Maternal Postnatal Depression and the Development of Depression in Offspring Up to 16 Years of Age

NEW RESEARCH

Maternal Postnatal Depression and the Development of Depression in Offspring Up to 16 Years of Age Lynne Murray, Ph.D., Adriane Arteche, Ph.D., Pasco Fearon, Ph.D., D.Clin.Psy., Sarah Halligan,

D.Phil.,

Ian Goodyer,

M.D.,

Peter Cooper,

D.Phil., D.Clin.Psych.

Objective: The aim of this study was to determine the developmental risk pathway to depression by 16 years in offspring of postnatally depressed mothers. Method: This was a prospective longitudinal study of offspring of postnatally depressed and nondepressed mothers; child and family assessments were made from infancy to 16 years. A total of 702 mothers were screened, and probable cases interviewed. In all, 58 depressed mothers (95% of identified cases) and 42 nondepressed controls were recruited. A total of 93% were assessed through to 16-year follow-up. The main study outcome was offspring lifetime clinical depression (major depression episode and dysthymia) by 16 years, assessed via interview at 8, 13, and 16 years. It was analysed in relation to postnatal depression, repeated measures of child vulnerability (insecure infant attachment and lower childhood resilience), and family adversity. Results: Children of index mothers were more likely than controls to experience depression by 16 years (41.5% versus 12.5%; odds ratio ⫽ 4.99; 95% confidence interval ⫽ 1.68 –14.70). Lower childhood resilience predicted adolescent depression, and insecure infant attachment influenced adolescent depression via lower resilience (model R2 ⫽ 31%). Family adversity added further to offspring risk (expanded model R2 ⫽ 43%). Conclusions: Offspring of postnatally depressed mothers are at increased risk for depression by 16 years of age. This may be partially explained by within child vulnerability established in infancy and the early years, and by exposure to family adversity. Routine screening for postnatal depression, and parenting support for postnatally depressed mothers, might reduce offspring developmental risks for clinical depression in childhood and adolescence. J. Am. Acad. Child Adolesc. Psychiatry, 2011;50(5):460 – 470. Key Words: maternal depression, adolescent depression, attachment, resilience, adversity

A

t least one-third of people experience a major depressive episode during their lifetime,1 and for many individuals the experience is persistent.2 Understanding the development of depression is, therefore, an important public health issue. This is especially true when first onset occurs in the school-age years, as such episodes are associated with particularly poor outcome in terms of severity, chronicity, and recurrence.3-5 The association between lifetime depression in mothers and offspring affective disorders is strong.6,7 Studying the develop-

This article is discussed in an editorial by Dr. David Reiss on page 431.

ment of children of depressed parents might therefore help to elucidate the mechanisms involved in transmission of disorder. Recent twin and adoption studies indicate that the association between parent depression and depression in juvenile offspring is mediated predominantly by environmental mechanisms,8,9 and suggest an important role for family adversity (e.g., parenting difficulties, marital conflict).6 Nevertheless, key questions remain. One question concerns timing of offspring exposure to maternal depression and, specifically, whether risk might be especially raised when exposure occurs in infancy, when dependency on the mother is maximal. The second question is the need to identify the psychological pathways to disorder in offspring, especially those established early in de-

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velopment. Here, we examine these issues in a longitudinal study of the development of children of postnatally depressed mothers. With regard to timing, three previous studies have found exposure before 2 years of age to be associated with increased offspring depression by adolescence10-12; however, whereas one study11 showed this to be sufficient albeit not necessary, the other two studies found overall duration of maternal depression to account for the association between early maternal depression and adolescent disorder. With regard to psychological pathways to depression, although none of the three previous reports examined early child psychological functioning, wider research suggests that insecure attachment to the mother in infancy, well-established as associated with PND,13 might confer initial psychological vulnerability. This is because attachment insecurity has been found to predict a constellation of cognitive, affective and behavioral processes in school-aged children, termed low “ego resiliency.”14,15 This constellation is characterised by inflexibility in the face of changing and stressful circumstances, and difficulty in recovering from challenge or failure.16 Notably, it shares core characteristics with a profile of cognitive vulnerability for depression (e.g., negative affect, feelings of unworthiness, low self-aspirations), as well as with temperamental dimensions considered to raise risk for depressive disorder (e.g., negative emotionality, failure to persist with endeavor, and low effortful control).17 To date, however, although infant insecurity has been found to predict clinical depression by age 17 years,18,19 this intervening developmental pathway through which depression might ultimately emerge has not been examined. Importantly, and consistent with evidence on family risk factors for offspring depression,6 longitudinal research has shown that poor child outcome following infant insecure attachment is substantially more likely when the child is exposed to further family problems.19,20 Because PND is commonly associated with family adversity, this suggests that any child psychological vulnerability for depression associated with PND is similarly likely to be increased by ongoing environmental adversities. Studying longer-term adversity effects is not only important for improving the prediction of child outcome but also for clarifying the clinical significance of the postnatal episode. As noted above,10-12 previous re-

