Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2013 Nov;25(4 Pt 2):1505-28.
doi: 10.1017/S0954579413000746.

Comorbidities and continuities as ontogenic processes: toward a developmental spectrum model of externalizing psychopathology

Affiliations

Comorbidities and continuities as ontogenic processes: toward a developmental spectrum model of externalizing psychopathology

Theodore P Beauchaine et al. Dev Psychopathol. 2013 Nov.

Erratum in

  • Dev Psychopathol. 2014 May;26(2):553

Abstract

Research on child and adolescent mental health problems has burgeoned since the inaugural issue of Development and Psychopathology was published in 1989. In the quarter century since, static models of psychopathology have been abandoned in favor of transactional models, following the agenda set by editor Dante Cicchetti and other proponents of the discipline. The transactional approach, which has been applied to autism, depression, self-injury, and delinquency, (a) specifies vulnerabilities and risk factors across multiple levels of analysis spanning genes to cultures, (b) identifies multifinal and equifinal pathways to psychopathology, and (c) transcends traditional disciplinary boundaries. However, as noted by Rutter and Sroufe (2000), specific mechanisms of continuity, discontinuity, and comorbidity of psychopathology must be identified if we wish to understand etiology fully. In this article, we present a model of early-onset externalizing behavior in which comorbidities and continuities are viewed as ontogenic processes: products of complex longitudinal transactions between interdependent individual-level vulnerabilities (e.g., genetic, epigenetic, allostatic) and equally interdependent contextual risk factors (e.g., coercive parenting, deviant peer group affiliations, neighborhood criminality). Through interactions across levels of analysis, some individuals traverse along the externalizing spectrum, beginning with heritable trait impulsivity in preschool and ending in antisociality in adulthood. In describing our model, we note that (a) the approach outlined in the DSM to subtyping externalizing disorders continues to obscure developmental pathways to antisociality, (b) molecular genetics studies will likely not identify meaningful subtypes of externalizing disorder, and (c) ontogenic trait approaches to psychopathology are much more likely to advance the discipline in upcoming years.

PubMed Disclaimer

Figures

Figure 1
Figure 1
A latent structure of externalizing behavior in which multiple first-order factors (attention-deficit/hyperactivity disorder, oppositional defiant disorder, conduct disorder, substance use disorderss, and antisocial personality disorder) load on a single higher order factor (externalizing liability).
Figure 2
Figure 2
An expanded model in which trait impulsivity serves as a common vulnerability to sequential development of externalizing spectrum disorders across the life span. Temperament and intermittent explosive disorder (IED) have been added. The latter is shaded because it is a new disorder, so its inclusion is based on theoretical rather than empirical grounds.
Figure 3
Figure 3
An ontogenic process model of externalizing spectrum behaviors in which levels of analysis are plotted on the y axis and relative age is plotted on the x axis. Heritable trait impulsivity is presumed to be the principal predisposing vulnerability to externalizing spectrum disorders, the syndromal manifestation (e.g., attention-deficit/hyperactivity disorder or conduct disorder) of which is influenced strongly by environmental risk mediators, which change and accrue across development. Trait impulsivity arises from factors specified in the top two panels. However, it is important to note that this heritable vulnerability is exacerbated through recursive feedback loops that span levels of analysis (dashed, bidirectional arrows). Through such mechanisms, high-risk behaviors (e.g., evocative effects on parenting or substance abuse) amplify inherited vulnerability. Emotion dysregulation emerges later in development and is influenced more by environmental influences than by heritability. Despite the daunting complexity of this model, many biological (e.g., head injury, taratogen exposure, serotonergic function) and environmental (e.g., abuse, neglect) etiological factors are left out, as are certain individual level of analysis predictors such as attributional biases and callous–unemotional traits. This illustrates why developmental psychopathology research on any complex trait needs to be conducted across disciplines and levels of analysis if we wish to understand multifinal and equifinal complexities of etiology. Solid arrows represent directional processes, and dashed arrows represent bidirectional processes.

References

    1. Achenbach T. Developmental psychopathology. New York: Ronald Press; 1974.
    1. Achenbach TM, Edelbrock CS. Psychopathology of childhood. Annual Review of Psychology. 1984;35:227–256. - PubMed
    1. Achenbach TM, Edelbrock CS. Manual for the Child Behavior Checklist/4-18 and 1991 profile. Burlington, VT: University of Vermont, Department of Psychiatry; 1991.
    1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 3rd, rev. Washington, DC: Author; 1987.
    1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th, text rev. Washington, DC: Author; 2000.

Publication types