Chronic stress involves a dynamic interplay of endocrine physiology, neural circuitry, and language. Sustained dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, the body's natural alarm system, results in loss of cortisol rhythmicity, cognitive rigidity, impaired emotional regulation, and changes in linguistic expression. Patterns of speech under chronic stress may exhibit features such as reduced fluency, fragmentation, or increased self-referential tendencies, reflecting both physiological and neurobiological dysregulation, including reactivity in the amygdala and hippocampus, as well as prefrontal cortical hypoactivity. This review integrates evidence from the neuroendocrinology of stress, psycholinguistics, cognitive neuroscience, and the language of trauma to advance a biopsycholinguistic loop model of chronic stress. This model highlights how patterns of communication may serve as behavioral biomarkers of internal regulation, while also acting as potential modulatory factors within stress-related processes. Furthermore, emerging evidence suggests that such approaches can regulate stress; however, direct causal relationships remain to be fully established. • Presents a novel integrative model bridging neuroendocrine and psycholinguistic dimensions of chronic stress. • Summarizes studies linking the overactive HPA-axis dysregulation and communication. • Highlights observable linguistic markers of somatic hyperarousal and trauma-related hypervigilance. • Suggests that re-establishing interpersonal and communicative safety may contribute to stress regulation.
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Mahmood et al. (2026) studied this question.
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