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Dev Psychopathol. Author manuscript; available in PMC 2020 November 11.
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Published in final edited form as:

Dev Psychopathol. 2020 October ; 32(4): 1287–1302. doi:10.1017/S0954579420000826.

Trajectories of co-occurring psychopathology symptoms in

autism from late childhood to adulthood
James B. McCauley, Rebecca Elias, Catherine Lord
Department of Psychiatry, University of California, Los Angeles, CA, USA

Abstract
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Given high rates of co-occurring conditions in youth and adults with autism spectrum disorder
(ASD), it is critical to examine the developmental trajectories of these symptoms of
psychopathology. Using data from a cohort of participants (n = 194), most of whom were first
assessed for ASD in very early childhood, we investigated the trajectories of co-occurring
depressive, anxiety, and attention-deficit hyperactivity disorder (ADHD) symptoms from late
childhood to adulthood. Additionally, childhood predictors and adult outcomes associated with
these symptom trajectories were examined. Using group-based trajectory modeling, we found two
distinct classes of individuals exhibiting each of these co-occurring symptom patterns: one class
exhibited fairly low symptoms across time, and one class with elevated symptoms with varied
fluctuation across time (ADHD symptoms starting high but decreasing, anxiety symptoms high
and stable, and depressive symptoms fluctuating but peaking at clinically significant levels in
young adulthood). All high trajectory classes were associated with age 9 adaptive skills; verbal IQ
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predicted higher anxiety and depressive symptom classes. After accounting for verbal IQ, all high
symptom trajectory classes were negative predictors of objective adult outcomes. These findings
call for wide-ranging considerations of the needs of individuals across ability levels, autism
symptoms, and behavioral and emotional challenges.

Keywords
autism; co-occurring symptoms; development; longitudinal data; outcomes; trajectories

Individuals with autism spectrum disorder (ASD) are at higher risk for developing co-
occurring mental health conditions compared to the general population. Although estimates
vary due to methodological differences, approximately 70% of children with ASD meet
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criteria for at least one co-occurring psychiatric condition (Leyfer et al., 2006; Simonoff et
al., 2008). Children, adolescents, and adults with ASD are at particularly high risk for co-
occurring clinical presentation of attention-deficit hyperactivity disorder (ADHD), anxiety,
and depression (Kim, Szatmari, Bryson, Streiner, & Wilson, 2000; Leyfer et al., 2006; Levy
et al., 2010; Simonoff et al., 2008; Strang et al., 2012). However, little is known about the
developmental trajectories of clinical symptom onset from late childhood into adulthood,

Author for Correspondence: Catherine Lord, George Tarjan Distinguished Professor of Psychiatry, David Geffen School of
Medicine, University of California, Los Angeles Jane & Terry Semel Institute for Neuroscience & Human Behavior, 760 Westwood
Plaza 68-265, Los Angeles, CA 90024, USA; clord@[Link].
 McCauley et al. Page 2

and early childhood factors have not been thoroughly examined to help identify individuals
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most at risk for developing psychopathology.

Co-occurring Psychopathology in ASD

Co-occurrence of psychiatric symptomatology is common throughout the lifespan of
individuals with ASD (Croen et al., 2015; Gordon-Lipkin, Marvin, Law, & Lipkin, 2018; Lai
et al., 2019; Matson & Goldin, 2013; Salazar et al., 2015; Simonoff et al., 2008; Stringer et
al., 2020). This is particularly salient because the presence of co-occurring psychiatric
disorders in ASD contributes to a variety of outcomes including poorer quality of life
(Sikora, Vora, Coury, & Rosenberg, 2012; Vannucchi et al., 2014), greater social impairment
(Chang, Quan, & Wood, 2012), and greater perceived distress (Ozsivadjian, Knott, &
Magiati, 2012). Despite documented prevalence in ASD and its impact on individual
functioning, little is known about the developmental trajectories of co-occurring conditions,
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including how co-occurring psychopathology presents across the lifespan in this population.
Further, capturing ‘pure’ co-occurring disorders among those with ASD is a difficult task;
differing measurement approaches, diagnostic overshadowing, and heterogeneity in clinical
presentation are pervasive (Gotham, Unruh, & Lord, 2015b; Hollocks, Lerh, Magiati,
Meiser-Stedman, & Brugha, 2019; Kerns et al., 2015; Rodriguez-Seijas et al., 2019; White
et al., 2015).

Anxiety disorders, mood disorders, obsessive-compulsive disorder (OCD), ADHD, and

oppositional defiant disorder (ODD) represent co-occurring psychopathologies most
commonly associated with a diagnosis of ASD (see Rosen, Mazefsky, Vasa, & Lerner, 2018
for a comprehensive review). Studies vary widely with regards to methodology employed,
including different assessment tools, age ranges captured, and cognitive abilities of the
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sample. Although these co-occurring psychiatric disorders align with fifth edition of
Diagnostic and Statistical Manual of Mental Disorders (DSM-5) guidelines for clinical
diagnosis (Lecavalier et al., 2011), subtle differences in the cognitive and behavioral
symptomatic presentations are apparent in those with ASD relative to that of neurotypical
peers with similar psychiatric conditions (Rosen et al., 2018). Individual factors such as age,
sex, and cognitive abilities have been hypothesized to impact the differing psychiatric
profiles of individuals with ASD. However, reports examining these characteristics are
somewhat inconsistent in the literature (e.g., de Bruin, Ferdinand, Meester, de Nijs, &
Verheij, 2007; Gadow, Devincent, Pomeroy, & Azizian, 2005; Kreiser & White, 2015;
Mazza, Rossetti, Crespi, & Clerici, 2019; Salazar et al., 2015). Greater examination of large
longitudinal studies of individuals with ASD has been proposed as an avenue for
determining factors associated with those with co-occurring psychiatric disorders across
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time. One prospective study from the Special Needs and Autism Project (SNAP; Stringer et
al., 2020) found high rates of psychiatric symptoms in a population-based sample of
individuals with ASD examined from age 12years to 23 years. Symptoms as measured by
the Strengths and Difficulties Questionnaire (SDQ; Goodman, Ford, Simmons, & Meltzer,
2000) showed a declining pattern from childhood to early adulthood. Higher adaptive
functioning early on was predictive of a faster decrease in conduct and ADHD symptoms
(Stringer et al., 2020). Similarly, Woodman and colleagues (2016) examined trajectories of
co-occurring psychopathology among individuals with ASD on the internalizing and

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externalizing scales from the Child Behavior Checklist (CBCL), and found declines in
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symptoms from late adolescence into adulthood. The high prevalence of multiple co-
occurring psychiatric disorders, and their relation to poor social-vocational outcomes,
highlights the need to characterize psychopathology across the lifespan of individuals with
ASD. Further, more information about the literature examining the symptom trajectories in
psychiatric symptom presentation in individuals with ASD across the lifespan is critically
needed to understand predictors, outcomes, and potential factors which may mitigate later
risks.

ADHD is a neurodevelopmental disorder which represents impairments in attention and/or

hyperactivity in a variety of contexts, beginning early in childhood (American Psychiatric
Association, 2013). In typically developing individuals, core symptoms decrease from
childhood into early adulthood (Spencer, Biederman, & Mick, 2007), and the rate of
trajectory changes varies as a factor of type of symptoms (i.e., hyperactivity vs. impulsivity;
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Spencer et al., 2007). The co-occurrence of ASD and ADHD has been demonstrated in
multiple studies (Lecavalier et al., 2019; Leitner, 2014; Rommelse, Franke, Geurts, Hartman,
& Buitelaar, 2010; Simonoff et al., 2008; Taurines et al., 2012). Reported prevalence rates of
diagnostic co-occurrence are somewhat variable, in part because only recently the DSM-5
criteria for concurrent diagnosis of the disorders were allowed (American Psychiatric
Association, 2013). Recent prevalence estimates of concurrent ASD and ADHD are veiy
high (i.e., 81% in a large treatment-seeking sample; Lecavalier et al., 2019). Further, the
clinical impact of co-occurring ASD and ADHD appeal’s significant (Gadow, DeVincent, &
Pomeroy, 2006; Zablotsky, Bramlett, & Blumberg, 2020). Individuals with ASD and co-
occurring ADHD are at greater risk for concomitant anxiety and mood disorders (Gordon-
Lipkin, Marvin, Law, & Lipkin, 2018; Lecavalier et al., 2019).
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The prevalence of anxiety in individuals with ASD is similarly high (White, Oswald,
Ollendick, & Scahill, 2009). Anxiety disorders represent a constellation of fears which are
disproportionate to the threat (see Craske & Stein, 2016). In typically developing youth, the
presence of an anxiety disorder is fairly stable across time. Those who are diagnosed with an
anxiety disorder in childhood are at higher risk for retaining anxiety across the lifespan
(Rapee, Schniering, & Hudson, 2009). For children and adolescents with ASD, prevalence
rates for presence of any anxiety disorder diagnosis hovers around 40% (van Steensel,
Bögels, & Perrin, 2011), making anxiety one of the most common co-occurring psychiatric
conditions. These prevalence estimates remain remarkably similar in adulthood (Hollocks et
al., 2019). However, symptom manifestations of the core features of ASD and anxiety are
shared in a number of contexts (Wood & Gadow, 2010) and the extent to which anxiety is
different in its presentation in people with ASD is not yet fully established (Kerns &
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Kendall, 2012; Kerns et al., 2015; Ollendick & White, 2012; White et al., 2015).

