Raw Whole Food B-Complex Ingredients & Drug Interactions

Goji can increase the effects of warfarin and possibly increase the risk of bleeding.
There are at least 5 case reports of increased international normalized ratio (INR) in patients stabilized on warfarin who began drinking goji juice, concentrated goji tea, or goji wine. Goji may inhibit the metabolism of warfarin by cytochrome P450 2C9 (CYP2C9).

Theoretically, concomitant use of goji root bark, but not goji fruit, with antihypertensive drugs might have additive effects.
Animal and in vitro research suggest that goji root bark has hypotensive effects. However, goji fruit juice does not appear to reduce systolic or diastolic blood pressure in humans.

Theoretically, goji berry might inhibit CYP2C19 and reduce metabolism of CYP2C19 substrates.
In vitro research shows that goji berry tincture and juice inhibit CYP2C19 enzymes. Concomitant use with goji may decrease metabolism and increase levels of CYP2C19 substrates. However, this has not been reported in humans.

Theoretically, goji berry might inhibit CYP2C9 and reduce metabolism of CYP2C9 substrates.
In vitro research shows that goji berry tincture and juice inhibit CYP2C9 enzymes. Additionally, multiple case reports suggest that goji berry concentrated tea and juice inhibit the metabolism of warfarin, a CYP2C9 substrate. Concomitant use with goji may decrease metabolism and increase levels of CYP2C9 substrates.

Theoretically, goji berry might inhibit CYP2D6 and reduce metabolism of CYP2D6 substrates.
In vitro research shows that goji berry juice inhibits CYP2D6 enzymes. Concomitant use with goji may decrease metabolism and increase levels of CYP2D6 substrates. However, this has not been reported in humans.

Theoretically, goji berry might inhibit CYP3A4 and reduce metabolism of CYP3A4 substrates.
In vitro research shows that goji berry juice inhibits CYP3A4 enzymes. Concomitant use with goji may decrease metabolism and increase levels of CYP3A4 substrates. However, this has not been reported in humans.

Theoretically, goji berry might increase the levels and clinical effects of flecainide.
In one case report, a 75-year-old patient stable on flecainide and warfarin presented to the emergency room with fainting and pleomorphic arrhythmia caused by flecainide toxicity. Flecainide toxicity was attributed to drinking 1-2 glasses of concentrated goji tea daily for 2 weeks. Theoretically, goji may have inhibited the cytochrome P450 2D6 (CYP2D6) metabolism of flecainide.

Theoretically, concomitant use of goji fruit polysaccharides or goji root bark with antidiabetes drugs might have additive effects.
Animal and in vitro research show that goji root bark and fruit polysaccharides might have hypoglycemic effects. However, clinical research has only shown that taking goji fruit polysaccharides with or without antidiabetes drugs modestly reduces postprandial glucose when compared with control, with no reports of hypoglycemia.

Grapefruit juice can increase blood levels of amiodarone, potentially increasing the effects and adverse effects of amiodarone.
Clinical research shows that grapefruit juice inhibits metabolism and increases absorption of amiodarone. Grapefruit juice increases amiodarone plasma levels by 50% and peak concentration by 84%.

Grapefruit juice can increase blood levels of oral artemether, potentially increasing the effects and adverse effects of artemether.
Clinical research shows that grapefruit juice increases the levels of oral artemether by 90% to 250% in healthy males.

Grapefruit juice might increase blood levels of some oral benzodiazepines, potentially increasing the effects and adverse effects of these drugs.
Clinical research shows that grapefruit juice can increase plasma triazolam concentrations. Repeated consumption of grapefruit juice greatly increases triazolam concentrations and prolongs the half-life, probably due to inhibition of cytochrome P450 3A4 (CYP3A4). Some studies show that grapefruit juice, particularly when taken in large quantities, reduces the clearance and increases the maximum blood levels, area under the plasma concentration curve (AUC), and duration of effect of midazolam. However, there is no effect on intravenous midazolam. Grapefruit juice has also been shown to increase the maximum blood levels and duration of effect of diazepam, but the clinical significance of this is not known. This interaction does not appear to occur with alprazolam.

Grapefruit juice can increase blood levels of buspirone, potentially increasing the effects and adverse effects of buspirone.
Clinical research shows that grapefruit juice increases absorption and plasma concentrations of buspirone.

Grapefruit juice can increase blood levels of oral calcium channel blockers, potentially increasing the effects and adverse effects of these drugs.
Clinical research shows that grapefruit juice increases absorption and plasma concentrations of amlodipine, nifedipine, nisoldipine, verapamil, felodipine, nimodipine, nicardipine, diltiazem, pranidipine, nitrendipine, and manidipine, This interaction is likely the result of the inhibition of intestinal metabolism of these drugs by CYP3A4, although some research suggests grapefruit may alter plasma drug levels by reducing the rate of gastric emptying. Consuming grapefruit juice 1 liter daily increases steady state concentrations of verapamil by as much as 50%. However, some references dispute the clinical relevance of the interactions with amlodipine, diltiazem, and verapamil. Other research in healthy individuals suggests plasma levels of felodipine and nifedipine are not affected when given intravenously. There is considerable interindividual variability in the effect of grapefruit juice on drug metabolism, which might account for inconsistent study results. In healthy older adults, the hemodynamic response to felodipine plus grapefruit juice might be influenced by altered autonomic regulation. In older healthy adults, a single dose of grapefruit juice and felodipine enhanced the blood pressure-lowering effects of felodipine. However, after a week of grapefruit juice and felodipine (steady state), the hypotensive activity was reduced, possibly due to compensatory tachycardia. Research indicates it is necessary to withhold grapefruit juice for as long as 3 days to avoid interactions with felodipine and nisoldipine.

Grapefruit juice can increase blood levels of carbamazepine, potentially increasing the effects and adverse effects of carbamazepine.
Clinical research shows that grapefruit juice increases absorption and plasma concentrations of carbamazepine.

