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. Author manuscript; available in PMC: 2026 Apr 8.
Published in final edited form as: Child Psychiatry Hum Dev. 2024 Oct 8;57(4):1025–1036. doi: 10.1007/s10578-024-01765-4

Parental Depression Symptoms, Skin Conductance Level Reactivity and Parenting: Associations with Youth Psychopathology

Allegra Skye Anderson 1, Rachel E Siciliano 2, Meredith A Gruhn 3, David Cole 1, Lauren M Henry 4, Allison J Vreeland 5, Kelly H Watson 6, Tarah Kuhn 6, Jon Ebert 6, Abagail Ciriegio 1, Bruce E Compas 1
PMCID: PMC11975721  NIHMSID: NIHMS2056863  PMID: 39379644

Abstract

Parental depression symptoms are a prevalent risk factor for internalizing and externalizing problems in youth, with parenting and parents’ physiological stress reactivity representing potential contributing factors in the intergenerational transmission of psychopathology symptoms. In a sample of adolescents (N = 97) and their parents, the current study examined parental depression symptoms, an observational measure of parenting, and parents’ physiological reactivity during a dyadic conflict discussion task in association with adolescents’ internalizing and externalizing psychopathology. Parental depression symptoms and harsh/insensitive parenting showed positive associations with youth psychopathology symptoms. Further, parental depression symptoms were associated with greater externalizing symptoms in youth, specifically for parents with higher physiological reactivity during the conflict task. The present study highlights risks associated with parental depression and harsh/insensitive parenting, and provides evidence for parental physiological reactivity as a moderator of the association between parent and youth psychopathology. Clinical implications, limitations, and directions for future research are discussed.

Keywords: Parenting, Depression, Adolescence, Internalizing, Externalizing

Introduction

Parental depressive disorders and symptoms represent a prevalent risk factor for youth internalizing and externalizing problems [1, 2]. Existing theories suggest that parental depression symptoms are unlikely to function alone in the intergenerational transmission of psychopathology; rather, several factors likely increase the risk in a moderated fashion [3, 4]. Two factors of interest include parenting behaviors and parental physiological stress reactivity. First, the role of parenting behaviors as a mechanism linking parental depression and youth psychopathology symptoms has been supported by extensive research [3]. Second, parental physiological reactivity has been linked to both elevated depression symptoms and hostile parenting behaviors [5]. However, prior research has often focused on categorical measures of parental psychopathology (e.g., MDD diagnosis vs. no diagnosis), self-report measures of parenting, and physiological measures collected from parents interacting with their young children (e.g., infants) [6]. The present study builds on this previous research by using a dimensional measure of parental depression symptoms, a gold-standard observational measure of parenting, measures of parental physiological reactivity during an ecologically valid dyadic conflict discussion task, and testing associations with youths’ symptoms of internalizing and externalizing psychopathology.

Parental Depression Symptoms and Youth Psychopathology

Parental depressive disorders and symptoms have consistently exhibited robust relations with child and adolescent internalizing and externalizing problems [1, 7, 8]. Children and adolescents of depressed parents are more likely to have increased negative cognitive biases [9], heightened levels of fear and irritability [10], impaired interpersonal relationships and behavioral dysregulation [11], and increased risk of depression and anxiety [8]. Further, longitudinal data support a strong association between parental depression and adolescent-onset depression [12]. Although prior research has provided valuable insights into the effects of depression within clinically depressed populations, there have been calls for dimensional approaches to the measurement of psychopathology that would allow researchers to quantify the degree to which symptoms are present for a given individual, regardless of diagnostic status [13, 14]. Accordingly, the present study utilizes a well-validated, continuous measure of parental depression symptoms in a non-clinical sample to provide a comprehensive assessment of the effects of parental depression symptoms across a broad range of clinical severity, thereby increasing the generalizability of findings [15].

Parenting

Parenting is a well-established mechanism in the intergenerational transmission of psychopathology [3, 11]. Numerous studies have shown that elevated levels of parental depression symptoms are linked with diminished quality of parenting, characterized by less warm, sensitive, and responsive parenting behaviors, and more intrusive, irritable, and harsh behaviors [3, 16, 17]. It is posited that these parenting difficulties are indicative of the cognitive, affective, and behavioral symptoms of depression including anhedonia, fatigue, depressed mood, and irritability [18]. For instance, parents who are experiencing depressed mood and fatigue may struggle to be sensitive and responsive to their children’s needs, while parents experiencing high levels of irritability may display more hostile parenting behaviors [17, 18]. Parents’ oscillation between insensitive, harsh, and intrusive parenting behaviors may create a chronically unpredictable and stressful environment for youth [17, 18]. It is posited that recurrent hostile interactions between children and parents may lead to increased internalizing problems in youth (i.e., feelings of hopelessness, worthlessness, and heightened anxiety) [18]. In addition, research suggests that both harsh and insensitive parenting behaviors are linked with heightened levels of externalizing problems [3], potentially as a function of parents’ inability to manage disruptive behavior [19].

