Our
Relationship With Food
Think 11
The Hunger Hormone:
Ghrelin
The
Fat Hormone: Leptin
Exercise vs. Drugs
Common Sense
Somewhere in your brain, there's a chocolate circuit. how
it works is not entirely clear, and you couldn't see it
even if you knew where to look. But it's there all the same
and it's a powerful thing. You didn't pop out of the womb
prewired for chocolate, but long ago, early in your babyhood,
you got your first taste of one, and instantly a series
of sensory, metabolic and neurochemical fireworks went off.
The
mesolimbic region in the center of your brain the area that
processes pleasure lit up. The vagus nerve flashed signals
to the stomach, which began to secrete digestive acids.
The pancreas began churning out insulin. The liver cranked
up to refine the body's chemistry to accommodate the sugar
and fat and starch that were coming in. As all those complex
processes were unfolding, your midbrain filed away a simple,
primal, unconscious idea: Chocolate is good. A lifetime love affair perhaps
pleasant, perhaps tortured began.
Our Relationship With Food
Human beings have always had a complicated relationship
with food. Staying alive from day to day requires our bodies
to keep a lot of systems running just so, but most of them
circulatory, respiratory, neurological, endocrine operate
automatically. Eating is different. Like sex, it's a voluntary
thing. And like sex, it's an essential element to keep the
species going. So nature cleverly rigs the game, making
sure we pursue them both by making sure we can't resist
them. In the case of food, that has lately spelled trouble.
Human history has usually been characterized by too little
to eat rather than too much. Nature never planned for what
could happen when unchecked appetites were suddenly matched
by unchecked resources. But we're seeing it now.
Postindustrial
humans as any trip to an all-you-can-eat buffet will tell
you have become a soft, sedentary, overfed lot. It's not
just that almost 70% of the U.S. population is either overweight
or obese, people
are getting fatter in all parts of the world. The fact
is, when faced with an abundance, we know that we're full,
but seem helpless to control ourselves. We lose weight and
routinely regain it; we vow to eat healthfully and almost
always lapse. Our doctors warn us about our rising blood
pressure and creeping cholesterol, and we get briefly spooked
until we're offered the next helping of cheesecake or curly
fries, our appetite shouts down our reason and before we
know it, we're at it again.
Just
why is our appetite such a powerful a driver of our behavior,
and, more important, how can we bring it to heel? If that
question has long defied easy answers, it's no wonder. Understanding
a single biological unit the heart, the lungs is hard enough.
Understanding a process as complex as appetite one that
involves taste, smell, sight, texture, brain chemistry,
gut chemistry, metabolism, evolution and, most confounding
of all, psychology is exponentially harder. But science
is trying to explain it.
Researchers
in labs and institutes around the world are peering into
the brain to understand the regions where appetite is perceived
and satisfied, and pinpointing the receptors on cell surfaces
that keep us hungry or get us sated. They're studying the
neural wiring of the stomach and intestines, as well as
the operation of the genes that drive our appetite, to track
how satiety signals are sent and determine why they sometimes
get lost. And they're peering back into human history to
understand better how we were booby-trapped for overeating
from the start and how we might be able, so many eons later,
to cut the trip wire at last. "The scourge of body-weight
disregulation has become a leading cause of death worldwide,"
says Dr. David Cummings, an associate professor of medicine
at the University of Washington. "Understanding it is perhaps
the most compelling agenda in the field of medical research."
If you're
among the millions who have ballooned past their target
weight, you can take some consolation from the fact
that your early ancestors would be very proud of you. Human
beings emerged into a world in which food often was scarce,
often spoiled and when we learned the art of hunting sometimes
bit back, making the idea of eating a lot when you could
both sensible and necessary. If you never knew when you
were going to have dinner again, it was best to gorge when
the food was there.
