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Perinatal Nutrition Interventions and Post-

Partum Depressive Symptoms

Article in Journal of Affective Disorders December 2016

DOI: 10.1016/j.jad.2016.12.014


0 136

4 authors, including:

Jacqueline F Gould Maria Makrides

South Australian Health and Medical Researc South Australian Health and Medical Researc


Karen Best
South Australian Health and Medical Researc


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Journal of Affective Disorders 224 (2017) 29

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Journal of Aective Disorders

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Perinatal nutrition interventions and post-partum depressive symptoms MARK

a,b a,c a,c,
Jacqueline F. Gould , Karen Best , Maria Makrides
Child Nutrition Research Centre, South Australian Health and Medical Research Institute, Adelaide, Australia
School of Psychology, University of Adelaide, Adelaide, Australia
Discipline of Paediatrics, University of Adelaide, Adelaide, Australia


Keywords: Background: Postpartum depression (PPD) is the most prevalent mood disorder associated with childbirth. No
Depression single cause of PPD has been identied, however the increased risk of nutritional deciencies incurred through
Nutrition the high nutritional requirements of pregnancy may play a role in the pathology of depressive symptoms. Three
Postpartum nutritional interventions have drawn particular interest as possible non-invasive and cost-eective prevention
and/or treatment strategies for PPD; omega-3 (n-3) long chain polyunsaturated fatty acids (LCPUFA), vitamin
D and overall diet.
Methods: We searched for meta-analyses of randomised controlled trials (RCT's) of nutritional interventions
during the perinatal period with PPD as an outcome, and checked for any trials published subsequently to the
Results: Fish oil: Eleven RCT's of prenatal sh oil supplementation RCT's show null and positive eects on PPD
symptoms. Vitamin D: no relevant RCT's were identied, however seven observational studies of maternal
vitamin D levels with PPD outcomes showed inconsistent associations. Diet: Two Australian RCT's with dietary
advice interventions in pregnancy had a positive and null result on PPD.
Limitations: With the exception of sh oil, few RCT's with nutritional interventions during pregnancy assess
Conclusions: Further research is needed to determine whether nutritional intervention strategies during
pregnancy can protect against symptoms of PPD. Given the prevalence of PPD and ease of administering PPD
measures, we recommend future prenatal nutritional RCT's include PPD as an outcome.

1. Introduction eect of PPD on child development outcomes (Conroy et al., 2012;

Field, 2010; Goodman et al., 2011; Zhu et al., 2014). A number of
Postpartum depression (PPD)1 is the most prevalent mood disorder caregiving activities are considered to be adversely impacted by PPD,
associated with childbirth. Clinically it is not dierent to depression at including infant feeding practices, sleep routines and routine infant
other times and symptoms include mood disturbances (such as and child health visits (Field, 2010), as well as disturbances to the
sadness, loss of pleasure, guilt or worthlessness), sleep disturbances mother-infant interaction such as less sensitivity or responsiveness to
(not related to the baby), appetite disturbances or weight loss, and infants (Field, 2010). A meta-analysis of 193 studies found that
suicidal ideation. Systematic reviews report that 19.2% of women maternal depression at any time is associated with increased ospring
experience depression within 12 weeks of birth (Gaynes et al., 2005) internalising and externalising behaviours and psychopathology
and 1020% of women experience PPD within the rst year, regardless (Goodman et al., 2011). International experts acknowledge that
of race, parity, age, education and socioeconomic status (Gavin et al., maternal depression has long-term adverse eects on child develop-
2005), with symptoms persisting beyond the rst year in 8% of eected ment (England and Sim, 2009). Public health preventive strategies to
mothers (Dennis et al., 2012). lower the prevalence of PPD would have wide ranging benets for
Minimising PPD is particularly important due to the implications mothers, children and families.
for the mother and child. Depression impairs social and psychological PPD is thought to be multifactorial, rather than due to a single
functioning and there is a body of evidence to suggest a deleterious causative factor (Beck, 2001; Bobo and Yawn, 2014), making preven-

