Interactions on record — worth a quick check against your medications. Based on 14 of 16 ingredients. Check your meds →
Dietary supplement

Soursop Bitters Ingredients & Drug Interactions

by Nature's Blooms

Liquid Category: Other Combinations
Most serious interaction: Moderate
The interaction bottom line Most serious interaction: Moderate

Soursop Bitters is a dietary supplement by Nature's Blooms with 16 active ingredients. Its ingredients are commonly taken for joint pain and arthritis, inflammation, digestive upset.Based on those ingredients, 1,564 medications have a known interaction with it, the most serious rated moderate. The ingredients most likely to interact are Ashwagandha Root Extract, Turmeric Root Extract, Black Pepper Extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Soursop Bitters by Nature's Blooms

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

From our pharmacy team — supplement deep dive

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 4 of its 16 active ingredients.
  • “Proprietary Extract Blend” is a proprietary blend — the label gives one combined amount (350 mg) without saying how much of each component you get.

Soursop Bitters by Nature's Blooms contains 16 active ingredients: Senna Leaf Extract, Honey, Turmeric Root Extract, Ashwagandha Root Extract, Black Pepper Extract, Hibiscus Flower Extract, Moringa Leaf Extract, Garlic Bulb Extract, Tamarind Fruit Extract, Cinnamon Bark Extract, Black Seed Extract, Irish Moss Extract, Soursop Leaf Extract, Goat Weed Extract, Lemon Root Extract, and Neem Tree Extract. The product is formulated as a liquid and contains no inactive ingredients listed.

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
Strong

Clinical evidence supports at least one of this product's ingredients for its stated purpose.

Why this rating?
  • The label markets this product for: Digestive health, energy, immune and cellular support.
  • We looked for evidence on: Common cold, Constipation, Bowel preparation, General wellness, Immune function, Energy metabolism — and 1 related terms.
  • The strongest evidence on file: Senna is rated "Likely Effective" for Constipation (Natural Medicines).
  • Also on file: Senna is rated "Possibly Effective" for Bowel preparation.
  • Also on file: Garlic is rated "Insufficient Reliable Evidence To Rate" for Common cold.

The evidence for Soursop Bitters is mixed. Senna Leaf Extract is likely effective for constipation and possibly effective for bowel preparation.

Honey is possibly effective for cough, cold sores, burns, dry eye, and oral mouth sores. Turmeric, Garlic, and Black Seed each show possibly effective evidence for several conditions—turmeric for depression and high cholesterol, garlic for high blood pressure and diabetes, and black seed for asthma and allergies.

Ashwagandha is possibly effective for anxiety, insomnia, and stress. Most of the other ingredients—including Moringa, Cinnamon, Neem, Irish Moss, and Soursop Leaf—have insufficient reliable evidence in our data to rate their effectiveness for any condition.

Lemon Root Extract and Tamarind Fruit Extract also lack established evidence for their listed uses.

The evidence, ingredient by ingredient Turmeric Senna Honey Black Pepper Moringa Garlic Tamarind Cassia Cinnamon

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 13 of the 14 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 14 of 14.
  • General safety write-ups exist for 14 of 14.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Short-term occasional use of Senna is generally well tolerated, but it's not for long-term daily use without medical advice. The most common side effects are abdominal pain, cramps, diarrhea, and nausea.

Honey is generally safe for adults and children over 1 year old, though some people may experience nausea or stomach pain. Turmeric, used in food amounts, is generally well tolerated, but concentrated supplements carry a small risk of liver damage with prolonged use—at least 70 cases have been reported.

Ashwagandha is generally well tolerated short-term but has rare reports of liver injury; the safety data advise against it in pregnancy and while breastfeeding. Black Pepper is generally safe as a food spice.

Garlic is well tolerated as food; supplements may cause stomach upset and increase bleeding risk. Black Seed, Neem, and Soursop Leaf all carry cautions: Black Seed is likely unsafe in pregnancy, Neem may affect fertility and should be avoided in pregnancy, and Soursop Leaf is possibly unsafe in pregnancy due to limited human safety data and lab concerns about nerve toxicity with long-term use.

Irish Moss (Sea Moss) should be avoided in pregnancy and while breastfeeding due to unpredictable iodine content.

Side effects, ingredient by ingredient Turmeric Senna Honey Black Pepper Moringa Garlic Tamarind Cassia Cinnamon

Meds to double-check

Moderate interaction found
Known Interaction Concern · database check
Moderate identified

The most serious documented interaction for these ingredients is Moderate. Check your medications for a personalized result.

Why this rating?
  • 14 of the 14 matched ingredients can interact with medications — Garlic, Lemon, Neem, Senna, Turmeric, among others.
  • The most serious interaction on file is rated Moderate.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 1,565 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 Soursop Bitters, check with your pharmacist or doctor if you take blood thinners (warfarin or others), diabetes medications, blood pressure medications, heart medications (digoxin, amiodarone), seizure medications (carbamazepine, phenytoin), thyroid hormones or antithyroid drugs, immunosuppressants, sedatives or anti-anxiety medications, cancer treatments, or any drug metabolized by your liver. The most serious interactions are Moderate in severity and involve estrogens (birth control), diuretics, sedatives, blood pressure drugs, and immune-related medications.

Check your own medication Run your meds through the checker above

The bottom line

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

Soursop Bitters may appeal to someone seeking a traditional herbal blend, but it's not for everyone—especially if you take medications for blood clotting, heart rhythm, seizures, diabetes, blood pressure, thyroid function, or immune suppression, since multiple ingredients interact with these drugs. If you're pregnant, breastfeeding, or taking any prescription medication, talk to your pharmacist or doctor before starting this product.

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

Assessment coverage: 14 of 16 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jun 25, 2025.

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

At a glance

General information

Key facts about Soursop Bitters, straight from the product label.

Brand Nature's Blooms
Barcode (UPC) 198715197877
Net contents 16 Fluid Ounce(s)
Market status On market
Date entered into DSLD Jun 25, 2025
DSLD ID 336373
Product type Other Combinations
Supplement form Liquid
Dietary claims / uses Nutrient, All Other, Structure/Function
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 Soursop Bitters by Nature's Blooms, 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:
15 mL
Maximum serving Sizes:
15 mL
Servings per container
32
UPC/BARCODE
198715197877
IngredientAmount% DV
Senna Leaf Extract0 NP--
Honey0 NP--
Turmeric Root Extract200 mg--
Proprietary Extract Blend350 mg--
Ashwagandha Root Extract200 mg--
Black Pepper Extract0 NP--
Hibiscus Flower Extract0 NP--
Moringa Leaf Extract0 NP--
Garlic Bulb Extract0 NP--
Tamarind fruit extract0 NP--
Cinnamon Bark Extract0 NP--
Black Seed Extract300 mg--
Irish Moss Extract0 NP--
Soursop Leaf Extract1500 mg--
Goat Weed extract0 NP--
Lemon Root Extract0 NP--
Neem Tree Extract0 NP--

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.
Formula

Potential Benefits Convenience and Effectiveness: Our multi-mineral drink simplifies your daily supplement regimen by combining the benefits of 17 powerful ingredients into one convenient serving. Say goodbye to the need for multiple supplements and hello to streamlined wellness with every sip. Boosts Immune Health: Our soursop supplement is a rich source of vitamin C, supporting a strong immune system, enhancing the body's ability to fight off infections and illnesses to help you stay healthy year-round. Anti-Inflammatory Effects: Our soursop contains compounds with anti-inflammatory properties that may help reduce inflammation in the body, potentially benefiting conditions like arthritis and inflammatory diseases promoting soothing relief and overall wellness. Digestive Health: Our soursop helps in supporting regular bowel movements, preventing constipation and bloating. It may also help improve gut health by nourishing beneficial gut bacteria, aids in gentle detoxification, supporting the body's natural cleansing processes while nurturing colon health for overall well-being. Elevates Energy Naturally: Experience a natural boost with our soursop supplement, due to its high vitamin and mineral content, revitalizing your energy levels for a vibrant lifestyle. Rich in Antioxidants: Our soursop supplement is packed with natural antioxidants to combat oxidative stress and promote overall health and vitality.

