Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35

Contents lists available at ScienceDirect

Best Practice & Research Clinical

Obstetrics and Gynaecology
journal homepage: www.elsevier.com/locate/bpobgyn

Maternal depression, anxiety and stress during

pregnancy and child outcome; what needs to be
done
Vivette Glover, PhD, Professor *
Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du
Cane Road, London W12 0NN, UK

Keywords:
Care for the emotional state of pregnant women remains a
prenatal neglected aspect of obstetric medicine. Many prospective studies
depression have shown that, if a mother is depressed, anxious, or stressed
anxiety while pregnant, this increases the risk for her child having a wide
stress range of adverse outcomes, including emotional problems, symp-
fetus toms of attention deficit hyperactivity disorder, or impaired
neurodevelopment cognitive development. Although genetics and postnatal care
cortisol
clearly affect these outcomes, evidence for an additional prenatal
causal component is substantial. Prenatal anxiety or depression
may contribute 10–15% of the attributable load for emotional and
behavioural outcomes. The Nurse Family Partnership remains the
only intervention that starts in pregnancy and has been shown to
have long-term benefits for the behaviour of the child. Several
other interventions, however, are likely to be helpful. Depression,
anxiety, and stress during pregnancy are frequently undetected by
health professionals, and untreated. Programmes to help with this
should eventually improve child outcome.
Ó 2013 Elsevier Ltd. All rights reserved.

Introduction

The physical care of pregnant women in the developed world has hugely improved over the past
100 years; however, the same has not been true of their emotional care. This is arguably the most

* Tel.: þ44 207 594 2136.

E-mail address: v.glover@imperial.ac.uk.

1521-6934/$ – see front matter Ó 2013 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.bpobgyn.2013.08.017
26 V. Glover / Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35

neglected aspect of obstetric medicine. It is important for the wellbeing of the pregnant woman herself,
and also for that of her future child. This aspect will be discussed here.
Considerable evidence from many prospective studies show that if the mother is depressed,
anxious, or stressed while she is pregnant her child is more likely to experience a range of adverse
neurodevelopmental outcomes than do the children of other mothers [1–3]. These include an
increased risk of emotional, behavioural and cognitive problems. It is also well-established that pre-
natal stress can cause lower birthweight for gestational age, earlier delivery and pregnancy, induced
hypertension [4], and altered physical outcomes, such as an increased risk of asthma [5].
With physical outcomes, the phenomenon of fetal programming is well established. This is when
the environment in utero during specific critical periods for different outcomes, can affect the
development of the fetus and the child in the long-term. Fetal programming has been especially
studied in relation to fetal growth and later vulnerability to cardiovascular and related diseases [6,7].
Fetal programming, however, seems to be equally important for the development of
psychopathology.
Here, I shall discuss the evidence for the association between maternal prenatal stress and child
outcomes (with a special focus on neurodevelopmental outcomes), and evidence that a component of
this association is causal. I will then briefly discuss what should be done but will not cover antide-
pressant and anti-anxiety medication or drug studies.

Types of stress associated with altered child outcome

It is clear that it is not just a diagnosable mental illness or extreme ‘toxic stress’ that is linked with
altered outcome. Stress is a generic term that includes a wide range of different types of exposure, and
can be acute and chronic. It is defined in different ways, including biologically. The types of prenatal
stress found to be associated with altered child outcome, however, have not been found to be asso-
ciated with any specific biological parameter, such as increased production of cortisol. The types of
stress are objective stressors and subjective stress, but this has not been studied in this context. It has
also been suggested that mild stress may have different effects from more severe stress, and may be
beneficial for some outcomes [8].
Exposures that have been shown to be associated with altered child outcome vary from the very
severe, such as the death of an older child, to quite mild stresses, such as daily hassles. They include
symptoms of maternal anxiety [9–13] and depression [9], as well as a diagnosis of depression [14],
pregnancy-specific anxiety and daily hassles [15], bereavement [16], and stress caused by a bad rela-
tionship with the partner [17]. They also include exposure to acute external disasters [18], the
September 11 attacks [19], Chernobyl [20], a Louisiana hurricane [21], or war [22,23]. Domestic abuse
during pregnancy has not been studied as such for its effects on the fetus and the child, but is also likely
to be important.
One issue of interest is whether some forms of stress have a greater effect than others, but little is
yet known about this. A few studies have examined both prenatal anxiety and depression, and have
found associations between both of them and child outcome [9,10], Of course, anxiety and depression
are quite strongly co-morbid, and it is hard to disentangle the effects of the two. It is possible that they
can affect outcome but in somewhat different ways. Barker et al. [24] found that, in the prenatal and
postnatal periods, maternal depression had a wider effect on different types of child maladjustment
than maternal anxiety, which appeared more specific to internalising difficulties in the child.

