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. Author manuscript; available in PMC: 2022 Mar 1.
Published in final edited form as: Res Child Adolesc Psychopathol. 2021 Jan 6;49(3):311–323. doi: 10.1007/s10802-020-00724-6

Early Development of Comorbidity Between Symptoms of ADHD and Anxiety

Shannon L Gair 1, Hallie R Brown 1, Sungha Kang 1, Adam S Grabell 1, Elizabeth A Harvey 1
PMCID: PMC7878348  NIHMSID: NIHMS1660810  PMID: 33404952

Abstract

Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder that shares a high comorbidity with anxiety disorders. However, the early development of comorbid ADHD and anxiety symptoms is not well-understood. In this study, the bidirectional relation between ADHD and anxiety symptoms was examined by testing two models of the development of ADHD and anxiety comorbidity: an anxiety effects model, which posits that anxiety symptoms contribute to the development of ADHD symptoms, and an ADHD effects model, which posits that ADHD symptoms contribute to the development of anxiety symptoms. Within the ADHD effects model, parenting practices were tested as mediators of this relation. Participants included children who were 3 years old at baseline (n = 258) and their caregivers who reported on their children’s ADHD and anxiety symptoms annually for 3 years. The bidirectional relation of parent-reported anxiety and ADHD symptoms was tested using a series of cross-lagged models. Results indicated that ADHD symptoms predicted later anxiety symptoms, but anxiety symptoms did not predict later ADHD symptoms. Parenting practices did not mediate the relation between ADHD and anxiety symptoms within the ADHD effects model. These findings suggest that ADHD-anxiety comorbidity may develop in part because early symptoms of ADHD contribute to the development of anxiety symptoms; future research should be conducted to elucidate the mechanisms of this relation.

Keywords: ADHD, anxiety, preschool, longitudinal, comorbidity

Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder characterized by excessive inattention and/or hyperactivity and impulsivity and is estimated to affect 5–10% of children (American Psychiatric Association, 2013; Polanczyk et al., 2014). In addition to these impairing core symptoms, ADHD also has a high comorbidity rate with other psychiatric disorders (Larson et al., 2011). Although conduct problems are the most common comorbid disorders (Elia et al., 2009), an estimated 25% to 40% of school-aged children with ADHD experience a co-occurring anxiety disorder (Jarrett & Olendick, 2008; Overgaard et al., 2016), which can impact ADHD symptom expression and prognosis in complex ways (Halldorsdottir & Ollendick, 2014; Hinshaw, 2007; Jarrett et al., 2016; Manassis et al., 2000; Overgaard et al., 2016). However, the processes by which comorbid ADHD and anxiety co-develop are poorly understood. Investigating the process by which comorbidity develops early in life, when these disorders are emerging, is necessary to advance theory regarding etiological underpinnings and to inform early intervention for comorbid problems among children with ADHD.

Two causal explanations for the development of comorbid ADHD/anxiety have been proposed that focus on bidirectional effects of ADHD and anxiety (Bubier & Drabick, 2009): 1) symptoms of anxiety exacerbate ADHD symptoms such as fidgetiness or distractibility (anxiety effects), and 2) negative social feedback and reduced executive functions related to ADHD symptoms contribute to the development of anxiety symptoms (ADHD effects). However, as described below, relatively few studies have empirically tested each of these effects and even fewer have simultaneously tested the bidirectional relation of anxiety and ADHD. To our knowledge, no studies have tested the bidirectional relation of anxiety and ADHD symptoms in a sample of preschoolers at risk for psychopathology.

Bidirectional Effects of ADHD and Anxiety

Anxiety Effects

Researchers have proposed several ways in which anxiety symptoms may exacerbate ADHD symptoms. For example, anxiety symptoms such as rumination and worry may directly interfere with attention and cause restlessness. Additionally, anxiety may lower the threshold for disruptive symptoms to be expressed; that is, in the context of anxiety, subthreshold ADHD symptoms may become clinical (Baldwin & Dadds, 2008; Bubier & Drabick, 2009). However, few empirical studies have longitudinally examined if anxiety predicts later ADHD symptoms, which would provide key evidence for the existence of anxiety effects.

The handful of studies that have examined anxiety as a predictor of later ADHD have yielded mixed results. Some studies have found that ADHD was not predicted by anxiety in toddlers (Overgaard et al., 2014), middle childhood (Burke et al., 2005), or late childhood to adolescence (Baldwin & Dadds, 2008; Costello et al., 2003), controlling for early ADHD symptoms. Bittner et al. (2007) found that anxiety predicted later ADHD diagnosis, but did not control for early ADHD symptoms. However, Speltz et al. (1999) did find that anxious-passive symptoms in preschoolers with ODD predicted ADHD diagnosis 2 years later, controlling for early ADHD symptoms. Although the majority of studies failed to find effects of anxiety on ADHD, Speltz and colleagues’ (1999) positive finding suggests that anxiety effects may occur specifically during the preschool years, which is a developmentally critical time for the development of behavior and affective regulation. Speltz and colleagues’ (1999) study was also one of the few to focus on a sample at risk for behavior problems and it may be that anxiety effects are most evident among at-risk preschoolers. However, further research on preschoolers with behavior problems is needed to establish if such a pattern exists.

