Top image

EMBL/EMBO Joint Conference 2004

Lloyd Demetrius, Harvard University, USA and Max Planck Institute for Molecular


Lloyd Demetrius did his undergraduate studies in mathematics at the University of Cambridge, England; graduate studies in mathematical biology, University of Chicago, Chicago, U.S.A; and post doctoral studies at the University of California, Berkeley. Demetrius was a faculty member in mathematics departments in the USA: University of California, Berkeley; Brown and Rutgers (1971-1979); and a research scientist at the Max Planck Institute for biophysical Chemistry, Goettingen (1980-1989) Since 1990, he has been with the Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, first as a visiting professor (1990-1992), and then as research scholar in population genetics. He has held visiting professoships at MIT, University of Paris, and was an occupant of a Chaire Municipale, a distinguished Visiting professorship at the University of Grenoble.

Main research interests: Theoretical and computational biology, mathematical studies of evolutionary theory, the structure and function of biological networks. In a recent issue of Journal of Gerontology, Demetrius has proposed a quantitative theory of aging which provides both a proximate mechanism and an evolutionary rationale for aging. The theory derives a quantitative explanation of the large variation in life span within and between species, and proposes a mechanism for the action of Caloric restriction (CR) on life span. CR has been thought to act by reducing the metabolic rate, the rate of oxygen consumption, a proposition which is a derivative of the rate of living theory advanced by Raymond Pearl in the 1920's. Demetrius argues that Caloric restriction acts to increase metabolic stability, the capacity of the organism to maintain steady state values of redox couples in the face of chance fluctuations due to the extremely low concentration of regulatory molecules in cells. The new theory indicates that in humans, CR will not lead to dramatic life extension as it does in laboratory rats and mice. The model predicts a 2-5 years gain in life span in non Çobese humans, derived primarily from a reduced incidence of cardiovascular disease and diabetes.