvANX/AP////n5+fnv7/Ly8vLf3+/v7+zs7OzPz+Tk5OS7u9/f393d3d2qqtfX19ea mtDQ0NCKis/Pz8jIyMh2dsLCwsJmZr+/v7u7u7tVVbW1tbVFRa+vr62tra0xMaampqYhIaCgoKAR EZ+fn5mZmZkAAI+Pj39/f3BwcGBgYFBQUEBAQDAwMCAgIBAQEAAAAAAAAAAAAAAAAAAAAAAAAAAA AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAACwAAAAAxwAvAEAG/0CAcEgsGo/IpHLJ bDqf0Kh0uvSUFKLSQGjFarnX7LaQaUREiIxIaClRAAj3oFFCnO31SJ1emA8UCggeGWRmJQUNFA0i AxQeAHd6eAhUlZaXmAAFLC6dnp0sKi2dFgAlLiqWnJ6lQiKfLq2ZBbApACYbK54oKgVUBSedqUsR o7CdK6KdEQUKmVEonb4mnrkuLRFC1C4sEdGgBcWdp+NFKZ7anwoWFgqr5C4pBeedmqu24i4lRN+f tyIWgpHKZ6GfixMnFBhjwanFBgAqhBVQYUKFChS+iDQUEnHZqBURTAiMd6Yfiw2fRHpa4etVp5Ft hImw2GKNq2MsjMUDMPLaTP+JJwyCLGKQ1ZCIAeFxW6NAha5OKJ5eM7HiIZJtLm6V6hgrBb1O51I4 g/iJxZp5n1as+2RzSFEXUl2YgJR2A0pPJ76qlVrTRL8WKbIdQzX2mWEoFToAYECCgBAIJEhAfiKC hawik4dATlCBhGYSCRwfgTyBhAYNED6HVo1B8eHXmERkG0AJtu3buHPr3s27t+8kJwBYYDG3gIkI ClDI2jbMklNPzdkhcZlxClett4xW6tg8iXFTNQEkFz9UU/jevizsyu4C4y0hKNgP4y581z4l3RV8 YrfLPRt0ZMnFESlHYIUdVvwRqB6BAXYX4Ao6WUUEPHNF1MJcEGkSnCcYNlj/H4HMpQNWWwXo0kIJ C2ZlSTTnOZFLh70tyAIvgzH4241GVIfjjjz26OOPQAbpGx0KlCBCA48QaSSSACh55CNDnKHABmsQ uUEDcWRDhx0iKKCHl1ds6QgAaiDQABF0NBLBGQWMKeWXkggp544RDDLnnXgecYYF2RBhQltC6EiF AoIaUdgzBZRgwmVsHCYhExZs0A4RxjF6Y0RVbVDRYCpYYIyDULCpkwkKpFDCp30aaukT1+FSonZT FPApExGlQOUJcXmSgjEtHMrbK4CtEst7Q4R4KjZFJLfMEca1AMBXLKQnS7P6YKWPJt/Ep8BTWTAq 1YGwUlueJrrI008E9PHk/4mzRMEFIYDNFcNSlCvMu60LNnmKbLLntKCjCaO0oMuHLjiD4ESphuhh iuaNK0QxTQ1x10sJDivKQwwHiGFHl52jKTqLshdLiqWQPCAqRXAFzhHwnJxVBNEOweFRwhBcisIG RgCXcTUDa5NB9xV7SnwK05diwoAa19AJGclKSopBi7AovJ1sbKOfIN/MSooYa5cuzSh/BaqwLqTK UTRrzHxyKibj7EmqyqFwggW+ADiEBSpPpaMI8pwcNAAiMH1ERPEBsEFwRMkSgVg5BjbEPI8aIYqO Z5xgkX8Pr/A3pSlYigKMAKBgdhGVwcLC5pATEfjjggeKgq8IEaECPmrlSf8FARA4QEQCEAiAOxG5 rquMgJhBYHwCQvAOgPLJGw8B8kZAwAAAEBzwe/PHYw+BaLbjCUEIAnyvmQYHRPZMZo95hv5mqx0R AmgkhEAE+6JNVlr3+Oev//78969/GZBAg/8GmAkqCechaDBgpACHAAUisDZNQpFsDJekDRgJDVKi gwU8cCURWMURHnBGATwgAkIQgQIi8IAvUBjCCG6wg5Ej4I0KkEIRpPANNCThDTVRwx0OYUsZ2AcN 1QCHIwXQTHnAIBrUkAU0FCkLZxICEaW4jy1tKRIClCGPztAICXGRAl5kBBiFgADZSGKKi6gNCbk0 iTSmsRE21BIJN1CAMmb/ow10hGMLJeHGLGrxj0VoQBQBSchCGvKQgVJZC07QJ1rMC3C2qERTOgEo SEoqBaC7xAZ0cjO6RSSTU7BAMpoAs7KQSggoKdyOlFIjUnwDVE/Qj7BW8DCdcMNRhxDWLVgQlxg+ oR+wNEcrYbGtffnmFSKUDQ2lMi+BBBMKXOlVoErgSyEEo1CsyprIVpVNlC0BBSyYZjNKICyMPAVx N3oFI79xM6x500tIwAJ+UuQCq0iHUmugBwvQ+Y/HraCSYMtKyBBUBOMIyqBCuEIzvnZKgIYOXxvo CEcoddAiXKYZSVhgshKSIfG8hGekmEd1tpGMdUlNQ2kxQimzopCZ3RNg/+vy1Loe6onSeSJoE4HF LSgirFI0S1gOYQdQPRFOo31ClaikZICyUqKbIMOCm0TGqWo6kr4IQVm6QiXZriEEAGFFBNwS0TBW wTZ0dCScRDgHQ4YgrE5VzAJYwQLViMcx2R3jFsmQylvVxSD6EGpt5+CmzrzJFXHsS20AeEoqCJou