StressCare Ingredients & Drug Interactions

Theoretically, taking ashwagandha with antidiabetes drugs might increase the risk of hypoglycemia.
There is preliminary clinical evidence suggesting that ashwagandha might lower blood glucose levels. Theoretically, ashwagandha might have additive effects when used with antidiabetes drugs and increase the risk of hypoglycemia.

Theoretically, taking ashwagandha with antihypertensive drugs might increase the risk of hypotension.
Animal research suggests that ashwagandha might lower systolic and diastolic blood pressure. Theoretically, ashwagandha might have additive effects when used with antihypertensive drugs and increase the risk of hypotension.

Theoretically, taking ashwagandha might increase the sedative effects of benzodiazepines.
There is preliminary evidence that ashwagandha might have an additive effect with diazepam (Valium) and clonazepam (Klonopin). This may also occur with other benzodiazepines.

Theoretically, taking ashwagandha might increase the sedative effects of CNS depressants.
Ashwagandha seems to have sedative effects. Theoretically, this may potentiate the effects of barbiturates, other sedatives, and anxiolytics.

Theoretically, taking ashwagandha with hepatotoxic drugs might increase the risk of liver damage.
Ashwagandha has been linked to cases of acute hepatitis, liver failure, hepatic encephalopathy, autoimmune hepatitis, the need for liver transplantation, and death due to liver failure.

Theoretically, taking ashwagandha might decrease the effects of immunosuppressants.
Ashwagandha has demonstrated immunostimulant effects in humans. Animal research has shown that ashwagandha can attenuate the immunosuppression caused by cyclophosphamide.

Ashwagandha might increase the effects and adverse effects of thyroid hormone.
Concomitant use of ashwagandha with thyroid hormones may cause additive therapeutic and adverse effects. Preliminary clinical research and animal studies suggest that ashwagandha boosts thyroid hormone synthesis and secretion. In one clinical study, ashwagandha increased triiodothyronine (T3) and thyroxine (T4) levels by 41.5% and 19.6%, respectively, and reduced serum TSH levels by 17.4% from baseline in adults with subclinical hypothyroidism.

Theoretically, ashwagandha might decrease the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that ashwagandha extract induces CYP1A2 enzymes.

Theoretically, ashwagandha might decrease the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that ashwagandha extract induces CYP3A4 enzymes.

Some animal studies have reported that ashwagandha can enhance serotonergic transmission by altering certain serotonin (5-HT) receptors. However, there is no evidence to suggest that ashwagandha increases the risk of serotonin-related effects, and there have been no published case reports of serotonin syndrome when combined with other serotonergic drugs. Nevertheless, due to the lack of extensive studies on the matter and the fact that ashwagandha appears to affect serotonergic pathways, it would be prudent to exercise caution when combining it with drugs that affect serotonin. [References: - Effects of Withania somnifera (Ashwaga ndha) on Stress and the Stress-Related Neuropsychiatric Disorders Anxiety, Depression, and Insomnia. Curr Neuropharmacol. 2021 Sep 14; 19: 1468–1495. - A Prospective, Randomized Double-Blind, Placebo-Controlled Study of Safety and Efficacy of a High-Concentration Full-Spectrum Extract of Ashwagandha Root in Reducing Stress and Anxiety in Adults. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573577/]

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research suggests that curcumin, a constituent of turmeric, inhibits mechlorethamine-induced apoptosis of breast cancer cells by up to 70%. Also, animal research shows that curcumin inhibits cyclophosphamide-induced tumor regression. However, some in vitro research shows that curcumin does not affect the apoptosis capacity of etoposide. Also, other laboratory research suggests that curcumin might augment the cytotoxic effects of alkylating agents. Reasons for the discrepancies may relate to the dose of curcumin and the specific chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have on alkylating agents.

Taking turmeric with amlodipine may increase levels of amlodipine.
Animal research shows that giving amlodipine 1 mg/kg as a single dose following the use of turmeric extract 200 mg/kg daily for 2 weeks increases the maximum concentration and area under the curve by 53% and 56%, respectively, when compared with amlodipine alone. Additional animal research shows that taking amlodipine 1 mg/kg with a curcumin 2 mg/kg pretreatment for 10 days increases the maximum concentration and area under the curve by about 2-fold when compared with amlodipine alone.

