30 Day Night Slim Skinny Tea Ingredients & Drug Interactions

Theoretically, due to potential diuretic effects, marshmallow might reduce excretion and increase levels of lithium.
Marshmallow is thought to have diuretic properties. To avoid lithium toxicity, the dose of lithium might need to be decreased when used with marshmallow.

Theoretically, marshmallow flower might have antiplatelet effects.
Animal research suggests that marshmallow flower extract has antiplatelet effects. However, the root and leaf of marshmallow, not the flower, are the plant parts most commonly found in dietary supplements. Theoretically, use of marshmallow flower with anticoagulant/antiplatelet drugs can have additive effects, and might increase the risk for bleeding in some patients.

Theoretically, mucilage in marshmallow might impair absorption of oral drugs.
Marshmallow contains mucilage which can affect oral drug absorption. To avoid changes in absorption, take marshmallow 30-60 minutes after oral medications.

Theoretically, black psyllium might reduce the effects of carbamazepine and increase the risk for convulsions.
Theoretically, black psyllium might reduce carbamazepine absorption. A preliminary study using blond psyllium reported decreased carbamazepine bioavailability due to binding of the drug to psyllium, as well as reduction of available fluid in the gut for dissolution of the drug. This interaction may also occur with black psyllium.

Theoretically, taking black psyllium at the same time as lithium might reduce lithium absorption.
The fiber in black psyllium might reduce lithium absorption and plasma levels. Some case reports describe a reduction in plasma lithium levels with concomitant administration of blond psyllium. This was reversed when psyllium was stopped. This interaction may also occur with black psyllium.

Theoretically, black psyllium might increase the therapeutic and adverse effects of metformin.
Animal research shows that concurrent consumption of blond psyllium with metformin slows and increases the absorption of metformin. This interaction may also occur with black psyllium. To avoid changes in absorption, take psyllium 30-60 minutes after metformin.

Theoretically, taking black psyllium at the same time as olanzapine might reduce olanzapine absorption.
The fiber in black psyllium might decrease the absorption of olanzapine. A single case report describes a reduction in the effectiveness of olanzapine when it was concomitantly administered with an unspecified type of psyllium 3 grams orally twice daily. This effect was reversed when psyllium was stopped.

Theoretically, taking black psyllium at the same time as digoxin might reduce digoxin absorption and decrease digoxin levels.
Psyllium might bind digoxin in the gut. However, some clinical evidence suggests that psyllium does not impact digoxin absorption.

Theoretically, taking black psyllium at the same time as ethinyl estradiol might alter levels of estradiol.
Concurrent use of blond psyllium with ethinyl estradiol results in a slight increase in the extent of ethinyl estradiol absorption and a slower rate of absorption. This is unlikely to be clinically significant.

Theoretically, psyllium might increase, decrease, or have no effect on the absorption of oral drugs.
Psyllium seems to have variable effects on drug absorption. To avoid changes in absorption, take psyllium 30-60 minutes after oral medications. Animal research shows that blond psyllium delays and increases the absorption of metformin and ethinyl estradiol. Case reports and animal research suggest that blond psyllium might reduce absorption of lithium, digoxin, olanzapine, and carbamazepine. Finally, some pharmacokinetic studies show that psyllium does not affect the absorption of levothyroxine or warfarin. Although many of these studies evaluated blond psyllium, the fiber content in black psyllium may have similar effects.

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, uva ursi may decrease the metabolism of CYP2C19 substrates.
In vitro, uva ursi appears to inhibit cytochrome CYP2C19. This effect has not been reported in humans.

Theoretically, uva ursi may decrease the metabolism of CYP3A4 substrates.
In vitro, uva ursi appears to inhibit CYP3A4. This effect has not been reported in humans.

Theoretically, uva ursi may increase levels of drugs metabolized by glucuronidation.
In vitro, uva ursi extract appears to strongly inhibit UDP-glucuronosyltransferase (UGT) 1A1 (UGT1A1). However, uva ursi extract does not appear to inhibit UGT1A1 in animal models. This effect has not been reported in humans.

