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Dietary supplement

Kava Calm Formula Ingredients & Drug Interactions

by Woodstock Herbal Products

Liquid Category: Botanical
Most serious interaction: Major
The interaction bottom line Most serious interaction: Major

Kava Calm Formula is a dietary supplement by Woodstock Herbal Products with 5 active ingredients. Its ingredients are commonly taken for fatigue and low energy, stress and adaptogen support, liver health.Based on those ingredients, 1,180 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Kava root extract, Chamomile flower extract, Hops strobile extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Kava Calm Formula by Woodstock Herbal Products

Our pharmacy team’s full take, with four database checks built into the cards below — a summary of what is known, not a grade of the product itself.

From our pharmacy team — supplement deep dive

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

Most active ingredients don't disclose an individual amount — you can't tell how much of each you're getting.

Why this rating?
  • The label discloses an exact amount for 0 of its 5 active ingredients.
  • “Proprietary Extract Blend” is a proprietary blend — the label gives one combined amount (440 mg) without saying how much of each component you get.

Kava Calm Formula contains 5 active ingredients: kava root extract, schisandra berry extract, passionflower aerial parts extract, hops strobile extract, and chamomile flower extract, blended in a proprietary proportion. Kava is included for relaxation; passionflower and hops have traditional uses for sleep and anxiety; schisandra is an adaptogenic herb; and chamomile is a common calming ingredient.

The liquid form also contains alcohol as an inactive ingredient.

Does it work?

Moderate evidence
Evidence for Intended Use · database check
By FDA rules, dietary supplements can’t claim to treat, cure, or prevent disease — so labels speak in careful marketing language. We discern each product’s intended use from its name, label claims, and label statements, then grade the clinical evidence for that use. How these ratings are computed
Moderate

Some clinical evidence supports this product's ingredients for its stated purpose, but it isn't conclusive.

Why this rating?
  • The label markets this product for: Calm and relaxation support.
  • We looked for evidence on: Anxiety, Generalized anxiety disorder (GAD), Stress, Insomnia, Pre-procedural anxiety, Psychological well-being — and 4 related terms.
  • The strongest evidence on file: Passion Flower is rated "Possibly Effective" for Pre-procedural anxiety (Natural Medicines).
  • Also on file: Passion Flower is rated "Possibly Effective" for Insomnia.
  • Also on file: Kava is rated "Possibly Ineffective" for Generalized anxiety disorder (GAD).

The evidence for most of these ingredients is limited. Passionflower is rated Possibly Effective for insomnia and pre-procedural anxiety.

Kava is rated Possibly Ineffective for generalized anxiety disorder—so the evidence doesn't support its use for that condition. For schisandra, hops, and chamomile, the data we hold shows Insufficient Reliable Evidence to rate them for conditions like cough, asthma, insomnia, anxiety, or attention issues.

In short, if you're hoping this formula will improve sleep or ease anxiety, the evidence backing it up is thin to nonexistent for most of the blend.

The evidence, ingredient by ingredient Schisandra German Chamomile Hops Passion Flower Kava

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

Adverse-effect, pregnancy, and general safety data are on file for most of these ingredients.

Why this rating?
  • We hold adverse-effect (side-effect) data for 5 of the 5 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 5 of 5.
  • General safety write-ups exist for 5 of 5.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Short-term use appears generally well tolerated, but long-term safety data are limited. Common side effects from these ingredients include drowsiness, decreased appetite, heartburn, stomach upset, dizziness, and confusion.

Kava carries a rare but serious risk: over 100 cases of liver damage have been reported with kava use, especially with prolonged or excessive use. Because kava is in this formula and has been linked to hepatotoxicity, you should be cautious if you have liver disease or take other medications that stress the liver.

Avoid this product during pregnancy—schisandra, hops, passionflower, and kava all lack reliable safety data or are suspected to affect the uterus. Do not use while breastfeeding; safety data are insufficient for all four of these ingredients.

Side effects, ingredient by ingredient Schisandra German Chamomile Hops Passion Flower Kava

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

At least one ingredient has a documented Major-severity interaction. Check your medications for a personalized result.

Why this rating?
  • 5 of the 5 matched ingredients can interact with medications — Schisandra, Hops, Passion Flower, Kava, German Chamomile.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs.
  • For scale: 1,181 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

Before taking this product, double-check these medication types with your pharmacist: CNS depressants (sedatives, sleeping pills, anti-anxiety drugs, opioids, alcohol)—kava has a Major interaction here. Also check any hepatotoxic drugs (drugs that can injure the liver), CYP3A4 substrates, CYP2C19 substrates, CYP2C9 substrates, P-glycoprotein substrates, warfarin (blood thinner), tacrolimus (immunosuppressant), voriconazole (antifungal), and midazolam (sedative).

These cover interactions from kava and schisandra. Hops and passionflower add further CNS depressant risk.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with some supporting evidence for its stated purpose. Major medication interactions have been identified, and safety information is well characterized.

This is a multi-ingredient herbal product with several major and moderate drug interactions—especially with sedatives and with drugs processed by your liver. If you take any prescription medications or have liver concerns, talk to your pharmacist or doctor before using it.

It's not safe in pregnancy or while breastfeeding. Check your exact medications with the tool on this page.

Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI

Assessment coverage: 5 of 5 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jun 25, 2025.

This Scorecard evaluates available label information, ingredient evidence, and known medication-safety considerations. It does not independently verify product identity, purity, potency, contamination, or manufacturing quality. How these ratings are computed

At a glance

General information

Key facts about Kava Calm Formula, straight from the product label.

Brand Woodstock Herbal Products
Barcode (UPC) 854245005241
Net contents 1 Fluid Ounce(s); 30 mL
Market status On market
Date entered into DSLD Jun 25, 2025
DSLD ID 335076
Product type Botanical
Supplement form Liquid
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Vegan, Vegetarian, Kosher, Women (not pregnant or lactating), Gluten Free, Dairy Free
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for Kava Calm Formula by Woodstock Herbal Products, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
0.2 mL
Maximum serving Sizes:
0.5 mL
Servings per container
60
UPC/BARCODE
854245005241
IngredientAmount% DV
Proprietary Extract Blend440 mg--
Schisandra Berry Extract0 NP--
Chamomile flower extract0 NP--
Hops strobile extract0 NP--
Passionflower aerial parts extract0 NP--
Kava root extract0 NP--

Other ingredients: Alcohol

Tap any ingredient to jump to its full detail below.

Label statements
These statements are the manufacturer’s wording, reproduced from the product label — the label is saying it, not HelloPharmacist. We don’t verify or endorse them.
FDA Disclaimer Statement

This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Seals/Symbols

Certified Vegan V Vegan.org KOF-K (Kosher) Parve

Formulation

Certified Vegan V Vegan.org

Gluten free

Traditionally Handcrafted Traditional Handcrafted Herbal Formula

Certified Organic Alcohol.

Formula

KOF-K (Kosher) Parve

Brand IP Statement(s)

Copyright 2016 Woodstock Herbal Products

FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Suggested Use: Shake well before each use. Take 10-25 drops in water or juice 2 to 5 times per day.

Precautions

Warning: Keep out of reach of children. Not for use by persons under 18 years of age, or by pregnant or breastfeeding women.

