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Parental Psychopathology and Childhood Atopic Disorders in the Community

From the Department of Psychiatry, Columbia University, New York, New York.

Address correspondence and reprint requests to Ramin Mojtabai, MD, 10 Waterside Plaza, Apt. 5J, New York, NY 10010. E-mail: rm322{at}columbia.edu

	ABSTRACT

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Objective: To examine the association of parental psychopathology and childhood atopic disorders in the general population.

Methods: In a sample of 9,240 parent–child dyads drawn from the 1999 US National Health Interview Survey, the association of childhood atopic disorders with parental major depression, generalized anxiety disorder, and panic attacks was examined. Parental DSM-IV psychiatric diagnoses were ascertained by the Composite International Diagnostic Interview, Short-Form (CIDI-SF).

Results: Parental major depression and panic attacks were associated with childhood atopic disorders only in biological parent–child dyads (adjusted odds ratios = 1.67 for major depression and 1.46 for panic attacks), and among these more strongly in mother–child dyads. Parental atopic disorders and parental psychopathology had an additive effect on the risk of atopic disorders in the offspring.

Conclusion: Findings from this study lend support to the "shared genetic liability" hypothesis for the association of childhood atopic disorders and parental major depression and panic attacks.

Key Words: atopic disorders • major depression • panic attacks

Abbreviations: NHIS = National Health Interview Survey; CIDI-SF = Composite International Diagnostic Interview, Short Form; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition; MD = major depression; GAD = generalized anxiety disorder; PA = panic attacks.

	INTRODUCTION

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Increased prevalence of mood and anxiety disorders in parents of children suffering from asthma and other atopic disorders has been noted for many years (1–6). The nature of this association, however, is still debated (6). Parental mental illness and stress may adversely impact parenting behavior, which in turn could potentially be a risk factor for early asthma (7–9) and perhaps other atopic disorders (10). There is some evidence, however, that this association is not mediated by behaviors that increase exposure to allergens such as smoking or formula feeding (8). Alternatively, the burden of caring for a sick child may contribute to development of mental health problems in the parents (11,12). It is also possible that a third factor, such as a shared genetic liability, underlies the association of childhood atopic disorders and parental psychopathology. Two studies found a shared genetic risk for atopy and behavioral and psychological symptoms in twins (13,14), suggesting that the association of psychopathology and childhood atopic disorders may be largely explainable by a shared genetic liability. In support of this hypothesis, Timonen and colleagues recently reported increased risk of depression in children of parents with atopic disorders in a longitudinal birth cohort study (15). These authors further noted that the increased risk of mood disorders was limited to children of mothers but not fathers with atopic disorders, and, based on this observation, suggested a maternal pattern of inheritance for the shared liability. This conclusion is further supported by the results of clinical and general population studies that record increased rates of comorbidity between atopic disorders and mood and anxiety disorders, more specifically, depression (16–19) and panic attacks (20–27).

The present study further explores the link between parental psychopathology and childhood atopic disorders in a large sample of biological and nonbiological parent–child dyads drawn from the general population. The study also tests Timonen and colleagues’ (15) maternal inheritance hypothesis by examining whether the link between parental psychopathology and childhood atopic disorders is limited to mother–child dyads or is found in father–child dyads as well.

	METHODS

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Sample
Data were drawn from the 1999 US National Health Interview Survey (NHIS), a national household survey of the US population, sponsored by the National Center for Health Statistics of the Centers for Disease Control and Prevention. NHIS is comprised of family, sample adult, and sample child interviews. The family interview collects information on household composition, sociodemographic characteristics, basic indicators of health status, activity limitations, injuries, health insurance coverage, and access to and utilization of health care services. All adult members of the household who are at home at the time of the interview are invited to participate and to respond to questions about themselves. For children and adults who are not at home during the interview, information is provided by a knowledgeable adult informant.

From each family in the NHIS, one sample adult and one sample child (if the family has a child) are randomly selected for more detailed interviews. Information for the sample child is obtained from a knowledgeable adult residing in the household, who is often a parent. The analyses in this paper use the intersection of the sample adult and sample child interviews in which the sample adult was a biological or adoptive/step parent of the sample child.

