654 FREDERICK S. HAMMETT 



investigations in an effort to determine the contributing factors to this 

 phenomenon. Although nerve impulses were at first considered as the 

 main source of stimuli for mammary hyperplasia, the experiments of de 

 Sinety, Goltz, Rohrig, Rein, Mironow, Ribbert, Pfister, Kehrer, and 

 others, demonstrated that this hypothesis was untenable since interference 

 with the nerve supply to the breasts produced no marked hindrance in 

 development. 



Clinical and experimental observations having indicated that castra- 

 tion inhibits the pubertal mammary development, Halban and Knauer 

 investigated the problem and found that when castration is followed by 

 ovarian implantation an apparently normal mammary development occurs. 

 From this they concluded that the pubertal impulse to mammary growth 

 in normal females is dependent upon material secreted by the ovary. 

 This idea was supported by the work of Fraenkel (a), Bouin and Ancel, 

 and later by O'Donoghue (a) (&) (c), and others. It was but natural that 

 the idea of an ovarian stimulus to mammary hyperplasia during preg- 

 nancy should be evolved. But Halban (c) (1905), reasoning from the 

 clinical evidence that puerperal involution does not follow bilateral ovari- 

 ectomy during pregnancy, opposed this view, and considered that "only the 

 recently fertilized ovum can be the cause for the initiation of the changes 

 in the maternal organism. 7 ' The problem thus being narrowed down to 

 two possible sources, Halban, by a process of reasoning, eliminated the 

 fetus as an influence, and evolved the hypothesis that the placenta during 

 pregnancy takes over the stimulating functions of the ovaries, the latter 

 having but little, if any, influence on mammary hyperplasia during this 

 period. This conclusion was apparently confirmed by Niklas and Fell- 

 ner, both of whom obtained changes in mammary tissue as the result of 

 injections of placenta! extracts. Nevertheless, later experiments by Mandl 

 and Kreidl, Lane-Claypon and Starling, Foa, Basch, Biedl and Konig- 

 stein, Frank and linger, and Biedl, gave either negative or at most slightly 

 positive results. Moreover, Foa and Basch showed that fetal extracts were 

 effective in producing mammary hyperplasia and, taking this in conjunc- 

 tion with the fact that Hammett (c) failed to find any increased mammary 

 development as the result of feeding desiccated placenta post partum to 

 lactating women, when compared with the course of development in women 

 not receiving the placental material, the evidence at hand can scarcely be 

 considered valid for assigning to the placenta alone the function of pro- 

 ducing a stimulus to mammary hyperplasia. 



The development of the mamma is the preparation of this tissue for as- 

 suming the function of milk secretion, and the question of the origin of the 

 source and stimulus to the production of milk has involved the possibility 

 that the placenta plays a significant part. From early times it has been 

 recognized that there exists a relationship between milk secretion and the 

 functioning of the genital organs. Hippocrates noted that with the cessa- 



