Abnormalities in plasma composition of essential fatty acids (EFAs) may be associated with the etiology of pruritus and other skin problems in patients undergoing hemodialysis. To study whether an oral supplementation with ω–6 (n–6) EFAs would restore deranged plasma EFAs and ameliorate skin symptoms, 9 and 7 dialysis patients were randomly assigned to receive either γ-linolenic acid (GLA)-rich evening primrose oil (EPO) or linoleic acid (LA) (2 g/day each) for 6 weeks. Plasma concentrations of EFA were analyzed by gas chromatography and uremic skin symptoms were assessed for dryness, pruritus and erythema by questionnaire and visual inspection in a double-blind manner. The patients given EPO exhibited a significant (p < 0.05) increase in plasma dihomo-γ-linolenic acid (a precursor of anti-inflammatory prostaglandin E1) with no concomitant change in plasma arachidonic acid (a precursor of pro-inflammatory prostaglandin E2 and leukotriene B4). In contrast, those given LA exhibited a significant (p < 0.05) increase in LA but not in any other n–6 EFAs, whereas they exhibited a significant (p < 0.05) decrease in plasma docosahexaenoic acid. The patients given EPO showed a significant (p < 0.05) improvement in the skin scores for the three different uremic skin symptoms over the baseline values and a trend toward a greater improvement (0.05 < p < 0.1) in pruritus scores than those given LA. Results indicate that GLA-rich EPO would be a more favorable supplemental source than LA in terms of shifting eicosanoid metabolism toward a less inflammation status through modifying plasma concentrations of their precursor n–6 EFAs. Further studies are required to confirm the efficacy and safety of EPO therapy for the treatment of uremic pruritus.
It has beem hypothesised that a depletion Of omega-3 PUFAs, particularly DHA, may be of aetiologic importance in depression This hypothesis is supported by epidemiological observationsand limited clinical data. We have fiuther investigated the hypothesis [2].PUFA composition of phospholipids in RBC membranes fiom 10 depressed cases and 14 matched controls were measured. Current dietary intake of PUFAs was also measured using the 7day weighed intake method.It was found that total omega3 PUFAs, EPA and DHA levels were significantly lower in the RBC membranes of the depressed subjectssee table I . These RBC PUFAs also correlated strongly and negatively with the Beck Depression Inventory scores of the depressed groupsee figure 1. In addition, the dietary levels of both A-LA and total omega-3 PUFAs in the depressed group correlated strongly and negatively with the Beck Depression Inventorysee figure 2. Significant positive correlations between the dietary and RBC membrane omega-3 PUFAs were also found in the depressed group. Table 1. RBC membrane omega-3 PUFA levels and absolute RBC values are presented as mg/100mg oftotal phospholipid total enerw intake-" (ATEI") Each value represents the mean-? S.E.M. for each subject group Patients (n = 10) Controls (n = 14) p* EPA 0.52 20.07 0.73 20.05 0.02 DHA 3.25 2 0.60 4.72 50.29 0.02 total omega-3 5.39 2 0.93 7.60 20.38 0.02 ATEI" 9153.73 5 769.44 8478.21 2 594.75 0.49 v) r n l w 20 I 3 w o 5 ! 10 1 2 3 5 6 RBC DHA: ns/1 OOmg ci :otal phospholipid Figure 1 Negative correlation between the severin of deuression and RBC DHA.p 30 0 0 cn W [2: 20 a W 0 : l r r = -0.75; p = 0.01 . 0 1000 2000 31 Dietary to:al omega-3 PUFAs: mg/lOOg of total 10 energy intake Figure 2 Negative correlation between the severitv O f deoression and total dietarv Omega -3 PLJF.4The results support the hypothesis of Hibbeln and Salem [ 11 and are consistent with the findings of others [2,3]. The difference in the omega-3 PUFA levels of the cases and controls cannot be explained by differences in smoking, alcohol consumption, stressful life events, reduced energy intake or physical health problems. The subjects were matched for these variables, plus age, gender and body mass index. It has also shown [4] that antidepressant drugs have no effect on omega-3 levels. Omega-3 PUFAs can only be obtained fiom the diet. These findings support the notion that a dietary deficiency of omega-3 PUFAs may be involved in the aetiology of depression. This is supported by the correlations we found in the depressed subjects between dietary A-LA intake and RBC membrane omega-3 PUFAssee table 4.Abnormal PUFA metabolism may also be present which could exacerbate the effect of depleted dietary omega-3 PUFAs.These findings provide the basis for studying the therapeutic effect of omega-3 PUFA supplementation in the treatment of depression.
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