IngredientsBoldo (Peumus boldus Molina), commonly known by its Mapuche name foḻo, is a species of tree in the family Monimiaceae and the only species in the genus Peumus. It is endemic to the central region of Chile, between 33° and 40° southern latitude. The boldo tree grows abundantly in the more humid ecosystems of the Mediterranean climatic region of central Chile and extends into the northern half of the much rainier Chilean lake district, between 33° and 39° South latitude.
It is a strongly aromatic, multibranched, evergreen shrub or tree, growing to about twenty feet in height and producing leathery, egg-shaped leaves, clusters of white or yellow bell-shaped flowers, and small yellow berries. The part of the species used medicinally is the leaf (boldo folium), which is simple, ovate, greyish-green on the upper side and whitish on the lower, shortly petioled, hard, and with a pleasant smell. The hallmark of boldo leaf is the presence of numerous bumps, corresponding to star-arranged protective hairs and a revolute margin. The spongy mesophyll is full of oil glands producing a brownish-yellow oil of camphoraceous odor and aromatic taste, containing 1,8-cineole, p-cymene, and ascaridole as major components.
Boldo has also been introduced to Europe and North Africa, though it is not often seen outside botanical gardens. Due to its common name, it is often confused with the species Plectranthus ornatus, known as falso boldo ("false boldo"), boldo paraguayo, or boldo rastrero, which has led to confusion about the uses, properties, and toxicity of both species.
The name "boldo" or "boldu" is presumably derived from the indigenous Mapuche verbs "weltum" (to sprout again) or "volitum" (to put out new roots), which may refer to this feature.
Peumus boldus is found in the official pharmacopoeias of Brazil, Chile, Germany, Spain, Portugal, and Switzerland as a reference in the treatment of liver diseases. Among Chilean medicinal plants, P. boldus stands out at the regulatory level, with leaves included in pharmacopoeias and official monographs due to their choleretic, hepatoprotective, and antioxidant effects. The European Medicines Agency's Committee on Herbal Medicinal Products (HMPC) has issued a community herbal monograph on Boldi folium, and the plant is recognized by ESCOP (European Scientific Co-operative on Phytotherapy).
Every year Chile exports about 2,000 tons of boldo folium (Peumus boldus), which is used around the world as a traditional herbal medicinal product (THMP), mostly to relieve gastrointestinal disorders. Boldo leaves (Boldi folium, from Peumus boldus Mol.) are very frequently used as a medicinal herb in Chile and are exported to many countries to be used in teas or as extracts included in herbal remedies, primarily as an aid to digestion and as a mild sedative.
The HMPC conclusions cover boldo leaf preparations obtained by drying and comminuting the leaves, or by putting the plant material in water to dissolve compounds and form a liquid extract, after which the solvent is evaporated to obtain a dry extract. Herbal medicines containing these boldo leaf preparations are usually available as herbal tea to be drunk and in solid forms to be taken by mouth. Standardized preparations must contain a minimum of 0.1% alkaloids expressed as boldine and at least 2.0% essential oils.
Boldo (Peumus boldus) is a Chilean evergreen tree known for its traditional medicinal use. Indigenous Mapuche people employed its leaves for centuries, particularly for digestive remedies. Boldo was a traditional remedy used by the Araucanian people of Chile as a tonic, and the berries are also eaten as a food. Boldo has a long history of use by the indigenous people of Chile as a liver tonic and in the treatment of gallstones.
Historically, boldo was used by Chilean indigenous peoples as a hepatic tonic, carminative, and diuretic, among other uses. In its native area, where it is most often consumed as a tea, boldo has been traditionally used to treat hangovers, gout, stomachache, and urogenital inflammation. Boldo is popularly used in cases of hepatitis, hepatic colic, biliary lithiasis, intestinal disorders, rheumatism, poor digestion, asthenia, dyspepsia, inappetence, and other disorders.
Known in Europe since the 1880s, boldo is especially valued for its beneficial action on hepatobiliary disorders. The leaves were progressively included in the French Pharmacopoeia (8th edition, 1965; 9th edition, 1979) and eventually received formal recognition across multiple national and European regulatory frameworks.
In Brazil, Argentina, Chile, Uruguay, and Paraguay, boldo is mixed with yerba mate or other teas to moderate its flavor. Native to Chile, boldo is one of the most widely used household herbs for preparing bitter infusions, traditionally associated with digestive and liver health.