Corresponding author at: Child Nutrition Research Centre, South Australian Health and Medical Research Institute, 72 King William Road, North Adelaide, SA 5006, Australia.
E-mail address: (M. Makrides).
125(OH)D: vitamin D, DHA: docosahexaenoic acid, EPDS: Edinburgh Postpartum Depression Scale, LCPUFA: long-chain polyunsaturated fatty acid, n-3: omega-3, PPD:
postpartum depression, RCT: randomised controlled trial.
Received 1 July 2016; Accepted 17 December 2016
Available online 18 December 2016
0165-0327/ 2016 Elsevier B.V. All rights reserved.
J.F. Gould et al. Journal of Affective Disorders 224 (2017) 29

tion problematic. However, nutrition is considered one of the likely 2008; Rees et al., 2008; Su et al., 2003), current PPD(Freeman et al.,
contributing factors and is modiable. Pregnancy and lactation are a 2006), at risk of PPD(Kaviani et al., 2014; Mozurkewich and Klemens,
time of particular stress on a woman's nutrient reserves, and nutrient 2012) or apparently healthy women (Doornbos et al., 2009; Krauss-
decits incurred may increase the likelihood of depression in the Etschmann et al., 2007; Llorente et al., 2003; Makrides and Gibson,
postpartum period. Nutritional interventions during the perinatal 2000; Mattes et al., 2009). Nine of these trials did not nd a signicant
period may oer a simple and cost eective strategy to prevent benet of n-3 LCPUFA supplementation administered either antena-
nutritional deciencies and hence reduce the prevalence of PPD. tally, postpartum or a combination of both periods. Two small trials
Three nutritional strategies that have drawn particular interest for including depressed women reported a signicant reduction in depres-
depressive symptoms are n-3 LCPUFA, vitamin D and overall diet. sion symptoms in the n-3 LCPUFA group (Kaviani et al., 2014; Su
This review evaluates possible nutritional interventions that may be et al., 2003). The majority of these trials conducted have been of low-
implemented as public health strategies for eective prevention of PPD to-moderate quality, mainly due to small sample size ( < 100) and
symptoms by summarising meta-analyses of randomised controlled failure to adhere to Consolidated Standards of Reporting Trials guide-
trials (RCT's), as the highest level of evidence, of omega-3 (n-3) long- lines (Jans et al., 2010). Perhaps the strongest evidence available
chain polyunsaturated fatty acids (LCPUFA), vitamin D and overall diet comes from the largest trial to date to investigate n-3 LCPUFA as a
interventions during pregnancy and/or lactation with PPD outcomes. preventative strategy. This double blind RCT included 2399 women
We also searched for any relevant RCT's with PPD that have been supplemented with DHA-rich sh oil or placebo from 20 weeks
published following the included reviews. gestation until delivery (Makrides and Gibson, 2000)Results demon-
strated that there was no statistically signicant benet of DHA
1.1. Omega-3 LCPUFA supplementation during pregnancy in preventing depressive symptoms
in the rst six months postpartum (Makrides and Gibson, 2000).
There has been considerable interest in the role n3 LCPUFA in As systematic reviews are generally considered to provide the best
mental health in the general population, however little is known about evidence to answer a research question we searched the databases and
their eects on maternal mental health. Pregnancy and the postpartum identied nine reviews of the literature examining the eect of n-3
period is a time when n-3 LCPUFA supply is particularly signicant. LCPUFA supplementation in the perinatal period on PPD. Six reviews
The metabolic demand for n-3 LCPUFA, in particular docosahexaenoic were narrative and three reviews combined studies with heterogeneous
acid (DHA) is increased as maternal tissue stores are used for the inclusion criteria, timing and duration of intervention in meta-analyses
developing fetus (Makrides and Gibson, 2000). Metabolic and post- (Table 2). One review including meta-analysis of 620 depressed or non-
mortem studies indicate that the fetus accumulates an average of depressed women with at least 4 weeks of n-3 LCPUFA supplementa-
67 mg of docosahexaenoic acid (DHA) per day during the last trimester tion (during pregnancy, the postpartum period or both) showed no
of pregnancy (Innis, 2003). Modern western diets are low in n-3 signicant eects of n-3 LCPUFA compared to placebo. A recent
