Child maltreatment and the development of psychopathology: The role of developmental timing and chronicity

Abstract

Background:

The effects of child maltreatment (CM) on psychopathology are well-established, yet the complex effects of timing and chronicity of maltreatment exposure on the development of psychopathology are still unclear.

Objective:

To elucidate developmental pathways from distinct dimensions of CM (chronicity and timing) to psychopathology during emerging adulthood using data from a longitudinal, multi-method study.

Participants and Setting:

Children with and without maltreatment exposure were recruited at wave 1 (age 10-12) to participate in a research summer camp. At wave 2, participants were recontacted during emerging adulthood (age 18-22). The current study includes 391 participants (51.3% female; 77.5% Black, 11.3% white, 7.4% Hispanic, 3.8% other race).

Methods:

Timing and chronicity of maltreatment exposures were coded from child protective services records using the Maltreatment Classification System. Childhood internalizing and externalizing symptoms were assessed using child- and camp counselor-report. Emerging adults completed self-report questionnaires and were interviewed about their current and past symptoms of psychopathology. Structural equation modeling was used to estimate direct and indirect links between childhood maltreatment dimensions (chronicity and timing) to adult psychopathology via childhood internalizing and externalizing.

Results:

Child maltreatment experiences that spanned several developmental periods, including both early and later childhood stages, predicted a cascade of both internalizing and externalizing symptoms in childhood that eventuated in greater symptoms of anxiety, depression, substance use disorder, and antisocial personality disorder in emerging adulthood.

Conclusions:

Results suggest that chronic childhood maltreatment exposure is associated with multifinality in psychopathology presentations that can be detected in childhood and extend into emerging adulthood. Early prevention and intervention efforts to promote positive and safe parenting are essential to decrease the burden of mental health symptoms conferred by chronic maltreatment exposures on individuals, families, and public health systems.

Introduction

Child maltreatment (CM) is a prevalent and destructive issue that poses substantial risk for derailing development across multiple domains of functioning throughout the life course (Cicchetti & Toth, 2016). Among the litany of adverse biological and psychological outcomes that follow CM, psychopathology is among the most salient sequelae (Zeanah & Humphreys, 2018). Specifically, CM sets in motion a path of vulnerability that broadly increases the likelihood of virtually all forms of psychopathology (McLaughlin et al., 2020), including forms that are complex, recurrent across the life course, and treatment resistant (Nanni et al., 2012). In fact, CM is among the most potent risks for adverse mental health outcomes, as children who experience maltreatment are three times more likely than children without CM histories to experience psychopathology, and approximately half of psychological disorders are attributable to CM experiences (Li et al., 2016; Zeanah & Humphreys, 2018).

The magnitude of mental health consequences of CM and the subsequent public health burden cannot be underestimated. One in four children experience CM (Stoltenborgh et al., 2015) and the aggregate lifetime economic cost incurred by CM survivors is an estimated $124 billion (Peterson et al., 2018). Further, psychopathology is set to become the leading burden of disease by the year 2030 (WHO, 2012), with trillions of dollars in economic loss. Given that CM and its sequelae are preventable, it is imperative that the field continues to augment the knowledge base regarding the etiology and sequelae of CM-related psychopathology to inform policy and prevention.

There is emerging evidence that CM confers non-specific risk for diverse forms of psychopathology (Cicchetti & Toth, 2016; McLaughlin et al., 2020), supporting the developmental psychopathology proposition of multifinality, defined as diversity in outcomes following the same risk (Cicchetti & Rogosch, 1996). However, CM is a multifaceted construct (English et al., 2005; Jackson et al., 2019; Manly, 2005), and it is still unclear if different dimensions of CM contribute to unique patterns of psychopathology. Specifically, it is unknown whether the development of psychopathology is non-specifically attributable to global categorizations of CM (i.e., presence vs absence), or if specific maltreatment dimensions (e.g., type, timing, chronicity) are more likely to shape risk for specific or diverse forms of psychopathology. Answers to these questions remain elusive, possibly resulting in an obfuscated or oversimplified understanding of the psychopathology sequela of CM (Jackson et al., 2019). Investigations that examine the differential impact of CM parameters have the potential to enlighten the field and advance intervention efforts. As such, the purpose of this study was to evaluate how the timing and chronicity of CM exposure differentially influence the development of psychopathology.

Maltreatment Dimensions

Dimensions of maltreatment include the type of exposure (i.e., sexual abuse, physical abuse, neglect, and emotional abuse), timing (i.e., age of onset or recency of maltreatment), severity, and chronicity. Additionally, much of the literature examining CM and psychopathology outcomes have modeled CM dichotomously (i.e., presence vs. absence of CM). However, there is no general consensus on which CM dimensions are most important in predicting adverse mental health outcomes and it is plausible that various parameters may have differing influences on the development of psychopathology. To date, CM subtypes have been the most commonly-studied dimension (Jackson et al., 2019). Although subtypes may be differentially associated with psychopathology symptoms (Cecil et al., 2017), multi-type exposure is frequently the norm (Vachon et al., 2015), and unique subtype effects are often found to be secondary to a linear association between the number of subtypes experienced and symptomatology (Cecil et al., 2017). In the presence of multi-type exposure (a pattern of maltreatment experiences shown to be common in CPS-recruited samples, including the present sample; Warmingham et al., 2019), other maltreatment parameters beyond presence versus absence (e.g., chronicity) may offer unique insights into the development of psychopathology. To this end, the present study focused on the effects of two of the least-commonly studied CM parameters, chronicity and timing (Jackson et al., 2019), on psychopathology outcomes. Investigation of these parameters and their effect on mental health functioning is important given that early onset CM and chronic CM are common patterns of exposure (Kim & Drake, 2019) and often portend the poorest mental health outcomes (Jaffee & Maikovich-Fong, 2011).

Chronicity.

CM chronicity is a complex construct itself and can be defined in several ways (English et al., 2005). Developmental definitions of chronicity attend to the number of developmental epochs in which CM occurred (Manly, 2005). This definition has been shown to be theoretically and conceptually sound, optimally sensitive to variation in outcomes, and may better account for how CM derails or undermines development (English et al., 2005). Exposure to CM over several developmental stages can interrupt the successful resolution of stage-salient developmental tasks relevant to psychopathology (e.g., attainment of a secure attachment and development of self-regulatory capacities). The compounded thwarting of adaptive development across domains throughout childhood may markedly increase risk for the development of psychopathology (Cicchetti & Toth, 2016).

