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ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Experimental Psychology (KMA, RCH, and PJR), the Department of Social Medicine (DG and ARN), and the Academic Unit of Primary Health Care, Department of Community Based Medicine (TJP and DK), University of Bristol, Bristol, United Kingdom
2 Supported by the Food Standards Agency, Government of the United Kingdom (grant no. NO5038) and The University of Bristol, United Kingdom. 3 Reprints not available. Address correspondence to KM Appleton, School of Psychology, Queen’s University, Belfast, 18-30 Malone Road, Belfast, BT9 5BP United Kingdom. E-mail: k.appleton{at}qub.ac.uk.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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Objective: This study aimed to systematically review all published randomized controlled trials investigating the effects of n–3 PUFAs on depressed mood.
Design: Eight medical and health databases were searched over all years of records until June 2006 for trials that exposed participants to n–3 PUFAs or fish, measured depressed mood, were conducted on human participants, and included a comparison group.
Results: Eighteen randomized controlled trials were identified; 12 were included in a meta-analysis. The pooled standardized difference in mean outcome (fixed-effects model) was 0.13 SDs (95% CI: 0.01, 0.25) in those receiving n–3 PUFAs compared with placebo, with strong evidence of heterogeneity (I2 = 79%, P < 0.001). The presence of funnel plot asymmetry suggested that publication bias was the likely source of heterogeneity. Sensitivity analyses that excluded one large trial increased the effect size estimates but did not reduce heterogeneity. Metaregression provided some evidence that the effect was stronger in trials involving populations with major depression—the difference in the effect size estimates was 0.73 (95% CI: 0.05, 1.41; P = 0.04), but there was still considerable heterogeneity when trials that involved populations with major depression were pooled separately (I2 = 72%, P < 0.001).
Conclusions: Trial evidence that examines the effects of n–3 PUFAs on depressed mood is limited and is difficult to summarize and evaluate because of considerable heterogeneity. The evidence available provides little support for the use of n–3 PUFAs to improve depressed mood. Larger trials with adequate power to detect clinically important benefits are required.
Key Words: n–3 Long-chain polyunsaturated fatty acids • depressed mood • randomized controlled trials • systematic review
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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There is biochemical evidence that n–3 PUFAs play an important role in neural structure and function. The brain and central nervous system contain high concentrations of n–3 PUFAs, and several studies suggest a role for n–3 PUFAs in neurotransmitter synthesis, degradation, release, reuptake, and binding (2-4). Low concentrations of n–3 PUFAs have been associated with lower concentrations of the neurotransmitter dopamine, lower density of neurotransmitter receptors D2, lower binding of D2 receptors (2-4), and increased serotonin activity and increased density of 5-HT2A receptors in the frontal cortex (2-4).
Epidemiologic evidence is also available from ecological and cross-sectional studies. Hibbeln (5) showed a strong negative association between fish intake and depression across 13 countries. Tanskanen et al (6) reported a higher prevalence of depressive symptoms in infrequent than in frequent fish consumers in Finland, Silvers and Scott (7) found lower mental health status in non-fish consumers than in fish consumers in New Zealand, and Timonen et al (8) showed an increased risk of developing depression in persons who rarely ate fish compared with regular fish eaters, although effects were only found for females.
A relation between n–3 PUFA intake and depressed mood has also been reported in clinical studies. Lower concentrations of n–3 PUFAs have been reported in the plasma or red blood cell membranes of persons with a Diagnostic and Statistical Manual of Mental Disorders 4th edition major depressive disorder diagnosis compared with matched nondepressed control subjects (9, 10). Depression severity has also been found to correlate positively with balance between n–3 PUFA and n–6 long-chain PUFAs in plasma and erythrocyte phospholipids (11, 12).
More recently, several trials have reported a beneficial effect of n–3 PUFA supplementation on depression in clinical populations. For example, Stoll et al (13) observed improvements in the depressive symptoms associated with bipolar disorder after supplementation with n–3 PUFAs compared with placebo, Nemets et al (14) reported benefits of n–3 PUFAs compared with placebo for treating unipolar depressive disorder, and Peet and Horrobin (15) found n–3 PUFAs to be effective in treating ongoing depression that remained unresponsive to standard therapies. These trials, however, have generally been small. Furthermore, not all studies have reported positive effects. Fenton et al (16) found no benefits of n–3 PUFAs on depressed mood compared with placebo for patients with schizophrenia, and Llorente et al (17) found no clinical improvement in patients with postpartum depression using n–3 PUFAs compared with placebo. The aim of the present review was to identify and combine all published randomized controlled trials investigating the effects of dietary supplementation with n–3 PUFAs on depressed mood.
