Hcg For The Treatment Of Benign Prostatic Hyperplasia
INTRODUCTION: ENDOGENOUS & EXOGENOUS hCG
Human Chorionic Gonadotropin, or hCG, is perhaps best known as either a fertility drug used to facilitate ovulation, or as an agent used by bodybuilders during or after a cycle of anabolic steroids (AAS) to help maintain or restore testicular function. It is well known that anabolic steroids suppress the hypothalamic-pituitary-testicular axis, preventing testicular Leydig cells from producing the body’s normal complement of testosterone, and leading to what is generally a temporary, reversible testicular shrinkage. The goal of the AAS using athlete or bodybuilder is to bring natural testosterone production back up to normal as quickly as possible after a steroid cycle, so as to maintain strength and size gains made during the cycle, and to avoid sexual dysfunction associated with low testosterone levels.
HCG is not produced in males; rather it is a hormone of human pregnancy secreted by cells of the fetal placenta shortly after the implantation of a fertilized ovum in the female womb. The hCG thus produced causes the female body to produce copious amounts of progesterone and estrogen. The high levels of progesterone maintain the function and growth of the endometrium, preventing menstruation. Clearly if menstruation were to occur, the pregnancy would be terminated. Thus hCG is critical for maintaining pregnancy.
HCG is capable of carrying out these functions because it is structurally similar to the naturally produced hormone LH, or luteinizing hormone. Similar enough in fact that it binds strongly to the body’s LH receptor, mimicking the actions of LH. During the normal menstrual cycle LH secreted by the pituitary ultimately leads to the maintenance of the endometrium. However if pregnancy fails to occur, LH levels decline during the cycle and the endometrium degenerates, leading to menstruation.
In a published study (1), a new and potentially exciting use for hCG in men is described: the treatment of benign prostatic hyperplasia, or BPH. It has been known for some time that hCG in vitro is capable of modulating the growth of prostatic cancer cells, leading to decreased growth rates, apoptosis, and cell death. Experiments leading up to this discovery were prompted by reports that hCG is capable of blocking metastasis of neoplastic Kaposi’s Sarcoma in immunodeficient mice. Further research showed that hCG administration led to regression of Kaposi lesions in AIDS patients. Interestingly, some recent research has suggested that contaminants present in some hCG preparations, rather than the hCG itself may be responsible for the effects of hCG on Kaposi’s lesions (2). These findings have led a number of experts to recommend against the use of hCG to treat Kaposi’s sarcoma. It would be ironic if “bad” science had actually contributed to the current research suggesting that hCG is beneficial in the treatment of BPH.