A review of studies using a developmental definition of chronicity demonstrates that, compared to nonmaltreated children, children who experienced chronic CM exhibit increased externalizing problems (English et al., 2005; Graham et al. 2010; Jaffee & Maikovich-Fong, 2011), internalizing symptoms (Warmingham et al., 2019; Ziobrowski, et al 2020), and an array of negative outcomes closely associated with the onset and maintenance of psychopathology symptoms, including poor inhibitory control (Cowell et al., 2015), cognitive deficits (Jaffee & Maikovich-Fong, 2011), emotion dysregulation (Warmingham et al., 2019), and peer difficulties (Graham et al., 2010). Importantly, chronic CM also results in more psychopathology symptoms than episodic CM (e.g., Jaffee & Maikovich-Fong, 2011; Manly et al., 2001), suggesting that children who experienced chronic CM evidence more problematic outcomes compared with those children who experienced episodic maltreatment.

Timing.

Consideration of the developmental timing of CM may also be critical to uncovering distinct pathways to the development of various forms of psychopathology (Manly, 2005). There is equivocal evidence regarding which developmental period is most sensitive to psychopathology-related effects of CM, and it is likely that CM experienced during unique developmental periods, or unique combinations of periods, may differentially affect the development of different forms of psychopathology (Dunn et al., 2018). Exposure in early childhood is associated with mechanisms relevant to mental health difficulties, such as childhood emotion dysregulation (Kim & Cicchetti, 2010), impulsivity, working memory (Cowell et al., 2015), and neuroendocrine dysregulation (Cicchetti et al., 2010). Early CM also predicts internalizing and externalizing symptoms in childhood (Keiley et al., 2001; Thompson & Tabone, 2010) and adulthood (Capretto, 2020; Dunn et al., 2017; Kaplow & Widom, 2007). Alternatively, CM occurring in later childhood or adolescence can be impactful, especially in regard to externalizing symptoms (Dunn et al., 2018; Thornberry et al., 2001). Still, others have found that it is a patterning of CM that is sustained across both early and later developmental stages that tends to have the greatest impact on mental health (English et al., 2005; Jaffee & Maikovich-Fong, 2011; Kaplow & Widom, 2007; Manly et al., 2001; Thornberry et al., 2010; Ziobrowski et al., 2020).

The developmental psychopathology perspective can explain why CM experienced at different times in development may lead to different psychopathology pathways and outcomes. Early CM may inhibit the successful resolution of early developmental tasks (e.g., tasks related to attachment associations and emotion regulation), which in turn prevents children from acquiring the skills needed for developmental gains in subsequent stages. Children from birth to age six may be particularly vulnerable to CM because it can interfere with sensitive windows of development, compromising salubrious brain architecture integral for social and emotional development (Teicher & Samson, 2016). On the other hand, those who experience CM for the first time in late childhood or adolescence may likely have acquired a foundation of consolidated skills that enables them to have more resilient outcomes (Cicchetti & Rizley, 1981). Conversely, it is also possible that CM occurring in later childhood may be more detrimental because these individuals have more advanced cognitive capacities that affect their conceptualization and understanding of their adversities, which can proximally influence psychological processes, behaviors, and distress (Newbury et al., 2018).

Advancing the Literature

Addressing the role of CM chronicity and timing has the potential to advance the field’s understanding of how specific aspects of maltreatment confer risk for diverse psychopathology outcomes. A developmental definition of chronicity is inextricably connected to the timing of CM. Children who experience CM in early development are also more likely to experience subsequent, chronic exposure, as early onset exposure is a predictor of recurrence in the next developmental period (Kim & Drake, 2019). As such, it can be difficult to disentangle whether it is the timing of CM, or if it is the association with some other characteristic of the CM, such as chronicity, that relates to specificity of psychopathology outcomes. For example, is early-onset CM predictive of specific mental health outcomes regardless of whether the exposure is contained within early development or persists into later childhood? Are specific psychiatric disorders more dependent on the recency of CM (i.e., the proximal context) than on the chronicity or distal exposures? There is evidence that the effects of chronic CM on mental health outcomes may be dependent on the child’s age at the time of abuse (Jaffee & Maikovich-Fong, 2011; Manly et al., 2001). However, research rarely considers the effects of both the developmental timing and the chronicity of CM in relation to psychopathology outcomes (Jackson et al., 2019). Nuanced investigations involving CM timing and chronicity are needed to determine whether various psychopathology outcomes and pathways are differentially influenced by CM that is restricted to early or later childhood, as opposed to CM that spans both early and later childhood in a more persistent, chronic pattern.

Thus far, a relatively small number of studies have examined both CM timing and chronicity as risk factors for the development of psychopathology outcomes (i.e., internalizing and externalizing domains). Collectively, these studies offer strong evidence that timing and chronicity are both important in predicting broad psychopathology outcomes (Capretto, 2020; Cicchetti et al., 2015; English et al., 2005; Jaffee & Maikovich-Fong, 2011; Kaplow & Widom, 2007; Kim & Cicchetti, 2010; Manly et al., 2001; Thornberry et al., 2010; Ziobrowski et al., 2020). However, these studies have at least one of the following limitations. First, many studies investigating the effect of timing or chronicity of CM on psychopathology have relied on self-reported CM. Although self-reported CM has utility in many contexts, it is limited by recall bias, mood effects, inaccuracy establishing the developmental timing of CM, and minimization of early exposures in infancy/toddlerhood (Widom, 2014). Second, some studies depend on a single informant for the assessment of psychopathology symptoms, limiting the breadth of knowledge about symptom presentation. Third, most studies lack a demographically-comparable, nonmaltreated control sample to draw comparisons. This is problematic because CM, especially early and chronic forms, occurs at higher levels within low-income and disadvantaged contexts (USDHHS, 2020) and exposure to poverty is associated with psychopathology (Peverill et al., 2020). Finally, studies examining CM timing and chronicity have typically focused on childhood or adolescent mental health outcomes. Extending the study of the effect of CM dimensions on psychopathology into emerging adulthood, a developmental period when psychopathology symptoms often emerge and tend to peak, is critical (Schulenberg & Zarrett, 2006). We are aware of only two studies that have prospectively examined the effects of both CM chronicity and timing on multiple mental health outcomes in adulthood (Kaplow & Widom, 2007; Thornberry et al., 2010). These longitudinal projects only examined the effect of chronicity and timing on outcomes at one timepoint (i.e., adulthood) and did not examine developmental pathways.

