Archive for the ‘Diabetes’ Category

WHO GETS TYPE II DIABETES?

Wednesday, June 1st, 2011
Type II diabetes occurs in both sexes, but women who have had a lot of children and those who have had unusually large babies seem to face a special risk. People who have relatives with diabetes (especially Type II diabetes) have a greater chance of developing the disease themselves.
Diabetes affects all the peoples of the earth, with a few exceptions: It is extremely rare among Eskimos, for example. In the United States, minority groups seem to be especially hard hit: Type II diabetes, the more common form, occurs about 60 percent more often in blacks than in whites, and its prevalence is also very high among Hispanic populations and certain Native American tribes such as the Pimas and Papagos.
The probability of getting Type II diabetes increases with age. The risk also increases with the amount of excess weight. At least three-quarters of the people who develop diabetes in middle or old age are overweight. Yet not all (or even most) overweight people develop diabetes.
What Goes Wrong
Although Type I diabetes is caused by damage to the beta cells of the pancreas, so that they cannot secrete enough insulin, some people with very serious cases of diabetes have beta cells that look perfectly normal. Tests of their blood show plenty of insulin—more than enough, it would seem, to keep the sugar metabolism running smoothly. Yet they too suffer from hyperglycemia.
High blood sugar could result if the pancreas is producing normal amounts of insulin, but the body’s needs for the hormone become far higher than normal and the gland cannot keep up. This might happen when people overeat to an extreme degree, flooding their bodies with more carbohydrates than their system can handle. (In general, any diet that results in a gain in weight will increase one’s chances of developing diabetes. A diet that causes weight reduction will decrease one’s chance of developing diabetes, or, if it is already present, will make it less severe.)
In some cases of diabetes, the insulin that the pancreas produces does not work properly. This may happen for several reasons. For example, the body normally produces a chemical called insulinase, which breaks down excess insulin when its job is done. If too much insulinase is produced, the insulin will be destroyed before it has had a chance to lower the body’s blood sugar level. Sometimes the body produces antibodies against insulin, in much the same way it makes them against disease germs. These anti-insulin antibodies may attack insulin or attach themselves to its molecules so that the hormone cannot work on the cells. Certain drugs, including cortisone, prednisone, contraceptive pills, nicotinic acid, and some diuretics (drugs that are used to rid the body of excess fluids), can interfere with the action of insulin.
Diabetes may also result from hormone disorders, in which the body produces too much glucagon or too much of another pancreatic hormone called somatostatin. This hormone, secreted by the delta cells in the islets, helps to regulate the secretion of both glucagon and insulin.
In non-insulin-dependent diabetes, insulin may not be able to allow glucose to pass into the cells effectively because something is wrong with the outer surface of the cells. Researchers have found that insulin normally reacts with specific chemicals, called receptors, on the cells’ outer membranes. If there are not enough of these receptors, or if they become less receptive to insulin, the hormone will not be able to help glucose get into the cells. This condition is called insulin resistance.
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WHAT CAUSES DIABETES: A VIRAL CAUSE?

