From: portsideMod <portsidemod@yahoo.com> 
Date: 2002/11/02 Sat AM 01:54:17 EST
To: ps <portside@yahoogroups.com>
Subject: Book Review: Why We Eat

Why We Eat

A review of Ellen Ruppel Shell's The Hungry Gene.

By Stephanie Mencimer
<http://www.washingtonmonthly.com/features/2001/0210.mencimer.html>

Two years ago, a young organ transplant doctor told me
a harrowing story. Recently he had stood by and watched
helplessly as a 15-year-old African-American girl died
from an enlarged heart. A transplant might have saved
her, but high blood pressure, diabetes, and a body mass
of more than 400 pounds made surgery impossible. The
memory haunted him as he continued to treat more and
more children experiencing the deadly effects of
chronic obesity. Mostly poor black kids, they marched
through his office suffering from high cholesterol,
high blood pressure, enlarged hearts, and adult-onset
diabetes that promised to fill their future with kidney
failure, amputations, blindness, and early heart
attacks and strokes.

Despite the staggering numbers of kids like this who
were showing up in District doctors' offices, little
was being done about it. The public schools had long
since sacrificed physical education to budget cuts;
understaffed cafeterias served students Domino's pizza
to be washed down with 20-ounce bottles of Powerade
from school vending machines. The American Diabetes
Association, headquartered in nearby Alexandria, Va.,
did not have a single program in the District for
adults, much less children. Even as the casualties
mounted, no one was sounding the alarm about all these
fat kids. Eventually, though, I discovered that one
group of people had taken a keen interest in the local
obesity epidemic: drug company researchers. D.C. had so
many fat kids, most of whom also had fat parents, that
it was a veritable gold mine for gene-hunters looking
for new drugs to treat Type 2 diabetes and obesity.

I thought about these kids--and the scientists pursuing
them--as I read Ellen Ruppel Shell's new book, The
Hungry Gene. As the co-director of the science
journalism program at Boston University, Shell's
specialty is scientists, and her book is largely a
story about them. Her characters run the gamut from
geneticists to nutritionists studying indigenous people
of Micronesia, where a traditional diet of fish and
breadfruit has been replaced by, of all things, Spam.
The sum of all their tales isn't particularly
heartening for those who may be carrying around a few
extra pounds.

As Shell explains, humans are hardwired to get fat. Put
us within arm's reach of too much junk food, liberate
us from manual labor, and very few will avoid gaining a
spare tire. "Obesity represents a triumph of instinct
over reason, and as such it embarrasses us," writes
Shell. "We prefer to think of ourselves as rational
beings, in firm control of our destinies or, at the
very least, of our bodies. But the deciphering of the
genetic underpinnings to weight regulation has
ascertained that it is to some degree biological, and
that our drive to eat can sometimes eclipse reason."

The difficulty of overcoming genetic imperatives,
though, hasn't prevented the nation from devoting its
tremendous scientific resources to finding a
pharmaceutical cure for excess poundage. While Shell
strives for balance, it's clear that she doesn't think
too highly of some of the scientists leading the race
to find an obesity drug. Some of those who specialize
in the study of gluttony also seem to suffer from
another deadly sin: greed. Foremost among them,
according to Shell, is Jeffrey Friedman, the head of
the Laboratory of Molecular Genetics at Rockefeller
University, who eventually helped discover--and
patent--the first obesity gene, ob, and the protein it
expressed, called leptin. Researchers believe that
leptin is the body's tool for regulating appetite,
alerting the brain when enough food has been consumed,
and have entertained high hopes that someday it could
be used as an appetite suppressant in humans.

In getting the gene patent, according to Shell,
Friedman screwed over the very people who had helped
him make the discovery in the first place, including
veterans in the field whose preeminence helped secure
the funding for his experiments and lab assistants who
had devoted their lives to the cause and labored in
horrible conditions for years. Shell says Friedman
conveniently took over one assistant's nearly finished
experiments while she was out of town, just before the
big discovery, thus ensuring that he would be the only
one credited with finding the gene. Friedman had also
ensconced himself on the scientific advisory board of a
drug company, anticipating a windfall from any drugs
produced as a result of the discovery of leptin.

Among the many people Friedman denied credit for the
achievement was Doug Coleman, who had done the
pioneering work on obesity in mice in the '70s, and who
had advised Friedman on his work. "Science was once
about the free exchange of ideas, about collaboration,"
Coleman told Shell bitterly. "But today it's about
intellectual property and confidentiality. It's all
about patents, about ownership."

