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. Author manuscript; available in PMC: 2021 Aug 11.
Published in final edited form as: Dev Psychobiol. 2021 Feb 11;63(5):1295–1308. doi: 10.1002/dev.22104

Trajectories of Internalizing Symptoms in Early Childhood: Associations with Maternal Internalizing Symptoms and Child Physiology

Anna M Zhou 1, Kristin A Buss 1
PMCID: PMC8355017  NIHMSID: NIHMS1665701  PMID: 33569780

Abstract

Research has shown that children’s internalizing symptom development during early childhood are shaped by biopsychosocial processes including physiology and parental symptoms. However, associations between maternal internalizing symptoms, child physiology and trajectories of child internalizing symptoms are not well understood. We used growth curve models to examine how maternal internalizing symptoms, child physiology and the interaction between maternal internalizing symptoms and child physiology may be associated with trajectories of internalizing symptoms during early childhood. Mothers reported their children’s internalizing symptoms when children were 3, 4, 5 and 6 years of age, and mothers self-reported their own internalizing symptoms when children were 3. Respiratory Sinus Arrhythmia (RSA) was collected when children were 3.5-years-old. Results showed that there is a non-linear, quadratic trajectory across all participants from age 3 to 6. Maternal internalizing symptoms were not associated with children’s internalizing symptoms at age 6, but were associated with both linear and quadratic change. Lower resting RSA was associated with greater increases in children’s internalizing symptoms over time. Interactions between maternal internalizing symptoms and RSA were not associated with children’s internalizing symptom development. The findings demonstrate that maternal internalizing symptoms and child physiology are independently associated with internalizing symptom development during early childhood.

Keywords: internalizing symptoms, toddlerhood, respiratory sinus arrhythmia, maternal anxiety, maternal depression


Approximately, 10% to 15% of US preschoolers meet diagnostic criteria for a DSM anxiety or depressive disorder (Egger & Angold, 2006). Research has shown that high levels of internalizing symptoms during early and middle childhood are more likely to lead to higher levels of internalizing disorders during adulthood (e.g. Bittner et al., 2007). Studies demonstrate that clinically significant levels of internalizing symptoms can be detected as early as toddlerhood (24–36 months), and subclinical levels of internalizing symptoms are present in toddlers and preschoolers (e.g. Luby et al., 2003; Sterba, Egger & Angold, 2007; Egger & Angold, 2006). However, many longitudinal studies on internalizing symptom development have often focused on middle childhood and adolescence (Dekovic, Buist, & Reitz, 2004; McLaughlin & King, 2015), and less is known about the early childhood period. Early identification of children who may be at greater risk of stable, high levels of internalizing symptoms throughout development may have long-term implications for subsequent socioemotional functioning (Sterba, Egger, & Angold, 2007).

In the present study, we examined trajectories of children’s internalizing symptoms from a biopsychosocial perspective (Gottlieb, Wahlsten, & Lickliter, 2007; Sameroff, 2010) – whereby development proceeds at different levels of analysis such as biological and environmental levels (Sameroff, 2010). Consistent with this model, we examined how individual differences in physiology may interact with maternal internalizing symptoms to be associated with trajectories of children’s internalizing symptom development from toddlerhood to school entry.

Trajectories of Internalizing Symptoms across Development

Though early internalizing symptoms (including anxiety, fear, depression, withdrawal and somatic complaints) are common, most children exhibit low levels of internalizing symptoms from ages 2 to 11 (Sterba, Prinstein, & Cox, 2007). Additional research has shown a curvilinear trajectory where internalizing symptoms decrease from age 7 to age 12 and then increase into adolescence (Cohen, Andrews, Davis, & Rudolph, 2017). Battaglia and colleagues (2016) found that children with higher levels of separation anxiety at age 1.5 years tended to exhibit lower levels of separation anxiety at around age 4–5, and highlight that children who show stable, high levels of separation anxiety into age 5 may be at greater risk of sustaining high levels of separation anxiety later into childhood and may be more likely to develop anxiety disorders.

Despite evidence for a general developmental trajectory, not all children follow the same trajectory of internalizing symptom development, suggesting that the development of internalizing symptoms during toddlerhood and preschool is multifaceted (e.g. Sterba, Prinstein, & Cox, 2007; Côte et al., 2009). For example, Sterba, Prinstein and Cox (2007) found that there are children who exhibit stable, high levels of internalizing symptoms from age 2 to 11, and a portion of children who exhibit a decreasing then increasing trajectory. Both individual characteristics in the child as well as variation in social and environmental influences have been associated with trajectories of internalizing symptom development, such as physiological reactivity to stress (Shanahan, Calkins, Keane, Kelleher, & Suffness, 2014), temperament (Côte et al., 2009) and maternal stress and psychopathology symptoms (Sterba, Prinstein & Cox, 2007; Bayer et al., 2006). Studies also demonstrate that early risk and protective factors are associated with developmental patterns of social withdrawal, fear and reticence (e.g. Brooker et al., 2013; Brooker, Kiel, & Buss, 2016; Degnan et al., 2014), which may also contribute to heterogeneity in internalizing symptom development. Taken together, the literature demonstrates that factors such as maternal internalizing symptoms and child physiology may account for differences in trajectories of child internalizing symptoms.

Associations between Maternal Internalizing Symptoms and Children’s Trajectories of Internalizing Symptoms

Children of parents with internalizing disorders are five times more likely to develop anxiety disorders than children of parents with no disorders (Beidel & Turner, 1997). Maternal depression and anxiety are associated with child trajectories characterized by high levels of internalizing symptoms during both early and middle childhood (Feng, Shaw & Silk, 2008; Côte et al., 2009; Sterba, Prinstein, & Cox, 2007).

There are multiple mechanisms by which maternal internalizing disorders are theorized to influence child socioemotional development, such as through heritability of psychopathology, dysfunctional biological mechanisms involved in regulation due to prenatal influences, exposure to mothers’ cognitions, behaviors and affect, as well as exposure to stressful environments (Goodman & Gotlib, 1999). In particular, mothers with high levels of depressive and anxiety symptoms may create increased stress for the child through exhibiting negative affect, utilizing over-intrusive and controlling parenting behaviors and exhibiting dysfunctional cognitions (Goodman & Gotlib, 1999; Bayer et al., 2006; Murray et al., 2008).

