| Yes, 100%. But apparently, there are cases where fluoroquinolones cause long-lasting oxidative damage or mitochondrial dysfunction. The recovery of mTOR signaling then may be slower. Even after the cessation of fluoroquinolones, prolonged oxidative stress can lead to chronic inflammation and collagen synthesis may remain impaired. Ongoing mitochondrial damage can reduce the cell's capacity to respond to anabolic signals, potentially leading to prolonged weakness in connective tissue and a higher risk of tendon damage. The slow recovery of mitochondrial function may lead to extended mTOR inhibition in tissues like tendons and ligaments. This bit is especially interesting: Fluoroquinolones also impact dopaminergic and adrenergic systems, which regulate the body's stress response (via dopamine and norepinephrine). This disruption can affect how the body handles both acute and chronic stress, with potential long-term changes in the hypothalamic-pituitary-adrenal (HPA) axis. Dysregulation in the HPA axis could affect cortisol production, impacting inflammation, immune function, and tissue repair over an extended period. Long-term impacts and the systemic nature of chronic inflammation, mitochondrial damage, and persistent oxidative stress can lead to structural or functional deficits in tissues that were secondarily affected during the acute phase of stress and disruption, which can manifest as persistent dysfunction, pain, or delayed healing. |