DRUSE

There’s a review paper that came out recently on Mechanisms of Ageing and Development journal ( Volume 129, Issue 12, December 2008, Pages 693-699). It is entitled “Does senescence give rise to disease?” by Bruce Carnes and colleagues. Here’s a portion of it:

“In a now classic paper, Strehler (1959) examined whether exposure to ionizing radiation actually “accelerated aging” or only mimicked the biological consequences of senescence. Although the radiation biology community was the target audience, this paper represents one of the earliest and most significant attempts to develop criteria that allow the biological effects of senescence to be distinguished from those arising from other causes. As such, it provides a useful starting point for determining whether a distinction can or should be made between senescence and disease.

Strehler focused on processes that have effects on biological structures and, hence their function. Although the acronym CUPID used to characterize senescence-induced changes in structure and function was not coined until later (e.g., Arking, 1991), Strehler identified the criteria that form the acronym: Cumulative (identified but not given separate status in the original paper), Universal, Progressive, Intrinsic and Deleterious.

These criteria have generated considerable debate among scientists. The “universal” criterion, in particular, has played a central role in the debates over the relationship between senescence and disease. Since age-associated pathologies (disease) are not universal, Hayflick (2004) argues that knowledge about disease will not advance our understanding of senescence. Conversely, Holliday (2004) argues that knowledge about the pathogenesis of disease provides invaluable insights into the changes in biological structure and function that accompany senescence.

Which of these alternative views is correct has considerable implications for public health and medicine, especially in an era of global population aging. If senescence and disease are unrelated, then treating one would have no impact on the health and life span consequences of the other. However, if they are causally related, then a single intervention for senescence could conceivably reap the cumulative health and life-extending benefits currently derived from multiple treatments applied to a spectrum of diseases ([Butler et al., 2008], [Tinetti and Fried, 2004] and [Holliday, 1984]).”

It also touched on some reasons to be optimistic in senescence research:
“(1) our bodies are not designed for indefinite survival, but neither are they designed to fail,
(2) genes evolved to promote health and vigor, not ensure decrepitude and death,
(3) senescence is ubiquitous, and is not driven by a single process, and
(4) senescence is a byproduct of evolutionary neglect, not evolutionary intent.”
Fig. 2. Schematic illustrating the relationship of observed life span to potential life span and the difference between interventions that reclaim survival time as opposed to those that extend survival by modifying senescence.
It concluded by stating:

“… the boundary between aging and disease is blurred. This blurring, however, is both inevitable and revealing. Although diseases have many causes (e.g., genetic, toxin and microbe), this review suggests that aging is one of them. Diseases not caused by aging arise from knowable causes with knowable pathogenesis. This class of disease can, in theory, be cured (e.g., appendicitis) or eliminated (e.g., smallpox). Aging, however, is not a single entity and its causes are deterministic and stochastic as well as omnipresent and ubiquitous. As such, aging can be mitigated but it can be neither “cured” nor eliminated.

… Our bodies are not designed for immortality; they are designed to replace themselves. Longevity provides the time for that to occur and aging is simply a byproduct of surviving beyond that timeframe.”