NUTRITION:
The Soft Science of Dietary Fat
Science Magazine Volume 291, Number 5513, Issue of 30 Mar 2001, pp. 2536-2545.

 Gary Taubes

     Mainstream nutritional science has demonized dietary fat, yet 50 years and
hundreds of millions of dollars of
                 research have failed to prove that eating a low-fat diet will
help you live longer

 When the U.S. Surgeon General's Office set off in 1988 to write the definitive
report on the dangers of dietary fat, the scientific
 task appeared straightforward. Four years earlier, the National Institutes of
Health (NIH) had begun advising every American old
 enough to walk to restrict fat intake, and the president of the American Heart
Association (AHA) had told Time magazine that if
 everyone went along, "we will have [atherosclerosis] conquered" by the year
2000. The Surgeon General's Office itself had just
 published its 700-page landmark "Report on Nutrition and Health," declaring fat
 the single most unwholesome component of the
 American diet.

 All of this was apparently based on sound science. So the task before the
project officer was merely to gather that science
 together in one volume, have it reviewed by a committee of experts, which had
been promptly established, and publish it. The
 project did not go smoothly, however. Four project officers came and went over
the next decade. "It consumed project officers,"
 says Marion Nestle, who helped launch the project and now runs the nutrition
and food studies department at New York
 University (NYU). Members of the oversight committee saw drafts of an early
chapter or two, criticized them vigorously, and
 then saw little else.

 Finally, in June 1999, 11 years after the project began, the Surgeon General's
Office circulated a letter, authored by the last of the project officers,
explaining that the
 report would be killed. There was no other public announcement and no press
release. The letter explained that the relevant administrators "did not
anticipate fully the
 magnitude of the additional external expertise and staff resources that would
be needed." In other words, says Nestle, the subject matter "was too
complicated." Bill
 Harlan, a member of the oversight committee and associate director of the
Office of Disease Prevention at NIH, says "the report was initiated with a
preconceived
 opinion of the conclusions," but the science behind those opinions was not
holding up. "Clearly the thoughts of yesterday were not going to serve us very
well."

 During the past 30 years, the concept of eating healthy in America has become
synonymous with avoiding dietary fat. The creation and marketing of reduced-fat
food
 products has become big business; over 15,000 have appeared on supermarket
shelves. Indeed, an entire research industry has arisen to create palatable
nonfat fat
 substitutes, and the food industry now spends billions of dollars yearly
selling the less-fat-is-good-health message. The government weighs in as well,
with the U.S.
 Department of Agriculture's (USDA's) booklet on dietary guidelines, published
every 5 years, and its ubiquitous Food Guide Pyramid, which recommends that fats
 and oils be eaten "sparingly." The low-fat gospel spreads farther by a kind of
societal osmosis, continuously reinforced by physicians, nutritionists,
journalists, health
 organizations, and consumer advocacy groups such as the Center for Science in
the Public Interest, which refers to fat as this "greasy killer." "In America,
we no
 longer fear God or the communists, but we fear fat," says David Kritchevsky of
the Wistar Institute in Philadelphia, who in 1958 wrote the first textbook on
 cholesterol.

 As the Surgeon General's Office discovered, however, the science of dietary fat
 is not nearly as simple as it once appeared. The proposition, now 50 years old,
 that
 dietary fat is a bane to health is based chiefly on the fact that fat,
specifically the hard, saturated fat found primarily in meat and dairy products,
 elevates blood
 cholesterol levels. This in turn raises the likelihood that cholesterol will
clog arteries, a condition known as atherosclerosis, which then increases risk
of coronary
 artery disease, heart attack, and untimely death. By the 1970s, each individual
 step of this chain from fat to cholesterol to heart disease had been
demonstrated
 beyond reasonable doubt, but the veracity of the chain as a whole has never
been proven. In other words, despite decades of research, it is still a
debatable
 proposition whether the consumption of saturated fats above recommended levels
(step one in the chain) by anyone who's not already at high risk of heart
disease
 will increase the likelihood of untimely death (outcome three). Nor have
hundreds of millions of dollars in trials managed to generate compelling
evidence that healthy
 individuals can extend their lives by more than a few weeks, if that, by eating
 less fat (see sidebar on p. 2538). To put it simply, the data remain ambiguous
as to
 whether low-fat diets will benefit healthy Americans. Worse, the ubiquitous
admonishments to reduce total fat intake have encouraged a shift to
high-carbohydrate
 diets, which may be no better--and may even be worse--than high-fat diets.

 Since the early 1970s, for instance, Americans' average fat intake has dropped
from over 40% of total calories to 34%; average serum cholesterol levels have
 dropped as well. But no compelling evidence suggests that these decreases have
improved health. Although heart disease death rates have dropped--and public
 health officials insist low-fat diets are partly responsible--the incidence of
heart disease does not seem to be declining, as would be expected if lower fat
diets made
 a difference. This was the conclusion, for instance, of a 10-year study of
heart disease mortality published in The New England Journal of Medicine in
1998, which
 suggested that death rates are declining largely because doctors are treating
the disease more successfully. AHA statistics agree: Between 1979 and 1996, the
 number of medical procedures for heart disease increased from 1.2 million to
5.4 million a year. "I don't consider that this disease category has disappeared
 or
 anything close to it," says one AHA statistician.