Main Variables
Parental psychopathology was assessed by Composite International Diagnostic Interview (CIDI) Short Form (CIDI-SF). The CIDI-SF is a structured diagnostic interview designed for use by trained nonclinician interviewers. The CIDI-SF was derived from the longer and more detailed Composite International Diagnostic Interview (28), and was revised to screen for disorders defined in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (29). In the 1999 NHIS, the CIDI-SF modules for three 12-month diagnoses were used: major depression, generalized anxiety disorder, and panic attacks.

Childhood atopic disorders were assessed by a set of questions asking if the child had had "hay fever," "respiratory allergies," "eczema or skin allergies," "wheeze or whistling sound in the chest," or "food allergies" in the past 12 months or had been diagnosed by a health professional as having asthma. For this report, a childhood atopic disorder was defined by the presence of any of these indicators.

It may be argued that "wheeze or whistling sound in the chest" is not as specific an indicator for atopic disorders as the other reported symptoms. However, it is noteworthy that 75.4% of the children with this symptom also had at least one of the other symptoms. Furthermore, there is some evidence that mild wheezing might be an indicator of a less severe forms of atopic disorder that is not diagnosed as such (3). Finally, further analysis after excluding this symptom produced results similar to those presented here.

Control Variables
Atopic disorders in adults were assessed by three questions about being diagnosed by a health professional with asthma or hay fever or having had a "wheezing or whistling sound in the chest" in the past 12 months. For this report, an adult atopic disorder was defined by the presence of any of these indicators. Similar to the case of children, 56.0% of the participants who reported "wheezing or whistling sound in the chest" also reported being diagnosed with asthma or hay fever. Further analyses after excluding this symptom produced results similar to those presented here.

Sociodemographic characteristics included the interviewed parent’s age, gender, race, parental smoking (number of cigarettes smoked per day), family size, family income, and the child’s gender and age.

Analyses
Analyses were conducted in two stages. First, the association of parental psychopathology with childhood atopic disorders was examined using a multiple logistic regression model in which the dichotomous variable of childhood atopic disorders was the outcome variable of interest and major depression, generalized anxiety disorder, and panic attacks were the independent variables of interest. Analyses adjusted for the control variables described above. In addition to statistical tests for the regression coefficients, Wald tests for the overall effects of psychopathology were also conducted. A statistically significant regression coefficient or overall Wald test for psychopathology among biological parents but not among nonbiological parents would lend support to the shared genetic liability hypothesis.

Second, the impact of the parent’s gender on the association of parental psychopathology and childhood atopic disorders was examined by running separate regressions for mother–child and father–child dyads similar to the one described above. These analyses were limited to biological parent–child dyads and parental mental health conditions found to be significantly related to childhood atopic disorders in the first stage of the analyses. Analyses adjusted for the control variables described above. A statistically significant regression coefficient or overall Wald test for maternal psychopathology, but not paternal psychopathology, would lend support to the maternal inheritance hypothesis.

The logistic regression models were fitted by the svylogit routine of STATA 8.0 (StataCorp., College Station, TX) statistical program, which accommodates complex survey data by taking survey weights and design elements into account. P < .05 was considered statistically significant.

	RESULTS

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Of 30,801 sample adults and 12,910 sample children interviewed in NHIS 1999, 9,240 involved a parent–child dyad—8,686 biological and 554 nonbiological (adoptive/step parent). The average age of children was 8.3 years (SD = 5.3); 51.8% (N = 4,785) were male and 48.2% (N = 4,455) female. Childhood atopic disorders were common in this sample, affecting 30.9% (N = 2,852) of the children.

