Depletion of Omega3 Fatty Acid Levels in Red Blood Cell Membranes of Depressive Patients
ABSTRACT Background: It has been hypothesized that depletion of cell membrane n3 polyunsaturated fatty acids (PUFA), particularly docosahexanoic acid (DHA), may be of etiological importance in depression.Methods: We measured the fatty acid composition of phospholipid in cell membranes from red blood cells (RBC) of 15 depressive patients and 15 healthy control subjects.Results: Depressive patients showed significant depletions of total n3 PUFA and particularly DHA. Incubation of RBC from control subjects with hydrogen peroxide abolished all significant differences between patients and controls.Conclusions: These findings suggest that RBC membranes in depressive patients show evidence of oxidative damage. Possible interpretations, and implications for the etiology and treatment of depression, are discussed.
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ABSTRACT: Ethyl-eicosapentaenoic acid (E-EPA) is an omega-3 fatty acid that has been used in a range of neuropsychiatric conditions with some benefits. However, its mechanism of action is unknown. Here, we investigate its effects on in vivo brain metabolism in first-episode psychosis (FEP). Proton magnetic resonance spectroscopy at 3 T was performed in the temporal lobes of 24 FEP patients before and after 12 weeks of treatment in the context of a larger double-blind, placebo-controlled E-EPA augmentation study. Treatment group effects for glutathione (F1,12=6.1, p=0.03), and a hemisphere-by-group interaction for glutamine/glutamate (F1,20=4.4, p=0.049) were found. Glutathione increased bilaterally and glutamate/glutamine increased in the left hemisphere following E-EPA administration. Improvement in negative symptoms correlated with metabolic brain changes, particularly glutathione (r=−0.57). These results suggest that E-EPA augmentation alters glutathione availability and modulates the glutamine/glutamate cycle in early psychosis, with some of the metabolic brain changes being correlated with negative symptom improvement. Larger confirmatory studies of these postulated metabolic brain effects of E-EPA are warranted.Neuropsychopharmacology 06/2008; 33(10). DOI:10.1038/npp.2008.62 · 7.83 Impact Factor
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ABSTRACT: Studies have shown that depression relates to biomarkers of both short-term and long-term polyunsaturated fatty acid intake. However, it is not known which of these two biomarkers is more closely related to depression. The aim of this study was to examine the relationship of depression with both adipose tissue and serum phospholipid polyunsaturated fatty acids and to assess the importance of each of these two biomarkers in relating to depression. This is a cross-sectional study of healthy adults from the island of Crete. Subjects were examined by the Preventive Medicine and Nutrition Clinic of the University of Crete. Subjects were 394 healthy adults (175 males, 219 females) aged 18-60. The sample consisted of farmers from a number of rural communities of Crete. Fatty acids were determined by gas chromatography in adipose tissue and serum phospholipids. Information about depression was obtained through the Beck Depression Inventory (BDI) and Zung Self-rating Depression Scale (ZSRDS). Adipose tissue alpha-linolenic acid (ALA) (C18:3n-3) was inversely correlated to BDI (r=-0.17, p<0.02). Multiple linear regression analysis taking into account the possible confounding effect of age, gender, body mass index (BMI), smoking and educational level did not confirm this association. The other polyunsaturated fatty acids in adipose tissue were not related to depression. Serum phospholipid polyunsaturated fatty acids did not correlate with depression. This study did not show that the polyunsaturated fatty acids in the adipose tissue are better predictors of depression than those in serum phospholipids.Pharmacology Biochemistry and Behavior 03/2008; 89(1):6-10. DOI:10.1016/j.pbb.2007.10.015 · 2.82 Impact Factor
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ABSTRACT: Oxidative stress has been implicated in the pathogenesis of diverse disease states, and may be a common pathogenic mechanism underlying many major psychiatric disorders, as the brain has comparatively greater vulnerability to oxidative damage. This review aims to examine the current evidence for the role of oxidative stress in psychiatric disorders, and its academic and clinical implications. A literature search was conducted using the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Preview, and Cochrane databases, with a time-frame extending to September 2007. The broadest data for oxidative stress mechanisms have been derived from studies conducted in schizophrenia, where evidence is available from different areas of oxidative research, including oxidative marker assays, psychopharmacology studies, and clinical trials of antioxidants. For bipolar disorder and depression, a solid foundation for oxidative stress hypotheses has been provided by biochemical, genetic, pharmacological, preclinical therapeutic studies and one clinical trial. Oxidative pathophysiology in anxiety disorders is strongly supported by animal models, and also by human biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine in cocaine dependence, while early evidence is accumulating for oxidative mechanisms in autism and attention deficit hyperactivity disorder. In conclusion, multi-dimensional data support the role of oxidative stress in diverse psychiatric disorders. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.The International Journal of Neuropsychopharmacology 02/2008; 11(6):851-76. DOI:10.1017/S1461145707008401 · 5.26 Impact Factor