Let
us begin with a short quiz: a few questions to ponder during the 30 (or
60 or 90) minutes a day you spend burning off excess calories at the
gym, or perhaps while feeling guilty because you’re not so engaged. If
lean people are more physically active than fat people—one fact in the
often-murky science of weight control that’s been established beyond
reasonable doubt— does that mean that working out will make a fat
person lean? Does it mean that sitting around will make a lean person
fat? How about a mathematical variation on these questions: Let’s say
we go to the gym and burn off 3,500 calories every week—that’s 700
calories a session, five times a week. Since a pound of fat is
equivalent to 3,500 calories, does that mean we’ll be a pound slimmer
for every week we exercise? And will we continue to slim down at this
pace for as long as we continue to exercise?
For most of
us, fear of flab is the reason we exercise, the motivation that drives
us to the gym. It’s also why public-health authorities have taken to
encouraging ever more exercise as part of a healthy lifestyle. If we’re
fat or fatter than ideal, we work out. Burn calories. Expend energy.
Still fat? Burn more. The dietary guidelines of the U.S. Department of
Agriculture, for instance, now recommend that we engage in up to 60
minutes daily of “moderate to vigorous intensity” physical activity
just to maintain weight—that is, keep us from fattening further.
Considering the ubiquity of the message, the hold it has on our lives,
and the elegant simplicity of the notion—burn calories, lose
weight—wouldn’t it be nice to believe it were true? The catch is that
science suggests it’s not, and so the answer to all of the above quiz
questions is “no.”
Just last month, the American Heart
Association and the American College of Sports Medicine published joint
guidelines for physical activity and health. They suggested that 30
minutes of moderate physical activity five days a week is necessary to
“promote and maintain health.” What they didn’t say, though, was that
more physical activity will lead us to lose weight. Indeed, the best
they could say about the relationship between fat and exercise was
this: “It is reasonable to assume that persons with relatively high
daily energy expenditures would be less likely to gain weight over
time, compared with those who have low energy expenditures. So far,
data to support this hypothesis are not particularly compelling.” In
other words, despite half a century of efforts to prove otherwise,
scientists still can’t say that exercise will help keep off the pounds.
The
30 minutes recommended by the AHA-ACSM report is a departure from the
recent guidelines of other authoritative organizations—the Institute of
Medicine of the National Academies and the International Association
for the Study of Obesity—both of which, like the USDA, have recommended
that we exercise for up to 60 minutes a day to avoid what the USDA
calls “unhealthy weight gain.” But the reason for this 60-minute
recommendation is precisely that so little evidence exists to support
the notion that exercising less has any effect.
The report
that these experts cite most often as grounds for their assessments was
published in 2000 by two Finnish researchers who surveyed all the
relevant research on exercise and weight of the previous twenty years.
Yet the Finnish report, the most scientifically rigorous review of the
evidence to date, can hardly be said to have cleared up the matter.
When the Finnish investigators looked at the results of the dozen
best-constructed experimental trials that addressed weight
maintenance—that is, successful dieters who were trying to keep off the
pounds they had shed—they found that everyone regains weight. And
depending on the type of trial, exercise would either decrease the rate
of that gain (by 3.2 ounces per month) or increase its rate (by 1.8
ounces). As the Finns themselves concluded, with characteristic
understatement, the relationship between exercise and weight is “more
complex” than they might otherwise have imagined.
This is
not to say that there aren’t excellent reasons to be physically active,
as these reports invariably point out. We might just enjoy exercise. We
may increase our overall fitness; we may live longer, perhaps by
reducing our risk of heart disease or diabetes; we’ll probably feel
better about ourselves. (Of course, this may be purely a cultural
phenomenon. It’s hard to imagine that the French, for instance, would
improve their self-esteem by spending more time at the gym.) But
there’s no reason to think that we will lose any significant amount of
weight, and little reason to think we will prevent ourselves from
gaining it.
The
one thing that might be said about exercise with certainty is that it
tends to makes us hungry. Maybe not immediately, but eventually. Burn
more calories and the odds are very good that we’ll consume more as
well. And this simple fact alone might explain both the scientific
evidence and a nation’s worth of sorely disappointing anecdotal
experience.
It’s difficult to get health authorities to
talk about the disconnect between their official recommendations and
the scientific evidence that underlies it because they want to
encourage us to exercise, even if their primary reason for doing so is
highly debatable. Steve Blair, for instance, a University of South
Carolina exercise scientist and a co-author of the AHA-ACSM guidelines,
says he was “short, fat, and bald” when he started running in his
thirties and he is short, fatter, and balder now, at age 68. In the
intervening years, he estimates, he has run close to 80,000 miles and
gained about 30 pounds.
