Major interaction on record — check this product against your medications before combining. Based on 9 of 11 ingredients. Check your meds →
Dietary supplement

Ultra Menoease With BioResponse DIM Ingredients & Drug Interactions

by Douglas Laboratories

Capsule Category: Other Combinations
Most serious interaction: Major
The interaction bottom line Most serious interaction: Major

Ultra Menoease With BioResponse DIM is a dietary supplement by Douglas Laboratories with 11 active ingredients. Its ingredients are commonly taken for bodybuilding and testosterone support, anxiety and stress, anti-inflammatory.Based on those ingredients, 1,317 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Red Clover flower extract, D-Alpha-Tocopheryl Succinate, Vitamin D3. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Ultra Menoease With BioResponse DIM by Douglas Laboratories

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 3 of its 11 active ingredients.
  • “Proprietary Blend” is a proprietary blend — the label gives one combined amount (300 mg) without saying how much of each component you get.
  • “BioResponse DIM Diindolylmethane Complex” is a proprietary blend — the label gives one combined amount (75 mg) without saying how much of each component you get.

Ultra Menoease contains 11 ingredients total. The active components include silica (from silicon), vitamin D3, chrysin, diindolylmethane (DIM), magnesium, vitamin E (D-alpha-tocopheryl succinate), phosphatidylcholine, a proprietary blend, genistein from geniVida, red clover flower extract, and black cohosh root extract.

These work together to address menopausal symptom support, with a focus on hormone metabolism and estrogen balance through ingredients like DIM and red clover. The inactive ingredients are pectin, hydroxypropyl methylcellulose, cellulose, and vegetable stearate.

Does it work?

Not established
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
Not established

The graded evidence we hold for these ingredients covers different conditions than the ones this product is marketed for, so there's no established rating for its stated use.

Why this rating?
  • The label markets this product for: menopause symptom support.
  • We looked for evidence on: Hot flashes, Night sweats, Menopause-related mood changes.
  • The closest evidence on file: Vitamin E is rated "Possibly Ineffective" for Breast cancer-related hot flashes (Natural Medicines).
  • Also on file: Red Clover is rated "Insufficient Reliable Evidence To Rate" for Breast cancer-related hot flashes.
  • Also on file: Black Cohosh is rated "Insufficient Reliable Evidence To Rate" for Breast cancer-related hot flashes.

The evidence for individual ingredients in this formula varies widely. Vitamin D is effective for certain bone and mineral disorders (familial hypophosphatemia, osteomalacia, rickets, renal osteodystrophy).

Magnesium is effective for constipation, dyspepsia, and certain pregnancy complications, and vitamin E is effective for vitamin E deficiency and related neurological conditions. Several other ingredients show possibly effective evidence: silica for osteoporosis, vitamin E for Alzheimer disease and some other conditions, and black cohosh for menopausal symptoms.

However, many of the specific claims related to hormone balance and menopausal support—including diindolylmethane, chrysin, red clover for menopausal symptoms, and genistein—lack sufficient reliable evidence to rate their effectiveness in available data. We hold no effectiveness data for starch or geniVida Genistein.

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

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

Why this rating?
  • We hold adverse-effect (side-effect) data for 8 of the 9 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 9 of 9.
  • General safety write-ups exist for 9 of 9.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Most ingredients are generally well tolerated at recommended doses. Magnesium, vitamin D3, and phosphatidylcholine are considered safe when used at typical amounts, though high-dose magnesium can cause diarrhea and other digestive upset.

Vitamin E is generally well tolerated but carries a caution about long-term high doses and bleeding risk. Silica, chrysin, and diindolylmethane are generally well tolerated short-term, though long-term safety is not well studied for the latter two.

Black cohosh and red clover are generally well tolerated short-term but warrant caution due to their estrogen-like effects and rare liver concerns with black cohosh. Pregnancy and breastfeeding: silica and diindolylmethane carry insufficient data and are best avoided in pregnancy and breastfeeding; vitamin D3 has no specific pregnancy/lactation rating on file, magnesium is likely safe in pregnancy under medical guidance, vitamin E recommends avoiding high-dose supplements unless directed by a doctor, phosphatidylcholine has insufficient supplement-specific data, red clover should be avoided in pregnancy and breastfeeding, and black cohosh should be avoided in both due to insufficient safety data and effects on the uterus.

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 9 matched ingredients can interact with medications — Red Clover, Black Cohosh, Vitamin D, Vitamin E, Magnesium, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications; Parkinson's medications.
  • For scale: 1,318 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.

Double-check with your pharmacist if you take levodopa/carbidopa (Parkinson's medication)—magnesium significantly reduces its levels. Also screen for thiazide diuretics, verapamil, digoxin, diltiazem, calcium channel blockers, blood thinners or antiplatelet drugs, warfarin, estrogen therapy or estrogen-containing contraceptives, skeletal muscle relaxants, quinolone antibiotics, bisphosphonates, sulfonylureas (diabetes drugs), methotrexate, tamoxifen, or serotonergic antidepressants.