search has suggested that the association between PND and adolescent depression may actually be mediated by the effects of later maternal depression, a conclusion with important implications for intervention strategies. The current paper reports a prospective longitudinal study of a community sample in which mothers either experienced PND, or else formed a control group of non–postnatally depressed mothers. Uniquely, the design incorporates directly observed measurements of infant attachment and a childhood behavioral profile akin to previous accounts of ego resilience, as well as assessment of family adversities (subsequent maternal depression, poor maternal support for the child, marital conflict), and repeated assessments of child psychiatric disorder (at 8, 13, and 16 years). The overarching aim was to identify a developmental risk pathway from infancy to the emergence of depression by 16 years of age. Specifically, we tested whether (i) relative to controls, offspring exposed to PND had an increased rate of depression (major depression or dysthymia); (ii) offspring depression was predicted by insecure infant attachment and expressions of lower ego resilience in childhood; and (iii) family adversity beyond the postpartum period increased risk for offspring depression. Because these different processes likely act in concert and influence each other over time, and could directly affect offspring outcome or operate by indirect, mediating, relationships, we took a developmental approach, using structural equation modeling (SEM). SEM is ideal for measuring relationships between variables across time while controlling for earlier influences, and for exploring multiple pathways simultaneously, including indirect effects. Here, we aimed to test two indirect effects: first, that insecure infant attachment would influence offspring depression via lower child resilience; and second, that longer-term family adversities would account for the association between PND and offspring depression.

METHOD Participants Mothers (and children) were recruited at 2 months postpartum, and assessments conducted at 18 months, and 5, 8, 13 and 16 years. Initially, a community sample of mothers on postnatal wards of the Cambridge (UK) maternity hospital (N ⫽ 702) was screened with the Edinburgh Postnatal Depression

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Scale21 at 6 weeks postpartum. The response rate was 97%. Mothers were primiparous, aged 18 to 42 years, were cohabiting or married, and had healthy, full-term infants. The Standardized Psychiatric Interview22 (SPI), modified according to Research Diagnostic Criteria,23 was administered to probable cases at 8 weeks. Of the women, 61 (9.4%) were identified as depressed, of whom 58 (95%) were recruited. A total of 42 mothers, randomly selected from the remaining women, were similarly interviewed and recruited as controls if they had no history of depression. We have previously reported that index group offspring showed more insecure attachment in infancy,24 signs of depressive cognitions at 5 years,25 and emergence of affective disorder, principally anxiety, by 13 years.10 Here, we provide novel data on adolescent psychiatric outcomes at age 16 years (53 index and 40 control) and the trajectory to depression from earlier psychological vulnerability and family adversity. The study was approved by the Cambridge Medical Ethics Committee; participants gave written informed consent.

Offspring Measures Infant Attachment. At 18 months, infant attachment was assessed using Ainsworth’s Strange Situation Procedure,26 a standardized observational measure of infant responses to maternal separation and reunion in an unfamiliar environment. This is a reliable measure that is used widely in research. Infants were classified as secure or insecure.24 Child Ego Resilience. At 5 and 8 years, the children were videotaped, with a same-aged friend, during a competitive card game, in which the aim is to accumulate “snap” deals (pairs of identical cards).25 Each child received the same number of losing and winning deals, administered in a predefined order. Trained researchers who were blinded to other information scored, on five-point scales, the study child’s behavior on losing deals. Ratings included emotional and behavioral responses (i.e., expressions of sadness and distress, failure to persist) and spoken cognitions expressing negative self-attributions or pessimism (e.g., “I always lose at card games”).25 The mean of negative minus positive scores (range ⫺5 to ⫹5) was computed as an index of low ego resilience comparable to that used in previous studies. Offspring Mental State. At 16 years, diagnostic interviews were conducted by a clinical researcher blind to maternal state using the Kiddie Schedule for Affective Disorders and Schizophrenia, Present and Lifetime Version (KSADs).27 The same assessments had been conducted at 8 and 13 years with mother and child.10 All interviews were discussed with a clinical team, and a consensus diagnosis made, with best estimate judgements made based on all available clinical information.

