Preventing postpartum depression: A meta-analytic review [615218]

Preventing postpartum depression: A meta-analytic review
Laura E. Sockola,b,c,*, C. Neill Eppersond, and Jacques P. Barbere
aWilliams College, Department of Psychology, United States
bAlpert Medical School of Brown University, Department of Psychiatry and Human Behavior,
United States
cUniversity of Pennsylvania, Department of Psychology, United States
dUniversity of Pennsylvania, Departments of Psychiatry and Obstetrics & Gynecology, United
States
eThe Derner Institute of Advanced Psychological Studies, Adelphi University, United States
Abstract
This meta-analysis assessed the efficacy of a wide range of preventive interventions designed to
reduce the severity of postpartum depressive symptoms or decrease the prevalence of postpartum
depressive episodes. A systematic review identified 37 randomized or quasi-randomized
controlled trials in which an intervention was compared to a control condition. Differences
between treatment and control conditions in the level of depressive symptoms and prevalence of
depressive episodes by 6 months postpartum were assessed in separate analyses. Depressive
symptoms were significantly lower at post-treatment in intervention conditions, with an overall
effect size in the small range after exclusion of outliers (Hedges' g = 0.18). There was a 27%
reduction in the prevalence of depressive episodes in intervention conditions by 6 months
postpartum after removal of outliers and correction for publication bias. Later timing of the
postpartum assessment was associated with smaller differences between intervention and control
conditions in both analyses. Among studies that assessed depressive symptoms using the EPDS,
higher levels of depressive symptoms at pre-treatment were associated with smaller differences in
depressive symptoms by 6 months postpartum. These findings suggest that interventions designed
to prevent postpartum depression effectively reduce levels of postpartum depressive symptoms
and decrease risk for postpartum depressive episodes.
Keywords
Postpartum depression; Prevention; Meta-analysis
© 2013 Elsevier Ltd. All rights reserved.
*Corresponding author at: Department of Psychology, Williams College, Bronfman Science Center, 18 Hoxsey St, Williamstown, MA
01267, United States. Tel: + 1 413 597 2120. [anonimizat] (L.E. Sockol).
NIH Public Access
Author Manuscript
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Published in final edited form as:
Clin Psychol Rev . 2013 December ; 33(8): 1205–1217. doi:10.1016/j.cpr.2013.10.004.
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1. Introduction
While the goal of treatment is to alleviate symptoms among individuals experiencing a given
disorder, preventive interventions are intended to avoid the initial onset of disorder.
Emotional and behavioral difficulties are commonly identified and treated only after the
onset of illness, but prevention of these disorders can significantly reduce the human and
economic costs associated with mental illness (National Research Council & Institute of
Medicine, 2009). A recent review of progress that has been made in the field of depression
prevention identified the implementation of interventions with strong evidence of
effectiveness as a major goal for ongoing research in this area (Muñoz, Beardslee, & Leykin,
2012). In order for this goal to be reached, it is necessary to identify characteristics of
effective preventive interventions.
Postpartum depression is a specific mental disorder for which preventive interventions could
yield dramatic benefits. Depression is one of the most common complications of
childbearing; a meta-analytic review found that approximately 13% of women will
experience a major depressive episode during the first postpartum year (O'Hara & Swain,
1996). According to the World Health Organization, depression is the leading cause of
disability worldwide (World Health Organization, 2012). Beyond the distress and
impairment experienced by women with depression during the postpartum period, research
also indicates that postpartum depression has negative consequences for the children of
depressed mothers. Postpartum depression limits a woman's ability to function effectively in
the maternal role: depressed mothers provide less responsive caregiving, are more likely to
discontinue breastfeeding early or have problems breastfeeding, are less likely to comply
with recommended safety practices such as use of car seats, and their children have lower
rates of preventive healthcare utilization and vaccination (Field, 2010). Infants of depressed
mothers show impairments in social engagement and emotional regulation, increased
negative emotionality, and high cortisol reactivity (Feldman et al., 2009). Impairments in
mother–infant bonding, including severe disorders of the mother–infant bond that may
include rejection of the infant or abusive behavior, are more common among women
experiencing postpartum depression (Brockington, Aucamp, & Fraser, 2006). Postpartum
depression is also associated with increased risk for long-term cognitive impairment,
emotional difficulties, and behavioral problems (Grace, Evindar, & Stewart, 2003).
The context in which postpartum depression occurs provides unique opportunities for
preventive interventions. Women with fewer financial resources may have greater access to
healthcare during pregnancy than during other points in the lifespan; for example, in the
United States, women are eligible for Medicaid during pregnancy and the first 60 days
postpartum (Centers for Medicare & Medicaid Services, 2012). More generally, pregnancy
is a time of increased healthcare utilization, which provides opportunities for screening and
intervention. Research has identified demographic groups at high risk for postpartum
depression, such as minority women and women of low socioeconomic status, which may be
used to target women at increased risk for the disorder (Beck, 2001; O'Hara & Swain, 1996).
Finally, there is some evidence that preventive interventions may be more acceptable than
treatment for depression, particularly among African-American women (Crockett, Zlotnick,
Davis, Payne, & Washington, 2008).Sockol et al. Page 2
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A wide range of interventions for preventing postpartum depression have been assessed in
randomized controlled trials. Many preventive interventions have modified treatments
demonstrated to be effective for postpartum depression. For example, psychotherapy –
particularly cognitive-behavioral and interpersonal psychotherapy – and antidepressant
medication have all been shown to be effective in the treatment of postpartum depression
(Sockol, Epperson, & Barber, 2011). Some studies have assessed whether implementation of
these interventions before the onset of a depressive episode can effectively prevent the
disorder (e.g., Austin et al., 2008; Wisner et al., 2001; Zlotnick, Capezza, & Parker, 2011).
Non-therapeutic social support and educational interventions have also been assessed as
preventive interventions (e.g., Dennis et al., 2008). Other research has investigated whether
modifications to standard postpartum care, such as having women attend their first
postpartum checkup at 1 week instead of 6 weeks postpartum, can reduce the incidence of
depression after childbirth (Gunn, Lumley, Chondros, & Young, 1998). Alternative
biological treatments, notably dietary supplements and hormonal interventions, have also
been assessed as potential preventive interventions for postpartum depression (e.g., Lawrie
et al., 1998; Llorente et al., 2003). Given the wide range of approaches that have been
utilized in prevention research, a comprehensive review of the research in this area is needed
to provide clinicians and researchers with important information regarding the absolute and
relative efficacy of these interventions.
While a great number of reviews of the literature on the prevention of postpartum depression
have been published, most of these reviews are qualitative in nature. Boath, Bradley, and
Henshaw (2005) reviewed evidence from twenty-one randomized controlled trials, including
both psychosocial interventions and biological interventions. Overall, this review found that
there is evidence for their short-term effectiveness, particularly for psychosocial
interventions, but that there was no evidence for long-term effectiveness. Dennis has
published two reviews evaluating the evidence for biological (Dennis, 2004a) and non-
biological (Dennis, 2004b) interventions. In the first review (Dennis, 2004a), she described
seven studies of biological interventions including antidepressant medications, hormonal
therapy, thyroid therapy, DHA, and calcium supplementation. Most of these studies found
no significant group differences; however, Dennis noted that given the methodological
limitations of the included studies no recommendations for clinical practice can be made on
the basis of existing evidence. In the second review (Dennis, 2004b), she described twenty-
nine studies of non-biological interventions including psychotherapy, psychological
debriefing, educational classes, social support, continuity of care and modifications to
postpartum care, and relaxation. This review found that the evidence for the efficacy of
these interventions is mixed and there is insufficient evidence to recommend any specific
intervention, particularly given the methodological limitations of many of the reviewed
studies.
