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Kava (Piper methysticum)



Interactions

Kava/Drug Interactions:
  • ACE inhibitorsACE inhibitors: According to secondary sources, kava may have diuretic properties and additive effects when taken with angiotensin-converting enzyme (ACE) inhibitors.
  • AlcoholAlcohol: Animal studies have demonstrated marked increases in alcohol's hypnosedative effects when taken with kava (79). However, this effect has not been confirmed in healthy human volunteers (76). In theory, an interaction between kava and alcohol may one of the mechanisms behind kava hepatotoxicity (141).
  • AnalgesicsAnalgesics: In theory, kava may have additive sedative effects when taken concomitantly with opioid analgesics. In animals, kava produced an analgesic effect that was not antagonized by naloxone (66; 142). In laboratory research, kavapyrones produced analgesic effects (143; 144; 145; 146; 147; 148; 149; 150).
  • AnestheticsAnesthetics: Kava may prolong the sedative action of anesthesia due to presumed MAOI-like action. While numerous anecdotal reports have circulated, there is a lack of clinical research that confirms this interaction (77). According to expert opinion, kava may increase anesthetic potency (78). In laboratory research, kavapyrones produced local anesthetic effects (143; 144; 145; 146; 147; 148; 149; 150). Anesthesiologists may recommend that patients stop taking kava 2-3 weeks prior to surgery.
  • Antianxiety agentsAntianxiety agents: Kava has been shown to have anxiolytic-like effects (151; 134). In animals, kava resulted in dose-related anxiolytic effects (151; 152) without sedation (134).
  • Anticoagulants and antiplateletsAnticoagulants and antiplatelets: Racemic kavain, present in kava preparations, has been shown to have antiplatelet effects due to cyclooxygenase inhibition and inhibition of thromboxane synthesis (67). In survey results, chronic and heavy use of kava has been associated with reduced platelet volume (24; 116).
  • Antidepressant agents, monoamine oxidase inhibitors (MAOIs)Antidepressant agents, monoamine oxidase inhibitors (MAOIs): The pyrone constituents of kava have been found to have weak MAO-inhibitory properties in vitro (155).
  • Antidepressant agents, selective serotonin reuptake inhibitors (SSRIs)Antidepressant agents, selective serotonin reuptake inhibitors (SSRIs): Kava may cause excessive drowsiness when taken with SSRIs. The sedative activity of kava resin and the pyrones dihydrokawain and dihydromethysticin has been reported (1; 66).
  • AntineoplasticsAntineoplastics: According to a review, kava may interact with anticancer drugs (153). Kava may participate in pharmacokinetic interactions with anticancer agents (154).
  • BenzodiazepinesBenzodiazepines: Kava may cause adverse neurological effects and excessive perioperative sedation. Such a reaction may be due to benzodiazepine and antidepressant activities on noradrenergic and/or serotonergic pathways that may potentiate benzodiazepine and induction anesthetic potency (78). In a case report, recommended doses of kava for three days in addition to alprazolam, cimetidine, and terazosin resulted in lethargy and disorientation for several hours (80).
  • BuspironeBuspirone: Kava-Kava LI150 has been used in the acute treatment of outpatients suffering from generalized anxiety disorder (GAD) (94). Therefore, kava may cause additive effects when taken concomitantly with these or other agents with similar effects.
  • Cardiovascular agentsCardiovascular agents: Tachycardia and electrocardiogram (ECG) abnormalities (tall P waves) have been reported in heavy kava users (24). It has been theorized that these P wave abnormalities reflect pulmonary hypertension, although research is lacking in this area. Treatment with kava resulted in a significant improvement in the baroreflex control of heart rate (BRC), although there was a lack of a significant difference in BRC between the kava and placebo groups (47; 87).
  • CNS depressantsCNS depressants: Kava may potentiate CNS depressants, including barbiturates and benzodiazepines (156). Lethargy and disorientation were reported in a 54 year-old man taking kava in combination with alprazolam (80). Kavalactones have been shown to potentiate the effects of CNS depressants, such as ethanol, benzodiazepines, low-potency neuroleptics, beta-blockers, and barbiturates in animals, with concurrent use being potentially toxic (79; 157).
  • ContraceptivesContraceptives: According to preliminary research, kava may decrease uterine tone (1).