Turmeric may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Curcumin, a constituent of turmeric, has demonstrated antiplatelet effects in vitro. Furthermore, two case reports have found that taking turmeric along with warfarin or fluindione was associated with an increased international normalized ratio (INR). However, one clinical study in healthy volunteers shows that taking curcumin 500 mg daily for 3 weeks, alone or with aspirin 100 mg, does not increase antiplatelet effects or bleeding risk. It is possible that the dose of turmeric used in this study was too low to produce a notable effect.

Theoretically, taking turmeric with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research and case reports suggest that curcumin, a turmeric constituent, can reduce blood glucose levels in patients with diabetes. Furthermore, clinical research in adults with type 2 diabetes shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg decreased postprandial glucose levels for up to 24 hours when compared with glyburide alone, despite the lack of a significant pharmacokinetic interaction. Other clinical studies in patients with diabetes show that taking curcumin daily can reduce blood glucose levels when compared with placebo.

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro and animal research shows that curcumin, a constituent of turmeric, inhibits doxorubicin-induced apoptosis of breast cancer cells by up to 65%. However, curcumin does not seem to affect the apoptosis capacity of daunorubicin. In fact, some research shows that curcumin might augment the cytotoxic effects of antitumor antibiotics, increasing their effectiveness. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effects, if any, antioxidants such as turmeric have on antitumor antibiotics.

Turmeric might increase or decrease levels of drugs metabolized by CYP3A4.
In vitro and animal research show that turmeric and its constituents curcumin and curcuminoids inhibit CYP3A4. Also, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking turmeric and cancer medications that are CYP3A4 substrates, including everolimus, ruxolitinib, ibrutinib, and palbociclib, and bortezomib. In another case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels after consuming turmeric powder at a dose of 15 or more spoonfuls daily for ten days prior. It was thought that turmeric increased levels of tacrolimus due to CYP3A4 inhibition.
Conversely, other in vitro research suggests that turmeric induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. An animal model suggests that induction of CYP3A4 occurs after daily curcumin use for 1 week. However, the induction of CYP3A4 by turmeric has not been reported in humans.

Theoretically, turmeric might increase the risk of liver damage when taken with hepatotoxic drugs.
There is concern that turmeric might cause hepatotoxicity, especially when highly bioavailable formulations are used in high doses.

Theoretically, turmeric might have additive effects when used with hepatotoxic drugs such as methotrexate.
In one case report, a 39-year-old female taking methotrexate, turmeric, and linseed oil developed hepatotoxicity.

Theoretically, turmeric might increase blood levels of OATP4C1 substrates.
In vitro research shows that the turmeric constituent curcumin competitively inhibits OATP4C1 transport. This transporter is expressed in the kidney and facilitates the renal excretion of certain drugs. Theoretically, taking turmeric might decrease renal excretion of OATP substrates.

Turmeric might increase the effects and adverse effects of sulfasalazine.
Clinical research shows that taking the turmeric constituent, curcumin, can increase blood levels of sulfasalazine by 3.2-fold.

Turmeric might increase the effects and adverse effects of tacrolimus.
In one case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels of 29 ng/mL. The patient previously had tacrolimus levels within the therapeutic range at 9.7 ng/mL. Ten days prior to presenting at the emergency room the patient started consumption of turmeric powder at a dose of 15 or more spoonfuls daily. It was thought that turmeric increased levels of tacrolimus due to cytochrome P450 3A4 (CYP3A4) inhibition. In vitro and animal research show that turmeric and its constituent curcumin inhibit CYP3A4.

Turmeric may reduce the absorption of talinolol in some situations.
Clinical research shows that taking curcumin for 6 days decreases the bioavailability of talinolol when taken together on the seventh day. The clinical significance of this effect is unclear.