Grapefruit juice can increase blood levels of carvedilol, potentially increasing the effects and adverse effects of carvedilol.
Clinical research shows that grapefruit juice increases the bioavailability of a single dose of carvedilol by 16%.

Grapefruit juice can decrease blood levels of celiprolol, potentially decreasing the clinical effects of celiprolol.
In human research, taking grapefruit juice within two hours of celiprolol appears to decrease absorption and blood levels of celiprolol by approximately 85%. This interaction is due to grapefruit-induced inhibition of organic anion transporting polypeptide (OATP). Grapefruit juice is thought to affect OATP for only a short time. Therefore, separating drug administration and consumption of grapefruit by at least 4 hours is likely to prevent this interaction.

Grapefruit juice can increase blood levels of cisapride, potentially increasing the effects and adverse effects of cisapride.
Clinical research shows that grapefruit juice increases the absorption and plasma concentrations of cisapride. According to the cisapride prescribing information, grapefruit juice is contraindicated in patients taking cisapride.

Theoretically, grapefruit juice might increase blood levels of clomipramine, potentially increasing the effects and adverse effects of clomipramine.
Case reports have shown that clomipramine trough levels increase significantly after the addition of grapefruit juice to the therapeutic regimen.

Grapefruit juice can decrease blood levels of the active metabolite of clopidogrel, thereby decreasing the antiplatelet effect of clopidogrel.
Clopidogrel is an antiplatelet prodrug that is metabolized primarily by cytochrome P450 2C19 (CYP2C19) to form the active metabolite. A small clinical study shows that taking grapefruit juice with clopidogrel decreases plasma levels of the active metabolite by more than 80% and impairs the antiplatelet effect of clopidogrel. This effect is possibly due to grapefruit-induced inhibition of CYP2C19.

Grapefruit juice can increase blood levels of oral cyclosporine, potentially increasing the effects and adverse effects of cyclosporine.
Clinical research shows that grapefruit juice increases the absorption and plasma concentrations of cyclosporine. The mechanism of action is unclear. However, there is no effect on intravenous cyclosporine.

Grapefruit juice can increase levels of drugs metabolized by CYP3A4.
Clinical research shows that grapefruit juice can inhibit CYP3A4 metabolism of drugs, causing increased drug levels and potentially increasing the risk of adverse effects. When taken orally, effects of grapefruit juice on CYP3A4 levels appear to last at least 48 hours. Grapefruit's ability to inhibit CYP3A4 has even been harnessed to intentionally increase levels of venetoclax, which is metabolized by CYP3A4, in an elderly patient with acute myeloid leukemia who could not afford full dose venetoclax. The lower dose of venetoclax in combination with grapefruit juice resulted in serum levels of venetoclax in the therapeutic reference range of full dose venetoclax and positive treatment outcomes for the patient.
Professional consensus recommends the consideration of patient age, existing medical conditions, additional medications, and the potential for additive adverse effects when evaluating the risks of concomitant use of grapefruit juice with any medication metabolized by CYP3A4. While all patients are at risk for interactions with grapefruit juice consumption, patients older than 70 years of age and those taking multiple medications are at the greatest risk for a serious or fatal interaction with grapefruit juice.

Grapefruit juice can increase blood levels of dextromethorphan, potentially increasing the effects and adverse effects of dextromethorphan.
Clinical research shows that grapefruit juice can inhibit cytochrome P450 3A4 (CYP3A4) metabolism, causing increased dextromethorphan levels.

Grapefruit juice can increase blood levels of estrogens, potentially increasing the effects and adverse effects of estrogens.
Clinical research shows that grapefruit increases the levels of endogenous and exogenous estrogens by inhibiting cytochrome P450 3A4 (CYP3A4) enzymes. Grapefruit juice increases exogenously administered 17-beta-estradiol by about 20% in females without ovaries and ethinyl-estradiol in healthy females.

Grapefruit juice can decrease blood levels of etoposide, potentially decreasing the clinical effects of etoposide.
Clinical research shows that grapefruit juice decreases the absorption and plasma concentrations of etoposide. There is some evidence that grapefruit juice co-administered with oral etoposide can reduce levels of etoposide by about 26%. Grapefruit juice seems to inhibit organic anion transporting polypeptide (OATP), which is a drug transporter in the gut, liver, and kidney. Grapefruit juice is thought to affect OATP for only a short time. Therefore, separating drug administration and consumption of grapefruit by at least 4 hours is likely to prevent this interaction.

Grapefruit juice can increase blood levels of halofantrine, potentially increasing the effects and adverse effects of halofantrine.
Clinical research shows that grapefruit juice inhibits cytochrome P450 3A4 (CYP3A4) metabolism, which increases halofantrine levels and peak concentration, as well as a marker of ventricular tachyarrhythmia potential.

Grapefruit juice can increase blood levels of statins that are metabolized by cytochrome P450 3A4 (CYP3A4), potentially increasing the effects and adverse effects of these statins. Additionally, grapefruit juice might interfere with the bioavailability of statins that are substrates of organic anion transporting polypeptides (OATP).
Clinical research shows that grapefruit juice inhibits metabolism and increases absorption and plasma concentrations of statins that are metabolized by CYP3A4. These include lovastatin, simvastatin, and atorvastatin. Keep in mind that there is considerable variability in the effect of grapefruit juice on drug metabolism, so individual patient response is difficult to predict.
Some statins, including pravastatin, fluvastatin, pitavastatin, and rosuvastatin, are not metabolized by CYP3A4. However, grapefruit juice might still affect the bioavailability of these statins. These statins are substrates of OATP. Grapefruit juice can inhibit OATP. Therefore, grapefruit juice may reduce the bioavailability or increase drug levels of these statins depending on the type of OATP. However, grapefruit juice affects OATP for only a short time. Therefore, separating drug administration by at least 4 hours is likely to avoid this interaction.

