Earlier posts on heat-created toxins focused on heterocyclic amines, acrylamide and polycyclic aromatic hydrocarbons. While these are all worrisome – and to a large degree avoidable – compounds, I’ve saved the group of heat-generated toxins that concern me most for this post: advanced glycation end products. These compounds, often abbreviated as AGEs, are created when sugar molecules or their byproducts react with a molecule with a free amino group, such as proteins, lipids or nucleic acids, in the absence of enzymes . While these compounds were first characterized in the 1950s, only since the 1980s has serious effort been invested to understand their role in human health, or more specifically their role in chronic, degenerative disease.
Advanced glycation end products form on their own in the human body, most commonly on long-lived tissues like the collagen fibers that compose our connective tissue and the myelin that forms the protective membranes surrounding our nerves. This is problematic because AGEs cause cross-linking in these tissues, reducing their flexibility and making them challenging to heal or rebuild. In addition to their native creation within the human body, AGEs are also formed in foods through cooking – particularly in grilling, frying and baking – and when ingested they add to the AGE burden of the body .
Excessive AGE levels in the body have been linked with the progression of many chronic, degenerative diseases, largely because the compounds and the cross-links they cause are inflammatory [2-4]. Because so many chronic degenerative diseases are linked to chronic inflammation, dietary AGE exposure and native AGE production within the body should be something health conscious people pay attention to. Diabetics, because of their inability to control their blood sugar, often have elevated levels of AGEs in their tissues that lead to a range of health complications, and additional intake of dietary AGEs doesn’t help [5, 6]. With heart disease, AGE-caused cross-links in the walls of blood vessels trap lipids like cholesterol, initiating and promoting the formation of the arteriosclerotic plaques that characterize this condition [2, 7].
Owing to the fact that dietary sources of AGEs are known to have health impacts, reducing our dietary intake of these compounds can have therapeutic value . Data is available on the AGE content of different foods prepared different ways, and, in general, dairy products, cooked meats, and foods containing processed, cooked grains contain the most AGEs, with fried meats – particularly bacon – containing the highest levels . Raw meats contain far lower levels of AGEs than cooked meats, although even raw meats have higher AGE contents than raw fruits and vegetables.
As with the previously listed heat-created toxins, I see value in reducing my exposure to AGEs. In fact, given AGEs’ role in inflammation and these compounds’ links to chronic degenerative diseases such as arteriosclerosis and diabetes, I find myself inspired to be even more conscientious about reducing my dietary intakes than of other heat-created toxins. It’s quite convenient that the very processes that yield high levels of AGEs in foods also yield high concentrations of other heat-created toxins, making my task of avoidance quite a bit easier.
- Advanced glycoxidation and lipoxidation end products (AGEs and ALEs): an overview of their mechanisms of formation. G. Vistoli et al, Free Radical Research, 2013, Vol. 47, Pgs. 3-27.
- Diet-derived advanced glycation end products are major contributors to the body’s AGE pool and induce inflammation in healthy subjects. J. Uribarri et al, Annals of the New York Academy of Science, 2005, Vol. 1043, Pgs. 461-466.
- Advanced glycoxidation end products in chronic diseases – clinical chemistry and genetic background. M. Kalousová et al, Mutation Research, 2005, Vol. 579, Pgs. 37-46.
- Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation. R. Ramasamy et al, Glycobiology, 2005, Vol. 15, Pgs. 16R-28R.
- Advanced glycation end products: a review. R. Singh et al, Diabetologia, 2001, Vol. 44, Pgs. 129-146.
- Advanced glycation endproducts – role in pathology of diabetic complications. N. Ahmed, Diabetes Research and Clinical Practice, 2005, Vol. 67, Pgs. 3-21.
- Glycoxidation and lipoxidation in atherogenesis. J. Baynes & S. Thorpe, Free Radical Biology & Medicine, 2000, Vol. 28, Pgs. 1708-1716.
- Food-derived advanced glycation end products (AGEs): a novel therapeutic target for various disorders. S. Yamagishi et al, Current Pharmaceutical Design, 2007, Vol. 13, Pgs. 2832-2836.
- Advanced glycation end products in foods and a practical guide to their reduction in diet. J. Uribarri et al, Journal of the American Dietetics Association, 2010, Vol. 110, Pgs. 911-916.