Brian M. Hicks,
Dr. Hicks is Research Assistant Professor of Psychiatry, Medical School
at the University of Michigan.
I am a Research Assistant Professor in University of Michigan Addiction Research Center (UMARC) in the Department of Psychiatry. I received my PhD in clinical psychology at the University of Minnesota and completed a post doc at the Minnesota Center for Twin and Family Research (MCTFR). I came to the UMARC in 2009 after being awarded a K01 Career Development Award “Integrating Genes, Environment, & Development in the Etiology of Substance Abuse” funded by NIDA, to receive additional training in statistical genetics and participate in genome wide association studies of substance use disorders (SUDs).
I have broad interests in SUDs, antisocial behavior, and personality, specifically, their developmental course and the interplay of genetic and environmental risk. Much of my work involves twin studies conducted at the MCTFR and longitudinal analyses. The major lines of research are described below:
Pre-morbid Liability to SUDs: Alternative Phenotype for Gene Association Studies
My K01 award entails developing a pre-morbid liability index for SUDs, that is, a measure of childhood behaviors and personality traits that predict later substance abuse. The pre-morbid liability index will be included as part of a genome wide association study funded by NIDA that will use large samples from longitudinal studies conducted by researchers at the University of Minnesota and Duke University. Using the longitudinal data, I will first identify the behaviors and traits present prior to substance initiation that best predict later SUDs and related outcomes such as antisocial behavior. This pre-morbid liability index will then be included in a genome association study of approximately 5500 people. This is project is based on the premise that a measure of underlying or pre-morbid risk will provide a useful complement to measures of manifest or “post-morbid” risk typically used in genetic association studies. We will then attempt to replicate any significant hits of risk genes in two independent samples of high-risk youth.
Externalizing Disorders: Genetic and Environmental Risk
I have participated in several studies that attempt to understand the co-occurrence among SUDs, antisocial behavior, and disinhibited personality traits. Much of this work supports the notion that a general externalizing factor accounts for this comorbidity such that these different disorders are different manifestations of a general liability to behavioral disinhibition. Based on data from the MCTFR twins studies, we have shown that this externalizing factor is highly heritable (80%) and accounts for much of the genetic risk of individual disorders. The externalizing factor also accounts for family resemblance among parents and their offspring; that is, rather than disorder-specific risk parents pass on a general risk to a number of disorders characterized by behavioral disinhibition. We have also demonstrated that gender differences in the general externalizing factor can account for gender differences in the prevalence of individual disorders, as well as much of the developmental change and stability of externalizing disorders from adolescence to adulthood. We have also examined gene-environment interplay in risk for externalizing disorders and found that genetic risk increases in the context of environmental adversity regardless of the environmental risk factor, suggesting a general mechanism of gene-environment interplay of risk for externalizing disorders.
Developmental Course of SUDs
I am also interested in the onset, persistence, and desistence of SUDs. At the population level, SUDs exhibit a normative developmental course of emerging in adolescence, a rapid escalation in young adulthood, followed by a plateau and relatively steep decline from the mid-20’s to early-30’s. Deviations from this normative course have important implications for the severity of SUD most notably an early onset (SUD present in adolescence) and persistent course (SUD still present by age 30). I am interested in examining the unique risk factors related to an early onset and persistent course as well as factors that influence desistence, that is, what individual-level and environmental factors contribute to the decline of SUDs? For example, in a study of male twins assessed from age 17 to 29, we found that an early onset of alcohol dependence was associated with various impairments in psychosocial functioning in adolescence, while specific risk factors related to behavioral disinhibition predicted a persistent course. Also, elements of the social environmental, in particular the substance use of peers and a romantic partner, were especially predictive of a persistent course.
