High concentrations of arachidonic acid (AA, C20:4 (n-6)) in cell membranes are increasingly being associated with chronic disease and degeneration. Arachidonic acid is released from cell membranes by the action of phospholipase A2, and converted to pro-inflammatory eicosanoids, that can promote cellular inflammation, platelet aggregation and thrombosis. Arachidonic acid can be derived endogenously from its precursor fatty acids such as the essential fatty acid linoleic acid (LA, C18:2 (n-6)), or its metabolites, γ-linolenic acid (GLA, C18:3 (n-6)) and dihomo-γ-linolenic acid (DGLA, C20:3 (n-6)). However, arachidonic acid can also be derived from the diet from foods of animal origin such as meat and eggs. Because vegetarian diets exclude these dietary sources of AA, it has been suggested that they should result in lower AA concentrations within cell membranes. However, a certain level of AA is needed for normal cellular function and it is unsure if dietary exclusion, as occurs in vegetarianism, is beneficial.
Researchers1 have investigated the effects of partial and complete animal product avoidance on the AA concentration of plasma phospholipids and cholesterol esters. Fasting plasma was analysed from 100 omnivorous subjects (ate meat and eggs more than twice a week) who acted as a control group, and then also from 16 low meat eaters (consumed meat and eggs less than once per week) and 25 vegetarians (ate meat or eggs less than once a month). The AA levels in the phospholipid fraction of plasma was lower in the vegetarian and low meat eating group that the omnivorous controls group. In addition, the AA levels of the cholesterol ester fraction was significantly lower in the vegetarian group than the other two groups. There was no difference in the LA content of any plasma fraction between the different groups, however, ALA concentrations were elevated in both the plasma fractions of the vegetarian and low meat eating groups.
These results suggest that dietary AA from meat and eggs contributes significantly to the accumulation of AA in human plasma. However, the 14% reduction in AA seen in the vegetarian group is difficult to quantify in terms of health benefits. Higher levels of α-linolenic acid (ALA, C18:3 (n-3)) were detected in the cholesteryl ester, triglyceride and phospholipid, and in the cholesteryl ester and phospholipid fraction of plasma in the low meat eaters and vegetarians, respectively. This would suggest that avoidance of meat results in higher intakes of plant foods that are sources of ALA. Higher levels of eicosapentanoic acid (EPA, C20:5 (n-3)), a metabolite of ALA, are associated with inhibition of the conversion of AA to its pro-inflammatory metabolites. However, it has been shown that ALA is a poor substrate for EPA and so the benefit of increased ALA concentrations in plasma is not fully understood.
Another interesting finding of this study was the fact that the vegetarian and low meat eating group had significantly higher levels of C20 and C22 non-essential derived fatty acids contained within their serum fatty acids. These fatty acids are metabolised by the elongase and desaturase enzyme system from non-essential precursors and can be used as a marker of essential fatty acid deficiency. However, as the levels of LA were not significantly lower compared to the omnivores, this may infer that the pathway is accelerated in vegetarians, and this then results in the flux of other non-essential fatty acids through the pathway, increasing their concentration. The authors suggest that this is because the lower dietary intakes of AA, cause the increased endogenous production and stimulation of this pathway. This lead to estimates by the authors of a necessary ≈500mg/d of AA to allow feedback inhibition to lower endogenous production.
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