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(February
6, 2003) - Rockefeller University - "Jack Sprat
could eat no fat, his wife could eat no lean," goes
the classic children's nursery rhyme, implying that Jack's
trim figure and his wife's portly profile were a
conscious choice, since "betwixt the two of them,
they licked the platter clean."
But as Jeffrey M. Friedman, M.D., Ph.D., argues in a
"Viewpoint" article in a special obesity issue
of the journal Science published Feb. 7, obesity
cannot be easily explained as simply a breakdown in
willpower. Genes and environment, explains the
Rockefeller University and Howard Hughes Medical
Institute researcher, both play important roles in
determining a person's body weight. He points put that
"in general, environmental factors account for
trends in a population over time, while genetic factors
account for most of the differences in weight among
individuals in present time.
"While answers are beginning to emerge as to why so
many of us are obese, there can be no meaningful
discussion on this subject until we resist the impulse to
assign blame," writes Friedman, who led the
laboratory team that discovered the obesity hormone
leptin in 1995. "Nor can we hold to the simple
belief that with willpower alone, one can consciously
resist the allure of food and precisely control one's
weight.
"Instead, we must look at the facts dispassionately
and uninfluenced by the numerous competing interests that
drive debate on this subject."
The facts, according to Friedman, are: increase in weight
does not fully account for the increase in the incidence
of obesity; the drive to eat is to a large extent hard-wired
and differences in weight are genetically determined; and
evolution exerts powerful forces that obese people need
to fight in order to lose weight.
An understanding of how genes and environment interact to
cause obesity, Friedman urges, requires a broad-based
research program that investigates not just the genes but
how they interact with the environment.
With nearly one-third of the U.S. population obese -- an
increase of 10 percent in the last decade -- public
health officials have been sounding an alarm, since
obesity carries an increased risk for heart disease, high
blood pressure and diabetes. And even more disturbing is
the increased incidence of type 2 diabetes in children --
which public health officials blame on the obesity
epidemic in young adults. Friedman points out that
although the incidence of obesity in the United States
has increased from 23.3 percent in 1991 to 30.9 percent
today, the weight of the average American has increased
about only seven to 10 pounds, on the average.
Why does an incremental increase in the average weight
have such a significant effect on the incidence of
obesity?
As Friedman explains, the reported incidence of obesity
is rooted in the definition of obesity, which is
described by the body mass index, or BMI. BMI is a
measure of body fat based on height and weight that
applies to both adult men and women. Obesity is
diagnosed when BMI passes a defined threshold: People are
said to be overweight if their BMI is greater than 25,
and obese if their BMI exceeds 30.
According to Friedman, since obesity is defined as a
threshold, an increase in average weight has a
disproportionate effect on the increasing incidence of
obesity.
Friedman suggests that there is a bright side: small,
achievable decrease in the average weight of the U.S.
population could have an enormous benefit to public
health.
In addition, Freidman cites a statistical analysis of BMI
trends by Katherine Flegal, Ph.D., an expert in the epidemiologist of obesity and overweight at the U.S.
Centers for Disease Control and Prevention, which shows
that in addition to an increase in average BMI, the
distribution of BMI in our population is also becoming
increasingly skewed at the higher end.
"Thus in modern times, some individuals have
manifested a much greater increase of BMI than others
strongly," Friedman writes, "suggesting the
possibility that in our population there is a subgroup
that is genetically susceptible to obesity and a
different subgroup that is relatively resistant."
Many factors have been cited as contributors to the rise in obesity: a
shift in American eating habits toward more fast food, increased
consumption of soft drinks, decreased physical activity and increased
inactivity.
But even with these environmental changes, Friedman poses a basic
question: how can anyone be thin in an environment where virtually
everyone has unfettered access to calories?
The answer lies in the interaction of the environment with the
biological system that our genes comprise.
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In 1995, Friedman and
his colleagues discovered the hormone leptin, which is produced by fat
tissue and signals the brain when to stop eating. As body fat increases,
more leptin is produced, which acts to reduce food intake. As body fat
decreases, less leptin is produced, which stimulates food intake and
reduces energy expenditure. Research by Friedman and other scientists
has shown that genetic mutations that lead to a full or partial loss of
leptin are associated with obesity in some humans.
In addition to leptin, Friedman and other scientists have identified a
number of hormones and genes that play a role in appetite and weight.
These hormones orchestrate the unconscious urge to eat, a basic
biological drive that is difficult to fight with the conscious desire to
eat less.
"Those who doubt the power of basic drives, however, might note that
while one can hold one's breath, this conscious act is soon overcome by
the compulsion to breathe," notes Friedman. "The feeling of hunger is
intense and, if not as potent as the drive to breathe, is probably no
less powerful than the drive to drink when one is thirsty.
"Who is it that can resist a drink of cold water when their lips are
parched? This is the feeling the obese must resist after they have lost
a significant amount of weight.
"The power of this drive is illustrated by the fact that, whatever ones
motivation, dieting is generally ineffective in for achieving
significant weight loss over the long term."
But what is the role of environment in all this? According to Friedman,
genes that compose the biological system that regulates weight should be
expected to vary depending on the environment due to intense selective
evolutionary pressure.
In other words, people who lived when food was sporadically available --
for example, hunters-gatherers -- benefited from genes that predisposed
them to obesity, since "these genes would increase energy stores and
provide a survival advantage during times of famine," Friedman says.
For those who lived in areas where the risk of starvation was low
because of farming, domestication of animals and the ability to store
food -- Western civilizations, for example -- the same genes that
protected people from starvation may have exposed the obese to
significant health consequences, such as diabetes and heart disease.
Modern-day humans, according to Friedman, "carry the genetic legacy of
both environments.
"In modern times, obesity and leptin resistance appear to be the residue
of genetic variants that were more adaptive in our previous
environments," he says. "It may be that the obese carry the
'hunter-gatherer' genes and the lean carry the 'Western' genes.
"The lean carry genes that protect them from the consequences of obesity
while the obese carry genes that are atavisms of a time of nutritional
privation in which they no longer live," he continues.
Taken together, our genes and our environment collaborate to build a
formidable barrier for those who want to lose weight.
"Obesity is not a personal failing," Friedman argues. "In trying to lose
weight, the obese are fighting a difficult battle -- a battle against
biology, a battle that only the intrepid take on and one in which only a
few prevail."
Friedman is the Marilyn M. Simpson Professor at The Rockefeller
University and an investigator at the Howard Hughes Medical Institute.
His research is supported by the National Institute of Diabetes and
Digestive and Kidney Diseases, part of the federal government's National
Institutes of Health.
News
release courtesy of Newswise
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