Uva Ursi (Bearberry)

Arctostaphylos uva-ursi belongs to the heather family, Ericaceae. Linnaeus named it Arbutus uva-ursi in 1753, and it received its current name in 1825, according to Kew’s Plants of the World Online (POWO). The genus name comes from the Greek for bear and grape, and the species name repeats the idea in Latin (Grieve). Common names include bearberry and kinnikinnick (FEIS) and, in nineteenth-century America, upland cranberry (King’s American Dispensatory). Its range circles the Northern Hemisphere: POWO records it as native from the subarctic south through northern, western, and central North America, and across Europe and Asia from Iceland and Norway to Spain, Greece, Siberia, and Mongolia. In North America it grows from Alaska and northern California across Canada to Newfoundland and New England, south in the Rocky Mountains to New Mexico, along the Atlantic coast to New Jersey, and down the Appalachians to Virginia (FEIS). In Britain, Grieve found it common in the Scottish Highlands and as far south as Yorkshire, and it also grows in northwest Ireland.

It is a prostrate evergreen shrub with long trailing stems that root where they touch the ground, forming dense mats, and its bark flakes with age (FEIS). The leaves are thick and leathery, dark glossy green above and paler beneath, about 1 to 3 cm long, rounded at the tip and narrowing toward the base; the European Pharmacopoeia’s description, quoted by EMA, notes a network of sunken veins that gives the upper surface a grainy look, and only young leaves have fine hairs at the margin. Small urn-shaped flowers, white or pinkish with a red lip, hang in drooping clusters of about 3 to 15 at the stem tips in spring (Grieve). They are followed by bright red berries 6 to 10 mm across, usually containing five hard seeds, with dry, mealy, tasteless flesh, and the fruit hangs on through winter (FEIS; Grieve). Bears eat the berries in autumn and especially in early spring, and grouse, wild turkey, songbirds, deer, and small mammals take them too, while hummingbirds visit the flowers (FEIS).

Bearberry is a plant of poor ground. It thrives on dry, acidic, nutrient-poor soils, on rocky outcrops, sand dunes, heaths, and alpine slopes, and forms the main ground cover in open jack pine, lodgepole pine, and ponderosa pine forests; its roots have been traced more than a meter down, and it spreads mainly by its rooting stems (FEIS). Gardeners and road builders use it as ground cover and for erosion control (FEIS). The leaf’s chemistry is dominated by arbutin, a molecule of glucose joined to hydroquinone. EMA reports 5% to 16% arbutin, varying with the season, up to 4% methylarbutin, less than 0.3% free hydroquinone, 10% to 20% tannins including gallotannins and corilagin, 0.8% to 1.5% of the flavonoid hyperoside, and triterpenes including ursolic acid. Medicinal leaf must contain at least 7% arbutin to meet the European Pharmacopoeia standard. Grieve gave a much lower tannin figure, 6% to 7%. Hydroquinone is not unique to bearberry: EMA notes that it occurs in pears, blueberries, coffee beans, and wheat products.

Bearberry’s medical history begins in northern Europe. Grieve records that it was used in the thirteenth century by the Welsh “Physicians of Myddfai,” and EMA’s assessment report notes that it seems to have been a folk remedy in northern regions long before it reached central Europe. The Flemish botanist Carolus Clusius described it in his Rariorum Plantarum Historia, published in Antwerp in 1601, and Linnaeus included it in his Materia Medica of 1749 (EMA). Gerhard of Berlin and others recommended it for medicinal use in 1763, and it entered the London Pharmacopoeia in 1788, though it was probably in use long before (Grieve). In Germany it was used on a larger scale from the middle of the eighteenth century and became official in the early nineteenth. Physicians once prescribed it for dropsy, stones, diabetes, and gonorrhea, but its use later narrowed to a urinary antiseptic and diuretic (EMA). The tannin-rich leaves had another job: they were used to tan leather in Sweden and Russia (Grieve) and in Scandinavia generally (FEIS).