Do not use if safety seal is damaged or missing. Caution: US FDA advises that a potential risk of rare, but severe, liver injury may be associated with kava-containing dietary supplements. Stop use and see a doctor if you develop symptoms that may signal liver problems (e.g.. unexplained fatigue, abdominal pain, loss of appetite, fever, vomiting. dark urine, pale stools, yellow eyes or skin). Not for use with alcoholic beverages. Excessive use, or use with products that cause drowsiness, may impair your ability to operate a vehicle or dangerous equipment.

Ask a healthcare professional before use if you have or have had liver problems, frequently use alcoholic beverages, are planning any medical procedure, have any medical condition, or are taking any medication. Not for use by persons under 18 years of age, or by pregnant or breastfeeding women.

See for yourself

Kava Calm Formula by Woodstock Herbal Products label

The label scan from the NIH Dietary Supplement Label Database. Tap to enlarge.

What’s inside

The Ingredients in Kava Calm Formula by Woodstock Herbal Products

These are the 5 active ingredients this product is made of. Select any to open its full monograph.

Serving size0.2 mL Dosage formLiquid Servings per container60 Amounts shown are per serving.

Most supplement products combine several ingredients, and a medication can interact with the product through any one of them. Each ingredient below shows whether it has known drug interactions.

Other (inactive) ingredients: Alcohol. These complete the product’s ingredient list but are not active constituents.

Interaction report

Kava Calm Formula by Woodstock Herbal Products Drug Interactions

Want to check YOUR meds against Kava Calm Formula?

Ask about interactions with your drugs in plain English — “Can I take it with lisinopril?” — and we find you the answer in seconds, ingredient by ingredient.

Go to the checker
1,180Drugs
248 Major 913 Moderate 19 Minor

Each ingredient & the kinds of drugs it affects

For each ingredient in Kava Calm Formula with known interactions, here are the types of medications they can affect. Open any type for the detail — or search your exact drug in the checker above.

Kava root extract12 drug types · 1,166 drugs

Cns Depressants

Combining kava with CNS depressants can have additive sedative effects.
Kava has CNS depressant effects. Concomitant use of kava with other CNS depressants can increase the risk of drowsiness and motor reflex depression. Clinical practice guidelines from a joint taskforce of the World Federation of Societies of Biological Psychiatry (WFSBP) and the Canadian Network for Mood and Anxiety Treatments (CANMAT) recommend that CNS depressants, including alcohol and benzodiazepines, not be used with kava.

Likelihood Probable Evidence A
Alcohol (Ethanol)

Combining kava with alcohol may increase the risk of sedation and/or hepatotoxicity.

Kava has CNS depressant effects. Concomitant use of kava with other CNS depressants can increase the risk of drowsiness and motor reflex depression. Additionally, kava has been associated with over 100 cases of hepatotoxicity. There is some concern that kava can adversely affect the liver, especially when used in combination with hepatotoxic drugs. Clinical practice guidelines from a joint taskforce of the World Federation of Societies of Biological Psychiatry (WFSBP) and the Canadian Network for Mood and Anxiety Treatments (CANMAT) recommend that alcohol not be used with kava.

Likelihood Possible Evidence A
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, kava might increase levels of CYP2C19 substrates.
In vitro research shows that kava significantly inhibits CYP2C19 enzymes. This effect has not yet been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, kava might increase levels of CYP2C9 substrates.
In vitro research shows that kava significantly inhibits CYP2C9 enzymes. This effect has not yet been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2E1 (Cyp2E1) Substrates

Kava might increase levels of CYP2E1 substrates.
In a clinical study in healthy volunteers, taking kava 1000 mg twice daily (containing a daily dose of 138 mg kavalactones) for 28 days inhibited the metabolism of CYP2E1 substrates.

Likelihood Probable Evidence B
Haloperidol (Haldol)

Combining kava and haloperidol might increase the risk of cardiovascular adverse effects and hypoxia.
Atrial flutter and hypoxia has been reported for a patient who received intramuscular injections of haloperidol and lorazepam after using kava orally. The side effects were attributed to kava-induced inhibition of CYP2D6, but might also have been related to additive adverse effects with the concomitant use of haloperidol, lorazepam, and kava.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, using kava with hepatotoxic drugs might increase the risk of liver damage.
Kava has been linked with over 100 cases of hepatotoxicity. Most cases occur with excessive and prolonged use. There is some concern that kava can adversely affect the liver, especially when used in combination with hepatotoxic drugs.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

It is unclear if kava inhibits P-glycoprotein (P-gp); research is conflicting.
In vitro research shows that kava can inhibit P-gp efflux. However, a clinical study in healthy volunteers shows that taking kava standardized to provide 225 mg kavalactones daily for 14 days does not affect the pharmacokinetics of digoxin, a P-gp substrate. It is possible that the use of other P-gp substrates or higher doses of kava might still inhibit P-gp.

Likelihood Possible Evidence D
Ropinirole (Requip)

Taking kava with ropinirole might increase the risk for dopaminergic toxicity.
A case of visual hallucinations and paranoid delusions has been reported for a patient who used kava in combination with ropinirole. The adverse effects were attributed to kava-induced inhibition of CYP1A2, which may have reduced the metabolism of ropinirole, resulting in excessive dopaminergic stimulation.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

It is unclear if kava inhibits CYP1A2; research is conflicting.
Although in vitro research and a case report suggest that kava inhibits CYP1A2, more robust clinical evidence shows that kava has no effect on CYP1A2. In a clinical study in healthy volunteers, taking kava 1000 mg twice daily (containing a daily dose of 138 mg kavalactones) for 28 days had no effect on CYP1A2 activity.

Likelihood Unlikely Evidence B
Cytochrome P450 2D6 (Cyp2D6) Substrates

It is unclear if kava inhibits CYP1A2; research is conflicting.
In vitro research shows that kava extract significantly inhibits CYP2D6. However, clinical research shows that kava does not affect the metabolism of CYP2D6 substrates in humans.

Likelihood Unlikely Evidence B
Cytochrome P450 3A4 (Cyp3A4) Substrates

It is unclear if kava inhibits CYP3AA; research is conflicting.
Although in vitro research suggests that kava inhibits CYP3A4, more robust clinical evidence shows that kava has no effect on CYP3A4. In a clinical study in healthy volunteers, taking kava 1000 mg twice daily (containing a daily dose of 138 mg kavalactones) for 28 days had no effect on CYP3A4 activity.

Likelihood Unlikely Evidence B

Chamomile flower extract9 drug types · 960 drugs

Cns Depressants

Theoretically, German chamomile might have additive effects when used with CNS depressants.
German chamomile has mild sedative effects. Theoretically, concomitant use with drugs with sedative properties can cause additive effects and side effects.

Likelihood Possible Evidence D
Contraceptive Drugs

Theoretically, large amounts of German chamomile might reduce the effectiveness of oral contraceptives.
In vitro, German chamomile has demonstrated antiestrogenic activity. Theoretically, concomitant use of large amounts of German chamomile might interfere with contraceptive drugs through competition for estrogen receptors.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, German chamomile might inhibit CYP2C9 and increase levels of drugs metabolized by these enzymes.
In vitro evidence shows that German chamomile might inhibit CYP2C9. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP2C9 in patients taking German chamomile.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, German chamomile might inhibit CYP2D6 and increase levels of drugs metabolized by these enzymes.
In vitro evidence shows that German chamomile might inhibit CYP2D6. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP2D6 in patients taking German chamomile.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, German chamomile might inhibit CYP3A4 and increase levels of drugs metabolized by these enzymes.
In vitro evidence shows that German chamomile might inhibit CYP3A4. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP3A4 in patients taking German chamomile.

