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Hypothesis: Vitamin E Complements Polyunsaturated Fatty Acids in Essential Fatty Acid Deficiency in Cystic Fibrosis

Discipline of Nutrition and Dietetics, University of Newcastle, Callaghan (L.G.W., M.L.G.), New South Wales, AUSTRALIA
Department of Respiratory Medicine, The Children’s Hospital at Westmead, Sydney (D.A.F.),New South Wales, AUSTRALIA

Address reprint requests to: Manohar L. Garg, PhD, Discipline of Nutrition & Dietetics, University of Newcastle, Callaghan, NSW, 2308, AUSTRALIA. E-mail: ndmg{at}mail.newcastle.edu.au

While several studies have demonstrated essential fatty acid (EFA) deficiency in plasma and tissue lipids of cystic fibrosis (CF) patients, the reasons for this deficiency are not well established. It is believed that reduced EFA intake, malabsorption of fat, altered desaturase/lipase activity and defective cystic fibrosis transmembrane conductance regulator (CFTR) altering utilisation of EFA in epithelial cells contribute to the development of EFA deficiency in CF. It is likely that increased metabolism of arachidonic acid to eicosanoids such as leukotrienes, thromboxane and prostaglandins may also be a contributing factor. Evidence is presented that elevated oxidative damage to EFA and impaired antioxidant defences, in particular vitamin E, may contribute to the development of EFA deficiency in CF. Furthermore, antioxidant supplementation in CF may improve EFA status.

Key words: cystic fibrosis, vitamin E, essential fatty acids, antioxidants, oxidative stress

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