THE USE OF HCG TO TREAT BENIGN PROSTATIC HYPERPLASIA

THE USE OF HCG TO TREAT BENIGN PROSTATIC HYPERPLASIA

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.
 

These observations, coupled with reports that LH/hCG receptor genes are present in human BPH tissue (3) prompted the authors of the current paper under discussion (1) to investigate whether hCG administration might halt or slow the progression of BPH, or at least improve symptoms associated with the disorder.

The authors of the current study performed a double blind placebo controlled trial involving 101 patients with BPH. 53 were given low-dose hCG, 0.5 IU sublingually 4 times daily; the remaining 48 were administered placebo. The fact that hCG was used sublingually is in itself somewhat interesting. HCG is not normally administered this way; rather it is injected subcutaneously or intramuscularly. The authors assumed that at such low doses the hCG would be unable to stimulate any significant increase in testosterone production, which might exacerbate existing BPH.

The primary determinant of the efficacy of treatment was based on the subjects’ responses to a standard set of questions ranking severity of symptoms before and after treatment, the so-called AUA Total Symptom Index Score. Symptoms described included both obstruction of urination (intermittency, force and straining) and irritative symptoms (incomplete voiding, frequency, urgency, and nocturia). Each question is scored from zero to five, with a total possible score between zero and 35. Mild BPH is generally associated with a score of less than 7; moderate 8 – 19; severe 20 – 35.

Another set of questions ranking sexual function was administered. Higher self-ratings indicated greater confidence in sexual competence. In addition, prostate volume, PSA, and peak urine flow were measured before and after treatment.

When the data were analyzed after 12 weeks of treatment, hCG had significantly improved AUA and sexual function scores compared to placebo. Subjects receiving hCG experienced a mean decline in AUA scores of –5.67 +/- 5.27 compared to a decline of –3.38 +/- 4.88 in the placebo group. The average percent improvement in AUA scores was 68% in subjects with mild to moderate prostatic disease and 99% in those with moderate to severe disease. Similarly, patients receiving hCG experienced a greater improvement in sexual functioning. Scores improved by an average of 5.57 in the hCG group but by only 0.72 in the placebo group. According to the authors,

“These data compare favorably with those in published reports [4] of the pivotal clinical trials for alpha 1 blockers and type II 5alpha-reductase inhibitors.”

There were no significant differences in peak urine flow volume between the two groups, and neither PSA nor prostate volume showed any significant changes during the study.

As for the mechanism by which hCG may be acting to improve BPH symptoms, the authors speculate that it may result from antiinflammatory actions attributed to hCG. HCG has been observed to reduce the proliferation of monocytes, immune cells that secrete proinflammatory cytokines. In animals and cell cultures treated with hCG, a decline in such proinflammatory compounds as tumor necrosis factor alpha, interleukin-6 and interleukin-1 has been observed. Inflammation is often associated with the proliferation of tissue near the focus of inflammation, and such proliferation of prostatic tissue could lead to enlargement of the gland and the associated obstructive symptoms.

The authors make another intriguing remark regarding the antiproliferative action of hCG, and that is that hCG has been shown to have a direct antiproliferative effect on cultured breast epithelial cells (5). Other researches have suggested that hCG might be used prophylactically to prevent breast cancer (6). Since gynecomastia in males represents a proliferation of ductal epithelial tissue, perhaps the possibility exists that hCG might help prevent this scourge among AAS using bodybuilders. At this point such a suggestion is pure speculation, but the possiblity should not be wholeheartedly dismissed either.

CONCLUSION

Low dose hCG administration to prevent or treat BPH may be a viable alternative for persons wishing to avoid the side effects associated with traditional BPH treatment such as finasteride and alpha 1 adrenergic blockers. Bodybuilders and athletes are often reluctant to use the former for fear of developing side effects such as sexual dysfunction and possibly gynecomastia. Moreover, dihydrotestosterone (DHT), the production of which is blocked by finasteride, is perceived as being beneficial to fueling the aggression necessary to get through grueling training sessions. There is also a general belief in the bodybuilding community that DHT plays a role in the neural adaptation to strength training that is responsible for a portion of the strength gains made in response to resistance training. Alpha 1 blockers in turn are associated with their own set of unpleasant side effects such as weight gain, sexual dysfunction, fatigue, and orthostatic hypotension. In the current study on the other hand, there were no significant differences in adverse side effects between the treatment and placebo groups.

Note that this is the first study of its kind to show that hCG is effective in treating BPH. The findings therefore should be considered preliminary, and in need of independent verification. A person who is currently using finasteride with or without an alpha blocker should NOT abandon that therapy without at least discussing these findings with his physician. HCG should be considered something that might be best used as an adjunct to existing treatments, or as a possible preventative therapy to be used by someone who is not suffering from BHP but is concerned about the possibility of developing it the disease.

(1) Godschalk MF, Unice KA, Bergner D, Katz PG, Mulligan T, McMichael J. A Trial Study: The Effect of Low Dose Human Chorionic Gonadotropin on the Symptoms of Benign Prostatic Hyperplasia. J Urol. 2003 Oct;170(4):1264-1269

(2) Bisacchi D, Noonan DM, Carlone S, Albini A, Pfeffer U. Kaposi's sarcoma and human chorionic gonadotropin: mechanisms, moieties and mysteries. Biol Chem. 2002 Sep;383(9):1315-20.

(3) Tao YX, Bao S, Ackermann DM, Lei ZM, Rao CV. Expression of luteinizing hormone/human chorionic gonadotropin receptor gene in benign prostatic hyperplasia and in prostate carcinoma in humans. Biol Reprod. 1997 Jan;56(1):67-72

(4) Lepor H, Williford WO, Barry MJ, Brawer MK, Dixon CM, Gormley G, Haakenson C, Machi M, Narayan P, Padley RJ. The efficacy of terazosin, finasteride, or both in benign prostatic hyperplasia. Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group. N Engl J Med. 1996 Aug 22;335(8):533-9.

(5) Lojun S, Bao S, Lei ZM, Rao CV. Presence of functional luteinizing hormone/chorionic gonadotropin (hCG) receptors in human breast cell lines: implications supporting the premise that hCG protects women against breast cancer. Biol Reprod. 1997 Nov;57(5):1202-10.

(6) Rao CV. Does full-term pregnancy at a young age protect women against breast cancer through hCG? Obstet Gynecol. 2000 Nov;96(5 Pt 1):783-6.