Likelihood Possible Evidence D
Estrogens

Theoretically, large amounts of German chamomile might reduce the effectiveness of estrogens.
In vitro, German chamomile has demonstrated antiestrogenic activity. Theoretically, large amounts of German chamomile might interfere with hormone replacement therapy through competition for estrogen receptors.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, large amounts of German chamomile might interfere with the activity of tamoxifen.
In vitro, German chamomile has demonstrated antiestrogenic activity.

Likelihood Possible Evidence D
Warfarin (Coumadin)

German chamomile might increase the effects of warfarin and increase the risk of bleeding.
In one case, a 70-year-old female taking warfarin developed retroperitoneal hematoma and bilateral recti muscle bleeding along with an INR of 7.9 following ingestion of German chamomile tea 4-5 cups daily and use of a topical chamomile-based lotion applied 4-5 times daily.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, German chamomile might inhibit CYP1A2 and increase levels of drugs metabolized by these enzymes.
In vitro and animal research shows that German chamomile might inhibit CYP1A2. So far, this interaction has not been reported in humans. However, there might be an increase in the levels of drugs metabolized by CYP1A2 in patients taking German chamomile.

Likelihood Possible Evidence D

Hops strobile extract4 drug types · 863 drugs

Cns Depressants

Theoretically, concomitant use of hops with sedative drugs might cause additive sedation.
Some animal research shows that hops has sedative effects.

Likelihood Possible Evidence D
Estrogens

Theoretically, concomitant use of large amounts of hops might interfere with hormone replacement therapy due to competition for estrogen receptors.
In vitro research suggests that certain hops constituents can competitively bind to estrogen receptors. However, most hops extracts contain very small amounts of these constituents.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Hops extract does not seem to affect the metabolism of CYP1A2 substrates.
In vitro research suggests that flavonoid constituents of hops inhibit CYP1A2 enzyme activity. However, a pharmacokinetic study in healthy postmenopausal patients shows that taking a standardized extract of spent hops containing prenylated phenols, as 59.5 mg twice daily for 2 weeks, does not affect levels of caffeine, a CYP1A2 probe substrate.

Likelihood Unlikely Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, hops extract might alter metabolism of CYP3A4 substrates; however, this effect may not be clinically significant.
Animal research suggests that specific constituents of hops, called lupulones, can induce hepatic CYP3A4 enzyme activity. However, a pharmacokinetic study in healthy postmenopausal patients with normal metabolism shows that taking a standardized extract of spent hops containing prenylated phenols, as 59.5 mg twice daily for 2 weeks, decreases the concentration of alprazolam, a CYP3A4 probe substrate, by 7.6%. This reduction is unlikely to be clinically relevant.

Likelihood Possible Evidence D

Passionflower aerial parts extract3 drug types · 836 drugs

Cns Depressants

Concomitant use of passion flower with sedative drugs might cause additive effects and side effects.
Research in animals and humans shows that passion flower has sedative effects which can be additive when used with sedative medications like lorazepam.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, passion flower might decrease the effects of CYP3A4 substrates.
In vitro research suggests that passion flower can induce CYP3A4 enzymes, albeit to a much lower degree than rifampin, a known CYP3A4 inducer.

Likelihood Possible Evidence D
Organic Anion-Transporting Polypeptide Substrates (Oatp)

Theoretically, passion flower might reduce the bioavailability of OATP2B1 and OATP1A2 substrates.
In vitro research shows that the passion flower constituents apigenin and vitexin inhibit OATP2B1 and OATP1A2. This inhibition may be dose-dependent. One specific high-flavonoid passion flower extract (Valverde) seems to inhibit OATP2B1 and OATP1A2, while another extract with a lower flavonoid concentration (Arkocaps) shows less potent inhibition. OATPs are responsible for the uptake of drugs and other compounds into the body; however, the specific activities of OATP2B1 and OATP1A2 are not well characterized.

Likelihood Possible Evidence D

Schisandra Berry Extract12 drug types · 803 drugs

Cyclophosphamide

Theoretically, schisandra might increase the levels and clinical effects of cyclophosphamide.
In vitro research shows that schisandra increases the concentration of cyclophosphamide, likely through inhibition of cytochrome P450 3A4. After multiple doses of the schisandra constituents schisandrin A and schisantherin A, the maximum concentration of cyclophosphamide was increased by 7% and 75%, respectively, while the overall exposure to cyclophosphamide was increased by 29% and 301%, respectively.

Likelihood Probable Evidence D
Cyclosporine (Neoral, Sandimmune)

Schisandra can increase the levels and clinical effects of cyclosporine.
A small observational study in children with aplastic anemia found that taking schisandra with cyclosporine increased cyclosporine trough levels by 93% without increasing the risk of adverse events. However, the dose of cyclosporine was reduced in 9% of children to maintain appropriate cyclosporine blood concentrations.

Likelihood Probable Evidence B
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, schisandra might increase the levels and clinical effects of CYP2C19 substrates.
In vitro research shows that schisandra inhibits CYP2C19, and animal research shows that schisandra increases the concentration of voriconazole, a CYP2C19 substrate. Theoretically, schisandra may also inhibit the metabolism of other CYP2C19 substrates. This effect has not been reported in humans.

Likelihood Probable Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, schisandra might decrease the levels and clinical effects of CYP2C9 substrates.
In vitro and animal research suggests that schisandra induces CYP2C9 enzymes. This effect has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Schisandra can increase the levels and clinical effects of drugs metabolized by CYP3A4.
Most clinical and laboratory research shows that schisandra, administered either as a single dose or up to twice daily for 14 days, inhibits CYP3A4 and increases the concentration of CYP3A4 substrates such as cyclophosphamide, midazolam, tacrolimus, and talinolol. Although one in vitro and animal study shows that schisandra may induce CYP3A4 metabolism, this effect appears to be overpowered by schisandra's CYP3A4 inhibitory activity and has not been reported in humans.

Likelihood Probable Evidence D
Midazolam (Versed)

Schisandra can increase the levels and clinical effects of midazolam.
A small pharmacokinetic study in healthy adults shows that taking schisandra extract (Hezheng Pharmaceutical Co.) containing deoxyschizandrin 33.75 mg twice daily for 8 days and a single dose of midazolam 15 mg on day 8 increases the overall exposure to midazolam by about 119%, increases the peak plasma level of midazolam by 86%, and decreases midazolam clearance by about 52%. This effect has been attributed to inhibition of CYP3A4 by schisandra.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Schisandra might increase the levels and clinical effects of P-glycoprotein substrates.
In vitro research shows that schisandra extracts and constituents such as schisandrin B inhibit P-glycoprotein mediated efflux in intestinal cells and in P-glycoprotein over-expressing cell lines. Additionally, a small clinical study shows that schisandra increases the peak concentration and overall exposure to talinolol, a P-glycoprotein probe substrate. Theoretically, schisandra might inhibit the efflux of other P-glycoprotein substrates.

