Inflammation may play an etiologic role in prostate cancer.
Several dietary factors influence inflammation; studies have shown that long-chain n-3 polyunsaturated fatty acids are anti-inflammatory, while n-6 and trans fatty acids are pro-inflammatory. We evaluated whether serum phospholipid n-3, n-6, and trans fatty acids were associated with intraprostatic inflammation, separately in 191 prostate cancer cases and 247 controls from the placebo arm of the in the Prostate Cancer Prevention Trial (PCPT). Men without a prostate cancer diagnosis underwent prostate biopsy at trial end, and benign prostate tissue inflammation was evaluated in approximately three biopsy cores per man; this was expressed as no, some, or all cores with inflammation. In controls, serum eicosapentaenoic acid (OR of all cores with inflammation versus none (95%CI): 0.35 (0.14, 0.89)), and docosahexaenoic acid (OR (95%CI): 0.42 (0.17, 1.02)) were inversely associated with, while linoleic acid (OR (95%CI): 3.85 (1.41, 10.55)) was positively associated with intraprostatic inflammation. Serum trans fatty acids were not associated with intraprostatic inflammation. No significant associations were observed in cases; however, we could not rule out a positive association with linoleic acid and an inverse association with arachidonic acid. Thus, in the PCPT, we found that serum n-3 fatty acids were inversely, n-6 fatty acids were positively, and trans fatty acids were not associated with intraprostatic inflammation in controls. While, in theory, inflammation could mediate associations of serum fatty acids with prostate cancer risk, our findings cannot explain the epidemiologic associations observed with n-3 and n-6 fatty acids.
Written by:
Nash SH, Schenk JM, Kristal AR, Goodman PJ, Lucia MS, Parnes HL, Thompson IM Jr, Lippman SM, Song X, Gurel B, De Marzo A, Platz EA. Are you the author?
Cancer Prevention Fellowship Program, National Cancer Institute; Cancer Prevention Program, Fred Hutchinson Cancer Research Center; Southwest Oncology Group Statistical Center; Pathology, University of Colorado; DCP, NCI; Cancer Therapy and Research Center, The University of Texas Health Science Center at San Antonio; University of California, San Diego, Moores Cancer Center; Department of Pathology, Kocaeli University School of Medicine; Department of Pathology, Johns Hopkins University; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health.
Reference: Cancer Prev Res (Phila). 2015 Apr 29. pii: canprevres.0398.2014.
doi: 10.1158/1940-6207.CAPR-14-0398
PubMed Abstract
PMID: 25926387