Major interaction on record — check this product against your medications before combining. Based on 8 of 14 ingredients. Check your meds →
Dietary supplement

Skull Dust Vanilla Mocha Ingredients & Drug Interactions

by Black Magic

Skull Dust Vanilla Mocha label
See full label image
Powder Category: Other Combinations
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 9, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Skull Dust Vanilla Mocha against your medications. The heart of this page is the interaction checker and the full interaction report — how this product’s ingredients may interact with prescription and over-the-counter medicines you may be taking.

Around that, we add a pharmacist’s high-level view of the product as a whole — what’s inside, the evidence for its stated use, how transparent the label is, and what safety data exists — so you can see the full picture in one place. It’s educational information from our licensed clinical databases and the clinical staff at HelloPharmacist — not medical advice — and we don’t sell or endorse products. Our editorial policy

The interaction bottom line Most serious interaction: Major

Skull Dust Vanilla Mocha is a dietary supplement by Black Magic with 14 active ingredients. Its ingredients are commonly taken for replacing fluids and electrolytes, preventing dehydration during exercise or illness, treating low blood sodium (under medical care).Based on those ingredients, 2,266 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Dietary Fiber, grass fed Collagen, Turmeric powder. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

Jump to a section

Check Your Meds Against Skull Dust Vanilla Mocha by Black Magic

Ask about any prescription or over-the-counter medication and we check it for interactions with Skull Dust Vanilla Mocha by Black Magic — and tell you which ingredient is responsible.

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HelloPharmacist Scorecard of Skull Dust Vanilla Mocha by Black Magic

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

From our pharmacy team — supplement deep dive

Generated from HelloPharmacist’s pharmacist-curated databases and editorial rules · Last generated Sep 10, 2026

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 3 of its 12 active ingredients.
  • “Keto Protein Blend” is a proprietary blend — the label doesn't break down how much of each component you get.

Skull Dust Vanilla Mocha contains 11 ingredients, including active minerals and botanicals. Sodium, potassium, and calcium provide electrolytes; caprylic acid and capric acid are medium-chain fatty acids; turmeric powder supplies the anti-inflammatory compound curcumin; the keto protein blend and collagen offer protein; ghee adds fat; espresso coffee powder brings caffeine for mental alertness; and MCT powder and omega oils round out the fat profile.

The inactive ingredients include natural flavors, disodium phosphate, xanthan gum, stevia (steviol glycosides), and silicon dioxide as a flow agent.

Does it work?

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

This product doesn't appear to be marketed for a specific use, so we graded its ingredients' overall clinical evidence instead.

Strong

Strong clinical evidence supports its ingredients for:

Why this rating?
  • We looked at the product name, claims, and label statements and couldn't find a stated purpose to grade.
  • Since the label doesn't commit to one use, we graded the ingredients' overall clinical evidence instead.
  • On file: Constipation — rated "Effective" (Black Psyllium) (Natural Medicines).
  • On file: Dyspepsia — rated "Effective" (Calcium) (Natural Medicines).
  • On file: Hypocalcemia — rated "Effective" (Calcium) (Natural Medicines).
  • On file: Kidney failure — rated "Effective" (Calcium) (Natural Medicines).
  • On file: Hyperkalemia — rated "Effective" (Calcium) (Natural Medicines).

The data we hold shows effectiveness ratings only for a few ingredients in this product. Calcium is effective for bone health (osteoporosis), kidney disease, and treating low calcium (hypocalcemia).

Turmeric powder is possibly effective for depression, hay fever, high cholesterol, and digestive upset. Coffee powder is likely effective for mental alertness and possibly effective for Parkinson disease, heart failure, and type 2 diabetes.

Sodium has evidence for cystic fibrosis (likely effective) and amphotericin B kidney toxicity (possibly effective), though normal dietary sodium is not a supplement goal. We hold no effectiveness data for potassium, caprylic acid, capric acid, the keto protein blend, collagen, ghee, MCT powder, or omega oils in this product.

The evidence, ingredient by ingredient Sodium Potassium Calcium Black Psyllium Caprylic Acid Turmeric Cannabis Coffee

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

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

Why this rating?
  • We hold adverse-effect (side-effect) data for 8 of the 8 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 8 of 8.
  • General safety write-ups exist for 8 of 8.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Calcium is generally well tolerated at recommended doses and is likely safe in pregnancy and breastfeeding. Turmeric powder is also generally well tolerated as a food, though concentrated supplement doses lack robust safety data — it's been linked to rare liver injury in isolated case reports when used as a supplement for weeks to months.

Coffee powder (caffeine) is well tolerated in moderate amounts and possibly safe in pregnancy at limited intake, though caffeine does pass into breast milk and high intake may cause fussiness in nursing infants. Sodium is essential in small amounts but too much is linked to high blood pressure and heart strain; normal dietary sodium is fine, but avoid supplements or very high intake without medical advice.

Potassium from food is safe, but supplements carry risks, especially for those with kidney disease, and should only be used under medical guidance. Caprylic acid is generally recognized as safe in food but lacks robust safety data at supplement doses.

We hold no pregnancy/breastfeeding safety data for capric acid, the keto protein blend, MCT powder, or omega oils. Grass-fed collagen and ghee are linked to cannabis monograph data showing calcium is unsafe in pregnancy and lactation, though these food ingredients are unlikely to carry active cannabis constituents.

Side effects, ingredient by ingredient Sodium Potassium Calcium Black Psyllium Caprylic Acid Turmeric Cannabis Coffee

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

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

Why this rating?
  • 8 of the 8 matched ingredients can interact with medications — Black Psyllium, Turmeric, Calcium, Potassium, Cannabis, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 2,267 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

Before taking Skull Dust, double-check with your doctor or pharmacist if you use: HIV medications like dolutegravir, elvitegravir, or raltegravir (calcium reduces their levels); blood thinners such as warfarin (calcium, caprylic acid, and the cannabis-linked ingredients may increase levels); blood pressure medications including ACE inhibitors, ARBs, or antihypertensive drugs (sodium and potassium may reduce effectiveness or cause dangerous electrolyte shifts); lithium (sodium alters its levels); levothyroxine or other thyroid medication (calcium reduces absorption); heart medications like sotalol or diltiazem (calcium interferes); immunosuppressants like tacrolimus (turmeric increases levels); chemotherapy drugs (turmeric may reduce effectiveness); and the stimulant ephedrine or CNS depressants (caffeine in coffee increases stimulant risk; cannabis-linked ingredients may have additive effects). If you take any prescription medication, run it through the checker on this page.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with strong clinical evidence behind its ingredients' uses. Major medication interactions have been identified, and safety information is well characterized.

