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While its precise etiology remains unclear, growing evidence implicates oxidative stress and mitochondrial dysfunction as key contributors to its pathophysiology ( Oxidative stress results from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, leading to cellular damage, lipid peroxidation, mitochondrial dysfunction, and neuroinflammationall of which may exacerbate pain sensitization and fatigue in FM ( Mitochondrial dysfunction in Redox imbalance is marked by decreased CoQ10 levels, reduced mitochondrial DNA content, and impaired electron transport chain activity, leading to excessive ROS production and decreased ATP synthesis

It is also used as sangrahi which acts as a catalyst with other given herbal medicine

There is considerable evidence suggesting that oxidative damage contributes to cone dysfunction and death and that treatments, including NAC, that reduce oxidative damage promote cone function and survival (59, 13, 2224)

Consult a qualified provider before beginning any peptide protocol

This inflammation can cause changes in the way that the brain and nervous system process pain signals, leading to increased sensitivity to pain