Major interaction on record — check this product against your medications before combining. Based on 8 of 10 ingredients. Check your meds →
Dietary supplement

Cruciferous Plus Ingredients & Drug Interactions

by NeoLife Nutritionals

Tablet Or Pill Category: Botanical
Most serious interaction: Major
The interaction bottom line Most serious interaction: Major

Cruciferous Plus is a dietary supplement by NeoLife Nutritionals with 10 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, 1,275 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Deglycyrrhizinated Licorice root extract, Soymilk powder, Orange Fruit Extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Cruciferous Plus by NeoLife Nutritionals

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 1 of its 10 active ingredients.
  • “Cruciferous Plus Blend” is a proprietary blend — the label gives one combined amount (525 mg) without saying how much of each component you get.

Cruciferous Plus contains 10 active and inactive ingredients. The active ones are sodium, deglycyrrhizinated licorice root extract (licorice with the potent compound glycyrrhizin removed), soymilk powder, a proprietary cruciferous blend, broccoli aerial parts extract, radish seed extract, kale aerial parts extract, orange fruit extract, mustard seed extract, mustard seed concentrate, and watercress aerial parts concentrate.

The inactive ingredients are microcrystalline cellulose, calcium carbonate, rice starch, sodium croscarmellose, stearic acid, silicon dioxide, hydroxypropyl methylcellulose, simethicone, and natural color.

Does it work?

Leans against
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
Leans against

The strongest graded evidence we hold for the stated purpose leans against a benefit.

Why this rating?
  • The label markets this product for: cell growth and renewal support in breast and prostate.
  • We looked for evidence on: Breast cancer, Breast cancer-related hot flashes, Benign prostatic hyperplasia (BPH), Prostate cancer, Cell differentiation, Hormone-responsive tissues.
  • The closest evidence on file: Soy is rated "Possibly Ineffective" for Benign prostatic hyperplasia (BPH) (Natural Medicines).
  • Also on file: Soy is rated "Possibly Ineffective" for Breast cancer-related hot flashes.
  • Also on file: Licorice is rated "Insufficient Reliable Evidence To Rate" for Prostate cancer.

Evidence for most of these ingredients remains limited. Broccoli extract is possibly effective for colorectal cancer prevention.

Soy is possibly effective for lowering blood sugar, cholesterol, blood pressure, and for osteoporosis. Deglycyrrhizinated licorice is possibly effective for canker sores and eczema.

Radish and kale lack established evidence for their claimed uses in our data. Sodium itself is likely effective for cystic fibrosis and possibly effective for amphotericin B kidney damage, though these are not typical reasons someone takes a supplement like this.

The evidence, ingredient by ingredient Sodium Licorice Soy Broccoli Radish Kale Sweet Orange Watercress

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 7 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.

Most of these ingredients are generally well tolerated in food amounts. Deglycyrrhizinated licorice—the form used here, with the glycyrrhizin removed—is well tolerated when used appropriately, though headache, nausea, and vomiting can occur.

Broccoli extract may cause loose stools, diarrhea, or abdominal cramping, especially at high doses. Radish can irritate your stomach if taken in large amounts.

Soy typically causes bloating, constipation, diarrhea, or nausea, and allergic reactions including rash and itching are possible. Watercress is well tolerated in food amounts but can cause stomach irritation at medicinal doses.

Sodium is essential but too much raises blood pressure and strains the heart. Avoid sodium supplements or very high intake without medical advice.

Pregnancy and breastfeeding safety varies by ingredient: broccoli and kale are likely safe in pregnancy; deglycyrrhizinated licorice has no pregnancy data on file; soy and radish pregnancy data is not on file; and watercress pregnancy data is not on file. Talk with your doctor or pharmacist before use during pregnancy or breastfeeding.

Side effects, ingredient by ingredient Sodium Licorice Soy Broccoli Radish Kale Sweet Orange Watercress

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?
  • 7 of the 8 matched ingredients can interact with medications — Watercress, Radish, Licorice, Sweet Orange, Soy, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 1,276 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.

Check the following medication types before taking this product, starting with the most serious: monoamine oxidase inhibitors (MAOIs)—major risk of dangerously high blood pressure; then antihypertensive drugs (blood pressure medications), antidiabetes drugs (including insulin and metformin), blood thinners including warfarin, lithium, corticosteroids, levothyroxine (thyroid hormone), digoxin (heart medication), estrogen or hormone replacement therapy, diuretics (water pills), and drugs processed by CYP1A2 or CYP2A6 liver enzymes. Use the checker on this page with your exact medications.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with graded evidence leaning against its stated purpose. Major medication interactions have been identified, and safety information is well characterized.

This product is a blend of cruciferous and related plant extracts plus sodium. If you take blood-pressure medications, diabetes drugs, blood thinners like warfarin, heart medications, thyroid hormone, or especially an MAOI antidepressant, you need to check your specific medications against the interaction tool below before taking it.

Even if you're on no medications, high sodium intake isn't ideal long-term. Talk to your pharmacist about whether it fits your health picture.

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

Assessment coverage: 8 of 10 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Dec 14, 2023.

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 Cruciferous Plus, straight from the product label.

Brand NeoLife Nutritionals
Barcode (UPC) 3301s
Net contents 60 Tablet(s)
Market status On market
Date entered into DSLD Dec 14, 2023
DSLD ID 303255
Product type Botanical
Supplement form Tablet Or Pill
Dietary claims / uses 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 Cruciferous Plus by NeoLife Nutritionals, 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:
1 Tablet(s)
Maximum serving Sizes:
1 Tablet(s)
Servings per container
60
UPC/BARCODE
3301s
IngredientAmount% DV
Calories0 Calorie(s)--
Total Carbohydrates1 Gram(s)1%
Sodium10 mg1%
Deglycyrrhizinated Licorice root extract0 NP--
Soymilk powder0 NP--
Cruciferous Plus Blend525 mg--
Broccoli Aerial Parts Extract0 NP--
Radish Seed Extract0 NP--
Kale Aerial Parts Extract0 NP--
Orange Fruit Extract0 NP--
Mustard Seed Extract0 NP--
Mustard Seed Concentrate0 NP--
Watercress Aerial Parts Concentrate0 NP--

Other ingredients: Microcrystalline Cellulose, Calcium Carbonate, Rice Starch, Sodium Croscarmellose, Stearic Acid, Silicon Dioxide, Hydroxypropyl Methylcellulose, Simethicone, Natural Color

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

Supports enzyme activity linked to normal cell growth and renewal, especially of breast and prostate tissues with sulforaphane and indolecarbinol (from broccoli and other crucifer extracts) and D-limonene (from oranges). Soy (from high isoflavone soy milk concentrate) provides isoflavones (e.g. genistein) that helps maintain healthy hormonal activity.

Protective phytonutrients from whole foods

Storage

Store in a cool, dry place away from direct sunlight.

Precautions

Packaged with safety seal

Contains soy.

Formulation

NeoLife products use only Gmo-free ingredients

Made in U.S.A.

General Statements

Based in nature

Not sold in retail stores. Available exclusively from NeoLife promoters.

FDA Disclaimer Statement

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

FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Suggested use: 1 tablet daily with food.

Brand IP Statement(s)

Leading edge nutrition since 1958. Based in nature, backed by science.

Seals/Symbols

SAB Scientific Advisory Board NeoLife Scientific Advisory Board

See for yourself

Cruciferous Plus by NeoLife Nutritionals label

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

What’s inside

The Ingredients in Cruciferous Plus by NeoLife Nutritionals

These are the 10 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Tablet(s) Dosage formTablet Or Pill Servings per container60 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.

Sodium

Interacts with
205 drugs
10 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

Cruciferous Plus Blend

525 mg per serving

Other (inactive) ingredients: Microcrystalline Cellulose, Calcium Carbonate, Rice Starch, Sodium Croscarmellose, Stearic Acid, Silicon Dioxide, Hydroxypropyl Methylcellulose, Simethicone, Natural Color. These complete the product’s ingredient list but are not active constituents.

Interaction report

Cruciferous Plus by NeoLife Nutritionals Drug Interactions

Want to check YOUR meds against Cruciferous Plus?

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
1,275Drugs
57 Major 1,092 Moderate 126 Minor

Each ingredient & the kinds of drugs it affects

For each ingredient in Cruciferous Plus 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.

Deglycyrrhizinated Licorice root extract18 drug types · 1,040 drugs

Antihypertensive Drugs

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

Likelihood Possible Evidence B
Cisplatin (Platinol-Aq)

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

Likelihood Possible Evidence D
Corticosteroids

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

Likelihood Possible Evidence D
Cytochrome P450 2B6 (Cyp2B6) Substrates

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

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

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

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

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

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

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

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

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

Likelihood Possible Evidence B
Digoxin (Lanoxin)

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

Likelihood Possible Evidence D
Diuretic Drugs

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

Likelihood Possible Evidence D
Estrogens

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

Likelihood Possible Evidence D
Loop Diuretics

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

Likelihood Possible Evidence D
Midazolam (Versed)

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

Likelihood Possible Evidence B
P-Glycoprotein Substrates

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

Likelihood Possible Evidence D
Paclitaxel (Abraxane, Onxol)

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

Likelihood Possible Evidence D
Warfarin (Coumadin)

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

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

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

Likelihood Possible Evidence D
Methotrexate (Trexall, Others)

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

Likelihood Unlikely Evidence D

Soymilk powder12 drug types · 611 drugs

Monoamine Oxidase Inhibitors (Maois)

Taking soy products containing high amounts of tyramine along with MAOIs can increase the risk of hypertensive crisis.
Fermented soy products such as tofu and soy sauce contain tyramine, a naturally occurring chemical that affects blood pressure regulation. The metabolism of tyramine is decreased by MAOIs. Consuming more than 6 mg of tyramine while taking an MAOI can increase the risk of hypertensive crisis. The amount of tyramine in fermented soy products is usually less than 0.6 mg per serving; however, there can be significant variation depending on the specific product used, storage conditions, and length of storage. Storing one brand of tofu for a week can increase tyramine content from 0.23 mg to 4.8 mg per serving. Advise patients taking MAOIs to avoid fermented soy products that contain high amounts of tyramine.

