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Its effects on inflammation run deep, operating through thiol-disulfide exchange reactions that modulate major signaling cascades such as NF-kB and MAPK pathways

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The constellation of SNS overactivity, parasympathetic withdrawal, glucocorticoid receptor insufficiency, and elevated inflammatory signaling may help account, at least in part, for the increased risk of metabolic syndrome, endocrine disorders, and vascular disease seen in bipolar patients (168, 177)