Prostate Cancer Prevention Policy
The causes of prostate cancer are poorly understood and there are no proven prevention measures. Researchers continue to examine possible risk factors and preventive approaches.
Non-modifiable risk factors
Increasing age is by far the most important risk factor for prostate cancer, with more than 80% of cases diagnosed in 2016 occurring in men 60 years of age or older. Younger men diagnosed with prostate cancer are more likely to die prematurely from the disease than older men, as there is, on average, more of their lifetime left in which the cancer can progress and they are less likely to die of other causes.
Family history of prostate cancer is a risk factor for the disease. Between five and 10% of prostate cancers may be due to an inherited genetic predisposition. Men with first-degree relatives diagnosed with prostate cancer are two to three times more likely to develop prostate cancer compared to men with no affected relatives, and the risk may be higher if a first-degree relative was diagnosed before the age of 60 years.
The genetic basis for familial prostate cancer is not fully understood. Men carrying mutations of the breast cancer susceptibility genes BRCA1 or BRCA2 have an increased risk of several types of cancer, including prostate cancer. Male carriers of BRCA2 mutations have a 3.5-fold increased risk of prostate cancer and an earlier age of onset and have been reported to have poorer survival rates than those without BRCA2 mutations.
A mutation of the gene HOXB13 has also been shown in recent research to substantially increase prostate cancer risk.
Analysis of NSW cancer registry data found that prostate cancer mortality 5-years after diagnosis was higher for Aboriginal men than non-Aboriginal men. Even after adjusting for differences in demographic factors, stage at diagnosis, health access and comorbidities, Aboriginal men were 49% more likely to die from prostate cancer.
Modifiable risk factors
Evidence on the links between prostate cancer risk and modifiable lifestyle factors is limited, with no conclusive evidence of an association identified by IARC. A comprehensive review of the impact of diet and physical activity on cancer by the World Cancer Research Fund in 2018 concluded that there is strong evidence that overweight/obesity is associated with increased risk of prostate cancer. While the association between higher pre-diagnosis body mass and higher risk of prostate cancer death is inconclusive, evidence suggests there is poorer treatment outcomes among overweight and obese men with prostate cancer.
There was limited suggestive evidence that dairy products, diets high in calcium, low plasma alpha-tocopherol concentrations (vitamin E) and low plasma selenium concentrations increase the risk of prostate cancer. This evidence falls below the threshold to make recommendations about dietary intake or supplement use.
Chemoprevention, or the use of natural or synthetic agents to reduce the incidence of cancer in those at increased risk, is being investigated but is not routinely used for prostate cancer.
The anti-androgen drug finasteride is thought to prevent prostate cancer, but this apparent benefit was limited to less aggressive cancers and it appeared that risk of more aggressive cancers was increased by the drug. Dutasteride showed a decrease in prostate cancer incidence but unlike finasteride, an increase in aggressive cancers was not observed. The United States Food and Drug Administration accepted the December 2010 advice of its Oncologic Drugs Advisory Committee that finasteride and dutasteride “do not have a favourable risk-benefit profile for the proposed use of chemoprevention of prostate cancer in healthy men”.
A trial examining selenium and vitamin E supplementation in healthy men (The SELECT trial) found that these agents did not prevent prostate cancer and that supplementation with vitamin E was associated with a significantly increased risk of prostate cancer of 17%.
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