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Diabetic angiopathy

Angiopathy is the generic term for a disease of the blood vessels (arteries, veins, and capillaries). The best known and most prevalent angiopathy is the diabetic angiopathy, a complication that may occur in chronic diabetes. more...

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There are two types of angiopathy: macroangiopathy and microangiopathy. In macroangiopathy, fat and blood clots build up in the large blood vessels, stick to the vessel walls, and block the flow of blood. In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body. The decrease of blood flow through stenosis or clot formation impair the flow of oxygen to cells and biological tissues (called ischemia) and lead to their death (necrosis and gangrene, which in turn may require amputation). Thus, tissues which are very sensitive to oxygen levels, such as the retina, develop microangiopathy and may cause blindness (so-called proliferative diabetic retinopathy). Damage to nerve cells may cause peripheral neuropathy, and to kidney cells, diabetic nephropathy (Kimmelstiel-Wilson syndrome).

Macroangiopathy, on the other hand, may cause other complications, such as ischemic heart disease, stroke and peripheral vascular disease which contributes to the diabetic foot ulcers and the risk of amputation.

Diabetes mellitus is the most common cause of adult kidney failure worldwide. It also the most common cause of amputation in the US, usually toes and feet, often as a result of gangrene, and almost always as a result of peripheral vascular disease. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US.

"Diabetic dermopathy" is a manifestation of diabetic angiopathy. It is often found on the shin.

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More on diet and C-reactive protein
From Townsend Letter for Doctors and Patients, 5/1/05 by Alan R. Gaby

Eleven patients with diabetes participated in a crossover study (2 weeks on each of 2 different diets), and 13 other patients with diabetes participated in a 6-week randomized trial of the same diets. The two diets had a similar content of protein, carbohydrate, and fat, but differed by approximately five-fold in their content of advanced glycation endproducts (AGEs), which was achieved by varying the cooking time and temperature. After two weeks on the high-AGE diet, the serum concentration of AGEs increased by 64.5% (p = 0.02) and on the low-AGE diet decreased by 30% (p = 0.02); the values at six weeks were +28.2% (p = 0.06) and -40% (p = 0.02), respectively. After six weeks, the mean C-reactive protein concentration increased by 35% relative to baseline on the high-AGE diet and decreased by 20% relative to baseline on the low-AGE diet (p = 0.014).

Comment: AGEs form during the heating of common foods. They result from reactions between reducing sugars and proteins or lipids. In contrast to the AGEs that are formed in vivo, dietary AGEs form much more rapidly in the presence of heat and in far greater concentrations. The infusion of AGEs into rabbits results in the formation of atheroma-like lesions. Approximately 10% of ingested AGEs are absorbed; of that 10%, two-thirds is retained in tissues in reactive forms. The results of the present study suggest that dietary AGEs (or some other substances that are formed along with AGEs during cooking) cause an inflammatory reaction in the body, and may contribute to the pathogenesis of cardiovascular disease.

The formation of AGEs in foods can be minimized by emphasizing certain methods of cooking (e.g., boiling or poaching, as opposed to grilling or frying). In addition, heating a protein in the presence of a reducing sugar (fructose, lactose, or glucose) accelerates the formation of AGEs. Eating as many raw foods as possible is probably the best way to reduce the AGE content of the diet. For additional information on the AGE content of foods, see J Am Diet Assoc 2004;104:1287-1291.

Vlassara H, et al. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. Proc Natl Acad Sci 2002;99:15596-15601.

COPYRIGHT 2005 The Townsend Letter Group
COPYRIGHT 2005 Gale Group

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