The Impact of Maternal Depression in Pregnancy on Early Child Development
Postpartum depression in mothers is associated with developmental problems in their children. Many women who are depressed following childbirth are also depressed during pregnancy. The aim of this study was to examine the associations between maternal depressive symptoms during pregnancy and child development at 18 months of age. A prospective cohort study, Avon Longitudinal Study of Parents and Children. The former county of Avon, southwest England. All pregnant women in the defined area with delivery dates between April 1991 and December 1992, 9244 women and their children. Data were collected antenatally, at 18 and 32 weeks of gestation and at 8 weeks and 8 months postnatally, through postal questionnaires, including a self-report measure of depression (Edinburgh Postnatal Depression Scale [EPDS]). By the time their child was 18 months old, women completed five further questionnaires about their children's health and development. Child development at 18 months using a modified Denver Developmental Screening Test (modified DDST). Applying the standard 12/13 cutoff, 1565 (14%) women were depressed antenatally but not at either time-points postnatally. Employing the modified DDST, 893 (9%) children were developmentally delayed at 18 months of age. Persistent depression (EPDS > or = 10 at both time-points) is associated with developmental delay (adjusted OR 1.34, 95% CI 1.11-1.62). Applying the 12/13 and 14/15 cutoffs gave similar results. After further adjustment for postnatal depression, the effect sizes were slightly attenuated. These findings highlight the importance of depression in pregnancy. Some effects on child development attributed to postpartum depression are caused in part by depressive symptoms during pregnancy.
The impact of maternal depression in pregnancy
on early child development
Centre for Child and Adolescent Health, University of the West of England, Bristol, UK
Department of Social Medicine, ALSPAC, University
of Bristol, Bristol, UK
Academic Unit of Psychiatry and
Centre for Child and Adolescent Health, University of Bristol, Bristol, UK
Correspondence: Dr T Deave, Centre for Child and Adolescent Health, University of the West of England, Bristol, Hampton House, Cotham Hill,
Bristol BS6 6JS, UK. Email firstname.lastname@example.org
Accepted 20 March 2008.
Objective Postpartum depression in mothers is associated with
developmental problems in their children. Many women who are
depressed following childbirth are also depressed during
pregnancy. The aim of this study was to examine the associations
between maternal depressive symptoms during pregnancy and
child development at 18 months of age.
Design A prospective cohort study, Avon Longitudinal Study of
Parents and Children.
Setting The former county of Avon, southwest England.
Population All pregnant women in the deﬁned area with delivery
dates between April 1991 and December 1992, 9244 women and
Methods Data were collected antenatally, at 18 and 32 weeks of
gestation and at 8 weeks and 8 months postnatally, through postal
questionnaires, including a self-report measure of depression
(Edinburgh Postnatal Depression Scale [EPDS]). By the time their
child was 18 months old, women completed ﬁve further
questionnaires about their children’s health and development.
Main outcome measure Child development at 18 months using
a modiﬁed Denver Developmental Screening Test (modiﬁed
Results Applying the standard 12/13 cutoff, 1565 (14%) women
were depressed antenatally but not at either time-points
postnatally. Employing the modiﬁed DDST, 893 (9%) children
were developmentally delayed at 18 months of age. Persistent
depression (EPDS ‡ 10 at both time-points) is associated with
developmental delay (adjusted OR 1.34, 95% CI 1.11–1.62).
Applying the 12/13 and 14/15 cutoffs gave similar results. After
further adjustment for postnatal depression, the effect sizes were
Conclusions These ﬁndings highlight the importance of depression
in pregnancy. Some effects on child development attributed to
postpartum depression are caused in part by depressive symptoms
Keywords ALSPAC, antenatal depression, child development,
pregnancy, postnatal depression.
Please cite this paper as: Deave T, Heron J, Evans J, Emond A. The impact of maternal depression in pregnancy on early child development. BJOG 2008;115:
It is widely recognised that depression is common during the
postpartum period and that maternal postnatal depression
can have a detrimental effect on child development (the term
‘depression’ and ‘depressed’ is used as a short-hand for those
women who scored above the speciﬁed cutoff on the Edin-
burgh Postnatal Depression Scale [EPDS]. The EPDS is not
a diagnostic tool and the women had not been assessed for-
mally, therefore they had not been diagnosed as clinically
Investigations of the inter-relationships
between maternal wellbeing and child development have
mostly been conducted after childbirth with few studies col-
lecting data prospectively, starting during pregnancy.
