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. Author manuscript; available in PMC: 2026 Feb 12.
Published in final edited form as: Res Child Adolesc Psychopathol. 2023 Oct 6;52(3):413–427. doi: 10.1007/s10802-023-01130-4

Parental Symptoms of Anhedonia, Parenting, and Youth Outcomes: A Multi-Method, Multi-Informant Investigation

Julianne M Griffith 1, Jami F Young 2,3, Benjamin L Hankin 1
PMCID: PMC12893203  NIHMSID: NIHMS2137441  PMID: 37801270

Abstract

Parental depression is a well-established risk factor for youth psychopathology; however, depression is highly heterogeneous, and different parental symptom profiles may be differentially associated with risk mechanisms and youth psychopathology outcomes. Thus, this study examined associations between parental anhedonic symptoms of depression, specifically, and (1) parenting and (2) youth outcomes using a multi-method, multi-informant approach. Participants included 595 parents (89% mothers) and youth (ages 8–16; M[SD] = 12.07[2.39]). Regression analyses indicated that parental self-reported anhedonic symptoms at baseline demonstrated relatively specific prospective associations with chronic parent–child stress assessed using contextual stress interview methods, as well as youth self-reported depressive symptoms at 18-month follow-up. Findings also indicated concurrent associations between parental anhedonic symptoms and observed parental criticism, conflict, and responsiveness in the context of a 5-min discussion task, as well as parent self-reported monitoring/supervision, although results were no longer significant after controlling for parental co-occurring non-anhedonic depressive symptoms. Findings suggest that parental anhedonic symptoms may contribute to relatively unique reductions in the quality of the parent–child relationship and may be a particularly salient risk factor for youth depression.

Keywords: Parental depression, Anhedonia, Parenting, Youth chronic stress, Youth depression, Intergenerational risk


Parental depression is a salient and influential factor contributing to transdiagnostic risk for psychopathology among youth (Goodman, 2020; Goodman et al., 2011; Gotlib et al., 2020). Models of intergenerational risk transmission propose several hypotheses concerning potential mechanisms catalyzing transdiagnostic, intergenerational risk (see Goodman, 2020; Gotlib et al., 2020). Individual differences in parenting behaviors represent a key process of intergenerational risk proposed in foundational theories of intergenerational risk transmission (e.g., Goodman & Gotlib, 1999) and supported by decades of empirical work (e.g., Nolen-Hoeksema et al., 1995; Pound et al., 1988; Weissman et al., 1972; see Lovejoy et al., 2000 and Wilson & Durbin, 2010 for meta-analyses). Such depression-related alterations in parenting include decreases in parental warmth, emotional involvement, and quality of communication, as well as increases in parental expressed hostile and irritable affects.

Studies of intergenerational risk processes have historically treated depression as a singular, unidimensional construct (see Goodman, 2020), although depression is a heterogeneous phenomenon (Zimmerman et al., 2015). This represents a notable opportunity for further inquiry, as it is possible that different facets of depression possess relatively unique explanatory power and predictive utility with respect to parenting and intergenerational risk outcomes. The present study sought to address this gap by focusing on parental anhedonia as an important facet of the broader parental depressive syndrome that may be especially salient in predicting parental patterns of parental engagement with child and adolescent offspring.

Parental Anhedonia and Intergenerational Risk: A Focus on Parenting and Outcomes

Anhedonia, traditionally conceptualized as the pervasive loss of interest or pleasure (American Psychiatric Association, 2013), serves as one of the criterial symptoms of depression and is associated with a host of negative correlates and outcomes, including impaired psychosocial functioning (Vinckier et al., 2017), reduced treatment response (Burkhouse et al., 2018; Khazanov et al., 2020; McMakin et al., 2012), more chronic and severe depressive symptoms (Buckner et al., 2008; Moos & Cronkite, 1999), and increased risk for suicidality (Auerbach et al., 2022; Ducasse et al., 2018). Further, anhedonia is associated with reductions in motivation, reward-based decision making, and effective reinforcement learning (Pizzagalli, 2014), with implications for parental patterns of attention and behavior. Taken together, there is a compelling literature to suggest that relative to depressive symptoms, broadly, parental anhedonia, specifically, may portend particularly deleterious psychosocial outcomes, with the potential for cascading effects across the family unit.

Dix and Meunier (2009) proposed an action-control model in which depressive symptoms undermine parenting via a number of mechanisms, spanning cognitive, attentional, motivational, and affective domains. This conceptual model suggests that depressive symptoms may lead parents to appraise their children more negatively, for example, and may reduce parental attention to children’s affective needs. Moreover, depressive symptoms are hypothesized to contribute to parental apathy, self-focused attention, and social withdrawal, thereby reducing parental capacity to demonstrate responsiveness to their children’s affective and behavioral cues, as well as constraining parental cognitive and behavioral flexibility in the context of parent–child interactions (Dix & Meunier, 2009). It is notable, however, that distinct facets of the broader depressive syndrome are likely to have varying influence on distinct parenting processes of interest. Relative to negative affect, positive affect has been conceptualized as relating particularly strongly with interpersonal relationships and behaviors (Fredrickson, 2004; Ramsey & Gentzler, 2015). That is, positive affect is proposed to play an important role in supporting the health and consolidation of interpersonal bonds, and parental deficits in positive affect might thus be expected to predict particularly weakened parenting responsiveness, availability, and active engagement—key components of effective parenting—relative to parental negative affects.