Irish sea moss, black seed oil, ashwagandha & turmeric

Suggested/Recommended/Usage/Directions

1 Shake Shake well before use to ensure even distribution of the supplement's ingredients. 2 Pour Carefully pour the suggested amount of 2 tablespoons once daily after meals. 3 Drink Consume as part of your daily routine.

Suggested Use: Take two tablespoons once daily after meals.

Formulation

Multi-Supplement Digestive health, energy, cellular regeneration & immune support benefits

Product of Ghana & Ivory Coast. Processed & packaged in the USA

FDA Statement of Identity

All-In-1 Dietary Supplement

Storage

Warning: Store in a cool, dry place.

Precautions

Keep out of reach of children.

Note: Before taking any new supplement, consult with your health care provider if you have medical conditions, take prescription medications or are pregnant or lactating.

FDA Disclaimer Statement

The statements on this product have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.

General Statements

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Nature's Blooms Bloom Naturally, Thrive Beautifully

See for yourself

Soursop Bitters by Nature's Blooms label

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

What’s inside

The Ingredients in Soursop Bitters by Nature's Blooms

These are the 16 active ingredients this product is made of. Select any to open its full monograph.

Serving size15 mL Dosage formLiquid Servings per container32 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.

Turmeric Root Extract

Interacts with
1,133 drugs
200 mg per serving

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

Turmeric Root Extract monograph & interactions

Proprietary Extract Blend

350 mg per serving

Ashwagandha Root Extract

Interacts with
1,372 drugs
200 mg per serving

Ashwagandha is an Ayurvedic herb most often taken to help with stress, anxiety, and sleep, and some small studies suggest it may help, though the evid...

Ashwagandha Root Extract monograph & interactions

Black Seed Extract

Interacts with
912 drugs
300 mg per serving

Black seed (Nigella sativa) is a traditional spice and remedy that has been studied for asthma, blood sugar, cholesterol, and blood pressure, with ear...

Black Seed Extract monograph & interactions

Soursop Leaf Extract

Interacts with
1 drug
1500 mg per serving

Graviola (soursop) is a tropical fruit tree whose leaves, fruit, and bark are used in traditional medicine, especially in parts of South America, Afri...

Soursop Leaf Extract monograph & interactions
Interaction report

Soursop Bitters by Nature's Blooms Drug Interactions

Want to check YOUR meds against Soursop Bitters?

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

Go to the checker
1,564Drugs
1,564 Moderate

Ingredients driving the most interactions

Each ingredient & the kinds of drugs it affects

For each ingredient in Soursop Bitters 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.

Ashwagandha Root Extract10 drug types · 1,372 drugs

Antidiabetes Drugs

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

Likelihood Possible Evidence B
Antihypertensive Drugs

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

Likelihood Possible Evidence D
Benzodiazepines

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

Likelihood Possible Evidence D
Cns Depressants

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

Likelihood Possible Evidence D
Hepatotoxic Drugs

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

Likelihood Possible Evidence D
Immunosuppressants

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

Likelihood Possible Evidence D
Thyroid Hormone

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

Likelihood Probable Evidence B
Cytochrome P450 1A2 (Cyp1A2) Substrates

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

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

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

Likelihood Possible Evidence D
Serotonergic Drugs

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

Likelihood Possible Evidence C

Turmeric Root Extract24 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

Black Pepper Extract17 drug types · 1,019 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, black pepper might increase the risk of bleeding when taken with antiplatelet or anticoagulant drugs.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit platelet aggregation. This has not been reported in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

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

Likelihood Possible Evidence D
Atorvastatin (Lipitor)

Theoretically, black pepper might increase blood levels of atorvastatin.
Animal research shows that taking piperine, a constituent of black pepper, 35 mg/kg can increase the maximum serum concentration of atorvastatin three-fold. This has not been reported in humans.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, black pepper might increase the effects and side effects of cyclosporine.
In vitro research shows that piperine, a constituent of black pepper, increases the bioavailability of cyclosporine. This has not been reported in humans.

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

Theoretically, black pepper might increase levels of drugs metabolized by CYP2D6.
In vitro research suggests that some constituents of black pepper inhibit CYP2D6. This has not been reported in humans.

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

Theoretically, black pepper might increase levels of drugs metabolized by CYP3A4.
In vitro research and pharmacokinetic simulation data suggest that piperine, a constituent of black pepper, as well as the pepper fruit seem to inhibit CYP3A4. This has not been reported in humans.

Likelihood Possible Evidence D
Lithium

Theoretically, black pepper might increase blood levels of lithium due to its diuretic effects. The dose of lithium might need to be reduced.
Black pepper is thought to have diuretic properties.

Likelihood Probable Evidence D
Nevirapine (Viramune)

Black pepper might increase blood levels of nevirapine.
Clinical research shows that piperine, a constituent of black pepper, increases the plasma concentration of nevirapine. However, no adverse effects were observed in this study.

Likelihood Probable Evidence D
P-Glycoprotein Substrates

Theoretically, black pepper might increase levels of P-glycoprotein substrates.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit P-glycoprotein.

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

Theoretically, black pepper might increase the sedative effects of pentobarbital.
Animal research shows that piperine, a constituent of black pepper, increases pentobarbital-induced sleeping time.

Likelihood Possible Evidence D
Phenytoin (Dilantin)

Black pepper might increase blood levels of phenytoin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption, slow elimination, and increase levels of phenytoin. Taking a single dose of black pepper 1 gram along with phenytoin seems to double the serum concentration of phenytoin. Consuming a soup with black pepper providing piperine 44 mg/200 mL of soup along with phenytoin also seems to increase phenytoin levels when compared with consuming the same soup without black pepper.

Likelihood Possible Evidence B
Propranolol (Inderal)

Black pepper might increase blood levels of propranolol.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of propranolol.

Likelihood Possible Evidence B
Rifampin (Rifadin)

Black pepper might increase blood levels of rifampin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and serum levels of rifampin.

Likelihood Possible Evidence B
Theophylline

Black pepper might increase blood levels of theophylline.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of theophylline.