Theoretically, uva ursi may increase lithium levels, necessitating a decrease in dose.
Uva ursi may have diuretic properties. Diuretics may increase lithium reabsorption with sodium in the proximal tubule of the kidney. Theoretically, uva ursi might reduce excretion and increase levels of lithium.

Effects of uva ursi in the urinary tract may be reduced by urinary acidifying agents.
Uva ursi seems to work best in alkaline urine. Theoretically, taking uva ursi with medications known to acidify the urine may decrease any effects of uva ursi on the urinary tract.

Theoretically, uva ursi may alter the levels of drugs transported by P-glycoprotein.
In vitro, uva ursi appears to inhibit the multi-drug transporter protein, P-glycoprotein. This effect has not been reported in humans.

Theoretically, cascara sagrada might increase the risk of hypokalemia when taken with corticosteroids.
Cascara sagrada has stimulant laxative effects, and long-term use has been associated with hypokalemia.

Theoretically, cascara sagrada might cause hypokalemia, potentially increasing the risk of digoxin toxicity.
Cascara sagrada has stimulant laxative effects, and long-term use has been associated with hypokalemia.

Theoretically, cascara sagrada might increase the risk of hypokalemia when taken with diuretic drugs.
Cascara sagrada has stimulant laxative effects, and long-term use has been associated with hypokalemia.

Theoretically, cascara sagrada might have additive adverse effects when taken with stimulant laxatives.
Cascara sagrada has stimulant laxative effects and might compound fluid and electrolyte losses when taken with stimulant laxatives.

Theoretically, cascara sagrada might increase the risk of bleeding when taken with warfarin.
Cascara sagrada has stimulant laxative effects. In some people, cascara sagrada can cause diarrhea. Diarrhea can increase the effects of warfarin, increase international normalized ratio (INR), and increase the risk of bleeding.

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

Theoretically, fennel might increase the risk of bleeding when used with antiplatelet or anticoagulant drugs.

Animal research suggests that fennel oil has antithrombotic and antiplatelet effects.

Theoretically, fennel might decrease the levels and clinical effects of ciprofloxacin.

Animal research shows that fennel reduces ciprofloxacin bioavailability by nearly 50%, possibly due to the metal cations such as calcium, iron, and magnesium contained in fennel. This study also found that fennel increased tissue distribution and slowed elimination of ciprofloxacin.

Theoretically, taking large amounts of fennel might decrease the effects of contraceptive drugs due to competition for estrogen receptors.

Some constituents of fennel have estrogenic activity.

Theoretically, fennel might increase levels of drugs metabolized by CYP3A4.

In vitro research suggests that fennel inhibits CYP3A4 enzyme activity. This effect has not been reported in humans.

Theoretically, taking large amounts of fennel might interfere with hormone replacement therapy due to competition for estrogen receptors.

Some constituents of fennel have estrogenic activity.

Theoretically, taking large amounts of fennel might decrease the antiestrogenic effect of tamoxifen.

Some constituents of fennel have estrogenic activity, which may interfere with the antiestrogenic activity of tamoxifen.

Vitamin D might increase aluminum absorption and toxicity, but this has only been reported in people with renal failure.
The protein that transports calcium across the intestinal wall can also bind and transport aluminum. This protein is stimulated by vitamin D, which may therefore increase aluminum absorption. This mechanism may contribute to increased aluminum levels and toxicity in people with renal failure, when they take vitamin D and aluminum-containing phosphate binders chronically.

Vitamin D might reduce absorption of atorvastatin.
A small, low-quality clinical study shows that taking vitamin D reduces levels of atorvastatin and its active metabolites by up to 55%. However, while atorvastatin levels decreased, total cholesterol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol levels did not substantially change. Atorvastatin is metabolized in the gut by CYP3A4 enzymes, and researchers theorized that vitamin D might induce CYP3A4, causing reduced levels of atorvastatin. However, this proposed mechanism was not specifically studied.