Monday, April 11th, 2011
In 1864, a Norwegian scientist reported that a patient developed diabetes after getting the mumps. Since then, more evidence has been found to link Type I diabetes with infectious diseases. Medical workers have noticed that diabetes in children, normally a rather rare disease (though it is growing ever more common), tends to occur in clusters. A number of cases will suddenly crop up in a particular area, and these outbreaks sometimes follow an epidemic of a viral disease, such as mumps or rubella (German measles). Coxsackie viruses (common viruses that can cause colds and intestinal infection) have also been implicated.
New cases of Type I diabetes seem to occur seasonally: most in the autumn and winter and least in the summer and spring—just like the incidence of many viral diseases. In some cases, diabetes “epidemics” follow virus epidemics closely; in others, there is a period of about three or four years between the outbreak of the viral disease and the appearance of diabetes symptoms.
Of course, it might be that the extra stress of the viral disease is just too much for a person who happens to have a weak pancreas, and the gland breaks down when the body is besieged by the disease germs. But researchers began to wonder whether the viral illness might actually damage the pancreas. Viruses might invade the pancreas and destroy the beta cells. Or there might be a more indirect effect, involving a mistaken attack by the body’s own defenses. The virus particles might happen to be chemically similar to part of the surface of the beta cells. (This kind of accidental similarity of environmental proteins to body biochemicals is called molecular mimicry.) Then antibodies produced by the body to attack the viruses would also attack and destroy beta cells. In any case, as beta cells are destroyed, the amount of insulin produced is greatly reduced. When 80 to 90 percent of the beta cells have been destroyed, the symptoms of diabetes develop quite suddenly.
There is a good deal of evidence to support the molecular mimicry theory. People with insulin-dependent diabetes usually make little or no insulin, and examinations of tissue from their pancreases show that beta cells have indeed been destroyed. Antibodies against these cells can be found circulating in the blood of a person with Type I diabetes. In fact, antibodies against one beta cell substance (glutamic acid decarboxylase, or GAD) may appear years before diabetes develops. Now researchers have confirmed that GAD is remarkably similar to a protein of the Coxsackie viruses.
All children catch viral diseases, usually quite a number of them during the growing years. Yet most children don’t develop diabetes. What determines that a virus infection will cause diabetes in one child, while another child will suffer the same infection and recover with full health?
If insulin-dependent diabetes is indeed an autoimmune disease—one in which the body makes antibodies against a virus that will also attack its own body cells—then a child who does not develop diabetes after a virus infection may just have been lucky enough not to produce those destructive antibodies. Each person produces his or her own unique antibodies against any particular germ or chemical. So some children may produce antibodies that simply cure them of the viral infection without affecting the pancreas.
Another possibility is that a person may inherit a pancreas or an immune system that is particularly susceptible to molecular mimicry. Researchers have found that most people with Type I diabetes have specific types of chemicals on the surfaces of their beta cells that are not usually found in other people. These cell-surface chemicals, which are hereditary, might be the chemicals against which a person’s body makes antibodies when viruses attack. (In Type II diabetes, this sort of correlation with special cell-surface chemicals is not seen.)
Although viruses may be implicated in Type I diabetes, this does not mean that diabetes is a contagious disease, like colds or mumps or TB. There is no “diabetes virus,” and you can’t catch diabetes by talking to, touching, or even kissing someone who has diabetes.
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SUMMARY OF INTENSIVE MANAGEMENT OF TYPE 1 DIABETES: SPECIAL ISSUES – ASPIRIN & FLOW SHEET

Saturday, February 19th, 2011

Aspirin
Aspirin therapy is indicated for some but not all patients with type 1 diabetes. There are limited data about people under age 30, and Reye’s syndrome can be an issue in younger patients. However, type 1 diabetic patients age 30 or older who are at high risk for cardiovascular events are candidates for aspirin therapy. High-risk patients are defined as those with strong family history of coronary heart disease, cigarette use, hypertension, albuminuria, BMI > 27 kg/m2, or altered lipid/lipoprotein profile (mg/dl: cholesterol > 200, LDL-C > 100, triglycerides > 150, and/or HDL-C < 45 (men) or < 55 (women). Many patients have hypertension and/or indicators of diabetic nephropathy.
Flow Sheet
Every type 1 diabetic patient who is under intensive management for glycemia and other micro- and macrovascular risk factors should have a serial flow sheet. Computerized systems are available. Reference to the flow sheet before and during patient visits is an effective way to keep preventive management and the regular evaluations current. The flow sheet is also an excellent tool for discussing with each patient the goals of therapy, their rationale, and the success in achieving them.
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SUGAR SUBSTITUTES AND DIABETES

Saturday, February 12th, 2011

Some doctors feel that people with diabetes shouldn’t use sugar substitutes because they simply maintain their “sweet tooth.” If the patients tried eating a more sensible diet, these doctors say, they would soon lose their taste for rich, sweet foods, and that would be a good thing. But some people feel that life just wouldn’t be worth living if they couldn’t have candy, a soft drink, or some other sweet-tasting treat at least occasionally. And some doctors feel that sugar substitutes are good because they permit people with diabetes, especially young ones, to enjoy some of the same treats as their friends, which can help them feel less “different.”
Nutritive sweeteners contain calories, and are usually carbohydrates that end in -ose, such as glucose, fructose, dextrose, and sucrose (sugars), or -ol, such as sorbitol and mannitol (sugar alcohols). They each contain four calories per gram.
Non-nutritive sweeteners provide almost no calories and do not affect blood glucose levels. Saccharin and aspartame (sold under the brand name NutraSweet) are the two major sugar substitutes. Aspartame actually contains the same four calories per gram as do the nutritive sweeteners; however, because it is 180 times sweeter than table sugar, much less has to be used. Saccharin is 300 times sweeter than sucrose and has no calories at all.
Dietetic foods are not necessarily good for people with diabetes. Some contain nutritive sweeteners such as fructose and sorbitol that need to be carefully monitored.
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THE CARBOHYDRATE ADDICT’S DIET: PLANNING AHEAD (MATTHEW’S STORY)