However, not all children of depressed and anxious mothers go on to develop internalizing disorders (Goodman et al., 2011). This suggests that other factors may be involved, and studies have shown that maternal internalizing symptoms often interact with moderators such as biological reactivity to stress (Poole, van Lieshout, & Schmidt, 2017), child temperament (Feng et al., 2008; Leve, Kim, & Pears, 2005) and poverty (Goodman et al., 2011; McLaughlin & King, 2015). Given the indirect effects of maternal internalizing symptoms on child development, individual differences in child self-regulation may moderate the association between maternal internalizing symptoms and child internalizing symptom development.

Resting Respiratory Sinus Arrhythmia as a Marker of Sensitivity to Environment

Children who are adept at down-regulating negative affect or up-regulating positive affect in the context of emotionally arousing family contexts may be less vulnerable to developing internalizing problems (Morris et al., 2002; Silk, Shaw, Forbes, Lane, & Kovacs, 2006). Autonomic nervous system (ANS) activity, such as heart rate variability, is often used as a biomarker of self-regulation, and has been associated with internalizing psychopathology (Beauchaine & Thayer, 2015). ANS activity may be a marker of children’s regulation of arousal associated with stressful environments.

The ANS plays an important role in how the body copes with stress, specifically in fight-or-flight responding (Porges, 2007; Zisner & Beauchaine, 2016). The parasympathetic branch (PNS) of the ANS responds very quickly to environmental cues as a first-response coping system, whereas the sympathetic nervous system responds less quickly (Zisner & Beauchaine, 2016). Porges’ polyvagal theory specifies that different physiological states support different classes of behavior (Porges, 2007) through activity of the vagus nerve and its influence on the parasympathetic nervous system. PNS activity is commonly assessed via respiratory sinus arrhythmia (RSA), a measure of the variation in inter-beat intervals of the heart at the frequency of breathing.

Different measures of RSA have been used as markers of regulation in children. Resting baseline RSA is a measure of parasympathetic activity during a period of non-engagement (Burt & Obradovic, 2013). Though resting RSA is often thought to measure an individual’s capacity for regulation, higher resting RSA is also posited as a marker of increased sensitivity to the environment (Beauchaine, 2001). Studies have shown that infants with higher resting RSA are more responsive to environmental stimuli than infants with lower resting RSA (e.g. Porges, Arnold & Forbes, 1973).

It has been demonstrated that high resting RSA is associated with better emotion regulation, and fewer internalizing and externalizing symptoms (Graziano & Derefinko, 2013; Beauchaine & Thayer, 2015). However, less is known about the associations between resting RSA and children’s developmental change in internalizing symptoms during early childhood. In addition, findings on RSA and internalizing symptoms are not always consistent, and some work demonstrates that other factors may interact with RSA to predict internalizing symptom development (Grazino & Derefinko, 2013). As some studies have shown that resting RSA may moderate relations between contextual risk and internalizing symptom development, it is important to consider how individual differences in RSA may interact with risk factors such as maternal internalizing symptoms to influence internalizing symptom development.

Interactions between Maternal Internalizing Symptoms and Child Resting RSA

Consistent with the biological sensitivity to context model (Ellis & Boyce, 2008), recent research demonstrates that individual differences in PNS activity may indicate sensitivity to maternal internalizing symptoms and lead to different developmental consequences, though there are some mixed findings. Studies have shown that both infants and children with higher resting RSA are more likely to be affected by maternal internalizing symptoms (Blandon, Calkins, Keane, & O’Brien, 2008; Peltola et al., 2017; Shanahan et al., 2014). For example, Blandon and colleagues (2008) demonstrated that children with higher resting RSA at age 4 exhibited poorer emotion regulation skills at age 7 in the presence of higher maternal depression symptoms. Although child internalizing symptoms were not directly measured in that study, prior literature has established that poor emotion regulation skills are often associated with development of internalizing symptoms (e.g., Eisenberg et al., 2001). Similarly, Peltola and colleagues (2017) showed that for infants with high resting RSA, there was a strong positive relation between maternal prenatal anxiety and later infant negative affectivity. This supports the hypothesis that infants and children with higher resting RSA are more susceptible to environmental effects. In addition, some research has examined these associations to predict trajectories of internalizing symptoms. Wetter and El-Sheikh (2012) found that preadolescent girls with high resting RSA and mothers with lower psychopathology symptoms showed the steepest decrease in internalizing symptoms from 8 to 10 years of age. In contrast, girls who had lower resting RSA and higher maternal internalizing symptoms had the highest level of internalizing symptoms at age 10.

These studies show that maternal internalizing symptoms and RSA interact to influence trajectories of internalizing symptom development in longitudinal studies, though there are some mixed findings in whether or it is higher or lower resting RSA that reflects vulnerability. Of note, Wetter and El-Sheikh (2012)’s finding that lower resting RSA exacerbates the negative effects of maternal internalizing symptoms is inconsistent with findings that suggest individuals with higher resting RSA are more susceptible to negative effects of maternal internalizing symptoms, though it is consistent with research demonstrating that low resting RSA is associated with greater internalizing symptoms as a standalone predictor (e.g. Hinnant & El-Sheikh, 2013). The mixed findings on how resting RSA may interact with maternal internalizing symptoms highlight the need for more studies to examine the relation between these variables to predict trajectories of children’s internalizing symptom development. In addition, many of the studies examining the interaction between RSA and maternal internalizing symptoms to predict trajectories of internalizing symptom development have samples of older children and preadolescents. It is unclear how RSA and maternal internalizing symptoms may be associated with internalizing symptom development during early childhood.

The Present Study

While it has been shown that individual differences in child physiology may interact with maternal depression and anxiety symptoms to predict children’s internalizing symptoms, less is known about how these factors interact to predict trajectories of internalizing symptom development in a temperamentally at-risk sample of children. The purpose of the present study was to examine how child resting RSA and maternal internalizing symptoms interact to predict trajectories of internalizing symptoms during early childhood.

