Hormones Most experts consider androgens (testosterone and related hormones) to play a permissive role in the development of<unk> . This means that androgens must be present for<unk>  to occur, but do not necessarily directly cause the condition. This is supported by evidence suggesting that castrated boys do not develop<unk>  when they age. In an unusual study of 26 eunuchs from the palace of the Qing dynasty still living in Beijing in 1960, the prostate could not be felt in 81% of the studied eunuchs. The average time since castration was 54 years (range, 41–65 years). On the other hand, some studies suggest that administering exogenous testosterone is not associated with a significant increase in the risk of<unk>  symptoms, so the role of testosterone in prostate cancer and<unk>  is still unclear. Further randomized controlled trials with more participants are needed to quantify any risk of giving exogenous testosterone. Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical mediator of<unk>  growth. DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2. DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is ten times more potent than testosterone because it dissociates from the androgen receptor more slowly. The importance of DHT in causing nodular<unk>  is supported by clinical observations in which an inhibitor of 5α-reductase such as finasteride is given to men with this condition. Therapy with a 5α-reductase inhibitor markedly reduces the DHT content of the prostate and, in turn, reduces prostate volume and<unk>  symptoms. Testosterone promotes prostate cell proliferation, but relatively low levels of serum testosterone are found in patients with<unk> . One small study has shown that medical castration lowers the serum and prostate hormone levels unevenly, having less effect on testosterone and dihydrotestosterone levels in the prostate. While there is some evidence that estrogen may play a role in the cause of<unk> , this effect appears to be mediated mainly through local conversion of androgens to estrogen in the prostate tissue rather than a direct effect of estrogen itself. In canine in vivo studies castration, which significantly reduced androgen levels but left estrogen levels unchanged, caused significant atrophy of the prostate. Studies looking for a correlation between<unk><unk>  and serum estrogen levels in humans have generally shown none. In 2008, Gat et al. published evidence that<unk>  is caused by failure in the spermatic venous drainage system resulting in increased hydrostatic pressure and local testosterone levels elevated more than 100 fold above serum levels. If confirmed, this mechanism explains why serum androgen levels do not seem to correlate with<unk>  and why giving exogenous testosterone would not make much difference. Diet Studies indicate that dietary patterns may affect development of<unk> , but further research is needed to clarify any important relationship. Studies from China suggest that greater protein intake may be a factor in development of<unk> . Men older than 60 in rural areas had very low rates of clinical<unk> , while men living in cities and consuming more animal protein had a higher incidence. On the other hand, a study in Japanese-American men in Hawaii found a strong negative association with alcohol intake, but a weak positive association with beef intake. In a large prospective cohort study in the US (the Health Professionals Follow-up Study), investigators reported modest associations between<unk>  (men with strong symptoms of<unk>  or surgically confirmed<unk>  and total energy and protein, but not fat intake. There is also epidemiological evidence linking<unk>  with metabolic syndrome (concurrent obesity, impaired glucose metabolism and diabetes, high triglyceride levels, high levels of low-density cholesterol, and hypertension). Degeneration<unk>  is an age-related disease. Misrepair-accumulation aging theory suggests that development of<unk>  is a consequence of fibrosis and weakening of the muscular tissue in the prostate. The muscular tissue is important in the functionality of the prostate, and provides the force for excreting the fluid produced by<unk>  glands. However, repeated contractions and dilations of myofibers will unavoidably cause injuries and broken myofibers. Myofibers have a low potential for regeneration; therefore, collagen fibers need to be used to replace the broken myofibers. Such misrepairs make the muscular tissue weak in functioning, and the fluid secreted by glands cannot be excreted completely. Then, the accumulation of fluid in glands increases the resistance of muscular tissue during the movements of contractions and dilations, and more and more myofibers will be broken and replaced by collagen fibers.
Benign prostatic hyperplasia
Prostate cancer
Chronic bacterial prostatitis
Heart failure
Acute prostatitis
Diabetes
Granulomatous prostatitis
Urinary bladder disease