Taken together, the effects of parental depression symptoms on youth psychopathology may be stronger in parents who engage in more harsh and insensitive parenting behaviors. However, many studies examining these associations have relied on self-report measures of parenting that are susceptible to social desirability bias, and a more rigorous examination of parenting using observational measures is warranted. To address this limitation in prior work, the present study uses a well-validated observational measure of parenting collected during an ecologically valid dyadic conflict discussion task to better understand the relations among parenting, depression symptoms, and youth psychological adjustment [20–22].

Physiological Reactivity

Psychophysiological reactivity to stress has been identified as a potential moderator of the association between the family environment and youth psychological adjustment [23, 24]. Specifically, the sympathetic nervous system (SNS) branch of the autonomic nervous system is responsible for producing the body’s “fight or flight” response to perceived stress or threat, and dysregulation of SNS activity may undermine an individual’s ability to regulate emotions in response to stress and parent effectively [5, 25, 26]. This, in turn, may influence the development of emotional and behavioral problems in youth. A body of research has emphasized the important role of SNS activity in the context of parenting behaviors, family stress, and parental depression [6, 23, 27, 28]. The present study examines skin conductance level (SCL), a well-studied measure of SNS function linked to emotional arousal [29, 30]. Prior research suggests that moderate levels of SCL reactivity (SCL-R) in response to stress may facilitate an individual’s ability to flexibly adapt to a stressor, low SCL-R may indicate a pattern of blunted or low responsivity, and high SCL-R may indicate physiological hyperreactivity and dysregulation [6, 23].

Some studies suggest that depressed adults have blunted physiological reactivity to both negative and positive stimuli [31, 32] a profile of responsivity that may relate to anhedonia. However, other studies have found increased SCL to be a biomarker for depression [33], a pattern of stress response that may be indicative of more negative emotional reactions [5, 27]. Although findings have been mixed in prior research, depression has generally been linked with reduced flexibility in autonomic stress reactivity [34]. It is also notable that most research examining SNS reactivity in parent–child dyads has focused on youth reactivity [35, 36], and additional research to inform how parental depression symptoms and parental physiological dysregulation may contribute to youth psychological adjustment is warranted.

Theoretical models have also linked parental physiological reactivity with the parenting behaviors they exhibit toward their children [5, 28, 37, 38]. A heightened SNS response to stress may be associated with greater negative emotional reactivity, diminished impulse control, and a greater risk for aggressive behavior in parents [5, 27, 39]. Additionally, parents exhibiting greater SNS reactivity to their children’s frustration report fewer supportive reactions to children’s negative emotions and less emotional availability [28]. Much of the research assessing physiological reactivity and parenting has been conducted with parent-infant dyads. Yet, late childhood and adolescence represent a highly sensitive period for the development of psychopathology [40]. A better understanding of these associations in parent-adolescent dyads may better inform intervention and prevention efforts.

Current Study

The present study builds upon existing research by utilizing a gold-standard observational measure of parenting, an ecologically valid conflict discussion task, and a continuous measure of parental depression symptoms. Using a multi-method and multi-informant design, the current study examines the direct associations between parental depression symptoms, parenting behaviors, and adolescent symptoms of internalizing and externalizing psychopathology. Further, the present study builds on existing research by examining parental SNS reactivity as a moderator of the associations between parental depression symptoms, parenting behaviors, and youth symptoms.

First, it was expected that parental depression symptoms would be associated with more symptoms of internalizing and externalizing psychopathology in youth (Hypothesis 1). Second, it was hypothesized that harsh/insensitive parenting would be associated with higher levels of internalizing and externalizing symptoms in youth (Hypothesis 2). Third, it was expected that harsh/insensitive parenting would moderate the association between parental depression symptoms and youth psychopathology, such that at higher levels of harsh/insensitive parenting, parental depression symptoms would show a stronger positive association with youth internalizing and externalizing symptoms (Hypothesis 3). Finally, exploratory aims were to examine two-way interactions between harsh/insensitive parenting × SCL-R and parental depression symptoms × SCL-R in association with youth symptoms. Given limited research examining these associations, no a priori hypotheses were made.