The dry leaves of Peumus boldus (Monimiaceae) are used in infusion or decoction as a digestive and to improve hepatic complaints. Traditional healers employed the leaves as infusions, decoctions, and tinctures, primarily for digestive and hepatobiliary support.
Eighteen alkaloids have been detected in the bark, leaves, wood, and roots of Peumus boldus, including traces of secoboldine, N-methylsecoboldine (boldine methine), glaucine, and norreticuline, not previously reported as constituents of this species. Boldine is dominant in the bark, and laurolitsine in the wood and roots. The alkaloid composition of the leaves, determined for 130 individually identified trees classified by age and sex, was highly variable, where N-methyllaurotetanine, laurotetanine, coclaurine, and in some cases isocorydine predominated, but not boldine.
The characteristic principal alkaloid is boldine, chemically identified as (S)-2,9-dihydroxy-1,10-dimethoxyaporphine, a major alkaloid found in the leaves and bark of boldo (Peumus boldus Molina), which has been shown to possess antioxidant activity and anti-inflammatory effects. Boldine's only commercial source today is the bark of the Chilean tree Peumus boldus Molina.
Boldine is not usually the major alkaloid of the leaves, and some of the medicinal properties of this herbal remedy are probably due to other, non-alkaloidal constituents. The preferential attention given to boldine's pharmacology has been to the detriment of structurally very similar 1,2,9,10-tetraoxygenated phenolic aporphine alkaloids, notably isoboldine and N-methyllaurotetanine. It is particularly noteworthy as a source of alkaloids such as boldine, laurolitsine, N-methyllaurotetanine, isocorydine, and coclaurine.
The phenolic constituents identified in infusions of the crude drug Boldi folium are mainly proanthocyanidins and flavonol glycosides. Nine quercetin glycosides, eight kaempferol derivatives, nine isorhamnetin glycosides, three phenolic acids, one caffeoylquinic acid glycoside, and twenty-one proanthocyanidins were identified by HPLC-DAD and ESI-MS. A small number of studies have addressed the polyphenolic constituents of boldo leaves. Flavon-3-ol glycosides, catechins and their oligomers (proanthocyanidins), and aromatic phenolic acids have been identified.
Catechin proved to be the main free-radical scavenger of hot-water extracts of boldo leaves. On the basis of dry starting material, the catechin content in the crude drug was 2.25%, while the total alkaloid calculated as boldine was 0.06%.
Boldo leaves contain between 2% to 3% essential oils, with components such as p-cymene and ascaridole, as well as flavonoids and a small amount of coumarin. A detailed GC-MS analysis showed that hydrodistillation of commercial boldo folium gave 1.5% (w/w) of a yellowish essential oil containing 1,8-cineole (20.7%), p-cymene (18.5%), limonene (9.1%), ascaridole (9.1%), and β-phellandrene (6.4%) as the main constituents.
Research conducted during the early 1990s led to the discovery that boldine is one of the most potent natural antioxidants. Boldine displays some important pharmacological activities, such as cytoprotective and anti-inflammatory activities, which may arise from its free radical scavenging properties. Lipid peroxidation in erythrocytes was inhibited by boldo extracts and fractions at 500 µg/ml with higher effect for the ethyl acetate soluble and alkaloid fractions. The IC50 for catechin and boldine in the lipid peroxidation test were 75.6 and 12.5 µg/ml, respectively. The activity of boldine was six times higher than catechin in the lipid peroxidation assay.
Studies conducted in the last 20 years indicate that boldine may interact with specific receptors and ion channels, most notably by blocking movement of small molecules through connexin (Cx) hemichannels (HC). The current consensus is that boldine's Cx HC blocking actions contribute much more to boldine's therapeutic effects than its antioxidant activity. Boldine inhibits connexin hemichannels (Cx HCs), pannexin 1 hemichannels (Panx1 HCs), and the purinergic receptor P2X7. This channel blockade significantly reduces Ca²⁺ influx and K⁺ efflux, both of which are key activators of the inflammasome. As a result, boldine reduces the activation of caspase-1, leading to decreased production of IL-1β, a key outcome of inflammasome activation. Importantly, boldine does not inhibit gap junction channels formed by connexins.
Boldine exhibits a dose-dependent anti-inflammatory activity in the carrageenan-induced guinea pig paw edema test with an oral ED50 of 34 mg/kg. Boldine also reduces bacterial pyrogen-induced hyperthermia in rabbits to an extent which varied between 51% and 98% at a dose of 60 mg/kg p.o. In vitro studies in rat aortal rings revealed that boldine is an effective inhibitor of prostaglandin biosynthesis, promoting 53% inhibition at 75 µM. This in vitro effect may be mechanistically linked to the anti-inflammatory and antipyretic effects of boldine exerted in vivo.