Anhedonia-related deficits in motivation, pleasure, and reward learning align well with the action-control model of mechanisms of depressed parenting. Expanding on the original model, parents experiencing elevated levels of anhedonia would be expected to demonstrate particularly impaired patterns of parenting with implications for youth socialization and susceptibility to affective dysfunction. Specifically, this elaboration suggests the hypothesis that anhedonic symptoms of depression are likely to associate with greater disengagement from children, as well as reduced warmth and responsiveness to children’s affective and behavioral cues. Such patterns of parental disengagement and reduced warmth and responsiveness would be posited to be more pronounced in anhedonia relative to depression symptoms more broadly, and are conceptually distinct from patterns of impaired parenting such as increased parental hostility and psychological control, that might be expected to associate with increased parental irritability or dysphoric affect. Moreover, anhedonia-related parental withdrawal may reduce parental capacities to engage in active and constructive ways with their children’s everyday small joys and simple pleasures, thereby robbing parents of commonly occurring, naturalistic opportunities to reinforce their children’s daily-life positive affective experience, as well as enhance their own intrapersonal experience of positive affect (Griffith & Hankin, 2021). In this way, individual differences in parenting may be particularly salient to the intergenerational transmission of risk within dyads affected by parental anhedonia.

Overview of Previous Research

At the syndrome level, parental depression has been found to predict multiple consequential outcomes, including youth internalizing symptom outcomes (e.g., anxiety, depression; Goodman et al., 2011; Spence et al., 2002), as well as other psychosocial risk processes, such as impaired parenting behaviors (Lovejoy et al., 2000; Wilson & Durbin, 2010) and youth increased exposure to stress (Griffith et al., 2023; Hammen et al., 2004, 2012). Indeed, epidemiological studies have found that children of depressed parents are approximately three times more likely to develop a depressive disorder, and approximately 1.5 times more likely to develop an anxiety disorder relative to children of never depressed parents (Lieb et al., 2002). Moreover, meta-analysis supports robust associations between parental depression and youth internalizing symptoms with a weighted mean effect size of r = 0.23 (Goodman et al., 2011).

Broad parental depression has also been found to associate with youth exposure to interpersonal stress–a potent risk factor for psychopathology and psychosocial impairment across the lifespan (Hammen, 2005; Hammen et al., 2004; Jenness et al., 2019; King & Merchant, 2008). In a case control study comparing adolescent children of mothers with and without a history of depression, for example, Hammen and Brennan (2001) found that children of mothers with a history of depression demonstrated impaired social functioning relative to children of mothers without a history of depression. Further, in a study of mother–child dyads assessed repeatedly across a 20-year period, Hammen and colleagues (2012) found that maternal depression prospectively predicted youth experience of chronic interpersonal stress across development. Moreover, youth experience of chronic interpersonal stress was found to subsequently predict youth odds of developing a depressive disorder by age 20 in this work. These findings align well with stress-generation theories of depression (Hammen, 2006; Liu & Alloy, 2010), which propose that depressive symptoms contribute to the occurrence of interpersonal stressors, with both individual-level as well as relational effects.

In summary, a large body of work demonstrates associations between parental depression, measured at the syndrome level, and a host of negative psychosocial outcomes including impaired parenting, increased interpersonal stress exposure, and youth symptoms of psychopathology. Given the heterogeneity of depression, however, there is a critical need for research evaluating associations between theoretically-based, salient facets of parental depression, such as parental anhedonia, and outcomes among youth (see e.g., Goodman, 2020). This more granular approach is essential to advancing theory and knowledge of processes involved in intergenerational risk transmission, as well as informing optimally targeted and sensitive interventions.

Developmental Considerations

The transition from middle childhood through late adolescence is characterized by a number of normative changes, including changes in the parent–child relationship (Steinberg, 2001), as well as risk for psychopathology (Paus et al., 2008). As youth navigate the adolescent transition, parent–child relationships tend to become less close and more conflictual (Collins & Laursen, 2004; Laursen et al., 1998; Marceau et al., 2015; Steinberg, 2001), although the parent–child relationship nevertheless remains closely related to youth emotional functioning and wellbeing (Griffith et al., 2021; Weinstein et al., 2006). In the context of these normative developmental processes, effects of parental depression in terms of parenting and psychosocial outcomes may vary depending on developmentally-specific expectations and demands. For example, it may be hypothesized that effects of parental withdrawal or lack of positive parenting might be especially pernicious among youth in middle childhood, when expectations for parental closeness are more salient. Poor monitoring/supervision, in contrast, might leave middle and late adolescents particularly vulnerable given heightened vulnerability to negative peer experiences during these developmental periods (Blakemore, 2008; Guyer et al., 2016). Empirical research is needed, however, to evaluate whether distinct depressive characteristics (e.g., anhedonia) associate with varying outcomes across childhood and adolescent development.

The Current Study

To advance knowledge on relatively specific relations between anhedonic symptoms of depression and intergenerational risk, the present work evaluated patterns of concurrent and prospective associations between parental anhedonic symptoms and (1) parenting behaviors, and (2) youth psychopathology symptoms and exposure to chronic interpersonal stress. We also evaluated whether observed patterns of association were relatively specific to anhedonic symptoms relative to broader, non-anhedonic symptoms of depressed mood. In this study, we incorporated multiple methods and informants to reduce the influence of common method variance and reporter bias (Podsakoff et al., 2003) based on best-practices in developmental psychopathology.

Specifically, we examined concurrent patterns of association between parental symptoms of anhedonia and parenting, as assessed via observed behaviors (i.e., parental responsiveness, support, criticism, and conflict) as well as parent-report (i.e., involvement, positive parenting, and poor supervision and monitoring). The selection of these particular aspects of parenting was theoretically-grounded and consistent with previous research implicating these parenting behaviors in youth adjustment and adaptation across development (Melnick & Hinshaw, 2000; NICHD Early Child Care Research Network, 1999; Pinquart, 2017; Sheeber et al., 2001; Yap et al., 2014). Parenting outcomes were selected to represent a relatively broad sampling of positive and negative parenting behaviors that are conceptually expected to relate to parental anhedonia (Dix & Meunier, 2009; Pizzagalli, 2014; Ramsey & Genztler, 2015), are theorized to contribute to youth risk and resilience, and have been found in meta-analysis to relate to youth internalizing symptoms (e.g., McLeod et al., 2007a, b; Yap et al., 2014). These parenting behaviors also broadly align with targets of evidence-based parenting interventions (e.g., Kehoe et al., 2014; Yap et al., 2016), increasing the potential translational value of findings.