Grapefruit juice can increase blood levels of methadone, potentially increasing the effects and adverse effects of methadone.
Clinical research shows that grapefruit juice inhibits the metabolism of methadone, increasing methadone levels and peak concentrations. In one case, a 51-year-old male taking methadone 90 mg daily and no other medications was found unresponsive. The patient reported drinking grapefruit juice 500 mL daily for 3 days prior to the event. Methadone is a substrate of cytochrome P450 3A4 (CYP3A4), and grapefruit juice-induced inhibition of CYP3A4 is the likely cause of this interaction.

Grapefruit juice can increase blood levels of methylprednisolone, potentially increasing the effects and adverse effects of methylprednisolone.
Clinical research shows that grapefruit juice can increase the plasma concentration of orally administered methylprednisolone. Grapefruit juice 200 mL three times daily given with methylprednisolone 16 mg increased methylprednisolone half-life by 35%, peak plasma concentration by 27%, and total area under the curve by 75%.

Grapefruit juice can decrease levels of drugs that are substrates of OATP.
In vitro and clinical research show that consuming grapefruit juice inhibits OATP, which reduces the bioavailability of oral drugs that are substrates of OATP. Various clinical studies have shown reduced absorption of OATP substrates when taken with grapefruit, including fexofenadine, acebutolol, aliskiren, celiprolol, levothyroxine, nadolol, and pitavastatin. Grapefruit juice is thought to affect OATP for only a short time. Therefore, separating drug administration and consumption of grapefruit by at least 4 hours is likely to prevent this interaction.

Grapefruit juice can increase blood levels of praziquantel, potentially increasing the effects and adverse effects of praziquantel.
Clinical research shows that grapefruit juice can inhibit cytochrome P450 3A4 (CYP3A4) metabolism of praziquantel. Plasma concentrations of praziquantel can increase by as much as 160% when administered with 250 mL of commercially available grapefruit juice.

Grapefruit or grapefruit juice, especially if consumed in large amounts, can cause additive QT interval prolongation when taken with QT interval-prolonging drugs, potentially increasing the risk of ventricular arrhythmias.
Clinical research in healthy volunteers shows that drinking 6 liters of grapefruit juice over 6 hours prolonged the QTc by a peak amount of 14 milliseconds (ms). This prolongation was similar to the QT prolongation caused by the drug moxifloxacin. In individuals with long QT syndrome, a smaller dose of grapefruit juice, 1.5 liters, resulted in a greater peak QTc prolongation of about 30 ms. The effect of smaller quantities of grapefruit juice on the QT interval is unclear.

Grapefruit juice may increase blood levels of quetiapine, increasing the effects and adverse effects of quetiapine.
Quetiapine is metabolized by cytochrome P450 3A4 (CYP3A4). Grapefruit can inhibit CYP3A4. In one case report, a healthy 28-year-old female with bipolar disorder stabilized on quetiapine 800 mg daily presented with quetiapine toxicity considered to be related to consuming a gallon of grapefruit juice over the past 24 hours.

Grapefruit juice can alter blood levels of quinidine, potentially increasing or decreasing the clinical effects of quinidine.
Clinical research shows that grapefruit juice decreases quinidine absorption, clearance, and metabolism, and prolongs the half-life by about 20%.

Theoretically, taking pomegranate with ACEIs might increase the risk of adverse effects.
Pomegranate juice is thought to have ACE inhibitor-like effects.

Theoretically, taking pomegranate with antihypertensive drugs might increase the risk of hypotension.
Consuming pomegranate juice can modestly lower blood pressure.

Theoretically, pomegranate might increase levels of drugs metabolized by CYP2D6.
In vitro, pomegranate juice inhibits CYP2D6. However, the clinical significance of this potential interaction in humans is not known.

Theoretically, taking pomegranate with rosuvastatin might increase the risk of adverse effects.
In one case, a patient taking rosuvastatin 5 mg every other day in combination with ezetimibe 10 mg daily developed rhabdomyolysis after drinking pomegranate juice 200 mL twice weekly for 3 weeks. This patient had a history of elevated creatine kinase levels while not receiving any statin treatment. This suggests a possible underlying myopathy and predisposition to rhabdomyolysis.

Theoretically, pomegranate might increase warfarin levels and increase the risk of bleeding. Also, discontinuing regular consumption of pomegranate juice might decrease warfarin levels.
In one case report, a patient had a stable, therapeutic bleeding time, as measured by international normalized ratio (INR), while taking warfarin in combination with pomegranate juice 2-3 times per week. The patient became subtherapeutic within about 10 days after discontinuing pomegranate juice, which required a warfarin dose increase. In another case report, a patient with a stable INR for over one year presented with an INR of 14. The patient noted no changes to medications or diet but did report consuming around 3 liters of pomegranate juice over the previous week. The patient's INR stabilized upon moderation of pomegranate juice consumption. The mechanism of this potential interaction is unclear.

Theoretically, taking pomegranate with carbamazepine might increase the risk of adverse effects, although research suggests this interaction is unlikely to be clinically significant.
Animal research shows that pomegranate juice may inhibit cytochrome P450 3A4 (CYP3A4) metabolism of carbamazepine and increase levels of carbamazepine by 1.5 times without prolonging the elimination half-life. This suggests that pomegranate juice inhibits intestinal CYP3A4, but might not inhibit hepatic CYP3A4. However, some human research suggests that pomegranate does not significantly inhibit CYP3A4 drug metabolism in humans.

Theoretically, pomegranate might increase levels of drugs metabolized by CYP2C9.
Some animal and in vitro research shows that pomegranate juice inhibits intestinal, but not hepatic, CYP2C9 isoenzyme activity. However, clinical research shows that neither pomegranate juice nor pomegranate extract have a significant effect on CYP2C9 activity in humans.