A dried hydroalcoholic extract of Peumus boldus has been evaluated for hepatoprotective, choleretic, and anti-inflammatory effects in mice and rats. This extract exerted a significant hepatoprotection of tert-butyl hydroperoxide-induced hepatotoxicity in isolated rat hepatocytes (in vitro technique) by reducing lipid peroxidation and the enzymatic leakage of LDH; this efficacy was reinforced by a significant hepatoprotection on CCl4-induced hepatotoxicity in mice (in vivo technique), with the plant extract reducing the enzymatic leakage of ALAT. Boldo has hepatoprotective properties, particularly against damage caused by hepatotoxic agents such as cisplatin. This protection is attributed to the catechins in boldo, which have significant antioxidant effects. These compounds effectively prevent lipid peroxidation in hepatic microsomes and reduce the activity of cytochrome P4502E1, thereby limiting oxidative damage to the liver.
Boldine exerts neuroprotective effects through a variety of mechanisms, including suppression of AChE and BuChE activity, blocking of connexin-43 hemichannels and pannexin 1 channels, reduction of NF-κβ mediated interleukin release, and reduction of glutamate excitotoxicity, which collectively reduce neuronal damage. A specific hemichannel inhibitor, boldine, derived from the boldo tree and shown to inhibit astrocytic and microglial hemichannels but not gap junctions, was evaluated in a murine model of Alzheimer's disease. The use of boldine in this model caused a reduction of ATP and glutamate release by astrocytes and activated microglia, alleviating hippocampal neuronal suffering.
Boldine may exert protective effects on the endothelium via several mechanisms, including protecting nitric oxide from degradation by reactive oxygen species in oxidative stress–related diseases. Available evidence supports a complementary therapeutic role of boldine against endothelial dysfunction associated with hypertension and diabetes mellitus by interfering with the oxidative stress–mediated signaling pathway. Boldine also protects against endothelial dysfunction through a mechanism proposed to result from anti-oxidant actions or inhibition of an angiotensin II-mediated BMP4-oxidative stress cascade.
Traditional basis and regulatory status: The HMPC concluded that, on the basis of its long-standing use, boldo leaf preparations can be used for the relief of symptoms of dyspepsia (indigestion) and mild spasms of the gut. The Committee on Herbal Medicinal Products (HMPC) has concluded that boldo leaf preparations available as herbal tea can be used for the relief of symptoms of dyspepsia and mild spasms of the gastrointestinal tract.
Human evidence: No studies in patients have been carried out with boldo leaf. The sole small human study identified involves intestinal transit: Gotteland et al. (1995) treated twelve healthy volunteers daily with 2.5 g of a dry boldo extract (ethanol 60% v/v) containing 0.12% of boldine and 0.4% of total alkaloids during two successive periods of four days, showing prolongation of oro-cecal transit time compared to placebo.
Preclinical evidence: The flavones boldoside and peumoside suppressed induced excitation in mice and demonstrated a marked spasmolytic effect in rabbits experiencing gut spasm.
Evidence strength: The EMA's HMPC classification for boldo leaf in the area of dyspepsia is traditional use — meaning it is supported by documented historical use but not by adequate clinical trial data. Scientific support for these uses is scanty.
Preclinical evidence: Multiple in vitro and animal studies support hepatoprotective properties. A dried hydroalcoholic extract exerted significant hepatoprotection of tert-butyl hydroperoxide-induced hepatotoxicity in isolated rat hepatocytes and on CCl4-induced hepatotoxicity in mice. Boldine, the main alkaloid of P. boldus, appears to be implicated in this hepatoprotective activity. Studies have demonstrated that polar extracts of Peumus boldus are able to display antioxidant activity and reduce hepatic lipoperoxidation induced by cisplatin.
Human evidence: No controlled clinical trials in human patients have demonstrated hepatoprotective effects. Clinical studies remain limited, with preclinical trials predominating and supporting its multifunctional profile.
Evidence strength: The hepatoprotective effect is well-supported in animal and in vitro models, but no human clinical trials are available. All hepatoprotective evidence in humans remains inferential.