Likelihood Possible Evidence D
Sirolimus (Rapamune)

Schisandra can increase the levels and clinical effects of sirolimus.
A small pharmacokinetic study in healthy volunteers shows that taking 3 capsules of schisandra (Hezheng Pharmaceutical Company) containing a total of 33.75 mg deoxyschizandrin twice daily for 13 days and then taking a single dose of sirolimus 2 mg increases the overall exposure and peak level of sirolimus by two-fold. This effect is thought to be due to inhibition of cytochrome P450 3A4 by schisandra, as well as possible inhibition of the P-glycoprotein drug transporter.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Schisandra can increase the levels and clinical effects of tacrolimus.
Clinical research in healthy children and adults, transplant patients, and patients with nephrotic syndrome and various rheumatic immunologic disorders shows that taking schisandra with tacrolimus increases tacrolimus peak levels by 183% to 268%, prolongs or delays time to peak tacrolimus concentrations, increases overall exposure to tacrolimus by 126% to 343%, and decreases tacrolimus clearance by 19% to 73%. This effect is thought to be due to inhibition of P-glycoprotein drug transporter and CYP3A4 and CYP3A5 by schisandra. Some clinical and observational studies suggest that schisandra increases tacrolimus levels similarly in both expressors and non-expressors of CYP3A5, while other studies suggest it does so to a greater degree in CYP3A5 expressors than non-expressors. Animal research suggests that the greatest increase in tacrolimus levels occurs when schisandra is taken either concomitantly or up to 2 hours before tacrolimus, and clinical and observational research in humans suggests that schisandra may increase whole blood levels of tacrolimus and decrease clearance of tacrolimus in a dose-dependent manner.

Likelihood Probable Evidence B
Talinolol

Schisandra can increase the levels and clinical effects of talinolol.
A small pharmacokinetic study in healthy volunteers shows that taking schisandra extract 300 mg twice daily for 14 days with a single dose of talinolol 100 mg on day 14 increases the peak talinolol level by 51% and the overall exposure to talinolol by 47%. This effect is thought to be due to the possible inhibition of cytochrome P450 3A4 and P-glycoprotein by schisandra. tly.

Likelihood Probable Evidence B
Voriconazole (Vfend)

Theoretically, schisandra might increase the levels and clinical effects of voriconazole.
Animal research shows that oral schisandra given daily for 1 or 14 days increases levels of intravenously administered voriconazole, a cytochrome P450 (CYP) 2C19 substrate. This effect is thought to be due to inhibition of CYP2C19 by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, schisandra might decrease the levels and clinical effects of warfarin.
Animal research suggests that oral schisandra extract, given daily for 6 days, reduces levels of intravenously administered warfarin. This effect might be due to the induction of cytochrome P450 (CYP) 2C9 metabolism by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for Kava Calm Formula, from the product label.

Woodstock Herbal Products

See all Woodstock Herbal Products products
Name
Woodstock Herbal Products LLC
City
Woodstock
State
NY
ZipCode
12498
Phone Number
855-573-1273
Web Address
www.woodstockherbalproducts.com
Pharmacist Counseling Corner

Kava Calm Formula by Woodstock Herbal Products: Common Questions

Does Kava Calm Formula by Woodstock Herbal Products interact with any medications?
Yes. Based on its ingredients, Kava Calm Formula has a known interaction with 1,180 medications, including 248 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Kava Calm Formula contains 5 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Is it safe to take this if I'm on a sleeping pill or anxiety medication?
No—not without checking first. Kava, hops, and passionflower all have documented interactions with sedatives and anti-anxiety drugs, which can cause dangerous additive drowsiness. Talk to your pharmacist before combining this product with any CNS depressant.
Will this help me sleep?
Passionflower in this blend is rated Possibly Effective for insomnia, but the evidence is limited. The other ingredients don't have strong evidence for sleep. This isn't the same as a proven sleep aid.
Can I take this for anxiety?
Kava is actually rated Possibly Ineffective for generalized anxiety disorder, so the research doesn't support using it for that. Passionflower may help with anxiety related to upcoming procedures, but again, evidence is limited.
What are the common side effects?
Drowsiness, dizziness, decreased appetite, heartburn, and stomach upset are the most commonly reported. These ingredients can also cause confusion. Kava specifically may cause memory problems and tremor.
Can I take this while pregnant or breastfeeding?
No. All four herbal ingredients in this product should be avoided during pregnancy due to lack of safety data or concerns about effects on the uterus. Do not use while breastfeeding; safety is unknown for all of them.
Should I worry about liver damage?
Kava has been linked to over 100 reported cases of liver injury, especially with long-term or excessive use. If you have liver disease or take other medications that stress the liver, mention this product to your doctor before using it.

Written and reviewed by the HelloPharmacist editorial staff. Our editorial policy

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The Full Monographs Behind Kava Calm Formula’s Ingredients

Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.

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Sources & How We Checked

Kava Calm Formula's label data comes from the NIH Dietary Supplement Label Database; the ingredient interaction data is from the Natural Medicines database, reviewed by our pharmacists.

Content is written and reviewed by licensed HelloPharmacist pharmacists. See our data sources and editorial standards for how this information is built and checked.

The 146 references behind this product’s interaction data

Every citation that drives the interaction findings for this product’s ingredients, from the evidence-graded Natural Medicines (TRC Healthcare) database. Open an ingredient to browse its citations — links open the study on PubMed or the publisher’s site.