Another of Shell's targets is George Bray, a professor
of medicine at Louisiana State University Medical
Center, an esteemed scientist, past president of the
International Association for the Study of Obesity, and
founding editor of both the International Journal of
Obesity and Obesity Research. He's also a guy who
thinks that obesity is so dangerous that half the
country should be taking diet drugs. As a result, his
services have been sought out by various drug companies
seeking to promote, or to protect from regulation,
highly dubious weight-loss products. According to
Shell, Bray has pimped fen-phen, Merida, and
Metabolife's dietary supplements containing ephedra, an
herb that works much like amphetamine and has been
linked to the deaths of more than 100 people.

Not all the scientists in the book are portrayed as
scoundrels. Shell finds several who got into the
obesity field because they were genuinely interested in
helping overweight people. One of them is Stephen
O'Rahilly, a professor of metabolic medicine at the
University of Cambridge, a doctor who actually likes
treating patients and specializes in hard cases. A few
years back, he treated a pair of cousins from Pakistan
who suffered from what could only be called a
pathological case of gluttony. The eight-year-old girl
weighed nearly 190 pounds, and, despite liposuction and
surgery, could no longer walk. The two-year-old, who
weighed 65 pounds, was heading down the same path. The
children behaved like "starving explorers," reports
Shell, devouring everything in sight. If their parents
padlocked the pantry at night, the kids would scavenge
"through the trash for soggy French fries and gnawed
frozen fish sticks from the freezer. There was no
stopping them."

Dozens of doctors had tried to help, but they could
find no explanation for such behavior. So the kids went
to see O'Rahilly. He was aware of Friedman's work on
the effects of leptin deficiency in mice, but
scientists had never been able to find a leptin
deficiency in humans. (In fact, most fat people have an
overabundance of the stuff.) But O'Rahilly located it
in the cousins and eventually also found the obesity
gene mutation--the first such discovery in humans--
which was telling the cousins' brains that they were
starving. In an unprecedented experiment, O'Rahilly
injected the cousins with leptin, with almost
instantaneous results. The cousins stopped their
nightly foraging in the kitchen, pushed away from the
table, and shed pound after pound. O'Rahilly's work
proved conclusively that the drive to overeat had deep
genetic roots.

While leptin may have cured the Punjabi cousins of
their ruinous cravings, its usefulness in treating
other overweight people has so far been limited only to
those with the specific, and rare, genetic mutation.
More recent studies have shown that leptin does not
serve as the body's tool for maintaining slimness, but
rather prevents the body from becoming too thin. It's
protective--if you're a hunter-gatherer subject to
great variations in the availability of food. That's
why, as one researcher told Shell, "For one or two
months people considered leptin the Great White Hope.
But we now know that leptin is not very good at
preventing people from eating too much."

Forever Fat

With more than 60 percent of Americans overweight,
Shell says scientists and drug companies alike see
obesity as the "trillion-dollar disease," which is why,
even when their products have failed to deliver, they
have resorted to devious and underhanded schemes to
deceive people into taking them anyway. Diet drugs have
proven notoriously ineffective at helping people lose
weight, and also usually rather dangerous. Fen-phen,
which caused hundreds of cases of deadly primary
pulmonary hypertension and heart-valve damage, is but
one example. Shell shows how drug companies manipulated
the Food and Drug Administration to get approval for
Meridia, a weight loss drug that raises the risk of
high blood pressure and stroke--the very things that
are supposed to be reduced by losing weight. Meridia
now has been linked to at least 19 deaths. And she
finds several examples of prominent doctors selling
drug companies the use of their names in order to get
misleading industry-written articles touting the
benefits of drugs like fen-phen into peer-reviewed
medical journals.

Not only does Shell hold out these stories as morality
tales about the dangers of greed in science, but she
also uses the diet drug failures to make a convincing
case that the scientific intellect will probably never
outsmart the hardwiring of the body to consume
excessive calories. Treat one angle of the problem, and
another will kick in to compensate for it. That's why
something drastic such as gastric bypass surgery--
stomach stapling--works, but only for a while.
Eventually, people who've undergone the surgery regain
their appetites, and find creative ways to circumvent
the problem of the smaller stomach, such as drinking
melted quarts of ice cream. "Mother Nature wants her
children to eat. Knock out a satiety gene like ob and
an animal will eat insatiably. But knock out an
appetite gene, and animals continue to eat normally,"
Shell writes. "For this reason, appetite-controlling
drugs like fen-phen and Meridia, while they may work
for some for a year or two, are not likely to
permanently alter the eating habits of millions."

