Depression as reversible biopsychosocial break up after schismogenesis.

• There is a need for biopsychosocial integrative hypotheses concerning depression. • The schismogenesis construct could be part of a potential hypothesis. • Such hypothesis could explain a common mechanism of action for all validated antidepressant therapies. In recent decades, an important amount of biomedical and psychosocial data regarding major depression etiology and treatment has emerged. Despite this wealth of information, a global hypothesis seeking to integrate all available data into a unified explanatory model of depression is still missing. The biopsychosocial model is a precedent in this endeavor. This model proposes a systemic conceptual framework, suggesting that the dynamic interactions of biological, psychological, and social factors constantly condition individuals' health status. However, it has been criticized for its lack of practical utility when it comes to understanding the onset and potential reversion of depression. Gregory Bateson proposed a systemic, transdisciplinary construct that may be useful for addressing these criticalities: schismogenesis. While this concept has found increasing application across different areas such as politics, ecology, or even psychotherapy, to the best of our knowledge, its use as a biopsychosocial etiology hypothesis for depression remains unexplored. The schismogenesis hypothesis suggests that depression can be considered as a switching process mediated by positive feedback curves, leading to a functional dissociation due to insufficient inhibitory control. Nonetheless, this process can be either reversed spontaneously or through external help, resulting in a rebalancing of the system. [ABSTRACT FROM AUTHOR]