This is a nature article discussing these theories.
http://www.nature.com/...ary/the-evolution-of-aging-23651151
The Mutation Accumulation Hypothesis
Following the logic outlined above, Medawar (1946, 1952) reasoned that, if the effects of a deleterious mutation were restricted to late ages, when reproduction has largely stopped and future survival is unlikely, carriers of the negative mutation would have already passed it on to the next generation before the negative late-life effects would become apparent. In such a situation, natural selection would be weak and inefficient at eliminating such a mutation, and over evolutionary time such effectively neutral mutations would accumulate in the population by genetic drift, which in turn would lead to the evolution of aging. This is known as Medawar's mutation accumulation (MA) hypothesis (Figure 3A). The effects of such a mutation accumulation process would only become manifest at the organismal level after the environment changes such that individuals experience less extrinsic mortality (e.g., due to decreased predation) and thus live to an age where they actually express the symptoms of aging.
The Antagonistic Pleiotropy Hypothesis If it is true that selection cannot counteract deleterious effects at old age, he argued, then mutations or alleles might exist that have opposite, pleiotropic effects at different ages: genetic variants that on the one hand exhibit beneficial effects on fitness early in life, when selection is strong, but that on the other hand have deleterious effects late in life, when selection is already weak. This idea is known today as the antagonistic pleiotropy (AP) hypothesis for the evolution of aging (see Rose 1991, Flatt & Promislow 2007, Figure 3B). Williams pointed out that, if the beneficial effects of such mutations early in life outweigh their deleterious effects at advanced age, such genetic variants would be favored and enriched in a population, thus leading to the evolution of aging. Thus, under Williams' hypothesis, the evolution of aging can be seen as a maladaptive byproduct of selection for survival and reproduction during youth.
A fundamental corollary of Williams’ AP hypothesis is that early fitness components such as reproduction should genetically trade-off with late fitness components such as survival at old age, so that, for example, genotypes with high early fecundity should be shorter lived than those with low reproduction (e.g., Williams 1957, Rose 1991, Charlesworth 1994, Hughes & Reynolds 2005). In a somewhat similar vein, Kirkwood’s 1977 "disposable soma" (DS) hypothesis predicts that the optimal level of investment into somatic maintenance and repair will evolve to be below that required for indefinite survival. The idea here is that the evolution of a higher investment is unlikely to pay off since the return from such an investment may never be realized due to extrinsic mortality. Moreover, investment into reproduction — or early fitness components in general — might withdraw limited resources that could otherwise be used for somatic maintenance and repair. Such resource allocation trade-offs can thus been seen as a physiological extension of Williams' AP model.
Although the relative frequency of MA versus AP is still debated (both may typically go hand in hand - see also Moorad & Promislow 2009), there is robust evidence today for the existence of fitness trade-offs that are consistent with the notion of AP (for a recent discussion of the positive evidence see Flatt & Promislow 2007, and Flatt 2011, but also see Moorad & Promislow 2009). Whether such trade-offs are physiologically caused by competitive energy or resource allocation — as would be expected under the DS hypothesis — remains somewhat controversial, but the trade-offs themselves are well established (see Flatt 2011). Most importantly, the kinds of trade-offs postulated by Williams, have been found at the evolutionary level: for example, fruit flies that were artificially selected for increased late-life reproductive success were found to be long-lived at the expense of reduced early fecundity in several, now classical, experiments in the labs of Michael Rose and Leo Luckinbill (Rose & Charlesworth 1980, Rose 1984, Luckinbill et al. 1984). These elegant experiments represent the first solid empirical tests of the evolutionary theory of aging (Rose 1991).
The classical evolutionary theory of aging has therefore two fundamental cornerstones: MA and AP. However, it is worth noting that both models are conceptually very similar: under MA, aging evolves through the accumulation of effectively neutral mutations with deleterious late-life effects, whereas, under AP, aging occurs due to mutations with beneficial early- and deleterious late-life effects. In reality, probably both types of mutations occur in populations, yet their relative frequencies remain unknown. Furthermore, the age distribution of mutational effects may be much more complicated than these two scenarios suggest (e.g., Moorad & Promislow 2008).
ps: I still have problems with quotes. I didnt write any of that.
Edited by CoolBeans, : No reason given.
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