Abstract 92 Developmental and Behavioral Pediatrics Topic Plenary, Monday, 5/3

Epidemiological studies suggest that populations with lower dietary intakes of DHA have higher rates of psychiatric disorders. This presumably reflects the lower levels of DHA in neuronal membranes secondary to low dietary DHA intake. Thus, since children with AD/HD have low plasma and erythrocyte phospholipid levels of DHA, it has been postulated that the DHA content of their neuronal membranes also is low and is responsible for the symptoms of AD/HD. If so, DHA supplementation of children with AD/HD will increase plasma levels of DHA and, if neuronal levels of DHA reflect plasma levels, should improve the symptoms of AD/HD. However, this possibility has not been evaluated by a controlled clinical trial. To do so, 70 children (6 to 12 years of age) with AD/HD were assigned randomly and blindly to receive a DHA supplement (345 mg/day) or placebo for 4 mo. All participants met DSM-IV criteria for AD/HD and were receiving an effective dose of stimulant medication. Outcome variables included plasma phospholipid DHA content, scores on objective measures of inattention and impulsivity (Test of Variables of Attention (TOVA); Color Trails Test) after the subjects had been off stimulant medication for at least 24 hr and parent/teacher behavioral rating scales (Child Behavior Checklist, Connor's Rating Scales). Fatty acid patterns were determined before and after the period of supplementation. Testing was done before and after both 2 and 4 mo. Forty-six subjects (23 assigned to each group) completed the entire 4-month study. Data from these subjects were analyzed by repeated measures analysis of covariance to compare longitudinal changes in each outcome variable between DHA-supplemented and placebo groups.

Plasma phospholipid DHA content of the DHA-supplemented group was 300% higher at the end of the study than that of the placebo group (3.98 ± 1.2 vs. 1.41 ± 0.3 mol percent of total fatty acids). However, this was not accompanied by improvement on objective measures of AD/HD symptomatology. TOVA errors of omission, an index of inattention, at baseline and after 4 mo were 31.7 ± 36.0 and 54.0 ± 62.0 vs. 25.7 ± 34.5 and 39.0 ± 51.5 in the DHA and placebo group, respectively; TOVA errors of commission, an index of impulsivity were 23.7 ± 20.5 and 18.1 ± 15.7 vs. 26.0 ± 15.4 and 10.4 ± 9.4 at the same times. The DHA group completed Part 2 of the Color Trails Test in 74.6 ± 37.8 sec at baseline and in 52.9 ± 24.9 sec after 4 mo; corresponding times required by the placebo group were 67.3 ± 27.7 and 50.5 ± 19.2 sec. Thus, despite theoretical arguments concerning the possible role of DHA in the etiology of AD/HD, data from this double-blind, placebo-controlled trial show that a 4 mo period of DHA supplementation does not improve symptoms of children with AD/HD.

Funded, in part, by Martek Biosciences Corporation, Columbia, MD