1: Diabetes: The Basics /
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Blood Sugars: The Nondiabetic
Versus the Diabetic
Our dietary sources
of blood sugar are carbohydrates and proteins. One
reason the taste of sugar—a simple form of carbohydrate—delights
us is that it fosters production of neurotransmitters
in the brain that relieve anxiety and can create a
sense of well-being, or even euphoria. This makes
carbohydrate quite addictive to certain people whose
brains may have inadequate levels of these neurotransmitters,
the chemical messengers with which the brain communicates
with itself and the rest of the body, or peripheral
nervous system. When blood sugar levels are low, the
liver can, through a process we will discuss shortly,
convert proteins into glucose, but very slowly and
inefficiently. The body cannot convert glucose back
into protein, nor can it convert fat into sugar. Fat
cells, however, with the help of insulin, do transform
glucose into fat.
The taste of protein doesn't
excite us as much as that of carbohydrate—it would
be the very unusual child who'd jump up and down in
the grocery store and beg his mother for a steak instead
of cookies. Protein gives us a much slower and smaller
blood sugar effect, which, as you will see, we diabetics
can use to our advantage in normalizing blood sugars.
In the fasting nondiabetic, and even in some Type
II diabetics, the pancreas constantly releases a steady,
low level of insulin. This baseline, or basal, insulin
level prevents the liver from inappropriately converting
bodily proteins (muscle, vital organs) into glucose
and thereby raising blood sugar, a process known as
gluconeogenesis. The nondiabetic ordinarily maintains
blood sugar immaculately within a narrow range—usually
between 80 and 100 mg/dl (milligrams per deciliter),*
with most people hovering near 85 mg/dl.* There are
times when that range can briefly stretch up or down—as
high as 160mg/dl and as low as 65—but generally, for
the nondiabetic, such swings are rare.
You will note that in some
literature on diabetes, "normal" may be
defined as 60–120 mg/dl, or even as high as 140 mg/dl.
This "normal" is entirely relative. No nondiabetic
will have blood sugar levels as high as 140 mg/dl
except after consuming a lot of carbohydrate. "Normal"
in this case has more to do with what is cost-effective
for the average physician to treat. Since a postmeal
(postprandial) blood sugar under 140 mg/dl is not
classified as diabetes, and since the individual who
experiences such a value will usually still have adequate
insulin production eventually to bring it down to
reasonable levels, many physicians would see no reason
for treatment. Such an individual will be sent off
with the admonition to watch his weight or her sugar
intake. Despite the designation "normal,"
an individual frequently displaying a blood sugar
level of 140 mg/dl is a good candidate for full-blown
Type II diabetes. I have seen "nondiabetics"
with sustained blood sugars averaging 120 mg/dl develop
Let's take a look at how
the average nondiabetic body makes and uses insulin.
Suppose that Jane, a nondiabetic, arises in the morning
and has a mixed breakfast, that is, one that contains
both carbohydrate and protein. On the carbohydrate
side, she has toast with jelly and a glass of orange
juice; on the protein side, she has a boiled egg.
Her basal (i.e., before-meals) insulin secretion has
kept her blood sugar level steady during the night,
inhibiting gluconeogenesis. Shortly after the sugar
in the juice or jelly hits her mouth, or the starchy
carbohydrates in the toast reach her saliva, glucose
begins to enter her bloodstream. The rise in Jane's
blood sugar is a chemical signal to her pancreas to
release the granules of insulin it has stored in order
to prevent a jump in blood sugar (see Figure
1-2). This rapid release of stored
insulin is called phase I insulin response. It quickly
corrects the initial blood sugar increase and can
prevent further increase from the ingested carbohydrate.
As the pancreas runs out of stored insulin, it manufactures
more, but it has to do so from scratch. The insulin
released now is known as the phase II insulin response,
and it's secreted much more slowly. As she eats her
boiled egg, the insulin of phase II can cover the
sugar that's slowly produced from the protein of the
Insulin acts in the nondiabetic
as the means to admit glucose—fuel—into the cells.
