By Melinda Beck at The Wall Street Journal: Imagine the typical office birthday party.
It's after lunch, so
everybody is full. Then, in comes a luscious chocolate confection. The
sight, the smell—even the sound of the word "cake!"—stimulate the
reward-and-pleasure circuits of the brain, activating memory centers and
salivary glands as well.
Melinda
Beck asks the age-old question: Do you eat to live, or live to eat?
Scientists, it turns out, have learned much more about how appetite
works in the brain - and the findings have major consequences.
Those reactions quickly drown out the subtle signals
from the stomach that are saying, in effect, "Still digesting down here.
Don't send more!" Social cues add pressure and permission to indulge.
Soon, everybody is having a slice—or two.
Scholars have
understood the different motives for eating as far back as Socrates, who
counseled, "Thou shouldst eat to live, not live to eat." But nowadays,
scientists are using sophisticated brain-imaging technology to
understand how the lure of delicious food can overwhelm the body's
built-in mechanism to regulate hunger and fullness, what's called
"hedonic" versus "homeostatic" eating.
One thing is clear: Obese
people react much more hedonistically to sweet, fat-laden food in the
pleasure and reward circuits of the brain than healthy-weight people do.
Simply seeing pictures of tempting food can light up the
pleasure-seeking areas of obese peoples' brains.
Two
conferences this week on obesity are each examining aspects of how
appetite works in the brain and why some people ignore their built-in
fullness signals. Scientists hope that breakthroughs will lead to ways
to retrain people's thinking about food or weight-loss drugs that can
target certain brain areas.
In a study presented this week at the
International Conference on Obesity in Stockholm, researchers from
Columbia University in New York showed pictures of cake, pies, french
fries and other high-calorie foods to 10 obese women and 10 non-obese
women and monitored their brain reactions on fMRI scans. In the obese
women, the images triggered a strong response in the ventral tegmental
area (VTA), a tiny spot in the midbrain where dopamine, the "desire
chemical," is released. The images also activated the ventral pallidum, a
part of the brain involved in planning to do something rewarding.
"When
obese people see high-calorie foods, a widespread network of brain
areas involved in reward, attention, emotion, memory and motor planning
is activated, and all the areas talk to each other, making it hard for
them to resist," says Susan Carnell, a research psychologist at the New
York Obesity Research Center at Saint-Luke's-Roosevelt Hospital and
Columbia University and one of the investigators.
Similar brain reactions occurred in
the obese subjects even when researchers merely said the words
"chocolate brownie"—but not when they saw or heard about lower calorie
foods such as cabbage and zucchini. Reactions were far less pronounced
in the non-obese subjects.
More such studies are being presented
in Pittsburgh this week at the annual meeting of the Society for the
Study of Ingestive Behavior. In one, neuroscientists from Yale
University's John B. Pierce Laboratory had 13 overweight and 13
normal-weight subjects smell and taste chocolate or strawberry
milkshakes and observed their brains with fMRI scans.
The
overweight subjects had strong reactions to the food in the amygdala—the
emotional center of the brain—whether they were hungry or not. The
healthy-weight subjects showed an amygdala response only when they were
hungry.
"If you are of normal weight, your homeostatic mechanisms
are functioning and controlling this region of the brain," says lead
investigator Dana Small. "But in the overweight group, there is some
sort of dysfunction in the homeostatic signal so that even though they
weren't hungry, they were vulnerable to these external eating cues."
Studies
have found that a diet of sweet, high-fat foods can indeed blunt the
body's built-in fullness signals. Most of them emanate from the
digestive tract, which releases chemical messengers including
cholecystokinin, glucagon-like peptide and peptide YY when the stomach
and intestines are full. Those signals travel up to the brain stem and
then the hypothalamus, telling the body to stop eating.
Obesity
also throws off the action of leptin, a hormone secreted by fat tissue
that tells the hypothalamus how much energy the body has stored. Leptin
should act as a brake against overeating, and it does in normal-weight
people. But most obese people have an overabundance of leptin, and
somehow their brains are ignoring the signal.
All these findings
beg the question, which came first? Does obesity disrupt the action of
leptin, or does a malfunction in leptin signaling make people obese?
Similarly,
are some people obese because their brains overreact to tempting food,
or do their brains react that way because something else is driving them
to overeat? Researchers at Yale and elsewhere are turning to such
questions next. "It's possible that these changes reflect how the brain
has adapted to eating patterns in obese people, and that could create a
vicious circle, putting them at risk for even more disordered eating,"
says Dr. Small.
There are plenty of other metabolic mysteries,
too: Why are some "foodies" who get intense pleasure from eating able to
stop when they're full and others aren't? Is the tendency to eat way
past fullness genetic or learned behavior, and how much can it be
changed?
The answers are still elusive, but neuroscientists and
behavioral experts are finding some tantalizing clues.
Some fMRI
studies have found that while tempting food stimulates the release of
dopamine in obese people, they actually have fewer dopamine receptors
than normal weight subjects do, so they may derive less pleasure from
actually eating, setting up a craving for more.
Curiously, several studies have shown
that some forms of gastric bypass surgery can actually create changes
in the brains of formerly obese people —and not just because their
stomachs are smaller and fill up more quickly. Levels of leptin and
glucose tend to drop in bypass patients, ending diabetes for many of
them. PET scans also show that bypass patients have more dopamine
circulating in their brains, which may help control appetite as well.
Bypass
surgery seems to make food less tempting, too. In a study in the
American Journal of Clinical Nutrition last month, Swiss researchers had
123 severely obese, 110 non-obese and 136 bypass patients take a test
that measures vulnerability to hedonistic eating, known as the "Power of
Food Scale." The bypass patients and the non-obese had scores far lower
than those who were currently obese. (Exactly why is still unclear, but
some experts think it could relate to "dumping syndrome," in which high
fat and sweet food creates nausea and dizziness in bypass patients.
They may have learned to associate such foods with discomfort rather
than pleasure.)
Some of the most intriguing imaging studies have
peered into the brains of people who have lost significant weight and
kept it off through diet and exercise alone—although researchers say
they're hard to find.
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