12
Weight Loss — If You’re Overweight
Weight loss can significantly reduce your insulin resistance. You may
recall from Chapter 1 that obesity, especially abdominal (truncal, or
visceral) obesity, causes insulin resistance and thereby can play a
major role in the development of both impaired glucose tolerance and
type 2 diabetes. If you have type 2 diabetes and are overweight, it
is important that weight loss become a goal of your treatment plan.Weight
reduction can also slow down the process of beta cell burnout by making
your tissues more sensitive to the insulin you still produce, allowing
you to require (and therefore to produce or inject) less insulin.
It may even be possible, under certain circumstances, to completely
reverse your glucose intolerance. Long before I studied medicine, I
had a friend, Howie, who gained about 100 pounds over the course of
a few years. He developed type 2 diabetes and had to take a large amount
of insulin (100 units daily) to keep it under control. His physician
pointed out to him the likely connection between his diabetes and his
obesity. To my amazement, during the following year, he was able to
lose 100 pounds. At the end of the year, he had normal glucose tolerance,
no need for insulin, and a new wardrobe. This kind of success may only
be possible if the diabetes is of short duration, but it is certainly
worth keeping in mind—weight loss can sometimes work miracles.
Before we discuss weight loss, it makes sense to consider obesity,
because if you don’t understand why and how you are overweight or obese,
it will be somewhat more difficult to reverse the condition.
THE THRIFTY GENOTYPE
When I see a very overweight person, I don’t think, “He ought to control
his eating.” I think, “He has the thrifty genotype.” What is the thrifty
genotype?
The hypothesis for the thrifty genotype was first proposed by the anthropologist
James V. Neel in 1962 to explain the high incidence of obesity and type
2 diabetes among the Pima Indians of the southwestern United States.
Evidence for a genetic determinant of obesity has increased over the
years. Photographs of the Pimas from a century ago show a lean and wiry
people. They did not know what obesity was and in fact had no word for
it in their vocabulary. Their food supply diminished in the early part
of the twentieth century, something that had occurred repeatedly throughout
their history. Now, however, they weren’t faced with famine. The Bureau
of Indian Affairs provided them with flour and corn, and an astonishing
thing happened. These lean and wiry people developed an astronomical
incidence of obesity—100 percent of adult Pima Indians today are grossly
obese, with a staggering incidence of diabetes. Fully 65 percent of
adults are type 2 diabetics. Since the publication of the first edition
of this book, even many Pima children have become obese, type 2 diabetic
teenagers. A similar scenario is now playing out across the United States
in the general population. The pace may be slower, but the result is
similar.
What happened to the Pimas? How did such apparently hardy and fit people
become so grossly obese? Though their society was at least in part agrarian,
they lived in the desert, where drought was frequent and harvests could
easily fail. During periods of famine, those of their forebears whose
bodies were not thrifty or capable of storing enough energy to survive
without food died out. Those who survived were those who could survive
long periods without food. How did they do it? Although it may be simplifying
somewhat, the mechanism essentially works like this: Those who naturally
craved carbohydrate and consumed it whenever it was available, even
if they weren’t hungry, would have made more insulin and thereby stored
more fat. Add to this the additional mechanism of the high insulin levels
caused by inherited insulin resistance, and serum insulin levels would
have become great enough to induce fat storage sufficient to enable
them to
live through famines. (See Figure 1-1.) Truly survival of the fittest—
provided famines would continue.
A strain of chronically obese mice created in the early 1950s demonstrates
quite vividly how valuable thrifty genes can be in famine. When these
mice are allowed an unlimited food supply, they balloon and add as much
as half again the body weight of normal mice. Yet deprived of food,
these mice can survive 40 days, versus 7–10 days for normal mice.
Recent research on these chronically obese mice provides some tantalizingly
direct evidence of the effect a thrifty genotype can have upon physiology.
In normal mice, a hormone called leptin is produced in the fat cells
(also a hormone human fat cells produce, with apparently similar effect).
The hormone tends to inhibit overeating, speed metabolism, and act as
a modulator of body fat. A genetic “flaw” causes the obese mice to make
a less effective form of leptin. In recent experiments, when injected
with the real thing they almost instantly slimmed down. Not only did
they eat less but they lost as much as 40 percent of their body weight,
their metabolism sped up, and they became much more active. Many were
diabetic, but their loss of weight (and the change in the ratio of fat
to lean body mass) reversed or even “cured” their diabetes. Normal mice
injected with leptin also ate less, became more active, and lost weight,
though not as much. Research on humans has not advanced sufficiently
to provide conclusive evidence that the mechanism is the same in obese
humans, but researchers believe it is at least equivalent and probably
related to more than one gene, and to different gene clusters in different
populations.