Taking calcipotriene with vitamin D increases the risk for hypercalcemia.
Calcipotriene is a vitamin D analog used topically for psoriasis. It can be absorbed in sufficient amounts to cause systemic effects, including hypercalcemia. Theoretically, combining calcipotriene with vitamin D supplements might increase the risk of hypercalcemia.

Theoretically, hypercalcemia induced by high-dose vitamin D can increase the risk of arrhythmia from digoxin.
High doses of vitamin D can cause hypercalcemia. Hypercalcemia increases the risk of fatal cardiac arrhythmias with digoxin. Avoid vitamin D doses above the tolerable upper intake level (4000 IU daily for adults) and monitor serum calcium levels in people taking vitamin D and digoxin concurrently.

Theoretically, hypercalcemia induced by high-dose vitamin D can reduce the therapeutic effects of diltiazem for arrhythmia.
High doses of vitamin D can cause hypercalcemia. Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically this could also occur with diltiazem. Avoid vitamin D doses above the tolerable upper intake level (4000 IU daily for adults) and monitor serum calcium levels in people taking vitamin D and diltiazem concurrently.

Theoretically, taking thiazide diuretics and high-dose vitamin D can increase the risk of hypercalcemia.
Thiazide diuretics decrease urinary calcium excretion, which could lead to hypercalcemia if vitamin D supplements are taken concurrently. This has been reported in people being treated with vitamin D for hypoparathyroidism, and also in elderly people with normal parathyroid function who were taking a thiazide, vitamin D, and calcium-containing antacids daily.

Hypercalcemia induced by high-dose vitamin D can reduce the therapeutic effects of verapamil for arrhythmia.
Hypercalcemia due to high doses of vitamin D can reduce the effectiveness of verapamil in atrial fibrillation. Avoid vitamin D doses above the tolerable upper intake level (4000 IU daily for adults) and monitor serum calcium levels in people taking vitamin D and verapamil concurrently.

Vitamin D might induce CYP3A4 enzymes and reduce the bioavailability of CYP3A4 substrates.
There is some concern that vitamin D might induce CYP3A4. In vitro research suggests that vitamin D induces CYP3A4 transcription. Additionally, observational research has found that increased UV light exposure and serum vitamin D levels are associated with decreased serum levels of CYP3A4 substrates such as tacrolimus and sirolimus, while no association between UV light exposure or vitamin D levels and levels of mycophenolic acid, a non-CYP3A4 substrate, was found. A small, low-quality clinical study shows that taking vitamin D reduces levels of the CYP3A4 substrate atorvastatin and its active metabolites by up to 55%; however, the clinical effects of atorvastatin were not reduced. While researchers theorized that vitamin D might induce CYP3A4, this proposed mechanism was not specifically studied.

Theoretically, lemongrass might decrease the metabolism of CYP3A4 substrates.
Animal research shows that lemongrass and its constituent citral inhibit CYP3A4.

Theoretically, lemongrass might increase the clearance and decrease the levels of glucuronidated drugs.
Animal research shows that lemongrass and its constituent citral induce uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation.

Theoretically, lemongrass might increase the effects and adverse effects of pentobarbital.
Animal research shows that high doses of lemongrass essential oil increases sleep time and decreases time to fall asleep in animals administered pentobarbital.

Theoretically, frequent and high doses of rhubarb might increase the risk of hypokalemia when taken with corticosteroids.
Rhubarb has stimulant laxative effects. Overuse of rhubarb might compound corticosteroid-induced potassium loss.

Theoretically, taking rhubarb with cyclosporine might reduce cyclosporine levels.
Animal research shows that co-administration of rhubarb decoction 0.25 or 1 gram/kg with cyclosporine 2.5 mg/kg, decreases cyclosporine maximum plasma concentration and overall exposure levels when compared with taking cyclosporine alone. The authors theorize that rhubarb might reduce cyclosporine bioavailability by inducing of P-glycoprotein and/or cytochrome P450 3A4. However, since rhubarb was administered as a single oral dose and enzyme induction usually occurs after multiple doses, it is possible that cyclosporine absorption was actually reduced via rhubarb's stimulant laxative effects. Also, the composition of the rhubarb decoction was not described.

