Diabetes: The Basics
This is the central problem for type 1 diabetics—the carbohydrate and
the drastic surge it causes in blood sugar. Because I know my body produces
no insulin, I have a shot of insulin before every meal. But I no longer
eat meals with fast-acting or large amounts of carbohydrate, because
the blood sugar swings they caused were what brought about my long-term
complications. Even injection by means of an insulin pump (see discussion
at the end of Chapter 19) cannot automatically fine-tune the level of
glucose in my blood the way a nondiabetic’s body does naturally.
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 small dose of insulin could
act quickly 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 (only the slow-acting
kind) and injected insulin that I use.
The Type 2 Diabetic
Let’s say Jim, a type 2 diabetic, is 6 feet tall and weighs 300 pounds,
much of which is centered around his midsection. Remember, at least
80 percent of type 2 diabetics are overweight. If Jim weighed only 170
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 overweight tend to be insulin-resistant as a group, a condition
that’s not only hereditary but also directly related to the ratio of
visceral and total body fat to lean body mass (muscle). The higher this
ratio, the more insulin-resistant a person will be. Whether or not an
overweight 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 less insulin than nonathletes.
An overweight type 2 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, his ability to store insulin is diminished
or gone, and his phase I insulin response is attenuated. Despite his
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. On examination, however,
most of these very obese “nondiabetics” have slight elevations of their
HgbA1C test for average blood sugar.)
Let’s take another look at that mixed breakfast and see how it affects
a type 2 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 may be 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
begins to rise. Unlike mine, Jim’s pancreas eventually 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 partially
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 centers
in the brain responsible for feeding behavior. Thus, in all likelihood,
Jim will grow even more overweight, as demonstrated by the cycle illustrated
in Figure 1-1.
Since he’s resistant to insulin, his pancreas has to work that much
harder to produce insulin to enable him to utilize 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 continues to rise, since his cells are unable to utilize all of
the glucose derived from his meal. 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 a few 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 (after-eating) blood sugar levels that I would call unacceptably
high—140 mg/dl, or even 200 mg/dl—may be considered by other physicians
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 2 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 can remain—a mild disease—elegantly
simple.-
* Waking, or fasting, blood sugars are frequently normal in mild type
2 diabetics. After they eat carbohydrate, however, their postprandial
blood sugars are usually elevated. † Beta cell burnout can be caused
both by overactivity of the cells and by the toxicity of high glucose
levels.
ON THE HORIZON
I include some hopeful forecasts of future treatments in this first
chapter because as you’re learning how to control your diabetes, hope
is a valuable asset. But your hope should be realistic. Your best hope
for controlling your diabetes is normalizing your blood sugars now.
That does not mean that the future will not bring great things. Diabetes
research progresses on a daily basis, and I hope as much as you do for
a cure, but it’s still on the horizon.
Researchers are currently trying to perfect methods for 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 patients’ 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, at least in theory, remain nondiabetic
for the rest of your life. If you had another autoimmune attack, you
would simply have to receive more of your replicated cells. Another
very hopeful approach currently undergoing clinical trials in humans
is the transformation of the precursors of beta cells (the cells that
line the ducts of the pancreas) into actual beta cells without even
removing them from your body. This apparently can be achieved by the
simple intramuscular injection of a special protein and is now being
tested for adverse effects at three centers.
Another potential approach might be to insert the genes for insulin
production into liver or kidney cells. These are potential opportunities
for a cure, and have successfully cured diabetes in rats, but there
are still obstacles to overcome.
Yet another approach to replacing lost beta cells has been used by
two competing companies to cure diabetes in animals. The technique involves
a series of ordinary injections of proteins that stimulate the remaining
beta cells to replicate until the lost ones have been replaced. With
respect to the replication of beta cells, the catch for me and other
diabetics who no longer have any insulin-producing capacity is that
the cells from which new beta cells would be replicated ideally should
be your own, and I have none. Had my diabetes been diagnosed, say, a
year earlier, 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, which is as
“natural” as one can go. 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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