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. Author manuscript; available in PMC: 2021 May 14.
Published in final edited form as: Dev Psychobiol. 2020 Jul 16;63(1):16–30. doi: 10.1002/dev.22013

Parent’s anxiety links household stress and young children’s behavioral dysregulation

Andrea Fields 1, Chelsea Harmon 1, Zoe Lee 1, Jennifer Y Louie 2, Nim Tottenham 1
PMCID: PMC8120989  NIHMSID: NIHMS1699759  PMID: 32671835

Abstract

Young children rely heavily on their caregivers to gain information about the environment, especially during times of duress. Therefore, considering parental assessments of behavior in the context of stressful environments may better facilitate our understanding of the longstanding association between early environmental stressors and changes in child behavior and physiology. Confirming many previous reports, a higher degree of household stress exposure was associated with elevated mental health symptoms in 2- to 6-year-old children (N = 115) (anxiety and externalizing behaviors), which were verified in a subset of children with laboratory-based behaviors (N = 46). However, these associations were mediated by parental anxiety symptoms, which was also associated with increased cortisol levels in children. A closer look at the stressors indicated that it was the adult-targeted, and not the child-targeted, stressors that correlated most with children’s behavior problems. These results highlight the importance of considering the mediating effect of parents, when examining associations between household stress and young children’s behavioral development.

Keywords: Stress, Parental Care, Intergenerational, Psychopathology, Children

Introduction:

Decades of research have established a link between childhood stress and heightened risk for emotional behavior problems, alterations in brain development and stress physiology, as well as psychopathology later in life (Hanson et al., 2015; McEwen, 2008; Green et al., 2010; Lupien et al., 2009; Werner et al., 1967). Extremely stressful experiences, including community violence, poverty, living in war-zones, and natural disasters have all been associated with these alterations (Amone-P’Olak et al., 2007; Fowler et al., 2009; Green et al., 1991; Huaqing Qi and Kaiser, 2003, McEwen, 2008; Noble et al., 2012; Swenson et al., 1996; Theall et al., 2017). Stressful events are unfortunately quite common during early childhood, with 46% of children in the United States having faced at least one adverse childhood experience (Sacks et al., 2014), and young children facing the greatest risk (CDC, 2019).

Previous research has highlighted parental psychopathology as a mediator of these associations, motivated by the logic that early instances of stress often include, and directly impact the caregiver as well as the child. Moreover, stress-induced alterations in the caregiver’s behavior can significantly impact the child’s development. The family stress model has posited that experiences of financial hardship indirectly influence problematic child behavior through increased emotional distress in caregivers and subsequent disrupted parenting practices (Conger et al., 2002). In line with this theoretical framework, parents’ symptomatology has been shown to mediate the association between financial hardship and preschoolers’ distress, internalizing behavior, and externalizing problems (Conger et al., 2002; Kiernan & Huerta, 2008; Rijlaarsdam et al., 2013). Similarly, following natural disasters and exposure to war, parental distress and posttraumatic stress disorder (PTSD) symptomatology have been linked to the presence and duration of preschool and school-age children’s emotional and behavioral problems (La Greca et al., 1996; Lewis, 1942; Scheeringa & Zeanah, 2008; Swenson et al., 1996). This link has also been demonstrated intergenerationally, with maternal anxiety and depressive behavior mediating the association between maternally-experienced adverse childhood events, and preschoolers’ internalizing and externalizing behaviors (Letourneau et al., 2019). Similarly, links between parental psychopathology and children’s outcomes have been observed at the level of stress physiology, with parental psychopathology showing associations with altered cortisol levels in children for both diurnal rhythms and in response to stressors (Brennan et al., 2008; Dougherty et al., 2013a; Dougherty et al., 2013b; Vänskä et al., 2016). Measures of physiology might be particularly useful to obtain in studies concerning the mediating effects of parental psychopathology on child outcome, as parental psychopathology may impact reporting validity. These studies highlight the mediating role of parental symptoms in the context of extreme stress, suggesting that the development of behavioral problems in young children is strongly tied to their caregivers’ responses to stressful events. The present study aimed to examine the role of parents’ behavior in linking more common, everyday household stressors and young children’s outcomes. Since parental behaviors should be especially influential for younger ages, the current study focused specifically on young children (2–6 year olds).

During early childhood, emotional responding is primarily regulated by the parent through multiple routes. For example, starting in infancy, children seek out parental cues when evaluating novel contexts and stimuli (i.e. social referencing) (Zarbatany & Lamb, 1985). Parents’ anxious or fearful behavior is often a readily visible and apparent cue, which can be transmitted via social referencing to young children (Burstein et al., 2010; Murray et al., 2008; Sorce et al., 1985). In contrast, parents’ regulated behaviors have been shown to successfully buffer young children’s responses to stressful environments (Katz & Gottman, 1997). This work supports the idea that parental cues can be important guides for young children’s behavioral and emotional development, and these behaviors can be especially salient during stressful times (Callaghan & Tottenham, 2016).

While extreme stressors have been shown to increase risk for negative outcomes in children, the links between more normative household stress and child symptoms have received considerably less attention. Less devastating and more routine experiences have also been associated with problematic behavior and later psychopathology. Household stressors, or life events as termed by Coddington (1972), represent a range of potentially stressful, but frequently encountered life-changing experiences, such as parental divorce, arguments with siblings, and changing schools. While experiencing a single household stressor, like parental divorce or unemployment, has been associated with behavioral and emotional problems in school-age children (Harland et al., 2002; Kroes et al., 2002), an accumulation of household stressors (e.g. school problems, familial illness, and arguments between parents) predicts school-age children’s anxiety symptoms (Platt et al., 2016). These findings suggest that even commonly-occurring household stressors are correlated with children’s behavior problems.

