Mitochondrial Retrograde Signaling in Fluoroquinolone Associated Disability, A Disease Theory

 Despite warnings from regulatory agencies urging conservative usage due to the potential for major adverse events, Fluoroquinolones remains one of the most commonly prescribed antibiotics worldwide. A large number of people who take this class of antibiotics become chronically or permanently disabled suffering from what the Federal Drug Administration has observationally identified as Fluoroquinolone Associated Disability or FQAD. FQAD is an idiopathic pathological presentation of numerous, disparate, symptoms that can literally number into several hundred. FQAD, in affected individuals, can cause an intractable long-term, progressive, multi-system condition that can be severely disabling or fatal. This multisystem involvement of symptoms is usually suspected as being genetic in origin. Despite this, most clinical genetic testing fails to identify any pathological phenotypes that would explain a progressive disease. Due to the lack of further research, the exact mechanism of FQAD remains unknown, even though many disparate pieces of academic research exist documenting the genotoxicity of fluoroquinolones. Based on over ten years of anecdotal evidence by citizen scientists, and the results of some recent research findings, this paper proposes a theory that, if proven true, would elucidate the mechanism behind FQAD in an otherwise healthy population in the absence of genetic predispositions.