Treatment of Parental Depression and Reduced Risk in Offspring-Does It Have Anything to Do with Offspring Gender?

Abstract

Objective

There is an increased risk for depression in the offspring of depressed parents. This is in part mediated by maladaptive parenting. Females are more vulnerable to parenting behavior and were found to be at increased risk of depression compared to male offspring of depressed parents. Previous work suggested a reduced risk for depression in the offspring of parents with remitted depression. Offspring gender differences in this association were rarely considered. Here, we are examining the hypothesis that female offspring are more likely to benefit from treating parental depression using data from the U.S. National Comorbidity Survey Replication (NCS-R).

Method

The NCS-R is a nationally representative household survey of adults 18 years and older carried out between February 2001 and April 2003. The World Health Organization World Mental Health Composite International Diagnostic Interview (WHO WMH-CIDI) was used to assess DSM-IV Major Depressive Disorder (MDD). Multiple logistic regressions were used to assess the association between parental treatment and offspring risk for MDD. An interaction term was added to study the effect of offspring’s gender on this risk.

Results

The age-adjusted odds ratio for treatment of parental depression was 1.15 (95% CI: 0.78, 1.72). There was no effect modification by gender (p = 0.42). Surprisingly, treatment of parental depression did not reduce their offspring’s risk for depression.

Conclusion

Gender of the offspring had no effect on the risk of depression in the adult offspring of treated versus untreated depressed parents. A focus on mediators like parenting behavior and its gender specific effect needs to be explored in future studies.

Introduction

Literature on major depressive disorder (MDD) has taken long strides recently as heaps of new data are pouring in through countless papers. The last few decades have witnessed major insights into the neurobiology, genetics, and environmental contribution to the causation of depression.^1–2 This also holds true for the rates and trends of depression. Delineating a set of risk factors for depression has become readily feasible. This is largely driven by landmark psychiatric epidemiologic studies that deployed standardized diagnostic instruments. Of these, the Epidemiologic Catchment Area Study and the National Co-morbidity Survey shed the light on the prevalence and risk factors of the major psychiatric disorders.^3–4

Depression is currently the world’s second leading cause of disability only after back pain.⁵ The estimated lifetime prevalence of depression is 15–17%.⁴ The prevalence of major depressive disorders was found to be approximately twice as high in women compared to men.^6–8

Understanding the gender differences in MDD unleashed a number of studies to identify the factors making women more vulnerable to depression. Biological, psychological, and socio-cultural factors were all proposed in an attempt to explain these differences. However, there were no consistent findings to favour one hypothesis over another.

The offspring of depressed parents have a higher risk and an earlier onset of MDD that continues into adulthood.^9–10 The underlying mechanisms for this association include both heritability and environmental effects of having a depressed parent.¹¹

Some findings suggested that a non-remitting course of parental depression is associated with a higher risk of impaired functioning and depressive symptoms in their offspring.¹² A finding that was challenged by other reports of similar levels of psychological impairment in children of chronically depressed mothers and their counterparts of mothers with remitted depression.¹³ These findings supported a notion that having a parent with depression is associated with psychopathology of the offspring regardless of the course of the illness thus shifting the focus to parenting and family functioning of a depressed parent as a possible causal mechanism.¹⁴ The negative family milieu and maladaptive parenting of depressed parents is a mediator in the effect of the parental depression on their offspring.¹⁵ Children of depressed mothers are exposed to the negative affect and cognition characteristics of a depressed mood state placing their offspring at elevated risk for developing depression.¹⁶

Although strong evidence of a gender difference in the risk of depression in the offspring of depressed parents is lacking, women are more vulnerable to parenting behavior than men. Levels of emotional ‘frigidity’ in particular, were related to increased risk of a broad range of psychiatric disorders in women.¹⁷ Female gender as a daughter of a depressed parent was associated with a higher risk for emotional problems.¹⁸ These findings may suggest that women are more likely to be effected by the course of parental depression than men.

Treatment is one of the factors on which the course and prognosis of depressive disorder depends. Targeting depressive symptoms by treatment and reducing its consequence of maladaptive family interaction may be a protective factor against depression in the offspring. Since women are more sensitive to the negative parenting and family interaction styles, they are more likely to benefit from treatment of parental depression.

