By Gary
Taubes
Eat less fat and more carbohydrates
may be the cause of the rampaging epidemic of obesity in America.
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.
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, 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.
New
York Times July 7, 2002
Continued
in the next issue of the newsletter