Likelihood Possible Evidence D
Amoxicillin (Amoxil, Trimox)

Theoretically, black pepper might increase the effects and side effects of amoxicillin.
Animal research shows that taking piperine, a constituent of black pepper, with amoxicillin increases plasma levels of amoxicillin. This has not been reported in humans.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, black pepper might increase blood levels of carbamazepine, potentially increasing the effects and side effects of carbamazepine.
One clinical study in patients taking carbamazepine 300 mg or 500 mg twice daily shows that taking a single 20 mg dose of purified piperine, a constituent of black pepper, increases carbamazepine levels. Piperine may increase carbamazepine absorption by increasing blood flow to the GI tract, increasing the surface area of the small intestine, or inhibiting cytochrome P450 3A4 (CYP3A4) in the gut wall. Absorption was significantly increased by 7-10 mcg/mL/hour. The time to eliminate carbamazepine was also increased by 4-8 hours. Although carbamazepine levels were increased, this did not appear to increase side effects. In vitro research also shows that piperine can increase carbamazepine levels by 11% in a time-dependent manner.

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

Theoretically, black pepper might decrease levels and clinical effects of drugs metabolized by CYP1A2.
In vitro research suggests that black pepper induces CYP1A2. This has not been reported in humans.

Likelihood Possible Evidence D

Neem Tree Extract7 drug types · 1,013 drugs

Antidiabetes Drugs

Neem might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Some clinical research shows that neem can lower blood glucose levels in adults with type 2 diabetes, including those already taking metformin.

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

Theoretically, neem leaf extract might increase the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that neem leaf extract inhibits CYP1A2 enzymes. So far, this reaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C8 (Cyp2C8) Substrates

Theoretically, neem leaf extract might increase the levels and clinical effects of CYP2C8 substrates.
In vitro research shows that neem leaf methanol extract inhibits CYP2C8 enzymes. So far, this reaction has not been reported in humans.

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

Theoretically, neem leaf extract might increase the levels and clinical effects of CYP2C9 substrates.
In vitro research shows that neem leaf methanol extract inhibits CYP2C9 enzymes. So far, this reaction has not been reported in humans.

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

Theoretically, neem leaf extract might increase the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that neem leaf methanol extract inhibits CYP3A4 enzymes. So far, this reaction has not been reported in humans.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, neem might decrease the effectiveness of immunosuppressants.
Animal research suggests that neem might have immunostimulant effects.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, neem leaf extract might increase the levels and clinical effects of P-glycoprotein substrates.
In vitro research shows that neem leaf methanol extract inhibits renal P-glycoprotein transport activity. So far, this reaction has not been reported in humans.

Likelihood Possible Evidence D

Garlic Bulb Extract12 drug types · 989 drugs

Anticoagulant/Antiplatelet Drugs

Garlic may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Raw garlic and a variety of garlic extracts have antiplatelet activity and can increase prothrombin time.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking garlic with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research suggests that garlic and garlic extract lower blood glucose levels in healthy and diabetic individuals.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking garlic with antihypertensive drugs might increase the risk of hypotension.
In human research, both garlic and garlic extracts have blood pressure-lowering effects.

Likelihood Possible Evidence D
Atazanavir (Reyataz)

Theoretically, garlic might decrease levels and effects of atazanavir.
In a case report, a patient consuming six stir-fried garlic cloves three times weekly developed suboptimal atazanavir levels and increases in HIV viral load. While the exact cause of this interaction is unclear, there is speculation that garlic might decrease the intestinal absorption of atazanavir or increase its metabolism by inducing cytochrome P450 3A4 (CYP3A4). Until more is known, advise patients not to consume large amounts of garlic while taking atazanavir.

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

Garlic might increase levels of drugs metabolized by CYP2E1.
Clinical research suggests garlic oil can inhibit the activity of CYP2E1 by 39%. Use garlic oil cautiously in patients taking drugs metabolized by these enzymes.

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

Theoretically, garlic products containing allicin might induce intestinal CYP3A4 and inhibit hepatic CYP3A4. This may increase or decrease levels of drugs metabolized by CYP3A4.
Some human research suggests that garlic may induce INTESTINAL CYP3A4, reducing levels of drugs metabolized by this enzyme. This is primarily based on a study showing that taking a specific allicin-containing garlic product (GarliPure Maximum Allicin Formula, Natrol Inc.) twice daily for 3 days reduces saquinavir levels by approximately 50%. It is speculated that the allicin constituent induced CYP3A4 in the gut mucosa. Another study shows that giving docetaxel intravenously, bypassing the CYP3A4 enzymes in the gut mucosa, along with the same specific garlic product for 12 consecutive days, does not affect docetaxel levels. Conversely, there is concern that garlic may inhibit HEPATIC CYP3A4. In a single case report, increased tacrolimus levels and liver injury occurred in a liver transplant patient after taking a specific garlic supplement (Garlicin Cardio, Nature's Way) at up to three times the manufacturer recommended dose for 7 days. Several other studies have evaluated the impact of other garlic formulations on CYP3A4 substrates and have found no effect. Most of the products in these studies provided little or no allicin.

Likelihood Possible Evidence B
Isoniazid

Theoretically, garlic might decrease levels of isoniazid.
Animal research suggests that an aqueous extract of garlic reduces isoniazid levels by about 65%. Garlic reduced the maximum concentration (Cmax) and area under the curve (AUC), but not the half-life, of isoniazid. This suggests that garlic extract might inhibit isoniazid absorption across the intestinal mucosa; however, the exact mechanism of this potential interaction is not known.

Likelihood Possible Evidence D
Protease Inhibitors (Pis)

Theoretically, garlic products containing allicin might decrease levels of PIs.
Protease inhibitors are metabolized by cytochrome P450 3A4 (CYP3A4) isoenzymes. There is concern that garlic products containing allicin might induce intestinal CYP3A4, reducing plasma levels of protease inhibitors. This is primarily based on a study showing that taking a specific garlic product (GarliPure Maximum Allicin Formula, Natrol Inc.) twice daily for 3 days reduces levels of saquinavir, a PI, by approximately 50%. It is speculated that the allicin constituent induce CYP3A4 in the gut mucosa. Several studies have evaluated the impact of other garlic formulations on CYP3A4 substrates and have found no effect. Most of the products in these studies provided little or no allicin.

Likelihood Possible Evidence B
Saquinavir (Fortovase, Invirase)

Theoretically, garlic containing allicin might decrease levels of saquinavir.
Saquinavir is a substrate of cytochrome P450 3A4 (CYP3A4) isoenzymes. There is concern that garlic products containing allicin might induce intestinal CYP3A4 and cause subtherapeutic levels of saquinavir. This is primarily based on a pharmacokinetic study showing that taking a specific garlic product (GarliPure Maximum Allicin Formula, Natrol Inc.) twice daily for 3 days reduces saquinavir levels by approximately 50%. It is speculated that the allicin constituent induces CYP3A4 in the gut mucosa. Several pharmacokinetic studies have evaluated the impact of other garlic formulations on CYP3A4 substrates and have found no effect. Most of the products in these studies provided little or no allicin. Until more is known about this potential interaction, use garlic containing allicin cautiously in patients taking saquinavir.

Likelihood Possible Evidence B
Sofosbuvir (Sovaldi)

Theoretically, taking garlic with sofosbuvir might decrease its effectiveness.
Animal research in rats shows that giving aged garlic extract 120 mg/kg orally daily for 14 days decreases the area under the concentration time curve (AUC) after a single sofosbuvir dose of 40 mg/kg by 36%, increases the clearance by 63%, and decreases the plasma concentrations at 1 and 8 hours by 35% and 58%, respectively. This interaction is hypothesized to be due to induction of intestinal P-glycoprotein expression by garlic.