Although parental symptoms have been examined within the context of household stressors, their role in explaining child outcome has not yet been established. In one study of older youth (i.e. school-age children and adolescents), parental symptomatology was not found to mediate the link between household stress and youth anxiety (Platt et al., 2016). However, the parent sample was clinically anxious, raising the possibility of ceiling effects due to a restricted range of parental anxiety. Additionally, parental anxiety itself was not tested in isolation, but rather a sum score of various parental psychopathology symptoms was used. While different forms of parental mental health problems, like depression, have shown strong ties to young children’s behavioral and physiological outcomes (Dougherty et al., 2013a; Dougherty et al., 2013b; Murray et al., 1996), anxiety might be particularly important to examine in isolation when considering the behavioral transmission of parental symptoms, as parental fear behaviors are available cues that have been shown to modulate young children’s behavior during stressful scenarios (Sorce et al., 1985). Instead of parental symptomatology, Platt and colleagues (2016) found that parenting-related stress mediated the link between household stress and youth. Parenting-related stress, or ‘parenting hassles’ (Crnic et al., 2005), has emerged as a mediator of this association in other studies as well, including samples of young children with previous clinical referrals (Östberg & Hagekull, 2013). This work suggests that parental phenotypes play an important role in explaining young children’s behavioral outcomes even in the context of normative household stress. However, directionality between parenting-related stress and child behavior can be particularly difficult to determine when children’s behavior is problematic (Neece et al., 2012), considering that parenting-related stress is evaluated using items specifically regarding the child.

The present study sought to assess whether, even within a normative range of household stress in a non-clinical sample, parental anxiety symptomatology mediated the link between household stress exposure and behavioral outcomes among young children (i.e. anxiety and externalizing behaviors). We anticipated that increased household stress and parent anxiety would be associated with heightened anxiety and externalizing behaviors in young children. To support the assessments of parent-reported behaviors, observable in-laboratory child behavior and child cortisol was measured. We also conducted exploratory analyses to examine the potential differential impacts of child-targeted versus adult-targeted stressors on child outcomes.

Methods:

Participants:

Participants included 115 young children 2 to 6 years of age (M = 4.26, SD =. 80) from the community and their parents, recruited originally from state birth records, posted flyers or friend referral for two separate studies, one to examine normative preschool temperament (N = 52) and the other to study fear conditioning (N = 104), with 41 participating in both studies (see Table 1 for demographic information). Parents were told the purpose of both studies was to examine normative emotional development. To increase sample size, we combined both cohorts into the current study, as no significant differences were noted in recruitment procedures or key variables between participants who had completed the temperament study, conditioning study and both studies (i.e. household stress, parent anxiety, child anxiety or externalizing behavior). During telephone prescreening, parents reported that children had never been diagnosed with any behavioral/psychological diagnoses, neurological problems or learning disabilities. We asked that the primary caregiver accompany the child to the visit. The Institutional Review Board at the University of California Los Angeles approved the protocol, and all parents provided written consent. In total, parents completed questionnaires concerning household stressors (N = 78), parental anxiety (N = 102), parenting-related stress (N = 81), and child behavior (N = 115), while subsets provided laboratory behavior (N = 46) and cortisol assessments. Salivary cortisol was collected from children at home across a two-day period (N = 56).

Table 1:

Demographics

Measure Descriptive Statistics N
Child Age (years) M ± SD: 4.26 ± .80 115
Yearly Household Income ($) Median: 100,001 – 150,000 111
Range: <10,000 – >200,001
Child Sex 54.8% F 63/52
Parent Sex 82.6% F 95/7
Child Race
 African-American/Black 11.3% 13
 Asian-American 20.9% 24
 Native Hawaiian/Other Pacific
Islander 1.7% 2
 European-American/Caucasian 79.1% 91
 Other 12.4% 11
Child Ethnicity
 Hispanic/Latinx 18.3% 21
 Non-Hispanic/Latinx 80.0% 92
 Missing 1.7% 2
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Note: Total exceeds 100% to account for those endorsing more than 1 race.

Measures

Household Stress:

Household stress was assessed using a version of the Coddington Life Events Scale (Coddington, 1972). This 40-item questionnaire assesses the presence and impact of a range of normative household stressors that could have occurred within the past 3 or 12 months. In the current study, we only chose to examine events that had been experienced within the past 3 months, as the majority of events endorsed for the 12 month period had occurred within the past 3 months. Parents rated the impact of each event using a 4-point scale with a score of 0 corresponding to an event that had “no impact” on the child, and a score of 3 corresponding to an event that had a “great deal” of impact on the child. Weighted scores were calculated by multiplying the presence of any endorsed item by the impact rating. These individual weighted scores were then summed to create a total sum score of weighted household stress exposure for each participant (see Table 2 for descriptive statistics). Natural log transformation was performed to normalize the distribution of the data (Skew = 1.87).