Depression is also common and clinically impairing in individuals with ASD (Kim et al.,
2000; Levy et al., 2010; Leyfer et al., 2006; Strang et al., 2012). Prevalence rates of
comorbid depression diagnoses and ASD range from approximately 1.4–38% (Hollocks et
al., 2019; Lainhart, 1999; Magnuson & Constantino, 2011) making clinical depression one
of the most common comorbidities in ASD, along with anxiety and ADHD (Gadow,
Guttmann-Steinmetz, Rieffe, & DeVincent, 2012; Strang et al., 2012). Prevalence of

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depression in ASD is thought to be higher for those individuals with greater cognitive
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capacity (Magnuson & Constantino, 2011; Mayes, Calhoun, Murray, Ahuja, & Smith, 2011;
Strang et al., 2012) and to follow the same developmental trajectory seen in typically
developing peers. Specifically, the rates of depression in individuals with ASD appear to
increase with age between childhood and adolescence (Kessler et al., 2010; Mayes et al.,
2011; Stewart, Barnard, Pearson, Hasan, & O’Brien, 2006; Thapar, Collishaw, Pine, &
Thapar, 2012). In previous analyses, increases in depressive symptoms across adolescence
appeared to be more prominent in females with ASD compared to males (Gotham,
Brunwasser, & Lord, 2015a). Further, verbal cognitive abilities were not found to be
predictor of depressive symptoms as measured by the CBCL/ Adult Behavior Checklist
(ABCL) measures. Still, higher depressive symptoms contribute to distinguishing poorer
outcomes in adults with ASD and higher IQs (McCauley, Pickles, Huerta, & Lord, in press).
For more cognitively able adolescents and adults, the most commonly endorsed items on
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depression measures reflected cognitive and emotional concerns, including feelings of guilt,
worthlessness, failure, pessimism, and sadness (Gotham et al., 2015b).

Developmental and Theoretical Considerations

ASD is a neurodevelopmental condition in which challenges with social communication and
restrictive and repetitive behaviors manifest early in development, but may not be apparent
until the social demands exceed capabilities (American Psychiatric Association, 2013). ASD
is a diagnosis that includes individuals with wide-ranging strengths, challenges, and
behavioral profiles. Around 30% of children with ASD in the United States have co-
occurring intellectual disability (Baio et al., 2018), and many, including individuals with
higher IQs, experience challenges in adaptive skills relative to same-aged peers (Alvares et
al., 2020). There are unique challenges, particularly with establishing peer relationships and
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developing adaptive skills, that individuals with ASD experience across development that
likely interact with the development of mental health concerns.

In early childhood, clinical concerns revolve around communication, social and adaptive
capabilities, and maladaptive behaviors associated with ASD, such as aggression, self-
injurious behavior, and hyperactivity (Zwaigenbaum et al., 2015). In preschool and later
school years, children with ASD often experience difficulties with forming relationships
with peers, exacerbated by co-occurring hyperactivity or problems with emotion regulation
(Bauminger & Kasari, 2000; Rotheram-Fuller, Kasari, Chamberlain & Locke, 2010).
Adolescence may be an especially vulnerable period for individuals with ASD, given the
influence of hormonal changes and increased social demands (Picci & Scherf, 2015). Early
challenges experienced by younger children become more pronounced as the social
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environment increases in complexity and as children are expected to have more autonomy
(Steinberg, 2008). Many adults with ASD live at home after high school, are not employed
or in education, and face challenges establishing friendships (Howlin, Mawhood, & Rutter,
2000; Orsmond, Shattuck, Cooper, Sterzing, & Anderson, 2013; Pickles, McCauley, Pepa,
Huerta, & Lord, 2020; Roux, Shattuck, Rast, & Anderson, 2017). As such, these
accumulating social and adaptive difficulties may likely contribute to the unique risks of
developing co-occurring psychopathology in ASD.

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Conceptually, there are similarities between symptoms of autism and symptoms of co-
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occurring psychopathology. Specifically, there is some overlap between dimensions of

hyperactivity/impulsivity and repetitive and restrictive behaviors (RRBs) in children with
ADHD (Martin, Hamshere, O’Donovan, Rutter, & Thapar, 2013) and there is evidence that
children with ADHD lack social awareness (Clark, Feehan, Tinline, & Vostanis, 1999). The
behavioral manifestations of both anxiety disorders and autism have overlapping features,
for example intense insistence on sameness or fear and avoidance to change (Wood &
Gadow, 2010). However, because anxiety is not always present, features of anxiety in people
with ASD are not simply a manifestation of the core symptomology of ASD (Kerns &
Kendall, 2012; Renno & Wood, 2013; White et al., 2015). Finally, depressive symptoms
include social isolation and withdrawal, which can be hard to distinguish from autism
symptoms (e.g., Biederman et al., 2011). The conceptual overlap between symptoms of
distinct forms of psychopathology and autism are likely to have reciprocal influences across
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development, yet there exists limited current information about how autism severity
influences the risks for different symptoms of co-occurring psychopathology.

Current Aims
The aims of the current study are to: (a) describe the trajectories of co-occurring symptoms
of three forms of psychopathology (ADHD, anxiety, and depression) in individuals referred
for an ASD assessment at an early age, (b) identify early childhood predictors of clinical
symptom trajectories, and (c) examine how symptom trajectories predict adult outcomes.

Using a longitudinal sample of individuals, most of whom who were diagnosed with ASD in
early childhood, we describe these trajectories from late childhood (age 9 years) to
adulthood (age 25 years). For each symptom, we hypothesize there will be one or more
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classes of individuals that exhibit clinically significant levels of psychopathology symptoms

across time, based on the prevalence estimates of co-occurring ADHD, anxiety, and
depression (although these estimates are variable). We then consider how cognitive and
adaptive skills and autism symptoms at ages 2 years, 5 years, and 9 years predict
membership in co-occurring trajectory classes, and we analyze symptom trajectories as
predictors of global adult outcomes at age 25 years. For ADHD symptom trajectories, we
hypothesize that symptom levels will abate over time similar to typically developing
children (Spencer et al., 2007), and that high symptoms will be associated with childhood
levels of adaptive behavior (e.g., Stringer et al., 2020). For anxiety symptoms, we expect
symptoms to be stable in accordance with typical development trajectories (e.g., Rapee et
al., 2009) and prevalence studies in ASD (e.g., Hollocks et al., 2019). For depressive
symptoms, we hypothesize increases across adolescence in accordance with other studies on
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individuals with ASD (e.g., Thapar et al., 2012). We expect negative associations between
verbal intellectual abilities and high levels of anxiety and depressive symptoms (e.g.,
Gotham et al., 2015a; White et al., 2009). Finally, we hypothesize that higher levels of
psychopathology symptoms will have a negative effect on the levels of outcomes adults
achieved. Altogether, we strive to increase the understanding of the development of these co-
occurring conditions and their associations with autism severity, cognitive ability, and
adaptive functioning across the lifespan.

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Method
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Participants
The current study draws from 253 individuals participating in a longitudinal study (Lord,
McCauley, Pepa, Huerta, & Pickles, 2020) recruited from three sites: 213 children under age
3 years (192 were referred for possible autism to two tertiary autism programs and 21
children of the same age with non-ASD developmental delays) from North Carolina and
Chicago, and 40 children from Michigan referred for possible autism at early ages who
joined the study at approximately age 13 and were followed for at the same intervals as the
initial recruits. Families from North Carolina and Chicago were seen for face-to-face
assessments at the following time points: age 2, 3 (ASD referrals only), 5 (North Carolina
only), 9, 19, and 25/26, with some young adults seen for an additional assessment at age 21
years. Families from Michigan were seen in early adolescence, and then at ages 19 and 26
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years at the same intervals as the initial families. In addition to face-to-face assessments,
telephone interviews and packets of questionnaires were sent to families in regular intervals
starting in early adolescence (ages 12–25 years). Of the 253 participants recruited across
sites, attrition occurred due to geographical relocation, unreachable status, and refusal. The
current analyses consist of 194 (79% male, 21% female) participants who had data from at
least one assessment after early childhood.