Some ingredients may also affect how your liver processes many other medications.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with no established evidence rating for its marketed use. Major medication interactions have been identified, and safety information is well characterized.

This product targets menopausal symptom support with multiple herbal and nutrient ingredients. If you take blood pressure medications (especially calcium channel blockers), blood thinners, diabetes medications, heart medications (digoxin, verapamil, diltiazem), Parkinson's disease medications, or chemotherapy, talk with your pharmacist before starting.

The product is generally well tolerated at recommended doses for short-term use in non-pregnant, non-breastfeeding adults, but the interaction profile is substantial—your exact medications matter here.

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

Assessment coverage: 9 of 11 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Feb 24, 2017.

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 Ultra Menoease With BioResponse DIM, straight from the product label.

Brand Douglas Laboratories
Barcode (UPC) 310539039533
Net contents 60 Vegetarian Capsule(s)
Market status On market
Date entered into DSLD Feb 24, 2017
DSLD ID 70915
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses All Other
Intended target group(s) Adult (18 - 50 Years), Gluten Free, Dairy Free, Sugar Free
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 Ultra Menoease With BioResponse DIM by Douglas Laboratories, 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:
2 Vegetarian Capsule(s)
Maximum serving Sizes:
2 Vegetarian Capsule(s)
Servings per container
30
UPC/BARCODE
310539039533
IngredientAmount% DV
Silica0 NP--
Proprietary Blend300 mg--
Starch0 NP--
Vitamin D31000 IU250%
Chrysin0 NP--
Diindolylmethane0 NP--
Magnesium100 mg25%
D-Alpha-Tocopheryl Succinate0 NP--
Phosphatidylcholine0 NP--
BioResponse DIM Diindolylmethane Complex75 mg--
geniVida Genistein30 mg--
Red Clover flower extract0 NP--
Black Cohosh root extract0 NP--

Other ingredients: Pectin, Hydroxypropyl Methylcellulose, Cellulose, Vegetable Stearate

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.
Precautions

Warning: Consult your healthcare professional before use if you are pregnant, nursing, taking prescription medications, have a liver disorder or develop symptoms of liver trouble.

Keep out of reach of children.

Tamper resistant package, do not use if outer seal is missing.

General Statements

Harmless changes in urine color may occur with the use of this product.

Brand IP Statement(s)

geniVida is a trademark of DSM BioResponse DIM is a trademark of BioResponse, L.L.C., Boulder, CO. U.S. Patent 6,086,915.

Storage

For optimal storage conditions, store in cool, dry place. (59(0)-77(0)F/15(0)-25(0)C) (35-65% relative humidity)

General

Formula #201938

FDA Statement of Identity

A Dietary Supplement

Formulation

This product contains no yeast, wheat, gluten, milk/dairy, sodium, sugar, artificial coloring, preservatives or flavoring.

Suggested/Recommended/Usage/Directions

Suggested Use: Adults take 2 capsules daily with a meal or as directed by a healthcare professional.

See for yourself

Ultra Menoease With BioResponse DIM by Douglas Laboratories label

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

What’s inside

The Ingredients in Ultra Menoease With BioResponse DIM by Douglas Laboratories

These are the 11 active ingredients this product is made of. Select any to open its full monograph.

Serving size2 Vegetarian Capsule(s) Dosage formCapsule Servings per container30 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.

Proprietary Blend

300 mg per serving

Vitamin D3

Interacts with
715 drugs
1000 IU per serving

Vitamin D is a fat-soluble vitamin that helps your body absorb calcium and is important for healthy bones, muscles, and immune function. Many people,...

Vitamin D3 monograph & interactions

Magnesium

Interacts with
295 drugs
100 mg per serving Form: Magnesium Amino Acid Chelate

Magnesium is an essential mineral your body needs for muscles, nerves, blood pressure, and many other functions, and supplements are useful for preven...

Magnesium monograph & interactions

BioResponse DIM Diindolylmethane Complex

75 mg per serving Form: Diindolylmethane

GeniVida Genistein

30 mg per serving

Other (inactive) ingredients: Pectin, Hydroxypropyl Methylcellulose, Cellulose, Vegetable Stearate. These complete the product’s ingredient list but are not active constituents.

Interaction report

Ultra Menoease With BioResponse DIM by Douglas Laboratories Drug Interactions

Want to check YOUR meds against Ultra Menoease With BioResponse DIM?

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
1,317Drugs
6 Major 1,249 Moderate 62 Minor

Ingredients driving the most interactions

Chrysin 358

Each ingredient & the kinds of drugs it affects

For each ingredient in Ultra Menoease With BioResponse DIM 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.

Red Clover flower extract9 drug types · 867 drugs

Estrogens

Theoretically, concomitant use of large amounts of red clover might interfere with estrogen therapy.
Red clover contains phytoestrogens which might have estrogenic activity in some people. Theoretically, red clover might compete for estrogen receptors and interfere with estrogen-containing drug therapy.

