
Men are diagnosed with prostate cancer each year. It is the most commonly diagnosed type of cancer in American males.
Some things, known as risk factors, increase your chances of getting the disease. For prostate cancer, the biggest risk factors are age and race. Men older than age 50 and African American men are at much higher risk. Another risk factor, which is perhaps less influential but more under your control, is your diet. For some time now, research has shown that diet and nutrition likely play an important role in contributing to or preventing certain types of cancer, including prostate cancer. Healthcare professionals have made prevention recommendations based on the latest and most trustworthy findings.
Research on nutrition and cancer is a complex field, and progress and results come with difficulty. The good news is that diet is a risk factor that everyone can control. It’s true that eating habits are hard to change. But what you eat, and how much of each type of food you eat, is your choice.
Most of the research seeking to identify the link between what men eat and their likelihood of getting prostate cancer has centered on saturated fat. Diets high in saturated fat are high in animal fat. Results of most studies indicate that men who eat a lot of saturated fat may have a greater chance of getting prostate cancer.
It isn’t completely known why there seems to be a link between high fat intake and prostate cancer. One theory is that a diet high in saturated fat may increase testosterone levels. In turn, these higher hormone levels contribute to a greater risk for developing prostate cancer.
The most compelling connection of a high-fat diet to prostate cancer is found when experts look at who gets the disease across races and nationalities. African American men, who have the highest incidence rate, often have a diet high in animal fat. On the other end of the scale are Asian males, especially Japanese men living in Japan. They have the lowest rates for getting and dying of prostate cancer. The traditional diet in Japan is mostly vegetarian, so the amount of animal fat eaten is very low. Also, a vegetarian diet reduces, rather than increases, levels of testosterone.
Even more striking is what happens when men emigrate from Japan to the United States. Within two generations, their rates of getting prostate cancer increases to that of American men. Typically, the traditional Japanese diet becomes more Americanized. That is, there’s an increased consumption of animal fat. This move away from the vegetarian diet may explain the changes in this prostate cancer rate.
However, a few researchers have questioned whether high fat consumption itself is the primary culprit in the American diet. Some studies have indicated that men with a high-fat diet generally consume significant amounts of diary products and low amounts of fruits and vegetables. Rather than high fat, the main connection to prostate cancer may be that this diet is high in dairy (or perhaps even calcium) and low in fructose, the sugar found in fruits.
The precise role that diet plays in the development of prostate cancer is still under study.
While studies of the amount of fat in a diet have been prostate cancer researchers’ primary focus, other findings about the effect of what men eat continue to be made.
Lycopene is a substance naturally found in tomatoes and other red fruits, such as grapefruit and watermelon. It may help lower the risk for prostate cancer. This discovery was made in a well-publicized Harvard University study in 1995. In it, the eating habits of 47,000 men were examined for six years.1 It was found that men who ate at least 10 servings a week of tomato-based food (all forms, cooked or uncooked) were up to 45% less likely to develop prostate cancer. Tomatoes and tomato products accounted for almost 90% of the lycopene in the diets of these men.
How does lycopene work? It’s a natural antioxidant. These are thought to prevent damage to a person’s DNA. This may in turn protect against certain changes in DNA, which can cause prostate cells to grow abnormally.
A recent review of the literature confirms that lycopene may lower the chance of getting prostate cancer.2 The incidence may be especially reduced in older men with a family history of prostate cancer.3 More research needs to be done before these antioxidants can be said to be preventive.
Some other studies have looked at the role that selenium, vitamins E and A, carotenoids, and other foods have in protecting against prostate cancer. Conclusions from these studies do not show that these are protective, but more research is needed.4
Based on the majority of research, the American Cancer Society (ACS) has developed nutritional guidelines for a healthy approach to eating that will help lower your risk for all types of cancer.
The ACS recommends a diet low in fat and high in fiber. Specifically, the guidelines recommend limiting food from high-fat animal sources and selecting most of the food you eat from plant sources. Following these recommendations should provide you with the majority of vitamins, minerals, and calories from fruit, vegetables, and grains. Increasing the amount of fruits and vegetables you eat usually means that you will eat less high-fat and high-calorie foods. This type of diet, along with regular exercise, will also help you maintain a balanced, healthy weight for your height.
References:
Giovannucci E, Ascherio A, et. al. “Intake of carotenoids and retinol in relation to risk of prostate cancer.” J Natl Cancer Inst. 1995; 87:1767-1776.
Dagnelie PC, Schuurman AG, et. al. “Diet, anthropometric measures and prostate cancer risk: a review of the prospective cohort and intervention studies.” BJU Int. 2004: May; 93(8): 1139-50.
Wu K, Erdman JW, et. al. “Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study.” Cancer Epidemiol Biomarkers Prev. 2004 Feb; 13(2):260-9.
Heinonen OP, Albanes D, Virtamo J, et al. “Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial.” J Natl Cancer Inst. 1998; 90:440-44