It is also important to acknowledge there are other individual difference factors that are associated with trajectories of internalizing symptom development. In particular, fearful temperament has been associated with child internalizing trajectories (e.g. Leve et al., 2005). Child sex has been shown to interact with maternal internalizing symptoms and child physiology in middle childhood and into adolescence (e.g. Wetter & El-Sheikh, 2012). The present study did not focus on these individual differences, but they were included as covariates in all analyses given that they may be associated with children’s internalizing symptom development. In particular, fearful temperament was specifically incorporated as a covariate as the present study oversampled for temperamentally fearful toddlers.

We hypothesized that after controlling for child fearful temperament and sex, maternal internalizing symptoms, child resting RSA and their interaction will be associated with child internalizing symptoms at age 6 and change in internalizing symptoms from ages 3 to 6. Specifically, we hypothesize that maternal internalizing symptoms will be positively associated with child internalizing symptoms at age 6, and associated with greater increases in internalizing symptoms across time. We hypothesize a negative association between resting RSA and child internalizing symptoms at age 6 and greater increases in internalizing symptoms across time. Although there have been mixed findings on the direction of effects in studies spanning from infancy to adolescence, longitudinal studies during infancy and early childhood demonstrate associations between higher resting RSA in the context of negative environmental experiences with outcomes associated with internalizing symptoms (Blandon et al., 2008; Peltola et al., 2017). Therefore, we hypothesized an interaction between resting RSA and mothers’ internalizing symptoms such that there will be a positive association between maternal internalizing symptoms and child internalizing symptoms at age 6 when children have higher levels of resting RSA relative to the mean, and there would be no association between maternal internalizing symptoms and child internalizing symptoms when children have lower levels of resting RSA. In addition, we hypothesize that maternal internalizing symptoms would be associated with greater increases in child internalizing symptoms across time when children have higher levels of resting RSA, and that there would be no association between maternal internalizing symptoms and change in children’s internalizing symptoms when children have lower levels of resting RSA.

Method

Participants.

Participants for the present study were recruited primarily from local birth records by mail and were enrolled as part of a larger longitudinal study of toddlers’ temperament and socioemotional development from 24 months to through Kindergarten. Institutional Board Review approval for this study was obtained from Penn State Office of Research Protections (IRB# 36563). Enrollment occurred following screening at 18-months, including oversampling for children high in fear (details described below). Participants in the 2-year laboratory visit included 125 children, 63 selected as fearful and 62 unselected/nonfearful. At later time-points, 45 more children who were identified as exuberant based on the 18-month screening were recruited in order to balance the sample to ensure full range of temperament traits. Data for the study included 170 children (50% female) and their parents. The sample consisted of 90% White, 0.5% African American/Black, 0.5% Asian, and 9% Biracial or Multiracial. On average, mothers who participated in the study reported 16.26 years of formal schooling (M = 16.26, SD = 2.33), with a range from 12 to 20 years. Fathers who participated in the study had an average of 15.63 years of formal schooling (M = 15.63, SD = 2.49), with a range from 10 to 20 years of formal schooling. 55% of the families reported a total family income above $60,000, 39% reported an income between $31,000 and $60,000, and 6% reported an income of less than $30,000.

Procedure.

Screening.

We recruited and screened 481 parents of full-term, healthy birth children between 18 and 20 months of age. Parents completed a six-item questionnaire about the toddler’s fearfulness in novel situations, and the Infant-Toddler Social Emotional Assessment (ITSEA; Carter, Briggs-Gowan, Jones, & Little, 2003). In order to be identified as a “high-fear” target for enrollment, toddlers had to meet the following criteria: 1 SD above the mean on at least two of three scales on the ITSEA (inhibition to novelty, separation distress, and anxiety/worry), and 1 SD above the mean on a six item on a toddler wariness scale (Buss et al., 2018). In total, 121 toddlers were identified as high fear, with 62 enrolling in the study. The non-fear participants were randomly selected from the remaining pool of screened, non-high fear children (n = 63). Additionally, children were identified as exuberant if they met two of the three following criteria from the 18-month ITSEA: 1 SD above the mean on the activity/impulsivity subscale, 1 SD below the mean on the inhibition to novelty subscale, and scored a 2 on the depression subscale (reverse score of children’s positive emotions). 81 toddlers were identified as exuberant, with 45 enrolling in the study.

Children participated in a laboratory visit at age 2, and behavioral measures of temperament were collected at this time. Mothers completed questionnaires when children turned 3, reporting on their own internalizing symptoms and their child’s internalizing symptoms. Participants were invited back to the laboratory when children were age 3.5 to complete laboratory tasks. Mothers then completed questionnaires on children’s internalizing symptoms at ages 4, 5 and 6.

Laboratory Visit at age 2.

When children were age 2, children and one parent visited the laboratory where they completed a series of structured tasks. In the present project, tasks designed to assess children’s fearful behavior were included, such as Puppet Show, Stranger Approach, Robot, Clown, Stranger Working and Spider presented in fixed order with other non-fear eliciting tasks occurring in between these. During the Puppet Show, exuberant puppets put on a show and engaged the child with games. A male stranger entered the room and talked to the child and tried to play with the child during Stranger Approach. During Robot, a remote-controlled robot moved around, lit up and made noises. During Clown, a friendly clown attempted to engage the child with games. A female stranger entered the room and worked in the corner during Stranger Working. Lastly, a remote-controlled spider approached the child.

Laboratory Visit at age 3.5.

When children were age 3.5, participants were invited back to the lab. Resting baseline RSA data was collected during this visit while the child sat quietly and colored, and read a book with an experimenter for 5 minutes.

Measures

Maternal Internalizing Symptoms.

Maternal self-report of depressive and anxiety symptoms was used to measure internalizing symptoms. A total count of internalizing symptoms endorsed across three questionnaires was used in analyses. The number of symptoms endorsed ranged from 7 to 41 (M = 21.25, SD = 7.93).