While much of The Hungry Gene is about the science of
fat, Shell doesn't overlook environment as a critical
factor in the world's obesity epidemic. It's the
interplay, she argues, between genetics and environment
that has created the current crisis in human
waistlines. Our hunter-gatherer genes, designed to
conserve energy and food to prepare for times of
famine, are clashing with a modern culture of ease and
plenty. To that end, she takes on car culture and the
fast-food industry, a subject that has been well
covered by Eric Schlosser in his bestselling Fast Food
Nation.

Like Schlosser, Shell ends with the now-familiar call
for a ban on marketing junk food to children. It's
absolutely the right prescription, but one that invokes
a "Yeah, right" response. This country will never ban
Happy Meal ads on TV. Shell might have done better to
suggest fighting fire with fire. Let the fast-food
industry continue to market to children, but require TV
stations to donate air time for anti-junk-food
messages, which might, say, show what really goes into
those burgers and fries. Or they might offer
testimonials on the value of exercise from young people
with Type 2 diabetes whose feet have been amputated. A
similar requirement in the late 1960s for tobacco ads
was so effective that it prompted the industry to
voluntarily remove cigarette ads from television all
together.

Another possibility would simply be warning labels,
stickers on the side of 7-11 Double Gulps that spell
out the dangers of consuming a full 64 ounces of Coke.
Warning labels may seem trite on cigarettes today, but
how many people really could say for sure how many
calories are in a Double Gulp? (Answer: 600, almost a
quarter of the proper full day's energy budget for an
average male.) The food industry lobby has ferociously
fought such labeling in the supermarket, a sign that
this might be effective, at least for a while.

But why wait for the government to get involved?
Instead, the food police at the Center for Science in
the Public Interest ought to station themselves outside
a busy McDonald's wearing sandwich boards that list the
calorie and fat content of a large Extra Value Meal
containing a Quarter Pounder with cheese (1,380
calories and 56 grams of fat). With the public duly
informed about the restaurant's products, sales might
plummet as people would no longer be able to delude
themselves that fast food isn't that bad. Again, it
might be only a temporary interruption, but it would
accomplish what consumer groups can't afford to do now:
counteract the onslaught of junk-food marketing. The
media would eat up a campaign like this, and give the
issue lots of free airtime. No doubt McDonald's would
also respond with some ham-fisted legal action that
would all but guarantee years of free fast-food bashing
to come.

Shell doesn't raise the possibility of such exercises,
but I'm sure she would approve. After all, they are far
safer than a dose of Xenical. And she concludes that
because of our genetic predisposition to amass
calories, it's imperative for the U.S. and other
countries to create an environment that at least makes
us work a little harder for our Krispy Kremes--or
shames us into avoiding them all together.

Stephanie Mencimer is an editor of The Washington
Monthly.

__________________________________________________

 

========================================================
University Of California - Berkeley 
Date:
10/31/2002


Popular Weed Killer Feminizes Native Leopard Frogs Across Midwest 

Berkeley - Native male leopard frogs throughout the nation's Corn Belt are
being feminized by an herbicide, atrazine, used extensively to kill weeds on
the country's leading export crops, corn and soybeans, according to a survey
conducted by University of California, Berkeley, biologists and reported
this week in Nature. 

The UC Berkeley scientists also showed that male leopard frogs raised in
laboratory tanks contaminated with atrazine develop egg cells in their
testes and essentially turn into hermaphrodites. These sexual abnormalities
were observed at atrazine levels as low as 0.1 parts per billion (ppb), 30
times lower than the current allowable limit for atrazine in drinking water
set by the Environmental Protection Agency. 

These findings, added to earlier evidence that atrazine demasculinizes two
other species of frog, suggest that the herbicide could be a factor in the
decline of frogs and other amphibians in the United States and around the
world, the authors say. Atrazine has been used on crops since 1956 and
currently is the most widely used herbicide in the nation. 

"These studies clearly indicate that atrazine is detrimental to amphibians,"
said study author Tyrone Hayes, associate professor of integrative biology
at UC Berkeley. 