ADHD Effects

ADHD symptoms may contribute to the development of anxiety symptoms. It has been argued that the negative feedback that children receive from their environment due to their ADHD symptoms may cause anxiety about these issues (Baldwin & Dadds, 2008; Bubier & Drabick, 2009). In addition, some executive function deficits that characterize ADHD (e.g., emotion regulation, cognitive inhibition) may reduce children’s ability to cope with stressors, contributing to the exacerbation of anxiety symptoms over time (Barkley, 2010; Nigg et al., 2004).

Few studies have longitudinally tested the ADHD effects model, and results have been mixed. Burke et al. (2005) found that early ADHD symptoms predicted later anxiety disorders, controlling for early anxiety. Similarly, in a retrospective study, Safren et al. (2001) found that generalized anxiety disorder emerged after ADHD for all cases except one, further lending support to the ADHD effects model. However, other studies have failed to find evidence for the ADHD effects model. When accounting for early anxiety, ADHD did not predict later anxiety in a clinical sample of toddlers (Overgaard et al., 2014), in a clinical sample in middle childhood (Foley et al., 2004), or in a community sample in late childhood across adolescence (Costello et al., 2003). In one community study, higher childhood ADHD symptoms actually predicted lower anxiety symptoms one year later (Baldwin & Dadds, 2008). Given this limited and mixed literature, additional research is needed to understand the impact of ADHD symptoms on the development of anxiety symptoms.

Even fewer studies have tested mechanisms that have been proposed in the ADHD effects model. Researchers have posited that ADHD symptoms elicit negative feedback from the environment which may in turn increase anxiety symptoms (Baldwin & Dadds, 2008; Bubier & Drabick, 2009). Negative parenting practices are one such form of negative environmental feedback that may mediate the relation between ADHD and anxiety symptoms. In particular, high levels of harsh/overreactive parenting and low warmth have been linked with both ADHD (e.g., Wymbs et al., 2015) and anxiety (Gallagher & Cartwright-Hatton, 2008). Parenting practices have been shown to mediate the relation between ADHD and other comorbidities (Breaux et al., 2017; Ostrander & Herman, 2006). There is considerably less research on the impact of parenting on the development of comorbid anxiety symptoms (Deault, 2010), but previous research suggests that it may mediate the relation between ADHD and anxiety symptoms. Child ADHD behavior predicts less positive parenting and more negative parenting (Shelleby & Ogg, 2020; Wymbs et al., 2015), and in children with ADHD, lack of positive parenting is associated with comorbid anxiety symptoms (Pfiffner & McBurnett, 2006). Research is needed to more directly test parenting as a mediator of the ADHD effects model. Such research could point to important dimensions of parenting to target to prevent or reduce the severity of anxiety symptom development in children with ADHD.

Relation Between ADHD and Anxiety Symptoms in Preschoolers

Much of the limited research assessing the relation between anxiety and ADHD comorbidity has focused on middle childhood to adolescence (Baldwin & Dadds, 2008; Bittner et al., 2007; Burke et al., 2005; Costello et al., 2003; Foley et al., 2004; Roza et al., 2003). However, the larger literature on externalizing and internalizing symptoms indicates that it is important to study the development of comorbidity of these symptoms during the preschool years, which may be a key developmental period for the emergence of these problems. Research has suggested that the relation between the development of internalizing and externalizing symptoms differs across time. For example, externalizing and internalizing symptoms have been found to be more strongly related in younger than older samples (Bird et al., 1993; Marmorstein, 2007; Russo & Beidel, 1994). Indeed, the handful of studies that have longitudinally assessed externalizing and internalizing symptoms beginning in the preschool years found a significant relation (Gilliom & Shaw, 2004; Keiley et al, 2000; Lavigne et al., 2001; Roza et al., 2003; Speltz et al., 1999). In contrast, the results of the studies with older children have been more mixed; only about half of the longitudinal studies assessing the development of internalizing and externalizing symptoms in older children have found a significant relation (Bittner et al., 2007; Burke et al. 2005; Foley et al., 2004; Last et al., 1996). It may be that ADHD and anxiety symptoms strongly influence each other in early childhood before patterns are stabilized in middle childhood. However, to our knowledge, no studies have tested the ADHD effects model across the preschool years, and only a single study has examined anxiety effects in preschoolers (Speltz et al., 1999). The only study of toddlers found no evidence supporting the anxiety or ADHD effects models (Overgaard et al., 2014). This finding suggests that toddlerhood, when children exhibit a wide range of disruptive yet normative behaviors, may be too young for transactional patterns to be detected. It is therefore important to develop a critical knowledge base of how ADHD and anxiety symptoms develop during the preschool years, which may be a critical time for the development of comorbidity.