  • CYP2D6 substratesCYP2D6 substrates: In a study of 16 healthy humans, kava did not significantly inhibit CYP2D6 (162).
  • CYP2E1 substratesCYP2E1 substrates: A review showed that kava (Piper methysticum) increased chlorzoxazone (a CYP2E1 substrate) clearance and may interact with paroxetine, alprazolam, and levodopa (163).
  • CYP3A substratesCYP3A substrates: In a study of 16 healthy volunteers, kava lacked significant effects on the activity of CYP3A (164).
  • Cytochrome P450 metabolized agentsCytochrome P450 metabolized agents: Preliminary evidence suggests that kava may significantly inhibit multiple cytochrome P450 enzymes, such as cytochrome P450 2C9 inhibitors, cytochrome P450 2D6 inhibitors, and cytochrome P450 3A(4,5,7) inhibitors (158; 159; 160). In 12 healthy humans, kava significantly reduced (by approximately 40%) serum concentrations of CYP2E1 (difference: -0.192; 95% CI: -0.325 to -0.060), while effects of kava on CYP3A4/5, CYP1A2, and CYP2D6 lacked statistical significance (161).
  • Dermatologic agentsDermatologic agents: Historically, chronic and excessive kava use has been shown to cause dry, scaly skin or yellow skin discoloration, also known as "kava dermopathy" (111; 1; 113). In case reports, use of kava for 2-3 weeks resulted in systemic or contact-type dermatitis, sebotropic reactions, and generalized erythema with papules (104; 105; 106). In case reports, kava ingestion resulted in urticaria (107).
  • DigoxinDigoxin: In a study of 20 healthy individuals, kava lacked an effect on pharmacokinetics of digoxin, a substrate of p-glycoprotein (P-gp), when compared to clarithromycin and rifampin. The authors concluded that kava therefore lacks an effect on P-gp (165).
  • DiureticsDiuretics: According to secondary sources, kava may have diuretic properties.
  • Dopamine agonistsDopamine agonists: Kava has been reported to antagonize the effect of dopamine and elicit extrapyramidal effects (55; 71; 73). Kava (Piper methysticum) increased "off" periods in Parkinson's patients taking levodopa and may cause a semicomatose state when given concomitantly with alprazolam (74).
  • Dopamine antagonistsDopamine antagonists: Kava has been reported to antagonize the effect of dopamine and elicit extrapyramidal effects (55; 71; 73). Kava (Piper methysticum) increased "off" periods in Parkinson's patients taking levodopa and may cause a semicomatose state when given concomitantly with alprazolam (74).
  • Gastrointestinal agentsGastrointestinal agents: Gastrointestinal upset has been reported as an infrequent adverse event in trials (6; 114; 91). In one study, patients experienced gastrointestinal problems, including nausea (88). In another study, a participant experienced mild nausea after taking kava; also gastrointestinal discomfort and symptoms resembling the flu began during the placebo phase but worsened during the kava treatment phase (17).
  • Heart rate regulating agentsHeart rate regulating agents: Tachycardia and electrocardiogram (ECG) abnormalities (tall P waves) have been reported in heavy kava users (24). It has been theorized that these P wave abnormalities reflect pulmonary hypertension, although research is lacking in this area. Treatment with kava resulted in a significant improvement in the baroreflex control of heart rate (BRC), although there was a lack of a significant difference in BRC between the kava and placebo groups (47; 87).
  • Hematologic agentsHematologic agents: In survey results, chronic and heavy use of kava has been associated with increased red blood cell volume, reduced platelet volume, reduced lymphocyte counts, and reduced serum albumin (24; 116). According to anecdotal reports, kava intake may lead to hematuria (24). In laboratory research, kavain, a kava constituent, had antiplatelet effects due to cyclooxygenase and thromboxane synthesis inhibition (67). In one case, a patient was taking kava, coltsfoot, and 10 or more other supplements and experienced a deep vein thrombosis and a pulmonary embolism (117).
  • Hepatotoxic agentsHepatotoxic agents: More than 30 cases of liver damage have been reported, including hepatitis (38; 39; 40; 103), cirrhosis, and fulminant liver failure (41; 42), and there have also been reports of death (43; 44). Anecdotally and according to human studies, heavy kava use may have resulted in increased levels of liver enzymes such as gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP) (24; 3; 81). In human research, kava has been connected to necrotizing hepatitis (125; 118; 26) and, upon overdose, to cholestatic hepatitis (26). In a case report, kava consumption resulted in severe toxic liver disease (132).
