Abstract
Dietary inclusion of fish and fish supplements as a means to improve cancer prognosis and prevent tumour growth is largely controversial. Long chain omega-3 polyunsaturated fatty acids (LCn-3 PUFA), eicosapentaenoic acid and docosahexaenoic acid, may modulate the production of inflammatory eicosanoids, thereby influencing local inflammatory status, which is important in cancer development. Although in vitro studies have demonstrated inhibition of tumour cell growth and proliferation by LCn-3 PUFA, results from human studies have been mainly inconsistent. Genes involved in the desaturation of fatty acids, as well as the genes encoding enzymes responsible for eicosanoid production, are known to be implicated in tumour development. This review discusses the current evidence for an interaction between genetic polymorphisms and dietary LCn-3 PUFA in the risk for breast, prostate and colorectal cancers, in regards to inflammation and eicosanoid synthesis.
Highlights
Cancer is a multifactorial, widely spread, variable and largely non-communicable disease, affecting populations in all parts of the world
The genes or family of genes under consideration include the fatty acid desaturase (FADS) genes involved in the desaturation of LCn-3 polyunsaturated fatty acids (PUFA) [46], the glutathione S-transferase (GST) family of genes involved in oxidative stress and inflammation [47], and the arachidonate lipoxygenase (ALOX) and c oxidase (COX) genes that generate pro- and anti-inflammatory mediators [48]
We propose that while the genotype of HCA-metabolizing enzymes may appear to interact with type of fatty acid intake and prostate cancer risk, it is the presence of HCAs that is interacting with genotype to influence disease risk
Summary
Widely spread, variable and largely non-communicable disease, affecting populations in all parts of the world. Some of the most significant cancers throughout the Western world include breast, colorectal and prostate cancers [1]. Intake of animal sources of fat, saturated and trans-unsaturated fatty acids are associated with all-cause mortality and death due to colorectal, breast and prostate cancers. Plant based oils and fish oils are associated with a decrease in the risk and death due to the aforementioned cancers [7,8,9]. The conversion of LA and ALA to longer-chain FAs is limited by the enzymatic capacity of the desaturases, as well as dietary levels of LA and ALA, which compete for the same enzymes. The conversion of ALA to eicosapentaenoic acid (EPA) (20:5n-3) ranges from between 0.2% and 21% [10]
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