Likelihood Likely Evidence C
Antidiabetes Drugs

Soy can lower blood glucose and have additive effects with antidiabetes drugs.
Clinical research shows that whole soy diets and soy-based meals reduce fasting glucose levels in diabetic and non-diabetic individuals. Also, individuals following a soy-based meal replacement plan seem to require lower doses of sulfonylureas and metformin to manage blood glucose levels when compared with individuals following a diet plan recommended by the American Diabetes Association.

Likelihood Possible Evidence A
Antihypertensive Drugs

Theoretically soy protein may have additive effects with antihypertensive drugs and increase the risk of hypotension.
Although some contradictory research exists, most clinical evidence suggests that consuming soy protein modestly reduces systolic and diastolic blood pressure in individuals with prehypertension or hypertension.

Likelihood Possible Evidence A
Caffeine

Theoretically, soy might reduce the clearance of caffeine.
Soy contains genistein. Taking genistein 1 gram daily for 14 days seems to inhibit caffeine clearance and metabolism in healthy females. This effect has been attributed to inhibition of the cytochrome P450 1A2 (CYP1A2) enzyme, which is involved in caffeine metabolism. It is unclear if this effect occurs with the lower amounts of genistein found in soy.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, soy might have additive effects when used with diuretic drugs.
Animal research suggests that genistein, a soy isoflavone, increases diuresis within 6 hours of subcutaneous administration in rats. The effects seem to be similar to those of furosemide. This effect has not been reported in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, soy might competitively inhibit the effects of estrogen replacement therapy.
Soy contains phytoestrogens and has been shown to have estrogenic activity in some patients. Although this has not been demonstrated in humans, theoretically, concomitant use of soy with estrogen replacement therapy might reduce the effects of the estrogen replacement therapy.

Likelihood Possible Evidence D
Levothyroxine (Synthroid, Others)

Soy products might reduce the absorption of levothyroxine in some patients.
Preliminary clinical research and a case report suggest that soy-based formulas inhibit the absorption of levothyroxine in infants with congenital hypothyroidism. A levothyroxine dosage increase may be needed for infants with congenital hypothyroidism while using soy-based formulas, and the dose may need to be reduced when soy-based formulas are no longer administered. However, in postmenopausal adults, clinical research shows that taking a single dose of soy extract containing isoflavones 60 mg along with levothyroxine does not affect the oral bioavailability of levothyroxine.

Likelihood Possible Evidence B
Progesterone

Theoretically, combining soy isoflavones with transdermal progesterone may worsen bone density.
Clinical research suggests that significant bone loss may occur in females with osteoporosis who receive a combination of transdermal progesterone with soy milk containing isoflavones when compared with placebo, soy milk alone, or progesterone alone.

Likelihood Possible Evidence A
Tamoxifen (Nolvadex)

Theoretically, estrogenic soy isoflavones might alter the effects of tamoxifen.
Laboratory research suggests that genistein and daidzen, isoflavones from soy, can antagonize the antitumor effects of tamoxifen under some circumstances; however, soy isoflavones might have different effects when used at different doses. A relatively low in vitro concentration of soy isoflavones such as 1 microM/L seems to interfere with tamoxifen, whereas high in vitro concentrations such as those >10 microM/L might actually enhance tamoxifen effects. People on a high-soy diet have soy isoflavones levels ranging from 0.1-6 microM/L. Until more is known, advise patients taking tamoxifen to avoid therapeutic use of soy products.

Likelihood Possible Evidence B
Warfarin (Coumadin)

Theoretically, soy might interfere with the effects of warfarin.
Soy milk has been reported to decrease the international normalized ratio (INR) in a patient taking warfarin. The mechanism of this interaction is not known. However, animal and in vitro research suggests that soy may also inhibit platelet aggregation. Dosing adjustments for warfarin may be necessary.

Likelihood Possible Evidence D
Antibiotic Drugs

Theoretically, antibiotics may decrease the activity of soy isoflavones.
Intestinal bacteria are responsible in part for converting soy isoflavones into their active forms. Antibiotics may decrease the amount of intestinal bacteria and decrease its ability to convert isoflavones.

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

Soy might modestly induce CYP2C9 enzymes. However, this effect does not seem to be clinically significant.
In vitro research suggests that an unhydrolyzed soy extract might induce CYP2C9. However, the significance of this interaction is likely minimal. In healthy females taking a specific extract of soy (Genistein Soy Complex, Source Naturals), blood levels of losartan, a CYP2C9 substrate, were not significantly affected.

Likelihood Unlikely Evidence D

Orange Fruit Extract7 drug types · 246 drugs

Celiprolol (Celicard)

Consuming sweet orange with celiprolol can decrease oral absorption of celiprolol.
A pharmacokinetic study in healthy volunteers shows that celiprolol levels, after a single dose of 100 mg, are decreased by up to 90% in people who drink sweet orange juice 200 mL three times daily. It's not known if lower consumption of sweet orange juice will have the same effect. Theoretically, this occurs due to short-term inhibition of organic anion transporting polypeptide (OATP). Recommend separating drug administration and consumption of sweet orange by at least 4 hours.

Likelihood Likely Evidence B
Ivermectin (Stromectol, Others)

Consuming sweet orange juice with ivermectin can decrease the oral absorption of ivermectin.
A pharmacokinetic study in healthy volunteers shows that taking ivermectin orally with sweet orange juice 750 mL over 4 hours reduces the bioavailability of ivermectin. This effect does not seem to be related to effects on P-glycoprotein. The effect on ivermectin is more pronounced in males compared to females.

Likelihood Likely Evidence B
Organic Anion-Transporting Polypeptide Substrates (Oatp)

Consuming sweet orange juice can decrease oral absorption of OATP substrates. Separate administration by at least 4 hours.
Clinical research shows that consuming sweet orange juice inhibits OATP, which reduces bioavailability of oral drugs that are substrates of OATP. For example, sweet orange juice decreases bioavailability of fexofenadine, a substrate of OATP, by about 72% and of celiprolol, another OATP substrate, by up to 90%. Since sweet orange juice seems to affect OATP for a short time, recommend separating drug administration and consumption of sweet orange juice by at least 4 hours.

Likelihood Likely Evidence B
Pravastatin (Pravachol)

Consuming sweet orange juice with pravastatin can increase the absorption of pravastatin.
A small pharmacokinetic study in healthy volunteers shows that consuming sweet orange juice 800 mL over 3 hours, including before, during, and after taking pravastatin 10 mg, increases pravastatin levels by about 149%, without affecting pravastatin elimination. Theoretically this effect might be due to modulation of organic anion transporting polypeptides (OATPs) by sweet orange juice. Sweet orange juice does not seem to affect simvastatin levels, but it is not known if sweet orange affects any of the other statins.

Likelihood Likely Evidence B
Fexofenadine (Allegra)

Consuming sweet orange juice with fexofenadine can decrease oral absorption of fexofenadine.
Clinical research shows that coadministration of sweet orange juice 1200 mL decreases bioavailability of fexofenadine by about 72%. In an animal model, sweet orange juice decreased bioavailability of fexofenadine by 31%. Fexofenadine manufacturer data indicates that concomitant administration of sweet orange juice and fexofenadine results in larger wheal and flare sizes in research models. This suggests that sweet orange reduces the clinical response to fexofenadine. Theoretically, this occurs due to short-term inhibition of organic anion transporting polypeptide (OATP). Recommend separating drug administration and consumption of sweet orange by at least 4 hours.

Likelihood Likely Evidence B
P-Glycoprotein Substrates

Sweet orange juice seems to modulate P-glycoprotein (P-gp), which might affect the blood levels of P-gp substrates.
Animal and in vitro research suggest that orange juice extract inhibits drug efflux by P-gp, increasing absorption and levels of P-gp substrates. In contrast, pharmacokinetic research in humans shows that drinking large amounts of sweet orange juice decreases absorption and levels of the P-gp substrate celiprolol. This suggests that orange juice actually induces drug efflux by P-gp or affects drug levels by another mechanism such as inhibiting the gut drug transporter called organic anion transporting polypeptide (OATP). Until more is known, sweet orange juice should be used cautiously in people taking P-gp substrates.

Likelihood Possible Evidence B
Quinolone Antibiotics

Calcium-fortified sweet orange juice might reduce quinolone absorption.
Calcium binds to quinolones in the gut. Theoretically, the calcium in certain fortified orange juices can also bind to quinolone antibiotics and reduce their absorption and levels.

Likelihood Possible Evidence D

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

Broccoli Aerial Parts Extract2 drug types · 187 drugs

Cytochrome P450 1A2 (Cyp1A2) Substrates

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

Likelihood Possible Evidence B
Cytochrome P450 2A6 (Cyp2A6) Substrates

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

Likelihood Possible Evidence B

Radish Seed Extract1 drug type · 86 drugs

Antidiabetes Drugs

Theoretically, radish might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research shows that radish extract, juice, and sprouts can reduce glucose levels. Animal research also shows that radish root juice 300 mg/kg reduces fasting and postprandial blood glucose in a rat model of diabetes, with effects similar to glibenclamide.

