Beyond oxytocin: A hypothalamic neuropeptide framework for socioaffective resonance and its dysregulation in psychiatry.

Oxytocin has emerged as a pivotal modulator of human social behavior, yet its effects are embedded within a broader hypothalamic neuropeptidergic network that also includes vasopressin, corticotropin-releasing hormone (CRH), orexin, and neuropeptide Y (NPY). These evolutionarily conserved systems jointly regulate socioaffective resonance - the dynamic alignment of emotional, physiological, and cognitive states between individuals - by tuning social salience, arousal, affective simulation, and stress regulation. Here, we synthesize evidence from animal and human research to outline an integrative model in which oxytocin's effects are amplified, attenuated, or redirected by the state of these other peptide systems. We introduce the Socioaffective Resonance Collapse Hypothesis, proposing that transdiagnostic social impairments in conditions such as autism, borderline personality disorder, depression, and schizophrenia may reflect maladaptive neuropeptide configurations that destabilize interpersonal alignment. By embedding oxytocin within this multi-system framework, we identify novel pathways for precision interventions, including pharmacological and behavioral strategies aimed at restoring the neurochemical balance that supports social connection. This conceptual synthesis complements oxytocin-focused perspectives by clarifying when and why oxytocin-based interventions may succeed or fail, and by offering a roadmap for translating basic neuropeptide science into clinical applications.