Schisandra 26 references
  1. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons, 1996.
  2. Iwata H, Tezuka Y, Kadota S, et al. Identification and characterization of potent CYP3A4 inhibitors in Schisandra fruit extract. Drug Metab Dispos 2004;32:1351-8. PubMed
  3. Mu Y, Zhang J, Zhang S, et al. Traditional Chinese medicines Wu Wei Zi (Schisandra chinensis Baill) and Gan Cao (Glycyrrhiza uralensis Fisch) activate pregnane X receptor and increase warfarin clearance in rats. J Pharmacol Exp Ther 2006;316:1369-77. PubMed
  4. Xin HW, Wu XC, Li Q, et al. Effects of Schisandra sphenanthera extract on the pharmacokinetics of tacrolimus in healthy volunteers. Br J Clin Pharmacol 2007;64:469-75.
  5. Qin XL, Bi HC, Wang XD, et al. Mechanistic understanding of the different effects of Wuhzi Tablet (Schisandra sphenanthera extract) on the absorption and first-pass intestinal and hepatic metabolism of tacrolimus (FK506). Int J Pharm 2010;389:114-21.
  6. Makino, T., Mizuno, F., and Mizukami, H. Does a kampo medicine containing schisandra fruit affect pharmacokinetics of nifedipine like grapefruit juice? Biol.Pharm.Bull. 2006;29(10):2065-2069. PubMed
  7. Fan L, Mao XQ, Tao GY, Wang G, Jiang F, Chen Y, Li Q, Zhang W, Lei HP, Hu DL, Huang YF, Wang D, Zhou HH. Effect of Schisandra chinensis extract and Ginkgo biloba extract on the pharmacokinetics of talinolol in healthy volunteers. Xenobiotica. 2009 Mar;39(
  8. Jiang W, Wang X, Xu X, Kong L. Effect of Schisandra sphenanthera extract on the concentration of tacrolimus in the blood of liver transplant patients. Int J Clin Pharmacol Ther. 2010 Mar;48(3):224-9. PubMed
  9. Xin HW, Wu XC, Li Q, Yu AR, Xiong L. Effects of Schisandra sphenanthera extract on the pharmacokinetics of midazolam in healthy volunteers. Br J Clin Pharmacol. 2009 May;67(5):541-6.
  10. Li J, Chen S, Qin X, et at. Wuzhi Tablet (<i>Schisandra sphenanthera</i> Extract) is a Promising Tacrolimus-Sparing Agent for Renal Transplant Recipients Who are CYP3A5 Expressers: a Two-Phase Prospective Study. Drug Metab Dispos. 2017;45(11):1114-1119.
  11. Qin XL, Li JL, Wang SH, Chen X, Huang M, Bi HC. Co-administration of Wuzhi tablet (Schisandra sphenanthera extract) alters tacrolimus pharmacokinetics in a dose- and time-dependent manner in rats. J Ethnopharmacol. 2020;263:113233. PubMed
  12. Yuan F, Liang X, Chen X, Qin X, Tan C, Wang L. CYP2C19 is involved in the effect of Wuzhi tablet (Schisandra sphenanthera extract) and its constituents on the pharmacokinetics of intravenous voriconazole. Pharmazie. 2020;75(11):559-564. DOI
  13. Zhang Z, Lu X, Dong L, Ma J, Fan X. Clinical observation on the effect of Wuzhi soft capsule on FK506 concentration in membranous nephropathy patients. Medicine (Baltimore). 2019;98(48):e18150. PubMed
  14. Yoo HH, Lee M, Lee MW, Lim SY, Shin J, Kim DH. Effects of Schisandra lignans on P-glycoprotein-mediated drug efflux in human intestinal Caco-2. Planta Med. 2007;73(5):444-50.
  15. Qiangrong P, Wang T, Lu Q, Hu X. Schisandrin B--a novel inhibitor of P-glycoprotein. Biochem Biophys Res Commun. 2005;335(2):406-11. PubMed
  16. Chen L, Ji N, Zhang M, Chen W. The influence of Wuzhi capsule on the pharmacokinetics of cyclophosphamide. Recent Pat Anticancer Drug Discov 2021. PubMed
  17. Cheng X, Ma J, Xu X, Zhang L, Wang X, Wu R. Effect of Wuzhi capsules on cyclosporine A concentration in children with aplastic anemia immunotherapy: a single-center observational study. Expert Rev Clin Pharmacol 2022:1-5. PubMed
  18. Cheng F, Li Q, Wang J, Zeng F, Zhang Y. Effects and safety evaluation of Wuzhi capsules combined with tacrolimus for the treatment of kidney transplantation recipients. J Clin Pharm Ther 2021;46(6):1636-49. PubMed
  19. Teng F, Wang W, Zhang W, et al. Effect of hepar-protecting Wuzhi capsule on pharmacokinetics and dose-effect character of tacrolimus in healthy volunteers. Biopharm Drug Dispos 2022.
  20. Kou K, Sun X, Li M, et al. Beneficial effects of Wuzhi capsule on tacrolimus blood concentrations in liver transplant patients with different donor-recipient CYP3A5 genotypes. J Clin Pharm Ther 2022;47(2):200-10. PubMed
  21. Peng Y, Jiang F, Zhou R, et al. Clinical evaluation of the efficacy and safety of co-administration of Wuzhi capsule and tacrolimus in adult Chinese patients with myasthenia gravis. Neuropsychiatr Dis Treat 2021;17:2281-9. PubMed
  22. Chen P, Dai R, She Y, et al. Prediction of tacrolimus and Wuzhi tablet pharmacokinetic interaction magnitude in renal transplant recipients. Clin Transplant 2022;36(12):e14807. PubMed
  23. Qu J, Bian R, Liu B, et al. The pharmacokinetic study of tacrolimus and Wuzhi capsule in Chinese liver transplant patients. Front Pharmacol 2022;13:956166. PubMed
  24. Zhou Y, Huang X, Liu L, et al. Effect of Wuzhi preparations on tacrolimus in CYP3A5 expressers during the early period after transplantation: A real-life experience from heart transplant recipients. Transpl Immunol 2023;76:101748. PubMed
  25. Huang Q, Lin X, Wang Y, et al. Tacrolimus pharmacokinetics in pediatric nephrotic syndrome: A combination of population pharmacokinetic modelling and machine learning approaches to improve individual prediction. Front Pharmacol 2022;13:942129. PubMed
  26. Wang CB, Zhang YJ, Zhao MM, Zhao LM. Population pharmacokinetic analyses of tacrolimus in non-transplant patients: a systematic review. Eur J Clin Pharmacol 2023;79(7):897-913. PubMed

See these in context on the Schisandra monograph →

German Chamomile 15 references
  1. Subiza J, Subiza JL, Hinojosa M, et al. Anaphylactic reaction after the ingestion of chamomile tea; a study of cross-reactivity with other composite pollens. J Allergy Clin Immunol 1989;84:353-8. PubMed
  2. Budzinski JW, Foster BC, Vandenhoek S, Arnason JT. An in vitro evaluation of human cytochrome P450 3A4 inhibition by selected commercial herbal extracts and tinctures. Phytomedicine 2000;7:273-82. PubMed
  3. Viola H, Wasowski C, Levi de Stein M, et al. Apigenin, a component of Matricaria recutita flowers, is a central benzodiazepine receptors-ligand with anxiolytic effects. Planta Med 1995;61:213-6.
  4. van Ketel WG. Allergy to Matricaria chamomilla. Contact Dermatitis 1982;8:143. PubMed
  5. van Ketel WG. Allergy to Matricaria chamomilla. Contact Dermatitis 1987;16:50-1. PubMed
  6. Hormann HP, Korting HC. Evidence for the efficacy and safety of topical herbal drugs in dermatology: part I: anti-inflammatory agents. Phytomedicine 1994;1:161-71. PubMed
  7. Avallone R, Zanoli P, Puia G, et al. Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla. Biochem Pharmacol 2000;59:1387-94. PubMed
  8. Kassi E, Papoutsi Z, Fokialakis N, et al. Greek plant extracts exhibit selective estrogen receptor modulator (SERM)-like properties. J Agric Food Chem 2004;52:6956-61. PubMed
  9. Maliakal PP, Wanwimolruk S. Effect of herbal teas on hepatic drug metabolizing enzymes in rats. J Pharm Pharmacol 2001;53:1323-9. PubMed
  10. Segal R, Pilote L. Warfarin interaction with Matricaria chamomilla. CMAJ 2006;174:1281-2. PubMed
  11. Loggia RD, Traversa U, Scarcia V, et al. Depressive effects of Chamomilla recutita (L.) Rausch, tubular flowers, on central nervous system in mice. Pharmacol Res Commun 1982;14(2):153-162. PubMed
  12. Ganzera M, Schneider P, Stuppner H. Inhibitory effects of the essential oil of chamomile (Matricaria recutita L.) and its major constituents on human cytochrome P450 enzymes. Life Sci 2006;78(8):856-861. PubMed
  13. Benito P, Rodríguez-Perez R, García F, Juste S, Moneo I, Caballero ML. Occupational allergic rhinoconjunctivitis induced by Matricaria chamomilla with tolerance of chamomile tea. J Investig Allergol Clin Immunol. 2014;24(5):369-70. No abstract available.
  14. Braga FT, Santos AC, Bueno PC, et al. Use of Chamomilla recutita in the prevention and treatment of oral mucositis in patients undergoing hematopoietic stem cell transplantation: a randomized, controlled, phase II clinical trial. Cancer Nurs 2015;38(4):32 PubMed
  15. Sarris J, Ravindran A, Yatham LN, et al. Clinician guidelines for the treatment of psychiatric disorders with nutraceuticals and phytoceuticals: The World Federation of Societies of Biological Psychiatry (WFSBP) and Canadian Network for Mood and Anxiety T