Additionally, the diverse psychopathology sequela of CM is known to unfold over time and not simply emerge with the onset of adulthood. Symptoms observed in childhood may be risk factors or early precursors of emergent disorder (Cicchetti & Toth, 2016). Thus, empirical investigations of CM chronicity and timing in the pathway to psychopathology outcomes in both childhood and adulthood are needed. Such investigations will contribute to our understanding of the persisting influence of CM on the course of psychopathology symptoms, and will further detail the existence of experience-driven differences in psychopathology outcomes. Such work can elucidate whether chronicity- or timing-specific risk for psychopathology begins in childhood and persists into adulthood and illuminate potentially distinct developmental patterns of symptom continuity and discontinuity (Rutter et al., 2006). This type of investigation is not only informative in examining the distal or proximal impacts of CM chronicity and timing, but also how those experiences initiate developmental pathways that may be sustained and maintained into later adulthood, via earlier symptoms.

Finally, people of color have been historically underrepresented in developmental psychology studies, including the extant literature on the psychopathology sequelae of CM. Yet, youth of color are disproportionately involved in the child welfare system (Hampton-Anderson et al., 2021), more likely to experience the negative mental health sequelae of CM (Metzger et al., 2021), and are consistently overrepresented among the economically-disadvantaged (Bullock, 2019). It is broadly agreed that the disproportionate rates of these adversities and the associated mental health inequities observed in historically marginalized populations reflects exposure to racism and race-related stressors (e.g., discrimination, historical trauma, systemic oppression; Metzger et al., 2021; Trent et al., 2019; Williams, 2018). Research suggests that, among populations of color, CM is similarly related to higher rates of internalizing and externalizing psychopathology (see Hampton-Anderson et al., 2021 for review), including depression (Crow et al., 2014), anxiety (Cross et al., 2015), substance use and ASPD symptoms (Kaslow & Thompson, 2008). However, it is critical to examine whether the timing and chronicity of CM predicts the development of psychopathology within racially and ethnically diverse samples to ensure findings are not overgeneralized from primarily middle class, white samples.

Present Study

The present investigation addresses the aforementioned gaps with a prospective, multi-informant, longitudinal design that traces the effect of documented CM on diverse psychopathology outcomes from childhood (ages 10-12) to emerging adulthood (ages 18-21) in an economically-disadvantaged sample that includes maltreated and demographically-matched nonmaltreated individuals. A primary objective was to evaluate the extent to which CM chronicity (i.e., number of developmental periods in which maltreatment occurred) and timing (i.e., age of onset and recency of exposure) predicted different forms of psychopathology in childhood and emerging adulthood, with a focus on developmental progression of internalizing and externalizing disorder symptoms from childhood to emerging adulthood. We expected that children exposed to chronic CM would exhibit both internalizing and externalizing psychopathology and diverse psychopathology presentations in emerging adulthood (symptoms of anxiety, depressive, substance use, and antisocial personality disorders). Given the mixed findings on CM timing and psychopathology, we had few a priori expectations about timing effects on specific psychopathology outcomes. To determine the unique influence of various maltreatment parameters on the development of psychopathology, we conducted three distinct models with different conceptualizations of maltreatment: 1) global classification (i.e., exposure vs. no exposure); 2) chronicity (i.e., number of developmental periods in which maltreatment occurred); and 3) developmental timing of maltreatment.

Methods

Participants

Participants (N = 391) were from a longitudinal follow-up study of emerging adults who participated in a research summer camp program as children. The original study (wave 1 [W1]) included 659 low-income maltreated (n = 339) and nonmaltreated (n = 320) children aged 10 to 12. The original sample was racially and ethnically diverse (71.6% Black, 11.8% White, 12.6% Hispanic, 4.0% biracial/other race) and evenly distributed by gender (50.1% male). The majority of children were from single parent families (68.7%) with a history of receiving public assistance (96.1%). At wave 2 (W2), participants were recontacted during emerging adulthood. Emerging adults were on average 19.66 years old (SD = 1.13), 51.3% female, 51.8% maltreated, and identified as Black (77.5%), White (11.3%), other race (3.8%), and Hispanic (7.4%). The current study included 391 participants who completed both waves of data collection. W2 participants did not significantly differ from W1 participants on maltreatment status (χ² (1) = .50, p = .48), income (t (678) = 1.23, p = .21), sex (χ² (1) = .60, p = .44), race (χ² (3) = 1.87, p = .17), or childhood internalizing (t (674) = 1.26, p = .21) and externalizing (t (674) = .43, p = .67) symptoms.

Procedures

W1 participants were recruited for a summer research camp from 2004-2007. Children in the maltreated group had substantiated investigations of child maltreatment according to Department of Human Services (DHS) Child Protective Services (CPS) records. Children without CPS involvement were recruited from families receiving Temporary Assistance to Needy Families (TANF) to ascertain a sociodemographically-comparable sample of children without maltreatment experiences. A DHS liaison identified eligible families and contacted a random sample from both groups via mail. Participation was voluntary. If families elected to participate, their contact information was shared with research staff. The demographics of families who declined participation were not disclosed by DHS.

Parents who chose to enroll their children in the research summer camp provided signed consent to study procedures. During the week of summer camp, camp counselors facilitated recreational activities with the same groups of 8-10 children (35 hours of direct contact and observation). Children also provided assent to study procedures. Children self-reported on their functioning and camp counselors provided independent ratings of childhood functioning after the end of the week. Maltreatment status was unknown to camp counselors. For a more detailed description of the summer research camp procedures, see Cicchetti and Manly (1990).

At W2 (~eight years after W1), a variety of strategies were used to relocate and recruit W1 participants for a follow-up study during emerging adulthood. Records of last known addresses, extensive public internet searches (e.g., LexisNexis), contact information from medical records, and neighborhood canvasing were part of a comprehensive recruitment design. Interested participants completed signed consents and then participated in three research visits.

Measures

Childhood measures (W1)

Childhood maltreatment.

The Maltreatment Classification System (MCS; Barnett et al., 1993) was used to code CPS records from birth until age 12. MCS reliable coders scored records based on the MCS and determined presence of subtypes for each child in the sample (average intraclass correlations [ICCs] between pairs of coders ranged from .86 to 1.0). The MCS identifies four different types of maltreatment (sexual abuse, physical abuse, emotional maltreatment, and neglect). Neglect ratings included lack of supervision, failure to provide, educational neglect, and moral/legal neglect. Developmental timing of each exposure was coded for the following periods: infancy (birth-17 months), toddlerhood (18 months-2 years), preschool age (3-5 years), early school age (6-7 years), and later school age (8-12 years). To derive a developmentally-informed index of chronicity, we totaled the number of developmental periods in which maltreatment was known to have occurred, spanning the five aforementioned periods. Among maltreated children (n = 202), 111 (55%) were exposed in one developmental period, 49 (24.3%) in two periods, 28 (13.9%) in three periods, 11 (5.4%) in four periods, and three (1.5%) in five periods.