Table 2:

Descriptive Statistics of Variables

Measure M SD Range N
Household Stress 2.19 2.73 0 – 14 78
Parent Anxiety Scores 33.97 8.74 20 – 65 102
Parenting-Related Stress Mean Scores 4.38 .45 2.85 – 5.00 81
Child Anxiety Scores 9.57 7.84 0 – 38.37 107
Child Externalizing Problems 43.11 9.59 28 – 79 109
Observed Internalizing Behavior (Factor 1) −.010 1.01 −2.05 – 2.27 46
 Snack Delay Fidgeting Score .30 .32 0 – 1.29 46
 Snack Delay Nonverbal Distraction Score .68 .36 0 – 1.49 46
 Tower of Patience Fidgeting Score .35 .34 0 – 1.39 46
 Tower of Patience Nonverbal Distraction Score 1.05 .34 .08 – 2.03 46
Observed Externalizing Behavior (Factor 2) .026 1.00 −1.50 – 2.10 46
 Snack Delay Anticipatory Score 1.52 .49 1.00 – 2.67 46
 Snack Delay Verbal Distraction Score .31 .35 0 – 1.39 46
 Tower of Patience Anticipatory Score 1.70 .62 .86 – 3.64 46
 Tower of Patience Verbal Distraction Score .59 .56 0 – 1.95 46
Cortisol Levels at Wake 18.97 8.49 7.31 – 46.50 46
Cortisol Levels at Wake + 45 15.61 6.16 6.39 – 33.59 46
Cortisol Levels at 5PM 4.44 2.35 1.50 – 12.58 46
Cortisol Levels at 8PM 2.61 1.86 .70 – 7.72 46
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In addition to this total score, we also separated items to create two additional subscales for an exploratory analysis: child-targeted and adult-targeted stressors. The child-targeted stressor score comprised the summed weighted total of items deemed to impact children more than adults based on those items encompassing child-targeted language and events directly experienced by children (i.e. increase in number of arguments between you and your siblings). The adult-targeted stressor score comprised the summed weighted total of items deemed to impact adults more than children based on those items encompassing adult-targeted language and events directly experienced by adults (i.e. change in parents’ financial status) (see Table 4). Note that items could be included in the child-targeted and adult-targeted stressor scales if they encompassed events equally targeted at children and adults (i.e. death of significant family member or friend). An independent-samples t-test revealed that there was no significant difference in the instrument-provided ‘trauma’ values (i.e. Life Change Units) for child-targeted stressors (M = 38.1, SD = 6.38) and adult-targeted stressors (M = 50.0, SD = 22.6); t(21) = −1.51, p = .15 (Coddington, 1972). However, in our sample, child-targeted stressors were rated overall as significantly more impactful (M = .22, SD = .21) than adult-targeted stressors (M = .13, SD = .22) by parents in the current study, t(77) = 3.99, p < .001. Due to a skewed, and zero-heavy, distribution of both the adult (Skew = 2.15) and child-targeted stressor scores (Skew = 1.56), these subscales were transformed into binary variables, representing the presence or absence of at least one child-targeted or adult-targeted stressor. Of the 78 children with household stress data, 43 children had experienced at least one child-targeted stressor and 22 children had parents who experienced at least one adult-targeted stressor (see Supplementary Materials for distributions).

Table 4:

Table of Adult-Targeted and Child-Targeted Stressors

Adult-Targeted Stressors Items Child-Targeted Stressor Items
Change in parents’ financial status Acquiring a visible deformity
Change of a parent’s occupation requiring his/her increased absence from home Change in your acceptance by peers
Change to a new school
Death of a parent Death of a close friend
Death of significant family member or friend Death of significant family member or friend
Decrease in number of arguments between parents Decrease in number of arguments with parents
Development by a parent of an emotional problem, such as depression, lasting 3 weeks or more Discovery of being an adopted child
Divorce of parents Having a visible congenital deformity
Increase in number of arguments between parents Increase in number of arguments between you and your siblings
Jail sentence of a parent for more than one year
Jail sentence of a parent for one year or less Increase in number of arguments with parents
Loss of job by a parent Outstanding personal achievement
Marital separation of parents Serious illness requiring your hospitalization
Marriage of a parent
Mother beginning to work
Mother being pregnant
Serious illness requiring hospitalization of a parent
Significant change in a parent’s state of health
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Parental Anxiety:

Parental trait anxiety was evaluated through the 20-item trait subscale of the Spielberger State/Trait Anxiety Inventory (STAI) (Spielberger, 1983). This measure assesses anxiety symptomatology using a 4-point scale with responses ranging from “almost never” to “almost always” and demonstrates high convergent validity (Spielberger, 1989) (see Table 2 for descriptive statistics).

Parenting-Related Stress:

Parenting-related stress was determined using the parenting stress index-short form (PSI-SF) (Abidin, 1990). The PSI-SF is a questionnaire used to determine the level of stress specifically associated with parenting by using a 5-point scale ranging from “strongly agree” to “strongly disagree” for 24 parenting-related stressors (Abidin, 1995). An average parenting stress score was obtained by calculating the mean score on this index from 81 participants. This scale is reverse coded, such that higher scores represent lower endorsement of parenting stress. Exponential transformation was performed to normalize the distribution of the data (Skew = −1.40).

Child Anxiety and Externalizing Symptomatology:

Child anxiety behaviors were assessed using the parent-reported Screen for Child Anxiety Related Disorder (SCARED-P) (Birmaher et al., 1997). Although the SCARED’s clinical cut-off scores were originally validated for use in children 9–18 years old (Birmaher et al., 1997), and more recently in children as young as 5-years-old (Sequeira et al., 2019), we were not interested in determining clinical cut-offs, but rather using it to provide a continuous measure of child anxiety behavior. Externalizing behavior was evaluated using the parent-reported form of the Child Behavior Checklist for ages 1.5–5 (Achenbach & Rescorla, 2001). The CBCL is a 120-item assessment in which child behaviors can be reported using a 3-point scale (Achenbach et al., 2003). In order to assess child externalizing symptomatology, the T-scores for the externalizing subscale of the CBCL were used.