Likelihood Possible Evidence D
Tacrolimus (Prograf)

Theoretically, garlic might increase levels of tacrolimus.
In one case report, a liver transplant patient taking tacrolimus experienced increased tacrolimus levels and liver injury after taking a specific garlic supplement (Garlicin Cardio, Nature's Way) at up to three times the manufacturer recommended dose for 7 days. It is speculated that garlic inhibited hepatic cytochrome P450 3A4 (CYP3A4), which increased plasma levels of tacrolimus.

Likelihood Possible Evidence B
Warfarin (Coumadin)

Theoretically, garlic might increase the risk of bleeding with warfarin.
Raw garlic and a variety of garlic extracts have antiplatelet activity and can increase prothrombin time. In addition, there is a report of two patients who experienced an increase in a previously stabilized international normalized ratio (INR) with concomitant garlic and warfarin use. However, this report has been subsequently debated due to limited clinical information. Other clinical studies have not identified an effect of garlic on INR, warfarin pharmacokinetics, or bleeding risk. More evidence is needed to determine the safety of using garlic with warfarin.

Likelihood Possible Evidence D

Black Seed Extract14 drug types · 912 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, black seed may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro and animal research suggests that black seed extract can inhibit platelet aggregation and clotting, and increase bleeding time. In addition, decreased platelet counts have occurred in a human case report and in animal research.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking black seed with antidiabetes drugs might increase the risk of hypoglycemia.
Some clinical research and numerous animal studies suggest that black seed, especially its constituent thymoquinone, can have hypoglycemic effects.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking black seed with antihypertensive drugs might increase the risk of hypotension.
Clinical research suggests that black seed powder and oil might reduce blood pressure by 2-3 mmHg. In animal research, black seed modestly reduces blood pressure and concomitant use of black seed and amlodipine (Norvasc) or metoprolol (Lopressor) increased the blood pressure lowering effects of these drugs.

Likelihood Possible Evidence B
Clopidogrel (Plavix)

Theoretically, black seed may increase the risk of bleeding if used with clopidogrel.
Animal research shows that taking black seed extract daily for 2 weeks prior to a single dose of clopidogrel increases maximum concentrations of clopidogrel by approximately 31% and modestly decreases oral clearance. Furthermore, bleeding time was increased by 12%. This has not been shown in humans.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, concomitant use with drugs that have sedative properties may cause additive effects.
Animal research suggests that black seed may have CNS depressant effects.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically taking black seed might reduce the levels and clinical effects of cyclosporine.
In animal research, black seed extract decreased the maximal levels of cyclosporine in the blood by 35.5%. This has not been shown in humans.

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

Theoretically, black seed might increase levels of drugs metabolized by CYP2C9.
In vitro research suggests that thymoquinone, a constituent of black seed, can decrease the metabolism of phenytoin by a mechanism possibly related to the inhibition of CYP2C9. The effect of black seed on CYP2C9 is unclear. This has not been shown in humans.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, taking black seed with diuretic drugs might increase potassium loss and the risk of hypokalemia.
Black seed extract has shown diuretic effects in animals, which could theoretically increase potassium loss. This has not been shown in humans.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, black seed might interfere with immunosuppressive therapy.
Animal and in vitro studies suggest that black seed might stimulate immune function. However, other animal studies suggest that black seed may suppress immune function.

Likelihood Possible Evidence D
Phenytoin (Dilantin)

Theoretically, black seed might increase or decrease levels and effects of phenytoin.
In vitro research suggests that thymoquinone, a constituent of black seed, can decrease the metabolism of phenytoin. This effect may be due to inhibition of cytochrome P450 2C9 (CYP2C9). However, animal research shows that black seed decreases the maximum concentration of and total systemic exposure to phenytoin by 57% and 87%, respectively. This seems to be related to increased clearance and steady state volume of distribution. This interaction has not been shown in humans.

Likelihood Possible Evidence D
Serotonergic Drugs

Theoretically, combining serotonergic drugs with black seed might increase the risk of serotonergic side effects, including serotonin syndrome and cerebral vasoconstrictive disorders.
Animal research suggests that black seed can increase brain serotonin levels. In one case report, a 35-year-old man undergoing endoscopic surgery experienced immediate postoperative serotonin syndrome that was likely associated with the use of black seed oil 600 mg daily starting 4 days before surgery, and precipitated by the use of serotonergic pain medications, including fentanyl and oxycodone. Monitor patients for signs of serotonin syndrome and other serotonergic side effects if using black seed with serotonergic drugs.

Likelihood Possible Evidence D
Sildenafil (Viagra)

Theoretically, black seed might reduce plasma levels and the therapeutic effects of sildenafil.
Animal research shows that black seed reduces the total systemic exposure to sildenafil by 43%. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, black seed might increase levels of warfarin and increase the risk of bleeding.
In vitro research suggests that thymoquinone, a constituent of black seed, can decrease the metabolism of warfarin. This effect may be due to inhibition of cytochrome P450 2C9 (CYP2C9). The effect of black seed on warfarin metabolism is unclear. This has not been shown in humans.

Likelihood Possible Evidence D
Prednisolone

Theoretically black seed might reduce plasma levels and therapeutic effects of prednisolone.
In animal research, oral administration of a single dose of black seed oil 15 minutes prior to oral prednisolone decreases the prednisolone maximum plasma concentration by 65% and area under the curve by 25%. This has not been shown in humans.

Likelihood Possible Evidence D

Moringa Leaf Extract6 drug types · 869 drugs

Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, moringa might increase or decrease levels of CYP3A4 substrates.
Some in vitro research suggests that moringa inhibits cytochrome P450 3A4 (CYP3A4). However, other in vitro research suggests that moringa extract induces CYP3A4 enzymes. A pharmacokinetic study in patients with HIV shows no change in the pharmacokinetics of nevirapine, which is partially metabolized by CYP3A4, when administered concomitantly with moringa leaf powder 1.85 grams daily for 14 days.

Likelihood Possible Evidence D
Levothyroxine (Synthroid, Others)

Theoretically, moringa leaf can antagonize the effects of levothyroxine.
Animal research suggests that moringa aqueous leaf extract might reduce serum triiodothyronine (T3) concentrations by inhibiting the peripheral conversion of thyroxine (T4) to T3.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, moringa leaf extract might increase the levels and clinical effects of P-glycoprotein substrates.
In vitro research shows that moringa leaf extract inhibits renal P-glycoprotein transport activity. So far, this reaction has not been reported in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, moringa might have additive effects when used with antidiabetes drugs; however, research is conflicting.
Animal research shows that moringa can lower blood glucose levels. However, research in humans has not shown consistent blood glucose lowering effects.

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

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

Likelihood Possible Evidence D
Nevirapine (Viramune)

Moringa leaf is unlikely to have a clinically significant interaction with nevirapine.
Nevirapine is partially metabolized by cytochrome P450 3A4 (CYP3A4). In vitro evidence suggests that moringa inhibits CYP3A4. However, a pharmacokinetic study in patients with HIV shows no change in nevirapine pharmacokinetics when administered concomitantly with moringa leaf powder 1.85 grams daily for 14 days.

Likelihood Unlikely Evidence B

Honey3 drug types · 736 drugs

Phenytoin (Dilantin)

Theoretically, honey might increase levels of phenytoin.
In an animal model, the rate and extent of absorption of phenytoin was increased by honey. This effect has not been reported in humans.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, honey may increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
In vitro, honey inhibits platelet aggregation and increases the time to clotting. Furthermore, animal research suggests that feeding mice large doses of honey for 12 days increases bleeding time when compared with no intervention. However, these effects have not been reported in humans.