In addition, we investigated prospective patterns of relations between parental symptoms of anhedonia and psychosocial functioning, specifically parent–child chronic stress and youth internalizing psychopathology symptoms. We focused on parent–child chronic stress, in particular, given previous work demonstrating associations with youths’ depressive and anxiety symptoms over time (e.g., Griffith et al., 2020). Chronic parent–child stress was assessed via gold-standard contextual stress interview methods (i.e., the Youth Life Stress Interview [YSLI]; Rudolph & Flynn, 2007). Relative to other measurement modalities, contextual stress interview methods provide a relatively “objective” index of youth stress exposure that is less influenced by various individual differences that can affect youth self-reported stress response (Harkness & Monroe, 2016). Adolescents self-reported various internalizing symptoms, including social anxiety, physical anxiety, and depression across an 18-month follow-up period. This suite of internalizing symptoms represents a collection of particularly developmentally salient outcomes, as symptoms of depression, social anxiety, and physical anxiety commonly onset and co-occur with one another across the adolescent transition (Brady & Kendall, 1992; Hamilton et al., 2016; Ranta et al., 2009) with potentially life-course persistent implications for youth psychosocial functioning (Bittner et al., 2007; Clayborne et al., 2019).

We conceptualized this study as descriptive and exploratory, rather than hypothesis-driven in nature, per se. Given Dix and Meunier’s (2009) model of depressed parenting, however, we tentatively expected that parental anhedonic symptoms would be associated with less parental responsiveness, support, involvement, and positive parenting, as well as poorer parental supervision and monitoring, and increased parent–child chronic stress. No specific a priori hypotheses were made with respect to relations between parental anhedonic symptoms and parental criticism or conflict nor with respect to prospective relations between parental anhedonic symptoms and prospective adolescent internalizing symptoms. We also explored the relative specificity of observed effects to parental anhedonic symptoms after controlling for parental non-anhedonic depressed mood. Given the relatively broad developmental range of the sample, as well as well-established gender differences in youth risk for internalizing psychopathology and interpersonal sensitivity across the adolescent transition (e.g., Crawford et al., 2001; Hankin et al., 2007, 2015; Merikangas et al., 2010), additional exploratory analyses were conducted examining youth grade cohort and gender as potential moderators of associations of interest. Grade cohort rather than age was selected as an indicator of development given that youth were recruited in discrete developmental cohorts; thus, chronological age was not distributed continuously within the study sample.

Methods

Participants and Procedures

Participants included parents and a participating adolescent child recruited in 3rd, 6th, and 9th grade cohorts (full study N = 680, youth age 8–16 at baseline, Mage = 11.87, SDage = 2.41, 56.7% girls, 43.3% boys) as part of the Genes, Environment, and Mood Study (Hankin et al., 2015). Inclusion criteria included youth English language fluency, absence of autism or psychotic disorder diagnosis, and IQ > 70 as assessed via parent report.1 Demographics of the study sample were approximately representative of the ethnic and racial characteristics of the United States population (68.3% White, 11.4% African American, 9.2% Asian/Pacific Islander, 5.7% Multi-racial, 5.6% Other racial identity, with 11.9% identifying as having a Latinx ethnic identity). Participating caregivers included predominantly mothers (89.4%), with smaller numbers of fathers (6.0%) and other caregivers (e.g., grandparents, aunts; 1.2%).2 Further details regarding sampling procedures and participant characteristics are described in Hankin et al. (2015). In instances in which parents participated with more than one child, parenting and outcome data related to one sibling was randomly chosen to be included in the present analyses. The final sample comprised 595 parent-adolescent dyads (Mage = 12.07, SDage = 2.39, 56.6% girls, 43.4% boys).

All procedures were approved by local Institutional Review Boards.3 Informed consent and assent were obtained from all participants prior to administration of study procedures. Participating parents and youth were invited to the laboratory to complete a baseline assessment, during which parents completed questionnaire measures of depression and parenting, as well as a standardized 5-min videotaped interaction task during which the parent–child dyad was instructed to discuss a source of disagreement in their relationship (e.g., completing homework; Feng et al., 2009; Kim Park et al., 2008). Videotapes were coded by trained research staff to yield observational measures of parenting behaviors, as described below. Eighteen months following this initial baseline visit, participating parents and youth were invited back to the lab to complete a follow-up assessment during which youth completed self-report questionnaire measures of internalizing symptoms. Parent–child chronic stress was also evaluated by trained interviewers at the 18-month follow-up assessment via child report.

Measures

Parental Anhedonic and Non-Anhedonic Depressive Symptoms

Parental anhedonic and non-anhedonic depressive symptoms were assessed at the baseline assessment via parent self-report on the Beck Depression Inventory (BDI-II; Beck et al., 1996). The BDI-II comprises 21 items assessing parents’ experience of a range of psychological, social, and somatic symptoms associated with depression. Items are scored on a 4-point Likert-style scale, with total scores ranging from 0 to 63, with higher scores indicating higher levels of depression. Of individuals included in the present analytic sample, 11.8% (n = 70) reported clinically significant levels of depression according to the clinical threshold BDI-II ≥ 14 (Beck et al., 1996).

Past work using factor analytic methods has found that the BDI-II comprises two factors corresponding to anhedonic and non-anhedonic depressed mood, respectively (e.g., Joiner et al., 2003; Kashdan et al., 2006; Treadway et al., 2009; Winer et al., 2014). Specifically, previous work has found items corresponding to loss of interest, loss of pleasure, loss of interest in sex, and loss of energy to comprise an “anhedonia subscale” of the BDI-II (e.g., Joiner et al., 2003; Kashdan et al., 2006; Pizzagalli et al., 2005; Treadway et al., 2009; Winer et al., 2014), with all other items representing generalized depressed mood.4 Thus, for the purposes of the present analyses, parental anhedonia was represented using sum scores of parental responses to anhedonic symptom items (McDonald’s ω = 0.70), and parental non-anhedonic symptoms of depression were represented using sum scores of parental responses to all other items (ω = 0.88).