The average age of parents was 36.7 years (SD = 8.3); 64.9% (N = 6,000) were female and 35.1% (N = 3,240) male; 58.6% (N = 5,411) were non-Hispanic white, 23.2% (N = 2,144) Hispanic, 14.8% (N = 1,370) non-Hispanic black, and 3.4% (N = 315) from other racial/ethnic groups. Major depression was the most common of the three psychiatric disorders ascertained, affecting 6.3% (N = 584) parents followed by panic attacks, affecting 3.3% (N = 309) and generalized anxiety disorder, affecting 3.2% (N = 292). Adult atopic disorders were more common, affecting 18.9% (N = 1,742).

The median size of the families from which the parent–child dyads were drawn was four members. The average income of 22.2% (N = 2,053) of the families was less than $20,000 per year.

In the multiple logistic regression analyses, parental major depression and panic attacks were associated with childhood atopic disorders at a statistically significant level only in biological parent-child dyads (Table 1). Parental atopic disorders, however, were associated with childhood atopic disorders both in biological and nonbiological parent–child dyads (Table 1). In biological parent–child dyads, the likelihood of childhood atopic disorders was lower in children of Hispanic parents, children who came from larger families and had lower income. Boys and older children had an increased risk of atopic disorders (Table 1).

In the multiple logistic regression analyses limited to biological parent–child dyads, major depression and panic attacks in mothers, but not fathers, were associated with childhood atopic disorders at a statistically significant level (Table 2). No such gender differences were observed in the association of parental and childhood atopic disorders (Table 2).

Further analyses, using adjusted probabilities obtained from the logistic regression models, indicated that parental atopic disorders and parental mental health conditions had additive effects on the risk of atopic disorders in children (Figure 1). Among parents who had atopic disorders but no major depression or panic attacks, atopic disorders were observed in 47.7% of the offspring. Among parents who had major depression or panic attacks but no comorbid atopic disorders, atopic disorders were observed in 36.7% and 36.0% of the offspring, respectively, whereas among parents with both atopic disorders and major depression and/or panic attacks, atopic disorders were observed in 63.0% of the offspring—considerably higher than either of the other groups (Figure 1) and 2.5 times higher than the group whose parents had neither condition (prevalence = 25.1%).

View larger version (29K): [in this window] [in a new window]   Figure 1. Prevalence (±95% confidence intervals) of childhood atopic disorders according to health conditions of the biological parents. The prevalence estimates are adjusted for parental age, race, gender, smoking, family size, family income, child’s sex, and child’s age. AD, atopic disorders; MD, major depression; PA, panic attacks. Significance tests were obtained from Wald tests for pairwise comparisons of groups. The "+" sign indicates that the health condition is present and the "–" that it is absent.

	DISCUSSION

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The results of this study should be interpreted in the context of the limitations of the data. First, the interviewed parent was in many cases the same person who provided information on the child’s health. If parents with mental health conditions are more alert to their children’s health conditions, a spurious relationship between parental psychopathology and childhood atopic disorders may be observed. To assess this possibility, further analyses were conducted in which the interaction terms for source of information (parent is source of information = 1; parent is not the source of information = 0) and major depression and panic attacks were entered into a logistic regression model similar to the model for biological parent–child dyads in Table 1. Adding the interaction terms did not improve the fit of the model (adjusted Wald test = 0.90, p = .407). Repeating this analysis in mother–child dyads (adjusted Wald test = 2.21, p = .111) and father–child dyads (adjusted Wald test = 0.05, p = .950) produced similar results. Thus, whether or not the parent was the informant had no appreciable impact on the relationship of parental psychopathology and childhood atopic disorders in mother–child or father–child dyads. A second limitation of the study is that atopic disorders were not substantiated by clinicians or objective tests. In past research, however, participants’ reports on atopic disorders were mostly found to be accurate. For instance, in a population study (30), response to a single question "do you have asthma?" had a sensitivity of 90% and specificity of 95% for detecting cases ascertained by a physician after a detailed interview. Third, information on parental psychopathology and atopic disorders were available only for one parent. Furthermore, since mothers are more likely than fathers to be the primary caregiver for their children, they were over-represented in the sample of parent-child dyads. However, since neither health nor gender was a condition for selection of participants, it is unlikely that the results would be affected by inclusion of only one parent and overrepresentation of mothers. Fourth, mental disorders in children were not assessed in NHIS. Future research needs to determine whether or not childhood psychopathology could be a mediator and explain the relationship between parental psychopathology and childhood atopic disorders. Fifth, the sample of nonbiological parent–child dyads was considerably smaller than that of biological parent-child dyads. As a result, the analysis in the group of nonbiological dyads is far less powerful than that in the biological dyads, and reliance on p values to assess the significance of findings in nonbiological dyads may not be justified. Similarly, the sample of father-child dyads were smaller than the sample of mother-child dyads. The findings need to be corroborated in larger samples of nonbiological parent–child dyads and of biological father-child dyads. Finally, only three mental health conditions were assessed in the 1999 NHIS. Although these conditions are quite common, they cover a limited range of adult psychopathology. However, the two mental health conditions most consistently associated with atopic disorders in past research, i.e., depression and panic attacks, were included in this study.