Theoretically, pomegranate might increase levels of drugs metabolized by CYP3A4, but most research suggests this interaction is unlikely to be clinically significant.
Pomegranate contains several polyphenols that have individually been shown to inhibit CYP3A4. However, there is contradictory evidence about the effect of whole pomegranate juice on CYP3A4 activity. In vitro, pomegranate juice significantly inhibits the CYP3A4 enzyme, with comparable inhibition to grapefruit juice. In an animal model, pomegranate juice inhibits CYP3A4 metabolism of carbamazepine and increases levels of carbamazepine by 1.5 times; however, in human volunteers, drinking a single glass of pomegranate juice 240 mL or taking 200 mL daily for 2 weeks does not significantly affect levels of the CYP3A4 substrate midazolam after oral or intravenous administration. Another study in healthy volunteers shows that consuming pomegranate juice 300 mL three times daily for three days also does not significantly affect levels of simvastatin, a CYP3A4 substrate This suggests that pomegranate is unlikely to significantly affect levels of CYP3A4 substrates in humans.

Theoretically, pomegranate might increase levels of tolbutamide, although research suggests this interaction is unlikely to be clinically significant.
Animal research shows that pomegranate juice inhibits the cytochrome P450 2C9 (CYP2C9) metabolism of tolbutamide. Pomegranate juice increased tolbutamide levels by 1.2 times without prolonging the elimination half-life. This suggests that pomegranate juice inhibits intestinal CYP2C9, but might not inhibit hepatic CYP2C9. Despite this evidence, clinical research shows that neither pomegranate juice nor pomegranate extract have a significant effect on CYP2C9 activity in humans. This interaction does not appear to be clinically significant in humans.

Theoretically, combining Fucus vesiculosus with amiodarone might cause excessively high iodine levels.
Fucus vesiculosus contains high concentrations of iodine. Amiodarone contains 37.3% iodine and can increase iodine levels. Concomitant use might increase the risk of having excessive iodine levels and adversely affecting thyroid function. Monitor thyroid function.

Due to its iodine content, Fucus vesiculosus might alter the effects of antithyroid drugs.
Fucus vesiculosus contains high concentrations of iodine. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Taking Fucus vesiculosus while using antithyroid drugs could alter the effects of the antithyroid drugs.

Concomitant use of Fucus vesiculosus and lithium has resulted in hyperthyroidism.
There is a case of hyperthyroidism occurring in a patient taking Fucus vesiculosus and lithium. Monitor thyroid hormones closely in patients taking lithium and Fucus vesiculosus concomitantly.

Due to its iodine content, Fucus vesiculosus might alter the effects of thyroid hormone.
Fucus vesiculosus contains high concentrations of iodine. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Taking Fucus vesiculosus while using thyroid hormone could alter the effects of thyroid hormone.

Theoretically, taking Fucus vesiculosus with antiplatelet or anticoagulant drugs might increase the risk of bruising and bleeding.
In vitro evidence suggests that a constituent of Fucus vesiculosus, known as fucoidan, has anticoagulant effects. However, in clinical research, fucoidan does not seem to have significant anticoagulant activity when taken orally, possibly due to poor absorption.

Theoretically, concomitant use of Fucus vesiculosus with CYP2C8 substrates might increase the risk for adverse effects.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, inhibits CYP2C8. This interaction has not been reported in humans.

Theoretically, concomitant use of Fucus vesiculosus with CYP2C9 substrates might increase the risk for adverse effects.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, inhibits CYP2C9. This interaction has not been reported in humans.

Theoretically, concomitant use of Fucus vesiculosus with CYP2D6 substrates might alter the effects of these substrates.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, both inhibits and induces CYP2D6. This interaction has not been reported in humans.

Theoretically, concomitant use of Fucus vesiculosus with CYP3A4 substrates might increase the risk for adverse effects.
In vitro research shows that fucoidan, a constituent of Fucus vesiculosus, inhibits CYP3A4. This interaction has not been reported in humans.

Concomitant use of alcohol and niacin might increase the risk of flushing and hepatotoxicity.
Alcohol can exacerbate the flushing and pruritus associated with niacin. Large doses of niacin might also exacerbate liver dysfunction associated with chronic alcohol use. A case report describes delirium and lactic acidosis in a patient taking niacin 3 grams daily who ingested 1 liter of wine. Advise patients to avoid large amounts of alcohol while taking niacin.

Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as allopurinol.
Large doses of niacin can reduce urinary excretion of uric acid, potentially resulting in hyperuricemia. Doses of uricosurics such as allopurinol might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.

Theoretically, niacin may have additive effects when used with anticoagulant or antiplatelet drugs.
Several cases of clotting factor synthesis deficiency and coagulopathy have been reported in patients taking sustained-release niacin. Also, thrombocytopenia has been reported in patients treated with niacin or niacin plus lovastatin.

Niacin can increase blood glucose levels and may diminish the effects of antidiabetes drugs.
Niacin impairs glucose tolerance in a dose-dependent manner, probably by causing or aggravating insulin resistance and increasing hepatic production of glucose. In diabetes patients, niacin 4.5 grams daily for 5 weeks can increase plasma glucose by an average of 16% and glycated hemoglobin (HbA1c) by 21%. However, lower doses of 1.5 grams daily or less appear to have minimal effects on blood glucose. In some patients, glucose levels increase when niacin is started, but then return to baseline when a stable dose is reached. Up to 35% of patients with diabetes may need adjustments in hypoglycemic therapy when niacin is added.

Theoretically, niacin may increase the risk of hypotension when used with antihypertensive drugs.
The vasodilating effects of niacin can cause hypotension. Furthermore, some clinical evidence suggests that a one-hour infusion of niacin can reduce systolic, diastolic, and mean blood pressure in hypertensive patients. This effect is not observed in normotensive patients.

Bile acid sequestrants can bind niacin and decrease absorption. Separate administration by 4-6 hours to avoid an interaction.
In vitro studies show that colestipol (Colestid) binds about 98% of available niacin and cholestyramine (Questran) binds 10% to 30%.

Theoretically, concomitant use of niacin and gemfibrozil might increase the risk of myopathy in some patients.
A case of myopathy from concomitant use of niacin and gemfibrozil has been reported. Niacin alone has also been associated with cases of myopathy. Using gemfibrozil with niacin might further increase the risk of developing myopathy.

Theoretically, concomitant use of niacin and hepatotoxic drugs might increase the risk of hepatotoxicity.
Niacin has been associated with cases of liver toxicity, especially when used in pharmacologic doses. Sustained-release niacin preparations appear to be associated with a higher risk of hepatotoxicity than immediate-release niacin.