Depressive symptoms were assessed using the Center for Epidemiological Studies - Depression Scale (CES-D; Radloff, 1977). Mothers rated how often they experienced various depressive symptoms over the past 6 months (e.g. “I felt sad.”) on a Likert scale from 0 (rarely to none of the time) to 3 (most or all of the time). All items scored 1 and above were considered endorsed symptoms, and included in the symptom count. The scale had good reliability (α = .87). Mothers also self-reported their general anxiety symptoms using the General Anxiety Disorder Questionnaire (GADQ; Newman et al., 2002) and the Social Interaction Anxiety Scale (SIAS; Mattick & Clarke, 1998). On the GADQ, mothers reported on their general anxiety symptoms over the past 6 months to indicate the presence of anxiety symptoms (e.g. “Do you experience excessive worry?”) on a dichotomous scale (yes or no). If participants responded yes then that item counted as endorsing the symptom. On the SIAS, mothers responded to 20 items (e.g. “I have difficulty talking with other people.”) on a Likert scale from 0 (not at all characteristic of me) to 4 (extremely characteristic of me). All items scored 1 and above were considered endorsed symptoms, and included in the symptom count. The SIAS had excellent internal reliability (α =.91), and the GADQ had acceptable reliability (α = .62).

Child Internalizing Symptoms.

Mothers reported on their children’s behaviors using the McArthur Health Behavior Questionnaire (HBQ; Armstrong et al., 2003) and the ITSEA (Carter et al., 2003). These measures are designed to measure mental health and functioning of children. The HBQ includes 172 items, and items ask about behaviors on either a dichotomous rating scale (yes or no) or on a Likert scale from 0 (never or not true) to 2 (often or very true). Participants completed the internalizing scale of the HBQ at ages 3, 4, 5 and 6. However, the internalizing scale of the HBQ does not include social withdrawal symptoms, which has often been identified as one of the major dimensions of dysfunctional behavior during childhood (Rubin, Coplan, & Bowker, 2009). To account for social withdrawal symptoms in our internalizing measure, the items “likes to be alone,” “shy with other children” and “shy with unfamiliar adults” from both the ITSEA (age 3) and HBQ social withdrawal scales (ages 4–6) were used to create a composite of internalizing symptoms that include depressive, general anxiety, separation anxiety and social withdrawal symptoms. These items were selected because they were identical across both the ITSEA and the HBQ. The mean of the composite score of children’s Internalizing Symptoms was used in analyses (the highest possible score for each scale is 2). Reliability for the internalizing composite score was good (α = .71 to .84) across all time points.

Physiological Data.

Measures of the physiological data was collected with the use of Mindware WiFi ACQ software, Version 1.0 (Mindware Technologies, Ltd., Westerville, OH). ECG was collected at a sampling rate of 500ms. Data was analyzed offline using the Mindware editing program Mindware HRV, Version 2.51, which identified interbeat-intervals (IBIs) and detected physiologically improbable intervals based on overall distribution using a validated algorithm (Berntson, Quigley, Jang, & Boysen, 1990). All data were visually inspected for artifact identification and editing by trained personnel. RSA was calculated in 30-second epochs as the natural log integral of high frequency 0.24–1.04 Hz power band, which reflects PNS influences on heart rate variability in phase with respiration for young children. The mean RSA value from across all usable epochs (M=5.62 epochs) during resting was used in analyses. Resting RSA ranged from 2.25 to 8.27 (M = 5.4, SD = 1.02).

Child Fear Sensitivity.

Fear sensitivity was used as a measure of fearful temperament. Fear sensitivity was calculated as a propensity to display fear relative to the threat of the task across six tasks designed to elicit object or social fear. Second-by-second microcoding of facial expressions of fear, bodily expressions of fear, freezing behavior, and close proximity to parent observed during the 24-month laboratory tasks were used to compute fear sensitivity. The percentage of the episode that was spent engaging in fearful behavior in each of the six fear tasks were standardized, and individual propensity to exhibit fear across all six tasks were derived using a measurement model based on a nonlinear growth model. Lower scores indicate lower thresholds for fear sensitivity (i.e. child more likely to exhibit fearful behaviors in contexts that are supposed to elicit less fear). Further details of how the fear sensitivity scores were computed is detailed in work by Buss and colleagues (2018).

Analytic Strategy.

Full Information Maximum likelihood (FIML) was used to account for missing data across participants in order to account for attrition under the assumption that data is missing at random as missing data analyses did not indicate that missingness was related to any covariates or variables of interest. Growth curve modeling was conducted using the lavaan package (Rosseel, 2012) in the R Environment for Statistical Computing. Age was centered at 6 years so that the intercept indicated the status at the end of the growth period examined, and growth coefficients indicated the change that occurred in 1-year increments starting at age 3. Growth curve analyses provide estimates pertaining to variability in children’s internalizing symptoms at age 6 (i.e., the intercept variance) as well as how internalizing symptoms may change at different rates (i.e. linear variance) (Delucia & Pitts, 2006). Once a baseline (or unconditional) model is established, inclusion of predictors of growth can be included to examine associations between predictors and growth (Curran, Obeidat, & Lorsado, 2010). We first examine an unconditional growth curve model that does not include predictors in order to examine the average trajectory of internalizing symptom development across all children. We then enter predictors and covariates to examine how maternal internalizing symptoms, resting RSA and their interaction may be associated with the intercept and slope variances.

Results

Descriptives Statistics.

Table 1 contains descriptives of children’s internalizing symptoms across all ages. The means and standard deviations in our sample are generally comparable to the means and standard deviations reported in the HBQ manual as population norms (Armstrong et al., 2003), though our sample reports lower child depressive symptomology. Of note, depressive symptoms were significantly positively skewed at ages 3 and 4. However, when included other internalizing symptoms in the composite score, data at all timepoints were not skewed and all participants were included in the analyses. Table 2 contains descriptives and correlations of maternal internalizing symptoms as measured by the total number of symptoms endorsed, child fear sensitivity, child resting RSA and child internalizing symptoms across all time points.

Table 1.

Descriptive statistics of mean scores for each subscale of child internalizing at each time point.