Method

Participants

Older children and adolescents between the ages of 10 and 15 (M = 12.21; SD = 1.68, 52.6% female) and their parents were enrolled in a study on stress and emotions in the lives of families. Data were collected from a total of 97 dyads (Nyouth = 97, Nparents = 97). Adolescents identified as White (72.2%), African American (15.5%), Asian (5.2%), and other (2.1%), with 5.0% identifying as Hispanic or Latino. Most parents were female (89.6%), married or living with a partner (71.1%), White (73%), and non-Hispanic or Latino (97.9%), with 15.5% identifying as Black or African American, 4.1% Asian, and 3% Other. See Table 1 for additional sociodemographic characteristics.

Table 1.

Demographic characteristics of study participants

Adolescents Parents
Age at assessment, M (SD) 12.22 (1.68) 42.04 (6.98)
Gender, n (%)
 Female 45 (46.4) 87 (89.7)
 Male 51 (52.6) 10 (10.3)
Ethnicity, n (%)
 Hispanic or Latino/a 5 (5.2) 2 (2.1)
 Not Hispanic or Latino/a 90 (92.8) 94 (96.4)
Race, n (%)
 Asian 5 (5.2) 4 (4.1)
 Black or African American 15 (15.5) 15 (15.5)
 White 70 (72.2) 73 (75.3)
 More than one race 5 (5.2) 3 (3.1)
 Other 2 (2.1) 2 (2.1)
Household income, n (%)
 $15,000 or under - 3 (3.1)
 $15,000-$29,999 - 6 (6.2)
 $30,000-$44,999 - 14 (14.4)
 $45,000-$59,999 - 12 (12.4)
 $60,000-$74,999 - 15 (15.5)
 $75,000-$89,999 - 5 (5.2)
 $90,000-$104,999 - 7 (7.2)
 $105,000-$119,999 - 6 (6.2)
 $120,000-$134,999 - 5 (5.2)
 $135,000-$149,999 - 6 (6.2)
 $150,000 or more - 17 (17.5)
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The sample included 97 adolescents and 97 parents

Procedure

Adolescents and their parents were recruited in a southern metropolitan area. To enroll a sample that varied regarding parent and adolescent symptoms of psychopathology, participants were recruited from outpatient clinics, university list-serv postings, and community sites. Trained research assistants screened parents who expressed interest in the study on the phone to determine eligibility. Exclusion criteria were: (a) the parent was not the adolescent’s legal guardian, (b) adolescents were outside the 10–15 years old age range, (c) the dyad did not live together at least 50% of the time for the previous six months, (d) diagnosis of schizophrenia (past or present) in parents or adolescents, or (e) diagnosis of autism spectrum disorder in the adolescent.

First, parents and adolescents completed a battery of online questionnaires. Dyads then completed a laboratory visit lasting approximately four hours, including questionnaires, interviews, and laboratory tasks (e.g., psychophysiological data acquisition and concurrent conflict discussion task). For the physiological data protocol, seven sensors were placed on participants’ torsos and hands. Participants completed a resting baseline phase (3 min), speaking baseline (3 min), conflict discussion task (10 min), stress recovery phase (3 min), and final baseline (3 min). During the conflict discussion task, dyads were instructed to (a) describe a chosen issue, (b) explain each of their positions on the issue, (c) discuss why it has become a source of conflict, and (d) attempt to resolve the issue for 10 min. The University Institutional Review Board approved all procedures and families were compensated.

Measures

Adolescent Internalizing and Externalizing Symptoms

The Youth Self-Report (YSR) was used to assess adolescent internalizing and externalizing symptoms within the previous six months [41]. The YSR is a 112-item self-report checklist of symptoms and behaviors on a 3-point scale (0 = not true, 1 = somewhat or sometimes true, 2 = very often or often true). The Internalizing and Externalizing Scales were used, including 31 items on depression, somatic complaints, and anxiety, and 32 items on aggressive behaviors and rule-breaking. The reliability and validity of the YSR are well-established [41]. The internal consistency reliability for the Internalizing (α = 0.77) and Externalizing (α = 0.81) scales in the full sample were adequate [42]. While the YSR was developed for use starting at age 11, adolescence is often conceptualized as the second decade of life [43], and the present sample included 18 10-year-olds. Internal consistency for this subgroup was good and these participants were retained in analyses (Internalizing α = 0.85, Externalizing α = 0.89).