When I asked Blair whether he
thought he might be leaner had he run even more, he had to think about
it. “I don’t see how I could have been more active,” he said. “Thirty
years ago, I was running 50 miles a week. I had no time to do more. But
if I could have gone out over the last couple of decades for two to
three hours a day, maybe I would not have gained this weight.” And
maybe he would have anyway. If we trust the AHA-ACSM report he
co-authored, there is little reason to believe that the amount he runs
makes any difference. Nonetheless, Blair personally believes he would
be fatter still if he hadn’t been running. Why?
There
was a time when virtually no one believed exercise would help a person
lose weight. Until the sixties, clinicians who treated obese and
overweight patients dismissed the notion as naïve. When Russell Wilder,
an obesity and diabetes specialist at the Mayo Clinic, lectured on
obesity in 1932, he said his fat patients tended to lose more weight
with bed rest, “while unusually strenuous physical exercise slows the
rate of loss.”
The problem, as he and his contemporaries
saw it, is that light exercise burns an insignificant number of
calories, amounts that are undone by comparatively effortless changes
in diet. In 1942, Louis Newburgh of the University of Michigan
calculated that a 250-pound man expends only three calories climbing a
flight of stairs—the equivalent of depriving himself of a
quarter-teaspoon of sugar or a hundredth of an ounce of butter. “He
will have to climb twenty flights of stairs to rid himself of the
energy contained in one slice of bread!” Newburgh observed. So why not
skip the stairs, skip the bread, and call it a day?
More-strenuous
exercise, these physicians further argued, doesn’t help matters—because
it works up an appetite. “Vigorous muscle exercise usually results in
immediate demand for a large meal,” noted Hugo Rony of Northwestern
University in his 1940 textbook, Obesity and Leanness.
“Consistently high or low energy expenditures result in consistently
high or low levels of appetite. Thus men doing heavy physical work
spontaneously eat more than men engaged in sedentary occupations.
Statistics show that the average daily caloric intake of lumberjacks is
more than 5,000 calories, while that of tailors is only about 2,500
calories. Persons who change their occupation from light to heavy work
or vice versa soon develop corresponding changes in their appetite.” If
a tailor becomes a lumberjack and, by doing so, takes to eating like
one, why assume that the same won’t happen, albeit on a lesser scale,
to an overweight tailor who decides to work out like a lumberjack for
an hour a day?
Credit for why we came to believe otherwise
goes to one man, Jean Mayer, who began his career at Harvard in the
early fifties, went on to become the most influential nutritionist in
the country, and then, for sixteen years, served as president of Tufts
University (where there is now a Jean Mayer USDA Human Nutrition
Research Center on Aging). As an authority on human weight regulation,
Mayer was among the very first of a new breed, a type that has since
come to dominate the field. His predecessors—Wilder, Rony, Newburgh,
and others—had all been physicians who worked closely with obese and
overweight patients. Mayer was not. His training was in physiological
chemistry; he had obtained a doctorate at Yale with a dissertation on
the interrelationship of vitamins A and C in rats. In the ensuing
decades, he would publish hundreds of papers on different aspects of
nutrition, including why we get fat, but he never had to reduce obese
patients as part of his clinical obligation, and so his hypotheses were
less fettered by anecdotal or real-life experience.
As
early as 1953, after just a few years of research on laboratory mice,
Mayer began extolling the virtues of exercise for weight control. By
1959, the New York Times was crediting him with having
“debunked [the] popular theories” that exercise played little role in
weight control. Mayer knew that the obese often eat no more than the
lean and occasionally even less. This seemed to exclude gluttony as a
cause of their weight gain, which meant that these fat people had to be
less physically active. Otherwise, how could they take in more calories
than they expend and so become fat?
Through the sixties, Mayer documented the
relationship between inactivity and the overweight. He noted that fat
high-school girls ate “several hundred calories less” than lean
classmates. “The laws of thermodynamics were, however, not flouted by
this finding,” he wrote, because the obese girls expended less energy
than the lean: They were much less active; they spent four times as
many hours watching television. Mayer also studied infants. “The
striking phenomenon is that the fatter babies were quiet, placid babies
that had moderate intake,” Mayer reported, “whereas the babies who had
the highest intake tended to be very thin babies, cried a lot, moved a
lot, and became very tense.” Thus, Mayer concluded, “some individuals
are born very quiet, inactive, and placid and with moderate intake get
fat, and some individuals from the very beginning are very active and
do not get particularly fat even with high intakes.”