The Present Study

In sum, the relation between ADHD and anxiety symptom development is poorly understood, and no studies have assessed the bidirectional relation of this comorbidity in preschoolers. The goal of the present study was to assess the development of comorbid anxiety and ADHD symptoms across the preschool years. Using a series of cross-lagged models, we tested the anxiety effects model and the ADHD effects model. In addition, we examined parenting as a potential mediator of the ADHD effects model. Because the preschool years are a period of rapid behavioral and emotional development, this study used longitudinal data assessed across multiple time points from ages 3 to 6 to explore whether effects vary across this developmental period. This study focused on data from families who were oversampled for parent-reported behavior problems to increase generalizability to children who are at risk for developing clinically significant difficulties. Although the empirical literature is mixed, based on existing theory we hypothesized that both models would be supported. In particular, we predicted support for the anxiety effects model, because anxiety may confer risk for ADHD symptoms by directly interfering with attention and increasing restlessness, or by lowering the threshold for ADHD symptoms to become clinical (Baldwin & Dadds, 2008; Bubier & Drabick, 2009). We hypothesized that we would find evidence of ADHD effects, as the negative environmental experiences that children with ADHD symptoms experience may increase anxiety (Bubier & Drabick, 2009). Finally, we predicted that ADHD effects would be mediated by maternal warmth and overreactive (harsh) parenting, such that ADHD symptoms at one time point would predict more overreactive parenting and less warmth at the next time point, which would in turn predict later anxiety.1

Method

Participants

Participants were 258 (138 boys; 120 girls) 3-year-old children (M = 44.13 months, SD = 3.39) and their caregivers who took part in a 3-year longitudinal study aimed at understanding the early development of ADHD. Children were oversampled for behavior problems; at screening, 199 children had significant externalizing problems (clinically elevated hyperactivity and/or aggression) and 59 children showed few behavior problems. Participants were from diverse ethnic backgrounds, including European American (55.4 %), Latino/a American (17.8 %; mostly Puerto Rican), African American (12 %), and multiethnic (14.7 %) children. The median family income was $48,000. Most mothers (87.5 %) and fathers (89.4 %) had high school diplomas, and a substantial minority (mothers: 33.5 %; fathers: 28.7 %) earned bachelor’s degrees or higher. Most families (86 %) were two-parent families. Of the 199 children with behavior problems, 168 completed a 3-year follow-up assessment during which more detailed diagnostic assessments were completed (for more details about this process see Harvey et al., 2009); assessments found that 36 children (20 boys) met criteria for ADHD only, 22 (13 boys) met criteria for ODD only, and 39 (26 boys) met criteria for ADHD and ODD.

Procedure

The study was conducted in compliance with the University of Massachusetts Amherst Institutional Review Board, and written informed consent was obtained from all participating parents. Participants were recruited over a 3-year period by distributing screening questionnaires through state birth records, pediatrician offices, child care centers, and community centers throughout western Massachusetts. Children with significant externalizing problems were recruited from 1752 3-year-old children whose parents completed a screening packet containing the Behavior Assessment System for Children–Parent Report Scale (BASC-PRS; Reynolds & Kamphaus, 1992) and a questionnaire assessing for exclusion criteria, parental concern about externalizing symptoms, and demographics. Inclusion criteria for the behavior problem group included: (a) parent responded yes or possibly to the question, “Are you concerned about your child’s activity level, defiance, aggression, or impulse control?” and (b) BASC–PRS hyperactivity and/or aggression subscale T scores fell at or above 65 (approximately 92nd percentile). Inclusion criteria for the control group included: (a) parent responded “no” to, “Are you concerned about your child’s activity level, defiance, aggression, or impulse control?” and (b) T scores on the BASC–PRS hyperactivity, aggression, attention problems, anxiety, and depression subscales fell at or below 60. Participants had no evidence of intellectual disability, hearing or visual impairment, language delay, cerebral palsy, epilepsy, autism, or psychosis, based on parent report, informal observations during the first home visit, and confirmed by administration of the McCarthy Scales of Children’s Abilities at Time 1 (T1). At T1, families were scheduled for two 3-hr home visits scheduled approximately 1 week apart. Each parent was paid for participation in the study. Home visits were then conducted annually, with 243 families participating at Time 2 (T2), 215 families participating at Time 3 (T3), and 223 families participating at Time 4 (T4). At each home visit, children completed tasks to assess their cognitive and behavioral functioning, and parents completed questionnaires and interviews. The present study focused on the following measures completed at these visits.