For the 8-year assessment, the current and previous 12 months’ mental state was determined; and at 13 and 16 years, both the current mental state and that since the previous assessment were ascertained. For major depressive disorder, timing of onsets was recorded on a month-by-month basis. Information from these three interviews was pooled to establish offspring lifetime occurrence of disorder.

Maternal and Family Adversity Measures Maternal Mental State. Maternal depression was assessed using the SPI at recruitment, the Schedule for Affective Disorder and Schizophrenia—Life-time version28 at 18 months and 5 years, and the Structured Clinical Interview for DSM-IV29 at 8, 13, and 16 years. Each time, maternal mental state since the previous occasion was assessed; timing of onsets and offsets was recorded by month and used to compute overall duration. Duration of child exposure exclusive of PND was defined as the number of months the mother was depressed beyond 4 months postpartum (when 55% had remitted) up to the child’s onset of depression (or to 16-year interview, if none). At 16 years, only 19.3% depressed mothers received treatment; of these, 64.3% were prescribed antidepressants. Interviews were administered by trained researchers, and reviewed by a clinical team blinded to child diagnoses. Maternal Support. At 5 and 8 years, mother– child interactions were video recorded in conditions requiring maternal support for the child. At 5 years, this comprised a 10-minute snack, in which the child needed help to manage the refreshments; at 8 years it comprised a 20-minute math problem task. Interactions were scored by trained raters, blinded to group, using a scheme tailored to child age and task demands, to measure maternal emotional support, and included ratings of warmth, acceptance, sensitive responsiveness, and availability.30,31 Marital Conflict. At each assessment, marital conflict was assessed using a combination of interview (the Life Events and Difficulties Schedule32) and questionnaire (the Dyadic Adjustment Scale33). Each provided a binary measure denoting significant conflict; these were summed to give a continuous measure of conflict up to 13 years. Conflict showed considerable continuity, the mean correlation between assessments being ␾ ⫽ 0.46 (range, 0.32– 0.63).

Data Analysis We first established whether PND was associated with offspring depression, then used logistic regression and analysis of variance to examine (i) main effects of PND on insecure infant attachment and lower ego resilience at 5 and 8 years, and (ii) the association between PND and family adversity (duration of maternal depression, poor maternal support, marital conflict). In turn, we

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TABLE 1

Prevalence of Lifetime Psychiatric Diagnosis by Maternal Group and by Child Gender % Total Sample

Axis 1 diagnosis Any Depressive disorder Any MDE Dysthymia Anxiety disorder Any Specific phobia GAD OCD Social phobia Separation anxiety Agoraphobia Panic PTSD Behavioral disorder Any ADHD ODD Conduct Disorder

Control

PND

Total (N ⴝ 93)

Female (n ⴝ 48)

Male (n ⴝ 45)

Total (n ⴝ 40)

Female (n ⴝ 20)

Male (n ⴝ 20)

Total (n ⴝ 53)

Female (n ⴝ 28)

Male (n ⴝ 25)