HBQ Subscale Age 3 Mean (SD) n = 101 Age 4 Mean (SD) n = 122 Age 5 Mean (SD) n = 109 Age 6 Mean (SD) n = 104
Depression 0.06 (0.13) 0.11 (0.18) 0.10 (0.14) 0.09 (0.14)
Overanxious 0.12 (0.12) 0.32 (0.22) 0.37 (0.24) 0.36 (0.22)
Separation Anxiety 0.17 (0.20) 0.35 (0.24) 0.33 (0.26) 0.30 (0.28)
Social Withdrawal 1.26 (0.39) 0.87 (0.46) 0.77 (0.39) 0.74 (0.45)
Internalizing Composite 0.22 (0.11) 0.32 (0.17) 0.32 (0.17) 0.30 (0.17)

Table 2.

Correlations between maternal internalizing symptoms, child resting RSA, and child internalizing symptoms across time, with means and standard deviations.

Variables 1 2 3 4 5 6 7
1. Maternal Internalizing Symptoms 1.00
2. Child Resting RSA −0.10 1.00
3. Fear Sensitivity −0.16 −0.08 1.00
4. Age 3 Child Internalizing Symptoms 0.28 * −0.04 −0.14 1.00
5. Age 4 Child Internalizing Symptoms 0.35 * −0.04 −.06 0.42 * 1.00
6. Age 5 Child Internalizing Symptoms 0.20 −0.06 0.05 0.26 * 0.63 * 1.00
7. Age 6 Child Internalizing Symptoms 0.11 −0.23 0.12 0.22 0.51 * 0.71 * 1.00
Mean 21.25 5.40 4.82 0.22 0.32 0.32 0.30
SD 7.93 1.02 1.15 0.11 0.17 0.17 0.17
*

indicates p < .05

Unconditional Growth Models.

An initial unconditional growth model with only intercept and linear change in internalizing symptoms was conducted to examine the overall trajectory of internalizing symptom development that the participants in the present study follow. However, this model did not fit the data well, χ2 = 18.09, p < .05, CFI = .88, RMSEA = .15, SRMR = .08. A quadratic term was entered, and fit indices for this model were good, χ2 = 0.11, p = .74, CFI = 1.00, RMSEA < .001, SRMR = .09. Figure 1 shows the mean trajectory of child internalizing symptoms from 3 to 6. There is also a significant variance component in the intercept factor, with an estimate of 0.02 (p = .04), highlighting significant individual variability in child internalizing symptoms at age 6. There was no significant variance component in the linear (−0.07, p =.01) or quadratic factors (−0.03, p < .01), suggesting that there were no inter-individual differences in the shape of change across participants. Figure 1 also shows the individual trajectories of internalizing symptom development across all participants. On average, internalizing symptoms increased from age 3 to age 4 and then remained stable through age 6. Although there were no inter-individual differences in the shape of change across participants in the unconditional growth model, adding predictors can increase power to predict variability in linear and quadratic factors.

Figure 1.

Figure 1.

Graph depicting all children’s’ internalizing symptoms from age 3 to age 6 in blue, with an average quadratic trajectory of all participants in black.

Conditional Growth Models.

Sex and Fear Sensitivity as Covariates.

Sex and fear sensitivity were entered as predictors in a preliminary conditional growth model in order to examine the role these variables may play as covariates (Table 3). This model fit well, χ2 = 3.50, p = .32, CFI = .99, RMSEA = .03, SRMR = .02. Neither sex nor fear sensitivity predicted child internalizing symptoms at age 6 or linear and non-linear changes in child internalizing symptoms across time (Table 3).

Table 3.

Growth Curve Model of Maternal Report of Child Internalizing Symptoms from 3 years to 6 with child sex and fear sensitivity included as covariates.

Child Internalizing Symptoms
Intercept Factor Slope Factor Quadratic Factor
Predictor B SE p B SE p B SE p
Sex 0.004 0.033 .90 0.005 0.031 .88 0.004 0.010 .73
Fear Sensitivity 0.015 0.016 .35 0.019 0.015 .20 0.003 0.005 .60
*

indicates p < .05

Maternal Internalizing Symptoms and Resting RSA.

Maternal internalizing symptoms and child resting RSA and their interaction were entered into the model to predict change in internalizing symptoms. Sex and child fearful temperament were included as covariates. Fit indices for this model were good, χ2 = 9.23, p = .16, CFI = .98, RMSEA = .05, SRMR = .03. Results for this model are displayed in Table 4.

Table 4.

Growth Curve Model of Maternal Report of Child Internalizing Symptoms from 3 years to 6 years as predicted by Maternal Internalizing Symptoms, Resting RSA and the interaction between Maternal Internalizing Symptoms and Resting RSA with child sex and fear sensitivity included as covariates.

Child Internalizing Symptoms
Intercept Factor Slope Factor Quadratic Factor
Predictor B SE p B SE p B SE p
Sex 0.029 0.036 .42 0.023 0.032 .46 0.007 0.011 .53
Fear Sensitivity 0.009 0.016 .57 0.002 0.016 .90 −0.002 0.005 .76
Resting RSA −0.037 0.024 .12 0.041 0.019 .03 * −0.009 0.007 .17
Maternal Internalizing Symptoms 0.008 0.016 .63 0.049 0.018 < .01 * 0.014 0.006 .01 *
Resting RSA × Maternal Internalizing Symptoms −0.036 0.026 .16 −0.041 0.027 .13 −0.008 0.009 .36
*

indicates p < .05

Child resting RSA significantly predicted linear change (slope) in internalizing symptoms from age 3 to age 6. Higher resting RSA predicted a flatter slope across time, β = −0.04, SE = 0.02, p = .03. Children with lower resting RSA increased more in internalizing symptoms than children with higher resting RSA. Figure 2 shows average trajectories for children with resting RSA values 1 standard deviation above and below the mean.

Figure 2.

Figure 2.

Line graph depicting average trajectories of children’s internalizing symptoms from age 3 to age 6 for children with resting RSA values 1 standard deviation above and below the mean.