In the current sample, 76% of the participants were White, 21% were African American,
with the remaining 3% from other racial backgrounds (Asian, Native American/Alaska
Native, Biracial). 52% of primary caregivers had a college degree or more advanced degree.
Of the current sample, 22% (n = 42) have never had a diagnosis of ASD after repeated
assessments by our team. We refer to them collectively as Never ASD, as opposed to Ever
ASD (e.g., individuals who received an ASD diagnosis at some point throughout the course
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of the study). The Never ASD group shares many similarities in functioning across
development and in adult outcomes with the Ever ASD group (Lord et al., 2020). Of the
individuals with a diagnosis of ASD, most of these individuals received a diagnosis in early
childhood that has been upheld in later assessments, but approximately 10% of the sample
were judged by a blinded clinician as no longer meeting clinical criteria for an autism
diagnosis in adulthood.

At their most recent adult assessments, the clinical characteristics of the current sample were
varied but at mean levels that typified broad impairments, including on the Adaptive
Behavior Composite on the Vineland-II (VABS-II; M = 54.47, SD = 28.04), the Autism
Diagnostic Observation Schedule-2 (ADOS-2; Calibrated Severity Score [CSS]: M = 5.63,
SD = 2.63, Social Affect [CSS SA]: M = 5.83, SD = 2.54, Restricted and Repetitive
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Behaviors [CSS RRB]: M = 6.00, SD = 2.92), and the Autism Diagnostic Interview-Revised
(ADI-R; Social Interaction Domain: M = 15.86, SD = 9.93, Communication Domain: M =
11.95, SD = 7.61, Restricted Repetitive Behavior Domain: M = 4.72, SD = 3.10).

Procedure
Data collection consisted of in-person assessments administered by a trained clinician,
standardized questionnaires, and phone interviews of caregivers and participants. When

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possible, participants reported on themselves and teachers, up through high school, were
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asked to report on participants in addition to information gathered from caregivers.

Personnel administering the test batteries were blind to information from previous
assessments, including diagnosis. The research was approved by the Institutional Review
Boards at the University of North Carolina, Chapel Hill, University of Chicago, University
of Michigan, Cornell University, and University of California, Los Angeles.

Diagnostic measures
The ADOS-2 (Bal et al., 2019; Lord, Rutter, DiLavore, Risi, Gotham, & Bishop, 2012) was
administered by an advanced graduate student, post-doctoral fellow, or clinical psychologist
trained to research-reliability at each in-person assessment (ages 2, 5, 9, 18, 21, and 25
years). In addition, the ADI-R (Lord, Rutter, & Le Couteur, 1994), a standard investigator-
based interview, was administered to caregivers at ages 2, 3, 5, 9, and 18 years. A best
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estimate autism diagnosis at each age was determined by the study team by reviewing
assessments and videos. Autism severity is calculated across modules using the CSS.

Cognitive and adaptive skills measures

During each in-person assessment, verbal and non-verbal IQs (VIQ, NVIQ respectively)
were determined from a hierarchy of cognitive tests. Choice of cognitive assessment was
primarily determined by expressive language abilities and age (most to least difficult to
complete: Wechsler Abbreviated Scale of Intelligence (Wechsler, 1999), Differential Ability
Scales (Elliott, 2007), Mullen Scales of Early Learning (Mullen, 1995). Children were
initially administered the test that most reflected their verbal abilities, but were given a more
or less difficult assessment when basal or ceiling scores were not achieved (see also,
Anderson et al., 2014). When standard scores were unable to be calculated (e.g., the score
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was outside the normed range or basal/ceiling limits), ratio IQs were calculated by dividing
the age equivalent score by the age of the participant and multiplying by 100 (Lord et al.,
2006). A best estimate of IQ was generated for each participant at each age that reflected the
best quality and most age appropriate test the team could administer. Adaptive skills were
assessed using the VABS-II (survey edition) at in-person visits in early childhood and in
adulthood (Sparrow, Cicchetti, & Balia, 2005).

Trajectory measures
The primary measures used to calculate trajectories of co-occurring psychopathology were
the CBCL (Achenbach & Rescorla, 2001) and the ABCL (Achenbach & Rescorla, 2003)
once participants were 18 years old (collectively referred to as the “ASEBA” scales). These
were selected for initial analysis because of their common use and standardization across the
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age range, despite some limitations with their use in samples of youth with ASD (e.g.,
Greenlee, Shui, Veenstra-VanderWeele, & Gotham, 2016). Parents reported on comorbid
symptoms of psychopathology via the ASEBA at five time points: T1: Late Childhood (M =
9.36 years, range 5.67–11.83), T2: Early Adolescence (M = 14.93 years, range 13.42–
15.92), T3: Late Adolescence (M = 17.40 years, range 16.00–18.67), T4: Early Adulthood
(M = 20.25 years, range 19.00–22.75), T5: Adulthood (M = 25.73 years, range 23.17–
30.08).

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To model ADHD symptoms, we used the Attention Problems T score of the ASEBA
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measures. This scale comprises items that measure concentration, impulsivity, hyperactivity,
and inattention. To model anxiety symptoms, we used the Anxious/Depressed T score. This
scale comprises items assessing fears, nervousness, worries, guilt, and feelings of
worthlessness. To model depressive symptoms, we used the Withdrawn/Depressed T score.
This scale measures depressive symptoms with items such as withdrawal from activities,
shyness, sadness, social isolation, and low energy. Previous analyses have found this
subscale to be congruent with a depression diagnosis when a clinical interview was also used
(Pandolfi, Magyar, & Norris, 2014). In samples of individuals with ASD, alpha reliability
estimates for these scales are high (Attention Problems: 0.83; Anxious/Depressed: 0.94;
Withdrawn/Depressed: 0.85; Pandolfi, Magyar, & Dill, 2012). In the normed sample,
correlations between these scales are high for the school-aged forms (Anxious/Depressed
and Withdrawn/Depressed: 0.52; Anxious/Depressed and Attention Problems: 0.39,
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Withdrawn/Depressed and Attention Problems: 0.40; Achenbach & Rescorla, 2001) and the
adult forms (Anxious/Depressed and Withdrawn, 0.54; Anxious/Depressed and Attention
Problems, 0.60; Withdrawn and Attention Problems, 0.42; Achenbach & Rescorla, 2003).

Additional psychopathology measures collected

Additional measures of psychopathology symptoms were collected at some of the same time
points as the ASEBA, including the Aberrant Behavior Checklist-Community (ABC; Aman,
Singh, Stewart, & Field, 1985), the Beck Depression Inventory (second edition) (BDI-II;
Beck, Steer, & Brown, 1996), the Adult Manifest Anxiety Scale (AMAS; Reynolds,
Richmond, & Lowe, 2003), and the Anxiety Depression and Mood Screen (ADAMS;
Esbensen, Rojahn, Aman, & Ruedrich, 2003). We elected not to generate composite/
summary or latent factor scores, given our focus on trajectories and the complexity of
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dealing with different measurements at developmental points and questions about

discrepancies between raters (which also likely changes with development). As a first step,
we wanted to begin with data that are relatively easily interpreted and allow simple
comparisons across measures over time including childhood and early adolescence.
However, in due course, latent classes (e.g., Pickles et al., 2020) are another important
approach that eventually will yield additional information about our sample in adulthood.

The ABC was administered to parents at the same time points as the CBCL/ABCL, and to
teachers at the same time points up to T3 (age 17 years). The ABC is a questionnaire that
contains five subscales: irritability, withdrawal, stereotypy, hyperactivity and inappropriate
speech. Internal consistency alpha coefficients among each subscale range from .86 to .94
(Aman et al., 1985). Further, the measure has been widely applied to autistic populations
(e.g., Kaat, Lecavalier, & Aman, 2014). The current study uses the withdrawal subscale to
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compare means across time by depressive symptom trajectory class, and the hyperactivity
subscale to compare means across time by ADHD symptom trajectory class.

The BDI-II was administered to participants and parents as informant reports starting in
adolescence (T3 to T5). The BDI-II is a 21-item measure that assesses depressive symptoms
in adolescents and adults. The BDI-II has adequate alpha reliability properties among
individuals with a diagnosis of ASD (α = 0.87; Gotham, Unruh, & Lord, 2015b). Although

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normed as a self-report measure, the present study adapted the measure to achieve
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concurrent caregiver ratings of their son or daughter. Higher scores on the BDI-II reflect
greater depressive symptom endorsement. The current study uses the self and parent report
total scores from the BDI-II to compare means across time by depressive symptom
trajectory class.

The AMAS was administered to participants and parents as informant reports stalling in
adolescence into adulthood (T3 to T5). The AMAS measures symptoms of anxiety in adults
and has adequate internal consistency (α = .90). On the AMAS, higher scores reflect greater
symptomology. The current study uses the total score derived from the AMAS to compare
means across time by anxiety trajectory class.