All children were also classified into four groups based on the timing of their maltreatment experiences. Children without maltreatment histories were classified as “nonmaltreated” (n= 189; 48.3%). Children who experienced maltreatment in infancy, toddlerhood or preschool periods (i.e., ages 0-5), but not since then, were classified as “early, not recently maltreated” (n = 25; 6.4%). Children who experienced maltreatment in infancy, toddlerhood, or preschool periods and since then (early and/or later school age) were classified as “early and recently maltreated” (n = 102; 26.1%). Children whose first maltreatment experience occurred during early or later school-age (ages 6-12) were classified as “recent onset maltreated” (n = 75; 19.2%).

We also compared information about chronicity and onset/recency to determine the extent of maltreatment experienced within each of the four timing groups. Among children exposed to maltreatment in more than one developmental period (N = 91), 3.3% were in the “early, not recent” group, 17.6% in “late onset,” and 79.1% in “early and recent.” All children who experienced maltreatment in three or more developmental periods (N = 42) were in the “early and recent” group. Individuals experiencing chronic child maltreatment (3+) were likely to be exposed in early and later childhood years, indicating both distal and proximal risk.

Teacher Report Form (TRF) of the Child Behavior Checklist.

(CBCL; Achenbach, 1991). The TRF/CBCL is a 113-item measure widely used to assess emotional and behavioral symptoms in children. Two counselors rated children in their group after the 35-hour week of direct observation and interaction. Each item was rated on a 0-2 scale (0 = not true, 1 = somewhat true, or 2 = very true or often true) and scores were averaged across two raters. The Internalizing (α = .70) and Externalizing (α = .76) subscale T-scores were used as indicators of internalizing and externalizing symptoms (higher scores represented more severe symptoms). The average intraclass correlation between raters for these scales indicated adequate reliability (Externalizing = .83; Internalizing = .79).

Child Depression Inventory

(CDI; Kovacs, 1982). The CDI is a widely used, reliable, and well-validated 27-item self-report questionnaire to assess depressive symptomatology in school-age children (Saylor et al., 1984). Children chose from three options (scored 0 to 2) for each item in order characterize their experiences and symptoms in the past two weeks, with higher scores representing more depressive symptomology. The 27-items were summed and used as an indicator of childhood internalizing symptoms (α = .85) and higher scores represented more severe symptoms.

Revised Children’s Manifest Anxiety Scale

(RCMAS; Reynolds & Richmond, 1997). The RCMAS is a 37-item self-report measure completed by children to assess symptoms of anxiety. Children responded “yes” or “no” to each item to indicate presence of each anxiety symptom. The RCMAS is a well-validated measure with good psychometric properties in samples of school-aged children (Muris et al., 2002; Reynolds & Richmond, 1997). A sum score was computed into a T-score (α = .84) and used as an indicator of childhood internalizing symptoms (higher scores represented more severe symptoms).

Pittsburgh Youth Survey

(PYS; Loeber et al., 1998). The PYS is a self-report measure of conduct behaviors in childhood. Children self-reported six-month prevalence of 25 behaviors (e.g., stealing, damaging property). This scale has strong evidence of convergent and predictive validity related to records of delinquency (Farrington et al., 1996). A count was computed for all endorsed items and used as an indicator of childhood externalizing symptoms.

Emerging adult measures (W2)

Diagnostic Interview Schedule for DSM-IV

(DIS-IV; Robins et al., 1995). The DIS-IV is a structured clinical interview administered in person with the help of a computer system to provide clinical psychiatric diagnoses and symptom counts based on DSM-IV criteria (APA, 1994). In the current study, modules of the DIS-IV were conducted with participants in a private room by administrators trained on this measure. Diagnostic symptom counts for each of the following DSM-IV disorders were used in the current study: Antisocial Personality Disorder (ASPD), Substance Dependence (Alcohol and Marijuana), Generalized Anxiety Disorder (GAD), Post-Traumatic Stress Disorder (PTSD), and Major Depressive Disorder (MDD).

Beck Depression Inventory-II

(BDI-II; Beck et al., 1996). The BDI-II is a widely-used 21-item measure that assesses depressive symptoms in the last two weeks. Participants rated their recent experiences by choosing one of four statements pertaining to different symptoms of depression (e.g., sadness, self-criticism). Items were scored from 0 to 3, and higher scores represented more severe symptoms. A sum score of the 21-items was computed (α = .88).

Adult Self-Report

(ASR; Achenbach, 1991). The ASR is a 123-item self-report scale that includes items relating to emotional and behavioral functioning. For each item, emerging adult participants rated themselves on a scale of 0 = not true, 1 = somewhat or sometimes true, or 2 = very true or often true. T-scores for ASPD (α = .80), Anxiety (α = .75), and Depression (α = .82) were used in the current study (higher scores represented more severe symptoms).

Data Analytic Plan

Descriptive data analyses were performed using SPSS 25 (see Table 1). To investigate the longitudinal relations between maltreatment, childhood internalizing and externalizing symptoms, and symptoms of anxiety, depression, substance dependence and antisocial personality disorders in emerging adulthood, we conducted structural equation modeling (SEM) with a maximum likelihood estimation method, using Mplus Version 8.3 (Muthén & Muthén, 2019). First, confirmatory factor analysis (CFA) was used to determine the factor structure of the six latent factors of psychopathology: Two using W1 data, including childhood internalizing (indicators: CDI sum score, RCMAS total anxiety score, TRF internalizing T-score) and childhood externalizing (indicators: PYS conduct problems, TRF externalizing T-score); and four using W2 data: Antisocial Personality Disorder (indicators: ASR ASPD subscale T-score, number of DIS-IV ASPD symptoms); Substance Use Disorders (SUDs; indicators: number of DIS-IV marijuana dependence symptoms and alcohol dependence symptoms); Anxiety (indicators: ASR Anxiety subscale T-score, number of DIS-IV Generalized Anxiety Disorder symptoms, number of DIS-IV PTSD symptoms); and Depression (indicators: ASR Depression subscale T-score, BDI-II sum score, number of DIS-IV Major Depressive Disorder symptoms).