Several quantitative systematic reviews have attempted to synthesize prior findings in this
area. Lumley, Austin, and Mitchell (2004) reviewed studies initiated during pregnancy and
the postpartum period; their meta-analysis found that only indicated postnatal interventions
were associated with decreased risk for postpartum depression. This metaanalysis did not
assess possible moderators of effect sizes. In another quantitative review, Dennis (2005)
conducted a meta-analysis of 15 psychological and psychosocial interventions forSockol et al. Page 3
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preventing postpartum depression. These analyses found that prevention programs did not
significantly reduce risk for postpartum depression. However, analyses of moderators
suggested that interventions were more effective when they targeted women at increased
risk, when they included a postnatal component, and when they were administered
individually. In their review of hormonal interventions for preventing and treating
postpartum depression, Dennis, Ross, and Herxheimer (2009) identified only one study in
which hormones were utilized as a preventive intervention. Similarly, a review of
antidepressant prevention of postnatal depression identified only two studies in which
medication was utilized for prevention, rather than treatment, of postpartum depression
(Howard, Hoffbrand, Henshaw, Boath, & Bradley, 2005). A protocol for a review of dietary
supplements for preventing postpartum depression has been published, but the review has
yet to be conducted (Miller, Murray, Beckmann, Kent, & Macfarlane, 2011).
Overall, existing meta-analyses suggest that preventive interventions for postpartum
depression may have limited efficacy. However, these analyses have several limitations.
Each of these analyses was limited to a single type of intervention (e.g., psychosocial,
hormonal, pharmacological), which precludes the comparison of these approaches. With the
exception of the Dennis (2005) meta-analysis, these studies have not assessed elements of
study design or interventions as potential moderators of the efficacy of these interventions.
These studies also fail to specify the timing of the postpartum assessments that were used to
calculate the effect sizes. A meta-analytic review of depression during the perinatal period
found that the prevalence of this disorder decreases after seven months postpartum, which
suggests that the timing of evaluation should be considered when evaluating the efficacy of
prevention programs (Gavin et al., 2005). Finally, a number of new prevention trials have
been published since these earlier meta-analyses were conducted.
The present meta-analysis addresses several limitations of the above studies. We included a
wide range of interventions, which allows for the direct comparison of the efficacy of
different approaches. We included interventions other than antidepressant medication and
psychotherapy, as complementary and alternative approaches to the treatment and
prevention of depression have high levels of acceptability among perinatal populations
(Battle, Uebelacker, Howard, & Castaneda, 2010). In order to assess whether these
alternative interventions are as effective as empirically supported treatments, we elected to
include as wide a range of preventive interventions as was possible. We limited our analyses
to those in which postpartum depression was assessed within the first 6 months postpartum.
We assessed characteristics of included studies and interventions as potential moderators of
effect size. We also included several studies that have been published since earlier
metaanalyses were conducted. The goal of the current meta-analysis was to assess the
efficacy of a range of preventive interventions for postpartum depression. We assessed both
the level of depressive symptoms in treatment conditions compared to control conditions
and the difference in the prevalence of depressive episodes by six months postpartum.Sockol et al. Page 4
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2. Method
2.1. Search procedures and selection of studies
Relevant studies were identified through searches of PsycInfo and PubMed through 2012
using postpartum depression and prevention as keyword search terms. The reference lists of
existing meta-analyses, relevant reviews, chapters, and retrieved articles were inspected for
further relevant studies. Clinical trial databases (including the Cochrane Pregnancy and
Childbirth Group, Cochrane Depression, Anxiety and Neurosis Group, and the International
Standard Randomised Controlled Trial Number Register) were also reviewed for eligible
studies.
To be included in the meta-analysis, studies had to meet the following inclusion criteria:
a.Study design included intervention and control group(s). Both randomized and
quasi-randomized controlled trials were eligible for inclusion. Due to the need to
compare separate treatment and control conditions for the calculation of effect
sizes, single-case designs were excluded.
b.Authors specified that the goal of the intervention was to reduce postpartum
depressive symptoms and/or the prevalence of postpartum major depressive
episodes. Interventions that did not explicitly target depressive symptoms, such as
smoking cessation programs, were excluded, even if authors reported outcome data
for depressive symptoms and/or major depressive episodes. Interventions in which
maternal depression was not the primary outcome of interest, such as studies of
infant development, were excluded. Interventions designed to treat postpartum
depression were excluded. Interventions were classified as treatment studies if all
subjects met criteria for a major depressive episode at pre-treatment or if all
subjects had depressive symptoms above a cutoff indicative of clinically significant
depressive symptoms at pre-treatment.
c.Intervention was initiated during pregnancy or within 4 weeks of childbirth.
d.Reported outcomes for depressive symptoms and/or prevalence of depressive
episodes between 1 and 6 months postpartum using a validated self-report or
clinician-administered measure.
e.Reported sufficient outcomes to allow for the calculation of effect size(s).
A flow chart summarizing the search process and exclusion of studies is presented in Fig. 1.
After removal of duplicates, the search procedure yielded 797 articles. Abstracts for these
articles were reviewed and the full text of 117 potentially relevant articles were obtained and
reviewed for inclusion. Of these 117 articles, 80 were excluded for the following reasons: 17
were excluded because the target outcome of the intervention was not depressive symptoms
or depression diagnosis, 16 were excluded because they were not randomized or quasi-
randomized controlled trials, 14 were excluded because they did not report outcome data or
reported insufficient data for the calculation of effect sizes, 11 were excluded because the
intervention was initiated after 4 weeks postpartum, 5 were excluded because they did not
include a postpartum assessment between 1 and 6 months postpartum, 4 were excluded
because they were treatment studies in which subjects were selected on the basis ofSockol et al. Page 5
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depressive symptoms and/or diagnosis, and 1 was excluded because the measure of
depressive symptoms was not validated. Secondary manuscripts were identified for 12
studies; all original manuscripts provided sufficient information for coding and calculation
of effect sizes so these articles were not utilized. The remaining 37 articles were eligible for
inclusion in the metaanalysis. Twenty-four studies reported sufficient outcome measures for
calculation of effect sizes representing the difference in depressive symptoms between
treatment and control conditions by 6 months postpartum, and 28 studies reported sufficient
outcome measures for calculation of effect sizes representing the difference in prevalence of
depressive episodes by 6 months postpartum.
2.2. Coding of studies
All studies were coded for intervention type (dietary supplement vs. educational vs.
hormonal vs. medication vs. modified care vs. therapy vs. social support). Interventions
were classified as educational when the intervention consisted of providing information,
either verbal or written, regarding postpartum depression and accessing treatment without
actively engaging participants in activities designed to change behavior or mood.
Interventions were coded as modified care whey they consisted of changes to standard
obstetric care (e.g., increasing frequency or changing timing of postnatal appointments).