Likelihood Possible Evidence D

Watercress Aerial Parts Concentrate3 drug types · 6 drugs

Chlorzoxazone (Parafon Forte, Paraflex)

Watercress might reduce the metabolism of chlorzoxazone and increase its effects and side effects. Clinical research in healthy volunteers shows that a single ingestion of watercress 50 grams increases the chlorzoxazone plasma concentration-time curve by about 56% and increases its half-life by about 53%.

Likelihood Probable Evidence B
Lithium

Watercress is thought to have diuretic properties. Theoretically, due to these potential diuretic effects, watercress might reduce excretion and increase levels of lithium.

Likelihood Probable Evidence D
Warfarin (Coumadin)

Watercress contains vitamin K. Consuming large amounts of watercress might antagonize the anticoagulant effects of warfarin.

Likelihood Possible Evidence B
The maker

Brand information

Manufacturer and brand details for Cruciferous Plus, from the product label.

NeoLife Nutritionals

See all NeoLife Nutritionals products
Name
NeoLife International, LLC
City
Fremont
State
CA
ZipCode
94538
Web Address
NeoLife.com
Pharmacist Counseling Corner

Cruciferous Plus by NeoLife Nutritionals: Common Questions

Does Cruciferous Plus by NeoLife Nutritionals interact with any medications?
Yes. Based on its ingredients, Cruciferous Plus has a known interaction with 1,275 medications, including 57 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Cruciferous Plus contains 10 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.
Does this product contain a filler, or is it just active ingredients?
This product contains inactive ingredients—microcrystalline cellulose, calcium carbonate, rice starch, and others. These are binders and fillers that help form the tablet. The active ingredients are the cruciferous and plant extracts plus sodium.
Is it safe to take this while pregnant?
Kale and broccoli are likely safe in pregnancy. We don't have enough safety data on file for the other plant extracts (soy, radish, watercress, licorice) in pregnancy, and high sodium is not ideal. Talk with your doctor or pharmacist before taking it during pregnancy.
What is deglycyrrhizinated licorice, and why is it in this product?
It's licorice root with glycyrrhizin, the compound that causes side effects, removed. The remaining licorice is possibly effective for canker sores and eczema, which is likely why it's included. It still has documented drug interactions, though.
Can this help with digestion or gut health?
The product facts focus on the cruciferous vegetables' potential roles in cancer prevention and soy's possible effects on blood sugar and cholesterol. There's no evidence on file that this product is effective for digestion or general gut health.
Will this raise my blood pressure?
The product contains sodium, which can raise blood pressure if taken in excess, especially if you already take blood pressure medications. Normal dietary sodium is fine, but avoid this supplement if you're salt-sensitive without checking with your doctor first.
What side effects are most common with this product?
Based on the individual ingredients, the most common are bloating, constipation, diarrhea, or nausea from the soy and plant extracts, and loose stools from broccoli at higher doses. Allergic reactions to soy are also possible in some people.

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

Not sure if Cruciferous Plus is safe with your meds?

Our pharmacists answer your medication & supplement questions — free.

Ask a pharmacist

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.

Cruciferous Plus label
Go deeper

The Full Monographs Behind Cruciferous Plus’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

Licorice

Interacts with 1,040 drugs

Licorice root is a traditional remedy used for sore throats, coughs, and digestive complaints, but solid human evidence is limited for most uses. Regular licorice contains glycyrrhizin, whic...

Read the full Licorice monograph →
Herb & supplement monograph

Soy

Interacts with 611 drugs

Soy is a nutritious bean that is a staple food and a popular source of plant protein and isoflavones. Eating soy foods as part of a balanced diet is generally considered safe for most people...

Read the full Soy monograph →
Herb & supplement monograph

Broccoli

Interacts with 187 drugs

Broccoli is a nutritious cruciferous vegetable rich in fiber, vitamins, and plant compounds like sulforaphane that have drawn scientific interest for health benefits. Eating broccoli as food...

Read the full Broccoli monograph →
Herb & supplement monograph

Radish

Interacts with 86 drugs

Radish is a common edible root vegetable that is nutritious and generally safe to eat as food. Some people use radish (especially black radish) and its extracts for digestion and liver suppo...

Read the full Radish monograph →
Herb & supplement monograph

Kale

Kale is a nutrient-dense leafy green vegetable that is rich in vitamins, minerals, fiber, and antioxidants. Eaten as a normal food it is very healthy for most people, but it is a whole food...

Read the full Kale monograph →
Herb & supplement monograph

Sweet Orange

Interacts with 246 drugs

Sweet orange is a common citrus fruit that is a good source of vitamin C, fiber, and antioxidants, and is enjoyed as a food worldwide. Its peel and essential oil are used in aromatherapy and...

Read the full Sweet Orange monograph →
Herb & supplement monograph

Watercress

Interacts with 6 drugs

Watercress is a nutrient-rich leafy green that provides vitamins A, C, and K plus minerals and antioxidant plant compounds. Eaten as a food it is generally safe and healthy for most people,...

Read the full Watercress monograph →
Sources

Sources & How We Checked

Cruciferous Plus'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 281 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
  1. Garabedian-Ruffalo SM, Ruffalo RL. Drug and nutrient interactions. Am Fam Physician 1986;33:165-74.
  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 →

