Prostate cancer has become so commonly diagnosed that a large study has been conducted to understand its etiological factors and how the onset of the disease can be prevented or delayed.

In 2002, the American Cancer Research Institute published a study in which a group of 16 experts reviewed 4,500 studies related to diet and cancer. They concluded that 200,000 of the 600,000 cancer deaths in the United States each year could be prevented through a combination of dietary changes, adequate physical activity, and maintaining appropriate body weight. They also noted that the cessation of tobacco and alcohol could prevent an additional one-third of cancers.

The concept of preventing or influencing the growth of cancer was studied in the early 1900s. Various animal studies have shown that the rate of cancer growth may have been affected by the type of diet that was applied to animals. In 1942, Tannenbaum demonstrated on animals that a diet high in fat stimulated the growth of cancer. In 1982, the American National Academy of Sciences presented compelling evidence regarding the relationship between dietary fat and cancer. All subsequent epidemiological studies, animal samples, and studies in biochemical and molecular biological processes that attract cancer have emphasized that diet plays a role in carcinogenesis in the process.

Prostate cancer is associated with various hormonal disturbances, genetic predisposition to cancer, oxidative DNA damage caused by chronic prostate inflammation, excessive food intake, obesity, excessive consumption of estrogens and phytoestrogens, and consumption of burnt or charred foods. Although when DNA is damaged, different treatment systems usually fix the problem. The unsuitability of various methods of DNA repair allows the altered cell to continue separating it instead of fixing the problem. One such system is glutatnon S, a P1-1 (GSTpi) recovery mechanism found to be functionally inactive in men with prostate cancer. The increase in data demonstrates the role of aging, diet, environment, lifestyle, and stress-related factors in the process.

Diet is perhaps the most important factor that a person can manage. The strongest association between diet and prostate cancer is obesity. The significant prevalence of gluttony and as a result of obesity, along with other risk factors, may explain the increasing prevalence of the disease. Numerous studies have shown that obese men have a greater risk of death from prostate cancer, developing more aggressive cancer and overcoming the recurent ratio of the disease after radiation therapy or surgery.

Heavy men who lose weight reduce the risk of prostate cancer. Obese men tend to have lower serum testosterone levels and a certain serum for prostate antigen (PSA) level and are more likely to experience an early cancer rate after primary therapy. A cancer prevention study showed that men with a body mass index (BMI) were 32.5 kg/m2, 35% more likely to die from prostate cancer than men whose BMI was less than 25%.

Each study of prostate cancer with survival eventually found that most patients die from causes other than prostate cancer, mainly cardiovascular disease. Therefore, the virtues of food measures are made up in that they are applicable to the prevention of prostate cancer and in the control of cardiovascular disease.

A lot of research has been done to understand the molecular biology that links diet to prostate cancer. These studies are difficult to implement and often lead to conflicting results. Obtaining data from animal research on humans is often a mistake, but it reduces the number of human studies.