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A war on obesity, not the obese
In their efforts to lose weight, obese
individuals are fighting biology, evolution
and a culture that misunderstands them
BY JEFFREY M. FRIEDMAN
Food consumes our interest. To the hungry, it
is the focal point of every thought and action. To hundreds of
millions of obese and overweight individuals, it is the
siren’s song, a constant temptation that must be avoided lest
one suffer health consequences and stigmatization. To the
non-obese, it is a source of sustenance and often pleasure. To the
food and diet industries, it is big business. And to those
interested in public health, it is at the root of one of the most
pressing public health problems in the developed and developing
world.
Alarm about the health crisis associated with
an emerging “obesity epidemic” is sounded almost weekly
in response to reports that its incidence has greatly increased
over the past decade. Many argue that this explosive increase over
a short period of time indicates that the obesity problem is
primarily a result of our modern lifestyle. The facts, however, do
not support this conclusion. For example this argument fails to
take into account that the increasing incidence of obesity in the
population, from 23.3 percent in 1991 to 30.9 percent today, is not reflected
by a proportionate increase in the weight of the average American,
which grew by just 7 to 10 pounds.
Thus while we can’t minimize the
importance of the fact that more than half of the U.S. population
is now overweight or obese, we should highlight the fact that the
change in weight attributable to any recent change in our
environment, such as a change in diet or a more sedentary
lifestyle, is much smaller than the enormous differences in weight,
often numbering in the hundreds of pounds, that can be observed
among individuals. The question might as well be, in our current
environment where almost everyone has essentially free access to
unrestricted calories, why is anyone thin?
The answer appears to reside in our genes and
the way in which they interact with environmental factors. Numerous
studies have shown that the heritability of obesity is equivalent
to that of height and exceeds that of many disorders for which a
genetic basis is generally accepted.
Consider the case of a 200-pound, 9-year-old
English girl whose legs were so large she could barely walk. She
was found to lack a weight-regulating hormone called leptin, and
often consumed as much as 1100 calories in a single meal,
approximately half the amount an average adult would require in an
entire day. After leptin treatment, this was reduced to 180
calories, the typical intake for a child her age. Her weight is now
normal. About five percent of severely obese children have been
shown to carry defects in known single genes, and there are likely
to be other forms of genetic obesity that have yet to be
identified.
In general, obesity genes encode the molecular
components of the system that regulates energy balance, matching
food intake to energy expenditure and maintaining constant energy
stores in the form of fat. Normally, the system is incredibly
precise. Over the course of a decade, a typical person consumes
approximately 10 million calories, generally with only a modest change in weight. To
accomplish this, energy intake and output must match with just a 0.17
percent margin for error. This extraordinary level of precision exceeds
by several orders of magnitude the ability of nutritionists to
accurately count calories and suggests that conscious factors alone are
incapable of precisely regulating caloric intake.
So why are some individuals obese and others
not? Feeding is a complex motivational behavior, and many factors
influence when we start eating and when we stop. These factors
include the unconscious urge to eat that is regulated by leptin and
other hormones, the conscious desire to eat less (or more), sensory
factors such as smell and taste, emotional state, and others. The
brain somehow processes this diverse information. Though there is
clearly cross-talk between brain regions that produce a basic drive
to eat and those that express your conscious wishes, the feeling of
hunger is intense and, even if not as potent as other basic drives,
such as the drive to breathe, it is the powerful force that the
obese must resist in order to sustain weight loss. For most
dieters, sooner or later a primal hunger trumps the conscious
desire to be thin.
There’s also an environmental component.
As a species, we carry the genetic legacy of two environments. One
is passed down from hunter-gatherers, who had only sporadic access
to food. In such an environment, genes that predispose to obesity
increase energy stores and provide a survival advantage in times of
famine. The second, passed down from more recent societies, is the
result of a decreased risk of starvation but a higher risk of
obesity related health problems. In this environment, genes that
resist obesity and its complications would have a selective
advantage. It may be that it is the obese who carry the
hunter-gatherer genes and the lean that carry the Western genes, an
idea supported by the observation that populations that were
historically more prone to starvation (Pima Indians, Pacific
Islanders and others) become the most obese when exposed to a
Western diet and lifestyle.
The challenge we face now is to build a
molecular framework for the system that regulates weight and to
identify these genes and genetic variants that cause obesity. As we
learn more about the physiologic system that balances energy, the
impact of the environment on its function will also become better
understood and new therapeutic approaches will be developed.
In the meantime, a different kind of
understanding is called for. Obesity is not a personal failing. In
trying to lose weight, the obese are fighting a difficult battle.
It is a battle against biology, a battle that only the intrepid
take on and one in which only a few prevail.
May 13, 2005
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