Table 1.

Correlation Analysis and Descriptive Statistics of Study Variables.

	1	2	3	4	5	6	7	8	9	10	11	12	13	14	15	16
1. Maltreatment Chron.	-
2. W1 TRF Internalizing	.06	-
3. W1 CDI	.14**	.19***	-
4. W1 Anxiety	.10	.11*	.64***	-
5. W1 TRF Externalizing	.18**	.23***	.10	.10	-
6. W1 CONDQ	.14**	−.03	.27***	.22***	.27***	-
7. W2 BDI	.10*	.07	.27***	.22***	.11*	.07	-
8. W2 ASR Depression	.11*	.11*	.24***	.25***	.04	.03	.65***	-
9. W2 DIS Depression	.03	.03	.14**	.17**	.05	.05	.30***	.35***	-
10. W2 ASR Anxiety	.07	.05	.26***	.21***	.01	.07	.48***	.61***	.26***	-
11. W2 DIS GAD	.09	−.04	.11*	.09	−.03	−.001	.27***	.30***	.20***	.27***	-
12. W2 DIS PTSD	.10*	−.01	.14**	.20***	.06	.11*	.34***	.29***	.33***	.27***	.23***	-
13. W2 ASR ASPD	.16**	.06	.26***	.22***	.18**	.14**	.46***	.53***	.24***	.38***	.19***	.14**	-
14. W2 DIS ASPD	.08	−.09	.15**	.13*	.16**	.24***	.28***	.25***	.21***	.24***	.12*	.17**	.53***	-
15. W2 DIS Alc Dep	.14**	−.04	.11*	.16**	.04	.17**	.20***	.20***	.24***	.14**	.15**	.12*	.31***	.45***	-
16. W2 DIS Mar Dep	.03	−.04	.09	.14**	.08	.15**	.06	.06	.16**	.14***	.03	.10	.27***	.50***	.28***	-
Mean	.90	47.47	7.99	46.45	52.14	4.77	12.25	55.79	2.15	56.38	.33	2.98	57.93	2.73	.71	.95
Percent (%)a,b		10.2%b	15.4%b	9.8%b	20.7%b		19.9%b	12.7%b	22.5%a	10.9%b	3.9%a	11.2%a	20.2%b	28.83%a	5.20%a	7.03%a
SD	1.12	8.29	6.85	10.35	8.81	4.34	8.61	6.93	3.16	6.50	1.22	4.95	7.73	2.12	1.22	1.36

Note. W1 = Wave 1, W2 = Wave 2, TRF = Teacher Report Form, CDI = Children’s Depression Inventory, CONDQ = Conduct Disorder Questionnaire, BDI = Beck Depression Inventory, ASR = Adult Self Report, DIS = Diagnostic Interview Schedule, GAD = Generalized anxiety disorder, PTSD = Post-traumatic stress disorder, ASPD = Antisocial personality disorder, Alc Dep = Alcohol dependence symptoms, Mar Dep = Marijuana dependence symptoms.

^aFor diagnostic variables, we show the percentage of participants who met criteria for the disorder.

^bFor variables with defined clinical thresholds, we show the percentage of participants with scores in the subclinical-clinical range.

^*p < .05

^**p < .01

^***p < .001.

Three SEMs were estimated each examining a unique conceptualization of maltreatment: In Model 1, CM was operationalized as a binary variable (yes/no) (See Figure 1a); In Model 2, chronicity of CM was operationalized as the number of developmental periods in which maltreatment occurred (See Figure 1b); and in Model 3, developmental timing of maltreatment was operationalized with three dummy coded variables representing the four categories: [a] early, not recent maltreated, [b] early and recent maltreated, [c] late onset maltreated, [reference] nonmaltreated; (See Figure 1c). The three models are differentiated by the exogenous maltreatment variable(s). Structural paths within the models remained the same.

Figure 1.

Structural equation model testing childhood externalizing and internalizing as mediators between chronic child maltreatment and emerging adult psychopathology (N = 391). The following were estimated, but not modeled to improve visual clarity: residual covariances between childhood latent factors and between all four adult latent factors; residual covariance between TRF-Ext and TRF-Intx indicators; residual covariance between marijuana dependence and ASPD symptom indicators Note. *p < .06, **p < .01, ***p < .001.

The amount of missing data from study variables was minimal, ranging from 5% (PYS) to < 1% (all remaining variables). Full information maximum likelihood estimation (FIML; Muthén & Muthén, 2019) was used to obtain parameter estimates for all 391 participants. Model fit for the CFA and SEM were determined using the following guidelines of McDonald and Ho (2002). RMediation (Tofigihi & MacKinnon, 2011) was used to produce 95% asymmetric confidence intervals (CI) and test the significance of indirect effects (intervals not including zero indicated significance at α=.05).

Results

Measurement Model

Modification indices from the initial CFA model indicated that correlating the residuals of the two counselor-reported indicators in childhood (TRF internalizing and TRF externalizing) would improve model fit and these modifications were incorporated. The measurement model exhibited satisfactory fit to the data, CFI = .93, RMSEA = .06 (.05 - .07), SRMR = .05. All factor loadings were statistically significant (p < .001). Residuals of all latent variables were significantly associated (p < .01) with the exception of W1 externalizing and W2 depression, β= .09, SE = .08, p = .27, and W1 externalizing and W2 anxiety, β = . 14, SE = .09, p = .11.

Binary Child Maltreatment and Psychopathology (Model 1)

See Figure 1a. The structural equation model (SEM) evidenced satisfactory fit to the data, CFI = .94, RMSEA = .05 (95% CI [.04, .06]), SRMR = .04. A binary variable representing child maltreatment presence/absence was associated with greater externalizing at W1, β = .33, SE = .07, p < .001, and marginally associated with greater internalizing at W1, β = .10, SE = .06, p = .09. In turn, internalizing psychopathology at W1 was associated with W2 outcomes including greater symptoms of depression, β = .39, SE = .07, p < .001, anxiety, β = .42, SE = .09, p < .001, and antisocial personality disorder, β = .19, SE = .08, p < .05. Externalizing at W1 predicted W2 antisocial personality disorder, β = .32, SE = .12, p < .01, and substance dependence, β = .34, SE = .14, p < .05. There were no statistically significant direct associations between child maltreatment and W2 psychopathology. Our model also estimated residual correlations between all endogenous variables.