Parental Depression Symptoms

The Patient Health Questionnaire-9 (PHQ-9) was used to assess parental depression symptoms over the past two weeks. The PHQ-9 is a nine-item self-report measure of depression symptoms on a four-point scale (0 = not at all, 1 = several days, 2 = more than half the days, 3 = nearly every day). The PHQ-9 evaluates the nine Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria for major depressive episodes [44]. Calculation of a summary score indicates the severity of depression symptoms: 0–4 (minimal depression), 5–9 (mild depression), 10–14 (moderate depression), 15–19 (moderately severe depression), and 20–27 (severe depression) [45]. The reliability and validity of the PHQ-9 are well-established [45, 46]. Internal consistency reliability for the PHQ-9 was good for the present sample (α = 0.85).

Conflict Discussion Task

Dyads completed an adapted version of the Issues Checklist [22] to guide their discussion task topic. This requires respondents to indicate which of 44 topics they discussed within the last four weeks (e.g., doing homework, talking back to parents), and rate how they felt during those discussions (1 = calm to 5 = angry). Research assistants compared parent and youth responses on the Issues Checklist to determine which topics were highly rated for both. If parent and adolescent responses were inconsistent, research assistants selected the topic that the adolescent rated highest.

SCL

Standard methods were followed for acquiring SCL [47, 48]. To collect SCL readings, two disposable silver/silver-chloride (Ag–AgCl) electrodes (1″ × 1″ foam, 0% chloride gel) were placed on the hypothenar and thenar eminences of parents’ non-dominant hand. Psychophysiological data were recorded using the MW1000A acquisition system, BioNex 8-slot chassis (MW50371108), BioNex Impedance Cardiography, and GSC (M371100–00), as well as disposable pediatric snap electrocardiogram (ECG) electrodes from MindWare, Technologies. Ltd (Gahanna, OH, USA). Parents completed an adaptation phase to acclimate to the lab setting (3 min), followed by a resting baseline (3 min) and conflict discussion task (10 min). During the acclimation and resting baseline phases, parents were instructed to rest quietly and refrain from moving or speaking. All psychophysiological data were processed and scored using MindWare’s electrodermal activity (EDA) software (MindWare Technologies Ltd., Gahanna, OH, USA). The MindWare program identified potential artifacts, and trained research assistants visually scanned all participant data to identify additional artifacts, and missing and/or misidentified psychophysiological responses. Identified artifacts and program issues were manually edited as needed. As suggested in the MindWare manual (https://support.mindwaretech.com/manuals/software/eda/3-2/), epochs requiring greater than 50% of data estimation and editing were excluded from analyses. Within-participant difference scores (i.e., SCL-R) were used, where SCL-R scores larger than zero suggest an increase relative to baseline, while scores less than zero indicate a decrease relative to baseline.

Parenting Behaviors

The Iowa Family Interaction Rating Scales (IFIRS) [21], a macro-level system, was used to code parental verbal and nonverbal behaviors during the videotaped discussion task on a 9-point scale (1 = absence of behavior, 9 = highest intensity and frequency of behavior). When discerning the score for each behavior, the intensity, frequency, contextual, and affective nature of the behavior are considered. The validity of IFIRS has been well-established in correlational analyses and confirmatory factor analyses [21, 49]. The parent-adolescent discussion tasks were coded by a team of trained graduate and undergraduate student research assistants. All trained coders passed a written test of code definitions and examples (90% accuracy) and reached 80% reliability on previously coded videos. All videos were double-coded; two trained research assistants independently coded all videos and then met to discuss and reach consensus. Per the IFIRS manual, when ratings differed by a single point, the higher score was utilized. Ratings that differed by two or more points were resolved through discussion.

A harsh/insensitive parenting composite was created by summing five parental codes (hostility, intrusive, lecture/moralize, reverse-scored child monitoring, and reverse-scored listener responsiveness). This was theoretically derived to represent behaviors that may be present in parents with elevated symptoms of depression based on prior research [18, 20, 50]. The internal consistency reliability for the harsh/insensitive parenting composite was adequate (α = 0.76). Interrater reliability for the individual codes within the observed harsh/insensitive composite ranged from 0.67 to 0.87 (M = 0.78). Code definitions and examples are presented in Supplementary Table 1.

Data Analytic Approach

SCL

Data were scored in 60-s epochs using MindWare analysis software (EDA version 3.2.4). Resting levels of skin conductance were obtained by averaging the 60-s mean SCL response during baseline conditions, while skin conductance during stress tasks was obtained by averaging responses during 60-s epochs of the conflict discussion task. SCL reactivity (SCL-R) was computed as a within-participant difference (i.e., change score) by subtracting pre-task resting SCL from the conflict discussion task SCL.