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METHODS |
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Identification of potentially relevant reports
Eight databases were searched over all years of records until June 2006. These databases were the following: MEDLINE, EMBASE, PsycInfo, CINAHL, Biosis, AMED, the Cochrane Controlled Trials Register, and the Cochrane Database of Systematic Reviews. Articles investigating the effects of n–3 PUFAs on depressed mood were identified by using the following search terms for n–3 PUFAs: "n–3," "omega-3," "
-3," "essential fatty acid," "ALA," "
-linolenic acid," "fish," "fatty fish," and "cod liver oil." These were combined with the following search terms for depressed mood: "depression," "depressive disorder," "depressed mood," "mood," "mood disorder," "affective disorder," "affect," "anxiety," "postpartum," "involutional," "dysthymic disorder," "seasonal affective disorder," in either the "Keyword" or "Abstract" sections of all databases. Duplicates were removed. Titles and abstracts were inspected independently by 2 researchers (KMA and RCH, HLS, or PLB), and articles clearly identified as not relevant were removed from the list. The reference lists of the relevant reports were also inspected to identify any additional trials not identified by the searches.
Report inclusion and data abstraction
Full copies of all relevant articles were acquired where possible over the duration of the data collection period. Some articles were not available through the British Library, so these articles were not acquired. Each article was independently assessed for inclusion in the review by 2 researchers (KMA and RCH, HLS, or PLB), using 5 inclusion criteria. These criteria were the following: exposure was n–3 PUFAs or fish, outcome measures included depressed mood, study was conducted on human participants, study included a comparison group, and reported a randomized controlled trial or a clinical controlled trial. Data were abstracted independently from each identified trial by 3 researchers (KMA; RCH, HLS, or PLB; and DG, DK, TJP, PJR, or ARN) using a standard data abstraction form. Discordances were discussed and resolved. Where data were incomplete, corresponding authors were contacted directly for relevant information.
Study quality
Study quality was assessed by using reports of adequate concealment of treatment allocation, blinding of study participants and researchers, and use of an intention-to-treat analysis.
Data analysis
The methods and results of all trials investigating the effects of n–3 PUFAs on depressed mood were tabulated. All trials reported continuous data (self-report ratings of depression) as opposed to dichotomous data, but trials used many psychometric instruments. Data from trials reporting means (±SDs) were combined (18). To include data from as many trials as possible, missing SD data for one trial were imputed from SD data from all other trials that used the same measure for depression (19), and the standardized mean effect for all trials was calculated by using Hedges’ adjusted g (20). Hedges’ adjusted g is a formulation of effect size used in the standardized mean difference method that includes an adjustment to correct for small sample bias (20). Both random- and fixed-effects models were used to estimate the overall effect size. Random-effects models are theoretically preferable when combining the results of studies when heterogeneity exists. However, where the heterogeneity is due to publication bias, fixed-effects models may be preferable because they give less weight to smaller studies (18, 20, 21). Heterogeneity was investigated by using Higgins’ I2 statistic (22, 23). The I2 statistic describes the proportion of total variation in study estimates that is due to heterogeneity. Three possible sources of heterogeneity were identified a priori—publication bias, the inclusion of one large trial in which depression was not a primary outcome measure, and the inclusion of trials involving different clinical populations. Possible publication bias was investigated by drawing a funnel plot to look for funnel plot asymmetry (24). Heterogeneity as a result of inclusion of one large trial in which depression was not a primary outcome measure was investigated by using sensitivity analyses (20). The effects of trial population were investigated with the use of metaregression (predictor: major or other depressive illness) and sensitivity analyses were also conducted. Analyses were performed in STATA version 8 (StataCorp, College Station, TX) by using the "METAN," "FUNNEL," and "METAREG" commands.