Licorice 92 references
  1. Farese RV Jr, Biglieri EG, Shackleton CH, et al. Licorice-induced hypermineralocorticoidism. N Engl J Med 1991;325:1223-7. PubMed
  2. Sigurjonsdottir HA, Ragnarsson J, Franzson L, Sigurdsson G. Is blood pressure commonly raised by moderate consumption of liquorice? J Hum Hypertens 1995;9:345-8.
  3. Armanini D, Lewicka S, Pratesi C, et al. Further studies on the mechanism of the mineralocorticoid action of licorice in humans. J Endocrinol Invest 1996;19:624-9. PubMed
  4. Zhang YD, Lorenzo B, Reidenberg MM. Inhibition of 11 beta hydroxysteroid dehydrogenase obtained from guinea pig kidney by furosemide, naringenin and some other compounds. J Steroid Biochem Mol Biol 1994;49:81-5.
  5. Strandberg TE, Jarvenpaa AL, Vanhanen H, McKeigue PM. Birth outcome in relation to licorice consumption during pregnancy. Am J Epidemiol 2001;153:1085-8. PubMed
  6. Sigurjonsdottir HA, Franzson L, Manhem K, et al. Liquorice-induced rise in blood pressure: a linear dose-response relationship. J Hum Hypertens 2001;15:549-52. PubMed
  7. Amato P, Christophe S, Mellon PL. Estrogenic activity of herbs commonly used as remedies for menopausal symptoms. Menopause 2002;9:145-50. PubMed
  8. Kent UM, Aviram M, Rosenblat M, Hollenberg PF. The licorice root derived isoflavan glabridin inhibits the activities of human cytochrome P450S 3A4, 2B6, and 2C9. Drug Metab Dispos 2002;30:709-15.. PubMed
  9. Yoshida S, Takayama Y. Licorice-induced hypokalemia as a treatable cause of dropped head syndrome. Clin Neurol Neurosurg 2003;105:286-7.. PubMed
  10. Strandberg TE, Andersson S, Jarvenpaa AL, et al. Preterm birth and licorice consumption during pregnancy. Am J Epidemiol 2002;156:803-5.. PubMed
  11. Hussain RM. The sweet cake that reaches parts other cakes can't! Postgrad Med J 2003;79:115-6.. PubMed
  12. Morris DJ, Davis E, Latif SA. Licorice, tobacco chewing, and hypertension. N Engl J Med 1990;322:849-50. PubMed
  13. Quinkler M, Stewart PM. Hypertension and the cortisol-cortisone shuttle. J Clin Endocrinol Metab 2003;88:2384-92. PubMed
  14. Westman EC, Guthrie GP. Licorice, tobacco chewing, and hypertension. N Engl J Med 1990;322:850. PubMed
  15. Mu Y, Zhang J, Zhang S, et al. Traditional Chinese medicines Wu Wei Zi (Schisandra chinensis Baill) and Gan Cao (Glycyrrhiza uralensis Fisch) activate pregnane X receptor and increase warfarin clearance in rats. J Pharmacol Exp Ther 2006;316:1369-77. PubMed
  16. Yasue H, Itoh T, Mizuno Y, Harada E. Severe hypokalemia, rhabdomyolysis, muscle paralysis, and respiratory impairment in a hypertensive patient taking herbal medicines containing licorice. Intern Med 2007;46:575-8. PubMed
  17. Brayley J, Jones J. Life-threatening hypokalemia associated with excessive licorice ingestion (letter). Am J Psychiatry 1994;151:617-8. PubMed
  18. de Klerk GJ, Nieuwenhuis G, Beutler JJ. Hypokalaemia and hypertension associated with use of liquorice flavoured chewing gum. BMJ 1997;314:731-2.
  19. Dellow EL, Unwin RJ, Honour JW. Pontefract cakes can be bad for you: refractory hypertension and liquorice excess. Nephol Dial Transplant 1999;14:218-20. PubMed
  20. Elinav E, Chajek-Shaul T. Licorice consumption causing severe hypokalemic paralysis. Mayo Clin Proc 2003;78:767-8. PubMed
  21. Eriksson JW, Carlberg B, Hillom V. Life-threatening ventricular tachycardia due to liquorice-induced hypokalemia. J Intern Med 1999;245:307-10.
  22. Janse A, van Iersel M, Hoefnagels WH, Olde Rikker MG. The old lady who liked liquorice: hypertension due to chronic intoxication in a memory-impaired patient. Neth J Med 2005;63:149-50.
  23. Lin SH, Yang SS, Chau T, Halperin ML. An unusual cause of hypokalemic paralysis: chronic licorice ingestion. Am J Med Sci 2003;325:153-6. PubMed
  24. van den Bosch AE, van der Klooster JM, Zuidgeest DM, et al. Severe hypokalemic paralysis and rhabdomyolysis due to ingestion of liquorice. Neth J Med 2005;63:146-8.
  25. van Uum SH. Liquorice and hypertension. Neth J Med 2005;63:119-20.
  26. Russo S, Mastropasqua M, Mosetti MA, et al. Low doses of liquorice can induce hypertension encephalopathy. Am J Nephrol 2000;20:145-8. PubMed
  27. Stormer FC, Reistad R, Alexander J. Glycyrrhizic acid in liquorice - evaluation of health hazard. Food Chem Toxicol 1993;31:303-12. PubMed
  28. Sontia B, Mooney J, Gaudet L, Touyz RM. Pseudohyperaldosteronism, liquorice, and hypertension. J Clin Hypertens (Greenwich) 2008;10:153-7. PubMed
  29. Francini-Pesenti F, Puato M, Piccoli A, Brocadello F. Liquorice-induced hypokalaemia and water retention in the absence of hypertension. Phytother Res 2008;22:563-5. PubMed
  30. Lapi F, Gallo E, Bernasconi S, et al. Myopathies associated with red yeast rice and liquorice: spontaneous reports from the Italian Surveillance System of Natural Health Products. Br J Clin Pharmacol 2008;66:572-4. PubMed
  31. Chen MF, Shimada F, Kato H, Yano S, Kanaoka M. Effect of glycyrrhizin on the pharmacokinetics of prednisolone following low dosage of prednisolone hemisuccinate. Endocrinol Jpn 1990;37:331-41. PubMed
  32. Teelucksingh S, Mackie AD, Burt D, McIntyre MA, Brett L, Edwards CR. Potentiation of hydrocortisone activity in skin by glycyrrhetinic acid. Lancet 1990;335(8697):1060-3. PubMed
  33. Heidemann HT, Kreuzfelder E. Hypokalemic rhabdomyolysis with myoglobinuria due to licorice ingestion and diuretic treatment. Klin Wochenschr 1983;61:303-5. PubMed
  34. Hukkanen J, Ukkola O, Savolainen MJ. Effects of low-dose liquorice alone or in combination with hydrochlorothiazide on the plasma potassium in healthy volunteers. Blood Press 2009;18:192-5. PubMed
  35. Bisogni V, Rossi GP, Calò LA. Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: case report and appraisal of the pathophysiology. Blood Press. 2014 Jun;23(3):189-92. PubMed
  36. Dehours E, Vallé B, Rougé-Bugat ME, Florent B, Bounes V, Franchitto N. Suspected hypokalaemia following liquorice ingestion on board ship. J Telemed Telecare. 2013 Jun;19(4):227-8. PubMed
  37. Kormann R, Languille E, Amiot HM, Hertig A. Dying for a cup of tea. BMJ Case Rep. 2012 Oct 19;2012. PubMed
  38. Panduranga P, Al-Rawahi N. Licorice-induced severe hypokalemia with recurrent torsade de pointes. Ann Noninvasive Electrocardiol. 2013 Nov;18(6):593-6. PubMed
  39. Räikkönen K, Seckl JR, Heinonen K, Pyhälä R, Feldt K, Jones A, Pesonen AK, Phillips DI, Lahti J, Järvenpää AL, Eriksson JG, Matthews KA, Strandberg TE, Kajantie E. Maternal prenatal licorice consumption alters hypothalamic-pituitary-adrenocortical axis fu
  40. Robles BJ, Sandoval AR, Dardon JD, Blas CA. Lethal liquorice lollies (liquorice abuse causing pseudohyperaldosteronism). BMJ Case Rep. 2013 Sep 19;2013. PubMed
  41. Chamberlain, J. J. and Abolnik, I. Z. Pulmonary edema following a licorice binge. West J Med 1997;167(3):184-185.
  42. Barrella, M., Lauria, G., Quatrale, R., and Paolino, E. Hypokaliemic rhabdomyolysis associated with liquorice ingestion: report of an atypical case. Ital.J Neurol.Sci 1997;18(4):217-220. PubMed
  43. Fugh-Berman, A. Herb-drug interactions. Lancet 2000;355(9198):134-138. PubMed
  44. Hasegawa, J., Suyama, Y., Kinugawa, T., Morisawa, T., and Kishimoto, Y. Echocardiographic findings of the heart resembling dilated cardiomyopathy during hypokalemic myopathy due to licorice-induced pseudoaldosteronism. Cardiovasc.Drugs Ther 1998;12(6):59 PubMed
  45. van Rossum, T. G., Vulto, A. G., Hop, W. C., Brouwer, J. T., Niesters, H. G., and Schalm, S. W. Intravenous glycyrrhizin for the treatment of chronic hepatitis C: a double-blind, randomized, placebo-controlled phase I/II trial. J Gastroenterol Hepatol 199 PubMed
  46. Lozano, P., Flores, D., Martinez, S., Artigues, I., Rimbau, E. M., and Gomez, F. Upper limb ischemia induced by chronic licorice ingestion. J Cardiovasc.Surg (Torino) 2000;41(4):631-632.
  47. Brouwers, A. J. and van der, Meulen J. ['Licorice hypertension' also caused by licorice tea]. Ned.Tijdschr Geneeskd. 4-14-2001;145(15):744-747.
  48. van Rossum, T. G., Vulto, A. G., Hop, W. C., and Schalm, S. W. Glycyrrhizin-induced reduction of ALT in European patients with chronic hepatitis C. Am J Gastroenterol 2001;96(8):2432-2437. PubMed
