54 General Discussion 



be found in skin exposed to light. Pigmentation must play a certain 

 part in the ageing process. Although it is not a product of ageing itself, 

 it becomes much more intensive in the ageing skin. The process of age- 

 ing is also manifested in a higher differentiation of the epidermis cells. 

 The tonohbrils are numerically increased. But they are increased in 

 other conditions as well, i.e. in the skin of animals painted with methyl- 

 cholanthrene and in precancerous stages. 



Tunbridge: Yes, I think we all agTce that where you have trauma as a 

 secondary factor — whether the trauma is physical, the result of disease, 

 or what you will — ^you will get changes. But where tissue is not exposed 

 to trauma, is there something inborn? I think Prof. Cameron con- 

 sidered that he could not find evidence of it. There is a pattern of 

 secondary degeneration, but is there a primary change? I think he even 

 said that the process manifests itself in the same way, be it in young or 

 old; only the degree changes with chronological age. 



Cameron: I think most pathologists recognize in ageing people two or 

 three different changes in cells, for example the wear and tear ])igment 

 found in cardiac muscle and in liver cells, and sometimes found in other 

 organ cells such as the spleen and kidney. That's one thing. Secondly 

 they claim to be able to recognize shrinkage or senile atrophy; I don't 

 believe they can but a lot of them say they can. Thirdly, in some 

 organs, for example the liver, they find these queer cells, called yellow 

 cells — ^Max Clara has studied them in great detail — which are shrinking 

 cells showing a change in their staining reactions and their cytoplasm 

 and nuclear changes which pathologists call pycnosis. All these changes 

 can be induced by vascular disease, and that is the whole point of my 

 talk. I want to know how can you distinguish these from arteriosclerotic 

 changes? You get exactly the same picture in young people with 

 arteriosclerosis, for example, or various other diseases. I frankly can't 

 say, and I don't believe that anyone can say whether these cells are 

 due to ageing or are specific changes. 



Rubin: My bias is functional as I'm a biochemist, but when techniques 

 become delicate enough to pick uj) differences of a biochemical nature 

 within the individual cell, for instance the concentrations of certain 

 enzymes and so on, which we can only get at indirectly now in func- 

 tional studies, I think probably you'd be able to find differences in 

 individual cells. 



Aub: Have any been found? 



Rubin: None that I know. 



Tunbridge: But might your changes be the result of a different 

 nutritional supply, conditioned by that and not fundamental to age? I 

 think that was Prof. Cameron's point. 



Medawar: Could I take up that point? Prof. Cameron maintains that 

 there is no pathological change specific to old age because all the changes 

 he considers, with a few trivial exceptions, are also found in young 

 people. Surely what is specific to old age is the frequeney of occurrence 

 of these various pathological conditions? The age-specific element in 

 cancer is the fact that its frequency of incidence does rise later in life. If 

 one translates that back to a statement about the individual, one can 