Choleretic effects, often mentioned in traditional indications, have not been confirmed in rats. Previous studies have failed to demonstrate choleretic activity after oral administration of 200–800 mg/kg of aqueous ethanolic boldo extract, or after intravenous administration of either ethanolic extract. The indications for the use of boldo are extremely broad in range and just as unsubstantiated.
Evidence strength: The choleretic claim is traditional in origin but has not been confirmed in available preclinical models, and no human trials have been conducted.
Preclinical evidence: Significant and dose-dependent anti-inflammatory effects were obtained in the acute carrageenan-induced edema test in rats. Boldine demonstrated anti-inflammatory properties in experimental colitis models. Mice with docusate sodium-induced ulcerative colitis treated with boldine 50 mg/kg orally for 7 days had less weight loss and better disease activity index scores compared with untreated mice. Boldine also decreased spleen weights, suppressed shrinkage of colon length, blocked inflammatory cell infiltration, and restored architecture of the colon epithelium.
Evidence strength: Evidence is preclinical (animal and in vitro only). No human clinical trials on inflammatory conditions have been conducted with boldo or boldine.
In vitro evidence: The anti-Helicobacter pylori effect of an aqueous extract from dried leaves of Peumus boldus Mol. (Monimiaceae) was evaluated. This extract displayed high inhibitory activity against H. pylori urease. The active fraction from aqueous extract was the most active against H. pylori urease with an IC50 = 15.9 µg gallic acid equivalents (GAE)/mL. HPLC analysis evidenced that this fraction was composed mainly of catechin-derived proanthocyanidins. The anti-adherent effect of boldo was assessed by co-culture of H. pylori and AGS cells. Both the aqueous extract and the active fraction showed an anti-adherent effect in a concentration-dependent manner.
Evidence strength: This evidence is entirely in vitro (cell-based laboratory studies). Certain chemical compounds such as flavonoids and antioxidants found in boldo leaves are associated with various activities attributed to these plants. However, the efficacy of these teas in treating peptic ulcers has not been scientifically established.
Boldine exerts antioxidant, hepatoprotective, anti-atherosclerotic, anti-diabetic, analgesic, antipyretic, anti-inflammatory, anti-epileptic, neuroprotective, nephroprotective, anti-arthritis, anticancer, and nootropic effects — though the majority of these are demonstrated in preclinical settings only. Research conducted during the early 1990s led to the discovery that boldine is one of the most potent natural antioxidants. A large and increasing number of studies emerged which focused on characterizing pharmacological properties that may arise from the free radical-scavenging properties of boldine.
Evidence strength: Strong evidence exists for antioxidant activity in vitro and in animal models. Human clinical evidence is absent.
Over the past decade, boldine has garnered attention for its efficacy in rodent models of human disease. Properties attributed to boldine include antioxidant activities, neuroprotective and analgesic actions, hepatoprotective effects, anti-inflammatory actions, cardioprotective effects, and anticancer potential. Long-term oral administration of boldine in Alzheimer's disease (AD) mice revealed prevention of increases in glial hemichannel activity, astrocytic Ca²⁺ signal, ATP and glutamate release, and alleviated hippocampal neuronal suffering. Another study investigating the neuroprotective effect of boldine in cellular models using primary hippocampal neurons and an HT22 hippocampal-derived cell line treated with amyloid beta peptide oligomers showed that boldine interacts with amyloid beta in silico, preventing its aggregation and defending hippocampus neurons against synaptic failure.
Evidence strength: Preclinical evidence (rodent models and in vitro) only. No human clinical trials have been conducted.
Available evidence supports a complementary therapeutic role of the phytochemical boldine against endothelial dysfunction associated with hypertension and diabetes mellitus by interfering with the oxidative stress–mediated signaling pathway. A randomized trial conducted by the Heart Protection Study Collaborative Group showed that a combined antioxidant regimen did not produce any significant effect on 5-year mortality from vascular and non-vascular diseases. Similarly, meta-analysis of several clinical trials demonstrated that supplementation of beta-carotene and vitamin E did not demonstrate any benefit. This context illustrates the general difficulty in translating antioxidant-based preclinical findings to human cardiovascular outcomes.
Evidence strength: Preclinical evidence only. No human clinical trials with boldo or boldine in cardiovascular endpoints have been reported.
Since current treatments for diabetic nephropathy do not prevent renal damage, researchers postulated an alternative treatment with boldine. Streptozotocin-induced diabetic and control rats were treated with boldine (50 mg/kg/day) for ten weeks. Mesangial cells were also cultured under control conditions or in high glucose concentration plus proinflammatory cytokines, with or without boldine (100 µmol/L). Boldine treatment in diabetic animals prevented the increase in glycemia, blood pressure, renal thiobarbituric acid reactive substances, and the urinary protein/creatinine ratio.
