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A legal system normally presumes the accused as innocent, until guilt is proven. In this context, the potential health risk of dietary AGEs must be discussed
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very carefully. Although there are indications that AGEs, either formed endogenously in the human body or taken up through the daily diet, may play a role in pathophysiological events, it is de nitely not proven that AGEs, either in total or one individual glycation compound, are toxic or may be the cause of any adverse effect. On the other hand, several arguments point against adverse effects, and the fact that glycation compounds may also have positive biological effects may support the theory that humans are not only accustomed to consuming cooked foods and their constituents for hundreds of thousands of years, but also that these compounds play a role as potential chemoprotective agents. The data available to date suggest that dietary AGEs are not harmful to healthy individuals. Of course it cannot be excluded that for certain subpopulations, dietary AGEs may pose a greater risk, although to date no studies have unequivocally shown this. Besides diabetics, these groups include for instance uremic patients, due to reduced elimination, or infants, whose gastrointestinal tract is more permeable and therefore may resorb more glycated peptides from the diet. Reports dealing with the physiological effects of glycation compounds, therefore, must be interpreted with caution. From a chemical viewpoint, only a very small fraction of the glycation compounds present in foods have been adequately characterized. Current data show that the metabolic transit may differ largely. Thus, reference to AGEs in total should be avoided and the research focused on individual compounds rather than on crude mixtures. Animal feeding studies or human intervention studies, in which effects of diets high or low in AGEs are presented, should only be accepted if the amount of individual glycation compounds in the said food items is quanti ed using reliable chromatographic techniques, ideally calibrated with pure reference standards. Calculations of an AGE content on the basis of awed data collections are out of the question. A risk assessment must be based on a data evaluation for individual Maillard compounds in common foods using reliable chromatographic techniques rather than screening methods such as ELISA. Furthermore, animal experiments and intervention studies must be based on in-depth chemical characterization of the individual compounds. Furthermore, knowledge on the structure activity relationships and the occurrence of the compounds is a prerequisite for any statement on biological effect. A real risk assessment must be based on sound science, considering all pertinent disciplines and joining the resources of biology, medicine, and chemistry.
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1. Balter, M. (1995). Archaeology did Homo erectus tame re rst Science, 268, 1570. 2. Ling, A.R. (1908). Malting. J. Inst. Brewery, 14, 494 521. 3. Maillard, L.C. (1912). Action of amino acids on sugars. Formation of melanoidins in a methodical way. Compt. Rend., 154, 66 68.
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4. Finot, P.A. (2006). Historical perspective of the Maillard reaction. Ann. N. Y. Acad. Sci., 1043, 1 8. 5. Doob, H., Willmann, A., Sharp, P.F. (1942). In uence of moisture on browning of dried whey and skim milk. Ind. Eng. Chem., 34, 1460 1468. 6. Finot, P.A., Deutsch, R., Bujard, E. (1981). The extent of the Maillard reaction during the processing of milk. Prog. Food Nutr. Sci., 5, 344 355. 7. Erbersdobler, H.F., Somoza, V. (2007). Forty years of furosine forty years of using Maillard reaction products as indicators of the nutritional quality of foods. Mol. Nutr. Food Res., 51, 423 430. 8. Mottram, D.S. (1994). Flavour compounds formed during the Maillard reaction. ACS Symp. Ser., 543, 104. 9. Van Boekel, M.A. (2006). Formation of avour compounds in the Maillard reaction. Biotechnol. Adv., 24, 230 233. 10. Rahbar, S., Blumenfeld, O., Ranney, H.M. (1969). Studies of an unusual haemoglobin in patients with diabetes mellitus. Biochem. Biophys. Res. Commun., 36, 838 843. 11. Brownlee, M., Vlassara, H., Cerami, A. (1984). Nonenzymatic glycosylation and the pathogenesis of diabetic complications. Ann. Intern. Med., 101, 527 537. 12. Raj, D.S., Choudhury, D., Welbourne, T.C., Levi, M. (2000). Advanced glycation end products: a nephrologist s perspective. Am. J. Kidney Dis., 35, 365 380. 13. Henle, T. (2003). AGEs in foods: do they play a role in uremia Kidney Int., (Suppl. 84), S145 S147. 14. Henle, T., Deppisch, R., Ritz, E. (1996). The Maillard reaction: from food chemistry to uremia research. Nephrol. Dial. Transplant., 11, 1719 1722. 15. Koschinsky, T., He, C.J., Mitsuhashi, T., Bucala, R., Liu, C., Buenting, C., Heitmann, K., Vlassara, H. (1997). Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy. Proc. Natl. Acad. Sci. U.S.A., 94, 6474 6479. 16. Uribarri, J., Cai, W., Peppa, M., Goodman, S., Ferrucci, L., Striker, G., Vlassara, H. (2007). Circulating glycotoxins and dietary advanced glycation endproducts: two links to in ammatory response, oxidative stress, and aging. J. Gerontol. A Biol. Sci. Med. Sci., 62, 427 433. 17. Hodge, J.E. (1953). Browning reactions in model systems. J. Agric. Food Chem., 1, 928 943. 18. Kroh, L.W. (1994). Caramelization in food and beverages. Food Chem., 51, 373 379. 19. Friedman, M. (2003). Nutritional consequences of food processing. Forum Nutr., 56, 350 352. 20. Penndorf, I., Biedermann, D., Maurer, S.V., Henle, T. (2006). Studies on N-terminal glycation of peptides in hypoallergenic infant formulas: quanti cation of alphaN-(2-furoylmethyl) amino acids. J. Agric. Food Chem., 55, 723 727. 21. Pilkova, L., Pokorny, J., Davidek, J. (1990). Browning reactions of Heyns rearrangement products. Nahrung/Food, 34, 759 764. 22. Brands, C.M.J., Van Boekel, M.A.J.S. (2001). Reactions of monosaccharides during heating of sugar-casein systems: building of a reaction network model. J. Agric. Food Chem., 49, 4667 4675.
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