Personality and SUDs
I am also interested in the inter-relationship between personality and SUDs. While there is substantial evidence that personality traits related to negative emotionality and behavioral disinhibition are risk factors for SUDs, much less is known about how SUDs influence personality development. For example, during the transition from adolescence to adulthood, people report major declines in mean-levels of negative emotionality and behavioral disinhibition, a trend often called the “maturity principle.” Does having a SUD during this time effect these normative developmental changes in personality change? Initial findings suggest that it depends on the type of personality trait. For negative emotionality, people who exhibit an early onset and persistent course of a SUD fail to show the normative declines such that the SUD seem to stunt personality growth. For behavioral disinhibition, people with SUDs are higher to begin with, but do show normative declines. The problem is that such people are always behind where they should be and so continue to struggle to complete normative developmental tasks as these tasks become more complex in adulthood.
I’ve also participated in several studies of psychopathy or psychopathic personality disorder. This work has focused on examining subtypes or facets of psychopathy. For example, there seem to be two broad subtypes or trait dimensions of psychopathy. The primary or factor 1 type is characterized by social dominance, lack of anxiety, and low fear. The secondary or factor 2 type is characterized by aggression, impulsivity, and associated with SUDs and other externalizing disorders. I’ve also participated in research that uses self-report measures of psychopathy and the MCTFR twin studies to examine the heritability, developmental change, and environmental risk associated with psychopathic traits.
Hicks, B. M., Iacono, W. G., & McGue, M. (in press). Index of the transmissible common liability to addiction: Heritability and prospective associations with substance abuse and related outcomes. Addiction.
Bornovalova, M. A., Hicks, B. M., Iacono, W. G., & McGue, M. (2010). Family transmission and heritability of childhood disruptive disorders. American Journal of Psychiatry, 167, 1066-1074.
Hicks, B. M., Iacono, W. G., & McGue, M. (2010). Consequences of an adolescent onset and persistent course of alcohol dependence in men: Adolescent risk factors and adult outcomes. Alcoholism: Clinical & Experimental Research, 34, 819-833.
Hicks, B. M., Vaidyanathan, U., & Patrick, C. J. (2010). Validating female psychopathy subtypes: Differences in personality, antisocial and violent behavior, substance abuse, trauma, and mental health. Personality Disorders: Theory, Research, & Treatment, 1, 38-57.
Hicks, B. M., South, S. C., DiRago, A. C., Iacono, W. G., & McGue, M. (2009). Environmental adversity and increasing genetic risk for externalizing disorders. Archives of General Psychiatry, 66, 640-648.
Hicks, B. M., Blonigen, D. M., Kramer, M. D., Krueger, R. F., Patrick, C. J., Iacono, W. G., & McGue, M. (2007). Gender differences and developmental change in externalizing disorders from late adolescence to early adulthood: A longitudinal twin study. Journal of Abnormal Psychology, 116, 433-447.
Johnson, W., Hicks, B. M., McGue, M., & Iacono, W. G. (2007). Most of the girls are alright but some aren’t: Personality trajectory classes from age 14 to 24 and some associations with outcomes. Journal of Personality and Social Psychology, 93, 266-284.
Blonigen, D. M., Hicks, B. M., Krueger, R. F., Patrick, C. J., & Iacono, W. G. (2006). Continuity and change in psychopathic personality traits as measured via normal range personality: A longitudinal-biometric study. Journal of Abnormal Psychology, 115, 85-95.
Hicks, B. M. & Patrick, C. J. (2006). Psychopathy and negative emotionality: Analyses of suppressor effects reveal distinct relations with emotional distress, fearfulness, and anger-hostility. Journal of Abnormal Psychology, 115, 276-287.
Hicks, B. M., Krueger, R. F., Iacono, W. G., McGue, M., & Patrick, C. J. (2004). Family transmission and heritability of externalizing disorders: A twin-family study. Archives of General Psychiatry, 61, 922-928.
Hicks, B. M., Markon, K. E., Patrick, C. J, Krueger, R. F., & Newman, J. P. (2004). Identifying psychopathy subtypes on the basis of personality structure. Psychological Assessment, 16, 276-288.
Krueger, R. F., Hicks, B. M., Patrick, C. J., Carlson, S. R., McGue, M., & Iacono, W. G. (2002). Etiological relationships among substance dependence, antisocial behavior, and personality: Modeling the externalizing spectrum. Journal of Abnormal Psychology, 111, 411-424.