Theoretically, turmeric might reduce the levels and clinical effects of tamoxifen.
In a small clinical trial in patients with breast cancer taking tamoxifen 20-30 mg daily, adding curcumin 1200 mg plus piperine 10 mg three times daily reduces the 24-hour area under the curve of tamoxifen and the active metabolite endoxifen by 12.8% and 12.4%, respectively, as well as the maximum concentrations of tamoxifen, when compared with tamoxifen alone. However, in the absence of piperine, the area under the curve for endoxifen and the maximum concentration of tamoxifen were not significantly reduced. Effects were most pronounced in patients who were extensive cytochrome P450 (CYP) 2D6 metabolizers.

Turmeric has antioxidant effects. There is some concern that this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research shows that curcumin, a constituent of turmeric, inhibits camptothecin-induced apoptosis of breast cancer cells by up to 71%. However, other in vitro research shows that curcumin augments the cytotoxic effects of camptothecin. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agents. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have.

Theoretically, turmeric might increase or decrease levels of tramadol.
Animal research suggests that a single dose of curcumin, a constituent of turmeric, may increase tramadol's maximum concentration (Cmax) by inhibiting metabolism, while continued daily use for 7 days may reduce the area under the curve (AUC) due to the induction of drug-metabolizing enzymes such as cytochrome P450 3A4 (CYP3A4). However, this interaction has not been reported in humans.

Turmeric might increase the risk of bleeding with warfarin.
One case of increased international normalized ratio (INR) has been reported for a patient taking warfarin who began taking turmeric. Prior to taking turmeric, the patient had stable INR measurements. Within a few weeks of starting turmeric supplementation, the patient's INR increased to 10. Additionally, curcumin, the active constituent in turmeric, has demonstrated antiplatelet effects in vitro, which may produce additive effects when taken with warfarin.

Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2. However, research is conflicting.
In vitro and animal research show that the turmeric constituent, curcumin, inhibits CYP1A2. However, other in vitro research suggests that curcumin does not significantly affect CYP1A2.

Theoretically, turmeric might increase blood levels of oral docetaxel.
Animal research suggests that the turmeric constituent, curcumin, enhances the oral bioavailability of docetaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Theoretically, large amounts of turmeric might interfere with hormone replacement therapy through competition for estrogen receptors.
In vitro research shows that curcumin, a constituent of turmeric, displaces the binding of estrogen to its receptors.

Theoretically, taking turmeric and glyburide in combination might increase the risk of hypoglycemia.
Clinical research shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg increases blood levels of glyburide by 12% at 2 hours after the dose in patients with type 2 diabetes. While maximal blood concentrations of glyburide were not affected, turmeric modestly decreased postprandial glucose levels for up to 24 hours when compared to glyburide alone, possibly due to the hypoglycemic effect of turmeric demonstrated in animal research.

Theoretically, turmeric might increase the effects of losartan.
Research in hypertensive rats shows that taking turmeric can increase the hypotensive effects of losartan.

Theoretically, turmeric might increase the effects and adverse effects of norfloxacin.
Animal research shows that taking curcumin, a turmeric constituent, can increase blood levels of orally administered norfloxacin.

Theoretically, turmeric might increase the absorption of P-glycoprotein substrates.
In vitro and animal research shows that curcuminoids and other constituents found in turmeric can inhibit P-glycoprotein expression and activity.

Theoretically, turmeric might alter blood levels of paclitaxel, although any effect may not be clinically relevant.
Clinical research in adults with breast cancer receiving intravenous paclitaxel suggests that taking turmeric may modestly alter paclitaxel pharmacokinetics. Patients received paclitaxel on day 1, followed by either no treatment or turmeric 2 grams daily from days 2-22. Pharmacokinetic modeling suggests that turmeric reduces the maximum concentration and area under the curve of paclitaxel by 12.1% and 7.7%, respectively. However, these changes are not likely to be considered clinically relevant. Conversely, animal research suggests that curcumin, a constituent of turmeric, enhances the oral bioavailability of paclitaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Theoretically, licorice might reduce the effects of antihypertensive drugs.
In human research, licorice increases blood pressure in a dose-dependent manner.

Theoretically, licorice might reduce the effects of cisplatin.
In animal research, licorice diminished the therapeutic efficacy of cisplatin.