This powder combines electrolytes, botanicals, protein, and fats in a single formula — potentially helpful for those seeking a keto-friendly, nutrient-dense drink mix. However, the sodium and potassium content make it important to check with your doctor before using it if you have high blood pressure, kidney disease, or take medications for heart rhythm or blood pressure control.

If you take any HIV medications, thyroid medication, blood thinners, or psychiatric drugs, talk with your pharmacist or doctor before starting, because several ingredients here have documented interactions that could affect how your medications work.

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

Assessment coverage: 9 of 12 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Mar 25, 2021.

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

At a glance

General information

Key facts about Skull Dust Vanilla Mocha, straight from the product label.

Brand Black Magic
Net contents 15.52 Ounce(s); 440 Gram(s)
Market status On market
Date entered into DSLD Mar 25, 2021
DSLD ID 242804
Product type Other Combinations
Supplement form Powder
Dietary claims / uses Nutrient
Intended target group(s) Adult (18 - 50 Years)
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for Skull Dust Vanilla Mocha by Black Magic, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
22 Gram(s)
Maximum serving Sizes:
22 Gram(s)
Servings per container
20
IngredientAmount% DV
Total Carbohydrates1 Gram(s)1%
Sugar0 Gram(s)--
Sodium150 mg6%
Potassium150 mg5%
Calcium25 mg3%
Total Fat4 Gram(s)6%
Protein12 Gram(s)24%
Caprylic Acid0 NP--
Capric Acid0 NP--
Cholesterol30 mg10%
Dietary Fiber0 Gram(s)--
Trans Fat0 mg--
Saturated Fat1.5 Gram(s)7%
Turmeric powder0 NP--
Keto Protein Blend0 NP--
grass fed Collagen0 NP--
grass fed Ghee0 NP--
Medium Chain Triglyceride powder0 NP--
natural Columbian Espresso Coffee powder0 NP--
Omega 3-6-9 powder0 NP--

Other ingredients: Natural flavors, Disodium Phosphate, Xanthan Gum, Steviol Glycosides, Silicon Dioxide

Tap any ingredient to jump to its full detail below.

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

From the other side Less luck More skill

Formula

Keto collagen creamer Essential fatty acids Grass-fed collagen Organic turmeric Vanilla Mocha Naturally flavored

FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Directions: As a dietary supplement, take 1 scoop with your morning coffee or 6-12 fl oz of hot or cold water.

Is this label outdated? Report a formula or label change and our pharmacy team will review it.

See for yourself

Skull Dust Vanilla Mocha by Black Magic label

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

Skull Dust Vanilla Mocha label

Label images are published by the NIH Dietary Supplement Label Database for the version of this product on file. Always read your actual product label.

View the full label (PDF)
What’s inside

The Ingredients in Skull Dust Vanilla Mocha by Black Magic

These are the 14 active ingredients this product is made of. Select any to open its full monograph.

Serving size22 Gram(s) Dosage formPowder Servings per container20 Amounts shown are per serving.

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

Sugar

0 Gram(s) per serving

Sodium

Interacts with
205 drugs
150 mg per serving

Sodium is an essential mineral and electrolyte your body needs to balance fluids, support nerves, and help muscles work. Most people in modern diets g...

Sodium monograph & interactions

Potassium

Interacts with
62 drugs
150 mg per serving

Potassium is an essential mineral your body needs for nerve signals, muscle function, and a steady heartbeat, and most people get enough from a balanc...

Potassium monograph & interactions

Calcium

Interacts with
168 drugs
25 mg per serving

Calcium is an essential mineral your body needs for strong bones, nerve signaling, and muscle function, and supplements can help fill gaps when diet f...

Calcium monograph & interactions

Protein

12 Gram(s) per serving

Dietary Fiber

Interacts with
2,025 drugs
0 Gram(s) per serving

Black psyllium is a soluble-fiber supplement made from the seeds of a Plantago plant, used mostly to ease constipation and support digestive health. I...

Dietary Fiber monograph & interactions

Keto Protein Blend

0 NP per serving

Other (inactive) ingredients: Natural flavors, Disodium Phosphate, Xanthan Gum, Steviol Glycosides, Silicon Dioxide. These complete the product’s ingredient list but are not active constituents.

Interaction report

Skull Dust Vanilla Mocha by Black Magic Drug Interactions

Want to check YOUR meds against Skull Dust Vanilla Mocha?

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

 Go to the checker
2,266Drugs
17 Major 1,584 Moderate 665 Minor

Ingredients driving the most interactions

Dietary Fiber 2,025
grass fed Collagen 1,136
Turmeric powder 1,133
natural Columbian Espresso Coffee powder 591
Caprylic Acid 262

Individual Drug Interactions

The ingredients in Skull Dust Vanilla Mocha interact with 2,266 drugs. Click any drug to see the details.

8 of the 14 ingredients in Skull Dust Vanilla Mocha interact with drugs. Each result below shows which ingredient is responsible. Dietary Fiber grass fed Collagen Turmeric powder natural Columbian Espresso Coffee powder Caprylic Acid Sodium Calcium Potassium

Each ingredient & the kinds of drugs it affects

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

Dietary Fiber7 drug types · 2,025 drugs

Carbamazepine (Tegretol)

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.

Likelihood Probable Evidence D
Lithium

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.

Likelihood Probable Evidence D
Metformin (Glucophage)

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.

Likelihood Possible Evidence D
Olanzapine (Zyprexa)

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.

Likelihood Possible Evidence D
Digoxin (Lanoxin)

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.

Likelihood Unlikely Evidence B
Ethinyl Estradiol

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.

Likelihood Unlikely Evidence D
Oral Drugs

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.

Likelihood Possible Evidence B
Dietary Fiber full monograph & interactions

grass fed Collagen18 drug types · 1,136 drugs

Warfarin (Coumadin)

Concomitant use with cannabis seems to increase the levels and clinical effects of warfarin.
In vitro research shows that the cannabis constituents delta-9-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol inhibit the cytochrome P450 2C9 (CYP2C9)-mediated 7-hydroxylation of S-warfarin in a concentration-dependent manner.
Additionally, there are multiple case reports of patients chronically taking warfarin that developed a spike in international normalized ratio (INR) after using cannabis in various forms, including smoking cannabis, taking medical cannabis orally, or drinking water infused with cannabis flower. One patient smoked 2-2.5 grams in one week and another patient had doubled the amount of THC consumed from 7.5 mg to 14.7 mg daily for one week.