41.9

47.9

35.6

27.5

35.0

20.0

52.8

57.1

48.0

29.0 26.9 4.3

35.4 33.3 6.3

22.2 20.0 2.2

12.5 12.5 2.5

20.0 20.0 5.0

5.0 5.0 0.0

41.5 37.7 5.7

46.4 42.9 7.1

36.0 32.0 4.0

24.7 12.9 5.4 5.4 3.2 2.2 2.2 1.1 1.1

33.3 14.6 6.3 8.3 4.2 2.1 2.1 2.1 2.1

15.6 11.1 4.4 2.2 2.2 2.2 2.2 0.0 0.0

15.0 7.5 0.0 2.5 2.5 0.0 0.0 0.0 2.5

20.0 10.0 0.0 5.0 0.0 0.0 0.0 0.0 5.0

10.0 5.0 0.0 0.0 5.0 0.0 0.0 0.0 0.0

32.1 17.0 9.4 7.5 3.8 3.8 3.8 1.9 0.0

42.9 17.9 10.7 10.7 7.1 3.6 3.6 3.6 0.0

20.0 16.0 8.0 4.0 0.0 4.0 4.0 0.0 0.0

8.6 5.4 3.2 2.2

4.2 2.1 2.1 0.0

13.3 8.9 4.4 4.4

7.5 5.0 2.5 0.0

5.0 0.0 5.0 0.0

10.0 10.0 0.0 0.0

9.4 5.7 3.8 3.8

3.6 3.6 0.0 0.0

16.0 8.0 8.0 8.0

Note: ADHD ⫽ attention-deficit/hyperactivity disorder; GAD ⫽ generalized anxiety disorder; MDE ⫽ major depressive episode; OCD ⫽ obsessive compulsive disorder; ODD ⫽ oppositional defiant disorder; PND ⫽ postnatal depression; PTSD ⫽ post-traumatic stress disorder.

investigated main effects of these variables on offspring depression, using logistic regression. We then conducted path analyses, using SEM, in two stages. First we examined the effects of PND on offspring depression, taking into account child vulnerability factors; second, we included family adversity factors. SEM analyses were performed using the maximum likelihood estimation with the Mplus 4.2 software.34

RESULTS Mean offspring age was 16.06 years (SD ⫽ 0.18 years; range, 15.75–17.00 years). There were minimal differences between index and control groups regarding socioeconomic status (I, II, and III nonmanual35: 61.5% for control versus 67.9% for PND), child gender (male 50% for control vs 47.2% for PND), and current family status (child resident with both biological parents, 87.5% for control versus 73.6% for PND).

Group Differences in Adolescent Psychiatric Disorder Psychiatric diagnoses occurring by 16 years are reported in Table 1. Index children were more likely than controls to experience Axis 1 disorder (52.8% versus 27.5%, respectively; Wald statistic ⫽ 5.83, odds ratio [OR] ⫽ 2.95, 95% confidence interval [CI] ⫽ 1.23–7.11, p ⬍ .05), and this was accounted for by elevated rates of depression (MDE and dysthymia) (41.5% versus 12.5%; Wald statistic ⫽ 8.39, OR ⫽ 4.99, 95% CI ⫽ 1.68 –14.70, p ⬍ .01), and anxiety disorders (32.1% versus 15%; Wald statistic ⫽ 3.43, OR ⫽ 2.68, 95% CI ⫽ 0.94 –7.59, p ⬍ .10). Although depression occurred in more girls than in boys, the difference was not significant (Wald statistic ⫽ 1.93, OR ⫽ 1.92, 95% CI ⫽ 0.77– 4.81, NS), and neither was the interaction PND by child gender (Wald statistic ⫽ 0.75, OR ⫽ 0.32, 95% CI ⫽ 0.03– 4.12, NS). Average age of first onset of depression was 13.81 years (SD ⫽ 1.40), the earliest being at 11.92; there was no gender difference in age of first

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episode (boys’ mean ⫽ 14.20, SD ⫽ 1.53; girls’ mean ⫽ 13.58, SD ⫽ 1.32; t(25) ⫽ 1.12, NS). Among those who were depressed, 59.3% (n ⫽ 16) had also had an anxiety diagnosis at some point. Girls more often experienced anxiety than boys (Wald statistic ⫽ 3.79, OR ⫽ 2.71, 95% CI ⫽ 0.99 –7.41, p ⬍ .05), but there was no interaction PND by gender on anxiety (Wald statistic ⫽ 0.06, OR ⫽ 1.33, 95% CI ⫽ 0.15–12.07, NS). Behavior disorders were uncommon and were comparable in the two groups (Wald statistic ⫽ 0.11, OR ⫽ 1.28, ⫽ 95% CI ⫽ 0.29 –5.72, NS). Group Differences in Child Vulnerability and Family Adversity, and Their Prediction to Adolescent Disorder Table 2 shows the effects of PND, child gender, and their interaction on child vulnerability and family adversity measures. Infant Attachment (Secure Versus Insecure). As reported previously,24 index group infants were more likely to be insecurely attached than were controls, and boys were more likely to be insecure than were girls. There was a trend for a PND by gender interaction, with boys of PND mothers being more frequently insecure. Child Ego Resilience (Lower Versus Higher). PND was associated with expressions of lower ego resilience at 5 years,25 and this tended to be the case at 8 years, with index group boys again being particularly affected. Prediction of Depression by 16 Years. As shown in Table 2, both infant insecure attachment and lower ego resilience at 8 years predicted offspring depression; lower ego resilience at 5 years tended to do the same. Family Adversity. As shown in Table 2, PND tended to be associated with poorer maternal support for the child at 5 years and was also associated with the duration of maternal depression and marital conflict. Poorer maternal support at 8 years was not predicted by PND. Prediction of Depression by 16 Years. As shown in Table 2, poor maternal support at 5 years predicted offspring disorder, but 8-year support did not, and so was not considered further. Marital conflict and duration of maternal depression were significantly associated with offspring lifetime depression. Path Analyses The first model focused on the child’s psychological trajectory. Figure 1a shows the hypothesized

