Potential role of omega-3 fatty acid in preventing psychological consequences of accidents

A report in the 5th 2011 issue of Psychotherapy and Psychosomatics suggests the potential role of omega-3 fatty acid in preventing the psychological consequences of an accident.

It is known that severity of depression is associated with low levels of erythrocyte omega-3 polyunsaturated fatty acids (n-3PUFA) and serum brain-derived neurotrophic factor (BDNF). Dietary n-3 PUFA promote the maturation of neurons and hippocampal neurogenesis in adult rats and have been found to increase the levels of BDNF in rat. BDNF exerts various effects on the nervous system, including neuronal outgrowth, differentiation, synaptic connectivity as well as neuronal repair and survival during development and in adulthood. These findings indicate that supplementation with n-3 PUFA enhances the effect of BDNF-related synaptic plasticity and neurogenesis. The investigators hypothesized that n-3 PUFA-induced neurogenesis occurring early in the transition period might, by increasing BDNF, facilitate the clearance of fear memory and attenuate posttraumatic distress as a consequence.

The aims of the present study were to answer the following questions: whether supplementation with n-3 PUFA increases serum levels of BDNF, and whether change in serum BDNF is associated with the alleviation of posttraumatic distress at follow up in the pilot trial. From among 122 consecutive patients who were recruitedfrom the intensive care unit of the National Disaster Medical Center within 240 h of accidental injury during a 23-week period, 27 met the inclusion criteria. Of these 27 eligible patients, 15 agreed to and provided prior written informed consent to participate in the study. Of the 15 patients enrolled, 11 completed the 12-week follow-up. A total of 7 n-3 PUFA capsules containing 1,470 mg docosahexaenoic acid and 147 mg eicosapentaenoic acid were administered daily for 12 weeks in an open-label fashion. Trained psychiatrists assessed posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) by structured clinical interviews at weeks 4 and 12. The interrater reliability for diagnosis of PTSD and MDD was reliable, with k values of 1.0 and 0.9, respectively.

To assess the serum BDNF levels, 7-10 ml of whole blood were obtained in ethylenediaminetetraacetic acid tubes in the emergency room (week 0), and in week 4 and week 12. Serum BDNF levels were measured using the BDNF Emax Immunoassay System Kit. The distress group consisted of those patients who met the criteria for MDD or PTSD during the trial. During the first 4 weeks after accident, 1 patient met the criteria for PTSD and remained essentially the same at week 12. Another patient met the criteria for MDD at the 4-week follow-up, but symptoms had disappeared at the 12-week follow-up. Overall, serum BDNF levels were significantly elevated from week 0 to week 12 [p = 0.001), although they were largely unchanged in the distress group. Changes in BDNF levels between weeks 0 and 12 were significantly greater in the nondistressed group than in the distress group (p = 0.037). Data confirmed that supplementation with n-3 fatty acids increased serum BDNF levels. The changes seen in serum BDNF levels might be associated with reduced posttraumatic distress on follow-up. Although the present study was not a placebo-controlled trial, the results suggest a potential role for BDNF in the prevention of posttraumatic distress by n-3 fatty acid supplementation. Against results from previous studies, the preventive effect on posttraumatic distress of n-3 PUFA supplementation seen in the present study may well be due to an antidepressant effect, alongside structural and molecular changes occurring in the hippocampus.