Greater maternal internalizing symptoms predicted a flatter slope across time, β = −0.05, SE = 0.02, p < .01, suggesting that children with mothers with more internalizing symptoms exhibit less increase in internalizing symptoms across time. Maternal internalizing symptoms also significantly predicted quadratic change across time, β = −0.02, SE = 0.01, p = .01. Greater maternal internalizing symptoms predicted greater negative quadratic change in children’s internalizing symptoms. Figure 3 shows the average trajectories for children with mothers with internalizing symptoms 1 standard deviation above and below the mean. Children exhibited greater increases followed by subsequent decreases in internalizing symptoms when their mothers were higher in internalizing symptoms when compared to children of mothers with lower internalizing symptoms.

Figure 3.

Figure 3.

Line graph depicting average trajectories of children’s internalizing symptoms from age 3 to age 6 for children of mothers with internalizing symptoms 1 standard deviation above and below the mean.

In addition, the interaction term between resting RSA and maternal internalizing symptoms did not significantly predict either the intercept, slope or quadratic latent factors.

Discussion

The current study was motivated by two gaps identified in the literature. First, most studies examining the developmental trajectories of children’s internalizing symptoms have often focused on older children, and less is known about the early childhood period leading up to school entry. Second, there have been mixed results how resting RSA and maternal internalizing symptoms may interact to predict internalizing symptoms across development. The present study used growth curve models to add to our understanding of how child RSA and maternal internalizing symptoms may be associated with developmental trajectories of internalizing symptoms from ages 3 to 6.

Results indicated that on average, a linear change did not adequately capture the developmental trajectories of internalizing symptoms, but there was support for a quadratic change in internalizing symptoms. On average, internalizing symptoms increased from age 3 to age 4 and then remained stable through age 6. This increase in internalizing symptoms coincides with the start of preschool for many children, and this is sustained throughout preschool through to school entry. The start of preschool may be accompanied by the introduction of new key developmental tasks such as making friends and learning social skills required in a preschool setting (Masten & Coatsworth, 1998; Denham et al., 2003), which may be linked to an increase in internalizing symptoms such as fear and anxiety.

While some studies find that anxiety disorders are prevalent during preschool (Eggers & Angold, 2006), research on trajectories of internalizing symptoms during this developmental period is mixed. Sterba and colleagues (2007) did not find an increase in internalizing symptoms from age 3 to 4 and Battaglia and colleauges (2016) showed that separation anxiety decreases at 4–5 years of age. However, Côte and colleagues (2009) found two groups that exhibited increases from age 2 to 5 with temperament distinguishing the high-rising group from the moderate-rising group. One possibility for the increase in internalizing from age 3 to 4 from the current study could be due to our sample being a temperamentally at-risk sample. Due to oversampling for fearful temperament during recruitment, we may see a greater number of children exhibiting increasing internalizing symptoms during this preschool period. Our lab has previously reported that fearful temperament during toddlerhood is predictive of social wariness and social anxiety symptoms during kindergarten (Buss et al., 2013). Specifically, fear sensitivity was associated with higher parental reports of social inhibition at 3 and 4 (Buss et al., 2018). Although fear sensitivity did not predict internalizing symptoms at age 6 or change in internalizing symptoms in the current study, it could be that temperamentally at-risk samples are more likely to demonstrate an overall increase in internalizing symptoms from age 3 to 4.

In addition, it is important to note that there was interindividual variability (Figure 1), highlighting the need to consider how factors such as RSA and maternal internalizing symptoms may be associated with different trajectories of internalizing symptom development.

Interactions between Child Physiology and Maternal Internalizing Symptoms

Child physiology and maternal internalizing symptoms independently predicted trajectories of child internalizing symptoms, but contrary to our hypothesis, their interaction did not. Prior literature has demonstrated that child physiology and maternal internalizing symptoms may interact to influence child internalizing symptom development (Wetter & El-Sheikh, 2012; Shanahan et al., 2014). However, given that the present study is the first to examine the interaction between child physiology and maternal internalizing symptoms in children during early development, one possibility is that child RSA and maternal internalizing symptoms do not interact to predict internalizing symptom development during the preschool years, but may later interact to predict trajectories of internalizing symptom development during adolescence. Rapid development in emotion regulation occurs during the preschool years (see Stifter & Augstine, 2019 for review). While innate mechanisms such as physiology help reduce emotional arousal during negatively-valenced experiences, they are difficult to sustain without the input of parents during the first three years of life. Parents continue to have an influence but play a less prominent role as children age due to the development of individual regulatory capabilities. It may be that the regulation of negative affect associated with internalizing symptom development is jointly influenced by physiological regulation and maternal internalizing symptoms during the preschool period, as younger children are partially reliant on their caregivers to regulate (Bariola, Gullone, & Hughes, 2011). As children in the present study may still be reliant on their caregivers to regulate, it could be that individual differences in RSA do not moderate the associations between maternal internalizing symptoms during this earlier developmental period, but RSA later moderates the associations between maternal and child internalizing symptoms as children become less reliant on caregivers to regulate.

Alternatively, RSA reactivity to stress-based tasks as opposed to resting RSA may evoke a wider range of responding that may be more representative of vulnerability to stressful environments associated with maternal internalizing symptoms. In particular, prior literature has shown that physiological regulation during tasks eliciting frustration and irritability are associated with children’s internalizing symptom development (Hinnant & El-Sheikh, 2009; Shanahan et al., 2014). There may be context-specific markers of physiological sensitivity to the environment that interact with maternal internalizing symptoms to predict trajectories of child internalizing symptoms. Future studies should examine whether RSA reactivity during stress-eliciting tasks may interact with maternal internalizing symptoms to predict trajectories of child internalizing symptoms during the preschool period.

Finally, there may be other measures of physiology that may moderate associations between maternal internalizing symptoms and trajectories of child internalizing symptom development. For example, measures of HPA axis functioning and sympathetic nervous system activity have been demonstrated to interact with environmental influences to predict children’s internalizing symptoms (e.g. Kalomiris, Phelps, & Kiel, 2019; Obradovic, Bush, & Boyce, 2011). Future work should examine if other measures of physiology better capture vulnerability to environmental stress associated with maternal internalizing symptoms to predict trajectories of child internalizing symptom development.