Theoretically, concomitant use of licorice and corticosteroids might increase the side effects of corticosteroids.
Case reports suggest that concomitant use of licorice and oral corticosteroids, such as hydrocortisone, can potentiate the duration of activity and increase blood levels of corticosteroids. Additionally, in one case report, a patient with neurogenic orthostatic hypertension stabilized on fludrocortisone 0.1 mg twice daily developed pseudohyperaldosteronism after recent consumption of large amounts of black licorice.

Theoretically, licorice might increase levels of drugs metabolized by CYP2B6.
In vitro research shows that licorice extract and glabridin, a licorice constituent, inhibit CYP2B6 isoenzymes. Licorice extract from the species G. uralensis seems to inhibit CYP2B6 isoenzymes to a greater degree than G. glabra extract in vitro. Theoretically, these species of licorice might increase levels of drugs metabolized by CYP2B6; however, these interactions have not yet been reported in humans.

Theoretically, licorice might increase levels of drugs metabolized by CYP2C19.
In vitro, licorice extracts from the species G. glabra and G. uralensis inhibit CYP2C19 isoenzymes in vitro. Theoretically, these species of licorice might increase levels of drugs metabolized by CYP2C19; however, this interaction has not yet been reported in humans.

Theoretically, licorice might increase levels of drugs metabolized by CYP2C8.
In vitro, licorice extract from the species G. glabra and G. uralensis inhibits CYP2C8 isoenzymes. Theoretically, these species of licorice might increase levels of drugs metabolized by CYP2C8; however, this interaction has not yet been reported in humans.

Theoretically, licorice might increase or decrease levels of drugs metabolized by CYP2C9.
There is conflicting evidence about the effect of licorice on CYP2C9 enzyme activity. In vitro research shows that extracts from the licorice species G. glabra and G. uralensis moderately inhibit CYP2C9 isoenzymes. However, evidence from an animal model shows that licorice extract from the species G. uralensis can induce hepatic CYP2C9 activity. Until more is known, licorice should be used cautiously in people taking CYP2C9 substrates.

Theoretically, licorice might increase or decrease levels of drugs metabolized by CYP3A4.
Pharmacokinetic research shows that the licorice constituent glycyrrhizin, taken in a dosage of 150 mg orally twice daily for 14 days, modestly decreases the area under the concentration-time curve of midazolam by about 20%. Midazolam is a substrate of CYP3A4, suggesting that glycyrrhizin modestly induces CYP3A4 activity. Animal research also shows that licorice extract from the species G. uralensis induces CYP3A4 activity. However, licorice extract from G. glabra species appear to inhibit CYP3A4-induced metabolism of testosterone in vitro. It is thought that the G. glabra inhibits CYP3A4 due to its constituent glabridin, which is a moderate CYP3A4 inhibitor in vitro and not present in other licorice species. Until more is known, licorice should be used cautiously in people taking CYP3A4 substrates.

Theoretically, concomitant use of licorice with digoxin might increase the risk of cardiac toxicity.
Overuse or misuse of licorice with cardiac glycoside therapy might increase the risk of cardiac toxicity due to potassium loss.

Theoretically, concomitant use of licorice with diuretic drugs might increase the risk of hypokalemia.
Overuse of licorice might compound diuretic-induced potassium loss. In one case report, a 72-year-old male with a past medical history of hypertension, type 2 diabetes, hyperlipidemia, arrhythmia, stroke, and hepatic dysfunction was hospitalized with severe hypokalemia and uncontrolled hypertension due to pseudohyperaldosteronism. This was thought to be provoked by concomitant daily consumption of a product containing 225 mg of glycyrrhizin, a constituent of licorice, and hydrochlorothiazide 12.5 mg for 1 month.

Theoretically, licorice might increase or decrease the effects of estrogen therapy.
Theoretically, licorice might interfere with estrogen therapy due to estrogenic and anti-estrogenic effects.

Theoretically, loop diuretics might increase the mineralocorticoid effects of licorice.
Theoretically, loop diuretics might enhance the mineralocorticoid effects of licorice by inhibiting the enzyme that converts cortisol to cortisone; however, bumetanide (Bumex) does not appear to have this effect.