There is increasing evidence that the mother’s mood during
pregnancy is important. For example, uterine blood ﬂow has
been observed to change in association with anxiety during
and antenatal anxiety in late pregnancy is
independently associated with children’s behavioural/emo-
tional problems at 4 years of age.
The children of women
in socio-economically deprived families, who are at risk of
depression antenatally, are at greater risk of developmental
delay at 2 years of age.
The strongest predictor of postnatal
depression is depression in pregnancy; however, antenatal
depression may be more common than postnatal depres-
Although severity and chronicity of maternal depres-
sion are related to increased developmental problems in their
less is known about the importance of timing of
ª 2008 The Authors Journal compilation ª RCOG 2008 BJOG An International Journal of Obstetrics and Gynaecology 1043
the exposure to maternal depression, in particular whether
pregnancy is a sensitive period.
Closing the gap in the evidence about associations between
parental depression and child health outcomes has important
implications for both families and healthcare practitioners.
The aim of this study was to assess the association between
maternal depression in pregnancy and child development.
Although fathers’ mood inﬂuences child development,
focus of this paper is on depressive symptoms in mothers. We
hypothesised that antenatal depression scores have an impact
on early childhood development that is independent of post-
natal depression. This was tested, ﬁrst, by investigating the
association between maternal antenatal depression and a mea-
sure of child development and second, by examining the
independent effects of antenatal depression. Data used to test
this hypothesis were derived from the Avon Longitudinal
Study of Parents and Children (ALSPAC),
a large commu-
nity sample in England that has been followed prospectively
since early pregnancy.
The ALSPAC study design included all pregnant women liv-
ing in the geographical area of Avon, England, who expected
to deliver their baby between April 1991 and December 1992,
resulting in 14 062 live births. Recruitment, dropout and
other methodologies have been described elsewhere.
line data, including socio-demographic and family details,
were collected from pregnant woman and their partners at
18 and 32 weeks of gestation using postal questionnaires.
Those women who did not complete the antenatal question-
naires at both 18 and 32 weeks of gestation were excluded
from these analyses, as were those children from multiple
The exposure of maternal depression was assessed using the
Although developed as a screening tool for depres-
sion following childbirth, this scale has been validated during
pregnancy as well as outside the postpartum period.
EPDS is a widely used 10-item self-rating questionnaire on
which women rate their feelings over the previous 7 days,
giving a score ranging from 0 to 30.
The EPDS has been
used in many studies of depression in childbearing women,
most typically in the ﬁrst year postpartum. Women com-
pleted the EPDS at 18 and 32 weeks of gestation and then
again at 8 weeks and 8 months postpartum. Women were
categorised into three ‘antenatal depression’ groups: those
with a score below the EPDS cutoff indicating the absence
of depression and those with EPDS scores at or above the
cutoff indicating depression either at 18 or 32 weeks (once),
or at 18 and 32 weeks (twice); the latter as a measure of
more persistent depression. A priori, to reﬂect the continuous
nature of the data, there were three stages of the analysis
undertaken. Each stage applied a different cutoff on the
EPDS: 9/10, 12/13 and 14/15; 12/13 is the standard cutoff.
Post hoc, another method was also applied in which women
were categorised at both 18 and 32 weeks of gestation into
four groups depending on their EPDS scores (0–9, 10–12, 13–
14 and 15–30) and data were scored as given in Table 1,
creating an ordinal scale from 0 to 6. This method combined
both levels of intensity (EPDS scores) and persistence
(depressed once, twice or at both time-points during preg-
nancy) and aimed to better characterise any dose–response
relationship, or threshold effect, between persistent antenatal
depression and developmental delay.
A modiﬁcation of the Denver Developmental Screening Test
(modiﬁed DDST) was used as the child outcome. This is
a screening questionnaire designed to identify cognitive and
behavioural problems in preschool children. The data are
presented as age norms. The more items a child fails to per-
form passed by 90% of his/her peers, the more likely the child
manifests a signiﬁcant developmental deviation. The items
used in the screening test were from the Denver II that has
been shown to be predictive of developmental delay.
been adapted for parental report through discussions with
focus groups and piloting, using the same cohort as this study
and found to signiﬁcantly relate to the Grifﬁths Scales classi-
for general development.
Parents completed a ques-
tionnaire at 18 months postpartum. The developmentally
delayed group were those who failed two or more items, which
was the case for 10% of the ALSPAC cohort.