  • Hormonal agentsHormonal agents: According to preliminary research, kava may decrease uterine tone (1). Kava may have estrogenic properties (117).
  • Mood stabilizersMood stabilizers: The pyrone constituents of kava have been found to have weak MAO inhibitory properties in vitro (155). Kava has been shown to have anxiolytic-like effects (151; 134).
  • Neurologic agentsNeurologic agents: In human studies, kava ingestion resulted in extrapyramidal side effects (55) and worsening of Parkinson's symptoms (71; 72). The extrapyramidal side effects caused by neuroleptic agents may be reduced by kava special extract WS 1490 (166). In a case study, kava intake resulted in choreoathetosis (73). In humans, excessive kava intake infrequently resulted in tremor, malcoordination, headache, drowsiness, and fatigue (6; 24). In three cases, kava resulted in meningismus, two of them with focal neurological manifestations (133). A review concluded that kava may affect electroconvulsive therapy (ECT) outcome (138). In human studies, kava resulted in mood elevation, anorexia, sleeplessness, palpitations, and paresthesias (92), and also dizziness and vivid dreams (98; 97; 17). In laboratory research, kavapyrones produced anticonvulsive, spasmolytic, antimycotic, and hypnotic effects (143; 144; 145; 146; 147; 148; 149; 150).
  • Ophthalmic agentsOphthalmic agents: Anecdotally, accommodative (ocular) disturbances are normally not associated with kava use; however, in a case report, a one-time use of kava was followed by impaired accommodation and convergence, increased pupil diameter, and oculomotor disturbance (139). In survey results, heavy kava use was followed by eye irritation (112). In a controlled study, excessive kava ingestion resulted in blepharospasm and saccadic dysmetria (81).
  • OpipramolOpipramol: Kava-Kava LI150 has been used in the acute treatment of outpatients suffering from generalized anxiety disorder (GAD) (94). Therefore, kava may cause additive effects when taken concomitantly with these or other agents with similar effects.
  • Renally eliminated drugsRenally eliminated drugs: There has been a case report of rhabdomyolysis in a 29 year-old man who consumed an herbal combination of kava, ginkgo, and guarana (69). It is unclear if renal failure occurred. In a case report, a large amount of ingested kava resulted in temporary rhabdomyolysis (70). The causal role of kava in both of these cases is unclear. Acute urinary retention secondary to kava ingestion has also been reported (140).
  • SedativesSedatives: Kava may potentiate CNS depressants, including barbiturates and benzodiazepines (156). Lethargy and disorientation were reported in a 54 year-old man taking kava in combination with alprazolam (80). Kavalactones have been shown to potentiate the effects of CNS depressants, such as ethanol, benzodiazepines, low-potency neuroleptics, beta-blockers, and barbiturates in animals, with concurrent use being potentially toxic (79; 157). In humans, kava has been reported to cause sedation (81) without neurologic impairment (21; 22; 23).

Kava/Herb/Supplement Interactions:
  • ACE inhibitorsACE inhibitors: According to secondary sources, kava may have diuretic properties and additive effects when taken with angiotensin-converting enzyme (ACE) inhibitors.
  • AnalgesicsAnalgesics: In theory, kava may have additive sedative effects when taken concomitantly with opioid analgesics. In animals, kava produced an analgesic effect that was not antagonized by naloxone (66; 142). In laboratory research, kavapyrones produced analgesic effects (143; 144; 145; 146; 147; 148; 149; 150).
  • AnestheticsAnesthetics: Kava may prolong the sedative action of anesthesia due to presumed MAOI-like action. While numerous anecdotal reports have circulated, there is a lack of clinical research that confirms this interaction (77). According to expert opinion, kava may increase anesthetic potency (78). In laboratory research, kavapyrones produced local anesthetic effects (143; 144; 145; 146; 147; 148; 149; 150). Anesthesiologists may recommend that patients stop taking kava 2-3 weeks prior to surgery.
  • Anticoagulants and antiplateletsAnticoagulants and antiplatelets: Racemic kavain, present in kava preparations, has been shown to have antiplatelet effects due to cyclooxygenase inhibition and inhibition of thromboxane synthesis (67). In survey results, chronic and heavy use of kava has been associated with reduced platelet volume (24; 116).
