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Willow bark comes from the bark of several willow tree species, most notably Salix alba (white willow). It has been used for at least 3,500 years — ancient Egyptians chewed willow leaves for pain, Hippocrates recommended it for fever, and Native American healers brewed it as a tea. The key active compound, salicin, was first isolated from willow bark in 1828, and its chemistry directly inspired the synthesis of aspirin (acetylsalicylic acid) in 1897.
When you take willow bark, salicin is converted in the body to salicylic acid, which works similarly to aspirin — it reduces the production of prostaglandins, the chemical messengers that trigger pain, inflammation, and fever. Because this conversion happens gradually in the gut and liver, willow bark tends to act more slowly than aspirin but may also be gentler on the stomach lining. The flavonoids and polyphenols in willow bark also contribute their own anti-inflammatory effects, meaning the whole herb may work better than isolated salicin alone.
Standardized capsules and tablets (240 mg salicin/day is the most studied dose) are the most reliable for consistent results. Tinctures and liquid extracts work well for those who prefer liquids. Traditional tea made from dried bark delivers lower, less predictable salicin levels but still provides some benefit. Topical creams are used for localized joint and muscle pain.
Willow bark's pain-relieving properties are documented in ancient Egyptian Ebers Papyrus (circa 1550 BCE), and Hippocrates wrote about it around 400 BCE. It remained a staple of European herbal medicine through the Middle Ages. The isolation of salicin in 1828 by Johann Buchner, and subsequent synthesis of aspirin from salicylic acid derivatives in 1897 by Felix Hoffmann at Bayer, made willow bark the direct ancestor of the world's most widely used drug.
What it is typically used for, usual dose, cautions, and the study behind it where real trial data exists.
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