Alpha-Linolenic Acid: Is It Essential to Cardiovascular Health?
Alpha-Linolenic Acid: Is It Essential to Cardiovascular Health?
Year: 2010
Authors: Geleijnse, J.M. de Goede, J. Brouwer, I.A.
Publication Name: Curr. Atheroscler. Rep.
Publication Details: Volume 12; Pages 359 – 367.
Abstract:
There is a large body of scientific evidence that has been confirmed in randomized controlled trials indicating a cardioprotective effect for omega-3 fatty acids from fish. For alpha-linolenic acid (ALA), which is the omega-3 fatty acid from plants, the relation to cardiovascular health is less clear. We reviewed the recent literature on dietary ALA intake, ALA tissue concentrations, and cardiovascular health in humans. Short-term trials (6 to 12 weeks) in generally healthy participants mostly showed no or inconsistent effects of ALA intake (1.2 to 3.6 g/d) on blood lipids, low-density lipoprotein oxidation, lipoprotein (a), and apolipoproteins A-I and B. Studies of ALA in relation to inflammatory markers and glucose metabolism yielded conflicting results. With regard to clinical cardiovascular outcomes, there is observational evidence for a protective effect against nonfatal myocardial infarction. However, no protective associations were observed between ALA status and risk of heart failure, atrial fibrillation, and sudden death. Findings from long-term trials of ALA supplementation are awaited to answer the question whether food-based or higher doses of ALA could be important for cardiovascular health in cardiac patients and the general population. (Authors abstract)
For ALA, the relation with cardiovascular health is less clear than for fish oils. Several large, prospective cohort studies in the United States have shown inverse associations of ALA intake with risk of cardiovascular diseases, but other epidemiologic studies have been inconclusive. This article summarizes the current literature (published after 2008) on dietary ALA intake, ALA tissue levels, and cardiovascular health in humans. The trials reviewed here consistently showed an increase in blood ALA levels after ALA supplementation, starting at low doses (<2 g/d). ALA supplementation also increased blood levels of EPA, but not of DHA, indicating conversion of ALA to EPA through elongation and desaturation. Short-term trials (6 to 12 weeks) in generally healthy individuals mostly showed no or inconsistent effects of ALA intake (1.2 to 3.6 g/d) on blood lipids, LDL oxidation, lipoprotein (a), and apolipoproteins A-I and B. The few studies that addressed ALA intake in relation to glucose metabolism or blood pressure yielded inconsistent results. There is, however, some observational evidence that a high ALA status may be related to a lower risk of metabolic syndrome. Long-term treatment with high ALA doses had a beneficial effect on body weight and blood LDL cholesterol, which warrants confirmation in future trials. Recent data provide support that ALA could protect against atherosclerosis but it should be noted that this evidence comes from relatively small cross-sectional studies and that conclusions on causality cannot be drawn. The authors conclude there is a need for long-term trials investigating the effect of ALA supplementation on cardiovascular risk factors and clinical end points to answer the question of whether a food-based dose of ALA affects cardiovascular health in high-risk individuals and, if so, whether this is comparable to the effect of marine n-3 fatty acids. (Editors comments)
For ALA, the relation with cardiovascular health is less clear than for fish oils. Several large, prospective cohort studies in the United States have shown inverse associations of ALA intake with risk of cardiovascular diseases, but other epidemiologic studies have been inconclusive. This article summarizes the current literature (published after 2008) on dietary ALA intake, ALA tissue levels, and cardiovascular health in humans. The trials reviewed here consistently showed an increase in blood ALA levels after ALA supplementation, starting at low doses (<2 g/d). ALA supplementation also increased blood levels of EPA, but not of DHA, indicating conversion of ALA to EPA through elongation and desaturation. Short-term trials (6 to 12 weeks) in generally healthy individuals mostly showed no or inconsistent effects of ALA intake (1.2 to 3.6 g/d) on blood lipids, LDL oxidation, lipoprotein (a), and apolipoproteins A-I and B. The few studies that addressed ALA intake in relation to glucose metabolism or blood pressure yielded inconsistent results. There is, however, some observational evidence that a high ALA status may be related to a lower risk of metabolic syndrome. Long-term treatment with high ALA doses had a beneficial effect on body weight and blood LDL cholesterol, which warrants confirmation in future trials. Recent data provide support that ALA could protect against atherosclerosis but it should be noted that this evidence comes from relatively small cross-sectional studies and that conclusions on causality cannot be drawn. The authors conclude there is a need for long-term trials investigating the effect of ALA supplementation on cardiovascular risk factors and clinical end points to answer the question of whether a food-based dose of ALA affects cardiovascular health in high-risk individuals and, if so, whether this is comparable to the effect of marine n-3 fatty acids. (Editors comments)
