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Benign Prostatic Hyperplasia (BPH)

Prostate Function and Causes of BPH

The main function of the prostate is to facilitate male fertility. This is accomplished through the liquid volume of ejaculate, rich in fructose, which functions as a fuel source for sperm, and also contains a protein called prostate-specific antigen (PSA). PSA is believed to help liquefy the ejaculate and promote sperm motility (McNicholas 2008).

The development of BPH is a multifactorial process. As men age, prostate cell growth becomes less well controlled by cell signaling activity. Also, the cells in the prostate become less responsive to signals that induce apoptosis or “programmed cell death”. This results in an overabundance of cells in the prostate, also known as prostate hyperplasia (McNicholas 2008).

This breakdown in cellular regulation that occurs with aging allows prostate cells to proliferate and promote the formation of additional tissue. This additional tissue is smooth muscle, and this tends to increase the overall muscle tone of the prostate, which can contribute to blockage of the urinary tract (McNicholas 2008).

Imbalanced hormone levels contribute to BPH. A derivative of testosterone called dihydrotestosterone (DHT) stimulates growth of the prostate. DHT is derived from testosterone via conversion by the enzyme 5α-reductase, which is an important pharmacologic target for BPH therapies (Lepor 2004). In addition, high levels of insulin-like growth factors and inflammatory markers (eg, C-reactive protein) can also contribute to BPH (Sarma 2012; McNicholas 2008).

Furthermore, ethnic differences have been reported, such as lower rates of BPH and prostate surgery among Asian men relative to Caucasian men. Furthermore, one study reported higher rates of moderate-to-severe lower urinary tract symptoms among Afro-Caribbean men relative to Caucasian men, whereas other studies have shown similar rates of BPH diagnosis and hospitalization among Afro-Caribbean men and Caucasian men (McNicholas 2008).

Estrogen and BPH

Estrogens appear to contribute to prostate tissue growth and may represent an underappreciated piece of the BPH puzzle (Ho 2008; Matsuda 2004).

As men age, estrogen (eg, estrone and estradiol) levels appear to increase. Aromatase, an enzyme which converts testosterone into estrogen, also increases with age in men (Vermeulen 2002). BPH risk also increases with age and studies have identified high concentrations of estradiol in cells from hyperplastic prostates (Jasuja 2012; Barnard 2009; Kozak 1982). Further investigations into the action of estrogen receptors in prostate cells led one group of researches to conclude that “…estrogens… may contribute at some level to the etiology of the most prevalent prostatic diseases including… BPH…” (Prins 2008).

Therefore, based on these and other findings, Life Extension suggests that aging men strive to maintain estradiol blood levels between 20 and 30 pg/mL for optimal prostatic and overall health.

A potentially useful strategy to help aging men control estradiol levels is to take an aromatase inhibiting drug like anastrazole (Arimidex®). One study showed that men 60 or older with low testosterone levels who took anastrazole for 12 months exhibited a reduction in serum estradiol levels without significant increases in BPH symptoms (Burnett-Bowie 2008). However, evidence is inconsistent regarding the efficacy of aromatase inhibitor therapy in BPH, as these drugs can increase DHT levels (Suzuki 1998). Fortunately, there are 5-alpha reductase-inhibiting drugs like Avodart® and finasteride that can block DHT formation and thus neutralize this factor behind so many cases of prostatic enlargement. Men who have BPH, and whose estradiol levels are above the optimal range of 20 – 30 pg/mL, are encouraged to discuss use of aromatase inhibiting drugs with their healthcare provider.