Diabetes: The Basics
At the time they are diagnosed, many type 1 diabetics still produce
a small amount of insulin. It’s important to recognize that if they
are treated early enough and treated properly, what’s left of their
insulinproducing capability frequently can be preserved. Type 1 diabetes
typically occurs before the age of forty-five and usually makes itself
apparent quite suddenly, with such symptoms as dramatic weight loss
and frequent thirst and urination. We now know, however, that as sudden
as its appearance may be, its onset is actually quite slow. Routine
commercial laboratory studies are available that can detect it earlier,
and it may be possible to arrest it in these early stages by aggressive
treatment. My own body no longer produces any insulin at all. The high
blood sugars I experienced during my first year with diabetes burned
out, or exhausted, the ability of my pancreas to produce insulin. I
must have insulin shots or I will rapidly die. I firmly believe— and
know from experience with my patients—that if the kind of diet and medical
regimen I prescribe for my patients had been utilized when I was diagnosed,
the insulin-producing capability left to me at diagnosis would have
been preserved. My requirements for injected insulin would have been
lessened, and it would have been much easier for me to keep my blood
sugars normal.
Blood Sugar Normalization: Restoring the Balance
According to the NIH, nearly 200,000 people die annually from both
type 1 and type 2 diabetes and their long-term complications—and it
is the NIH’s contention that diabetes is grossly underreported on death
certificates. (Is a diabetic’s death from heart disease, kidney disease,
or stroke, for example, really a death from diabetes?) 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 support this.
The Diabetes Control and Complication Trial (DCCT), conducted by the
NIH’s National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), began in 1983 as a ten-year study of type 1 diabetics to gauge
the effects of improved control of blood sugar levels. Patients whose
blood sugars were nearly “normalized” (my patients’ blood sugars are
usually closer to normal than were those in the intensive care arm of
the trial because of our low-carbohydrate diet) 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 more than
a 75 percent reduction in the progression of early retinopathy. They
found similarly dramatic results in other diabetic complications and
announced the results of the study early in order to make the good
news immediately 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.
I believe that with truly normal blood sugars, which many of my patients
have, these reductions can be 100 percent.
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 remotely as high as was suggested in
the DCCT’s findings.
The Insulin-Resistant Diabetic: Type 2
Different from type 1 diabetes is what is officially known as type
2. This is by far the more prevalent form of the disease.According to
statistics from the American Diabetes Association, 90–95 percent of
diabetics are type 2. Furthermore, as many as a quarter of Americans
between the ages of sixty-five and seventy-four have type 2 diabetes.
A recent study, published by Yale University, discovered that 25 percent
of obese teenagers now have type 2 diabetes.
(A new category of “pre-diabetes” has been recently called latent autoimmune
diabetes, or LADA. This category applies to mild diabetes with onset
after the age of thirty-five, in which the patient has been found to
produce an antibody to the pancreatic beta cell protein called GADA,
just as in type 1 diabetes. Eventually these people may develop overt
diabetes and require insulin.)
Approximately 80 percent of those with type 2 diabetes are overweight
and are affected by a particular form of obesity variously known as
abdominal, truncal, or visceral obesity. It is quite possible that the
20 percent of the so-called type 2 diabetics who do not have visceral
obesity actually suffer from a mild form of type 1 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 true
type 2 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 1 diabetes may still be somewhat mysterious,
the cause of type 2 is less so. As noted previously, another designation
for type 2 diabetes is insulin-resistant diabetes. Obesity, particularly
visceral obesity, and insulin resistance—the inability to fully utilize
the glucose-transporting effects of insulin—are interlinked. For reasons
related to genetics (see Chapter 12, “Weight Loss—If You’re Overweight”),
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 released
from abdominal fat—in the branch of the bloodstream that feeds the liver.
(Transient insulin resistance can be created in laboratory animals by
injecting triglycerides—fat—directly into their liver’s blood supply.)*
Insulin resistance by its very nature increases the body’s need 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.
* New evidence demonstrates a role for fat contained in muscle cells
(intramyocyte fat) as another important factor in causing insulin resistance.
High levels of insulin in the blood down-regulate the affinity for
insulin that insulin receptors all over the body have naturally. This
“tolerance” to insulin causes even greater insulin resistance.
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.
Truncal
Obesity
Insulin Overeating
Resistance
Hereditary Craving
for Carbohydrate Foods
High Dietary High
Carbohydrate Blood Hunger
Sugar
Excessive
Insulin
Production
by Reduced
Number of
Beta Cells
Beta Cell Burnout
If that sounds circular, it is. But note that the fat that is the culprit
here is not dietary fat.
Triglycerides are in circulation at some level in the bloodstream at
all times. High triglyceride levels 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 actually
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 obese individuals and especially those 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 adverse
effects of elevated blood sugar are the same—type 2 diabetes differs
from type 1 in several important ways.
The onset of type 2 diabetes is slower and more stealthy, but even
in its earliest stages the abnormal blood sugar levels, though not skyhigh,
can cause damage to nerves, blood vessels, heart, eyes, and more. Type
2 diabetes is often called the silent killer, and it is quite frequently
discovered through one of its complications, such as hypertension, visual
changes, or recurrent infection.*
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