Likelihood Probable Evidence D
Methotrexate (Trexall, Others)

Theoretically, red clover might increase the risk of methotrexate toxicity.
In a case report, a 52-year-old female receiving weekly methotrexate injections for psoriasis developed symptoms of methotrexate toxicity, including severe vomiting and epigastric pain, after three days of taking red clover 430 mg daily. Toxicity resolved after red clover was discontinued. However, no liver function tests or methotrexate levels were reported.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, the phytoestrogens in red clover might interfere with tamoxifen.
In vitro and animal research suggests that genistein, a constituent of red clover, might antagonize the antitumor effects of tamoxifen. However, there is some evidence from an animal study that red clover does not reduce the efficacy of tamoxifen. Until more is known, tell patients taking tamoxifen to avoid red clover.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Although some laboratory research suggests that red clover may have anticoagulant and antiplatelet activity, clinical research has not shown this effect.
In vitro research suggests that genistein in red clover has antiplatelet effects, and historically, red clover was thought to have anticoagulant effects due to its coumarin content. However, some experts state that this is unlikely as most natural coumarins have not been shown to have anticoagulant effects, and their content in red clover is low. Additionally, some clinical research in postmenopausal patients found no effect on coagulation or prothrombin time with the use of red clover flowering tops 378 mg daily for 12 months or red clover isoflavone (Rimostil) 50 mg daily for 2 years.

Likelihood Unlikely Evidence B
Caffeine

Theoretically, soy might reduce the clearance of caffeine; however, a small clinical study found no effect.
Red clover contains genistein. Taking genistein 1 gram daily for 14 days seems to inhibit caffeine clearance and metabolism in healthy females. However, this effect does not seem to occur with the lower amounts of genistein found in red clover. A clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of caffeine.

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

Theoretically, red clover might increase levels of drugs metabolized by CYP1A2; however, a small clinical study found no effect.
In vitro evidence shows that red clover inhibits CYP1A2. However, a clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of caffeine, a CYP1A2 probe substrate.

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

Theoretically, red clover might increase the levels and clinical effects of drugs metabolized by CYP2C19.
In vitro evidence suggests that red clover weakly inhibits CYP2C19. This interaction has not been reported in humans.

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

Theoretically, red clover might increase levels of drugs metabolized by CYP2C9; however, a small clinical study found no effect.
In vitro evidence suggests that red clover might inhibit CYP2C9. However, a clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of tolbutamide, a CYP2C9 probe substrate.

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

Theoretically, red clover might increase levels of drugs metabolized by CYP3A4; however, a small clinical study found no effect.
In vitro evidence shows that red clover might inhibit CYP3A4 isoenzymes. However, a clinical study in healthy postmenopausal individuals shows that taking red clover capsules standardized to contain 60 mg isoflavones twice daily for 14 days does not affect the pharmacokinetics of alprazolam, a CYP3A4 probe substrate.

Likelihood Unlikely Evidence B

D-Alpha-Tocopheryl Succinate8 drug types · 764 drugs

Alkylating Agents

Theoretically, antioxidant effects of vitamin E might reduce the effectiveness of alkylating agents.
There's concern that antioxidants could reduce the activity of chemotherapy drugs which generate free radicals, such as cyclophosphamide, chlorambucil, carmustine, busulfan, and thiotepa. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as vitamin E have on chemotherapy. Advise patients to consult their oncologist before using vitamin E supplements, especially in high doses.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Concomitant use of vitamin E and anticoagulant or antiplatelet agents might increase the risk of bleeding.
Vitamin E seems to inhibit of platelet aggregation and antagonize the effects of vitamin K-dependent clotting factors. These effects appear to be dose-dependent, and are probably only likely to be clinically significant with doses of at least 800 units daily. Mixed tocopherols, such as those found in food, might have a greater antiplatelet effect than alpha-tocopherol. RRR alpha-tocopherol (natural vitamin E) 1000 IU daily antagonizes vitamin K-dependent clotting factors. Advise patients to avoid high doses of vitamin E, especially in people with low vitamin K intake or other risk factors for bleeding.

Likelihood Possible Evidence B
Antitumor Antibiotics

Theoretically, antioxidant effects of vitamin E might reduce the effectiveness of antitumor antibiotics.
There's concern that antioxidants could reduce the activity of antitumor antibiotic drugs such as doxorubicin, which generate free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as vitamin E have on chemotherapy involving antitumor antibiotics. Advise patients to consult their oncologist before using vitamin E supplements, especially in high doses.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

A specific form of vitamin E might increase absorption and levels of cyclosporine.
There is some evidence that one specific formulation of vitamin E (D-alpha-tocopheryl-polyethylene glycol-1000 succinate, TPGS, tocophersolan, Liqui-E) might increase absorption of cyclosporine. This vitamin E formulation forms micelles which seems to increase absorption of cyclosporine by 40% to 72% in some patients. However, this interaction is unlikely to occur with the usual forms of vitamin E.

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

Theoretically, vitamin E might induce metabolism of CYP3A4, possibly reducing the levels CYP3A4 substrates.
Vitamin E appears to bind with the nuclear receptor, pregnane X receptor (PXR), which results in increased expression of CYP3A4. Although the clinical significance of this is not known, use caution when considering concomitant use of vitamin E and other drugs affected by these enzymes.

