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Prostate Cancer Prostatic Dis. 2017 Mar;20(1):48-54. doi: 10.1038/pcan.2016.39. Epub 2016 Sep 6.

Saturated fat intake and prostate cancer aggressiveness: results from the population-based North Carolina-Louisiana Prostate Cancer Project.

Author information

1
Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
2
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
3
David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
4
Winthrop P Rockefeller Cancer Institute and College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
5
School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
6
Department of Urology, Roswell Park Cancer Institute, Buffalo, NY, USA.
7
Department of Urology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
8
Department of Epidemiology and Biostatistics, University of South Carolina, Columbia, SC, USA.

Abstract

BACKGROUND:

Epidemiologic and laboratory evidence supports a role for cholesterol in prostate cancer (PC). Dietary saturated fat content impacts serum cholesterol levels. However, epidemiologic associations between saturated fat and PC aggressiveness are inconsistent. We hypothesized that high saturated fat intake would be associated with increased PC aggressiveness, and that statin use would modify this association.

METHODS:

Of 1854 PC cases in the North Carolina-Louisiana PC Project, 321 (17%) were classified as high aggressive (Gleason sum ⩾8, PSA>20 ng ml-1, or Gleason sum ⩾7 and clinical stage T3-4) or low/intermediate aggressive (all other cases). Using low/intermediate aggressive cases as the referent group, we examined the association between tertiles of total fat-adjusted saturated fat intake and high aggressive PC using logistic regression, overall and stratified by race and statin use. We examined total fat-adjusted polyunsaturated and monounsaturated fatty acids (PUFA and MUFA, respectively), trans fat and cholesterol intake in secondary analysis.

RESULTS:

High total fat-adjusted saturated fat intake was associated with an elevated odds ratio (OR) for aggressive PC (ORT3vsT1 1.51; 95% CI 1.10-2.06; P-trend=0.009), with an attenuated association in statin users (ORT3vsT1 1.16; 95% CI 0.67-2.01; P-trend=0.661) compared with non-users (ORT3vsT1 1.71; 95% CI 1.16-2.51; P-trend=0.053). High total fat-adjusted cholesterol intake was associated with aggressive PC in European Americans (ORT3vsT1 1.62; 95% CI 1.02-2.58; P-trend=0.056), but not African Americans (ORT3vsT1 0.92; 95% CI 0.60-1.42; P-trend=0.750). High total fat-adjusted PUFA was inversely associated with PC aggressiveness (ORT3vsT1 0.75; 95% CI 0.55-1.03), although this was not significant. No associations were found between total fat-adjusted MUFA or trans fat and PC aggressiveness.

CONCLUSIONS:

High total fat-adjusted saturated fat intake was associated with increased PC aggressiveness, with a suggestion of a stronger effect in men not using statins. The association between total fat-adjusted cholesterol intake and PC aggressiveness was most pronounced in European Americans.

PMID:
27595916
DOI:
10.1038/pcan.2016.39
[Indexed for MEDLINE]

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