The ADAMS was administered to parents of participants who could not report for
themselves in late adolescence (T3 and T4). The ADAMS is a 28-item questionnaire
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addressing an individual’s behavior over a six-month period. This measure was designed to
assess affective behaviors in individuals with intellectual disabilities. The informant is asked
to provide information for items covering the following five subscales: manic/hyperactive
behavior, depressed mood, social avoidance, general anxiety, and obsessive/compulsive
behavior. Psychometric properties of the scale are adequate (test–retest reliability = .80, α
= .80; Esbensen et al., 2003). Although only a subset of the current participants was assessed
using the ADAMS (T3 n = 45; T4 n = 60), the current study uses the depressed mood
subscale and the general anxiety subscales to compare means across time by trajectory class,
for less verbally fluent participants.

Adult outcomes measures

Adult outcomes were calculated separately for more (Adult VIQ ≥ 70) and less cognitively
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able (Adult VIQ < 70) adults using a method described in (McCauley et al., in press).
Information about adult outcomes was collected through caregiver and participant interviews
using the Social and Emotional Functioning Interview—Revised (SEFI-R; Rutter et al.,
1988). For more cognitively able adults, positive outcomes were defined as living
independently, having employment, and having at least one true friend (someone whom
participants see frequently and relies on for emotional support). A count variable was
created to describe how many outcomes each individual met. For less cognitively able
adults, positive outcomes were defined as having at least one peer or regular nonfamilial,
nonpaid acquaintance whom they enjoy seeing regularly, daily living skills above an 8-year-
old level, and regular activities to do outside the house (e.g., work, volunteering). A count
variable was created to describe how many outcomes each less cognitively able individual
met. Adult outcome data were available for 123 adults within the current study.
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Data analysis plan

Missing data—Attrition was statistically associated with having lower parent education (p
< .002) and being non-white (p < .001), but not significantly associated with gender, IQ, or
ASD diagnosis when first recruited. Sample size and missing data patterns across the five
time points of ASEBA collection were variable, T1: n = 115; T2: n = 73; T3: n = 119; T4; n
= 71; T5: n = 95. Most participants (n = 124, 66%) received two or more measurements

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across the five time points (Completed 1 assessment: n = 66, 34%; Completed 2
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assessments: n = 40, 21%; Completed 3 assessments: n = 34, 18%; Completed 4

assessments: n = 45 (23%); Completed 5 assessments: n = 9, 5%).

Aim 1—Estimating trajectories of comorbid psychopathology in ASD—Group

based trajectory modeling was performed using the traj plugin in Stata Version 16 (Jones &
Nagin, 2007; 2013; Jones, Nagin, & Roeder, 2001). Group-based trajectory modeling is a
type of pattern-mixture modeling in which relatively homogenous developmental trajectories
are estimated. These are estimated using maximum likelihood estimation using a general
quasi-Newton procedure, and missing data are handled by estimating the model using all
available information.

The five time points of CBCL data collection were used as independent variables to analyze
the latent grouping of individuals in their trajectories of ADHD symptoms, anxiety
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symptoms, and depressive symptoms. For each group of symptoms, unconditional 2-, 3-, and
4-class models were first compared using the Bayesian information criterion (BIC) and by
examining the smallest group membership percentage. After the number of classes were
determined, higher order effects were tested to establish whether cubic, quadratic, linear, or
intercept modeling best explained variation over time. To aid in model selection, the average
posterior probabilities were evaluated to determine if they met adequate model fit (above
0.70; Nagin, 2005). For each model, the best estimate of VIQ from age 9 years was included
as a time-stable covariate. We then compared whether the composition of these classes
differed by diagnosis (Ever or Never ASD), gender, race, and caregiver education with chi
square analyses.

Aim 2—predicting trajectory class from early childhood data—We used

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multinomial logistic regression models to test how the characteristics of participants in early
childhood distinguished the trajectory classes. For each symptom trajectory, separate models
were estimated using age 2, 5, and 9-year-old data.

Aim 3—Predicting adult outcomes from trajectory classes—We conducted

ordinal regressions to examine whether trajectory class probabilities were associated with
the number of positive adult outcomes achieved which were defined separately for more
cognitively able adults (VIQ > 70), and less cognitively able adults (VIQ < 70) as defined
above. These models included interaction terms for adult ability level and trajectory class,
and included age 9 VIQ, ASD diagnosis, race, caregiver education, and age 9 CSS as
covariates. All analyses reported in the current paper were conducted in Stata Version 16.
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Results
ADHD symptoms trajectory classes
Table 1 displays the fit statistics and smallest group percentage for each symptom trajectory.
As seen in Table 1, although the BIC indicated a better fit for the 4-class model, the
differences in BIC were small and the smallest group membership in the 4-class model was
under 1%, so we chose the 2-class model as the best fit for ADHD symptoms trajectory
classes. The groups were labeled “Low Decreasing ADHD Symptoms” (59.1% of sample,

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 McCauley et al. Page 11

highest order function: quadratic, p = .03) and “High Decreasing ADHD Symptoms” (40.9%
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of the sample, highest order function: quadratic, p = .005). The average posterior
probabilities were 0.87 for the Low Decreasing ADHD Symptoms and 0.84 for the High
Decreasing ADHD Symptoms trajectory classes.

The Low Decreasing ADHD Symptoms class had slightly elevated levels of ADHD
symptoms as defined by the ASEBA norms at T1 (Age 9, M = 59.95, SD = 7.81), with
steady decreases at each time point up to T5 (age 25, M = 54.58, SD = 3.72). The High
Decreasing ADHD Symptoms class had a clinically significant T score means at T1 (age 9
years, M = 75.11, SD = 8.64), and borderline means at T2 (age 14 years, M = 69.72, SD =
8.09) and T3 (age 17 years, M = 64.65, SD = 6.41), which continued to decrease by T4 (age
20 years, M = 63.54, SD = 4.24) and T5 (age 25 years, M = 61.97, SD = 5.12). These classes
did not differ by ‘Ever’ or ‘Never’ diagnosis of ASD, χ2 (1) = 0.76, p = .38, gender, χ2 (1) =
3.16, p = .08, race, χ2 (4) = 2.01, p = 0.73, nor primary caregiver education levels, χ2 (4) =
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6.82, p = 0.15. Supplementary Table 1 contains the counts and descriptive characteristics of
early childhood data by trajectory classes. Figure 1 displays the observed means and
confidence intervals of the two trajectory classes across time.

Convergent validity of trajectory classes with other measures of ADHD symptoms

Table 2 displays the means of hyperactivity symptoms as measured by the ABC from the
current sample, indicating sample size, time point, and reporter. There were significant
trajectory class differences in parent-reported hyperactivity symptoms at each time point in
the same directions (decreasing) as we found for the ASEBA scale. For teacher-reported
hyperactivity symptoms, the significant differences occurred only between classes at T2 (age
14).
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Predicting high ADHD symptom trajectory class from early childhood characteristics
Multinomial logistic regression models were conducted to measure whether age 2, age 5,
and age 9 characteristics predicted ADHD trajectory class membership, using the Stable
Low ADHD Symptoms trajectory as the reference group. Table 3 displays the results of each
model by age. At ages 2, 5, and 9 years, higher adaptive skills were significantly associated
with lower odds of being in the High Decreasing ADHD Symptoms class.

Predicting adult outcomes from ADHD symptom trajectory class membership

An ordinal regression model was conducted to examine whether the ADHD Symptom
trajectory class was associated with the number of positive outcomes adults achieved, while
controlling for race, caregiver education, ASD diagnosis, CSS, and VIQ measured at age 9
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years. There was a significant interaction between trajectory class and adult ability level,
indicating that for more cognitively able adults in the High Decreasing ADHD Symptoms
class (n = 16 in High Decreasing vs. n = 40 in Low Decreasing class), there were lower odds
of achieving positive adult outcomes (B = −1.49, Odds ratio [OR] = 0.23, SE = 0.63, p
= .02). For less able adults (n = 35 in High Decreasing vs. n = 32 in Low Decreasing class),
membership in the High Decreasing ADHD Symptoms class was not associated with the
number of adult outcomes achieved (p =.32).

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Anxiety Symptoms trajectory classes

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The model fit statistics indicated a 2-class model as the best fit for Anxiety symptom
trajectory classes (see Table 1). The groups were labeled “Stable Low Anxiety Symptoms”
(74.23% of sample, N = 144, highest order function: quadratic, p = .02) and “Stable High
Anxiety Symptoms” (25.77% of the sample, N = 50, highest order function: intercept, p
< .001). The average posterior probabilities were 0.84 for the Stable Low Anxiety
Symptoms and 0.89 for the Stable High Anxiety Symptoms trajectory classes.