Likelihood Possible Evidence D
Selumetinib (Koselugo)

Taking selumetinib with vitamin E can result in a total daily dose of vitamin E that exceeds safe limits and therefore might increase the risk of bleeding.
Selumetinib contains 48-54 IU vitamin E per capsule. The increased risk of bleeding with vitamin E appears to be dose-dependent. Be cautious when using selumetinib in combination with supplemental vitamin E, especially in patients at higher risk of bleed, such as those with chronic conditions and those taking antiplatelet drugs.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Using vitamin E with warfarin might increase the risk of bleeding.
Due to interference with production of vitamin K-dependent clotting factors, use of more than 400 IU of vitamin E daily with warfarin might increase prothrombin time (PT), INR, and the risk of bleeding,. At a dose of 1000 IU per day, vitamin E can antagonize vitamin K-dependent clotting factors even in people not taking warfarin. Limited clinical evidence suggests that doses up to 1200 IU daily may be used safely by patients taking warfarin, but this may not be applicable in all patient populations.

Likelihood Possible Evidence B
Niacin

Vitamin E might decrease the beneficial effects of niacin on high-density lipoprotein (HDL) cholesterol levels.
A combination of niacin and simvastatin (Zocor) effectively raises high-density lipoprotein (HDL) cholesterol levels in people with coronary disease and low HDL levels. Clinical research shows that taking a combination of antioxidants (vitamin C, vitamin E, beta-carotene, and selenium) along with niacin and simvastatin (Zocor) attenuates this rise in HDL, specifically the HDL-2 and apolipoprotein A1 fractions, by more than 50%. Vitamin E alone combined with a statin does not seem to decrease HDL levels. It is not known whether the adverse effect on HDL is due to one of the other antioxidants or to the combination. It also is not known whether it will occur in other patient populations.

Likelihood Possible Evidence A

Vitamin D38 drug types · 715 drugs

Aluminum

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

Likelihood Probable Evidence B
Atorvastatin (Lipitor)

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

Likelihood Probable Evidence B
Calcipotriene (Dovonex)

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

Likelihood Probable Evidence D
Digoxin (Lanoxin)

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

Likelihood Possible Evidence D
Diltiazem (Cardizem, Others)

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

Likelihood Probable Evidence B
Thiazide Diuretics

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

Likelihood Probable Evidence D
Verapamil (Calan, Others)

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

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

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

Likelihood Possible Evidence D

Black Cohosh root extract7 drug types · 652 drugs

Atorvastatin (Lipitor)

Taking black cohosh with atorvastatin might increase the risk for elevated liver function tests.
In one case report, a patient taking atorvastatin (Lipitor) developed significantly elevated liver function enzymes after starting black cohosh 100 mg four times daily. Liver enzymes returned to normal when black cohosh was discontinued. It is unclear whether the elevated liver enzymes were due to black cohosh itself or an interaction between atorvastatin and black cohosh.

Likelihood Possible Evidence D
Cisplatin (Platinol-Aq)

Theoretically, black cohosh may reduce the clinical effects of cisplatin.
Animal research suggests that black cohosh might decrease the cytotoxic effect of cisplatin on breast cancer cells.

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

Some research suggests that black cohosh might inhibit CYP2D6, but there is conflicting evidence.
Some clinical research suggests that black cohosh might modestly inhibit CYP2D6 and increase levels of drugs metabolized by this enzyme. However, contradictory clinical research shows a specific black cohosh product (Remifemin, Enzymatic Therapy) 40 mg twice daily does not significantly inhibit metabolism of a CYP2D6 substrate in healthy study volunteers. Until more is known, use black cohosh cautiously in patients taking drugs metabolized by CYP2D6.

Likelihood Possible Evidence B
Estrogens

Theoretically, black cohosh may alter the effects of estrogen therapy.
Some research suggests that black cohosh has estrogenic effects. This may enhance or inhibit the effects of estrogen therapy.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, taking black cohosh with hepatotoxic drugs may increase the risk of liver damage.
There is concern that black cohosh might be linked to cases of liver failure and autoimmune hepatitis.

Likelihood Possible Evidence D
Serotonergic Drugs

Combining serotonergic drugs with black cohosh might cause additive serotonergic effects.
Black cohosh might increase the risk of serotonin syndrome when combined with other serotonergic drugs. Black cohosh acts as an agonist at several serotonin receptor subtypes and might interact with other serotonergic medications. In one case, a 55-year-old female who had been on stable treatment with sertraline 50 mg and duloxetine 60 mg daily developed serotonin syndrome after taking black cohosh extract 40 mg daily for 3 days.

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

Black cohosh may inhibit one form of OATP, OATP2B1, which could reduce the bioavailability and clinical effects of OATP2B1 substrates.
In vitro research shows that black cohosh modestly inhibits OATP2B1. OATPs are expressed in the small intestine and liver and are responsible for the uptake of drugs and other compounds into the body. Inhibition of OATP may reduce the bioavailability of oral drugs that are substrates of OATP.

