Study Offers Ways to Minimize Cell Damage from Cooked Foods

by | Apr 22, 2016 | 2015, Digestive Health, Food Safety

Written by Greg Arnold, DC, CSCS. Study discusses food preparation methods that protect against cell damage due to AGE’s (advanced glycation end products).

At the heart of the chronic diseases that affect our society, from heart disease to arthritis to diabetes, is a cumulative effect of damage to cells called “oxidation” by substances called “free radicals” that is the primary driver of aging and disease (1).   A component of this oxidation-driven process of cell damage are compounds called “advanced glycation end products”, or AGEs (2, 3), formed when sugars, proteins, and fats interact with each other in the body (4).

So while oxidation by free radicals occurs in our body through natural processes, we can also accelerate the forming of AGEs in our body in how we prepare our food. Cooking, specifically grilling, broiling, roasting, searing, and frying accelerate AGE formation (4). And given how much of the Western diet is filled with “dead food” from heating and processing, research conclusively shows that much of the modern diet is “a large source of AGEs” (5).

Fortunately, the American Dietetic Association (6) has released information on how to minimize your exposure to AGEs during food preparation. Measuring AGE content of 549 foods obtained between 2003 and 2008 from various New York City hospitals, supermarkets, and restaurants, as well as the methods used to prepare these foods, the researchers discovered the following:

  • Scrambled eggs prepared in an open pan over medium-low heat had about one half the AGEs of eggs prepared in the same way but over high heat.
  • Poached or steamed chicken had less than one fourth the AGEs of roasted or broiled chicken.
  • In all food categories, frying, broiling, grilling, and roasting yielded more AGEs compared to boiling, poaching, stewing, and steaming.
  • Microwaving did not raise AGE content to the same extent as other dry heat cooking methods for the relatively short cooking times (6 minutes or less) that were tested.
  • AGE formation in cooked meat was inhibited following exposure to acidic solutions (marinades) of lemon juice and vinegar. Beef that was marinated for 1 hour in these solutions formed less than half the amount of AGEs during cooking than the untreated samples.

In addition, the researchers started to quantify levels of dietary AGE intake and to suggest levels that may increase disease risk. The average dietary AGE intake in a cohort of healthy adults from the New York City area was recently found to be 14,700 AGE kiloUnits/day (7). And while they admit that “A safe and optimal dietary AGE intake for the purposes of disease prevention has yet to be established”, they did cite research in mice showing a 50% reduction of dietary AGE to reduce oxidative stress, have a lesser deterioration of insulin sensitivity and kidney function with age while also resulting in a longer life span (8).

For the researchers, “Ongoing studies are needed to further expand the dietary AGE database and investigate additional methods for reducing AGE generation during home cooking and food processing”. In addition, “future studies continue to investigate the health effects of AGEs and refine recommendations for safe dietary intakes” and that “current data support the need for a paradigm shift that acknowledges that how we prepare and process food may be equally important as nutrient composition.”

Source: Jiao, Li, et al. “Dietary consumption of advanced glycation end products and pancreatic cancer in the prospective NIH-AARP Diet and Health Study.” The American journal of clinical nutrition 101.1 (2015): 126-134.

© 2015 American Society for Nutrition

Posted October 28, 2015.

Greg Arnold is a Chiropractic Physician practicing in Hauppauge, NY.  You can contact Dr. Arnold directly by emailing him at PitchingDoc@msn.com or visiting his web site at www.PitchingDoc.com

References:

  1. Sanz A. The mitochondrial free radical theory of aging: a critical view. Curr Aging Sci 2008 Mar;1(1):10-21
  2. Huebschmann AG, Regensteiner JG, Vlassara H, Reusch JEB. Diabetes and advanced glycoxidation end products. Diabetes Care. 2006; 29:1420-1432.
  3. Bohlender JM, Franke S, Stein G, Wolf G. Advanced glycation end products and the kidney
  4. O’Brien J, Morrissey PA. Nutritional and toxicological aspects of the Maillard browning reaction in foods. Crit Rev Food Sci Nutr. 1989;28: 211-248
  5. Goldberg T, Cai W, Peppa M, Dardaine V, Baliga BS, Uribarri J, Vlassara H. Advanced glycoxidation end products in commonly consumed foods. J Am Diet Assoc. 2004;104:1287-1291
  6. Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. J Am Diet Assoc. 2010 Jun;110(6):911-16.e12. doi: 10.1016/j.jada.2010.03.018
  7. Uribarri J, Cai W, Peppa M, Goodman S, Ferruci L, Striker G, Vlassara H. Circulating glycotoxins and dietary advanced glycation endproducts: Two links to inflammatory response oxidative stress, and aging. J Gerontol A Biol Sci Med Sci. 2007;62:427-433
  8. Cai W, He JC, Zhu L, Chen X, Zheng F, Striker GE, Vlasara H. Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan. Am J Pathol. 2008;173:327-336