Theoretically, overuse of rhubarb might increase the risk of adverse effects when taken with digoxin.
Rhubarb has stimulant laxative effects. Overuse of rhubarb might cause potassium depletion, increasing the risk of digoxin toxicity.

Theoretically, frequent and high doses of rhubarb might increase the risk of hypokalemia.
Rhubarb has stimulant laxative effects. Overuse of rhubarb might cause potassium depletion and compound diuretic-induced potassium loss.

Theoretically, concomitant use of rhubarb with potentially hepatotoxic drugs might increase the risk of developing liver damage.
Some animal research suggests that anthraquinones in rhubarb might have hepatotoxic effects. Also, rhubarb use has been linked to at least 24 cases of liver injury, although details on the dose of rhubarb and duration of use in these cases is unclear.

Theoretically, long-term use of anthraquinones from rhubarb might increase the risk of nephrotoxicity when used with nephrotoxic drugs.
The anthraquinone constituents of rhubarb have been shown to induce nephrotoxicity in animal research. Additionally, in a case report, a 23-year old female presented with kidney failure after taking 6 tablets of a proprietary slimming agent (found to contain the anthraquinones emodin and aloe-emodin from rhubarb) daily for 6 weeks and then adding diclofenac 25 mg 4 times daily for 2 days. The authors postulate that the anthraquinone constituents of rhubarb contributed to the renal dysfunction, and the addition of diclofenac, a nephrotoxic drug, led to renal failure. Until more is known, advise patients to avoid taking rhubarb if they are taking other potentially nephrotoxic drugs.

Theoretically, rhubarb might increase the risk for fluid and electrolyte loss when taken with other stimulant laxatives.
Rhubarb has stimulant laxative effects. Concomitant use with stimulant laxatives might compound fluid and electrolyte loss.

Theoretically, excessive use of rhubarb might increase the risk of bleeding when taken with warfarin.
Rhubarb has stimulant laxative effects and can cause diarrhea. Diarrhea can increase the effects of warfarin, increase international normalized ratio (INR), and increase the risk of bleeding. Advise patients who take warfarin not to take excessive amounts of rhubarb.

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, spearmint might alter the sedative effects of CNS depressants.
Animal research suggests that (-)-carvone, a major constituent of spearmint, has sedative effects. However, in humans, chewing spearmint-flavored gum induced arousal effects.

Theoretically, high doses of spearmint might increase the risk of liver damage when taken with hepatotoxic drugs.
Animal research suggests that drinking spearmint tea for 30 days can increase markers of liver damage, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and cause liver degeneration and necrosis, in a dose-dependent manner. This effect has not been reported 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, the antioxidant effects of rose hip might reduce the effectiveness of alkylating agents but might also reduce the oxidative damage caused by certain alkylating agents.
Rose hip contains vitamin C. The use of antioxidants like vitamin C during chemotherapy is controversial. There is concern that antioxidants could reduce the activity of chemotherapy drugs that generate free radicals, such as cyclophosphamide, chlorambucil, carmustine, busulfan, and thiotepa. In contrast, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that could interfere with apoptosis (cell death) of cancer cells. Further, some animal research suggests that the antioxidant effects of rose hip might attenuate cyclophosphamide-induced testicular toxicity. More evidence is needed to determine what effect, if any, antioxidants found in rose hip, such as vitamin C, have on the effectiveness and adverse effects of chemotherapy.

Theoretically, rose hip might increase the amount of aluminum absorbed from aluminum compounds.
Rose hip contains vitamin C. Theoretically, vitamin C increases the absorption of aluminum. Concomitant use might increase aluminum absorption, but the clinical significance of this is unknown. Administer rose hip two hours before or four hours after antacids.

