ALEX COMFORT 
faulty copying in cells which divide clonally, and that it is a 
mechano-physical process involving the “setting’’ of low- 
turnover colloids and other macromolecules. 
It would be a very brief and satisfying explanation of age 
changes if they were due simply to the steady loss of vital and 
irreplaceable cells. One difficulty in assessing this view, apart 
from that of counting cells, and knowing what cells to count, is 
that we do not know what makes fixed post-mitotic cells die, 
or how far their enzyme system can be damaged by events 
analogous to mutation. Certainly animals such as insect 
imagos, which have little or no cell division, are inordinately 
resistant to life-shortening by radiation. It may be that the rat 
experiments carried out by McCay, in which life was prolonged, 
effectively, by lengthening childhood through calorie restric- 
tion, are in a sense irrelevant to the problem of prolonging 
human adult vigour, for in all probability this type of manoeuvre 
acts by delaying development, and perhaps merely by post- 
poning the age at which certain timekeeping cells reach their 
fixed post-mitotic state; and it may be that the real problem 
will prove to be one of conserving these cells as we conserve 
irreplaceable teeth—not so much of postponing the age at 
which the permanent set erupts, as of preventing decay and 
filling biochemical cavities as they develop. It would be 
tempting to look on loss of neurones per se as a possible time- 
keeping mechanism, for both between species and between 
breeds within a species it is the index of cephalization—the 
excess of brain over the expected amount—which is correlated 
most closely with longevity, and next to the biochemical infor- 
mation store in cell nuclei the central nervous system is our 
main and overriding homoeostatic system. If this were so, if 
the deterioration of fixed post-mitotic cells were the timing 
mechanism for mammalian senescence, the prospect of slowing 
it seems by no means hopeless, for the very diversity in the rate 
of ageing between similar mammalian species suggests that the 
rate of spoilage might be accessible. When typical ageing can 
be produced by experimental damage to the brain, I shall be 
prepared to take this particular speculation further. At the 
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