Interventions were coded as therapy when they were clinician-led and participants were
engaged in activities with a goal of modifying behavior, cognition, or mood. Interventions in
which participants were provided with nonspecific support were coded as social support
interventions. For moderator analyses, interventions were also coded as biological
interventions (dietary supplement, hormonal, and medication) or psychosocial interventions
(educational, modified care, therapy, and social support) and as established treatments for
postpartum depression (cognitive-behavioral therapy, interpersonal psychotherapy, and
antidepressant medication) and non-established treatments for postpartum depression
(dietary supplements, educational interventions, hormonal interventions, modified care,
other psychotherapies, and social support).
Studies were also coded for type of control group (active vs. educational vs. placebo vs.
treatment-as-usual), timing of intervention (pregnancy vs. labor vs. postpartum), outcome
measure, and timing of postpartum assessment (in weeks). The type of prevention study was
classified using the criteria proposed by the Institute of Medicine report on prevention
research (Mrazek & Haggerty, 1994): indicated interventions target individuals with
subclinical symptoms who do not meet diagnostic criteria, selected interventions target
individuals with risk factors for a disorder but without symptoms of the disorder, and
universal interventions are administered to all members of a given population. Several
studies included subjects who were either at-risk or exhibiting sub-clinical symptoms of
depression; we classified these studies as selected/indicated . While a conservative definition
of preventive interventions would have required us to exclude studies in which subjects were
experiencing major depressive episodes at pre-treatment, over a third of the potential studies
either did not assess for the presence of a major depressive episode at pre-treatment or did
not exclude subjects on the basis of a positive screening. Given the large number of studies
that would have been excluded on the basis of this criterion, we elected to include these
studies and to assess this as a potential moderator of effect size (excluded subjects withSockol et al. Page 6
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MDE at pre-treatment vs. did not assess/did not exclude subjects with MDE at pre-
treatment). We also coded the average level of depressive symptoms at pre-treatment across
treatment and control conditions.
Because studies did not consistently report sample characteristics (ethnicity, parity, and
marital status), these variables were not coded.
The only intervention type for which enough studies were included to assess potential
moderators of effect size was therapeutic interventions. These studies were also coded for
therapeutic orientation (cognitive-behavioral therapy vs. eclectic vs. interpersonal
psychotherapy), whether therapy was conducted individually or in a group format, and the
number of therapy sessions.
Effect sizes were calculated using the study's designated primary outcome measure. When
more than one postpartum assessment was conducted between 1 and 6 months postpartum,
the latest assessment point was used.
2.3. Analyses
Two separate analyses were conducted. The first analysis compared the difference in
depressive symptoms by 6 months postpartum between treatment and control conditions
using the standardized mean group difference. While this effect size does not account for
possible differences in depressive symptoms between treatment and control conditions at
pre-treatment, too few studies reported pre-treatment depressive symptoms for effect sizes
that take these potential differences into account to be calculated. Effect sizes were
calculated by dividing the difference between treatment and control means by the pooled
standard deviation, corrected for upward bias using Hedges' g (Hedges, 1981):
where the pooled standard deviation is defined as
and cm is defined as
Effect sizes were calculated so that positive effect sizes represent lower scores in the
intervention group compared to the control group.
The second analysis compared the prevalence of depressive episodes by 6 months
postpartum between treatment and control conditions using the odds ratio:Sockol et al. Page 7
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Where PT is the proportion of depressed subjects in treatment conditions and PC is the
proportion of depressed subjects in treatment conditions. Odds ratios less than 1 indicate
lower rates of depression among treated conditions compared to control conditions.
The heterogeneity of effect sizes was examined using the Q statistic and the I2 index.
Significant Q statistics indicate that the observed range of effect sizes is significantly larger
than would be expected based on within-study variance. The I2 value indicates the
proportion of variance in effect sizes accounted for by between-study variance. The index
has a range from 0 to 100; Higgins, Thompson, Deeks, and Altman (2003) suggest that 25,
50 and 75% I2 values indicate low, medium and high levels of hetereogeneity, respectively.
When analyses indicated significant heterogeneity among effect sizes, exploratory analyses
were conducted to assess for moderators of effect size. Categorical moderators were
assessed using an analysis of variance (ANOVA) of mixed-effects models for each variable
hypothesized to influence the effect size. Meta-regression analyses were conducted to assess
the effects of continuous moderators.
Publication bias was assessed by visual examination of funnel plots, Duval and Tweedie's
(2000) trim-and-fill procedure, and classic failsafe N values (Rosenthal, 1979). First, the
effect size for each study was plotted against the study standard error. An asymmetric
distribution suggests missing studies due to publication bias (Lipsey & Wilson, 2001). We
used Duval and Tweedie’s trim-and-fill procedure (2000) to identify asymmetric
distributions of effect sizes. When this test indicated significant asymmetry in the funnel
plot, the overall estimates for the model were calculated using the trim-and-fill correction
(Duval & Tweedie, 2000). Using the fail-safe N value, we determined the number of studies
with null findings that would be necessary to produce a nonsignificant overall effect size.
Using Rosenthal’s (1991) recommendation, a value of 5K + 10, where K is the number of
observed studies, was used as the cutoff for an unlikely number of studies.
For each of these analyses, outliers were identified using the sample-adjusted meta-analytic
deviance (SAMD) statistic (Huffcutt & Arthur, 1995). A conservative cutoff score of 2.58
was used to consider studies for exclusion from the analyses, since extreme values can result
from either true population variability or error, and removing outliers whose effects
represent true variability limits the ability to assess the role of moderators (Beal, Corey, &
Dunlap, 2002). The SAMDs were rank-ordered and the scree plots examined to confirm the
outlier status of studies with SAMDs above this cutoff. In cases where the SAMD value was
greater than 2.58 but the scree plot suggested that the SAMD was not discrepant from the
overall distribution, the study was retained to maximize the variance available to assess the
role of moderators.
Calculations of weighted mean effect sizes, heterogeneity, and moderators were conducted
using Comprehensive Meta-Analysis, version 2.2.046 (Borenstein, Hedges, Higgins, &
Rothstein, 2005). We estimated overall effect sizes using random effects models, based onSockol et al. Page 8
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the assumption that the included studies represent a distribution of true intervention effects.
Considerable heterogeneity of effect sizes was expected given the differences in
interventions and samples across the included studies. As the Q statistic is underpowered in
cases of small sample size (Lipsey & Wilson, 2001), random effects models were estimated
regardless of the observed heterogeneity.
3. Results
3.1. Characteristics of included studies
Table 1 presents characteristics of the studies included in the analyses. Studies included a
wide range of intervention types, including therapy ( n = 18), modified care ( n = 6), social
support (n = 6), antidepressant medication ( n = 2), educational programs ( n = 2), dietary
supplements ( n = 2), and hormonal interventions ( n = 1). Control group types included
treatment-as-usual ( n = 24), educational programs ( n = 7), placebo ( n = 5), and a nonspecific
active treatment ( n = 1). Interventions were initiated during pregnancy ( n = 23), the first four
weeks postpartum ( n = 13), or during labor ( n = 1). Prevention types included indicated
interventions ( n = 3), selected/ indicated interventions ( n = 9), selected interventions ( n =
12), and universal interventions ( n = 13). The timing of the postpartum assessment ranged
from 4 to 24 weeks, with the average assessment taking place at 14.6 weeks postpartum ( SD
= 6.7).
