What if It's All Been a Big Fat Lie? (Part 1)
By GARY TAUBES
July 7, 2002
nytimes.com
If the members of the American medical establishment were to have a collective find-yourself-standing-naked-in-Times-Square-type
nightmare, this might be it. They spend 30 years ridiculing Robert Atkins, author of the phenomenally-best-selling ''Dr. Atkins' Diet
Revolution'' and ''Dr. Atkins' New Diet Revolution,'' accusing the Manhattan doctor of quackery and fraud, only to discover that the
unrepentant Atkins was right all along. Or maybe it's this: they find that their very own dietary recommendations -- eat less fat and more
carbohydrates -- are the cause of the rampaging epidemic of obesity in America. Or, just possibly this: they find out both of the above are
true.
When Atkins first published his ''Diet Revolution'' in 1972, Americans were just coming to terms with the proposition that fat -- particularly
the saturated fat of meat and dairy products -- was the primary nutritional evil in the American diet. Atkins managed to sell millions of copies
of a book promising that we would lose weight eating steak, eggs and butter to our heart's desire, because it was the carbohydrates, the
pasta, rice, bagels and sugar, that caused obesity and even heart disease. Fat, he said, was harmless.
Atkins allowed his readers to eat ''truly luxurious foods without limit,'' as he put it, ''lobster with butter sauce, steak with bearnaise sauce . . .
bacon cheeseburgers,'' but allowed no starches or refined carbohydrates, which means no sugars or anything made from flour. Atkins banned
even fruit juices, and permitted only a modicum of vegetables, although the latter were negotiable as the diet progressed.
Atkins was by no means the first to get rich pushing a high-fat diet that restricted carbohydrates, but he popularized it to an extent that the
American Medical Association considered it a potential threat to our health. The A.M.A. attacked Atkins's diet as a ''bizarre regimen'' that
advocated ''an unlimited intake of saturated fats and cholesterol-rich foods,'' and Atkins even had to defend his diet in Congressional hearings.
Thirty years later, America has become weirdly polarized on the subject of weight. On the one hand, we've been told with almost religious
certainty by everyone from the surgeon general on down, and we have come to believe with almost religious certainty, that obesity is caused
by the excessive consumption of fat, and that if we eat less fat we will lose weight and live longer. On the other, we have the ever-resilient
message of Atkins and decades' worth of best-selling diet books, including ''The Zone,'' ''Sugar Busters'' and ''Protein Power'' to name a few.
All push some variation of what scientists would call the alternative hypothesis: it's not the fat that makes us fat, but the carbohydrates, and if
we eat less carbohydrates we will lose weight and live longer.
The perversity of this alternative hypothesis is that it identifies the cause of obesity as precisely those refined carbohydrates at the base of the
famous Food Guide Pyramid -- the pasta, rice and bread -- that we are told should be the staple of our healthy low-fat diet, and then on the
sugar or corn syrup in the soft drinks, fruit juices and sports drinks that we have taken to consuming in quantity if for no other reason than that
they are fat free and so appear intrinsically healthy. While the low-fat-is-good-health dogma represents reality as we have come to know it,
and the government has spent hundreds of millions of dollars in research trying to prove its worth, the low-carbohydrate message has been
relegated to the realm of unscientific fantasy.
Over the past five years, however, there has been a subtle shift in the scientific consensus. It used to be that even considering the possibility of
the alternative hypothesis, let alone researching it, was tantamount to quackery by association. Now a small but growing minority of
establishment researchers have come to take seriously what the low-carb-diet doctors have been saying all along. Walter Willett, chairman of
the department of nutrition at the Harvard School of Public Health, may be the most visible proponent of testing this heretic hypothesis. Willett
is the de facto spokesman of the longest-running, most comprehensive diet and health studies ever performed, which have already cost
upward of $100 million and include data on nearly 300,000 individuals. Those data, says Willett, clearly contradict the low-fat-is-good-health
message ''and the idea that all fat is bad for you; the exclusive focus on adverse effects of fat may have contributed to the obesity epidemic.''