It does this by activating the production of glucose
"transporters" within the cells. These specialized
protein molecules emerge from the nuclei of the cells
to grab glucose from the blood and bring it to the
interiors of the cells. Once inside the cell, glucose
can be utilized to power energy-requiring functions.
Without insulin, the cells can absorb only a very
small amount of sugar, not enough to sustain the body.
As Jane's blood continues
to accumulate sugar, and the beta cells in her pancreas
continue to release insulin, some of her blood sugar
is transformed to glycogen, a starchy substance stored
in the muscles and liver. Once glycogen storage sites
in the muscles and liver are filled, excess glucose
remaining in the bloodstream is converted to and stored
as fat. Later, as lunchtime nears but before Jane
eats, if her blood sugar drops too low, the alpha
cells of her pancreas will release another pancreatic
hormone, glucagon, which will "instruct"
her liver and muscles to begin converting glycogen
to glucose, to raise blood sugar. When she eats again,
her store of glycogen will be replenished.
This pattern of basal,
phase I, then phase II insulin secretion is perfect
for keeping Jane's blood glucose levels in a healthy
range. Her body is nourished, and things work according
to design. Her mixed meal is handled beautifully.
This is not, however, how things work for either the
Type I or Type II diabetic.
The Type I Diabetic
Let's look at what would happen to me, a Type I diabetic,
if I had the same breakfast as Jane, our nondiabetic.
Unlike Jane, because of
a condition peculiar to diabetics, if I take insulin,
I might awaken with normal blood sugar levels, but
if I spend some time awake before breakfast, my blood
sugar may rise, even if I haven't had anything to
eat. Ordinarily, the liver is constantly removing
some insulin from the bloodstream, but during the
first few hours after waking from a full night's sleep,
it clears insulin out of the blood at an accelerated
rate. This dip in insulin level is called the dawn
phenomenon (see Chapter 6, "Strange Biology").
Because of it, my blood glucose can rise even though
I haven't eaten. A nondiabetic just makes more insulin
to take care of the increased clearance. Those of
us who are severely diabetic have to track the dawn
phenomenon carefully by monitoring blood glucose levels,
and can learn how to prevent its effect upon blood
As with Jane, the minute
the meal hits my mouth, the enzymes in my saliva begin
to break down the sugars in the toast and juice, and
almost immediately my blood sugar begins to rise.
Even if the toast had no jelly, the enzymes in my
saliva and stomach would begin to rapidly transform
the toast into glucose upon ingestion.
Since my beta cells have
completely ceased functioning, there is no stored
insulin to be released by my pancreas, so I have no
phase I insulin response. My blood sugar (in the absence
of injected insulin) will rise while I digest my meal.
None of the glucose will be converted to fat, nor
will any be converted to glycogen. Eventually much
will be filtered out by the kidneys and passed out
through the urine, but not before my body has endured
damagingly high blood sugar levels—which won't kill
me on the spot but will over the years be an incremental
step in the slow, "silent" death from diabetic
complications. The natural question is, wouldn't injected
insulin "cover" the carbohydrate in such
a breakfast? No. This is a common misconception—even
by those in the health care profession. Normal phase
I insulin is almost instantly in the bloodstream.
Rapidly it begins to hustle blood sugar off to where
it's needed. Injected insulin, on the other hand,
is injected either into fat or muscle (not into a
vein) and absorbed slowly. The fastest insulin we
have, lispro, starts to work in about 15 minutes,
but that isn't fast enough to prevent a damaging upswing
in blood sugars if fast-acting carbohydrate, like
bread, is consumed.
This is the central problem
for Type I 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 complications. Even injection by means of
an insulin pump (see discussion at the end of Chapter
18) cannot fine-tune the level of glucose in my blood
the way a nondiabetic's body does naturally.