White Willow

Salix alba L. belongs to Salicaceae, the willow family, and was first published by Linnaeus in Species Plantarum in 1753 (Kew’s Plants of the World Online, POWO). POWO gives its native range as Europe to northern China and north-west Africa, from Portugal, Spain, and Morocco through central Europe, Türkiye, Iran, and Central Asia to Xinjiang, Tibet, and Inner Mongolia. It has been introduced far beyond that, including Great Britain, Ireland, Scandinavia, much of the United States, parts of Canada, south-eastern Australia, Argentina, and Chile, and POWO accepts a subspecies, subsp. micans, alongside the typical plant. The Woodland Trust, which treats it as non-native in Britain, describes white willow as the largest of the willows, reaching up to 25 m, with an irregular, often leaning crown, grey-brown bark that develops deep fissures with age, and slender, flexible grey-brown twigs. Like most willows it grows on wet ground, along rivers and streams, where its branches make good nesting sites for birds.

The name white refers to the leaves. The Woodland Trust describes them as slender and oval, hairy all over when young and later downy underneath, and paler than most other willows because of a felty covering of fine, silky, silvery-white hairs on the underside. White willow is dioecious: male and female catkins grow on separate trees and appear in early spring, the male catkins 4–5 cm long and the female 3–4 cm. After pollination by insects, the female catkins lengthen into small capsules whose tiny seeds are wrapped in white down and carried by the wind. In winter the tree can be recognized by narrow, hairy, green to yellow-brown buds pressed close to the twig. Willows hybridize freely, which makes identification tricky; the Woodland Trust notes that the cricket bat willow is a hybrid of white willow and crack willow. The catkins are an early source of nectar and pollen for bees, and the leaves feed the caterpillars of moths such as the puss moth and eyed hawk-moth.

Medicinal willow bark is not one species. The EMA assessment report notes that there are about 500 Salix species; those of medical interest include white willow, black willow (S. nigra), and purple willow (S. purpurea), but violet willow (S. daphnoides), crack willow (S. fragilis), and purple willow give the greatest yield of salicin precursors. The European Pharmacopoeia defines willow bark as the dried bark of young branches, or pieces of current-year twigs, of various Salix species, containing at least 1.5% total salicylic derivatives expressed as salicin, and the EU monograph names purple, violet, and crack willow. Content varies widely: the assessment report puts total salicin at about 0.5% in white willow, 1–10% in crack willow, 4–8% in purple willow, and more than 4% in violet willow, with further shifts by season, growing conditions, and processing. According to the same report, the extracts in the main clinical trials were made from violet and purple willow bark, even though reviews such as Cochrane’s file the results under Salix alba. A label reading “white willow bark” therefore says little about how much salicin a product contains.

Besides salicin, the bark’s characteristic constituents are related salicylate glycosides, mainly salicortin, 2′-O-acetylsalicortin, and tremulacin, together with flavonoids, catechins, and condensed tannins, which make up 8–20% of the bark (EMA). The tannins give the bark its astringency, and EMA notes that they may interfere with the absorption of salicylic acid. An analysis of 57 white willow bark samples, cited by EMA, found its procyanidins, the building blocks of condensed tannins, dominated by procyanidins B3 and B4. The leaves are chemically different. Piątczak and colleagues (Biomolecules 2020) identified 29 phenolic compounds in white willow leaves and 34 in the bark. The leaves held more than twice the total phenolic content, about 5,576 versus 2,330 mg per 100 g of dry weight, and nearly half of their compounds were flavonols such as quercetin glycosides, whereas the bark was dominated by procyanidins. That study did not measure salicin, and neither the EU monograph nor the European Pharmacopoeia covers the leaf.

Willow’s ancient reputation is real but often exaggerated. Reviews of aspirin’s history, such as Mahdi and colleagues (Cell Proliferation 2006), report that Assyrian clay tablets describe willow leaves for pain and inflammation, that the Ebers Papyrus of ancient Egypt lists willow leaves to “draw the heat out” of inflamed wounds, and that Chinese medicine used willow shoots (from Salix babylonica) and poplar bark for rheumatic fever, colds, and wounds. Many histories add that Hippocrates told patients to chew willow bark for fever and pain. Philippa Martyr, a pharmacology lecturer at the University of Western Australia, checked the Hippocratic writings and found essentially one reference to willow: burning the leaves to make smoke for fumigating the uterus after a miscarriage. Dioscorides recommended willow for stomach ache, tuberculosis, and contraception, rubbed burned bark soaked in vinegar on corns, and used a hot pack of willow leaves for gout, while Celsus applied warm willow poultices for prolapse. Martyr points out that many such remedies were used externally, and that their salicin content is impossible to judge.

