Diet/Lifestyle Strategies for Preventing Benign Prostatic Hyperplasia

Although benign prostatic hyperplasia (BPH) is often viewed as an inevitable concomitant of the aging process, recent research establishes that this syndrome is significantly more common in men with metabolic syndrome. Moreover, twentienth century epidemiology focusing on quasi-vegan rural China reveals that this syndrome may in fact be substantially preventable. The decline in cellular apoptosis which appears to be a key driver of BPH should be counteracted in part by diet/lifestyle measures which minimize systemic IGF-I activity. Diets moderate in protein and very low in animal products are associated with low plasma IGF-I levels, reflecting decreased hepatic production of this hormone. Leanness, exercise training, and other lifestyle measures which minimize diurnal insulin secretion, have been found to correlate with reduced BPH risk, and can be expected to reduce systemic and prostatic IGFI/IGF-II bioactivity by increasing hepatic secretion of IGFBP-1. Apoptosis of prostate cells can also be promoted by selective agonists for estrogen receptor-β; high dietary intakes of soy isoflavones can function as such agonists. Conversion of prostate epithelial and stromal cells to a myofibroblast phenotype by transforming growth factor-β contributes importantly to the expansion of the stromal compartment in BPH; there is reason to suspect that this transition could be opposed by the antioxidant activity of spirulina, AMPK-activating drugs or nutraceuticals, and possibly adiponectin (suggesting a further benefit of leanness). Although calcitriol analogs appear to have potential for preventing and treating BPH, there is no current evidence that dietary modulation of vitamin D status can be beneficial in this regard. Prospects for prevention of BPH may be good in individuals who adopt optimally healthprotective diet, lifestyle, and nutraceutical strategies. Benign Prostatic Hyperplasia – A Component of the Metabolic Syndrome Benign prostatic hyperplasia (BPH) is often thought of as an inevitable concomitant of aging, as prostate volume increases progressively with age; in the U.S., prevalence of symptomatic BPH has been estimated as 50% at age 60 and 80% at age 85. Nonetheless, recent studies demonstrate that, at any given age, BPH and associated lower urinary tract symptoms (LUTS) are significantly more common in men with metabolic syndrome. 3 Pioneering research by Hammersten and Hogstedt demonstrated that both prevalent BPH and annual prostate growth rate correlate positively with fasting serum insulin as well as other typical features of this syndrome, including waist circumference, blood pressure, and low HDL; 5 subsequent research has confirmed these associations, and has also demonstrated that LUTS is more common in metabolic syndrome. The link between hyperinsulinemia and BPH risk remains strong in multiple regression analyses. 11 Moreover, regular exercise and moderate alcohol consumption, independent of body weight, are associated with decreased BPH risk, and of course tends to downregulate insulin levels by favorably impacting muscle insulin sensitivity. These findings suggest that elevated diurnal insulin may play a pathogenic role in BPH and LUTS, and may be largely responsible for the association of these conditions with metabolic syndrome. Commentators have suggested that hyperinsulinemia may both promote prostate growth, while also abetting LUTS via its stimulatory impact