LCPUFA and this level of DHA exceeds the intake of many pregnant Cochrane review examining the eect of dietary supplements for the
women highlighting a potential dietary insuciency. During the prevention of postpartum depression (Miller et al., 2013) included one
postpartum period there is further risk of DHA deciency as depletion trial that compared n-3 LCPUFA's DHA and eicosapentaenoic acid to
of maternal serum DHA declines following delivery (Otto et al., 2001). placebo in women at high risk of PPD. This trial including 126 women
Alterations in fatty acid metabolism and the composition of found no eect of either DHA or eicosapentaenoic acid on the
phospholipids in serum and membranes have been implicated in the prevention of PPD in at risk women. The only other review with
pathophysiology of depression in the general population. Observational meta-analysis included pregnant women as a subgroup of their report
studies in the general population have shown that levels of DHA in on the eects of n-3 fatty acids on depressive disorders (Grosso et al.,
serum and cell membranes are lower in people who suer from 2014). The authors reported inconclusive results from RCTs including
depression compared to healthy controls (Edwards et al., 1998). women with a major depressive disorder (Freeman et al., 2006; Rees
Studies during the perinatal period also suggest an association between et al., 2008; Su et al., 2003) and RCTs including apparently healthy
decreased maternal n-3 LCPUFA intake during pregnancy (Gow and women (Doornbos et al., 2009; Llorente et al., 2003; Mozurkewich
Hibbeln, 2014) (or low or DHA status following delivery) and the et al., 2013) (primary prevention). Not all reviews were systematic or
occurrence of postpartum depression (De Vriese et al., 2003; Golding comprehensive of the relevant studies (as illustrated in Table 2) and the
et al., 2009). Epidemiological studies observing the association of inclusion of small scale studies with high risk of bias combined with the
higher intakes of n-3 LPCUFA during pregnancy have appeared heterogeneity of available RCTs of perinatal n-3 LCPUFA supplemen-
promising and suggest a reduction of depressive symptoms in the tation prevents consistent conclusions.
postnatal period (Hibbeln, 1998; Oken and Belfort, 2010), however There is considerable biological plausibility to support a role of n-3
these studies are unable to establish causality because of the diculty LCPUFA in PPD and some evidence for observational studies however
in adjusting for complex confounding factors (Lawlor et al., 2004). the current evidence from RCTs is inconclusive. RCTs reporting the
Emerging evidence from randomised trials indicates that DHA eects of perinatal n-3 LCPUFAs on PPD has increased in recent years
interventions in patients with major depression improve depressive though remains dicult to summarise because of small sample size,
symptoms compared with control (Marangell et al., 2003; Stoll et al., low-to-moderate quality, and considerable heterogeneity between
1999; Su et al., 2003). A recent systematic review and meta-analysis studies. Overall, the evidence shows that supplementation with marine
including 35 randomised controlled trials (RCTs) concluded that the oil or n-3 LCPUFA is safe in the perinatal period and is generally well
evidence available provides some support of a benet of n-3 PUFAs in tolerated. However, more work is needed to understand the optimal
individuals with depressive illness but no evidence of any benet in maternal n-3 LCPUFA status for the prevention and/or treatment of
individuals without a diagnosis of depressive illness (Appleton et al., PPD. Questions remain in regard to optimal dose (amount and type of
2010). n-3 LCPUFA i.e. DHA vs eicosapentaenoic acid) and timing of
Supplementation of pregnant women with n-3 LCPUFA has been supplementation as well as which sub-populations may benet most.
proposed as a potential strategy to prevent and/or treat PPD. The eect Currently, there is not enough evidence to support the routine use of
of perinatal n-3 LCPUFA supplementation on PPD has been studied in marine oil, or other prostaglandin precursor, supplements in the
11 RCTs (Table 1). Supplementation of women has occurred either perinatal period to reduce the risk of PPD.
during pregnancy (antenatally), postpartum or a combination of both
time periods. Participant inclusion criteria varies greatly with trials
including women with major depressive disorder (Freeman et al.,

