Bruce Ames - Understanding Aging

Bruce Ames (born December 16, 1928) is a professor of Biochemistry and Molecular Biology at the University of California, Berkeley, and a senior scientist at Children's Hospital Oakland Research Institute (CHORI). He is the inventor of the Ames test, a system for easily and cheaply testing the mutagenicity of compounds.

His research focuses on cancer and aging and he has authored over 500 scientific publications. He is among the few hundred most-cited scientists in all fields.

Ames' current research includes identifying agents that delay the mitochondrial decay of aging, understanding the role of mitochondrial decay in aging, particularly in the brain, optimizing micronutrient intakes in the population to prevent disease, malnutrition, and obesity. He is also interested in mutagens as they relate to cancer prevention and aging.

He is a recipient of the Bolton S. Corson Medal in 1980, Tyler Prize for Environmental Achievement in 1985, the Japan Prize in 1997, the National Medal of Science in 1998 and the Thomas Hunt Morgan Medal in 2004[1], among many others.

He was born and raised in New York City. He is a graduate of the Bronx High School of Science. His undergraduate studies were at Cornell University in Ithaca, New York, and his graduate studies were completed at the California Institute of Technology.

Mitochondrial decay, (a decrease in membrane potential, respiratory control ratio, cardiolipin, and cellular oxygen consumption, and an increase in oxidant by-products) appears to be a major contributor to aging and associated degenerative diseases. Oxidative damage to DNA, RNA, proteins, and lipids in mitochondrial membranes is a major consequence of this decay, resulting in functional decline of mitochondria, cells, and organs. Feeding the mitochondrial metabolites acetyl carnitine and lipoic acid to old rats rejuvenates the mitochondria and improves brain and other function. The degenerative diseases accompanying aging, such as immune dysfunction, cancer, cognitive decline, and stroke, might be delayed by an inexpensive intervention. About 40 essential micronutrients are required for metabolism and include minerals, vitamins, amino acids and fatty acids.

Micronutrient inadequacy (2 standard deviations below the RDA) is unusually widespread in the U.S. population (especially in the poor, children, adolescents, the obese, and the elderly) because of high consumption of calorie-rich micronutrient-poor unbalanced diets. Most of the world's population, particularly the poor, has inadequate intake of one or more micronutrients. Societal concern is low because no overt pathology has been associated with these levels of deficiency, e.g. 56% of the U.S. have intakes below the EAR for Mg and almost all African-Americans for vitamin D. My triage theory explains why the pathology is insidious. When a micronutrient is inadequate, nature selects for a rebalancing of metabolism, that ensures survival of the organism at the expense of metabolism whose lack has only longer term consequences. I propose that during evolution micronutrient shortages were very common, e.g. the 15 essential minerals, which are not distributed evenly on the earth. The consequences of this homeostatic response are, for example, DNA damage (future cancer), adaptive immune dysfunction (future severe infection), and mitochondrial decay (future cognitive dysfunction and accelerated aging). Much evidence supports this idea that micronutrient shortages accelerate aging.