This study also had several strengths that complement and extend findings from previous studies that were mostly based on small clinical samples, including a well-characterized, large, and representative population sample, structured interviews for mental disorders, and availability of both biological and nonbiological parent–child dyads. In the context of these strengths and limitations, data from this study provide further support for the role of parental mental health in childhood atopic disorders. The association appears to be specific to two of the mental health conditions covered in the study, i.e., major depression and panic attacks. This finding is consistent with past research suggesting an association between childhood atopic disorders and parental panic disorder (1,6). However, to our knowledge these data are the first general population data that indicate a similar relationship between childhood atopic disorders and parental major depression, ascertained by a structured interview instrument and according to DSM-IV criteria.

Furthermore, the observation that the association of parental psychopathology and childhood atopic disorders is limited to biological parent–child dyads is consistent with the hypothesis that a shared genetic liability underlies the intergenerational association of these conditions (1,15). It is interesting to note that although the relationship of parental mental health conditions and childhood atopic disorders was fully dependent on the biological relationship of parent–child dyads, the relationship of parental atopic disorder with childhood atopic disorder was only partially dependent on the biological relationship. This finding may suggest that the relationship of parental and childhood atopic disorders is, in part, mediated by current environmental factors such as household exposure to allergens that are shared by all parent–child dyads, whereas the relationship of parental mental health conditions and childhood atopic disorders is not mediated by such common environmental exposures. This possibility needs to be tested in future parent–child studies.

It is also noteworthy that parental major depression and panic attacks confer additional risk of atopic disorders in offspring, beyond that of parental atopic disorders (Figure 1). This finding is consistent with past research, which noted that parents with both mental health conditions and atopic disorders are at increased risk of atopic disorders compared with children of parents with atopic disorders alone (7,9).

Although the nature of the shared genetic liability remains unknown, it is noteworthy that the association is more pronounced in mother–child than in father–child dyads. This finding is consistent with the maternal inheritance hypothesis proposed by Timonen and colleagues for explaining the association of maternal atopic disorders and depression in the offspring (15). These authors suggest that this pattern of inheritance may reflect mitochondrial inheritance. Mutations in mitochondrial DNA have been reported both in atopic and other skin disorders (31) and in bipolar mood disorder (32). The other potential explanation for this pattern of inheritance put forth by Timonen and colleagues is genomic imprinting (33) in which the same gene would have a different effect, depending on its maternal or paternal origin. A competing explanation for the mother–child genetic transmission of liability is fetal exposure. However, an increased risk of mood disorders in offspring of mothers with atopic disorders has also been observed (15). Although shared genetic liability appears to be a parsimonious explanation for the reciprocal transgenerational association of mental health and atopic disorders, other potential explanations such as the mediating role of childhood psychopathology or direct impact of adult psychopathology in the perinatal period merit further exploration (34). As Simonof notes (34), distinguishing between these competing models is often difficult and requires additional information from other sources. A more definitive answer may emerge only from triangulation of evidence from a number of different approaches.

	NOTES

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Received for publication June 22, 2004; revision received November 23, 2004.

DOI:10.1097/01.psy.0000160460.59505.db

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