3.1.1. Characteristics of therapy interventions— Eighteen studies assessed
therapeutic interventions. One study assessed training in guided relaxation provided via
videotape; this study was excluded from moderator analyses of therapy characteristics due to
differences in the method of administration of the intervention. The remaining studies
assessed cognitive-behavioral ( n = 10), interpersonally-oriented ( n = 5), and eclectic ( n = 2)
interventions. Studies included both group therapy ( n = 10) and individually-administered
therapy (n = 7). The average number of therapy sessions was 5.9 ( SD = 3.0). Study
therapists came from a variety of fields including midwifery ( n = 4), psychology ( n = 4),
nursing (n = 2), social work ( n = 2), occupational therapy ( n = 1) and psychiatry ( n = 1).
There was also considerable variability in the level of educational attainment of therapists,
which ranged from bachelors'-level research staff ( n = 1), to graduate-level students ( n = 4),
to psychiatrists ( n = 1). Many studies included therapists from multiple backgrounds. For
example, the intervention developed by Austin et al. (2008) was implemented by a clinical
psychologist with a midwife who acted as a co-therapist.
3.2. Methodological quality
Table 2 presents characteristics of the included studies related to methodological quality.
Two studies were quasi-randomized trials; the remaining 35 studies were randomized
controlled trials. 62% of studies reported results on the basis of intent-to-treat analyses. 95%
of studies provided some information characterizing the included sample. 28% of studies
excluded participants with current major depressive episodes. Of the 19 studies that included
a clinician-administered measure, 63% reported that assessors were blind to treatment status.
Of the 35 randomized controlled trials, 83% specified the method by which participants
were randomized.Sockol et al. Page 9
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3.2.1. Methodological quality of therapy interventions— Eighteen studies included
therapeutic interventions. One of these interventions was provided via videotape. Of the
remaining 17 studies, 83% provided information about the therapists who provided the
intervention, 56% indicated that an intervention manual was utilized, 78% indicated that
therapists received training in the intervention, 67% indicated that therapists received
supervision during the study, and 44% assessed sessions for adherence to the intervention.
3.2.2. Methodological quality of pharmacological interventions— Five studies
included pharmacological interventions (antidepressant medication, dietary supplements, or
hormonal interventions). For these studies, 80% reported that clinicians were blind to
treatment status and 100% reported that participants were blind to treatment status.
3.3. Postpartum depressive symptoms
Table 3 presents the results of the random effects model for postpartum depressive
symptoms, representing results from 24 studies. These effect sizes represent the difference
between depressive symptoms at the postpartum assessment closest to 6 months postpartum;
positive effect sizes indicate superiority of treatment to control conditions. Effect sizes
(Hedges' g) ranged from −0.20 to 12.10; eight studies had significant effect sizes, all in favor
of the treated condition. There was a significant overall effect of treatment ( g = 0.37, 95%
CI 0.15–0.60, p < 0.001). Two studies had SAMD values greater than 2.58. Visual
inspection of the scree plot of the rank-ordered SAMD scores suggested that the SAMD
values for the studies by Small, Lumley, Donohue, Potter, and Waldonstrom (2000) and
Wolman, Chalmers, Hofmeyr, and Nikodem (1993) were discrepant with the overall
distribution of SAMD scores. These studies were excluded from subsequent analyses; the
average effect size excluding these outliers was g = 0.18 (95% CI 0.09–0.27, p< 0.001).
We also used meta-analysis to assess the average level of depressive symptoms by six
months postpartum in treatment and control conditions. In the 14 studies that utilized the
EPDS as a measure of depressive symptoms, the average EPDS score was 7.06 in treatment
conditions, compared to 7.69 in control conditions. In the five studies that used the BDI-II as
a measure of depressive symptoms, the average BDI score was 8.99 in treatment conditions,
compared to 8.55 in control conditions. In the two studies that used the CES-D as a measure
of depressive symptoms, the average CES-D score was 1.49 in treatment conditions,
compared to 1.57 in control conditions.
Results of tests for publication bias were acceptable. The fail-safe N value was 129, which
exceeds the tolerance value of 120. While the funnel plot was slightly asymmetric (see Fig.
2); trim-and-fill procedures suggested no missing studies. The Q statistic indicated that there
was significant heterogeneity among effect sizes ( p < 0.05). The I2 value indicated a
medium level of heterogeneity, with 37% of the variance in effect sizes attributable to
between-study variance (Higgins et al., 2003).Sockol et al. Page 10
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3.4. Moderator analyses: postpartum depressive symptoms
Because both the Q statistic and I2 index indicated significant heterogeneity of effect sizes,
exploratory analyses of potential moderators were conducted. Subgroups including only one
study were excluded from moderator analyses.
3.4.1. Study characteristics— Nine characteristics of the included studies were assessed
as potential moderators: intervention type (general, biological vs. psychosocial, and EST vs.
non-EST), control group type, timing of intervention, type of prevention, measure, whether
the study excluded women with a current major depressive episode, timing of postpartum
assessment, and average pre-treatment depressive symptoms (see Table 4). No categorical
variables were significant moderators of effect size. There was a trend for later assessment
timing to be associated with smaller effect sizes, indicating a smaller difference between
treatment and control conditions at later assessment points; slope = −0.01, p = 0.05. In
studies that assessed depressive symptoms using the EPDS, higher levels of depressive
symptoms at pre-treatment were associated with smaller effect sizes, indicating a smaller
difference between treatment and control conditions at later assessment points; slope =
−0.07, p < 0.01. There was no relationship between depressive symptoms at pre-treatment
and effect size in studies that assessed depressive symptoms using the BDI-II, slope = 0.01,
p >0.05.
3.4.2. Intervention variables— Three characteristics of interventions for studies
assessing psychotherapeutic interventions were assessed as potential moderators: therapeutic
orientation, method of administration, and number of sessions. There were not enough
studies representing other types of interventions to assess moderators for these interventions.
No categorical characteristics of psychotherapeutic interventions were significant
moderators of effect size. There was a trend for studies with more therapy sessions to have
smaller effect sizes, indicating a smaller difference between treatment and control conditions
at later assessment points; slope = −0.04, p = 0.06.
3.5. Postpartum depression diagnosis
Table 5 presents the results of the random effects model for postpartum depression
diagnoses, representing results from 28 studies. Odds ratios for individual studies ranged
from 0.02 to 1.79. Odds ratios were significant for eight individual studies; seven in favor of
the treated condition and one in favor of the control condition. There was a significant
overall positive effect of treatment ( OR = 0.72, 95% CI 0.0.56–0.94, p = 0.01), representing
a 28% reduction in risk for postpartum depression in treatment groups compared to control
groups. Nine studies had SAMD values greater than 2.58. Visual inspection of the scree plot
of the rank-ordered SAMD scores indicated that the value for the studies by Kozinszky et al.
(2012) and Small et al. (2000) were discrepant. These studies were excluded from
subsequent analyses. The average effect size, excluding these outliers, was OR = 0.67 (95%
CI 0.52–0.85, p < 0.01), which represents a 33% reduction in risk for treatment groups
compared to control groups.
