276 /. /. Christian 



substance, such as adrenal hormones, contained in the milk were responsible 

 for the decrease in weights of the progeny. The mechanism by which these 

 effects were carried over into the second generation of progeny is not known. 

 Presumably the second generation of young may reflect the inanition suf- 

 fered by the first generation of progeny as a result of deficient lactation. 

 However, the fact that androgens can produce subsequent permanent 

 sterility when injected into mice less than 10 days old suggests the possibil- 

 ity that increased amounts of adrenal androgens may reach the nursing 

 young via the milk and exert similar partial effects if some escape metabo- 

 lism in the liver. The weights of the young at birth were unaffected by the 

 earlier crowding of their mothers. Although the precise mechanisms are not 

 understood, these results support and extend D. Chitty's results with voles 

 and help in providing an explanation for the prolonged effects of high 

 density on surviving young observed in natural populations, such as 

 Chitty's (1952, 1954) observations on young voles from natural popula- 

 tions. 



5. Growth 



The effects of increased population density on growth have not been 

 studied to the same degree as its effects on other aspects of endocrine 

 physiology, although suppression of the secretion of pituitary growth 

 hormone presumably is a part of the response to stimuli which also result 

 in the increased secretion of ACTH (Selye, 1950) . However, there are a few 

 experiments which clearlj^ indicate that the growth of house mice is de- 

 pressed in response to increased population density (Vetulani, 1931; 

 Christian, 1955b) . It has been shown also that there is suppression of 

 growth in all but the dominant and second-ranking mice in a group of six 

 (Christian, 1961). The degree of inhibition was related to rank. 



6. Inflammation, Resistance to Infection, and Population Den- 

 sity 



In earlier sections of this account the inhibition of the inflammatory re- 

 response, granulation, and antibody formation, and therefore resistance to 

 disease, by adrenal carbohydrate-active corticoids was discussed. Most of 

 the experimental evidence cited was based on the results of injecting corti- 

 cal hormones. A few examples of decreased resistance to infectious agents 

 brought about by stimuli, such as cold, which stimulated increased adreno- 

 cortical secretion were given. However, even though these experiments 

 indicated that such effects might occm- under natural circumstances, they 

 did not establish this possibility, and especially they did not show that 

 increased population density could stimulate a sufficient increase in the 



