Journal Name:
Cancer Causes Control
Article Title:
A prospective study of dietary alpha-linolenic acid and the risk of prostate cancer (United States)
Date Written:
2006
Volume:
17
Number:
NA
Page:
783
Author(s):
Koralek, D.O.; Peters, U.; Andriole, G.; Reding, D.; Kirsh, V.; Subar, A.; Schatzkin, A.; Hayes, R.; Leitzmann, M.F.
Article:
Some epidemiologic studies have suggested that increased dietary intake of alpha-linolenic acid (ALA) enhances the risk of prostate cancer. Further, the association between ALA intake and prostate cancer appeared to be related to mortality from prostate cancer, suggesting that ALA may stimulate progression from latent prostate cancer to invasive disease. However, what many of these studies failed to recognize is that ALA does not represent a single dietary source.
The objective of this study was to evaluate the association of total ALA and ALA from specific food sources with prostate cancer risk in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Different food sources of ALA were examined including from animal products. Animal products are a source of ALA and have been associated with increased prostate cancer risk. It has been hypothesized that positive associations between ALA and prostate cancer may be accounted for by intake of animal products or other unknown factors in animal fat.
A cohort of 29,592 male participants (age 55–74 years) in the screening arm of the PLCO Cancer Screening Trial was followed for an average of 5.1 years. There were 1,898 cases of total prostate cancer, of which 1,631 were organ-confined cases and 285 were advanced stage cases. In this study population, ALA from animal sources contributed 42.5% of total ALA consumed while ALA from plant sources contributed 57.5% of total ALA intake. The largest individual food sources of ALA in the PLCO study population were regular salad dressings, mayonnaise, and milk.
No association was found between total ALA intake and overall prostate cancer (multivariate RR comparing extreme quintiles = 0.94). The corresponding RRs for organ-confined and advanced prostate cancer were 0.94 and 0.83, respectively. In addition, ALA intake from any specific food source was not associated with the risks of total, organ confined, or advanced prostate cancer. ALA intake also showed no association with low grade (Gleason sum < 7; 1,221 cases) tumors or high grade (Gleason sum >/= 7; n = 677 cases) tumors.
Previous experimental studies have yielded inconsistent findings which may be attributable to variations in cell culture growth conditions or differences in the concentrations of ALA and serum used in the cell culture medium. Other studies have suffered from the methodological difficulties related to the measurement of dietary exposure to ALA. Current food composition databases are limited with respect to specific fatty acids and may not always reflect the fatty acid composition of foods over time.
In this study, no association between dietary intake of total ALA or ALA from specific food sources and risk of prostate cancer was found. No observations between ALA and the risk of prostate tumors characterized by stage or grade were noted. The data support that the dietary intake of ALA does not appear to be related to prostate cancer risk and suggests that better attention needs to be paid to the sources of ALA in dietary assessment.
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