Saturday, December 11th, 2010

When Matthew P. came to us, we knew already he was a busy man. He’d called from his car phone to make an appointment, and despite a certain urgency in his voice, he had told us that he couldn’t fit in a meeting with us for two weeks. His schedule was too jammed.
Matthew’s easy manner upon meeting him came as a surprise. He was a finance attorney whose rugged good looks and solid build would have fit a man in a more physical line of work. But the extra pounds (perhaps twenty-five) he was carrying were unmistakable.
He told us a good deal about himself (he’d struggled with his weight much of his life), his job (his work kept him on the road a great deal), and his family (his father was very much overweight: “His doctor says it’s killing him”). And he confided in us his fear that his own eating and weight would get truly out of control.
We tested Matthew, and he proved to be a moderate carbohydrate addict. We recommended that he follow the diet, and he agreed. When we explained to him how the diet works, he did express one concern.
His worry was how to fit low-carbohydrate lunches into his hectic business schedule. He had several meetings a week that took the form of business lunches, and the times and places were often chosen by other people. As he described the problem, we felt that he wanted us to allow him to be an exception to the rules—but of course we could not.
We reminded him that his primary concerns had to be with his weight, his eating control, and his addiction. Matthew rose to the challenge.
“Certainly,” he decided then and there, “I know I can work this out if I really want to.”
At our next appointment, a relaxed Matthew appeared. He began telling of his triumphs while we were still walking through the halls into our office.
“I did it,” he said, beaming. “It was really terrific. It wasn’t as hard as I thought. Except for one time, I didn’t have any trouble.”
He had devised a series of sensible strategies. He would call ahead to the people with whom he was to meet and suggest restaurants in which he knew he would be able to get a tasty Low-Carbohydrate Meal. For a meeting in another city in which he knew of no restaurant, Matthew called ahead and asked his host if they might meet at a Japanese restaurant. He knew that there he could get a meal of simple protein (chicken, beef, or fish) and plain vegetables (no rice). Sometimes he would suggest that they have a seafood lunch so that he could enjoy shrimp or lobster or the catch of the day—and a large salad.
Matthew proved even more resourceful and was really enjoying being in control. At one conference lunch, he told us, everyone was served the same casserole dish, one in which the foods—including some that were rich in carbohydrates—were mixed together. Matthew ate his salad, drank a diet soda, and then excused himself. He went down the street, found a fast-food restaurant, and ordered another diet soda and two hamburgers with cheese. He removed the buns and completed his Low-Carbohydrate Meal. He said that he felt great. Then he returned to the conference and enjoyed a cup of coffee knowing that his Reward Meal was coming later that evening.
Matthew used his wits to stay on his eating plan. He didn’t allow himself to be bullied by circumstance.
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WHY IS THE G.I. FACTOR RELEVANT TO SPORTING PERFORMANCE?

Friday, May 8th, 2009

The G.I. Factor ranks foods on the basis of their measured blood sugar response to a specific food. The rate at which glucose enters the bloodstream affects the insulin response to that food and ultimately affects the fuels available to the exercising muscles. There are times when low G.I. Foods provide an advantage and times when high G.I. Foods are better. For best performance, a serious athlete needs to learn about which foods have high and low G.I. factors and when to eat them.

High G.I. Factor foods like potatoes will produce a rapid increase in glucose and insulin levels, something which is not desirable just before a race when glycogen stores should already be fully charged. Low G.I. Foods, such as pasta, which are digested and absorbed much more slowly, are able to provide glucose to the working muscle towards the end of exercise when glycogen stores are running low. They can be likened to a continuous injection of glucose during the event. This can boost energy when fatigue begins to set in. After the event, high G.I. Foods are best because they stimulate more insulin, the hormone responsible for putting glycogen back into the muscles.

Manipulating the G.I. Of your diet can give you the winning edge!

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