Descriptive statistics and frequencies were used to examine
the characteristics of the study population. The three cutoffs
Table 1 . Categories allocated to each woman according to their
antenatal EPDS scores. A woman’s category at each time-point was
then summed to indicate the severity and persistence of her
EPDS score at
18 weeks of
EPDS score at 32 weeks of gestation
EPDS 0–9 EPDS 10–12 EPDS 13–14 EPDS ‚ 15
EPDS 0–9 0 1 2 3
EPDS 10–12 1 2 3 4
EPDS 13–14 2 3 4 5
EPDS 15 3 4 5 6
Category 0, EPDS 0–9; category 1, EPDS 10–12; category 2,
EPDS 13–14; category 3, EPDS 15.
Deave et al.
1044 ª 2008 The Authors Journal compilation ª RCOG 2008 BJOG An International Journal of Obstetrics and Gynaecology
on the women’s EPDS scores (9/10, 12/13 and 14/15) were
applied at three different stages of the analysis. Bivariable tests
of association and multivariable regression analyses were
undertaken for each stage to quantify the individual relation-
ships between maternal depression, potential confounding
factors and developmental delay. Potential confounding fac-
tors entered into the analysis included demographic details
for both parents, previous maternal depression, maternal anx-
iety, paternal depression and anxiety, life events in the pre-
vious year, gestation, gender and ethnicity of child, feeding
method, postnatal mood of parents and life events postnatally
(Table 2). Individual unadjusted odds ratios were calculated
for each potential confounding and explanatory variable. For
the multivariable analysis, because of the complex inter-
relationship between antenatal depression and child deve-
lopment, a conceptual framework was used to describe the
hierarchical relationships between risk factors (Table 3).
This framework uses ﬁndings from previous research and
guides the decision about which variables to include in the
analysis. A multivariable regression analysis was undertaken
applying the steps of the conceptual framework one by one
starting with step 1. Following the inclusion of each step,
variables were removed if, individually, they had minimal
impact on the relationship between women with antenatal
depression and developmental delay (less than 5% change
in the odds ratio).
Those variables remaining in the model
were carried forward and included together with the variables
in the next step of the framework. Each variable was then
individually re-entered at the end. The evidence for any neg-
ative effect of young maternal age on developmental delay is
conﬂicting, therefore maternal age was retained.
also be a proxy variable for some other factor that has not
been, or cannot be, measured. Due to missing data for the
exposure and for potential confounding variables, a sensitivity
analysis was undertaken using imputed data. In the multivari-
able models of our primary analyses, missing data on con-
founding variables resulted in a loss of almost 10% of the
sample when the fully adjusted models were derived. To avoid
any potential bias that might result when incorporating these
confounding variables into the model, a missing data impu-
tation technique was employed (missing imputation for
using the procedure in STATA known
Imputation was restricted to confounding variables
(no imputation of the outcome variables was performed). The
results from the regression using imputed data were similar to
those using unimputed data. This suggests that the missing
data were not substantially biasing the ﬁndings and therefore
only the analysis using the unimputed data is reported. Data
Table 2. Details of the potential confounding factors that were
included in the conceptual framework and analysis
women EPDS < 13
(n 5 8799),
EPDS ‚ 14
(n 5 2299),
Primiparous women 3911 (44.5) 922 (40.1)
Owned/mortgaged housing 6943 (78.9) 1417 (61.6)
Overcrowding 1272 (14.5) 591 (25.7)
No use of car 1749 (19.9) 771 (33.5)
No smoking ﬁrst trimester 7035 (79.9) 1464 (63.7)
No alcohol ﬁrst trimester 3938 (44.8) 1038 (45.2)
Mother less than 20 years 234 (2.7) 146 (6.4)
Father less than 20 years 52 (0.6) 53 (2.6)
3091 (35.3) 802 (35.1)
Father unemployed 495 (6.4) 233 (12.6)
Have partner 8372 (98.4) 2040 (95.6)
Mother: previous depression 463 (5.3) 454 (19.7)
Mother: anxious 920 (10.5) 1562 (67.8)
Father: depressed 185 (2.7) 135 (8.2)
Father: anxious 274 (3.1) 118 (5.1)
,3 life events in past year 2135 (24.5) 189 (8.4)
Preterm 462 (5.3) 150 (6.5)
Ever breastfed 6163 (77.9) 1344 (70.3)
Male child 4510 (51.3) 1194 (51.9)
Ethnicity: white 8545 (97.1) 2183 (94.9)
Mother: no low mood 7176 (81.5) 1282 (55.9)
Father: no low mood 4378 (49.8) 876 (38.1)
,3 life events in past year 2456 (31.1) 1052 (54.7)
*These percentages represent the percentage response for the total
number of answers for that particular question.
