The clinical and physiological phenomenon where a state of chronic, low-grade systemic inflammation contributes directly to the onset, severity, or persistence of anxiety symptoms. This concept moves beyond a purely psychological model, recognizing the bidirectional communication between the immune system and the central nervous system. Elevated circulating inflammatory markers are increasingly viewed as key biological drivers of mood and anxiety disorders.
Origin
This is a modern, integrative term synthesizing the concepts of “systemic inflammation,” a measurable immunological state, and “anxiety,” a psychological and neurological state. The link emerged from psychoneuroimmunology research, which demonstrated that pro-inflammatory cytokines can cross the blood-brain barrier and directly influence neurocircuitry.
Mechanism
Inflammatory cytokines, such as interleukin-6 and TNF-alpha, can cross the blood-brain barrier and interfere with the synthesis and metabolism of key neurotransmitters, including serotonin and dopamine. They also activate the HPA axis, increasing cortisol release, which can further exacerbate anxiety. Furthermore, inflammation can compromise the integrity of the gut barrier, leading to increased permeability and a heightened inflammatory response that continually feeds back to the brain.
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