Theoretically, rose hip might reduce the effectiveness of anticoagulant or antiplatelet drugs.
In vitro and animal research suggests that a constituent of rose hip, rugosin E, can induce platelet aggregation. This has not been shown in humans. Theoretically, concomitant use of rose hip might reduce the effectiveness of antiplatelet or anticoagulant drugs.

Theoretically, the antioxidant effects of rose hip might reduce the effectiveness of antitumor antibiotics.
Rose hip contains the antioxidant vitamin C. 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, rose hip might increase blood levels of estrogens.
Rose hip contains vitamin C. Increases in plasma estrogen levels of up to 55% have occured 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, rose hip might increase blood levels of lithium.
Rose hip is thought to have diuretic properties. Theoretically, due to these potential diuretic effects, rose hip might reduce excretion and increase levels of lithium. The dose of lithium might need to be decreased.

Theoretically, rose hip might reduce the clearance of aspirin; however, its vitamin C content is likely too low to produce clinically significant effects.
Rose hip 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 rose hip is typically about 500 mg per 100 grams. Thus, a clinically significant interaction between rose hip and aspirin is unlikely.

Theoretically, rose hip might reduce the effectiveness of warfarin; however, its vitamin C content is likely too low to produce clinically significant effects.
Rose hip 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 rose hip is typically about 500 mg per 100 grams. Thus, a clinically significant interaction between rose hip and warfarin is unlikely.

Theoretically, a high intake of dietary sodium might reduce the effectiveness of antihypertensive drugs.
High intake of dietary sodium can increase systolic and diastolic blood pressure. Also, high intake of sodium may necessitate increased use of antihypertensive medications to achieve blood pressure control in some patients, such as those with chronic kidney disease.

Concomitant use of mineralocorticoids and some glucocorticoids with sodium supplements might increase the risk of hypernatremia.
Mineralocorticoids and some glucocorticoids (corticosteroids) cause sodium retention. This effect is dose-related and depends on mineralocorticoid potency. It is most common with hydrocortisone, cortisone, and fludrocortisone, followed by prednisone and prednisolone.

Concomitant use of didanosine with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia.
Didanosine formulations contain a significant amount of sodium.

Altering dietary intake of sodium might alter the levels and clinical effects of lithium.
High sodium intake can reduce plasma concentrations of lithium by increasing lithium excretion. Reducing sodium intake can significantly increase plasma concentrations of lithium and cause lithium toxicity in patients being treated with lithium carbonate. Stabilizing sodium intake is shown to reduce the percentage of patients with lithium level fluctuations above 0.8 mEq/L. Patients taking lithium should avoid significant alterations in their dietary intake of sodium.

Theoretically, concomitant use of sodium phosphate with sodium supplements might increase the risk of hypernatremia.
Use of high doses (> 45 mL in 24 hours) of sodium phosphate, such as those used for bowel cleansing before surgery, can lead to serious electrolyte disturbances, including hypernatremia. The risk of hypernatremia is highest in the elderly and people with other risk factors for electrolyte disturbances.

Concomitant use of sodium-containing drugs with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia and long-term sodium-related complications.
The Chronic Disease Risk Reduction (CDRR) intake level of 2.3 grams of sodium daily indicates the intake at which it is believed that chronic disease risk increases for the apparently healthy population. Some medications contain high quantities of sodium. When used in conjunction with sodium supplements or high-sodium diets, the CDRR may be exceeded. Additionally, concomitant use may increase the risk for hypernatremia; this risk is highest in the elderly and people with other risk factors for electrolyte disturbances.

Theoretically, concomitant use of tolvaptan with sodium might increase the risk of hypernatremia.
Tolvaptan is a vasopressin receptor 2 antagonist that is used to increase sodium levels in patients with hyponatremia. Patients taking tolvaptan should use caution with the use of sodium salts such as sodium chloride.

Theoretically, taking horsetail with antidiabetes drugs might increase the risk of hypoglycemia.
Equisetum myriochaetum has demonstrated hypoglycemic activity in clinical research. In an animal diabetic model, Equisetum giganteum had hypoglycemic effects. It is unclear whether other horsetail species have hypoglycemic effects.