Very little is known about the effect of the treatment of paternal depression on the risk of psychopathology in the offspring and whether this effect will be different by gender.

Here, we hypothesize that treatment of parental depression will protect women against depression more than men. These results will help predict gender specific protective factors in accordance with an integrative bio-psycho-socio-cultural model to explain the gender differences in rates of depression.

Materials and Methods

Data

The NCS-R is a nationally representative survey of English-speaking household residents aged 18 years and older in the coterminous United States.¹⁹

The study was conducted a decade after the original National Co-morbidity Survey with an expanded questionnaire that included assessments based on the DSM-IV diagnostic system.⁴ Face-to-face interviews were carried out by professional interviewers from the Institute for Social Research at the University of Michigan, Ann Arbor, between February 2001 and April 2003. The survey was administered using laptop computer-assisted personal interview (CAPI) methods.

The response rate was 70.9%. The survey was administered in two parts. Part I included a core diagnostic assessment of all respondents (n = 9282) that took an average of about one hour to administer. Part II included questions about risk factors, consequences, other correlates, and additional disorders. In an effort to reduce respondent burden and control study costs, Part II was administered only to 5692 of the 9282 Part I respondents, including all Part I respondents with a lifetime disorder plus a probability subsample of other respondents. Interviewers explained the study and obtained verbal informed consent prior to beginning each interview. The Human Subjects Committees of Harvard Medical School, Boston, Mass, and the University of Michigan approved recruitment and consent.

Measures

The NCS-R diagnoses are based on the World Mental Health Survey Initiative Version of the World Health Organization Composite International Diagnostic Interview (WMH-CIDI),²⁰ a fully structured lay-administered diagnostic interview that generates both International Classification of Diseases, 10th Revision and DSM-IV diagnoses.^21–22

CIDI was used to measure the lifetime prevalence of MDD. The CIDI has acceptable inter-rater reliability and test–retest reliability for most diagnoses including major depression.²³ The CIDI is considered to have an acceptable validity, however only few studies examined its validity.²⁴

Subjects were asked whether in their childhood they grew up with either parent having depressive symptoms. Depressive symptoms were defined as having a period of sadness for more than two weeks. Information on whether either parent received professional treatment for his/her depressive disorder was obtained. Sociodemographic characteristics including education, marital status, family income and age were collected. Education was divided into four categories (0–11, 12, 13–15, 16 or more). Current marital status was also divided into three categories (married, divorced/separated/widowed, never married). Family income was defined in relation to the federal poverty line.²⁵ Low income was less than or equal to 1.5 times the poverty line, low average was more than 1.5 to 3 times the poverty line, high average was more than 3 to 6 times the poverty line, and high was greater than 6 times the poverty line. Age was treated as a continuous variable. Although, these sociodemographic characteristics are thought to be independent predictors of depression in community samples, they are unlikely to confound the association of treated parental depression and later developmentt of major depressive disorder. Accordingly they will not be adjusted for.

Young individuals are more likely than older individuals to remember history of parental depression and treatment. However, older individuals are more likely to have experienced at least one depressive episode during their lifetime thus, making age a potential confounder of this association.

Statistical Analysis

All statistical analysis was carried out using SAS (Statistical Analysis System) version 9.1 software for Windows (SAS Institute, Inc., Cary, North Carolina). All p values are two sided, with a 0.05 level of significance.

This analysis is restricted to those with either parent with a depressive disorder (n = 1693). The association between lifetime prevalence of MDD and treatment of depressive disorder in either parent will be examined using logistic regression models. The primary outcome is whether parental treatment will have a more protective effect on women than men. An interaction term between both parent receiving treatment and gender was added to the model to answer this question. Treatment of parental depression will be added as an independent variable to explore the risk of depression in treated versus untreated parental depression. The results will be adjusted for the age of the offspring as it is considered a confounder in the association under study.

Associations between variables were expressed as odds ratios and 95 percent confidence intervals.

Missing data on treatment for parental depression were considered as not having treatment and those who refused to answer the question were excluded from the analysis.

