Does Alpha-linolenic Acid intake reduce the risk of coronary heart disease? A review of the evidence.

January 1, 2005 Human Health and Nutrition Data 0 Comments

Does Alpha-linolenic Acid intake reduce the risk of coronary heart disease? A review of the evidence.

Year: 2005
Authors: D Mozaffarian.
Publication Name: Alternative Therapies in Health & Medicine.
Publication Details: Volume 11; Page 3.

Abstract:

In this significant review article, the question as to whether (and if so, how?) alpha-linolenic acid (ALA) intake affects coronary heart disease (CHD) risk is presented. The author indicates that answers to these queries are of considerable public health importance, particularly for populations with a dislike, a low consumption or availability of fatty fish. It has been presented in some publications that conversion of ALA to the longer chain n-3 fatty acid, EPA occurs to some extent in humans, but further conversion to DHA is very low. Conversion of ALA to longer chain n-3 metabolites varies due to numerous factors including background diet (high levels of n-6 fatty acids will reduce conversion) and by gender, with conversion possibly being greater in women than in men. Trials evaluating secondary outcomes in humans and experimental animal studies indicate that, similar to long-chain fatty acids from fish, ALA has several effects, which might reduce cardiovascular risk. It is unclear to what extent these experimentally observed effects of ALA may be related to a direct physiologic effect versus conversion to more active long-chain metabolites such as EPA; nevertheless, on either case, a diet enriched with ALA appears to favorably affect cardiovascular risk factors as per findings from both experimental studies in human and animal models. These effects include decreased heart rate; reduced systematic vascular resistance; increased arterial compliance; improved autonomic tone; attenuated response to arterial vasoconstrictors; improved left ventricular diastolic function; increased threshold for cardiac arrhyrhmias; improved endothelial cell function; decreased systemic inflammation; reduction in serum triglycerides; inhibition of platelet aggregation and thrombosis and altered adipocyte insulin sensitivity. In one study among US men, the strongest relationship between ALA intake and CHD risk was seen among participants who consumed very little seafood. Among men with little to no seafood intake (EPA + DHA intake <100 mg per day), each 1 g per day ALA intake was associated with –50% lower risk of both nonfatal myocardial infarction (MI) and total CHD. The risk estimate was similar for sudden death, but fewer numbers of events limited the ability to confirm this association. If benefits of ALA are greatest when EPA + DHA intake is very low, then consumption of plant sources of n-3 fatty acids may be particularly important for CHD prevention among individuals who do not regularly consume fatty fish or in areas in which fatty fish is not readily available. Further investigation of this relationship and potential underlying mechanisms is necessary. Data from secondary prevention trials have shown that diets rich in ALA intake markedly reduced recurrent coronary events and clearly indicate that a healthy dietary pattern that includes foods rich in ALA substantially decreases the risk of CHD. *The author concludes that evidence from experimental, observational, and clinical studies suggests that consumption of ALA, found in flaxseed oil, canola oil, walnuts, and other plant sources, reduces CHD risk. ALA may reduce cardiovascular risk via a variety of biologic mechanisms, including effects on platelet function, inflammation, endothelial cell function, arterial compliance, and arrhythmia. Although clinical benefits have not been seen consistently in all studies, most prospective observational studies suggest that ALA intake reduces the incidence of CHD, and two randomized trials have demonstrated that a dietary pattern that includes fruits, vegetables, whole grains, nuts or legumes, and foods rich in ALA substantially reduces the recurrence of CHD events. Additional observational and clinical studies will further establish the effects of ALA on CHD risk and determine whether such effects vary based on gender, duration of intake, background dietary intake of seafood, other factors. At the present time, the weight of the evidence favors recommendations for modest dietary consumption of ALA (2 to 3 g per day) for the primary and secondary prevention of CHD.



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