We chose to use the SCARED anxiety scale over the CBCL internalizing scale to assess anxiety symptomatology because previous research has indicated significant shared variance between the internalizing and externalizing subscales of the CBCL, thus potentially representing “contaminated” scales rather than comorbidity (Goodman & Scott, 1999; Goodman, 2001). Our own analyses confirmed this shared variance, (r(109) = .68, p < .001), while the correlation between the SCARED anxiety scale and the CBCL externalizing subscale was weaker (r(101) = .35, p < .001). Moreover, a regression analysis that included both CBCL internalizing and SCARED anxiety showed that CBCL internalizing problems remained a significant predictor of CBCL externalizing problems (B = .69 t = 7.55, p < .001, R2 = .43), while the SCARED did not (B = .008, t = .34, p = .73, R2 = .43), showing independence from the CBCL externalizing measure. Therefore, we opted to use the SCARED anxiety and CBCL externalizing scales to assess distinct dimensions of anxiety and externalizing behavior. Log transformation was utilized to normalize the distribution of both scores (see Table 2 for descriptive statistics).

Child In-Laboratory Behavior:

Child behaviors were additionally assessed in a subsample to support measurements of parent-reported behavior using in-laboratory observations of two episodes adapted from the Laboratory Temperament Assessment Battery (Lab-TAB): Snack Delay and Tower of Patience (Goldsmith & Rothbart, 1996). For the Snack Delay episode, a piece of candy was placed under a cup by the experimenter, and the child was told to wait until the experimenter rang a bell before picking up the cup to eat the candy. The Tower of Patience episode involved an experimenter and child taking turns building a tower with blocks, with the experimenter increasingly delaying the length of her turn. Each episode was coded by two independent coders according to a standardized coding scheme for representative behaviors (Table 3). Coders rated both the presence and intensity of each behavior during the episodes. According to Lab-TAB protocols, each episode was divided into epochs based on task-based markers, and the presence and presentation of each behavior was summed and then divided by the number of epochs to create mean behavior scores (Gagne et al., 2011). Because the Tower of Patience episode was completed twice, each tower behavior score was averaged into a single variable. Behavioral data were coded by two independent, trained coders, who double coded 93% of the data and demonstrated high inter-rater reliability (Cronbach’s αs = .839 – .995). For cases when scores from both coders were available, behavior scores were averaged between coders to create one mean score for each behavior. For the remaining cases, individual coder scores were used as the behavioral score.

Table 3:

Table of LabTAB Behaviors for Factor Analysis

Snack Delay and Tower of Patience Behaviors Factor Loadings for Factor 1 Observed Internalizing Behavior Factor Loadings for Factor 2 Observed Externalizing Behavior
Snack Delay
 Anticipatory behavior −.197 .607
 Engagement −.016 .137
 Fidgeting .611 −.040
 Nonverbal Distraction .810 −.090
 Verbal Distraction .294 .538
Tower of Patience
 Anticipatory behavior −.169 .805
 Fidgeting .820 .078
 Nonverbal distraction .640 −.207
 Verbal distraction .041 .720
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Note: Factor loadings on the varimax rotated component matrix for two factors with sufficient primary loadings

Behavioral Factor Creation:

A factor analysis was performed with scores from the Snack Delay and Tower of Patience behavior episodes to extract their common variance. Nine behaviors from the Lab-TAB, which had face-validity for the behaviors of interest (anxiety and externalizing behavior), were selected for factor analysis (Table 3). It was determined that all nine behaviors of interest from the Snack Delay and Tower of Patience were correlated at a minimum absolute value of .3 with at least one other behavior. These nine behaviors were then entered into a principal components factor analysis. The Kaiser-Meyer Olkin measure of sample adequacy was just below the recommended cutoff of .5, at .47, and Bartlett’s test of sphericity was significant (χ2(36) = 111.3, p < .001). Finally, communalities were all greater than the recommended value of .4.

Initial eigenvalues indicated that factors 1 to 3 exceeded the standard threshold of 1, and explained 29.0%, 21.6%, and 12.3% of the variance respectively. Factors were examined using the varimax rotation matrix, and all variables were required to load onto at least one factor at >.5. Cross-loading of variables to different factors was allowed. Factor 3 was subsequently eliminated from analyses because of insufficient primary loading (only 2 variables or less loading to factor; Hatcher, 1994). Factors 1 and 2 demonstrated sufficient primary loading, with loading values to the rotated component matrix exceeding .61 for at least 3 variables for each factor, and were saved as individual items characterized based on investigation of the primary loading variables. The first factor was termed “internalizing behavior”, encompassing the nonverbal distraction and fidgeting behaviors from both episodes, and was deemed representative of anxiety symptoms as both fidgeting and distractibility are considered symptoms of anxiety in young children (Ronan, 1996; Volbrecht & Goldsmith, 2010). The second factor was termed “externalizing behavior”, encompassing the anticipatory and verbal distraction behaviors from both episodes, and was deemed representative of externalizing behavior, as young children with externalizing problems are prone to outward displays of impulsivity, poor behavioral regulation (Eisenberg et. al, 2001) and distraction (Liu, 2004).