It
was Mayer who pioneered the now-ubiquitous practice of implicating
sedentary living as the “most important factor” leading to obesity and
the chronic diseases that accompany it. Modern Americans, said Mayer,
were inert compared with their “pioneer forebears” who were “constantly
engaged in hard physical labor.” Every modern convenience, by this
logic, from power windows to the electric toothbrush, only serves to
minimize the calories we expend. “The development of obesity,” Mayer
wrote in 1968, “is to a large extent the result of the lack of
foresight of a civilization which spends tens of billions annually on
cars, but is unwilling to include a swimming pool and tennis courts in
the plans of every high school.”
Mayer’s hypothesis always
had shortcomings, but they were ignored for the same reasons they still
are—who wants to openly question the idea that physical activity is a
panacea? The first issue is a logical one: That conclusion that the
fatter we are, the more sedentary we’re likely to be is actually a
correlation; it tells us nothing about what is cause and what is
effect. “It is a common observation,” noted Rony in 1941, “that many
obese persons are lazy, i.e., show decreased impulse to muscle
activity. This may be, in part, an effect that excess weight would have
on the activity impulse of any normal person.” Equally possible is that
obesity and physical inactivity are both symptoms of the same
underlying cause.
This logical problem was then obscured
by Mayer’s all-out attack on the role of hunger. Mayer acknowledged
that exercise could make us hungrier, but he said it wasn’t necessarily
the case. This was the heart of Mayer’s message—a purported loophole in
the relationship between appetite and physical activity. “If exercise
is decreased below a certain point, food intake no longer decreases,”
said Mayer. “In other words, walking one half-hour a day may be
equivalent to only four slices of bread, but if you don’t walk the
half-hour, you still want to eat the four slices.”
Mayer
based this conclusion on two (and only two) of his own studies from the
mid-fifties. The first purported to demonstrate that laboratory rats
exercised for a few hours every day will eat less than rats that don’t
exercise at all. But this would never be replicated. In more recent
experiments, the more rats run the more rats eat; weights remain
unchanged. And when rats are retired from these exercise programs, they
eat more than ever and gain weight with age more rapidly than rats that
were allowed to remain sedentary. With hamsters and gerbils, exercise
increases body weight and body-fat percentage. So exercising makes
these particular rodents fatter, not leaner.
Mayer’s
second study was an assessment of the diet, physical activity, and
weights of workers and merchants at a mill in West Bengal, India. This
article is still cited—by the Institute of Medicine, for instance—as
perhaps the only existing evidence that physical activity and appetite
do not necessarily go hand in hand. But it, too, has never been
replicated, despite (or perhaps because of) a half-century of
improvements in methods of assessing diet and energy expenditure in
humans.
It helped that Mayer promoted his pro-exercise
message with a fervor akin to a moral crusade. In 1966, Mayer was the
primary author of a U.S. Public Health Service report advocating
increased physical activity along with diet as the best way to lose
weight. In 1969, Mayer chaired Richard Nixon’s White House Conference
on Food, Nutrition, and Health. “The successful treatment of obesity
must involve far-reaching changes in lifestyle,” the conference report
concludes. “These changes include alterations of dietary patterns and
patterns of physical activity.” In 1972, Mayer began writing a
syndicated newspaper column on nutrition: Exercise, Mayer now wrote,
sounding suspiciously like a diet doctor selling a patent claim, will
make “weight melt away faster,” and “contrary to popular belief,
exercise won’t stimulate your appetite.”
Our culture of
physical exercise began only in the late sixties, coincident with
Mayer’s crusade, which explains why our parents might not have been
quite so devoted to the idea of spending their leisure time perspiring
profusely. In 1977, the New York Times was covering the
“exercise explosion” that had come about because the conventional
wisdom of the sixties that exercise was “bad for you” had been
transformed into the “new conventional wisdom—that strenuous exercise
is good for you.” When the Washington Post estimated in 1980
that 100 million Americans were partaking in the “new fitness
revolution”—coincident with the start of the current obesity
epidemic—it also noted that most of them “would have been derided as
‘health nuts’" only a decade earlier.
Meanwhile, the
evidence simply never came around to support Mayer’s hypothesis, even
though our beliefs did. My favorite study of the effect of physical
activity on weight loss was published in 1989 by a team of Danish
researchers. Over the course of eighteen months the Danes trained
nonathletes to run a marathon. At the end of this training period, the
eighteen men in the study had lost an average of five pounds of body
fat. As for the nine women subjects, the Danes reported, “no change in
body composition was observed.” That same year, F. Xavier Pi-Sunyer,
then director of the St. Luke’s–Roosevelt Hospital Obesity Research
Center in New York, reviewed the studies on exercise and weight, and
his conclusion was identical to that of the Finnish review’s eleven
years later: “Decreases, increases, and no changes in body weight and
body composition have been observed,” Pi-Sunyer reported.