Results of tests for publication bias indicated potential bias in the included studies. The fail-
safe N value was 147, which exceeds the tolerance limit of 140. The funnel plot wasSockol et al. Page 11
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asymmetric (see Fig. 3), and the trim-and-fill correction suggested 5 studies missing to the
right of the mean. After correction for publication bias, the overall effect size was 0.73 (95%
CI 0.56–0.95), which represents a 27% reduction in the risk for treatment groups compared
to control groups. The Qstatistic indicated that there was significant heterogeneity among
the effect sizes ( p < 0.01). The I2 value indicated a medium level of heterogeneity, with 46%
of the variance in effect sizes attributable to between-study variance (Higgins et al., 2003).
3.6. Moderator analyses: postpartum depression diagnosis
3.6.1. Study characteristics— Ten characteristics of the included studies were assessed
as potential moderators: intervention type (general, biological vs. psychosocial, and EST vs.
non-EST), control group type, timing of intervention, type of prevention, method of
diagnosing depression, whether the study excluded women with a current major depressive
episode, timing of postpartum assessment, and baseline depressive symptoms (see Table 6).
No categorical variables were significant moderators of effect size. Studies with later
assessments had larger effect sizes, indicating a smaller difference between treatment and
control conditions at later assessment points; slope = 0.02, p < 0.05. There was no
relationship between depressive symptoms at pre-treatment and effect size in studies that
assessed depressive symptoms using the EPDS, slope = 0.04, p > 0.05.
3.6.2. Intervention variable— Three characteristics of interventions for studies assessing
psycho-therapeutic interventions were assessed as potential moderators: therapeutic
orientation, method of administration, and number of sessions. There were not enough
studies representing other types of interventions to assess moderators for these interventions.
None of these variables was a significant moderator of effect size.
4. Discussion
Results of these meta-analyses suggest that a wide range of interventions may be effective in
the prevention of depression during the first 6 months postpartum. These interventions result
in small but significant reductions in depressive symptoms ( g = 0.18) and the prevalence of
depressive episodes ( OR = 0.73). Although the magnitude of the effects of preventive
interventions are modest compared to treatments for postpartum depression, which a
previous meta-analysis found to be in the medium range ( g = 0.65, Sockol et al., 2011), the
efficacy of these interventions is comparable to, or exceeds, the efficacy of preventive
interventions for anxiety and depression from other meta-analyses (Cuijpers, van Straten,
Andersson, & van Oppen, 2008; Zalta, 2011). The overall level of depressive symptoms by
six months postpartum in both treatment and control conditions were below generally
accepted cutoffs for clinically significant depressive symptoms (Cox, Chapman, Murray, &
Jones, 1996; Dozois & Dobson, 2002).
For both depressive symptoms and depression diagnosis, a later assessment was associated
with a smaller difference between intervention and control conditions. This is consistent
with the results of a meta-analysis of treatments for postpartum depression, which found that
greater treatment length was associated with smaller effect sizes (Sockol et al., 2011).
Moreover, it is consistent with evidence that postpartum depression tends to naturally remit
over time (Heron, O'Connor, Evans, Golding, & Glover, 2004). Given that the naturalSockol et al. Page 12
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course of postpartum depression is for symptom severity to decrease over time, it is
unsurprising that preventive interventions appear to be most efficacious when they are
assessed early during the postpartum period. However, this should not be taken as an
indication that preventive interventions are unnecessary. Given the adverse impact of
depression on depressed women and their children (Grace et al., 2003), even a self-limiting
depressive episode may be extremely distressing and increase the risk for long-term negative
outcomes.
Higher levels of depressive symptoms at pre-treatment were associated with smaller
differences in depressive symptoms by six months postpartum between treatment and
control conditions in studies that used the EPDS as a measure of depressive symptoms. As
this result was only found in one of our analyses, and for only one measure of depressive
symptoms, this result should be interpreted with caution. However, if this finding represents
a true difference in the efficacy of preventive interventions, this suggests that preventive
interventions might be more effective for women who are not yet experiencing significant
levels of depressive symptoms. The duration or intensity of preventive interventions may not
be sufficient to prevent the onset of depressive episodes or worsening of symptoms among
this population.
Interestingly, we found that intervention type was not related to the effectiveness of
treatments for either reducing depressive symptoms or preventing depressive episodes. A
lack of social support is an established risk factor for postpartum depression (Beck, 2001). It
may be that nonspecific social contact and support is sufficient for reducing risk for
depression among this population and that the specific active elements of treatment are less
important. However, further research assessing the efficacy of less well-studied
interventions is necessary to determine whether our failure to identify moderators simply
results from a lack of sufficient evidence. Given the small number of studies representing
antidepressant medication and non-traditional interventions, particularly dietary supplements
and hormonal interventions, further research is necessary to establish whether these
approaches are truly equally efficacious.
One limitation of this meta-analysis was the use of uncontrolled effect sizes. This raises the
concern that differences at post-treatment may actually reflect pre-existing differences
between treatment and control conditions. A separate meta-analysis was conducted assessing
the average change in depressive symptoms between treatment and control conditions,
controlling for pre-treatment symptom levels, using the 13 studies for which this effect size
could be calculated (Morris, 2008). The fail-safe N for this analysis was 17, which is well
below the tolerance value, so the results should be interpreted with caution. With this caveat,
this analysis also found a small but significant difference in the reduction of depressive
symptoms between treatment and control conditions at post-treatment, Hedges' g = 0.15, p =
0.01,95% CI 0.03–0.27. The results of this analysis suggest that our findings are unlikely to
simply reflect preexisting differences between treatment and control conditions.
While the number of studies included in these meta-analyses is comparable to other meta-
analyses of preventive interventions (e.g., Cuijpers et al., 2008; Zalta, 2011), moderator
analyses assessed small subgroups of studies. Because of this, moderator analyses should beSockol et al. Page 13
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interpreted with caution. This is particularly true for the analyses of intervention type. There
were relatively few studies assessing antidepressant medication, dietary supplements,
educational interventions, hormonal interventions, and social support programs. More
research assessing the efficacy of these interventions is necessary in order to establish
whether there are systematic differences between types of interventions. Similarly,
psychotherapy was the only type of intervention for which enough studies were present to
assess for potential moderation of specific aspects of the intervention. Further evaluation of
other types of interventions would allow for similar questions to be asked of these
interventions; for example, whether phone-based social support programs have comparable
efficacy to in-person support groups. Due to inconsistencies across studies in the reporting
of demographic characteristics, we were also unable to assess these as potential moderators.
Future research should help clarify whether particular interventions are more effective for
specific populations, especially women of low socioeconomic status, ethnic/racial
minorities, and single women who are at higher risk for postpartum depression (Beck, 2001;
O'Hara & Swain, 1996; Robertson, Grace, Wallington, & Stewart, 2004).
A significant concern raised by these analyses is the evidence that published studies are
biased in favor of studies with significant positive findings. While the overall effect for
preventive interventions remained significant even after correction for publication bias, there
is no statistical approach that can take the place of real data for moderator analyses. While
our analyses found no evidence that types of interventions or characteristics of interventions
were associated with efficacy, it is possible that there are systematic characteristics of
ineffective interventions that we were unable to assess because these results have not been
published. This may have limited our ability to identify moderators of effect size. While the
“file-drawer problem” is well-known, these analyses provide further evidence that null
findings from well-designed prevention studies are vitally important to a full understanding
of these interventions.