J.F. Gould et al. Journal of Affective Disorders 224 (2017) 29

Table 1
Characteristics of individual omega-3 long-chain polyunsaturated fatty acids randomised controlled trials and postpartum depression (PPD).

Author/ref Study location Participants/Inclusion Intervention PPD measure Result


Kaviani et al., 2014 Iran 80 primiparous women with n-3 fatty acid 1000 mg (type not reported) vs placebo BDI Positive
mild depression > 20w for 6 weeks

Mozurkewich et al., USA 126 women with EPDS > 9 or DHA 274 mg+EPA 1060 mg vs. DHA 900 mg+ BDI, MINI Null
2013 history of depression EPA 180 mg vs. placebo

Makrides et al., 2010 Australia 2399 Apparently healthy women DHA 800 mg+EPA 100 mg vs. placebo EPDS Null
< 20w gestation to delivery

Doornbos et al., 2009 The Netherlands 119 Apparently healthy women DHA 220 mg OR DHA 220 mg+AA 220 mg vs. placebo EPDS & Blues Null
16w gestation to 3 m postpartum questionnaire

Mattes et al., 2009 Australia 83 Apparently healthy women Fish oil 4000 mg (56% DHA, 27.7% EPA) vs. placebo BDI Null
20w gestation to delivery

Rees et al., 2008 Australia 26 women with MDD Fish oil 6000 mg (27.3% DHA, 6.9% EPA) vs. placebo EPDS, HSM-F, Null
Between third trimester and 6 m postpartum for 6 MADRAS
Su et al., 2008 Taiwan 33 women with MDD DHA 1200 mg+EPA 2200 mg vs. placebo EPDS, HAM-D, BDI Positive

Freeman et al., 2008 USA 59 women with perinatal MDD DHA 800 mg+EPA 1100 mg+psychotherapy vs. EPDS & HAM-D Null
Between 12w-32w gestation for 8 weeks

Krauss-Etschmann Germany Hungary 170 Apparently healthy women DHA 500 mg+EPA 150 mg vs. DHA 500 mg+EPA EPDS Null
et al., 2007 Spain 150 mg vs.+400 mg MTHF vs. 400 mg MTHF vs.
22w gestation until Delivery

Freeman et al., 2006 USA 16 women with PPD n-3 LCPUFA 500 mg vs. 1050 mg vs. 1400 mg vs. EPDS & HRDS Null
2800 mg (EPA: DHA 1.5 :1)
214w postpartum

Llorente et al., 2003 USA 138 Apparently healthy women DHA 200 mg vs. placebo EPDS, BDI SCID Null
Delivery to 3 m postpartum

DHA, docosahexaenoic acid; AA, arachidonic acid; MDD, major depressive disorder; EPDS, Edinburgh Postpartum Depression Scale; BDI, Beck Depression Inventory; w, weeks; HAM-
D, Hamilton Rating Scale for Depression; MINI, Mini-International Neuropsychiatric Interview; MTHF, methyltetrahydrofolic

1.2. Vitamin D number of vitamin D interventions during pregnancy (a total of 65

RCT's (42 published and a further 23 unpublished or underway on
Vitamin D (25(OH)D) acts as a neurosteroid hormone. It has identied in a recent Cochrane review (De-Regil
receptors throughout the brain and is involved in a number of et al., 2016)), we were not able to nd any RCT's that have intervened
neurologic process that support the hypothesis that vitamin D is with vitamin D during pregnancy or lactation and assessed PPD
involved in the pathology of mood disorders. Despite the interest in symptoms.
the role of vitamin D in the pathogenesis of depression, and the Instead, we found seven observational studies (see Table 3) that

Table 2
Reviews of the various omega-3 long-chain polyunsaturated fatty acids randomised controlled trials and postpartum depression (PPD).

