Instantiating the multiple levels of analysis perspective in a program of study on externalizing behavior

Abstract

During the last quarter century, developmental psychopathology has become increasingly inclusive and now spans disciplines ranging from psychiatric genetics to primary prevention. As a result, developmental psychopathologists have extended traditional diathesis-stress and transactional models to include causal processes at and across all relevant levels of analysis. Such research is embodied in what is known as the multiple levels of analysis perspective. We describe how multiple levels of analysis research has informed our current thinking about antisocial and borderline personality development among trait impulsive and therefore vulnerable individuals. Our approach extends the multiple levels of analysis perspective beyond simple Biology × Environment interactions by evaluating impulsivity across physiological systems (genetic, autonomic, hormonal, neural), psychological constructs (social, affective, motivational), developmental epochs (preschool, middle childhood, adolescence, adulthood), sexes (male, female), and methods of inquiry (self-report, informant report, treatment outcome, cardiovascular, electrophysiological, neuroimaging). By conducting our research using any and all available methods across these levels of analysis, we have arrived at a developmental model of trait impulsivity that we believe confers a greater understanding of this highly heritable trait and captures at least some heterogeneity in key behavioral outcomes, including delinquency and suicide.

Figure 1

A transactional model of antisocial personality development in which (left) specific genetic vulnerabilities (primarily those affecting dopaminergic neurotransmission) are either amplified by familial reinforcement of emotional lability/emotion dysregulation, resulting in (right) escalation of externalizing behavior across development, or attenuated by development of strong emotion regulation skills, resulting in attention-deficit/hyperactivity disorder. Adapted from “Polyvagal Theory and Developmental Psychopathology: Emotion Dysregulation and Conduct Problems From Preschool to Adolescence,” by T. P. Beauchaine, L. Gatzke-Kopp, and H. K. Mead, 2007, Biological Psychology, 74. Copyright 2007 Elsevier. Adapted with permission.

Figure 2

A broadened model of externalizing conduct in which neural vulnerability interacts with contextual risk to produce externalizing spectrum behaviors. In this model, no assumptions are made about specific sources (e.g., genetic, epigenetic, allostatic) of neural dysfunction. Nevertheless, neural deficiencies primarily in the mesolimbic dopamine system (described in text) provide the principal mechanism through which impulsivity is expressed. Adapted from “The Canary in the Coal Mine: The Sensitivity of Mesolimbic Dopamine to Environmental Adversity During Development,” by L. M. Gatzke-Kopp, 2011, Neuroscience and Biobehavioral Reviews, 35. Copyright 2011 Elsevier. Adapted with permission.

Figure 3

The association between age and probability of alcohol use in the past year for at-risk participants scoring below the 25th percentile and above the 75th percentile on PEP reactivity to incentives (N = 206). Greater sympathetic nervous system responding is marked by preejection period (PEP) shortening. Thus, those scoring below the 25th percentile exhibited less PEP shortening than those scoring above the 75th percentile. Adapted from “Cardiac Pre-Ejection Period Reactivity and Psychiatric Comorbidity Prospectively Predict Substance Use Initiation Among Middle-Schoolers: A Pilot Study,” by S. L. Brenner and T. P. Beauchaine, 2011, Psychophysiology, 48. Copyright 2011 Wiley Blackwell. Adapted with permission.

Figure 4

The associations among (top) facial expressions of sadness and skin conductance level (SCL), (middle) preejection period (PEP), and (bottom) respiratory sinus arrhythmia (RSA) for (dashed lines) boys with disruptive behavior disorders and (solid lines) controls. Facial sadness ranged from 0 (no sadness) to 3 (highest level of sadness) for SCL and from 0 (no sadness) to 6 (highest level of sadness) for PEP and RSA because of the different temporal resolutions of measures. Adapted from “Dissociation of Sad Facial Expressions and Autonomic Nervous System Responding in Boys With Disruptive Behavior Disorders,” by P. Marsh, T. P. Beauchaine, and B. Williams, 2008, Psychophysiology, 45. Copyright 2008 Wiley Blackwell. Adapted with permission.