The modern story begins with an English clergyman. Around 1757, Martyr recounts, the Reverend Edward Stone of Chipping Norton in Oxfordshire chewed some white willow bark out of curiosity, was struck by its bitterness, and wondered whether it might work like cinchona, the bitter bark that yields quinine. He dried about half a kilogram of bark, ground it to powder, and took small doses every four hours for his own fever, then tried it on sick parishioners. In 1763 he reported his results to the Royal Society in a letter published in its Philosophical Transactions as an account of the success of the bark of the willow in the cure of agues, ague meaning fevers usually taken to be malaria (Mahdi). The EMA assessment report likewise dates willow bark’s tradition as a fever remedy to the 18th century. Martyr adds that by early modern times willow had come to be considered largely useless as a medicine, so Stone was rediscovering it rather than continuing an unbroken ancient tradition.

Chemists then went looking for the active substance. According to Mahdi and colleagues, the Italians Brugnatelli and Fontana obtained a crude active extract in the 1820s; Johann Andreas Buchner at the University of Munich purified a yellowish substance in 1828 and named it salicin, after Salix; and the French pharmacist Henri Leroux obtained pure crystalline salicin in 1829. Raffaele Piria showed that salicin is made of glucose and salicyl alcohol, which can be oxidized to salicylic acid. A parallel route ran through meadowsweet, then called Spiraea ulmaria: in 1835 the Swiss pharmacist Pagenstecher extracted a compound from its flowers that the German chemist Löwig oxidized to salicylic acid. The Science History Institute records that Hermann Kolbe determined the structure of salicylic acid and synthesized it in 1859, and that from 1874 the Heyden company near Dresden sold synthetic salicylic acid more cheaply than extracts from willow bark. In 1876 the Scottish physician Thomas MacLagan treated acute rheumatism with salicin (Mahdi). Salicylic acid worked, but it irritated the stomach, and some patients simply could not tolerate it.

In 1897 Felix Hoffmann, a chemist at Bayer, acetylated salicylic acid to make acetylsalicylic acid. The Science History Institute notes the legend that he wanted something for his father’s rheumatic pains, and evidence that his colleague Arthur Eichengrün played a significant role that was later written out of the story. Bayer named the drug Aspirin, the A for acetyl and spirin from Spiraea, and registered the trade name on 6 March 1899 (Mahdi). Interest in willow bark then fell away, the EMA assessment report says, until demand for better-tolerated painkillers revived research. Germany’s Commission E approved willow bark in 1984 for feverish illnesses, rheumatic complaints, and headache. EMA’s herbal committee adopted its first willow bark monograph in 2009 and a revised version on 31 January 2017, which turned an earlier warning about use under 18 into an outright contraindication; in April 2025 it opened a call for new data for a further periodic review. In the United States, the US Pharmacopeia’s Salix species monograph now includes a cautionary labeling statement, described in its 2019 safety review.

Salicin is a prodrug: it does little until the body changes it. According to the EU monograph, the salicylate glycosides in willow bark break down to salicin, salicin is split into saligenin (salicyl alcohol) and glucose, and saligenin is oxidized in the blood and liver to salicylic acid. The EMA assessment report notes that rat studies suggested gut bacteria in the lower intestine do the splitting, but that human studies found salicylic acid in the blood within an hour, pointing to absorption higher in the gut. In the key human study, summarized by EMA, Schmid and colleagues (European Journal of Clinical Pharmacology 2001) gave 10 healthy volunteers 1,360 mg of a standardized extract, equal to 240 mg of salicin, in two doses three hours apart. Salicylic acid made up 86% of the salicylates in their blood, peaking within two hours at an average of 1.2 mg per liter, and total exposure matched what about 87 mg of aspirin would produce. EMA concludes that the salicylate levels reached at recommended doses are too low to explain willow’s pain-relieving effect on their own.