Measures

Child ADHD

ADHD symptoms were assessed using the ADHD section of the NIMH-Diagnostic Interview Schedule for Children-IV (DISC-IV; Shaffer et al., 2000), which was administered at all time points to parents jointly when available, or to one parent when not. The DISC-IV2 is a highly structured diagnostic instrument which asks parents to respond yes/no regarding their child’s psychiatric symptoms. Minor modifications were made to school-related questions for preschoolers (e.g., “school” was changed to “preschool/daycare” in questions asking about school behavior, and references to schoolwork or homework as examples were removed). Symptom counts for hyperactivity/impulsivity and inattention were used in the present study; possible scores for each domain range from 0 to 9 symptoms. Internal consistency was high (Kuder–Richardson 20 ranged from .80 to .87 across time points for hyperactivity/impulsivity and inattention).

Child Anxiety

At each time point, mothers completed the BASC-PRS (Reynolds & Kamphaus, 1992), a broadband measure of psychopathology. The BASC-Preschool Version, designed for children 2 to 5 years old, and the BASC-Child Version, designed for children 6 to 12 years old, were administered as appropriate. At T1 and T2, all mothers were administered the BASC-Preschool Version. At T3, 39 children were 6 years old, and their mothers were administered the BASC-Child Version, and the rest were administered the BASC-Preschool Version. At T4, all mothers were administered the BASC-Child Version. The BASC subscales show good internal consistency and test-retest reliability (Reynolds & Kamphaus, 1992). The anxiety subscale was used for present analyses3 and showed good internal consistency for both the BASC-Preschool version (Cronbach’s ✓: T1 = .73; T2 = .80; T3 = .78) and the BASC-Child Version (Cronbach’s ✓ = .77).

Parenting Practices

Maternal Warmth.

Mothers and children were videotaped annually during a 5-min free play task and a clean-up task. Tasks were rated separately and then averaged to create one warmth score per mother. All tapes were coded by two undergraduate research assistants, whose scores were averaged. Global ratings of warmth were used, with Likert-scale scores ranging from 1 (complete absence of warmth) to 7 (high warmth). Warmth was defined as the extent to which mothers positively attended to their children; used praise, encouragement, and terms of endearment; conveyed affection; were supportive and available; were cheerful in mood and tone of voice; and conveyed interest, joy, and enthusiasm in the interactions. Inter-rater reliability, as measured by intraclass correlations, averaged .68 across the four time points.

Maternal Overreactivity4.

The Parenting Scale (Arnold et al., 1993), a 30-item scale measuring parenting practices, was used to measure maternal overreactivity. The overreactivity subscale includes items measuring harsh discipline and negative emotion (e.g., “I get so frustrated or angry that my child can see I’m upset”). On the Parenting Scale, mothers reported the frequency with which they use various discipline strategies on a 7-point Likert scale, where a 7 represents a greater frequency of overreactivity. The present study used mean scores for mothers’ self-reported overreactivity, which demonstrated good internal consistency at T1 (✓ = .72), at T2 (α = .80), at T3 (α = .76), and at T4 (α = .83).

Data Analyses

MPlus (Muthén & Muthén, 2017) was used to test a series of cross-lagged path models examining the direction of paths across time between ADHD and anxiety. Full information maximum likelihood was used to account for missing data. Children who did not participate in any follow-up visits after T1 (n = 21) did not significantly differ on any of the target variables (i.e., ADHD symptoms, anxiety symptoms, parenting variables) from children who completed at least one follow-up visit (ps from .346 to .944). Additionally, Little’s MCAR test (χ2 = 23.54, df = 14, p = .052) showed that there was not sufficient evidence that results were missing systematically, although this result was a trend. Analyses were originally conducted separately for hyperactivity and inattention (scores out of 9 for each), but results were essentially identical. Thus, hyperactivity and inattention were summed into one ADHD variable (scores out of 18) that was used for all analyses.

Traditional cross-lagged models have been critiqued due to limitations distinguishing between within-subjects and between-subjects change (e.g., Hamaker et al., 2015). Modified cross-lagged models (e.g., Besemer et al., 2016; Hamaker et al., 2015) have been used, although these models typically remove between-subjects variance, which was of interest in the present study. Specifically, we were interested in testing whether children with above average symptoms relative to peers at one time point would be at risk for above average symptoms of the other disorder at a later time point, controlling for early symptoms. By focusing only on within-subjects variance, we would have instead been testing whether children with above average symptoms relative to their own mean would be at risk for above average symptoms of the other disorder relative to their own mean). As such, we used the traditional cross-lagged design.

First, a baseline model was estimated with auto-regressive paths from anxiety and ADHD symptoms at each time point predicting their respective symptoms at the following time point. The correlation between ADHD and anxiety at T1 was estimated, and the covariances between residuals of ADHD and anxiety at T2 through T4 were estimated. Next, the ADHD effects model was tested by adding paths to the baseline model from ADHD symptoms at one time point to anxiety at the next time point. The anxiety effects model was tested by adding paths to the baseline model from anxiety at one point to ADHD at the next time point. For each of these models, a constrained model in which cross-lagged paths were set to be equal across time was compared to one in which paths were free, using a χ2 difference test. In all models, errors were allowed to covary for non-adjacent time points within each type of symptom. Model fit was assessed using model χ2 (χ2 /df below 5.0 indicates acceptable fit though smaller is better; Hooper et al., 2008), the comparative fit index (CFI > .90 indicates good fit; Hu & Bentler, 1999), standardized root mean residuals (SRMR < .08 is acceptable fit; Hu & Bentler, 1999), and the root mean square error of approximation (RMSEA < .08 is acceptable fit; Hooper et al., 2008; Hu & Bentler, 1999). χ2 difference tests were used to compare nested models.