Types of outcome altered

A wide range of different outcomes have been shown to be associated with prenatal stress in studies
examining the children from birth until adulthood. At birth, an increase in congenital malformations
has been found to be associated with severe stress in the first trimester, such as the death of an older
child [25]. Many studies have shown that less severe stress is associated with somewhat lower
birthweight and reduced gestational age [26,27]. Another finding at birth is an altered sex ratio, with
fewer males to females being born than in an unstressed population [28,29]. Mothers scoring in the
 V. Glover / Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35 27

upper quartile of the General Health Questionnaire had 47% boys compared with 52% in the undis-
tressed groups [28].
Most studies have looked at neurodevelopmental and psychopathological outcomes. Some in-
vestigators have looked at the newborns of mothers who report stress during pregnancy and found a
poorer performance on the Neonatal Behavioural Assessment Scale relative to newborns of mothers
who do not report stress during pregnancy [30], showing that adverse behavioural outcomes are
observable from the very beginning. Studies of infants and toddlers have shown them to have a more
difficult temperament [10,31], sleep problems [32], and lower cognitive performance and increased
fearfulness [17] associated with higher maternal stress during pregnancy.
Many studies have examined the association between prenatal stress and neurodevelopmental
outcomes in children ages 3–16 years, rather than babies, infants or adults. Many independent groups
have shown that prenatal stress increases the risk for child emotional problems, especially anxiety and
depression, and symptoms of attention deficit hyperactivity disorder (ADHD) and conduct disorder
[9,23,26,33–36]. Other studies have shown a reduction in cognitive performance [12,18] associated
with prenatal stress.
Some studies have found an association between prenatal stress and increased risk of autism
[21,37], with exposure in mid- to late-gestation, although a large population study has failed to confirm
the increased autism [38]. Two studies have found an increased risk of schizophrenia in adults born to
mothers who experienced stress during pregnancy. Both showed effects with severe stress, the death
of a relative [16] or exposure to the invasion of the Netherlands in 1940 [22], and both showed that the
sensitive period of exposure was during the first trimester.
A further set of studies have shown associations between prenatal stress and a range of altered
physical and physiological outcomes. These include an altered fingerprint pattern [39], more mixed
handedness [40,41], and specific regional reductions in brain grey-matter density [42]. Such altered
grey matter may be associated with neurodevelopmental and psychiatric disorders, and cognitive and
intellectual impairment.
Several studies have shown that prenatal stress is associated with an altered diurnal pattern or
altered function of the hypothalamic–pituitary-adrenal (HPA) axis although the pattern of alteration is
quite complex [43]. Finally, recent studies have shown that prenatal anxiety is associated with reduced
telomere length [44,45]. This is an intriguing finding, as well as of concern, as reduced telomere length
is associated with a reduced life span.
Research on the most sensitive time in gestation for the influence of prenatal stress is inconsistent.
It is likely that sensitivity can occur at different times depending on the outcome studied and the stage
of development of the relevant brain or other structures. Two studies of schizophrenia found that the
most sensitive period was in the first trimester. This is when neuronal cells are migrating to their
eventual site in brain, a process previously suggested to be disrupted in schizophrenia. In contrast, two
studies of conduct disorder, or antisocial behaviour, found the greatest associations with stress later in
pregnancy [26,33]. It is clear that these effects are not all over by the first trimester, but this is an area
where much more research is needed.

Is maternal stress and altered outcome causal?

