The article retraces the shifting conceptualizations of psychological trauma in experimental psychopathological research in the middle decades of the twentieth century in the United States. Among researchers studying so-called experimental neuroses in animal laboratories, trauma was an often-invoked category used to denote the clash of conflicting forces believed to lead to neurotic suffering. Experimental psychologists, however, soon grew skeptical of the traumatogenic model and ultimately came to reject neurosis as a disease entity. Both theoretical differences and practical circumstances, such as the technical challenge of stabilizing neurotic symptoms in rats, led to this demise. Yet, despite their reservations, experimental psychologists continued to employ traumatic stimuli to produce psychopathological syndromes. In the 1960s, a new understanding of trauma evolved, which emphasized the loss of control experienced by traumatized animal subjects. These shifting ideas about trauma, I argue, reflect both varying experimental cultures, epistemic norms as well as changing societal concerns.

Sensation Seekers zijn personen die vrijwillig levensgevaarlijke situaties opzoeken. Sensation Seeking gedrag kan sociaal en lichamelijk schadelijke effecten hebben. In vergelijking met controlegroepen zijn bij Sensation Seekers significante ver-schillen aangetoond in verscheidene psychobiologische reacties die optreden bij informatieverwerking.

Adolf Meyer (1866–1950) exercised considerable influence over the development of Anglo-American psychiatry during the first half of the twentieth century. The concepts and techniques he implemented at his prominent Phipps Psychiatric Clinic at Johns Hopkins remain important to psychiatric practice and neuro-scientific research today. In the 1890s, Meyer revised scientific medicine’s traditional notion of clinical skill to serve what he called the ‘New Psychiatry’, a clinical discipline that embodied social and scientific ideals shared with other ‘new’ progressive reform movements in the United States. This revision conformed to his concept of psychobiology – his biological theory of mind and mental disorders – and accorded with his definition of scientific medicine as a unity of clinical–pathological methods and therapeutics. Combining insights from evolutionary biology, neuron theory and American pragmatist philosophy, Meyer concluded that subjective experience and social behaviour were functions of human biology. In addition to the time-honoured techniques devised to exploit the material data of the diseased body – observing and recording in the clinic, dissecting in the morgue and conducting histological experiments in the laboratory – he insisted that psychiatrists must also be skilled at wielding social interaction and interpersonal relationships as investigative and therapeutic tools in order to conceptualise, collect, analyse and apply the ephemeral data of ‘social adaptation’. An examination of his clinical practices and teaching at Johns Hopkins between 1913 and 1917 shows how particular historical and intellectual contexts shaped Meyer’s conceptualisation of social behaviour as a biological function and, subsequently, his new vision of clinical skill for twentieth-century psychiatry.

Although racial disparities in health have been documented both historically and in more contemporary contexts, the frameworks used to explain these patterns have varied, ranging from earlier theories regarding innate racial differences in biological vulnerability, to more recent theories focusing on the impact of social inequalities. However, despite increasing evidence for the lack of a genetic definition of race, biological explanations for the association between race and health continue in public health and medical discourse. Indeed, there is considerable debate between those adopting a “social determinants” perspective of race and health and those focusing on more individual-level psychological, behavioral, and biologic risk factors. While there are a number of scientifically plausible and evolving reasons for the association between race and health, ranging from broader social forces to factors at the cellular level, in this essay we argue for the need for more transdisciplinary approaches that specify determinants at multiple ecological levels of analysis. We posit that contrasting ways of examining race and health are not necessarily incompatible, and that more productive discussions should explicitly differentiate between determinants of individual health from those of population health; and between inquiries addressing racial patterns in health from those seeking to explain racial disparities in health. Specifically, we advance a socio-psychobiological framework, which is both historically grounded and evidence-based. This model asserts that psychological and biological factors, while playing a central role in determining individual risk for poor health, are relatively less consequential for understanding racial disparities in health at the population level. Such a framework emphasizes the etiologic role of social inequities in generating and perpetuating racial disparities in health and highlights their impact on psychological, behavioral, and biological disease processes.

L’étude de la fonction hypothalamo-hypophyso-cortico-surrénalienne (HHS) occupe une place de choix dans l’étude du stress, de l’anxiété et d’autres pathologies psychiatriques telle la dépression. Mais les procédures d’investigation actuellement utilisées sont difficiles à mettre en œuvre et susceptibles d’interférer avec les phénomènes étudiés. Les auteurs présentent ici l’adaptation et les applications du dosage du cortisol dans la salive dans diverses conditions statiques et dynamiques chez des patients et des sujets sains qui devraient permettre une approche fructueuse dans l’étude des corrélations clinico-biologiques en psychiatrie et en psychobiologie.