A major limitation of research in this area is that most studies do not report infant outcomes.
As postpartum depression is associated with a range of negative infant and child outcomes
(Grace et al., 2003), it is important to investigate whether interventions that prevent or
reduce the severity of depressive symptoms during the postpartum are able to lessen the
impact of maternal psychopathology on infant development. Only one study that was
eligible for these metaanalyses reported infant outcomes. Armstrong, Fraser, Dadds, and
Morris (1999) found no differences in breastfeeding rates, knowledge or practice of SIDS-
preventing behavior, or use of health services by the mother or infant at six weeks
postpartum. While some studies have shown that intervention may improve both maternal
depression and infant outcomes (e.g., Field et al., 1996; Murray, Cooper, Wilson, &
Romaniuk, 2003), others find that treatment for postpartum depression is not sufficient to
improve infant outcomes (Forman et al., 2007). Future studies investigating preventive and
treatment interventions for perinatal depression should endeavor to assess infant outcomes in
order to determine whether these interventions result in improved infant outcomes.
In summary, these analyses suggest that a wide range of interventions are effective in the
prevention of postpartum depression. By six months postpartum, these interventions are
associated with a 27% reduction in the prevalence of depressive episodes and a reduction inSockol et al. Page 14
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levels of depressive symptoms compared to control conditions. Effect sizes were larger in
studies that assessed depression earlier in the postpartum period; this is consistent with
natural remission of depressive symptoms over the course of the postpartum period. In these
meta-analyses, we found no differences between types of interventions, and different types
of psychotherapeutic interventions appeared to have comparable efficacy. There were few
studies assessing antidepressant medication and other non-therapeutic interventions; more
research is necessary to assess whether these interventions are effective and to establish
whether characteristics of other intervention types are related to efficacy. Although more
research is needed to confirm and extend the results of these meta-analyses, these results
suggest that a wide range of interventions should be targeted for further investigation as
preventive interventions for this disorder.
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HIGHLIGHTS
•The perinatal period is an opportune time to reduce psychological morbidity.
•Many types of interventions may prevent postpartum depression.
•These interventions result in significantly lower levels of depressive symptoms.
•These interventions significantly reduce the risk of major depressive episodes.Sockol et al. Page 20
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Fig. 1.
Flow chart illustrating identification of included studies.Sockol et al. Page 21
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Fig. 2.
Funnel plot for studies assessing the difference between depressive symptoms between
treatment and control conditions by 6 months postpartum. The asymmetric distribution of
studies in the lower half of the funnel plot suggests that there are missing studies with
negative effect sizes, in which control conditions would be superior to treatment conditions.Sockol et al. Page 22
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Fig. 3.
Funnel plot for studies assessing the difference in prevalence of depressive episodes
between treatment and control conditions by 6 months postpartum. The asymmetric
distribution of studies in the lower half of the funnel plot suggests that there are missing
studies with odds ratios greater than 0, in which control conditions would be superior to
treatment conditions.Sockol et al. Page 23
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NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 24Table 1
Characteristics of included studies.
Study Country Intervention type Contra1
typeIntervention
timingPrevention type Symptom
measureDiagnosis
criteriaPostpartum assessment
timing (weeks)Psychotherapy
orientationPsychotherapy
administrationNumber of
sessions
Armstrong et
al. (1999)AUS Modified care TAU POST Selected EPDS EPDS >12 6
Austin et al.
(2008)AUS Therapy EDUC PREG Selected/indicated MINI 16 CBT Group 6
Brugha et al.
(2000)UK Therapy TAU PREG Selected/indicated SADS 12 CBT Group 6
Chabrol et al.
(2002)FR Therapy TAU POST Indicated EPDS EPDS > 11 4–6 CBT Individual 1
Dennis,
Hodnett et al.
(2009)CAN Social support TAU POST Indicated EPDS EPDS > 12 24
Elliott et al.
(2000)UK Social support TAU PREG Selected PSE 12
Gao, Chan,
and Sun (2012)CHINA Therapy EDUC PREG Universal EPDS 12 IPT Group 2
Gorman (1997) USA Therapy TAU PREG Selected/indicated EPDS SCID 24 IPT Individual 5
Gunn et al.
(1998)AUS Modified care TAU POST Universal EPDS EPDS ≥ 13 24
Hagan, Evans,
and Pope
(2004)AUS Therapy EDUC POST Selected SADS 24 CBT Group 6
Hayes, Muller,
and Bradley
(2001)AUS Educational TAU PREG Universal POMS 16–24
Ho et al.
(2009)CHINA Educational TAU POST Universal EPDS 12
Kozinszky et
al. (2012)HUN Therapy EDUC PREG Universal LQ≥12 6–8 Eclectic Group 4
Lara, Navarro,
and Navarrete
(2010)MEX Therapy EDUC PREG Selected/Indicated SCID 16–24 Eclectic Group 8
Lawrie et al.
(1998)SAFR Hormonal PLA POST Universal EPDS EPDS ≥ 12 12
Le, Perry, and
Stuart (2011)USA Therapy TAU PREG Selected/indicated BDI-II BDI-II ≥ 20 16 CBT Group 8
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 25Study Country Intervention type Contra1
typeIntervention
timingPrevention type Symptom
measureDiagnosis
criteriaPostpartum assessment
timing (weeks)Psychotherapy
orientationPsychotherapy
administrationNumber of
sessions
Llorente et al.
(2003)USA Dietary supplement PLA POST Universal BDI-II 16
Logsdon,
Birkimer,
Simpson, and
Looney (2003)USA Social support TAU PREG Selected CES-D 6
Marks, Siddle,
and Warwick
(2003)UK Modified care TAU PREG Selected/indicated EPDS SCID 12
Meeker (1985) USA Social support TAU PREG Universal BDI-II 7
Milgrom,
Schembri,
Ericksen,
Ross,
and Gemmill
(2011)AUS Therapy TAU PREG Selected/indicated BDI-II ≥ 14 12 CBT Individual (Phone) 8
Mokhber et al.
(2011)IRAN Dietary supplement PLA PREG Universal EPDS 8
Munoz et al.
(2007)USA Therapy TAU PREG Selected/indicated EPDS MMS 24 CBT Group 12
Nalepka and
Coblentz
(1995)USA Social support EDUC PREG Universal EPDS ≥ 10 12
Ngai, Chan,
and Ip (2009)CHINA Therapy EDUC PREG Universal EPDS 24 CBT Group 6
Rees(1995) USA Therapy ACT POST Universal CES-D 4 Guided Relaxation Individual (Home) N/A
Shields and
Reid (1997)UK Modified care TAU PREG Universal 9 Item EPDS EPDS > 13 7
Silverstein et
al. (2011)USA Therapy TAU POST Selected QJDS ≥ 11 24 CBT Individual 4
Small et al.
(2000)AUS Modified care TAU POST Selected EPDS EPDS ≥ 13 24
Stamp,
Williams, and
Crowther
(1995)AUS Social support TAU PREG Selected EPDS EPDS > 12 24
Webster et al.
(2003)AUS Educational TAU PREG Selected EPDS > 12 16
Wisner et al.