Table 3. Conceptual hierarchical framework of risk factors for
Step Label for steps
1 Socio-economic Parity, housing tenure, overcrowding,
use of car, mother’s smoking habit,
mother’s alcohol intake
2 Parental Mother’s age, partner’s age, mother’s
education, partner’s employment,
Previous maternal depression, maternal
anxiety, life events in previous year,
paternal depression and anxiety
4 Birth Gestation, breastfeeding, gender,
ethnicity of child
5 Postnatal Postnatal mood of parents, life events
Modiﬁed from Victora et al.
Antenatal depression: impact on child development
ª 2008 The Authors Journal compilation ª RCOG 2008 BJOG An International Journal of Obstetrics and Gynaecology 1045
analysis was performed using STATA (STATA version 8)
(Stata Corporation, College Station, TX, USA).
Ethics approval for the study was obtained from the
ALSPAC Law and Ethics Committee and the Local Research
Complete antenatal EPDS data (18 and 32 weeks of gestation)
were available for 11 098 women, of whom 4833 (44%) were
expecting their ﬁrst child. Women with incomplete antenatal
EPDS data were excluded from the study. There were few
demographic differences between these women and those
retained in the analysis. The main differences were that, com-
pared with the women who were excluded, a higher percent of
included women had a partner, a lower percent achieved
O’level or equivalent qualiﬁcations or had partners who were
unemployed (Table 4).
Child developmental outcomes
Parental report on the modiﬁed DDST (n = 10 125) identiﬁed
893 (9%) children who were developmentally delayed. The
children were mainly White British (97.7%), 612 (5.5%) were
preterm, 5704 (51.4%) were male children and 7505 (76.4%)
ever breastfed. There were just 36 (0.4%) children whose
parents reported that their child was usually unwell.
Using the standard 12/13 cutoff, 8262 (74.4%) women were
not depressed either antenatally or postnatally, 1565 (14.1%)
women were depressed on at least one occasion antenatally
but at neither postnatally. Five hundred and thirty-seven
(4.8%) women were depressed on at least one of the two
measurement occasions postnatally but at neither antenatally
(Table 5). There were just 156 (1.4%) women who were per-
sistently depressed antenatally and postnatally.
When combined with the modiﬁed DDST data, of the
11 098 women with complete EPDS scores, antenatal data
were available on 9244 (83%) women and children.
For the ﬁrst stage of the analysis, complete case analyses for
the EPDS 9/10 cutoff were applied. Those women whose
EPDS scores were <10 at both 18 and 32 weeks of gestation
formed the baseline comparison group. The ﬁnal model pro-
vided adjusted estimates of the odds of developmental delay
of tobacco smoked in the ﬁrst trimester, mothers’ age and life
events at 8 months. The odds ratio for developmental delay
associated with antenatal depression at both time-points was
1.24 (95% CI 1.04–1.49) and when adjusted for smoking,
maternal age and life events was 1.34 (95% CI 1.11–1.62).
For the second stage, the EPDS 12/13 cutoff was applied
and the results followed a similar pattern, with a 50% increase
in the odds of developmental delay (adjusted odds ratio 1.50;
95% CI 1.15–1.96) (Table 6). For the third stage, applying the
14/15 cutoffs gave similar results, although with wider and
nonsigniﬁcant conﬁdence intervals. For each cutoff, after fur-
ther adjustment for postnatal depression, the effect sizes were
similar to those of the unadjusted models for each cutoff
Applying the conceptual framework, paternal depression
and antenatal anxiety were included in the analysis. However,
as they both had minimal impact on the relationship between
antenatal depression and the odds of developmental delay,
they were removed from the model.
