by emily zola

Created on: June 11, 2008

Willow was first used by the ancient Greeks. As early as 400 BC, the Greek physician Hippocrates prescribed the bark and leaves of the willow to reduce fever and pain. Proponents of willow used extracts in antiseptics, mouthwashes, and tea. The bark of willow was used to clean teeth by many Native American Tribes in the US. The Comanche burned the bark and used the ashes to treat eye ailments. The Ojibwe Indians rubbed prairie willow bark extract on skin to treat rashes.

The active ingredient of willow, salicin, was identified in the mid-1820s, by Johann Buchner in Germany and by Luigi Brugnatelli and Joanes de Fontana in Italy, but the compound was not very pure and had been extracted in small amounts. A number of subsequent investigators worked on the problem. Raffaele Pira was able to obtain a pure crystalline form of salicylic acid in 1838. But the "acid" portion of the compound was problematic for patients, causing gastric upsets. In 1853, Charles Frederic Gerhardt was able to buffer the acid portion of salicylic acid to create acetylsalicylic acid. This is the active ingredient of aspirin. However, Gerhardt was not successful at bringing the product to market and his synthesis method was too complex.

It was over forty years later, in 1897, that Felix Hoffman who worked at Bayer in Germany synthesized acetylsalicylic acid successfully for mass production of the drug aspirin. The name "aspirin" is derived from the scientific name of the willow plant, "spirea." The "a" was added to reflect that the active ingredient contains an acetyl group. The "in" suffix was commonly used at the end of drug names at that time.

Two years later, Bayer began selling aspirin powder to physicians. The drug became available over the counter without a prescription in 1915. And it was as early as 1948 that a physician by the name of Dr. Lawrence Craven detected an association between aspirin and reductions in risk of heart attack. Forty years later, a placebo-controlled trial of over 20,000 patients determined that risk for myocardial infarction was reduced as much 44% n patients taking aspirin. Even more recently, aspirin, along with other NSAIDs, has been implicated in reduction of risk for early-onset Alzheimer's disease. In a recent study, patients who took aspirin, Ibuprofen, or Advil long-term (eg, greater than 2 years, four times a week) had a 45% risk of reduction of Alzheimer's disease.

Aspirin, like other NSAIDs, inhibits cylcooxygenase (COX) enzymes in the body. COX enzymes participate in the synthesis of inflammatory agents called prostaglandins. Inhibition of COX enzymes thus reduces inflammation, pain, fever, and blood clotting. It's not clear how aspirin reduces risk for Alzheimer's disease, but it is speculated that Alzheimer's may be caused by an inflammatory process in the brain. Another theory proposes that NSAIDs may reduce the formation plaques.

Aspirin acts on both forms of COX enzymes that exist in the body, COX-1, and COX-2, like Ibuprofen, and unlike Celebrex, which acts only on COX-2. However, unlike Ibuprofen, aspirin irreversibly inhibits these enzymes. That means that once an enzyme molecule's activity is shut off, it's shut off for good. Side effects associated with non-specific NSAIDs include stomach sensitivity and increased bleeding.

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