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Douglas Watt and Jaak Panksepp present a very thorough, thoughtful, and thought-provoking review of the neurobiology and treatment of depression. Based on this review, the authors propose an overarching hypothesis of depression as an evolutionarily selected-for mechanism in mammals for terminating separation distress. This hypothesis is offered as a potential explanatory model for the available and diverse neurobiological findings in depression research; furthermore, the authors hope this model can serve as a guide for future investigation into the neurobiological underpinnings of depression and antidepressant-treatment development.
The authors' argument relies on several premises:
Separation-distress behaviors (e.g., crying) in response to social loss occur in most mammals, including humans.
Mechanisms to inhibit separation-distress behaviors exist in mammals.
These mechanisms have been evolutionarily selected for since the inability to inhibit such behaviors in infants would have an untenable survival/reproductive cost.
In susceptible individuals, these inhibitory mechanisms—what the authors refer to as a fundamental shutdown process—are not properly regulated, leading to a protracted abnormal state; this protracted state is what is clinically referred to as depression.
The authors provide support for this argument by citing a wealth of data relating depression to social loss/stress. Additionally, the authors show that the response of animals to a separation-distress testing paradigm has significant phenomenological overlap with the clinical depressive syndrome in humans. Finally, the authors note that separation-distress responses in animals are associated with changes in biological systems (endo-crinological, immunological, etc.) similar to those tied to human depression. While the proposed model has much to support it—and does indeed provide a novel framework to guide future depression research—there are several questions that need to be addressed to strengthen this