 Meanwhile, obesity in America, which remained constant from the early 1960s
through 1980, has surged upward since then--from 14% of the population to over
 22%. Diabetes has increased apace. Both obesity and diabetes increase heart
disease risk, which could explain why heart disease incidence is not decreasing.
 That
 this obesity epidemic occurred just as the government began bombarding
Americans with the low-fat message suggests the possibility, however distant,
that low-fat
 diets might have unintended consequences--among them, weight gain. "Most of us
would have predicted that if we can get the population to change its fat intake,
 with its dense calories, we would see a reduction in weight," admits Harlan.
"Instead, we see the exact opposite."

 In the face of this uncertainty, skeptics and apostates have come along
repeatedly, only to see their work almost religiously ignored as the mainstream
medical
 community sought consensus on the evils of dietary fat. For 20 years, for
instance, the Harvard School of Public Health has run the Nurses' Health Study
and its two
 sequelae--the Health Professionals Follow-Up Study and the Nurses' Health Study
 II--accumulating over a decade of data on the diet and health of almost 300,000
 Americans. The results suggest that total fat consumed has no relation to heart
 disease risk; that monounsaturated fats like olive oil lower risk; and that
saturated fats
 are little worse, if at all, than the pasta and other carbohydrates that the
Food Guide Pyramid suggests be eaten copiously. (The studies also suggest that
trans fatty
 acids are unhealthful. These are the fats in margarine, for instance, and are
what many Americans started eating when they were told that the saturated fats
in butter
 might kill them.) Harvard epidemiologist Walter Willett, spokesperson for the
Nurses' Health Study, points out that NIH has spent over $100 million on the
three
 studies and yet not one government agency has changed its primary guidelines to
 fit these particular data. "Scandalous," says Willett. "They say, 'You really
need a
 high level of proof to change the recommendations,' which is ironic, because
they never had a high level of proof to set them."

 Indeed, the history of the national conviction that dietary fat is deadly, and
its evolution from hypothesis to dogma, is one in which politicians,
bureaucrats, the media,
 and the public have played as large a role as the scientists and the science.
It's a story of what can happen when the demands of public health policy--and
the
 demands of the public for simple advice--run up against the confusing ambiguity
 of real science.

 Fear of fat
 During the first half of the 20th century, nutritionists were more concerned
about malnutrition than about the sins of dietary excess. After World War II,
however, a
 coronary heart disease epidemic seemed to sweep the country (see sidebar on p.
2540). "Middle-aged men, seemingly healthy, were dropping dead," wrote
 biochemist Ancel Keys of the University of Minnesota, Twin Cities, who was
among the first to suggest that dietary fats might be the cause. By 1952, Keys
was
 arguing that Americans should reduce their fat intake to less than 30% of total
 calories, although he simultaneously recognized that "direct evidence on the
effect of
 the diet on human arteriosclerosis is very little and likely to remain so for
some time." In the famous and very controversial Seven Countries Study, for
instance, Keys
 and his colleagues reported that the amount of fat consumed seemed to be the
salient difference between populations such as those in Japan and Crete that had
 little
 heart disease and those, as in Finland, that were plagued by it. In 1961, the
Framingham Heart Study linked cholesterol levels to heart disease, Keys made the
 cover
 of Time magazine, and the AHA, under his influence, began advocating low-fat
diets as a palliative for men with high cholesterol levels. Keys had also become
 one
 of the first Americans to consciously adopt a heart-healthy diet: He and his
wife, Time reported, "do not eat 'carving meat'--steaks, chops, roasts--more
than three
 times a week."

 Nonetheless, by 1969 the state of the science could still be summarized by a
single sentence from a report of the Diet-Heart Review Panel of the National
Heart
 Institute (now the National Heart, Lung, and Blood Institute, or NHLBI): "It is
 not known whether dietary manipulation has any effect whatsoever on coronary
heart
 disease." The chair of the panel was E. H. "Pete" Ahrens, whose laboratory at
Rockefeller University in New York City did much of the seminal research on fat
and
 cholesterol metabolism.

 Whereas proponents of low-fat diets were concerned primarily about the effects
of dietary fat on cholesterol levels and heart disease, Ahrens and his panel--10
 experts in clinical medicine, epidemiology, biostatistics, human nutrition, and
 metabolism--were equally concerned that eating less fat could have profound
effects
 throughout the body, many of which could be harmful. The brain, for instance,
is 70% fat, which chiefly serves to insulate neurons. Fat is also the primary
component
 of cell membranes. Changing the proportion of saturated to unsaturated fats in
the diet changes the fat composition in these membranes. This could conceivably
 change the membrane permeability, which controls the transport of everything
from glucose, signaling proteins, and hormones to bacteria, viruses, and
tumor-causing
 agents into and out of the cell. The relative saturation of fats in the diet
could also influence cellular aging as well as the clotting ability of blood
cells.

 Whether the potential benefits of low-fat diets would exceed the potential
risks could be settled by testing whether low-fat diets actually prolong life,
but such a test
 would have to be enormous. The effect of diet on cholesterol levels is subtle
for most individuals--especially those living in the real world rather than the
metabolic
 wards of nutrition researchers--and the effect of cholesterol levels on heart
disease is also subtle. As a result, tens of thousands of individuals would have
 to switch to
 low-fat diets and their subsequent health compared to that of equal numbers who
 continued eating fat to alleged excess. And all these people would have to be
 followed for years until enough deaths accumulated to provide statistically
significant results. Ahrens and his colleagues were pessimistic about whether
such a
 massive and expensive trial could ever be done. In 1971, an NIH task force
estimated such a trial would cost $1 billion, considerably more than NIH was
willing to
 spend. Instead, NIH administrators opted for a handful of smaller studies, two
of which alone would cost $255 million. Perhaps more important, these studies
would
 take a decade. Neither the public, the press, nor the U.S. Congress was willing
 to wait that long.

