The Promise of Human Life Span Extension

By Estep, Preston W., III | Annual Review of Gerontology & Geriatrics, January 1, 2007 | Go to article overview

The Promise of Human Life Span Extension


Estep, Preston W., III, Annual Review of Gerontology & Geriatrics


The eminent evolutionary biologist George C. Williams once famously entitled a publication "Mother Nature is a wicked old witch!" in which he described the efficient brutality of natural selection as morally reprehensible (Williams, 1995). Williams rightly thought that one of the most brutal and unforgiving selective acts is death itself, although he thought it unavoidable (Nesse & Williams, 1996). Throughout history, humans have had no real control over senescence and death, and, to deal with this ever-present burden, they have turned to various diversions and increasingly elaborate mythmaking (Holliday, 2001). We still do not have a clear overall physiological model of the senescent mechanisms that lead ultimately to death, but evolutionary biology and gerontology have made impressive progress in understanding many aspects of this process.

In theory, there is no known physical law or other scientific barrier to prevent complete control over senescence and death. Despite the absence of proof that death is an immutable part of human life, there is an equal absence of proof that it can be controlled to this degree. From our current perspective, the known scientific and technological challenges that must be overcome to approach this level of control appear so daunting, and our current states of ignorance and biomedical incapacity so obvious, that most biomedical scientists restrict their research and development efforts to more perceptible therapeutic horizons with more certain near-term benefits. The vast majority focus their efforts on increasing healthy life span (health span) through disease treatment and prevention and through basic research and development of approaches to slowing senescent processes.

WHAT IS SENESCENCE?

Senescence is the progressive deterioration that most people refer to as aging. It is somewhat difficult to define more explicitly, and both organisms and their cells can be said to senesce, but it is widely accepted that death results from the accumulation of deleterious molecular damage, possibly accompanied by depletion of certain important reserves such as stem cells (Holliday, 2006). I will restrict the analyses herein mostly to senescence and damage of the soma, the collection of all non-germline cells of the body, even though there is no absolute division between germline and soma. In theory, individuals of a senescing species exhibit a progressive increase in mortality risk with increasing age under environmental circumstances that support a lower rate of mortality for the less aged (Medawar, 1955). This phenomenological explanation applies equally well to all organisms, from bacteria to humans, even though the underlying molecular damage that causes senescence and death might be different (Stewart, Madden, Paul, & Taddei, 2005). Finch has suggested the possibility that some organisms might display negligible senescence and have indeterminate life spans, but the recent demonstration of aging even in bacteria seriously undermines this general hypothesis (Finch, 1990; Stewart et al., 2005).

There are both physiological (mechanistic, proximate cause) and evolutionary (ultimate cause) models of senescence. see the work by Steven Austad (2001) for reviews of the competing, overlapping, and complementary physiological theories. A leading physiological model of senescence is the mitochondrial free-radical theory of aging, in which reactive oxygen species are primary contributors to several kinds of downstream life span-limiting damage, including DNA damage and mutation and epigenetic damage (also known as epimutation) (Harman, 1956; Holliday, 2006). Some of these pathologies are the focus of other physiological theories, including the somatic mutation and dysdifferentiative theories of aging, although it is unclear whether mitochondrial free-radical generation is the primary cause of damage (Cutler, 1991; Szilard, 1959).

The modern evolutionary view of senescence and death began in the 1930s with the ideas of Fisher and Haldane, leading in 1941 to Haldane s suggestion that selection against harmful alleles would decline dramatically after the oldest age of reproduction (Haldane, 1941, pp. …

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