Maternal Internalizing Symptoms and Trajectories of Child Internalizing Symptoms

Main effects of maternal internalizing symptoms demonstrated that maternal internalizing symptoms predicted both linear and quadratic change in child internalizing symptoms from age 3 to 6, but did not predict levels of internalizing symptoms in children at age 6.

Higher maternal internalizing symptoms were associated with a steeper increase followed by a greater decrease in child internalizing symptoms, which resulted in and overall flatter slope (i.e., less linear increase from age 3 to age 6). In addition, there was no association between maternal internalizing symptoms and child internalizing symptoms at age 6. The association between higher maternal internalizing symptoms and steeper increase from ages 3 to 5 shows that maternal symptoms may be more salient during this preschool period. This is consistent with literature that highlights the importance of considering how these early risk factors may be related to internalizing symptoms during the preschool period (e.g. Mesman & Koot, 2001).

The positive association between maternal internalizing symptoms and a steeper increase in child internalizing symptoms could be due to parenting behaviors such as overprotection or parental modeling of emotion regulation strategies. We know from other literature that parents with higher internalizing symptoms utilize more parenting behaviors such as overprotection that lead to higher levels of child internalizing symptoms later in development (Bayer et al., 2006; Murray et al., 2008). During childhood, parents have an influence over children’s emotion regulation through instruction, modeling, and interpretation of different emotional events (Stifter & Augustine, 2019; Kiel & Kalomiris, 2015). One study has demonstrated that mothers who engaged in joint regulation with their child during preschool were more likely to demonstrate lower levels of anger and sadness (Morris et al., 2011). Mothers with more internalizing symptoms may influence their children’s emotion regulation strategies differently than mothers with less internalizing symptoms, as mothers with more internalizing symptoms may model less effective emotion regulation strategies or engage in joint regulation less. This could lead to children exhibiting higher levels of internalizing symptoms during this early childhood period, as they are less effective at emotion regulation.

In addition, greater decreases in internalizing symptoms from age 5 to 6 characterized by the quadratic change in children with mothers with more internalizing symptoms (see Figure 3) may be due to exposure to social relationships beyond the immediate family, such as teachers and peers, that may influence the development of internalizing symptoms. The decrease in internalizing symptoms observed in the current study coincides with the participants entering kindergarten. During this period of time, children may be getting exposure to other forms of emotion socialization and social relationships beyond maternal influences that may be associated with the development of internalizing symptoms (Dunsmore & Karn, 2004; Denham, Bassett, & Zinsser, 2012). Teachers also play a role in the socialization of emotion through modeling, teaching explicitly about emotions and through their own behaviors in reaction to children’s emotions (Denham et al., 2012). In addition, peer interactions and relationships during kindergarten was also demonstrated to influence children’s emotion knowledge (Dunsmore & Karn, 2004). Taken together, this suggests that there may be other social influences such as peers and teachers that may influence children’s internalizing symptom development during the kindergarten period such that maternal internalizing symptoms does not significantly impact the level of children’s internalizing symptoms by the spring of kindergarten.

Given that maternal internalizing symptoms predicted change in children’s internalizing symptoms but did not predict symptoms at age 6, post-hoc analyses (not reported) were conducted with age 3 as the intercept. Results showed that maternal internalizing symptoms significantly predicted children’s internalizing symptoms at age 3, with greater maternal internalizing symptoms significantly predicting more internalizing symptoms at age 3. While there may be other influences on children’s internalizing symptoms during school entry, this post-hoc analysis may be indicative that mothers’ self-reported symptoms are most strongly associated with more proximal measures of children’s internalizing symptoms. Future research should examine how repeated measures of maternal internalizing symptoms may be associated with children’s trajectories of internalizing symptoms.

Additionally, findings from the current study are not entirely consistent with prior literature that has demonstrated that higher levels of maternal internalizing symptoms are associated with stable high levels of internalizing symptoms or increasing symptoms over time (Sterba, Prinstein, & Cox, 2007; Côte et al., 2009). Our findings could potentially be consistent with work by Côte and colleagues (2009) as both studies demonstrated increased maternal internalizing symptoms were associated with increases in child internalizing symptoms from ages 3 to 5. However, trajectories in Côte and colleagues’ work (2009) did not extend to age 6. On the other hand, Sterba and colleagues (2007) did not find that maternal covariates (including maternal anxiety and depressive symptoms) were associated with a group increasing in internalizing symptoms during this age range. The lack of consistency may be due to key methodological differences between the current study and prior literature. Most studies that have examined trajectories of internalizing symptoms during early childhood have taken a group-based perspective by identifying whether or not maternal internalizing symptoms was more strongly associated with specific types trajectories identified using a person-centered approach. The current study utilized latent growth curve modeling, which allow us to examine how varying levels of maternal internalizing symptoms may be associated with varying levels of change in child internalizing symptoms. Inconsistency with prior studies could be due to differences in methodological approaches to modeling how factors such as maternal internalizing symptoms may be associated with children’s internalizing symptom development.

An additional future direction is to examine child internalizing symptoms from age 3 to beyond early childhood. Given the present study’s results, there is a possibility that higher maternal internalizing symptoms may be associated with a greater decline in child symptoms beyond early childhood, whereas those with lower maternal internalizing may flatten out, or increase in child symptoms. This may also help establishing consistency with other studies that examine trajectories extending into middle childhood and pre-adolescence.

The main effect of maternal internalizing symptoms provides more insight to how the risk factor of maternal internalizing symptoms may be associated with changes in internalizing symptoms in children aged 3 to 6, and highlights that these changes occur in children’s internalizing symptom development before school entry.