Likelihood Possible Evidence D

Chrysin9 drug types · 358 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, chrysin might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that chrysin might inhibit platelet aggregation.

Likelihood Possible Evidence D
Aromatase Inhibitors

Theoretically, chrysin might increase the effects and adverse effects of aromatase inhibitors.
In vitro research suggests that chrysin might decrease estrogen synthesis by acting as an aromatase (estrogen synthetase) inhibitor..

Likelihood Possible Evidence D
Contraceptive Drugs

Theoretically, chrysin might reduce the efficacy of estrogen-containing contraceptive drugs.
In vitro research suggests that chrysin might have antiestrogenic activity.

Likelihood Possible Evidence D
Diclofenac (Voltaren, Others)

Theoretically, chrysin might increase the effects and adverse effects of diclofenac.
In vitro research suggests that chrysin and its sulfate conjugate inhibit diclofenac metabolism. It is speculated that chrysin and its sulfate conjugate reduce the metabolism of diclofenac by inhibiting cytochrome P450 2C9. This effect has not been reported in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, chrysin might decrease the effects of estrogen therapy.
In vitro research suggests that chrysin might have antiestrogenic activity.

Likelihood Possible Evidence D
Mephenytoin (Mesantoin)

Theoretically, chrysin might increase the effects and adverse effects of mephenytoin.
In vitro research suggests that chrysin and its sulfate and glucuronide conjugates inhibit S-mephenytoin metabolism. It is speculated that chrysin and its conjugates reduce the metabolism of S-mephenytoin by inhibiting cytochrome P450 2C19. This effect has not been reported in humans.

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

Theoretically, chrysin might increase levels of drugs metabolized by CYP1A2.
In vitro research suggests that chrysin inhibits CYP1A2 isozymes. However, chrysin does not appear to inhibit CYP1A2-dependent caffeine metabolism in animals. Due to chrysin's low bioavailability and rapid metabolism to glucuronide and sulfate conjugates, this interaction is unlikely.

Likelihood Unlikely Evidence D
Glucuronidated Drugs

Theoretically, chrysin might increase the clearance of drugs that are UGT1A1 substrates, thereby reducing their effectiveness.
In vitro research suggests that chrysin might induce UDP-glucuronosyltransferase 1A1 (UGT1A1).

Likelihood Unlikely Evidence D
Testosterone

Theoretically, chrysin might increase the effects and adverse effects of testosterone.
In vitro research suggests that chrysin and its sulfate conjugate inhibit testosterone metabolism. It is speculated that chrysin and its sulfate conjugate reduce the metabolism of testosterone by inhibiting cytochrome P450 3A4. This effect has not been reported in humans.

Likelihood Possible Evidence D

Magnesium15 drug types · 295 drugs

Levodopa/Carbidopa (Sinemet)

Magnesium can reduce the bioavailability of levodopa/carbidopa.
Clinical research in healthy volunteers shows that taking magnesium oxide 1000 mg with levodopa 100 mg/carbidopa 10 mg reduces the area under the curve (AUC) of levodopa by 35% and of carbidopa by 81%. In vitro and animal research shows that magnesium produces an alkaline environment in the digestive tract, which might lead to degradation and reduced bioavailability of levodopa/carbidopa.

Likelihood Probable Evidence B
Aminoglycoside Antibiotics

Concomitant use of aminoglycoside antibiotics and magnesium can increase the risk for neuromuscular weakness.
Both aminoglycosides and magnesium reduce presynaptic acetylcholine release, which can lead to neuromuscular blockade and possible paralysis. This is most likely to occur with high doses of magnesium given intravenously.

Likelihood Possible Evidence D
Antacids

Use of acid reducers may reduce the laxative effect of magnesium oxide.
A retrospective analysis shows that, in the presence of H2 receptor antagonists (H2RAs) or proton pump inhibitors (PPIs), a higher dose of magnesium oxide is needed for a laxative effect. This may also occur with antacids. Under acidic conditions, magnesium oxide is converted to magnesium chloride and then to magnesium bicarbonate, which has an osmotic laxative effect. By reducing acidity, antacids may reduce the conversion of magnesium oxide to the active bicarbonate salt.

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

Magnesium might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide should be taken at least 2 hours before or 6 hours after magnesium containing products.

Likelihood Probable Evidence D
Bisphosphonates

Magnesium can decrease absorption of bisphosphonates.
Cations, including magnesium, can decrease bisphosphonate absorption. Advise patients to separate doses of magnesium and these drugs by at least 2 hours.

Likelihood Probable Evidence B
Calcium Channel Blockers

Magnesium can have additive effects with calcium channel blockers, although evidence is conflicting.
Magnesium inhibits calcium entry into smooth muscle cells and may therefore have additive effects with calcium channel blockers. Severe hypotension and neuromuscular blockades may occur when nifedipine is used with intravenous magnesium, although some contradictory evidence suggests that concurrent use of magnesium with nifedipine does not increase the risk of neuromuscular weakness. High doses of magnesium could theoretically have additive effects with other calcium channel blockers.