Theoretically, licorice might decrease levels of midazolam.
In humans, the licorice constituent glycyrrhizin appears to moderately induce the metabolism of midazolam. This is likely due to induction of cytochrome P450 3A4 by licorice. Until more is known, licorice should be used cautiously in people taking midazolam.

Theoretically, licorice might decrease the absorption of P-glycoprotein substrates.
In vitro research shows that licorice can increase P-glycoprotein activity.

Theoretically, licorice might decrease plasma levels and clinical effects of paclitaxel.
Multiple doses of licorice taken concomitantly with paclitaxel might reduce the effectiveness of paclitaxel. Animal research shows that licorice 3 grams/kg given orally for 14 days before intravenous administration of paclitaxel decreases the exposure to paclitaxel and increases its clearance. Theoretically, this occurs because licorice induces cytochrome P450 3A4 enzymes, which metabolize paclitaxel. Notably, a single dose of licorice did not affect exposure or clearance of paclitaxel.

Theoretically, licorice might decrease plasma levels and clinical effects of warfarin.
Licorice seems to increase metabolism and decrease levels of warfarin in animal models. This is likely due to induction of cytochrome P450 2C9 (CYP2C9) metabolism by licorice. Advise patients taking warfarin to avoid taking licorice.

Theoretically, licorice might decrease the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that licorice induces CYP1A2 enzymes.

Theoretically, licorice might increase levels of methotrexate.
Animal research suggests that intravenous administration of glycyrrhizin, a licorice constituent, and high-dose methotrexate may delay methotrexate excretion and increase systemic exposure, leading to transient elevations in liver enzymes and total bilirubin. This interaction has not yet been reported in humans.

Theoretically, concomitant use of clove extracts with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical and laboratory research suggest that polyphenol extracts from clove flower buds might lower blood glucose levels. Dosing adjustments for insulin or oral hypoglycemic agents may be necessary when taken with clove. Monitor blood glucose levels closely.

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP1A2.
In vitro research shows that eugenol, the principal constituent of clove, can inhibit CYP1A2 in a dose-dependent manner,. This effect has not been reported in humans.

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP2C9.
In vitro research shows that eugenol, the principal constituent of clove, inhibits CYP2C9 in a dose-dependent manner. This effect has not been reported in humans.

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP2D6.
In vitro research shows that eugenol, the principal constituent of clove, can inhibit CYP2D6 in a dose-dependent manner. This effect has not been reported in humans.

Theoretically, concomitant use of clove may increase levels of drugs metabolized by CYP3A4.
In vitro research shows that eugenol, the principal constituent of clove, can inhibit CYP3A4 in a dose-dependent manner. This effect has not been reported in humans.

Theoretically, clove oil may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Laboratory research suggests that eugenol, a constituent of clove, has antiplatelet activity. This interaction has not been reported in humans.

Theoretically, topical application of clove oil with ibuprofen might increase the absorption and side effects of topical ibuprofen.
Laboratory research shows that topical application of clove oil increases the absorption of topical ibuprofen. This interaction has not been reported in humans.

Bergapten, a constituent of bishop's weed, has antiplatelet activity. Theoretically, bishop's weed might have additive effects with anticoagulant or antiplatelet drugs and possibly increase the risk of bleeding.
Some anticoagulant or antiplatelet drugs include aspirin, clopidogrel (Plavix), dalteparin (Fragmin), enoxaparin (Lovenox), heparin, ticlopidine (Ticlid), warfarin (Coumadin), and others.

Bergapten, a constituent of bishop's weed, has been shown to inhibit cytochrome P450 3A4 (CYP3A4) in vitro. Theoretically, bishop's weed might inhibit elimination and increase blood levels of drugs metabolized by CYP3A4.
Some drugs metabolized by CYP3A4 include alprazolam (Xanax), amitriptyline (Elavil), amiodarone (Cordarone), buspirone (Buspar), cerivastatin (Baycol), citalopram (Celexa), felodipine (Plendil), fexofenadine (Allegra), itraconazole (Sporanox), ketoconazole (Nizoral), lansoprazole (Prevacid), losartan (Cozaar), lovastatin (Mevacor), ondansetron (Zofran), prednisone (Deltasone, Orasone), sertraline (Zoloft), sibutramine (Meridia), sildenafil (Viagra), simvastatin (Zocor), verapamil (Calan, Covera-HS, Isoptin), and many others.