These researchers point out that there are plenty of reasons to suggest that the low-fat-is-good-health hypothesis has now effectively failed the
test of time. In particular, that we are in the midst of an obesity epidemic that started around the early 1980's, and that this was coincident with
the rise of the low-fat dogma. (Type 2 diabetes, the most common form of the disease, also rose significantly through this period.) They say
that low-fat weight-loss diets have proved in clinical trials and real life to be dismal failures, and that on top of it all, the percentage of fat in the
American diet has been decreasing for two decades. Our cholesterol levels have been declining, and we have been smoking less, and yet the
incidence of heart disease has not declined as would be expected. ''That is very disconcerting,'' Willett says. ''It suggests that something else
bad is happening.''
The science behind the alternative hypothesis can be called Endocrinology 101, which is how it's referred to by David Ludwig, a researcher at
Harvard Medical School who runs the pediatric obesity clinic at Children's Hospital Boston, and who prescribes his own version of a
carbohydrate-restricted diet to his patients. Endocrinology 101 requires an understanding of how carbohydrates affect insulin and blood sugar
and in turn fat metabolism and appetite. This is basic endocrinology, Ludwig says, which is the study of hormones, and it is still considered
radical because the low-fat dietary wisdom emerged in the 1960's from researchers almost exclusively concerned with the effect of fat on
cholesterol and heart disease. At the time, Endocrinology 101 was still underdeveloped, and so it was ignored. Now that this science is
becoming clear, it has to fight a quarter century of anti-fat prejudice.
The alternative hypothesis also comes with an implication that is worth considering for a moment, because it's a whopper, and it may indeed
be an obstacle to its acceptance. If the alternative hypothesis is right -- still a big ''if'' -- then it strongly suggests that the ongoing epidemic of
obesity in America and elsewhere is not, as we are constantly told, due simply to a collective lack of will power and a failure to exercise.
Rather it occurred, as Atkins has been saying (along with Barry Sears, author of ''The Zone''), because the public health authorities told us
unwittingly, but with the best of intentions, to eat precisely those foods that would make us fat, and we did. We ate more fat-free
carbohydrates, which, in turn, made us hungrier and then heavier. Put simply, if the alternative hypothesis is right, then a low-fat diet is not by
definition a healthy diet. In practice, such a diet cannot help being high in carbohydrates, and that can lead to obesity, and perhaps even heart
disease. ''For a large percentage of the population, perhaps 30 to 40 percent, low-fat diets are counterproductive,'' says Eleftheria
Maratos-Flier, director of obesity research at Harvard's prestigious Joslin Diabetes Center. ''They have the paradoxical effect of making
people gain weight.''
Scientists are still arguing about fat, despite a century of research, because the regulation of appetite and weight in the human body
happens to be almost inconceivably complex, and the experimental tools we have to study it are still remarkably inadequate. This
combination leaves researchers in an awkward position. To study the entire physiological system involves feeding real food to real human
subjects for months or years on end, which is prohibitively expensive, ethically questionable (if you're trying to measure the effects of foods
that might cause heart disease) and virtually impossible to do in any kind of rigorously controlled scientific manner. But if researchers seek to
study something less costly and more controllable, they end up studying experimental situations so oversimplified that their results may have
nothing to do with reality. This then leads to a research literature so vast that it's possible to find at least some published research to support
virtually any theory. The result is a balkanized community -- ''splintered, very opinionated and in many instances, intransigent,'' says Kurt
Isselbacher, a former chairman of the Food and Nutrition Board of the National Academy of Science -- in which researchers seem easily
convinced that their preconceived notions are correct and thoroughly uninterested in testing any other hypotheses but their own.
What's more, the number of misconceptions propagated about the most basic research can be staggering. Researchers will be suitably
scientific describing the limitations of their own experiments, and then will cite something as gospel truth because they read it in a magazine.
The classic example is the statement heard repeatedly that 95 percent of all dieters never lose weight, and 95 percent of those who do will not
keep it off. This will be correctly attributed to the University of Pennsylvania psychiatrist Albert Stunkard, but it will go unmentioned that this
statement is based on 100 patients who passed through Stunkard's obesity clinic during the Eisenhower administration.