Likelihood Possible Evidence D
Digoxin

Magnesium salts may reduce absorption of digoxin.
Clinical evidence suggests that treatment with oral magnesium hydroxide or magnesium trisilicate reduces absorption of digoxin from the intestines. This may reduce the blood levels of digoxin and decrease its therapeutic effects.

Likelihood Possible Evidence B
Potassium-Sparing Diuretics

Potassium-sparing diuretics decrease excretion of magnesium, possibly increasing magnesium levels.
Potassium-sparing diuretics also have magnesium-sparing properties, which can counteract the magnesium losses associated with loop and thiazide diuretics. Theoretically, increased magnesium levels could result from concomitant use of potassium-sparing diuretics and magnesium supplements.

Likelihood Probable Evidence D
Quinolone Antibiotics

Magnesium decreases absorption of quinolones.
Magnesium can form insoluble complexes with quinolones and decrease their absorption. Advise patients to take these drugs at least 2 hours before, or 4 to 6 hours after, magnesium supplements.

Likelihood Probable Evidence D
Skeletal Muscle Relaxants

Parenteral magnesium alters the pharmacokinetics of skeletal muscle relaxants, increasing their effects and accelerating the onset of effect.
Parenteral magnesium shortens the time to onset of skeletal muscle relaxants by about 1 minute and prolongs the duration of action by about 2 minutes. Magnesium potentiates the effects of skeletal muscle relaxants by decreasing calcium-mediated release of acetylcholine from presynaptic nerve terminals, reducing postsynaptic sensitivity to acetylcholine, and having a direct effect on the membrane potential of myocytes. Magnesium also has vasodilatory actions and increases cardiac output, allowing a greater amount of muscle relaxant to reach the motor end plate. A clinical study found that low-dose rocuronium (0.45 mg/kg), when given after administration of magnesium 30 mg/kg over 10 minutes, has an accelerated onset of effect, which matches the onset of effect seen with a full-dose rocuronium regimen (0.6 mg/kg). In another clinical study, onset times for rocuronium doses of 0.3, 0.6, and 1.2 mg/kg were 86, 76, and 50 seconds, respectively, when given alone, but were reduced to 66, 44, and 38 seconds, respectively, when the doses were given after a 15-minute infusion of magnesium sulfate 60 mg/kg. Giving intraoperative intravenous magnesium sulfate, 50 mg/kg loading dose followed by 15 mg/kg/hour, reduces the onset time of rocuronium, enhances its clinical effects, reduces the dose of intraoperative opiates, and prolongs the spontaneous recovery time. It does not affect the activity of subsequently administered neostigmine.

Likelihood Probable Evidence A
Sulfonylureas

Magnesium increases the systemic absorption of sulfonylureas, increasing their effects and side effects.
Clinical research shows that administration of magnesium hydroxide with glyburide increases glyburide absorption, increases maximal insulin response by 35-fold, and increases the risk of hypoglycemia, when compared with glyburide alone. A similar interaction occurs between magnesium hydroxide and glipizide. The mechanism of this effect appears to be related to the elevation of gastrointestinal pH by magnesium-based antacids, increasing solubility and enhancing absorption of sulfonylureas.

Likelihood Probable Evidence B
Tetracycline Antibiotics

Magnesium decreases absorption of tetracyclines.
Magnesium can form insoluble complexes with tetracyclines in the gut and decrease their absorption and antibacterial activity. Advise patients to take these drugs 1 hour before or 2 hours after magnesium supplements.

Likelihood Probable Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, magnesium may have antiplatelet effects, but the evidence is conflicting.
In vitro evidence shows that magnesium sulfate inhibits platelet aggregation, even at low concentrations. Some preliminary clinical evidence shows that infusion of magnesium sulfate increases bleeding time by 48% and reduces platelet activity. However, other clinical research shows that magnesium does not affect platelet aggregation, although inhibition of platelet-dependent thrombosis can occur.

Likelihood Unlikely Evidence B
Gabapentin (Neurontin)

Gabapentin absorption can be decreased by magnesium.
Clinical research shows that giving magnesium oxide orally along with gabapentin decreases the maximum plasma concentration of gabapentin by 33%, time to maximum concentration by 36%, and area under the curve by 43%. Advise patients to take gabapentin at least 2 hours before, or 4 to 6 hours after, magnesium supplements.

Likelihood Unlikely Evidence B
Sevelamer (Renagel, Renvela)

Sevelamer may increase serum magnesium levels.
In patients on hemodialysis, sevelamer use was associated with a 0.28 mg/dL increase in serum magnesium. The mechanism of this interaction remains unclear.

Likelihood Possible Evidence B

Diindolylmethane3 drug types · 269 drugs

Diuretic Drugs

Theoretically, diindolylmethane might increase the risk of hyponatremia if used with sodium-depleting diuretics.
Large doses of diindolylmethane (600 mg daily) have been associated with two cases of asymptomatic hyponatremia in clinical research.