Theoretically, taking horsetail with diuretic drugs might increase potassium loss and the risk of hypokalemia.
Laboratory research shows that various species of horsetail have diuretic properties. Due to its diuretic effects, there has been concern that taking horsetail along with potassium-depleting diuretics might increase the risk for hypokalemia. However, pharmacokinetic research in humans shows that taking horsetail 900 mg daily for 4 days does not affect urinary excretion of electrolytes, including potassium and sodium, despite having a diuretic effect similar to taking hydrochlorothiazide 25 mg daily. It is unclear if taking horsetail for a longer duration would affect electrolyte levels. Until more is known, use with caution.

Theoretically, horsetail might decrease the levels and clinical effects of efavirenz.
In two case reports, patients were found to have detectable viral loads when taking horsetail-containing supplements along with an antiretroviral regimen that included efavirenz. In one case, the antiretroviral regimen included zidovudine, lamivudine, and efavirenz; in the other case, the regimen consisted of emtricitabine, tenofovir disoproxil fumarate, and efavirenz. One month after discontinuing horsetail, the viral loads became undetectable in both cases. The exact mechanism of this interaction is unknown. It is also unclear if this interaction is specific to efavirenz or if it is related to various components of antiretroviral therapy.

Theoretically, horsetail might increase the levels and adverse effects of lithium.
Animal research suggests that horsetail has diuretic properties. Theoretically, due to these potential diuretic effects, horsetail might reduce excretion and increase levels of lithium. The dose of lithium might need to be decreased.

Theoretically, horsetail might decrease the levels and clinical effects of NRTIs.
In two case reports, patients were found to have detectable viral loads when taking horsetail-containing supplements along with an antiretroviral therapy. In one case, the antiretroviral regimen included zidovudine, lamivudine, and efavirenz; in the other case, the regimen consisted of emtricitabine, tenofovir disoproxil fumarate, and efavirenz. One month after discontinuing the supplement, the viral loads became undetectable in both cases. The exact mechanism of these interactions is unknown. It is also unclear if these interactions are specific to NRTIs or if they are related to various components of antiretroviral therapy.

Co-administration of intravenous calcium and ceftriaxone can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys.
Avoid administering intravenous calcium in any form, such as parenteral nutrition or Lactated Ringers, within 48 hours of intravenous ceftriaxone. Case reports in neonates show that administering intravenous ceftriaxone and calcium can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys. In several cases, neonates have died as a result of this interaction. So far there are no reports in adults; however, there is still concern that this interaction might occur in adults.

Calcium seems to reduce levels of dolutegravir.
Advise patients to take dolutegravir either 2 hours before or 6 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium carbonate 1200 mg concomitantly with dolutegravir 50 mg reduces plasma levels of dolutegravir by almost 40%. Calcium appears to decrease levels of dolutegravir through chelation.

Calcium seems to reduce levels of elvitegravir.
Advise patients to take elvitegravir either 2 hours before or 2 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium along with elvitegravir can reduce blood levels of elvitegravir through chelation.

Calcium citrate might increase aluminum absorption and toxicity. Other types of calcium do not increase aluminum absorption.
Calcium citrate can increase the absorption of aluminum when taken with aluminum hydroxide. The increase in aluminum levels may become toxic, particularly in individuals with kidney disease. However, the effect of calcium citrate on aluminum absorption is due to the citrate anion rather than calcium cation. Calcium acetate does not appear to increase aluminum absorption.

Calcium might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption when taken in a fasting state.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide and calcium can be taken together if taken with food. However, if taken on an empty stomach, bictegravir/emtricitabine/tenofovir alafenamide should not be taken with, or 2 hours after, calcium containing products.

Calcium reduces the absorption of bisphosphonates.
Advise patients to take bisphosphonates at least 30 minutes before calcium, but preferably at a different time of day. Calcium supplements decrease absorption of bisphosphonates.

