PATHOLOGICAL STATES IN EVOLUTION. 



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immense functional and structural results; not on changes which 

 can in any sense be called spontaneous, by which we may suppose 

 is meant those no cause can be assigned to, but on variations, 

 which, though they occurred ages ago, were obviously due to the 

 very same causes that the pathologist can demonstrate to be 

 working at the present day. Only such organisms as respond by 

 direct reactions in a manner that finally turns out to be useful, 

 or at the very least compatible with life and reproduction, are 

 able to survive. The whole of growth and development thus 

 becomes largely a function of effective morphogenetic repair to 

 organic failure and disease. 



Though this is not the place to deal at length with the vexed 

 question of transmission of modifications, it may be remarked 

 that the foregoing arguments seem to imply that such alterations 

 as a matter of fact are inherited. I think some progress can be 

 made if we simply assume provisionally that organisms do tend 

 to repeat themselves and that it is unlikeness rather than likeness 

 which requires explanation. We know that gross unlikeness is 

 almost always due to a lack or excess of some internal secretion, 

 hormone, or enzyme, and from this it may be inferred that 

 likeness is due to such catalytic machinery coming over in the 

 zygote, and to each differentiation producing anew its own 

 peculiar products which stimulate or inhibit further growth and 

 differentiation. Some time ago I was struck by a remark of 

 Starling's that each new organism seemed a fresh "creation." 

 He gave this up on account of the difficulty he found in the 

 " time element " of the problem, but I venture to think lie was 

 right in his surmise. There is a growing body of opinion in 

 support of this view, as the names of Cunningham, McBride, 

 Dendy, and Bourne seem to bear witness. We must certainly 

 take into account these regulators of metabolism, and if w T e 

 accept the view that hypo-thyroidism determines cretinism, or, 

 in the adult, myxoedema ; that hyper- thyroidism is the direct 

 cause of the phenomena seen in Graves' disease, just as hyper - 

 or hypo-pituitarism causes giantism or infantilism in children 

 while a later overgrowth of the gland causes acromegaly, I see 

 no difficulty in accepting th,e hypothesis that growth is deter- 

 mined, i. e. stimulated or finally inhibited, by non-living catalysts 

 or secretions not necessarily confined to the endocrine organs. 

 In this way a bridge may perl) aps be built between the orthodox 

 Weismannian and the Lamarckian. Growth and character cure 

 caused by determinants, but these are not part of the cytoplasm 

 itself, they are the machinery by and through which living 

 matter acts. The organism is not built up try special protoplasm 

 or by entelechies or by any mysterious elan creatif. It arises 

 from the definite influence of definite catalysts originating, in an 

 orderly sequence, as the organs become differentiated, while the 

 individual is as a whole exposed in an infinite progression to 

 the internal and external stimuli of a like but slowly changing 