(2001)USA ADM nortriptyline PLA POST Selected RDC 17
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NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 26Study Country Intervention type Contra1
typeIntervention
timingPrevention type Symptom
measureDiagnosis
criteriaPostpartum assessment
timing (weeks)Psychotherapy
orientationPsychotherapy
administrationNumber of
sessions
Wisner et al.
(2004)USA ADM sertraline PLA POST Selected DSM-IV 17
Wolman et al.
(1993)SAFR Modified care TAU BIRTH Universal PITT PITT ≥ 35 6
Zayas, McKee,
and jankowski
(2004)USA Therapy TAU PREG Indicated BDI-II 12 CBT Individual 12
Zlotnick et al.
(2011)USA Therapy TAU PREG Selected EPDS LIFE 12 IPT Individual 4
Zlotnick
Johnson,
Miller,
Pearlstein,
and Howard
(2001)USA Therapy TAU PREG Selected/indicated SCID 12 IPT Group 4
Zlotnick
Miller,
Pearlstein,
Howard, and
Sweeney
(2006)USA Therapy TAU PREG Selected BDI-II LIFE 12 IPT Group 4
Note . AUS = Australia, CAN = Canada, CHINA = China, FR = France, HUN = Hungary, IRAN = Iran, MEX = Mexico, S AFR = South Africa, UK = United Kingdom, USA = United States, ACT =
Active, EDUC = Educational, PLA = Placebo, TAU = Treatment As Usual, BIRTH = During labor, POST = Postpartum, PREG = Pregnancy, BDI-II = Beck Depression Inventory, CES-D = Center for
Epidemiological Studies Depression Scale, DSM-IV = DSM-IV depression criteria, EPDS = Edinburgh Post-Natal Depression Scale, PITT = Pittsburgh Depression Inventory, LIFE = Longitudinal
Interview Follow-Up Examination, LQ = Leverton Questionnaire, MINI = MINI-International Neuropsychiatry: Interview, MMS = Maternal Mood Screener, QJDS = Quick Inventory of Depressive
Symptomatology, RDC = Research Diagnostic Criteria, SADS = Schedule for Affective Disorders and Schizophrenia, SCID = Structured Clinical Interview for DSM-IV, CBT = Cognitive-Behavioral
Therapy, IPT = Interpersonal Psychotherapy.
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 27Table 2
Methodological quality of included studies.
Study ITT Char sample Excl curr MDE Blind assess Spec random Therapy Pharmacological
Spec ther Manual Training Super Adher Blind clin Blind pt
Armstrong et al. (1999) − + − + +
Austin et al. (2008) + + − + + + + + − −
Brugha et al. (2000) + + − + + + + + + −
Chabrol et al. (2002) + + − N/A + + + + + +
Dennis, Hodnett et al. (2009) + + − N/A +
Elliott et al. (2000) + − − + QR
Gao et al. (2012) + + − N/A + + − + + −
Gorman (1997) − + − + + − + − − +
Gunn et al. (1998) + + − N/A +
Hagan et al. (2004) − + + + + + − + + −
Hayes et al. (2001) − + + − +
Ho et al. (2009) − + − N/A +
Kozinszky et al. (2012) + + − + + + − + − +
Lara et al. (2010) + + + − + + + + + +
Lawrie et al. (1998) + + − + + + +
Le et al. (2011) + + + − + + + + + +
Llorente et al. (2003) − + − N/A + − +
Logsdon et al. (2003) − + − N/A +
Marks et al. (2003) + + − − +
Meeker (1985) + + − N/A −
Milgrom et al. (2011) + + − N/A + + + − + +
Mokhber et al. (2011) − + + N/A − + +
Muñoz et al. (2007) − + + − + + + + + +
Nalepka and Coblentz (1995) − + − N/A +
Ngai et al. (2009) + + − N/A QR + − + − −
Rees (1995) + + − N/A − N/A N/A N/A N/A N/A
Shields and Reid (1997) − + − N/A −
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 28Study ITT Char sample Excl curr MDE Blind assess Spec random Therapy Pharmacological
Spec ther Manual Training Super Adher Blind clin Blind pt
Silverstein et al. (2011) + + − + + + + + + +
Small et al. (2000) + + − N/A +
Stamp et al. (1995) + + − N/A +
Webster et al. (2003) + + N/A +
Wisner et al. (2001) + − + + + + +
Wisner et al. (2004) + + + + + + +
Wolman et al. (1993) − + − + +
Zayas et al. (2004) − + − N/A − + − + + −
Zlotnick et al. (2011) + + + − + + + + + −
Zlotnick et al. (2001) − + + − − − − − − −
Zlotnick et al. (2006) − + + − + + − + + −
Note . ITT = report intent-to-treat analyses, Char Sample = specify characteristics of sample, Excl Curr MDE = assess for depressive episode pre-treatment and exclude subjects who meet diagnostic criteria,
Blind Assess = clinician-administered diagnostic measures conducted by independent evaluator blind to treatment condition, Spec Random = specification of method of randomization, Spec Ther = specify
therapist characteristics, Manual = specify use of therapy manual, Training = describe therapist training, Super = describe therapist supervision, Adher = indicate therapy was assessed for adherence to
manual, Blind Clin = clinician blind to treatment status, Blind Pt = patient blind to treatment status, + = Yes, − = No, N/A = Not Applicable, QR = Quasi-Randomized.
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 29Table 3
Random weighted effect sizes (Hedges' g) comparing depressive symptoms between treatment and control conditions by 6 months postpartum.
Study n Hedges' g 95% CI SAMD
Armstrong et al. (1999) 1810.44** 0.14–0.73 1.97
Chabrol et al. (2002) 211042** 0.15–0.70 2.05
Dennis, Hodnett et al. (2009) 600 0.13 −0.03–0.29 −0.17
Gao et al. (2012) 1940.34* 0.06–0.62 1.39
Gorman (1997) 30 0.02 −0.68–0.72 −0.33
Gunn et al. (1998) 475 0.02 −0.16–0.20 −1.38
Hayes et al. (2001) 188 0.1 −0.18–0.39 −0.27
Ho et al. (2009) 168 0.39’ 0.09–0.70 1.61
Lawrie et al. (1998) 168 −0.12 −0.42–0.19 −1.67
Le et al. (2011) 174 −0.09 −0.38–0.21 −1.52
Llorente et al. (2003) 89 −0.15 −0.56–0.26 −1.38
Logsdon et al. (2003) 109 −0.2 −0.65–0.25 −1.76
Marks et al. (2003) 85 0 −0.42–0.42 −0.65
Mokhber et al. (2011) 85 0.39 −0.03–0.82 1.15
Muñoz et al. (2007) 41 0.24 −0.36–0.84 0.30
Ngai et al. (2009) 1840.42** 0.13–0.71 1.89
Rees (1995) 600.61* 0.10–1.12 1.78
Shields and Reid (1997) 7880.18** 0.04–0.32 0.60
Small et al. (2000)a 917 −0.08 −0.21–0.05 −3.55
Wolman et al. (1993)a 14912.10*** 10.69–13.51 70.69
Zayas et al. (2004) 57 0.07 −0.44–0.59 −0.25
Zlotnick et al. (2011) 35 0.32 −0.21–0.85 0.86
Zlotnick et al. (2001) 86 0.44 −0.22–1.10 −0.22
Zlotnick et al. (2006) 54 0.09 −0.33–0.51 0.64
k Hedges' g 95% CI Q(df) I2
Total (all studies) 240.37*** 0.15–0.60321.40(23)*** 92.84
Total (outliers excluded) 220.18*** 0.09–0.2733.32(21)* 36.98
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 30*p < 0.05.
