Bidder’s Hypothesis Revisited

Abstract

In this paper I consider three major difficulties associated with the general molecular theory of ageing, namely: (1) How can molecular damage accumulate in the face of the constellation of repair mechanisms that is found in cells? (2) How can the obvious programmatic nature of ageing be reconciled with underlying stochastic processes? (3) How do some organisms avoid ageing? As a solution to points 1 and 2, I propose that the repair mechanisms themselves deteriorate in a programmed fashion with age. However, I argue that this programming is unlikely to be a result of direct selection for life-shortening but, rather, is more likely to be a result of an indirect selection for other characters. This idea is very similar to the theory of senescence first formulated by Bidder. The solution to point 3 is that the repair mechanisms in systems which avoid ageing, in particular cellular and molecular turnover, are not impaired with age. The rejuvenating capacities of sexual and asexual reproduction are also discussed.

Implications of Protein Degradation in Aging

“…Although this theory has not gained experimental support so far (see, e.g., Refs. 10–12), an important realization has been advanced that one of the reasons errors do not increase is that error‐containing molecules would be largely degraded, thus preventing their accumulation 13–15. Nevertheless, altered proteins do increase with age 16,17.…”

No Time to Age: Uncoupling Aging from Chronological Time

“…Whether or not aging is programmed or is the result of accumulated damage has been the subject of debate for many decades. Early twentieth-century theories favoring programming proposed that aging was a consequence of differentiation as put forth by Minot [ 1 ] or factors leading to the cessation of growth as proposed by Bidder [ 2 ]. The evolution of a genetic program for aging seemed unlikely because there is little selective pressure for gene variants once reproductive maturity is reached.…”