"We
were hardwired to eat and eat and particularly eat fatty
foods because we didn't get them often," says Sharman Apt
Russell, author of Hunger: An Unnatural History. We're programmed
not only to overeat but also to fail to recognize immediately
just when we've reached that point. Mothers tell kids not
to wolf their food because it's harder to enjoy it that
way and also because even after you've had enough, it can
take a while for your brain to get the message. By the time
it does, you're not just full; you're stuffed. "The people
who didn't immediately lose their appetites, who could gorge
themselves and keep going, those people would survive longer
during the next famine," says Dr. Jeffrey Flier, obesity
scientist and professor at Harvard Medical School.
That's
not to say that your body doesn't work hard to keep itself
balanced. Over the course of a year, the average adult male
consumes about 900,000 calories, yet his weight may not
rise or fall by more than a pound. Since a pound equals
about 4,000 calories, that means his annual intake is just
0.4% or 11 calories a day above or below precisely what
he needs to keep going. "You are within a potato chip a
day of matching your intake with expenditure," says Randy
Seeley, professor of psychiatry and associate director of
the Obesity Research Center at the University of Cincinnati.
Think 11
That's
why exercise is so critical to the equation. The burning
of fuel is essential to our total
energy requirement. If for example, our total energy
requirement is equal to 2000 calories per day and we've
ingested 2011 calories per day. We need to have a plan to
get rid of those extra 11 calories, since we've ingested
more than we've expended. Regardless of what types of foods
these extra 11 calories consist of, whether it be a liquid
or solid, fat or protein, fruit or chocolate bar, salad
or french fries, our body is inevitably programmed to turn
these extra calories into fat. We will then store this fat
until it is needed for energy.
In theory, if we continue to maintain this calorie surplus
daily, we would end up storing an additional 84 calories
per week, 336 calories per month and 4368 calories per year
(that's over 1 pound of fat). Keep in mind that this calculation
is based on exceeding your daily energy expenditure by only
11 calories. That's equivalent to just over 1 cup of lettuce,
2 cups of plain black coffee, 1 M&M peanut or 1 glass
of Kool-Aid. Since most people exceed their calorie expenditure
by far more than 11 calories per day, it's no surprise that
obesity is becoming the number one health problem in developed
nations.
It takes
a lot to maintain such a precisely balanced cycle of fueling
and burning, and in most cases, it all starts with the clock.
Like other animals, we are creatures of dietary habit. Feed
us at 8 a.m., 1 p.m. and 7 p.m., and we learn to get hungry
as those hours approach. Throw in a snack at 3:30 or before
bedtime, and we get the itch then too. At all these moments,
what's fueling the feeling is a substance called ghrelin.
The Hunger Hormone: Ghrelin
Identified in 1999, ghrelin is often called the hunger hormone
because that precisely captures what it does. Ghrelin is
produced in the gut in response to meal schedules and, according
to some theories, the mere sight or smell of food and is
designed to give rise to the empty feeling we recognize
as wanting to eat. When ghrelin hits the brain, it heads
straight for three areas: the hindbrain, which controls
the body's automatic, unconscious processes; the hypothalamus,
which governs metabolism; and the mesolimbic reward center
in the midbrain, where feelings of pleasure and satisfaction
are processed. That's a neural triple play that guarantees
that when ghrelin talks, the brain will listen.
Cummings
has conducted studies in which he measured the hormone in
people's blood every 20 min. and found that levels reliably
spike as mealtimes approach. Add or subtract a daily meal,
and you soon gain or lose a surge. "Grazing animals have
little spikes of ghrelin all day long 20 to 30 in the case
of a rat," Cummings says. One of the reasons gastric-bypass
surgery can work in severely obese people apart from the
fact that it reduces the carrying capacity of the stomach
is that it also appears to turn down the ghrelin spigot.
An Italian study even looked at ghrelin in anorexics and
found that levels of the hormone were chronically high a
chemical alarm that the self-starvers trained themselves
to ignore. All this research confirmed ghrelin's role in
driving appetite, both when we really need to eat and when
we merely expect to.
