Statins may reduce inflammation related to advanced prostate cancer risk

May 9, 2017

Nearly one-third of U.S. adults take cholesterol-lowering drugs known as statins to lower their risk of heart attack or stroke, studies have found. These cholesterol-lowering drugs also are linked to lowered risk for advanced prostate cancer. Now, researchers may better understand why.

In a study of 6,655 men who were at high risk for prostate cancer but who had a biopsy showing no prostate cancer, researchers found lower levels of prostate inflammation in statin users compared with men who did not use statins. While epidemiologic evidence links statins with lower risk of advanced prostate cancer, the new study, published in the journal Cancer Prevention Research, points to prostate inflammation as a possible mechanism for the link.

Dr. Emma Allott

Dr. Emma Allott

“By measuring prostate inflammation, we were able to look at a possible intermediate or contributing mechanism linking statins with lower advanced prostate cancer risk,” said Emma Allott, PhD, research assistant professor of nutrition at the UNC Gillings School of Global Public Health and first author of the study. “We found that statin users were less likely to have histologic inflammation in their prostate tissue.”

Already, studies have linked high levels of cholesterol in the blood to increased risk of prostate cancer recurrence and death. Researchers wanted to know whether there could be a reason, in addition to cholesterol-lowering effects, for the link between statins and lower prostate cancer risk.

In the new study, Allott and her collaborators studied levels of prostate inflammation in 6,655 men who participated in the REduction by DUtasteride of prostate Cancer Events (REDUCE)  trial, with a prostate biopsy negative for cancer.

The authors used REDUCE data to examine the association between cholesterol levels in the blood, statin use and histologic prostate inflammation. Their goal was to study men who tested negative for prostate cancer to better understand molecular pathways linking statins with lower risk of advanced prostate cancer.

“Studying the effect of risk factors on pre-cancerous prostate biology will improve our understanding of prostate cancer development and inform prostate cancer prevention efforts,” Allott said.

They found chronic inflammation in 77 percent of men enrolled in the trial, and acute inflammation in 15 percent, based on a pathologist’s assessment of histologic inflammation in prostate biopsies found to be negative for prostate cancer.

Causes of histologic prostate inflammation are largely unknown but may include lifestyle factors such as smoking, diet and, as shown for the first time in this study, statin use. Statin users had lower chronic inflammation and were less likely to have severe chronic or severe acute inflammation. With the exception of HDL (“good”) cholesterol, where high levels correlated with lower levels of acute inflammation, blood cholesterol levels were not linked with prostate inflammation.

Inflammation, which helps to recruit other immune cells to the site of infection or disease, has been studied as a driver of multiple cancer types. Studies have had conflicting findings, however, as to the relationship between histologic inflammation in negative prostate biopsies and subsequent risk of prostate cancer.

Allott said that an important future line of research should examine specific types of inflammation that could be helping to drive cancer risk. She also called for additional studies to examine the relationship between statin use, inflammation and prostate cancer.


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Gillings School of Global Public Health contact: David Pesci, director of communications, (919) 962-2600 or dpesci@unc.edu