 Science by committee
 Like the flourishing American affinity for alternative medicine, an antifat
movement evolved independently of science in the 1960s. It was fed by distrust
of the
 establishment--in this case, both the medical establishment and the food
industry--and by counterculture attacks on excessive consumption, whether
manifested in
 gas-guzzling cars or the classic American cuisine of bacon and eggs and marbled
 steaks. And while the data on fat and health remained ambiguous and the
scientific
 community polarized, the deadlock was broken not by any new science, but by
politicians. It was Senator George McGovern's bipartisan, nonlegislative Select
 Committee on Nutrition and Human Needs--and, to be precise, a handful of
McGovern's staff members--that almost single-handedly changed nutritional policy
 in
 this country and initiated the process of turning the dietary fat hypothesis
into dogma.

 McGovern's committee was founded in 1968 with a mandate to eradicate
malnutrition in America, and it instituted a series of landmark federal food
assistance
 programs. As the malnutrition work began to peter out in the mid-1970s,
however, the committee didn't disband. Rather, its general counsel, Marshall
Matz, and
 staff director, Alan Stone, both young lawyers, decided that the committee
would address "overnutrition," the dietary excesses of Americans. It was a
"casual
 endeavor," says Matz. "We really were totally na



ïve, a bunch of kids, who just
thought, 'Hell, we should say something on this subject before we go out of
business.'
 " McGovern and his fellow senators--all middle-aged men worried about their
girth and their health--signed on; McGovern and his wife had both gone through
 diet-guru Nathan Pritikin's very low fat diet and exercise program. McGovern
quit the program early, but Pritikin remained a major influence on his thinking.

 McGovern's committee listened to 2 days of testimony on diet and disease in
July 1976. Then resident wordsmith Nick Mottern, a former labor reporter for The
 Providence Journal, was assigned the task of researching and writing the first
"Dietary Goals for the United States." Mottern, who had no scientific background
 and
 no experience writing about science, nutrition, or health, believed his Dietary
 Goals would launch a "revolution in diet and agriculture in this country." He
avoided the
 scientific and medical controversy by relying almost exclusively on Harvard
School of Public Health nutritionist Mark Hegsted for input on dietary fat.
Hegsted had
 studied fat and cholesterol metabolism in the early 1960s, and he believed
unconditionally in the benefits of restricting fat intake, although he says he
was aware that
 his was an extreme opinion. With Hegsted as his muse, Mottern saw dietary fat
as the nutritional equivalent of cigarettes, and the food industry as akin to
the tobacco
 industry in its willingness to suppress scientific truth in the interests of
profits. To Mottern, those scientists who spoke out against fat were those
willing to take on the
 industry. "It took a certain amount of guts," he says, "to speak about this
because of the financial interests involved."

 Mottern's report suggested that Americans cut their total fat intake to 30% of
the calories they consume and saturated fat intake to 10%, in accord with AHA
 recommendations for men at high risk of heart disease. The report acknowledged
the existence of controversy but insisted Americans had nothing to lose by
 following its advice. "The question to be asked is not why should we change our
 diet but why not?" wrote Hegsted in the introduction. "There are [no risks]
that can
 be identified and important benefits can be expected." This was an optimistic
but still debatable position, and when Dietary Goals was released in January
1977, "all
 hell broke loose," recalls Hegsted. "Practically nobody was in favor of the
McGovern recommendations. Damn few people."

 McGovern responded with three follow-up hearings, which aptly foreshadowed the
next 7 years of controversy. Among those testifying, for instance, was NHLBI
 director Robert Levy, who explained that no one knew if eating less fat or
lowering blood cholesterol levels would prevent heart attacks, which was why
NHLBI
 was spending $300 million to study the question. Levy's position was awkward,
he recalls, because "the good senators came out with the guidelines and then
called
 us in to get advice." He was joined by prominent scientists, including Ahrens,
who testified that advising Americans to eat less fat on the strength of such
marginal
 evidence was equivalent to conducting a nutritional experiment with the
American public as subjects. Even the American Medical Association protested,
suggesting
 that the diet proposed by the guidelines raised the "potential for harmful
effects." But as these scientists testified, so did representatives from the
dairy, egg, and cattle
 industries, who also vigorously opposed the guidelines for obvious reasons.
This juxtaposition served to taint the scientific criticisms: Any scientists
arguing against the
 committee's guidelines appeared to be either hopelessly behind the paradigm,
which was Hegsted's view, or industry apologists, which was Mottern's, if not
both.

 Although the committee published a revised edition of the Dietary Goals later
in the year, the thrust of the recommendations remained unchanged. It did give
in to
 industry pressure by softening the suggestion that Americans eat less meat.
Mottern says he considered even that a "disservice to the public," refused to do
 the
 revisions, and quit the committee. (Mottern became a vegetarian while writing
the Dietary Goals and now runs a food co-op in Peekskill, New York.)

 The guidelines might have then died a quiet death when McGovern's committee
came to an end in late 1977 if two federal agencies had not felt it imperative
to
 respond. Although they took contradictory points of view, one message--with
media assistance--won out.

 The first was the USDA, where consumer-activist Carol Tucker Foreman had
recently been appointed an assistant secretary. Foreman believed it was
incumbent on
 USDA to turn McGovern's recommendations into official policy, and, like
Mottern, she was not deterred by the existence of scientific controversy. "Tell
us what you
 know and tell us it's not the final answer," she would tell scientists. "I have
 to eat and feed my children three times a day, and I want you to tell me what
your best
 sense of the data is right now."