See these in context on the German Chamomile monograph →

Hops 15 references
  1. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.
  2. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
  3. Zava DT, Dollbaum CM, Blen M. Estrogen and progestin bioactivity of foods, herbs, and spices. Proc Soc Exp Biol Med 1998;217:369-78. PubMed
  4. Milligan SR, Kalita JC, Heyerick A, et al. Identification of a potent phytoestrogen in hops (Humulus lupulus L.) and beer. J Clin Endocrinol Metab 1999;84:2249-52.. PubMed
  5. Milligan SR, Kalita JC, Pocock V, et al. The endocrine activities of 8-prenylnaringenin and related hop (Humulus lupulus L.) flavonoids. J Clin Endocrinol Metab 2000;85:4912-5.. DOI
  6. Henderson MC, Miranda CL, Stevens JF, et al. In vitro inhibition of human P450 enzymes by prenylated flavonoids from hops, Humulus lupulus. Xenobiotica 2000;30:235-51.. PubMed
  7. Mannering, G. J., Shoeman, J. A., and Deloria, L. B. Identification of the antibiotic hops component, colupulone, as an inducer of hepatic cytochrome P-4503A in the mouse. Drug Metab Dispos 1992;20(2):142-147. DOI
  8. Skorska, C., Mackiewicz, B., Gora, A., Golec, M., and Dutkiewicz, J. Health effects of inhalation exposure to organic dust in hops farmers. Ann.Univ Mariae.Curie Sklodowska [Med] 2003;58(1):459-465.
  9. Schiller, H., Forster, A., Vonhoff, C., Hegger, M., Biller, A., and Winterhoff, H. Sedating effects of Humulus lupulus L. extracts. Phytomedicine. 2006;13(8):535-541. PubMed
  10. van Hunsel, F. P. and Kampschoer, P. [Postmenopausal bleeding and dietary supplements: a possible causal relationship with hop- and soy-containing preparations]. Ned.Tijdschr.Geneeskd. 2012;156(41):A5095.
  11. Fenselau, C. and Talalay, P. Is oestrogenic activity present in hops? Food Cosmet.Toxicol. 1973;11(4):597-602. PubMed
  12. Godnic-Cvar, J., Zuskin, E., Mustajbegovic, J., Schachter, E. N., Kanceljak, B., Macan, J., Ilic, Z., and Ebling, Z. Respiratory and immunological findings in brewery workers. Am J Ind Med 1999;35(1):68-75. DOI
  13. Lee KM, Jung JS, Song DK, and et al. Effects of Humulus lupulus extract on the central nervous system in mice. Planta Med 1993;59(Suppl):A691.
  14. Assessment report on Humulus lupulus L., flos. European Medicines Agency, 2014. Available at: https://www.ema.europa.eu/en/documents/herbal-report/final-assessment-report-humulus-lupulus-l-flos_en.pdf. Accessed September 29, 2021.
  15. van Breemen RB, Chen L, Tonsing-Carter A, et al. Pharmacokinetic Interactions of a Hop Dietary Supplement with Drug Metabolism in Perimenopausal and Postmenopausal Women. J Agric Food Chem. 2020;68(18):5212-5220. PubMed

See these in context on the Hops monograph →

Passion Flower 19 references
  1. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.
  2. The Review of Natural Products by Facts and Comparisons. St. Louis, MO: Wolters Kluwer Co., 1999.
  3. Fisher AA, Purcell P, Le Couteur DG. Toxicity of Passiflora incarnata L. J Toxicol Clin Toxicol 2000;38:63-6.
  4. Akhondzadeh S, Naghavi HR, Shayeganpour A, et al. Passionflower in the treatment of generalized anxiety: a pilot double-blind randomized controlled trial with oxazepam. J Clin Pharm Ther 2001;26:363-7. PubMed
  5. Farnsworth N, Bingel A, Cordell G, et al. Potential value of plants as sources of new antifertility agents I. J Pharm Sci 1975;64:535-98. DOI
  6. Mori A, Hasegawa K, Murasaki M, et al. Clinical evaluation of Passiflamin (passiflora extract) on neurosis - multicenter double blind study in comparison with mexazolam. Rinsho Hyoka (Clinical Evaluation) 1993;21:383-440.
  7. Miyasaka LS, Atallah AN, Soares BG. Passiflora for anxiety disorder. Cochrane Database Syst Rev 2007;(1):CD004518. DOI
  8. Speroni E., Minghetti A. Neuropharmacological activity of extracts from Passiflora incarnata. Planta Med. 1988;54:488-91.
  9. Capasso A., Sorrentino L. Pharmacological studies on the sedative and hypnotic effect of Kava kava and Passiflora extracts combination. Phytomedicine. 2005;12:39-45. PubMed
  10. Carrasco MC, Vallejo JR, Pardo-de-Santayana M, et al. Interactions of Valeriana officinalis L. and Passiflora incarnata L. in a patient treated with lorazepam. Phytother Res. 2009 Dec;23:1795-6.
  11. Smith, G. W., Chalmers, T. M., and Nuki, G. Vasculitis associated with herbal preparation containing Passiflora extract. Br J Rheumatol. 1993;32(1):87-88.
  12. Soulimani, R., Younos, C., Jarmouni, S., Bousta, D., Misslin, R., and Mortier, F. Behavioural effects of Passiflora incarnata L. and its indole alkaloid and flavonoid derivatives and maltol in the mouse. J Ethnopharmacol. 1997;57(1):11-20. PubMed
  13. Nojoumi M, Ghaeli P, Salimi S, Sharifi A, Raisi F. Effects of Passion Flower Extract, as an Add-On Treatment to Sertraline, on Reaction Time in Patients ?with Generalized Anxiety Disorder: A Double-Blind Placebo-Controlled Study. Iran J Psychiatry. 2016;1
  14. Rokhtabnak F, Ghodraty MR, Kholdebarin A, et al. Comparing the Effect of Preoperative Administration of Melatonin and Passiflora incarnata on Postoperative Cognitive Disorders in Adult Patients Undergoing Elective Surgery. Anesth Pain Med. 2016;7(1):e4123 PubMed
  15. Dantas LP, de Oliveira-Ribeiro A, de Almeida-Souza LM, Groppo FC. Effects of passiflora incarnata and midazolam for control of anxiety in patients undergoing dental extraction. Med Oral Patol Oral Cir Bucal. 2017;22(1):e95-e101. PubMed
  16. Ozturk Z, Kalayci CC. Pregnancy outcomes in psychiatric patients treated with passiflora incarnata. Complement Ther Med. 2018 Feb;36:30-32. PubMed
  17. da Cunha RS, Amorim KS, Gercina AC, et al. Herbal medicines as anxiolytics prior to third molar surgical extraction. A randomized controlled clinical trial. Clin Oral Investig. 2020. PubMed
  18. Schäfer AM, Gilgen PM, Spirgi C, et al. Constituents of Passiflora incarnata, but Not of Valeriana officinalis, Interact with the Organic Anion Transporting Polypeptides (OATP)2B1 and OATP1A2. Planta Med. 2021. PubMed
  19. Mazzari ALDA, Lacerda MG, Milton FA, et al. In vitro effects of European and Latin-American medicinal plants in CYP3A4 gene expression, glutathione levels, and P-glycoprotein activity. Front Pharmacol 2022;13:826395. PubMed

