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Honoring obesity
Rockefeller’s Jeffrey Friedman
wins Gairdner and Passano awards for research on how hormones
regulate body weight
BY JOSEPH BONNER
Considering he’s a scientist, Jeffrey Friedman has
quite a following among average Joes, especially the overweight ones. After
public events he’s approached by grateful attendees eager to thank
him for relieving a bit of the stigma they experience regarding their
weight, which Friedman’s research has shown is more a product of
genetics than bad habits.
This spring, Friedman also received some unexpected
attention from his scientific colleagues. On April 5, it was announced that
he had won the prestigious Gairdner Award, one of the top international
prizes in biomedical science. A few weeks later, at a banquet in Baltimore,
he was presented with the highly selective Passano Foundation Award.
Both awards have a history of recognizing truly
outstanding scientists. Founded by a Toronto businessman, James Gairdner,
in 1959, Gairdners are awarded to between three and six scientists each
year to recognize the achievements of medical researchers whose work
contributes significantly to improving the quality of human life. Of the
274 Gairdner winners, 64 have gone on to win the Nobel Prize.
The Passano Foundation Award has been given since 1945
to just one exceptional scientist each year who has done outstanding
research in the United States. More than 20 Passano award winners have gone
on to win the Nobel Prize.
Prior to Friedman’s research, little was known
about the components of the biologic system that controls weight. Many
scientists, in fact, questioned the very existence of such a system. Then,
in December 1994, Friedman, who is Marilyn M. Simpson Professor and
director of the Starr Center for Human Genetics at Rockefeller, and his
colleagues published a landmark paper in the journal Nature in which they identified a gene
in mice and humans called obese (ob)
that codes for a hormone he later named leptin, after the Greek word
leptos, for thin. Friedman and colleagues showed that leptin is a hormonal
signal made by the body’s fat cells that regulates food intake and
energy expenditure.
Over the last decade, as his research has progressed,
Friedman has learned much about leptin. Mice that lack ob, and thus do not produce
leptin, are massively obese. So are humans — those lacking leptin eat
copious amounts of food and often weigh several times what normal adults
do. In patients with leptin mutations and in a subset of obese patients in
the general population, treatment with leptin can lead to substantial
weight loss. But the majority of obese individuals have high, not low,
levels of leptin in their blood. Friedman’s studies have indicated
that such high levels are associated with leptin resistance, and further
evidence suggests that animals destined to become obese increase their
production of leptin in order to satisfy a higher set point for weight.
Leptin has also proven to be an effective therapy for
a number of conditions, including several forms of human diabetes and
hypothalamic amennorhea, a condition which develops in extremely thin women
— often ballet dancers and long-distance runners — that is one
of the most common causes of infertility in women. More recently, Friedman
and his colleagues at Rockefeller and the University of Wisconsin at Madison have begun to
understand how leptin functions at a molecular level; in 2002 they showed
that an enzyme called SCD-1 works through leptin to signal the body to
either store fat or burn it. They believe leptin acts in part by
suppressing SCD-1’s activity, which in turn activates a metabolic
pathway that promotes the burning of fat.
What has made Friedman something of a celebrity for
the overweight, however, is his fight against the stigmatization of the
heavy-set. Friedman’s long experience with the genetics of obesity
— including his clinical research of obese patients in The
Rockefeller University Hospital and his collaboration in a long-term study
of obesity-related health problems among the remote population of the south
Pacific island of Kosrae — have in recent years led him to become an
outspoken advocate for the obese. In editorials published in scientific
journals and the lay press, Friedman has argued that obesity cannot be
simply ascribed to a breakdown in willpower or poor lifestyle choices, as
many of the world’s thin would have us believe. It is primarily genes
modified by environmental factors, he explains, that determine a
person’s weight. (See A War on Obesity,
Not the Obese.)
“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,” Friedman says.
“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.”
May 13, 2005
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