Likelihood Probable Evidence D
Alcohol (Ethanol)

Theoretically, cannabis might have additive effects when used with alcohol.
Cannabis can have CNS depressant effects, similar to synthetic delta-9-tetrahydrocannabinol (THC). Theoretically, concomitant use of alcohol with cannabis can have additive effects including psychomotor impairment, sedation, and changes in mood and behavior.

Likelihood Possible Evidence D
Anesthesia

Cannabis use might alter the safety and clinical effects of various forms of anesthesia.
A small clinical study shows that higher doses of propofol may be needed to achieve relaxation and loss of consciousness in chronic cannabis users compared with nonusers. Another small clinical study shows that use of cannabis within 72 hours prior to undergoing surgery requiring atropine anesthesia may increase the risk of sustained postoperative tachycardia. The exact mechanisms of these interactions are unclear. Obtain a patient's history of cannabis use preoperatively and advise patients to discontinue cannabis use for at least 2 weeks prior to undergoing surgery.

Likelihood Possible Evidence B
Anticoagulant/Antiplatelet Drugs

Theoretically, cannabis might increase the risk of bleeding when used concomitantly with anticoagulant/antiplatelet drugs.
In vitro research shows that the cannabis constituents delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) inhibit platelet aggregation.

Likelihood Possible Evidence D
Barbiturates

Theoretically, cannabis might increase the levels and adverse effects of barbiturates.
Some research shows that synthetic delta-9-tetrahydrocannabinol (THC) increases the elimination half-life of pentobarbital by 4 hours when dosed concomitantly.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, cannabis might have additive effects if used with other CNS depressants.
Cannabis can have CNS depressant effects. Combining cannabis with other CNS depressants might result in additive or synergistic effects. A small clinical trial in healthy adults shows that inhaling a high-grade cannabis (Bedrocan International B.V., Veendam, The Netherlands) 100 mg, containing delta-9-tetrahydrocannabinol 21.8% and cannabinol 0.1%, modestly increases subjective feelings of sedation when compared with cannabis alone.

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

Cannabis may increase levels of drugs metabolized by CYP2C19.
Research shows that cannabidiol (CBD), a constituent of cannabis, inhibits CYP2C19. In clinical studies and case reports, cannabidiol use resulted in significant increases in the serum levels of topiramate, methadone, citalopram, omeprazole, and N-desmethylclobazam, the primary active metabolite of clobazam. These chemicals are metabolized by CYP2C19. Concomitant use of cannabis with CYP2C19 substrates may increase the risk for adverse effects from these substrates.

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

Theoretically, drugs that are CYP2C9 inducers might decrease the effects of cannabis.
Delta-9-tetrahydrocannabinol (THC), an active constituent of cannabis, is a substrate of CYP2C9 enzymes.

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

Theoretically, drugs that are CYP2C9 inhibitors might increase the adverse effects of cannabis.
Delta-9-tetrahydrocannabinol (THC), an active constituent of cannabis, is a substrate of CYP2C9 enzymes.

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

Theoretically, cannabis might increase the levels and adverse effects of CYP2C9 substrates.
In vitro research shows that the cannabis constituents delta-9-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol moderately inhibit the CYP2C9-mediated 7-hydroxylation of S-warfarin in a concentration-dependent manner. In vitro research also shows that cannabis extracts modestly inhibit the CYP2C9 metabolism of tolbutamide; extracts providing the specific cannabinoids CBD and cannabigerol (CBG) had stronger inhibitory effects than extracts containing THC and CBD.

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

Theoretically, cannabis might decrease the levels and clinical effects of CYP2E1 substrates.
In vitro research shows that cannabis can induce the activity of CYP2E1, which might increase the metabolism of CYP2E1 substrates.

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

Theoretically, CYP3A4 inducers might reduce the levels and clinical effects of cannabis.
Delta-9-tetrahydrocannabinol (THC), an active constituent of cannabis, is a substrate of CYP3A4 enzymes.

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

Theoretically, CYP3A4 inhibitors might increase the levels and adverse effects of cannabis.
Delta-9-tetrahydrocannabinol (THC), an active constituent of cannabis, is a substrate of CYP3A4 enzymes.

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

Theoretically, cannabis may increase the levels and adverse effects of CYP3A4 substrates.
In vitro research shows that cannabis can inhibit the activity of CYP3A4 enzymes, which might decrease the metabolism of CYP3A4 substrates. In vitro research also shows that cannabis extracts modestly inhibit the CYP3A4 metabolism of testosterone; extracts providing the specific cannabinoids CBD and cannabigerol (CBG) had stronger inhibitory effects than extracts containing THC and CBD.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, cannabis might alter levels of drugs that are substrates of P-glycoprotein (P-gp).
Most in vitro research suggests that constituents of cannabis, including cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC), can inhibit P-gp and increase the accumulation of probe compounds by reducing P-gp mediated drug efflux. In vitro studies in kidney cell lines show that a 1-hour exposure to CBD and THC inhibits P-gp. Cannabis may also alter the expression of P-gp, although this effect appears to vary based on duration of exposure. Some in vitro research in lymphoblastoid leukemia cell lines indicates that a 1-hour exposure to cannabinoids does not affect P-gp expression, while a prolonged 72-hour exposure decreases P-gp expression. Other in vitro research in these cell lines shows that a 4-hour exposure to THC and CBD induces P-gp gene expression, while exposure for longer than 4 hours and up to 48 hours does not induce P-gp gene expression.

Likelihood Possible Evidence D
Theophylline

Smoking cannabis while taking theophylline might reduce the levels and clinical effects of theophylline.
Similar to smoking tobacco, smoking cannabis seems to increase the metabolism of theophylline.

Likelihood Possible Evidence D
Thrombolytic Drugs

Cannabis might augment the effects of thrombolytic drugs and increase the risk of severe bleeding.
A case of cerebral hemorrhage has been reported for a 51-year-old female and chronic cannabis user who had consumed a large amount of cannabis prior to receiving recombinant tissue plasminogen activator (rtPA) for ischemic stroke. Hemorrhage had been ruled out prior to providing the rtPA. The exact mechanism of this interaction is unclear.

