Ok, this is a very simple rule: Don't take Tylenol (acetaminophen, paracetamol, whatever) when you've been drinking, or you'll do horrible damage to your liver, and possibly die. Death by complete liver failure isn't a fun way to go either, unless you really dig crippling pain, vomiting, and blindness. Daily alcohol users are most susceptible to the damage, including both wine-with-dinner drinkers and hardcore alcoholics. Even if you don't drink much but take acetaminophen after you've had a few, it'll still do damage.

Most acetaminophen metabolism, about 95%, is done by specialized glucuronide and sulfate routes, which don't have any harmful end products. The remaining 5% is done by oxidase enzymes in the liver, particularly cytochrome p-4502E1. Metabolizing acetaminophen via this route produces the compound N-acetyl-p-benzoquinoneimine, also known as NAPQI, which is quite deadly to liver tissue.

Normally, NAPQI is made non-toxic by being combined with glutathione, and circulated harmlessly out of the liver. When alcohol (or an overdose of acetaminophen) is taken , too much NAPQI builds up to be handled by the body's supply of glutathione, and liver damage results. Risk from NAPQI can last up to five days after taking alcohol, especially once there is no more alcohol in the system to compete for the cytochrome enzyme.

This toxicity can be completely avoided by taking the supplements N-acetyl-cysteine and L-glutlamine, 500 mg once or twice a day. These amino acids limit glutathione production, so having them highly available means that glutathione will be available to process the NAPQI. Even people taking acetaminophen regularly for chronic pain would be wise to take these, and avoid the chance for any liver damage at all. I still can't figure out why commercial acetaminophen producers don't put both of these precursors in every Tylenol pill they sell -- it seems like a simple way to reduce their liability.

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