**p < 0.01.
***p < 0.001.
aOutlier excluded from subsequent analyses.
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 31Table 4
Analyses of moderation for depressive symptoms by 6 months postpartum.
Moderator N Hedges’
g95% CI Q(df) p
Intervention type 2.73(4) 0.60
Dietary supplement 2 0.12 −0.42–0.65
Educational 2 0.24 −0.04–0.53
Modified care 4 0.16 −0.01–0.33
Therapy 110.27*** 0.14–0.40
Social support 2 0.04 −0.25–0.33
Intervention type 1.06(1) 0.30
Biological 3 0.02 −0.30–0.35
Psychosocial 190.20*** 0.11–0.29
Intervention type 1.56(1) 0.21
EST 100.25*** 0.12–0.38
Non-EST 120.14* 0.03–0.25
Control group type 4.89(2) 0.09
Educational 20.38*** 0.18–0.58
Placebo 3 0.02 −0.30–0.35
TAU 160.16*** 0.07–0.25
Intervention timing 0.06(1) 0.81
Pregnancy 140.18*** 0.09–0.26
Postpartum 80.20* 0.03–0.36
Type of prevention 2.17(3) 0.54
Indicated 30.22* 0.01–0.44
Selected 4 0.18 −0.10–0.47
Selected/indicated 5 0.03 −0.11–0.23
Universal 100.19** 0.07–0.32
Measure 4.34(2) 0.11
BDI-II 5 0.00 −0.19–0.18
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 32Moderator N Hedges’
g95% CI Q(df) p
CES-D 2 0.20 −0.60–.99
EPDS 130.23*** 0.12–0.34
Exclude current MDE 0.32(1) 0.58
No 150.19*** 0.08–0.29
Yes 7 0.13 −0.02–0.29
Psychotherapy orientation 0.06(1) 0.80
CBT 5 0.23 0.00–0.46
IPT 50.27** 0.07–0.47
Method of psychotherapy 0.39(1) 0.53
administration
Group 60.23* 0.04–0.41
Individual 40.31** 0.11–0.52
*p < 0.05.
**p <0.01.
***p < 0.001.
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 33Table 5
Random weighted effect sizes (odds ratio) comparing prevalence of depressive episodes between treatment and control conditions by 6 months
postpartum.
Study n OR 95% CI SAMD
Armstrong et al. (1999) 1810.24** 0.09–0.65 −3.30
Austin et al. (2008) 277 0.94 0.50–1.76 1.79
Brugha et al. (2000) 190 0.49 0.12–2.02 −1.54
Chabrol et al. (2002) 2110.46** 0.26–0.81 −1.95
Dennis, Hodnett et al. (2009) 600 0.80 0.49–1.31 1.00
Elliott et al. (2000) 990.38* 0.15–0.94 −1.73
Gorman (1997) 37 0.57 0.11–3.03 −0.43
Gunn et al. (1998) 475 1.26 0.76–2.09 5.63
Hagan et al. (2004) 192 1.02 0.47–2.23 2.04
Kozinszky et al. (2012)a 1719 1.79 1.30–2.48 18.00
Lara et al. (2010) 116 0.36 0.13–1.01 −1.95
Lawrie et al. (1998) 168 1.13 0.59–2.18 2.60
Le et al. (2011) 174 1.38 0.52–3.67 4.18
Marks et al. (2003) 87 1.05 0.41–2.73 1.51
Milgrom et al. (2011) 890.24** 0.08–0.69 −2.31
Muñoz et al. (2007) 41 0.17 0.01–3.82 −1.68
Nalepka and Coblentz (1995) 72 0.94 0.18–4.98 0.88
Shields and Reid (1997) 7880.66* 0.47–0.94 −0.70
Silverstein et al. (2011) 42 0.40 0.11–1.51 −1.01
Small et al. (2000)a 917 1.26 0.88–1.80 7.39
Stamp et al. (1995) 121 1.62 0.54–4.89 4.79
Webster et al. (2003) 369 0.80 0.50–1.28 0.81
Wisner et al. (2001) 51 0.95 0.26–3.45 0.77
Wisner et al. (2004) 220.08* 0.01–0.90 −1.44
Wolman et al. (1993) 1490.02** 0.00–0.40 −4.17
Zlotnick et al. (2011) 35 1.68 0.36–7.86 2.68
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 34Study n OR 95% CI SAMD
Zlotnick et al. (2001) 86 0.06 0.00–1.08 −3.00
Zlotnick et al. (2006) 540.17* 0.03–0.88 −2.01
kOR 95% CI Q(df) I2
Total (all studies) 280.72* 0.56–0.9474.83(27)*** 63.92
Total (outliers excluded) 260.67** 0.52–0.8545.95(25)** 45.60
Total (trim-and-fill correction)0.73* 0.56–0.95 61.93
*p < 0.05.
**p < 0.01.
***p < 0.001.
aOutlier excluded from subsequent analyses.
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 35Table 6
Analyses of moderation for depressive episodes by 6 months postpartum.
Moderator nOR 95% CI Q(df) p
Intervention type 1.13(3) 0.77
Medication 2 0.34 0.03–3.85
Modified care 5 0.61 0.31–1.19
Therapy 130.57** 0.38–0.84
Social support 4 0.77 0.46–1.31
Intervention type 0.02(1) 0.88
Biological 3 0.71 0.24–2.12
Psychosocial 230.61** 0.50–0.84
Intervention type 0.82(1) 0.37
EST 140.58** 0.39–0.87
Non-EST 120.73* 0.54–1.00
Control group type 1.13(2) 0.57
Educational 4 0.82 0.53–1.25
Placebo 3 0.71 0.24–2.12
TAU 190.62** 0.46–0.83
Intervention timing 0.03(1) 0.87
Pregnancy 16 0.70 0.47–1.05
Postpartum 90.67** 0.50–0.90
Type of prevention 1.05(3) 0.79
Indicated 2 0.62 0.36–1.07
Selected 100.60* 0.38–0.97
Selected/indicated 90.60* 0.36–0.99
Universal 5 0.84 0.48–1.46
Criterion for diagnosis 0.03(1) 0.87
Clinical 120.64* 0.42–0.99
Cutoff 140.67* 0.50–0.92
Exclude current MDE 0.27(1) 0.60
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.

NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSockol et al. Page 36Moderator nOR 95% CI Q(df) p
No 170.68** 0.53–0.89
Yes 9 0.56 0.29–1.10
Psychotherapy orientation 0.41(1) 0.52
CBT 80.63* 0.41–0.97
IPT 4 0.40 0.11–1.51
Method of psychotherapy administration 0.71(1) 0.40
Group 8 0.62 0.36–1.07
Individual 50.46** 0.29–0.73
*p < 0.05
**p <0.01.
Clin Psychol Rev . Author manuscript; available in PMC 2014 July 21.