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

Theoretically, honey might decrease levels of drugs metabolized by CYP3A4, but research is conflicting.
Some clinical research shows that honey induces CYP3A4. However, other clinical studies found no effect on CYP3A4 activity. Different honey preparations may have different effects on CYP3A4.

Likelihood Possible Evidence B

Cinnamon Bark Extract2 drug types · 442 drugs

Antidiabetes Drugs

Theoretically, cassia cinnamon may have additive effects with antidiabetes drugs.
Cassia cinnamon may lower blood glucose levels, and have additive effects in patients treated with antidiabetic agents. Dose adjustments to diabetes medications might be necessary.

Likelihood Possible Evidence B
Hepatotoxic Drugs

Theoretically, large doses of cassia cinnamon might cause additive effects when used with hepatotoxic drugs.
There is some concern that ingesting large amounts of cassia cinnamon for an extended duration might cause hepatotoxicity in some people. Cassia cinnamon contains coumarin, which can cause hepatotoxicity in animal models. In humans, very high doses of coumarin from 50-7000 mg/day can result in hepatotoxicity that resolves when coumarin use is discontinued. Lower amounts might also cause liver problems in sensitive people, such as those with liver disease or those taking potentially hepatotoxic agents.

Likelihood Possible Evidence D

Senna Leaf Extract5 drug types · 140 drugs

Digoxin (Lanoxin)

Theoretically, senna might increase the risk of adverse effects when taken with digoxin.
Overuse/abuse of senna increases the risk of adverse effects from cardiac glycosides, such as digoxin, due to potassium depletion.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, senna might increase the risk of hypokalemia when taken with diuretic drugs.
Overuse of senna might compound diuretic-induced potassium loss and increase the risk for hypokalemia.

Likelihood Possible Evidence D
Estrogens

Theoretically, taking senna may interfere with the absorption of exogenous estrogens.
Some preliminary clinical evidence suggests that senna reduces the absorption of estradiol and decreases serum concentrations of estrone and estrone sulfate by decreasing intestinal transit time.

Likelihood Possible Evidence B
Stimulant Laxatives

Theoretically, senna might increase the risk for fluid and electrolyte loss when taken with other stimulant laxatives.
Senna is a stimulant laxative; concomitant use with other stimulant laxatives might compound fluid and electrolyte loss.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, excessive use of senna might increase the effects of warfarin.
Senna 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. In one case report, excessive use of senna for 3 weeks resulted in diarrhea, bloody stools, and an elevated INR of 11.9.

Likelihood Possible Evidence D

Tamarind fruit extract3 drug types · 130 drugs

Antidiabetes Drugs

Theoretically, tamarind seed extract might have additive effects when used with antidiabetes drugs.
Animal research suggests that an extract of tamarind seed can reduce fasting blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Aspirin

Theoretically, tamarind fruit extract might increase the effects and side effects of aspirin.
Taking tamarind fruit extract as a component of millet porridge concurrently with aspirin seems to increase aspirin absorption and blood levels.

Likelihood Possible Evidence B
Ibuprofen (Advil, Others)

Theoretically, tamarind fruit extract might increase the effects and side effects of ibuprofen.
Taking tamarind fruit extract as a component of millet porridge concurrently with ibuprofen seems to increase ibuprofen absorption and blood levels.

Likelihood Possible Evidence B

Irish Moss Extract3 drug types · 22 drugs

Amiodarone (Cordarone)

Theoretically, combining sea moss with amiodarone might cause excessively high iodine levels.
Amiodarone contains 37.3% iodine and can increase iodine levels. Concomitant use with sea moss, which contains approximately 4-7 mcg of iodine per gram, might increase the risk of adverse effects from iodine, including altered thyroid function.

Likelihood Possible Evidence D
Antithyroid Drugs

Due to its iodine content, sea moss might alter the effects of antithyroid drugs.
Sea moss contains approximately 4-7 mcg of iodine per gram. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Taking sea moss could theoretically alter the effects of antithyroid drugs.

Likelihood Possible Evidence D
Thyroid Hormone

Due to its iodine content, sea moss might alter the effects of thyroid hormone.
Sea moss contains approximately 4-7 mcg of iodine per gram. Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Taking sea moss could theoretically alter the effects of thyroid hormone.

Likelihood Possible Evidence D

Lemon Root Extract1 drug type · 1 drug

Itraconazole (Sporanox)

Theoretically, taking itraconazole capsules or tablets with a beverage containing lemon might increase the levels and clinical effects of itraconazole.
In one case report, dissolving itraconazole tablets in a small amount of specific beverages containing lemon prior to administration increased the level of itraconazole in a lung transplant patient. In this case, the increased bioavailability was desirable and was likely due to improved tablet dissolution in the acidic beverage.

Likelihood Possible Evidence D

Soursop Leaf Extract1 drug type · 1 drug

Carbamazepine (Tegretol)

Theoretically, graviola might decrease concentrations of carbamazepine when used concomitantly.
A study in rats shows that graviola extract reduces the area under the curve of carbamazepine by 46% and maximum concentration by 35% when compared with carbamazepine alone.

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for Soursop Bitters, from the product label.

Nature's Blooms

See all Nature's Blooms products
Name
Nature's Blooms LLC
City
Bronx
State
NY
ZipCode
10467
Web Address
www.natures-blooms.com
Pharmacist Counseling Corner

Soursop Bitters by Nature's Blooms: Common Questions

Does Soursop Bitters by Nature's Blooms interact with any medications?
Yes. Based on its ingredients, Soursop Bitters has a known interaction with 1,564 medications. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Soursop Bitters contains 16 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 Soursop Bitters safe to take while I'm pregnant or breastfeeding?
No, it's not recommended. Ashwagandha, Black Seed, Neem, and Soursop Leaf are all likely unsafe or possibly unsafe in pregnancy, and most have insufficient or cautionary data for breastfeeding. Talk to your doctor or pharmacist before using this product if you're pregnant or nursing.
What is senna in this product supposed to do?
Senna Leaf Extract is a stimulant laxative. It's likely effective for treating constipation and possibly effective to prepare the bowel before medical procedures. It works by speeding up intestinal movement, which is why the most common side effects are cramps, diarrhea, and abdominal pain.
Does this bitters really help with digestion?
Some of the ingredients—turmeric, ginger, and garlic—have evidence suggesting they may help with digestion-related symptoms, but the data in our files don't establish that the combination in this product works for digestion overall. Senna will promote bowel movements, but that's different from aiding healthy digestion.
Can I take this if I'm on blood thinners like warfarin?
No, not without talking to your doctor first. Both Senna and Garlic can increase the effects of warfarin and raise your bleeding risk. Your doctor may need to adjust your dose or monitor you more closely if you use both.
What are the most common side effects of senna in this product?
The most common side effects from Senna are abdominal pain, cramps, diarrhea, and nausea. Serious side effects are rare but can include skin reactions. Because senna is a strong laxative, it's meant for short-term use only, not daily long-term use.
Is there any iodine in this bitters?
Yes. Irish Moss Extract (Sea Moss) contains approximately 4–7 micrograms of iodine per gram. If you have thyroid disease or take thyroid or antithyroid medications, this could affect how those drugs work, so check with your pharmacist first.