Salicylic acid can block cyclo-oxygenase (COX) enzymes, which make the prostaglandins involved in pain, fever, and inflammation, and EMA’s public summary says willow may work partly in this way, like aspirin. There are important differences, though. Aspirin permanently disables COX-1 by attaching an acetyl group to it, which is the basis of its lasting effect on platelets, whereas the assessment report notes that salicylic acid does not irreversibly acetylate COX-1. When three healthy volunteers took an extract equal to 240 mg of salicin, it did not significantly inhibit COX-1, COX-2, or the release of the inflammatory messengers TNF-alpha and IL-1beta in their blood (Wagner and colleagues, cited by EMA). Platelets are affected, but mildly. In a double-blind study by Krivoy and colleagues, summarized by EMA, arachidonic acid-induced platelet aggregation reached 61% of maximum in back pain patients taking willow extract with 240 mg of salicin a day, 78% on placebo, and 13% in heart patients on 100 mg of aspirin a day; collagen-induced aggregation was unaffected by either.

Researchers therefore look to the rest of the bark. The EMA assessment report suggests that flavonoids such as naringenin and eriodictyol, catechins, and salicin esters may contribute, and Knuth and colleagues, cited by EMA, detected catechol, a compound described as anti-inflammatory, in the blood of volunteers after an extract supplying 240 mg of salicin, peaking at about 1.5 mg per liter after 1.2 hours. In laboratory studies summarized by MSKCC, willow bark extract inhibited the inflammatory messengers TNF-alpha and COX-2 and the activation of NF-κB, a master switch for inflammatory genes, and raised low glutathione levels. For safety, though, the salicylate is what counts. The US Pharmacopeia review by Oketch-Rabah and colleagues (Planta Medica 2019) calculated that metabolizing 240 mg of salicin could yield 113 mg of salicylic acid, more than the 62 mg delivered by an 81 mg low-dose aspirin tablet, which must by law carry warnings. That is why regulators treat willow bark as a salicylate even though it is too weak and variable to replace aspirin.

What is white willow used for? Mainly pain. MSKCC lists arthritis, fever, headaches, inflammation, influenza, pain, and weight loss among its purported uses, and the EMA assessment report records traditional use for muscle and joint rheumatism, influenza, gouty arthritis, and rheumatoid arthritis, with Germany’s Commission E approving it for feverish illness, rheumatic complaints, and headache. Modern regulation is narrower. EMA recognizes a single type of standardized extract as a well-established medicine for short-term low back pain, and other willow bark preparations as traditional medicines for minor joint pain, fever with a cold, and headache in adults. Those traditional indications rest on long use: EMA considered trials in joint pain and headache but judged them too small and too short to prove benefit. Willow bark is also added to weight-loss and sports products. MSKCC finds no studies showing that it aids weight loss, and notes a serious allergic reaction in a woman with an aspirin allergy who took a weight-loss product containing willow bark.

Low back pain has the strongest evidence. Chrubasik and colleagues (American Journal of Medicine 2000) randomized 210 adults with a flare-up of chronic low back pain, rated at least 5 out of 10, to willow bark extract supplying 120 mg or 240 mg of salicin a day, or placebo, for four weeks, with the painkiller tramadol as the only rescue medicine. In the final week, 39% of the high-dose group, 21% of the low-dose group, and 6% of the placebo group were pain-free without tramadol for at least five days. The high dose separated from placebo after the first week, and the low dose by the second. EMA’s assessor judged the study to be of good quality. An open trial in 228 patients by the same group (Rheumatology 2001) found no significant difference between 240 mg of salicin and 12.5 mg of the anti-inflammatory drug rofecoxib, but patients could use other treatments freely and the open design invites bias. Rofecoxib was withdrawn from the market in 2004, so that comparison is now mainly of historical interest.

Systematic reviews agree that the effect is real but only moderately well supported. Oltean and colleagues’ Cochrane review (2014), covering 14 trials of herbal medicines for low back pain, concluded that daily doses of willow bark standardized to 120 mg or 240 mg of salicin are probably better than placebo for short-term improvements in pain and in the use of rescue medicine, based on two trials with 261 participants and moderate-quality evidence; the rofecoxib comparison was graded very low quality. The review also found that willow minimally affected platelets compared with a heart-protective dose of aspirin, and that no significant adverse events were reported in the included trials. EMA adds that no new willow trials appeared between its first assessment and its 2016 review, and Cochrane’s authors suggested comparing willow with paracetamol (acetaminophen) rather than a withdrawn drug. In practical terms, willow bark is a reasonable short-term option for some adults with flare-ups of back pain, but it has not been tested over months or against today’s first-line treatments.

