La compréhension contemporaine des troubles psychiques tend à les assimiler à des troubles cérébraux. Cet article vise à distinguer deux thèses souvent confondues : l’existence de corrélats biologiques des troubles mentaux, et l’idée que leur cause première serait cérébrale. Il propose, en alternative, un modèle « sociopsychobiologique » qui déplace l’organe pertinent de la psychiatrie vers la personne indissociable de son milieu.

Analyse conceptuelle et épistémologique adossée à une revue critique de travaux en philosophie de la médecine, histoire et épistémologie de la psychiatrie, anthropologie médicale, et sciences sociales. L’argumentaire examine successivement : les débats sur la définition du trouble mental, la nature interactive et hybride des catégories psychiatriques, les limites de la quête de biomarqueurs, et les effets cliniques et identitaires des récits d’origine biologisante.

L’article montre que l’absence de causes neurobiologiques nécessaires et suffisantes pour la majorité des troubles psychiatriques rend insuffisante une étiologie exclusivement biologique. Les catégories diagnostiques sont décrites comme des cibles mouvantes, réactives à leur propre classification, et comme des objets hybrides dont la composante sémantique et contextuelle est décisive. La recherche de marqueurs biologiques, même lorsqu’elle identifie des corrélats, ne tranche pas la frontière entre le normal et le pathologique. Sur le plan clinique, l’hypothèse d’une origine biologique première peut produire une « double peine » : déresponsabilisation et fatalisation, au détriment de l’agentivité et de l’horizon thérapeutique. Le modèle sociopsychobiologique propose un critère de démarcation : lorsqu’une cause cérébrale est nécessaire et suffisante et que sa correction abolit la souffrance, la situation relève principalement de la neurologie ; dans le cas contraire, la ou les causalités distales doivent être cherchées dans les contraintes et désaccords entre la personne et son monde, tout en reconnaissant des effets somatiques et des vulnérabilités individuelles. Le modèle sociopsychobiologique se présente donc à la fois comme une proposition alternative mais aussi potentiellement complémentaire au modèle biopsychosocial.

L’approche défendue ne nie ni la pertinence de la biologie, ni l’intérêt du modèle biopsychosocial pour décrire des boucles de rétroaction, mais critique sa hiérarchisation biologisante en étiologie. Elle ajoute par ailleurs un garde-fou contre tout réductionnisme socioculturel et plaide pour une transdisciplinarité effective entre psychiatrie et sciences humaines et sociales.

Le modèle sociopsychobiologique vise à rééquilibrer la recherche et la clinique : privilégier l’analyse des milieux et des trajectoires, circonscrire la portée étiologique des explications biologiques, refonder la nosographie sur la personne-dans-son-milieu, et orienter les soins vers des interventions psychothérapeutiques et environnementales autant que biomédicales.

Contemporary public and scientific discourse increasingly frame mental disorders as brain disorders. Our article aimed to disentangle two frequently conflated claims: that there are biological correlates of mental suffering and that the primary cause of mental disorders is located in the brain. Instead, we argue that, in psychiatry, our framework should not be reduced to the brain. Rather, we should focus on the person as a whole, inseparable from their environment. Building on this premise, we have proposed a “sociopsychobiological” model designed to reorient etiological reasoning and nosological practices.

We adopted a conceptual and epistemological approach grounded in a critical review of findings in the philosophy of medicine, the history and epistemology of psychiatry, medical anthropology, and the social sciences. The analysis had five steps: (1) we revisited major debates regarding the definition of a mental disorder and the limits of purely biological criteria; (2) we examined why psychiatric categories are unstable and self-reactive, shaped by classificatory practices and social expectations; (3) we discussed the emblematic quest for biological markers and explained why such markers, even if identified, cannot by themselves delineate the boundary between pathological and non-pathological; (4) we analyzed the clinical and identity-related consequences of biology-based narratives; and (5) we formulated a sociopsychobiological model with practical implications for research and care.

We argue that most psychiatric conditions do not have clearly defined neurobiological causes whose treatment could reliably eliminate suffering. While biological changes may accompany mental distress, they are often better understood as correlates, consequences, mediators, or vulnerabilities rather than as primary causes. Psychiatric diagnoses can be seen as “moving targets” because they interact with clinical practices, institutions, and lay discourse; they also function as hybrid objects whose meaning depends on narrative, culture, and prevalent norms. Consequently, a research program that relies on fixed diagnostic entities to identify a single biological cause will face structural difficulties. Discourse around biological markers highlights an asymmetry: in somatic medicine, markers are typically sought for already delineated natural objects, whereas, in psychiatry, markers are often expected to prove that diagnostic categories are naturally delineated objects. Moreover, the presence of a marker does not determine whether a condition is harmful, disabling, or socially recognized as an illness because such judgments remain value-laden and context-dependent. In this article, wehave clinically described the “double bind” produced by biology-based etiology: first, the patient is positioned as a passive victim (“you are not responsible”), and second, the patient is symbolically imprisoned by their condition (“it is biological and therefore inescapable”), which can undermine agency and narrow therapeutic possibilities.

Our sociopsychobiological model does not reject the existence of biology, biomedical interventions, or feedback loops among bodily states, psychological experiences, and social responses. Instead, it challenges the hierarchical assumption that biological explanations should dominate etiological reasoning in psychiatry. The sociopsychobiological model is thus put forward both as an alternative to the biopsychosocial model and as a potential complement to it. A pragmatic demarcation is proposed: when a strictly cerebral cause is well-defined and of sufficient consequence and its treatment eliminates symptoms, the case squarely lands in the domain of neurology. However, when suffering emerges from a mismatch between a person's disposition and their life/world, the primary causal focus should be the person in their environment, where the distal cause or causes are to be sought, while also acknowledging potential biological vulnerabilities and bodily symptoms. With our model, we also caution against “sociocultural reductionism”: we wish to underscore that social explanations can become just as totalitarian as neurobiological reductionism. Finally, we advocate for a productive reconciliation between psychiatry and the humanities and social sciences through true transdisciplinary work.

Redefining the target “organ” in psychiatry as the person in their environment could help rebalance research priorities and clinical practices. Greater attention could be paid to the study of environments and life trajectories, while treating biological research as heuristically valuable but etiologically limited for many psychiatric phenomena. There could be development of revised and contextualized descriptive classifications, and care could be oriented toward psychotherapeutic and environmental interventions as much as toward biomedical tools.