Chapter 1: Diabetes: The Basics / Read It Online!

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Blood Sugars: The Nondiabetic Versus the Diabetic

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.
 
The Nondiabetic
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 diabetic complications.

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 egg.

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 sugar.

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.

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