Polyunsaturated Fat Intake and Prostate Cancer Public Deposited

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  • March 19, 2019
  • Koralek, Daniel
    • Affiliation: Gillings School of Global Public Health, Department of Epidemiology
  • While the burden of prostate cancer is high, few well-established risk factors exist. Recent efforts have focused on elucidating the role of diet in prostate carcinogenesis, including the roles of individual fatty acids. Evidence has been inconsistent for the relations between specific fatty acids and prostate cancer risk. However, recent evidence suggests that high intakes of alpha-linolenic acid may increase prostate cancer risk while high intakes of longer chain omega-3 fatty acids may reduce prostate cancer risk. We investigated the relations between incident prostate cancer and intakes of specific polyunsaturated fatty acids and their ratios within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial and in the National Institutes of Health-AARP Diet and Health Study, two large prospective cohort studies of diet and cancer. Cox proportional hazards models were used to estimate hazard ratios and their 95% confidence intervals. In the PLCO population, we found that intake of linoleic acid, the most common !-6 fatty acid, was inversely associated with total prostate cancer (multivariable-adjusted hazard ratio (HR) for a 4g increment of intake = 0.94; 95% iv confidence interval (CI)= 0.89 - 1.00). Dietary intakes of !-3 fatty acids were positively associated with low-grade prostate cancer (HR for a 0.1g increment of intake = 1.04; 95% CI = 0.99 - 1.09) and trans fatty acid intakes were positively associated with high-grade disease (HR for a 2g increment of intake of total trans fatty acids = 1.07; 95% CI = 0.96 - 1.19). In the NIH-AARP population, we found that intakes of long-chain !-3 fatty acids were positively associated with total prostate cancer (MV-adjusted HR comparing C5 to C1 = 1.07; 95% CI = 1.02 - 1.12) and inversely associated with fatal tumors (MV-adjusted HR for a 0.1g increment of intake = 0.87; 95% CI = 0.78 - 0.98). Total TFA intake was inversely associated with high-stage disease (MV-adjusted HR for a 2g increment of intake total TFA = 0.95; 95% CI = 0.89 - 1.02) and TFA 16:1 intake was positively associated with fatal disease (MV-adjusted HR for a 0.04g increment of intake = 1.07; 95% CI = 0.97 - 1.18). More research, involving additional prospective studies using instruments with better estimation of PUFA intakes may be used to clarify the role that dietary intakes of these highly interrelated fatty acids may play in prostate carcinogenesis and suggest avenues for primary prevention through the identification of modifiable risk factors for this high burden disease in men.
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  • In Copyright
  • Poole, Charles
  • Su, L. Joseph
  • Schroeder, Jane C.
  • Satia, Jessie
  • Leitzmann, Michael
  • Doctor of Philosophy
Degree granting institution
  • University of North Carolina at Chapel Hill Graduate School
Graduation year
  • 2008
  • This item is restricted from public view for 1 year after publication.

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