Arthritis results are disappointing. Schmid and colleagues (Phytotherapy Research 2001) gave 78 people with hip or knee osteoarthritis an extract supplying 240 mg of salicin a day or placebo for two weeks. Pain scores fell 14% with willow and rose 2% with placebo, a difference that only just reached statistical significance (p = 0.047). Biegert and colleagues (Journal of Rheumatology 2004) then ran a larger six-week trial in 127 people with hip or knee osteoarthritis, comparing the same salicin dose with 100 mg of diclofenac a day and with placebo. Pain fell 17% with willow, 47% with diclofenac, and 10% with placebo; diclofenac clearly beat placebo, but willow did not, and the authors concluded that the extract showed no relevant efficacy. In a parallel trial in 26 people with active rheumatoid arthritis, willow did no better than placebo. A 2009 systematic review by Vlachojannis and colleagues called the osteoarthritis evidence conflicting, described the rheumatoid trial as grossly underpowered, and asked whether doses above 240 mg of salicin a day might be needed.

For headache and fever the evidence is thinner still. MSKCC notes that willow bark is thought to lower fever as aspirin does, but that clinical trials have not been performed. The only headache study EMA describes was an open trial without a control group, in which 12 people with migraine took a combination of feverfew and white willow for 12 weeks and had fewer attacks, a design that cannot separate the herbs from placebo or from each other. Willow should not be used for heart protection: MSKCC states that it should not be substituted for aspirin because its potency varies, and Krivoy’s platelet study shows that it lacks aspirin’s strong antiplatelet effect. Laboratory studies have found anti-inflammatory and anticancer effects of willow extracts and salicin, but MSKCC stresses that human data are limited. In folk use, the EMA assessment report records dried willow bark applied to warts in central Italy and willow bark decoctions used to help wounds heal, though neither has been tested in modern trials.

Most of the evidence comes from one type of product: a dry extract made with 70% ethanol at a ratio of 8–14 parts bark to 1 part extract, containing on average 15% total salicin. The EU monograph doses it at 393–786 mg up to twice a day (393–1,572 mg daily) for adults only. The main back pain trial used 786 mg (120 mg of salicin) or 1,572 mg (240 mg of salicin) a day, divided into two doses, and EMA’s assessor advised the 240 mg daily dose. The monograph says to see a doctor or pharmacist if pain persists during the first week, and EMA limits use for back or joint pain to four weeks. ESCOP recommends extracts equivalent to 120–240 mg of total salicin a day and Commission E 60–120 mg (EMA). The European Pharmacopoeia requires willow bark dry extracts to contain at least 5% total salicin, but EMA stresses that extracts differ in their mix of salicylates and other constituents, so results for one extract cannot be assumed for another. The practical rule is to choose a product that states its salicin content per daily dose.

Teas, powders, and tinctures are covered by EMA only as traditional medicines. The monograph gives an infusion of 1–3 g of chopped bark in 150 ml of boiling water three times a day, or a decoction of 4 g boiled, covered, in 200 ml of water for 15 minutes, left to stand for 15 minutes, strained, and drunk warm three times a day after meals. Other traditional forms include powdered bark (260–500 mg three to eight times a day, after meals with plenty of hot water), dry water extracts (480–600 mg twice a day), a 1:1 liquid extract (1–3 ml three times a day), and a 1:5 tincture in 25% ethanol (15–24 ml a day). These deliver far less salicin than the trial extract. The assessment report cites an estimate that 1–3 g of bark three times a day supplies about 60–120 mg of salicin daily, and warns that bark decoctions will usually not match the doses used in trials. Expect a bitter, astringent drink: Martyr notes that white willow’s bitter tannins would cause stomach pain long before chewing or brewing delivered an effective dose.

In the United States willow bark is sold as a dietary supplement, and the USP review points out that, unlike low-dose aspirin, supplements are not required to carry warnings. USP’s Salix species monograph now asks that products bear the statement “Not for use in children, women who are pregnant or nursing, or by persons with known sensitivity to aspirin.” Check whether a label names the species and states the salicin per dose, and be wary of multi-ingredient weight-loss formulas that list willow among many other ingredients; the anaphylaxis case described by Boullata and colleagues involved such a product. Follow EMA’s time limits: no more than four weeks for back or joint pain, a doctor if fever lasts more than three days or headache more than one day, and prompt medical advice for fever above 39°C, fever with a severe headache, or symptoms that worsen. Do not combine willow with aspirin, other NSAIDs, or other salicylate products, and do not strip bark from wild trees: willows hybridize freely, and the species and salicin content of a wild tree are unknown.