Chapter
1: Diabetes: The Basics /
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Now, if I ate
only the protein portion of the meal, my blood sugar
wouldn't have the huge, and potentially toxic, surge
that carbohydrates cause. It would rise less rapidly,
and a smaller dose of insulin could act rapidly enough
to cover the glucose that's slowly derived from the
protein. My body would not have to endure wide swings
in blood sugar levels. (Dietary fat, by the way, has
no effect on blood sugar levels, except that it can
slightly slow the digestion of carbohydrate.)
In a sense, you could look
at my insulin shot before eating only the protein
portion of the meal as mimicking the nondiabetic's
phase II response. This is much easier to accomplish
than trying to mimic phase I, because of the much
lower levels of dietary carbohydrate and injected
insulin.
The
Type II Diabetic
Let's say Jim, a Type II diabetic, is 6 feet tall
and weighs 300 pounds, much of which is centered around
his midsection. Remember, at least 80 percent of Type
II diabetics are obese. If Jim weighed only 150 pounds,
he might well be nondiabetic, but because he's insulin-resistant,
Jim's body no longer produces enough excess insulin
to keep his blood sugar levels normal.
The obese
tend to be insulin-resistant as a group, a condition
that's not only hereditary but also directly related
to the ratio of visceral fat to lean body mass (muscle).
The higher this ratio, the more insulin-resistant
a person will be. Whether or not an obese individual
is diabetic, his weight, intake of carbohydrates,
and insulin resistance all tend to make him produce
considerably more insulin than a slender person of
similar age and height (see Figure 1-3). Many athletes,
because of their low fat mass and high percentage
of muscle, tend as a group to require and make low
levels of insulin. An obese Type II diabetic like
Jim, on the other hand, typically makes two to three
times as much insulin as the slender nondiabetic.
In Jim's case, from many years of having to overcompensate,
his pancreas has partially burned out, and despite
the huge output of insulin, he no longer can keep
his blood sugars within normal ranges. (In my medical
practice, a number of patients come to me for treatment
of their obesity, not diabetes. However, on examination,
most of these very obese "nondiabetics"
have slight elevations of their test for average blood
sugar.)
Let's take another look
at that mixed breakfast and see how it affects a Type
II diabetic. Jim has the same toast and jelly and
juice and boiled egg that Jane, our nondiabetic, and
I had. Jim's blood sugar levels at waking are normal.*
Since he has a bigger appetite than either Jane or
I, he has two glasses of juice, four pieces of toast,
and two eggs. As soon as the toast and juice hit his
mouth, his blood sugar level begins to rise. Unlike
mine, Jim's pancreas releases insulin, but he has
very little or no stored insulin (his pancreas works
hard just to keep up his basal insulin level), so
he has impaired phase I secretion. His phase II insulin
response, however, may be intact. So very slowly,
his pancreas will struggle to produce enough insulin
to bring his blood sugar down toward the normal range.
Eventually it may get there, but not until hours after
his meal, and hours after his body has been exposed
to high blood sugars. Insulin is not only the major
fat-building hormone, it also serves to stimulate
the center in the brain responsible for feeding behavior.
Thus, in all likelihood, Jim may well grow even more
obese, as demonstrated by the cycle illustrated in
Figure
1-1.
Since he's resistant to
insulin, his body has to work that much harder to
metabolize the carbohydrate he consumes. Because of
insulin's fat-building properties, his body stores
away some of his blood sugar as fat and glycogen;
but his blood sugar level continues to rise, since
his cells are unable to utilize adequate amounts.
Jim, therefore, still feels hungry. As he eats more,
his beta cells work harder to produce more insulin.
The excess insulin and the "hungry" cells
in his brain prompt him to want yet more food. He
has just one more piece of toast with a little more
jelly on it, hoping that it will be enough to get
him through until lunch. Meanwhile, his blood sugar
goes even higher, his beta cells work harder, and
perhaps some of them burn out. Even after all this
food, he still may feel many of the symptoms of hunger.
His blood sugar, however, will probably not go as
high as mine would if I took no insulin. In addition,
his phase II insulin response could even bring his
blood sugar down to normal after many hours without
more food.
Postprandial
blood sugar levels that I would call unacceptably
high—140 mg/dl, or even 200 mg/dl—may be considered
by other doctors to be unworthy of treatment because
the patient still produces adequate insulin to bring
them periodically down to normal, or "acceptable,"
ranges. If Jim, our Type II diabetic, had received
intensive medical intervention before the beta cells
of his pancreas began to burn out, he would have slimmed
down, brought his blood sugars into line, and eased
the burden on his pancreas. He might even have "cured"
his diabetes by slimming down, as I've seen in several
patients. But many doctors might decide such "mildly"
abnormal blood sugars are only impaired glucose tolerance
(IGT), and do little more than "watch" them.
Again, it's my belief that aggressive treatment at
an early stage can save most patients considerable
lost time and personal agony by preventing complications
that will occur if blood sugar levels are left unchecked.
Such intervention can make subsequent treatment of
what remains—a mild disease—elegantly simple.
On the Horizon
Researchers are
currently trying to perfect a method for cloning,
or replicating, insulin-producing pancreatic beta
cells in the laboratory. Doing this in a fashion that's
comparatively easy and cost effective should not be
an insurmountable task, and indeed the preliminary
results are quite encouraging. Once cells are replicated,
they can be transplanted back into patients to actually
cure their diabetes. After such treatment, unless
you were to have another autoimmune event that would
destroy these new beta cells, you would remain nondiabetic
for the rest of your life. If you had another autoimmune
attack, you would simply have to transplant more cloned
cells. This is the single best opportunity we have
for a cure, immeasurably better than all the electronic
insulin pumps, and the only one I'd personally have
any part of—except I can't.
The catch here for me and
other diabetics who no longer have any insulin-producing
capacity is that the cells from which new beta cells
would be cloned have to be your own, and I have none.
Had I gone on insulin, say, a year before I was diagnosed
with diabetes, or had my blood sugars been immaculately
controlled immediately upon diagnosis, the injected
insulin might have taken much of the strain off my
remaining beta cells and allowed them to survive.
Many people (including
the parents of diabetic children) view having to use
insulin as a last straw, a final admission that they
are (or their child is) a diabetic and seriously ill.
Therefore they will try anything else—including things
that will burn out their remaining beta cells—before
using insulin. Many people in our culture have the
notion that you cannot be well if you are using medication.
This is nonsense, but some patients are so convinced
that they must do things the "natural" way
that I practically have to beg them to use insulin.
In reality, nothing could be more natural. Diabetics
who still have beta cell function left may well be
carrying their own cure around with them—provided
they don't burn it out with high blood sugars and
the refusal to use insulin.
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