- 07-05-2004, 05:20 PM
- 07-05-2004, 05:25 PM
07-05-2004, 05:27 PM
Especially anything else that can be hard on the liver. Alcohol, most antiinflamatories, etc. Keep it liver friendly when on M1T, 'cause it's hostile enough on its own.Originally Posted by Jarconis
07-05-2004, 05:27 PM
Well, since Tylenol (acetaminophen) stresses the liver and can actually cause liver damage all by itself, using it at the same time as taking M1T is a bad idea, IMO. Of course, I don't know how much Tylenol you take daily, but it definitely isn't a good idea to combine the two IMO.Originally Posted by rebo
07-05-2004, 06:13 PM
if you already have a bad back, i hope you dont experience some of those back aches that some M1T users have. usually taurine/potassium helps, but if you have back problems going in, it could be real bad.Originally Posted by rebo
07-05-2004, 06:50 PM
Much of the research in the area of hepatotoxicity centers on acetaminophen and alcohol, since those are the two most common ways people induce liver damage in themselves. Combining it with another substance that is hard on the liver like M 1-T is not a good idea. The following article deals with large doses, to show how destructive Tylenol can be.
http://www.ncbi.nlm.nih.gov/entrez/q..._uids=14625346Drug Metab Dispos. 2003 Dec;31(12):1499-506. Related Articles, Links
James LP, Mayeux PR, Hinson JA.
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA. [email protected]
The analgesic acetaminophen causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. The initial phases of toxicity were described in Dr. Gillette's laboratory in the 1970s. These findings indicated that acetaminophen was metabolically activated by cytochrome P450 enzymes to a reactive metabolite that depleted glutathione (GSH) and covalently bound to protein. It was shown that repletion of GSH prevented the toxicity. This finding led to the development of the currently used antidote N-acetylcysteine. The reactive metabolite was subsequently identified to be N-acetyl-p-benzoquinone imine (NAPQI). Although covalent binding has been shown to be an excellent correlate of toxicity, a number of other events have been shown to occur and are likely important in the initiation and repair of toxicity. Recent data have shown that nitrated tyrosine residues as well as acetaminophen adducts occur in the necrotic cells following toxic doses of acetaminophen. Nitrotyrosine was postulated to be mediated by peroxynitrite, a reactive nitrogen species formed by the very rapid reaction of superoxide and nitric oxide (NO). Peroxynitrite is normally detoxified by GSH, which is depleted in acetaminophen toxicity. NO synthesis (serum nitrate plus nitrite) was dramatically increased following acetaminophen. In inducible nitric oxide synthase (iNOS) knockout mice, acetaminophen did not increase NO synthesis or tyrosine nitration; however, histological evidence indicated no difference in toxicity. Acetaminophen did not cause hepatic lipid peroxidation in wild-type mice but did cause lipid peroxidation in iNOS knockout mice. These data suggest that NO may play a role in controlling lipid peroxidation and that reactive nitrogen/oxygen species may be important in toxicity. The source of the superoxide has not been identified, but our recent finding that NADPH oxidase knockout mice were equally sensitive to acetaminophen and had equal nitration of tyrosine suggests that the superoxide is not from the activation of Kupffer cells. It was postulated that NAPQI-mediated mitochondrial injury may be the source of the superoxide. In addition, the significance of cytokines and chemokines in the development of toxicity and repair processes has been demonstrated by several recent studies. IL-1beta is increased early in acetaminophen toxicity and may be important in iNOS induction. Other cytokines, such as IL-10, macrophage inhibitory protein-2 (MIP-2), and monocyte chemoattractant protein-1 (MCP-1), appear to be involved in hepatocyte repair and the regulation of proinflammatory cytokines.
PMID: 14625346 [PubMed - in process]
07-05-2004, 06:53 PM
http://www.ncbi.nlm.nih.gov/entrez/q..._uids=14523675Semin Liver Dis. 2003 Aug;23(3):217-26. Related Articles, Links
Acute liver failure in the United States.
