Abstract
Fatty acid composition in plasma captures both dietary intake and endogenous synthesis. Prospective analyses of plasma fatty acid composition are needed to establish the role of monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) on risk of developing colorectal cancer. To evaluate associations between plasma fatty acid composition and colon or rectal cancer risk separately, a nested case-control study of 350 colorectal (211 colon and 139 rectal) cancer cases and an equal number of individually matched control subjects was conducted within the Singapore Chinese Health Study, a cohort of 63,257 men and women recruited between 1993 and 1998. Fatty acids in pre-diagnostic plasma were quantified using gas chromatography–tandem mass spectrometry. Conditional odds ratios (ORs) and 95% confidence intervals (CIs) comparing highest to lowest quartiles are presented. For colon cancer, inverse associations were reported with higher essential PUFAs, α-linolenic acid (OR = 0.41; 95% CI: 0.23, 0.73; Ptrend = 0.005) and linoleic acid (OR = 0.43; 95% CI: 0.23, 0.82; Ptrend = 0.008). Higher desaturase activity in the n-6 PUFA synthesis pathway estimated by the arachidonic:linoleic acid ratio was associated with increased colon cancer risk (OR = 3.53; 95% CI: 1.82, 6.85; Ptrend = 0.006), whereas higher desaturase activity in the MUFA synthesis pathway estimated by the oleic:stearic acid ratio was associated with decreased colon cancer risk (OR = 0.42; 95% CI: 0.19, 0.92; Ptrend = 0.024). There was no significant association between the essential fatty acids or the desaturase indices and rectal cancer risk. Endogenous synthesis of arachidonic and oleic acids has an impact on colon cancer development.
Highlights
Colorectal cancer is the fourth most common cancer in the US.[1]Worldwide, a trend of increasing incidence is observed among recently developed countries.[2]
Fatty acids may contribute to colorectal carcinogenesis through a variety of mechanisms including the modulation of immunity, inflammation, and cell signaling.[5,6,7]
There is a large body of evidence supporting the role of lipid metabolism, the effects of various eicosanoids generated from the cyclooxygenase and lipoxygenase metabolisms of arachidonic acid, an n-6 polyunsaturated fatty acid (PUFA), in the development and progression of colorectal cancer.[8]
Summary
A trend of increasing incidence is observed among recently developed countries.[2] Historically, Singapore had lowincidence rates of colorectal cancer, but most recent rates (33.3 per 100,000 from 2008 to 2012) have nearly reached those observed among Asians in the US.[1,3] While it is undisputed that diet is an important contributor to colorectal cancer risk, the specific foods and nutrients that can be translated for prevention remain elusive.[4]. Epidemiologic studies have, for the most part, relied on self-reported recall of usual diet to evaluate potential dietary fat–colorectal cancer associations, with only limited evidence for a positive association with animal fats.[9]
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