Results

The baseline characteristics of the study participants are shown in Table 1. Men and women had similar distribution of number of years of education and family income. Compared to men, women were more likely to be divorced, separated or widowed. However, men were more likely to never marry. In both men and women, the highest proportion was married.

Table 1. Background Characteristics of Subjects with At Least One Parent with Depressive Symptoms in the National Comorbidity Survey Replication, USA 2001.

		Women				Men
Characteristics		No.*		Proportion or mean (SD†)		No.*		Proportion or mean (SD)
Age		1038		42.98 (15.68)		655		41.54 (15.24)
Years of education
0–11 years		131		12.62		104		15.88
12		283		24.43		160		27.26
13–15 years		333		32.08		210		32.06
≥ 16		291		28.03		181		27.63
Marital status (%)
Married		511		49.23		351		53.59
Separated/divorced/Widowed		294		28.32		117		17.86
Never married		233		22.45		187		28.55
Family income
Low		314		30.25		190		29.01
Low average		221		21.29		106		16.18
High average		308		29.67		227		34.66
High		195		18.79		132		20.15

* Number of subjects with a measurement.

^† SD, standard deviation.

In this sample, 583 participants reported having a major depressive episode at one point in their lives. Accordingly, the prevalence estimate of lifetime depression was 34.44 percent (95 percent CI: 32.21, 36.73) among adults who grew up with a parent or a caregiver with depressive symptoms. This compares with a prevalence of 13.03 percent (95 percent CI: 12.28, 13.8) among adults who did not grow up with a parent with depressive symptoms. The prevalence of depression among women was 38.15 percent (95 percent CI: 35.24, 41.14) compared to 28.55 percent (95 percent CI: 25.22, 32.13) in men.

Only 24.45 percent of depressed parents received treatment. There was no difference in the prevalence of depression between the offspring of treated versus untreated depressed parents (Z score = 0.246, p = 0.8057) This is shown in Table 2. Women had a slightly higher prevalence of depression among those with treated parental depression. For men, however, there was a decrease in the prevalence of depression when a parent received treatment for depressive symptoms. The groups with the untreated parental depression had a narrower 95 percent confidence interval compared to the groups with the treated parental depression.

Table 2. Prevalences of Depression of Subjects with At Least One Parent with Depressive Symptoms in the National Comorbidity Survey Replication, USA.

		Lifetime major depressive disorder
		No.*		Prevalence (%)		95% CI
Total
Treated parental depression		145		34.93		30.51, 39.65
Untreated parental depression		438		34.27		31.72, 36.92
Women
Treated parental depression		103		40.23		34.41, 46.34
Untreated parental depression		293		37.47		34.14, 40.91
Men
Treated parental depression		42		26.42		20.16, 33.79
Untreated parental depression		145		29.23		25.4, 33.39

* Number of subjects with a measurement.

^† Confidence Interval.

Among the population under investigation, treatment of parental depression was not significantly associated with the risk of MDD in their adult offspring (age-adjusted OR = 1.15, 95 percent CI: 0.78, 1.72). There was no difference by gender of the offspring on the effect of treatment of parental depression in the adult offspring risk for MDD (p for the interaction = 0.42).

Discussion

Our analysis found that the prevalence of MDD is expectedly higher among adult offspring of parents with depressive symptoms compared with those whose parents did not have these symptoms. This result is in concordance with earlier findings that offspring of depressed parents have a 2-3-fold increase in the risk of MDD compared to controls and that this risk continues into adulthood.^9–10

A non-remitting course of parental depression was suggested to increase the risk of psychopathology in the offspring.¹¹ Also, remission or improvement in parental depression decreases the risk for depression in their children.^26–27 However, our analysis of the data suggested that receiving professional treatment for parental depression did not have a protective effect against the development of depression in adulthood. These results are supported by the other body of evidence suggesting no difference in psychopathology in the offspring of depressed parents when comparing those with remitting versus non-remitting courses.^13,29

The majority of previous reports on the protective effect of a remitting course of parental depression did not follow the offspring into adulthood to study whether this effect is a transient one due to an immediate improvement in some parenting functions or has a more enduring long-lasting effect. Of those with a longer follow-up period extending up to ten years, offspring of parents with remitted depression were functioning at a comparable level to those whose parents had non-remitting depression.¹⁴

Although the evidence is well-established for the efficacy of different treatment modalities in improving the course of adult depression, our data does not include a direct measure of remission or improvement of parental depression and its relation to subsequent risk of depression in the adult offspring. However, from a public health perspective the data on the effect of treatment rather than the course of depression carries more weight in highlighting the need for implementing intervention plans to protect against the effect of parental depression on the offspring psychopathology.