  49. Sigurjonsdottir, H. A., Manhem, K., Axelson, M., and Wallerstedt, S. Subjects with essential hypertension are more sensitive to the inhibition of 11 beta-HSD by liquorice. J Hum Hypertens 2003;17(2):125-131.
  50. Shintani, S., Murase, H., Tsukagoshi, H., and Shiigai, T. Glycyrrhizin (licorice)-induced hypokalemic myopathy. Report of 2 cases and review of the literature. Eur Neurol 1992;32(1):44-51. PubMed
  51. Chen, M. F., Shimada, F., Kato, H., Yano, S., and Kanaoka, M. Effect of oral administration of glycyrrhizin on the pharmacokinetics of prednisolone. Endocrinol Jpn 1991;38(2):167-174. PubMed
  52. Lee, C. K., Park, K. K., Lim, S. S., Park, J. H., and Chung, W. Y. Effects of the licorice extract against tumor growth and cisplatin-induced toxicity in a mouse xenograft model of colon cancer. Biol Pharm Bull 2007;30(11):2191-2195. PubMed
  53. Isaia, G. C., Pellissetto, C., Ravazzoli, M., and Tamone, C. Acute adrenal crisis and hypercalcemia in a patient assuming high liquorice doses. Minerva Med 2008;99(1):91-94.
  54. Bocker, D. and Breithardt, G. [Induction of arrhythmia by licorice abuse]. Z Kardiol 1991;80(6):389-391.
  55. Tacconi, P., Paribello, A., Cannas, A., and Marrosu, M. G. Carpal tunnel syndrome triggered by excessive licorice consumption. J Peripher.Nerv.Syst. 2009;14(1):64-65. PubMed
  56. Tu, J. H., He, Y. J., Chen, Y., Fan, L., Zhang, W., Tan, Z. R., Huang, Y. F., Guo, D., Hu, D. L., Wang, D., and Hong-Hao Zhou. Effect of glycyrrhizin on the activity of CYP3A enzyme in humans. Eur J Clin Pharmacol 2010;66(8):805-810. PubMed
  57. Goultschin, J., Palmon, S., Shapira, L., Brayer, L., and Gedalia, I. Effect of glycyrrhizin-containing toothpaste on dental plaque reduction and gingival health in humans. A pilot study. J Clin Periodontol 1991;18(3):210-212. PubMed
  58. Scali, M., Pratesi, C., Zennaro, M. C., Zampollo, V., and Armanini, D. Pseudohyperaldosteronism from liquorice-containing laxatives. J Endocrinol Invest 1990;13(10):847-848. PubMed
  59. Chatterjee, N., Domoto-Reilly, K., Fecci, P. E., Schwamm, L. H., and Singhal, A. B. Licorice-associated reversible cerebral vasoconstriction with PRES. Neurology 2010;75(21):1939-1941. PubMed
  60. Imtiaz, K. E. Sweet root, bitter pill: liquorice-induced hyperaldosteronism. QJM 2011;104(12):1093-1095. PubMed
  61. van Beers, E. J., Stam, J., and van den Bergh, W. M. Licorice consumption as a cause of posterior reversible encephalopathy syndrome: a case report. Crit Care 2011;15(1):R64. PubMed
  62. MacKenzie, M. A., Hoefnagels, W. H., Jansen, R. W., Benraad, T. J., and Kloppenborg, P. W. The influence of glycyrrhetinic acid on plasma cortisol and cortisone in healthy young volunteers. J Clin Endocrinol Metab 1990;70(6):1637-1643. PubMed
  63. Bardhan, K. D., Cumberland, D. C., Dixon, R. A., and Holdsworth, C. D. Clinical trial of deglycyrrhizinised liquorice in gastric ulcer. Gut 1978;19(9):779-782. PubMed
  64. Koster, M. and David, G. K. Reversible severe hypertension due to licorice ingestion. N Engl J Med 1968;278(25):1381-1383. PubMed
  65. Corse, F. M., Galgani, S., Gasparini, C., Giacanelli, M., and Piazza, G. Acute hypokalemic myopathy due to chronic licorice ingestion: report of a case. Ital J Neurol Sci 1983;4(4):493-497. PubMed
  66. Berlango Jimenez A., Jimenez Murillo L., Montero Perez F. J., Munoz Avila J. A., Torres Murillo J., and Calderon de la Barca Gazquez J. M. [Acute rhabdomyolysis and tetraparesis secondary to hypokalemia due to ingested licorice]. An Med Interna 1995;12(1)
  67. Bernardi, M., D'Intino, P. E., Trevisani, F., Cantelli-Forti, G., Raggi, M. A., Turchetto, E., and Gasbarrini, G. Effects of prolonged ingestion of graded doses of licorice by healthy volunteers. Life Sci 1994;55(11):863-872. PubMed
  68. van der Zwan A. Hypertension encephalopathy after liquorice ingestion. Clin Neurol Neurosurg 1993;95(1):35-37. PubMed
  69. Werner, S., Brismar, K., and Olsson, S. Hyperprolactinaemia and liquorice. Lancet 2-10-1979;1(8111):319.
  70. Nishioka, K. and Seguchi, T. Contact allergy due to oil-soluble licorice extracts in cosmetic products. Contact Dermatitis 1999;40(1):56. PubMed
  71. Yoshino T, Yanagawa T, Watanabe K. Risk factors for pseudoaldosteronism with rhabdomyolysis caused by consumption of drugs containing licorice and differences between incidence of these conditions in Japan and other countries: case report and literature r
  72. Li G, Simmler C, Chen L, et al. Cytochrome P450 inhibition by three licorice species and fourteen licorice constituents. Eur J Pharm Sci. 2017;109:182-190. PubMed
  73. Li J, Fan X, Wang Q. Hypertensive crisis with 2 target organ impairment induced by glycyrrhizin: a case report. Medicine (Baltimore) 2018;97(11):e0073. PubMed
  74. Foster CA, Church KS, Poddar M, Van Uum SH, Spaic T. Licorice-induced hypertension: a case of pseudohyperaldosteronism due to jelly bean ingestion. Postgrad Med 2017;129(3):329-31. PubMed
  75. Gallacher SD, Tsokolas G, Dimitropoulos I. Liquorice-induced apparent mineralocorticoid excess presenting in the emergency department. Clin Med (Lond) 2017;17(1):43-5. PubMed
  76. Dai DW, Singh I, Hershman JM. Lozenge-induced hypermineralcorticoid state--a unique case of licorice lozenges resulting in hypertension and hypokalemia. J Clin Hypertens (Greenwich) 2016;18(2):159-60.
  77. O'Connell K, Kinsella J, McMahon C, Holian J, O'Riordan S. Posterior reversible encephalopathy syndrome (PRES) associated with liquorice consumption. Ir J Med Sci 2016;185(4):945-7. PubMed
  78. Hataya Y, Oba A, Yamashita T, Komatsu Y. Hyponatremia in an elderly patient due to isolated hypoaldosteronism occurring after licorice withdrawal. Intern Med 2017;56(2):175-9. PubMed
  79. Ha Y, Wang T, Li J, et al. Herb-Drug Interaction Potential of Licorice Extract and Paclitaxel: A Pharmacokinetic Study in Rats. Eur J Drug Metab Pharmacokinet. 2020;45(2):257-264. PubMed
  80. Edelman ER, Butala NM, Avery LL, Lundquist AL, Dighe AS. Case 30-2020: A 54-Year-Old Man with Sudden Cardiac Arrest. N Engl J Med. 2020;383(13):1263-1275. PubMed
  81. Wang H, Dong L, Qu F, et al. Effects of glycyrrhizin on the pharmacokinetics of nobiletin in rats and its potential mechanism. Pharm Biol. 2020 Dec;58(1):352-356. PubMed
  82. Attou R, Redant S, Honore PM, Preseau T, Hantson P, De Bels D. Liquorice intoxication can lead to cardiac arrest! Case Rep Emerg Med. 2020;2020:3727682. PubMed
  83. Benge E, Shah P, Yamaguchi L, Josef V. Trick or Treat? Licorice-Induced Hypokalemia: A Case Report. Cureus 2020;12(11):e11656. PubMed
  84. Abe K, Higurashi T, Takahashi M, et al. Concomitant Use of High-dose Methotrexate and Glycyrrhizin Affects Pharmacokinetics of Methotrexate, Resulting in Hepatic Toxicity. In Vivo 2021;35(4):2163-2169. PubMed
  85. Awad N, Makar G, Burroughs V, Ravi P, Burroughs SR. Licorice-induced apparent mineralocorticoid excess causing persistent hypertension and hypokalemia. Acta Endocrinol (Buchar) 2020;16(4):508-510. PubMed
  86. Patel P, Aknouk M, Dawson A, et al. How Much Is Too Much? Exploring Pseudohyperaldosteronism in Glycyrrhizic Acid Toxicity From Chronic Licorice Root Consumption. Cureus 2021;13(7):e16454. PubMed
  87. Fan ZJ, Liu JM, Li XX, et al. Glycyrrhizin-Induced Pseudohyperaldosteronism: A Case Report. Chin J Integr Med 2022. PubMed
  88. Gatica-Ortega ME, Pastor-Nieto MA. Allergic contact dermatitis to Glycyrrhiza inflata root extract in an anti-acne cosmetic product. Contact Dermatitis 2021;85(4):454-455.
  89. Wang JB, Huang A, Wang Y, et al. Corticosteroid plus glycyrrhizin therapy for chronic drug- or herb-induced liver injury achieves biochemical and histological improvements: a randomised open-label trial. Aliment Pharmacol Ther 2022;55(10):1297-1310. PubMed
  90. Puaratanaarunkon T, Washrawirul C, Chuenboonngarm N, Noppakun N, Asawanonda P, Kumtornrut C. Efficacy and safety of a facial serum containing snail secretion filtrate, Calendula officinalis, and Glycyrrhiza glaba root extract in the treatment of maskne: A
  91. 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
  92. Han EJ, Park JS. Lethal Arrhythmia Induced by Licorice. J Korean Med Sci 2023;38(12):e107. PubMed

