Fat and Fatty Acid Terminology, Methods of Analysis and Fat Digestion and Metabolism: A Background Review Paper

Nutrition Research Division, Food Directorate, Health Products and Food Branch, Health Canada, Ottawa, Ontario, Canada.
Annals of Nutrition and Metabolism (Impact Factor: 2.62). 09/2009; 55(1-3):8-43. DOI: 10.1159/000228994
Source: PubMed
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    • "The recommended n-6:n-3 ratio ranges from 1:1 to 4:1 in order to avoid adverse effects on metabolism. However, the Western diets provide ratios of between 10:1 and 20:1, and there are reports of 50:1 (Ratnayake & Galli, 2009). "
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    • "In experimental studies, higher n-3 PUFAs levels alter cell membrane fluidity and receptor responses, regulate gene transcription, and serve as metabolic precursors to potent anti-inflammatory molecules [24]. These molecular effects may underline their systemic and cardiac benefits such as inflammatory responses, autonomic control, vascular and cardiac hemodynamics, endothelial function, blood lipids, and possibly thrombosis [24,25]. Data from intervention studies have also identified a lower risk of cardiovascular events associated with purified EPA (1800 mg/day) [26] as well as EPA+DHA (1 g/day) [27]. "
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    ABSTRACT: Diabetes mellitus (DM) accelerates plaque progression despite the use of statin therapy. The purpose of the present study was to evaluate the determinants of atheroma progression in statin-treated patients with DM. Coronary atherosclerosis in nonculprit lesions in a vessel undergoing percutaneous coronary intervention (PCI) was evaluated using virtual histology intravascular ultrasound. The study included 50 patients with DM who had been taking statin therapy for 8 months at the time of PCI. Twenty-six patients (52%) showed atheroma progression (progressors) and the remaining 24 patients (48%) showed atheroma regression (regressors) after 8 months of follow-up. Fewer progressors than regressors received intensive lipid-lowering therapy with pitavastatin (31% vs. 50%, p = 0.17) and the frequency of insulin use was higher in progressors (31% vs. 13%, p = 0.18). However, neither of these differences reached statistical significance. Risk factor control at baseline and at the 8-month follow-up did not differ between the 2 groups except for serum levels of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA). Univariate regression analysis showed that serum EPA (r = -0.317, p = 0.03) and DHA (r = -0.353, p = 0.02) negatively correlated with atheroma progression. Multivariate stepwise regression analysis showed that low serum DHA and pravastatin use were significant independent predictors for atheroma progression during statin therapy (DHA: beta = -0.414, type of statin: beta = -0.287, p = 0.001). Low serum DHA is associated with progression of coronary atherosclerosis in statin-treated patients with DM.Trial registration: UMIN Clinical Trials Registry, UMIN ID: C000000311.
    Cardiovascular Diabetology 01/2014; 13(1):13. DOI:10.1186/1475-2840-13-13 · 4.02 Impact Factor
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    • "The first step in the pathway requires Δ6 Desaturase [3] [4] which has a higher affinity for ALA than LA but due to the typically higher intake and concentration of LA there is greater conversion of n-6 PUFA producing the predominant product of the n-6 pathway, arachidonic acid (AA or 20 : 4n-6) [1, 5–7]. Thus the capacity of human metabolism to derive EPA and DHA by the desaturation of ALA is negligible in normal circumstances [1]. The efficiency of conversion is particularly poor in relation to DHA [6] [8]. "
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    ABSTRACT: Omega-3 polyunsaturated fatty acids, in particular eicosapentaenoic acid, and docosahexaenoic acid have been shown to have multiple beneficial antitumour actions that affect the essential alterations that dictate malignant growth. In this review we explore the putative mechanisms of action of omega-3 polyunsaturated fatty acid in cancer protection in relation to self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion, and how these will hopefully translate from bench to bedside.
    05/2013; 2013(11):261247. DOI:10.1155/2013/261247
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