Taxometric Methods: Enhancing Early Detection and Prevention of Psychopathology by Identifying Latent Vulnerability Traits

Beauchaine, Theodore P.; Marsh, Penny

doi:10.1002/9780470939383.ch23

Cited by 11 publications

(7 citation statements)

References 231 publications

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“…Such pathways may have different responses to treatment and different prognoses (Beauchaine et al, 2008;Faja & Dawson, 2015;Iacono et al, 2017). Ignoring biological and neuropsychological underpinnings forfeits the opportunity to develop targeted interventions based on valid etiological subtypes (Beauchaine & Marsh, 2006;Beauchaine et al, 2008). Some features of ASD make this disorder a particularly good candidate for identifying endophenotypes.…”

Section: Biomarkers and Endophenotypes In Autism Spectrum Disorder (Asd)mentioning

confidence: 99%

Social endophenotypes in autism spectrum disorder: A scoping review

Tiede

Walton

2020

Dev Psychopathol

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Endophenotypes are measurable markers of genetic vulnerability to current or future disorder. Autism spectrum disorder (ASD) is well-suited to be examined within an endophenotype framework given past and current emphases on the broader autism phenotype and early detection. We conducted a scoping review to identify potential socially-related endophenotypes of ASD. We focused on paradigms related to sociality (e.g., theory of mind (TOM), social attention), which comprise most of this literature. We integrated findings from traditional behavioral paradigms with brain-based measures (e.g., electroencephalography, functional magnetic resonance imaging). Broadly, infant research regarding social attention and responsivity (Research Domain Criteria (RDoC) domain of affiliation) and attention to faces and voices (social communication) finds consistent abnormality in vulnerable infant siblings. Several additional paradigms that have shown differences in vulnerable infants and young children include animacy perception tasks (perception and understanding of others), measures of recognition and response to familiar faces (attachment), and joint attention and false-belief tasks (understanding mental states). Research areas such as alexithymia (the perception and understanding of self), empathic responding, and vocal prosody may hold interest; however, challenges in measurement across populations and age ranges is a limiting factor. Future work should address sex differences and age dependencies, specificity to ASD, and heterogeneous genetic pathways to disorder within samples individuals with ASD and relatives.

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Section: Biomarkers and Endophenotypes In Autism Spectrum Disorder (Asd)mentioning

confidence: 99%

Social endophenotypes in autism spectrum disorder: A scoping review

Tiede

Walton

2020

Dev Psychopathol

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“…Lacking such specification, we are forced to infer psychopathology solely from symptoms, which are often insensitive and nonspecific indicators of disease state (see Beauchaine, Lenzenweger, & Waller, 2008; Meehl, 1995). As a result, etiology-based diagnosis is often a necessary condition for determining whether apparent comorbidity is artifactual, spurious, or true (see Beauchaine & Marsh, 2006; Preskorn & Baker, 2002). For example, even though obsessive–compulsive disorder (OCD) is similar to other DSM-IV-TR (APA, 2000) anxiety disorders phenomenologically, it appears to be distinct etiologically, with differences in longitudinal course, patterns of heritability, and implicated neural circuitry (e.g., Stein et al, 2010).…”

Section: Homotypic Comorbiditymentioning

confidence: 99%

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

2013

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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.

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“…Although these approaches yield important descriptive information about diagnostic co-occurrence and about heritabilities of comorbidity, they provide no information about neurobiological mechanisms. This is a significant limitation because etiology-based diagnosis is often a precondition for determining whether apparent comorbidity is artifactual, spurious, or true (see Beauchaine & Marsh, 2006; First, 2005; Jensen, 2003; Preskorn & Baker, 2002). Lacking specification of etiology, we must infer psychopathology solely from symptoms, which are often nonspecific, insensitive markers of disease state (see Beauchaine, Lenzenweger, & Waller, 2008; Meehl, 1995).…”

Section: Artifactual Spurious and True Comorbiditymentioning

confidence: 99%

Neural substrates of trait impulsivity, anhedonia, and irritability: Mechanisms of heterotypic comorbidity between externalizing disorders and unipolar depression

Zisner

Beauchaine

2016

Dev Psychopathol

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Trait impulsivity, which is often defined as a strong preference for immediate over delayed rewards and results in behaviors that are socially inappropriate, maladaptive, and short-sighted, is a predisposing vulnerability to all externalizing spectrum disorders. In contrast, anhedonia is characterized by chronically low motivation and reduced capacity to experience pleasure, and is common to depressive disorders. Although externalizing and depressive disorders have virtually nonoverlapping diagnostic criteria in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, heterotypic comorbidity between them is common. Here, we review common neural substrates of trait impulsivity, anhedonia, and irritability, which include both low tonic mesolimbic dopamine activity and low phasic mesolimbic dopamine responding to incentives during reward anticipation and associative learning. We also consider how other neural networks, including bottom-up emotion generation systems and top-down emotion regulation systems, interact with mesolimbic dysfunction to result in alternative manifestations of psychiatric illness. Finally, we present a model that emphasizes a translational, transdiagnostic approach to understanding externalizing/depression comorbidity. This model should refine ways in which internalizing and externalizing disorders are studied, classified, and treated.

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Taxometric Methods: Enhancing Early Detection and Prevention of Psychopathology by Identifying Latent Vulnerability Traits

Cited by 11 publications

References 231 publications

Social endophenotypes in autism spectrum disorder: A scoping review

Social endophenotypes in autism spectrum disorder: A scoping review

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

Neural substrates of trait impulsivity, anhedonia, and irritability: Mechanisms of heterotypic comorbidity between externalizing disorders and unipolar depression

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