 Of course, given the controversy, the "best sense of the data" would depend on
which scientists were asked. The Food and Nutrition Board of the National
 Academy of Sciences (NAS), which decides the Recommended Dietary Allowances,
would have been a natural choice, but NAS president Philip Handler, an
 expert on metabolism, had told Foreman that Mottern's Dietary Goals were
"nonsense." Foreman then turned to McGovern's staffers for advice and they
 recommended she hire Hegsted, which she did. Hegsted, in turn, relied on a
state-of-the-science report published by an expert but very divergent committee
of the
 American Society for Clinical Nutrition. "They were nowhere near unanimous on
anything," says Hegsted, "but the majority supported something like the McGovern
 committee report."

 The resulting document became the first edition of "Using the Dietary
Guidelines for Americans." Although it acknowledged the existence of controversy
 and
 suggested that a single dietary recommendation might not suit an entire diverse
 population, the advice to avoid fat and saturated fat was, indeed, virtually
identical to
 McGovern's Dietary Goals.

 Three months later, the NAS Food and Nutrition Board released its own
guidelines: "Toward Healthful Diets." The board, consisting of a dozen nutrition
 experts,
 concluded that the only reliable advice for healthy Americans was to watch
their weight; everything else, dietary fat included, would take care of itself.
The advice
 was not taken kindly, however, at least not by the media. The first
reports--"rather incredulously," said Handler at the time--criticized the NAS
advice for conflicting
 with the USDA's and McGovern's and thus somehow being irresponsible. Follow-up
reports suggested that the board members, in the words of Jane Brody, who
 covered the story for The New York Times, were "all in the pocket of the
industries being hurt." To be precise, the board chair and one of its members
consulted for
 food industries, and funding for the board itself came from industry donations.
 These industry connections were leaked to the press from the USDA.

 Hegsted now defends the NAS board, although he didn't at the time, and calls
this kind of conflict of interest "a hell of an issue." "Everybody used to
complain that
 industry didn't do anything on nutrition," he told Science, "yet anybody who
got involved was blackballed because their positions were presumably influenced
by the
 industry." (In 1981, Hegsted returned to Harvard, where his research was funded
 by Frito-Lay.) The press had mixed feelings, claiming that the connections
"soiled"
 the academy's reputation "for tendering careful scientific advice" (The
Washington Post), demonstrated that the board's "objectivity and aptitude are in
 doubt" (The
 New York Times), or represented in the board's guidelines a "blow against the
food faddists who hold the public in thrall" (Science). In any case, the NAS
board
 had been publicly discredited. Hegsted's Dietary Guidelines for Americans
became the official U.S. policy on dietary fat: Eat less fat. Live longer.

 Creating "consensus"
 Once politicians, the press, and the public had decided dietary fat policy, the
 science was left to catch up. In the early 1970s, when NIH opted to forgo a $1
billion
 trial that might be definitive and instead fund a half-dozen studies at
one-third the cost, everyone hoped these smaller trials would be sufficiently
persuasive to
 conclude that low-fat diets prolong lives. The results were published between
1980 and 1984. Four of these trials --comparing heart disease rates and diet
within
 Honolulu, Puerto Rico, Chicago, and Framingham--showed no evidence that men who
 ate less fat lived longer or had fewer heart attacks. A fifth trial, the
Multiple
 Risk Factor Intervention Trial (MRFIT), cost $115 million and tried to amplify
the subtle influences of diet on health by persuading subjects to avoid fat
while
 simultaneously quitting smoking and taking medication for high blood pressure.
That trial suggested, if anything, that eating less fat might shorten life. In
each study,
 however, the investigators concluded that methodological flaws had led to the
negative results. They did not, at least publicly, consider their results reason
 to lessen
 their belief in the evils of fat.

 The sixth study was the $140 million Lipid Research Clinics (LRC) Coronary
Primary Prevention Trial, led by NHLBI administrator Basil Rifkind and
biochemist
 Daniel Steinberg of the University of California, San Diego. The LRC trial was
a drug trial, not a diet trial, but the NHLBI heralded its outcome as the end of
 the
 dietary fat debate. In January 1984, LRC investigators reported that a
medication called cholestyramine reduced cholesterol levels in men with
abnormally high
 cholesterol levels and modestly reduced heart disease rates in the process.
(The probability of suffering a heart attack during the seven-plus years of the
study was
 reduced from 8.6% in the placebo group to 7.0%; the probability of dying from a
 heart attack dropped from 2.0% to 1.6%.) The investigators then concluded,
 without benefit of dietary data, that cholestyramine's benefits could be
extended to diet as well. And although the trial tested only middle-aged men
with cholesterol
 levels higher than those of 95% of the population, they concluded that those
benefits "could and should be extended to other age groups and women and ...
other
 more modest elevations of cholesterol levels."

 Why go so far? Rifkind says their logic was simple: For 20 years, he and his
colleagues had argued that lowering cholesterol levels prevented heart attacks.
They had
 spent enormous sums trying to prove it. They felt they could never actually
demonstrate that low-fat diets prolonged lives--that would be too expensive, and
 MRFIT
 had failed--but now they had established a fundamental link in the causal
chain, from lower cholesterol levels to cardiovascular health. With that, they
could take the
 leap of faith from cholesterol-lowering drugs and health to
cholesterol-lowering diet and health. And after all their effort, they were
eager--not to mention urged by
 Congress--to render helpful advice. "There comes a point when, if you don't
make a decision, the consequences can be great as well," says Rifkind. "If you
just allow
 Americans to keep on consuming 40% of calories from fat, there's an outcome to
that as well."