  • Antidepressant agents, monoamine oxidase inhibitors (MAOIs)Antidepressant agents, monoamine oxidase inhibitors (MAOIs): The pyrone constituents of kava have been found to have weak MAO-inhibitory properties in vitro (155).
  • Antidepressants, selective serotonin reuptake inhibitors (SSRIs)Antidepressants, selective serotonin reuptake inhibitors (SSRIs): Kava may cause excessive drowsiness when taken with SSRIs. The sedative activity of kava resin and the pyrones dihydrokawain and dihydromethysticin has been reported (1; 66).
  • AntineoplasticsAntineoplastics: According to a review, kava may interact with anticancer drugs (153). Kava may participate in pharmacokinetic interactions with anticancer agents (154).
  • AnxiolyticsAnxiolytics: Kava has been shown to have anxiolytic-like effects (151; 134). In animals, kava resulted in dose-related anxiolytic effects (151; 152) without sedation (134).
  • Bee pollenBee pollen: In women, ingestion of kava in conjunction with bee pollen, black cohosh, valerian, and nettle resulted in elevated serum lead levels (68).
  • Black cohoshBlack cohosh: In women, ingestion of kava in conjunction with bee pollen, black cohosh, valerian, and nettle resulted in elevated serum lead levels (68).
  • Cardiovascular agentsCardiovascular agents: Tachycardia and electrocardiogram (ECG) abnormalities (tall P waves) have been reported in heavy kava users (24). It has been theorized that these P wave abnormalities reflect pulmonary hypertension, although research is lacking in this area. Treatment with kava resulted in a significant improvement in the baroreflex control of heart rate (BRC), although there was a lack of a significant difference in BRC between the kava and placebo groups (47; 87).
  • ContraceptivesContraceptives: According to preliminary research, kava may decrease uterine tone (1).
  • CYP2D6 substratesCYP2D6 substrates: In a study of 16 healthy humans, kava did not significantly inhibit CYP2D6 (162).
  • CYP2E1 substratesCYP2E1 substrates: A review showed that kava (Piper methysticum) increases chlorzoxazone (a CYP2E1 substrate) clearance and may interact with alprazolam, levodopa, and paroxetine (163).
  • CYP3A substratesCYP3A substrates: In a study of 16 healthy volunteers, kava lacked significant effects on the Supplementation with goldenseal (Hydrastis canadensis), but not kava kava (Piper methysticum), inhibited human activity of CYP3A activity in vivo (164).
  • Cytochrome P450 metabolized herbs and supplementsCytochrome P450 metabolized herbs and supplements: Preliminary evidence suggests that kava may significantly inhibit multiple cytochrome P450 enzymes such as cytochrome P450 2C9 inhibitors, cytochrome P450 2D6 inhibitors, and cytochrome P450 3A(4,5,7) inhibitors (158; 159). In 12 healthy humans, kava produced significantly reductions (by approximately 40%) in serum concentrations of CYP2E1 (difference: -0.192; 95% CI: -0.325 to -0.060), while effects of kava on CYP3A4/5, CYP1A2, and CYP2D6 lacked statistical significance (161).
  • Dermatologic agentsDermatologic agents: Historically, chronic and excessive kava use has been shown to cause dry, scaly skin or yellow skin discoloration, also known as "kava dermopathy" (111; 1; 113). In case reports, use of kava for 2-3 weeks resulted in systemic or contact-type dermatitis, sebotropic reactions, and generalized erythema with papules (104; 105; 106). In case reports, kava ingestion resulted in urticaria (107).
  • DiureticsDiuretics: According to secondary sources, kava may have diuretic properties.
  • Dopamine agonistsDopamine agonists: Kava has been reported to antagonize the effect of dopamine and elicit extrapyramidal effects (167; 71; 73). Kava (Piper methysticum) increased "off" periods in Parkinson's patients taking levodopa and may cause a semicomatose state when given concomitantly with alprazolam (74).
  • Dopamine antagonistsDopamine antagonists: Kava has been reported to antagonize the effect of dopamine and elicit extrapyramidal effects (167; 71; 73). Kava (Piper methysticum) increased "off" periods in Parkinson's patients taking levodopa and may cause a semicomatose state when given concomitantly with alprazolam (74).
