This issue of the Journal includes an article on posttraumatic stress disorder (PTSD) in children and adolescents that deserves special attention because it is an example of a step forward in conceptualizing and examining the etiology of psychopathology. Silva et al. attempt to take into consideration both the external stress and the predisposing vulnerabilities that together produce this clinical disorder. In my own training in psychiatry there was no diagnosis such as PTSD, but we did refer to "war neurosis" as a consequence of exposure to severe and acute and/or prolonged stress in military combat. It was common wisdom that in the face of sufficient stress anyone could develop such a disorder. This was useful in attempting to remove stigma and any suggestion that the affected serviceman was weak or unmasculine or was complicit in his illness. However, it was a more or less obvious observation that, exposed to the same degree of stress, some developed the symptoms of what was later classified as PTSD (in DSM-III) but that many, indeed most, others did not. From the point of view then of understanding etiology and prevention, those who do not develop a disorder are at least as important as those who do, when in the presence of very similar or identical external circumstances.
Although Freud certainly included considerations of constitution and predisposition in his concepts of causality, his initial theory of psychopathology, such as hysteric or obsessive-compulsive symptoms, was one of a repressed actual childhood sexual trauma, the effects of which were subsequently rekindled at puberty or later and expressed in the form of symptoms. As is well known, Freud reversed himself after his own self-analysis and assigned causality to the conflict between innate instinctual drives pressing for discharge and the internal psychic forces opposing such discharge. As such, real events and the external environment took a prolonged backseat to the interplay of internal forces. Childhood physical trauma did not become an acknowledged issue until the early 1970s, and sexual abuse did not do so until a decade later, in the 1980s, and then once again it became unseemly to suggest or explore any causality that implied "blame" in the victim. The trauma itself was the only predisposing factor that could be considered. So despite consistent lip service to the contrary, the nature versus nurture paradigm has persisted, and if anything, it has intensified with the combination of biological psychiatry’s advent, increasing awareness of familial transmission and its genetic underpinnings, and the emphasis of patient advocacy groups on referring to psychiatric disorders as "brain diseases." In a way, biological psychiatry has returned the field closer to Freud’s position after he rejected his original theory of causation by trauma in favor of the interplay of internal forces; only now those forces are represented by the influence of genetic predisposition on the proper balance of certain neurotransmitters across the synaptic cleft, in what might be thought of as a new topographic theory of psychopathology.
But in fact there is now rapidly expanding research that examines the interaction of genetic predispositions on the one hand and psychosocial influences on the other, both of which have been demonstrated to be associated with individual differences in behavior, including such outcomes as antisocial behavior in children and adolescents. The questions now being asked and examined have to do with the mutual influences of genetic endowment and the psychosocial factors, particularly within the family, that lead to individual differences even between identical twins, who are genetically identical and grow up presumably in the same psychosocial environment.
In a series of studies, Reiss, Plomin, Heatherington, and their many colleagues and co-workers have proposed understanding the influence of genetic predispositions on the organization of the environment vis-à-vis the family, from infancy into adolescence. Conversely, they have studied also how and how much the family’s organization either reinforces genetic predispositions or diverts them into behavioral organizations. The importance of this paradigm can be seen in the study of sibling pairs who vary all the way from 100% shared genes to 0% shared genes (step-siblings) who are reared within the same and different families, a method allowing for an understanding of the influence of genetic sharing, the shared environment, and the nonshared environment in determining the variance in developmental outcome, including psychopathology such as adolescent depression.
When looked at within this paradigm, the findings of the study in this issue on PTSD and vulnerabilities take on additional dimensions. For example, Silva et al. report that preexisting physical aggression was more often related to physical abuse and that preexisting anxiety was related to sexual abuse and more elaborated PTSD symptoms. Both aggression and anxiety are associated with familial genetic predispositions, and both often are aspects of parental behaviors and familial organization. The authors point out that almost one-half of the study group did not develop PTSD despite exposure to the same types of abuse and family violence as those who did, so the authors state that "DSM-IV presumes a causal path from exposure to a stressor to the development of PTSD, but that does not seem to be the case." The question of what determines resilience is as critical as what determines vulnerability, and those questions can now be approached together by use of the genetic/nonshared environment paradigm.
Address reprint requests to Dr. Wiener, Department of Psychiatry, The George Washington University Medical Center, 2150 Pennsylvania Ave., N.W., Washington, DC 20037; firstname.lastname@example.org (e-mail).