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
Due to its unique waterless nature, it may feel 'oily' for a few seconds to some
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Much as stratification of responders in trials of heart failure and hypertension therapies has revealed targetable subtypes, allowing more effective pharmacologic management for some patients, the same could feasibly be seen with ME/CFS
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