In North America, bearberry was part of daily life long before it entered pharmacy. EMA notes its use by Native Americans for urinary diseases, and LiverTox describes Native American use for urinary symptoms and as a diuretic. FEIS reports that smoking the leaves as a tobacco substitute is the most widely mentioned human use of the plant, and that Native Americans also powdered the leaves for sores and ate the berries fried or mixed into pemmican. The word kinnikinnick, first recorded in English in 1799, comes from an Algonquian language and means a mixture; it named a blend of dried leaves and bark, sometimes with tobacco, smoked by Indigenous Americans and pioneers, and then the plants used in it, especially bearberry (Merriam-Webster). By 1898, King’s American Dispensatory listed uva ursi as official in the United States Pharmacopoeia, recommended it for chronic bladder irritation and catarrh, and warned that the leaves were often adulterated with whortleberry or cowberry leaves, which can be told apart because only uva ursi has a fine network of veins beneath.

Chemistry gradually explained the old remedy. King’s records that Kawalier announced the isolation of arbutin in 1852, that an earlier chemist had attributed the leaf’s diuretic power to a crystalline substance he called ursin, and that acids split arbutin into sugar and hydroquinone. EMA dates the idea that hydroquinone released from arbutin is the active antibacterial agent to 1883. In the twentieth century, Germany’s Commission E endorsed bearberry for inflammatory disorders of the lower urinary tract, with no more than a week’s use and no more than five times a year without a doctor, and WHO and ESCOP published monographs in 2002 and 2003. EMA adopted its first European Union monograph in 2011, revised it in 2012, and issued the current second revision in January 2018, restricting use to women and to one week. In March 2025, EMA’s herbal committee completed a periodic review that summarized the two new clinical trials, but judged that they did not trigger a revision at that time.

Arbutin is a prodrug, a compound that does little until the body changes it. In a study by Schindler and colleagues (Journal of Clinical Pharmacology 2002), 16 healthy volunteers took a bearberry extract as film-coated tablets or as a solution; on average about two-thirds of the arbutin dose was recovered in the urine as hydroquinone and its conjugates, peaking around 4 hours after the dose, with considerable variation between individuals. Almost all of it arrives in the urine bound to glucuronic acid or sulfate, forms that are not themselves antibacterial. In a study of 12 volunteers given 420 mg of arbutin, Siegers and colleagues, summarized by EMA, found that only about 0.6% of the dose appeared as free hydroquinone, and in half the volunteers none could be detected. The theory is that free hydroquinone, released from these conjugates within the bladder, is what acts against bacteria, which would explain why bearberry was always described as a urinary antiseptic rather than a general antibiotic.

How free hydroquinone is released has been argued over for decades. Laboratory work in the 1970s found that urine collected after arbutin or bearberry tea inhibited Staphylococcus aureus and Escherichia coli when it was alkaline, at pH 8, but not at pH 6 (Frohne 1970; Kedzia 1975, summarized by EMA). This is why older handbooks told patients to take sodium bicarbonate or eat a vegetable diet. But keeping urine alkaline is hard: in one experiment, 10 g of sodium bicarbonate raised urine pH from 6.5 to 7.4 on average, and therapeutic levels of free hydroquinone were reached only when the pH reached 8, which happened in one case for an hour. EMA concludes that whether alkalizing helps in the body is doubtful. Siegers’s group offered another explanation: E. coli itself released hydroquinone from its conjugates more efficiently than a laboratory enzyme mixture, suggesting that bacteria free the active compound where they are, without any need to alter urine pH. All of this comes from laboratory and volunteer studies, not from trials in people with infections.