Post hoc analysis
In the post hoc analysis, an ordinal scale combining both
intensity (EPDS scores) and persistence (above EPDS cutoff
at both 18 and 32 weeks of gestation) of symptoms was
applied. The odds ratios and 95% CIs show a consistent pat-
tern between the multivariable models without and with
adjustment (Figure 1). There is a suggestion of a threshold
Table 4. Demographic descriptions for the women who were retained in the analysis and those who were excluded from the study
(n 5 11 098), n (%)
(n 5 3370), n (%)
Primiparous [missing data for variable] 4833 (44.3) [180 (1.6)] 971 (47.3.) [1317 (39.1)]
Average age (SD) 28 (4.8) 27 (5.3)
Age in years (range) 15–44 15–44
Achieved O’levels/equivalent [missing data for variable] 6002 (54.4) [60 (0.5)] 892 (63.2) [1958 (58.1)]
No partner [missing data for variable] 227 (2.1) [459 (4.1)] 63 (5.7) [2267 (67.3)]
Partner unemployed [missing data for variable] 728 (7.4) [1228 (11.1)] 215 (14.1) [1840 (54.6)]
Each variable have missing data and therefore percentages are presented for both missing data and for the variable in question. For the variable
itself (e.g. no partner) what is taken as 100% 5 11 098 (or 3370)—missing data. For ‘partner unemployed’, the data for no partner are excluded
from the missing data figures.
Deave et al.
1046 ª 2008 The Authors Journal compilation ª RCOG 2008 BJOG An International Journal of Obstetrics and Gynaecology
effect between the groups who scored 3 and 4 on the ordinal
scale, indicating an underlying effect of antenatal depression,
although none of the results are statistically signiﬁcant and
the wide conﬁdence intervals arise from the small numbers
involved, especially in the severe and persistent depression
Summary of the study ﬁndings
This study set out to test the hypothesis that antenatal depres-
sion has an adverse impact on early childhood development.
This was tested, ﬁrst, by investigating the association between
women’s antenatal depression and a child development
measure and second, by examining the effects of antenatal
depression independent of postnatal depression. Applying
the modiﬁed DDST at 18 months of age as a measure of
development, an association was found between persistent
depression during pregnancy and developmental delay with
a 50% increase in the odds of developmental delay associated
with persistent antenatal depression. While the presence of
postnatal depression had a modifying effect on the odds,
we found evidence of an independent and statistically signiﬁ-
cant 34% increase in the odds of developmental delay when
the standard 12/13 cutoff on the EPDS was used to indicate
However, postnatal depression may be either a factor on
the causal pathway between antenatal depression and child
development, in which case it would be inappropriate to
adjust for its effects, or it may act as an independent inﬂuence
on child development, in which case it would be appropriate
to adjust for its effects. This study set out to examine speciﬁc
effects of antenatal depression on child development, inde-
pendent of postnatal depression, rather than to investigate
any potential link between the two. The observed threshold
effect is difﬁcult to explain by confounding factors; moreover,
Table 5. Women’s depression scores during pregnancy (18 and 32 weeks of gestation) and postnatally (8 weeks and 8 months) using
the EPDS and the standard 12/13 cutoff (n = 11 098)
Antenatally PN EPDS <13,
PN EPDS at
8 weeks, n (%)*,***
PN EPDS at 8 months,
PN EPDS at 8 weeks
and 8 months, n (%)*,***
Total, n (%)**
AN EPDS , 13** 8262 (74.4) 247 215 75 8799 (79.3)
AN EPDS at 18 weeks** 518 69 55 33 675 (6.1)
AN EPDS at 32 weeks** 603 88 73 81 845 (7.6)
AN EPDS at 18 and 32 weeks** 444 103 76 156 779 (7)
Total 9827 (88.5) 507 (4.6) 419 (3.8) 345 (3.1) 11 098 (100)
*Percentages given relative to total sample.