Granted,
all this still doesn’t explain why we bought into Mayer’s idea that we
could exercise more and not compensate by eating more. One simple
reason is that the health reporters bought it, and we were reading
their articles, not the research literature itself. In 1977, for
instance, the National Institutes of Health hosted its second
conference on obesity and weight control. “The importance of exercise
in weight control is less than might be believed,” the assembled
experts concluded, “because increases in energy expenditure due to
exercise also tend to increase food consumption, and it is not possible
to predict whether the increased caloric output will be outweighed by
the greater food intake.” That same year, The New York Times Magazine
reported that there was “now strong evidence that regular exercise can
and does result in substantial and—so long as the exercise is
continued—permanent weight loss.” By 1990, a year after Pi-Sunyer’s
pessimistic assessment of the evidence, Newsweek was declaring exercise an “essential” element of any weight-loss program, and the Times
had stated that on those infrequent occasions “when exercise isn’t
enough” to lose weight, “you must also make sure you don’t overeat.”
As
for the authorities themselves, the primary factor fueling their belief
in the weight-maintaining benefits of exercise was their natural
reluctance to acknowledge otherwise. Although one couldn’t help but be
“underwhelmed by” the evidence, as Mayer’s student Judith Stern, a UC
Davis nutritionist, wrote in 1986, it would be “shortsighted” to say
that exercise was ineffective because it meant ignoring the possible
contributions of exercise to the prevention of obesity and to the
maintenance of weight loss that might be induced by diet. These, of
course, had never been demonstrated either, but they hadn’t been ruled
out. This faith-based philosophy came to dominate scientific
discussions on exercise and weight, but it couldn’t be reconciled with
the simple notion that appetite and calories consumed will increase
with an increase in physical activity. Hence, the idea of working up an
appetite was jettisoned. Clinicians, researchers, exercise
physiologists, even personal trainers at the local gym took to thinking
and talking about hunger as though it were a phenomenon exclusive to
the brain, a question of willpower (whatever that is), not the natural
consequence of a body trying to replenish itself with energy.
Ultimately,
the relationship between physical activity and fatness comes down to
the question of cause and effect. Is Lance Armstrong excessively lean
because he burns off a few thousand calories a day cycling, or is he
driven to expend that energy because his body is constitutionally set
against storing calories as fat? If his fat tissue is resistant to
accumulating calories, his body has little choice but to burn them as
quickly as possible: what Rony and his contemporaries called the
“activity impulse”—a physiological drive, not a conscious one. His body
is telling him to get on his bike and ride, not his mind. Those of us
who run to fat would have the opposite problem. Our fat tissue wants to
store calories, leaving our muscles with a relative dearth of energy to
burn. It’s not willpower we lack, but fuel.
For the last
60 years, researchers studying obesity and weight regulation have
insisted on treating the human body as a thermodynamic black box:
Calories go in one side, they come out the other, and the difference
(calories in minus calories out) ends up as either more or less fat.
The fat tissue, in this thermodynamic model, has nothing to say in the
matter. Thus the official recommendations to eat less and exercise more
and assuredly you’ll get thinner. (Or at least not fatter.) And in the
strict sense this is true—you can starve a human, or a rat, and he will
indeed lose weight—but that misses the point. Humans, rats, and all
living organisms are ruled by biology, not thermodynamics. When we
deprive ourselves of food, we get hungry. When we push ourselves
physically, we get tired.
Our bodies, like all living
organisms, have evolved a fantastically complex web of feedback loops.
These physiological mechanisms serve fundamentally to work against the
inevitable pull of thermodynamics (which is entropy, a.k.a. death) and
so make life possible. The necessary condition of life, as the great
French physiologist Claude Bernard noted 140 years ago, is to keep the
internal environment of an organism stable and conducive to life,
regardless of what’s happening on the outside. This is what the Harvard
physiologist Walter Cannon, in the thirties, called homeostasis—or the
“wisdom of the body,” as he put it. “Somehow the unstable stuff of
which we are composed,” Cannon wrote, “had learned the trick of
maintaining stability.”
The key is that among the many things
regulated in this homeostatic system—along with blood pressure and
blood sugar, body temperature, respiration, etc.—is the amount of fat
we carry. From this biological or homeostatic perspective, lean people
are not those who have the willpower to exercise more and eat less.