Evidence strength: Evidence is preclinical (animal models and cell culture). No human clinical trials are available.
No quality clinical trials exist to support therapeutic dosing of boldo leaf extract. Traditional doses include 1 to 2 teaspoons (2 to 3 g) of dry leaf per cup of water; 0.1 to 0.3 mL of liquid extract (1:1 in 45% alcohol) 3 times a day.
The volatile oil of boldo is not recommended due to its high ascaridole content. The dried leaf can be used as an infusion at 3 grams per day.
The single small human trial on oro-cecal transit used 2.5 g per day of a dry boldo extract (ethanol 60% v/v) containing 0.12% of boldine and 0.4% of total alkaloids, administered over two successive periods of four days.
The key preclinical anti-inflammatory dose in animal models was an oral ED50 of 34 mg/kg for boldine's anti-inflammatory activity in the carrageenan-induced paw edema test, and 60 mg/kg p.o. for antipyretic effects in rabbits.
In the nephroprotective rat study, streptozotocin-induced diabetic and control rats were treated with boldine at 50 mg/kg/day for ten weeks.
As reported in one phytotherapy reference, an infusion of 1–2 g of crushed herb in 150 mL of boiling water, taken 2–3 times a day, and a dry extract daily dose of 60–200 mg have been described.
The volatile oil (2.5% in the leaf) contains ascaridole, a hepatotoxic toxin. Ascaridole is a matter of concern due to its toxicity, so that ascaridole-containing boldo preparations should be managed carefully for human use. Boldo should be used with caution as the leaves contain ascaridole, which can be toxic to the liver. There are ascaridole-free preparations available, and only those should be used medicinally.
Published case reports have documented hepatotoxicity associated with boldo use. Piscaglia et al. published a case report titled "Caution in the use of boldo in herbal laxatives: a case of hepatotoxicity" in Scandinavian Journal of Gastroenterology, 2005; 40:236–9. Additional published case series document boldo-related adverse events including anaphylaxis, prolonged QT interval, ventricular tachycardia, and hepatotoxicity.
A case of anaphylaxis to a boldo infusion was documented: Monzon S, Lezaun A, Saenz D, et al., "Anaphylaxis to boldo infusion, a herbal remedy," published in Allergy, 2004; 59:1019–20.
A published case report documented behavioural impairments and hallucinations after consumption of boldo leaf infusions, published in Therapie, 2014; 69(5):465–467.
Boldo ingestion may enhance the anticoagulant effect of warfarin; caution is warranted. This interaction is supported by a published pharmacotherapy case report: Lambert J, Cormier J., "Potential interaction between warfarin and boldo-fenugreek," Pharmacotherapy, 2001; 21:509–12. The proposed mechanism involves increased anticoagulant effect of warfarin due to anticoagulant coumarins present in boldo.
A possible interaction with tacrolimus has been documented, resulting in decreased plasma levels. This was reported in: Carbajal R, Yisfalem A, Pradhan N, Baumstein D, Chaudhari A., "Case report: boldo (Peumus boldus) and tacrolimus interaction in a renal transplant patient," Transplant Proceedings, 2014; 46(7):2400–2402.
Boldo leaf medicines must not be taken by patients with obstruction of the bile duct, cholangitis (inflammation of the bile duct), liver disease, gallstones, and any other disorders of the bile ducts. Boldo is contraindicated in liver disease and diseases of the bile duct, including gallstones.
Boldo leaf medicines should only be used in adults. Hypersensitivity (allergic) reactions have been reported with boldo medicines.
The indications for the use of boldo are extremely broad in range and just as unsubstantiated. Future assessments of new boldine analogues — with structural modifications leading to longer half-lives — might merit a more detailed in vivo evaluation of their potential hepatoprotective usefulness. For P. boldus, clinical studies remain limited, with preclinical trials predominating and supporting its multifunctional profile.
Health conditions that Boldo may help support.
Boldo (Peumus boldus) leaves contain boldine with documented choleretic activity—stimulating bile secretion from the liver. Recognized by ESCOP for biliary complaints and used in South American traditional medicine for hepatobiliary disorders. Animal pharmacology studies confirm boldine-induced increases in bile secretion.
Body systems that Boldo may help support.
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