Likelihood Possible Evidence D
Antipsychotic Drugs

Cannabis does not seem to affect blood levels or effects of some antipsychotic drugs.
Human research shows that cannabis use does not affect blood levels or clinical effects of amisulpride, aripiprazole, or olanzapine in patients with schizophrenia and related disorders.

Likelihood Unlikely Evidence B
grass fed Collagen full monograph & interactions

Turmeric powder24 drug types · 1,133 drugs

Alkylating Agents

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

Likelihood Possible Evidence D
Amlodipine (Norvasc)

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

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

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

Likelihood Possible Evidence B
Antidiabetes Drugs

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

Likelihood Possible Evidence B
Antitumor Antibiotics

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

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

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

Likelihood Possible Evidence D
Hepatotoxic Drugs

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

Likelihood Possible Evidence D
Methotrexate (Trexall, Others)

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

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

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

Likelihood Possible Evidence D
Sulfasalazine (Azulfidine)

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

Likelihood Probable Evidence B
Tacrolimus (Prograf)

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

Likelihood Possible Evidence D
Talinolol

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

Likelihood Probable Evidence B
Tamoxifen (Nolvadex)

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

Likelihood Possible Evidence B
Topoisomerase I Inhibitors

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

Likelihood Possible Evidence D
Tramadol (Ultram)

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

Likelihood Possible Evidence D
Warfarin (Coumadin)

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

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

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

Likelihood Possible Evidence D
Docetaxel (Taxotere)

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

Likelihood Possible Evidence D
Estrogens

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

Likelihood Possible Evidence D
Glyburide (Diabeta, Others)

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

Likelihood Possible Evidence B
Losartan (Cozaar)

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

Likelihood Possible Evidence D
Norfloxacin (Noroxin)

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

Likelihood Possible Evidence D
P-Glycoprotein Substrates

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

Likelihood Possible Evidence D
Paclitaxel (Abraxane, Onxol)

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

Likelihood Possible Evidence D
Turmeric powder full monograph & interactions

natural Columbian Espresso Coffee powder33 drug types · 591 drugs

Ephedrine

Theoretically, concomitant use might increase the risk of stimulant adverse effects.
Coffee contains caffeine. There is evidence that using ephedrine with caffeine might increase the risk of serious life-threatening or debilitating adverse effects such as hypertension, myocardial infarction, stroke, seizures, and death. Tell patients to avoid taking caffeine with ephedrine and other stimulants.

Likelihood Probable Evidence D
Adenosine (Adenocard)

Theoretically, coffee might decrease the vasodilatory effects of adenosine and interfere with its use prior to stress testing.
Coffee contains caffeine. Caffeine is a competitive inhibitor of adenosine at the cellular level. However, caffeine does not seem to affect supplemental adenosine because high interstitial levels of adenosine overcome the antagonistic effects of caffeine. It is recommended that methylxanthines such as caffeine, as well as methylxanthine-containing products, be stopped 24 hours prior to pharmacological stress tests. However, methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.

Likelihood Possible Evidence B
Alendronate (Fosamax)

Coffee reduces alendronate bioavailability.
Separate coffee ingestion and alendronate administration by two hours. Coffee reduces alendronate bioavailability by 60%.

Likelihood Probable Evidence B
Anticoagulant/Antiplatelet Drugs

Theoretically, coffee may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Coffee contains caffeine. Caffeine is reported to have antiplatelet activity. Theoretically, the caffeine in coffee might increase the risk of bleeding when used concomitantly with these agents. However, this interaction has not been reported in humans. There is some evidence that caffeinated coffee might increase the fibrinolytic activity in blood.

Likelihood Unlikely Evidence D
Beta-Adrenergic Agonists

Theoretically, concomitant use of large amounts of coffee might increase cardiac inotropic effects of beta-agonists.
Coffee contains caffeine. Caffeine can increase cardiac inotropic effects of beta-agonists.

Likelihood Probable Evidence D
Cimetidine (Tagamet)

Theoretically, cimetidine might increase the effects and adverse effects of caffeine in coffee.
Coffee contains caffeine. Cimetidine can reduce caffeine clearance by 31% to 42%.

Likelihood Likely Evidence B
Clozapine (Clozaril)

Theoretically, coffee might increase the levels and adverse effects of clozapine and acutely exacerbate psychotic symptoms.
Coffee contains caffeine. Caffeine can increase the effects and toxicity of clozapine. Caffeine doses of 400-1000 mg daily inhibit clozapine metabolism. Clozapine is metabolized by cytochrome P450 1A2 (CYP1A2). Researchers speculate that caffeine might inhibit CYP1A2. However, there is no reliable evidence that caffeine affects CYP1A2. There is also speculation that genetic factors might make some patients be more sensitive to the interaction between clozapine and caffeine.

Likelihood Possible Evidence B
Contraceptive Drugs

Theoretically, concomitant use might increase the effects and adverse effects of caffeine found in coffee.
Coffee contains caffeine. Oral contraceptive drugs can decrease caffeine clearance by 40% to 65%.

Likelihood Probable Evidence B
Dipyridamole (Persantine)

Theoretically, coffee might decrease the vasodilatory effects of dipyridamole and interfere with its use prior to stress testing.
Coffee contains caffeine. Caffeine is a methylxyanthine that may inhibit dipyridamole-induced vasodilation. It is recommended that methylxanthines such as caffeine, as well as methylxanthine-containing products such as coffee, be stopped 24 hours prior to pharmacological stress tests. Methylxanthines appear more likely to interfere with dipyridamole (Persantine) than adenosine-induced stress testing.

Likelihood Probable Evidence B
Disulfiram (Antabuse)

Theoretically, disulfiram might increase the risk of adverse effects from caffeine.
Coffee contains caffeine. In human research, disulfiram decreases the clearance and increases the half-life of caffeine.

Likelihood Probable Evidence B
Diuretic Drugs

Theoretically, concomitant use might increase the risk of hypokalemia.
Coffee contains caffeine. Caffeine, especially in excessive amounts, can reduce potassium levels due to stimulation of the sodium-potassium pump. Diuretics can also cause lower potassium levels.

Likelihood Possible Evidence D
Estrogens

Theoretically, estrogens might increase the levels and adverse effects of caffeine.
Coffee contains caffeine. Estrogen inhibits caffeine metabolism.