Likelihood Possible Evidence B
Estrogens

Theoretically, diindolylmethane might increase or decrease the effects of estrogens.
Diindolylmethane might have mild estrogenic or antiestrogenic effects. Theoretically, large amounts of diindolylmethane might interfere with hormone replacement therapy.

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

Theoretically, diindolylmethane might lower serum levels of CYP1A2 substrates.
In vitro evidence suggests that diindolylmethane can induce CYP1A2. Theoretically, it might increase metabolism of CYP1A2 substrates and lower serum concentrations. This interaction has not been reported in humans.

Likelihood Unlikely Evidence D
The maker

Brand information

Manufacturer and brand details for Ultra Menoease With BioResponse DIM, from the product label.

Douglas Laboratories

See all Douglas Laboratories products
Name
Douglas Laboratories
Street Address
600 Boyce Road
City
Pittsburgh
State
PA
ZipCode
15205
Phone Number
1-800-245-4440
Web Address
www.douglaslabs.com
Pharmacist Counseling Corner

Ultra Menoease With BioResponse DIM by Douglas Laboratories: Common Questions

Does Ultra Menoease With BioResponse DIM by Douglas Laboratories interact with any medications?
Yes. Based on its ingredients, Ultra Menoease With BioResponse DIM has a known interaction with 1,317 medications, including 6 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Ultra Menoease With BioResponse DIM contains 11 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Is this safe to take if I'm pregnant or breastfeeding?
Several ingredients should be avoided in pregnancy and breastfeeding due to insufficient safety data or estrogen-like effects—silica, chrysin, red clover, and black cohosh fall into this category. Magnesium is likely safe in pregnancy under medical guidance, and diindolylmethane is rated likely safe, but you should discuss this product with your doctor or pharmacist before using it while pregnant or nursing.
What is diindolylmethane (DIM) and why is it in this product?
DIM is a compound derived from cruciferous vegetables like broccoli. It's included because it's theorized to influence estrogen metabolism, which is relevant for menopause support. However, evidence for its effectiveness in menopausal symptoms is not yet established in our data.
Can I take this with birth control?
Not without checking first. Chrysin, diindolylmethane, red clover, and black cohosh all have documented moderate interactions with estrogen-containing contraceptives and may reduce their effectiveness. Talk to your pharmacist or doctor before combining them.
Will this product affect my cholesterol or heart medications?
Yes, potentially. Vitamin D3 may reduce absorption of atorvastatin (Lipitor), and magnesium can have additive effects with calcium channel blockers. Vitamin E may increase bleeding risk if you're on blood thinners. If you take any heart or cholesterol medication, check your exact prescriptions before starting.
What side effects might I experience?
Diindolylmethane commonly causes diarrhea, gas, headache, nausea, and rash. Magnesium frequently causes diarrhea, gastrointestinal irritation, and nausea. Phosphatidylcholine may cause bloating, diarrhea, altered taste, and nausea. Black cohosh and red clover typically cause nausea and mild gastrointestinal symptoms. Most side effects are mild and digestive.
Can I take this with my diabetes medication?
Magnesium increases the absorption of sulfonylureas (a type of diabetes drug) and can raise insulin response significantly, increasing hypoglycemia risk. If you take glyburide or similar medications, talk with your pharmacist before starting this product.

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

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

Ultra Menoease With BioResponse DIM label
Go deeper

The Full Monographs Behind Ultra Menoease With BioResponse DIM’s Ingredients

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

Herb & supplement monograph

Chrysin

Interacts with 358 drugs

Chrysin is a plant flavonoid sold mainly as a bodybuilding supplement claimed to raise testosterone or block estrogen, but human studies have not shown these benefits, largely because the bo...

Read the full Chrysin monograph →
Herb & supplement monograph

Red Clover

Interacts with 867 drugs

Red clover is a plant rich in isoflavones (plant compounds with weak estrogen-like activity) that is most often used for menopause symptoms like hot flashes. The evidence is mixed and genera...

Read the full Red Clover monograph →
Herb & supplement monograph

Black Cohosh

Interacts with 652 drugs

Black cohosh is a North American plant most often used to ease menopause symptoms like hot flashes, but the research is mixed and far from settled. It is generally well tolerated for short-t...

Read the full Black Cohosh monograph →
Herb & supplement monograph

Vitamin D

Interacts with 715 drugs

Vitamin D is a fat-soluble vitamin that helps your body absorb calcium and is important for healthy bones, muscles, and immune function. Many people, especially those with low sun exposure,...

Read the full Vitamin D monograph →
Herb & supplement monograph

Magnesium

Interacts with 295 drugs

Magnesium is an essential mineral your body needs for muscles, nerves, blood pressure, and many other functions, and supplements are useful for preventing or correcting deficiency. Some othe...

Read the full Magnesium monograph →
Herb & supplement monograph

Silicon

Silicon is a trace mineral found in the body and in foods like oats, barley, and certain fruits and vegetables, and it is popular in supplements for hair, skin, nail, and bone health. Some s...