Theoretically, concomitant use of niacin and statins might increase the risk of myopathy and rhabdomyolysis in some patients.
Some case reports have raised concerns that niacin might increase the risk of myopathy and rhabdomyolysis when combined with statins. However, a significantly increased risk of myopathy has not been demonstrated in clinical trials, including those using an FDA-approved combination of lovastatin and niacin (Advicor).

Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as probenecid.
Large doses of niacin reduce urinary excretion of uric acid, potentially causing hyperuricemia. Doses of uricosurics such as probenecid might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.

Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as sulfinpyrazone.
Large doses of niacin reduce urinary excretion of uric acid, potentially causing hyperuricemia. Doses of uricosurics such as sulfinpyrazone might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.

Theoretically, niacin might antagonize the therapeutic effects of thyroid hormones.
Clinical research and case reports suggests that taking niacin can reduce serum levels of thyroxine-binding globulin by up to 25% and moderately reduce levels of thyroxine (T4). Patients taking thyroid hormone for hypothyroidism might need dose adjustments when using niacin.

Theoretically, concomitant use of niacin and transdermal nicotine might increase the risk of flushing and dizziness.
Niacin and nicotine can both cause flushing and dizziness.

There is limited evidence that niacin may increase the anticoagulant effects of warfarin.
In a case report, a patient on warfarin developed an elevated international normalized ratio (INR) of 3.9 after taking niacin for two weeks. The patient's INR was previously stable, ranging between 2 and 3 in recent months, and no other medication changes were identified. The elevated INR returned to therapeutic range within 4 days following the discontinuation of niacin.

Large doses of aspirin might alter the clearance of niacin.
Aspirin is often used with niacin to reduce niacin-induced flushing. Doses of 80-975 mg aspirin have been used, but 325 mg appears to be optimal. Aspirin also seems to reduce the clearance of niacin by competing for glycine conjugation. Taking aspirin 1 gram seems to reduce niacin clearance by 45%. This is probably a dose-related effect and not clinically significant with the more common aspirin dose of 325 mg.

Theoretically, cranberry might increase levels and adverse effects of atorvastatin.
In one case report, a patient taking atorvastatin experienced upper back pain, rhabdomyolysis, and abnormal liver function after drinking cranberry juice 16 ounces daily for 2 weeks. Theoretically, this may have been caused by inhibition of cytochrome P450 3A4 (CYP3A4) enzymes by cranberry juice, as atorvastatin is a CYP3A4 substrate. Creatinine kinase and liver enzymes normalized within 2 weeks of stopping cranberry juice. Patients taking atorvastatin should avoid large quantities of cranberry juice.

Theoretically, cranberry might increase the levels and adverse effects of CYP3A4 substrates.
A case of upper back pain, rhabdomyolysis, and abnormal liver function has been reported for a patient taking atorvastatin, a CYP3A4 substrate, in combination with cranberry juice 16 ounces daily for 2 weeks. Creatinine kinase and liver enzymes normalized within 2 weeks of stopping cranberry juice. Also, animal research suggests that cranberry juice, administered intraduodenally 30 minutes prior to nifedipine, a CYP3A4 substrate, inhibits nifedipine metabolism and increases the area under the concentration-time curve by 1.6-fold compared to control.

Theoretically, cranberry might increase the levels and adverse effects of nifedipine.
Animal research suggests that cranberry juice, administered intraduodenally 30 minutes prior to nifedipine treatment, inhibits nifedipine metabolism and increases the area under the concentration-time curve by 1.6-fold compared to control. This interaction has not been reported in humans.

Theoretically, cranberry might increase the levels and adverse effects of warfarin. However, research is conflicting.
There is contradictory evidence about the effect of cranberry juice on warfarin. Case reports have linked cranberry juice consumption to increases in the international normalized ratio (INR) in patients taking warfarin, resulting in severe spontaneous bleeding and excessive postoperative bleeding. Daily consumption of cranberry sauce for one week has also been linked to an increase in INR in one case report. In a small study in healthy young males, taking a high dose of 3 grams of cranberry juice concentrate capsules, equivalent to 57 grams of fruit daily, for 2 weeks produced a 30% increase in the area under the INR-time curve after a single 25-mg dose of warfarin. However, 3 very small clinical studies in patients stabilized on warfarin reported that cranberry juice 250 mL once or twice daily for 7 days (27% cranberry juice or pure cranberry juice) or 240 mL once daily for 14 days does not significantly increase INR or affect plasma warfarin levels. The reasons for these discrepant findings are unclear. It is possible that the form and dose of cranberry may play a role, as cranberry extracts and juices contain different constituents. Additionally, an in vitro study evaluating 5 different cranberry juices found varying effects, with only a cranberry concentrate, and not diluted cranberry juices, inhibiting CYP2C9. However, this concentrate did not inhibit CYP2C9 activity in humans.

Theoretically, cranberry might increase the levels and adverse effects of CYP2C9 substrates. However, research is conflicting.
There is contradictory evidence about the effect of cranberry on CYP2C9 enzymes. In vitro evidence suggests that flavonoids in cranberry inhibit CYP2C9 enzymes. However, clinical research shows that cranberry juice does not significantly affect the levels, metabolism, or elimination of the CYP2C9 substrates flurbiprofen or diclofenac. Also, in patients stabilized on warfarin, drinking cranberry juice 250 mL daily for 7 days does not significantly increase the anticoagulant activity of warfarin, a CYP2C9 substrate. Additional pharmacokinetic research shows that cranberry juice does not increase peak plasma concentrations or area under the concentration-time curve of warfarin.

Theoretically, cranberry might modestly increase the levels and adverse effects of diclofenac.
In vitro evidence suggests that cranberry juice inhibits diclofenac metabolism by human liver microsomes. However, drinking cranberry juice does not seem to affect diclofenac metabolism in humans.

