Nutrition & Prevention Strategies: Prostate Ca

Nutrition and Prevention Strategies for Prostate Cancer

The goal of primary cancer prevention strategies is to prevent persons with no evidence of clinical disease, including those with premalignant lesions, from developing invasive, life-threatening cancer. In prostate cancer, this goal has not yet been achieved, despite significant progress in research over the past 15 years.

Both genetic and environmental risk factors for prostate cancer have been identified; however, at present, the evidence is neither strong enough nor coherent enough to provide a clinically useful means to stratify men according to level of risk.

Furthermore, notwithstanding the encouraging but potentially confusing results from the Prostate Cancer Prevention Trial (PCPT) with finasteride, we do not yet have established means for interrupting the early carcinogenic process in high-risk individuals.

Secondary prevention, specifically screening with prostate-specific antigen (PSA) testing to detect and treat prostate cancer at a curable stage, has probably contributed to the recent steady decline in prostate cancer mortality in the United States,[1] but the associated costs are high, due to false-positive results and, to some degree, detection and treatment of clinically insignificant cancers.

Given the widespread use of PSA screening and the typically slow but unpredictable growth of prostate cancer, an increasingly large pool of men with early disease are being faced with difficult decisions about treatments that confer significant side effects and lifestyle ramifications.[2]

Thus, researchers have begun to look at effective "preventive" strategies to remove or mitigate risk factors, and thereby delay disease progression.

This chapter of the Report to the Nation on Prostate Cancer will review the latest research efforts in the identification of risk factors for disease and the stratification of risk groups, as well as the attempts made to date to recognize nutritional elements and chemopreventive agents that can help prevent prostate cancer and/or slow disease progression.

Identifying Risk Factors for Prostate Cancer

As noted above, the goal of primary prevention strategies is to prevent persons with no evidence of clinical disease, including those with premalignant lesions, from developing cancer. In the last decade, abundant circumstantial evidence has been collected to suggest that prostatic intraepithelial neoplasia (PIN) is one, although perhaps not the only, premalignant lesion for prostate cancer.

However, PIN does not cause a characteristic change in PSA or imaging signature, so detection of PIN requires a random needle biopsy. Once detected, surgical removal is clearly unfeasible, and the risk-benefit ratio for potentially effective drug treatment of PIN, such as androgen ablation, is not well understood.

Because of the typically slow progression of prostate cancer, the presence of high-grade PIN on biopsy can precede clinically detected carcinoma by decades, leaving room to question the utility of identifying PIN as premalignant disease.[3]

As an alternative, research efforts have focused on identifying high-risk populations that can be targeted for secondary preventive strategies, namely more intense screening for disease. In prostate cancer, as in nearly all cancers, three of the strongest predictors for disease are age, race, and family history.

Much study has been done over the years to better identify how each of these factors affects the risk of development and progression of disease.

The probability of developing prostate cancer rises with age, such that only 1 in nearly 13,000 men under age 40 years will be diagnosed with prostate cancer, vs 1 in 44 in men aged 40-59 years, 1 in 7 in men aged 60-79 years, and finally 1 in 6 in men over age 70 years.[4,5] Accordingly, more than 70% of prostate cancers are diagnosed in men over age 65 years; it is the third leading cause of cancer death in men aged 60-79 years, and the second leading cause of cancer death in men aged 80 years and above.[2]

Race or ethnicity as a predictor for prostate cancer is most clearly demonstrated in African-American men. The incidence of prostate cancer in African-American men is about 1.5 times higher than among white men, and is 2.7 times higher than among Asian/Pacific Islander men.[6]

In addition, a higher prevalence of more aggressive disease and higher PSA levels at diagnosis have been noted in African-American men vs white men.[7,8] Accordingly, some screening guidelines recommend that African-American men begin annual PSA and digital rectal exam (DRE) screening at age 45 years rather than at age 50 years.

The risk for Hispanic men is not as clear. SEER data from 11 geographic areas in 1992-1996 show a lower incidence of prostate cancers among Hispanic men compared with white men.[9]

Results from the Prostate Cancer Outcomes Study, a population-based longitudinal study initiated in 1994 by the National Cancer Institute using SEER data from six cancer registries, demonstrated that Hispanic men were more likely than white men to present with clinically advanced stage disease,[10] suggesting that Hispanic men might be at greater risk for more advanced disease.

