Western diets are too high in the n-6 essential fatty acid linoleic acid (LA, C18:2 (n-6)) and too low in the n-3 essential fatty acid α-linolenic acid (ALA, C18:3 (n-3)). This imbalance in essential fatty acids, in addition to high intakes of arachidonic acid from high saturated fat intakes, is believed to result in systemic inflammation that leads to disease and chronic ill health. Increasing dietary levels of n-3 fatty acids has been shown to reduce the risk of cardiovascular disease, diabetes and other inflammatory conditions because it restores the required n-6 to n-3 ratio which reduces inflammation. One method of achieving this rebalancing is to increase consumption of the fish oils eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)). However, vegetarians cannot consume these fish oils and so recommendations are to increase dietary consumption of ALA containing seeds, such as flax.
However, consumption of ALA from flax seed is controversial because the conversion of to EPA, the fatty acid required inhibit the pro-inflammatory action of arachidonic acid, is slow due to a widespread inherited deficiency of the required delta 5-desaturase enzyme. Consumption of ALA tends to increase ALA concentrations in phospholipid membranes, but this does not increase EPA concentrations as much as consumption of EPA from fish oil. The problem with consumption of flax, or other similar seeds, is that they must be milled or have their oil extracted in order to be bioavailable. This is because the seed coating is resistant to digestion. This relates to the biological seed dispersal mechanism of the flax plant that required they survive the digestive processes of mammals and birds. Therefore the bioavailability of flax when consumed as whole seeds, milled seeds or oil has been investigated by researchers.
Researchers1 have administered 30g of flax as either milled, or whole seeds or an equivalent amount (6g) of flax seed oil, to healthy male and female subjects in cooked muffins for 3 months. After 1 month the flaxseed oil and milled flax seed oil groups had significant rises in their plasma levels of ALA, with the oil group showing the greatest increase. However, the consumption of whole seeds did not cause an increase in plasma levels of ALA compared to baseline. The plasma levels of ALA in all groups remained stable from 1 month and no further increases in plasma levels were recorded. Importantly though, none of the groups had any increase in EPA or DHA levels throughout the study, supporting previous research that suggests that ALA is not effective at raising plasma levels of EPA in humans due to deficiency of delta 5-desaturase enzyme.
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