> Research into the therapeutic benefits of aspirin (acetylsalicylic acid) has been recently reignited by the observation that it may help prevent complex diseases such as diabetes and cancer [1–3]. Mechanisms invoked to explain the benefits of salicylates include increased mitochondrial biogenesis and increased mitochondrial energy metabolism via activation of key metabolic regulators such as AMP-activated protein kinase (AMPK), NF-Kb, and SIRT1, among others [4–8]. However, these findings contradict an older literature from the 1970s and 1980s that focused on the link between aspirin and Reye Syndrome. Several published papers from that era demonstrated that aspirin can uncouple mitochondria and inhibit mitochondrial fatty acid oxidation (FAO), among other negative effects [9–12]. This research led to the discontinuation of aspirin as an analgesic in children. Many Reye Syndrome patients were later found to be suffering from undiagnosed genetic disorders, particularly in the pathway of mitochondrial FAO, and aspirin usage was apparently a triggering factor in their metabolic decompensation rather than the root cause [13]. While aspirin use in children has declined sharply in recent decades, there are still instances of severe metabolic decompensation and even death in patients with undiagnosed metabolic disorders after ingestion of aspirin [14–16]. You really delivered on that one. Not only largely addressed my question but current events too. Kudos.