The Stable Low Anxiety Symptoms class had overall low levels of anxiety symptoms
sustained throughout adolescence and early adulthood, from T1 (age 9 years, M = 51.40, SD
= 3.27) to T2 (age 14 years, M = 52.29, SD = 3.59) to T3 (age 17 years, M = 53.41, SD =
4.35), and remained stable in adulthood (T4 M = 52.99, SD = 4.41; T5 M = 52.81, SD =
4.12). The Stable High Anxiety group had higher stable levels of anxiety symptoms from T1
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to T5, with means that ranged from 62.95 (SD = 7.76) to 66 (SD = 8.31). These classes did
not differ by Ever or Never diagnosis of ASD, χ2(1) = 0.22, p = .63, primary caregiver
education, χ2(4) = 5.87, p = .21, race, χ2(4) = 3.30, p = .51, but did differ on gender, χ2(1)
= 5.01, p = .03 (25% female in Stable Low vs. 10% female in Stable High class). Due to the
distributions of VIQ in the classes (see Supplementary Table 1), we examined whether this
relation was significant after accounting for VIQ in an analysis of covariance (ANCOVA)
model, and found gender to no longer be significant, F (1, 165) = 0.11, p = .75). Figure 2
displays the two classes of anxiety symptom trajectories and their confidence intervals.

Convergent validity of trajectory classes with other measures of anxiety symptoms

Table 4 displays the means of other measures of anxiety symptoms from the current sample,
indicating sample size, time point, and reporter. Here, only parent-reported anxiety
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symptoms are significantly elevated in the Stable High Anxiety trajectory group compared
to the Stable Low Anxiety Symptom class from late adolescence into adulthood, although
trends for means on self-reported anxiety symptoms show generally similar patterns to the
parent measures, especially by T5 (age 25).

Predicting High Anxiety Symptom trajectory class from early childhood characteristics
Multinomial logistic regression models were conducted to measure whether age 2, age 5,
and age 9 characteristics predicted the probability of anxiety symptom trajectory class
membership, with the Stable Low Anxiety Symptom class as the reference group. Table 5
displays the results of each model by age. At ages 5 years and 9 years higher VIQ was a
significant predictor of membership in the Stable High Anxiety Symptom class. At age 9
years, higher levels of adaptive skills were associated with decreased odds of being in the
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Stable High Anxiety Symptom class.

Predicting adult outcomes from anxiety symptom trajectory class membership

An ordinal regression model was conducted to examine whether the Anxiety symptom
trajectory class was associated with the number of outcomes adults achieved, while
controlling for race, caregiver education, ASD diagnosis, and CSS and VIQ measured at age
9 years. There was a significant interaction between trajectory class and adult ability level,
indicating that for more able adults in the Stable High Anxiety Symptom class (n = 32 in

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 McCauley et al. Page 13

Stable High vs. n = 24 in Stable Low class), there were lower odds of achieving positive
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adult outcomes (B = −1.37, OR = 0.25, SE = 0.60, p = .02). For less able adults (n = 4 in
Stable High vs. n = 63 in Stable Low class, membership in the Stable High Anxiety
Symptom class was not associated with the number of adult outcomes achieved (p = .12).

Depressive symptoms trajectory classes

A 2-class model for depressive symptoms was the best fit. The groups were labeled “Stable
Low Depressive Symptoms” (68.04% of sample, N = 132, highest order function: intercept,
p < .001) and “High/Fluctuating Depressive Symptoms” (31.96% of the sample, N = 62,
highest order function: cubic, p = −.03). The average posterior probabilities were 0.90 for
the Stable Low Depressive Symptoms and 0.85 for the High/Fluctuating Depressive
Symptoms trajectory classes.

The Stable Low Depressive Symptoms class had overall low levels of depressive symptoms
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throughout adolescence and early adulthood with means ranging from 54.96 (SD = 5.22) to
55.60 (SD = 5.36). The High/Fluctuating Depressive Symptoms class had stable levels of
depressive symptoms from T1 (age 9 years; M = 68.45, SD = 8.02) to T2 (age 14 years; M =
64.29, SD = 5.24), increasing from T2 (age 9 years) to T3 (age 17 years; M = 67.75, SD =
7.81) and T3 to T4 (age 20 years; M = 70.21, SD = 8.31), with decreasing symptoms from
T4 to T5 (age 25 years; M = 66.72, SD = 7.74). These classes did not differ by Ever or
Never diagnosis of ASD, χ2 (1) = 2.73, p = .09, gender, χ2 (1) = 0.63, p = .43, race, χ2 (4) =
3.41, p = .49, nor primary caregiver education, χ2 (4) = 1.73, p = .79. Figure 3 displays the
two classes of trajectories and their confidence intervals.

Convergent validity of trajectory classes with other measures of depressive symptoms

Table 6 displays the means of other measures of depressive symptoms from the current
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sample, indicating sample size, time point, and reporter. Overall, the trends across other
measures of depressive symptoms show trends similar to the latent trajectories found in the
group-based trajectory modeling. In addition, at least with the parent-reported ABC
withdrawal, the pattern of changes across adolescence and adulthood was veiy similar to the
pattern in the high trajectory from the ASEBA measures, except that they peaked in late
adolescence rather than early adulthood. Individuals in the High/Fluctuating Depressive
Symptoms class had significantly higher levels of depressive symptoms across other
measures, with some exceptions (i.e., parent-reported BDI-II at T3 and T4, the self-reported
BDI-II at T4 and T5, and the teacher-reported withdrawal scores on the ABC at T3 and T4).

Predicting High Depressive Symptom trajectory class from early childhood characteristics
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Multinomial logistic regression models were conducted to measure whether age 2, age 5,
and age 9 characteristics predicted class membership, using the Stable Low Depressive
Symptoms class as the reference group. Table 7 displays the results of each model by age. At
age 2 years, none of the individual characteristics tested were significant predictors of class
membership. At age 5 years, higher VIQ was associated with greater odds of being in the
High/Fluctuating Depressive Symptoms class, an effect that was not significant at age 2
years or age 9 years but with similar ranges of odds ratios. At age 9 years, higher levels of
autism severity-social affect (CSS SA) were associated with increased odds of being in the

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High/Fluctuating Depressive Symptoms trajectory class. In contrast, higher levels of

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adaptive skills at age 9 years were negatively associated with the odds of being in the High/
Fluctuating Depressive Symptoms trajectory class.

Predicting adult outcomes from depressive symptom trajectory class membership

An ordinal regression model was conducted to examine whether the probability of belonging
to the High/Fluctuating Depressive Symptoms class was associated with the number of
positive outcomes adults achieved, while controlling for race, caregiver education, ASD
diagnosis, CSS, and VIQ measured at age 9 years. There was a significant interaction
between trajectory class and adult ability level. For more cognitively able adults in the high
depressive trajectory class (n = 20 in Higher/Fluctuating vs. n = 36 in Stable Low class),
there were less odds of achieving positive adult outcomes (B = −1.77, OR = 0.17, SE = 0.58,
p = .002). For less cognitively able adults (n = 19 in High Fluctuating vs. n = 48 in Stable
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Low class), the Higher/Fluctuating Depressive Symptom class was not associated with the
number of adult outcomes achieved ( p = .32).

Commonalities across symptom trajectories

Table 8 displays the proportions of individuals with one or more high trajectory class in the
whole sample and in the ASD ever subsample. The distributions of trajectory classes in the
ASD ever subsample are reflective of the whole sample distributions, with 57% (ASD Ever)
to 60% (Whole Sample) in at least one high symptom trajectory class, and 9% of the sample
in all three.

We then examined whether the probabilities of being in the symptom trajectory classes were
associated with one another using partial correlations that accounted for age 9 years VIQ.
We found significant relations between the probabilities of being in the high ADHD and
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depressive symptom trajectories (r = .42, p < .001), between the High Decreasing ADHD
and Stable High Anxiety Symptom trajectories (r = .32, p < .001) and between the High/
Fluctuating Depressive and Stable High Anxiety Symptoms probabilities (r = .31, p < .001).
These relations were similar without including VIQ as a covariate, except the relation
between the Stable High Anxiety and High Decreasing ADHD Symptoms probabilities was
no longer significant (r = .12)

Finally, we explored the possibility that baseline levels of each symptom group could
influence membership in the other symptom trajectories using multinomial logistic
regressions. Baseline levels of depressive symptoms (OR = 1.10, p < .001) but not anxiety
symptoms (OR = 0.98, p = .41) were associated with being in the High Decreasing ADHD
Symptoms class over the Stable Low ADHD Symptoms class. Neither baseline levels of
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depressive symptoms (OR = 1.04, p = .10) nor ADHD symptoms (OR = 1.02, p = .28) were
predictive of the Stable High Anxiety Symptoms trajectory probability. Baseline levels of
ADHD symptoms (OR = 1.08, p < .001) and anxiety symptoms (OR = 1.06, p = .03) were
positively associated with the membership in the High/Fluctuating Depressive Symptoms
class over the Stable Low Depressive Symptoms class.

