Science
30. mars 2001:
NUTRITION:
The Soft Science of Dietary Fat
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 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 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 naïve, 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" 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 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 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 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 naïve" 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." ----------------------------------------------------------------------------------------------------------- What
If Americans Ate Less Saturated Fat?
Gary
Taubes
Eat
less saturated fat, live longer. For 30 years, this has stood as one
cornerstone of nutritional advice given to Americans (see main
text). But how much longer? Between 1987 and 1992, three independent
research groups used computer models to work out the answer. All three
analyses agreed, but their conclusions have been buried in the literature,
rarely if ever cited. All
three models estimated how much longer people might expect to live, on
average, if only 10% of their calories came from saturated fat as
recommended. In the process their total fat intake would drop to the
recommended 30% of calories. All three models assumed that LDL
cholesterol--the "bad cholesterol"--levels would drop accordingly
and that this diet would have no adverse effects, although that was
optimistic at the time and has become considerably more so since then. All
three combined national vital statistics data with cholesterol risk factor
data from the Framingham Heart Study. The
first study came out of Harvard Medical School and was published in the Annals
of Internal Medicine in April 1987. Led by William Taylor, it concluded
that individuals with a high risk of heart disease--smokers, for instance,
with high blood pressure--could expect to gain, on average, one extra year
by shunning saturated fat. Healthy nonsmokers, however, might add 3 days to
3 months. "Although there are undoubtedly persons who would choose to
participate in a lifelong regimen of dietary change to achieve results of
this magnitude, we suspect that some might not," wrote Taylor and his
colleagues. The
following year, the U.S. Surgeon General's Office funded a study at the
University of California, San Francisco, with the expectation that its
results would counterbalance those of the Harvard analysis. Led by
epidemiologist Warren Browner, this study concluded that cutting fat
consumption in America would delay 42,000 deaths each year, but the
net increase in life expectancy would average out to only 3 to 4 months. The
key word was "delay," for death, like diet, is a trade-off:
Everyone has to die of something. "Deaths are not prevented, they are
merely delayed," Browner later wrote. "The 'saved' people mainly
die of the same things everyone else dies of; they do so a little later in
life." To be precise, a woman who might otherwise die at 65 could
expect to live two extra weeks after a lifetime of avoiding saturated fat.
If she lived to be 90, she could expect 10 additional weeks. The third
study, from researchers at McGill University in Montreal, came to virtually
identical conclusions. Browner
reported his results to the Surgeon General's Office, then submitted a paper
to The Journal of the American Medical Association (JAMA). Meanwhile, the
Surgeon General's Office--his source of funding--contacted JAMA and tried to
prevent publication, claiming that the analysis was deeply flawed. JAMA
reviewers disagreed and published his article, entitled "What If
Americans Ate Less Fat?" in June 1991. As for Browner, he was left
protecting his work from his own funding agents. "Shooting the
messenger," he wrote to the Surgeon General's Office, "or creating
a smoke screen--does not change those estimates." ---------------------------------------------------------------------------------------------------------- The
Epidemic That Wasn't?
Gary
Taubes
For
half a century, nutritionists have pointed to soaring death rates as the
genesis of their research into dietary fat and heart disease and as reason
to advise Americans to eat less fat (see main
text). "We had an epidemic of heart disease after World War
II," obesity expert Jules Hirsch of Rockefeller University in New York
City said just 3 months ago in The New York Times. "The rates
were growing higher and higher, and people became suddenly aware of that,
and that diet was a factor." To
proponents of the antifat message, this heart disease epidemic has always
been an indisputable reality. Yet, to the statisticians at the mortality
branch of the National Center for Health Statistics (NCHS), the source of
all the relevant statistics, the epidemic was illusory. In their view, heart
disease deaths have been steadily declining since the late 1940s. According
to Harry Rosenberg, director of the NCHS mortality branch since 1977, the
key factor in the apparent epidemic, paradoxically, was a healthier American
population. By the 1950s, premature deaths from infectious diseases and
nutritional deficiencies had been all but eliminated, which left more
Americans living long enough to die of chronic diseases such as heart
disease. In other words, the actual risk of dying from a heart attack at any
particular age remained unchanged: Rather, the rising number of 50-year-olds
dropping dead of heart attacks was primarily due to the rising number of
50-year-olds. The
secondary factor was an increase from 1948 to 1968 in the probability that a
death would be classified on a death certificate as arteriosclerotic disease
or coronary heart disease. This increase, however, was a figment of new
diagnostic technologies--the wider use of electrocardiograms, for
instance--and the changing terminology of death certificates. In 1949, the
International Classification of Diseases (ICD) added a new category,
"arteriosclerotic heart disease," under the more general rubric
"diseases of the heart." The result, as a 1958 report to the
American Heart Association noted, was dramatic: "In one year, 1948 to
1949, the effect of this revision was to raise coronary disease death rates
by about 20% for white males and about 35% for white females." In 1965,
the ICD added a category for coronary heart disease, which added yet more
deaths and capped off the apparent epidemic. To Rosenberg and others at NCHS, the most likely explanation for the postwar upsurge in coronary heart disease deaths is that physicians slowly caught on to the new terminology and changed the wording on death certificates. "There is absolutely no evidence that there was an epidemic," says Rosenberg.
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