ALEX COMFORT 
artificially. Burnet has recently suggested that the particular 
mutations responsible may be those which accumulate in 
lymphocytes, giving rise to clones which ignore the ban on the 
production of antibodies against body constituents. This 
hypothesis may or may not be correct, and I give it here simply 
as an instance of a mutative process which it might conceivably 
be possible to modify. A process of this sort could meet the 
statistical objection to point mutation as a cause of ageing by 
simple cell loss. Maynard Smith has computed that, given rates 
similar to the apparent rate of germinal mutation, about 
two million cells would have been affected by the age of 30, 
and perhaps four million by the age of 60. If loss were 
the cause of ageing, this is not enough. If, however, harmful 
properties and a selective power of clonal multiplication were 
also involved, the numerical possibility seems rather better. 
We can still hope, therefore, for a more localized and tractable 
cause for the rise in mortality with age than generalized somatic 
mutation. 
The longevity of human tissues in storage is not, perhaps, 
likely to have a great influence on our longevity as individuals. 
There is the same fallacy in the conception of spare parts as a 
fundamental remedy for senescence as in the idea that better 
medical services will push up the limit of the lifespan; some of 
us certainly age more rapidly in one system than in another, 
but ageing is characteristically an increase in the number and 
variety of homoeostatic faults. For this reason alone the interest 
of grafting and storage techniques for age studies is still much 
more for their contribution to theory than for the chance of 
using them as a prosthetic remedy for ageing. Professor Krohn’s 
work in making age chimeras by grafting mouse ovaries from 
old to young and from young to old is an elegant example of 
this kind, but it was found that a transplanted ovary did not 
gain in longevity from being in a young environment. 
Both organ culture and organ storage might throw some light 
on the réle of somatic ageing in mutation, and on the related 
problem of the general stability of somatic cell-clones. I must 
confess to being somewhat lost in the literature of tissue and 
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