About Dr. AmesDr. Ames is a Senior Scientist at Childrens Hospital Oakland Research Institute (CHORI), director of their Nutrition & Metabolism Center, and a Professor Emeritus of Biochemistry and Molecular Biology, University of California, Berkeley.
He is a member of the National Academy of Sciences and he was on their Commission on Life Sciences. He was a member of the board of directors of the National Cancer Institute, the National Cancer Advisory Board, from 1976 to 1982. He was the recipient of the General Motors Cancer Research Foundation Prize (1983), the Tyler Environmental Prize (1985), the Gold Medal Award of the American Institute of Chemists (1991), the Glenn Foundation Award of the Gerontological Society of America (1992), the Lovelace Institutes Award for Excellence in Environmental Health Research (1995), the Honda Prize of the Honda Foundation, Japan (1996), the Japan Prize, (1997), the Kehoe Award, American College of Occup. and Environ. Med. (1997), the Medal of the City of Paris (1998), the U.S. National Medal of Science (1998), The Linus Pauling Institute Prize for Health Research (2001), and the American Society for Microbiology Lifetime Achievement Award (2001).
His over 555 publications have resulted in his being among the few hundred most-cited scientists (in all fields).
The Laboratory of Bruce Ames, PhDThe research of the lab involves various aspects of tuning-up metabolism to optimize health.
The Nutrition and Metabolism group at Children's Hospital of Oakland Research Institute under the direction of U.S. National Medal of Science recipient, Prof. Bruce N. Ames, is clarifying the mechanisms, and proposing solutions, by which Most of the world’s population, even in developed countries, has inadequate intake of one or more of the ~30 essential vitamins and minerals (V/M), mostly used as cofactors by the proteins/enzymes of metabolism. A varied and balanced diet should provide enough V/M; an unbalanced diet with too much refined food provides calories, but not enough V/M. Triage theory (1,2) posits that, as a result of recurrent shortages of V/M during evolution, natural selection developed a strategic rationing response to moderate shortages so that the scarce V/M is preferentially retained by V/M-dependent proteins that are essential for short-term survival and reproduction. In contrast, proteins needed for long-term health, which I term "longevity proteins" because they defend against the diseases associated with aging, are starved for the V/M and thus are disabled. Moreover, since the damage from moderate deficiency is insidious, its importance for long-term health is not clinically apparent. Strong support for triage theory comes from our analyses of published data on proteins dependent on vitamin K (3) and on selenium (4). Both of these V/M have built into metabolism a triage-like trade-off between short-term survival and long-term health; each uses a different mechanism to accomplish this end. Mechanistic, genetic, and epidemiological evidence suggests that this metabolic trade-off accelerates aging-associated diseases, such as cancer, cardiovascular disease, immune dysfunction, and cognitive decline. Importantly, by the official U.S. Institute of Medicine measure of inadequacy, the Estimated Average Requirement (EAR), most of the U.S. population is below the EAR for one or more V/M (5). The RDA is set at 2SD above the EAR. The percentages of the U.S. population that are currently below the EAR (including fortifications and supplements) are (5): vitamin D 70%, vitamin E 60%, magnesium 45%, calcium 38%, vitamin K 35%, vitamin A 34%, vitamin C 25%, zinc 8%, vitamin B6 8%, folic acid 8%, etc. These low intakes are especially true for children, adolescents, elders, and the obese. The U.S. population also has a very low intake of DHA/EPA omega-3 intake. These official estimates of population inadequacy are likely to be underestimates, as EARs do not take long-term triage effects into account, which is likely to lead to increased EAR estimates. An assay for a longevity protein concentration/activity in a finger prick of blood may be useful for early detection of a functional effect of a low intake of each V/M, and could be used for prevention. About half of the proteins we have studied are longevity proteins. This implies an undiscovered class of longevity V/Ms may exist, which we are exploring and discovering (6). Most of the obese eat very poor diets, as judged by the calorie to V/M ratio (7-11). They are starving for V/M, which may overrule satiety signals or activate triage mechanisms. (10-13). The frequency of every age-associated disease that has been examined is increased in the obese. Our Choribar (V/M-dense, low-calorie, high-fiber, fruit-based) markedly improves metabolism in those with less than optimal diets (most subjects) in many human trials (14, 15).
References Cited1. Ames BN (2006) Proc. Natl. Acad. Sciences, U.S.A., 103:17589-94. doi:10.1073/pnas.0608757103
2. Ames BN. (2010) J Nucleic Acids. doi:10.4061/2010/725071
3. McCann JC and Ames BN. (2009) Am J Clin Nutr. 90:889-907. doi:10.3945/ajcn.2009.27930
4. McCann JC and Ames BN. (2011) FASEB J. 25:1793-1814. doi:10.1096/fj.11-180885
5. Fulgoni VL., et al. (2011) 141:1847-54. doi:10.3945/jn.111.142257
6. Ames B., et al. "Rethinking Vitamins and Minerals as Factors in Optimizing Longevity" in preparation.
7. Damms-Machado A., et al. (2012) Nutr J. 11:34. doi:10.1186/1475-2891-11-34
8. Via, M. (2012) ISRN Endocrinol 2012:103472. doi:10.5402/2012/103472
9. Asfaw A. (2007) Econ Hum Biol 5:471-83. doi:10.1016/j.ehb.2007.03.004
10. Garcis OP., et al. (2009) Nutr Rev. 67:559-72. doi:10.1111/j.1753-4887.2009.00228.x
11. Amara NB., et al. (2014) Genes Nutr 9:410. doi:10.1007/s12263-014-0410-x
12. Major GC., et al. (2008) Br J Nutr. 99:1157-67. doi:10.1017/S0007114507853335
13. Major GC., et al. (2009) Br J Nutr. 101:659-63. doi:10.1017/S0007114508030808
14. Mietus-Snyder M., et al. (2012) 26:3515-27. FASEB J. doi:10.1096/fj.11-201558
15. McCann JC., et al. (2015) FASEB J. [Epub ahead of print]. doi: 10.1096/fj.15-271833 fj.15-271833