Every man has some level of risk for getting prostate cancer, yet many other factors also make some men more susceptible to prostate cancer than others. For the general population, a man has about a 17 percent chance of getting prostate cancer and a three percent chance of dying from it.
Knowing your level of risk can help you develop your plan of attack. In general, men should begin testing for prostate cancer at age 45. If you have one ore more of the risk factors listed on this page (not including age), you should begin annual prostate cancer testing at age 40.
Age is the strongest risk factor for getting prostate cancer. One in every six men gets prostate cancer at some point. The probability of prostate cancer varies greatly by age.
For those age 30 to 39, the risk is 0.01 (1 in 12,288) for white men and 0.02 (1 in 4,379) for African Americans. For those age 40 to 49, the risk is 0.27 (1 and 375) for white men and 0.60 (1 in 168) for African Americans. For those age 50 to 59, the risk is 2.14 (1 in 47) for white men and 3.78 (1 in 26) for African Americans. For those age 60 to 69, the risk is 6.23 (1 in 16) for white men and 9.75 (1 in 10) for African Americans. For those age 70 to 79, the risk is 8.02 (1 in 12) for white men and 11.17 (1 in 9) for African Americans.
As studies into aging continue, scientists may find that the aging process produces biochemical reactions that contribute to abnormal cell growth. This is an area of intense research.
While it is rare for younger men to get prostate cancer, those cases tend to be more aggressive.
Compared with men who have no family history of the disease, men with a father or brother who has been diagnosed with prostate cancer have more than twice the risk of being diagnosed. Men with two or more relatives have about five times the risk. Men with three or more relatives are almost guaranteed to get prostate cancer.
Scientists are looking at genes that may be responsible for inherited prostate cancer. The genes under investigation are called Hereditary Prostate Cancer Genes 1 and 2 (HPC1, HPC2) and HPCX. It is not yet known to what degree these genes are responsible for prostate cancer. It may be that genetically acquired prostate cancer develops differently than cancer from other causes, but more research into this theory is needed.
Rates of prostate cancer in the U.S. are 60 percent higher among African-American men, and their mortality rate is two-and-a-half times that of Caucasian men. Studies are being done on potential differences in physiology, diet and access to care.
Rates for Asian men in the U.S. are lower than average, which may be a result of traditional diets.
Hispanic men have a risk of getting prostate cancer similar to the general population; however, rates of death due to the disease have not declined over recent years as they have for Caucasian and African-American men.
Diet and Obesity
The "Western or Cowboy diet," which is high in fat, meat and sugar and low in fruits, vegetables and fiber, may be one of the greatest factors contributing to prostate cancer. Studies suggest a strong relationship between consumption of saturated fat or dairy fat and prostate cancer, while polyunsaturated fats such as Omega-3 fatty acids may help prevent the disease.
Obese men, those with a body mass index (BMI) of over 32.5, are 33 percent more likely to die from prostate cancer if diagnosed. Some studies suggest a relationship between obesity and higher risk, but it is difficult to prove a direct link. Consumption of saturated fat and meat may be the determining factor, but the effect of obesity on hormone function may also play a significant role. Further studies are needed to determine the exact relationship between obesity and prostate cancer development.
People exposed to certain chemicals such as pesticides and herbicides may have higher than average rates of prostate cancer. One pesticide, methyl bromide, has shown a clear link to increased prostate cancer among exposed farm workers.
Veterans exposed to herbicides like Agent Orange may be at higher risk of prostate cancer. Studies of Vietnam veterans potentially provide the most direct evidence of the health effects on Agent Orange exposure. While most studies have shown to be inconclusive because of the small number of participants, one notable Air Force Health Study specifically compared about 1,200 Ranch Hand veterans directly involved in herbicide distribution to 1,300 veterans not involved. This 20-year study, launched in 1982, involved periodic physical exams, medical record reviews, and blood dioxin measurements; it suggests those with direct contact with the herbicide may be twice as likely to get prostate cancer and die from it. However, the relatively small number of subjects, and the even smaller number with elevated blood dioxin levels, greatly limited the study's power to detect increases in cancer incidence.
Much research is being conducted to determine whether or not there is a genetic link to prostate cancer. In particular, researchers are looking to identify biomarkers in one's DNA which may lead to a diagnosis of prostate cancer. Men with BRCA-2 mutations are at increased risk for prostate cancer that typically is more aggressive and develops at a younger age. Several genetic studies have identified locations on chromosome 8 (in a region called 8q24) that are associated with an increased risk of developing prostate cancer and with more aggressive prostate cancer.
Bad cholesterol may be linked to prostate cancer risk.
Early studies suggest a link between high cholesterol and prostate cancer, as bad cholesterol or low-density lipoprotein (LDL) contributes to increases in dyhydrotestosterone or what some scientists call bad testosterone. High levels of testosterone or bad testosterone may impact the chance of having prostate cancer and prostate cancer severity.
Cholesterol plays a role in cell growth in the body and in cancer. Accumulation of cholesterol within the prostate membrane may stimulate signals that promote cancer progression.
Leading researchers are suggesting that doctors should screen for cardiovascular disease along with prostate cancer because evidence is strong enough to indicate a link.
Exercise is associated with increased metabolism and weight loss which can contribute to lowering the risk of prostate cancer.
While studies are inconclusive that exercise has a direct impact on prostate cancer risk, exercise results in the temporary reduction in testosterone chief contributor to male hormone dependent cancers such as prostate cancer and helps lower one’s weight when applied with a healthy diet.
By lowering your weight through diet and exercise, PSA levels may go down and some studies suggest that tumor growth is slowed by as much as 30 percent. However, in order to fully determine direct links to exercise and the reduction of prostate cancer, a long and extensive randomized trial is needed.
Smoking may contribute to the growth of prostate cancer tumors. Studies also show nicotene may also interfere with the process of chemotherapy.
Smoking influences the progression of prostate cancer through a process that affects certain genes in the body and is also likely to alter your hormonal balance by creating an environment conducive to tumor growth. It can increase the amount of steroid hormones, called androgens, which can fuel the growth of malignant prostate cells in your body. Also, tobacco is a source of cadmium, a heavy metal that interacts with zinc found in the prostate, which leads to prostate cancer. This human carcinogenic metal inhibits DNA repair in your body, which allows cancer cells to mutate and multiply.
Several research have shown that men under age 65 those who smoke a pack of cigarettes a day for 40 years face a 100 percent increased risk of developing the more aggressive forms of prostate cancer as compared to nonsmokers. Also, compared to nonsmokers, current smokers face a 40 percent increase in the risk of prostate cancer.
In addition, smoking cigarettes could lead to severe side-effects in your body when undergoing treatment for prostate cancer, just as in case of cancers of the head and neck, cervix, lung and breast. Patients who smoke during treatment normally develop acute gastrointestinal side-effects such as diarrhea, much more severe than nonsmokers. This highlights the importance of quitting smoking before starting radiation therapy.