Saccone and Szajewska et al., Miller (Horvath Larqu et al., Wojcicki and Jans et al., Ramakrishnan et al., BorjaHart and
Berghella, 2015 2006 et al., 2007) 2012 Heyman, 2011 2010 2010 Marino, 2010

2015 2014 2013 2012 2011 2010 2010 2010

AN AN+PP AN AN+PP or AN+PP or AN or AN+PP or AN AN+PP or AN or
Kaviani et al., 2014
Mozurkewich et al.,
Makrides et al., 2010
Doornbos et al., 2009
Mattes et al., 2009
Rees et al., 2008
Su et al., 2008
Freeman et al., 2008
Freeman et al., 2006
Llorente et al., 2003
et al., 2007

AN, Antenatal; PP, Postpartum

J.F. Gould et al. Journal of Affective Disorders 224 (2017) 29

Table 3
Observational studies of vitamin D level during pregnancy and postpartum depression (PPD).

Author, year Setting, sample Vitamin D measure and PPD measure and denition Result

Murphy et al., 2010 Sample: Serum 25(OH)D measured EPDS (English and Spanish versions) measured N=97
monthly from 46 weeks PP to 7 mo PP monthly from 46 weeks PP to 7 mo PP Low PP serum 25(OH)D
U.S.: Women taking 800, 2400 or 6400 IU Sample analysis: Radioimmunoassay Depression=EPDS > 9 increased risk of PPD during
vitamin D/day, excluded births < 35 weeks Sucient: 33 ng/mL the rst 7 month PP
gestation, pre-existing diabetes or a multiple Insucient: 21-32 ng/mL
birth Decient: 20 ng/mL
Nielsen et al., 2013 Sample: Serum 25(OH)D mid- Danish Register of Medicinal Product Statistics N=1480
pregnancy (25 weeks gestation)
Denmark: Singleton pregnancy with live-born Sample analysis: Liquid Depression=prescription for any anti-depressant Null association
infant, excluded women with previous chromatography-tandem mass medication within 1 yr of delivery
registered mental illness or anti-depressant spectroscopy
N=605 with PPD
N=875 without PPD
Robinson et al., 2014 Sample: Serum 25(OH)D early- EPDS (English version-6 questions only) at 3 N=706
pregnancy (18 weeks gestation) days PP
Australia: Caucasian women Sample analysis: Liquid Depression=EPDS > 6 Low serum 25(OH)D
chromatography-tandem mass increased risk of PPD at 3 days
N=2900 Quartile 1: < 47 nmol/L
Quartile 2: 4758 nmol/L
Quartile 3: 5970 nmol/L
Quartile 4: > 70 nmol/L
Fu et al., 2014 Sample: Serum 25(OH)D 2448 h after EPDS (Chinese version) at 3 mo PP N=213
China: full-term, singleton, excluded if Sample analysis: E601 modular analyser Depression=EPDS 12 Low serum 25(OH)D
psychiatric care during pregnancy Sucient: > 30 ng/mL increased risk of PPD at 3 mo
N=248 Insufficient: 2030 ng/mL
Decient: < 20 ng/mL
Gur et al., 2014 Sample: Serum 25(OH)D mid- EPDS (Turkish version) at 1 week, 6 weeks and 6 N=179
pregnancy (2428 weeks gestation) mo PP
Turkey: Normal pregnancy and delivery, with Sample analysis: NR Depression=EPDS 12 Low serum 25(OH)D
low risk of PPD Sucient: > 50 nmol/L (20 g/mL) increased risk of PPD at 1 and
N=208 Insufficient: 26-50 nmol/L (10 6 weeks and 6 mo
20 ng/mL)
Decient: 25 nmol/L (10 ng/mL)
Huang et al., 2014 Sample: Serum 25(OH)D early- DASS and PHQ-9, time point NR N=498
pregnancy (mean 15.4 weeks gestation)
U.S.: Part of pregnancy migraine study Sample analysis: Liquid Depression=DASS 14=PHQ-919 Null association
chromatography-tandem mass
N=500 Sufficient: 33 ng/mL
Insucient: 21-32 ng/mL
Decient: 20 ng/mL
Gould et al., 2015 Sample: Cord blood 25(OH)D at birth EPDS (English version) at 6 weeks and 6 mo PP N=1040
Australia: singletons, healthy women with or Sample analysis: Liquid Depression=EPDS > 12 Null association at 6 weeks
without history of depression chromatography-tandem mass and 6 mo
N=2,399 Sufficient: > 50 nmol/L
Insucient: 2550 nmol/L
Decient: < 25 nmol/L