Observed Parenting

Reliable, independent raters including post-baccalaureate research assistants, graduate students, and post-doctoral scholars coded parental support, responsiveness, conflict, and criticism during the baseline parent–child interaction task. Raters were blind to study hypotheses, as well as parental depression status.

During the interaction task, parent–child dyads were instructed to discuss a source of disagreement in their relationship (e.g., completing homework; Feng et al., 2009; Kim Park et al., 2008). To facilitate selection of a topic, youth and their parents were asked to rate how “hot” (i.e., anger-eliciting) they found a number of topics on which parents and youth normatively disagree (e.g., telephone calls, bedtime, clothing) within their relationship. The dyad was then instructed to discuss the topic mutually rated as the “hottest” for a period of 5 min. Global codes for each parenting construct (support, responsiveness, conflict, and criticism) were assigned on a scale of 1 to 5 (1 = not at all characteristic of the parenting behavior during the interaction and 5 = highly characteristic of the parenting behavior during the interaction). Codes were based on validated parent–child coding systems and reflect theoretically grounded dimensions of parenting (Melnick & Hinshaw, 2000; NICHD Early Child Care Research Network, 1999) described by leading conceptual models describing relations between parenting and youth depression (Sheeber et al., 2001). Parents rated as high in support demonstrated engaged and affirming behavior, providing validating comments (e.g., “I can see that”) as well as praise or recognition of their child. High levels of responsiveness were demonstrated by parents who followed their child’s lead and matched their child’s affect throughout the discussion, remaining undistracted and displaying appropriately responsive social gestures (e.g., nodding). Parental conflict was indicated by displays of hostility or anger. Parental criticism was indicated by such behaviors as statements of disapproval or insults directed toward the child, as well as parental blaming or inappropriately critical behavior. Codes are consistent with prior work assessing positive and negative parenting (Chi & Hinshaw, 2002; Corona et al., 2005; Davidov & Grusec, 2006). Approximately 20% of videotaped observations were double coded. Intraclass correlations between coders ranged from 0.71 to 0.85 on all subscales in this study, indicating good interrater reliability.

Parent-Reported Parenting

Parental involvement, positive parenting, and poor monitoring and supervision were assessed at baseline via parent self-report on the Alabama Parenting Questionnaire (APQ; Frick, 1991). The APQ comprises 42 items assessing different dimensions of parenting. For each item, parents are asked to rate how frequently they engage in a number of parenting behaviors on a 5-point Likert scale from (1) never to (5) always. The present analyses specifically included data corresponding to the involvement (10 items), positive parenting (6 items), and poor monitoring and supervision (10 items) subscales. Subscale scores were computed by summing all items belonging to each respective scale. The parental involvement subscale includes such items as “You have a friendly talk with your child,” “You volunteer to help with special activities that your child is involved in,” and “You play games and do other fun things with your child.” The positive parenting subscale includes such items as “You let your child know they are doing a good job with something,” “You reward or give something extra to your child for obeying you or behaving well,” and “You compliment your child when they do something well.” The poor supervision and monitoring subscale includes such items as “You get so busy that you forget where your child is and what they are doing,” “Your child plays with children you don’t know,” and “Your child goes outside without a set time to come in.” The APQ has been found to be a valid and reliable measure of parenting (e.g., Dadds et al., 2003; Essau et al., 2006; Hawes & Dadds, 2006). McDonald’s omega indicated good internal reliability across subscales in the present sample (ω’s = 0.77-0.81).

Parent–Child Chronic Stress

Parent–child chronic stress was assessed at the 18-month follow up assessment, to cover the degree of chronic stress exposure experienced from baseline to the 18-month time point, using the Youth Life Stress Interview (YLSI; Rudolph & Flynn, 2007). The YSLI is semi-structured contextual stress interview designed to provide an objective measure of youths’ ongoing experience of stress. Previous work demonstrates strong interrater reliability in samples of children and adolescents, as well as concurrent and predictive validity; interpersonal domains of the YSLI, specifically, have been demonstrated to positively associate with both concurrent and prospective measures of psychopathology among youth (Conley & Rudolph, 2009; Gershon et al., 2011; Rudolph & Flynn, 2007).

In the context of the present study, interviewers included post-baccalaureate research assistants, graduate students, and post-doctoral scholars who were extensively trained and supervised by primary investigators. Interviewers asked youth standardized questions targeting aspects of parent–child relationships (e.g., interpersonal closeness, communication and trust, conflict, etc.). Sample questions in the domain of parent–child relationships include: “Do you get along with your parent?,” “Do you argue or fight with your parent?,” and “Do you spend time with your parent?” Severity of chronic stress was rated via a consensus score assigned by a team of three or more masked raters. Rating teams included post-baccalaureate research assistants, graduate students, and post-doctoral scholars.5 The consensus score approach used in the present work required that team members collectively converge on a single stress rating for each interview based on detailed scoring criteria, maximizing reliability. Severity scores ranged from 1 (little/no stress) to 5 (severe stress) and were based on behaviorally-specific anchors regarding such aspects of interpersonal relationships as interpersonal closeness, communication, and conflict. The scoring manual additionally instructed coders to take into account the age and developmental context of each participant when making their objective rating. Chronic stress ratings are adjusted based on normative development, and what would constitute average to severe stress for youth of different ages.

Youth Symptoms of Depression

Youth depressive symptoms were assessed at the 18-month follow-up assessment via self-report on the Children’s Depression Inventory (CDI; Kovacs, 1985). The CDI comprises 27-items assessing youths’ experience of a range of psychological, social, and somatic symptoms associated with depression. Each item is scored on a 3-point Likert-style scale ranging from 0 to 2, and total depressive symptom scores were computed using the sum of all items, with higher scores indicating higher levels of depressive symptoms. The CDI demonstrates good psychometric properties, including convergent validity, as evidenced by correlations with other measures of depression and related constructs (Klein et al., 2005). Internal reliability in the present study was good (ω = 0.88). At 18-months, 6.9% (n = 34) of youth who provided data reported clinically significant levels of depression (i.e., CDI ≥ 16; Timbremont et al., 2004).