Cortisol Measurement:

Families provided cortisol samples at four time points across two successive (or near successive) days at home: wake, 45 minutes after wake, 5PM, and 8PM. They were informed that cortisol should be collected before, or at least 15 minutes after eating and drinking, and not to collect samples on days when children felt ill. For collection, parents were instructed to place two sorbettes under their child’s tongue for 1 minute, according to Salimetrics protocol. Samples were then stored in a locked −20° C freezer, until being shipped on dried ice to Dr. Clemens Kirschbaum’s Biological Psychology Laboratory at the Technical University Dresden for analyses. Using a daily diary, parents reported that children had no major illnesses or fever, and were not taking any medication on days when cortisol was collected. While past work has suggested trait-like stability in diurnal cortisol in slightly older children (Shirtcliff et al., 2012), in the current study, we included two days of cortisol measurements when possible to increase the reliability of the measurements.Values between the two successive days were averaged to create one cortisol value for each time point of interest. For cases when one of two cortisol values was missing due to data loss (N = 12) it was replaced with the individual value of cortisol at the corresponding time point. Averaged cortisol levels for each time point were subjected to log transformation to normalize the distribution of the data. Outliers which fell 1.5 times above the top or below the bottom quartile of the log transformed mean cortisol levels for each time point were removed (N = 10), leaving us with a final sample of 46 children with usable, home, diurnal cortisol data.

Analysis Plan:

Primary analyses were centered on the question of whether parental anxiety statistically explained the association between household stress and children’s outcomes. Therefore, two separate linear regressions tested associations between household stress and child a) anxiety scores and b) externalizing problems, and mediation tests assessed whether parental anxiety mediated these associations. Parenting-related stress was not the focus of the current paper, but motivated by past research on parenting-related stress (Östberg & Hagekull, 2013; Platt et al., 2016), we additionally tested whether the associations described above between parental anxiety and children’s behavior problems were mediated by parenting-related stress. To strengthen our confidence in the parent reports of children’s behavior, we assessed the associations between parent-reported children’s behavior in the subsample that also had in-laboratory behavior. Associations between parental anxiety and children’s cortisol levels were also tested in the subset with these data. A repeated-measures ANCOVA was used to assess interactions between parental anxiety and time of day for children’s home cortisol. Finally, exploratory ANCOVAs examined associations between child-targeted and adult-targeted stressors with child behaviors (see Supplementary Materials for full Data Analysis Plan).

Results:

Household Stress Exposure and Behavior:

Linear regression analyses were conducted to investigate the association between degree of household stress exposure and parent and child behavior, controlling for child age and sex (see Table 2 for descriptive information). There were significant associations between household stress and child anxiety scores and child externalizing problems (Figure 1a), such that increased exposure to household stress was associated with increased child anxiety scores (B = .15, β = .37, t = 3.32, p = .001, R2 = .20) and externalizing problems (B = .042, β = .31, t = 2.79, p = .007, R2 = .16). There was also a significant association between stress exposure and parent anxiety scores, such that increased household stress exposure was associated with higher parental anxiety scores (B = 4.40, β = .38, t = 3.24, p = .002, R2 = .15). See Table 5 for a bivariate correlation table of variables.

Figure 1:

Figure 1:

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a. Association between household stress and child anxiety and externalizing problems. The x axis represents natural-log-transformed household stress impact scores. The y axes represent log-transformed child anxiety t-scores and log-transformed externalizing raw scores. The ribbons represent 95% confidence intervals. N = 73. b. Parental anxiety mediation models. The values in the mediation paths represent unstandardized coefficients and standard error. † p < .10; * p < .05; ** p < .01.

Table 5:

Bivariate Correlation Table for Key Variables

1 2 3 4 5 6 7 8 9 10 11
1. Household Stress Scores 1
2. Parent Anxiety Scores .389** 1
3. Parenting-Related Stress Mean Scores −.305** −.617*** 1
4. Child Anxiety Scores .470*** .472*** −.510*** 1
5. Child Externalizing Problems .260* .414*** −.431*** .348*** 1
6. Observed Internalizing Behavior (Factor 1) .048 .308 −.019 .407** .097 1
7. Observed Externalizing Behavior (Factor 2) .200 .238 −.216 −.015 .444** .012 1
8. Raw Cortisol Levels at Wake .238 −.170 .020 −.022 .004 −.248 .436* 1
9. Raw Cortisol Levels at Wake + 45 −.217 −.238 .261 −.400** −.257 .128 .072 −.003 1
10. Raw Cortisol Levels at 5PM −.161 −.229 .187 −.244 .019 −.349 .427 .092 .335* 1
11. Raw Cortisol Levels at 8PM .164 .178 −.137 .030 .066 −.162 .304 .242 .232 .332* 1
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Note:

*

p < .05

**

p < .01

***

p < .001

Association between Parent-Reported Behaviors and Observed In-Laboratory Behaviors:

To confirm parent reports of child behavior, observed behavioral factor scores (from Lab-TAB) were entered into two separate linear regression analyses predicting parent-reported behaviors of interest, controlling for child age and sex. There was a significant association between Factor 1 (observed internalizing behavior) and parent-reported child anxiety, such that increased observed internalizing behavior was associated with increased parent-reported anxiety behavior (i.e. SCARED) (B = .094, β = .35, t = 2.25, p = .031, R2 = .18). Similarly, there was a significant association between Factor 2 (observed externalizing behavior) and parent-reported child externalizing symptoms, such that increased observed externalizing behavior was associated with increased parent-reported externalizing symptoms (i.e. CBCL) (B = .033, β = .42, t = 2.86, p = .007, R2 = .19) (Figure 2).

Figure 2:

Figure 2:

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Association between observed behavior factors, and child anxiety and externalizing problems. N = 43. The x axis represents behavior factor scores. The y axes represent log-transformed child anxiety t-scores and log-transformed externalizing raw scores. The ribbons represent 95% confidence intervals.