See these in context on the Licorice monograph →

Soy 88 references
  1. Franke AA, Custer LJ, Tanaka Y. Isoflavones in human breast milk and other biological fluids. Am J Clin Nutr 1998;68:1466-73. PubMed
  2. Albertazzi P, Pansini F, Bonaccorsi G, et al. The effect of dietary soy supplementation on hot flushes. Obstet Gynecol 1998;91:6-11. PubMed
  3. Lu LJ, Anderson KE, Grady JJ, et al. Decreased ovarian hormones during a soya diet: implications for breast cancer prevention. Cancer Res 2000;60:4112-21.
  4. Pino AM, Valladares LE, Palma MA, et al. Dietary isoflavones affect sex hormone-binding globulin levels in postmenopausal women. J Clin Endocrinol Metab 2000;85:2797-800. DOI
  5. Nisley N, Klepser T. Phytoestrogens for the prevention and treatment of osteoporosis. Alt Med Alert 1999 Dec;138-42.
  6. McMichael-Phillips DF, Harding C, Morton M, et al. Effects of soy-protein supplementation on epithelial proliferation in the histologically normal human breast. Am J Clin Nutr 1998;68:1431S-5S. PubMed
  7. Petrakis NL, Barnes S, King EB, et al. Stimulatory influence of soy protein isolate on breast secretion in pre- and postmenopausal women. Cancer Epidemiol Biomarkers Prev 1996;5:785-94.
  8. Baird DD, Umbach DM, Lansdell L, et al. Dietary intervention study to assess estrogenicity of dietary soy among postmenopausal women. J Clin Endocrinol Metab 1995;80:1685-90. DOI
  9. Duncan AM, Underhill KE, Xu X, et al. Modest hormonal effects of soy isoflavones in postmenopausal women. J Clin Endocrinol Metab 1999;84:3479-84. PubMed
  10. Ginsburg J, Prelevic GM. Lack of significant hormonal effects and controlled trials of phyto-oestrogens. Lancet 2000;355:163-4. PubMed
  11. Anthony MS. Soy and cardiovascular disease: Cholesterol lowering and beyond. J Nutr 2000;130:662S-3S. PubMed
  12. Hargreaves DF, Potten CS, Harding C, et al. Two-week dietary soy supplementation has an estrogenic effect on normal premenopausal breast. J Clin Endocrinol Metab 1999;84:4017-24. DOI
  13. Lamartiniere CA. Protection against breast cancer with genistein: a component of soy. Am J Clin Nutr 2000;71:1705S-7S. PubMed
  14. Electronic Code of Federal Regulations. Title 21. Part 182 -- Substances Generally Recognized As Safe. Available at: https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=182
  15. Codina R, Ardusso L, Lockey RF, et al. Sensitization to soybean hull allergens in subjects exposed to different levels of soybean dust inhalation in Argentina. J Allergy Clin Immunol 2000;105:570-6. PubMed
  16. Anto JM, Sunyer J, Rodriguez-Roisin R, et al. Community outbreaks of asthma associated with inhalation of soybean dust. Toxicoepidemiological Committee. N Engl J Med 1989;320:1097-1102. PubMed
  17. White MC, Etzel RA, Olson DR, Goldstein IF. Re-examination of epidemic asthma in New Orleans, Louisianna, in relation to the presence of soy at the harbor. Am J Epidemiol 1997;145:432-8.
  18. Murkies A, Dalais FS, Briganti EM, et al. Phytoestrogens and breast cancer in postmenopausal women: a case control study. Menopause 2000;7:289-96. PubMed
  19. Setchell KD, Cassidy A. Dietary isoflavones: biological effects and relevance to human health. J Nutr 1999;129:758S-67S. PubMed
  20. Teixeira SR, Potter SM, Weigel R, et al. Effects of feeding 4 levels of soy protein for 3 and 6 wk on blood lipids and apolipoproteins in moderately hypercholesterolemic men. Am J Clin Nutr 2000;71:1077-84. PubMed
  21. White LR, Petrovitch H, Ross GW, et al. Brain aging and midlife tofu consumption. J Am Coll Nutr 2000;19:242-55. PubMed
  22. Grodstein F, Mayeux R, Stampfer MJ. Tofu and cognitive function: food for thought. J Am Coll Nutr 2000;19:207-9. PubMed
  23. Divi RL, Chang HC, Doerge DR. Anti-thyroid isoflavones from soybean: isolation, characterization, and mechanisms of action. Biochem Pharmacol 1997;54:1087-96. PubMed
  24. de Lemos ML. Effects of soy phytoestrogens genistein and daidzein on breast cancer growth. Ann Pharmacother 2001;35:1118-21. PubMed
  25. Strom BL, Schinnar R, Ziegler EE, et al. Exposure to soy-based formula in infancy and endocrinological and reproductive outcomes in young adulthood. JAMA 2001;286:807-14. PubMed
  26. Goodman MT, Wilkens LR, Hankin JH, et al. Association of soy and fiber consumption with the risk of endometrial cancer. Am J Epidemiol 1997;146:294-306. PubMed
  27. Wu AH, Yang D, Pike MC. A meta-analysis of soyfoods and risk of stomach cancer: the problem of potential confounders. Cancer Epidemiol Biomarkers Prev 2000;9:1051-8.
  28. Ji BT, Chow WH, Yang G, et al. Correspondence re: AH Wu et al, A meta-analysis of soyfoods and risk of stomach cancer: the problem of potential confounders. Cancer Epidemiol Biomarkers Prev 2001;10:570.
  29. Foth D, Cline JM. Effects of mammalian and plant estrogens on mammary glands and uteri of macaques. Am J Clin Nutr 1998;68:1413S-7S. PubMed
  30. Duncan AM, Merz BE, Xu X, et al. Soy isoflavones exert modest hormonal effects in premenopausal women. J Clin Endocrinol Metab 1999;84:192-7. DOI
  31. Morito K, Hirose T, Kinjo J, et al. Interaction of phytoestrogens with estrogen receptors alpha and beta. Biol Pharm Bull 2001;24:351-6. PubMed
  32. Persky VW, Turyk ME, Wang L, et al. Effect of soy protein on endogenous hormones in postmenopausal women. Am J Clin Nutr 2002;75:145-53. PubMed
  33. Ju YH, Doerge DR, Allred KF, et al. Dietary Genistein Negates the Inhibitory Effect of Tamoxifen on Growth of Estrogen-dependent Human Breast Cancer (MCF-7) Cells Implanted in Athymic Mice. Cancer Res 2002;62:2474-7 .
  34. Cambria-Kiely JA. Effect of soy milk on warfarin efficacy. Ann Pharmacother 2002;36:1893-6.. PubMed
  35. Ziegler RG, Hoover RN, Pike MC, et al. Migration patterns and breast cancer risk in Asian-American women. J Natl Cancer Inst 1993;85:1819-27.. PubMed
  36. Brown BD, Thomas W, Hutchins A, et al. Types of dietary fat and soy minimally affect hormones and biomarkers associated with breast cancer risk in premenopausal women. Nutr Cancer 2002;43:22-30.. PubMed
  37. Sun CL, Yuan JM, Arakawa K, et al. Dietary soy and increased risk of bladder cancer: the Singapore Chinese Health Study. Cancer Epidemiol Biomarkers Prev 2002;11:1674-7.
  38. Balk JL, Whiteside DA, Naus G, et al. A pilot study of the effects of phytoestrogen supplementation on postmenopausal endometrium. J Soc Gynecol Investig 2002;9:238-42.. DOI
  39. Horn-Ross PL, John EM, Canchola AJ, et al. Phytoestrogen intake and endometrial cancer risk. J Natl Cancer Inst 2003;95:1158-64.. PubMed
  40. Kumar NB, Cantor A, Allen K et al. The specific role of isoflavones in reducing prostate cancer risk. Prostate 2004;59:141-7. PubMed
  41. Chen A, Rogan WJ. Isoflavones in soy infant formula: a review of evidence for endocrine and other activity in infants. Annu Rev Nutr 2004;24:33-54. PubMed
  42. Chen YM, Ho SC, Lam SS, et al. Soy isoflavones have a favorable effect on bone loss in Chinese postmenopausal women with lower bone mass: a double-blind, randomized, controlled trial. J Clin Endocrinol Metab 2003;88:4740-7. PubMed
  43. Unfer V, Casini ML, Costabile L, et al. Endometrial effects of long-term treatment with phytoestrogens: a randomized, double-blind, placebo-controlled study. Fertil Steril 2004;82:145-8. PubMed
  44. Bruce B, Messina M, Spiller G. Isoflavone supplements do not affect thyroid function in iodine-replete postmemopausal women. J Med Food 2003;6:309-16.
  45. He J, Gu D, Wu X, et al. Effect of soybean protein on blood pressure: A randomized, controlled trial. Ann Intern Med 2005;143:1-9. PubMed
  46. Kaari C, Haidar MA, Junior JMS, et al. Randomized clinical trial comparing conjugated equine estrogens and isoflavones in postmenopausal women: a pilot study. Maturitas 2006;53:49-58. PubMed
  47. Sacks FM, Lichtenstein A, Van Horn L, et al. Soy protein, isoflavones, and cardiovascular health. An American Heart Association Science Advisory for Professionals from the Nutrition Committee. Circulation 2006;113:1034-44. PubMed
  48. Jones JL, Daley BJ, Enderson BL, et al. Genistein inhibits tamoxifen effects on cell proliferation and cell cycle arrest in T47D breast cancer cells. Am Surg 2002;68:575-7. DOI
  49. Shulman KI, Walker SE. Refining the MAOI diet: tyramine content of pizzas and soy products. J Clin Psychiatry 1999;60:191-3. DOI
  50. Gardner DM, Shulman KI, Walker SE, Tailor SA. The making of a user friendly MAOI diet. J Clin Psychiatry 1996;57:99-104.
  51. Walker SE, Shulman KI, Tailor SA, Gardner D. Tyramine content of previously restricted foods in monoamine oxidase inhibitor diets. J Clin Psychopharmacol 1996;16:383-8. PubMed
  52. Krebs EE, Ensrud KE, MacDonald R, Wilt TJ. Phytoestrogens for treatment of menopausal symptoms: a systematic review. Obstet Gynecol 2004;104:824-36. PubMed
  53. Wang G, Xiao CQ, Li Z, et al. Effect of soy extract administration on losartan pharmacokinetics in healthy female volunteers. Ann Pharmacother 2009;43:1045-9. PubMed
  54. Jabbar MA, Larrea J, Shaw RA. Abnormal thyroid function tests in infants with congenital hypothyroidism: the influence of soy-based formula. J Am Coll Nutr. 1997;16(3):280-2. PubMed
  55. Conrad SC, Chiu H, Silverman BL. Soy formula complicates management of congenital hypothyroidism. Arch Dis Child. 2004;89(1):37-40. PubMed
  56. Chen, Y., Xiao, C. Q., He, Y. J., Chen, B. L., Wang, G., Zhou, G., Zhang, W., Tan, Z. R., Cao, S., Wang, L. P., and Zhou, H. H. Genistein alters caffeine exposure in healthy female volunteers. Eur.J Clin.Pharmacol. 2011;67(4):347-353. PubMed
  57. Whelan, A. M., Jurgens, T. M., and Naylor, H. Herbs, vitamins and minerals in the treatment of premenstrual syndrome: a systematic review. Can.J.Clin.Pharmacol. 2009;16(3):e407-e429.
  58. Lydeking-Olsen, E., Beck-Jensen, J. E., Setchell, K. D., and Holm-Jensen, T. Soymilk or progesterone for prevention of bone loss--a 2 year randomized, placebo-controlled trial. Eur.J Nutr. 2004;43(4):246-257. PubMed
  59. Hill, D. J., Heine, R. G., Cameron, D. J., Francis, D. E., and Bines, J. E. The natural history of intolerance to soy and extensively hydrolyzed formula in infants with multiple food protein intolerance. J.Pediatr. 1999;135(1):118-121. PubMed
  60. Fitzpatrick, M. Soy formulas and the effects of isoflavones on the thyroid. N.Z.Med J 2-11-2000;113(1103):24-26.
  61. Li, Z., Hong, K., Saltsman, P., DeShields, S., Bellman, M., Thames, G., Liu, Y., Wang, H. J., Elashoff, R., and Heber, D. Long-term efficacy of soy-based meal replacements vs an individualized diet plan in obese type II DM patients: relative effects on w
  62. Post-Skagegard, M., Vessby, B., and Karlstrom, B. Glucose and insulin responses in healthy women after intake of composite meals containing cod-, milk-, and soy protein. Eur J Clin Nutr 2006;60(8):949-954. PubMed
  63. Mclachlan, J. A., Simpson, E., and Martin, M. Endocrine disrupters and female reproductive health. Best.Pract Res Clin Endocrinol.Metab 2006;20(1):63-75. PubMed
  64. Messina, M. and Redmond, G. Effects of soy protein and soybean isoflavones on thyroid function in healthy adults and hypothyroid patients: a review of the relevant literature. Thyroid 2006;16(3):249-258. PubMed
  65. Rozman, K. K., Bhatia, J., Calafat, A. M., Chambers, C., Culty, M., Etzel, R. A., Flaws, J. A., Hansen, D. K., Hoyer, P. B., Jeffery, E. H., Kesner, J. S., Marty, S., Thomas, J. A., and Umbach, D. NTP-CERHR expert panel report on the reproductive and dev
  66. Azadbakht, L., Kimiagar, M., Mehrabi, Y., Esmaillzadeh, A., Padyab, M., Hu, F. B., and Willett, W. C. Soy inclusion in the diet improves features of the metabolic syndrome: a randomized crossover study in postmenopausal women. Am J Clin Nutr 2007;85(3):7 PubMed
  67. Berseth, C. L., Johnston, W. H., Stolz, S. I., Harris, C. L., and Mitmesser, S. H. Clinical response to 2 commonly used switch formulas occurs within 1 day. Clin.Pediatr.(Phila) 2009;48(1):58-65. PubMed
  68. Altorf-van der Kuil, W., Engberink, M. F., Brink, E. J., van Baak, M. A., Bakker, S. J., Navis, G., van, 't, V, and Geleijnse, J. M. Dietary protein and blood pressure: a systematic review. PLoS.One. 2010;5(8):e12102. PubMed
  69. Clement, Y. N., Onakpoya, I., Hung, S. K., and Ernst, E. Effects of herbal and dietary supplements on cognition in menopause: a systematic review. Maturitas 2011;68(3):256-263. PubMed
  70. Liu, Z. M., Chen, Y. M., and Ho, S. C. Effects of soy intake on glycemic control: a meta-analysis of randomized controlled trials. Am.J.Clin.Nutr. 2011;93(5):1092-1101. PubMed
  71. Iyngkaran, N., Yadav, M., Looi, L. M., Boey, C. G., Lam, K. L., Balabaskaran, S., and Puthucheary, S. D. Effect of soy protein on the small bowel mucosa of young infants recovering from acute gastroenteritis. J Pediatr.Gastroenterol.Nutr 1988;7(1):68-75. DOI
  72. Freni-Titulaer, L. W., Cordero, J. F., Haddock, L., Lebron, G., Martinez, R., and Mills, J. L. Premature thelarche in Puerto Rico. A search for environmental factors. Am.J Dis.Child 1986;140(12):1263-1267. PubMed
  73. Halpin, T. C., Byrne, W. J., and Ament, M. E. Colitis, persistent diarrhea, and soy protein intolerance. J Pediatr. 1977;91(3):404-407. PubMed
  74. Chorazy, P. A., Himelhoch, S., Hopwood, N. J., Greger, N. G., and Postellon, D. C. Persistent hypothyroidism in an infant receiving a soy formula: case report and review of the literature. Pediatrics 1995;96(1 Pt 1):148-150. DOI
  75. Gimenez, I., Martinez, R. M., Lou, M., Mayoral, J. A., Garay, R. P., and Alda, J. O. Salidiuretic action by genistein in the isolated, perfused rat kidney. Hypertension 1998;31(2):706-711. PubMed
  76. Van Wyk JJ, Arnold MB, Wynn J, and et al. The effects of a soybean product on thyroid function in humans. Pediatrics 1959;24:752-760. DOI
  77. Fruzza AG, Demeterco-Berggren C, Jones KL. Unawareness of the effects of soy intake on the management of congenital hypothyroidism. Pediatrics. 2012;130(3):e699-702. PubMed
  78. EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS). Risk assessment for peri- and post-menopausal women taking food supplements containing isolated isoflavones. EFSA J. 2015;13(10):4246. DOI
  79. Vitolins MZ, Griffin L, Tomlinson WV, et al. Randomized trial to assess the impact of venlafaxine and soy protein on hot flashes and quality of life in men with prostate cancer. J Clin Oncol. 2013;31(32):4092-8. PubMed
  80. Persiani S, Sala F, Manzotti C, et al. Evaluation of levothyroxine bioavailability after oral administration of a fixed combination of soy isoflavones in post-menopausal female volunteers. Drug Res (Stuttg). 2016;66(3):136-40. PubMed
  81. Wu AH, Spicer D, Garcia A, et al. Double-blind randomized 12-month soy intervention had no effects on breast MRI fibroglandular tissue density or mammographic density. Cancer Prev Res (Phila). 2015;8(10):942-51. PubMed
  82. Yagami A, Suzuki K, Nakamura M, et al. Case of anaphylactic reaction to soy following percutaneous sensitization by soy-based ingredients in cosmetic products. J Dermatol. 2015;42(9):917-8. PubMed
  83. Zhang XM, Zhang YB, Chi MH. Soy protein supplementation reduces clinical indices in type 2 diabetes and metabolic syndrome. Yonsei Med J. 2016;57(3):681-9. PubMed
  84. Barni S, Mori F, Pantano S, Novembre E. Adverse reaction to benzathine benzylpenicillin due to soy allergy: a case report. J Med Case Rep. 2015;9:134. PubMed
  85. Gao M, Wang H. Frequent milk and soybean consumption are high risks for uterine leiomyoma: A prospective cohort study. Medicine (Baltimore). 2018;97(41):e12009. PubMed
  86. Upson K, Sathyanarayana S, Scholes D, Holt VL. Early-life factors and endometriosis risk. Fertil Steril. 2015;104(4):964-971.e5. PubMed
  87. Mumford SL, Weck J, Kannan K, Buck Louis GM. Urinary phytoestrogen concentrations are not associated with incident endometriosis in premenopausal women. J Nutr. 2017;147(2):227-234. PubMed
  88. Yamagiwa Y, Sawada N, Shimazu T, et al. Soy Food Intake and Pancreatic Cancer Risk: The Japan Public Health Center-based Prospective Study. Cancer Epidemiol Biomarkers Prev. 2020;29(6):1214-1221. PubMed