relationships between model variables: insecure infant attachment and lower ego resilience at 5 and 8 years were each expected to increase risk of offspring depression. PND was hypothesized to have an adverse effect on infant attachment, and on 5- and 8-year ego resilience. Finally, insecure attachment was expected to have an adverse effect on ego resilience. The correlations between these variables, as well as those concerning family adversity, supported these predictions (Table 3). Model acceptability was estimated from the ␹2 statistic, the comparative fit index (CFI), the Tucker-Lewis coefficient (TLI), and the root mean-square error of approximation (RMSEA).36 CFI and TLI values closer to 1.0, and RMSEA values of 0.08 or less, indicate acceptable model fit.37 The initial model including child vulnerability factors showed good fit [␹2(1) ⫽ 0.02, p ⫽ .89; CFI ⫽ 1.0; TLI ⫽ 1.27; RMSEA ⫽ 0.00]. Nevertheless, three paths were weak (r ⬍ 0.10), suggesting their low contribution; therefore we ran a subsequent model without them. This showed similarly good fit [␹2(3) ⫽ 0.43, p ⫽ .93; CFI ⫽ 1.0; TLI ⫽ 1.24; RMSEA ⫽ 0.00]. Figure 1b shows the second model’s standardized regression weights, as well as the three excluded paths (dashed lines). Notably, we had hypothesised that one of these, from insecure infant attachment to offspring depression, would be mediated by lower child ego resilience. Consistent with this, the association between insecure infant attachment and offspring depression dropped substantially when lower ego resilience was included (Sobel’s test Z ⫽ 1.72, p ⫽ .08). In turn, and in line with predictions, the relationship between lower 8-year ego resilience and offspring depression remained substantial (0.32). In combination, child vulnerability factors accounted for 19% of the effect of PND on offspring depression, increasing the explained variance from R2 ⫽ 18% to R2 ⫽ 31%; and the effect of PND on offspring depression dropped from 0.42 (direct association, no potential mediators) to 0.34 when insecure attachment and lower resilience were included. We next extended the model to include family adversity. This showed good fit, and the explained variance in depression increased by 12% [␹2(9) ⫽ 12.66, p ⫽ .18; CFI ⫽ 0.92; TLI ⫽ 0.84; RMSEA ⫽ 0.060; offspring depression R2 ⫽ 43%]. As seen in Figure 2, the direct effect of PND on offspring depression dropped from 0.34 when

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TABLE 2 Postnatal Depression, Gender, and Postnatal Depression by Gender Effects on Child Vulnerability and Family Adversity, and Effects of Each of These on Child Depression Outcome

Control (n ⴝ 40)

PND (n ⴝ 53)

PND, Gender, and PND ⴛ Gender Effects on Child Vulnerability and Family Adversity

Female

Male

Female

PND Effects

Gender Effects

PND ⴛ Gender Effects

25.0%

25.0%

84.0%

46.4%

Ego resilience, 5 y, mean (SD)

1.17 (0.66)

0.67 (0.89)

0.74 (0.83)

0.43 (0.69)

Wald ⫽ 13.11*** OR ⫽ 5.37 CIb ⫽ 2.16-13.33 F(1, 88) ⫽ 4.22*

Wald ⫽ 3.78* OR ⫽ 0.44 CI ⫽ 0.19–1.01 F(1, 88) ⫽ 6.30**

Wald ⫽ 3.33† OR ⫽ 0.16 CI ⫽ 0.02–1.14 F(1, 88) ⫽ 0.35

Ego resilience 8 y, mean (SD)