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

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Label information is sourced from the NIH Dietary Supplement Label Database and reflects the product version on file; always read your actual product label. This page is for education only and is not a substitute for professional medical advice. Confirm with your pharmacist or doctor before combining supplements and medications.

Soursop Bitters label
Go deeper

The Full Monographs Behind Soursop Bitters’s Ingredients

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

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

Senna

Interacts with 140 drugs

Senna is a plant-based stimulant laxative that is widely used and generally effective for short-term relief of constipation. It is best used occasionally and for only a few days at a time, s...

Read the full Senna monograph →
Herb & supplement monograph

Honey

Interacts with 736 drugs

Honey is a natural food with some real, modest evidence for easing coughs and helping certain wounds, especially when special medical-grade or Manuka honey is used. It is generally safe for...

Read the full Honey monograph →
Herb & supplement monograph

Black Pepper

Interacts with 1,019 drugs

Black pepper is a common kitchen spice that is generally safe in the amounts used in food. Its extract, piperine, is mostly added to supplements to help the body absorb other ingredients (li...

Read the full Black Pepper monograph →
Herb & supplement monograph

Moringa

Interacts with 869 drugs

Moringa is a nutrient-rich plant whose leaves are widely used as a food and supplement, especially in parts of the world where malnutrition is common. Early research hints at possible benefi...

Read the full Moringa monograph →
Herb & supplement monograph

Garlic

Interacts with 989 drugs

Garlic is a common food and supplement that may modestly help with blood pressure and cholesterol, though the evidence is mixed and effects are usually small. It is generally safe in food am...

Read the full Garlic monograph →
Herb & supplement monograph

Tamarind

Interacts with 130 drugs

Tamarind is a tangy tropical fruit widely used in cooking and traditional medicine, mainly for digestion and as a mild laxative. While it is a nutritious food, strong human evidence for most...

Read the full Tamarind monograph →
Herb & supplement monograph

Cassia Cinnamon

Interacts with 442 drugs

Cassia cinnamon is the common, inexpensive cinnamon used in cooking, and it is also taken as a supplement, most often for blood sugar support. The evidence for its health benefits is mixed a...

Read the full Cassia Cinnamon monograph →
Herb & supplement monograph

Sea Moss

Interacts with 22 drugs

Sea moss is a type of red seaweed that is naturally rich in iodine and several minerals, and it is popular as a 'whole-food' supplement. Strong human evidence for most of its health claims i...

Read the full Sea Moss monograph →
Herb & supplement monograph

Lemon

Interacts with 1 drug

Lemon is a common citrus fruit that is a good source of vitamin C and citric acid, and it is widely used in food, drinks, and home remedies. While it can support hydration and a healthy diet...

Read the full Lemon monograph →
Herb & supplement monograph

Neem

Interacts with 1,013 drugs

Neem is a tree from India used for centuries in traditional medicine, especially for skin, dental, and antimicrobial purposes. Some small studies are promising for oral health and skin, but...

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Herb & supplement monograph

Ashwagandha

Interacts with 1,372 drugs

Ashwagandha is an Ayurvedic herb most often taken to help with stress, anxiety, and sleep, and some small studies suggest it may help, though the evidence is still limited. It is generally w...

Read the full Ashwagandha monograph →
Herb & supplement monograph

Black Seed

Interacts with 912 drugs

Black seed (Nigella sativa) is a traditional spice and remedy that has been studied for asthma, blood sugar, cholesterol, and blood pressure, with early research showing some promise but no...

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Herb & supplement monograph

Graviola

Interacts with 1 drug

Graviola (soursop) is a tropical fruit tree whose leaves, fruit, and bark are used in traditional medicine, especially in parts of South America, Africa, and Asia. Despite popular online cla...

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Sources

Sources & How We Checked

Soursop Bitters'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 542 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.