Likelihood Probable Evidence B
Fluvoxamine (Luvox)

Theoretically, fluvoxamine might increase the levels and adverse effects of caffeine.
Coffee contains caffeine. Fluvoxamine reduces caffeine metabolism.

Likelihood Probable Evidence B
Lamotrigine (Lamictal)

Coffee consumption can decrease the levels and clinical effects of lamotrigine.
A pharmacokinetic study in patients taking lamotrigine shows that consumption of coffee, both caffeinated and decaffeinated, can decrease the area under the concentration-time curve (AUC) and the peak plasma level (Cmax) of lamotrigine. Each additional cup of coffee reduced the AUC and Cmax by 4% and 3%, respectively. It is unclear whether this interaction is due to induction of lamotrigine metabolism or inhibition of lamotrigine absorption.

Likelihood Probable Evidence B
Levothyroxine (Synthroid, Others)

Coffee can reduce the absorption of levothyroxine.
In some patients, coffee can reduce levothyroxine absorption, possibly through the formation of non-absorbable complexes. A pharmacokinetic study in these patients found that 25-30 mL of espresso coffee consumed with levothyroxine tablets delayed the time to peak plasma levels by 38-43 minutes, reduced the peak plasma level (Cmax) by 19% to 36%, and reduced the area under the curve (AUC) by 27% to 36%. Coffee consumed one hour after levothyroxine did not affect absorption. It is not known whether this interaction occurs with other types of coffee. Tell patients to avoid drinking coffee at the same time that they take their levothyroxine, and for up to an hour afterwards.

Likelihood Possible Evidence B
Lithium

Theoretically, abrupt coffee withdrawal might increase the levels and adverse effects of lithium.
Coffee contains caffeine. Abrupt caffeine withdrawal can increase serum lithium levels. Two cases of lithium tremor that worsened with abrupt coffee withdrawal have been reported. There is also one case of a 2.8-fold increase in blood lithium levels after a patient taking lithium reduced his coffee consumption from 13-20 cups daily to 10 cups daily.

Likelihood Probable Evidence D
Monoamine Oxidase Inhibitors (Maois)

Theoretically, concomitant use might increase the risk of a hypertensive crisis.
Coffee contains caffeine. Caffeine has been shown to inhibit monoamine oxidase (MAO) A and B in laboratory studies. Concomitant intake of large amounts of caffeine with MAOIs might precipitate a hypertensive crisis. In a case report, a patient that consumed 10-12 cups of caffeinated coffee and took the MAOI tranylcypromine presented with severe hypertension. Hypertension was resolved after the patient switched to drinking decaffeinated coffee.

Likelihood Possible Evidence D
Nicotine

Theoretically, concomitant use might increase the risk of hypertension.
Coffee contains caffeine. Concomitant use of caffeine and nicotine has been shown to have additive cardiovascular effects, including increased heart rate and blood pressure. Blood pressure was increased by 10.8/12.4 mmHg when the agents were used concomitantly.

Likelihood Probable Evidence B
Pentobarbital (Nembutal)

Theoretically, coffee might reduce the effects of pentobarbital.
Coffee contains caffeine. Theoretically, caffeine might negate the hypnotic effects of pentobarbital.

Likelihood Possible Evidence B
Phenylpropanolamine

Theoretically, phenylpropanolamine might increase the risk of hypertension, as well as the levels and adverse effects of caffeine.
Coffee contains caffeine. Concomitant use of phenylpropanolamine and caffeine might cause an additive increase in blood pressure. Phenylpropanolamine also seems to increase caffeine serum levels.

Likelihood Probable Evidence B
Pioglitazone (Actos)

Theoretically, coffee might increase the levels and clinical effects of pioglitazone.
Coffee contains caffeine. Animal research suggests that caffeine can modestly increase the maximum concentration, area under the curve, and half-life of pioglitazone, and also reduce its clearance. This increased the antidiabetic effects of pioglitazone. However, the exact mechanism of this interaction is unclear.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, quinolone antibiotics might increase the levels and adverse effects of caffeine.
Coffee contains caffeine. Concomitant use of caffeine and quinolones can decrease caffeine clearance and increase effects and risk of adverse effects.

Likelihood Probable Evidence B
Riluzole (Rilutek)

Theoretically, concomitant use might increase the levels and adverse effects of both caffeine and riluzole.
Coffee contains caffeine. Caffeine and riluzole are both metabolized by cytochrome P450 1A2 (CYP1A2), and concomitant use might reduce metabolism of one or both agents.

Likelihood Possible Evidence D
Stimulant Drugs

Theoretically, concomitant use might increase stimulant adverse effects.
Coffee contains caffeine. Due to the central nervous system (CNS) stimulant effects of caffeine, concomitant use with stimulant drugs can increase the risk of adverse effects.

Likelihood Probable Evidence C
Theophylline

Theoretically, coffee might increase the levels and adverse effects of theophylline.
Coffee contains caffeine, which can increase theophylline levels.

Likelihood Probable Evidence B
natural Columbian Espresso Coffee powder full monograph & all 33 interactions

Caprylic Acid3 drug types · 262 drugs

Antihypertensive Drugs

Theoretically, caprylic acid might increase the risk of hypotension when used with antihypertensive drugs.
Animal research suggests that caprylic acid might have positive inotropic effects, resulting in reduced arterial pressure and vascular resistance and increased cardiac output.

Likelihood Possible Evidence D
Nonsteroidal Anti-Inflammatory Drugs (Nsaids)

Theoretically, caprylic acid might increase plasma concentrations of NSAIDs.
In vitro research suggests that caprylic acid might displace NSAIDs from binding sites on albumin. This effect has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, caprylic acid might increase plasma concentrations of warfarin.
In vitro research suggests that high doses of caprylic acid might displace warfarin from albumin binding sites. This effect has not been reported in humans.

Likelihood Possible Evidence D
Caprylic Acid full monograph & interactions

Sodium7 drug types · 205 drugs

Antihypertensive Drugs

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.

Likelihood Probable Evidence A
Corticosteroids

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.

Likelihood Possible Evidence D
Didanosine (Videx)

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.

Likelihood Probable Evidence C
Lithium

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.

Likelihood Probable Evidence B
Sodium Phosphates

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.

Likelihood Possible Evidence D
Sodium-Containing Drugs

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.