Preliminary Analyses

Means and standard deviations were calculated for key study variables and the distributions of scores were examined for skewness, kurtosis, and outliers. Bivariate correlations were conducted to assess associations between study variables. Paired samples t-tests to compare SCL values during the conflict task and resting baseline were computed to determine that the conflict discussion task successfully elicited physiological responses. All tests were conducted at α = 0.05.

Power

Power analyses using α = 0.05 and power = 0.80 suggested sufficient power to detect small-to-medium correlations (r = 0.27) with a total sample of n = 97, two-tailed (G*Power 5) [51]. The sample size was sufficient to detect small effects for t-tests (d = 0.28). Models testing Hypotheses 1–2, with n = 97, α = 0.05, power = 0.80, and a potential of two covariates (e.g., adolescent age and gender) for each model, yielded power to detect small-to-medium effects (f2 = 0.08). For models testing Hypothesis 3 and exploratory two-way interactions, the present sample of n = 97 yielded power to detect small-to-medium effects (f2 = 0.12).

Missing Data

Two parents did not complete the discussion task that was coded for parenting behaviors, and seven parents had unusable SCL data. Little’s MCAR test showed that the data were missing completely at random (p = 0.88). Multiple imputation was used in all analyses using these variables to minimize potential bias [52].

Hypothesis Testing

A series of multiple linear regression (MLR) models were used to examine the main effects of parental depression symptoms (Hypothesis 1), harsh/insensitive parenting (Hypothesis 2), and their interaction (Hypothesis 3) on youth internalizing and externalizing symptoms. Additional MLR models were conducted to predict youth symptoms from the interactions between (1) parental depression symptoms × SCL-R and (2) harsh/insensitive parenting × SCL-R. To construct the regression models, all variables defining products to test interactions were mean-centered before computing interaction terms. Separate models were conducted for internalizing and externalizing symptoms and controlled for adolescent age and gender in all models.

Results

Preliminary Analyses

Table 2 presents means, standard deviations, and value ranges for key study variables. Adolescent internalizing symptoms were approximately one-half standard deviation above the normative mean (MT-score = 54.72, SD = 10.01), and adolescent externalizing symptoms approximated the normative mean (MT-score = 51.15, SD = 9.71) [41]. Consistent with efforts to recruit parents with a broad range of severity of depression symptoms, parental PHQ-9 scores ranged from minimal depression to severe depression, with a mean score of minimal-to-mild depression (M = 4.93, SD = 4.53). Correlations between key study variables are reported in Table 3. Paired samples t-tests revealed that SCL, t(89) = 7.27, p < 0.001, significantly increased from parents’ mean resting baseline (M = 4.57, SD = 4.42) to their mean conflict discussion task measurement (M = 7.00, SD = 5.31). This demonstrates that the conflict discussion task elicited an SNS response in parents.

Table 2.

Descriptive statistics for key study variables

Variable M SD Min Max
Adolescent internalizing symptomsa 54.72 10.01 32 81
Adolescent externalizing symptomsa 51.15 9.71 30 81
Parent depression symptoms 4.93 4.53 0 24
Harsh/insensitive parenting 20.73 5.43 9 36
Parent SCL-R 2.53 3.31 − 5.76 16.90
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SCL-R skin conductance level reactivity

a

Values presented are T scores (M = 50; SD = 10)

Table 3.

Correlations among key study variables

Variables 1 2 3 4 5 6
1. Adolescent Internalizing Symptoms -
2. Adolescent Externalizing Symptoms 0.46*** -
3. Parent Depression Symptoms 0.21* 0.23* -
4. Harsh/Insensitive Parenting 0.09 0.23* − 0.01 -
5. Parent Skin Conductance Level Reactivity 0.01 0.01 − 0.02 − 0.10 -
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*

p < 0.05

**

p < 0.01

***

p < 0.001

†

p < 0.10

Multiple Linear Regression Analyses

Hypothesis 1: Parental Depression and Adolescent Symptoms

Separate models were conducted to examine associations among parental depression symptoms with adolescent symptoms (Table 4, Models 1–2). Parental depression symptoms were positively associated with youth internalizing (β = 0.22, p = 0.02) and externalizing symptoms (β = 0.23, p = 0.03), where higher parental depression symptoms corresponded to higher adolescent internalizing and externalizing problems.

Table 4.

