Anxiety is a clinical state characterized by excessive worry, apprehension, and fear, often accompanied by somatic symptoms resulting from heightened autonomic nervous system activation. Physiologically, it reflects a dysregulation within the hypothalamic-pituitary-adrenal (HPA) axis, leading to an overproduction or sustained elevation of stress hormones like cortisol. This chronic activation can disrupt the delicate balance of the endocrine system, impacting mood, sleep, and metabolic function.
Origin
The term “anxiety” derives from the Latin anxietas, meaning distress or trouble of mind, reflecting its ancient recognition as a state of psychological unease. Clinically, its formal definition and classification have evolved through psychological and psychiatric frameworks, but its physiological underpinnings are rooted in the body’s fundamental fight-or-flight stress response. The modern understanding emphasizes the interplay between neurochemistry, genetic predisposition, and environmental stressors.
Mechanism
The core mechanism involves the limbic system, particularly the amygdala, which initiates the fear response, triggering the release of corticotropin-releasing hormone (CRH) and subsequent cortisol secretion from the adrenal glands. Persistent anxiety maintains this HPA axis hyper-responsiveness, leading to allostatic overload and potential receptor downregulation in the hippocampus and prefrontal cortex. This sustained hormonal imbalance, particularly elevated cortisol, can negatively influence neurotransmitter systems, perpetuating the anxious state and contributing to endocrine disruption.
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