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In general, depressed mothers experience more environmental and family risk factors, and lead riskier lifestyles, than mothers who are not depressed.
To test whether the exposure of the child to risk factors associated with mental health adds to the prediction of child psychopathology beyond exposure to maternal depression.
In 7,429 mother-offspring pairs participating in the Avon Longitudinal Study of Parents and Children in the United Kingdom, maternal depression was assessed at child age 1.5 years; multiple risk factor exposures were examined between birth and child age 2 years; and DSM-IV based externalizing and internalizing diagnoses were evaluated at child age 7.5 years.
Children of depressed mothers were exposed to more risk factors associated with maternal mental health. Maternal depression increased diagnoses of externalizing and internalizing disorders, but a substantial portion of these associations was explained by increased risk factor exposure (37% and 41%, respectively). At the same time, these risk exposures significantly increased the odds of both externalizing and internalizing diagnoses, over and above the influence of maternal depression.
Children of depressed mothers are exposed to both maternal psychopathology and risks that are associated with maternal mental health. These results may explain why treating depressed mothers shows beneficial effects for children, but does not completely neutralize the increased risk of psychopathology and impairment.
Maternal depression is a significant public health concern due to its negative impact on both the mothers and their children (1). Rates of depression in females peak during pregnancy and in the early postnatal years (2). Though this is an established trend, depression is not randomly distributed across mothers; instead, past studies suggest that compared to women who are not depressed, depressed mothers are exposed to higher rates of cumulative life-stressors including socio-economic disadvantage (3), family violence and low social support (1) and they tend to follow riskier life-course pathways characterized by low educational attainment, teen pregnancy, substance use, and criminal behaviors (4).
The behavior and life circumstances of a depressed individual can affect the lives of others around them (5). Maternal depression is thought to disrupt normative child development by impairing the ability of the mother to parent in a warm, consistent and sensitive manner (6). Indeed, it is well established that young children of mothers who are depressed are at increased risk for emotional problems, disruptive behaviors, and attention and cognitive problems (4, 7). Yet, to our knowledge, very few studies have examined the alternative explanation that psychopathology in the offspring of depressed mothers may in part be due to higher exposure to the environmental, family and maternal risks. Research has suggested that children of depressed mothers may be exposed to a number of risks closely associated with maternal dysfunction (8, 9) – and that these risks may have equal or greater impact on early child psychopathology than depression in the mother (10-12). Moreover, although it has been reported that remission of a mother’s major depression (after treatment) is significantly associated with reductions in her child’s symptoms of psychopathology, these reductions were significantly less for children of depressed mothers who were experiencing the most severe environmental risks, and were less responsive to treatment (13). Hence, from a clinical perspective, risks associated with mental health in the mother may contribute to child psychiatric diagnosis, in addition to depression in the mother.
In the present research, we sought to examine, within a prospective epidemiological sample of 7,429 mother-child pairs from varied socio-economic and risk backgrounds, the predictive impact of maternal depression (child age 1.5 years) and risk exposure of the child (0-2 years) on the child’s externalizing and internalizing DSM-IV-based diagnoses at 7.5 years. We focused on maternal depression and associated risks within the first few years of the child’s life because during this age period the child is particularly dependent on the parenting/behavior of the mother (14), which relates to achieving developmental milestones, such as cognitive maturation and development, and early social and emotional competence (15). We expected that exposure to risk factors associated with mental health in the mother would increase risk for child psychopathology above and beyond effects directly attributable to depression in the mother.
The Avon Longitudinal Study of Parents and Children (ALSPAC) is an ongoing population-based study designed to investigate the effects of a wide range of influences on the health and development of children. Pregnant women resident in the former Avon Health Authority in southwest England, having an estimated date of delivery between 1 April 1991 and 31 December 1992, were invited to take part, resulting in a cohort of 14,541 pregnancies and 13 988 singletons/twins alive at 12 months of age. When compared to 1991 National Census Data, the ALSPAC sample was found to be similar to the UK population as a whole (15). Ethical approval for the study was obtained from the ALSPAC Law and Ethics Committee and the Local Research Ethics Committees. More detailed information on ALSPAC is available from the website: http://www.bris.ac.uk/alspac/.
Mothers completed questionnaires at multiple time points during their pregnancy and their child’s infancy and childhood. The early risk factors examined here were drawn from questionnaires completed between birth and approximately 2 years of child age. Our previous research has demonstrated the validity of the risks presented below (16, 17).