Likelihood Possible Evidence D
Tolvaptan (Samsca)

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.

Likelihood Probable Evidence C
Sodium full monograph & interactions

Calcium18 drug types · 168 drugs

Ceftriaxone (Rocephin)

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.

Likelihood Probable Evidence D
Dolutegravir (Tivicay)

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.

Likelihood Probable Evidence B
Elvitegravir (Vitekta)

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.

Likelihood Probable Evidence B
Aluminum

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.

Likelihood Possible Evidence B
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)

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.

Likelihood Probable Evidence D
Bisphosphonates

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.

Likelihood Probable Evidence C
Calcipotriene (Dovonex)

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.

Likelihood Possible Evidence B
Digoxin (Lanoxin)

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.

Likelihood Possible Evidence B
Diltiazem (Cardizem, Others)

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.

Likelihood Probable Evidence D
Levothyroxine (Synthroid, Others)

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.

Likelihood Probable Evidence B
Lithium

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.

Likelihood Possible Evidence B
Quinolone Antibiotics

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.

Likelihood Probable Evidence B
Raltegravir (Isentress)

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.

Likelihood Possible Evidence B
Sotalol (Betapace)

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.

Likelihood Possible Evidence B
Tetracycline Antibiotics

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.

Likelihood Probable Evidence C
Thiazide Diuretics

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.

Likelihood Probable Evidence C
Verapamil (Calan, Others)

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.

Likelihood Probable Evidence D
Calcium Channel Blockers

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.

Likelihood Unlikely Evidence D
Calcium full monograph & interactions

Potassium3 drug types · 62 drugs

Ace Inhibitors (Aceis)

Using ACEIs with high doses of potassium increases the risk of hyperkalemia.
ACEIs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia. However, concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels.

Likelihood Likely Evidence C
Angiotensin Receptor Blockers (Arbs)

Using ARBs with high doses of potassium increases the risk of hyperkalemia.
ARBs block the actions of the renin-angiotensin-aldosterone system and reduce potassium excretion. Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia. However, concomitant use of these drugs with moderate dietary potassium intake (about 3775-5200 mg daily) does not increase serum potassium levels.

Likelihood Likely Evidence C
Potassium-Sparing Diuretics

Concomitant use increases the risk of hyperkalemia.
Using potassium-sparing diuretics with potassium supplements increases the risk of hyperkalemia.

Likelihood Likely Evidence C
Potassium full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Skull Dust Vanilla Mocha, from the product label.

Black Magic

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Black Magic
Pharmacist Counseling Corner

Skull Dust Vanilla Mocha by Black Magic: Common Questions

Does Skull Dust Vanilla Mocha by Black Magic interact with any medications?
Yes. Based on its ingredients, Skull Dust Vanilla Mocha has a known interaction with 2,266 medications, including 17 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Skull Dust Vanilla Mocha contains 14 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Is this safe during pregnancy?
The data on individual ingredients is mixed. Calcium and turmeric are likely safe in pregnancy at normal amounts, and coffee is possibly safe in limited quantities — but discuss your total caffeine intake with your doctor. However, the Cannabis monograph data linked to the collagen and ghee ingredients rate those as unsafe or likely unsafe in pregnancy, though these food ingredients typically don't contain active cannabis constituents. Talk with your doctor before using this product if you're pregnant.
Is this safe while breastfeeding?
Calcium and turmeric are likely safe during breastfeeding at normal amounts. Coffee (caffeine) is possibly safe but passes into breast milk and may cause fussiness or sleep problems in infants — keep intake low and watch your baby. The Cannabis monograph data linked to collagen and ghee rates them as likely unsafe during lactation, though food-grade ingredients are unlikely to carry active constituents. Discuss with your doctor or pharmacist before using while breastfeeding.
Can this help with joint pain or inflammation?
The turmeric powder in this product is possibly effective for reducing inflammation and may help with conditions like arthritis, but the evidence isn't definitive. Collagen and the omega oils may support joint structure, though we have no effectiveness ratings for them in our data. This product is not a proven treatment for joint disease — if you have arthritis or chronic inflammation, talk with your doctor about whether it fits your care plan.
Will this give me an energy boost?
Yes — the coffee powder contains caffeine, which is likely effective for mental alertness. However, the amount of caffeine in one serving of this powder isn't stated on the label provided, so you won't know exactly how much stimulant you're getting. If you're sensitive to caffeine or take medications that interact with it (such as certain antidepressants or heart drugs), check with your pharmacist first.
What are the side effects of turmeric in this powder?
Most people tolerate turmeric well. The most common side effects are mild digestive issues — constipation, diarrhea, nausea, or stomach upset — especially at higher doses. Rarely, turmeric supplements have been associated with liver damage when used daily for weeks or longer; most cases resolved when the supplement was stopped. If you experience persistent nausea, vomiting, or abdominal pain, stop and talk with your doctor.
Is there a lot of sodium in this powder?
Yes — sodium is listed as a primary ingredient. The exact amount per serving isn't provided in the facts here, but if you have high blood pressure, heart disease, or kidney disease, or take blood pressure medications or diuretics, check the nutrition label closely or ask your pharmacist whether this product fits your sodium limits.

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

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Go deeper

The Full Monographs Behind Skull Dust Vanilla Mocha’s Ingredients

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

Herb & supplement monograph

Sodium

Interacts with 205 drugs

Sodium is an essential mineral and electrolyte your body needs to balance fluids, support nerves, and help muscles work. Most people in modern diets get more than enough—often too much—from...

Read the full Sodium monograph → Herb & supplement monograph

Potassium

Interacts with 62 drugs

Potassium is an essential mineral your body needs for nerve signals, muscle function, and a steady heartbeat, and most people get enough from a balanced diet rich in fruits and vegetables. P...

Read the full Potassium monograph → Herb & supplement monograph

Calcium

Interacts with 168 drugs

Calcium is an essential mineral your body needs for strong bones, nerve signaling, and muscle function, and supplements can help fill gaps when diet falls short. Most people do best getting...

Read the full Calcium monograph → Herb & supplement monograph

Black Psyllium

Interacts with 2,025 drugs

Black psyllium is a soluble-fiber supplement made from the seeds of a Plantago plant, used mostly to ease constipation and support digestive health. It is best known and most studied for rel...