Theoretically, alfalfa might reduce the anticoagulant activity of warfarin.
Alfalfa contains a large amount of vitamin K. This could theoretically interfere with the activity of warfarin.

Theoretically, alfalfa might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research suggests that alfalfa decreases blood sugar in diabetic mice. Also, in one case report, a diabetic patient experienced hypoglycemia after consuming alfalfa extract. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Theoretically, alfalfa might interfere with the activity of contraceptive drugs.
Alfalfa contains coumestrol, a phytoestrogen, and isoflavonoids, which have estrogenic effects.

Theoretically, alfalfa might interfere with hormone therapy.
Alfalfa contains coumestrol, a phytoestrogen, and isoflavonoids, which have estrogenic effects.

Theoretically, alfalfa might decrease the efficacy of immunosuppressive therapy.
In vitro research and human case reports suggest that alfalfa may have immunostimulant effects.

Theoretically, concomitant use of alfalfa with photosensitizing drugs might have additive effects.
Animal research suggests that excessive doses of alfalfa may increase photosensitivity, possibly due to its chlorophyll content. It is unclear if this effect would be clinically relevant in humans.

Theoretically, taking dandelion root along with anticoagulant or antiplatelet drugs might increase the risk of bruising and bleeding.
In vitro research suggests that dandelion root inhibits platelet aggregation.

Theoretically, dandelion might increase the risk for hypoglycemia when used with antidiabetes drugs.
Laboratory research suggests that dandelion extract may have moderate alpha-glucosidase inhibitor activity and might also increase insulin secretion. Also, in a case report, a 58-year-old woman with type 2 diabetes who was being treated with insulin developed hypoglycemia 2 weeks after beginning to eat salads containing dandelion.

Theoretically, dandelion might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that dandelion might inhibit CYP1A2. So far, this interaction has not been reported in humans. However, until more is known, watch for an increase in the levels of drugs metabolized by CYP1A2 in patients taking dandelion.

Theoretically, dandelion might increase the clearance of drugs that are UDP-glucuronosyltransferase substrates.
There is some preliminary evidence that dandelion might induce UDP-glucuronosyltransferase, a phase II enzyme.

Theoretically, through diuretic effects, dandelion might reduce excretion and increase levels of lithium.
Animal research suggests that dandelion has diuretic properties. As diuretics can increase serum lithium levels, the dose of lithium might need to be decreased when taken with dandelion.

Theoretically, dandelion might increase the risk of hyperkalemia when taken with potassium-sparing diuretics.
Dandelion contains significant amounts of potassium.

Theoretically, dandelion might lower fluoroquinolone levels.
Animal research shows that dandelion reduces absorption of ciprofloxacin and can lower levels by 73%. However, this effect has not been reported in humans.

Theoretically, parsley might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
Animal research suggests that parsley has antiplatelet effects.

Theoretically, parsley might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research suggests that parsley might decrease blood glucose. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Theoretically, parsley might increase serum levels of CYP1A2 substrates.
Laboratory research suggests that parsley can inhibit CYP1A2.

Theoretically, parsley might enhance or interfere with the effects of diuretic drugs.
Animal research suggests that parsley seed extract increases urine elimination. Parsley leaf and root might also interfere with diuretic therapy due their purported aquaretic effects.

Theoretically, parsley might increase the duration of pentobarbital effects.
Animal research suggests that parsley juice prolongs the action of pentobarbital, perhaps by decreasing cytochrome P450 levels. It is not known if this occurs in humans or if this applies to other barbiturates or sedatives.

Theoretically, large quantities of parsley might increase sirolimus levels.
In one case report, an adult female with a history of kidney transplant presented with elevated blood sirolimus levels, approximately 4-7 times greater than previous measures, after daily consumption of a juice containing approximately 30 grams of parsley for 7 days. Sirolimus levels returned to normal a week after the parsley juice was discontinued.

Theoretically, large amounts of parsley leaf and root might decrease the effects of warfarin.
Parlsey contains vitamin K.

Theoretically, aspirin might increase the severity of allergic reactions to parsley.
In one case, severe urticaria and swelling were reported after taking aspirin with parsley in an individual with a known mild parsley allergy.

Theoretically, chlorella might have additive effects with photosensitizing drugs.
Chlorella has been reported to cause photosensitization. In five case reports, patients who had ingested chlorella exhibited swelling followed by erythematopurpuric lesions on sun-exposed areas of the body. Theoretically, concomitant use with photosensitizing drugs may exacerbate effects.

Theoretically, chlorella might reduce the clinical effects of warfarin.
Chlorella contains significant amounts of vitamin K. There is at least one case report of warfarin therapy becoming sub-therapeutic after initiation of chlorella supplements.

Theoretically, spirulina blue-green algae might increase the risk of bleeding if used with other anticoagulant or antiplatelet drugs. However, this is unlikely.
Spirulina blue-green algae have shown antiplatelet and anticoagulant effects in vitro. However, one preliminary study in 24 patients receiving spirulina blue-green algae 2.3 grams daily for 2 weeks showed no effect on platelet activation or measures of clotting time.

Theoretically, taking blue-green algae with antidiabetes drugs might increase the risk of hypoglycemia.
Human research shows that spirulina blue-green algae can have hypoglycemic effects in patients with diabetes, at least some of whom were using antidiabetes drugs. However, blue-green algae does not seem to improve glycated hemoglobin (HbA1c) levels in patients with diabetes. A meta-analysis of animal studies also suggests that spirulina blue-green algae have hypoglycemic effects.

Theoretically, concurrent use of blue-green algae might interfere with immunosuppressive therapy.
Blue-green algae have been shown to stimulate the immune system.

Cabbage might increase clearance and reduce the effects of acetaminophen.
A small clinical study shows that daily consumption of cabbage and Brussels sprout decreases acetaminophen levels by as much as 16%, with some evidence suggesting that this effect is due to increased elimination through glucuronide conjugation.

Theoretically, cabbage might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal and in vivo research suggests that cabbage might have hypoglycemic effects.