However, the difference between the groups was no longer significant after adjustment for socioeconomic factors.[10] Studies of other ethnic groups have also shown that environmental factors can affect risk profiles: one study found that duration of residence in North America independently increased prostate cancer incidence in Asian-born men living in the United States and Canada,[11] while a second found that mortality from prostate cancer in Japanese-born men living in the United States tends to match the higher rates seen in the overall US population rather than the lower rates seen in the overall Japanese population.[12]

Although the precise mechanisms remain unclear, these data clearly indicate that the effects of diet, lifestyle, and other factors on the development of prostate cancer cannot be overlooked.

The third primary risk factor, family history, has also been shown to affect the risk of prostate cancer development.

Hereditary prostate cancer that is attributable to high-penetrance gene mutations and is reflected in obvious family clustering accounts for approximately 5% to 10% of cases in the entire population, and for up to 40% in men under age 55 years.[13]

Data from a population-based case-control study of 563 men under age 70 years with prostate cancer and 703 age-matched controls with no history of disease indicate that the risk of prostate cancer varies depending upon the number of first-degree relatives affected and upon the relationship of the affected family members to the case.

[14] Men with a single relative with a history of prostate cancer had a 2.2-fold risk of cancer, while those with two or more relatives with a history of prostate cancer had a 3.9-fold risk of cancer; the risk was higher if the brother had prostate cancer than if the father had prostate cancer.[14]

Of note, early age of onset of prostate cancer in the affected family members increased the risk, with the highest risk seen in those with family members diagnosed under age 60 years.[14]

Because of this increased risk, the American Cancer Society guidelines recommend that men with a strong family history of prostate cancer initiate regular screening 5 years earlier than the general population, at age 45 years.[15]

As with other epithelial cell cancers, somatic genetic alterations underlie prostate cancer development. A wide variety of alterations have been identified in patients with prostate cancer, but the heterogeneity of these mutations has made study of the genetic underpinnings of prostate cancer challenging.

In addition, genetic alterations have been shown to accumulate over time, suggesting that environmental factors not only affect risk profiles and disease incidence rates but can also induce further somatic genetic abnormalities.[16]

The link between genetic mutations and dietary or lifestyle factors remains unconfirmed, but data to date clearly suggest that both genetic and environmental factors play a role in prostate cancer development and progression.

Unfortunately, the role of environmental factors that have been associated with an increased risk in other cancers, particularly obesity, is not yet well understood in prostate cancer. Data from two large retrospective, multicenter studies found that body mass index (BMI) >/= 30 independently predicted higher tumor grade and higher risk of biochemical recurrence in patients undergoing radical prostatectomy (RP),[17,18] while moderately and severely obese men (BMI >/= 35) had a 4-fold higher risk for PSA failure.[18]

In addition, a Swedish study evaluating 135,000 men followed for 18 years found that an increased risk of death from prostate cancer -- but not the incidence of prostate cancer -- was associated with higher BMI.[19]

However, analysis of data from the Health Professionals Follow-up Study on nearly 3000 men with prostate cancer showed an inverse relationship between BMI >/= 30 and prostate cancer risk when detected in patients under age 60 years or in patients with a family history of prostate cancer: a 48% decrease in cancer risk was noted for obese patients under age 60 years and a 26% decrease was noted for obese patients among those with a positive family history of prostate cancer.[20]

Taken together, these data indicate that, in some populations, obese patients are at decreased risk for developing prostate cancer, but that, overall, they are at increased risk for worse outcomes following RP, and are at increased risk of death from prostate cancer.

This complex relationship between obesity and prostate cancer likely results from the interplay of multiple environmental and genetic factors, which may vary by age, and which are yet to be elucidated.

Research into the role of environmental factors in the development and progression of prostate cancer is ongoing, particularly focusing on identifying modifiable factors that can be targeted with nutrition and pharmacologic preventive strategies.


Dean Ornish, Nutrition & Prostate Cancer, Fall, 2005

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