Deficiency of the essential fatty acids can occur with the feeding of high glucose enteral or parenteral nutrition in as little as two weeks. This is because of the absence of dietary essential fatty acid precursors as well as the fact that glucose suppresses the mobilisation of stored essential fatty acids from triglycerides in adipose tissue. When the glucose is withdrawn, the lowered insulin levels allows oxidation of fatty acids from adipose tissue and essential fatty acids stored in this tissue are released to circulation, thus reversing the deficiency as measured by the triene to tetraene ratio*. Adipose tissue is predominantly composed of linoleic acid (LA, C18:2 (n-6)), with only trace amounts (<0.5%) arachidonic acid (AA, C20:4 (n-6)). It is thought that during calorie restriction, the LA in adipose tissue is mobilised and may contribute towards the production of series 2 prostaglandins and thromboxanes and the series 4 leukotrienes, which may increase inflammation, thrombosis and platelet aggregation.
Researchers1 have investigated the effects of extreme calorie restriction (1000 kcal/d with 90g protein) on the levels of serum fatty acids in obese women. Following 2 weeks of the low calorie diet, subjects were allocated to receive either a lean meat and fish diet providing 450 to 550 kcal and 2 gram of EFAs per day, or a commercial product meal of 420 kcal with less than 1 gram per of EFAs per day (EFAs mainly as LA), which was followed for a further 28 weeks. Mean weight loss on the subject during the study was 17.6 kg. At baseline the obese women subjects had similar phospholipid levels of gamma linolenic acid (GLA, C18:3 (n-6)), dihomo gamma linolenic acid (DGLA, C20:4 (n-6)) and alpha linolenic acid (ALA, C18:3 (n-3)) as lean women. However, the obese subjects had lower levels of AA in their phospholipid membranes compared to controls. During the extreme calorie restriction diet, phospholipid levels of LA while AA levels rose to normal control values, whereas AA in cholesteryl esters rose above normal.
Upon refeeding at the end of the calorie restriction phase, all levels of LA and AA in serum phospholipids and cholesteryl esters returned to baseline. In this study, mead acid (MA, C20:3 (n-9)), which is considered a marker of EFA deficiency when levels rise in relation to AA phospholipid levels, fell significantly within 1 month of the extreme calorie restriction period. This decline in MA did not return to normal during the entire calorie restriction period despite the very low fat content of the diets. These results suggest that obese individuals have low levels of AA in their plasma phospholipids, which rise during calorie restriction but return to abnormal levels following weight loss. The levels of AA in phospholipids in the obese subjects was lower than would be found in vegetarians, who have low dietary intakes of AA. The normal levels of LA and AA in cholesteryl esters suggests that a deficiency of either of these fatty acids was not the cause of the low levels of AA in phospholipid fraction of serum.
The authors suggested that the rise in plasma phospholipid AA levels during the very low calorie phase of the study may have been due to increased mobilisation of AA from triglycerides in adipose tissue, which were then able to raise plasma phospholipid levels. Evidence from this comes from the fact that both dieting groups experienced the same rise in phospholipid AA, but one of these diets was devoid of preformed AA, which hints at endogenous synthesis from LA. Despite the diet reducing the weight of the subjects from 159 % to 129 % of their ideal body weight, the AA in phospholipids did not return to control following refeeding. This suggests that the abnormal levels of AA were not a secondary effect of the adiposity but perhaps indicate a metabolic dysfunction that may be the cause of the obesity. Obesity is increasingly being seen as a disease of systemic inflammation, and AA and the eicosanoids it forms are part of the cellular mechanism for regulation of that inflammation.
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1Phinney, S. D., Davis, P. G., Johnson, S. B. and Holman, R. T. 1991. Obesity and weight loss alter serum polyunsaturated lipids in humans. American Journal of Clinical Nutrition. 53: 831-838
*the triene tetraene ratio, also called the Holman index, is a measure of the amount of eicosatrienoic acid (ETA, C20:3 (n-9)) to arachidonic acid (AA, C20:4 n-6)). During an essential fatty acid deficiency the amount of arachidonic acid in plasma phospholipid membranes decreases while the amount of eicosatrienoic acid (also called mead) in plasma phospholipid membranes increases. A triene to tetraene ratio of less than ~ 0.2 to 0.4 is considered a clinical essential fatty acid deficiency.