Child Physiology and Trajectories of Child Internalizing Symptoms

There was also a main effect of child resting RSA on children’s trajectories of internalizing symptoms. Children with lower levels of resting RSA had greater increases in internalizing symptoms from ages 3 to 6 than children with higher levels of resting RSA. Our findings are consistent with prior research that has shown lower resting RSA is associated with increasing levels of internalizing symptoms over time from third to fifth grade, though it is also important to note Hinnant and El-Sheikh (2009) examined how both resting RSA and RSA reactivity predict trajectories of symptom development. Beauchaine (2015) suggests that low resting RSA is a marker for poor executive control over behavior and poor emotion regulation. Lower resting RSA may be a physiological marker for children with poorer regulatory capabilities such that children with lower resting RSA are developing more internalizing symptoms across time than their peers with higher resting RSA.

It is also important to note that resting RSA did not significantly predict the levels of child internalizing symptoms at age 6, though prior studies have demonstrated that higher resting RSA is often associated with lower internalizing symptoms (Graziano & Derefinko, 2013; Beauchaine & Thayer, 2015). This may be due to including maternal internalizing symptoms in the same model and controlling for sex and temperament, thus highlighting the importance of examining resting RSA from a biopsychosocial perspective and accounting for both individual factors as well as environmental factors such as maternal internalizing symptoms. Prior studies that have found associations between resting RSA and internalizing symptoms have often not accounted for both biological and environmental factors and their interaction. In addition, children often have multiple risk or protective factors across development, so it is important to consider multiple factors as the development of internalizing symptoms is multifaceted. To our knowledge, this is the first study to examine the role of resting RSA on trajectories of internalizing symptom development during this age range.

Strengths, Limitations and Future Directions

Findings from the present study should be considered within the strengths and limitations of the study. The longitudinal design of the study with multiple time-points is a strength, which allows us to utilize the statistical models of latent growth curve models to examine the developmental changes in internalizing symptoms. We were able to capture a quadratic pattern of change, in addition to examining how different risk factors may influence the patterns of change as opposed to taking a group-based trajectory approach. In addition, the oversampling for children with fearful temperament allowed us to examine greater variability in internalizing symptom development during early childhood. However, one limitation of the present study consisted primarily of White, middle-class families, so future work should examine these associations with a larger, more diverse sample for generalizability.

Maternal internalizing symptoms was conceptualized as a time-invariant predictor in the current study – though internalizing symptoms may remain stable during adulthood, there is literature demonstrating that there may be transactional influences between child and maternal internalizing symptoms across time (Nicholson, Deboeck, Farris, Boker, & Borkowski, 2011). Future research should consider examining transactional relations between child physiology, child internalizing and maternal internalizing across time to better understand the dynamic relations between biological and social processes to inform children’s trajectories of internalizing symptom development. A study conducted by Feldman and colleagues (2009) found that the differences between groups of children with different numbers of “risk” indicators based on maternal depressive symptoms and neonatal resting RSA increased with age. It is important to examine at which point during development that groups start to diverge. Longitudinal research will elucidate how factors such as maternal psychopathology and physiological reactivity may interact to increase or decrease children’s risk of developing psychopathology and inform the design of targeted interventions.

In addition, resting RSA was also considered as a time-invariant predictor and was only assessed at 42-months. While prior research suggests that resting RSA increases linearly across development, recent work has demonstrated that there is stability in resting RSA from toddlerhood through adolescence (Dollar et al., 2020). In particular, resting RSA was shown to have greater stability from Age 2 to Age 7 (Dollar et al., 2020), which encompasses the ages of assessment in the present study.

Another limitation of the present study is that both child and maternal internalizing symptoms were reported by mothers. There have been some studies that have shown that mothers with internalizing symptoms such as depression overreport child behavior problems (Najman et al., 2000; Xerxa et al., 2020). Though there were no strong correlations between maternal internalizing symptoms and child internalizing symptoms in the present study (Table 2), future research should aim to replicate the findings of the present study by examining utilizing multiple reporters, such as fathers and teachers or incorporating a measure of internalizing symptoms assessed via a clinical interview.

A related line of research demonstrates that maternal internalizing symptoms are associated with variations in parenting behaviors, such as overprotection (Bayer et al., 2006; Murray et al., 2008; Kiel, & Buss, 2011). There were no measures of overprotective parenting that were included in the present study, which is an additional limitation to the study. Some studies have demonstrated that overprotective parenting is a primary predictor of child internalizing symptom development, especially in children under the age of 6 (Bayer et al., 2006). Hastings and colleagues (2008) found that resting RSA moderated the associations between maternal protective overcontrol to predict social wariness in preschoolers. Given that resting RSA did not moderate associations between maternal internalizing symptoms and trajectories of child internalizing symptoms, one possibility is that resting RSA may moderate the associations between variations in parenting behaviors and trajectories of child internalizing symptoms instead. Future research should examine if maternal internalizing symptoms and children’s developmental trajectories of internalizing symptoms may be indirectly associated via variations in parenting behaviors to better understand the mechanisms by which maternal internalizing symptoms may influence internalizing symptom development. This can help us identify potential targets for intervention, as aspects of parenting are modifiable. For example, overprotective parenting may be a target for interventions, as these parenting behaviors are often linked with both maternal internalizing symptoms and child anxiety (e.g. Ginsburg, Grover, & Ialongo, 2005).

Conclusions

Understanding the early risk factors associated with different developmental trajectories of internalizing symptoms will help elucidate the etiologies. A better understanding of the factors influencing the developmental trajectories of children’s internalizing symptoms can also help us identify which children are at greatest risk of developing depression and anxiety, and has implications for creating more targeted prevention and intervention programs for these children.

This study demonstrates that both social and biological factors, such as maternal internalizing symptoms and child physiology, are associated with the development of internalizing symptoms during early childhood. Both child physiology and maternal internalizing symptoms predicted the developmental trajectories of children’s internalizing symptoms, though neither predicted levels of internalizing symptoms at age 6. These findings highlight the need to consider both environmental and biological factors in shaping children’s internalizing symptom development.

Acknowledgments

Data for this study is supported by a grant from National Institutes of Health (MH075750). Anna M. Zhou and Kristin A. Buss declare they have no conflicts of interest. The data that support the findings of this study are available on request from Kristin A. Buss. The data are not publicly available due to privacy or ethical restrictions.

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