How Tylenol Works

More on how Tylenol works

• History of Tylenol
• History of Painkillers
• How the Body Processes Tylenol
• Tylenol Is Not Always Safe to Take
• FDA's Recommended Dose of Tylenol

Acetaminophen is an analgesic, or pain reliever, as well as an antipyretic, or fever reducer. It relieves pain by elevating the pain threshold, meaning that a user must experience more pain than usual to feel it. It also lowers the body’s temperature, which helps combat fevers.

Tylenol is one of the most popular forms of pain reliever in the US. Every year, Americans take more than 8 billions doses of Tylenol in capsule or tablet forms. The generic name for Tylenol is acetaminophen. Even though acetaminophen is present in more than 200 types of medication, many do not have the name Tylenol included in the label.

The greatest danger of a Tylenol overdose is liver damage. Tylenol’s active ingredient—acetaminophen—is toxic to the liver in large doses. When acetaminophen is metabolized (or processed) by the liver, the toxic chemic byproduct N-acetyl-p-benzo-quinone imine, or NAPQI, is produced. When taking Tylenol or other acetaminophen-containing products in safe amounts, the liver produces a manageable quantity of NAPQI, which the liver almost immediately detoxifies and removes from the body in the form of bile or urine.

However, under some conditions the liver cannot adequately detoxify NAPQI, whether by being overloaded by too much of the toxic chemical—which occurs in the case of an overdose, or by being too weak to handle the normal amount of NAPQI—which occurs when taking certain medications or by drinking alcohol. Medications like isoniazid, carbamazepine, phenytoid and Phenobarbital compromise the liver’s ability to process Tylenol and acetaminophen.

Normally, acetaminophen is metabolized when it bonds with glucuronic acid, a process called glucuronidation. The combination causes a chemical reaction, which splits the new compound into two substances. The majority becomes a relatively non-toxic metabolite, which is excreted into bile and passed out of the body. The small remaining amount of the drug, about 10%, becomes NAPQI, which is extremely toxic to liver tissue.

Normally, NAPQI immediately combines with the complex amino acid glutathione. Chronic alcoholics may not have enough glutathione to inactivate all of the NAPQI produced. The most frequent problem, however, is when a person ingests of large amounts of acetaminophen due to accidental or intentional overdose.

A toxic dose of acetaminophen usually varies between 4 grams (g) in special populations (like alcoholics) and 6 g in the average person. The lethal dose is usually between 10 g and 15 g, however if a person is drinking alcohol at the same time, it will lower that figure significantly.

When a person takes too much acetaminophen, the sheer quantity of the drug will overwhelm the normal metabolic pathway, causing large amounts of NAPQI to be produced instead. Some of this will be detoxified by glutathione, but eventually the excessive quantity of NAPQI will use up all of the glutathione reserves in the liver. With the normal metabolic pathway shut off, and the liver out of glutathione, the NAPQI builds up undeterred in the liver, which in these large quantities kills liver cells very effectively. The effects become apparent 3-4 days after the original acetaminophen was ingested, and results in permanent liver damage, liver failure, and sometimes death.