Introduction

It is evident from many chapters in this volume that the origins and maintenance of conduct problems in childhood entail transactional processes between the individual and the environment (see also Caspi & Moffitt, 1995). Equally it is clear that many of the children who are at highest risk have problems that appear early and are remarkably predictive of antisocial behaviour in adolescence and early adult life, which suggests that stable individual vulnerabilities may be important. These have been characterized in terms of genetic influences (Simonoff, chapter 8, this volume), neuropsychological deficits (Lynam & Henry, chapter 9, this volume) perceptual processes (Pettit et al., chapter 11, this volume) and attachment status (DeKlyen & Speltz, chapter 12, this volume). At this stage we cannot be sure to what extent these accounts reflect different processes that might contribute independently or in combination to risk, or overlapping processes viewed from different standpoints. If they are different, and they do contribute independently, we need models of the way in which this might happen, and one route is via consideration of biosocial and biopsychological processes.

The distinction between the ‘bio’ and the ‘social’ is in many respects artificial. There is nothing intrinsically less biological about social interactions than physiological processes (Bolton & Hill, 1996). We will take ‘biological’ to refer principally to neuroanatomy, neurochemistry and neurophysiology, and ‘social’ to family, peer and wider social processes. Psychological processes may be seen as mediating between the biological and the social.