Jonathan B. Britten 10/22/03 1:20 AM Wrote: > List, > > Please see this month's Esquire magazine to learn that Acetaminophen is the > leading cause of liver failure in the USA today. Tens of thousands of > people each year suffer serious, sometimes irreversible, sometimes fatal toxic > reactions from this powerful and popular drug -- which of course is approved > by the FDA. > > I am busy and will stop here: if you read the entire article, you will > understand clearly the grotesque contrast between the FDA tolerance of toxic > OTC remedies from the big pharmaceutical companies, as opposed to the FDA > attacks on effective, largely harmless non-pharmaceutical substances and > devices,. > > Read it and weep, or laugh bitterly, depending on your inclinations. *************************** Hi Jon,
Man, Esquire is cheap -- you can,t read an article on-line without paying. BUT -- that turns out to be a good thing, because I then went looking for supportive evidence of acetaminophen toxicity-- and I found it, but no normal person coming anywhere near the recommended dosage would be in any danger of harm from the use of acetaminophen; Esguire must have been hard-up for a filler article. The complete information can be found at: http://www.emedicine.com/emerg/topic819.htm a portion of the reference follows: Pathophysiology: The maximum daily dose of APAP is 4 g in adults and 90 mg/kg in children. The toxic dose of APAP after a single acute ingestion is 150 mg/kg or approximately 7 g in adults, although the at-risk dose may be lower in persons with alcoholism and other susceptible individuals. When dosing recommendations are followed, the risk of hepatotoxicity is extremely small. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents, which then are eliminated in the urine. In acute overdose or when maximum daily dose is exceeded over a prolonged period, the normal pathways of metabolism become saturated. Excess APAP is then metabolized in the liver via the mixed function oxidase P450 system to a toxic metabolite, N-acetyl-p-benzoquinone-imine (NAPQI). NAPQI has an extremely short half-life and is rapidly conjugated with glutathione, a sulfhydryl donor, and removed from the system. Under conditions of excessive NAPQI formation or reduced glutathione stores, NAPQI is free to covalently bind to vital proteins and the lipid bilayer of hepatocytes; this results in hepatocellular death and subsequent centrilobular liver necrosis. The antidote for APAP poisoning is N-acetylcysteine (NAC). NAC is theorized to work by a number of protective mechanisms. Early after overdose, NAC prevents the formation and accumulation of NAPQI. NAC increases glutathione stores, combines directly with NAPQI as a glutathione substitute, and enhances sulfate conjugation. NAC also functions as an anti-inflammatory and antioxidant and has positive inotropic and vasodilating effects, which improve microcirculatory blood flow and oxygen delivery to tissues. Vasodilating effects decrease morbidity and mortality once hepatotoxicity is well established. The same thing was done to Ephedrin ( sp?) those athletes that had trouble were probably of the mind set -- If a little does good, then a lot will do gooder -- duh? Jack Be Nice -- Be Nice -- The silver-list is a moderated forum for discussion of colloidal silver. Instructions for unsubscribing may be found at: http://silverlist.org To post, address your message to: [email protected] Silver-list archive: http://escribe.com/health/thesilverlist/index.html List maintainer: Mike Devour <[email protected]>