At the least, he said, atrazine is altering amphibian populations in large
areas of the United States. His field studies show that frogs seem to adapt,
since leopard frogs (Rana pipiens) - the most common frogs in the Midwest -
are often abundant in some of the corn growing areas region where atrazine
is used most. Atrazine may feminize male tadpoles and turn them into female
frogs, he said, or it may render some males infertile. Alternatively,
atrazine may favor tadpoles that delay sexual differentiation until after
they've turned into frogs and leave the contaminated water. 

"Atrazine is potentially destroying biodiversity," said Hayes, now engaged
in studies to determine the ultimate fate of these feminized tadpoles. "In
my opinion, this is an unacceptable risk." 

Hayes and his colleagues sampled leopard frog tadpoles in eight separate
ponds, ditches, rivers and streams in the Midwest during the summer of 2001
and found feminized male frogs at every site with measurable levels of
atrazine. The current laboratory detection limit is 0.1 parts per billion
(ppb). 

The sites were scattered through the Corn Belt and beyond, including in
Utah, Wyoming, Nebraska and near the Iowa-Illinois border. Several ponds
chosen as controls because they are in nonagricultural areas also had
measurable levels of atrazine and feminized frogs, while only one, in Utah,
had neither detectable atrazine nor affected frogs. 

The site with the highest concentration of feminized frogs was along the
North Platte River in Wyoming. There, 92 percent of male frogs showed sex
reversal. This area of Wyoming reports little use of atrazine, but the river
is fed by streams that carry runoff from Colorado farms, which do use
significant amounts of the herbicide. 

Earlier this year, Hayes and his colleagues reported that a common
laboratory frog, the African clawed frog (Xenopus laevis), became
demasculinized when raised in lab tanks with concentrations of atrazine of
0.1 ppb or higher. The current allowable limit set by the Environmental
Protection Agency for atrazine in drinking water is 3 ppb, and the proposed
chronic exposure limit for aquatic life is 12 ppb. 

The new experiment, reported in the Oct. 31 issue of Nature, is a repeat of
these experiments using the leopard frog . The new report also contains a
summary of Hayes' survey of Midwestern frog ponds. 

A field study by another group showed similar gonadal abnormalities in
atrazine-exposed northern cricket frogs (Acris crepitans). 

Just as in Hayes' earlier experiment, the male tadpoles developed female
characteristics in their sex organs, or gonads. Up to 29 percent of males
developed female egg cells (oocytes) in their testes, becoming
hermaphrodites. In one experiment, more than a third of the male frogs
exposed to 0.1 ppb atrazine showed under-developed testes. 

Details of the experiment are reported in the November issue of the journal
Environmental Health Perspectives (EHP). 

"The testes in these male frogs are obviously not functioning normally,
because if they were, egg cells would not be able to grow in them," Hayes
said. "Some testes are so invaded by ovary cells it looks like they are
converted, and technically, they could be considered ovaries." 

Hayes suspects that atrazine boosts the activity of an enzyme, aromatase,
that converts male sex hormones, or androgens, to female hormones, or
estrogens. The lowered androgens and increased estrogens allow egg cells to
grow within the testes, which is normally impossible. Atrazine's effects on
aromatase have been demonstrated in fish, reptiles and mammals, but not yet
in amphibians. 

Atrazine is so widespread that it can be found far from agricultural areas
and even in rainwater and snow. At one site in Nebraska, Hayes found that
rain and tap water contained enough atrazine to disrupt normal male
development in amphibians. 

"The current data raise concern about the effects of atrazine on amphibians
in general and the potential role of atrazine and other endocrine-disrupting
pesticides in amphibian declines," the authors wrote in their EHP article. 

The leopard frog studies are supported by various private grants and by the
National Science Foundation. Hayes' coauthors are former or current
undergraduate students - Kelly Haston, Mable Tsui and Cathryn Haeffele -
postdoctoral fellow Anhthu Hoang and research associate Aaron Vonk. 

Hayes is a member of UC Berkeley's Health Sciences Initiative, a broad-based
effort to bring the physical and biological sciences together to tackle
health problems of the 21st century. 


Editor's Note: The original news release can be found here.


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Note: This story has been adapted from a news release issued for journalists
and other members of the public. If you wish to quote any part of this
story, please credit University Of California - Berkeley as the original
source. You may also wish to include the following link in any citation:


http://www.sciencedaily.com/releases/2002/10/021031074404.htm