**AN EPDS: antenatal EPDS scores.
***PN EPDS: postnatal EPDS scores.
Table 6. Unadjusted and adjusted odds ratios of the relationship between antenatal depression and developmental delay
Variables Unadjusted Adjusted* Adjusted* 1 PN depression**
OR (95% CI) P OR (95% CI) P OR (95% CI) P
EPDS 10 at 18 or 32 weeks 0.99 (0.84–1.19) 0.996 1.06 (0. 88–1.27) 0.557 1.11 (0.85–1.23) 0.819
EPDS 10 at 18 and 32 weeks 1.24 (1.04–1.49) 0.023 1.34 (1.11–1.62) 0.003 1.23 (1.00–1.51) 0.047
EPDS 12 at 18 or 32 weeks 1.04 (0.86–1.29) 0.641 1.14 (0.92–1.40) 0.231 1.07 (0.86–1.33) 0.530
EPDS 12 at 18 and 32 weeks 1.35 (1.04–1.76) 0.025 1.50 (1.15–1.96) 0.003 1.34 (1.01–1.78) 0.043
EPDS 14 at 18 or 32 weeks 1.16 (0.92–1.47) 0.218 1.26 (0.99–1.60) 0.065 1.16 (0.90–1.49) 0.245
EPDS 14 at 18 and 32 weeks 1.34 (0.91–1.98) 0.140 1.49 (1.00–2.20) 0.050 1.27 (0.84–1.92) 0.254
*Adjusted for tobacco used in ﬁrst 3/12 of pregnancy, mothers’ age, life events at 8 months.
**Adjusted for postnatal depression as well.
Antenatal depression: impact on child development
ª 2008 The Authors Journal compilation ª RCOG 2008 BJOG An International Journal of Obstetrics and Gynaecology 1047
adjustment for suspected confounders did not markedly
change the estimates for the effect of cumulative exposure
to antenatal depression. So, although not statistically signiﬁ-
cant, the consistent association between antenatal depression
and child development seems credible. While the link between
antenatal and postnatal depression is widely recognised,
aspects of both antenatal and postnatal depression in mothers
are likely to be important in relation to early child develop-
ment. Any persistent depression during pregnancy has the
potential to be an important risk factor for developmental
delay in childhood. On the basis of the threshold effect, these
ﬁndings suggest that, for those women who reach this thres-
hold during pregnancy, there is a risk of developmental delay
in early childhood.
Strengths and limitations
This study uses a large prospective, longitudinal design and
recruited a large community sample that is broadly represen-
tative of the UK population when compared with the 1991
Many potential confounding variables were con-
trolled for during the process of the analysis. However, all
but three were removed by the confounder selection strategy
for the ﬁnal model. The evidence for an adverse affect of
young maternal age on child development is conﬂicting and
therefore maternal age was included.
It may also be a proxy
variable for some other factor that has not been, or cannot be,
measured. Nevertheless, there remains a possibility of residual
confounding of some unmeasured variables, in particular
mother–child interaction, a measure of which was not avail-
able for these analyses. This has been shown to be related to
both maternal depression and lead to poor cognitive devel-
opment in children.
A conceptual framework was used to manage the complex
hierarchical inter-relationship between antenatal depression
and child development and to describe the relationships be-
tween risk factors. The framework guided the multivariable ana-
lysis and was thus not based on purely statistical association.
To reﬂect the continuous nature of the data and to explore
the possibility of a dose–response effect between antenatal
depression and developmental delay, separate stages of the
analysis used different cutoffs on the EPDS: 9/10, 12/13 and
14/15. Using these three cutoffs do not necessarily deal with
the problem of misclassification of cases but rather shifts the
balance of false positives (women classified as having depres-
sion but who are not depressed) and false negatives (women
classified as not having depression but who are depressed) by
a particular cutoff. A post hoc analysis tried to address this by
creating an ordinal scale combining both intensity and per-
sistence of symptoms. Analysing the data in this way allowed
us to explore the possibility of a dose–response relationship to
be investigated further. However, underlying this method is
the assumption that the association with developmental delay
is the same for women in each category on the ordinal scale.
.7 .8 .9 1 1.2 1.5 2
± 95% CI
Unadjusted Adjusted Adjusted + PN EPDS
0123456 0123456 0123456
EPDS 7 category scale
0 = No depressive symptoms.
6 = Greatest intensity and persistence of symptoms.
*Adjusted for tobacco used in first trimester of pregnancy, mothers’ age and life events at 8 months.
Figure 1. Association of antenatal depression (using an ordinal scale) and developmental delay (post hoc analysis). Results for the unadjusted
analyses, adjusted for confounding factors* and further adjusted for postnatal depression (PN EPDS) are illustrated.
Deave et al.
1048 ª 2008 The Authors Journal compilation ª RCOG 2008 BJOG An International Journal of Obstetrics and Gynaecology
Despite the overall size of the cohort because of the relatively
small number of women with severe and persistent depres-
sion, our analysis has limited power to detect modest but
clinically important effects. The modiﬁed DDST is a binary
outcome and, by the nature of any population, there were few
women who experienced more severe depression that further
limits the power.