Bishop's weed constituents seem to cause photosensitivity. Theoretically, concomitant use of bishop's weed with photosensitizing drugs might result in increased photosensitivity.
Some drugs that cause photosensitivity include amitriptyline (Elavil), quinolones (Ciprofloxacin, others), sulfa drugs (Septra, Bactrim, others), and tetracycline.

Theoretically, concomitant use of Terminalia arjuna with anticoagulant or antiplatelet drugs may increase the risk of bleeding in some patients.
In vitro, Terminalia arjuna bark extract inhibits platelet aggregation, decreases platelet activation, and shows antithrombotic properties.

Theoretically, concomitant use of Terminalia bellirica or Terminalia chebula with antidiabetes drugs could affect blood sugar control and increase the risk of hypoglycemia.
Animal and in vitro research shows that Terminalia bellirica and Terminalia chebula fruit and seed extract have hypoglycemic effects.

Theoretically, use of Terminalia chebula may increase the risk of adverse effects from chlorzoxazone.
Animal research shows that enteral administration of Terminalia chebula for 15 days prior to administration of chlorzoxazone increases blood levels of chlorzoxazone and decreases chlorzoxazone clearance. It is speculated that Terminalia chebula reduces the metabolism of chlorzoxazone by inhibiting cytochrome P450 2E1.

Theoretically, use of Terminalia arjuna may increase the levels and clinical effects of CYP2C9 substrates.
In vitro research shows that Terminalia arjuna extract inhibits CYP2C9 enzymes and reduces CYP2C9 substrate metabolism.

Theoretically, use of Terminalia arjuna may increase the levels and clinical effects of CYP2D6 substrates.
In vitro research shows that Terminalia arjuna extract inhibits CYP2D6 enzymes and reduces CYP2D6 substrate metabolism.

Theoretically, use of Terminalia arjuna may increase the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that Terminalia arjuna extract inhibits CYP3A4 enzymes and reduces CYP3A4 substrate metabolism.

Theoretically, use of Terminalia chebula may increase the risk of adverse effects from omeprazole.
Animal research shows that enteral administration of Terminalia chebula for 15 days prior to administration of omeprazole increases blood levels of omeprazole and decreases omeprazole clearance. It is speculated that Terminalia chebula reduces the metabolism of omeprazole by inhibiting cytochrome P450 2C19.

Theoretically, Indian long pepper might increase the risk of bleeding when taken with anticoagulant/antiplatelet drugs.
In vitro research shows that Indian long pepper extract inhibits platelet aggregation.

Theoretically, Indian long pepper might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research shows that piperine, a constituent of Indian long pepper, can reduce blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Theoretically, Indian long pepper might increase the effects and adverse effects of cyclosporine.
In vitro research shows that piperine, a constituent of Indian long pepper, increases the bioavailability of cyclosporine.

Theoretically, Indian long pepper might increase the effects and adverse effects of CYP3A4 substrates.
In vitro research shows that piperine, a constituent of Indian long pepper, inhibits CYP3A4.

Theoretically, Indian long pepper might increase blood levels of nevirapine.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases the plasma concentration and systemic exposure of nevirapine. However, no adverse effects were associated with the elevated plasma levels of nevirapine.

Theoretically, Indian long pepper might increase levels of P-glycoprotein substrates.
In vitro research shows that piperine, a constituent of Indian long pepper, can inhibit P-glycoprotein.

Theoretically, Indian long pepper might increase the sedative effects of pentobarbital.
Animal research shows that piperine, a constituent of Indian long pepper, can increase pentobarbitone-induced sleeping time.

Theoretically, Indian long pepper might increase blood levels of phenytoin.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases phenytoin serum levels and slows its elimination.