Regression analyses predicting adolescent internalizing and externalizing symptoms from parent depression and parenting

DV: Internalizing Sx β t p DV: Externalizing Sx β t p
Model 1 F(3,93) = 5.41**; adjusted R2 = 0.12** Model 2 F(3,93) = 1.90; adjusted R2 = 0.03
Adolescent gender 0.28 2.92** 0.001 Adolescent gender 0.07 0.72 0.473
Adolescent age 0.18 1.90† 0.061 Adolescent age 0.00 0.03 .974
Parent depression 0.22 2.32* 0.023 Parent depression 0.23 2.26* 0.026
Model 3 F(3,93) = 3.97*; adjusted R2 = 0.09* Model 4 F(3,93) = 2.05; adjusted R2 = 0.03
Adolescent gender 0.29 2.99** 0.004 Adolescent gender 0.10 0.98 0.331
Adolescent age 0.16 1.59 0.116 Adolescent age − 0.03 − 0.28 0.781
H/I Parenting 0.12 1.21 0.229 H/I Parenting 0.24 2.35* 0.021
Model 5 F(5,91) = 3.54**; adjusted R2 = 0.12** Model 6 F(5,91) = 2.98*; adjusted R2 = 0.09*
Adolescent gender 29 3.02** 0.003 Adolescent gender 0.11 1.12 0.265
Adolescent age 0.18 1.87† 0.065 Adolescent age 0.00 − 0.00 0.998
Parent depression 0.22 2.31* 0.023 Parent depression 0.25 2.50* 0.014
H/I Parenting 0.12 1.23 0.222 H/I Parenting 0.28 2.76** 0.007
Dep × H/I 0.01 0.11 0.913 Dep × H/I 0.17 1.68† 0.095
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DV dependent variable, Sx symptoms, H/I harsh/insensitive, Dep depression

†

p < 0.10

*

p < 0.05

**

p < 0.01

Hypothesis 2: Harsh/insensitive Parenting and Adolescent Symptoms

Separate models examined associations among harsh/insensitive parenting with adolescent internalizing and externalizing symptoms (Table 4, Models 3–4). Harsh/insensitive parenting showed a significant positive association with adolescent externalizing symptoms (β = 0.24, p = 0.02), but not with internalizing symptoms (β = 0.12, p = 0.23).

Hypothesis 3: Interaction Between Parental Depression and Harsh/insensitive Parenting

Separate models were conducted to examine the association between adolescent symptoms and the interaction between parental depression symptoms and harsh/insensitive parenting. Within the interaction models, main effects for parental depression symptoms in association with adolescent internalizing (β = 0.22, p = 0.02) and externalizing symptoms were retained (β = 0.25, p = 0.01). Further, the main effect for harsh/insensitive parenting in association with externalizing symptoms remained significant in the interaction model (β = 0.28, p = 0.01). However, there were no significant interactions between harsh/insensitive parenting and parental depression symptoms (Table 4, Models 5–6).

Exploratory Analyses: Parenting, Parental Depression, and Parental SCL

There were no significant interactions between harsh/insensitive parenting and SCL-R in association with adolescent symptoms (ps > 0.05; Table 5, Models 3–4). However, there was a significant interaction between parental depression symptoms and SCL-R in association with youth externalizing symptoms (β = 0.24, p = 0.04; Table 4, Model 2), where at moderate (b = 0.34, t(91) = 2.16, p = 0.03) and high (b = 0.62, t(91) = 3.10, p = 0.003) levels of SCL-R, parental depression symptoms were associated with greater externalizing symptoms in adolescents (Fig. 1).

Table 5.

Regression analyses predicting adolescents’ symptoms from parent depression and SCL-R

DV: Internalizing Sx β t p DV: Externalizing Sx β t p
Model 1 F(5,91) = 3.68**; adjusted R2 = 0.12** Model 3 F(5,91) = 2.06†; adjusted R2 = 0.05†
Adolescent gender 0.29 3.01** 0.003 Adolescent gender 0.09 0.84 0.402
Adolescent age 0.19 2.01* 0.047 Adolescent age 0.02 0.21 0.831
Parent depression 0.21 2.22* 0.029 Parent depression 0.22 2.16* 0.034
SCL-R − 0.10 − 0.92 0.359 SCL-R − 0.11 − 0.96 0.341
Dep × SCL-R 0.16 1.44 0.154 Dep × SCL-R 0.24 2.11* 0.038
Model 1 F(5,91) = 2.38*; adjusted R2 = 0.07* Model 5 F(5,91) = 1.33; adjusted R2 = 0.02
Adolescent gender 0.30 2.95** 0.004 Adolescent gender 0.10 0.92 0.361
Adolescent age 0.15 1.56 0.121 Adolescent age − 0.03 − 0.28 0.778
H/W Parenting 0.12 1.21 0.231 H/W Parenting 0.25 2.40* 0.019
SCL-R − 0.02 − 0.17 0.863 SCL-R 0.03 0.28 0.782
H/W × SCL-R 0.04 0.39 0.696 H/W × SCL-R 0.08 0.74 0.463
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DV dependent variable, Sx symptoms, Dep depression, SCL-R skin conductance level reactivity, H/W Harsh/withdrawn

†

p < 0.10

*

p < 0.05

**

p < 0.01

Fig. 1.