With these caveats, one of the few reasonably reliable facts about the obesity epidemic is that it started around the early 1980's. According to
Katherine Flegal, an epidemiologist at the National Center for Health Statistics, the percentage of obese Americans stayed relatively constant
through the 1960's and 1970's at 13 percent to 14 percent and then shot up by 8 percentage points in the 1980's. By the end of that decade,
nearly one in four Americans was obese. That steep rise, which is consistent through all segments of American society and which continued
unabated through the 1990's, is the singular feature of the epidemic. Any theory that tries to explain obesity in America has to account for that.
Meanwhile, overweight children nearly tripled in number. And for the first time, physicians began diagnosing Type 2 diabetes in adolescents.
Type 2 diabetes often accompanies obesity. It used to be called adult-onset diabetes and now, for the obvious reason, is not.
So how did this happen? The orthodox and ubiquitous explanation is that we live in what Kelly Brownell, a Yale psychologist, has called a
''toxic food environment'' of cheap fatty food, large portions, pervasive food advertising and sedentary lives. By this theory, we are at the
Pavlovian mercy of the food industry, which spends nearly $10 billion a year advertising unwholesome junk food and fast food. And because
these foods, especially fast food, are so filled with fat, they are both irresistible and uniquely fattening. On top of this, so the theory goes, our
modern society has successfully eliminated physical activity from our daily lives. We no longer exercise or walk up stairs, nor do our children
bike to school or play outside, because they would prefer to play video games and watch television. And because some of us are obviously
predisposed to gain weight while others are not, this explanation also has a genetic component -- the thrifty gene. It suggests that storing extra
calories as fat was an evolutionary advantage to our Paleolithic ancestors, who had to survive frequent famine. We then inherited these
''thrifty'' genes, despite their liability in today's toxic environment.
This theory makes perfect sense and plays to our puritanical prejudice that fat, fast food and television are innately damaging to our humanity.
But there are two catches. First, to buy this logic is to accept that the copious negative reinforcement that accompanies obesity -- both
socially and physically -- is easily overcome by the constant bombardment of food advertising and the lure of a supersize bargain meal. And
second, as Flegal points out, little data exist to support any of this. Certainly none of it explains what changed so significantly to start the
epidemic. Fast-food consumption, for example, continued to grow steadily through the 70's and 80's, but it did not take a sudden leap, as
obesity did.
As far as exercise and physical activity go, there are no reliable data before the mid-80's, according to William Dietz, who runs the division of
nutrition and physical activity at the Centers for Disease Control; the 1990's data show obesity rates continuing to climb, while exercise
activity remained unchanged. This suggests the two have little in common. Dietz also acknowledged that a culture of physical exercise began in
the United States in the 70's -- the ''leisure exercise mania,'' as Robert Levy, director of the National Heart, Lung and Blood Institute,
described it in 1981 -- and has continued through the present day.
As for the thrifty gene, it provides the kind of evolutionary rationale for human behavior that scientists find comforting but that simply cannot
be tested. In other words, if we were living through an anorexia epidemic, the experts would be discussing the equally untestable ''spendthrift
gene'' theory, touting evolutionary advantages of losing weight effortlessly. An overweight homo erectus, they'd say, would have been easy
prey for predators.
It is also undeniable, note students of Endocrinology 101, that mankind never evolved to eat a diet high in starches or sugars. ''Grain products
and concentrated sugars were essentially absent from human nutrition until the invention of agriculture,'' Ludwig says, ''which was only 10,000
years ago.'' This is discussed frequently in the anthropology texts but is mostly absent from the obesity literature, with the prominent exception
of the low-carbohydrate-diet books.
What's forgotten in the current controversy is that the low-fat dogma itself is only about 25 years old. Until the late 70's, the accepted wisdom
was that fat and protein protected against overeating by making you sated, and that carbohydrates made you fat. In ''The Physiology of
Taste,'' for instance, an 1825 discourse considered among the most famous books ever written about food, the French gastronome Jean
Anthelme Brillat-Savarin says that he could easily identify the causes of obesity after 30 years of listening to one ''stout party'' after another
proclaiming the joys of bread, rice and (from a ''particularly stout party'') potatoes. Brillat-Savarin described the roots of obesity as a natural
predisposition conjuncted with the ''floury and feculent substances which man makes the prime ingredients of his daily nourishment.'' He added
that the effects of this fecula -- i.e., ''potatoes, grain or any kind of flour'' -- were seen sooner when sugar was added to the diet.