A mediational ADHD effects model was tested in separate models for parental warmth and overreactivity. Paths were added to the ADHD effects model from ADHD symptoms at each time point to the target parenting practice at the next time point, and from parenting practice to subsequent anxiety symptoms. Indirect effects were estimated between ADHD symptoms and later anxiety symptoms via parenting. Thus, parenting behavior at T2 was tested as a mediator for ADHD symptoms at T1 and anxiety symptoms at T3, and parenting behavior at T3 was tested as a mediator for ADHD symptoms at T2 and anxiety symptoms at T4.

Maternal education and child gender were tested as potential covariates by examining correlations with anxiety and ADHD symptoms. Higher maternal education was related to lower ADHD symptoms at each time point (ps from < .001 to .017). Maternal education was not related to anxiety symptoms (ps from .244 to .860). Cross-lagged analyses were repeated, controlling for maternal education and there were no major differences in terms of size or significance of effects; analyses are therefore reported without maternal education as a covariate. There were no significant gender differences on any target variable (ps from .223 to .941), so it was not included as a control. However, cross-lagged models were tested for gender invariance.

Results

Descriptive Results

See Table 1 for intercorrelations, means, and standard deviations of all variables. ADHD and anxiety scores at each time point appeared to be normally distributed and showed low skewness (ranged from .11 to .71) and kurtosis (ranged from −1.04 to .73). ADHD scores may have been less skewed than in the general population because children were oversampled for behavior problems. As expected, ADHD symptoms at each time point were strongly related to ADHD symptoms at all other time points and showed small- to medium-sized relations to anxiety symptoms at all time points. Anxiety symptoms at each time point were moderately to strongly related to anxiety symptoms at all other time points. The mean anxiety score at all time points fell in the average range, but there was substantial variability; 22% of children fell at or above the at-risk range (T = 60) at T1, 24% at T2, 21% at T3, and 7% at T4. A higher proportion of children showed elevated ADHD symptoms; 44% of children showed inattention or hyperactivity/impulsivity above the clinical cutoff of six symptoms at T1, 45% at T2, 41% at T3, and 29% at T4.

Table 1.

Intercorrelations, Means, and Standard Deviations

Variable 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17
1. ADHD T1 -
2. ADHD T2 .70*** -
3. ADHD T3 .59*** .79*** -
4. ADHD T4 .54*** .67*** .74*** -
5. Anxiety T1 .25*** .20** .20** .22** -
6. Anxiety T2 .23*** .27*** .23** .22** .63*** -
7. Anxiety T3 .25*** .31*** .32*** .26*** .48*** .56*** -
8. Anxiety T4 .23*** .17* .21** .20** .51*** .53*** .55*** -
9. Warmth T1 −.19** −.23** −.16* −.07 −.04 −.09 −.09 .06 -
10. Warmth T2 −.30*** −.30*** −.27*** −.18** −.15* −.12 −.17** −.10 .40** -
11. Warmth T3 −.13 −.11 −.05 −.03 −.03 −.12 −.06 −.04 .45** .23** -
12. Warmth T4 −.21** −.22** −.18 −.15* −.09 −.03 .07 .00 .36*** .22** .34*** -
13. Overreactivity T1 .20** .24*** .26*** .29*** .15* .15* .13 .11 .04 −.23** .04 .01 -
14. Overreactivity T2 .14* .21** .21** .28*** −.02 .03 .12 −.01 .02 −.10 .01 .08 .53*** -
15. Overreactivity T3 .20** .22** .31*** .30*** .09 .17* .19** .17* −.00 −.16* −.02 .02 .54*** .67*** -
16. Overreactivity T4 .19** .25*** .30*** .31*** .11 .13 .06 .08 −.10 −.20** −.07 −.08 .52*** .66*** .70*** -
17. Maternal Education (years) −.34*** −.32*** −.26*** −.16** .07 .02 .01 .03 .28*** .22** .23** .32*** .03 −.01 .02 −.10 -
M 8.21 7.98 7.33 5.44 50.45 50.01 50.16 46.68 4.39 4.32 4.45 4.26 2.69 2.70 2.59 2.67 13.46
SD 7.73 4.79 5.20 4.92 10.67 11.30 11.13 8.89 1.12 .95 .58 .54 .74 .76 .75 .78 2.75
N 257 237 192 217 255 238 212 216 230 220 174 185 242 232 210 216 257
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Note. ADHD = Attention Deficit/Hyperactivity Disorder: summed hyperactivity/impulsivity and inattention symptoms from the Diagnostic Interview for School Children; Anxiety = Behavior Assessment System for Children – Parent Rating Scale T scores. T1 = Time 1, T2 = Time 2, T3 = Time 3, T4 = Time 4