Youth Symptoms of Social and Physical Anxiety

Youth social and physical anxiety symptoms were assessed at the 18-month follow-up assessment via adolescent self-report using the Multidimensional Anxiety Scale for Children (MASC; March et al., 1997). The MASC assesses physical symptoms of anxiety, social anxiety, separation anxiety, and harm avoidance, and shows good reliability and validity (March et al., 1997). Items are scored on a 4-point Likert scale, with higher scores indicating greater anxiety. The present study included the physical symptoms and social anxiety subscales, which are associated with risk for their specific disorders and demonstrate discriminant validity (March et al., 1997; van Gastel & Ferdinand, 2008; Wei et al., 2014). Subscale scores for physical symptoms and social anxiety were generated by computing a sum score of the items in each subscale, with higher scores indicate higher levels of each type of anxiety symptoms. McDonald’s omega across subscales and assessment points indicated good internal reliability in the present sample (social anxiety ω = 0.87, physical anxiety ω = 0.85). At 18-months, 4.5% (n = 22) of youth who provided data reported clinically significant levels of physical anxiety (i.e., MASC-PH ≥ 19; Baldwin & Dabbs, 2007) and 4.9% of youth (n = 24) reported clinically significant levels of social anxiety (i.e., MASC-SA ≥ 19; Baldwin & Dabbs, 2007).

Data Analytic Plan

Hypotheses and data analytic plan were pre-registered using the Open Science Framework prior to analysis (https://osf.io/g3ztp/). Analyses were conducted using a structural regression approach implemented in the ‘lavaan’ library in R (Rosseel, 2012; R Core Team, 2013) using full-information maximum likelihood (FIML) estimation to account for missing data and maximum likelihood robust (MLR) estimation due to non-normality of data (Savalei & Rosseel, 2022). To examine concurrent associations between parental anhedonia and parenting behaviors, we conducted a series of linear regressions in which each parenting outcome of interest was regressed on parental symptoms of anhedonia. Prospective associations between adolescent outcomes at 18-months and parental anhedonia were similarly evaluated using a series of linear regressions.

Sensitivity Analyses

To examine the specificity of observed associations to parental symptoms of anhedonia relative to parental non-anhedonic symptoms of depression, a series of sensitivity analyses were conducted in which parental non-anhedonic symptoms of depression were included as a covariate.

Exploratory Moderation Analyses

To address potential moderation by youth development and gender, separate Grade Cohort x Parental Anhedonia, and Gender x Parental Anhedonia, interaction terms were created to evaluate grade cohort and gender, respectively, as moderators of concurrent and prospective associations. Continuous parental anhedonia scores were mean-centered prior to calculation of interaction terms, and parental non-anhedonic symptoms of depression were included as a covariate in all models. Significant interactions were probed using multiple group models to evaluate patterns of association separately within each group (i.e., grade cohort or gender category).

Results

Preliminary Analyses

Means and standard deviations describing primary variables of interest, as well as bivariate correlations between primary variables of interest, are reported in Table 1.6 Parental anhedonic and non-anhedonic symptoms of depression were positively correlated with observed parental criticism and conflict, as well as poor parental monitoring/supervision and chronic parent–child stress. Both parental anhedonic and non-anhedonic symptoms of depression were negatively correlated with observed parental responsiveness. Relative to parental non-anhedonic symptoms of depression, parental anhedonic symptoms of depression were uniquely related to adolescent self-reported depressive symptoms at 18 months (see Table 1).

Table 1.

Descriptive Statistics and Bivariate Correlations Describing Primary Variables of Interest

1 2 3 4 5 6 7 8 9 10 11 12 13
1. Parental Anhedonic Symptoms 1.50 (1.74)
2. Parental Non-Anhedonic Symptoms 0.70* 3.83 (4.96)
3. Observed Parental Criticism 0.11* 0.13* 2.12 (1.04)
4. Observed Parental Conflict 0.09* 0.10* 0.58* 1.79 (0.99)
5. Observed Parental Support −0.01 −0.04 −0.36* −0.43* 2.88 (1.03)
6. Observed Parental Responsiveness −0.10* −0.12* −0.18* −0.26* 0.31 4.09 (0.84)
7. Parent-reported Positive Parenting 0.001 0.02 −0.03 −0.05 0.02 0.04 24.95 (2.93)
8. Parent-reported Parental Involvement −0.06 −0.06 −0.10* −0.11* 0.09 0.12* 0.61* 39.09 (4.68)
9. Parent-reported Parental Poor Monitoring/Supervision 0.16* 0.21* 0.09* 0.07 −0.04 −0.08 −0.17* −0.25* 20.28 (4.52)
10. Parent-Child Chronic Stress at 18mo 0.15* 0.10* 0.15* 0.25* −0.18* −0.18* −0.13* −0.10 0.13* 1.89 (0.73)
11. Youth Depressive Symptoms at 18mo 0.12* 0.08 0.11* 0.14* −0.14* −0.07 −0.01 −0.02 0.19* 0.29* 5.35 (5.83)
12. Youth Social Anxiety Symptoms at 18mo 0.04 0.004 −0.01 0.05 0.02 0.002 −0.05 0.03 0.07 0.19* 0.41* 7.66 (5.88)
13. Youth Physical Anxiety Symptoms at 18mo 0.06 0.04 0.14* 0.15* −0.10* −0.06 −0.05 −0.06 0.14* 0.22* 0.50* 0.51* 6.55 (5.81)

Means (standard deviations) are reported along the diagonal.