Many human studies, as discussed above, have shown an association between maternal stress
during pregnancy and a risk for altered outcome for the child. The evidence for this is strong, and has
been shown in many independent prospective studies from around the world. What is harder to
establish is that the association is causal. If a mother is stressed while she is pregnant she may well be
stressed postnatally and this could affect her parenting. Other associated confounding factors include
smoking or alcohol consumption, which may affect behaviour and birthweight. Genetic continuity
could also occur. The mother may have certain genes that make her more likely to become anxious or
depressed, and she may pass these genes on to her child, which in turn makes them more prone to
emotional or behavioural problems.
Several studies have tried to address these issues. These include animal studies, human studies
showing changes at birth, human studies that have allowed for many possible confounders, and human
studies that are starting to uncover possible underlying mechanisms.
28 V. Glover / Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35

With animal studies, it is much easier to establish that prenatal stress has a direct effect on the
outcome for the offspring. Newborn rat pups of prenatally stressed mothers can be cross fostered to
non-stressed mothers on the first day after birth, with control pups of unstressed mothers cross-
fostered also. This can establish that any differences in outcome are caused by stress in the pre-
natal period. Many such studies have shown definite programming effects of prenatal stress on
behaviour, cognitive development, the HPA axis, and brain structure and function of the offspring
[46–49]. The nature of the effects can be affected by the timing of the exposure in gestation, the type
of the stress, the strain of the animal, the age at which the offspring was tested, and the sex of the
offspring [48]. Some altered outcomes are not observed in the youngest offspring, but become
apparent as they mature. In general, although not always, prenatal stress increases anxiety and
depressive behaviour to a greater extent in female offspring, and impairs learning and cognition
more in the males [50]. The effects of prenatal stress on the offspring can often be mimicked by
giving the stress hormone corticosterone or a synthetic glucocorticoid to the pregnant animal [49].
Some of the effects of prenatal stress can also be moderated by the quality of the postnatal maternal
care [51].
In humans, an association between the mother’s emotional state and the behaviour or heart rate of
her fetus is supported by good evidence. Monk et al. [52], for example, have conducted experiments in
which a pregnant mother is asked to carry out a stressful computer task, while the fetal heart rate is
monitored [52]. They showed that the fetal heart rate went up during the task, but only in the mother’s,
who rated themselves as anxious. Thus, even before birth, the fetus can be affected by the maternal
emotional state, although we do not know what the mechanism is. The effects are too fast to be caused
by cortisol, which takes 10–20 mins to rise, and catecholamines do not cross the placenta. Evidence
shows continuity from fetal behaviour and neurological maturation in the first weeks after birth. For
example, fetal parameters, such as heart-rate variability and fetal movement, predicted neonatal motor
behaviour and reflexes [53].
Several studies have shown that maternal stress during pregnancy is associated with altered out-
comes at birth, including reduced birthweight [26], reduced scores on the Brazelton assessment [54],
and a more difficult temperament [55] soon afterwards. Recently, an alteration in telomere length in
cord blood leukocytes has been shown to be associated with pregnancy-specific anxiety [45]. These
studies all provide some evidence for prenatal, independent of postnatal, effects.
Another approach is to carry out prospective human studies allowing for as many potential
confounders as possible, such as prenatal smoking and alcohol consumption, and for postnatal
maternal mood. Several studies have found a strong signal remaining for prenatal anxiety or
depression on child emotional and behavioural problems [9,34,17] after controlling for many con-
founders, including postnatal depression and anxiety. In our study (unpublished data), we found
that these effects are also apparent when allowing for paternal pre- and postnatal mood. If the
observed associations are primarily due to an anxious mother passing on predisposing genes to her
child, it would not be expected to be specifically associated with prenatal compared with postnatal
mood, or maternal compared with paternal mood. One recent study, which just looked at the
outcome of ADHD, found that the effect of prenatal maternal mood remained after controlling for
paternal mood in one cohort, the Avon Longitudinal Study of Parents and Children, but not in
another, Generation R [56]. Differences in design and the measuring instruments used may help to
explain this discrepancy. Postnatal maternal mood and parenting both have clear effects. For
example, the association between prenatal anxiety and child fearfulness was found to be greater in
those children with an insecure attachment [57]. Most of the prospective cohort studies, allowing for
confounders, also suggest a prenatal causal component.
In a study by Rice et al. [26] in children born after in-vitro fertilisation [26], prenatal stress and child
outcome in babies who were genetically related to the mother was compared with those who were not
[26]. They showed an association between maternal stress in pregnancy and child symptoms of ADHD
and conduct disorder, and that the association with conduct disorder was apparent in the unrelated
mothers. This gives strong support to the idea that the association between prenatal stress and child
conduct disorder is independent of genetic factors. The fact that the increase in symptoms of ADHD
was apparent only in those with related mothers does not conclusively rule out a prenatal environ-
mental component. A gene environment interaction may also be involved. Prenatal stress may only
 V. Glover / Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35 29