 With the LRC results in press, the NHLBI launched what Levy called "a massive
public health campaign." The media obligingly went along. Time, for instance,
 reported the LRC findings under the headline "Sorry, It's True. Cholesterol
really is a killer." The article about a drug trial began: "No whole milk. No
butter. No fatty
 meats ..." Time followed up 3 months later with a cover story: "And Cholesterol
 and Now the Bad News. ..." The cover photo was a frowning face: a breakfast
 plate with two fried eggs as the eyes and a bacon strip for the mouth. Rifkind
was quoted saying that their results "strongly indicate that the more you lower
 cholesterol and fat in your diet, the more you reduce your risk of heart
disease," a statement that still lacked direct scientific support.

 The following December, NIH effectively ended the debate with a "Consensus
Conference." The idea of such a conference is that an expert panel, ideally
unbiased,
 listens to 2 days of testimony and arrives at a conclusion with which everyone
agrees. In this case, Rifkind chaired the planning committee, which chose his
LRC
 co-investigator Steinberg to lead the expert panel. The 20 speakers did include
 a handful of skeptics --including Ahrens, for instance, and cardiologist
Michael Oliver
 of Imperial College in London--who argued that it was unscientific to equate
the effects of a drug with the effects of a diet. Steinberg's panel members,
however, as
 Oliver later complained in The Lancet, "were selected to include only experts
who would, predictably, say that all levels of blood cholesterol in the United
States are
 too high and should be lowered. And, of course, this is exactly what was said."
 Indeed, the conference report, written by Steinberg and his panel, revealed no
 evidence of discord. There was "no doubt," it concluded, that low-fat diets
"will afford significant protection against coronary heart disease" to every
American over
 2 years old. The Consensus Conference officially gave the appearance of
unanimity where none existed. After all, if there had been a true consensus, as
Steinberg
 himself told Science, "you wouldn't have had to have a consensus conference."

 The test of time
 To the outside observer, the challenge in making sense of any such long-running
 scientific controversy is to establish whether the skeptics are simply on the
wrong
 side of the new paradigm, or whether their skepticism is well founded. In other
 words, is the science at issue based on sound scientific thinking and
unambiguous
 data, or is it what Sir Francis Bacon, for instance, would have called "wishful
 science," based on fancies, opinions, and the exclusion of contrary evidence?
Bacon
 offered one viable suggestion for differentiating the two: the test of time.
Good science is rooted in reality, so it grows and develops and the evidence
gets increasingly
 more compelling, whereas wishful science flourishes most under its first
authors before "going downhill."

 Such is the case, for instance, with the proposition that dietary fat causes
cancer, which was an integral part of dietary fat anxiety in the late 1970s. By
1982, the
 evidence supporting this idea was thought to be so undeniable that a landmark
NAS report on nutrition and cancer equated those researchers who remained
 skeptical with "certain interested parties [who] formerly argued that the
association between lung cancer and smoking was not causational." Fifteen years
and
 hundreds of millions of research dollars later, a similarly massive expert
report by the World Cancer Research Fund and the American Institute for Cancer
Research
 could find neither "convincing" nor even "probable" reason to believe that
dietary fat caused cancer.

 The hypothesis that low-fat diets are the requisite route to weight loss has
taken a similar downward path. This was the ultimate fallback position in all
low-fat
 recommendations: Fat has nine calories per gram compared to four calories for
carbohydrates and protein, and so cutting fat from the diet surely would cut
pounds.
 "This is held almost to be a religious truth," says Harvard's Willett.
Considerable data, however, now suggest otherwise. The results of
well-controlled clinical trials
 are consistent: People on low-fat diets initially lose a couple of kilograms,
as they would on any diet, and then the weight tends to return. After 1 to 2
years, little has
 been achieved. Consider, for instance, the 50,000 women enrolled in the ongoing
 $100 million Women's Health Initiative (WHI). Half of these women have been
 extensively counseled to consume only 20% of their calories from fat. After 3
years on this near-draconian regime, say WHI sources, the women had lost, on
 average, a kilogram each.

 The link between dietary fat and heart disease is more complicated, because the
 hypothesis has diverged into two distinct propositions: first, that lowering
cholesterol
 prevents heart disease; second, that eating less fat not only lowers
cholesterol and prevents heart disease but prolongs life. Since 1984, the
evidence that
 cholesterol-lowering drugs are beneficial--proposition number one--has indeed
blossomed, at least for those at high risk of heart attack. These drugs reduce
serum
 cholesterol levels dramatically, and they prevent heart attacks, perhaps by
other means as well. Their market has now reached $4 billion a year in the
United States
 alone, and every new trial seems to confirm their benefits.

 The evidence supporting the second proposition, that eating less fat makes for
a healthier and longer life, however, has remained stubbornly ambiguous. If
anything, it
 has only become less compelling over time. Indeed, since Ancel Keys started
advocating low-fat diets almost 50 years ago, the science of fat and cholesterol
 has
 evolved from a simple story into a very complicated one. The catch has been
that few involved in this business were prepared to deal with a complicated
story.



 Researchers initially preferred to believe it was simple--that a single
unwholesome nutrient, in effect, could be isolated from the diverse richness of
human diets; public
 health administrators required a simple story to give to Congress and the
public; and the press needed a simple story--at least on any particular day--to
give to
 editors and readers in 30 column inches. But as contrarian data continued to
accumulate, the complications became increasingly more difficult to ignore or
exclude,
 and the press began waffling or adding caveats. The scientists then got the
blame for not sticking to the original simple story, which had, regrettably,
never existed.

