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Diabetics die from heart failure at a rate far exceeding that of people with normal glucose tolerance. Heart failure involves a weakening of the cardiac muscle so that it cannot pump enough blood. Most long-term, poorly controlled diabetics have a condition called cardiomyopathy. In diabetic cardiomyopathy, the muscle tissue of the heart is slowly replaced by scar tissue over a period of years. This weakens the muscle so that it eventually "fails." There is no evidence linking cardiomyopathy with dietary fat intake or serum lipids.

A fifteen-year study of 7,038 French policemen in Paris reported that "the earliest marker of a higher risk of coronary heart disease mortality is an elevation of serum insulin level." A study of middle-aged nondiabetic women at the University of Pittsburgh showed an increasing risk of heart disease as serum insulin levels increased. Other studies in nondiabetics have shown strong correlations between serum insulin levels and other predictors of cardiac risk such as hypertension, elevated triglyceride, and low HDL. The importance of elevated serum insulin levels (hyperinsulinemia) as a cause of heart disease and hypertension has taken on such importance that a special symposium on this subject was held at the end of the 1990 annual meeting of the ADA. A report in a subsequent issue of the journal Diabetes Care quite appropriately points out that "there are few available methods of treating diabetes that do not result in systemic hyperinsulinemia" unless the patient is following a low-carbohydrate diet.

Although the AHA and the ADA have been recommending low-fat, high-carbohydrate diets for diabetics for many decades, no one had compared the effects on the same patients of low- versus high-carbohydrate diets until the late 1980s. Independent studies performed in Texas and California demonstrated lower levels of blood sugar and improved blood lipids when patients were put on lower-carbohydrate, high-fat diets. It was also shown that, on average, for every 1 percent increase in HgbA1C (the test for average blood sugar over the prior four months), total serum cholesterol rose 2.2 percent and triglycerides increased 8 percent.

The National Health Examination Follow-Up Survey, which followed 4,710 people, reported in 1990 that "in the instance of total blood cholesterol, we found no evidence in any age-sex group of a risk associated with elevated values." That's right—they found no risk associated directly with elevated total cholesterol. On the same page, this study lists diabetes as by far the single most important risk factor affecting mortality. In males aged 55–64, for example, diabetes was associated with 60 percent greater mortality than smoking and double the mortality associated with high blood pressure.

The evidence is now simply overwhelming that elevated blood sugar is the major cause of the high serum lipid levels among diabetics and, more significantly, the major factor in the high rates of various heart and vascular diseases associated with diabetes. Many diabetics were put on low-fat diets for so many years, and yet these problems didn't stop. It is only logical to look elsewhere, to elevated blood sugar and hyperinsulinemia, for the cause of what kills and disables so many of us.

My personal experience with diabetic patients is very simple. When we reduce dietary carbohydrate, blood sugars improve dramatically. After about two months of improved blood sugars, we repeat our studies of lipid profiles and thrombotic risk factors. In the great majority of cases, I see normalization or improvement of abnormalities. This parallels what happened to me nearly thirty years ago when I abandoned the high-carbohydrate, low-fat diet that I had been following since 1947.*

Why Is Protein Restriction So Common?

By looking at how the kidney functions, one can better understand the relative roles of glucose and protein in kidney failure of diabetes. The kidney filters wastes, glucose, drugs, and other potentially toxic materials from the blood and deposits them into the urine. It is the urine-making organ. A normal kidney contains about 6 million microscopic blood filters, called glomeruli. Figure A-1 illustrates how blood enters a glomerulus through a tiny artery called the incoming arteriole. The arteriole feeds a bundle of tiny vessels called capillaries. The capillaries contain tiny holes or pores that carry a negative electrical charge. The downstream ends of the capillaries merge into an outgoing arteriole, which is narrower than the incoming arteriole. This narrowing results in high fluid pressure when blood flows through the capillary tuft. The high pressure forces some of the water in the blood through the pores of the capillaries. This water dribbles into the capsule surrounding the capillary tuft. The capsule, acting like a funnel, empties the water into a pipelike structure called the tubule. The pores of the capillaries are of such a size that small molecules in the blood, such as glucose and urea, can pass through with the water to form urine. In a normal kidney, large molecules, such as proteins, cannot readily get through the pores. Since most blood proteins carry negative electrical charges, even the smaller proteins in the blood cannot easily get through the pores, because they are repelled by the negative charge on each pore.

The glomerular filtration rate (GFR) is a measure of how much filtering the kidneys perform in a given period of time. Anyone with a high blood sugar and normal kidneys will have an excessively high GFR. This is in part because blood glucose draws water into the bloodstream from the surrounding tissues, thus increasing blood volume, blood pressure, and blood flow through the kidneys. A GFR that is one-and-a-half to two times normal is commonplace in diabetics with high blood sugars prior to the onset of permanent injury to their kidneys. These people may typically have as much glucose in a 24-hour urine collection as the weight of 5 to 50 packets of sugar. According to an Italian study, an increase in blood sugar from 80 mg/dl to 272 mg/dl resulted in an average GFR increase of 40 percent even in diabetics with severe kidney disease. Before we knew about glycosylation of proteins and the other toxic effects of glucose upon blood vessels, it was speculated that the cause of diabetic kidney disease (nephropathy) was this excessive filtration (hyperfiltration).

The metabolism of dietary protein produces waste products such as urea and ammonia, which contain nitrogen. It therefore had been speculated that in order to clear these wastes from the blood, people eating large amounts of protein would have elevated GFRs. As a result, diabetics have been urged to reduce their protein intake to low levels. Studies by an Israeli group, however, of people on high-protein (meat-eating) and very low protein (vegetarian) diets, disclosed no difference in GFR. Furthermore, over many years on these diets, kidney function was unchanged between the two groups. A report from Denmark described a study in which Type I diabetics without discernible kidney disease were put on protein-restricted diets, and experienced a very small change in GFR and no change in other measures of kidney function. These would suggest that the currently prevailing admonition to all diabetics to reduce protein intake is unjustified.

Recent studies on diabetic rats have shown the following: Rats with blood sugars maintained at 250 mg/dl rapidly develop diabetic nephropathy. If their dietary protein is increased, kidney destruction accelerates. Diabetic rats at the same laboratory, with blood sugars maintained at 100 mg/dl, live full lives and never develop nephropathy, no matter how much protein they consume. Diabetic rats with high blood sugars and significant nephropathy have shown total reversal of their kidney disease after blood sugars were normalized for several months.

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