14 March 2008
Fatty Acid Status and Behavioral Symptoms of Attention Deficit Hyperactivity Disorder in Adolescents: A Case-Control Study
Colter et al. Nutrition Journal. 7(1):8, epub ahead of print. (2008)
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Previous studies (case-control) have reported reduced levels of omega-3 fatty acids including DHA/EPA in the circulation of children with ADHD (Attention Deficit Hyperactivity Disorder). However, the various studies have been somewhat inconsistent and have usually not controlled for the dietary intake for the long-chain omega-3 fatty acids as DHA (docosahexaenoic acid) + EPA (eicosapentaenoic acid). Consequently, it has been difficult to differentiate between the impact of ADHD itself on the abnormal fatty acid profiles when reported vs. differences in intakes of these fatty acids in the control (healthy) children as compared to those with ADHD.
The present study compared 12 age-matched controls with 11 adolescents with ADHD (average age of 14 years) with the diet record analysis indicating non-significant differences in the dietary intakes of DHA (average of 31mg in the ADHD group as compared to 39 mg/day in the control group) and EPA (average of 22 mg vs. 14 mg/day). Furthermore, no significant differences were found in the intake of alpha-linolenic acid (ALA) with intakes averaging 660 mg in the ADHD group as compared to 710 mg/day in the control group. Analysis by capillary gas-liquid chromatography of the fatty acids in the red blood cell phospholipid revealed a significantly lower level of DHA (by 29% on average in the ADHD group as compared to controls amounting to 3.12% of total fatty acids vs. 4.39%) with no significant differences in the levels of EPA between the two groups. Furthermore, the omega-3 fatty acid levels (summed) were lower in the ADHD group (by 22%) whereas no significant differences in the AA (arachidonic acid, 20:4 n-6)/ EPA ratio was found. Additional correlational analysis by the investigators indicated that a lower omega-3 status in the blood correlated with higher scores on several Conners’ behavioural scales. The authors concluded that adolescents with ADHD expressed abnormal fatty acid profiles (including lower DHA levels) as compared to similar age which cannot be explained by differences in dietary intakes thereby suggesting metabolic differences in fatty acid metabolism between ADHD adolescents and normal controls.
Dr. Holub's Comments:
The present study (albeit with a small number of subjects)is of particular interest in this field since the authors utilized ADHD vs. control subjects who exhibited no significant differences in their overall intakes of long-chain omega-3 fatty acids as DHA and EPA. The lower levels of DHA in the biomarker (red blood cell phospholipid) could result from an impaired formation of DHA via metabolic conversion (desaturation + desaturation reactions) of ALA to DHA and/or an accelerated catabolism of DHA by a yet to be defined metabolic processes and/or an increased retroconversion of DHA to EPA. In this regard, it is interesting to note that the ratio of EPA/DHA in the ADHD group was 0.71 overall as compared to a much lower ratio of 0.36 in the control group. Future randomized placebo-controlled cross-over trials (double-blinded) will be of interest using differing doses (DHA and/or EPA) and durations to determine if such omega-3 supplementation can improve various measures of ADHD behaviours.