Theoretically, Indian long pepper might increase blood levels of propranolol.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, accelerates absorption and increases serum concentrations of propranolol.

Theoretically, Indian long pepper might increase blood levels of rifampin.
Piperine, a constituent of Indian long pepper, seems to increase absorption and serum levels of rifampin.

Indian long pepper might increase blood levels of theophylline.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases serum concentrations and slows elimination of theophylline.

Theoretically, Indian long pepper might increase the effects and adverse effects of amoxicillin.
Evidence from animal research shows that piperine, a constituent of Indian long pepper, increases the plasma levels of amoxicillin when taken concomitantly.

Theoretically, Indian long pepper might increase blood levels of carbamazepine.
A small pharmacokinetic study in patients taking carbamazepine 300 mg or 500 mg twice daily shows that a single 20 mg dose of purified piperine, which is a constituent of Indian long pepper, increases carbamazepine levels. Piperine may increase absorption by increasing blood flow to the GI tract, increasing the surface area of the small intestine, or by cytochrome P450 3A4 (CYP3A4) inhibition in the gut wall. Absorption was significantly increased by 7-10 mcg/mL/hour. The time to eliminate carbamazepine was also increased by 4-8 hours. Although carbamazepine levels were increased, this did not appear to increase side effects.

Theoretically, Indian long pepper might increase the effects and adverse effects of cefotaxime.
Animal research shows that piperine, a constituent of Indian long pepper, increases the plasma levels of cefotaxime when taken concomitantly.

Theoretically, taking gotu kola might increase the sedative effects of CNS depressants.
In vitro research suggests that gotu kola may have sedative effects via binding of GABA receptors.

Theoretically, taking gotu kola with hepatotoxic drugs might have additive adverse effects.
There are at least four case reports of hepatotoxicity associated with the use of gotu kola. However, more information is needed to determine if gotu kola was the causative factor in these cases.

Theoretically, concomitant use of nutmeg and anticholinergic drugs might decrease the effectiveness of either agent.
Animal research suggests that nutmeg extract can inhibit acetylcholinesterase and might increase acetylcholine levels.

Theoretically, concomitant use of nutmeg with other cholinergic drugs might have additive effects and increase the risk of cholinergic side effects.
Animal research suggests that nutmeg extract can inhibit acetylcholinesterase and might increase acetylcholine levels.

Theoretically, nutmeg might increase the risk of additive sedation when taken with CNS depressants.
Animal studies suggest that nutmeg extracts and several volatile oils in nutmeg, such as methyleugenol, isoeugenol, safrole, myristicin, trimyristin, 1,8-cineole, and geranyl acetate, have sedative effects. One animal study shows that petroleum ether extracts of nutmeg can potentiate the effects of pentobarbital or phenobarbital. However, evidence from other animal research suggests that the nutmeg constituent myristicin can actually reduce sleeping time in rats pretreated with phenobarbital.

Theoretically, nutmeg might decrease levels of drugs metabolized by CYP1A2.
Animal research suggests that intraperitoneal injections of myristicin, a constituent of nutmeg, can induce CYP1A2.

Theoretically, nutmeg might increase or decrease the effects and adverse effects of phenobarbital.
Some animal research suggests that myristicin, a constituent of nutmeg, can reduce sleeping time in rats pretreated with phenobarbital. However, other animal research suggests that petroleum ether extract of nutmeg can potentiate the effects of phenobarbital.

Theoretically, concomitant use of saffron with antidiabetes drugs might increase the risk of hypoglycemia.
Some clinical research shows that taking saffron extract reduces fasting levels of glucose when used in addition to hypoglycemic agents. However, saffron powder itself has not been shown to reduce fasting glucose levels.

Theoretically, concomitant use of saffron with antihypertensive drugs might have additive effects.
Animal and human research suggests that saffron extract can decrease blood pressure.

Theoretically, saffron might inhibit the metabolism of caffeine.
A small clinical study suggests that taking saffron powder 300 mg in 150 mL water daily for 5 days and then taking caffeine 200 mg seems to reduce caffeine metabolite levels in the saliva and urine in males, but not females. Theoretically, this may be due to the inhibition of cytochrome P450 1A2 by saffron.