*

significantly different from zero at p < 0.05

With respect to gender differences, independent samples t-tests revealed that girls were higher in symptoms of social (M[SD] = 8.68[6.12]) and physical anxiety (M[SD] = 7.12[6.24]) at 18-months relative to boys (M[SD] = 6.31[5.25] and M[SD] = 5.80[5.10], respectively). No other gender differences were observed (all p’s > 0.05; see Supplemental Table S2 for full results). Results of one-way analysis of variance (ANOVA) tests evaluating differences based on grade cohort are reported in Supplemental Table S3. Significant grade differences were found for observed parental conflict, as well as parental self-reported positive parenting and poor monitoring/supervision, parent–child chronic stress, and youth symptoms of depression and social anxiety, Post-hoc tests conducted using Tukey’s HSD indicated that parents of 9th graders demonstrated greater conflictual behavior and self-reported more poor monitoring/supervision relative to parents of 3rd and 6th graders (p’s < 0.01). Parents of 3rd graders self-reported greater positive parenting relative to parents of 6th and 9th graders (p’s < 0.01). Youth in the grade 3 cohort experienced less parent–child chronic stress and reported lower social anxiety symptoms relative to youth in the grade 6 and 9 cohorts at 18-months (p’s < 0.001). Symptoms of depression significantly increased across successive cohorts (p’s < 0.05). No grade differences were found in parental anhedonic or non-anhedonic symptoms of depression (p’s > 0.05).

Concurrent Associations between Parental Anhedonic Symptoms and Parenting

Results of linear regression models evaluating concurrent associations between parental anhedonic symptoms of depression and both observed and self-reported parenting are reported in Table 2. Regression results indicated that parental anhedonic symptoms of depression were positively associated with observed parental criticism (β = 0.11, p = 0.010), observed parental conflict (β = 0.09, p = 0.025), and parental self-reported poor monitoring/supervision (β = 0.17, p < 0.001). Parental anhedonic symptoms were negatively associated with observed parental responsiveness (β = −0.10, p = 0.012). Parental anhedonic symptoms were not significantly related to observed parental support, nor were they related to parental self-reported positive parenting or involvement (β’s ≤|.06|, p’s > 0.05; see Table 2).

Table 2.

Results of Regression Analyses Examining Associations between Parental Anhedonic Symptoms and Outcomes of Interest

β b SE(b) [95% CI b] p
Concurrent Associations
Observed Parental Criticism 0.11 0.07 0.03 [0.02, 0.11] 0.010
Observed Parental Conflict 0.09 0.05 0.02 [0.01, 0.10] 0.025
Observed Parental Support −0.01 −0.01 0.02 [−0.05, 0.04] 0.728
Observed Parental Responsiveness −0.10 −0.05 0.02 [−0.09, −0.01] 0.012
Parent-reported Positive Parenting 0.001 0.001 0.09 [−0.17, 0.17] 0.991
Parent-reported Parental Involvement −0.06 −0.15 0.14 [−0.43, 0.13] 0.285
Parent-reported Parental Poor Monitoring/Supervision 0.17 0.43 0.12 [0.20, 0.67] < 0.001
Prospective Associations
Parent–Child Chronic Stress at 18 months 0.16 0.07 0.02 [0.03, 0.11] 0.001
Youth Depressive Symptoms at 18 months 0.12 0.41 0.16 [0.09, 0.72] 0.012
Youth Social Anxiety Symptoms at 18 months 0.04 0.14 0.17 [−0.18, 0.47] 0.387
Youth Physical Anxiety Symptoms at 18 months 0.06 0.20 0.17 [−0.14, 0.54] 0.244

β = standardized coefficient; b = unstandardized coefficient; 95% CI b = 95% confidence interval of the unstandardized effect

Prospective Associations between Parental Anhedonic Symptoms and Youth Outcomes

As reported in Table 2, results of linear regression analyses indicated that parental anhedonic symptoms were positively related to interviewer-assessed parent–child chronic stress (β = 0.16, p = 0.001) and youth self-reported depressive symptoms (β = 0.12, p = 0.012) at 18-months. Parental anhedonic symptoms were not significantly related to youth self-reported symptoms of social or physical anxiety (β’s ≤ 0.06, p’s > 0.05; see Table 2).

Sensitivity Analyses

Results of sensitivity analyses controlling for parental non-anhedonic symptoms of depression are reported in Table 3. After controlling for parental non-anhedonic symptoms of depression, concurrent associations between parental anhedonic symptoms and parenting behaviors were no longer significant. Parental anhedonic symptoms of depression continued to predict interviewer-rated parent–child chronic stress (β = 0.16, p = 0.018) and youth self-reported depressive symptoms (β = 0.12, p = 0.047) at 18 months.

Table 3.

Results of Sensitivity Analyses Controlling for Parental Non-Anhedonic Symptoms

β b SE(b) [95% CI b] p
DV: Observed Parental Criticism
Parental Anhedonic Symptoms 0.04 0.02 0.04 [−0.05, 0.10] 0.552
Parental Non-anhedonic Symptoms 0.10 0.02 0.01 [−0.01, 0.05] 0.118
DV: Observed Parental Conflict
Parental Anhedonic Symptoms 0.05 0.03 0.04 [−0.04, 0.10] 0.459
Parental Non-anhedonic Symptoms 0.07 0.01 0.02 [−0.01, 0.04] 0.255
DV: Observed Parental Responsiveness
Parental Anhedonic Symptoms −0.04 −0.02 0.03 [−0.08, 0.04] 0.483
Parental Non-anhedonic Symptoms −0.09 −0.02 0.01 [−0.04, 0.01] 0.169
DV: Parent-reported Parental Poor Monitoring/Supervision
Parental Anhedonic Symptoms 0.02 0.05 0.18 [−0.30, 0.41] 0.766
Parental Non-anhedonic Symptoms 0.20 0.18 0.07 [0.04, 0.33] 0.013
DV: Parent–Child Chronic Stress at 18mo
Parental Anhedonic Symptoms 0.16 0.07 0.03 [0.02, 0.12] 0.018
Parental Non-anhedonic Symptoms −0.01 −0.001 0.01 [−0.02, 0.02] 0.894
DV: Adolescent Depressive Symptoms at 18mo
Parental Anhedonic Symptoms 0.12 0.41 0.21 [0.01, 0.81] 0.047
Parental Non-anhedonic Symptoms −0.002 −0.002 0.08 [−0.15, 0.14] 0.976

β = standardized coefficient; b = unstandardized coefficient; 95% CI b = 95% confidence interval of the unstandardized effect; DV = dependent variable