Senna 42 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. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  3. American Academy of Pediatrics. The transfer of drugs and other chemicals into human milk. Pediatrics 2001;108:776-89. PubMed
  4. Nusko G, Schneider B, Schneider I, et al. Anthranoid laxative use is not a risk factor for colorectal neoplasia: results of a prospective case control study. Gut 2000;46:651-5. PubMed
  5. Seybold U, Landauer N, Hillebrand S, Goebel FD. Senna-induced hepatitis in a poor metabolizer. Ann Intern Med 2004;141:650-1. PubMed
  6. Vanderperren B, Rizzo M, Angenot L, et al. Acute liver failure with renal impairment related to the abuse of senna anthraquinone glycosides. Ann Pharmacother 2005;39:1353-7. PubMed
  7. Xing JH, Soffer EE. Adverse effects of laxatives. Dis Colon Rectum 2001;44:1201-9. PubMed
  8. Prior J, White I. Tetany and clubbing in patient who ingested large quantities of senna. Lancet 1978;2:947. PubMed
  9. Langmead L, Rampton DS. Review article: herbal treatment in gastrointestinal and liver disease--benefits and dangers. Aliment Pharmacol Ther 2001;15:1239-52. PubMed
  10. Joo JS, Ehrenpreis ED, Gonzalez L, et al. Alterations in colonic anatomy induced by chronic stimulant laxatives: the cathartic colon revisited. J Clin Gastroenterol 1998;26:283-6. PubMed
  11. Godding EW. Laxatives and the special role of senna. Pharmacology 1988;36:230-6. PubMed
  12. van Os FH. Anthraquinone derivatives in vegetable laxatives. Pharmacology 1976;14:7-17. PubMed
  13. Sondheimer JM, Gervaise EP. Lubricant versus laxative in the treatment of chronic functional constipation of children: a comparative study. J Pediatr Gastroenterol Nutr 1982;1:223-6. DOI
  14. Perkin JM. Constipation in childhood: a controlled comparison between lactulose and standardized senna. Curr Med Res Opin 1977;4:540-3. PubMed
  15. Shelton MG. Standardized senna in the management of constipation in the puerperium: A clinical trial. S Afr Med J 1980;57:78-80.
  16. [No authors listed] Senna in the puerperium. Pharmacology 1992;44:23-5. PubMed
  17. Passmore AP, Davies KW, Flanagan PG, et al. A comparison of Agiolax and lactulose in elderly patients with chronic constipation. Pharmacology 1993;47:249-52. PubMed
  18. Passmore AP, Wilson-Davies K, Stoker C, Scott ME. Chronic constipation in long stay elderly patients: a comparison of lactulose and a senna-fibre combination. BMJ 1993;307:769-71. PubMed
  19. MacLennan WJ, Pooler AFWM. A comparison of sodium picosulphate ("Laxoberal") with standardised senna ("Senokot") in geriatric patients. Curr Med Res Opin. 1974;2:641-7. PubMed
  20. Kittisupamongkol W, Nilaratanakul V, Kulwichit W. Near-fatal bleeding, senna, and the opposite of lettuce. Lancet 2008;371:784. PubMed
  21. Prather CM. Pregnancy-related constipation. Curr Gastroenterol Rep 2004;6:402-4. PubMed
  22. Werthmann WM Jr, Krees SV. Quantitative excretion of Senokot in human breast milk. Med Ann Dist Columbia 1973;42:4-5.
  23. Hagemann TM. Gastrointestinal medications and breastfeeding. J Hum Lact 1998;14:259-62. PubMed
  24. Faber P, Strenge-Hesse A. Senna-containing laxatives: excretion in the breast milk? Geburtshilfe Frauenheilkd 1989;49:958-62.
  25. Faber P, Strenge-Hesse A. Relevance of rhein excretion into breast milk. Pharmacology 1988;36 Suppl 1:212-20. PubMed
  26. Duncan AS. Standardized senna as a laxative in the puerperium; a clinical assessment. Br Med J 1957;1:439-41. PubMed
  27. Stickel, F. and Schuppan, D. Herbal medicine in the treatment of liver diseases. Dig.Liver Dis. 2007;39(4):293-304. PubMed
  28. BALDWIN, W. F. CLINICAL STUDY OF SENNA ADMINISTRATION TO NURSING MOTHERS: ASSESSMENT OF EFFECTS ON INFANT BOWEL HABITS. Can.Med Assoc.J 9-14-1963;89:566-568. DOI
  29. Sonmez, A., Yilmaz, M. I., Mas, R., Ozcan, A., Celasun, B., Dogru, T., Taslipinar, A., and Kocar, I. H. Subacute cholestatic hepatitis likely related to the use of senna for chronic constipation. Acta Gastroenterol.Belg. 2005;68(3):385-387.
  30. Beuers, U., Spengler, U., and Pape, G. R. Hepatitis after chronic abuse of senna. Lancet 2-9-1991;337(8737):372-373. PubMed
  31. Lim, A. K., Hooke, D. H., and Kerr, P. G. Anorexia nervosa and senna misuse: nephrocalcinosis, digital clubbing and hypertrophic osteoarthropathy. Med J Aust. 1-21-2008;188(2):121-122. PubMed
  32. McLaughlin, A. F. Anorexia nervosa and senna misuse: nephrocalcinosis, digital clubbing and hypertrophic osteoarthropathy. Med J Aust. 9-15-2008;189(6):348. PubMed
  33. Soyuncu, S., Cete, Y., and Nokay, A. E. Portal vein thrombosis related to Cassia angustifolia. Clin.Toxicol.(Phila) 2008;46(8):774-777.
  34. Levine, D., Goode, A. W., and Wingate, D. L. Purgative abuse associated with reversible cachexia, hypogammaglobulinaemia, and finger clubbing. Lancet 4-25-1981;1(8226):919-920. PubMed
  35. Malmquist, J., Ericsson, B., Hulten-Nosslin, M. B., Jeppsson, J. O., and Ljungberg, O. Finger clubbing and aspartylglucosamine excretion in a laxative-abusing patient. Postgrad.Med J 1980;56(662):862-864. PubMed
  36. Lewis, S. J., Heaton, K. W., Oakey, R. E., and McGarrigle, H. H. Lower serum oestrogen concentrations associated with faster intestinal transit. Br.J Cancer 1997;76(3):395-400. PubMed
  37. Lewis, S. J., Oakey, R. E., and Heaton, K. W. Intestinal absorption of oestrogen: the effect of altering transit-time. Eur.J Gastroenterol.Hepatol. 1998;10(1):33-39. PubMed
  38. Vilanova-Sanchez A, Gasior AC, Toocheck N, et al. Are Senna based laxatives safe when used as long term treatment for constipation in children? J Pediatr Surg 2018;53(4):722-7. PubMed
  39. Cogley K, Echevarria A, Correa C, De la Torre-Mondragón L. Contact Burn with Blister Formation in Children Treated with Sennosides. Pediatr Dermatol 2017;34(2):e85-e88. PubMed
  40. Coskun Y, Yuksel I. Polyethylene glycol versus split high-dose senna for bowel preparation: A comparative prospective randomized study. J Gastroenterol Hepatol 2020;35(11):1923-1929.
  41. Haoudar A, Chekhlabi N, El Kettani C, Dini N. Acute Hepatitis and Pancytopenia in a Child With Chronic Abuse of Senna. Cureus 2021;13(1):e12436. PubMed
  42. Irazábal B, Sánchez de Vicente J, Galán C, et al. Anaphylaxis Due to Senna (Cassia angustifolia). J Investig Allergol Clin Immunol 2021;31(1):71-73. PubMed