Division of Digestive Liver Diseases, University of Texas Southwestern Medical Center Dallas, Texas, USA. [email protected]
In the last 5 years the use of a multicenter approach has helped to define acute liver failure (ALF) in the United States. Drug-related hepatotoxicity comprises more than 50% of cases of ALF, including acetaminophen toxicity (40%) and idiosyncratic drugs (approximately 12%). Nearly 20% of cases remain of unknown etiology. Outcome of ALF is determined by etiology; by the degree of hepatic encephalopathy present on admission; and by complications, principally infection. More than 43% survive without a transplant, 28% die, and 29% undergo liver transplantation. Liver support machines have had no impact on this condition to date. A trial of N-acetylcysteine for the treatment of ALF not related to acetaminophen toxicity is underway. Future research in ALF in the United States should focus on limiting the number of cases related to drugs, searching for causes of the indeterminate cases, and developing more effective temporary liver support.
* Review, Multicase
PMID: 14523675 [PubMed - indexed for MEDLINE]
07-05-2004, 09:21 PM
Recently my best friend lost his sister from Tylenol abuse...if you need to take it everyday, you should see a doctor...Acetaminiphn (sp?) is not ment to be taken on a daily basis for extended periods of time..
07-05-2004, 11:12 PM
Tylenol VS Muscle Gain
I believe there was also a study that showed tylenol or maybe it was aspirin (can't remember which) interfers with protein synthesis. Since I can't remember which it is I stay away from both. I work too hard to keep growing to let a little thing like some pain get in the way. Of course a migraine headache will invariably sway me to the dark side.
07-06-2004, 12:59 AM
Sorry to hear about her death. But out of professional curiosity, can i ask you why she was abusing tylenol on a daily basis? how long? did she drink alcohol often? was she in chronic pain from a health condition? why didn't she go see a doctor?Originally Posted by willieman
07-06-2004, 01:04 AM
Go see a good Chiropractor for your back problem. pain killers will do nothing to cure your back problem. it will only hide the pain temporarily. you need your lumbar spine and hips adjusted to re-align your bones and muscles stripped and rehabed.Originally Posted by rebo
07-07-2004, 01:06 PM
You are correct regarding this side effect.Originally Posted by uridium245
As a brief background, when tissues are damaged, white blood cells flood to the site to try to minimize tissue destruction. Prostaglandins, which are produced by a biochemical synthesis from the fatty acid, arachidonic acid, are produced as a result. The production of a particular prostaglandin is believed to be tied into the synthesis of skeletal muscle (see quote).
http://www.google.com/search?q=cache...c%2520Acid.docStudies point to PGF2a, specifically, as being the prostaglandin most closely tied to increase skeletal muscle protein synthesis. Skeletal muscle tissue has no capacity to actually store prostaglandins, so the only local source for PGF2a is the arachidonic acid that is retained in the outer phospholipids layer of each cell. It is the stretching of muscle fibers during intense physical exercise that causes arachidonic acid to be released and metabolized to active prostaglandins. Arachidonic acid is actually the chemical messenger first released by your muscles during intense weight training, controlling the core physiological response to exercise and regulating the intensity of all growth signals to follow. Also, anytime you have tissue injury, inflammation is involved in healing the wound. Some prostaglandins have pro-inflammatory affects. The fact is, if you work out, you have tissue injury - micro trauma to the muscle tissue. As your delayed onset muscle soreness will tell you, inflammation is involved in the healing of this micro trauma.
However, aspirin, acetaminophen, and ibuprofen block an enzyme called cyclooxygenase (COX-1 and COX-2), which is involved with the ring closure and inhibits arachidonic acid from converting to prostaglandins. This is good for decreasing pain, but it also stops muscle synthesis, since the mechanism telling the body it needs to be repaired has been stopped.
07-07-2004, 01:34 PM
Nice info,i take 2 tylenol a day for bad disk in my back.And i am taking m1t at low dose(10mg).Havnt had any problems as of yet.I will keep doses of both low.Thanks for the info.
07-07-2004, 02:45 PM
She originally was on pain killers for a neck and back injury from a vicious car accident, the Dr. cut her off of the meds without weening her off of them, or solving the problem of the pain...she turned to Tylenol, and then Advil too.She was not a drinker drug abuser at all.Was on the donation list for a liver, went from a 9 to a 1 in about a week and a half.I think this was over about a 9 month period.She was on the list for a while though before her condition disingrated rapidly.Originally Posted by lancelot
07-07-2004, 02:52 PM
again, sorry to hear about her death. but, the stupid azz doctor should have refered her to a PT or better yet a Chiropractor for her musculoskeletal problems incurred in the accident. pain killers don't do **** to cure her health condition.Originally Posted by willieman
07-07-2004, 05:40 PM
Unfortunately it seems that most doctors these days treat the symptoms rather than the actual condition.Originally Posted by lancelot
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