Fig. 1

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Interaction between parent depression symptoms and skin conductance level reactivity predicting adolescent externalizing symptoms. Note. *indicates statistically significant slopes

Discussion

The current study examined relations between parental depression symptoms and harsh/insensitive parenting in association with adolescent psychopathology and parental SNS reactivity as a potential moderator of these associations. Results showed positive associations among parental depression symptoms and harsh/insensitive parenting with youth psychopathology symptoms. Further, associations between parental depression symptoms and youth psychopathology were stronger for parents with greater SNS reactivity, emphasizing the interactive roles of parental physiological reactivity and parental depression symptoms. Findings build upon prior research by leveraging a multi-method and multi-informant design to test associations, including an observational parenting measure collected during an ecologically valid task, a measure of SNS reactivity, and parent- and child-report of symptoms.

Parental Depression Symptoms and Adolescent Symptoms

Consistent with well-established associations between parental depression symptoms and youth psychopathology [1, 2, 7, 8], parental depression symptoms were positively associated with adolescent internalizing and externalizing problems. Importantly, a body of research has shown that remission of parental depression is associated with decreased symptoms of psychopathology in youth, regardless of whether children receive their own psychological treatment [53, 54]. If parents engage in their own treatment, this may enable them to strengthen parenting behaviors, subsequently improve parent–child relationship quality, and support positive outcomes in youth [53]. In contrast, children of parents with chronic, untreated depression show worsening psychopathology over time, as well as decreased compliance and reduced efficacy of mental health treatment [54]. Thus, treatment of parental depression symptoms may serve as a robust preventative intervention that benefits both parents and their adolescents.

Observed Parenting and Adolescent Symptoms

In partial support of Hypothesis 2, higher observed harsh/insensitive parenting was associated with more externalizing problems in adolescents, though not adolescent internalizing psychopathology. This is consistent with prior work showing stronger associations between harsh parenting behaviors and externalizing versus internalizing problems in youth [20, 55, 56]. Harsh parenting may impede the development of adolescents’ emotion- and self-regulation abilities, which may contribute to externalizing problems in youth [57]. Thus, interventions that focus on reducing harsh/insensitive parenting behaviors may be beneficial for families.

Contrary to hypotheses, parenting behaviors did not moderate the association between parental depression and adolescent symptoms. There are several potential interpretations of this null finding. First, the interactive effects of parental depression symptoms and parenting behaviors are likely more salient over time, and the present study’s cross-sectional design may have precluded the ability to detect the joint effects of parenting and parental depression symptoms on adolescent symptoms. Second, effect sizes for some nonsignificant interactions were comparable to the statistically significant main effects of parental depression symptoms and parenting behaviors. Thus, analyses may have been underpowered to detect interaction effects that may have reached statistical significance in a larger sample. Finally, although the present findings support well-established direct associations between parental depression symptoms, parenting behaviors, and adolescents’ symptoms of psychopathology [3, 7, 11, 12, 20], parents with elevated levels of depression symptoms were not statistically more likely to engage in harsh/insensitive parenting behaviors. Given the significant interaction between parental depression symptoms and physiological reactivity, it is possible that other factors were more salient in the present sample.

SCL-R, Parental Depression Symptoms, and Adolescent Externalizing Problems

The present findings add to an emerging body of research indicating physiological hyperreactivity as a moderator of the association between parental and youth psychological problems [6, 58]. Specifically, parental depression symptoms were associated with more adolescent externalizing symptoms only for parents with higher SNS reactivity during the conflict task. Although there is some evidence that depressed individuals tend to exhibit blunted patterns of physiological stress reactivity [26, 31, 32], increased SCL-R has also been identified as a biomarker for depression and may be indicative of more negative emotional reactions [5, 27, 33].

