Hormones play an important part in prostate health; both in the promotion of prostate disease as well as in the treatment of specific disorders with hormone therapy. Prostate cancer is influenced by hormones and the relationship and balance of those hormones to each other; specifically, testosterone (and its conversion into dihydrotestosterone (DHT)) and estrogen/estradiol (see Testosterone and Prostate Cancer). Dihydrotestosterone (DHT) is involved in noncancerous growth of the prostate (BPH) as well as the development of prostate cancer. DHT also stimulates growth of prostate cells, and is reportedly as much as 30 times more potent than testosterone. Hormones can also influence the growth of the prostate in cases of BPH (see Causes and Risk Factors for BPH).
Male hormones are like fuel for prostate tumors, which cannot grow without them. Conventional hormone therapy, as treatment for prostate cancer, is designed to reduce the levels of the fueling male hormones—primarily testosterone and dihydrotestosterone (DHT)—and thereby starve the tumor. Although hormone therapy does not cure cancer, it can slow the growth of prostate cancers, or even cause them to shrink.
Hormone therapy is not for every man who has prostate cancer. It is typically recommended:
- For men whose prostate cancer has already moved beyond the gland and has invaded nearby or distant parts of the body
- Before surgery or radiation in an attempt to shrink the tumor and enhance the effectiveness of the other therapies
- In combination with radiation therapy in certain men whose cancers are likely to return after therapy
- For men who have already had surgery or radiation and their cancer has returned
Three additional hormones have an impact on how testosterone and estrogen/estradiol behave and affect prostate health:
Follicle-stimulating hormone (FSH)
Follicle-stimulating hormone (FSH), important for sperm production, is produced by the pituitary gland.
Luteinizing hormone (LH)
Luteinizing hormone (LH), also produced by the pituitary gland, stimulates secretion of testosterone.
Gonadotropin-releasing hormone, also known as luteinizing-hormone-releasing-hormone (LH-RH), is produced and released from the hypothalamus in the brain. LH-RH stimulates secretion of LH, which in turn stimulates secretion of testosterone.
If secretion of either LH or FSH declines, testosterone production also falls off, and a deficiency of testosterone (increase in estrogen) can result.
Testosterone levels are also affected by an enzyme called aromatase, which is found in fat tissues. Aromatase converts testosterone into estrogen, which alters the ratio of estrogen to testosterone. All of these factors are involved in a delicate balancing act to maintain prostate health.
Although our knowledge of prostate cancer has improved since the days of Charles Huggins, MD, the surgeon who treated prostate cancer with surgical castration, there are still unanswered questions about the relationship between hormones and prostate cancer. Here is what the experts generally say:
- Evidence strongly indicates that while testosterone is in the prostate cancer equation, it is not the cause of prostate cancer alone.
- One of the main contributing causes of prostate cancer appears to be an imbalance in the ratio of testosterone to estrogen (estradiol).
- If you achieve optimal hormone balance, you will have a healthier prostate and reduce your risk of prostate disease.
Finasteride (Proscar) is a 5-alpha-reductase inhibitor used to treat benign prostatic hypertrophy (BPH). When scientists noticed that finasteride inhibited the conversion of testosterone to DHT, they initiated a study called the Prostate Cancer Prevention Trial (PCPT) in the early 1990s. (Thompson 2003) The trial evaluated 18,000 men age 55 and older and lasted seven years. The results, published in 2003, found that:
- 18.4 percent of men who took finasteride developed prostate cancer over the study’s course
- 24.4 percent who took placebo developed prostate cancer over the study’s course
- Men in the finasteride group had a 28 percent reduction in prevalence in prostate cancer and a smaller prostate volume than men in the placebo group
- The rate of high-grade cancers was greater in the finasteride group (6.5%) than in the placebo group (5.1%). The reason for this is unknown.
- Most cancers in the finasteride group were small and localized.
The incidence of high grade cancers in the finasteride group during this study is one reason medical professionals are reluctant in most instances to prescribe finasteride for prostate cancer treatment.
Since the PCPT, subsequent studies have reinterpreted the findings. Some research confirmed the reduced risk of prostate cancer (Thompson 2008), while others re-examined the increased risk of high-grade tumors and determined that finasteride actually reduced the risk of developing aggressive cancer when compared with placebo. (Pinsky 2008; Redman 2008)
However, two physicians from Johns Hopkins evaluated all the findings and note that the decrease in prostate cancer related to finasteride was much smaller than originally reported and not statistically significant. Therefore, they believe finasteride will not significantly help reduce the risk of prostate cancer among men who are monitored regularly and who have a biopsy when they experience an elevated PSA or abnormal digital rectal exam. They recommend men not take 5-alpha-reductase inhibitors as a means to prevent prostate cancer, and warn that because 5-alpha reductase inhibitors reduce PSA levels by about 50 percent, men should multiply their PSA numbers during the first two years they use the drugs, by 2.3 for years 2 through 7, and by 2.5 for 7 years or longer to get a more accurate indication of their prostate cancer risk that may require a biopsy. (Johns Hopkins)
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Updated June 1, 2011