Child Maltreatment Chronicity and Psychopathology (Model 2)

See Figure 1b. The structural equation model (SEM) evidenced satisfactory fit to the data, CFI = .94, RMSEA = .05 (95% CI [.04, .06]), SRMR = .04. Chronic child maltreatment significantly predicted higher levels of W1 internalizing, β = .16, SE = .06, p < .01, and W1 externalizing, β = .26, SE = .08, p < .001. Chronic child maltreatment was not directly associated with any W2 latent factors, controlling for W1 symptoms. Higher levels of child internalizing symptoms predicted higher levels of W2 depression, β = .37, SE = .01, p < .001, W2 anxiety, β = .41, SE = .09, p < .001, and W2 antisocial personality disorder, β = .19, SE = .08, p < .05. Additionally, higher levels of childhood externalizing significantly predicted higher levels of W2 antisocial personality disorder, β = .29, SE = .11, p < .01, and W2 substance dependence disorder, β = .32, SE = .13, p < .05. Correlated residuals were estimated for all endogenous variables, and the associations between correlated residuals were consistent in magnitude to results from Model 1.

Child Maltreatment Timing and Psychopathology

See Figure 1c. The structural equation model (SEM) evidenced satisfactory fit to the data, CFI = .94, RMSEA = .05 (95% CI [.04, .06]), SRMR = .04. At W1, children who experienced early childhood maltreatment and also recent maltreatment had elevated levels of W1 internalizing psychopathology, β = .15, SE = .06, p < .05, and externalizing psychopathology, β = .21, SE = .08, p < .001. Additionally, having only recent experiences of maltreatment were associated with higher levels of W1 externalizing psychopathology, β = .35, SE = .08, p < .001. Early CM only (vs. no CM) was not associated with internalizing psychopathology, and marginally associated with externalizing psychopathology at W1, β = .14, SE = .08, p = .07. Higher levels of child internalizing symptoms predicted higher levels of W2 depression, β = .39, SE = .08, p < .001, W2 anxiety, β = .43, SE = .09, p < .001, and W2 antisocial personality disorder, β = .20, SE = .08, p < .05. Additionally, higher levels of W1 externalizing significantly predicted higher levels of W2 antisocial personality disorder, β = .29, SE = .12, p < .01, and W2 substance dependence disorder, β = .34, SE = .14, p < .05.

Tests of Indirect Effects

See Table 2 for a summary of indirect effects evaluated in Models 2 and 3. Using the distribution of the product of coefficients method and 95% asymmetric confidence intervals (RMediation; Tofigihi & MacKinnon, 2011), we found that internalizing and externalizing at W1 significantly mediated several pathways in the model. Specifically, in Model 2, W1 internalizing mediated the association between chronic child maltreatment and adult symptoms of depression, anxiety, and antisocial personality disorders. Additionally, W1 externalizing mediated the association between chronic child maltreatment and adult symptoms of substance dependence and antisocial personality disorders. In Model 3 using childhood maltreatment onset and recency groups, externalizing symptoms in childhood mediated the effect of later maltreatment onset (compared to no maltreatment) on adult antisocial personality disorder symptoms and substance use disorder symptoms. Childhood externalizing symptoms also mediated the effect of early and recent maltreatment (vs. no maltreatment) on adulthood antisocial personality disorder symptoms. Childhood internalizing symptoms were a mechanism explaining the link between early and recent maltreatment exposure (vs no maltreatment) and multiple adulthood symptoms presentations, including antisocial personality disorder symptoms, depression, and anxiety.

Table 2.

Indirect Effects

Chronic Maltx Model	α*β	SE	95% CI
MalChron → Ext → ASPD	0.43	0.23	[0.063, 0.953]
MalChron → Ext → SUD	0.04	0.03	[0.002, 0.10]
MalChron → Ext → Anxiety	−0.05	0.13	[−0.33, 0.20]
MalChron → Ext → Depression	−0.13	0.16	[−0.50, 0.17]
MalChron → Int → ASPD	0.17	0.10	[0.013, 0.39]
MalChron → Int → SUD	0.01	0.01	[−0.007, 0.035]
MalChron → Int → Anxiety	0.27	0.12	[0.071, 0.52]
MalChron → Int → Depression	0.35	0.15	[0.093, 0.67]
Onset/Recency Model	α*β	SE	95% CI
RecentMal → Ext → ASPD	1.53	0.79	[0.24, 3.294]
RecentMal → Ext → SUD	0.17	0.096	[0.013, 0.38]
Early/RecentMal → Ext → SUD	0.094	0.062	[0, 0.24]
Early/RecentMal → Int → SUD	0.027	0.027	[−0.017, 0.088]
Early/RecentMal → Ext → ASPD	0.84	0.53	[0.033, 2.05]
Early/RecentMal → Int → ASPD	0.40	0.25	[0.013, 0.98]
Early/RecentMal → Int → Depression	0.87	0.42	[0.16, 1.78]
Early/RecentMal → Int → Anxiety	0.62	0.30	[0.11, 1.30]

Note: RMediation was used to compute indirect effect estimates with asymmetric 95% confidence intervals. Bolded paths indicate significance at α=.05. Note for the Onset/Recency model, indirect effects were tested if a and b paths were significant. MalChron = # developmental periods with exposure to maltreatment, RecentMal = recent onset maltreatment only; Early/Recent Mal = early and recent Maltreatment; Int = W1 internalizing, Ext = W1 externalizing, ASPD = W2 antisocial personality disorder, SUD = substance use disorder.

Discussion

The current study advances knowledge on the ways in which various dimensions of CM exposures affect differential psychopathology outcomes in childhood and emerging adulthood. Our analyses reveal that, although comparing the effect of maltreatment exposure vs no exposure identified pathways of greater externalizing symptoms in childhood and symptoms of multiple externalizing disorders (i.e., ASPD and substance dependence) in emerging adulthood, more precise information on the developmental timing and chronicity of CM exposure illuminated critical nuances in these developmental outcomes. Only CM experiences that spanned several developmental periods, including both early and later childhood stages, predicted a cascade of both internalizing and externalizing symptoms in childhood that eventuated in greater anxiety, depression, substance dependence, and ASP disorder symptoms in emerging adulthood. We found that this type of exposure resulted in developmental pathways of homotypic (within-disorder) and heterotypic (between-disorder) symptom continuity. In contrast, maltreatment exposures that were limited to later childhood stages (i.e., school age) predicted pathways to greater childhood externalizing symptoms and ASPD and substance dependence symptoms in emerging adulthood. Finally, CM limited to early childhood (ages 0-5; vs no maltreatment) did not significantly predict greater psychopathology symptoms in childhood or adulthood.

