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May 24, 1947


JAMA. 1947;134(4):348-351. doi:10.1001/jama.1947.02880210026006

The theory that benign hyperplasia of the prostate gland is the result of hormonal imbalance is supported by much experimental and clinical observation. The fact that benign hypertrophy does not develop except in the presence of a functioning testis is the strongest evidence yet offered, according to Moore,1 that the disease is an endocrinologic dystrophy. It is also well established that the testes are the main center of androgenic activity and exert a powerful influence on the development and function of the entire genital organs, for without the natural male hormone (testosterone) atrophy, hypogonadism, eunuchoidism and degrees thereof result. There is no record of prostatic obstruction ever developing in a true eunuch, although Young2 and others have performed prostatectomy on men previously castrated in early life. Barron and Huggins3 consider that removal of testicular androgens by excision causes atrophy of the prostate gland and cessation of secretion,

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