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Diabetes: The Basics

Type 2 diabetes is, at the beginning, a less serious disease—patients don’t melt away into sugar water and die in a few months’ time. Type 2, however, can through chronically but less dramatically elevated blood sugars be much more insidious. Because so many more people are affected, it probably causes more heart attacks, strokes, and amputations than the more serious type 1 disease. Type 2 is a major cause of hypertension, heart disease, kidney failure, blindness, and erectile dysfunction. That these serious complications of type 2 diabetes can progress is no doubt because it is initially milder and is often left untreated or treated more poorly.

Individuals with type 2 still make insulin, and most will never require injected insulin to survive, though if the disease is treated poorly, they can eventually burn out their pancreatic beta cells and require insulin shots. Because of their resistance to the blood sugar– lowering effects of insulin (though not its fat-building effects), many overweight type 2 diabetics actually make more insulin than slim nondiabetics.

* A common early sign of mild chronic blood sugar elevation in women is recurrent vaginal yeast infections that cause itching or burning.


Since high blood sugar is the hallmark of diabetes, and the cause of every long-term complication of the disease, it makes sense to discuss where blood sugar comes from and how it is used and not used.

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 or sensitivity to these neurotransmitters, the chemical messengers with which the brain communicates with itself and the rest of the body. When blood sugar levels are low, the liver, kidneys, and intestines 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 steak or fish instead of cookies. Dietary 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 most type 2 diabetics, the pancreas constantly releases a steady, low level of insulin. This baseline, or basal, insulin level prevents the liver, kidneys, and intestines 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 160 mg/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 considered “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 may 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 of 140 mg/dl is a good candidate for full-blown type 2 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 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 certain enzymes in 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 Jane eats her boiled egg, the small amount of insulin of phase II can cover the glucose that, over a period of hours, is 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 movement of glucose“transporters” within the cells. These specialized protein molecules protrude from the cytoplasm of the cells and their surfaces to grab glucose from the blood and bring it to the interiors of the cells. Once inside the cells, glucose can be utilized to power energy requiring functions. Without insulin, the cells can absorb only a very
small amount of glucose, not enough to sustain the body.

As glucose continues to enter Jane’s blood, 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 slightly 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 safe 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 1 or type 2 diabetic.

The Type 1 Diabetic

Let’s look at what would happen to me, a type 1 diabetic, if I had the same breakfast as Jane, our nondiabetic.

Unlike Jane, because of a condition peculiar to diabetics, if I take a long-acting insulin at bedtime, I might awaken with a normal blood sugar, 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 the level of my previously injected insulin 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 offset the increased insulin 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 use injected insulin 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 would begin to rise. Even if the toast had no jelly, the enzymes in my saliva and intestines and acid in my stomach would begin to transform the toast rapidly into glucose shortly after 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 my 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 do so over many years. The natural question is, wouldn’t injected insulin “cover” the carbohydrate in such a breakfast? Not adequately! This is a common misconception— even by those in the health care professions. Injected insulin— even with an insulin pump—doesn’t work the same as insulin created naturally in the body. Conventional insulin therapy resulting in high blood sugar after meals is a guaranteed incremental, “silent” death from the ravages of diabetic complications.

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 20 minutes, but its full effect is drawn out over a number of hours, not nearly fast enough to prevent a damaging upswing in blood sugars if fast-acting carbohydrate, like bread, is consumed.

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Quick Reference
This quick index helps you zoom in on chapter/article references dealing with a symptom or complication of diabetes. There may be other references throughout the site; always read the paragraphs or pages surrounding the reference in order to obtain proper context. A key to abbreviations is featured at the bottom of the chart.

amputation Ch.1
anemia B&A
arm pain B&A
arthritis B&A
cardiomyopathy /
cardiovascular disease
50yrs Ch.1 AppA 
cardiac neuropathy B&A B&A
cataracts / blindness 50yrs Ch.1 Ch.1 Ch.1 B&A App.A Articles
convulsions B&A
diarrhea, chronic Articles Articles
digestive problems B&A
erectile dysfunction (impotence) Ch.1 B&A B&A Ch.23
fatigue / fainting B&A B&A
feet, general App.E Articles Articles
feet, altered gait B&A Articles
feet, deformity 50yrs
feet, neuropathy B&A B&A B&A Ch.23 Articles Articles
feet, numbness B&A B&A
feet, pain Ch.1 B&A B&A
feet, scaly B&A
feet, ulcers B&A Articles
flatulence B&A
frozen shoulder 50yrs Ch.1
glaucoma B&A Articles
gluconeogenesis Ch.1
hand numbness B&A 
heart attack / blood clots Ch.1 App.A
headaches B&A
heart / arterial disease B&A B&A App.A
heartburn / belching / gastroparesis B&A Articles Articles
high cholesterol 50yrs B&A
hypertension / high blood pressure Ch.1 App.A App.A Ch.23 Articles Articles
hyperglycemia Ch.9
hyperinsulinemia Ch.1
hypoglycemia 50yrs 50yrs B&A B&A B&A Ch.1 Ch.9 Articles Articles Articles
ilio-tibial band/tensor fascia lata syndrome 50yrs
impaired glucose tolerance (IGT) Ch.1
joint inflammation / tightness Ch.1
ketoacidosis 50yrs B&A Articles Articles
kidney stones / kidney disease / nephropathy / infections 50yrs Ch.1 B&A B&A B&A B&A App.A App.A App.A Ch.9 Articles
leg pain B&A
macular edema 50yrs
microaneurysms 50yrs 50yrs
mood changes B&A
night blindness 50yrs
nerve damage Ch.1 Ch.1
obesity / weight gain B&A B&A B&A B&A  Ch.1 Ch.1 Ch.12 Articles
osteoporosis Ch.1
periodontal disease  Articles
peripheral vascular disease 50yrs
proteinuria 50yrs 50yrs
retinopathy Ch.1 B&A
salivary duct stones 50yrs
short-term memory loss / loss of mental activity  B&A Articles
skin tightness / skin conditions Ch.1 B&A
sleepiness B&A
sweating B&A B&A
thirst B&A
twitching limbs B&A
ulcers B&A
vision changes / diseases B&A B&A B&A B&A Ch.23 Articles Articles Articles

50yrs: "My First 50 Years as a Diabetic"
B&A: "Before & After: 14 Patients Share Their Experiences"
Ch.1: "Chapter 1", etc.
App.A: "Appendix A", etc.
Articles: References an item in the "Articles" section of the site.

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