The essential fatty acid α-linolenic acid (ALA, C18:3 (n-3)) is required for human health because it enters the metabolic pathway that synthesises hormones required to regulate cellular inflammation and immunity. Flaxseeds and walnuts are good sources of ALA but smaller quantities are found in vegetable oils, nuts, seeds and green leafy vegetables. Western diet are generally deficient in n-3 fatty acids while intakes of the n-6 fatty acid linoleic acid (LA, C18:2 (n-6)) are too high. Current estimates suggest that the ratio of n-6 to n-3 fatty acids is ~6 to 10:1, but should be closer to 3 to 1. The result of the imbalance in this fatty acid ratio is an increase in cellular inflammation that may predispose individuals to cardiovascular disease, cancer and other degenerative conditions. Researchers are therefore interested in the effects of supplementing n-3 fatty acids on known biomarkers for cardiovascular disease.
For example, research published in the journal Heart1, investigated the effects of ALA supplementation on the modification of cardiovascular risk factors using a meta-analysis of previous studies. In particular, the researchers were interested in the effects of ALA supplementation from clinical trails and their effects on total cholesterol, low density lipoprotein cholesterol (LDL), high density cholesterol (HDL), very low density cholesterol (VLDL), triglycerides, fibrinogen, fasting plasma glucose, changes in body mass, changes in weight and systolic and diastolic blood pressure. The analysis included 14 studies with treatment durations of over 4 weeks. The results showed that ALA supplementation only had effects on 3 of the 32 outcomes tested in those studies. These included a reduction in fasting plasma glucose, a reduction in fibrinogen and small reduction in HDL concentration. However, there was no significant effect on any other cardiovascular disease marker.
These results suggests that ALA does have some benefits on biomarkers for cardiovascular disease. However, the benefits of ALA appear not to be as great as those seen following supplementation with fish oils. Fish oils contain high concentrations of eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)), both of which accumulate in cell membranes and regulate of cellular inflammation through production of eicosanoids and docosanoids, respectively. Dietary ALA accumulates in cell membranes, and cells can metabolise ALA to both EPA and DHA. However, the conversion of ALA to EPA and DHA is not efficient in humans due to low activity of the required desaturase enzyme. Supplementation with ALA is therefore not as efficient at increasing plasma membrane levels of EPA and DHA, when compared to fish oils. This explains the lack of cardiovascular benefits following ALA supplementation seen in this study.
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