***

p < .001;

**

p < .01;

*

p < .05

Baseline Model

In the baseline model with autoregressive paths for each ADHD and anxiety variable, ADHD symptoms significantly predicted subsequent ADHD symptoms from T1 to T2, T2 to T3, and T3 to T4. Anxiety symptoms significantly predicted subsequent anxiety symptoms from T1 to T2, T2 to T3, and T3 to T4 (see Figure 1). The baseline model displayed adequate fit based on CFI (.99), RMSEA (.06), and χ2 /df (1.97), though SRMR was not adequate (.09). All subsequent models were built on this baseline model.

Figure 1.

Figure 1

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Baseline Model. Unstandardized coefficients are on top and standardized coefficients are on the bottom. Correlated errors were estimated for non-adjacent time points, but are not pictured for ease of presentation.

*p < .05, **p < .01, ***p < .001

Anxiety Effects Model: Does Anxiety Predict Later ADHD?

ADHD symptoms at T2, T3, and T4 were each regressed on anxiety symptoms from the previous time point. A model in which paths from anxiety to ADHD symptoms were constrained to be equal across time was not significantly different from a model in which these paths were free, Δχ2 (2) = .29, p = .865, suggesting the paths from anxiety to ADHD symptoms did not significantly differ across time. The simpler constrained model was thus chosen as the better model. In this model, anxiety symptoms were not a significant predictor of ADHD symptoms at each time point (see Figure 2). This model showed adequate CFI (.99), RMSEA (.07), and χ2 /df (2.12), but not adequate SRMR (.09). The anxiety effects model was not a significantly better fit than the baseline model, Δχ2 (1) = .28, p = .597. The anxiety effects model was also tested for gender invariance. A model in which all parameters were set to be equal for boys and girls was not a significantly worse fit compared to a model in which boys and girls were allowed to vary in their parameters, Δχ2(3) = 0.91, p = .823, suggesting that these paths across time are not different for boys and girls. Thus, the model was not separated by gender.

Figure 2.

Figure 2

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Anxiety Effects Model. Unstandardized coefficients are on top and standardized coefficients are on the bottom. Correlated errors were estimated for non-adjacent time points, but are not pictured for ease of presentation.

*p < .05, **p < .01, ***p < .001

ADHD Effects Model: Does ADHD Predict Later Anxiety?

Anxiety symptoms at T2, T3, and T4 were regressed on ADHD symptoms from the previous time point. A model in which paths from ADHD to anxiety were constrained to be equal across time was not significantly different from a model in which these paths were free, Δχ2 (2) = 3.20, p = .202, suggesting that the paths from ADHD symptoms to anxiety symptoms did not significantly differ across time. The simpler constrained model was thus chosen as the better model. In this model, greater ADHD symptoms predicted greater anxiety symptoms at the subsequent time point (see Figure 3). This model showed adequate CFI (.99), RMSEA (.04), SRMR (.05), and χ2 /df (1.51) and was a significantly better fit than the baseline model, Δχ2 (1) = 7.02, p = .008. The ADHD effects model was also tested for gender invariance. A model in which all parameters were set to be equal for boys and girls was not a significantly worse fit compared to a model in which boys and girls were allowed to vary in their parameters, Δχ2(3) = 1.94, p = .548, suggesting that these paths across time are not significantly different for boys and girls. Thus, the final ADHD effects model was not separated by gender.

Figure 3.

Figure 3

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ADHD Effects Model. Unstandardized coefficients are on top and standardized coefficients are on the bottom. Correlated errors were estimated for non-adjacent time points, but are not pictured for ease of presentation.

*p < .05, **p < .01, ***p < .001

Do Parenting Practices Mediate ADHD Effects?

Overreactivity at T2 did not mediate the relation between ADHD symptoms at T1 and anxiety symptoms at T3 (indirect path; b = .056, β = .002, SE = .004, p = .562), nor between ADHD symptoms at T2 and anxiety symptoms at T4 (indirect path; b = .006, β = .003, SE = .001, p = .489). Warmth at T2 did not mediate the relation between ADHD symptoms at T1 and anxiety symptoms at T3 (indirect path; b = .03, β = .02, SE = .02, p = .344), nor between ADHD symptoms at T2 and anxiety symptoms at T4 (indirect path; b =− .003, β = −.002, SE = .004, p = .670).

Disentangling Effects from Other Forms of Psychopathology

Because ODD is highly comorbid with ADHD, and depression is highly comorbid with anxiety (e.g., Bird et al., 1993), we also considered if ADHD effects could be accounted for by ODD or depression. We estimated two 3-way cross-lagged models, by adding BASC Depression subscales at each time point and DISC ODD symptoms at each time point to the ADHD effects model. In both models, ADHD symptoms showed trend-level significance in predicting later anxiety symptoms (ODD model: b = .16, SE = .08, p = .061; depression model: b = .14, SE = .08, p = .066). Note that the addition of highly correlated covariates often increases standard errors, which would account for some of the increase in the p-value; the magnitude of the ADHD effects was only slightly reduced suggesting that ODD and depression do not appear to account for ADHD effects.