Considering findings suggesting that the combination of physiological dysregulation and parental depression symptoms is particularly harmful to youth, clinical interventions utilizing biofeedback may be useful for improving the efficacy of parent–child interventions. Providing individuals with real-time physiological information may be an effective way to support emotion identification and enhance emotion regulation skills [59]. For instance, a recent RCT demonstrated that children and adolescents who successfully learned SCL self-regulation showed reduced aggression over time [60]. While additional research is warranted within the context of family therapy, dyadic biofeedback may enable parent–child dyads to learn to understand the mind–body connection, attend to each other’s physiology, tolerate the other’s stressed behavior while supporting regulatory behaviors, and generalize these skills to their routine dyadic interactions (i.e., attachment-informed biofeedback) [61]. As a supplement to treating parental depression symptoms and supporting the use of more effective parenting strategies, dyadic biofeedback may also improve the families’ understanding of the mechanisms that regulate their interpersonal interactions [62].

Strengths, Limitations, and Future Directions

The present study has several notable strengths, including the use of a multi-informant and multi-method design to test associations among parental depression symptoms, observed parenting behaviors, and SNS reactivity during an ecologically valid task with adolescent psychological problems. Further, the current study leveraged an observational measure of parenting, a dimensional measure of parental depression, and is among the first to examine interactions between parental depression symptoms and parental SNS reactivity in association with adolescent symptoms of psychopathology. These strengths notwithstanding, several limitations can be addressed in future research.

Given the cross-sectional design, causal inferences cannot be made regarding the relations among parental depression symptoms, parenting behaviors, physiological reactivity, and adolescent symptoms of psychopathology. Longitudinal research can provide a more rigorous assessment of the temporal associations among these variables. While the present study focused on parental factors, child-focused characteristics such as youths’ behavior, self-reported emotional reactivity to stress, and physiological reactivity likely also contribute to youth adjustment [35, 36, 63]. Future research should examine the joint influences of parent and child behaviors, child emotional and physiological reactivity, and child psychopathology to better inform intervention and prevention efforts. Further, while analyses were able to detect small-to-medium effects for complex regression models assessing interaction effects, future research using larger samples is warranted to better understand the nature of these associations. Finally, the present study focused on parents with a broad range of severity in depression symptoms to increase the generalizability, reliability, and validity of findings [15]. However, it is important to note that several parents in the present sample reported minimal or mild levels of depression, and thus, findings may not generalize to parents with more severe levels of depression symptoms. Future research should seek to replicate findings in samples of parents with clinically significant depression.

Conclusion

Parental depression, harsh parenting, and physiological stress reactivity have been examined as risk factors for the development of youth psychopathology. The present findings highlight the risks associated with parental depression symptoms and harsh/insensitive parenting behaviors, and provide evidence for SNS hyperreactivity as a moderator of the association between parent and youth psychopathology. These findings have significant clinical implications, motivating parental depression symptoms and parenting behaviors as intervention and prevention targets, and supporting the use of dyadic biofeedback in family therapy.

Summary

Parental depression symptoms represent a salient risk factor for youth psychopathology, and existing theories suggest that several factors likely increase the risk of intergenerational transmission of psychopathology in a moderated fashion. There is extensive research supporting the role of parenting behaviors as a mechanism linking parental depression symptoms and youth psychopathology, and parental physiological reactivity has been linked to both elevated depression symptoms and hostile parenting behaviors [3–5]. In a sample of adolescents (N = 97) and their parents, the present study examined relations between parental depression symptoms and harsh/insensitive parenting in association with adolescent internalizing and externalizing psychopathology and parental SNS as a potential moderator of these associations. Results showed significant positive associations between parental depression symptoms and adolescent internalizing and externalizing symptoms. Harsh/insensitive parenting was associated with adolescent externalizing, but not internalizing symptoms. Further, associations between parental depression symptoms and youth psychopathology were stronger for parents with greater SNS reactivity, emphasizing the interactive roles of parental physiological reactivity and parental depression symptoms. This study builds upon previous research by leveraging a multi-method and multi-informant design to test associations, including an observational parenting measure collected during an ecologically valid task, a measure of SNS reactivity, and parent- and child-report of symptoms. Findings have significant clinical implications, motivating parental depression symptoms and parenting behaviors as intervention and prevention targets, and supporting the use of dyadic biofeedback in family therapy.

Supplementary Material

Supplementary Table 1

Footnotes

Declarations

Conflict of interest The authors declare no competing interests.

Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/s10578-024-01765-4.

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Data Availability

No datasets were generated or analysed during the current study.

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Associated Data

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Supplementary Materials

Supplementary Table 1
NIHMS2056863-supplement-Supplementary_Table_1.docx (13.3KB, docx)

Data Availability Statement

No datasets were generated or analysed during the current study.

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