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One of the primary functions of the neuroendocrine system is the regulation of male sex hormones and androgens, especially testosterone and human growth hormone, to enable sperm development and for sperm retention. When a fertilised egg implants in the uterus, the ovaries secrete progesterone from the pituitary gland that prevents the egg from getting too far along its way to the uterus, and stimulates the ovaries to release luteinising hormone and follicle stimulating hormone. This stimulates the development of the adrenal cortex, which produces both sex hormone binding globulin (SHBG) and FSH (FSH stimulates synthesis of testosterone), and the conversion of androstenedione to DHT. While these functions of the CNS are only partially relevant to the functioning of the testes, a direct influence of these chemicals on the testes results in the formation of scrotal hyperplasia, which leads to an increased risk of prostate cancer. The direct effect of these testosterone-progesterone hormones on the penis is not known. In a similar situation, in the absence of gonadal hormone or estradiol, testicular cancer is increased in men who do not undergo surgical male changes, but who nevertheless carry a testosterone level above the normal range [37–42]. A possible explanation could be a genetic predisposition that makes men with higher testosterone levels, who have had more sexual exposure to androgens, more prone to developing scrotal hyperplasia, or an inability to produce androstenedione.
In summary, when there is a direct relationship between a man’s blood type (e.g. A, B, O, OA, T, D), and semen chemistry and testicular function, men in the group with A blood type are at increased risk of developing testicular cancer. The direct effect of sex hormones on testicular function could be a potential trigger for prostate cancer in men of OA type.
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