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Old Sun, Jul-07-02, 17:24
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Atkid Atkid is offline
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Plan: Atkins
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Default New York Times

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

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


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


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

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


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


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


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


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


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


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


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


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


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


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


This theory makes perfect sense and plays to our
puritanical prejudice that fat, fast food and television
are innately damaging to our humanity. But there are two
catches. First, to buy this logic is to accept that the
copious negative reinforcement that accompanies obesity --
both socially and physically -- is easily overcome by the
constant bombardment of food advertising and the lure of a
supersize bargain meal. And second, as Flegal points out,
little data exist to support any of this. Certainly none of
it explains what changed so significantly to start the
epidemic. Fast-food consumption, for example, continued to
grow steadily through the 70's and 80's, but it did not
take a sudden leap, as obesity did.


As far as exercise and physical activity go, there are no
reliable data before the mid-80's, according to William
Dietz, who runs the division of nutrition and physical
activity at the Centers for Disease Control; the 1990's
data show obesity rates continuing to climb, while exercise
activity remained unchanged. This suggests the two have
little in common. Dietz also acknowledged that a culture of
physical exercise began in the United States in the 70's --
the ''leisure exercise mania,'' as Robert Levy, director of
the National Heart, Lung and Blood Institute, described it
in 1981 -- and has continued through the present day.


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


The answer provided by Endocrinology 101 is that we are
simply hungrier than we were in the 70's, and the reason is
physiological more than psychological. In this case, the
salient factor -- ignored in the pursuit of fat and its
effect on cholesterol -- is how carbohydrates affect blood
sugar and insulin. In fact, these were obvious culprits all
along, which is why Atkins and the low-carb-diet doctors
pounced on them early.


The primary role of insulin is to regulate blood-sugar
levels. After you eat carbohydrates, they will be broken
down into their component sugar molecules and transported
into the bloodstream. Your pancreas then secretes insulin,
which shunts the blood sugar into muscles and the liver as
fuel for the next few hours. This is why carbohydrates have
a significant impact on insulin and fat does not. And
because juvenile diabetes is caused by a lack of insulin,
physicians believed since the 20's that the only evil with
insulin is not having enough.


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


In all five studies, cholesterol levels improved similarly
with both diets, but triglyceride levels were considerably
lower with the Atkins diet. Though researchers are hesitant
to agree with this, it does suggest that heart-disease risk
could actually be reduced when fat is added back into the
diet and starches and refined carbohydrates are removed.
''I think when this stuff gets to be recognized,'' Stunkard
says, ''it's going 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, perhaps, we might have some long-awaited answers
as to why we grow fat and whether it is indeed preordained
by societal forces or by our choice of foods. For the first
time, the N.I.H. is now actually financing comparative
studies of popular diets. Foster, Klein and Hill, for
instance, have now received more than $2.5 million from
N.I.H. to do a five-year trial of the Atkins diet with 360
obese individuals. At Harvard, Willett, Blackburn and
Penelope Greene have money, albeit from Atkins's nonprofit
foundation, to do a comparative trial as well.


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


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


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


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

*****
Gary Taubes is a correspondent for the journal Science and
author of ''Bad Science: The Short Life and Weird Times of
Cold Fusion.''
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  #2   ^
Old Sun, Jul-07-02, 23:39
Soinwi's Avatar
Soinwi Soinwi is offline
Senior Member
Posts: 1,170
 
Plan: Atkins
Stats: 293/288.2/199 Female 5 foot 11 inches
BF:38%/??/25%
Progress: 5%
Location: Milwaukee
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Thanks for posting that article..I found it very interesting and really informational.


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  #3   ^
Old Sun, Jul-07-02, 23:45
akelley akelley is offline
Registered Member
Posts: 27
 
Plan: Atkins
Stats: 180/168/160 Male 67 inches
BF:
Progress: 60%
Location: Westchester NY
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Very good article. Can you post the source link? When was this published?

Thanks.
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  #4   ^
Old Mon, Jul-08-02, 04:05
Vickolien Vickolien is offline
Registered Member
Posts: 40
 
Plan: Atkins
Stats: 224/206/140
BF:47%/45.5%/29%?
Progress: 21%
Location: The Netherlands
Thumbs up Interesting!

Thanks so much for posting this....it took me a while to read it though! This gives me alot of info I can use to explain to people why i think this is a right WOL!

Vickolien
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