See these in context on the Passion Flower monograph →

Kava 71 references
  1. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  2. Strahl S, Ehret V, Dahm HH, Maier KP. [Necrotizing hepatitis after taking herbal medication]. Dtsch Med Wochenschr 1998;123:1410-4.
  3. Spillane PK, et al. Neurological manifestations of kava intoxication. Med J Aust 1997;167:172-3. PubMed
  4. Swensen JN. Man convicted of driving under the influence of kava. Salt Lake City, UT: Deseret News, 1996.
  5. Pittler MH, Ernst E. Efficacy of kava extract for treating anxiety: systematic review and meta-analysis. J Clin Psychopharmacol 2000;20:84-9. PubMed
  6. Volz HP, Kieser M. Kava-kava extract WS 1490 versus placebo in anxiety disorders--a randomized placebo-controlled 25-week outpatient trial. Pharmacopsychiatry 1997;30:1-5. PubMed
  7. Heinze HJ, Munthe TF, Steitz J, Matzke M. Pharmacopsychological effects of oxazepam and kava-extract in a visual search paradigm assessed with event-related potentials. Pharmacopsychiatry 1994;27:224-30. PubMed
  8. Munte TF, Heinze HJ, Matzke M, Steitz J. Effects of oxazepam and an extract of kava roots (Piper methysticum) on event-related potentials in a word recognition task. Neuropsychobiology 1993;27:46-53.
  9. Wheatley D. Stress-induced insomnia treated with kava and valerian: singly and in combination. Hum Psychopharmacol 2001;16:353-6. PubMed
  10. Schelosky L, Raffaup C, Jendroska K, Poewe W. Kava and dopamine antagonism. J Neurol Neurosurg Psychiatry 1995;58:639-40. PubMed
  11. Norton SA, Ruze P. Kava dermopathy. J Am Acad Dermatol 1994;31:89-97.
  12. Pizzorno JE, Murray MT, eds. Textbook of Natural Medicine. 2nd ed. Edinburgh:Churchill Livingstone, 1999.
  13. Mathews JD, Riley MD, Fejo L, et al. Effects of heavy usage of kava on physical health: Summary of a pilot survey in an aboriginal community. Med J Aust 1988;148:548-55.
  14. Escher M, Desmeules J, Giostra E, Mentha G. Hepatitis associated with Kava, a herbal remedy for anxiety. BMJ 2001;322:139.
  15. Russmann S, Lauterburg BH, Helbling A. Kava hepatotoxicity [letter]. Ann Intern Med 2001;135:68-9.
  16. Liver Toxicity With Kava. Pharmacist's Letter/Prescriber's Letter. January 2001.
  17. Consultation letter MLX 286: Proposals to prohibit the herbal ingredient Kava-Kava (Piper methysticum) in unlicensed medicines. Medicines Control Agency, United Kingdom, July 19, 2002.
  18. Meseguer E, Taboada R, Sanchez V, et al. Life-threatening parkinsonism induced by kava-kava. Mov Disord 2002;17:195-6. PubMed
  19. Ruze P. Kava-induced dermopathy: a niacin deficiency? Lancet 1990;335:1442-5. PubMed
  20. Singh YN. Kava: an overview. J Ethnopharmacol 1992;37:13-45.
  21. Bilia AR, Gallori S, Vincieri FF. Kava-kava and anxiety: growing knowledge about the efficacy and safety. Life Sci 2002;70:2581-97. PubMed
  22. Wooltorton E. Herbal kava: reports of liver toxicity. CMAJ 2002;166:777.
  23. Mathews JM, Etheridge AS, Black SR. Inhibition of human cytochrome P450 activities by kava extract and kavalactones. Drug Metab Dispos 2002;30:1153-7. PubMed
  24. Logan JL, Ahmed J. Critical hypokalemic renal tubular acidosis due to Sjogren's syndrome: association with the purported immune stimulant echinacea. Clin Rheumatol 2003;22:158-9.
  25. Teschke R, Gaus W, Loew D. Kava extracts: safety and risks including rare hepatotoxicity. Phytomedicine 2003;10:440-6. PubMed
  26. Schmidt P, Boehncke WH. Delayed-type hypersensitivity reaction to kava-kava extract. Contact Dermatitis 2000;42:363-4.
  27. Schulze J, Raasch W, Siegers CP. Toxicity of kava pyrones, drug safety and precautions--a case study. Phytomedicine 2003;10:68-73.. PubMed
  28. Pittler MH, Ernst E. Kava extract for treating anxiety. Cochrane Database Syst Rev 2003;(1):CD003383.
  29. Cairney S, Maruff P, Clough AR, et al. Saccade and cognitive impairment associated with kava intoxication. Hum Psychopharmacol 2003;18:525-33. PubMed
  30. Moulds RF, Malani J. Kava: herbal panacea or liver poison? Med J Aust 2003;178:451-3. PubMed
  31. Gow PJ, Connelly NJ, Hill RL, et al. Fatal fulminant hepatic failure induced by a natural therapy containing kava. Med J Aust 2003;178:442-3. PubMed
  32. Unger M, Frank A. Simultaneous determination of the inhibitory potency of herbal extracts on the activity of six major cytochrome P450 enzymes using liquid chromatography/mass spectrometry and automated online extraction. Rapid Commun Mass Spectrom 2004;1 PubMed
  33. Gurley BJ, Gardner SF, Hubbard MA, et al. In vivo effects of goldenseal, kava kava, black cohosh, and valerian on human cytochrome P450 1A2, 2D6, 2E1, and 3A4/5 phenotypes. Clin Pharmacol Ther 2005;77:415-26. PubMed
  34. Weiss J, Sauer A, Frank A, Unger M. Extracts and kavalactones of Piper methysticum G. Forst (kava-kava) inhibit P-glycoprotein in vitro. Drug Metab Dispos 2005;33:1580-3. PubMed
  35. Gurley BJ, Swain A, Barone GW, et al. Effect of goldenseal (Hydrastis canadensis) and kava kava (Piper methysticum) supplementation on digoxin pharmacokinetics in humans. Drug Metab Dispos 2007;35:240-5. PubMed
  36. Gurley BJ, Swain A, Hubbard MA, et al. Clinical assessement of CYP2D6-mediated herb-drug interactions in humans: Effects of milk-thistle, black cohosh, goldenseal, kava kava, St. John's wort, and Echinacea. Mol Nutr Food Res 2008;52:755-63.
  37. Li XZ, Ramzan I. Role of ethanol in kava hepatotoxicity. Phytother Res 2010;24:475-80. PubMed
  38. Bodkin R, Schneider S, Rekkerth D, et al. Rhabdomyolysis associated with kava ingestion. Am J Emerg Med 2012;30:635.el-3. PubMed
  39. Donadio V, Bonsi P, Zele I, et al. Myoglobinuria after ingestion of extracts of guarana, Ginkgo biloba and kava. Ginkgo biloba and kava. Neurol Sci 2000;21:124. PubMed
