Compared with white men, African-American men are twice as likely to develop prostate cancer in their early 50s and twice as likely to die of the disease. (American Cancer Society) They are also more likely to be in an advanced stage of the disease when diagnosed. (Winterich 2009). Recent findings released at the American Urological Association annual meeting also showed that black men also appear to be more likely to develop aggressive forms of prostate cancer.
On the other end of the spectrum, Asian-Americans and Hispanic/Latino men are less likely to develop prostate cancer than are non-Hispanic white men.
What makes African American men so susceptible to prostate cancer? There are several possible reasons:
Genetics: Differences in the androgen (male hormone) receptor genes related to the prostate may play a role. (Platz 2000)
Environment: Blacks living in Africa have a lower rate of prostate cancer and death related to prostate cancer than do African-Americans. This gives researchers reason to suggest that African-Americans may be exposed to dietary habits, chemicals, or other factors which, when combined with genetic changes, increase the risk for prostate cancer among African-Americans compared to white men.
Medical care: Prostate cancers are less likely to be detected in the early stages among African-Americans because research shows they are generally less likely to have health insurance and have less access to health care.
Mistrust: Research has shown that African-American men are less trustful of their physicians than are white men, less likely to see the same doctor each time they go a visit or care, and less likely to be screened for prostate cancer. (Carpenter 2009)
Research by University of Michigan Comprehensive Cancer Center showed that five-year survival rates varied by 10 percent between blacks and whites with colorectal cancer and by 25 percent among uterine cancer patients. These are both cancers that can generally be cured with appropriate surgery and medical treatments and tended to be fatal without treatment. The report noted the following items as reasons for the disparities:
Black men as patients: Blacks are often diagnosed with more advanced cancer and are more likely to have other underlying health problems
Underuse of care: Black patients are less likely to be advised about cancer screenings and less likely to receive surgery or chemotherapy
Hospital systems: Hospitals that treat primarily black patients tend to have fewer resources and offer lower quality care
Another factor in higher prostate cancer rates for black men is their levels of vitamin D; which has been shown to have a protective effect against prostate cancer. One theory that has a lot of support is that black men living in North America may not produce sufficient vitamin D, as they are not getting the necessary sunlight to maintain adequate levels and synthesis is inhibited through higher levels of melanin in the skin. If you are a black man, then having your vitamin D serum levels checked using the 25-hydroxy vitamin D test is a good first step.
In addition, getting adequate sunlight and maintaining a diet rich in vitamin D based foods such as fish and egg yolks will help in natural vitamin D supplementation. If your levels of vitamin D are low, then supplementation will most likely be recommended with retesting after 6 months. Your doctor will advise the correct dose of vitamin D supplementation (usually in the form of D3) as well as follow up screening.
It seems that the first step for all black men is getting better and earlier screening given the trend of late diagnosis and the disparities in death rates combined with black men generally having more advanced forms of the disease.
References
American Cancer Society. Cancer facts & figures for African Americans.
Morris AM et al. Understanding racial disparities in cancer treatment and outcomes. Journal of the American College of Surgeons 2010 Jul; 211(1): 105-13
Winterich JA et al. Men’s knowledge and beliefs about prostate cancer: education, race, and screening status. Ethnicity & Disease 2009 Spring; 19(2): 199-203