Discussion

The present study sought to contribute to the small body of literature examining the development of comorbid ADHD and anxiety symptoms. Specifically, we examined the temporal relation between ADHD and anxiety symptoms for preschoolers across four time points. Results supported an ADHD effects model, suggesting that greater ADHD symptoms at an earlier time point predicted greater anxiety at subsequent time points, controlling for earlier anxiety. The anxiety model was not supported; anxiety at earlier time points did not predict subsequent ADHD.

ADHD Effects Model

The ADHD effects model was best supported in explaining the temporal relation between ADHD and anxiety symptoms. ADHD at an earlier time point predicted subsequent anxiety in preschool children across 4 time points, and these effects appeared to be distinct from effects of co-occurring ODD and depression symptoms. The model was not significantly different across gender, suggesting that ADHD effects on anxiety impact boys and girls similarly. These results are in line with existing literature that has found more robust evidence of externalizing behaviors contributing to exacerbation of internalizing symptoms in early childhood than vice versa in both community- and clinic-based samples (see Bubier & Drabick, 2009 for review). They are also consistent with Burke et al. (2005) who found that ADHD predicted later anxiety in older children. However, this is the first study to longitudinally demonstrate that ADHD symptoms predict later anxiety symptoms in early childhood.

This finding is in contrast to some previous research that has not found ADHD symptoms to predict later anxiety symptoms. However, these studies either used community samples (Baldwin & Dadds, 2008; Costello et al., 2003) or different age ranges (Bagwell et al., 2006; Overgaard et al., 2014). The present study’s findings may differ from these prior studies because the impact of ADHD symptoms on subsequent anxiety symptoms may be dependent on severity of ADHD symptoms as well as stage of development. The present study used a sample with elevated ADHD symptoms; ADHD symptoms may lead to the development of anxiety symptoms when ADHD symptoms are high, but not in subclinical samples. Additionally, the preschool years may be a particularly important period for the co-development of ADHD and anxiety symptoms; we found ADHD effects on anxiety from the preschool to early school-age years that have not been evident in studies of effects from middle childhood to adolescence (Bagwell et al., 2006) or from the toddler to preschool years (Overgaard et al., 2014).

Several mechanisms may underlie ADHD predicting later anxiety symptoms. For example, disruptive behaviors of children with ADHD may elicit more negative reactions from their environments, which may exacerbate feelings of worry and rumination over time (Dodge et al., 1997; Little & Garber, 1995). We did not find support for parenting practices as one of these negative environmental reactions that mediates this relation. This is the first study to test parenting as a mediator of the relation between ADHD and anxiety symptoms, and this lack of support is both theoretically and clinically important. Parenting does mediate the relation between ADHD and other comorbidities (e.g., depression, ODD; Breaux et al., 2017; Ostrander & Herman, 2006), and our results suggest that the development of comorbid anxiety symptoms develop differently from other comorbidities. However, there is evidence that specific subdomains of parenting practices, such as autonomy-granting, have stronger effects on anxiety than other aspects of parenting, such as warmth (McLeod et al., 2007). Our analyses focused on warmth and overreactivity, and it is possible that other dimensions of parenting do mediate the relation between ADHD and anxiety symptoms. Alternatively, other forms of negative environmental reactions, such as from peers or teachers, may have a greater effect on the development of anxiety symptoms than parenting.

Another proposed mechanism posits that the executive function deficits underlying ADHD symptoms (e.g., reduced cognitive inhibition) may reduce children’s ability to cope with anxiety, contributing to the exacerbation of internalizing symptoms over time (Barkley, 2015; Nigg et al., 2004). It is also possible that what are perceived as early ADHD symptoms are in fact expressions of anxiety that children are too young to express (e.g., in some children, restlessness may be a manifestation of anxiety, rather than a symptom of ADHD); thus, what appear to be ADHD effects may in fact be effects of anxiety mimicking ADHD symptoms. It is important for future research to elucidate these possible mechanisms that may explain this temporal relation between ADHD and anxiety symptoms in young children.