Theoretically, cabbage might decrease levels of drugs metabolized by CYP1A2.
Some animal research suggests that cabbage or its constituent indole-3-carbinol might increase drug metabolism and elimination by stimulating CYP1A2 activity.

Theoretically, cabbage might increase clearance and decrease the effects of drugs metabolized through glucuronide conjugation.
A small clinical study shows that daily consumption of cabbage and Brussels sprout decreases levels of some drugs metabolized through glucuronide conjugation.

Cabbage might increase clearance and reduce the effects of oxazepam.
A small clinical study shows that daily consumption of cabbage and brussels sprout decreases oxazepam levels by as much as 17%, with some evidence suggesting that this effect is due to increased elimination through glucuronide conjugation.

Theoretically, cabbage might decrease the anticoagulant effects of warfarin.
Cabbage contains vitamin K. If consumed in large quantities, cabbage might decrease the anticoagulant effects of warfarin.

Theoretically, vitamin B6 might increase the photosensitivity caused by amiodarone.
Despite initial case reports suggesting that pyridoxine may have a protective effect against amiodarone-induced photosensitivity, preliminary clinical research suggests that pyridoxine may actually exacerbate this adverse effect.

Theoretically, vitamin B6 may have additive effects when used with antihypertensive drugs.
Research in hypertensive rats shows that vitamin B6 can decrease systolic blood pressure. Similarly, clinical research in patients with hypertension shows that taking high doses of vitamin B6 may reduce systolic and diastolic blood pressure, possibly by reducing plasma levels of epinephrine and norepinephrine.

High doses of vitamin B6 may reduce the levels and clinical effects of phenobarbital.
Preliminary clinical evidence suggests that vitamin B6 200 mg daily can reduce plasma levels of phenobarbital, possibly by increasing metabolism. It is not known whether lower doses have any effect. Advise people taking phenobarbital to avoid high doses of vitamin B6.

High doses of vitamin B6 may reduce the levels and clinical effects of phenytoin.
Preliminary clinical evidence suggests that vitamin B6 200 mg daily can reduce plasma levels of phenytoin, possibly by increasing metabolism. It is not known whether lower doses have any effect. Advise people taking phenytoin to avoid high doses of vitamin B6.

Vitamin B6 may increase the metabolism of levodopa when taken alone, but not when taken in conjunction with carbidopa.
Vitamin B6 (pyridoxine) enhances the metabolism of levodopa, reducing its clinical effects. However, this interaction does not occur when carbidopa is used concurrently with levodopa (Sinemet). Therefore, it is not likely to be a problem in most people.

Theoretically, broccoli might reduce the levels and effects of drugs metabolized by CYP1A2.
Pharmacokinetic research in humans shows that eating 500 grams of fresh broccoli daily for 6-12 days can increase CYP1A2 activity by 10% to 200%. Induction of CYP1A2 activity by broccoli is attributed to its glucosinolate constituents.

Theoretically, broccoli might reduce the levels and effects of drugs metabolized by CYP2A6.
Pharmacokinetic research in humans shows that eating 500 grams of broccoli daily for 6 days increases CYP2A6 activity by 135% to 550%. Induction of CYP2A6 activity is attributed to its glucosinolate constituents.

Theoretically, black currant seed oil might increase the risk of bleeding if used in combination with anticoagulant or antiplatelet drugs.
Gamma-linolenic acid (GLA), a constituent of black currant seed oil, appears to have antiplatelet effects.

Theoretically, black currant seed oil might increase the risk of seizure in patients receiving phenothiazines.
Black currant seed oil contains gamma-linolenic acid (GLA). There is some concern that taking supplements containing GLA might cause seizures, or lower the seizure threshold, when taken with phenothiazines, although there is no evidence that black currant seed oil causes seizures. In one report, three patients with schizophrenia who had received phenothiazines developed EEG changes suggestive of temporal lobe epilepsy after starting treatment with GLA, although none experienced an actual seizure. In another report, two patients with schizophrenia who were stabilized on phenothiazines developed seizures when evening primrose 4 grams daily, which contains GLA, was added. One of these patients had a prior history of seizures.

Theoretically, the antioxidant effects of acerola might reduce the effectiveness of alkylating agents.
Acerola contains vitamin C, an antioxidant. There is concern that antioxidants might reduce the activity of chemotherapy drugs that generate free radicals, such as alkylating agents. In contrast, other researchers theorize that antioxidants might make alkylating chemotherapy more effective by reducing oxidative stress that could interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as vitamin C have on chemotherapy.

Theoretically, the antioxidant effects of acerola might reduce the effectiveness of antitumor antibiotics.
Acerola contains vitamin C, an antioxidant. There is concern that antioxidants might reduce the activity of chemotherapy drugs that generate free radicals, such as antitumor antibiotics. In contrast, other researchers theorize that antioxidants might make antitumor antibiotic chemotherapy more effective by reducing oxidative stress that could interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effects, if any, antioxidants such as vitamin C have on antitumor antibiotic chemotherapy.

Theoretically, concomitant use of acerola with aluminum salts might increase the amount of aluminum absorbed.
Acerola contains vitamin C. It is thought that vitamin C chelates aluminum, keeping it in solution and available for absorption. In people with normal renal function, urinary excretion of aluminum likely increases, making aluminum retention and toxicity unlikely. However, patients with renal failure who take aluminum-containing compounds, such as phosphate binders, should avoid acerola in doses that provide more vitamin C than the recommended dietary allowances.

Theoretically, acerola might reduce the clearance of aspirin; however, its vitamin C content is likely too low to produce clinically significant effects.
Acerola contains vitamin C. It has been suggested that acidification of the urine by vitamin C can decrease the urinary excretion of salicylates, increasing plasma salicylate levels. However, short-term use of up to 6 grams daily of vitamin C does not seem to affect urinary pH or salicylate excretion. The vitamin C content of acerola is typically about 2000 mg per 100 grams. Thus, a clinically significant interaction between acerola and aspirin is unlikely.