If ghrelin
were all there was to it, we and the rats would eat ourselves
to death. But even as one system is gunning our hunger higher,
another is standing by to slow things down. The first step
in that appetite-taming process occurs in the stomach and
upper intestine, where nerves that sense stretching and
distension eventually alert the brain that we're getting
full. That message is reinforced by three substances that
travel northward from the gut. The first, a peptide released
by the upper intestine called cholecystokinin (CCK), is
the most fleeting of the three, reaching the brain and increasing
the feeling of heavy satisfaction that prods you to push
away from the table. But CCK does not last long, certainly
not long enough to prevent you from eating again well before
your body needs more fuel.
Racing
in after CCK are two hormones, GLP-1 and PYY, that really
slam on the brakes. Produced in the lower gut, they not
only tell your brain you've had enough but also tell your
stomach to stop what it's doing and not move anything further
along into the intestines where the real business of digestion
takes place until what's there has been broken down some.
If you've ever finished a heavy meal at 8:30 p.m. and realized
that you still feel stuffed when you climb into bed at 11,
that's why. What's more, GLP-1 adjusts blood chemistry,
stimulating the pancreas to release more insulin, which
soaks up sugars released into the blood by the in rushing
food and stores them in the body's fat deposits. "These
two hormones go beyond meal intake and regulate overall
energy balance," says Hans-Rudolf Berthoud, head of the
neurobiology and nutrition laboratory at the Pennington
Biomedical Research Center in Baton Rouge, La.
The Fat Hormone: Leptin
If despite all those obstacles in the path of overeating
you still pack in too much food and as a result pack on
too much fat the body has one other, much bigger gun it
can roll out: leptin. An appetite-suppressing hormone discovered
in 1994, leptin is produced by body fat itself, usually
in direct proportion to how much of the tissue you're carrying.
The fatter you are, the more leptin you produce. Once in
the bloodstream, the hormone travels to the hypothalamus,
one of the same brain regions targeted by ghrelin, seeks
out a pair of neuropeptides known to stimulate appetite
and partly muffles their signals. The result is, or should
be, that fatter people want to eat less. Not surprisingly,
the discovery of leptin was huge news in the diet community.
Maybe obese people were simply suffering from a shortage
of leptin; supplement the hormone with periodic injections,
and the fat would dissolve away.
As it
turned out, things weren't so easy. For one thing, there
are hundreds of millions of obese people in the world, but
even after 13 years of study, researchers have found only
a handful on the order of 10 to 20 with a congenital deficit
in leptin production or function. In fact, the leptin system
in most overweight people works precisely the way it's supposed
to, with hormone levels climbing more or less in lockstep
with weight. The problem is, at some point the stuff simply
stops working or at least stops keeping pace with the numbers
on the scale. When the few people born with a leptin deficit
are given supplemental injections, they respond to the treatment.
But in other obese people whose systems have been overexposed
to the hormone over the years and thus grown resistant to
it the treatments do no good at all. Once again that's where
exercise comes to the rescue. Studies have shown that leptin
sensitivity can be improved by exercising and losing body
fat. Exercise will lower the levels of leptinin the body
- no matter how fat a person is. A team at the Harvard School
of Public Health found that, fat or thin, men who exercised
the most had lower levels of leptin in their blood.
If we
get more exercise, we can lower your leptin levels, even
if our BMI stays the same. BMI
stands for body mass index, and although not an accurate
measurement of health, it is used by some researchers to
calculate obesity. Scientists have been intrigued since
the hormone leptin was discovered, and became excited when
they found that injecting leptin into rats could cause them
to lose weight. Sadly, the same is not true for humans.
They found that the human metabolism was most effective
at reducing the amount of leptin in our blood by decreasing
body fat through exercise and a good diet.
Exercise vs. Drugs
If we haven't yet figured out how to tame our need to eat,
one reason may be that ghrelin, leptin and the handful of
other gut chemicals are only the big dogs of the appetite-control
system. Researchers have discovered at least two dozen other
hormones and peptides that play a role too. Adjusting the
levels of just the few we know best is a little like upgrading
the quality of the gas in your car and thinking that is
going to boost it from 20 m.p.g. to 75 m.p.g. You may notice
some improvement, but if you really want a better, more
efficient machine, you have to open the hood and retool
things in a much more fundamental way...exercise.