Read the full Black Psyllium monograph → Herb & supplement monograph

Caprylic Acid

Interacts with 262 drugs

Caprylic acid is a medium-chain fatty acid found in coconut oil and palm kernel oil that is popularly used for yeast overgrowth and gut health. While laboratory studies show it has antimicro...

Read the full Caprylic Acid monograph → Herb & supplement monograph

Turmeric

Interacts with 1,133 drugs

Turmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising, but quality is mixed and curcumin is po...

Read the full Turmeric monograph → Herb & supplement monograph

Cannabis

Interacts with 1,136 drugs

Cannabis contains many active compounds, mainly THC (which causes a 'high') and CBD (which does not). Some uses, such as chemotherapy-related nausea, certain seizure disorders, and muscle sp...

Read the full Cannabis monograph → Herb & supplement monograph

Coffee

Interacts with 591 drugs

Coffee is a widely consumed beverage made from roasted coffee beans, valued mainly for its caffeine, which boosts alertness and energy. For most healthy adults, moderate coffee intake is gen...

Read the full Coffee monograph →
Sources

Sources & How We Checked

Skull Dust Vanilla Mocha's label data comes from the NIH Dietary Supplement Label Database; the ingredient interaction data is from the Natural Medicines database, reviewed by our pharmacists.

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

The 673 references behind this product’s interaction data

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

Sodium 38 references
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  2. Food and Drug Administration Science Background: Safety of Sodium Phosphates Oral Solution. September 17, 2001. Available at: http://www.fda.gov/cder/drug/safety/sodiumphospate.htm
  3. Coton T, Mallaret C, Coilliot C, Carre D, Guisset M. Severe acute ulcerated gastritis induced by salt. Presse Med 2009;38(3):499-500. PubMed
  4. Frings-Meuthen P, Buehlmeier J, Baecker N, et al. High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses. J Appl Physiol 2011;111(2):537-542. PubMed
  5. Frings-Meuthen P, Baecker N, Heer M. Low-grade metabolic acidosis may be the cause of sodium chloride-induced exaggerated bone resorption. J Bone Miner Res 2008;23(4):517-524. PubMed
  6. Alam S, Johnson AG. A meta-analysis of randomised controlled trials (RCT) among healthy normotensive and essential hypertensive elderly patients to determine the effect of high salt (NaCl) diet of blood pressure. J Hum Hypertens 1999;13(6):367-74.
  7. Boudville N, Ward S, Benaroia M, House AA. Increased sodium intake correlates with greater use of antihypertensive agents by subjects with chronic kidney disease. Am J Hypertens 2005;18(10):1300-5. PubMed
  8. Bennett WM. Drug interactions and consequences of sodium restriction. Am J Clin Nutr 1997;65(2 Suppl):678S-681S. PubMed
  9. Okusa MD, Crystal LJ. Clinical manifestations and management of acute lithium intoxication. Am J Med 1994;97(4):383-9. PubMed
  10. Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for water, potassium, sodium, chloride, and sulfate. Washington, DC: National Academy Press, 2005. Available at: http://www.nap.edu/openbook.php?record_id=10925. DOI
  11. D'Elia L, Rossi G, Ippolito R, Cappuccio FP, Strazzullo P. Habitual salt intake and risk of gastric cancer: a meta-analysis of prospective studies. Clin Nutr 2012;31(4):489-98. PubMed
  12. Goldsmith SR. Hyponatremia in heart failure: time for a trial. J Card Fail 2013;19(6):398-400. PubMed
  13. Willocks L, Brettle R, Keen J, Valentine C, Pinching AJ. Formulations of didanosine (ddI) and salt overload. Lancet 1992;339(8786):190.
  14. Chen L, Zhang Z, Chen W, Whelton PK, Appel LJ. Lower Sodium Intake and Risk of Headaches: Results From the Trial of Nonpharmacologic Interventions in the Elderly. Am J Public Health. 2016;106(7):1270-5. PubMed
  15. Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014;129(9):981-9. PubMed
  16. Cook NR, Appel LJ, Whelton PK. Sodium Intake and All-Cause Mortality Over 20 Years in the Trials of Hypertension Prevention. J Am Coll Cardiol. 2016;68(15):1609-1617. PubMed
  17. Mente A, O'Donnell M, Rangarajan S, et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. Lancet. 2016;388(10043):465-75. PubMed
  18. Moosavian SP, Haghighatdoost F, Surkan PJ, Azadbakht L. Salt and obesity: a systematic review and meta-analysis of observational studies. Int J Food Sci Nutr. 2017;68(3):265-277. PubMed
  19. O'Donnell M, Mente A, Rangarajan S, et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014;371(7):612-23. DOI
  20. Poggio R, Gutierrez L, Matta MG, Elorriaga N, Irazola V, Rubinstein A. Daily sodium consumption and CVD mortality in the general population: systematic review and meta-analysis of prospective studies. Public Health Nutr. 2015;18(4):695-704. PubMed
  21. Stallings VA, Harrison M, Oria M; Committee to Review the Dietary Reference Intakes for Sodium and Potassium, Food and Nutrition Board, Health and Medicine Division, National Academies of Sciences, Engineering, and Medicine. Washington (DC): National Acad
  22. Mahtani KR, Heneghan C, Onakpoya I, et al. Reduced Salt Intake for Heart Failure: A Systematic Review. JAMA Intern Med. 2018 Dec 1;178(12):1693-1700. PubMed
  23. Yancy CW. Sodium Restriction in Heart Failure: Too Much Uncertainty-Do the Trials. JAMA Intern Med. 2018 Dec 1;178(12):1700-1701. PubMed
  24. He FJ, Campbell NRC, Ma Y, MacGregor GA, Cogswell ME, Cook NR. Errors in estimating usual sodium intake by the Kawasaki formula alter its relationship with mortality: implications for public health. Int J Epidemiol. 2018;47(6):1784-1795. PubMed
  25. Murthy K, Ondrey GJ, Malkani N, et al. THE EFFECTS OF HYPONATREMIA ON BONE DENSITY AND FRACTURES: A SYSTEMATIC REVIEW AND META-ANALYSIS. Endocr Pract. 2019;25(4):366-378. PubMed
  26. Messerli FH, Hofstetter L, Syrogiannouli L, et al. Sodium intake, life expectancy, and all-cause mortality. Eur Heart J 2021;42(21):2103-2112. PubMed
  27. Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database Syst Rev 2020;12(12):CD004022. PubMed
  28. Giatti S, Santos RB, Aielo AN, et al. Association of sodium with obstructive sleep apnea. The ELSA-Brasil study. Ann Am Thorac Soc 2021;18(3):502-510. PubMed
  29. Nan X, Lu H, Wu J, et al. The interactive association between sodium intake, alcohol consumption and hypertension among elderly in northern China: a cross-sectional study. BMC Geriatr 2021;21(1):135. PubMed
  30. Kyozuka H, Fukusda T, Murata T, et al. Impact of preconception sodium intake on hypertensive disorders of pregnancy: The Japan Environment and Children's study. Pregnancy Hypertens 2021;23:66-72. PubMed
  31. Zhao L, Ogden CL, Yang Q, et al. Association of usual sodium intake with obesity among US children and adolescents, NHANES 2009-2016. Obesity (Silver Spring) 2021;29(3):587-594. PubMed
  32. Ma Y, He FJ, Sun Q, et al. 24-Hour urinary sodium and potassium excretion and cardiovascular risk. N Engl J Med 2022;386(3):252-263. PubMed
  33. Liu J, Yang X, Zhang P, et al. Association of urinary sodium excretion and left ventricular hypertrophy in people with type 2 diabetes mellitus: A cross-sectional study. Front Endocrinol (Lausanne) 2021;12:728493. PubMed
  34. Filippini T, Malavolti M, Whelton PK, Vinceti M. Sodium intake and risk of hypertension: A systematic review and dose-response meta-analysis of observational cohort studies. Curr Hypertens Rep 2022;24(5):133-144. PubMed
  35. Wang DD, Li Y, Nguyen XT, et al. Dietary sodium and potassium intake and risk of non-fatal cardiovascular diseases: The million veteran program. Nutrients 2022;14(5):1121. PubMed
  36. Kwak JH, Park CH, Eun CS, et al. The associations of dietary intake of high sodium and low zinc with gastric cancer mortality: A prospective cohort study in Korea. Nutr Cancer 2022;74(10):3501-3508. PubMed
  37. George S, Maiti R, Mishra BR, Jena M, Mohapatra D. Effect of regulated add-on sodium chloride intake on stabilization of serum lithium concentration in bipolar disorder: A randomized controlled trial. Bipolar Disord 2023;25(1):66-75. PubMed
  38. Zhou TL, Schütten MTJ, Kroon AA, et al. Urinary Sodium Excretion and Salt Intake Are Not Associated With Blood Pressure Variability in a White General Population. J Am Heart Assoc 2023;12(1):e026578. PubMed