  • FoxgloveFoxglove: In a study of 20 healthy individuals, kava lacked an effect on pharmacokinetics of digoxin, a substrate of p-glycoprotein (P-gp), when compared to clarithromycin and rifampin. The authors concluded that kava therefore lacks an effect on P-gp (165).
  • Gastrointestinal herbs and supplementsGastrointestinal herbs and supplements: Gastrointestinal upset has been reported as an infrequent adverse event in trials (6; 114; 91). In one study, patients experienced gastrointestinal problems, including nausea (88). In another study, a participant experienced mild nausea after taking kava; also gastrointestinal discomfort and symptoms resembling the flu began during the placebo phase but worsened during the kava treatment phase (17).
  • GinkgoGinkgo: Cases of rhabdomyolysis have been reported with kava use in combination with guarana and Ginkgo biloba (69; 70).
  • GuaranaGuarana: Cases of rhabdomyolysis have been reported with kava use in combination with guarana and Ginkgo biloba (69; 70).
  • Heart rate regulating agentsHeart rate regulating agents: Tachycardia and electrocardiogram (ECG) abnormalities (tall P waves) have been reported in heavy kava users (24). It has been theorized that these P wave abnormalities reflect pulmonary hypertension, although research is lacking in this area. Treatment with kava resulted in a significant improvement in the baroreflex control of heart rate (BRC), although there was a lack of a significant difference in BRC between the kava and placebo groups (47; 87).
  • Hematologic herbs and supplementsHematologic herbs and supplements: In survey results, chronic and heavy use of kava has been associated with increased red blood cell volume, reduced platelet volume, reduced lymphocyte counts, and reduced serum albumin (24; 116). According to anecdotal reports, kava intake may lead to hematuria (24). In laboratory research, kavain, a kava constituent, had antiplatelet effects due to cyclooxygenase and thromboxane synthesis inhibition (67). In one case, a patient was taking kava, coltsfoot, and 10 or more other supplements and experienced a deep vein thrombosis and a pulmonary embolism (117).
  • Hepatotoxic herbs and supplementsHepatotoxic herbs and supplements: More than 30 cases of liver damage have been reported, including hepatitis (38; 39; 40; 103), cirrhosis, and fulminant liver failure (41; 42), and there have also been reports of death (43; 44). Anecdotally and according to human studies, heavy kava use may have resulted in increased levels of liver enzymes such as gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP) (24; 3; 81). In human research, kava has been connected to necrotizing hepatitis (125; 118; 26) and, upon overdose, to cholestatic hepatitis (26). In a case report, kava consumption resulted in severe toxic liver disease (132).
  • Hormonal herbs and supplementsHormonal herbs and supplements: According to preliminary research, kava may decrease uterine tone (1). Kava may have estrogenic properties (117).
  • MelatoninMelatonin: Theoretically, kava and melatonin taken concomitantly may have additive sedative effects.
  • Mood stabilizersMood stabilizers: The pyrone constituents of kava have been found to have weak MAO inhibitory properties in vitro (155). Kava has been shown to have anxiolytic-like effects (151; 134).
  • NettleNettle: In women, ingestion of kava in conjunction with bee pollen, black cohosh, valerian, and nettle resulted in elevated serum lead levels (68).
  • Neurologic agentsNeurologic agents: In human studies, kava ingestion resulted in extrapyramidal side effects (55) and worsening of Parkinson's symptoms (71; 72). The extrapyramidal side effects caused by neuroleptic agents may be reduced by kava special extract WS 1490 (166). In a case study, kava intake resulted in choreoathetosis (73). In humans, excessive kava intake infrequently resulted in tremor, malcoordination, headache, drowsiness, and fatigue (6; 24). In three cases, kava resulted in meningismus, two of them with focal neurological manifestations (133). A review concluded that kava may affect electroconvulsive therapy (ECT) outcome (138). In human studies, kava resulted in mood elevation, anorexia, sleeplessness, palpitations, and paresthesias (92), and also dizziness and vivid dreams (98; 97; 17). In laboratory research, kavapyrones produced anticonvulsive, spasmolytic, antimycotic, and hypnotic effects (143; 144; 145; 146; 147; 148; 149; 150).
  • Ophthalmic herbs and supplementsOphthalmic herbs and supplements: Anecdotally, accommodative (ocular) disturbances are normally not associated with kava use; however, in a case report, a one-time use of kava was followed by impaired accommodation and convergence, increased pupil diameter, and oculomotor disturbance (139). In survey results, heavy kava use was followed by eye irritation (112). In a controlled study, excessive kava ingestion resulted in blepharospasm and saccadic dysmetria (81).