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RESULTS |
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. The methods of the 18 relevant randomized controlled trials are displayed in Table 1. The number of persons enrolled in the trials ranged from 11 (32) to 452 (29). Some trials recruited males only (29), some females only (17, 31, 33), some trials recruited both sexes (13-16, 25-28, 30, 32, 34-37), and all trials involved adults, excepting one conducted on children (37). Trial participants either had a diagnosis of various different clinical conditions, including unipolar depression (14, 15, 28, 30, 34, 37), bipolar disorder (13, 27, 33, 36), schizophrenia (16), chronic fatigue symdrome (25, 26), postpartum depression (17), borderline personality disorder (31), obsessive compulsive disorder (32), and angina (29), or were healthy volunteers (35). The intervention varied considerably between studies. The daily dose ranged from 0.2 g PUFA (17) to 9.6 g PUFA (13) and was composed of eicosapentaenoic acid only (14-16, 27, 31, 32, 36), docosahexanoic acid only (17, 28), or a combination of eicosapentaenoic acid and docosahexanoic acid (13, 25, 26, 29, 30, 33-35, 37). Duration of supplementation ranged from 28 d (14, 33) to 180 d (29). In some studies, n–3 PUFA supplementation was given alone (eg, 26), and in others n–3 PUFA supplementation was given in addition to a range of existing treatments (eg, 31). Depressed mood was also measured differently in different studies. Most studies used the Hamilton Depression Rating Scale (HDRS; 38)(13-15, 28, 30, 32, 33, 36), the Montgomery-Asberg Depression Rating Scale (MADRS; 39) (15, 16, 28, 31), or the Beck Depression Inventory (BDI; 40) (15, 17, 26, 34), but the short form of the Hamilton Depression Rating Scale (HRDS-SF; 41) (34), the Inventory of Depressive Symptomatology (IDS-C; 42) (27), the Children’s Depression Rating Scale (CDRS; 43), the Children’s Depression Inventory (CDI; 44), the Clinical Global Impression (CGI; 45) (37), the Depression scale of the Derogatis Stress Profile (DSP; 46) (29), the Depression scale of the Profile of Mood States (POMS; 47) (35), and a 4-point Likert scale (25) were also used. Most studies reported that they had used blinding (13-17, 25-27, 30, 31, 33-37), 8 studies described adequate allocation concealment (14, 16, 17, 26, 34-37), and 9 had clearly used intention-to-treat analyses (15, 17, 28, 29, 32-36). The results, as reported for all studies, are shown in Table 2, along with the effect sizes and CIs used in the meta-analyses.
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The pooled standardized difference in means (ie, the pooled effect size) obtained with a fixed-effects model was 0.13 SDs (95% CI: 0.01, 0.25). The pooled standardized difference in means obtained with a random-effects model was 0.50 SDs (95% CI: 0.19, 0.81). Results of the meta-analysis obtained with the use of a fixed-effect model are summarized in Figure 2.
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. The funnel plot shows evidence of considerable asymmetry.
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Second, a meta-regression was conducted on all 12 trials to investigate the effect of trial population on the combined estimate. This provided some evidence that the effect was stronger in trials that involved populations with major depression—the difference in the effect size estimates was 0.73 SDs (95% CI: 0.05, 1.41; P = 0.04). This explained some of the heterogeneity—I2 reduced from 79% to 66%, although significant heterogeneity remained (P < 0.001). To investigate this further, sensitivity analyses were conducted for each population type. The analysis of effects of n–3 PUFAs on depressed mood in a trial population with major depressive illness diagnoses involved only trials that were conducted in participants who had a diagnosis of unipolar or bipolar depressive illness (13-15, 28, 30, 34, 36, 37). By using these 8 trials, the pooled standardized difference in means obtained with a fixed-effects model was 0.57 SDs (95% CI: 0.37, 0.77), and the pooled standardized difference in means obtained with a random-effects model was 0.73 SDs (95% CI: 0.35, 1.12). Evidence of heterogeneity and funnel plot asymmetry remained (I2 = 72%, P < 0.001). For the analysis of effects of n–3 PUFAs in trials on persons without major depressive illness (16, 17, 29, 31), the pooled standardized difference in means obtained with a fixed-effects model was –0.13 SDs (95% CI: –0.29, 0.03), and the pooled standardized difference in means obtained with a random-effects model was –0.13 SDs (95% CI: –0.29, 0.02). No evidence of heterogeneity was found (I2 = 3%, P = 0.38). Results of the sensitivity analysis of the effects of n–3 PUFAs on depressed mood in a trial population with a diagnosis of major depressive illness obtained with a fixed-effects model are summarized in Figure 4.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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From the meta-analyses here, the pooled estimate from the fixed-effects model provides little evidence of a beneficial effect of n–3 PUFAs on depressed mood, whereas the combined estimate from the random-effects model suggests a beneficial effect of n–3 PUFAs on depressed mood. There was, however, statistical evidence of substantial heterogeneity and funnel plot asymmetry, which suggests that the combined estimates should be interpreted with considerable caution.
There are several possible causes of heterogeneity and funnel plot asymmetry as seen here (18, 20), the most common source of which is publication bias. If publication bias exists, random-effects models, which place greater weight on small studies, tend to produce estimates of effect size that are biased in the direction of the positive effects of the smaller published studies (18, 20). As publication bias seems likely in these data, the more informative analysis presented in the present review is likely to be the fixed-effects analysis. This analysis suggests that there is little evidence of a beneficial effect of n–3 PUFA for depressed mood.