They are people whose bodies are programmed to send the calories they
consume to the muscles to be burned rather than to the fat tissue to be
stored—the Lance Armstrongs of the world. The rest of us tend to go the
other way, shunting off calories to fat tissue, where they accumulate
to excess. This shunting of calories toward fat cells to be stored or
toward the muscles to be burned is a phenomenon known as fuel
partitioning.
The job of determining how fuels (glucose
and fatty acids) will be used, whether we will store them as fat or
burn them for energy, is carried out primarily by the hormone insulin
in concert with an enzyme known technically as lipoprotein lipase—LPL,
for short. (Sex hormones also interact with LPL, which is why men and
women fatten differently.)
In the eighties, biochemists
and physiologists worked out how LPL responds to exercise. They found
that during a workout, LPL activity increases in muscle tissue, and so
our muscle cells suck up fatty acids to use for fuel. Then, when we’re
done exercising, LPL activity in the muscle tissue tapers off and LPL
activity in our fat tissue spikes, pulling calories into fat cells.
This works to return to the fat cells any fat they might have had to
surrender—homeostasis, in other words. The more rigorous the exercise,
and the more fat lost from our fat tissue, the greater the subsequent
increase in LPL activity in the fat cells. Thus, post-workout, we get
hungry: Our fat tissue is devoting itself to restoring calories as fat,
depriving other tissues and organs of the fuel they need and triggering
a compensatory impulse to eat. The feeling of hunger is the brain’s way
of trying to satisfy the demands of the body. Just as sweating makes us
thirsty, burning off calories makes us hungry.
This
research has never been controversial. It’s simply been considered
irrelevant by authorities, all too often lean, who have been dead set
on blaming fatness on some combination of gluttony, sloth, and perhaps
a little genetic predisposition thrown in on the side. But
contemplating the means by which we might lose weight without
considering the hormonal regulation of fat tissue is like wondering why
children grow taller without considering the role of growth hormones.
Or, for that matter, like trying to explain the record-breaking
triumphs of modern athletes—Barry Bonds, say—and never considering the
possibility that steroid hormones (or human growth hormone or insulin)
might be involved.
If it’s
biology, and not a lack of willpower, that explains why exercise fails
so many of us as a weight-loss tool, then we can still find reason for
optimism. Since insulin is the primary hormone affecting the activity
of LPL on our cells, it’s not surprising that insulin is the primary
regulator of how fat we get. “Fat is mobilized [from fat tissue] when
insulin secretion diminishes,” the American Medical Association Council
on Foods and Nutrition explained back in 1974, before this fact, too,
was deemed irrelevant to the question of why we gain weight or the
means to lose it. Because insulin determines fat accumulation, it’s
quite possible that we get fat not because we eat too much or exercise
too little but because we secrete too much insulin or because our
insulin levels remain elevated far longer than might be ideal.
To
be sure, this is the same logic that leads to other unconventional
ideas. As it turns out, it’s carbohydrates—particularly easily
digestible carbohydrates and sugars—that primarily stimulate insulin
secretion. “Carbohydrates is driving insulin is driving fat,” as George
Cahill Jr., a retired Harvard professor of medicine and expert on
insulin, recently phrased it for me. So maybe if we eat fewer
carbohydrates—in particular the easily digestible simple carbohydrates
and sugars—we might lose considerable fat or at least not gain any
more, whether we exercise or not. This would explain the slew of recent
clinical trials demonstrating that dieters who restrict carbohydrates
but not calories invariably lose more weight than dieters who restrict
calories but not necessarily carbohydrates. Put simply, it’s quite
possible that the foods—potatoes, pasta, rice, bread, pastries, sweets,
soda, and beer—that our parents always thought were fattening (back
when the medical specialists treating obesity believed that exercise
made us hungry) really are fattening. And so if we avoid these foods
specifically, we may find our weights more in line with our desires.
As
for those people who insist that exercise has been the key to their
weight-loss programs, the one thing we’d have to wonder is whether they
changed their diets as well. Rare is the person who decides the time
has come to lose weight and doesn’t also decide perhaps it’s time to
eat fewer sweets, drink less beer, switch to diet soda, and maybe
curtail the kind of carb-rich snacks—the potato chips and the candy
bars—that might be singularly responsible for driving up their insulin
and so their fat.
For the rest of us, it may be time to
take a scientific or biological view of our excesses rather than a
biblical one. The benefits of exercise include the joys of
virtuousness. I worked out today, therefore I can eat fattening foods
to my heart’s content. But maybe the causality is reversed here too.
Maybe it’s because we eat foods that fatten us that the workout becomes
a necessity, the best we can do in the battle against our own fat
tissue.
Gary Taubes is the author of Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease (Knopf, October 2), from which this article is adapted.