Docosahexaenoic acid deficiency

Martinez, M. (1996) Docosahexaenoic acid therapy in docosahexaenoic acid-deficient patients with disorders of peroxisomal biogenesis. Lipids. 31 S145-S152. 

There is some evidence that, in these patients, the interconversion between the polyunsaturated fatty acids is disturbed, which restricts the formation of eicosapentaenoic and docosahexaenoic acids. Such children are less likely to have been breastfed (breast milk contains these omega-3 fatty acids) they are more likely to suffer from allergies associated with essential fatty acid deficiency and also dry skin and hair and the membranes of the erythrocytes contain less omega-3 fatty acids compared with normal children. So far, the results of supplementation of the diet of these children with this disorder have not been conclusive. 

Deficiency can lead to lower levels of docosahexaenoic acid, leading to abnormal brain and eye function Optimizes nutrition, growth, and feeding efficiency of children suffering from cystic fibrosis Attenuates diabetic complications... 

Martinez M (1990) Severe deficiency of docosahexaenoic acid in peroxisomal disorders a defect of delta 4 desaturation Neurology 40 1292-1298... 

Schiefermeier M. and Yavin E. (2002). n-3 Deficient and docosahexaenoic acid-enriched diets during critical periods of the developing prenatal rat brain. J. Lipid Res. 43 124-131. 

Gronn, M., Christensen, E., Hagve, T.A. and Christophersn, B.O. (1990) The Zellweger syndrome deficient conversion of docosahexaenoic acid (22 6(n-3)) to eicosapen-taenoic acid (20 5(n-3)) and normal delta 4-desaturase activity in cultured skin fibroblasts. Biochim. Biophys. Acta. 1044 249-254. 

Martinez, M. (1991) Developmental profiles of polyunsaturated fatty acids in the brain of normal infants and patients with peroxisomal diseases severe deficiency of docosahexaenoic acid in Zellweger s and pseudo-Zellweger s syndomes. World Rev. Nutr. Diet. 66 87-102. 

Stinson AM, Wiegand RD, and Anderson RE. Recycling of docosahexaenoic acid in rat retinas during n-3 fatty acid deficiency. J Lipid Res 1991 32 2009-2017. 

Connor WE, Neuringer M, and Lin DS. Dietary Effects on brain fatty acid composition The reversibility of n-3 fatty acid deficiency turnover of docosahexaenoic acid in the brain eiy throcytes and plasma of rhesus monkeys. J Lipid Res 1990 31 237-247. 

Wiegand RD, Koutz A, Stinson AM, Anderson RE. Conservation of docosahexaenoic acid in rod outer segments of rat retina during n-3 and n-6 fatty acid deficiency. J Neurochem 1991 57 1690-1699. 

Owens SP, Innis SM. Docosahexaenoic acid and arachidonic acid prevent a decrease in dopaminergic and serotoninergic neurotransmitters in frontal cortex caused by a 1 inoleic and a-linolenic acid deficient diet in formula-fed piglets. J Nutr 1999 129 2088-2093. 

Janssen A, Baes M, Gressens P, Mannaerts GP, Declercq P, Van Veldhoven PP. Docosahexaenoic acid deficit is not a major pathogenic factor in peroxisome-deficient mice. Lab Invest 2000 80(l) 31-35. 

Important in this respect is that 18 2, n-6 18 3, n-3 20 3, n-9 FA and varions cis-trans isomers show competitive inhibition with 20 3, n-6 20 4, n-6 and 20 5, n-3, which are the precursors for the known biologically active prostaglandins and lencotrienes. Administration of an EFA-deficient diet leads to partial replacement of AA by 20 3, n-9, which is a substrate for lipoxygenase bnt not for cyclooxygenase. Feeding a diet high in PUFA of the n-3 type (e.g., linseed oil, fish oil) resnlts in an enrichment of membrane phospholipids with EPA and docosahexaenoic acid (DHA). This may explain why the FA composition of tissue lipids, including membrane PF, can be modified to some extent by the amount of each class of FA in the diet. 

Cao DH, Xue RH, Xu J, Liu ZL (2005) Effects of docosahexaenoic acid on the survival and neurite outgrowth of rat cortical neurons in primary cultures. J Nutr Biochem 16 538-546 Casha S, Yu WR, Fehhngs MG (2005) FAS deficiency reduces apoptosis, spares axons and improves function after spinal cord injury. Exp Neurol 196 390-400 Chan CC (2008) Inflammation beneficial or detrimental after spinal cord injury Recent Pat CNS Drug Discov 3 189-199... 

Docosahexaenoic acid (22 6n-3, DHA) is essential for normal brain and retinal development (1). A 22 6n-3 deficiency is associated with impaired neurological functions, including reduced learning ability in rats (2,3), impaired visual acuity in infant monkeys (4), and abnormal brain development in human infants with Zellweger syndrome (ZS) (5,6). 

A specific deficiency of docosahexaenoic acid (C22 6n-3 DHA) has been noted in some children with TCHAD, TFP, and VLCAD deficiency [14, 35, 38]. DHA is an essential component of cell membranes and is necessary for normal retinal and brain function. Whether the cause of the DHA deficiency is related to the low-fat diet or to poor synthesis of DHA from its precursor a-linolenic acid is not known. Supplementing children with TCHAD, TFP, and VTCAD deficiency with preformed DHA (60 mg/day for children less than 20 kg 100 mg/day for patients >20 kg 100-200 mg/ day for adults) should normalize plasma DHA levels and may slow progression of pigmentary retinopathy and peripheral neuropathy in TCHAD/TFP deficiency [15, 39, 40]. DHA supplements derived from algae rather than fish oils provide good amounts of DHA without other fatty acids. 

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