Despite substantial increases in pharmacological and psychotherapeutic treatment availability, global rates of psychological distress continue to rise, a pattern existing frameworks, taken individually, cannot fully explain. Current dominant models frequently conceptualize distress primarily as neurochemical dysfunction, emphasizing symptom reduction while leaving broader neurobiological signaling processes insufficiently addressed. For a clinically significant subset of individuals, this contributes to recurring symptom patterns, escalating treatment requirements, and eventual treatment resistance that existing literature has not yet fully accounted for. This paper introduces Adaptive Signal Theory (AST), an integrative evolutionary, ecological, and intergenerational framework proposing that psychological distress must be understood simultaneously across four nested levels: the evolutionary origin of distress signals, the autonomic mechanisms of their expression, the contemporary ecological conditions that chronically sustain them, and the intergenerational pathways through which dysregulation may transmit across generations. Critically, AST argues these levels are not parallel explanations for the same phenomenon; rather, they are nested layers of a single adaptive system, and failure to integrate them may produce predictable and clinically recognizable patterns of treatment limitation. Drawing on Polyvagal Theory (Porges, 2011), allostatic load theory (McEwen and Stellar, 1993), hormesis (Calabrese and Mattson, 2011), somatic trauma theory (Levine, 1997; van der Kolk, 2014), attachment theory (Bowlby, 1969), evolutionary psychiatry (Nesse, 2019; Hollon, 2020), and interpersonal neurobiology (Siegel, 2012), AST advances four central propositions: that psychological distress reflects functional neurobiological signaling; that exclusive symptom suppression may fail to resolve underlying threat-detection processes; that contemporary post-industrial environments may systematically deprive nervous systems of the relational, sensory, and co-regulatory inputs necessary for baseline neuroception of safety; and that chronic disruption of adaptive signal processing in caregivers may contribute to intergenerational consequences for infant neurobiological development. The perinatal period is examined as a clinically significant context in which all four propositions converge simultaneously, with implications for dyadic intervention, maternal regulatory restoration, and co-regulatory treatment approaches. A central clinical implication follows across populations and presentations: treatment effectiveness depends on alignment between the level at which a signal is generated and the level at which intervention is applied. Directions for future empirical investigation and interdisciplinary clinical application are discussed.
Amanda Suncire-Nerison (Wed,) studied this question.