Subject: What if It's All Been a Big Fat Lie?
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    <TD vAlign=3Dtop align=3Dleft><IMG=20
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<BR><BR=20
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      <H5>July 7, 2002</H5><NYT_HEADLINE type=3D" " version=3D"1.0">
      <H2>What if It's All Been a Big Fat =
Lie?</H2></NYT_HEADLINE><NYT_BYLINE=20
      type=3D" " version=3D"1.0"><FONT size=3D-1><STRONG>By GARY=20
      TAUBES</STRONG></FONT><BR><BR></NYT_BYLINE><NYT_TEXT>
      <P><IMG alt=3DI =
src=3D"http://graphics7.nytimes.com/images/dropcap/i.gif"=20
      align=3Dleft border=3D0>f 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. </P>
      <P>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. </P>
      <P>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 . . . <EM>bacon</EM> 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
      </P>
      <P>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
      </P>
      <P>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. </P>
      <P>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. </P>
      <P>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.'' </P>
      <P>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.'' </P>
      <P>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. </P>
      <P>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.'' </P>
      <P><IMG alt=3DS src=3D"http://graphics7.nytimes.com/images/s.gif"=20
      align=3Dleft>cientists 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. </P>
      <P>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. </P>
      <P>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. </P>
      <P>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. </P>
      <P>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. =
</P>
      <P>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. </P>
      <P>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. </P>
      <P>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. </P>
      <P>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. </P>
      <P>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.'' </P>
      <P>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. </P>
      <P>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. </P>
      <P>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.'' </P>
      <P>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?'' </P>
      <P>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 &amp; 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. </P>
      <P><IMG alt=3DF src=3D"http://graphics7.nytimes.com/images/f.gif"=20
      align=3Dleft>ew 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. </P>
      <P>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. </P>
      <P>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
      </P>
      <P>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. </P>
      <P>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.'' </P>
      <P>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. </P>
      <P>''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.'' </P>
      <P>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. </P>
      <P>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. </P>
      <P>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? </P>
      <P>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. =
</P>
      <P>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. </P>
      <P>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. </P>
      <P>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.'' </P>
      <P>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. =
</P>
      <P>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.'' </P>
      <P>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. </P>
      <P>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. </P>
      <P>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 <ORG=20
      value=3D"KO" idsrc=3D"NYSE">Coca-Cola</ORG>, 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.) </P>
      <P>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. </P>
      <P>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. </P>
      <P><IMG alt=3DT src=3D"http://graphics7.nytimes.com/images/t.gif"=20
      align=3Dleft>he 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. </P>
      <P>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.'' </P>
      <P>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. </P>
      <P>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. </P>
      <P>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 <ORG value=3D"MCD"=20
      idsrc=3D"NYSE">McDonald's</ORG> and a delicatessen around every =
corner. It's=20
      normal to starve.'' </P>
      <P>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. </P>
      <P>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. </P>
      <P>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. </P>
      <P>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.'' </P>
      <P>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. </P>
      <P>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.'' </P>
      <P>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. </P>
      <P>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!' '' </P>
      <P>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. </P>
      <P>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. </P>
      <P>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?''<BR>
</P>
      <P><EM></P>
      <P>Gary Taubes is a correspondent for the journal Science and =
author of=20
      ''Bad Science: The Short Life and Weird Times of Cold =
Fusion.''</P></EM>
      <P></P></NYT_TEXT><BR>
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