25(OH)D: 25-hydroxyvitamin D (vitamin D)

CES-D: Centre for Epidemiological Studies Depression scale
DASS: Depression, Anxiety and Stress Scale
EPDS: Edinburgh Postnatal Depression Scale
NR: not reported
PHQ-9: Patient Health Questionnaire Depression Module
PP: Post-partum
PPD: postpartum depression

examined the association between 25(OH)D status and PPD; two symptoms simultaneously measured monthly after birth from four-
cohort studies which reported associations between PPD and low six weeks to seven months postpartum (Murphy et al., 2010). The two
maternal serum vitamin D in mid-pregnancy (Gur et al., 2014; largest studies reported no association between PPD symptoms and
Robinson et al., 2014), one cohort study which reported no association cord serum vitamin D at birth (Gould et al., 2015) or when cases of
between PPD symptoms and low maternal serum vitamin D in early- PPD were compared to women without PPD (Nielsen et al., 2013).
pregnancy (Huang et al., 2014), one cohort study which reported an However, limitations and methodological dierences (including varia-
association between PPD symptoms and maternal serum shortly after tions in cut-os for 25(OH)D suciency, sample size, control of
birth (Fu et al., 2014) and one vitamin D intervention trial that found confounders, analysis of vitamin D status, assessment of PPD, and
an association between low maternal serum vitamin D and PPD timing of PPD assessment), complicate comparison between studies.

