The effects of obesity, energy expenditure, and specific nutrients are being vigorously studied in both the development and the outcomes of prostate cancer. In fact, countries with historically lower incidences of prostate cancer are now beginning to recognize increases in its diagnosis as their lifestyles become more "Westernized."
With 1 in 3 adults in the United States considered obese, it is clear this epidemic could have a very marked effect in the way we think about prostate cancer. Even though obesity by itself is not clearly associated with an increased risk of developing prostate cancer, it has been linked to the diagnosis of more advanced prostate cancer, higher risk of dying of prostate cancer, and progression after prostatectomy.[86,87,88] The mechanism for this is not clear, but difficulties in examining the prostate, inaccurate nodal staging during prostatectomy, lower prostate-specific antigen (PSA) values in obese patients, a low-testosterone/high-estradiol environment, leptin, adiponectin, and insulin-like growth factor have all been implicated as potential contributors to these findings.
Obese patients have increased caloric and fat intake. The increased intake of calories has been prospectively linked to an increased prostate cancer mortality. Conversely, increased physical activity does not appear to have either a positive or a negative correlation. Preadulthood height and obesity may indeed be associated with the above risk in mortality. This implies that efforts to control the effect of obesity on cancer mortality should start during childhood and adolescence.
The US diet is rich in linoleic acid, a fatty acid commonly found in corn oil. In vitro studies show that androgen-sensitive prostate cancer cell lines exhibit increased growth when exposed to this ubiquitous fatty acid. Again, there is no apparent relationship to fat intake in terms of prostate cancer incidence, yet one study linked the consumption of saturated fat to increased relapse rates after prostatectomy.
The Western diet, in addition to being rich in calories and saturated fat, may lack certain specific nutrients. Particular attention has been paid to those that may have antioxidant properties, under the hypothesis that excessive oxidative damage to nucleic acids is likely to lead to carcinogenesis and cancer progression.
Particular attention has been paid to lycopene, an antioxidant commonly found in tomatoes. Most of the US intake of lycopene is derived from tomato sauce consumption. Results from a 2004 meta-analysis initially showed a possible decrease in incidence of 10% to 20%. However, a recent analysis from the Prostate, Lung, Colorectal and Ovarian Screening Trial shows no relationship between this nutrient and prostate cancer incidence. Moreover, consumption of beta-carotenoids, a related group of antioxidants, was associated with an increased risk of aggressive prostate cancer in the same study.
Selenium has received much attention as well. This stems from an initial trial of selenium supplementation in skin cancer patients residing in areas with low dietary selenium. As a secondary endpoint, it was noted that there were fewer prostate cancers in participants assigned to selenium.[97,98] The possible preventive role of selenium has been recently investigated by the National Cancer Institute in the SELECT trial, where 35 533 participants were given placebo, selenium, and/or vitamin E for up to 7 years. After a negative planned second interim analysis, the Data and Safety Monitoring Committee recommended the discontinuation of these supplements.
High milk consumption has been associated with increased risk of prostate cancer. To test whether this was related to calcium intake and vitamin D levels, the Health Professionals Follow-up Study assessed 47 750 men. The results showed that high calcium intakes of more than 1500 mg/d were associated with the development of high-grade prostate cancer but not low-grade, organ-confined prostate cancer. In addition, those patients with an intake of more than 1500 mg/d did indeed have lower levels of circulating vitamin D. This led to the hypothesis that lower levels of vitamin D may impair the differentiation of prostate cancer cells toward a less aggressive, more confined cancer.
With respect to diet, review of the published evidence does not support the viewpoint that the development of prostate cancer is the direct result of increased caloric intake, fat intake, or nutritional deficiencies. However, the studies indicate that our dietary habits Sep o Oct 2009 may modify the biologic behavior of pre-existent foci of less aggressive prostate cancers. The implications are that this impact will be noted mostly in terms of detection of aggressive cancers, rates of relapse after curative treatment, and, ultimately, risk of death.
At this point, it is impossible to make evidence-based recommendations toward the ingestion or avoidance of any specific nutrient. But based on the information presented on caloric and fat intake, it would appear wise to support a dietary regimen that would avoid obesity and excess fat as early as possible in one's life.
Am J Lifestyle Med. 2009;3(5):337-348. © 2009 Sage Publications, Inc.
Cite this: Lifestyle Interventions in the Prevention and Treatment of Cancer - Medscape - Sep 01, 2009.