Comparing the effect of different treatment modalities of parental depression on the offspring risk for MDD is beyond the scope of this paper. Accordingly, considering “receiving professional treatment” as an aggregate of all treatment modalities in one measure is not considered a limitation of this paper. A variety of treatment modalities such as psychopharmacology and psychotherapy are known to be efficacious in the treatment of adult depression. This does not rule out that different treatment modalities of parental depression may affect parenting styles differentially.

To our surprise, our data suggested no difference in the effect of treatment of parental depression by the gender of the offspring. The data on the effect of the offspring gender on the relation between parents’ depression and their offspring’s risk for depression is scant. Most of the data focused on the risk in the offspring during their childhood prior to the emergence of the gender differences in the rates of depression during puberty.⁷ However, studies done on adolescents reported a higher risk of psychopathology in daughters of depressed parents compared to sons.^18,28,29 Data on adult offspring of depressed parents are lacking. Equally, the evidence to support or refute the effect of treated parental depression on the risk of depression in their offspring by their gender is deficient.

Moreover, our data does not examine the role of other proposed mediators between the treatment and the improvement of offspring psychopathology. These include parenting behaviors, affect and cognitive styles among others that might better explain the gender differences in depression rates as highlighted in the introduction.

This analysis did not include a chronological assessment of the time of onset and course of depression in the offspring by gender. Such analysis could enable us to identify a high-risk gender for an increased burden of parental depression. Moreover, the data had no formal assessment of the parental depression and lacked information on possible moderators such as its timing, severity, and chronicity.

Other limitations of this analysis are the ones commonly encountered in cross-sectional designs where temporality cannot be assessed and where results could be subject to recall bias, although young children’s self-reports have been recently suggested to minimize this bias.³⁵

The results of this study argue in favor of the body of evidence suggesting that although offspring of depressed parents are at an increased risk for depression over different periods in their lifetime, this risk does not decrease by treating parental depression. Furthermore, it finds no evidence for a gender difference in the effect of treatment of parental depression. Thus, we failed to identify women as a high-risk gender that may benefit from treating parental depression more than their male counterparts.

These findings support a stronger toll of heritability in the determination of offspring risk of depression rather than the environmental and social effect of having a parent with depressive symptoms. Twin studies estimated the heritability of MDD to be moderate, in the range of 35–40%,^30–31 which was found to be higher among women.^32–33

Another explanation is that the unavoidable effect of parenting behavior early in the course of a parent’s depression causes an irreversible insult in the emotional development of the offspring leading to an increased risk for psychopathology. It is also possible that the currently available treatment modalities, although effective in treating depressive symptoms, are less likely to reduce the maladaptive parenting and negative milieu characteristic of a family with a depressed parent. Subsequently, the offspring is continuously exposed to these negative effects regardless of treatment.

Despite our findings and in the realm of controversial, non-consistent evidence supporting treatment of parental depression to mitigate the risk of depression in their offspring, we recommend continuing intervention strategies that target parents with depression and consider female offspring as a high risk gender. Such strategies are supported by the strong evidence for increased risk of depression in the offspring of depressed parents and increased vulnerability for depression in women in general.

Further studies should examine the efficacy of implementing specific treatment modalities for parental depression to reduce the risk of depression in their offspring using large samples, longer follow-up periods, and should further assess the effect of the gender of the offspring and their parents on this association. More focus on the mediating effect of family milieu and parenting behavior (e.g., marital discord) is also necessary.^34–36 Studies examining the gene-environment interaction in the risk of depression in the offspring of depressed parents may better explain this complex relation.