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Increased ω-3 polyunsaturated fatty acid/arachidonic acid ratios and upregulation of signaling mediator in individuals with autism spectrum disorders
- Yui, Kunio, Imataka, George, Kawasak, Yohei, Yamada, Hiroshi
- Life sciences 2016 v.145 pp. 205-212
- arachidonic acid, autism, biomarkers, brain damage, copper, ferroxidase, food intake, iron, neurons, neuroprotective effect, nutrients, omega-3 fatty acids, omega-6 fatty acids, pathophysiology, superoxide dismutase, transferrin
- The investigation of links between the ratio of omega-3/omega-6 PUFAs and neuronal signaling is a research priority in autism spectrum disorders (ASD).We examine the relationships between the plasma ratios of docosahexaenoid acid (DHA)/arachidonic acid (AA) and eicopentaenoic acid (EPA)/AA and biomarkers of AA-related signaling mediators such as ceruloplasmin, transferrin and superoxide dismutase, in the behavioral symptoms of 28 individuals with ASD (mean age 13.5±4.6years) and 21 age- and gender-matched normal healthy controls (mean age 13.9±5.7years). Behavioral symptoms were assessed using the Aberrant Behavior Checklists (ABC). We conducted controlling for dietary intake and assessed the dietary intake of nutrients.There were no significant differences in intake of nutrients such as omega-3 and omega-6 PUFAs, saturated and unsaturated fatty acid, DHA, AA, iron and copper. Plasma EPA, DHA, and arachidic acid levels, and plasma DHA/AA and EPA/AA ratios were significantly higher, while plasma AA and adrenic acid were significantly lower in the 28 individuals with ASD than in the 21 normal controls. The ABC scores were significantly higher in the ASD group compared to the control group. The plasma ceruloplasmin levels in the ASD group were significantly reduced compared to those in the control group.Increased plasma DHA/AA and EPA/AA ratios may be related to low plasma levels of ceruloplasmin which has neuroprotective properties. Reduced plasma ceruloplasmin levels may diminish the protective capacity against brain damage, and may contribute to the pathophysiology of behavioral symptoms in individuals with ASD.