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The Soft Science of Dietary Fat
In March 2001, Gary Taubes wrote of the lack of evidence that a fatty diet causes heart disease. That article, published in the journal, Science, is The Soft Science Of Dietary Fat.
It sparked a riposte from Dr Scott Grundy on behalf of the 'conventional' medical world.
However, an international group of 'cholesterol sceptics', led by Dr Uffe Ravnskov, pointed out that the references which Grundy relied on to back his letter, didn't! Read their letter to Science.
Have you ever wondered why 200 mg/dl (5.2 mmol/l) came to be the recommended 'healthy' blood cholesterol level? Dr Mary Enig enlightens us.
The Soft Science of Dietary Fat
Gary Taubes  |
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 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"
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
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."
Last updated 22 April 2002
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