Exploratory Moderation Analyses

Controlling for parental non-anhedonic symptoms of depression, youth grade cohort was found to interact with parental anhedonia to predict parental self-reported monitoring/supervision (β = 0.29, b = −0.11, SE = 0.05, p = 0.015). Follow-up analyses evaluating associations separately by cohort, however, found no significant associations between parental anhedonic symptoms and parental monitoring/supervision in 3rd (β = −0.13, b = −0.34, SE = 0.29, p = 0.236), 6th (β = 0.13, b = 0.30, SE = 0.32, p = 0.347), or 9th grade cohorts (β = −0.04, b = −0.12, SE = 0.30, p = 0.684). Youth gender was observed to interact with parental anhedonic symptoms (β = −0.34, b = −0.55, SE = 0.28, p = 0.048) to predict parental self-reported involvement such that associations between parental anhedonia and parental involvement were in opposite directions among boys (β = 0.05, b = 0.11, SE = 0.30, p = 0.701) and girls (β = −0.09, b = −0.24, SE = 0.24, p = 0.314), although effects were not statistically significant in either group. No other moderation effects were observed (all p’s > 0.05).

Discussion

Exposure to parental depression has far-ranging implications for youth adjustment and adaptation across development (see e.g., Goodman et al., 2011). Importantly, depression is a heterogenous syndrome (Zimmerman et al., 2015), and scholars are increasingly recognizing the need to evaluate relatively specific patterns of association between distinct facets of parental depression (e.g., parental anhedonia) and diverse psychosocial sequalae (Goodman, 2020). In order to advance a more granular, nuanced understanding of intergenerational risk transmission in parent–child dyads, the present work evaluated associations between a particularly salient and influential facet of parental depression—that is, parental anhedonia—and both potential mechanisms (i.e., parenting), as well as indicators (i.e., chronic stress, youth symptoms) of risk using a multi-method, multi-informant approach. Results found that parental anhedonic symptoms demonstrate relatively unique, prospective associations with individual differences in parent–child chronic stress, as well as youth depressive symptoms across an 18-month period. Further, results were not moderated by youth development or gender, indicating that patterns of effects were robust across grade cohorts, as well as boys and girls. Findings also demonstrated concurrent associations between parental anhedonic symptoms and varied domains of positive and negative parenting, although these associations were no longer significant after controlling for parental non-anhedonic symptoms of depression. Together, results suggest that diverse parental depressive symptom profiles may be associated with relatively distinct patterns of risk among offspring, with implications for prevention and intervention efforts.

The present results demonstrated that prospective associations between parental anhedonic symptoms and parent–child chronic stress, as well as youth depressive outcomes were retained after controlling for parental non-anhedonic symptoms of depression. This pattern of findings suggests that parental anhedonia predicts unique variance in these important psychosocial outcomes above and beyond variance explained by parental symptoms of depressed mood more broadly. Clinically, this suggests that children of depressed parents high in anhedonia may be especially vulnerable to experiencing enduring disruptions in the parent–child relationship across development relative to children of depressed parents low in anhedonia. Further, it suggests that children of depressed parents high in anhedonia may be at particularly enhanced risk for the development of depression in adolescence. These findings are consequential, given associations between parent–child chronic stress and youth psychopathology (e.g., Griffith et al., 2020; Starr & Davila, 2008), as well as the potentially life-course persistent negative psychosocial sequalae of depression onsetting during the adolescent transition (Clayborne et al., 2019; Keenan-Miller et al., 2007; Sawyer et al., 2012). Screening for anhedonic symptom levels among populations of depressed and/or dysphoric parents, for example, may represent a time- and resource-efficient strategy for identifying those youth at highest risk for these negative outcomes across development.

Interestingly, parental anhedonic symptoms did not prospectively predict individual differences in youth symptoms of social or physical anxiety. This finding may be somewhat surprising given a wealth of previous work implicating parental depression in transdiagnostic risk for psychopathology among offspring (see Goodman et al., 2011). This finding is consistent, however, with recent work highlighting the utility of symptom-focused, rather than syndrome-focused, approaches to the study of depression (Fried, 2015; Hankin & Griffith, 2023). That is, by demonstrating that parental anhedonic symptoms may confer relatively specific risk for depression relative to anxiety among offspring, the present findings make an incremental contribution to a more granular, precise understanding of intergenerational risk processes in parent–child dyads, and may help to inform optimally targeted and effective research and prevention efforts.

Consistent with previous research demonstrating robust associations between parental depression and individual differences in parenting behaviors (see Lovejoy et al., 2000 and Wilson & Durbin, 2010), results of the present study demonstrate that parental anhedonic symptoms are concurrently associated with both observed and self-reported parenting behaviors, although these associations were not retained after controlling for parental non-anhedonic symptoms. Specifically, parents high in anhedonia were observed to engage in greater conflict and critical behavior, as well as less responsiveness, in the context of a 5-min parent–child interaction task, and parents higher in anhedonia self-reported poorer monitoring and supervision relative to parents lower in anhedonia in the present work. Notably, however, results of sensitivity analyses controlling for parental co-occurring non-anhedonic depressive symptoms indicate that associations between parental depressive symptoms and individual differences in parenting are not specific to parental anhedonia. In contrast, results suggest that parenting is most affected by the elements of depressive phenomenology shared across both anhedonic and non-anhedonic symptom presentations. Future research may be interested in examining specific mechanisms linking these overlapping dimensions of anhedonic- and non-anhedonic depressive symptoms to deficits in parental efficacy.

Contrary to expectations, parental anhedonic symptoms were not associated with parental self-reported positive parenting or involvement in the present work, nor were parental anhedonic symptoms related to observed parental support. It may be that patterns of self-report questionnaire responses were affected by social desirability bias (Podsakoff et al., 2003), or that parents high in anhedonia have impaired insight into these aspects of their own parenting behavior. Additionally, it is possible that the laboratory-based interaction task in which parenting behavior was observed in the present work was not structured in such a way to sensitively detect individual differences in parental support. Future research may wish to replicate findings using behavioral observations of parenting as it unfolds across diverse, naturalistic settings (e.g., using ambulatory assessment methods) to further clarify patterns of effects.

