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Dietary supplements for preventing postnatal depression

  1. Brendan J Miller1,*,
  2. Linda Murray2,
  3. Michael M Beckmann3,
  4. Terrence Kent4,
  5. Bonnie Macfarlane3

Editorial Group: Cochrane Pregnancy and Childbirth Group

Published Online: 24 OCT 2013

Assessed as up-to-date: 4 SEP 2013

DOI: 10.1002/14651858.CD009104.pub2


How to Cite

Miller BJ, Murray L, Beckmann MM, Kent T, Macfarlane B. Dietary supplements for preventing postnatal depression. Cochrane Database of Systematic Reviews 2013, Issue 10. Art. No.: CD009104. DOI: 10.1002/14651858.CD009104.pub2.

Author Information

  1. 1

    Flinders Medical Centre, Department of Obstetrics and Gynaecology, Bedford Park, South Australia, Australia

  2. 2

    University of Tasmania, School of Medicine, Hobart, Australia

  3. 3

    Mater Health Services, Brisbane, Queensland, Australia

  4. 4

    Raceview Surgery, Raceview, Queensland, Australia

*Brendan J Miller, Department of Obstetrics and Gynaecology, Flinders Medical Centre, Flinders Drive, Bedford Park, South Australia, 5042, Australia. brendan_miller@hotmail.com.

Publication History

  1. Publication Status: New
  2. Published Online: 24 OCT 2013

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Characteristics of included studies [ordered by study ID]
Mokhber 2011

MethodsRandomised controlled trial. Method of randomisation not described. Method of allocation concealment was not described.

218 assessed for eligibility. 39 were excluded or refused to participate in the trial.

179 were randomised to either 100 µg selenium tablets or matched placebo tablets.

13 were excluded after the first consumption of tablets due to intolerance to selenium tablets or bad smell of selenium tablets.

22 withdrew from selenium arm. 19 withdrew from the placebo arm. 61 completed the selenium arm of the trial. 64 completed the placebo arm of the trial.

44 from the selenium arm completed the EPDS test. 41 from the placebo arm of the study completed the EPDS test.

Outcomes were serum selenium tests at baseline and at end of trial, and self-reported EPDS after the end of the trial.


ParticipantsIranian primigravid women aged 16-35 years attending the Obstetrics and Gynaecology department of OM-Albanin Hospital (Mashhad, Iran) between June 2006 and August 2008.

Inclusion criteria were women gestational age up to 12 weeks with a live fetus, and with no serious physical or mental disease and no indications for terminating the pregnancy.

Exclusion criteria were use of any drugs, but not routine supplementation of folic acid and ferrous sulphate, and occurrence of any severe disease or stressful life events according to the Holmes and Rahe stress scale. Also excluded were those women with intolerance to the tablets or the unpleasant aroma associated with the tablets and women with a BDI score greater than or equal to 31, indicating moderate to severe depression.


Interventions100 µg selenium yeast tablets or matched placebo yeast tablets were given daily.  Selenium yeast tablets were provided by Pharma Nord, Vejle (Denmark).

Tablets were given from the first trimester of pregnancy until delivery (approximately 6 months).


OutcomesThe mean serum selenium level (µg/dL ± SD) was measured pretrial and post-trial.

The self reported mean EPDS score (± SD) post-trial for the selenium group was 8.8 ± 5.1 and for the placebo group post-trial was 10.7 ± 4.4.


NotesNo power calculation reported.


Risk of bias

BiasAuthors' judgementSupport for judgement

Random sequence generation (selection bias)Low riskStudy authors were emailed. They replied that block randomisation was performed from a table.

Allocation concealment (selection bias)Unclear riskStudy authors were emailed. They replied that a person not involved in the trial placed and labelled the treatment and placebo boxes. However, no specific information regarding allocation concealment was given.

Blinding of participants and personnel (performance bias)
Personnel
Low riskStudy authors were emailed. They replied that both personnel having contact with participants and participants were blinded as to treatment and placebo.

Blinding of participants and personnel (performance bias)
Participants
Low riskParticipants received either selenium yeast tablets or matched placebo yeast tablets in identical packaging as this is a double-blind design.  Provided the taste of the tablets was the same and there are no obvious side-effects to this dosage of selenium then there would be a low risk of unblinding.    

Blinding of outcome assessment (detection bias)
Outcome of Self reported EPDS
Low riskIf women were aware they received the intervention (selenium) rather than placebo this might introduce a significant risk of bias on the outcome assessment (self-reported EPDS). However, it is our judgement that this would be unlikely and hence there is a low risk of bias for this outcome assessment.

Incomplete outcome data (attrition bias)
Self-reported EPDS
High riskMissing outcome data are balanced across intervention groups. Similar numbers of women withdrew from treatment for similar reasons. Reasons are given for why women withdrew from treatment. However, no reasons are specified for why so many women failed to complete their EPDS test, although similar numbers failed to complete the EPDS in each treatment group.

