Prostate cancer is one of the most common cancers of older men, with a median age of onset of 72 years. It is the sixth most common cancer in the world and represents the third most common cause of cancer death in American men. However, because its age of onset is usually so late in life and because a variety of treatment options exist for both localized and advanced disease, many men with prostate cancer ultimately end up dying of other causes. In fact, many believe that if all men lived long enough, they would ultimately develop prostate cancer. (Davis 2005 23)
The normal prostate encircles the neck of the bladder and urethra and consists of variously sized glandular spaces lined by two layers of epithelium and separated from the fibromuscular stroma by a distinct basement membrane. Both epithelial and stromal cells have receptors for testosterone and its metabolite, dihydrotestosterone (DHT), produced largely by the stromal cells, and respond to these growth factors with cell proliferation. While the initial causes of prostate cancer are not known, it is likely that the initial neoplastic change involves cumulative damage to deoxyribonucleic acid (DNA). Evidence that obesity plays a major role in the pathogenesis of prostate cancer risk is inconsistent. Possible reasons for inability to detect an association include the difficulty in screening obese patients and the confounding influence of diabetes mellitus, known to increase risk for prostate cancer. However, many lines of evidence suggest that abdominal obesity, even in lean patients, is associated with increased risk for cancer progression, and that obesity facilitates conversion to androgen-independent growth patterns. Such tumors tend be high grade, aggressive and resistant to treatment, and contribute to high mortality from prostate cancer. (Michiko 2003 56)
Abdominal adipose tissue actively secretes endocrine hormones or adipokines. Leptin regulates body weight by central actions on food intake and energy expenditure and also known to be important in events such as reproduction, hematopoiesis, angiogenesis, and insulin secretion through receptor binding and downstream signaling pathways, known to be involved in cell proliferation and survival in androgen-independent prostate cancer cells. Other adipokines, including interleukin-6 (IL-6) and insulin-like growth factor (IGF), have also been implicated in prostate cancer risk. (Singh 2004 11)
Obesity in both men and women is associated with increased conversion of adrenal androgens to estrogens via an aromatase enzyme located in adipose tissue. Increased local or paracrine production of estrogens by breast adipose tissue has been associated with increased risk for breast cancer. Thus, while circulating adipokines may facilitate prostate cancer progression, it is also likely that transformed prostate cells may be exposed to paracrine secretions from adjacent retropubic adipose tissue. This possibility would explain the clinical observation that obesity contributes more to prostate cancer progression than to its initiation. (Davis 2005 18)
Further, consumption of a high-fat, low-fiber, nutrient-poor “Western” diet increases risk for both obesity and prostate cancer. Epidemiological and laboratory studies have shown that diets containing large amounts of green vegetables, fruits, grains, and legumes reduce risk for many ...