Taking calcipotriene with calcium might increase the risk for hypercalcemia.
Calcipotriene is a vitamin D analog used topically for psoriasis. It can be absorbed in sufficient amounts to cause systemic effects, including hypercalcemia. Theoretically, combining calcipotriene with calcium supplements might increase the risk of hypercalcemia.

Using intravenous calcium with digoxin might increase the risk of fatal cardiac arrhythmias.
Hypercalcemia increases the risk of fatal cardiac arrhythmias with digoxin. However, one retrospective analysis of clinical data suggests that intravenous calcium does not increase the risk of dysrhythmias or mortality in patients receiving digoxin.

Theoretically, calcium may reduce the therapeutic effects of diltiazem.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, calcium might increase this risk of hypercalcemia and reduce the effectiveness of diltiazem.

Calcium seems to reduce the absorption and effectiveness of levothyroxine.
Advise patients to take levothyroxine and calcium supplements at least 4 hours apart. Calcium reduces levothyroxine absorption, probably by forming insoluble complexes. Calcium carbonate supplements reduce effectiveness of levothyroxine in patients with hypothyroidism.

Theoretically, concomitant use of calcium and lithium may increase this risk of hypercalcemia.
Clinical research suggests that long-term use of lithium may cause hypercalcemia in 10% to 60% of patients. Theoretically, concomitant use of lithium and calcium supplements may further increase this risk.

Calcium seems to reduce the absorption of quinolone antibiotics.
Advise patients to take oral quinolones at least 2 hours before or 4-6 hours after calcium supplements or calcium-fortified foods. Taking calcium at the same time as oral quinolones can reduce quinolone absorption. Calcium binds to quinolones in the gut.

Calcium may reduce levels of raltegravir.
Pharmacokinetic research shows that taking a single dose of calcium carbonate 3000 mg along with raltegravir 400 mg twice daily modestly decreases the mean area under the curve of raltegravir, but the decrease does not necessitate a dose adjustment of raltegravir. However, a case of elevated HIV-1 RNA levels and documented resistance to raltegravir has been reported for a patient taking calcium carbonate 1 gram three times daily plus vitamin D3 (cholecalciferol) 400 IU three times daily in combination with raltegravir 400 mg twice daily for 11 months. It is thought that calcium reduced raltegravir levels by chelation, leading to treatment failure.

Calcium seems to reduce the absorption of sotalol.
Advise patients to separate doses by at least 2 hours before or 4-6 hours after calcium. Calcium appears to reduce the absorption of sotalol, probably by forming insoluble complexes.

Calcium seems to reduce the absorption of tetracycline antibiotics.
Advise patients to take oral tetracyclines at least 2 hours before, or 4-6 hours after calcium supplements. Taking calcium at the same time as oral tetracyclines can reduce tetracycline absorption. Calcium binds to tetracyclines in the gut.

Taking calcium along with thiazides might increase the risk of hypercalcemia and renal failure.
Thiazides reduce calcium excretion by the kidneys. Using thiazides along with moderately large amounts of calcium carbonate increases the risk of milk-alkali syndrome (hypercalcemia, metabolic alkalosis, renal failure). Patients may need to have their serum calcium levels and/or parathyroid function monitored regularly.

Theoretically, calcium may reduce the therapeutic effects of verapamil.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, use of calcium supplements may increase this risk of hypercalcemia and reduce the effectiveness of verapamil.

Intravenous calcium may decrease the effects of calcium channel blockers; oral calcium is unlikely to have this effect.
Intravenous calcium is used to decrease the effects of calcium channel blockers in the management of overdose. Intravenous calcium gluconate has been used before intravenous verapamil (Isoptin) to prevent or reduce the hypotensive effects without affecting the antiarrhythmic effects. But there is no evidence that dietary or supplemental calcium when taken orally interacts with calcium channel blockers.

Theoretically, taking juniper berry with antidiabetes medications might cause additive hypoglycemia.
Animal research shows that juniper berry can lower blood glucose.

Theoretically, juniper berry might increase the risk of adverse effects from diuretic drugs.
Juniper berry is thought to have mild diuretic effects.