No mention is made regarding whether an attempt was made to impute data for the women who failed to complete the EPDS but had completed the trial into the EPDS mean calculation.

The numbers of women that failed to complete their EPDS is such a high proportion of the participants that this could have a high risk of introducing bias.  Approximately half of the women either withdrew from the study or failed to complete their EPDS in both arms of the study.     

Selective reporting (reporting bias)Low riskWith regard to postnatal depression, this article only provides continuous data with a comparison between the mean score for EPDS between selenium and control group as a primary outcome measure.  It would have been possible for dichotomous data to be presented with for example numbers of women with an EPDS ≥ 13 (indicating they were at risk of depression). This may have given an indication of whether selenium has a clinically significant effect as well as a statistically significant effect on postnatal depression. At this time these data are not yet available from the study authors, but we are seeking it.

Otherwise, this appears to have a very simple trial design and it is our judgement that the published report includes all expected outcomes, including those that were pre-specified, even though the study protocol is not available. The study authors have stated in an email that the trial did not deviate from outcomes listed in the original University ethics application.

Mozurkewich 2013

MethodsThis was a double-blind, placebo-controlled, randomised controlled trial to assess whether omega-3 fatty acid supplementation prevents antenatal and postpartum depressive symptoms among pregnant women at risk for depression. The plan was to recruit 126 pregnant women at less than 20 weeks' gestation from prenatal clinics at 2 health systems in Ann Arbor, Michigan and the surrounding communities. They were followed prospectively over the course of their pregnancies and up to 6 weeks postpartum.


ParticipantsThe women participating in this study were receiving prenatal care at 2 health systems in southeastern Michigan, the University of Michigan Hospitals and Clinics and St Joseph Mercy Health System/Integrated Health Associates. These health systems are located in Ann Arbor, Michigan and Ypsilanti, Michigan and the surrounding communities.

Women were 18 years of age or older, have a confirmed, live, intrauterine pregnancy of greater than 12 weeks' gestation but less than 20 weeks' gestation, and be enrolled in prenatal care at 1 of the 2 participating health systems. They must have been planning to deliver at 1 of the 2 participating hospitals and plan to remain in the southeastern Michigan area through 6 weeks after delivery. To qualify for the study, women must be at risk for depression, based on (i) a history of MDD, (ii) a history of postpartum depression, or (iii) an EPDS score between 9 and 19.
Women were excluded from participating in the study if they were currently taking an omega-3 fatty acid supplement; taking antidepressant or other psychiatric medications; using therapeutic or prophylactic anticoagulation medication; or consuming more than 2 fish meals per week. In addition, pregnant women with a diagnosis of current major depressive disorder, or other psychiatric diagnoses, including current substance abuse, schizophrenia, and bipolar disorder were excluded from study. Pregnant women with known multiple gestation or a history of bleeding disorder such as von Willebrand’s Disease were also to be excluded.


InterventionsEnrolled participants were randomised to 1 of 3 groups: a) EPA-rich fish oil supplement (1060 mg EPA plus 274 mg DHA); b) DHA-rich fish oil supplement (900 mg DHA plus 180 mg EPA; or c) a placebo.


OutcomesThe primary outcome for this study was the BDI score at 6 weeks postpartum. Secondary outcome measures include: omega-3 fatty acid concentrations in maternal plasma and cord blood, pro-inflammatory cytokine levels (IL-1b, IL-6, and TNF-a) in maternal and cord blood, need for and dosage of antidepressant medications, and obstetrical outcomes.


NotesPlan was to randomise 126 women to have 80% power to detect a 50% reduction in participants’ mean BDI scores with EPA or DHA supplementation compared with placebo.


Risk of bias

BiasAuthors' judgementSupport for judgement

Random sequence generation (selection bias)Low riskRandomisation was carried out using a random number table maintained in the University of Michigan investigational drug service.

Allocation concealment (selection bias)Low riskThe research team provided the investigational drug service staff with a list of unique identifying numbers prior to the start of recruitment. At the time of randomisation the research team informed the investigational drug service staff of the study identification number of each participant to be randomised. The investigational drug service staff then randomised participants to 1 of 3 study arms using a random number table: intervention #1, intervention #2 or placebo and will maintain randomisation records until the last participant has completed the protocol.

Blinding of participants and personnel (performance bias)
Personnel
Low riskThe research team was blinded to the results of randomisation. The supplements or placebo were dispensed by the investigational drug service and hence the research team had no way of knowing which participants received intervention or placebo.

Blinding of participants and personnel (performance bias)
Participants
Low riskPlacebos were formulated to be identical in appearance to both DHA and EPA rich supplements, and contained 98% soybean oil and 1% each of lemon and fish oil. A double-dummy design was used to maintain blinding as EPA and DHA containing capsules were different sizes. Hence each participant received 4 small capsules and 2 large capsules, regardless of which arm they were randomised to.