  • Renally eliminated herbs and supplementsRenally eliminated herbs and supplements: There has been a case report of rhabdomyolysis in a 29 year-old man who consumed an herbal combination of kava, ginkgo, and guarana (69). It is unclear if renal failure occurred. In a case report, a large amount of ingested kava resulted in temporary rhabdomyolysis (70). The causal role of kava in both of these cases is unclear. Acute urinary retention secondary to kava ingestion has also been reported (140).
  • SedativesSedatives: Kavalactones have been shown to potentiate the effects of CNS depressants (156; 79; 157). In humans, kava has been reported to cause sedation (81) without neurologic impairment (21; 22; 23).
  • St. John's wortSt. John's wort: In a telephone survey, one woman reported nausea, diaphoresis, muscle cramping, weakness, and elevated pulse and blood pressure after a single dose of an herbal combination of kava, St. John's wort (Hypericum perforatum), and valerian (168). In a case report, kava taken with St. John's wort daily for 10 weeks resulted in acute immunologic idiosyncratic hepatitis, which also involved increased transaminase levels and normal hepatitis serology (103).
  • ValerianValerian: In a telephone survey, one woman reported nausea, diaphoresis, muscle cramping, weakness, and elevated pulse and blood pressure after a single dose of an herbal combination of kava, St. John's wort, and valerian (Valeriana officinalis) (168). In women, ingestion of kava in conjunction with bee pollen, black cohosh, valerian, and nettle resulted in elevated serum lead levels (68).

Kava/Food Interactions:
  • Bee pollenBee pollen: In women, ingestion of kava in conjunction with bee pollen, black cohosh, valerian, and nettle resulted in elevated serum lead levels (68).
  • NettleNettle: In women, ingestion of kava in conjunction with bee pollen, black cohosh, valerian, and nettle resulted in elevated serum lead levels (68).
  • Tyramine/tryptophan-containing foodsTyramine/tryptophan-containing foods: Tyramine- or tryptophan-containing foods may pose a risk of hypertensive crisis if eaten while taking kava, due to the monoamine oxidase inhibitory (MAOI) activity of kava found in vitro (155). However, this interaction has not been reported in humans.

Kava/Lab Interactions:
  • Heart rateHeart rate: Tachycardia and electrocardiogram (ECG) abnormalities (tall P waves) have been reported in heavy kava users (24). It has been theorized that these P wave abnormalities reflect pulmonary hypertension, although research is lacking in this area. Treatment with kava resulted in a significant improvement in the baroreflex control of heart rate (BRC), although there was a lack of a significant difference in BRC between the kava and placebo groups (47; 87).
  • Coagulation panelCoagulation panel: In laboratory research, kavain, a kava constituent, had antiplatelet effects due to cyclooxygenase and thromboxane synthesis inhibition (67). In survey results, chronic and heavy use of kava has been associated with reduced platelet volume (24; 116).
  • Complete blood countComplete blood count: Chronic heavy use of kava has been associated with increased red blood corpuscle volume and reduced platelet volume (24). It is not clear if poor nutrition or iron deficiency coincides with chronic kava use, thus confounding these findings. Chronic heavy use of kava has been associated with decreased lymphocyte counts (24; 116).
  • Serum albumin, total proteinSerum albumin, total protein: Chronic heavy use of kava has been associated with decreased albumin and total protein (24). Causality is unclear and may be due to poor nutrition in chronic kava users or hepatic damage.
  • Serum bilirubinSerum bilirubin: Chronic heavy use of kava has been paradoxically associated with decreased bilirubin (24).
  • Serum leadSerum lead: Women using kava, bee pollen, black cohosh, valerian, and nettle had serum lead levels that were 23% (95% CI: 4-46%; p=0.02) higher than in women that did not use these herbs (68).
  • Serum transaminasesSerum transaminases: Kava use has been associated with elevations of liver function tests in animals and humans (24; 116; 34; 35).
  • Urine red blood cellsUrine red blood cells: Hematuria of unclear etiology has been reported anecdotally with kava use, although scientific data are scant (24).

Copyright © 2011 Natural Standard (www.naturalstandard.com)


The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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