Genetics May Explain Why Calcium Increases Risk for Prostate Cancer

September 15, 2011

Researchers target gene common among African-American men  

A study by epidemiologists at Wake Forest Baptist Medical Center and colleagues suggests that a high intake of calcium causes prostate cancer among African-American men who are genetically good absorbers of the mineral. 

“High dietary intake of calcium has long been linked to prostate cancer but the explanation for this observation has been elusive,” said Gary G. Schwartz, Ph.D., associate professor of cancer biology, urology, and public health sciences at Wake Forest Baptist and co-author on the study.  

Schwartz and colleagues from the Keck School of Medicine at the University of Southern California (USC) and the Cancer Prevention Institute of California studied 783 African-American men living in the San Francisco and Los Angeles areas, 533 of whom were diagnosed with prostate cancer. They studied the effects of genotype, calcium intake and diet-gene interactions. 

The study is one of the few to explore genes related to calcium absorption or to examine diet in a large African-American population. Although prostate cancer is 36 percent more common among African-Americans than in non-Hispanic whites, data on the diet-cancer link primarily comes from Caucasian populations. The team targeted a genetic allele that is more common in populations of African origin than in other populations and which is associated with regulating the absorption of calcium. 

In the United States, more than 240,000 men are diagnosed annually with prostate cancer and about 33,720 die from the disease, according to the National Cancer Institute. Only lung cancer kills more American men. According to the Prostate Cancer Foundation, there are no proven strategies for preventing the disease, but changes in diet and lifestyle have shown to reduce the risk of disease progression. 

The study, which is now available in the online issue of the Journal of Bone and Mineral Research, found that men who reported the highest intake of calcium were two times more likely to have localized and advanced prostate cancer than those who reported the lowest. Men with a genotype associated with poor calcium absorption were 59 percent less likely to have been diagnosed with advanced prostate cancer than men who genetically were the best absorbers of calcium. And, among men with calcium intake below the median, genetically poor absorbers had a 50 percent decreased risk of having advanced prostate cancer than the best absorbers. The final paper is scheduled to appear in the January 2012 print issue.  

The results pose somewhat of a “conundrum,” said Sue Ann Ingles, Dr.P.H., associate professor of preventive medicine at USC and principal investigator of the study. Although calcium appears to increase risk for prostate cancer, it is essential for bone health and appears to protect against colorectal cancer, she said.  

“It may be possible in the future to personalize prevention using this type of genetic knowledge,” Schwartz said of the research findings. “But first, we will need to confirm this genetic result among men of other races to be sure that it is the allele that increases the risk of disease, rather than the possibility that we’re seeing this result simply because we are studying an allele that is highly associated with African-American men.” 

He added the findings provide some clarity about the link between calcium and prostate cancer. Unlike age and race, which are fixed risk factors for prostate cancer, diet is modifiable. 

“We now have a better understanding of why calcium in diet may increase the risk for prostate cancer and who is at increased risk,” Schwartz said. “If our results are confirmed, it gives much better insight into the preventable causes of prostate cancer. So if I know I’m a good absorber of calcium, I may want to be careful about my diet and about the use of calcium supplements.” 

The study was funded by grants from the National Institute of Environmental Health Sciences, The Cancer Research Fund of the California Department of Health Services Cancer Research Program and the National Cancer Institute. Co-authors on the paper, in addition to Schwartz and Ingles, include: Glovioell W. Rowland, from USC; and Esther M. John, from the Cancer Prevention Institute and the Department of Health Research and Policy at Stanford University School of Medicine and Stanford Cancer Center.

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