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Discussion
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The current study documents trajectories of symptoms characteristic of ADHD, anxiety, and
depression in a sample of children referred for ASD at an early age who were followed into
young adulthood. Our goals were to define individuals at risk of having higher symptoms of
psychopathology throughout adolescence and into adulthood, examine predictors of these
risks from early childhood characteristics, and consider how having higher symptom
trajectories relate to objective adult outcomes. Overall, 60% of the current sample (63%
when looking at only individuals with an ASD diagnosis) belonged to one or more of the
higher symptom trajectory classes, which corroborates past research looking at the
prevalence of co-occurring conditions in ASD (Leyfer et al., 2006; Simonoff et al., 2008;
Stringer et al., 2020). Using group-based trajectory modeling, we found two classes of each
symptom trajectory that were similar in composition, one that represented overall low levels
of symptoms, and one that represented more symptoms across adolescence and into
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adulthood. For ADHD symptoms, the higher symptom trajectory class decreased from late
childhood to early adolescence, and stabilized across adolescence into adulthood. For
anxiety symptoms, the higher symptom trajectory class appeared stable. For depressive
symptoms, the higher symptom trajectory class fluctuated in severity, but appeared to peak
during the transition to adulthood.

Higher VIQ was a predictor of higher anxiety and depressive symptom trajectory classes.
This finding is consistent with past work on internalizing symptomatology in individuals
with ASD (e.g., Mayes et al., 2011). This finding lends itself to a variety of interpretations.
First, select symptoms of psychiatric conditions such as anxiety and depression may
necessitate greater insight (including social and self-awareness; Mayes et al., 2011). This
insight into potential failures to meet social demands may contribute to distress which
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manifests in the broad symptom classes identified by the ASEBA. Second, the effects of
verbal IQ may be an artifact of measurement. Internalizing symptoms in children and adults
who are minimally verbal can be difficult to assess using instruments normed for the general
populations. In a recent study, individuals with cognitive impairments were most commonly
diagnosed with specific phobias and separation anxiety, whereas a much wider range of
anxiety disorders were found in individuals with IQs over 70 (Kerns et al., 2020). Thus, the
ASEBA measures may not have been sensitive to detect the quality of anxiety in individuals
with ASD and lower cognitive capacity. Indeed, the ABC subscales may better identify
elevations in the behavior problems of minimally verbal autistic individuals (Fok & Bal,
2019), although we found similar stability in the withdrawal subscale as our depressive
symptom trajectory analysis.
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Notably, we did not find trajectory class probabilities to be influenced by gender in the
current analyses. There were significantly fewer females than males in our High Stable
Anxiety trajectory class, but this effect was accounted for by differences in IQ distributions.
This is in contrast to an earlier report that females had greater increases in depressive and
anxiety symptoms in early adulthood (Gotham et al., 2015a; Stringer et al., 2020). This
discrepancy is likely reflective of differences in analytic techniques (e.g., trajectory models
as opposed to generalized mixed effects models and the use of T scores over raw scores). A
potential limitation in the present study is the relatively small sample of female participants.

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Future research should further examine the unique contributions that sex and gender may
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play in individuals with ASD of different cognitive abilities.

Psychopathology is a distinct and persistent challenge across development for individuals

with ASD. This is evidenced from associations with early developmental factors, most
notably adaptive skills. By age 9 years (age 2 years for the ADHD trajectory), early and
higher adaptive skills were associated with lower odds of membership in the higher ADHD,
anxiety, and depressive symptom trajectories. This finding is similar to the finding by
Stringer et al. (2020) which found higher adaptive skills at age 12 to be predictive of greater
declines in ADHD symptoms into young adulthood. Other studies have found similar
patterns: individuals with ASD face significant challenges in adaptive skills that remain
across childhood and into adulthood when compared to typically developing peers, or to
cognitively matched individuals with other developmental disabilities (Lord et al., 2020;
Matthews, Smith, Pollard, Ober-Reynolds, Kirwan, & Malligo, 2015; Smith, Maenner,
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Seltzer, 2012). For individuals with ASD, particularly individuals with higher IQ, levels of
adaptive functioning fall significantly below IQ estimates (Alvares et al., 2020; Charman et
al., 2011), and a recent study has found associations between the discrepancy between IQ
and adaptive skills in adulthood and co-occurring anxiety and depressive symptoms (Kraper,
Kenworthy, Popal, Martin, & Wallace, 2017). Adaptive functioning is a target well-suited for
intervention across time, and the current evidence suggests that these skills are related to
psychopathology across the lifespan, yet further examination is needed concerning the
causality of these associations.

ADHD Symptom trajectories

Around 40% of our sample fell in the High Decreasing ADHD Symptoms trajectory class.
This class was characterized by levels above clinical threshold in late childhood which
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gradually abated in adulthood. Previous studies have also described reductions in problems
associated with ADHD in people with ASD (Anderson et al., 2011; Gray, Keating, Taffe,
Brereton, Einfeld, & Tonge, 2012). This also mirrors the trajectory of ADHD symptoms in
the general population (e.g., Döpfner et al., 2015). In previous analyses of this sample using
the ABC, reductions in ADHD symptoms (hyperactivity) were associated with higher levels
of VIQ (Anderson et al., 2011), but we did not find that association in our ASEBA trajectory
classes.

However, despite reductions in ADHD over time, the High Decreasing ADHD Symptom
class continued to have significantly more attention problems at each time point. In addition,
more cognitively able adults in the higher symptom trajectory class had fewer positive adult
outcomes. Greater attention problems in childhood may be a barrier to learning opportunities
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that can potentially cascade into difficulties for individuals to gain friends, live
independently, or work independently in adulthood.

Anxiety Symptom trajectories

Around 30% of current participants had a stable trajectory of elevated anxiety symptoms,
although the mean levels fell under clinical significance (T scores around 65). VIQ
measured at ages 2, 5, and 9 was a positive predictor of the high anxiety symptom trajectory

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class, indicating that anxiety problems, at least as measured from parent-report on the
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CBCL, may be more pertinent for individuals with ASD and higher IQs. This corroborates
past research on individuals with ASD (Hallett et al., 2013). The presentation of anxiety
symptoms may indeed be different in individuals with lower IQs (especially when
considering individuals with minimal language) and thus it may be difficult to assess via
informant. For example, in individuals with lower IQs, anxiety may present as increased
repetitive behaviors or aggressive behavior (Appleton, Roberts, & Simpson, 2019). We used
one measure of anxiety specific to individuals with limited language, the ADAMS, but the
number of participants in the high symptom trajectory group who completed this measure
was too small for us to interpret trajectory differences.

Depressive Symptom trajectories

The current analyses revealed that over a third of individuals had a high depressive symptom
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trajectory, characterized by fluctuations peaking at a clinically significant level in early

adulthood. It is important to note that in previous analyses of this verbally fluent subset of
this sample, 14% received clinical diagnoses of major depressive disorder and that measures
of depressive symptoms tended to “over-identify” clinical concerns associated with true co-
occurrence (Gotham et al., 2015a). Parents report more concerns than diagnostic instruments
are capturing (Gotham et al., 2015b), so these analyses could also be overestimating
depressive symptoms. However, because this trajectory class was negatively associated with
objective measures of adult outcomes (e.g., participation in work, independent living, and
friendships) for more cognitively able individuals, elevated depressive symptoms are still of
concern.

Although early childhood data did not account for much of the variation in this trajectory
class probability, social affect as measured on the ADOS at age 9 years was a significant
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predictor of the high/fluctuating depressive symptom trajectory. Although this finding could
reflect the conceptual similarities between autism symptoms and depressive symptoms as
they are measured by the ASEBA, particularly social withdrawal (e.g., Biederman et al.,
2011), the ADOS is clinician administered and measures qualities of interactions and not so
much elements of social withdrawal. We also found that other measures of depression
demonstrated similar patterns as the trajectory analyses. The trajectory classes were
corroborated by parent reports of depressive symptoms across a variety of measures,
including the ABC withdrawal across all time points, the BDI-II in adulthood, and for the
less cognitively able subsample, the ADAMS. We also found similar differences between
trajectory classes on the teacher-reported withdrawal scale on the ABC in late childhood and
early adolescence. For the smaller subset of participants for which we were able to collect
self-reports, trajectory class differences were not significant but were in the same direction.
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The findings of depressive symptoms peaking in early adulthood and the association
between trajectory class and adult outcomes warrant further examination. At least in the US,
there are few supports available for individuals and families transitioning out of high school
in early adulthood (Taylor & Seltzer, 2011). Adults with ASD are less likely to be working
or attending higher education, to be living independently, and to have supportive friendships
than typically developing adults or adults with other developmental disabilities (Orsmond,