Anxiety Effects Model

The anxiety effects model posited that anxiety symptoms exacerbate ADHD symptoms. This model was not supported by this study; anxiety did not significantly predict subsequent ADHD at any time point, suggesting that anxiety symptoms, such as worry, may not increase ADHD symptoms such as restlessness and distractibility. Findings are consistent with some previous literature that has not found a significant relation between anxiety symptoms and subsequent ADHD symptoms (Baldwin & Dadds, 2008; Burke et al., 2005; Costello et al., 2003; Overgaard et al., 2014) and are consistent with a recent review of internalizing and externalizing symptom development that found more robust evidence of externalizing symptoms predicting later internalizing symptoms than vice versa in early childhood (Bubier & Drabick, 2009). However, this lack of support for the anxiety effects model is in contrast to some previous literature, which has found that anxious symptoms predict later ADHD symptoms (Bittner et al., 2007; Speltz et al., 1999). Notably, these studies used samples with different clinical characteristics and age ranges. Speltz et al. (1999) used a sample of preschoolers with oppositional defiant disorder (ODD), and it may be that the relation between ADHD and anxiety symptoms is different for children with ODD. Bittner et al. (2007) found that childhood social phobia was associated with ADHD in adolescence. However, because they did not control for early ADHD symptoms, it is possible that this relation was due to childhood comorbidity. Further research is needed to examine whether anxiety effects may vary as a function of age or clinical characteristics.

Limitations

These results should be interpreted in the context of several limitations. First, parent report was used to measure both anxiety and ADHD, so relations could have been inflated by shared method variance. However, because we controlled for earlier symptoms in our models and because we used two different assessment strategies (interview and questionnaire), the impact of shared method variance on lagged paths should have been minimal. Second, participants were over-sampled for externalizing behaviors. Although participants displayed a range of anxiety symptoms, it is possible that relations would be different in a sample specifically recruited for elevated internalizing behaviors. Third, this study assessed anxiety symptoms broadly, and not specific anxiety disorders. It is possible that the bidirectional relation of anxiety and ADHD symptoms varies based on different presentations of anxiety. Finally, although this study design was longitudinal, care should be used in drawing causal conclusions, as third variables could have influenced our findings.

Implications and Future Directions

This study has important theoretical implications, as it offers insight into the early development of ADHD and anxiety symptoms, filling a gap by empirically testing models that might explain comorbidity of these disorders. Findings suggest that, in a clinically at-risk sample during the preschool years, ADHD symptoms predict the subsequent development of anxiety symptoms, but not vice-versa. Results indicate that, in the preschool years, the relation may be unidirectional. Future research studies should explore shared risk factors that contribute to the development of ADHD/anxiety comorbidity, as ADHD and anxiety symptoms were correlated beginning from the first time point, when children were 3 years old. Such factors may include shared genetic risk or shared environmental factors (Bubier & Drabick, 2009), which may contribute to the development of each disorder and account for their comorbidity.

The findings of this study have important implications for clinical interventions. Because results suggested a unidirectional effect of ADHD symptoms on anxiety symptoms, clinicians working with preschoolers with ADHD should be aware that these early ADHD symptoms may increase risk for future anxiety symptoms and conduct periodic assessments of children’s anxiety. Preschool-age ADHD interventions designed to reduce ADHD symptomatology, such as parent training interventions (see Mulqueen et al., 2015 for review), might help mitigate future risk of developing anxiety symptoms. Some preschool-age ADHD interventions include an emphasis on teaching parents about supportive emotion socialization techniques, as well as teaching children emotion regulation skills (Herbert et al., 2013; Webster-Stratton et al., 2011). It is possible that these emotion-focused aspects of the interventions could reduce later anxiety symptoms. It is also possible that preschool interventions for ADHD symptoms, which often involve increasing desired behaviors and decreasing undesired behaviors, help reduce the amount of negative feedback children with ADHD symptoms receive from their environment. In order to bolster such effects, further research is needed to elucidate the mechanisms underlying ADHD effects, such as emotion dysregulation and peer influences, as our findings did not find support for maternal warmth or overreactivity as mechanisms. Identifying such mechanisms may help us develop more targeted ADHD interventions to specifically reduce the development of co-occurring anxiety symptoms.

Funding

This work was supported by a grant from NIMH to the 5th author (MH60132).

Footnotes

Publisher's Disclaimer: This Author Accepted Manuscript is a PDF file of an unedited peer-reviewed manuscript that has been accepted for publication but has not been copyedited or corrected. The official version of record that is published in the journal is kept up to date and so may therefore differ from this version.

Availability of data and material

The data that support the findings of this study are available from the corresponding author, EH, upon reasonable request.

Code availability: Not applicable.

Conflicts of interest

The authors declare that they have no conflict of interest or competing interests.

1

We did not test parenting as a mediator of anxiety effects because theoretical explanations of anxiety effects do not point to parenting as a likely mechanism.

2

Note that DSM-IV ADHD symptoms are identical to DSM-5 ADHD symptoms, except that additional examples are provided in DSM-5 to aid clinicians in identifying symptoms.

3

Both the DISC and BASC can be used to measure ADHD and anxiety symptoms. However, although diagnostic interviews are considered a gold standard for assessing ADHD, they do not readily yield a symptom count for anxiety symptoms. Therefore, two different assessment methods were chosen; this methodology has the added advantage of reducing the effects of shared method variance.

4

There was too little variation in harsh/overreactive parenting during the observational task, so self-report of overreactivity was used. There was not a self-report measure of warmth available at all time points.

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