Leonard Hayflick

American anatomist

Leonard Hayflick (born May 20, 1928 in Philadelphia) is a professor of anatomy at the UCSF School of Medicine and was a professor of medical microbiology at Stanford University School of Medicine. He is known for the Hayflick limit and has won more than 25 major awards.

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  • Age-related sensory changes can be traced to degeneration in some of the cells and cell products that compose the sense organ itself.
  • Natural selection favors animals that are most likely to become reproductively successful by developing better survival strategies and greater reserve capacity in vital systems to better escape predation, disease, accidents, and environmental extremes. Natural selection diminishes after reproductive success because the species will not benefit from members favored for greater longevity. The level of physiological reserve remaining after reproductive maturity determines longevity and evolves incidental to the selection process that acts on earlier developmental events. Physiological reserve does not renew at the same rate that it incurs losses because molecular disorder increases at a rate greater than the capacity for repair. These are age changes, and they increase vulnerability to predation, accidents, or disease.
  • Since the first cell culture was set at the beginning of the twentieth century it was believed that all cultured cells, if provided with the proper conditions, would replicate indefinitely. Sixty years later we overthrew this dogma by finding that normal cells have a finite capacity to replicate and that only abnormal or cancer cell populations can replicate indefinitely. We interpreted these findings to bear on our understanding of the aging process. If, as had been previously thought, normal cells can replicate indefinitely, then age changes could not have an intracellular origin. Our findings demonstrated that, on the contrary, age changes do have an intracellular origin. The hundreds of changes that were subsequently found to precede the loss of replicative capacity have been interpreted to be age changes and the finitude of replication to be an expression of longevity determination. Subsequent findings by others have determined the molecular mechanism that governs the finitude of normal cell replicative capacity and how immortal cancer cells escape this inevitability.

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