1.40 (0.65)

1.35 (0.55)

0.83 (0.79)

1.34 (0.85)

F(1, 80) ⫽ 3.17†

F(1, 80) ⫽ 2.08

F(1, 80) ⫽ 2.94†

2.54 (1.05)

2.88 (0.89)

3.06 (0.93)

3.09 (1.02)

F(1, 84) ⫽ 2.91†

F(1, 84) ⫽ 0.81

F(1, 84) ⫽ 0.55

Poor maternal support, 8 y, mean (SD)

1.36 (0.11)

1.40 (0.14)

1.36 (0.10)

1.41 (0.12)

F(1, 81) ⫽ 0.15

F(1, 81) ⫽ 2.48

Duration of MD (mo), mean (SD)

3.00 (4.49)

2.65 (4.54)

13.84 (12.50)

20.61 (15.57)

F(1, 89) ⫽ 37.90***

F(1, 89) ⫽ 1.88

Marital conflict, mean (SD) 1.10 (1.25)

1.10 (1.02)

2.08 (1.32)

2.46 (1.34)

F(1, 89) ⫽ 19.82***

F(1, 89) ⫽ 0.53

a. Child vulnerability Infant insecure attachment (% of insecure)

b. Family adversity Poor maternal support, 5 y, mean (SD)a

Wald ⫽ 3.64* OR ⫽ 2.45, CI ⫽ 0.98–6.18 Wald ⫽ 3.36† OR ⫽ 1.07, CI ⫽ 0.99–1.16 Wald ⫽ 7.67** OR ⫽ 1.07, CI ⫽ 1.02–1.13

Wald ⫽ 3.68* OR ⫽ 1.62, CI ⫽ 0.99–2.65 F(1, 81) ⫽ 0.004 Wald ⫽ 2.00 OR ⫽ 0.08, CI ⫽ .002-4.17 F(1, 89) ⫽ 2.31 Wald ⫽ 7.54** OR ⫽ 1.05, CI ⫽ 1.01–1.08 F(1, 89) ⫽ 0.53 Wald ⫽ 6.78** OR ⫽ 1.58, CI ⫽ 1.12–2.24

Note: CI ⫽ confidence interval; KSADs ⫽ Kiddie Schedule for Affective Disorders and Schizophrenia, Present and Lifetime Version; MD ⫽ maternal depression; PND ⫽ postnatal depression; Wald ⫽ Wald statistic. a Higher scores indicate poorer maternal support. b All confidence intervals at 95%. *p ⬍ .05; **p ⬍ .01; ***p ⬍ .001; †p ⬍ .10.

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Effects of Child Vulnerability and Family Adversity on Child Depression Outcome (KSADs)

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FIGURE 1 (a.) The hypothesized relationship between postnatal depression (PND) and offspring depression, including infant attachment and child resilience. (b.) The final model linking PND to offspring depression, taking into account infant attachment and child resilience. Note: Dashed lines represent weak paths excluded from the final model. Coefficients represent standardized regression weights. Offspring depression n ⫽ 93.

only the child’s psychological trajectory was considered to 0.08 when additional family adversity was included, suggesting that child vulnerability and family adversity accounted for 81% of the effect of PND on offspring depression. Because

TABLE 3

1 2 3 4 5 6 7 8

this model took the intercorrelations among the three adversity factors into account, we examined their individual paths to identify the contribution of each. This showed that duration of maternal depression (Z ⫽ 2.61, p ⫽ .008) and

Relationship Among All Variables

PND Insecure attachment Lower ego resilience, 5 y Lower ego resilience, 8 y Poor maternal support, 5 y Marital conflict Duration of MD Offspring lifetime depression

2

3

4

5

6

7

8

0.39***

0.22* 0.08

0.17 0.25* 0.14

0.18† 0.15† 0.14 0.14

0.28** 0.31** 0.12 0.14 0.23*

0.64** 0.21* 0.28** 0.10 0.29** 0.33**

0.32** 0.20* 0.19† 0.31** 0.20* 0.28** 0.31*

Note: Coefficients represent Pearson or ␾ correlations, as appropriate. Postnatal depression (PND) scored as 0 ⫽ control/1 ⫽ index. Attachment scored as 0 ⫽ secure/1 ⫽ insecure. Offspring lifetime depression scored as 0 ⫽ no depression/1 ⫽ depression. *p ⬍ .05; **p ⬍ .01; ***p ⬍ .001; †p ⬍ .10.