have the effect of increasing symptoms of ADHD in the genetically vulnerable mother and child pairs.
More research is needed to disentangle the role of genetic factors for all outcomes.
Another indication that the effects of prenatal stress are not just caused by genetic continuity are
the group of studies that have studied children of mothers exposed to acute disasters. These have
included a Canadian ice storm [18], the September 2011 attacks [19] and Chernobyl [20]. With these
‘natural or man-made experiments’, as for example in the ice storm study, the level of stress was
objectively assessed, and the exposure was of a specific duration. This reduces the confounding effects
of pre-existing emotional problems and genetic continuity.

Underlying biological mechanisms

Little is understood about the mechanisms that may underlie fetal programming by prenatal stress
in humans. One early suggestion was a decrease in blood flow to the fetus [58]. It is not clear, however,
if the decrease observed in that study would be clinically significant, and others have failed to replicate
the original finding [59].
Another possible mediating factor is increased exposure of the fetus to cortisol. Glucocorticoids (e.g.
cortisol in humans and primates, corticosterone in rodents) are known to have a range of effects on the
developing fetus, including on the brain [60]. Although they are essential for fetal development and
tissue maturation, overexposure can have effects that predispose to ill health in later life. [61] Fetal
overexposure to glucocorticoids could occur through increases in maternal cortisol associated with
anxiety and during periods of stress, which then crosses the placenta into the fetal environment. In
animal models, this has been shown to be one mechanism. The human HPA axis functions differently in
pregnancy from most animal models, because of the placental production of corticotropin-releasing
hormone, which in turn causes an increase in maternal cortisol. The maternal HPA axis becomes
gradually less responsive to stress as pregnancy progresses [62], and there is only a weak, if any, as-
sociation between maternal mood and the woman’s cortisol level, especially later in pregnancy [63]. It
thus seems unlikely that an increase in maternal cortisol is the mediating mechanism between pre-
natal maternal stress, anxiety or depression in later pregnancy and altered fetal outcome.
It is possible that fetal programming may be partially mediated by cortisol without increases in
maternal levels. Depression, stress, or anxiety may cause increased transplacental transfer of maternal
cortisol to the fetal compartment. The placenta clearly plays a crucial role in moderating fetal exposure
to maternal factors, and presumably in preparing the fetus for the environment in which it is going to
find itself [63]. Thus, another mechanism by which the fetus could become overexposed to gluco-
corticoids is through changes in placental function, especially the enzyme 11b-hydroxysteroid dehy-
drogenase type II (11b-HSD2), the barrier enzyme which converts cortisol to the inactive cortisone. If
there is less of this barrier enzyme then the fetus will be exposed to more maternal cortisol, inde-
pendently of any change in the maternal level. Some evidence in rat models shows that prenatal stress
can down-regulate placental 11b-HSD2. Restraining pregnant rats in the last week of pregnancy, a
procedure they find stressful, has been shown to result in decreased placental 11b-HSD2 expression
and activity [64]. Our laboratory has found direct evidence that maternal prenatal anxiety and
depression are also associated with a down-regulation of 11b-HSD2 in humans [65].
It is unclear which changes in maternal chemistry associated with maternal mood in pregnancy
have this influence on placental function. One possibility is the cytokines. Psychosocial stress during
pregnancy has been shown to be associated with raised levels of inflammatory cytokines such as
interleukin-6 [66]. How, if at all, these affect placental function remains to be determined.
Serotonin is another possible mediator of programming effects induced by prenatal stress on the
offspring’s neurocognitive and behavioural development. During gestation, serotonin acts as a trophic
factor regulating cell division, differentiation and synaptogenesis [67]. Animal studies have shown that
increased serotonin exposure during gestation is associated with alterations in many neuronal pro-
cesses and subsequent changes in offspring behaviour. Recent work has identified an endogenous
serotonin biosynthetic pathway in the human placenta [68], suggesting a possible role for alterations in
placental serotonin in human fetal programming.
Epigenetic changes, which involve reversible changes to the structure of DNA, such as the
addition of a methyl group, control the amount of mRNA and protein produced. Such
30 V. Glover / Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35

epigenetic changes can be induced by the environment, and may underlie many of the pro-
cesses of fetal programming. Prenatal stress has been shown to cause epigenetic changes in the
rodent brain, in the DNA, which codes for the receptor that binds the stress hormone cortisol
[69]. In humans, stress during pregnancy caused by violence from the partner, has been shown
to cause epigenetic changes in the DNA for this same receptor, in the blood of their adolescent
children [70].