The present work demonstrated several strengths that advance the existing literature. First, the present study employed a multi-method, multi-informant design incorporating both parent and youth self-report questionnaires, as well as behavioral observation and gold-standard contextual stress interview measures (Harkness & Monroe, 2016). The present study design reduces the influence of common method variance and reporter bias (Podsakoff et al., 2003) and permitted us to evaluate study aims in an appropriately rigorous manner. Additionally, the present study is among the first to account for the heterogeneity of parental depression in examinations of intergenerational risk. Indeed, the present work aimed to respond to calls within the field of intergenerational risk research (e.g., Goodman, 2020), as well as within the field of developmental psychopathology, more broadly (e.g., Hankin & Griffith, 2023), for symptom-focused studies of depression-related processes and phenomena. Finally, the present study evaluated associations between parental anhedonic symptoms, parenting, and youth psychosocial outcomes during an especially important and vulnerable period of the lifespan (i.e., middle childhood through adolescence; Paus et al., 2008; Sawyer et al., 2012).

The present work also had several limitations that represent important areas for future research. First, participants in the present study predominantly identified as white/European-American, which may limit the generalizability of findings. Future work should strive to examine associations between parental anhedonic symptoms, parenting, and youth outcomes among samples of more diverse racial and ethnic backgrounds. Further, given research demonstrating individual differences in associations between parenting and emotional processes both within- and between- cultural groups (see e.g., Friedlmeier et al., 2011; Lansford, 2022; Raval & Walker, 2019), future research should evaluate potential cultural differences in observed patterns of effects. Additionally, parents included in the present work were primarily mothers, and future work should aim to include larger numbers of fathers and other caregivers, and to examine whether anhedonia-related deficits in parenting replicate across diverse parental genders and family structures. Further, the present sample was recruited in an unselected manner from the general community. This sampling design has several strengths, including providing insight into patterns of association as they are observed in dyads with a range of clinical histories and symptoms; however, generalizability to clinical populations of parent–child dyads may be limited. Thus, future research is needed to replicate findings in clinical samples to clarify whether mechanisms and indicators of transdiagnostic risk may be differentially influenced by clinically-elevated levels of parental anhedonia. Finally, the selection of parenting variables included in the present work was theoretically-grounded and selected to ensure a broad sampling of parenting behaviors relevant to youth risk and resilience; however, it must be noted that other aspects of parenting outside the scope of the present work (e.g., parental consistency, guilt induction, etc.) may also be affected by parental anhedonia. This represents an exciting area for future research.

Clinical Implications

Together the present findings suggest that assessing for parental anhedonia may be a particularly useful strategy for identifying youth most at risk for the experience of chronic stress, as well as the onset of depressive symptoms during childhood and adolescence. Further, given that anhedonia is related to poorer treatment response (Burkhouse et al., 2018; Khazanov et al., 2020; McMakin et al., 2012), results support the need for enhanced treatment efforts aimed at alleviating parental anhedonic symptoms in order to promote both individual- and familial well-being. Moreover, results suggest that parents affected by diverse presentations of depression, including but not limited to parental anhedonia, may benefit from interventions aimed at reducing negative parenting and enhancing parental responsiveness.

Conclusion

In summary, using multiple methods including self-report questionnaires, behavioral observations, and contextual stress interviews, the present work demonstrated that parental anhedonic symptoms prospectively predict relatively unique variance in parent–child chronic stress, as well as youth risk for depression above and beyond variance explained by parental non-anhedonic symptoms of depression. Together, these findings suggest that parental anhedonic symptoms may be a fruitful target for interventions aimed at reducing youth risk for depression and interrupting intergenerational transmission of psychopathology. Future work investigating different facets and mechanisms of intergenerational risk across units of analysis (e.g., neurobiological, cognitive, etc.) should continue to account for the heterogeneity of parental depression in order to inform optimally efficacious and targeted risk identification and intervention efforts.

Supplementary Material

Supplement

The online version contains supplementary material available at https://doi.org/10.1007/s10802-023-01130-4.

Acknowledgements

This material is based upon work supported by the National Science Foundation Graduate Research Fellowship Program under Grant No. DGE – 1746047.

Funding

The research reported in this article was supported by grants from the National Institute of Mental Health to Benjamin L. Hankin, R01MH077195, and to Jami F. Young, R01MH077178.

Footnotes

Conflicts of Interest The authors declare no conflicts of interest. Dr. Young has developed Interpersonal Psychotherapy—Adolescent Skills Training (IPT-AST) and has received royalties from sales of the book she co-authored that describes the program.

Ethical Approval The study has been conducted in accordance with the ethical standards of the American Psychological Association. The research was approved by the University of Denver and the Rutgers University Institutional Review Boards.

Informed Consent All participants provided written consent as well as assent to participation.

1

Specifically, parental report of IQ was obtained during an initial phone screening assessment during which parents were asked to report on whether their child had any history of diagnoses of autism or intellectual disability (i.e., IQ < 70). No formal tests of IQ were administered in the context of the present work.

2

Data concerning the participating caregiver’s relationship to the participating youth was not available in 3.4% of cases.

3

Study procedures specifically received the following Institutional Review Board approvals: University of Illinois at Urbana-Champaign, Children’s Hospital of Philadelphia, University of Denver, and Rutgers University.

4

For more details regarding this previous work and evidence for the validity of the specific disaggregation of the BDI-II implemented in the present study, please see Supplemental Materials.

5

To preserve the independence of chronic stress ratings, the individual who conducted any given interview was excluded from the coding team for that respective interview. A sufficient number of staff were trained such that three independent raters were available to code each interview.

6

Please see Supplemental Table S1 for additional details regarding the skew and kurtosis describing primary variables of interest.

Data Availability

The datasets analysed during the current study may be available from the senior author on reasonable request.

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Data Availability Statement

The datasets analysed during the current study may be available from the senior author on reasonable request.

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