Of the additional potential sources of heterogeneity that were investigated, the inclusion in the meta-analysis of one large trial where depressed mood was not a primary outcome measure is unlikely to be important. This trial found no effect of n–3 PUFAs on depressed mood compared with placebo and pulled the pooled standardized difference in means toward the null; the meta-analyses conducted excluding this trial resulted in a small beneficial effect of n–3 PUFAs on depressed mood. Heterogeneity, however, was not reduced by the removal of this trial.
The meta-regression, however, provided some evidence that the effect of n–3 PUFA on depressed mood was stronger in trials that involved populations with major depression than in trials conducted on other populations. The meta-analysis performed with only trials that involved populations with a diagnosis of depressive illness (13, 14, 28, 30, 34, 36, 37) showed a beneficial effect of n–3 PUFAs on depressed mood, whereas the meta-analysis performed with the other trials (16, 17, 29, 31) found no evidence of a beneficial effect of n–3 PUFAs on depressed mood. The strong evidence of heterogeneity in the analysis of populations with major depressive illness and the small number of subjects in the analysis of populations without major depressive illness highlight the lack of interpretable evidence. However, these results do suggest that trial population is a modifier of the effects of n–3 PUFAs on depressed mood and that pooling across trials with differing study populations may not be appropriate.
Important additional causes of heterogeneity may also exist in these data. Key potential sources of heterogeneity include measure of depression used (HDRS, HDRS-SF, ADRS, BDI, BDI-II, DSP, or CDRS), the nature of the intervention (n–3 PUFA used, n–3 PUFA dosage, relative proportions of different n–3 PUFAs, and duration of supplementation), characteristics of the trial population (sex, age, and treatment status), and aspects of trial quality. It has been previously suggested that differences in study outcome may be explained by these variables (48). Furthermore, evidence of different effects depending on different measures of depression and different doses of n–3 PUFA supplementation is available within the studies analyzed here (15, 28, 36). These additional sources of heterogeneity were not investigated here because of the small number of trials available. Only 18 trials were included in the review and only 12 trials included in the meta-analysis; therefore, the ability to explore heterogeneity in the present review was limited. The potential importance of these factors, however, should not be underestimated. The mechanisms underlying any effect of n–3 PUFAs on mood are still far from clearly understood (eg, see 49).
Considering the many potential sources of heterogeneity and the small number of trials for which complete data are available, a reliable combined estimate of effects of n–3 PUFAs on depressed mood is difficult to achieve. Additional large, well-conducted trials that have adequate power to detect clinically important differences are required. Power calculations suggest that sample sizes of 
100 participants per group are necessary to achieve evidence of a clinically meaningful change in depressed mood (3–4 points) as measured by scales such as the HRDS and MADRS. Trial quality is also of paramount importance. Various methodologic aspects of a trial can hugely affect trial outcomes (48). Intervention concealment, the use of blinding, and the use of intention-to-treat analyses were just 3 measures of trial quality assessed here, yet only 3 of 18 studies demonstrated all 3 aspects of trial quality. Recent guidelines for the conduct and reporting of randomized controlled trials (50) will hopefully improve trial quality. The exact trials required are difficult to suggest considering our current lack of knowledge of the mechanisms through which n–3 PUFAs may affect depressed mood. Trials conducted on populations with particularly low n–3 PUFA biochemical status have been previously suggested (48), and, considering the differences found here, trials conducted on populations with diagnoses of major depressive illness may be of value.
It is unfortunate that suitable data (means and SDs of outcome measures) were not available to allow the inclusion of all trials in the meta-analysis. All corresponding authors were contacted, yet relevant data could not be obtained for 6 trials. Two of the 6 trials excluded from the analyses reported positive effects of n–3 PUFAs on depressed mood (25, 35); the other 4 trials reported no beneficial effects (26, 27, 32, 33). It is difficult to assess the impact of these trials. The present review also did not attempt to locate unpublished work or hand search journals to locate additional trials. Other potentially eligible trials, therefore, may have been missed. These trials, however, are likely to be few; the database searches were systematic, thorough, and likely to identify all relevant trials.
In conclusion, little trial evidence is currently available to investigate the effects of n–3 PUFAs on depressed mood, and the evidence that was available is difficult to summarize and evaluate due to the heterogeneous nature of the populations studied and the interventions used. The lack of evidence and the marked heterogeneity between studies highlights the need for well-designed, adequately powered, randomized controlled trials.
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ACKNOWLEDGMENTS |
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All authors were involved in the collection of data for this article and provided intellectual input throughout the project development, analysis, and write-up. The authors had no conflicts of interest.
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, The weighting given to the trial in the overall pooled estimate, taking into account the number of participants and the amount of between-study variation (heterogeneity); error bars indicate 95% CIs. —, The combined effect size estimate of 0.13; rhombus, 95% CI (0.01, 0.25).
