The Biology of Senescence 



between related species, and between genetic races of the same 

 species. The mechanism which determines specific size has long 

 been believed by some workers to intervene more actively in 

 mammalian development and to be more selective in its action 

 on tissues, than the mechanism which leads to the more gradual 

 decline of growth in some reptiles and fish. In these forms, 

 according to this view, the die-away curve of growth, which is 

 generally exponential in relation to body weight, suggests a far 

 more general process of size-limitation affecting all the tissues 

 approximately equally, and reaching the virtual limiting size 

 without much alteration in the general physiology of the animal. 

 'It is the rule in fishes and other cold-blooded vertebrates that 

 growth is asymptotic and size indeterminate, while in warm- 

 blooded animals, growth comes, sooner or later, to an end. But 

 the characteristic form is established earlier in the former case, 

 and changes less, save for . . . minor fluctuations. In the higher 

 animals, such as ourselves, the whole course of life is attended 

 by constant alteration and modification of form' (D'Arcy 

 Thompson, 1942). The form of the mammalian, and especially 

 the human, cycle both of growth and of senescence has fre- 

 quently been interpreted as an active process of negative feed- 

 back, which operates unequally, which may contribute to the 

 relatively sharp arrest of growth at the level represented by the 

 specific size, but which results in a 'morphogenetic' senescence 

 depending in turn upon a rather limited number of key physio- 

 logical changes. 



With the hypothetical relationship between growth-cessation 

 and senescence in mind, a number of attempts have been made 

 in the past to interpret senile changes in terms of endogenous 

 'growth inhibitors', whether these are regarded as substances 

 or as physico-chemical conditions (Baker and Carrel, 1926; 

 Carrel and Ebeling, 1921; Simms and Stillman, 1936). The 

 case for such an inhibiting system was stated by Bidder (1932) 

 in the passage already quoted (p. 12). The nature of influences 

 determining mammalian organ size is virtually unknown. Some 

 of these appear to be extra-cellular and inhibitory. In cultures, 

 e.g. of diatoms, growth may be arrested by the accumulation 

 of a metabolite (Denffer, 1948). The most primitive types of 

 morphogenesis, such as that found in hydroids, depend on the 



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