Is excessive masterbation linked to prostate hyperplasia? .
BPH (hyperplasia) is not related to prostate cancer - seperate problems. BPH does not cause cancer - different zones of the prostate.
Estrogen is one strong link to prostate cancer (as are vasectomies). Testosterone (endogenous or exogenous has not been linked to increased rates of prostate cancer), in fact low testosterone is linked to the most aggresive prostate cancers.
Minerva Endocrinol. 2006 Mar;31(1):1-12.
Links
Aromatase and prostate cancer.
Ellem SJ,
Risbridger GP.
Centre for Urological Research, Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia.
The normal growth and development of the prostate requires the presence and action of androgens, which are also known risk factors in the origins of benign and malignant prostate disease. Paradoxically, the incidence of prostate disease increases with age when serum androgen levels are in decline and emerging evidence suggests that estrogens may also be important in the normal prostate, as well as in the etiology of prostate disease. Both estrogen receptor subtypes are present in the prostate, demonstrating that the gland responds directly to estrogens. Recent data suggests that estrogens play a role in prostate disease and has demonstrated that high doses of estrogens induce premalignant dysplasia and in combination with high doses of androgens, malignancy. The production of estrogens from androgens is mediated by the aromatase enzyme, the aberrant expression of which plays a critical role in the disease process in other tissues, most notably the breast. The prostate expresses aromatase within the stroma of benign tissue, while in malignancy there is an induction of epithelial expression with altered promoter utilisation. Although the presence of aromatase in the prostate and its aberrant expression in prostate cancer is significant, its role and contribution to prostate carcinogenesis remains unclear. Transgenic mouse models lacking aromatase (ArKO) and over-expressing aromatase (AROM+) have provided an ideal means to examine aromatase expression in the prostate. Studies using these animals may lead to a better understanding of the role that aromatase--and therefore estrogen--plays in the development and progression of prostate disease.
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Vasectomy and prostate cancer:
JAMA. 1993 Feb 17;269(7):873-7.
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A prospective cohort study of vasectomy and prostate cancer in US men.
Giovannucci E,
Ascherio A,
Rimm EB,
Colditz GA,
Stampfer MJ,
Willett WC.
Channing Laboratory, Department of Medicine, Harvard Medical School, Boston, MA 02115.
OBJECTIVE--To examine prospectively the relationship between vasectomy and prostate cancer. DESIGN--Cohort study. SETTING--Health professionals (dentists, veterinarians, osteopaths, optometrists, pharmacists, and podiastrists) in the United States. PARTICIPANTS--There were 10,055 male members of the Health Professionals Follow-up Study, aged 40 to 75 years, who had had a vasectomy, and 37,800 members who had not had a vasectomy at the time of study entry in 1986. These participants had provided detailed information on various life-style variables including diet. MAIN OUTCOME MEASURE--Diagnosis of prostate cancer. RESULTS--Between 1986 and 1990, 300 new cases of prostate cancer were diagnosed in participants who were initially free of diagnosed cancer. Vasectomy was associated with an elevated risk of prostate cancer (age-adjusted relative risk, 1.66; 95% confidence interval, 1.25 to 2.21; P = .0004). This elevated risk persisted after excluding 21 stage A1 cases (age-adjusted relative risk, 1.56; 95% confidence interval, 1.15 to 2.11; P = .004). Among men who had their vasectomy at least 22 years in the past (before 1965), the risk of prostate cancer was even higher (relative risk, 1.85; 95% confidence interval, 1.26 to 2.72; P = .002). This elevated risk among men with vasectomy did not appear to be caused by detection bias and persisted when we controlled for diet, level of physical activity, smoking, alcohol consumption, educational level, body mass index, and geographical area of residence. CONCLUSIONS--These results support evidence from other epidemiologic studies that vasectomy increases risk of prostate cancer. The consistency of results among various epidemiologic studies, the increase of risk over time following vasectomy, the apparent lack of confounding or bias, and the existence of physiological changes in the prostate following vasectomy suggest that the association may be causal.
