By James L McGaugh and Sara B. Kiesler (Eds.)
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Finch has also proposed that age-related changes after sexual maturation occur result from an extension of the neural and endocrine mechanisms that control earlier development (Finch 1976). He has organized an impressive argument suggesting that time-dependent changes in neural, endocrine, and target-tissue interactions can lead to senescence by creating an imbalance of proper neuroendocrine control processes. In effect this would create a so-called regulatory cascade of hormonal imbalance, much in the same manner as suggested by Dilman and Everitt.
Most important, there is the serious possibility that restricted nutrition might not actually extend maximum life-span potential beyond that which is normal for the animal in the wild (Wulf and Cutler 1975). For example, it appears unnatural for animals to eat ad libitum (to have all they want to eat all the time) as they do in the laboratory. A more natural feeding situation is feast and famine. It is therefore possible that ad libitum feeding produces a complex spectrum of diseases and dysfunctions that restricted nutrition and periodic fasting-feeding programs eliminate.
Given a history at least somewhat along these lines, how should the evolution be interpreted? The increase in cranial capacity is clear from well-preserved and well-dated specimens, but estimates of body weight are very uncertain. It is possible to make the case that the small Australopithecus was small, more or less the size of contemporary chimpanzees, and that there had already been some increase in brain size-body size. It is also possible to place the large form of Australopithecus well within the range of contemporary human beings and to think that there has been little or no important increase in body size over the last 2 million years.
Aging. Biology and Behavior by James L McGaugh and Sara B. Kiesler (Eds.)