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FIGURE 2 The relationship between postnatal depression (PND) and offspring depression, accounting for child vulnerability and family adversity. Note: Coefficients represent standardized regression weights. Offspring depression n ⫽ 93.

marital conflict (Z ⫽ 2.23, p ⫽ .03) were partial mediators of PND on offspring depression, with PND still being marginally significant when the former was entered in the model (p ⫽ .074), and significant (p ⫽ .03) when marital conflict was included; no such effect obtained for poor maternal support at 5 years (Z ⫽ 1.28, NS). Duration of Exposure to Maternal Depression Given the effect on offspring depression of the overall duration of maternal depression, we were interested in identifying the threshold (if any) whereby such exposure starts to increase risk, over and above the PND effect itself. Thus we disaggregated the total duration of depression beyond 4 months postpartum into quartiles: never subsequently depressed, and depressed between 1 and 7, 8 and 16, and 17 or more months. Only four PND mothers had no subsequent depression (first quartile), and therefore only the remaining quartiles were examined. Effects on offspring depression of exposure versus nonexposure to each of these depression durations was examined in terms of direct and indirect (controlling for PND) ef-

fects. The second and third quartiles showed no effects; however, a main effect of the fourth was observed (Wald statistic ⫽ 10.21, OR ⫽ 5.20 (95% CI ⫽ 1.88 –14.29), p ⬍ .01). Furthermore, when controlling for PND, the fourth quartile was still significantly associated with offspring depression (Wald ⫽ 3.67, OR ⫽ 3.03, 95% CI ⫽ 0.97–9.44), p ⫽ .05; PND Wald ⫽ 3.12, OR ⫽ 3.00 (95% CI ⫽ 0.89 –10.16), p ⫽ .078). We also examined whether the effect of long duration of maternal depression might actually be explained by recent exposure (defined as episodes in the year before offspring onset). Although there was a modest association between the two measures (r ⫽ .23, p ⫽ .028), recent maternal episodes were unrelated to offspring depression (t ⫽ ⫺1.20, NS); and when both variables were considered jointly, only the fourth quartile duration was significant, indicating that its effects were not explained by recent exposure (recency: Wald statistic ⫽ 0.43, OR ⫽ 1.07, 95% CI ⫽ 0.87–1.31, NS; fourth quartile duration: Wald statistic ⫽ 9.57, OR ⫽ 5.27, 95% CI ⫽ 1.83–15.12, p ⫽ .002).

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Anxiety ⫻ Depression Lifetime Diagnosis Given the association between PND and offspring anxiety, we explored whether our model also applied to anxiety, testing each target predictor in relation to this outcome. Only marital conflict was significant (Wald statistic ⫽ 8.34, OR ⫽ 1.73, 95% CI ⫽ 1.19 –2.52, p ⬍ .01), suggesting that this form of adversity might contribute to the development of both disorders, whereas the child developmental trajectory elucidated in the present study may be relatively specific to depression.

DISCUSSION We report the occurrence of clinical depression in a community sample of adolescents within a prospective longitudinal study that uniquely included direct investigation of interpersonal psychology (mother–infant attachment) and indices of low resilience under social stress. Furthermore, we examined the role of ongoing family adversity to establish the extent to which it added to child risk, and accounted for any association between maternal PND and child disorder. In line with other studies,11,12 we found offspring of postnatally depressed mothers to be at substantially increased risk for depression themselves; furthermore, their rate of life-time depression by age 16 was slightly more than 40%, consistent with evidence on adolescent offspring of depressed parents in general,6,7 as was their age at first onset (typically after age 12), and frequent anxiety disorder.3,4 As predicted, we found insecure attachment to the mother in infancy to predict depression in adolescence; furthermore, this association arose largely via lower child ego resilience, as expressed in a constellation of cognitive–affective– behavioral features, elicited under conditions of social challenge, some years before first onset of depression. To our knowledge, this represents the first demonstration of this trajectory from infancy through to adolescence. Notably, however, continuing family adversity (poor maternal support, marital conflict and prolonged maternal depression) added substantially to offspring risk. In our sample, boys of depressed mothers were rather more likely than girls to be insecure and less resilient, possibly reflecting a more general vulnerability to PND.38 This might account for the somewhat smaller than usual gender difference in the rate of depression in our sample.39