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Shattuck, Cooper, Sterzing, & Anderson, 2013; Pickles et al., 2020; Wei, Wagner, Hudson,
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Yu, & Shattuck, 2015). Another consideration is that schooling provides individuals with
predictable and stable opportunities for social interactions, and individuals with ASD may
have difficulty establishing these connections without structure, contributing to heightened
feelings of isolation and depressed mood. Our trajectories, particularly the increase of
depressive symptoms from late adolescence into young adulthood, may be describing a
potential period of vulnerability for adults, in which shifts in support and expectations could
lead to heightened feelings of depressed mood or withdrawal. These trajectories also mirror
what is found in typical development, with the exception that our high symptom trajectory
group peaked in early adulthood and not late adolescence (e.g., Garber et al., 2002)

Commonalities among symptom trajectories

The presence of two or more co-occurring psychiatric conditions is commonly reported
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among individuals with ASD (e.g., Lecavalier et al., 2019). For example, children with
anxiety and ASD may display more elevated depressive symptoms, such as withdrawal
(Kerns et al., 2015), and higher levels of ADHD symptoms in children with ASD are related
to increased rates of being diagnosed with an additional co-occurring condition, such as
anxiety, mood disorder, and disruptive behavioral disorders (Mansour, Dovi, Lane,
Loveland, & Pearson, 2017). In the current study, 29% of participants belonged to more than
one high symptom trajectory class, but the amount of overlap was variable across conditions.
There did not appear to be a distinct profile of multiple co-occurring symptoms.

The probability of being in the high depressive symptom trajectory class was positively
associated with being in the high symptom ADHD and anxiety trajectory classes, indicating
the possibility of some shared risk between having depressive symptoms and other co-
occurring disorders. We also explored whether baseline levels of each symptom influenced
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the probabilities of being in other high symptom trajectory classes. We found the higher
depressive symptom trajectory class to be positively associated with baseline levels of
anxiety and attention problems, and the higher but decreasing ADHD trajectory class to be
predicted by higher levels of withdrawn/depressed symptoms. The relation between
depression and ADHD in ASD is not yet well understood, and future research should
examine how these symptoms influence each other earlier in development, whether they
share etiology, or perhaps whether together they represent psychopathology not well
captured by the measures available.

Measurement considerations
The ASEBA trajectory classes were corroborated by other measures via parent report and
teacher report, but not consistently by self-report. Specific to internalizing symptomatology,
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concerns have been raised about the validity of self-report by individuals with ASD, in that
parent and clinician reports appear to be more often in agreement with each other than self-
reports (e.g., Storch et al., 2012). In research on ASD, parents are frequent sources of
information about their child’s behaviors and symptoms, but it is fair to question how
accurately parents can report on their children’s internal states. Typically, although not as
apparent using the BDI in these analyses, parents tend to endorse higher rates of symptoms
than children (e.g., Lopata et al., 2010; Nicpon et al., 2010; White et al., 2012), but it is

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important to acknowledge that these reports can be distorted by parent’s own mental health
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concerns (Bitsika & Sharpley, 2016). Another measurement complication is the relevance of
these measures to minimally verbal individuals. For example, parents may be less likely to
endorse some items on the ASEBA that involve complaining if their son or daughter does
not use words. Research has yet to establish best practices for how best to get information
about these conditions from individuals themselves while also incorporating a diverse range
of cognitive profiles.

Further compounding concerns about measurement validity, most existing measures of

psychopathology—including the ASEBA—were developed, scaled, and normed for the
general population. Studies have found inconsistent support for the factor structure of the
syndrome scales in ASD samples across early and late childhood (e.g., Medieiros, Mazurek,
& Kanne, 2017; Pandolfi et al., 2012); and some evidence suggests the specificity and
sensitivity of syndrome scales are low in this population (Fok, & Bal, 2019; Hoffman et al.,
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2016). Nevertheless, the ASEBA is a widely used tool used in clinics for screening
emotional and behavior problems and for possible autism (e.g., Havdahl et al., 2016;
Mazefsky, Anderson, Connor, & Minshew, 2010).

Future studies, perhaps using larger existing datasets, should address these concerns about
measurement invariance using statistical techniques designed to account for differences
across reporters, measures, and time. Moderated nonlinear factor analyses offer one
approach to account for differences on item functioning within and across populations,
reporters, measures, and time (see Curran et al., 2014, 2020). These models could address
empirical questions about how best to adjust available measurement tools to produce more
robust representations of psychopathology constructs in ASD samples. However, there
remains a great need of more valid and comprehensive assessments of psychopathology that
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better reflect the symptoms experienced of individuals with ASD across varying abilities.

Strengths and limitations

Trajectory classes are empirically derived constructs and thus may not be entirely reflective
of the course of development for a co-occurring condition. Previous studies have reported
concerns that the established ASEBA scales are complicated measures of psychopathology
for studies of individuals with ASD, in that syndrome scales do not always directly match up
with clinical diagnoses (e.g., Greenlee et al., 2016; Medeiros et al., 2017). Two scales from
the ASEBA, Withdrawn/Depressed and Anxious/Depressed were used in the current study
despite their conceptual overlap, yielding distinctive class memberships. One strength of the
current study is that we were able to compare empirically derived ASEBA trajectory classes
with other measures of symptoms and across multiple reporters. However, we did not
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account for the differences across raters and measures using more advanced methods, such
as nonlinear factor analysis referenced above, to produce more precise estimates of
psychopathology (e.g., Curran et al., 2014).

One particular limitation of measures that are normed for the general population is that they
may not be as valid in other contexts or populations (see Meehl 1990). Particularly
concerning are measures that assess subjective and internal symptoms in individuals who are
minimally verbal or less cognitively able. For informant-reported symptoms, more visible

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 McCauley et al. Page 20

behaviors and constructs, such as irritability as assessed by the ABC, may better capture
Author Manuscript

variations in mood in minimally verbal individuals than existing measures of anxiety or

depressive symptoms that reflect internal states (Fok & Bal, 2019).

Another limitation is that we do not address whether the observed stability or change in the
levels of symptoms across time represents natural fluctuations in response to changes in
environmental demands, the effects of services received or medications, or individual
changes in coping skills. These questions are important developmental and treatment
considerations.

The cohort of the current participants is small, and our sample of children diagnosed in the
early 1990s is likely different than a similar sample of consecutively referred children at
early ages diagnosed today due to changes in ASD awareness and treatment availability.
This limits our ability to generalize these findings. However, one strength of the current
Author Manuscript

study is that it consists of individuals who were referred for ASD in early childhood, rather
than adolescents and adults who are recruited from clinics and are likely to be biased by
current clinical concerns.

Conclusions
Variation in the trajectories of co-occurring psychopathology from late childhood into
adulthood is informative to understanding the development of people with ASD. Early
characteristics, particularly adaptive skills, predict trajectories of different co-occurring
symptoms, and, for more cognitively able adults, predict fewer positive outcomes associated
with these trajectories. We hope these patterns help contextualize changes in symptoms an
individual or family may report. Developmental trajectories are a starting point in our search
for mechanisms that explain changes occur across time and provide clues to how we can
Author Manuscript

address them in clinical practice.

Supplementary Material
Refer to Web version on PubMed Central for supplementary material.

Acknowledgments.
We would like to extend our gratitude to the participants and families for the time they have given to this study, as
well as all the research staff over the years. This study was funded by the National Institute of Child Health and
Human Development R01 HD081199 (PI: CL), and National Institute of Mental Health R01MH081873 (PI: CL).
CL acknowledges the receipt of royalties from the sale of the Autism Diagnostic Observation Schedule-2
(ADOS-2) and the Autism Diagnostic Interview-Revised (ADI-R). Royalties generated from this study were
donated to a not-for-profit agency, Have Dreams. JM and RE have no potential conflicts to declare.
Author Manuscript

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Figure 1.
Trajectory classes derived from the attention problems symptom T score. Both groups have
significant quadratic effects in the model. Dots represent observed means, lines represent
estimated trajectories, and dotted lines represent the 95th confidence interval for estimated
trajectories.
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Figure 2.
Trajectory classes derived from the anxious/depressed symptom T score. Group 1 has a
significant quadratic slope, and Group 2 is an intercept model. Dots represent observed
means, lines represent estimated trajectories, and dotted lines represent the 95th confidence
interval for estimated trajectories.
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 McCauley et al. Page 30
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Figure 3.
Trajectory classes derived from the withdrawn/depressed symptom T score. Group 1 is
typified by a significant intercept model, Group 2 is typified by a significant cubic model.
Dots represent observed means, lines represent estimated trajectories, and dotted lines
represent the 95th confidence interval for estimated trajectories.
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Table 1.