The leaf’s other main constituents, its tannins, act on the gut rather than the bladder. EMA attributes bearberry’s nausea and vomiting to tannins and notes that boiling the leaf extracts much more of them than steeping it in cold water, which is why it recommends an infusion or cold macerate rather than a decoction. Arbutin also blocks tyrosinase, the enzyme that makes melanin pigment: EMA cites laboratory work in which both a bearberry extract and arbutin inhibited the enzyme, and this is the basis of arbutin’s use in skin-lightening cosmetics. Germany’s Federal Institute for Risk Assessment (BfR) considers such cosmetic use a health concern, because arbutin can be broken down in the skin, partly by skin bacteria, into hydroquinone. The same melanin-blocking effect was suggested as the cause of retinal damage in a long-term tea drinker. EMA also notes laboratory evidence that leaf extracts inhibit CYP3A drug-metabolizing enzymes, but no clinical reports of interactions.

Relief of mild bladder infection symptoms is bearberry’s one accepted use, and it rests on tradition rather than proof. EMA’s monograph allows it as a traditional herbal medicine for relief of symptoms of mild recurrent lower urinary tract infections, such as a burning sensation during urination and frequent urination, in women, after serious conditions have been excluded by a doctor, on the strength of long-standing use. EMA’s assessors concluded that there were no clinical studies to support a well-established use, but that laboratory evidence of antibacterial activity, together with centuries of use, made short-term traditional use plausible. Earlier references cast the net wider: Commission E listed inflammatory disorders of the lower urinary tract, ESCOP listed uncomplicated lower urinary tract infections such as cystitis when antibiotic treatment is not considered essential, and the British Herbal Pharmacopoeia of 1983 named acute catarrhal cystitis with painful urination and highly acid urine. The European indication is deliberately narrow: it covers mild, recurrent, lower urinary infections in women whose doctor has already excluded serious causes, not a first episode of unexplained symptoms or a possible kidney infection.

The first large placebo-controlled trial was disappointing. In the ATAFUTI trial, Moore and colleagues (Clinical Microbiology and Infection 2019) randomized 382 women aged 18 to 70 who consulted in primary care with a suspected uncomplicated UTI. Using a factorial design, they tested uva ursi extract against placebo and, separately, advice to take ibuprofen against no such advice; every woman also received a delayed, or back-up, antibiotic prescription. On days 2 to 4, symptom scores for frequency of urination barely differed between uva ursi and placebo (a difference of 0.06 points, with a confidence interval from 0.33 lower to 0.21 higher). Antibiotics were used by 39.9% of women on uva ursi and 47.4% on placebo, a difference that was not statistically significant. Advice to take ibuprofen, by contrast, did reduce antibiotic use, from 51.0% to 34.9%. There were no safety concerns and no upper urinary tract infections. EMA’s 2025 review notes that the extract contained 20% arbutin and that only 286 symptom diaries were returned.

REGATTA asked whether uva ursi could replace an antibiotic as the first treatment. Gágyor and colleagues (Clinical Microbiology and Infection 2021) randomized 398 women with suspected uncomplicated UTIs in 42 German family practices to two 105 mg uva ursi tablets three times a day for five days or a single 3 g dose of fosfomycin, each with a matching placebo so that neither the women nor their doctors knew who had which. Over 28 days, the uva ursi group used 63.6% fewer antibiotic courses. But their total symptom burden was 136.5% of that in the fosfomycin group, so uva ursi failed the test of being no worse than the antibiotic, and eight women in the uva ursi group developed pyelonephritis, a kidney infection, compared with two on fosfomycin, a difference that narrowly missed statistical significance. Other adverse events were similar. The authors concluded that starting with uva ursi reduced antibiotic use but led to a higher symptom burden and more safety concerns. Taken together, the two trials do not show that bearberry relieves symptoms, and REGATTA raises the concern that relying on it instead of an antibiotic may let some infections reach the kidneys.

Prevention has even less evidence, and it sits awkwardly with the safety limits. The only trial usually cited is a preliminary report by Larsson and colleagues (Current Therapeutic Research 1993), as summarized by LiverTox: 57 women with recurrent cystitis took UVA-E, a combination of uva ursi with dandelion, or placebo for one month, and in the following year none of the 30 on the combination had cystitis, against 5 of the 27 on placebo. The dose is not known. IQWiG, in a 2022 health technology assessment of herbal remedies for recurrent bladder infections, found only a hint of benefit for this uva ursi and dandelion preparation, noted that it and another combination of uva ursi with birch were either unavailable or inadequately described, and concluded that, apart from cranberry, the data were too limited to judge whether herbal preventives are a good option. Because EMA limits use to one week at a time, daily bearberry is not a prevention strategy, and the one known case of retinal damage occurred in a woman who drank bearberry tea for three years to ward off infections.