Descriptive statistics for the sample overall are presented in Table 1. Mother ethnicity was recorded at 18 weeks gestation. Child birth weight and birth complications (e.g., abruption, preterm rupture, cervical suture) were recorded at birth. Birth complications were dichotomized to contrast mothers with any complications (1) versus those without (0). Parity was obtained at 18 weeks gestation from a series of questions about previous pregnancies. Multiparous mothers were coded 1 and primiparous mothers were coded 0.
Maternal depression at child age 21 months (1.5 years) was assessed with the Edinburgh Postnatal Depression Scale, a widely used 10-item self report questionnaire that has been shown to be valid in and outside the postnatal period (18, 19). A cutoff of 13 was used because it predicts a clinical diagnosis of depression (19). Nine percent of the mothers included in this study (n = 662 of 7,429) were identified as clinically depressed at child age 1.5 years.
Environmental risk factors consisted of mother reports of low SES (assessed at 18 weeks) and inadequate living conditions (assessed at 8 and 21months). Poverty was coded via the Registrar General’s social class scale (20); we compared mothers in classes IV and V (low SES) with those in classes I, II and III. Inadequate living conditions were coded via any indication of not having a working bath/shower, no hot water, no indoor toilet and/or no working kitchen.
Family risk factors consisted of maternal reports of: (i) being a single care-giver (e.g., not cohabiting, not in a relationship [assessed at 8 months]); (ii) experiencing partner cruelty (e.g., any indication of emotional and/or physical abuse from partner [assessed at 2, 6 and 21 months]); (iii) low partner affection (e.g., partner does not show affection, does not hug/kiss, low intimate bond [assessed at 8 months]); (iv) low emotional support (e.g., having no one to discuss feelings with [assessed at 2 and 8 months]); and (v) low practical support (i.e., whether there is anyone who could lend the mother £100 and/or the mother could turn to in times of trouble [assessed at 2 and 8 months]).
Maternal lifestyle risk factors consisted of mother reports of: (i) early parenthood (19 years or younger [assessed at 18 weeks]); (ii) low educational attainment (e.g., did not finish mandatory schooling [assessed at 32 weeks prenatal]); (iii) substance use (e.g., any indication of the use of hard drugs, alcoholism, and/or consuming more than 2 pints of beer a day [assessed 2, 8 and 21 months]); and (iv) crime trouble with police (any indication that this has happened [assessed at 2, 8 and 21 months]).
A cumulative risk index was created by summing the individuals risks described above (range: 0-11). A cumulative risk index is consistent with the idea that: (i) although the effect of one risk might be weak, the effects of multiple risks can be quite large; and (ii) because risks tend to cluster together, the number of risks, but not a particular risk, will explain greater variance in the adjustment outcome (21).
DSM-IV psychiatric child diagnoses at ages 7-8 years (7.5 years), were measured using the Development and Well-Being Assessment (DAWBA), a well-validated measure developed for the British Child Mental Health surveys (22). The DAWBA generates preliminary DSM-IV psychiatric diagnoses for ages 5-17 years using a well defined computerized algorithm (see www.dawba.com) drawing on symptom reports from all available reporters. Experienced clinical raters then review all the data available for each child (including free text comments made by respondents), and decide whether to accept or overturn the computer-generated diagnoses. Chance-corrected agreement between the two clinical raters who independently rated DAWBA data for 500 children in the first British Child Mental Health Survey was 0.86 for any disorder (SE 0.04), 0.57 for internalizing disorders (SE 0.11), and 0.98 for externalizing disorders (SE 0.02) (Ford, Goodman & Meltzer, 2003).
An adapted self-completion version of the DAWBA (including prompts for free-form comments) was devised for use in ALSPAC, and the clinical ratings were undertaken by the same two experienced clinicians as completed the ratings in the British national survey (Professor Robert Goodman, who developed the DAWBA, and Dr Tamsin Ford). For externalizing disorders (reported by parents and teachers), we examined diagnoses of conduct disorder (CD), oppositional defiant disorder (ODD) and any attention deficit-hyperactivity disorder (ADHD) (including hyperactive, inattentive and combined sub-types, and ADHD not otherwise specified). With regard to internalizing disorders (reported by parents), we used diagnoses of anxiety and depression.
