Chapter
1: Diabetes: The Basics /
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Blood
Sugar Normalization: Restoring the Balance
According to the American Diabetes Association (ADA),
more than 150,000 people die annually from both Type
I and Type II diabetes and their long-term complications.
Certainly everyone has to die of something, but you
needn't die the slow, torturous death of diabetic
complications, which often include blindness and amputations.
My history and that of my patients supports this.
The recently completed Diabetes Control and Complication
Trial (DCCT) began as a ten-year study of Type I diabetics
to gauge the effects of improved control of blood
sugar levels (see the foreword, by Dr. Frank Vinicor).
Patients whose blood sugars were nearly "normalized"
(my patients' blood sugars are usually closer to normal
than were those in the trial) had dramatic reductions
of long-term complications. Researchers began the
DCCT trying to see if they could, for example, lessen
the frequency of diabetic retinopathy by at least
33.5 percent. Instead of a one-third reduction in
retinopathy, they found a more than 75 percent reduction
in the progression of early retinopathy. They found
similarly dramatic results in other diabetic complications
and halted the study early in order to make the results
available to all. They found a 50 percent reduction
of risk for kidney disease, a 60 percent reduction
of risk for nerve damage, and a 35 percent reduction
of risk for cardiovascular disease.
The patients followed in
the DCCT averaged twenty-seven years of age at the
beginning of the trial, so reductions could easily
have been greater in areas such as cardiovascular
disease if they had been older or followed for a longer
period of time. The implication is that full normalization
of blood sugar could totally prevent these complications.
In any case, the results of the DCCT are good reason
to begin aggressively to monitor and normalize blood
sugar levels. The effort and dollar cost of doing
so does not have to be so high as was suggested in
the DCCT's findings.
The Insulin-Resistant Diabetic:
Type II
Different from Type I diabetes is what is commonly
known as Type II. This is by far the more prevalent
form of the disease. According to ADA statistics,
90–95 percent of diabetics are Type II. Furthermore,
as many as a quarter of Americans between the ages
of sixty-five and seventy-four have Type II.
Approximately
80 percent of those with Type II diabetes are overweight
and suffer from a particular form of obesity known
as truncal, or visceral, obesity. It is quite possible
that the 20 percent of the so-called Type II diabetics
who do not have visceral obesity actually suffer from
a form of Type I diabetes that causes only partial
loss of the pancreatic beta cells that produce insulin.
If this proves to be the case, then fully all of those
who have Type II diabetes may be overweight. (Obesity
is usually defined as being at least 20 percent over
the ideal body weight for one's height, build, and
sex.)
While the cause of Type
I diabetes may still be somewhat mysterious, the cause
of Type II is less so. As noted earlier, another name
for Type II diabetes is insulin-resistant diabetes.
Obesity, particularly visceral obesity, and insulin
resistance—the inability to fully utilize the glucose-transporting
qualities of insulin—are interlinked. For reasons
related to genetics (see Chapter 12, "Weight
Loss"), a substantial portion of the population
has the potential when overweight to become sufficiently
insulin-resistant that the increased demands on the
pancreas burn out the beta cells that produce insulin.
These people enter the vicious circle depicted in
Figure
1-1. Note in the figure the crucial
role of dietary carbohydrate in the development and
progression of this disease. This is discussed in
detail in Chapter 12.
Insulin
resistance appears to be caused at least in part by
inheritance and in part by high levels of fat—in the
form of triglycerides—in the branch of the bloodstream
that feeds the liver. (Transient insulin resistance
can be created in laboratory animals by injecting
triglycerides directly into their liver's blood supply.)
Insulin resistance by its very nature increases the
body's needs for insulin, which therefore causes the
pancreas to work harder to produce elevated insulin
levels (hyperinsulinemia), which can indirectly cause
high blood pressure and damage the circulatory system.
So, to simplify somewhat, fat in the blood feeding
the liver causes insulin resistance, which causes
elevated serum insulin levels, which cause the fat
cells to build even more abdominal fat, which raises
triglycerides in the liver's blood supply, which causes
insulin levels to increase because of increased resistance
to insulin.
If that sounds circular,
it is. The fat that is the culprit here is not dietary
fat. High levels of triglycerides in the blood—which
are in circulation at some level in the bloodstream
at all times—are not so much the result of intake
of dietary fat as they are of carbohydrate consumption
and existing body fat. (We will discuss carbohydrates,
fat, and insulin resistance more in Chapter 9, "The
Basic Food Groups.") The culprit is rather a
particular kind of body fat. Visceral obesity is a
type of obesity in which fat is concentrated around
the middle of the body, particularly surrounding the
intestines (the viscera). A man who is viscerally
obese has a waist of greater circumference than his
hips. A woman who is viscerally obese will have a
waist at least 80 percent as big around as her hips.
All individuals with visceral obesity are insulin-resistant.
The ones who eventually become diabetic are those
who cannot make enough extra insulin to keep their
blood sugars normal.
Though treatment has many
similar elements—and many of the effects are the same—Type
II diabetes differs from Type I in several important
ways.
The onset of Type II diabetes
is slower and more stealthy, but even in its earliest
stages, the abnormal blood sugar levels, though not
sky-high, can cause damage to nerves, blood vessels,
heart, eyes, and more. Type II diabetes is often called
the silent killer, and it is quite frequently discovered
through one of its complications, such as hypertension
or a defect in vision.*
Type II
diabetes is, at the beginning, a less serious disease—patients
don't melt away into sugar water and die in a few
months' time. Type II, however, can through chronically
but less dramatically elevated blood sugars be much
more insidious. It probably causes more heart attacks,
strokes, and amputations than the more serious Type
I disease. Type II is a major cause of hypertension,
heart disease, blindness, and amputation due to impaired
sensation (nerve damage) in feet with poor circulation
that do not heal when injured. That these serious
complications of Type II diabetes can proliferate
is no doubt because it is initially milder and is
often left untreated or treated poorly.
Individuals with Type II
still make insulin, and most will never require injected
insulin to survive, though if the disease is treated
poorly, they can eventually burn out their pancreatic
beta cells and require insulin shots. Because of their
resistance to the blood sugar–lowering effects of
insulin (though not its fat-building effects), many
obese Type II diabetics actually make more insulin
than nondiabetics.
Since high blood sugar
is the hallmark of diabetes, and the cause of every
long-term complication of the disease, it makes sense
to discuss where blood sugar comes from and how it
is used and not used.
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