See these in context on the Senna monograph →

Honey 40 references
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  3. Bose B. Honey or sugar in treatment of infected wounds? Lancet 1982;1:963. PubMed
  4. Ozhan H, Akdemir R, Yazici M, et al. Cardiac emergencies caused by honey ingestion: a single centre experience. Emerg Med J 2004;21:742-4. PubMed
  5. Centers for Disease Control. Botulism in the Unites Sates, 1899-1996. Handbook for epidemiologists, clinicians, and laboratory workers, 1998. Available online: http://www.cdc.gov/ncidod/dbmd/diseaseinfo/botulism.PDF.
  6. Simon A, Traynor K, Santos K, et al. Medical honey for wound care - still the 'latest resort'? Evid Based Complement Alternat Med 2009;6:165-73. PubMed
  7. Gethin G, Cowman S. Case series of use of Manuka honey in leg ulceration. Int Wound J 2005;2:10-15. PubMed
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  9. Johnson DW, van Eps C, Mudge DW, et al. Randomized, controlled trial of topical exit-site application of honey (Medihoney) versus mupirocin for the prevention of catheter-associated infections in hemodialysis patients. J Am Soc Nephrol 2005;16:1456-62. PubMed
  10. Sukriti and Garg, S. K. Influence of honey on the pharmacokinetics of phenytoin in rabbits. Ind J Pharmacol 2002;34(147).
  11. Jung, A. and Ottosson, J. [Infantile botulism caused by honey]. Ugeskr Laeger 2001;163(2):169.
  12. Gunduz, A., Turedi, S., Uzun, H., and Topbas, M. Mad honey poisoning. Am J Emerg.Med 2006;24(5):595-598.
  13. van der Vorst, M. M., Jamal, W., Rotimi, V. O., and Moosa, A. Infant botulism due to consumption of contaminated commercially prepared honey. First report from the Arabian Gulf States. Med Princ.Pract. 2006;15(6):456-458. PubMed
  14. Tushar, T., Vinod, T., Rajan, S., Shashindran, C., and Adithan, C. Effect of honey on CYP3A4, CYP2D6 and CYP2C19 enzyme activity in healthy human volunteers. Basic Clin Pharmacol Toxicol 2007;100(4):269-272. PubMed
  15. Nilforoushzadeh, M. A., Jaffary, F., Moradi, S., Derakhshan, R., and Haftbaradaran, E. Effect of topical honey application along with intralesional injection of glucantime in the treatment of cutaneous leishmaniasis. BMC Complement Altern Med 2007;7:13. PubMed
  16. Koca, I. and Koca, A. F. Poisoning by mad honey: a brief review. Food Chem Toxicol 2007;45(8):1315-1318. PubMed
  17. Akinci, S., Arslan, U., Karakurt, K., and Cengel, A. An unusual presentation of mad honey poisoning: acute myocardial infarction. Int J Cardiol 2008;129(2):e56-e58. PubMed
  18. Yildirim, N., Aydin, M., Cam, F., and Celik, O. Clinical presentation of non-ST-segment elevation myocardial infarction in the course of intoxication with mad honey. Am J Emerg Med 2008;26(1):108.e-2. PubMed
  19. Shrestha, P., Vaidya, R., and Sherpa, K. Mad honey poisoning: a rare case report of seven cases. Nepal Med Coll J 2009;11(3):212-213.
  20. Fetzner, L., Burhenne, J., Weiss, J., Völker, M., Unger, M., Mikus, G., and Haefeli, W. E. Daily honey consumption does not change CYP3A activity in humans. J Clin Pharmacol 2011;51(8):1223-1232. PubMed
  21. Thamboo, A., Thamboo, A., Philpott, C., Javer, A., and Clark, A. Single-blind study of manuka honey in allergic fungal rhinosinusitis. J Otolaryngol Head Neck Surg 2011;40(3):238-243.
  22. Ahmed, A., Khan, R. A., Azim, M. K., Saeed, S. A., Mesaik, M. A., Ahmed, S., and Imran, I. Effect of natural honey on human platelets and blood coagulation proteins. Pak.J Pharm Sci 2011;24(3):389-397.
  23. Yarlioglues, M., Akpek, M., Ardic, I., Elcik, D., Sahin, O., and Kaya, M. G. Mad-honey sexual activity and acute inferior myocardial infarctions in a married couple. Tex.Heart Inst.J 2011;38(5):577-580.
  24. Biberoglu, S., Biberoglu, K., and Komsuoglu, B. Mad honey. JAMA 4-1-1988;259(13):1943.
  25. Biberoglu, K., Biberoglu, S., and Komsuoglu, B. Transient Wolff-Parkinson-White syndrome during honey intoxication. Isr.J.Med.Sci. 1988;24(4-5):253-254.
  26. Gössinger, H., Hruby, K., Pohl, A., Davogg, S., Sutterlütti, G., and Mathis, G. [Poisoning with andromedotoxin-containing honey]. Dtsch Med Wochenschr 1983;108(41):1555-1558.
  27. Fenicia, L., Ferrini, A. M., Aureli, P., and Pocecco, M. A case of infant botulism associated with honey feeding in Italy. Eur J Epidemiol 1993;9(6):671-673. PubMed
  28. Sutlupinar, N., Mat, A., and Satganoglu, Y. Poisoning by toxic honey in Turkey. Arch.Toxicol. 1993;67(2):148-150. PubMed
  29. von Malottki, K. and Wiechmann, H. W. [Acute life-threatening bradycardia: food poisoning by Turkish wild honey]. Dtsch.Med.Wochenschr. 7-26-1996;121(30):936-938.
  30. Abdulla CO, Ayubi A, Zulfiquer F, Santhanam G, Ahmed MA, Deeb J. Infant botulism following honey ingestion. BMJ Case Rep. 2012 Sep 7;2012.
  31. Johnson DW, Badve SV, Pascoe EM, Beller E, Cass A, Clark C, de Zoysa J, Isbel NM, McTaggart S, Morrish AT, Playford EG, Scaria A, Snelling P, Vergara LA, Hawley CM; HONEYPOT Study Collaborative Group. Antibacterial honey for the prevention of peritoneal-d
  32. Matos D, Serrano P, Menezes Brandão F. A case of allergic contact dermatitis caused by propolis-enriched honey. Contact Dermatitis. 2015 Jan;72(1):59-60. PubMed
  33. Oduwole O, Meremikwu MM, Oyo-Ita A, Udoh EE. Honey for acute cough in children. Cochrane Database Syst Rev. 2014 Dec 23;12:CD007094. PubMed
  34. Vezir E, Kaya A, Toyran M, Azkur D, Dibek Misirlioglu E, Kocabas CN. Anaphylaxis/angioedema caused by honey ingestion. Allergy Asthma Proc. 2014 Jan-Feb;35(1):71-4. PubMed
  35. Wang YT, Qi Y, Tang FY, et al. The effect of cupping therapy for low back pain: A meta-analysis based on existing randomized controlled trials. J Back Musculoskelet Rehabil. 2017;30(6):1187-1195. PubMed
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  37. Wong D, Albietz JM, Tran H, et al. Treatment of contact lens related dry eye with antibacterial honey. Cont Lens Anterior Eye. 2017;40(6):389-393. PubMed
  38. Martina SJ, Ramar LAP, Silaban MRI, Luthfi M, Govindan PAP. Antiplatelet Effectivity between Aspirin with Honey on Cardiovascular Disease Based on Bleeding Time Taken on Mice. Open Access Maced J Med Sci. 2019 Oct 14;7(20):3416-3420. PubMed
  39. Jhawar N, Gonzalez-Estrada A. Honey-induced anaphylaxis in an adult. QJM 2022;115(5):325-326. PubMed
  40. Di Costanzo M, De Paulis N, Peveri S, Montagni M, Berni Canani R, Biasucci G. Anaphylaxis caused by artisanal honey in a child: a case report. J Med Case Rep 2021;15(1):235. PubMed

See these in context on the Honey monograph →

Turmeric 102 references
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  13. Monera-Penduka TG, Maponga CC, Wolfe AR, Wiesner L, Morse GD, Nhachi CF. Effect of Moringa oleifera Lam. leaf powder on the pharmacokinetics of nevirapine in HIV-infected adults: a one sequence cross-over study. AIDS Res Ther. 2017;14:12. doi: 10.1186/s1 PubMed
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  15. Nur R, Demak IPK, Radhiah S, Rusydi M, Mantao E, Larasati RD. The effect of moringa leaf extracton increasing hemoglobin and bodyweight in post-disaster pregnant women. Enferm Clin. 2020;30 Suppl 4:79-82. DOI
  16. Taweerutchana R, Lumlerdkij N, Vannasaeng S, Akarasereenont P, Sriwijitkamol A. Effect of Moringa oleifera Leaf Capsules on Glycemic Control in Therapy-Naïve Type 2 Diabetes Patients: A Randomized Placebo Controlled Study. Evid Based Complement Alternat M
  17. Sumiaty, Tahir A, Burhanuddin B, Nurhaedar J, Veni H. The effect of moringa leaves on pregnancy on growth and morbidity of 6-11 month. Enferm Clin. 2020;30 Suppl 4:104-108. DOI
  18. Ulmy MN, Tahir A, Arsunan AA, Burhanuddin B, Veni H. Effect of moringa leaves during pregnancy on growth and morbidity in 0-5 months. Enferm Clin. 2020;30 Suppl 4:61-65. DOI
  19. Amaeze O, Marques ES, Wei W, et al. Evaluation of Nigerian Medicinal Plants Extract on Human P-glycoprotein and Cytochrome P450 Enzyme Induction: Implications for Herb-drug Interaction. Curr Drug Metab. 2021;22(14):1103-1113. PubMed
  20. Ebhohon E, Miller D. Moringa Oleifera leaf extract induced pulmonary embolism-a case report. Int J Emerg Med 2022;15(1):16. PubMed
  21. Basri H, Hadju V, Zulkifli A, Syam A, Indriasari R. Effect of Moringa oleifera supplementation during pregnancy on the prevention of stunted growth in children between the ages of 36 to 42 months. J Public Health Res 2021;10(2):2207.
  22. Haron MH, Dale O, Martin K, et al. Evaluation of the Herb-Drug Interaction Potential of Commonly Used Botanicals on the US Market with Regard to PXR- and AhR-Mediated Influences on CYP3A4 and CYP1A2. J Diet Suppl 2022. PubMed
  23. Amsler E, Mahevas T, Soria A, Barbaud A. Fixed food eruption to Moringa oleifera. Contact Dermatitis 2023;89(4):301-302.

See these in context on the Moringa monograph →

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

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