Ok this is the first post read this and then scroll below for the next one -- DietLowCarb.com

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Date Posted: 08:42:09 07/08/02 Mon
Author: Nancy
Subject: Ok this is the first post read this and then scroll below for the next one

Ok I apologize, I had to post this on my board and then break it up, too large to put into one post.

Complements of AOL and the New York Times.

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

f 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.''

cientists 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.

ew 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.

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