Clinical magnitude of the effects of prenatal stress

The magnitude of many of the effects described above are not just statistically significant but also
clinically significant. In the large Avon Longitudinal Study of Parents and Children population study,
it was found that, if the mother was in the top 15% for anxiety, her child was at double the risk for
emotional and behavioural problems at ages 4 and 7 years [9,33] after controlling for a wide range of
possible confounders, including postnatal maternal mood. The risk was raised from about 5% in the
general population to about 10% in the children of the high anxiety group. Most children were not
affected, and those that were, were affected in different ways. It is possible to calculate from this that
the attributable risk of childhood behavioural problems caused by prenatal stress is about 10–15%
[2]. Similar results have been reported at age 13 years (unpublished data). The effects of prenatal
stress on cognitive development also seem to be clinically significant. In a study correlating prenatal
life events with child cognitive development at 17 months, Bergman et al. [17] found that prenatal
stress accounted for 17% of the variance in cognitive ability, after allowing for a range of con-
founders, including postnatal maternal mood. Prenatal partner relationship strain accounted for
most (73%) of the variance in cognitive ability related to life-event stress. If the woman said she had
suffered from three or more partner-related life events (e.g your partner was emotionally cruel to
you), her infant had a mean Bayley Mental Developmental index of 89, compared with 98 for the
rest of the group (the general population norm being 100). King and Laplante [71] found even
greater effects on cognitive ability. They examined 2-year old children of mothers who had been
exposed to a Canadian Ice storm during pregnancy, and compared the outcome for those who had
been exposed to high or low stress. For children of mothers exposed to high stress in the first or
second trimesters, the Bayleys’ scores were 14 and 19 points respectively, lower than the children of
the low stress mothers.

What should be done?

These findings have important clinical implications. If maternal depression, anxiety, or stress during
pregnancy can increase the risk for an adverse outcome for the child, then interventions to reduce such
stress should improve the outcome. It is clear that not all the adverse effects described above are
caused in the first trimester. Many also seem to be caused by changes in the second and third tri-
mesters. Therefore, although it is best to start interventions as early as possible, later interventions are
likely to be beneficial too.
No study has yet been conducted on interventions specifically designed to reduce maternal
depression, anxiety, or stress during pregnancy with a long-term follow-up study of outcomes for
the child. The only intervention that starts during pregnancy and that has included long-term follow
up studies is the Nurse Family Partnership. This is targeted at deprived, especially teenage, and poor
single mothers, and includes multiple home visits by specially trained nurses during pregnancy and
for the first 2 years. It was not designed to target stress but to help the mothers with diet, health
care, their own education, reduction in smoking, and with parenting. These special nurses, however,
do provide much support for these mothers from early pregnancy onwards. The results of this
intervention have been impressive, with many long-term improvements in self care and parenting
behaviour, as well as child outcome [72–74]. A notable finding was a reduction of criminal behav-
iour, especially in girls [75]. Compared with the comparison group, by 19 years of age, girls in the
pregnancy and infancy nurse-visited group were less likely to have been arrested (10% v 30%) and
convicted (4% v 20%). No comparable benefit was observed for boys. As prenatal stress causes an
increased risk for conduct disorder, ADHD, and cognitive problems, and all these are major risk
 V. Glover / Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35 31

