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From the Townsend Letter
July 2015

How Your Food Is Cooked May Affect Your Health

by Alan R. Gaby, MD

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Considering that we existed before we discovered fire, it would be reasonable to assume that humans were designed to subsist on raw foods. There is evidence that consuming more raw foods can have various health benefits, including improvements in hypertension, rheumatoid arthritis, and fibromyalgia; a reduction in inflammation; and an increase in antioxidant activity.
Of course, cooking foods has some beneficial effects. For example, cooking kills pathogenic microorganisms and inactivates undesirable substances in certain foods (such as the trypsin inhibitor in soybeans). However, cooking also has deleterious effects, particularly when foods are heated to high temperatures. Cooking can alter the structure of proteins, thereby decreasing their digestibility and potentially increasing their immunogenicity. Moreover, a number of toxic compounds are produced during cooking, including lipid peroxides, polymerized fats, cholesterol oxides, advanced glycation end products, heterocyclic amines, polycyclic aromatic hydrocarbons, and acrylamide. Each of these compounds may play a role in the pathogenesis of one or more chronic diseases (including cardiovascular disease and cancer), and some may accelerate the aging process. In addition, cooking can lead to the destruction or leaching of essential nutrients, thereby lowering the nutritional value of food. Thus, the manner in which foods are cooked may be an important determinant of whether those foods are beneficial or harmful.

Advanced Glycation End Products (AGEs)
Perhaps the best studied of the molecules formed during harsh cooking are advanced glycation end products (AGEs). These compounds are produced by a reaction between a reducing sugar (glucose, fructose, or lactose) and a protein or amine-containing lipid. AGEs are absorbed from food intact and persist in tissues, where they can modify protein structures. AGEs appear to promote inflammation and insulin resistance, both of which play a role in the pathogenesis of many chronic illnesses. In addition, AGEs are thought to contribute to the development of cardiovascular disease, diabetes complications, and fibromyalgia, and to accelerate the aging process.1,2

AGEs, Diabetes, and Inflammation
In an animal model of type 1 diabetes, feeding a low-AGE diet (as compared with a standard diet) significantly decreased the incidence and delayed the onset of diabetes, decreased the degree of inflammation of pancreatic islet cells, decreased the severity of nephropathy, and prolonged survival.3,4 Consumption of a low-AGE diet also improved insulin sensitivity, decreased islet cell destruction, reduced the severity of nephropathy, and promoted weight loss in an animal model of type 2 diabetes and obesity.5
The potential of AGEs to promote inflammation and insulin resistance has also been demonstrated in humans. In one study, 74 overweight women were randomly assigned to consume a diet high or low in AGEs. The difference in dietary AGE content was achieved primarily by differences in cooking methods. Compared with the high-AGE diet, the low-AGE diet significantly decreased insulin resistance, as determined by the homeostasis model assessment of insulin resistance (HOMA-IR).6 In another study, 13 patients with diabetes were randomly assigned to consume a diet for 6 weeks that was high or low in AGE content. The two diets had a similar amount of protein, carbohydrate, and fat, but differed by approximately 5-fold in AGE content, which was achieved by varying the cooking time and temperature. After 6 weeks, the mean C-reactive protein concentration (an indicator 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). Levels of other inflammatory mediators also increased on the high-AGE diet and decreased on the low-AGE diet.7

How to Reduce the Amount of Dietary AGEs
Raw foods are virtually devoid of AGEs, so eating more raw foods will decrease AGE intake. Cooking at lower temperatures and in the presence of water results in relatively little AGE formation, whereas more AGEs are formed when foods are cooked at higher temperatures and in the absence of water. Temperature and cooking method seem to be more important factors for AGE formation than cooking time. Emphasizing boiling, poaching, and stewing over frying, broiling, and roasting may decrease daily AGE intake by up to 50%. Microwaving foods increases their AGE content only modestly, to about the same extent as boiling.8

High-fat and high-protein foods (such as meat and cheese) tend to have the highest AGE content. High-carbohydrate foods typically contain much less AGEs. However, within the carbohydrate group, commercially prepared breakfast foods and snacks have a high AGE content compared with oatmeal. This relatively high AGE content is presumably due to the fact that processing of some ready-to-eat cereals includes heating to temperatures over 230 ºC. In addition, many cereals and snack foods undergo an extrusion process under high pressure, which can promote the formation of AGEs.8

1.   Hein G, Franke S. Are advanced glycation end-product-modified proteins of pathogenetic importance in fibromyalgia? Rheumatology. 2002;41:1163–1167.
2.   Ruster M et al. Detection of elevated N epsilon-carboxymethyllysine levels in muscular tissue and in serum of patients with fibromyalgia. Scand J Rheumatol. 2005;34:460–463.
3.   Peppa M et al. Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice. Diabetes. 2003;52:1441–1448.
4.   Zheng F et al. Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products. Diabetes Metab Res Rev. 2002;18:224–237.
5.   Hofmann SM et al. Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse. Diabetes. 2002;51:2082–2089.
6.   Mark AB et al. Consumption of a diet low in advanced glycation end products for 4 weeks improves insulin sensitivity in overweight women. Diabetes Care. 2014;37:88–95.
7.   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.
8.   Goldberg T et al. Advanced glycoxidation end products in commonly consumed foods. J Am Diet Assoc. 2004;104:1287–1291.

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