rLwKLgoTQeG4tk1iiXVtBAMc5oiAnO6o7K2LG0vGOmK1YT2uUwYa6NaMYjIP2bUWBfKEM67T0a5W DWxlBVHNRHYLxG1DYP4AwH5mV5i5lICWRatZa/FTBJhAzaJzLe2qUqu1p7HWa7vF7cSkyVmibmBG hUkFCuKDWKPq1ptYGf/dJrJBi3p4dF0myIg7liWQbkwSZS65Bh1RAKj5lmUYLonUJ/bhF8PdNEDd IEvfjEDdbdITIG8jFzKK8BRaOq1qgJqYTzKyIH8JFyyBUqyBO/EQgbSAT1VlhgqoZNJOsCuhrZwX i7mRjY5EEnDI8FWAolKOu5k2qsYswGPXENV4YFMTVOGFCkKBAr1oAseguGgEnnIfIT9lwdRwyBHe sp5b5ANDLsHIq+b1KmO+0he0aEFHTpSEM5ggZEpwGneZkEoc6QytD5Oakm21RUWhyDcT4WasLMdR /dFzmKBEpKKTkAASTKADGvjMBBpNKWCeoEtXvdpjNCAZ6E1mfZJ53hF8WtPoCUAAA5/JHvUk04EP 4MiGF2wirG0o61rH+ta0xvWsd23rXPsa1kM4zfJAs+kOvO8Jo8OMZz4TmWWvWgO6O0L5TBOZA3wG 2tcOQWpc0Wte67rb4N7cAAXQmQ9Mb9OrPp+z0w3qyGzbCBhw9QdQzWzJpM/di863vo8QBAA7 ------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: image/gif Content-Transfer-Encoding: base64 Content-Location: http://graphics7.nytimes.com/images/dropcap/i.gif R0lGODlhCwAhAMQAAP/////v7++9va0AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAACH5BAEA AAAALAAAAAALACEAQAU2oCCOYwAMaJoKp6qy7tvGA0zXc2zTu567PeBPdsMVg8QbcjVkHpuoZRRq VFKlVd51++xavdoQADs= ------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: image/gif Content-Transfer-Encoding: base64 Content-Location: http://graphics7.nytimes.com/images/s.gif R0lGODlhIQAiAJEAAP///6oAAAAAAAAAACH5BAEAAAAALAAAAAAhACIAAAJchI8Qy5EPUZszWoqr lbmvbXiic41iaWJg91BrVoIhLL90HZ14bu5c+sEBXbKhxmYkbZKNGlNZTPoUwGlCZ/0RL1EVCnls ha838vbggTzP2udy3ZU6h9lRVg3FFQAAOw== ------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: image/gif Content-Transfer-Encoding: base64 Content-Location: http://graphics7.nytimes.com/images/f.gif R0lGODlhHAAiAJEAAP///6oAAAAAAAAAACH5BAEAAAAALAAAAAAcACIAAAJNhI+pG+0PY0uyVmqz wzrzfiGgJ4bLaVjoqq5n6ypwXEq0bN7puKF8//oFWELiz8hDQnS1CPMw00VvU1o1dnVllY/nzubd +nJSsvecKAAAOw== ------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: image/gif Content-Transfer-Encoding: base64 Content-Location: http://graphics7.nytimes.com/images/t.gif R0lGODlhHwAiAJEAAP///6oAAAAAAAAAACH5BAEAAAAALAAAAAAfACIAAAJMhI+pe+EPo4xp2usq 3lBz7n1YKFoMSZ0qMK5n6y5wjHa0Mt9GrvO3TwPGhC7iyqhCvi662qOJUDKkMiZ0Z71ScVno1pm5 srrNr3hRAAA7 ------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: image/gif Content-Transfer-Encoding: base64 Content-Location: http://graphics.nytimes.com/images/misc/pixel.gif R0lGODlhAQABAIAAAP///////yH5BAUUAAAALAAAAAABAAEAAAICRAEAOw== ------=_NextPart_000_0000_01C2273A.858A3950 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.nytimes.com/js/csssniff.js =0A= =0A= =0A= ------=_NextPart_000_0000_01C2273A.858A3950--