Maltreatment Chronicity and Timing

A primary objective of the investigation was to determine if various dimensions of child maltreatment differentially affect psychopathology presentations in childhood and emerging adulthood. This basic aim was achieved, as our results demonstrate that a global classification of CM (presence vs. absence) was less sensitive to the diversity of psychopathology pathways present in the data (i.e., only predicting externalizing disorder symptoms); whereas classifications that incorporated developmental information on timing and chronicity revealed greater diversity in predicted outcome pathways (i.e., externalizing and internalizing pathways of homotypic and heterotypic symptom continuity). Specifically, more chronic CM predicted both greater internalizing and externalizing childhood symptoms, as well as indirect pathways that resulted in greater anxiety, depression, substance dependence and ASP disorder symptoms in adulthood. This is consistent with previous evidence that chronic CM predicts negative child and adult outcomes across a range of mental health domains (English et al., 2005; Jaffee & Maikovich-Fong, 2011; Jonson-Reid et al., 2012).

Taking the developmental timing (i.e., onset and recency) of the CM exposure into account yielded additional insight and information beyond the established finding that chronic CM potentiated worse mental health outcomes. Children who experienced maltreatment limited to early development (birth to age 5) did not evince patterns of greater internalizing or externalizing symptoms in childhood or emerging adulthood, compared to nonmaltreated peers. This finding is inconsistent with some studies (e.g., Dunn et al., 2013; Manly et al., 2001) and consistent with others (Kaplow & Widom, 2007; Thornberry et al., 2010). There are several possible explanations for this finding. When CM exposure is truly limited to early development, children may have a chance to rebound through self-righting tendencies that redirect developmental trajectories towards healthy outcomes, especially when early intervention occurs. Alternatively, only a minority of children in our sample experienced early CM without later maltreatment (12% of the maltreated sample), complicating our ability to isolate the effects of early exposure due to power limitations. This suggests those exposed to CM early in life are more likely to be exposed later, and studies focusing on developmental timing effects without attending to chronicity may be misconstruing timing effects with what are chronicity effects. Finally, it is possible that the influence of early childhood-limited maltreatment on psychopathology outcomes is moderated by the type of maltreatment exposure or by other factors, such as genetic variation (e.g., Handley et al., 2019). Future studies should investigate this finding in more detail.

Alternatively, school-aged only CM exposure was related to greater risk for externalizing symptoms in childhood, which in turn predicted greater ASPD and substance dependence disorder symptoms in emerging adulthood. This finding is in accordance with other studies that have evidenced how maltreatment that begins when children are school-aged has a pronounced effect on subsequent externalizing symptoms, but not internalizing symptoms, in childhood (Kim & Cicchetti, 2010), adolescence (Thornberry et al., 2001), and adulthood (Kaplow & Widom, 2007; Thornberry et al., 2010). Our results bring together these lines of research and further demonstrate how late-onset CM predicts developmental pathways of externalizing symptoms that are identifiable in childhood and persist into emerging adulthood. Although children who are not exposed to CM in the early years may have a greater probability of establishing a strong developmental foundation that could buffer against some of the harmful sequalae of later CM, they are not fully inoculated from the detrimental effects. It may be that the recent CM exposures are reverberating in the child and their distress and frustration with the more recent/current circumstances they cannot escape becomes outwardly expressed as misconduct and aggressive or oppositional behaviors (Agnew, 1992). This may also be related to the proximity of the outcome assessment and the CM timing. Further, by virtue of their age, these children may simply be developmentally poised to exhibit greater behavioral expressions of their distress after CM exposure (Thornberry et al., 2010).

Our results also highlight that children who experienced both early onset CM and recent CM are at distinct risk for developmental progressions of both internalizing and externalizing symptoms. This finding attests to the pervasive impact of CM that is distributed across early and later childhood stages in potentiating transdiagnostic risk for adverse mental health outcomes. Findings are also consistent with other studies evidencing that CM spanning early and later development is more sensitive to internalizing outcomes (Cicchetti et al., 2015; English et al., 2005; Manly et al., 2001). The nuanced timing and chronicity distinctions in our findings align with an organizational perspective on child development and suggest that CM derails optimal development and potentiates multiple forms of psychopathology that persist into emerging adulthood (Sroufe & Rutter, 1984). When maltreatment experiences are episodic or isolated to early development, individuals are provided with respite and the opportunity to recover from detrimental effects or course-correct developmental trajectories and evade heightened symptomatology (Cicchetti & Rizley, 1981). However, if CM is unremitting and persists across early and later developmental periods, then it follows that the repeated disruptions would compound, compromising consolidated organization of various developmental systems, and ultimately increasing the probability of developmental pathways that eventuate in a broad range of psychopathology symptoms. Therefore, an obvious explanation for why CM that spanned early and later childhood would predict psychopathology multifinality, as opposed to specific effects (e.g., only externalizing symptoms), is that this type of developmentally-extensive exposure impairs an equally broad range of developmental processes known to influence both internalizing and externalizing outcomes. Additionally, CM occurring across several developmental periods often exists, and is more likely to occur, within high-risk contexts characterized by several familial risk factors (e.g., intergenerational trauma, parental psychopathology, and sociological influences; Russotti et al., 2021). Thus, a more chronic pattern of CM may be associated with a broader range of pathways that potentiate multiple forms of psychopathology because it is a marker of high-risk environments and the accumulation of family-level risk factors that broadly influence psychopathology risk.

Developmental Pathways of Psychopathology

Our use of longitudinal modeling extending from childhood to emerging adulthood significantly advances the previous research examining CM timing/chronicity and psychopathology outcomes (Cicchetti et al., 2015; English et al., 2005; Jaffee & Maikovich-Fong, 2011; Kaplow & Widom, 2007; Manly et al., 2001; Thornberry et al., 2010). Analysis of multi-method data drawn from a prospective, longitudinal study not only provides the opportunity to explore the distal or proximal impacts of chronic maltreatment, but also how those experiences initiate developmental pathways that may be sustained and maintained into emerging adulthood via earlier symptoms. For example, our findings suggest that the externalizing and internalizing sequela of chronic CM shows notable stability from childhood to adulthood. Internalizing symptoms in childhood were predictive of more specific internalizing symptom profiles in emerging adulthood such as depression and anxiety, while childhood externalizing symptoms were predictive of more specific externalizing symptom profiles in emerging adulthood such as ASPD and substance dependence. These patterns of homotypic (within-disorder/domain) symptom continuity are well-documented (e.g., Copeland et al., 2013).