See these in context on the Sodium monograph →

Potassium 12 references
  1. McEvoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
  2. Gennaro A. Remington: The Science and Practice of Pharmacy. 19th ed. Lippincott: Williams & Wilkins, 1996.
  3. Whelton PK, He J, Cutler JA, et al. Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials. JAMA 1997;277:1624-32. PubMed
  4. Phillips, C. O., Kashani, A., Ko, D. K., Francis, G., and Krumholz, H. M. Adverse effects of combination angiotensin II receptor blockers plus angiotensin-converting enzyme inhibitors for left ventricular dysfunction: a quantitative review of data from ra DOI
  5. Altieri, P. I., Herrero, C., Suero, R., and Ortiz, A. Bleeding duodenal ulcer in a patient taking slow-releasing potassium tablets. Bol.Asoc.Med P.R. 1977;69(8):276.
  6. Raf, L. E. Enteric-coated potassium chloride tablets and ulcer of the small intestine. Acta Chir Scand Suppl 1967;(374):1-87.
  7. Potassium chloride oral solution [package insert]. Allentown, PA: Lehigh Valley Technologies, Inc.; 2014.
  8. Potassium chloride injection [package insert]. Lake Forest, IL: Hospira Inc.; 2009.
  9. Patel RB, Tannenbaum S, Viana-Tejedor A, et al. Serum potassium levels, cardiac arrhythmias, and mortality following non-ST-elevation myocardial infarction or unstable angina: insights from MERLIN-TIMI 36. Eur Heart J Acute Cardiovasc Care 2017 Feb;6(1):1 PubMed
  10. Malta D, Arcand J, Ravindran A, Floras V, Allard JP, Newton GE. Adequate intake of potassium does not cause hyperkalemia in hypertensive individuals taking medications that antagonize the renin angiotensin aldosterone system. Am J Clin Nutr 2016 Oct;104(4 PubMed
  11. Keskin M, Kaya A, Tatlisu MA, et al. The effect of serum potassium level on in-hospital and long-term mortality in ST elevation myocardial infarction. Int J cardiol. 2016 Oct 15;221:505-10.
  12. Stallings VA, Harrison M, Oria M; Committee to Review the Dietary Reference Intakes for Sodium and Potassium, Food and Nutrition Board, Health and Medicine Division, National Academies of Sciences, Engineering, and Medicine. Washington (DC): National Acad

See these in context on the Potassium monograph →

Calcium 62 references
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  33. Calcium supplementation and vascular events. Pharmacist's Letter / Prescriber's Letter 2008;24(3):240306.
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See these in context on the Calcium monograph →

Caprylic Acid 5 references
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  3. Hayball PF, Holman JW, Nation RL. Influence of octanoic acid on the reversible protein binding of ketorolac enantiomers to human serum albumin (HSA): comparative liquid chromatographic studies using a HSA chiral stationary phase. J Chromatogr B Biomed App PubMed
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See these in context on the Caprylic Acid monograph →

Black Psyllium 18 references
  1. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
  2. Gruenwald J, Brendler T, Jaenicke C. PDR for Herbal Medicines. 1st ed. Montvale, NJ: Medical Economics Company, Inc., 1998.
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  16. Diez R, Garcia JJ, Diez MJ, Sierra M, Sahagun AM, Fernandez N. Influence of Plantago ovata husk (dietary fiber) on the bioavailability and other pharmacokinetic parameters of metformin in diabetic rabbits. BMC Complement Altern Med. 2017 Jun 7;17(1):298. PubMed
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  18. Merrick C, Madden CA, Capurso NA. A Case of Blunted Orally Disintegrating Olanzapine Effect Due to Coadministered Psyllium. J Clin Psychiatry 2021;82(2):20cr13633. PubMed

See these in context on the Black Psyllium monograph →

Turmeric 102 references
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See these in context on the Cannabis monograph →

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