Of the original 14,541 mothers, a total of 10,141 mothers reported on their depression at child age 1.5 years. Diagnostic DAWBA assessment was available for 8,110 (externalizing) and 8,141 (internalizing) children. A total of 7,429 mothers had reports on depression and internalizing disorders and the DAWBA diagnoses. In a multivariate logistic regression, we tested the study variables as predictors of exclusion (n = 7112) versus inclusion (n = 7,429). Odds ratios (ORs) showed that mothers excluded from the present analysis were more likely to be depressed (OR = 1.22; 95% CI: 1.08 – 2.01), to be young mothers (OR = 1.91; 95% CI: 1.83-2.54), to have financial difficulties (OR = 1.32; 95% CI = 1.18 – 1.87), to have reported low partner affection (OR = 1.65; 95% CI: 1.42 – 1.92), and to have reported crime trouble with police (OR = 1.51; 95% CI: 1.05 – 2.23) than mothers included in the analyses; their children were also more likely to have an externalizing disorder (OR = 1.70; 95% CI: 1.54 – 1.90). Nine of the 11 risks had minimal missing responses (i.e., n = 0 to 3), whereas substance use (n = 122) and partner affection (n = 443) showed higher rates. Missing data in substance use and partner affection, within the cumulative risk scale, was replaced by a one-off imputation using a multiple imputation procedure (PROC MI) in the statistical software, SAS v9.1 (23).
The analysis proceeded in two main steps. In the first step, we compared the children of mothers with and without depression on exposure to each risk factor. We also verified that early maternal depression was associated with increased odds of externalizing (i.e., ADHD, ODD, CD) and/or internalizing (anxiety, depression) disorders. In the second step, to maximize power, we collapsed ADHD, ODD and CD into Any Externalizing Diagnosis, and anxiety and depression into Any Internalizing Diagnosis. We then examined: (i) the effect of maternal depression alone; and (ii) the reduction in the effect of maternal depression when controlling for cumulative risk as well as the independent effect of risk. The cumulative risk index was treated as continuous in this analysis, and the significance of the reduction in risk for a child psychiatric diagnosis was assessed with Sobel’s test (24). The percentage decrease in the OR was computed as (ORuncorrected − ORcorrected)/(ORuncorrected − 1)*100%.
Analyses were conducted in SAS v9.1 (23). ORs from logistic regressions are reported in the Results.
The top portion (part A) of Table 2 presents the rates of risk factor exposure in children of mothers with and without depression. Children of depressed mothers were significantly more likely to be exposed to 10 of the 11 risk factors, compared to their counterparts with non-depressed mothers. The middle portion of Table 2 (part B), contains the cumulative risk index (i.e., the sum of all risk factors). The difference in exposure to cumulative risks for the children of depressed vs. non-depressed mothers was large. On average, children of depressed mothers were exposed to 2.3 risk factors, whereas children of non-depressed mothers were exposed to 1 risk factor.
The bottom portion of Table 2 (part C) presents the extent to which maternal depression (compared to non-depression) was associated with an increase in the odds of diagnoses of ADHD, ODD, CD, anxiety and/or depression in children. Maternal depression increased the odds of all diagnoses. We note here, however, that the base rates for CD and depression were low.
Table 3 contains the effect of maternal depression on diagnoses of externalizing and internalizing disorder, with and without controlling for the cumulative risk index as a covariate. Maternal depression increased the odds of both externalizing and internalizing disorders (Step 1 in Table 3). When the cumulative risk index was added to the equation (Step 2), the impact of maternal depression was significantly reduced (i.e., 41% reduction for externalizing and 37% reduction for internalizing). Yet, both exposure to maternal depression and exposure to the cumulative risks remained significant predictors of increased odds of both externalizing and internalizing disorder in the child (see Step 2).
Using a large longitudinal cohort, we provide evidence that psychopathology in the offspring of depressed mothers is influenced by additional risk exposures closely associated with maternal mental health. More specifically, the present study underscores that, in addition to the debilitating effects of depression in the mother, multiple risk exposures strongly affect child psychopathology – with exposure to each additional risk factor there was at least a 20% increase in the odds for an externalizing and internalizing disorder in boys and girls (see Table 3). For example, a child with three risks factors increased his or her odds for a disorder by approximately 80% (i.e., 1.20*1.20*1.20). These epidemiological data suggest that addressing both maternal depression and associated risk factors may be the most effective manner by which to prevent adverse outcomes in the offspring, and that studies that consider the effect of maternal depression may benefit from also considering other risk factors associated with the mother’s mental health.
As stated, few published research efforts have examined the degree to which additional risk exposures impact child psychopathology above the influence of depression in the mother. Three studies (9-11) reported that multiple contextual risks (e.g., low social support, family conflict) had as large an effect on psychopathology in the child as did depression in the mother. However, this research was generally limited by small sample sizes and low rates of contextual risks, such as poverty, housing inadequacy, single motherhood, teen motherhood, and criminal lifestyles. In addition, they typically did not examine clinical levels of child psychopathology. The present research, supports and extends these earlier findings through examining a similar research question in a prospective epidemiological birth cohort of 7,429 mother-child pairs from varied socio-economic and risk backgrounds; and by assessing the predictive impact of maternal depression (child age 1.5 years) and risk exposure of the child (0-2 years) on the child’s externalizing and internalizing DSM-IV based diagnoses at 7.5 years.