 More fats, fewer answers
 The original simple story in the 1950s was that high cholesterol levels
increase heart disease risk. The seminal Framingham Heart Study, for instance,
which revealed
 the association between cholesterol and heart disease, originally measured only
 total serum cholesterol. But cholesterol shuttles through the blood in an array
 of
 packages. Low-density lipoprotein particles (LDL, the "bad" cholesterol)
deliver fat and cholesterol from the liver to tissues that need it, including
the arterial cells,
 where it can lead to atherosclerotic plaques. High-density lipoproteins (HDLs,
the "good" cholesterol) return cholesterol to the liver. The higher the HDL, the
 lower
 the heart disease risk. Then there are triglycerides, which contain fatty
acids, and very low density lipoproteins (VLDLs), which transport triglycerides.

 All of these particles have some effect on heart disease risk, while the fats,
carbohydrates, and protein in the diet have varying effects on all these
particles. The
 1950s story was that saturated fats increase total cholesterol, polyunsaturated
 fats decrease it, and monounsaturated fats are neutral. By the late 1970s--when
 researchers accepted the benefits of HDL--they realized that monounsaturated
fats are not neutral. Rather, they raise HDL, at least compared to
carbohydrates, and
 lower LDL. This makes them an ideal nutrient as far as cholesterol goes.
Furthermore, saturated fats cannot be quite so evil because, while they elevate
LDL, which
 is bad, they also elevate HDL, which is good. And some saturated fats--stearic
acid, in particular, the fat in chocolate--are at worst neutral. Stearic acid
raises HDL
 levels but does little or nothing to LDL. And then there are trans fatty acids,
 which raise LDL, just like saturated fat, but also lower HDL. Today, none of
this is
 controversial, although it has yet to be reflected in any Food Guide Pyramid.

 To understand where this complexity can lead in a simple example, consider a
steak--to be precise, a porterhouse, select cut, with a half-centimeter layer of
 fat, the
 nutritional constituents of which can be found in the Nutrient Database for
Standard Reference at the USDA Web site. After broiling, this porterhouse
reduces to a
 serving of almost equal parts fat and protein. Fifty-one percent of the fat is
monounsaturated, of which virtually all (90%) is oleic acid, the same healthy
fat that's in
 olive oil. Saturated fat constitutes 45% of the total fat, but a third of that
is stearic acid, which is, at the very least, harmless. The remaining 4% of the
fat is
 polyunsaturated, which also improves cholesterol levels. In sum, well over
half--and perhaps as much as 70%--of the fat content of a porterhouse will
improve
 cholesterol levels compared to what they would be if bread, potatoes, or pasta
were consumed instead. The remaining 30% will raise LDL but will also raise HDL.
 All of this suggests that eating a porterhouse steak rather than carbohydrates
might actually improve heart disease risk, although no nutritional authority who
 hasn't
 written a high-fat diet book will say this publicly.

 As for the scientific studies, in the years since the 1984 consensus
conference, the one thing they have not done is pile up evidence in support of
the low-fat-for-all
 approach to the public good. If anything, they have added weight to Ahrens's
fears that there may be a downside to populationwide low-fat recommendations. In
 1986, for instance, just 1 year after NIH launched the National Cholesterol
Education Program, also advising low-fat diets for everyone over 2 years old,
 epidemiologist David Jacobs of the University of Minnesota, Twin Cities,
visited Japan. There he learned that Japanese physicians were advising patients
to raise
 their cholesterol levels, because low cholesterol levels were linked to
hemorrhagic stroke. At the time, Japanese men were dying from stroke almost as
frequently as
 American men were succumbing to heart disease. Back in Minnesota, Jacobs looked
 for this low-cholesterol-stroke relationship in the MRFIT data and found it
 there, too. And the relationship transcended stroke: Men with very low
cholesterol levels seemed prone to premature death; below 160 milligrams per
deciliter
 (mg/dl), the lower the cholesterol level, the shorter the life.

 Jacobs reported his results to NHLBI, which in 1990 hosted a conference to
discuss the issue, bringing together researchers from 19 studies around the
world. The
 data were consistent: When investigators tracked all deaths, instead of just
heart disease deaths, the cholesterol curves were U-shaped for men and flat for
women.
 In other words, men with cholesterol levels above 240 mg/dl tended to die
prematurely from heart disease. But below 160 mg/dl, the men tended to die
prematurely
 from cancer, respiratory and digestive diseases, and trauma. As for women, if
anything, the higher their cholesterol, the longer they lived (see graph on p.
2540).

 These mortality data can be interpreted in two ways. One, preferred by low-fat
advocates, is that they cannot be meaningful. Rifkind, for instance, told
Science that
 the excess deaths at low cholesterol levels must be due to preexisting
conditions. In other words, chronic illness leads to low cholesterol levels, not
 vice versa. He
 pointed to the 1990 conference report as the definitive document on the issue
and as support for his argument, although the report states unequivocally that
this
 interpretation is not supported by the data.

 The other interpretation is that what a low-fat diet does to serum cholesterol
levels, and what that in turn does to arteries, may be only one component of the
 diet's
 effect on health. In other words, while low-fat diets might help prevent heart
disease, they might also raise susceptibility to other conditions. This is what
always
 worried Ahrens. It's also one reason why the American College of Physicians,
for instance, now suggests that cholesterol reduction is certainly worthwhile
for those
 at high, short-term risk of dying of coronary heart disease but of "much
smaller or ... uncertain" benefit for everyone else.

