Generalized anxiety disorder (GAD) is a chronic and disabling mental health condition characterized by excessive, uncontrollable worry and persistent psychological and somatic tension. Affecting approximately 3-6 % of the global population, GAD significantly impairs daily functioning and often coexists with other psychiatric conditions. Among its many symptoms, sleep disturbances-particularly insomnia-are among the most frequently reported and debilitating. Individuals with GAD commonly experience difficulties with sleep initiation, maintenance, and restorative rest, making insomnia one of the most pervasive features of the disorder. Emerging research highlights a bidirectional relationship between GAD and insomnia: while anxiety contributes to cognitive and physiological arousal that interferes with sleep, insomnia in turn exacerbates emotional dysregulation, amplifies worry, and may even precede the development of anxiety disorders. Neurobiological and neuroimaging studies support this reciprocal link, showing shared dysfunctions such as heightened hypothalamic-pituitary-adrenal (HPA) axis activity, increased amygdala reactivity, reduced prefrontal cortical control, and GABAergic deficits. These overlapping mechanisms underscore a common pathophysiological substrate that reinforces both conditions. Recognizing and addressing this interplay is critical, as untreated insomnia may perpetuate or intensify GAD symptoms. Notably, cognitive behavioral therapy for insomnia (CBT-I) has been effective in improving sleep and reducing anxiety severity-even without directly targeting anxiety-supporting a shift toward integrating sleep-focused interventions in the treatment of GAD. This review aimed to elucidate clinical and neurobiological evidence on the bidirectional link between insomnia and GAD, emphasizing shared mechanisms and treatment implications.
Keywords: Anxiety; Anxiety disorders; Generalized anxiety disorder; Insomnia; Sleep deprivation; Sleep disturbances.
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