Household Stress and Child Behavior: Mediation by Parental Anxiety Scores

Two separate mediation analyses were conducted using the PROCESS macro in SPSS version 25 (Hayes, 2017), testing parental anxiety as a mediator between the independent variable of household stress and two dependent variables, child anxiety scores and externalizing problems (see Figure 1b). Significant mediations were determined using bias-corrected bootstrapped confidence intervals. The association between household stress and child anxiety scores, without mediation, was significant (path c) (B = .15, SE = .046, t = 3.32, p = .001), as was the association between household stress and parent anxiety (path a) (B = 4.69, SE = 1.39, t = 3.37, p = .001), with the association between parental anxiety and child anxiety falling just above the .05 significance threshold (path b) (B = .009, SE = .004, t = 1.99, p = .052). The confidence interval for the indirect effect did not include zero (B = .040, CI [.002, .11]), although the association between household stress and child anxiety scores (path c’) remained significant (B = .12, SE = .051, t = 2.30, p = .025). Thus, the association between household stress and child anxiety was partially statistically mediated by parental anxiety scores. For the second mediation model testing child externalizing problems as the outcome, the initial association between household stress and child externalizing problems, without mediation, was significant (path c) (B = .042, SE = .015, t = 2.79, p = .007). The association between household stress and parent anxiety (path a) was significant (B = 3.69, SE = 1.41, t = 2.61, p = .011), as was the association between parental anxiety scores and child externalizing problems (path b) (B = .005, SE = .001, t = 3.33, p = .002). The confidence interval for the indirect effect did not include zero (B = .017, CI [.004, .039]), and the association between household stress and child externalizing problems was no longer significant when including parental anxiety as the mediator (path c’) (B = .026, SE = .016, t = 1.62, p = .11). Thus, the association between household stress and child externalizing problems was fully statistically mediated by parental anxiety scores.

Parent Anxiety Scores and Child Behavior: Mediation by Parenting-Related Stress

Two separate mediation analyses were conducted using the PROCESS macro (Hayes, 2017), testing parenting-related stress as a mediator between parental anxiety scores and the two dependent variables, child anxiety scores and externalizing problems. Significant mediations were determined using bias-corrected bootstrapped confidence intervals. For the first mediation model testing child anxiety as the outcome, the initial association between parent anxiety scores and child anxiety scores, without mediation, was significant (path c) (B = .016, SE = .004, t = 4.19, p < .001). The association between parent anxiety scores and parenting-related stress (path a) was significant (B = −2.18, SE = .35, t = −6.19, p < .001), as was the association between parenting-related stress and child anxiety scores (path b) (B = −.005, SE = .001, t = −3.40, p = .001). The association between parental and child anxiety scores was no longer significant when including parenting-related stress as the mediator (path c’) (B = .003, SE = .005, t = .54, p = .59), and the confidence interval for the indirect effect did not contain zero (B = .010, CI [.004, .018]). Thus, the association between parental and child anxiety scores was fully statistically mediated by parenting-related stress. For the second mediation model, the association between parental anxiety scores and child externalizing problems, without mediation, was significant (path c) (B = .005, SE = .001, t = 4.59, p < .001). The association between parent anxiety scores and parenting-related stress (path a) (B = −2.13, SE = .36, t = −5.88, p < .001) and the association between parenting-related stress and child externalizing problems (path b) (B = −.001, SE = .0004, t = −2.02, p = .048) were significant. The association between parent anxiety scores and child externalizing problems remained significant when including parenting-related stress as the mediator (path c’) (B = .004, SE = .002, t = 2.19, p = .032), but the confidence interval for the indirect effect did not contain zero (B = .002, CI [.0004, .005]). Thus, the association between parental anxiety scores and child externalizing problems was partially statistically mediated by parenting-related stress.

Serial Multiple Mediation:

Serial mediation analyses were conducted using the PROCESS macro (Hayes, 2017), testing both parental anxiety and parenting-related stress as mediators of the associations between household stress and a) child anxiety scores and b) externalizing problems. Significant mediations were determined using bias-corrected bootstrapped confidence intervals. The association between household stress and parent anxiety was significant (path a) (B = 4.69, SE = 1.39, t = 3.37, p = .001), as was the association between parental anxiety and parenting-related stress (path d) (B = −2.02, SE = .39, t = −5.14, p < .001), and the association between parenting-related stress and child anxiety scores (path b) (B = −.004, SE = .001, t = −3.17, p = .002). The confidence interval for the indirect effect of the full model did not include zero (B = .039, CI [.009, .093]), although the association between household stress and child anxiety scores (path c’) remained significant (B = .10, SE = .048, t = 2.08, p = .041). For the second mediation model, the association between household stress and parent anxiety was significant (path a) (B = 3.69, SE = 1.41, t = 2.61, p = .011), as was the association between parental anxiety and parenting-related stress (path d) (B = −1.98, SE = .39, t = −5.05, p < .001), with the association between parenting-related stress and child externalizing problems falling above the .05 significance threshold (path b) (B = −.0008, SE = .0005, t = −1.84, p = .071). The confidence interval for the indirect effect of the full model did not include zero (B = .006, CI [.0002, .018]), and the association between household stress and child externalizing problems was no longer significant when including parental anxiety and parenting-related stress as mediators (path c’) (B = .022, SE = .016, t = 1.39, p = .17).