factor for later criminal behaviour, one would expect a reduction in prenatal stress to reduce crime
as well as improving other outcomes. It may be that, for boys, a ‘top up’ intervention in the teenage
years is needed. Olds et al. [76] have shown that this programme is of great benefit and is cost
effective. After assessment when the children were 12 years old, the government spent less on
various types of aid to the families than the cost of the programme, with a net saving of about $800
per family.
Although no other long-term follow-up studies have been published, several studies of in-
terventions that reduce aspects of depression, anxiety and stress during pregnancy have been con-
ducted [77]. Interpersonal therapy has been shown to be effective at reducing depression during
pregnancy [78]. A randomised-controlled trial of cognitive–behavioural therapy for anxious or
depressed pregnant women is being conducted [79]. New models of perinatal care are being developed
[80], and evidence shows that interventions delivered in the home setting may be especially helpful
[81].
Listening to music has been found to decrease maternal plasma cortisol and self-reported state
anxiety score in pregnant women awaiting amniocentesis [82]. Maternal relaxation has also been
shown to improve indices of fetal neurobehaviour, such as heart rate variability [83]. One study
compared active (directed by a therapist) and passive (sitting in a chair) relaxation [84]. Both active
and passive relaxation significantly reduced state anxiety and maternal heart rate, but the effect was
significantly greater with the active relaxation. In contrast, the passive relaxation significantly
reduced noradrenaline levels, whereas active did not. Both methods significantly reduced cortisol.
Overall, however, a striking lack of correlation existed between the psychometric and biological
indices. To reduce specific biological effects of anxiety or depression during pregnancy, different
methods may be needed from those which are most effective at reducing subjective psychological
symptoms.
It is still true that most depression, anxiety, and emotional and physical abuse experienced by
pregnant women is undetected by health professionals, and little help seems to be available [85].
Symptoms of anxiety and depression are at least as common during pregnancy as postnatally [86],
and domestic abuse can increase. Midwives and obstetricians need to be trained to detect all this
and offer appropriate support or help. If women are anxious or depressed they should be referred to
their general practitioner, as recommended in the National Institute for Health and Clinical Excel-
lence 2007 guidelines on antenatal and postnatal mental health. If suffering abuse, they should be
referred to specific agencies focusing on domestic abuse. Up to 15% of pregnant women and their
children would benefit from this type of support. For most depressed or anxious women, some sort
of counselling or talking therapy, such as cognitive– behavioural therapy [87] will be most appro-
priate. For the more severely depressed, more specialised care may be necessary, and antidepres-
sants may be the best option. Although the use of antidepressants has not been discussed here,
some evidence shows that their use in anxious women may benefit at least some aspects of child
outcome [88].

Conclusion

Good evidence shows that the emotional state of the mother during pregnancy, as well as in the
postnatal period, can have long-term effects on her child, especially on neurodevelopmental out-
comes. The mechanisms underlying such fetal programming are only just starting to be uncovered
and, often, a limited correlation between psychometric indices and biological ones. Research is still
needed to determine which interventions during pregnancy are most effective at improving child
outcome. More needs to be done to detect and treat emotional problems and disorders during
pregnancy. This will benefit the woman herself, and eventually will benefit the next generation
also.

Conflict of interest

None declared.
32 V. Glover / Best Practice & Research Clinical Obstetrics and Gynaecology 28 (2014) 25–35

Practice points

 Mental health is fundamental to health.

 A psychosocial assessment that includes enquiring about the woman’s overall wellbeing,
including stressors, important relationships and strengths, should be part of her routine
maternity care. This discussion can open the conversation about psychosocial issues,
including intimate partner violence and people who may be able to support her.
 Routinely use a screening instrument, such as the Edinburgh Postnatal Depression scale
(EPDS), which also assesses symptoms of anxiety, and is validated for use in pregnancy. This
does not give a diagnosis but, if the woman’s score is of concern (13 or above), she should be
receive additional evaluation for the presence of an episode of major depression or other
mental disorder and intervention.
 Evidence suggests that fetal development can be affected in women in the top 15% for
symptoms of anxiety, depression, or stress, even if they do not meet criteria for a disorder. An
optimal service will provide an appropriate intervention or help for such women.
 A system of care, ideally including a perinatal mental health care team, should be in place so
that health professionals know to whom they should refer a women in need of mental health
assessment and treatment.

Research agenda

 The effects of domestic abuse on child outcome needs to be investigated.

 More research is needed on the underlying mechanisms by which maternal stress affects
child outcome.
 Interventions that help the mother may not necessarily help the outcome for the child.
Research is needed to follow up children of depressed, anxious, or stressed mothers after
different specific interventions to determine their effects on different child outcomes.

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