 This interpretation--that the connection between diet and health far transcends
 cholesterol--is also supported by the single most dramatic diet-heart trial
ever
 conducted: the Lyon Diet Heart Study, led by Michel de Lorgeril of the French
National Institute of Health and Medical Research (INSERM) and published in
 Circulation in February 1999. The investigators randomized 605 heart attack
survivors, all on cholesterol-lowering drugs, into two groups. They counseled
one to
 eat an AHA "prudent diet," very similar to that recommended for all Americans.
They counseled the other to eat a Mediterranean-type diet, with more bread,
 cereals, legumes, beans, vegetables, fruits, and fish and less meat. Total fat
and types of fat differed markedly in the two diets, but the HDL, LDL, and total
 cholesterol levels in the two groups remained virtually identical. Nonetheless,
 over 4 years of follow-up, the Mediterranean-diet group had only 14 cardiac
deaths
 and nonfatal heart attacks compared to 44 for the "Western-type" diet group.
The likely explanation, wrote de Lorgeril and his colleagues, is that the
"protective
 effects [of the Mediterranean diet] were not related to serum concentrations of
 total, LDL or HDL cholesterol."

 Many researchers find the Lyon data so perplexing that they're left questioning
 the methodology of the trial. Nonetheless, says NIH's Harlan, the data "are
very
 provocative. They do bring up the issue of whether if we look only at
cholesterol levels we aren't going to miss something very important." De
Lorgeril believes the
 diet's protective effect comes primarily from omega-3 fatty acids, found in
seed oils, meat, cereals, green leafy vegetables, and fish, and from antioxidant
 compounds,
 including vitamins, trace elements, and flavonoids. He told Science that most
researchers and journalists in the field are prisoners of the "cholesterol
paradigm."
 Although dietary fat and serum cholesterol "are obviously connected," he says,
"the connection is not a robust one" when it comes to heart disease.

 Dietary trade-offs
 One inescapable reality is that death is a trade-off, and so is diet. "You have
 to eat something," says epidemiologist Hugh Tunstall Pedoe of the University of
 Dundee,
 U.K., spokesperson for the 21-nation Monitoring Cardiovascular Disease Project
run by the World Health Organization. "If you eat more of one thing, you eat a
lot
 less of something else. So for every theory saying this disease is caused by an
 excess in x, you can produce an alternative theory saying it's a deficiency in
y." It
 would be simple if, say, saturated fats could be cut from the diet and the
calories with it, but that's not the case. Despite all expectations to the
contrary, people tend
 to consume the same number of calories despite whatever diet they try. If they
eat less total fat, for instance, they will eat more carbohydrates and probably
less
 protein, because most protein comes in foods like meat that also have
considerable amounts of fat.

 This plus-minus problem suggests a different interpretation for virtually every
 diet study ever done, including, for instance, the kind of metabolic-ward
studies that
 originally demonstrated the ability of saturated fats to raise cholesterol. If
researchers reduce the amount of saturated fat in the test diet, they have to
make up the
 calories elsewhere. Do they add polyunsaturated fats, for instance, or add
carbohydrates? A single carbohydrate or mixed carbohydrates? Do they add green
leafy
 vegetables, or do they add pasta? And so it goes. "The sky's the limit," says
nutritionist Alice Lichtenstein of Tufts University in Boston. "There are a
million
 perturbations."

 These trade-offs also confound the kind of epidemiological studies that
demonized saturated fat from the 1950s onward. In particular, individuals who
eat copious
 amounts of meat and dairy products, and plenty of saturated fats in the
process, tend not to eat copious amounts of vegetables and fruits. The same
holds for entire
 populations. The eastern Finns, for instance, whose lofty heart disease rates
convinced Ancel Keys and a generation of researchers of the evils of fat, live
within 500
 kilometers of the Arctic Circle and rarely see fresh produce or a green
vegetable. The Scots, infamous for eating perhaps the least wholesome diet in
the developed
 world, are in a similar fix. Basil Rifkind recalls being laughed at once on
this point when he lectured to Scottish physicians on healthy diets: "One said,
'You talk about
 increasing fruits and vegetable consumption, but in the area I work in there's
not a single grocery store.' " In both cases, researchers joke that the only
green leafy
 vegetable these populations consume regularly is tobacco. As for the purported
benefits of the widely hailed Mediterranean diet, is it the fish, the olive oil,
 or the fresh
 vegetables? After all, says Harvard epidemiologist Dimitrios Trichopoulos, a
native of Greece, the olive oil is used either to cook vegetables or as dressing
 over
 salads. "The quantity of vegetables consumed is almost a pound [half a
kilogram] a day," he says, "and you cannot eat it without olive oil. And we eat
a lot of
 legumes, and we cannot eat legumes without olive oil."

 Indeed, recent data on heart disease trends in Europe suggest that a likely
explanation for the differences between countries and over time is the
availability of fresh
 produce year-round rather than differences in fat intake. While the press often
 plays up the French paradox--the French have little heart disease despite
seemingly
 high saturated fat consumption--the real paradox is throughout Southern Europe,
 where heart disease death rates have steadily dropped while animal fat
consumption
 has steadily risen, says University of Cambridge epidemiologist John Powles,
who studies national disease trends. The same trend appears in Japan. "We have
this
 idea that it's the Arcadian past, the life in the village, the utopia that
we've lost," Powles says; "that the really protective Mediterranean diet is what
 people ate in the
 1950s." But that notion isn't supported by the data: As these Mediterranean
nations became more affluent, says Powles, they began to eat proportionally more
 meat
 and with it more animal fat. Their heart disease rates, however, continued to
improve compared to populations that consumed as much animal fat but had less
access
 to fresh vegetables throughout the year. To Powles, the antifat movement was
founded on the Puritan notion that "something bad had to have an evil cause, and
 you
 got a heart attack because you did something wrong, which was eating too much
of a bad thing, rather than not having enough of a good thing."

