BY SIDNEY CROWN , FEMI OYEBODE and ROSALIND RAMSAY
نویسنده
چکیده
In this book Mike Rutter sets out to explain how genes might influence behaviour and how this might be important in understanding the causal pathways leading to various behavioural traits and psychiatric disorders. This is an ambitious and challenging project, not just because the issues themselves are so complex and our current understanding so rudimentary, but also because this area has suffered from a polarisation of views between the proponents of Nature and Nurture that has been most unhelpful. The great majority of researchers have realised for some time that the key to understanding individual differences in susceptibility to behavioural disorders will come from understanding how the effects of genetic variation and environmental exposure interact over the lifespan, but the grumbling guerrilla war between behaviour geneticists and psychosocial researchers has been sustained by the fact that the different schools have approached their subjects from different theoretical and methodological perspectives and spoken different languages in which apparently similar terms actually describe crucially different concepts. As with many intellectual disputes the differences have had a lot to do with reciprocal misunderstandings of methodology and language, but the flames have been fanned by evangelists on both sides. What is needed, therefore, is someone with an understanding not just of genetics, but also of psychosocial and developmental research – to integrate the results from these areas, to illuminate the misunderstandings and to point out where, in their enthusiasm, the evangelists have strayed from the path of righteousness and, in some cases, common sense. As such, Mike Rutter is probably one of the few people in the world who could have written this book. Most of the readers of the Journal will be familiar with his work and will not be surprised to learn that he brings to the task his formidable analytical approach whereby the problems and issues are dissected and the bones laid bare. He has worked hard to present a clear and non-technical account of a number of different areas of research including behaviour genetics, psychiatric genetics and research into environmentally mediated risks. Crucially, the treatment of these issues includes clear descriptions of the underlying assumptions, careful consideration of the strengths and weaknesses of the methodology and cautious interpretation of the findings. This is complemented by two chapters that serve as a non-technical primer in genetics and that illustrate how genes might influence behaviour and, equally importantly, show the limits of simple genetic explanations. Finally, having brought the reader to a level where they can understand the issues and interpret the findings, he brings together genes and environment and reaches the heart of his argument: the effects of genes and environment are inextricably interwoven. With rare exceptions, human traits and disorders, medical as well as psychiatric, are multifactorial, with good evidence of both genetic and environmental influences. On the one hand, this means that genetic influences are pervasive, though not necessarily predominant, across virtually all behaviours. This applies not just to disorders but also to psychological traits that are present to various degrees across the general population. The latter include temperamental and cognitive characteristics and even socially defined behaviours such as criminality and divorce to the extent that they are influenced by underlying temperamental and cognitive characteristics. On the other hand, it seems that in many, and perhaps most, instances the effects of genes are likely to manifest through various types of interplay with the environment. Thus, some genetically influenced behaviours will affect the extent to which individuals are exposed to environmental risk (so-called gene–environment correlation). To give one example, antisocial behaviour in a parent, which is influenced by genetics, can disrupt family function, which in turn will contribute to a child’s risk of developing antisocial traits. In other words, the parent’s genes are contributing to a child’s risk via an environmental mechanism. There are also other forms of gene–environment correlation by which an individual’s own behaviour, again partly influenced by genes, can influence exposure to environmental risks either directly or by evoking risk-imposing behaviour on other people such as family members. The other main way in which the effects of genes and the environment collide is via so-called gene–environment interaction. This describes the situation whereby genes influence a person’s susceptibility to environmental risk. For example, there is an accumulating body of evidence that variation in the gene encoding the serotonin transporter might modulate the extent to which depression occurs as a consequence of exposure to adverse experiences such as stressful life events and childhood maltreatment. Rutter argues persuasively that gene– environment interactions of this sort are likely to be common and that we must take this into account in our research. Thus, genes are not deterministic and they do not ‘cause’ behaviours or psychiatric disorders such as autism and schizophrenia in any direct way. Rather their effects on behaviour are indirect and mediated to a considerable extent via the environment. The challenge now is to delineate gene–environment interplay more widely and to begin to determine the causal
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تاریخ انتشار 2006