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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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Dietary factors in inflammation and autoimmune disease
From Townsend Letter for Doctors and Patients, 5/1/04 by Alan R. Gaby

A growing body of evidence suggests that diet plays an important role in the pathogenesis of autoimmune diseases and other chronic inflammatory conditions. In my experience, dietary modification alone can produce marked clinical improvement in some cases. While we still have a long way to go before this diet-disease connection can be considered "proven," there is reason to believe that a few basic dietary changes have great potential, not only to ameliorate autoimmune disease and chronic inflammation, but to improve overall health, as well.

Identify and avoid allergenic foods

The absorption of antigens from foods may result in the production of antibodies that cross-react with specific tissues, resulting in an autoimmune or inflammatory reaction. Disorders with an autoimmune or inflammatory component that have been reported to be relieved by the avoidance of allergenic foods include rheumatoid arthritis, inflammatory bowel disease, migraine, systemic lupus erythematosus, hypertension, multiple sclerosis, asthma, perennial allergic rhinitis, atopic dermatitis, thrombophlebitis, nephrotic syndrome, chronic bronchitis, and aphthous ulceration. Although there is no universally reliable test for food allergies, I have successfully used an elimination diet, followed by individual food challenges, with more than 1,500 patients.

Avoid excessive consumption of fructose

While fructose is touted as a safe alternative to sucrose because it causes little or no increase in blood-glucose levels, it has a definite downside. Fructose is the most potent reducing sugar in the human diet (lactose and glucose are the other, less potent, reducing sugars) and, as such, is capable of interacting with the amino acid side chains of tissue proteins, in a chemical reaction known as glycation (or fructosylation). The glycation of proteins can alter their function (for example, a glycated trypsin molecule might lose some of its antiinflammatory activity). In addition, glycation changes the structure of proteins, which can cause them to be recognized by the immune system as "foreign" and to be subjected to autoimmune attack. Moreover, glycated proteins have been implicated in the pathogenesis of atherosclerosis and in the end-organ damage seen in diabetics. To the extent that dietary fructose makes its way into the body intact, it is capable of promoting these undesirable effects via its enhancement of glycation reactions. Fortunately, most orally ingested fructose is converted to glucose in the intestinal wall or in the liver before it reaches the general circulation. Consumption of very large amounts of fructose, however (as one would obtain from a large soft drink or from other gluttonous imbibements or repasts), overwhelms the body's fructose-metabolizing capacity, resulting in the spillage of fructose into the bloodstream. In addition to its possible adverse effects on autoimmune disease and inflammation, consumption of large amounts of fructose has been shown to accelerate the aging process in laboratory animals.

Avoid dietary sources of advanced glycation endproducts (AGEs)

AGEs are irreversible products of glycation that form during the heating of common foods. They result from reactions between "reducing sugars" (e.g., fructose, glucose, or lactose), which occur naturally in or are added to food, and proteins or lipids. The amount of AGEs produced increases with higher cooking temperature and duration of cooking; consequently, overcooked food tends to contain large amounts of these toxic compounds. In contrast to AGEs formed in vivo, dietary AGEs form much more rapidly in the presence of heat and in far greater concentrations. A substantial amount of dietary AGEs is absorbed and persists in tissues in reactive forms. As with endogenously formed AGEs, those derived from the diet have the potential to evoke an immune or inflammatory response in the body and have been implicated in the pathogenesis of atherosclerosis and diabetic end-organ damage.

In a recent study, a group of diabetic patients consumed one of two diets for six weeks. The diets contained similar amounts of protein, carbohydrate, and fat, but differed by approximately five-fold in AGE content, which was achieved by varying the cooking time and temperature. (1) After six weeks, the mean concentration of C-reactive protein (a marker of inflammation) increased by 35% relative to baseline on the high-AGE diet and decreased by 20% relative to baseline on the low-AGE diet (p < 0.02 for the difference between groups). Other inflammatory mediators also increased on the high- and decreased on the low-AGE diet, respectively. Changes in the levels of inflammatory markers paralleled changes in the serum concentration of AGEs. These results suggest that excessive heating of food results in the formation of AGEs, which in turn evokes an inflammatory response


Other studies have suggested that eating a raw-food diet can reduce the severity of inflammation in conditions such as rheumatoid arthritis. According to one report, some foods become allergenic only after they have undergone glycation as a result of cooking. While eating only raw foods is not practical for most individuals, avoiding overcooked foods is certainly a good start. At restaurants I always ask that my steak be cooked midway between E. coli and heterocyclic amines.

The presence of a reducing sugar greatly increases the formation of AGEs during the heating of food. Thus, a pastry, pie, cake, doughnut, funnelcake, cookie, cracker, pot pie, or piece of bread that is sweetened with high-fructose corn syrup would be expected to contain large amounts of AGEs, particularly if baked at a high temperature. Baking with sucrose (which is not a reducing sugar) in the presence of yeast may also promote the formation of AGEs, because sucrose is converted to glucose and fructose during fermentation by the yeast. In addition, cooking with milk might cause similar problems, as the lactose present in milk is a reducing sugar.

Other factors

Various micronutrients in the diet may also influence the inflammatory response. There is some evidence that arachidonic acid, which is present in meat, is pro-inflammatory. In contrast, long-chain omega-3 fatty acids found in fish and fish oil are anti-inflammatory. Omega-6 fatty acids have been reported to exert both pro- and anti-inflammatory effects. Nutrients such as vitamin C, vitamin E, vitamin B6, magnesium, selenium, zinc, and copper have anti-inflammatory activity.


The importance of food allergy as a factor in autoimmune and inflammatory disorders has repeatedly been demonstrated in published (albeit usually uncontrolled) studies and in the clinical experience of many practitioners. While the evidence implicating the other factors mentioned above is largely circumstantial, it seems logical to avoid becoming petrified and calcified by advanced glycation endproducts (i.e., don't become a rock of AGEs).


1. 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.

Alan R. Gaby, MD

COPYRIGHT 2004 The Townsend Letter Group
COPYRIGHT 2004 Gale Group

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