 The other salient trade-off in the plus-minus problem of human diets is
carbohydrates. When the federal government began pushing low-fat diets, the
scientists and
 administrators, and virtually everyone else involved, hoped that Americans
would replace fat calories with fruits and vegetables and legumes, but it didn't
 happen. If
 nothing else, economics worked against it. The food industry has little
incentive to advertise nonproprietary items: broccoli, for instance. Instead,
says NYU's Nestle,
 the great bulk of the $30-billion-plus spent yearly on food advertising goes to
 selling carbohydrates in the guise of fast food, sodas, snacks, and candy bars.
 And
 carbohydrates are all too often what Americans eat.

 Carbohydrates are what Harvard's Willett calls the flip side of the calorie
trade-off problem. Because it is exceedingly difficult to add pure protein to a
diet in any
 quantity, a low-fat diet is, by definition, a high-carbohydrate diet--just as a
 low-fat cookie or low-fat yogurt are, by definition, high in carbohydrates.
Numerous
 studies now suggest that high-carbohydrate diets can raise triglyceride levels,
 create small, dense LDL particles, and reduce HDL--a combination, along with a
 condition known as "insulin resistance," that Stanford endocrinologist Gerald
Reaven has labeled "syndrome X." Thirty percent of adult males and 10% to 15% of
 postmenopausal women have this particular syndrome X profile, which is
associated with a several-fold increase in heart disease risk, says Reaven, even
 among
 those patients whose LDL levels appear otherwise normal. Reaven and Ron Krauss,
 who studies fats and lipids at Lawrence Berkeley National Laboratory in
 California, have shown that when men eat high-carbohydrate diets their
cholesterol profiles may shift from normal to syndrome X. In other words, the
more
 carbohydrates replace saturated fats, the more likely the end result will be
syndrome X and an increased heart disease risk. "The problem is so clear right
now it's
 almost a joke," says Reaven. How this balances out is the unknown. "It's a
bitch of a question," says Marc Hellerstein, a nutritional biochemist at the
University of
 California, Berkeley, "maybe the great public health nutrition question of our
era."

 The other worrisome aspect of the carbohydrate trade-off is the possibility
that, for some individuals, at least, it might actually be easier to gain weight
 on
 low-fat/high-carbohydrate regimens than on higher fat diets. One of the many
factors that influence hunger is the glycemic index, which measures how fast
 carbohydrates are broken down into simple sugars and moved into the
bloodstream. Foods with the highest glycemic index are simple sugars and
processed grain
 products like pasta and white rice, which cause a rapid rise in blood sugar
after a meal. Fruits, vegetables, legumes, and even unprocessed starches--pasta
al dente,
 for instance--cause a much slower rise in blood sugar. Researchers have
hypothesized that eating high-glycemic index foods increases hunger later
because insulin
 overreacts to the spike in blood sugar. "The high insulin levels cause the
nutrients from the meal to get absorbed and very avidly stored away, and once
they are, the
 body can't access them," says David Ludwig, director of the obesity clinic at
Children's Hospital Boston. "The body appears to run out of fuel." A few hours
after
 eating, hunger returns.

 If the theory is correct, calories from the kind of processed carbohydrates
that have become the staple of the American diet are not the same as calories
from fat,
 protein, or complex carbohydrates when it comes to controlling weight. "They
may cause a hormonal change that stimulates hunger and leads to overeating,"
says
 Ludwig, "especially in environments where food is abundant. ..."

 In 1979, 2 years after McGovern's committee released its Dietary Goals, Ahrens
wrote to The Lancet describing what he had learned over 30 years of studying fat
 and cholesterol metabolism: "It is absolutely certain that no one can reliably
predict whether a change in dietary regimens will have any effect whatsoever on
the
 incidence of new events of [coronary heart disease], nor in whom." Today, many
nutrition researchers, acknowledging the complexity of the situation, find
themselves
 siding with Ahrens. Krauss, for instance, who chairs the AHA Dietary Guidelines
 Committee, now calls it "scientifically na



ïve" to expect that a single dietary
regime
 can be beneficial for everybody: "The 'goodness' or 'badness' of anything as
complex as dietary fat and its subtypes will ultimately depend on the context of
 the
 individual."

 Given the proven success and low cost of cholesterol-lowering drugs, most
physicians now prescribe drug treatment for patients at high risk of heart
disease. The
 drugs reduce LDL cholesterol levels by as much as 30%. Diet rarely drops LDL by
 more than 10%, which is effectively trivial for healthy individuals, although
it may
 be worth the effort for those at high risk of heart disease whose cholesterol
levels respond well to it.

 The logic underlying populationwide recommendations such as the latest USDA
Dietary Guidelines is that limiting saturated fat intake--even if it does little
 or nothing
 to extend the lives of healthy individuals and even if not all saturated fats
are equally bad--might still delay tens of thousands of deaths each year
throughout the entire
 country. Limiting total fat consumption is considered reasonable advice because
 it's simple and easy to understand, and it may limit calorie intake. Whether
it's
 scientifically justifiable may simply not be relevant. "When you don't have any
 real good answers in this business," says Krauss, "you have to accept a few not
 so
 good ones as the next best thing."