Many
health experts predict that most future studies will inevitably
conclude that exercise will do more and better than any
drug, hormone or chemical therapy ever can to tweak our
metabolism. Between researching appetite-controlling receptor
sites, genetic variances, mutations, blocking pathways and
other physiological entities that control our metabolism,
it's obvious that drug therapy is the underlying goal for
most studies which are funded by drug companies. The problem
is, with each drug that is developed to tweak a specific
chemical in the body, there is always an unwanted side-effect
from its very specific action. It's kind of like trying
to fix specific components of an engine, when the real problem
is the gas itself.
The body has an innate ability to fine tune every chemical
process in unison to effectively control our energy-burning
motor, something a drug has never been able to do without
serious side-effects. It's just the way our body is designed.
Artificial chemical intervention has consistently created
more problems than benefits, and probably always will.
Exercise time and time again is proving to control our health
better than any drug. We know that exercise alone thwarts
pre-diabetic
syndrome and prevents
diabetes by improving markers for glucose and fat metabolism.
A large randomized clinical trial proved that lifestyle
modification is better than drugs. Exercise also helps
control and reduce dangerous levels of cholesterol and high
blood pressure by directly preventing
these diseases. There is also mounting evidence that
vigorous
exercise and bursts of exercise are extremely valuable
for long-term weight loss and controlling visceral fat which
also influences appetite. The benefits to exercise are endless
and postively impact the human body and our appetite naturally
without chemical intervention, without side-effects and
with all the enhancements we need to propel our health where
we need it most.
Common Sense
So besides exercise, what can we do on the diet front? At
the moment, some of the research in the kitchen involves
trying to find a more precise way to balance the glucose
loads various foods deliver to the body. That's important,
since the bigger the glucose hit, the greater the sense
of satiation, but only for a little while. Afterward, hunger
returns stronger than ever. "High
glycemic foods" like refined breads and sugars
push the body to refuel," says nutrition scientist Marlene
Most, head of the metabolic kitchen. "In low
glycemic foods, there is a constant flow of glucose
and insulin, so we don't need to refuel as much."
It's
all about common sense. Barbara Rolls, a professor of nutritional
sciences at Pennsylvania State University, advocates another
way to attack hunger even more aggressively. Rolls currently
tops the best-seller lists with a book about what she calls
the "volumetrics" eating plan the kind of prefab word that
cries out diet fad but in this case describes a sensible
idea, provided that it's followed in moderation. The key
to volumetrics, Rolls explains, is to consume foods that
are high in volume but not in calories in order to stimulate
the digestive system's distension nerves. It's the difference
between, say, a large, filling salad with a low-calorie
load and a small, unfilling brownie with a high one.
"This
whole idea of eating smaller portions I'm really fed up
with it," Rolls says. "It's not big portions that make you
eat more. It's big portions of calories. If you eat big
portions of fruits and vegetables, they displace other foods."
Rolls stresses that it's important to eat a variety of tastes
and textures. If you overload on one thing say, the heavy
dose of meats that the low-carbohydrate Atkins plan recommends
you're going to crave the sweet or crunchy or doughy experience
of the fruits and breads you're forbidden. "It's called
sensory-specific satiety," she says, and it's one of the
reasons we still have the appetite for a sweet dessert even
after we stuff ourselves with a heavy dinner.
The
very discordance between a mouthful term like sensory-specific satiety and the uncomplicated
joy of a crème brûlée at the end of
a meal speaks to the puzzle that is the human appetite.
We may always be pleasure-seeking creatures, intoxicated
by the very experience of food with its colors and textures
and notes of flavor but that doesn't mean our ancient impulse
to eat whenever we can must always yield to our modern ability
to satisfy that urge. The same human brain that invented
the food court and the supermarket must now develop ways
to control how and when we use them. Physical activity and
balanced nutrition are key to our survival. Just as when
we were learning to hunt and eat on the savanna, our health
was at stake then, just as it is today.