ω-3 Fatty acids for major depressive disorder in adults: an abridged Cochrane review
What this study found
Overall, the evidence is insufficient and of very low quality to determine whether omega-3 fatty acids are effective for major depressive disorder. Pooled analyses suggested a small-to-modest benefit on depressive symptoms versus placebo, but the estimate was imprecise and may not be clinically important. Adverse events appeared similar between groups, although safety evidence was uncertain. In the single available comparison with antidepressants, there was no clear difference.
- Study & population
- Cochrane systematic review and meta-analysis of 26 independent studies involving 1458 adults with major depressive disorder.
- Intervention
- Oral omega-3 fatty acid regimens, mainly eicosapentaenoic acid (EPA) alone or EPA/docosahexaenoic acid (DHA) combinations, were tested across trials at doses ranging from EPA 1 g/day to EPA 3 g/day and EPA/DHA combinations such as 0.93/0.75 g/day and 1.05/0.15 g/day.
- Key limitation
- The evidence base was very low quality, with imprecise estimates and concern for bias.
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Open PDFOriginal abstract
Objective To assess the effects of n-3 polyunsaturated fatty acids (n-3PUFAs; also known as ω-3 fatty acids) compared with comparator for major depressive disorder (MDD) in adults. Design Systematic review and meta-analyses. Data sources The Cochrane Depression, Anxiety and Neurosis Review Group's Specialised Registers (CCDANCTR) and International Trial Registries searched to May 2015. CINAHL searched to September 2013. Trial selection Inclusion criteria: a randomised controlled trial (RCT); that provided n-3PUFAs as an intervention; used a comparator; measured depressive symptomology as an outcome; and was conducted in adults with MDD. Outcomes Primary outcomes were depressive symptomology and adverse events. Results 20 trials encompassing 26 relevant studies were found. For n-3PUFAs versus placebo, n-3PUFA supplementation resulted in a small-to-modest benefit for depressive symptomology: SMD=−0.32 (95% CI −0.52 to −0.12; 25 studies, 1373 participants, very low-quality evidence), but this effect is unlikely to be clinically meaningful, is very imprecise and, based on funnel plot inspection, sensitivity analyses and comparison with large well-conducted trials, is likely to be biased. Considerable evidence of heterogeneity between studies was also found, and was not explained by subgroup or sensitivity analyses. Numbers of individuals experiencing adverse events were similar in intervention and placebo groups (OR=1.24, 95% CI 0.95 to 1.62; 19 studies, 1207 participants; very low-quality evidence). For n-3PUFAs versus antidepressants, no differences were found between treatments in depressive symptomology (MD=−0.70 (95% CI −5.88 to 4.48); 1 study, 40 participants, very low-quality evidence). Conclusions At present, we do not have sufficient evidence to determine the effects of n-3PUFAs as a treatment for MDD. Further research in the form of adequately powered RCTs is needed.