Abstract
Objective: This study reviews epidemiological and experimental works dealing with the effects of dietary n–6 or n–3 polyunsaturated fatty acids (PUFA) on prostate cancer (PCa) development and PCa risk.
Methods: Systematic literature searches were made using Medline. The epidemiological studies reviewed (ecological, case–control, cohorts, and nested case–control) were those having tested the association of PCa risk with the dietary intake or the blood or adipose tissue levels of PUFA (n–6 PUFA, n–3 PUFA, long-chain n–3 PUFA, linoleic acid, α-linolenic acid, arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid), and with the dietary intake of fish and seafood. Experimental studies dealing with the effects of PUFA on PCa development in animal models or with PCa cell growth in vitro were also reviewed, as well as studies on the mechanisms of the effects of PUFA on PCa.
Results: There is no or little evidence of an association of linoleic or arachidonic acids with PCa risk. Most epidemiological studies failed to find an association of PCa risk with fish or long-chain n–3 PUFA intake, but two recent cohort studies did find an inverse association of fish consumption with the risk of the latest stages of PCa. α-linolenic acid intake was associated with an increase of PCa risk in a majority of epidemiological studies, but other studies did not find this association. Experimental work in vitro and in vivo, as well as mechanistic studies, support a protective effect of long-chain n–3 PUFA on PCa, but data on the effects of linoleic and α-linolenic acids are scarce.
Conclusions: Long-chain n–3 PUFA from fish are possible promising nutrients for the dietary prevention of PCa, but to-date with little epidemiological support. In contrast, studies suggest that α-linolenic acid intake might be a risk factor. New work, both epidemiological and experimental, is awaited to clarify these results.
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Astorg, P. Dietary n – 6 and n – 3 Polyunsaturated Fatty Acids and Prostate Cancer Risk: A Review of Epidemiological and Experimental Evidence. Cancer Causes Control 15, 367–386 (2004). https://doi.org/10.1023/B:CACO.0000027498.94238.a3
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DOI: https://doi.org/10.1023/B:CACO.0000027498.94238.a3