Maternal low mood may make completion of the modiﬁed
women who successfully completed the ques-
tions relating to their child’s development may be less likely to
experience depression than those nonrespondents. However,
this would probably result in an underestimation of any asso-
ciation. Moreover, the identiﬁcation of those women with
depression was undertaken prior to the analysis of the out-
come. Typically, within large-scale studies, most of the data
relied on maternal (or parental) report. There is always the
potential for some effect of reporter bias, e.g. depressed
mothers not recognising their children’s abilities. However,
the ﬁndings are broadly consistent with an earlier study that
looked at associations between women at risk of antenatal
depression and child development in a socio-economically
deprived population, independent of postpartum depression,
where child development was assessed using a trained assessor,
not by parental completion as in this study.
analysis was undertaken imputing missing data, which sug-
gested missing data were not biasing the results.
Generalisability of the study ﬁndings
This was a large community-based population sample that
was followed-up for 18 months. The prevalence estimates
of probable depression, as assessed by a screening tool both
antenatally and postpartum, are similar to those reported in
Comparison is difﬁcult because few studies
have been undertaken on prospectively collected antenatal
depression data. Those that have, found no association with
antenatal depression and preschool children’s development
after adjusting for postpartum depression.
number of women with antenatal depression in these studies
was small. As mentioned above, the ﬁndings are broadly con-
sistent with an earlier study that looked at associations
between women at risk of antenatal depression and child
development in a socio-economically deprived population,
independent of postpartum depression.
Our results also ﬁt
with other studies that reported associations between post-
partum depression and child development
and, using the
ALSPAC data, between antenatal anxiety and children’s emo-
tional and behavioural problems.
Our ﬁndings are also consistent with studies on rodents and
nonhuman primates, which indicate that maternal anxiety
during pregnancy can inﬂuence the developing fetus, resulting
in delay in motor and cognitive development and impaired
adaptation to stressful situations.
Moreover, studies have
shown a link between antenatal anxiety and cognitive, behav-
ioural and emotional problems in children, after adjusting for
These results support a fetal program-
ming hypothesis whereby biological systems adapt to environ-
mental input during sensitive periods of development, e.g. the
anxiety experienced by the mother has a direct
inﬂuence on the development of the hypothalamic–pituitary–
adrenal axis in the fetus.
Chronic maternal distress compro-
mises the normal regulations of hormonal activity during
pregnancy. Additionally, children of depressed mothers may
inherit directly a vulnerability to depression.
It has also been
suggested that the magnitude of the long-term effects of ante-
natal maternal anxiety in the child could be substantial.
Postpartum depression is a known risk factor for behav-
ioural/emotional problems in children, but it is less clear
whether postnatal depression leads to cognitive delay in chil-
dren unless it is prolonged or severe.
depression was included in these analyses, persistent antenatal
depression remained an important risk factor for develop-
mental delay and this is likely to be magniﬁed for those
who might be diagnosed as clinically depressed. This implies
that this association is unlikely to be fully explained by raised
postnatal depression in those women who experienced ante-
natal depression. Therefore, some effects on child develop-
ment attributed to postpartum depression may be caused in
part by depression in pregnancy.
Implications of the study
These ﬁndings add to the growing body of research, suggest-
ing that maternal psychological wellbeing during pregnancy
has important consequences for child development. Women
who are between 15 and 44 years form a group in which
depression is the leading cause of disease burden worldwide.
Therefore, obstetricians, midwives and GPs can play an active
role in assessing and identifying maternal depression.
Family and personal histories of depression and postpartum
depression are known risk factors, and therefore, the use of
these by healthcare professionals may be helpful in identifying
women at risk. This is highly relevant for practice because
maternal mental health problems are associated with the
health of women’s partners, their children’s health, develop-
ment and use of health services.
We are extremely grateful to all the families who took part in
this study, the midwives for their help in recruiting them and
the whole ALSPAC team, which includes interviewers, com-
puter and laboratory technicians, clerical workers, research
scientists, volunteers, managers, receptionists and nurses.
The UK Medical Research Council, the Wellcome Trust and
the University of Bristol provide core support for ALSPAC.
Antenatal depression: impact on child development
ª 2008 The Authors Journal compilation ª RCOG 2008 BJOG An International Journal of Obstetrics and Gynaecology 1049
This publication is the work of the authors and will serve as
guarantors for the contents of this paper. T.D. is funded by
a Higher Education Funding Council for England postdoc-
toral fellowship from the University of the West of England,
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