Blinding of outcome assessment (detection bias)
Outcome of Self reported EPDS
Low riskThe research team was blinded to the results of randomisation.

Incomplete outcome data (attrition bias)
Self-reported EPDS
Low riskSmall numbers were lost to follow-up in each arm: EPA n = 3, DHA n = 4, placebo n = 1. These were not included in the intention to treat analysis. There were no significant differences between randomised groups in measures of adherence. Results of participants who discontinued the intervention but were not lost to follow-up were included in the intention to treat analysis (EPA n = 5, DHA n = 4, placebo n = 7).

Selective reporting (reporting bias)Low riskThe outcomes discussed in the protocol appear to be addressed in the final paper.

 
Characteristics of excluded studies [ordered by study ID]

StudyReason for exclusion

Beard 2005Participants with depression at time of recruitment were not excluded from the study.

Doornbos 2009Participants with depression at time of recruitment were not excluded from the study.

Dunstan 2003Participants with depression at time of recruitment were not excluded from the study.

Freeman 2004All participants had depression at time of recruitment.

Freeman 2006All participants had depression at time of recruitment.

Freeman 2007All participants had depression at time of recruitment.

Freeman 2008All participants had depression at time of recruitment.

Freeman 2010All participants had depression at time of recruitment.

Harrison-Hohner 2001Participants with depression at time of recruitment were not excluded from the study.

Llorente 2003Participants with depression at time of recruitment were not excluded from the study.

Makrides 2010Participants with depression at time of recruitment were not excluded from the study.

Rees 2008All participants had depression at time of recruitment.

Smith 2007Participants with depression at time of recruitment were not excluded.

Su 2008All participants had depression at time of recruitment.

 
Characteristics of studies awaiting assessment [ordered by study ID]
Judge 2011

MethodsRandomised, double-blind placebo-controlled trial.

Participants52 women between 24 and 40 weeks of pregnancy.

InterventionsPlacebo (corn oil capsule) or DHA (300 mg DHA fish oil capsule). 26 women were assigned to each group for consumption 5 days per week between 24 and 40 weeks of pregnancy.

OutcomesPostpartum depression symptoms were assessed at 2 and 6 weeks, and at 3 and 6 months with the Postpartum Depression Screening Scale.

There was a significant group difference (P = 0.0057) for the Postpartum Depression Screening Scale between the 2 groups. Compared with controls DHA was associated with a consistent 6-point lower mean depression score across all time points.

NotesThis was a meeting abstract only.

Have made contact with study authors and emailed study authors seeking more information but have not received all the required information to classify this study.

 
Comparison 1. Selenium versus placebo

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 EPDS score185Mean Difference (IV, Fixed, 95% CI)-1.90 [-3.92, 0.12]

 
Comparison 2. EPA versus placebo

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 Beck Depression Inventory Score180Mean Difference (IV, Fixed, 95% CI)0.70 [-1.78, 3.18]

 2 Presence of Major Depressive Disorder180Risk Ratio (M-H, Fixed, 95% CI)1.58 [0.28, 8.94]

 3 Started antidepressant180Risk Ratio (M-H, Fixed, 95% CI)1.58 [0.48, 5.17]

 4 Maternal estimated blood loss (ml)180Mean Difference (IV, Fixed, 95% CI)53.0 [-123.06, 229.06]

 5 NICU admission of neonate180Risk Ratio (M-H, Fixed, 95% CI)1.5 [0.46, 4.91]

 
Comparison 3. DHA versus placebo

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 Beck Depression Inventory Score179Mean Difference (IV, Fixed, 95% CI)-0.20 [-2.61, 2.21]

 2 Presence of Major Depressive Disorder179Risk Ratio (M-H, Fixed, 95% CI)1.08 [0.16, 7.28]

 3 Started antidepressant179Risk Ratio (M-H, Fixed, 95% CI)1.89 [0.60, 5.94]

 4 Maternal estimated blood loss (ml)179Mean Difference (IV, Fixed, 95% CI)54.0 [-83.43, 191.43]

 5 NICU admission of neonate178Risk Ratio (M-H, Fixed, 95% CI)0.53 [0.10, 2.71]

 
Comparison 4. EPA versus DHA

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 Beck Depression Inventory Score177Mean Difference (IV, Fixed, 95% CI)0.90 [-1.33, 3.13]

 2 Presence of Major Depressive Disorder177Risk Ratio (M-H, Fixed, 95% CI)1.46 [0.26, 8.26]

 3 Started antidepressant177Risk Ratio (M-H, Fixed, 95% CI)0.84 [0.31, 2.26]

 4 Maternal estimated blood loss (ml)177Mean Difference (IV, Fixed, 95% CI)-1.0 [-183.94, 181.94]

 5 NICU admission of neonate178Risk Ratio (M-H, Fixed, 95% CI)2.85 [0.61, 13.26]