See these in context on the Soy monograph →

Broccoli 5 references
  1. Kristal AR, Lampe JW. Brassica vegetables and prostate cancer risk: a review of the epidemiological evidence. Nutr Cancer 2002;42:1-9. PubMed
  2. Chakrabarti A, Prais L, Foulds IS. Allergic contact dermatitis to broccoli. Br J Dermatol 2003;148:172-3. PubMed
  3. Hakooz, N. and Hamdan, I. Effects of dietary broccoli on human in vivo caffeine metabolism: a pilot study on a group of Jordanian volunteers. Curr Drug Metab 2007;8(1):9-15. PubMed
  4. Kall MA, Vang O, Clausen J. Effects of dietary broccoli on human drug metabolising activity. Cancer Lett. 1997;114(1-2):169-70. PubMed
  5. Bauman JE, Hsu CH, Centuori S, et al. Randomized Crossover Trial Evaluating Detoxification of Tobacco Carcinogens by Broccoli Seed and Sprout Extract in Current Smokers. Cancers (Basel). 2022;14(9):2129. Published 2022 Apr 24. PubMed

See these in context on the Broccoli monograph →

Radish 5 references
  1. Gruenwald J, Brendler T, Jaenicke C. PDR for Herbal Medicines. 1st ed. Montvale, NJ: Medical Economics Company, Inc., 1998.
  2. Damiani E, Aloia AM, Priore MG, Nardulli S, Ferrannini A. Generalized urticaria after ingestion of Raphanus sativus. Ann Allergy Asthma Immunol. 2011 Feb;106(2):168. PubMed
  3. Evans M, Paterson E, Barnes DM. An open label pilot study to evaluate the efficacy of Spanish black radish on the induction of phase I and phase II enzymes in healthy male subjects. BMC Complement Altern Med. 2014 Dec 9;14:475. PubMed
  4. Banihani SA. Radish (Raphanus sativus) and diabetes. Nutrients. 2017;9(9). pii: E1014. PubMed
  5. Shukla S, Chatterji S, Mehta S, Rai PK, Singh RK, Yadav DK, Watal G. Antidiabetic effect of Raphanus sativus root juice. Pharm Biol. 2011 Jan;49(1):32-7.

See these in context on the Radish monograph →

Kale 2 references
  1. Vitamin K - Health Professional Fact Sheet — NIH Office of Dietary Supplements Source
  2. Lutein and Zeaxanthin — NIH Office of Dietary Supplements Source

