What if It's All Been a Big Fat Lie?
The New York Times Magazine
By Gary Taubes
Published: Sunday, July 7, 2002
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 b�arnaise 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?''
Photos: Spaghetti in olive oil: Which one is the culprit? (Lendon
Flanagan); From pyramid to pear: The Agriculture Department's
recommendations may be partly responsible for
America's increasing obesity
rates. Milk made whole: Is the full-fat kind healthier than
skim? (Jennifer Durham/Getty Images)
Gary Taubes is a correspondent for the journal Science and
author of ''Bad Science: The Short Life and Weird Times of
Cold Fusion.''
|