An Integrative Common Liabilities Model for the Comorbidity of Substance Use Disorders with Externalizing and Internalizing Disorders

Abstract

This paper presents an integrative research-derived model to explain comorbidity among SUDs, externalizing disorders, and internalizing disorders. This hierarchical model is based on phenotypic covariance among the disorders and latent common genetic liability. At the highest level of the hierarchy, general genetically-influenced biological dispositions to negative emotionality and behavioral disinhibition each give rise to spectra of related personality traits, cognitive processes, behavioral tendencies, and psychopathology that account for the pattern of co-occurrence among mental disorders. At the lowest level of the hierarchy, disorder-specific genetic and environmental effects explain the presence of some and not other disorders associated with a given general liability. Interplay between the general liabilities and both other genes and environmental factors throughout development affect the likelihood of developing specific mental disorders.

Changes in genetic and environmental influences on trait anxiety from middle adolescence to early adulthood

“…In other words, developmentally stable sources of genetic risk that became relatively more important compared to environmental risks were responsible for the increased heritability, and genetic innovation did not contribute to increased heritability. Consistent with etiological models positing genetic influences on traits that underlie symptoms of psychological disorders (Iacono et al, 2008; Tully and Iacono, in press), our findings indicate that stable genetic influences on trait anxiety contribute to anxiety across adolescence and into adulthood, and previous research by Kendler and colleagues provides evidence of genetic innovation on recent symptoms of anxious-depression (Kendler et al, 2008b) and phobias/fears (Kendler et al, 2008a). Thus, our findings support the usefulness of trait measures of anxiety in molecular genetic studies aimed at identifying genes involved in risk for anxiety disorders (e.g., Fakra et al, 2009; Zhou et al, 2008).…”

“…Etiological models of psychopathology (e.g., Iacono et al, 2008; Tully and Iacono, in press) suggest that stable traits are more proximal to risk genes than manifest behaviors or symptoms, and stable traits are increasingly understood to underlie internalizing psychopathology throughout development (De Pauw, 2010; Kendler and Gardner, 2011; Mineka and Zinbarg, 2006; Van Ameringen et al, 1998). For example, trait anxiety proneness has demonstrated stability from adolescence into adulthood (Usala and Hertzog, 1991) and is predictive of anxiety symptoms across development (Watson and Walker, 1996).…”

Appropriate Use of Bifactor Analysis in Psychopathology Research: Appreciating Benefits and Limitations

“…Researchers sometimes prefer to use a higher-order model if their theoretical model conceptualizes the narrow factors as components of the general factor, rather than distinct entities. For example, one common liabilities model posits that individuals first develop a general liability for psychopathology, which then differentiates into more specific pathologies in response to environmental experiences (90).…”

Beauchaine ontogenic process model of externalizing psychopathology a biosocial theory of crime and delinquency

“…9 For example, in a recent longitudinal study (Sibley et al, 2014) growth in ADHD symptoms over childhood was the strongest predictor of growth in CD symptoms, which in turn was the most consistent predictor of adolescent substance use. Indeed, CD confers a six-fold increase in risk for developing an SUD (Tully & Iacono, 2014). This increased risk for progression to SUD conferred by CD is mediated by two major processes: increased risk for academic failure and association with deviant peers.…”

“…Hence, it is not surprising that aggregate data from studies in the United States yield prevalence rates ranging from 38% to 50% of ADHD among adolescents in treatment for SUD (Wilens & Morrison, 2011).There are of course other pathways that lead to SUDs. For example, some focus on stress/negative affective or the effects of substances (Chassin et al, 2014) as well as other biologically based vulnerabilities that increase risk for SUDs (Tully & Iacono, 2014). The BOPM model presents one developmental pathway that is solidly anchored in developmental theory and robustly supported by empirical research.…”