In a full-blown famine, the Pima Indian’s ability to survive long enough
to find food is nothing short of a blessing. But when satisfying carbohydrate
craving is suddenly just a matter of going to the grocery or making
fried bread, what was once an asset becomes a very serious liability.
Although current statistics estimate slightly more than 60 percent
of the overall population of the United States as chronically overweight,
there is even greater reason to be concerned, because the number has
been increasing by 1 percent each year. Some researchers attribute rising
obesity in the United States at least in part to increasing numbers
of former smokers. Others attribute it to the recent increase in carbohydrate
consumption by those trying to avoid dietary
fat. Whatever the reasons, overweight and obesity can lead to diabetes.
The thrifty genotype has its most dramatic appearance in isolated populations
like the Pimas, which have recently been exposed to an unlimited food
supply after millennia of intermittent famine. The Fiji Islanders, for
example, were another lean, wiry people, accustomed to the rigors of
paddling out against the
Pacific to fish. Their diet, high in protein and low in carbohydrate,
suited them perfectly. After the onset of the tourist economy that followed
World War II, their diet changed to our high-carbohydrate western diet,
and they too began (and continue) to suffer from a high incidence of
obesity and type 2 diabetes.
The same is true of the Australian Aborigines after the Aboriginal
Service began to provide them with grain. Ditto for South African blacks
who migrated from the bush into the big cities. Interestingly, a study
that paid obese, diabetic South African blacks to go back to the countryside
and return to their traditional high-protein, low-carbohydrate diet
found that they experienced dramatic weight loss and regression of their
diabetes.
It’s clear that thrifty genotypes work in isolated populations to make
metabolism supremely energy-efficient, but what happens when the populations
have unrestricted access to high-carbohydrate foods? It would appear
that the mechanism of the thrifty genotype works something like this:
Certain areas of the brain associated with satiety—that sensation of
being physically and emotionally satisfied by the last meal—may have
lower levels of certain brain chemicals known as neurotransmitters.
A number of years ago, Drs. Richard and Judith Wurtman at the Massachusetts
Institute of Technology (MIT) discovered that the level of the neurotransmitter
serotonin is raised in certain parts of the hypothalamus of the animal
brain when the animal eats carbohydrate, especially fast-acting concentrated
carbohydrate like bread. Serotonin is a neurotransmitter that seems
to reduce anxiety as it produces satiety. Other neurotransmitters such
as dopamine, norepinephrine, and endorphins can also affect our feelings
of satiety and anxiety. There are now more than one hundred known neurotransmitters,
and many more of them may affect mood in response to food in ways that
are just beginning to be researched and understood.
In persons with the thrifty genotype, deficiencies of these neurotransmitters
(or diminished sensitivity to them in the brain) causes both a feeling
of hunger and a mild dysphoria—often a sensation of anxiety, the opposite
of euphoria. Eating carbohydrates temporarily causes the individual
to feel not only less hungry but also more at ease. A frequent television
sitcom scenario is the woman just dumped by her boyfriend who plops
down on the couch with a pie or half a gallon of ice cream, a spoon,
and the intention of eating the whole thing. She’s not really hungry.
She’s depressed and trying to make herself feel better. She’s indulging
herself, we think, rewarding herself in a way for enduring one of life’s
traumas, and we laugh because we understand the feeling. But there is
a very real biochemical mechanism at work here. She craves the sugar
in the pie or the ice cream not because she’s hungry but because she
knows, consciously or not, that it really will make her feel better.
Contrary to popular belief, the fat in the ice cream or in the crust
of the pie doesn’t make much of a difference. It’s the carbohydrate
that will increase the level of certain neurotransmitters in her brain
and make her feel better temporarily. The side effect of the carbohydrate
is that it also causes her blood sugar to rise and her body to make
more insulin; and, as she sits on the couch, the elevation in her serum
insulin level will facilitate the storage of fat.
On television the actress may never get fat. But for the real-life
woman, high serum insulin levels from eating high-carbohydrate foods
will cause her to crave carbohydrate again. If she is a type 1 diabetic
making no insulin, she’ll have to inject a lot of insulin to get her
blood sugar down, with the same effect—more carbohydrate craving and
building up of fat reserves.
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