Cortisol:

A repeated measures ANCOVA was conducted to examine the association between home-cortisol across the day, entered as four time points (wake, wake + 45, 5PM and 8PM) as the within-subjects factor, and parental anxiety scores, controlling for child age and sex. Because Mauchly’s Test of Sphericity was not significant (p = .69), the assumption of sphericity was not violated. As hypothesized, there was a significant effect of time on cortisol values, F(3, 114) = 7.03, p < .001, ηp2 = .16, such that cortisol decreased across the 4 times points. There was also an interaction of time and parental anxiety scores on cortisol values, F(3, 114) = 3.02, p = .033, ηp2 = .074. To examine the source of the interaction, a post-hoc hierarchical linear regression was conducted, which revealed that 8PM cortisol was significantly associated with parental anxiety scores. Specifically, higher parental anxiety scores were associated with increased child 8PM cortisol, when controlling for child age, sex, and cortisol measurements during the alternate time points (B = .013, β = .39, SE = .005, t = 2.49, p = .018) (Figure 3).

Figure 3:

Figure 3:

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Association between parental anxiety, and child evening cortisol N = 42. The x axis represents raw parent anxiety scores. The y axis represents log-transformed cortisol levels. The ribbon represents the 95% confidence interval.

Binary Categorizations of Adult vs. Child Stressors:

To further understand how household stressors impact children, we conducted an exploratory analysis that split household stress items into child-targeted and adult-targeted stressor variables (see Table 4). Univariate ANCOVAs, adjusted for child age, sex, and alternate child-targeted or adult-targeted stressor subscales, were used to investigate changes in child behavior associated with child-targeted and adult-targeted stressors. Child-targeted stressors were not significantly associated with children’s anxiety scores F(1,67) = .074, p = .79, ηp2 = .001, or externalizing problems F(1,68) = .35, p = .56, ηp2 = .005. We followed up these analyses with Bayesian Independent Samples T-Test models in JASP (JASP Team, 2018) to assess the likelihood of the null hypothesis. For child anxiety scores, the Bayes factor indicated that the data were 2.26 times more likely to be observed under the null hypothesis than the alternative hypothesis. For child externalizing problems, the Bayes factor indicated that the data were 3.96 times more likely to be observed under the null hypothesis than the alternative hypothesis. These analyses are consistent with there being no significant difference in children’s behavioral outcomes between those exposed to a child-targeted stressor and those who were not. In contrast to the null findings for the child-targeted stressors, adult-targeted (i.e. to the parent) stressors were significantly associated with increased anxiety scores F(1,67) = 4.97, p = .029, ηp2 = .069, and externalizing problems in children F(1,68) = 16.8, p < .001, ηp2 = .20 (Figure 4).

Figure 4:

Figure 4:

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Binary split between presence or absence of at least 1 child-targeted and adult-targeted stressor. N = 73. The y axes represent log-transformed child anxiety t-scores and log-transformed externalizing raw scores. Error bars represent 95% confidence intervals. * p < .05; *** p < .001.

Discussion:

Here, we showed that increasing exposures to stress, even when within a normative range, are associated with heightened behavioral problems (i.e. anxiety symptoms and externalizing problems) and elevated stress hormone production in young children. However, children’s phenotypes (which were supported through in-lab observation of behavior) were also correlated with parents’ anxiety symptoms, which statistically mediated those links between exposure to household stressors and child symptoms. These associations support the hypothesis that household stress relates to child outcomes (at least in part) via parental routes. Further adding to this claim was the finding that adult-targeted—but not child-targeted stressors—were those associated with child symptoms. In other words, the stressors directly targeting the child did not correspond to their anxiety or externalizing behaviors, but instead the stressors targeting their parents did. This is especially noteworthy because parents rated the child-targeted stressors as more impactful for their children than the adult-targeted stressors. Although there always exists a concern that parent reports of child behavior will be biased, the parent-reported behaviors in the current study received empirical support through direct observations of children’s behavior in the laboratory. Additionally, parental anxiety scores were positively correlated with children’s evening cortisol levels, paralleling our parent-reported measures. The multiple metrics, including parent report, laboratory observations, and cortisol measures, suggest parents’ reporting was a fairly accurate description of children’s phenotypes. Overall, our findings indicate that parents, and specifically parental anxiety symptoms, may be a mechanistic link between normative household stressors and children’s outcomes.

This work expands upon the prior literature illuminating the important role caregivers play in modulating their children’s stress response (Gee et al., 2014; Hostinar et al., 2015; Moriceau & Sullivan, 2006; Tong et al., 2015). However, the majority of previous work in this domain has focused on school-age children and adolescents. Although parents play a significant role in older children’s and adolescents’ behavior, relative to early childhood, their dependence is declining (Callaghan et al., 2019). Importantly, adult-targeted stressors and parental anxiety symptoms may be particularly salient for very young populations, and thus, our sample was restricted to young children (2–6 year olds). This developmental period is especially meaningful to study in the context of stress and parenting because young children are highly reliant on caregivers for both physiological and behavioral regulation (Callaghan & Tottenham, 2016; Hostinar et al., 2015). Our findings support this notion, demonstrating that parental anxiety symptoms statistically mediated the associations between household stress exposure and children’s anxiety symptoms and externalizing problems. Notably, adult-targeted stressors were a better predictor of child symptomatology than child-targeted stressors, consistent with the hypothesis that parental emotion is particularly potent for young children. This also suggests that children rely on parents to guide their emotional behavior, harkening to social referencing effects that have been well documented throughout infancy. As our study was restricted to a very young age range, these findings raise further questions concerning the specific age at which children gain independence from this observed parental stress cascade, to modulate behavior in direct response to their own environments.

