[Stress and allostatic load: perspectives in psycho-oncology]

Since its origins as a scientific field back in the late seventies, psycho-oncology has remained notably descriptive. Few conceptual advances have been achieved in the study of psychodynamics and biological underpinnings of psychological adjustment to the experience of cancer. Moreover, the specific aspects of psychopathological responses to cancer, as well as their optimal pharmacological management remain poorly understood. On the other hand, recent years have been characterized by significant progress in the delineation of biological mechanisms of stress and its consequences for the brain, body, and general health. In this paper, we examine the applicability of the concept of allostatic load to the study of stress and psychopathology related to the cancer experience. While homeostasis refers to maintaining specific biological parameters constant, allostasis can be defined as the process of maintaining stability through change. In this context, excessive or dysregulated activity of allostatic (adaptive) systems leads to deleterious effects for the brain (reduced neurogenesis, altered cell death processes, and dendritic branching) and body (increased cardiovascular risk). These damaging effects of cumulated stress have been refered to as the allostatic load, or the cost inflicted to the organism in order to maintain stability. We hypothesize that the concept of allostatic load is particularly relevant to the multiple, repeated and chronic stressors associated with the experience of cancer. In the light of this model, we propose a new classification of psychopathological conditions in psycho-oncology: the cancer-specific stress syndrome, with its three clinical subtypes (depressive, post-traumatic, and dysallostatic). Suggestions are formulated for some biological correlates of psychodynamic processes and for the study of innovative pharmacological approaches in the treatment of stress-related disorders in oncology (anticonvulsants, CRH antagonists, 5HT-1A receptor agonists...).