J.F. Gould et al. Journal of Affective Disorders 224 (2017) 29

Both (Gur et al., 2014) and (Robinson et al., 2014) applied the One of the RCT's involved only women at risk of developing gestational
Edinburgh Postpartum Depression Scale (EPDS) within one week of diabetes and was designed to reduce perinatal complications (Crowther
birth, although it is not recommended for use within 14 days of delivery et al., 2005). Whilst the authors found that the intervention success-
(Cox et al., 1987), and Robinson et al. shortened the EPDS to just six fully reduced the risk of perinatal complications including PPD
items (Robinson et al., 2014). Nielsen et al. reported prescription for symptoms, whether or not women successfully improved their diet
antidepressant medication within one year of delivery, rather than was not reported (Crowther et al., 2005). The other RCT was conducted
measuring symptoms of PPD (Nielsen et al., 2013). in overweight women with the aim of reducing gestational weight gain
These inconsistent ndings are in accordance with the rst to improve maternal and infant outcomes (Dodd et al., 2016). In
systematic review and meta-analyses of observational studies pairing contrast to Crowther et. al., the authors reported that although
vitamin D status with any depressive symptoms at any time (Anglin intervention group women improved their diet, there was no dierence
et al., 2013). Anglin et al. identied one case-control, three cohort and in PPD symptoms between the groups (Dodd et al., 2016). Despite
10 cross-sectional studies, all of which had dierent results and similarities between these RCT's, including being conducted in
methodologies (Anglin et al., 2013). Interestingly none of the observa- Australia, using the EPDS and having large sample sizes (n > 1000),
tional studies investigating PPD were included in the review. Two other neither trial was designed with PPD as a primary outcome and the
relevant cohort studies not included in the review by Anglin et al. results were inconsistent.
linked antenatal 25(OH)D status to antenatal depressive symptoms A recent review of nutrition and perinatal depression identied
(Brandenbarg et al., 2012; Cassidy-Bushrow et al., 2012). three cohort studies of dietary patterns during pregnancy with incon-
A more recent review of the evidence of vitamin D supplementation sistent associations with PPD (Sparling et al., 2016). The largest
for a number of health outcomes reported that eight RCT's in general observational study (n=7814: the British Avon Longitudinal Study of
populations showed no meaningful change in depression even when Parents and Children) found no association between antenatal diet and
25(OH)D) levels were low (Allan et al., 2016). The subgroup analysis of symptoms of PPD (Pina-Camacho et al., 2015). Similarly, in a cohort of
three RCT's with depressed patients was inconclusive and the authors Japanese women, a high-glycaemic index diet (Murakami et al., 2008),
concluded that there was insucient evidence for the prevention or and Western, healthy, or Japanese dietary patterns (Okubo et al., 2011)
reduction of depressive symptoms with vitamin D supplementation were not associated with PPD. In contrast, a cohort study in Greece
(Allan et al., 2016). We found four additional meta-analyses of vitamin linked a healthy antenatal diet (high intake of fruits, vegetables,
D interventions for the prevention or treatment of depression at any seafood, nuts) to a reduced risk of PPD symptoms whilst a high intake
time, the largest and most recent of which included nine RCT's in of sugar and sugar products was associated with higher EPDS scores
n=4923 depressed patients (Gowda et al., 2015). No review identied a (Chatzi et al., 2011). Antenatal RCT's of dietary and lifestyle interven-
clear benet of vitamin D supplementation for the prevention or tions have similarly had inconsistent eects on symptoms of depression
treatment of depressive symptoms (Gowda et al., 2015; Li et al., measured with the EPDS during pregnancy (Bogaerts et al., 2013;
2014; Shaer et al., 2014; Spedding, 2014) and it is noteworthy that Poston et al., 2013).
PPD was not addressed in these reviews. Although biologically plausible, the current evidence does not
To summarise, the current evidence does not support vitamin D conclusively support the use of dietary guidance as a means of
interventions to prevent or treat symptoms of depression, however preventing PPD. Further RCT's that are specically designed to prevent
little research has focused on PPD. Given that measures of PPD, such PPD are needed.
as the EPDS, can be easily administered, we recommend that PPD is
included as an outcome in current incomplete RCT's of prenatal 2. Discussion
vitamin D and future trials.
Whilst causes of depressive symptoms are considered multifactorial
1.3. Diet (Beck, 2001; Bobo and Yawn, 2014), nutrition (and nutritional
deciencies) have been hypothesised to play a role in the pathology
Nutrients do not work alone, and are rarely consumed in isolation of depression. We reviewed the evidence for the prevention of PPD
so that individual's decient in one nutrient are likely have suboptimal symptoms by nutritional interventions during pregnancy. The current
levels of other nutrients. Numerous nutrients, in sucient quantities, evidence does not support the use of sh oil, vitamin D or dietary
are needed to maintain many processes for normal brain functioning, interventions during pregnancy for the prevention of PPD symptoms,
such as enzymatic activities, signal transmission, cellular processes and however due to the quality of the evidence, the possibility of a
maintenance, and the synthesis and functioning of neurotransmitters. nutritional intervention preventing PPD cannot be ruled out.
Individuals with depression often have low levels of nutrients such Our results are in accordance with an earlier Cochrane review of
as folate, iron, zinc and vitamin B12 (Bodnar and Wisner, 2005). nutritional RCT's during the antenatal or post-natal period, or both for
However, it is unclear whether these deciencies are the result of the prevention symptoms of depression in the antenatal or postpartum
depressive symptoms or a cause of them. Pregnancy and lactation are period, or both (Miller et al., 2013). The authors only identied two
major nutritional stressors for a woman's body due to the high relevant trials, one of sh oil and one of selenium, and concluded that
requirements of the fetus or infant as well as the woman's increased there was insucient evidence to recommend dietary supplements for
needs. Ensuring a healthy, nutritious diet during pregnancy and prevention of depressive symptoms (Miller et al., 2013).
lactation may prevent nutrient deciencies, and will likely infer a wide We attempted to focus our review on RCT's and systematic reviews
range of benets to the health of the mother and infant by ensuring all to provide a comprehensive overview of the evidence. A major
nutritional requirements are met. This may lower the risk of PPD, both limitation we found was the scarcity of adequate of perinatal nutri-
by ensuring optimal nutrition for neurologic functioning but also tional RCT's that measure PPD. Surprisingly, we found that only sh oil
through minimising other adverse health outcomes that may increase interventions had received reasonable attention in relation to PPD with
the risk of PPD. Additionally, healthy perinatal eating habits may be nine reviews of 11 RCT's. A recent Cochrane review identied 42
continued to confer ongoing benet to the mother and infant. published antenatal vitamin D RCT's (De-Regil et al., 2016), none of
None of the identied PPD reviews reported the eects of dietary which assessed PPD despite widespread beliefs that vitamin D is
interventions on PPD, however we found two RCT's with dietary advice involved in the pathogenesis of mood disorders. Further, although we
interventions and assessment of PPD symptoms (Crowther et al., 2005; found several reviews of RCT's and observational studies of vitamin D
Dodd et al., 2016). Both trials randomised pregnant women to receive and depression, PPD was not addressed in any and seven observational
individualised dietary advice compared or standard care (see Table 4). studies of vitamin D and PPD identied by us were absent from all