Other uses are untested. The WHO monograph, as summarized by EMA, records folk use as a diuretic, to stimulate uterine contractions, and for diabetes, poor eyesight, kidney and bladder stones, rheumatism, and venereal disease, and topically to lighten the skin; none has clinical support. LiverTox concludes that, despite extensive traditional use, there is no convincing medical evidence that uva ursi is effective for urinary infections or urinary symptoms, and notes that it now appears in multi-ingredient supplements marketed for weight loss, wellness, anti-aging, and energy. Long-term use of such products goes beyond anything EMA considers acceptable for bearberry. Its reputation as a diuretic is also shaky: King’s American Dispensatory remarked in 1898 that the leaf was said not to act as a diuretic in healthy people. Laboratory studies summarized by EMA report antiviral activity and anti-inflammatory effects in mice, but these have not been studied in people. For preventing repeat UTIs, cranberry has better evidence (see the FAQs below).

EMA’s monograph covers five preparations, all for adult women and all for no more than one week; if symptoms last more than four days, a doctor should be consulted. As a tea, 1.5 to 4 g of the cut leaf is steeped in 150 ml of boiling water as an infusion, or soaked in 150 ml of water as a macerate, two to four times a day, up to 8 g a day; the macerate should be drunk immediately after it is made. The powdered leaf is taken at 700 to 1,050 mg twice a day, up to 1.75 g a day. Two standardized dry extracts, one made with 60% ethanol and one with water, are dosed by their content of hydroquinone derivatives calculated as arbutin: 100 to 210 mg two to four times a day, or 200 to 840 mg a day in total. A 1:1 liquid extract in 25% ethanol is taken at 1.5 to 4 ml up to three times a day, to a maximum of 8 ml. EMA’s assessors judged doses corresponding to 840 mg of arbutin a day for one week to be safe, based on long experience. ESCOP allowed up to two weeks.

How the tea is made matters. EMA notes that decoction, or boiling, extracts large amounts of tannin, while cold maceration prevents it, and recommends infusion or maceration to keep stomach upset to a minimum. Older recipes were stronger: Grieve gave an ounce of leaves to a pint of boiling water, and German pharmacy handbooks described boiling the powdered leaf for 15 minutes (EMA). The arbutin content of the leaf varies with the season, from about 5% to 16% (EMA), so an unstandardized tea delivers an uncertain dose, while the clinical trials used standardized extracts; REGATTA’s two 105 mg tablets three times a day kept women within EMA’s daily limit. LiverTox notes that supplements are typically sold as tablets and capsules of 150, 455, and 505 mg, taken one to three times a day. EMA’s assessment also lists many combination bladder and kidney teas and tablets in which bearberry is mixed with birch leaf, horsetail, goldenrod, juniper, buchu, and other herbs, and taking several such products together can add up to more arbutin than intended.

In practice, bearberry is for short courses, not daily use. Commission E’s rule of no more than a week at a time and no more than five times a year without a doctor is a sensible ceiling, and needing it more often is a reason to discuss recurrent infections with a doctor, who can offer prevention strategies (MedlinePlus). Expect urine to turn greenish-brown, which EMA attributes to hydroquinone oxidizing on contact with air. There is no need to take sodium bicarbonate or follow a special alkaline diet: bicarbonate raises urine pH only briefly, and EMA doubts that alkalizing helps in the body. WHO and ESCOP advised drinking plenty of fluids during treatment. If symptoms worsen, or fever, painful urination, cramps, or blood in the urine appear, stop and see a doctor (EMA), and anyone whose symptoms come back soon after a course of antibiotics should also be seen (MedlinePlus).