This is what my mother taught me 40 years ago, backed up by the vague observation that Italians tended toward corpulence because they ate
so much pasta. This observation was actually documented by Ancel Keys, a University of Minnesota physician who noted that fats ''have
good staying power,'' by which he meant they are slow to be digested and so lead to satiation, and that Italians were among the heaviest
populations he had studied. According to Keys, the Neapolitans, for instance, ate only a little lean meat once or twice a week, but ate bread
and pasta every day for lunch and dinner. ''There was no evidence of nutritional deficiency,'' he wrote, ''but the working-class women were
fat.''
By the 70's, you could still find articles in the journals describing high rates of obesity in Africa and the Caribbean where diets contained
almost exclusively carbohydrates. The common thinking, wrote a former director of the Nutrition Division of the United Nations, was that the
ideal diet, one that prevented obesity, snacking and excessive sugar consumption, was a diet ''with plenty of eggs, beef, mutton, chicken,
butter and well-cooked vegetables.'' This was the identical prescription Brillat-Savarin put forth in 1825.
It was Ancel Keys, paradoxically, who introduced the low-fat-is-good-health dogma in the 50's with his theory that dietary fat raises
cholesterol levels and gives you heart disease. Over the next two decades, however, the scientific evidence supporting this theory remained
stubbornly ambiguous. The case was eventually settled not by new science but by politics. It began in January 1977, when a Senate
committee led by George McGovern published its ''Dietary Goals for the United States,'' advising that Americans significantly curb their fat
intake to abate an epidemic of ''killer diseases'' supposedly sweeping the country. It peaked in late 1984, when the National Institutes of
Health officially recommended that all Americans over the age of 2 eat less fat. By that time, fat had become ''this greasy killer'' in the
memorable words of the Center for Science in the Public Interest, and the model American breakfast of eggs and bacon was well on its way
to becoming a bowl of Special K with low-fat milk, a glass of orange juice and toast, hold the butter -- a dubious feast of refined
carbohydrates.
In the intervening years, the N.I.H. spent several hundred million dollars trying to demonstrate a connection between eating fat and getting
heart disease and, despite what we might think, it failed. Five major studies revealed no such link. A sixth, however, costing well over $100
million alone, concluded that reducing cholesterol by drug therapy could prevent heart disease. The N.I.H. administrators then made a leap of
faith. Basil Rifkind, who oversaw the relevant trials for the N.I.H., described their logic this way: they had failed to demonstrate at great
expense that eating less fat had any health benefits. But if a cholesterol-lowering drug could prevent heart attacks, then a low-fat,
cholesterol-lowering diet should do the same. ''It's an imperfect world,'' Rifkind told me. ''The data that would be definitive is ungettable, so
you do your best with what is available.''
Some of the best scientists disagreed with this low-fat logic, suggesting that good science was incompatible with such leaps of faith, but they
were effectively ignored. Pete Ahrens, whose Rockefeller University laboratory had done the seminal research on cholesterol metabolism,
testified to McGovern's committee that everyone responds differently to low-fat diets. It was not a scientific matter who might benefit and who
might be harmed, he said, but ''a betting matter.'' Phil Handler, then president of the National Academy of Sciences, testified in Congress to
the same effect in 1980. ''What right,'' Handler asked, ''has the federal government to propose that the American people conduct a vast
nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?''
Nonetheless, once the N.I.H. signed off on the low-fat doctrine, societal forces took over. The food industry quickly began producing
thousands of reduced-fat food products to meet the new recommendations. Fat was removed from foods like cookies, chips and yogurt. The
problem was, it had to be replaced with something as tasty and pleasurable to the palate, which meant some form of sugar, often high-fructose
corn syrup. Meanwhile, an entire industry emerged to create fat substitutes, of which Procter & Gamble's olestra was first. And because these
reduced-fat meats, cheeses, snacks and cookies had to compete with a few hundred thousand other food products marketed in America, the
industry dedicated considerable advertising effort to reinforcing the less-fat-is-good-health message. Helping the cause was what Walter
Willett calls the ''huge forces'' of dietitians, health organizations, consumer groups, health reporters and even cookbook writers, all
well-intended missionaries of healthful eating. |