Theoretically, concomitant use of saffron and CNS depressants might have additive sedative effects.
Clinical research shows that taking saffron extract 60 mg orally daily for 26 weeks can cause drowsiness and sedation. Animal research suggests that adding saffron to hexobarbital further increases sleeping and slows motor activity.

Concomitant use can increase the risk of levodopa-related adverse effects.
Cowhage contains levodopa. Some cowhage products have been standardized to contain 75-400 mg of levodopa per dose.

Theoretically, concomitant use of cowhage and methyldopa might increase the risk of hypotension.
Cowhage contains levodopa. Use of levodopa with methyldopa might cause additive hypotension. In addition, methyldopa may inhibit peripheral decarboxylation of levodopa and increase levodopa levels in the central nervous system; avoid using.

Theoretically, concomitant use of cowhage and non-selective MAOIs might increase the risk of hypertensive crisis.
Cowhage contains levodopa. Use of levodopa with non-selective MAOIs might cause hypertensive crisis. However, this interaction has not been reported with MAO-B selective inhibitors such as selegiline.

Theoretically, concomitant use of cowhage and anesthesia might increase the risk of arrhythmias.
Cowhage contains levodopa. Use of levodopa with cyclopropane or halogenated hydrocarbon anesthesia has led to arrhythmias. Other anesthetics have not been implicated. Use other anesthetics in patients taking cowhage or tell patients to stop taking cowhage at least 2 weeks before surgery.

Theoretically, concomitant use of cowhage and antidiabetes drugs might increase the risk of hypoglycemia.
Animal research shows that cowhage might have hypoglycemic effects.

Theoretically, use of cowhage might decrease the clinical effects of antipsychotic drugs.
Cowhage contains levodopa. Use of levodopa might counteract the antidopaminergic effects of antipsychotic medications.

Theoretically, concomitant use of cowhage and guanethidine might increase the risk of hypotension.
Cowhage contains levodopa. Use of levodopa with guanethidine might cause additive hypotension; avoid using.

Theoretically, use of TCAs might reduce the levels and clinical effects of cowhage.
Cowhage contains levodopa. Use of TCAs might reduce the absorption of levodopa. Some case reports describe patients that developed hypertension and dyskinesia when taking both levodopa and TCAs.

Taking shilajit with antidiabetes drugs might increase the risk of hypoglycemia.
Most human and animal research shows that shilajit can decrease fasting plasma glucose levels. In an animal model, shilajit 100 mg per kg daily enhanced the glucose-lowering ability of both glibenclamide and metformin when given in combination over a 4 week period. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Some preliminary clinical research shows that taking caper fruit extract 1200 mg daily for 2 months can lower fasting blood glucose and glycated hemoglobin (HbA1c) in patients with type 2 diabetes who are already taking antidiabetes drugs. However, other research does not support this effect. Until more is known, monitor blood glucose levels closely. Medication dose adjustments may be necessary.
Some antidiabetes drugs include glimepiride (Amaryl), glyburide (DiaBeta, Glynase PresTab, Micronase), insulin, pioglitazone (Actos), rosiglitazone (Avandia), and others.

Theoretically, chicory might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal and in vitro research shows that chicory extracts have antidiabetic effects.

Theoretically, asparagus racemosus root might increase diuresis and electrolyte loss when used with diuretic drugs.
Animal studies show that asparagus racemosus root has diuretic effects when used in high doses. This effect has not been reported in humans.

Theoretically, Asparagus racemosus root could reduce excretion and increase levels of lithium.
Animal research suggests that Asparagus racemosus root has diuretic properties when used in high doses. Therefore, it might reduce excretion and increase levels of lithium. The dose of lithium might need to be decreased.

Theoretically, taking yarrow with lithium might increase the levels and adverse effects of lithium.
Animal research shows that yarrow has diuretic activity. Theoretically, due to these potential diuretic effects, yarrow might reduce excretion and increase levels of lithium. The dose of lithium might need to be decreased.