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Biosocial studies of antisocial and violent behavior in children and adults: a review - 1

Journal of Abnormal Child Psychology,  August, 2002  by Adrian Raine

INTRODUCTION

Over the past 50 years, important progress has been made in delineating replicable psychosocial risk factors for antisocial and violent behavior (Farrington, 2000; Hinshaw & Anderson, 1996; Loeber & Farrington, 1998; McCord, 2001; Rutter, Giller, & Hagell, 1998). Within the past 15 years, important progress has also been made in uncovering biological risk factors that predispose to antisocial behavior (Lahey, McBurnett, Loeber, & Hart, 1995; Moffitt, 1990a; Rutter et al., 1998; Susman & Finkelstein, 2001). Despite this progress, we know surprisingly little about how these different sets of risk factors interact in predisposing to antisocial behavior. Furthermore, although passing heuristic and theoretical references are frequently made to such interactional influences, there are remarkably few investigators who are conducting serious empirical research on this interface in humans (Raine, Brennan, & Farrington, 1997).

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The goal of this paper is to review the known facts on biosocial interaction effects in relation to antisocial and violent behavior in order to highlight this important yet un-derresearched field. The focus is placed on documenting empirical examples of interaction effects within the areas of genetics, psychophysiology, obstetrics, brain imaging, neuropsychology and neurology, hormones, neurotransmitters, and environmental toxins, rather than describing heuristic conceptualizations or theoretical perspectives. Only research on humans will be reviewed as perspectives from the animal literature are given in Miczek (2001), Suomi (1999), and Niehoff (1999). Although more complex transactional perspectives are potentially very important (Hinshaw & Anderson, 1996; Susman & Ponirakis, 1997), they are not the focus of this particular review because there are few empirical long-term outcome studies of serious antisocial and violent behavior.

The emphasis is placed on empirical knowledge because research in this area of antisocial behavior is sorely lacking hard empirical data on the nature of interactions, whereas in contrast speculation is rampant. By documenting these findings at this point in time, the field will be better placed in the future to develop more sophisticated and specific biosocial theories of violence, which are empirically testable, as opposed to overly amorphous and all-encompassing. Nevertheless, good theory is also critical for scientific advance, and theoretical perspectives will be returned to in the conclusion section.

To serve as a heuristic guide to this review, Fig. 1 illustrates a simple biosocial model of violent behavior that highlights the key influences of genetic and environmental processes in giving rise to social and biological risk factors that both individually and interactively predispose to antisocial behavior. The model also incorporates social and biological protective factors, influences that will be touched upon briefly in this review. Inevitably, this model is overly simplistic, but it does provide a framework within which the research reviewed below can be viewed. It should also be noted that what constitutes a biological variable and what constitutes a social variable is open to question. There is much that is social about biological variables (e.g., head injuries leading to brain dysfunction are caused by the environment) and much that is biological about social variables (e.g., genetic factors, and their biological predispositions, contribute to bad parenting). Although "biological" and "social" are in strict terms false dichotomies, they are retained here for illustrative purposes.

GENETICS

There is now clear evidence from twin studies, adoption studies, twins reared apart, and molecular genetic studies to support the notion that there are genetic influences on antisocial and aggressive behavior (Raine, 1993; Rowe, 2001; Rutter, 1997). The more challenging issue now concerns if and how genetic processes interact with environmental processes in predisposing to antisocial behavior. Twin studies find stronger evidence for heritability of antisocial behavior than adoption studies (Raine, 1993), and because interaction effects will influence heritability estimates from twin but not adoption designs, there is prima facie evidence that such interactions exist. Indeed, it is a truism that genetic processes need an environment in which to become expressed. As such, environmental changes will turn these genetic influences on and off across the life-span (Plomin & Rutter, 1998). Genetic factors likely give rise to biological risk factors for antisocial behavior such as low arousal, and if gene x environment interactions are found, this would suggest that interaction effects may well exist at the level of biological influences, a view that will be returned to later.

Gene by Environmental Interactions

One of the most striking examples of gene by environment interactions in genetic studies of crime is a cross-fostering analysis of petty criminality (Cloninger, Sigvardsson, Bohman, & von Knorring, 1982), results of which are illustrated in Fig. 2. Male Swedish adoptees (N = 862) were divided into four groups depending on the presence or absence of (a) a congenital predisposition (i.e., whether biological parents were criminal) and (b) a postnatal predisposition (how the children were raised by their adoptive parents). When both heredity and environmental predispositional factors were present, 40% of the adoptees were criminal compared to 12.1% with only genetic factors present, 6.7% for those with only a bad family environment, and 2.9% when both genetic and environmental factors were absent. The fact that the 40% rate for criminality when both biological and environmental factors are present is greater than the 18.8% rate given by a combination of "congenital only" and "postnatal only" conditions indicates that genetic and environmental factors interact. Further analyses indicated that occupational status of both biological and adoptive parents were the main postnatal variables involved in this nonadditive interaction.