Theoretically, concomitant use of acerola with estrogens might increase estrogenic effects.
Acerola contains vitamin C. Increases in plasma estrogen levels of up to 55% have occurred under some circumstances when vitamin C is taken concurrently with oral contraceptives or hormone replacement therapy, including topical products. It is suggested that vitamin C prevents oxidation of estrogen in the tissues, regenerates oxidized estrogen, and reduces sulfate conjugation of estrogen in the gut wall. When tissue levels of vitamin C are high, these processes are already maximized and supplemental vitamin C does not have any effect on estrogen levels. However, increases in plasma estrogen levels may occur when women who are deficient in vitamin C take supplements.

Theoretically, acerola might reduce the effectiveness of warfarin; however, its vitamin C content is likely too low to produce clinically significant effects.
Acerola contains vitamin C. High doses of vitamin C may reduce the response to warfarin, possibly by causing diarrhea and reducing warfarin absorption. This occurred in two people who took up to 16 grams daily of vitamin C, and resulted in decreased prothrombin time. Lower doses of 5-10 grams daily of vitamin C can also reduce warfarin absorption, but this does not seem to be clinically significant. The vitamin C content of acerola is typically about 2000 mg per 100 grams. Thus, a clinically significant interaction between acerola and warfarin is unlikely.

Theoretically, blueberries or blueberry leaf extracts might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal and in vitro research suggests that blueberry and/or blueberry leaf extracts can lower blood glucose levels.

Theoretically, blueberry juice might increase blood levels of buspirone.
In vitro research shows that blueberry juice can inhibit the metabolism of buspirone, possibly by inhibiting cytochrome P450 3A (CYP3A) enzymes. However, pharmacokinetic research in humans shows that drinking 300 mL of blueberry juice 30 minutes before taking buspirone hydrochloride 10 mg does not significantly affect the concentration or clearance of buspirone.

Theoretically, blueberry juice might increase blood levels of flurbiprofen.
In vitro research shows that blueberry juice can inhibit the metabolism of flurbiprofen, possibly by inhibiting cytochrome P450 2C9 (CYP2C9) enzymes. However, pharmacokinetic research in humans shows that drinking 300 mL of blueberry juice 30 minutes before taking flurbiprofen 100 mg does not significantly affect the concentration or clearance of flurbiprofen.

Theoretically, maqui fruit extract may increase the risk of hypoglycemia when used with antidiabetes drugs.
Animal research shows that maqui berry reduces fasting blood glucose. However, maqui berry extract taken orally, either as a single dose or daily for 3 months, does not decrease fasting blood glucose in prediabetic patients. It is unknown whether it might reduce blood glucose levels in patients with diabetes.

Theoretically, oats may have additive effects with antidiabetic agents and might increase the risk of hypoglycemia.
Consuming oats can decrease blood glucose in patients with diabetes. In those who require insulin, taking oats 100 grams daily for 2 days reduces the insulin dose required to achieve metabolic control.

Concomitant use of oats and insulin might increase the risk of hypoglycemia.
In patients with insulin-dependent type 2 diabetes, taking oats 100 grams daily for 2 days reduces the insulin dose required to achieve metabolic control.

Theoretically, taking acai with antidiabetes drugs might interfere with glycemic control.
Preliminary clinical research in healthy adults has shown that taking acai may increase or decrease levels of fasting blood glucose.

Theoretically, combining dulse with amiodarone might cause excessively high iodine levels.
Dulse is rich in iodine, and amiodarone contains 37.3% iodine and can increase iodine levels.

Theoretically, due to its iodine content, dulse might alter the effects of antithyroid drugs.
Dulse is rich in iodine. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history.

Theoretically, dulse might increase the risk of hyperkalemia when taken with digoxin.
Dulse is rich in potassium, and digoxin can increase potassium levels in the blood. This interaction has not been demonstrated in humans.

Theoretically, due to its iodine content, dulse might alter the effects of thyroid hormone.
Dulse is rich in iodine. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Although dulse has been associated with a statistically significant increase in thyroid stimulating hormone (TSH) levels in clinical research, clinically significant increases have not been documented.

Theoretically, dulse might increase the risk of hyperkalemia when taken with ACEIs.
Dulse is rich in potassium. ACEIs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels. However, using these drugs while consuming dulse in quantities that provide larger amounts of potassium daily might increase the risk of hyperkalemia. Additionally, in vitro research suggests that dulse protein hydrolysates inhibit the activity of ACE. However, these effects have not been demonstrated in humans.

Theoretically, dulse might increase the risk of hyperkalemia when taken with ARBs.
Dulse is rich in potassium. ARBs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels. However, using these drugs while consuming dulse in quantities that provide higher amounts of potassium daily might increase the risk of hyperkalemia. Additionally, in vitro research suggests that dulse protein hydrolysates inhibit the activity of angiotensin converting enzyme (ACE). However, these effects have not been demonstrated in humans.

Theoretically, dulse might increase the risk of hyperkalemia when taken with potassium-sparing diuretics.
Dulse is rich in potassium, and potassium-sparing diuretics can increase potassium levels in the blood. This interaction has not been shown in humans.

Theoretically, taking riboflavin with tetracycline antibiotics may decrease the potency of these antibiotics.
In vitro research suggests that riboflavin may inhibit the potency of tetracycline antibiotics. It is not clear if this effect is clinically significant, as this interaction has not been reported in humans.

Metformin, a common medication used to manage type 2 diabetes, has been associated with lower vitamin B12 levels in some individuals. Prolonged use of metformin can interfere with the absorption of B12 in the digestive system, potentially leading to a deficiency in this essential vitamin.

Trimethoprim might increase blood levels of thiamine.
In vitro, animal, and clinical research suggest that trimethoprim inhibits intestinal thiamine transporter ThTR-2, hepatic transporter OCT1, and renal transporters OCT2, MATE1, and MATE2, resulting in paradoxically increased thiamine plasma concentrations.

Theoretically, barley might decrease the clinical effects of triclabendazole.
Animal research suggests that a diet supplemented with barley can reduce the bioavailability of triclabendazole when taken concomitantly. This effect has not been shown in humans.