See these in context on the Kale monograph →

Sweet Orange 17 references
  1. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons, 1996.
  2. FDA, CFSAN. FDA-approved potassium health claim notification for potassium containing foods. 2000. Available at: www.cfsan.fda.gov/~dms/hclm-k.html.
  3. Kurowska EM, Spence JD, Jordan J, et al. HDL-cholesterol-raising effect of orange juice in subjects with hypercholesterolemia. Am J Clin Nutr 2000;72:1095-100. PubMed
  4. Murry JJ, Healy MD. Drug-mineral interactions: a new responsibility for the hospital dietician. J Am Diet Assoc 1991;91:66-73.
  5. Bailey DG, Dresser GK, Munoz C, et al. Reduction of fexofenadine bioavailability by fruit juices. Clin Pharmacol Ther 2001;69:P21.
  6. Pletz MW, Petzold P, Allen A, et al. Effect of calcium carbonate on bioavailability of orally administered gemifloxacin. Antimicrob Agents Chemother 2003;47:2158-60.. PubMed
  7. Lilja JJ, Juntti-Patinen L, Neuvonen PJ. Orange juice substantially reduces the bioavailability of the beta-adrenergic-blocking agent celiprolol. Clin Pharmacol Ther 2004;75:184-90.
  8. Tian R, Koyabu N, Takanaga H, et al. Effects of grapefruit juice and orange juice on the intestinal efflux of P-glycoprotein substrates. Pharm Res 2002;19:802-9. PubMed
  9. Vanapalli SR, Chen Y, Ellingrod VL, et al. Orange juice decreases the oral bioavailability of ivermectin in health volunteers. Clin Pharmacol Ther 2003;73 (Abstract PDII-A-10):P94.
  10. Huang SM, Lesko LJ. Drug-drug, drug-dietary supplement, and drug-citrus fruit and other food interactions: what have we learned? J Clin Pharmacol 2004;44:559-69. PubMed
  11. Koitabashi Y, Kumai T, Matsumoto N, et al. Orange juice increased the bioavailability of pravastatin, 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, in rats and healthy human subjects. Life Sci 2006;78:2852-9. PubMed
  12. Takanaga H, Ohnishi A, Yamada S, et al. Polymethoxylated flavones in orange juice are inhibitors of P-glycoprotein but not cytochrome P450 3A4. J Pharmacol Exp Ther 2000;293:230-6. DOI
  13. Greenblatt DJ. Analysis of drug interactions involving fruit beverages and organic anion-transporting polypeptides. J Clin Pharmacol 2009;49:1403-7. PubMed
  14. Bailey DG. Fruit juice inhibition of uptake transport: a new type of food-drug interaction. Br J Clin Pharmacol 2010;70:645-55. PubMed
  15. Kamath AV, Yao M, Zhang Y, Chong S. Effect of fruit juices on the oral bioavailability of fexofenadine in rats. J Pharm Sci 2005;94:233-9. PubMed
  16. Kays MB, Overholser BR, Mueller BA, et al. Effects of sevelamer hydrochloride and calcium acetate on the oral bioavailability of ciprofloxacin. Am J Kidney Dis. 2003;42(6):1253-9. PubMed
  17. Neuhofel, A. L., Wilton, J. H., Victory, J. M., Hejmanowsk, L. G., and Amsden, G. W. Lack of bioequivalence of ciprofloxacin when administered with calcium-fortified orange juice: a new twist on an old interaction. J Clin Pharmacol. 2002;42(4):461-466. DOI

See these in context on the Sweet Orange monograph →

Watercress 34 references
  1. Gruenwald J, Brendler T, Jaenicke C. PDR for Herbal Medicines. 1st ed. Montvale, NJ: Medical Economics Company, Inc., 1998.
  2. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  3. Leclercq I, Desager JP, Horsmans Y. Inhibition of chlorzoxazone metabolism, a clinical probe for CYP2E1, by a single ingestion of watercress. Clin Pharmacol Ther 1998;64:144-9. PubMed
  4. Bolton-Smith C, Price RJ, Fenton ST, et al. Compilation of a provisional UK database for the phylloquinone (vitamin K1) content of foods. Br J Nutr 2000;83:389-99.
  5. Rondelaud, D., Dreyfuss, G., Bouteille, B., and Darde, M. L. Changes in human fasciolosis in a temperate area: about some observations over a 28-year period in central France. Parasitol.Res 2000;86(9):753-757. PubMed
  6. Sanchez-Sosa, S., Rojas-Ortega, S., Reed-San Roman, G., and Torres-Santana, M. A. [Massive hepatobiliary fascioliasis]. Rev Gastroenterol.Mex. 2000;65(4):179-183.
  7. van Daele, P. L., Madretsma, G. S., and van Agtmael, M. A. [Stomach ache and fever after consumption of watercress in Turkey: fascioliasis]. Ned.Tijdschr.Geneeskd. 9-29-2001;145(39):1896-1899.
  8. Cosme, A., Ojeda, E., Cilla, G., Torrado, J., Alzate, L., Beristain, X., Orive, V., and Arenas, J. [Fasciola hepatica. study of a series of 37 patients]. Gastroenterol.Hepatol. 2001;24(8):375-380.
  9. Martinez-Bebert, K., Rodriguez-Baez, R., Pila-Perez, R., Pila-Pelaez, R., and Tamakloe, K. [Hepatic hematoma caused by fascioliasis]. Gac.Med Mex. 2002;138(3):271-274.
  10. Dreyfuss, G., Vignoles, P., Abrous, M., and Rondelaud, D. Unusual snail species involved in the transmission of Fasciola hepatica in watercress beds in central France. Parasite 2002;9(2):113-120.
  11. Christmann, M., Henrich, R., Mayer, G., and Ell, C. [Infection with fasciola hepatica causing elevated liver-enzyme results and eosinophilia - serologic and endoscopic diagnosis and therapy]. Z.Gastroenterol. 2002;40(9):801-806.
  12. Cosme, A., Ojeda, E., Poch, M., Bujanda, L., Castiella, A., and Fernandez, J. Sonographic findings of hepatic lesions in human fascioliasis. J Clin Ultrasound 2003;31(7):358-363. PubMed
  13. Sapunar, J., Latorre, R., Guerra, M., and Defilippi, C. [Clinical considerations on 2 cases of hepatic fascioliasis. Importance of the imaging examinations]. Bol.Chil.Parasitol. 1992;47(3-4):70-76.
  14. de Gorgolas, M., Torres, R., Verdejo, C., Garay, J., Robledo, A., Ponte, M. C., and Fernandez Guerrero, M. L. [Fasciola hepatica infestation. Biopathology and new diagnostic and therapeutic aspects]. Enferm.Infecc.Microbiol.Clin 1992;10(9):514-519.
  15. Carrada-Bravo, T. [Fascioliasis: diagnosis, epidemiology and treatment]. Rev Gastroenterol.Mex. 2003;68(2):135-142.
  16. Yilmaz, H. and Godekmerdan, A. Human fasciolosis in Van province, Turkey. Acta Trop. 2004;92(2):161-162.
  17. Dobrucali, A., Yigitbasi, R., Erzin, Y., Sunamak, O., Polat, E., and Yakar, H. Fasciola hepatica infestation as a very rare cause of extrahepatic cholestasis. World J Gastroenterol. 10-15-2004;10(20):3076-3077. PubMed
  18. Alvarez-Chacon, R., Garcia-Rosales, J. J., de la Cruz-Otero MC, Wong-Chio, M., Cabrera-Bravo, M., Gomez-Gomez, J. V., and Gamez-Aranda, V. [Fascioliasis in children. A study of 10 cases]. Bol.Med Hosp.Infant Mex. 1992;49(6):365-371.
  19. Mailles, A., Capek, I., Ajana, F., Schepens, C., Ilef, D., and Vaillant, V. Commercial watercress as an emerging source of fascioliasis in Northern France in 2002: results from an outbreak investigation. Epidemiol.Infect. 2006;134(5):942-945.
  20. Cruz, Lopez O., Adan, Pimentel A., Tamariz Cruz, O. J., Munoz, Lopez A., Cruz Lopez, M. C., Cruz Lopez, M. E., and Munoz, Lopez S. [Hepatic fasciolasis diagnosed in state phase]. Rev Gastroenterol Mex. 2006;71(1):59-62.
  21. el Shazly, A. M., Handousa, A. E., Youssef, M. E., Rizk, H., and Hamouda, M. M. Human fascioliasis: a parasitic health problem in Dakahlia Governorate, Egypt. J Egypt.Soc Parasitol. 1991;21(2):553-559.
  22. Cosme, A., Alzate, L., Orive, V., Recasens, M., Torrado, J., Ruiz, I., and Arenas, J. [Laparoscopic findings in liver fascioliasis. Study of 13 cases]. Rev Esp.Enferm.Dig. 1990;78(6):359-362.
  23. Diaz, J., Pina, B., Lastre, M., Rivera, L., and Perez, O. [Epidemic human fascioliasis. Cuba 1983. VI. Clinical study of 40 children in the Hospital Provincial of Sagua la Grande]. G.E.N. 1990;44(4):385-388.
  24. Borie, C., Corona, S., Garin, A., Olea, P., Salcedo, M., Perez, C., and Apt, W. [A family outbreak of acute hepatic fascioliasis]. Rev Med Chil. 1990;118(1):67-72.
  25. Diamond, S. P., Wiener, S. G., and Marks, J. G., Jr. Allergic contact dermatitis to nasturtium. Dermatol.Clin. 1990;8(1):77-80. DOI
  26. Delasalle, P., Beytout, J., Cambon, M., and Bommelaer, G. [Distomatosis: diagnosis and treatment]. Rev Prat. 1-21-1990;40(3):230-236.
  27. Rivera, J. V. and Bermudez, R. H. Radionuclide imaging of the liver in human fascioliasis. Clin Nucl.Med 1984;9(8):450-453. PubMed
  28. Croese, J., Chapman, G., and Gallagher, N. D. Evolution of fascioliasis after eating wild watercress. Aust.N.Z.J.Med. 1982;12(5):525-527. PubMed
  29. Bendezu, P., Frame, A., and Hillyer, G. V. Human fascioliasis in Corozal, Puerto Rico. J Parasitol. 1982;68(2):297-299. DOI
  30. Derrick, E. and Darley, C. Contact dermatitis to nasturtium. Br.J Dermatol 1997;136(2):290-291. PubMed
  31. Narain, K., Biswas, D., Rajguru, S. K., and Mahanta, J. Human distomatosis due to Fasciola hepatica infection in Assam, India. J Commun.Dis 1997;29(2):161-165.
  32. Brinker, F. Herb Contraindications and Drug Interactions. 1998;2nd edition.
  33. Gruenwald, J. PDR for Herbal Medicines. 1998;1st ed.
  34. Clemente M, Miguel MD, Felipe KB, et al. Effect of watercress extract supplementation on lipid profile and oxidative stress markers in overweight people with physical disability: A randomized, double-blind, and placebo-controlled trial. Phytother Res. 202 PubMed

See these in context on the Watercress monograph →

Parts of this content are provided by the Therapeutic Research Center, LLC.

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.

© 2021 Therapeutic Research Center, LLC

Keep exploring