In addition to the homotypic pathways, chronic CM also indirectly affected ASPD symptoms in adulthood through childhood internalizing symptoms. In previous research, childhood-onset internalizing symptoms have been linked with later antisocial behavior (Rutter et al., 2006). Two developmental psychopathology concepts explain why internalizing symptoms in childhood may be predictive of ASPD symptoms in emerging adulthood: heterotypic continuity and psychopathological progression (Rutter et al., 2006). For some, this developmental pattern may exemplify heterotypic symptom continuity, wherein there is meaningful continuity in the course of certain symptoms relevant to ASPD, but the ways in which symptoms manifest change with increasing age (Rutter, et al., 2006). For example, features of irritability may manifest as symptoms of depression in childhood and then as symptoms of ASPD in adulthood (Thapar & Rigbin, 2020). This finding may also illustrate psychopathological progressions, in which internalizing symptoms in childhood actually create risk for the development of ASPD symptoms in the transition to adulthood (Rutter et al., 2006). For example, social isolation or low self-worth in childhood may result in affiliation with other marginalized peers (e.g., deviant peers) that contribute to later antisocial behaviors.

Taken together, the present findings support the developmental psychopathology adage that mental health problems do not simply occur, they develop (Cicchetti, 1993; Sroufe, 2009). In this case, observable symptoms of ASPD, anxiety, depressive, and substance dependence disorders in adulthood have a developmental history that, at least partially, may originate with chronic CM exposure that begins in early childhood and also occurs in later childhood. Despite the possibility for change and resilience throughout life, our results suggest that chronic CM generates maladaptive pathways that, once started, place constraints on subsequent adaptation within the domain of mental health and limit the capacity to reclaim normal developmental trajectories (Cicchetti, 1993; Rutter et al., 2006; Sroufe, 2013).

Implications

This paper has clear implications for the study and conceptualization of CM, highlighting the criticality of considering CM dimensions in research studies and acknowledging that variability in CM experiences matters in terms of the development of psychopathology. Our results also underscore that preventing CM and its recurrence may have an impactful role in reducing the mental health burden for individuals living in economically-disadvantaged contexts. First and foremost, interventions designed to prevent the onset of CM offer the greatest benefit in preventing the psychopathology sequela (Toth & Manly, 2019; van IJzendoorn et al., 2020). Moreover, there is a need for secondary prevention approaches that aim to interrupt chronic patterns of CM following initial episodes (Valentino, 2017). Relatedly, providers should strive to conduct comprehensive assessments of CM experiences that evaluate the pattern of CM across developmental epochs when considering relative risk for mental health problems and intervention needs (English et al., 2005).

The results of this study also highlight the need for early therapeutic intervention in instances when chronic CM has already occurred. Delivering CM-related mental health interventions in childhood may not only alleviate current suffering but also prevent the progression of symptoms into adulthood (Copeland et al., 2013; Toth & Manly, 2019). Further, while childhood externalizing symptoms are typically easier to detect and often demand greater attention from adults (e.g., problem behaviors in the classroom), it is essential that we attend to less noticeable, but equally powerful, childhood internalizing symptoms, as they may portend mental and behavioral health challenges during the transition to adulthood, including greater anxiety, depressive, and antisocial symptoms.

Finally, given that most individuals in the current study identified as Black or Hispanic, our findings should be interpreted through an intersectional lens that considers how child maltreatment influences the development of psychopathology within the contexts of systemic oppression, racial injustice, and unfair economic disenfranchisement that historically marginalized individuals may endure (Trent et al., 2019; Williams, 2018). Race-related stressors have documented effects on the mental health of people of color throughout the lifespan (Hampton-Anderson et al., 2021; Williams, 2018), and race-related stress may compound or exacerbate the effects of child maltreatment on psychopathology. Unfortunately, the current study did not assess race-related stressors and was unable to account for their influence. Future research examining the psychopathology sequelae of child maltreatment timing and chronicity would do well to conceptualize and measure race-related stressors (e.g., discrimination, historical trauma, and structural/personally-mediated/internalized racism; Trent et al., 2019) to effectively address the sources of stress that influence mental health outcomes in populations of color. Further, it is essential that interventions aimed at preventing and treating the mental health sequelae of maltreatment in low income, minoritized communities use a culturally-grounded biopsychosocial formulation to understand the strengths and challenges faced by families (Hampton-Anderson et al., 2021) and deliver adapted interventions that integrate culturally-relevant techniques (see Metzger et al., 2021).

Limitations and Future Directions

Strengths of this study include the prospective, multi-informant, longitudinal design that traces the effect of multiple CM parameters across childhood and emerging adulthood within an ethnically-diverse, economically-disadvantaged sample that includes maltreated and demographically-matched nonmaltreated individuals. However, there are several limitations that may be addressed with future research. It is possible that children we classified into timing groups experienced prior or subsequent abuse that was not detected by CPS records. Also, statistical power necessitated that we collapse CM exposures occurring between birth and age 5 into an “early” category and ages 6 to 12 into a “recent” category. However, it may be that identifying specific ages within those groups (e.g., age 3 exposure) would be more sensitive to psychopathology outcomes. Additionally, although our study could examine developmental progressions in psychopathology symptoms, our variable-centered approach limits our ability to address individual patterns of symptom stability and change. Person-centered approaches, such as latent transition analysis, may offer additional information. Also, this study focuses on the implications of various dimensions of CM on the development of psychopathology. A critical next step would be the identification of mechanistic processes that link various forms of CM to internalizing and externalizing symptoms and disorders throughout development. This might include hypervigilance to threat, deficits in emotion regulation, social cognition, or biological processes (Cicchetti, 2016; Kim & Ciccehtti, 2010; McLaughlin et al., 2020).

Conclusion

In conclusion, our results highlight the need to examine diverse dimensions of maltreatment exposure when considering the development of psychopathology. Global categorizations of maltreatment may obscure important predictive differences on broad and specific psychopathology risk that are better revealed when accounting for patterning of exposure that includes developmental timing and chronicity. Early detection of CM and comprehensive assessment of timing and chronicity of exposure is highly relevant to the conceptualization of mental health problems in children and emerging adults. Finally, risk trajectories for adult psychopathology are observable in childhood, where the presence of externalizing and internalizing symptoms represent precursors to subsequent anxiety, depression, ASPD, and substance dependence disorder symptoms. Systems and practitioners have opportunities to assess for the initial emergence of these deleterious pathways and potentially revive youth from maladaptive trajectories before they become entrenched.