Fit statistics for different class models tested by symptom

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ADHD symptom model selection

Model BIC Smallest group %

2-class model −1561.43 40.90

3-class model −1556.70 18.52

4-class model −1556.38 0.67

Anxiety symptom model selection

Model BIC Smallest group %

2-class model −1249.96 30.60

3-class model −1235.61 1.91

4-class model −1234.74 1.82

Depressive symptom model selection

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Model BIC Smallest group %

2-class model −1522.70 33.80

3-class model −1510.85 10.82

4-class model −1514.34 3.71

Note: Final selected models in bold

BIC: Bayesian information criteria

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Table 2.

Descriptive statistics for other attention-deficit/hyperactivity disorder (ADHD) measures by ADHD trajectory class

Stable low trajectory High decreasing trajectory

Variable N Mean (SD) N Mean (SD) p value

McCauley et al.

T1 ABC Hyperactivity–IR 86 10.18 (8.62) 53 20.46 (10.59) .000

T2 ABC Hyperactivity–IR 92 6.86 (7.12) 56 15.34 (7.93) .000

T3 ABC Hyperactivity–IR 76 5.14 (6.85) 53 13.38 (8.85) .000

T4 ABC Hyperactivity–IR 68 5.01 (7.26) 49 12.19 (8.62) .000

T5 ABC Hyperactivity–IR 59 3.54 (4.57) 46 11.43 (8.31) .000

T1 ABC Hyperactivity–TR 56 11.87 (10.4) 37 14.27 (9.32) .260

T2 ABC Hyperactivity–TR 77 7.95 (6.43) 49 14.5 (9.69) .000

T3 ABC Hyperactivity–TR 50 9.7 (8.8) 41 11.96 (10.69) .271

T4 ABC Hyperactivity–TR 15 10.39 (8.78) 20 10.74 (8.46) .907

Note: ABC = Aberrant Behavior Checklist, IR = Informant report, TR = Teacher report,

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Table 3.

Multinomial logistic models predicting attention-deficit/hyperactivity disorder (ADHD) symptom trajectory membership

Age 2 data (N = 151) Age 5 data (N = 92) Age 9 data (N = 142)

Class Variable OR (95th CI) OR (95th CI) OR (95th CI)
McCauley et al.

Class 1: Low decreasing Reference group Reference group Reference group

Class 2: High decreasing VIQ 1.00 (0.98–1.02) 1.02 (0.98–1.05) 1.02 (1.00–1.04)

CSS SA 1.00 (0.83–1.20) 0.87 (0.69–1.08) 0.96 (0.80–1.15)

CSS RRB 0.94 (0.78–1.12) 1.07 (0.85–1.34) 1.12 (0.92–1.36)

VABS ABC 0.94 (0.88–0.99)* 0.93 (0.88–0.98)* 0.94 (0.91–0.97)***

Note: CSS SA = Calibrated Severity Score Social Affect; CSS RRB = Calibrated Severity Score Restricted and Repetitive Behaviors; VABS ABC = Vineland Adaptive Behavior Scale Adaptive Behavior
Composite; VIQ = verbal IQ

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Table 4.

Descriptive statistics for other anxiety measures by anxiety trajectory class

Low increasing trajectory High stable trajectory

Variable N Mean (SD) N Mean (SD) p value

McCauley et al.

T3 AMAS Total–SR 14 12.88 (7.37) 15 14.68 (8.01) .54

T4 AMAS Total–SR 18 13.05 (6.7) 13 13.27 (5.51) .92

T5 AMAS Total–SR 13 13.5 (6.87) 19 18.03 (7.45) .09

T3 AMAS Total–IR 72 8.24 (5.31) 23 17.21 (6.07) .000

T4 AMAS Total–IR 76 8.98 (5.86) 21 18.1 (6.45) .000

T5 AMAS Total–IR 74 7.78 (4.63) 23 17.87 (6.33) .000

T3 ADAMS Anxiety Symptoms–IR 46 3.71 (3.08) 2 2.5 (3.54) .589

T4 ADAMS Anxiety Symptoms–IR 55 3.92 (4.05) 5 8.6 (3.21) .015

Note: AMAS = Adult Manifest Anxiety Scale, ADAMS = Anxiety Depression and Mood Screen, IR = Informant Report, SR = Self-Report

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Table 5.

Multinomial logistic models predicting anxiety symptom trajectory membership

Age 2 data (N = 151) Age 5 data (N = 92) Age 9 data (N = 142)

Class Variable OR (95th CI) OR (95th CI) OR (95th CI)

McCauley et al.

Class 1: Low Stable Reference group Reference group Reference group

Class 2: High Stable VIQ 1.01 (0.99–1.04) 1.08 (1.03–1.13)** 1.06 (1.03–1.09)***

CSS SA 1.1 (0.89–1.37) 1.08 (0.83–1.42) 1.09 (0.90–1.32)

CSS RRB 0.94 (0.76–1.16) 1.23 (0.94–1.62) 0.84 (0.69–1.02)

VABS ABC 1.04 (0.98–1.1) 0.98 (0.93–1.04) 0.95 (0.92–0.99)**

Note: CSS RRB = Calibrated Severity Score Restricted and Repetitive Behaviors; CSS SA = Calibrated Severity Score Social Affect; VABS ABC = Vineland Adaptive Behavior Scale Adaptive Behavior
Composite; VIQ = verbal IQ

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Table 6.

Descriptive statistics for other depression measures by depression trajectory class

Stable low trajectory High trajectory

Variable N Mean (SD) N Mean (SD) p value

McCauley et al.

T1 ABC Withdrawal–IR 93 5.66 (6.35) 46 13.88 (6.98) .000

T2 ABC Withdrawal–IR 103 4.75 (4.65) 45 12.51 (7.65) .000

T3 ABC Withdrawal–IR 88 4.65 (4.9) 41 14.99 (8.99) .000

T4 ABC Withdrawal–IR 81 6.07 (7.07) 36 12.08 (5.94) .000

T5 ABC Withdrawal–IR 72 5.98 (6.68) 33 12.27 (8.78) .000

T1 ABC Withdrawal–TR 63 8.79 (7.52) 30 14.59 (8.96) .002

T2 ABC Withdrawal–TR 83 8.64 (6.64) 43 12.64 (7.44) .003

T3 ABC Withdrawal–TR 60 10.9 (9.21) 31 12.63 (8.83) .392

T4 ABC Withdrawal–TR 25 10.6 (9.17) 10 13.2 (8.08) .439

T3 BDI II- IR 46 7.93 (7.36) 18 8.5 (6.2) .774

T4 BDI II- IR 36 5.71 (7.36) 22 9.7 (8.53) .065

T5 BDI II- IR 73 3.54 (4.54) 33 7.31 (7.11) .001

T3 BDI II- SR 16 6.95 (8.8) 3 22.28 (6.29) .011

T4 BDI II- SR 20 7.15 (7.74) 14 9.99 (6.94) .280

T5 BDI II- SR 21 9.74 (9.13) 14 15.2 (10.55) .113

T3–ADAMS Depressive Symptoms–IR 36 1.98 (2.55) 12 3.71 (2.95) .056

T4–ADAMS Depressive Symptoms–IR 43 2.12 (2.52) 17 6.42 (5.62) .000

Note: ADAMS = Anxiety Depression and Mood Screen; ABC = Aberrant Behavior Checklist; BDI II = Beck Depression Inventory; IR = Informant Report; TR = Teacher Report; SR = Self-Report

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Table 7.

Multinomial logistic models predicting depressive symptom trajectory membership

Age 2 data (N = 151) Age 5 data (N = 92) Age 9 data (N = 142)

Class Variable OR (95th CI) OR (95th CI) OR (95th CI)

McCauley et al.

Class 1: Low Stable Reference group Reference group Reference group

Class 2: High Fluctuating VIQ 1.01 (0.99–1.04) 1.05 (1.01–1.09)* 1.02 (1–1.04)

CSS SA 1.05 (0.87–1.27) 1.25 (0.99–1.59) 1.32 (1.09–1.60)**

CSS RRB 1.02 (0.85–1.23) 1.04 (0.82–1.31) 0.95 (0.80–1.13)

VABS ABC 0.97 (0.92–1.03) 0.96 (0.91–1.01) 0.97 (0.94–1.00)*

Note: VABS ABC = Vineland Adaptive Behavior Scale Adaptive Behavior Composite

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Table 8.

Percentage of sample in one or more trajectory class

N (whole sample) % of whole sample N (ASD Ever) % of ASD Ever sample

One high symptom trajectory (high depressive, anxiety, or ADHD symptoms) 62 32% 51 34%
McCauley et al.

High depressive and anxiety symptom trajectory 9 5% 6 4%

High depressive and ADHD symptom trajectory 23 12% 22 14%

High anxiety and ADHD symptom trajectory 4 2% 3 2%

High depressive, anxiety, and ADHD symptom trajectory 18 9% 14 9%

One or more high Symptom trajectory 116 60% 95 63%

No high symptom trajectory 78 40% 57 37%

Note: ADHD = attention-deficit/hyperactivity disorder

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