J.F. Gould et al. Journal of Affective Disorders 224 (2017) 29

Table 4
Randomised controlled trials of perinatal dietary counselling and multivitamin interventions with postpartum depression (PPD) outcomes.

Author, year Setting, sample Randomisation and Intervention PPD measure and Result

Crowther et al., 2005 Randomisation method: computer generated Measure: EPDS at 3 mo N=573
Australia: Singleton or twin pregnancy 1630 weeks Intervention group: individualised dietary advice PPD=EPDS > 12 Fewer intervention group women with
gestation, 1 risk factor for gestational diabetes and blood glucose monitoring PPD (8% vs. 17%, p=0.001)
Excluded: gestational diabetes or previously treated Control group: standard care
gestational diabetes
Dodd 2016(Dodd et al., 2016) Randomisation method: computer generated Measure: EPDS at 4 mo N=1221
Australia: Singleton pregnancy 1620 weeks Intervention group: individualised lifestyle and PPD=EPDS > 12 Null effect on PPD (7.9% vs. 6.6%,
gestation, maternal BMI25 kg/m2, dietary advice p=0.95)
N=2212 Control group: standard care

BMI: Body mass index

EPDS: Edinburgh Postnatal Depression Scale
PP: Post-partum
PPD: postpartum depression

reviews (Anglin et al., 2013; Gowda et al., 2015; Li et al., 2014; Shaer nutrition for the prevention of PPD symptoms. However, the potential
et al., 2014; Spedding, 2014). Only two RCT's with prenatal dietary for appropriate nutrition to minimise PPD warrants further research as
interventions and PPD outcomes were identied, and both included nutritional interventions may be a simple, cost-eective method of
depressive symptoms as a secondary outcome (Crowther et al., 2005; preventing or reducing the symptoms of PPD with likely benets to
Dodd et al., 2016). other aspects of health due to avoided deciencies. Future high quality
There is disparity between the interests in preventing PPD as one of RCT's will be needed to determine whether nutrition is an eective
the most prevalent maternal morbidities stemming from pregnancy, means of minimising PPD.
and in the role of nutrition in pregnancy. PPD symptoms can be quickly
and easily assessed with many freely available measures such as the References
commonly used EPDS (Boyd et al., 2005), yet very few perinatal
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