We found marital conflict and further maternal depression to be partial mediators of the effects of PND on adolescent depression. With regard to the latter, however, only maternal depression accumulating for more than 17 months beyond the postnatal period added significantly to offspring risk, and even such prolonged subsequent maternal depression did not entirely eliminate the association between the postnatal episode and offspring depression. In our study, therefore, the presence of PND does seem to have been of particular importance for offspring outcome. It should be noted, though, that we recruited a relatively low-risk sample; given greater socio-economic adversity,12 such unique effects of the postnatal episode might be eclipsed by subsequent family difficulties. Although our study focussed on the development of depression, we investigated whether the same trajectory held for anxiety. Offspring anxiety was also predicted by PND, and it occurred in more than half those offspring who experienced depression. Nevertheless, apart from PND, the only predictor associated with both offspring disorders was marital conflict, an established risk for child anxiety, as well as depression.40 The fact that neither insecure attachment nor lower child ego resilience predicted anxiety was not surprising: With regard to attachment, insecure infants in our sample showed either an avoidant or a resistant pattern (with avoidant being far more common (86% of insecure infants),24 the same combination that predicted depression in the Minnesota study.19 Anxiety, by contrast, has been linked more commonly to resistant insecure attachment.41 Moreover, our measure of low ego resilience, as in the wider literature,15,16 subsumed cognitions and temperamental features associated with vulnerability to depression (e.g., pessimism, low self-worth, lack of persistence, and flexibility), as well as sad affect, rather than behaviors and cognitions more specific to anxiety. Thus, although anxiety and depression are highly comorbid, our findings, in common with those of others,42 do suggest some etiological specificity. Our study had a number of strengths, including direct assessments through childhood, repeated diagnostic interviews, and high sample retention. Nevertheless, some limitations applied. First, our relatively small sample size restricted the analyses that could be conducted (e.g., insecure attachment subtype effects). Fur-

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thermore, although recent research has shown that the association between parent and juvenile depression is mediated predominantly by the environment,8,9 it was a study limitation that we could not address the issue of possible genetic contributions to offspring disorder; and information was not collected on maternal antenatal risk (e.g., alcohol/drug use) or mental state, factors increasingly recognized as important in understanding effects of postnatal disorder.43 The substantially raised risk for depression among offspring of postnatally depressed mothers underlines the importance of screening for PND and of delivering early interventions. Moreover, as this risk could, in part, be traced back to infant insecure attachment to the mother, and as treatments directed only at alleviating maternal depression do not appear to benefit the mother– child relationship,44 interventions focussing on promoting good parental care are desirable. Evidence for the benefits of these is accumulating.45-47 Our findings regarding subsequent maternal depression also suggest, however, that where mothers experience postnatal depression, long-term monitoring and support might also be important. Furthermore, as marital conflict con-

stituted an important component of risk for both offspring depression and anxiety and, in line with wider research,32 was significantly associated with maternal depression, interventions might need to be tailored accordingly, possibly also encompassing the paternal depression commonly associated with maternal disorder and marital conflict.48 & Accepted February 3, 2011. Drs. Murray, Arteche, Fearon, Halligan, and Cooper are with the University of Reading, School of Psychology and Clinical Language Sciences, Reading, UK. Dr. Goodyer is with University of Cambridge, Cambridge, UK. The study was supported by grants from the Medical Research Council (G9324094) and the Tedworth Charitable Trust (TED76). The authors thank Sheelah Seeley, Janet Edwards, and Joseph Murray of the University of Cambridge for assistance in manuscript preparation. Disclosure: Drs. Murray, Arteche, Fearon, Halligan, Goodyer, and Cooper report no biomedical financial interests or potential conflicts of interest. Correspondence to Dr. Lynne Murray, School of Psychology, University of Reading, Reading, RG6 6AL, UK; e-mail: lynne. [email protected] 0890-8567/$36.00/©2011 American Academy of Child and Adolescent Psychiatry DOI: 10.1016/j.jaac.2011.02.001

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