THE SECOND LAW OF THERMODYNAMICS AND THE ETIOLOGY OF BIOLOGICAL AGING

(This conference is dedicated to the memory of Dr. Robin Holliday)

Washington D.C., November 5, 2014

This conference will be held from 8:00 AM to 5:45 PM on the day of the evening start of the Annual Meeting of the Gerontological Society of America. The hotel site and conference room is not yet determined. Registration is to be made at the GSA website or at the conference site.

Sponsored by the Glenn Foundation for Medical Research, Executive Director, M. Collins

Co-organized by L. Hayflick, UCSF and W. Bortz, Stanford, University

The premise of this conference is that the origin of biological aging is at the molecular level and that this has been rarely the subject of a conference.

Presentations will focus on the fundamental cause(s) of biological aging and not on longevity determinants or age-associated diseases.

One major concept in this area is that the Second Law of Thermodynamics plays a significant, if not the only, role in the accumulation of miss-folded, dysfunctional molecules that leads to age changes at higher levels of complexity. Put simply, the law says that energy tends to dissipate unless restrained.

There are only two fundamental ways in which age changes can occur. They can arise either as the result of a purposeful program driven by genes or by random stochastic or accidental events.

There appears to be little, if any, evidence that a deteriorative, catabolic process like aging is driven by a genetic program. However, there is ample evidence that the genome drives the anabolic processes that govern the determinants of longevity.

Many believe that age changes result from the accumulation of dysfunctional molecules including those in the maintenance systems of repair, synthesis and turnover. The slow, but escalating increase in dysfunctional molecules is thought, ultimately, to exceed maintenance or repair capacity at about the time of reproductive maturity. This condition then increases vulnerability to age-associated pathology or disease.

Because the purpose of this conference is to discuss the etiology of age changes at the molecular level, the roles of longevity determinants and age associated diseases in the finitude of life will be deemphasized.

Leonard Hayflick, Ph.D.
Professor of Anatomy
University of California, San Francisco

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