  40. Sarris J, Kavanagh DJ, Byrne G, et al. The Kava Anxiety Depression Spectrum Study (KADSS): a randomized, placebo-controlled crossover trial using an aqueous extract of Piper methysticum. Psychopharmacology 2009;205:399-407. PubMed
  41. Hannam S, Murray M, Romani L, Tuicakau M, J Whitfeld M. Kava dermopathy in Fiji: an acquired ichthyosis? Int J Dermatol 2014;53(12):1490-4. PubMed
  42. Huynh JC, Asgari MM, Moore MM. Sebotropic eruption associated with use of oral kava kava supplement. Clin Exp Dermatol 2014;39(7):816-8. PubMed
  43. Teschke R, Sarris J, Schweitzer I. Kava hepatotoxicity in traditional and modern use: the presumed Pacific kava paradox hypothesis revisited. Br J Clin Pharmacol 2012;73(2):170-4. PubMed
  44. Scherer, J. Kava-kava extract in anxiety disorders: an outpatient observational study. Adv.Ther. 1998;15(4):261-269.
  45. Humberston, C. L., Akhtar, J., and Krenzelok, E. P. Acute hepatitis induced by kava kava. J Toxicol.Clin Toxicol. 2003;41(2):109-113. PubMed
  46. Schmidt, M. Are kavalactones the hepatotoxic principle of kava extracts? The pitfalls of the glutathione theory. J Altern Complement Med 2003;9(2):183-187. PubMed
  47. Stickel, F., Baumuller, H. M., Seitz, K., Vasilakis, D., Seitz, G., Seitz, H. K., and Schuppan, D. Hepatitis induced by Kava (Piper methysticum rhizoma). J Hepatol. 2003;39(1):62-67. PubMed
  48. Grace, R. Kava-induced urticaria. J Am Acad Dermatol 2005;53(5):906. PubMed
  49. Christl, S. U., Seifert, A., and Seeler, D. Toxic hepatitis after consumption of traditional kava preparation. J.Travel.Med. 2009;16(1):55-56. PubMed
  50. Teschke, R., Genthner, A., and Wolff, A. Kava hepatotoxicity: comparison of aqueous, ethanolic, acetonic kava extracts and kava-herbs mixtures. J.Ethnopharmacol. 6-25-2009;123(3):378-384. PubMed
  51. Jappe, U., Franke, I., Reinhold, D., and Gollnick, H. P. Sebotropic drug reaction resulting from kava-kava extract therapy: a new entity? J Am Acad Dermatol. 1998;38(1):104-106. PubMed
  52. Gessner B and Cnota P. Extract of the kava-kava rhizome in comparison with diazepam and placebo. Z Phytother 1994;15(1):30-37.
  53. Johnson D, Frauendorf A, Stecker K, and et al. Neurophysiological active profile and tolerance of kava extract WS 1490, A pilot study with randomized evaluation. TW Neurolgie Psychiatrie 1991;5(6):349-354.
  54. Keller F and Klohs M. A review of the chemistry and pharmacology of the constituents of Piper methysticum. Lloydia 1963;26:1-15.
  55. Siegers CP, Honold E, Krall B, and et al. Results of the drug monitoring L 1090 with Laitan capsules. Arztl Forsch 1992;39:7-11.
  56. Chanwai, L. G. Kava toxicity. Emergency Medicine 2002;12:142-145.
  57. Leung, N. Acute urinary retention secondary to kava ingestion. Emerg Med Australas 2004;16(1):94. PubMed
  58. Teschke R. Kava hepatotoxicity: pathogenetic aspects and prospective considerations. Liver Int 2010;30(9):1270-9. PubMed
  59. Toohey TP, Lu BY, Wada C. Toxic effects of psychotropics related to possible p450 enzyme inhibition by kava:report of 2 cases. Prim Care Companion CNS Disord 2013;15(5). PubMed
  60. Ostermayer D. News: Kava, Popular as Alcohol Alternative, May Cause Toxicity. Emerg Med News. 2016;38(1B).
  61. Kuchta K, Schmidt M, Nahrstedt A. German Kava Ban Lifted by Court: The Alleged Hepatotoxicity of Kava (Piper methysticum) as a Case of Ill-Defined Herbal Drug Identity, Lacking Quality Control, and Misguided Regulatory Politics. Planta Med. 2015;81(18):16 PubMed
  62. Schmidt M. German Court Ruling Reverses Kava Ban; German Regulatory Authority Appeals Decision. HerbalEGram. 2014;11(7).
  63. Wainiqolo I, Kool B, Nosa V, Ameratunga S. Is driving under the influence of kava associated with motor vehicle crashes? A systematic review of the epidemiological literature. Aust N Z J Public Health 2015;39(5):495-9. PubMed
  64. Wainiqolo I, Kafoa B, Kool B, et al. Driving following kava use and road traffic injuries: a population-based case-control study in Fiji (TRIP 14). PLoS One 2016;11(3):e0149719. PubMed
  65. Asher GN, Corbett AH, Hawke RL. Common Herbal Dietary Supplement-Drug Interactions. Am Fam Physician. 2017;96(2):101-107.
  66. Sarris J, Byrne GJ, Bousman CA, et al. Kava for generalised anxiety disorder: A 16-week double-blind, randomised, placebo-controlled study. Aust N Z J Psychiatry. 2020 Mar;54(3):288-297. PubMed
  67. Aporosa AS, Atkins M, Brunton R. Kava drinking in traditional settings: towards understanding effects on cognitive function. Hum Psychopharmacol. 2020;35(2):e2725. PubMed
  68. Sarris J, Ravindran A, Yatham LN, et al. Clinician guidelines for the treatment of psychiatric disorders with nutraceuticals and phytoceuticals: The World Federation of Societies of Biological Psychiatry (WFSBP) and Canadian Network for Mood and Anxiety T
  69. Aporosa S', Ballard H, Pandey R, McCarthy MJ. The impact of traditional kava (Piper methysticum) use on cognition: Implications for driver fitness. J Ethnopharmacol 2022;291:115080. PubMed
  70. Savage K, Sarris J, Hughes M, et al. Neuroimaging insights: Kava's (Piper methysticum) effect on dorsal anterior cingulate cortex GABA in generalized anxiety disorder. Nutrients 2023;15(21):4586. PubMed
  71. du Plessis Nisbet J, Xie D, Thompson R, Wark K, Lamrock E, Scurry J. Kava-induced dermatitis: A detailed histopathological analysis. Australas J Dermatol 2024. PubMed

See these in context on the Kava monograph →

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DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.

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