Our findings also indicate that the characteristic changes in child behavior problems following stress may be attenuated by addressing parent behavior. If parental anxiety serves as a link between household stress and children’s mental health symptomatology, clinical interventions geared towards children may yield best results if parent symptoms are also addressed, if not prioritized, following stress exposure. This strategy would not only benefit the parent, but also provide a practical method to address psychopathology and behavior problems that start in early childhood.

Previous research has highlighted an association between stress and children’s stress physiology (i.e. cortisol). Exposure to increased family conflict and/or parental psychopathology has been linked to heightened cortisol production in children (Doom et al., 2018; Dougherty et al., 2013a; Dougherty et al., 2013b). The current study used cortisol to further support the parent-reported variables of interest, to address potential issues of reporting biases, and demonstrated a significant association between increased parental anxiety symptoms and elevated evening cortisol levels. Although based on a correlational design with a small sample size, this association may indicate that behaviorally as well as physiologically, young children are sensitive to their parents’ anxiety, even if in the normative range. These hypotheses should be further tested in larger samples with measures of timing compliance, which we did not have access to in the present study. However, consistent with this interpretation, rodent models have shown that maternal fear expression increases pups’ stress hormone corticosterone and fear behaviors (Debiec & Sullivan, 2014). Both stress exposure and heightened cortisol levels in childhood have been linked to a number of poor health outcomes including cardiovascular disease and disrupted immune function (Barr, 2017; Lundberg, 2005). Therefore, addressing parental anxiety may have important effects on children beyond behavior, promoting improvements in child health and well-being following stressful experiences.

Though the findings in the current study are based on cross-sectional, correlational data, causality between parental stress and offspring outcomes has been established in rodent models. For example, exposure to a stressor in the form of limited nesting material causes anxiety-like behaviors and subsequent aberrant caregiving in dams (Ivy et al., 2008), which produces physiological changes in pups (Gilles et al., 1996) and anxiety-like behaviors in adult offspring (Dalle Molle et. al, 2012). It has therefore been suggested that environmental stress is signaled to offspring through changes in maternal caregiving behavior (Champagne & Meaney, 2006). This series of events in rodents can be interpreted as following a similar stress cascade as observed in our study, such that exposure to stress is associated with increased parental anxiety and changes in parenting behavior, which is in turn linked to heightened behavior problems and cortisol levels in children. Taken together, this cross-species evidence informs our current working theory that anxious behavior in caregivers may serve as a mechanism by which stress in the environment is translated to young. However, it is important to note that our data were collected at one time point, and thus, further longitudinal replications are necessary to validate the directionality of these associations.

The limited past work in this domain has overwhelmingly focused on stress related to parenting as a mediator, with mixed results. Importantly, when assessing parenting-related stress, it is impossible to dissociate changes in parent behavior from child behavior, as parenting-related stress is assessed through questions related to child behavior. Therefore, the current study considered both measures of parent anxiety and parenting-related stress. Our findings suggest that household stressors impact children through parental anxiety, and these characteristic changes in parental anxiety behaviors were associated with heightened risk for behavioral problems in children via increased parenting-related stress. This work begins to reconcile the discrepancies in prior literature by assessing both parental anxiety symptoms and parenting-related stress, to disentangle the reciprocal influence of stress related to parenting and child behavior symptoms. These results help us provide a novel framework to understand how household stress influences parental symptomatology and parenting behavior, and increases children’s risk for negative outcomes.

Our study was constrained by several limitations. Because our sample did not strive to include families exposed to extreme forms of stress or adversity, we could not obtain a robust distribution of child and adult-targeted stress exposure, limiting us to binary categorizations for these analyses. Further, the incidence of parental anxiety was relatively low, and mostly fell within a normative range, rather than a clinically significant one. Moreover, the median income of our sample was relatively high ($100,001 – $150,000), which may limit the generalizability of our findings. Additionally, since this was a secondary data analysis using information collected from two separate study samples, there was missing data that limited sample sizes for some analyses (e.g., behavioral assessments and diurnal cortisol measures, in particular). Due to the relatively small sample, these findings should be replicated in larger cohorts. This is especially important for the measures used to support parent report i.e. lab behavior and child cortisol. Finally, while we have presented a mediation model here, our data were cross-sectional and longitudinal samples are therefore needed to establish the true directionality of the pathways investigated.

Taken together, these data show that adult-targeted stressors and parental anxiety symptoms are associated with young children’s behavior and physiology, supporting the hypothesis that parents are significant translators of household stress to children. If this hypothesis continues to receive support, one implication would be that the route between household stress and child outcome is not direct. The converse, then, would also be true; namely parents are able to prevent the transmission of stressful events to their children. This study has practical implications in that, in the context of stressful households, addressing parental behavior could have beneficial effects for both the parent and the child. It may even be that supporting the parent is the most effective way to promote mental health in the child, as has been shown in populations at high-risk for depression (Pilowsky et al., 2014). By investigating the role of the parent as a mediator between household stress exposure and child outcomes, we were able to gain a greater understanding of the mechanism by which household stress may impact early development, and underscore the critical role that parents play as conduits between young children and their environments.

Supplementary Material

supplemental

Acknowledgements:

This research was supported in part by grant number R01MH091864 from the National Institute of Mental Health. The content is solely the responsibility of the author and does not necessarily represent the views of funding agencies. The authors have no conflicts of interest to declare.

Footnotes

Data Availability Statement: The data that support the findings of this study are not publicly available due to privacy or ethical restrictions.

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