The prospective study, led by Yaacov Richard Lawrence, MD, of the Sheba Medical Center, Ramat Gan, Israel, included 11,541 men with coronary heart disease screened to participate in a secondary cardiac prevention trial. Investigators classified subjects into one of four groups: 6,119 with neither diabetes mellitus nor metabolic syndrome (MS); 3,376 with MS but not diabetes; 560 with diabetes but not MS; and 1,486 with both conditions.
During a median follow-up was 12.7 years (range 0-15.7 years), 459 new cases of PCa developed. In age-adjusted analyses, diabetes was associated with a 46% reduced risk of PCa compared with the absence of diabetes, researchers reported online ahead of print in Prostate Cancer and Prostatic Disease. In multivariate analysis, diabetes continued to be associated with a decreased risk of PCa, especially in the absence of MS. Among men who did not have MS, diabetes was associated with a significant 57% decreased risk. In the presence of MS, diabetes was associated with a nonsignficant 36% decreased risk.
Dr. Lawrence’s group observed that the protective effect of diabetes started after five years of follow-up.
The new study confirms the findings of a number of previous investigations, which have demonstrated an inverse relationship between diabetes and PCa development.
Dr. Lawrence and his colleagues pointed out that, compared with previous studies, their study included men screened at a relatively older age (meant 59 years) and followed up for a relatively longer period. As the protective effect of diabetes was observed only after more than five years of follow up, they explained, it is possible that studying a younger cohort for a shorter period will not allow full recognition of the protective effect of diabetes.
“Our findings emphasize the critical importance of sugar metabolism to the cancer cell, providing a clinical corollary to laboratory data,” Dr. Lawrence told Renal & Urology News. “Modulation of glucose pathways is an area of very active research in cancer therapeutics. Exposing prostate cancer cells to ‘a diabetic intracellular-environment’ may be a new way to fight cancer.”