What You Don't Know About Fat

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What You Don't Know About Fat

 

Fat cells: The average person has 40 billion of them.

They multiply, they're almost impossible to kill and

they're sending messages to your body that can ruin

your health.

By Anne Underwood And Jerry Adler

Newsweek

 

Aug. 23 issue - It was one of the biggest medical

stories of the 1990s and, consequently, one of the

biggest disappointments. In 1994, researchers at

Rockefeller University, working with mutant mice that

grew to be three times the size of normal ones,

discovered what made them different: the absence of a

hormone they named " leptin. " When injected with leptin

the mice suddenly changed their eating habits and

began shedding those unsightly grams. Not since

Charles Atlas had there been such a convincing set of

before-and-after pictures; to millions of Americans

who secretly identified with the tangerine-size balls

of fur, leptin seemed like the long-sought

willpower-in-a-pill. But what worked in mice didn't

work in people—or, rather, it worked only in a handful

of people who, like the mice, lacked the gene to

produce leptin on their own. For a young woman in

England who had weighed 207 pounds at the age of 9, it

has been a lifesaver. For everyone else who thought it

might succeed where low-carb diets, low-fat diets,

Slim-Fast and Richard Simmons had failed, it's been a

bust.

 

It was a bust because obesity researchers are up

against a phenomenally complex and robust system,

devised by evolution precisely for the purpose of

hoarding fat against the certainty of future famine.

The search for a simple cure for obesity failed for

decades, in part because researchers regarded fat as

merely the product of an equation whose other terms

were greed and guilt. Now they recognize fat tissue as

a discrete, active organ in its own right,

continuously exchanging messages with the rest of the

body by way of the bloodstream. The messages are,

generally, of two kinds: either " I'm full " or " Isn't

there a Wendy's two-for-one coupon in the glove

compartment? " " We like to think that eating is a

voluntary act, " says Dr. Michael Schwartz of the

University of Washington. " But the amount you eat is

controlled in part by how much fat you have. "

 

The search for a simple cure for obesity is still

failing. Ask any researcher, no matter how esoteric

his specialty, for the best way to lose weight and he

will reply, " Eat less and exercise more. " But now we

have a much better understanding of why the search is

so difficult—and where we should look, not just to

treat obesity as such, but also to recognize that some

people are likely to stay fat to minimize the negative

effects on their health.

 

The work begins at the level of the fat cell itself, a

glistening oleaginous sphere so tiny that it takes a

million of them to store the calories in a Life Saver,

yet functioning like little chemical factories

continually absorbing or releasing substances in

response to the body's energy needs. " Few systems are

more critical to survival, " says Dr. Rudolph Leibel of

Columbia, than the energy storage-and-management

system that includes not just fat but the brain,

stomach, liver, pancreas and thyroid. The problem, of

course, is that the system evolved millions of years

before the first food court made its appearance on

earth. That, says Bruce Spiegelman of the Harvard

Medical School, is why it is so much easier for most

people to gain weight than to lose it: " For most of

evolution, getting enough to eat was a driving force

for survival. How many individuals were lost to morbid

obesity? "

 

When calorie intake exceeds expenditures, fat cells

swell, to as much as six times their minimum size, and

begin to multiply, from 40 billion in an average adult

up to 100 billion, the threshold to get your picture

on the front page of the supermarket tabloids. (Losing

weight causes them to shrink in size and become less

metabolically active, but their number goes down only

slowly, if at all.) Some of the resulting problems are

familiar, and essentially mechanical. Fat requires a

copious supply of blood in tiny capillaries (compared

with an equal weight of lean muscle, which is supplied

by larger blood vessels); this puts a strain on the

cardiovascular system. Obesity creates wear on the

joints, leading to osteoarthritis. The accumulation of

fat around the windpipe can interfere with breathing

when muscles relax in sleep. And fat discourages

exercise by reminding the brain: no way am I going out

of doors in a jogging suit, unless there's a blackout.

 

But the discovery of leptin helped create a paradigm

shift: increasingly, researchers believe that the

biochemistry of fat holds clues both to its tenacity

and to the diseases associated with obesity, including

heart disease, diabetes and even certain cancers.

Leptin is one of a half-dozen or so chemical

messengers produced by fat cells, including thrombotic

(pro-clotting) agents, vasoconstrictors (which raise

blood pressure) and both inflammatory and

anti-inflammatory agents that have powerful effects

throughout the body. It just goes to show, says Dr.

Gokhan Hotamisligil of the Harvard School of Public

Health, " in the human body, as in the world, if you

control fuel resources, you influence a lot of other

things as well. "

 

CONTINUED>>

 

Page 2: The Implications of Fat Placement in the Body

 

Page 3: Will Leptin Lead a Shortcut Path to Weight

Loss?

© 2004 Newsweek, Inc.

 

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