Both the present study and the former studies (10), however, are correlational and were not designed to examine the reasons underlying the overlap of maternal depression with risk factors. For example, risk factors could cause depression in the mother, but depression and risk could also work in a bidirectional manner, whereby increases in one relate to increases in the other, thereby increasing child exposure to both maternal psychopathology and risks associated with mental health in the mother (25). There is, however, growing evidence from natural experiments, randomized control trials, and other statistically innovative designs that both maternal depression and contextual risk factors like poverty have causal effects on children’s mental health (13, 26). In future, studies of these kinds could be used to test whether some risk factors have a greater effect than others on child and maternal mental health. For example, it may be that proximal risk factors (e.g., family violence) have a stronger effect on child psychopathology than distal risk factors (e.g., poverty). In the present study, however, we examined a cumulative risk factor, where all risks were equally weighted.
In addition, the present results also help to validate findings that programs that successfully intervene on maternal depression are also associated with improvements – but generally not complete remission – in adverse child outcomes (13, 27, 28). For example, certain associated risk factors may be more responsive to intervention than others – targetable risks include trying to increase social support network density and to decrease maternal alcohol use and dysfunction in the family. The risk of poverty, which is robustly associated with adverse child outcomes (29), on the other hand, has been shown to be less responsive to intervention (e.g., 30), but can be successfully buffered by attentive parents who are actively involved in their child’s life (31). Hence, interventions aimed at reducing depression in the mother and its adverse effects on the children likely need to be informed by the nature of specific risks, their respective impacts on the child, and how they may directly or indirectly respond to an intervention.
Incomplete intervention effects on the child may also be related to at least two developmental sources: (i) the timing of the exposures, and (ii) reciprocal relationships between the mother and the child. With regard to the timing of exposures, the emergence of risk factors in certain periods of development may influence and change a child’s developmental pathway. In the present study, we assessed risk exposure from birth to 2 years of age, a critical developmental period when, for example, brain maturation (i.e., the hippocampus), mother-child attachment and the foundations of cognitive and socio-emotional competence are in play (32). Early disturbances in normative development can have lasting effects on child well-being (26). With regard to reciprocal effects, the relationship between maternal depression and child disturbance appears to be bidirectional, such that the child’s problems can contribute to mother’s symptoms which then, in turn, can further increase the child’s problems (33). If such reciprocal patterns are established early in the life course, an intervention on the child, as well as the mother, is likely necessary (20-22).
The present results should be interpreted in the context of seven main limitations. First, as stated, this research is correlational in nature, hence no causative relationship have been identified. Second, most measures were based on maternal reports, raising the possibility of shared method variance. Future studies should incorporate multiple informants. Third, we relied on self-reports of depressed mothers, which calls into question the accuracy of the reports. That said, studies have found that depressed mothers can be as accurate as other informants about their children’s behavior (34) and a recent meta-analyses suggested that the size of the effect of maternal depression on child outcomes, as measured by maternal reports on scale formats versus clinical diagnoses, do not significantly differ (35). Fourth, although the mothers and children of ALSPAC represent a broad spectrum of SES backgrounds, the sample includes relatively low rates of ethnic minorities. The present results will need replication with more ethnically diverse samples. Fifth, like most large longitudinal cohorts, ALSPAC has faced attrition over time. As expected, younger and more socially disadvantaged mothers were more likely to be lost to follow-up. However, although attrition affected prevalence rates of depression in the mother and the externalizing and internalizing disorders in the children, past studies have suggested that the associations between risks and outcomes remained intact, though conservative estimates of the likely true effects (36). Sixth, we focused on maternal depression and associated risks in the early postnatal period. Earlier (prenatal effects) and later mother, child- and family-based risks may also contribute to differentiating and maintaining early psychopathology in the child, and are important targets for future study. Seventh, in addition to maternal depression, paternal psychopathology has been shown to negatively affect child development (9). Future research should examine the additive and interactive effects of psychopathology from the mother and father on child wellbeing.
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, computer 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. Barbara Maughan is supported by the Medical Research Council. Edward D. Barker had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Authorship credit and contribution:
Financial Disclosure/Competing Interests: None reported.