Read the full Silicon monograph →
Herb & supplement monograph

Diindolylmethane

Interacts with 269 drugs

Diindolylmethane (DIM) is a compound made when your body digests cruciferous vegetables, and it is sold as a supplement mainly for hormone balance and cancer prevention. Although early lab s...

Read the full Diindolylmethane monograph →
Herb & supplement monograph

Vitamin E

Interacts with 764 drugs

Vitamin E is an essential fat-soluble vitamin and antioxidant that most people get in adequate amounts from a normal diet. Supplements can help correct a true deficiency, but high-dose vitam...

Read the full Vitamin E monograph →
Herb & supplement monograph

Phosphatidylcholine

Phosphatidylcholine is a phospholipid that is part of every cell membrane and a source of choline. People take it for liver, brain, and gut health, but solid human evidence is limited for mo...

Read the full Phosphatidylcholine monograph →
Sources

Sources & How We Checked

Ultra Menoease With BioResponse DIM'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 335 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.

Silicon 19 references
  1. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002.
  2. Jugdaohsingh R, Anderson SH, Tucker KL, et al. Dietary silicon intake and absorption. Am J Clin Nutr 2002;75:887-93. PubMed
  3. Ichiyanagi O, Sasagawa I, Adachi Y, et al. Silica urolithiasis without magnesium trisilicate intake. Urol Int 1998;61:39-42. PubMed
  4. Levison DA, Crocker PR, Banim S, Wallace DM. Silica stones in the urinary bladder. Lancet 1982;1:704-5. PubMed
  5. Lee MH, Lee YH, Hsu TH, et al. Silica stone--development due to long time oral trisilicate intake. Scand J Urol Nephrol 1993;27:267-9. PubMed
  6. Cruz Guerra, N. A., Gomez Garcia, M. A., Lovaco, Castellano F., Saez Garrido, J. C., Garcia, Cuerpo E., and Escudero, Barrilero A. [Silica urolithiasis: report of a new case]. Actas Urol.Esp 2000;24(2):202-204.
  7. Merget, R., Bauer, T., Kupper, H. U., Philippou, S., Bauer, H. D., Breitstadt, R., and Bruening, T. Health hazards due to the inhalation of amorphous silica. Arch Toxicol. 2002;75(11-12):625-634. PubMed
  8. Khuder, S. A., Peshimam, A. Z., and Agraharam, S. Environmental risk factors for rheumatoid arthritis. Rev Environ Health 2002;17(4):307-315. PubMed
  9. McLaughlin, J. K., Chow, W. H., and Levy, L. S. Amorphous silica: a review of health effects from inhalation exposure with particular reference to cancer. J Toxicol.Environ Health 4-25-1997;50(6):553-566. DOI
  10. Pelucchi, C., Pira, E., Piolatto, G., Coggiola, M., Carta, P., and La, Vecchia C. Occupational silica exposure and lung cancer risk: a review of epidemiological studies 1996-2005. Ann.Oncol. 2006;17(7):1039-1050. PubMed
  11. Gillissen, A., Gessner, C., Hammerschmidt, S., Hoheisel, G., and Wirtz, H. [Health significance of inhaled particles]. Dtsch.Med Wochenschr. 3-24-2006;131(12):639-644.
  12. Hu, J. F., Qu, H., and Wang, J. Z. [Meta analysis for relationship between exposure of free silicon dioxide and lung tumor]. Zhonghua Lao.Dong.Wei Sheng Zhi.Ye.Bing.Za Zhi. 2006;24(7):415-417.
  13. Jugdaohsingh, R. Silicon and bone health. J Nutr Health Aging 2007;11(2):99-110.
  14. Lacasse, Y., Martin, S., Gagne, D., and Lakhal, L. Dose-response meta-analysis of silica and lung cancer. Cancer Causes Control 2009;20(6):925-933. PubMed
  15. McCormic, Z. D., Khuder, S. S., Aryal, B. K., Ames, A. L., and Khuder, S. A. Occupational silica exposure as a risk factor for scleroderma: a meta-analysis. Int Arch Occup.Environ Health 2010;83(7):763-769. PubMed
  16. Haddad, F. S. and Kouyoumdjian, A. Silica stones in humans. Urol.Int 1986;41(1):70-76. PubMed
  17. Tervaert, J. W., Stegeman, C. A., and Kallenberg, C. G. Silicon exposure and vasculitis. Curr Opin.Rheumatol 1998;10(1):12-17. PubMed
  18. Steenland, K. and Stayner, L. Silica, asbestos, man-made mineral fibers, and cancer. Cancer Causes Control 1997;8(3):491-503. PubMed
  19. Boqué N, Valls RM, Pedret A, Puiggrós F, Arola L, Solà R. Relative absorption of silicon from different formulations of dietary supplements: a pilot randomized, double-blind, crossover post-prandial study. Sci Rep 2021;11(1):16479. PubMed

See these in context on the Silicon monograph →

Vitamin D 26 references
  1. McEvoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
  2. Tatro DS, ed. Drug Interactions Facts. Facts and Comparisons Inc., St. Louis, MO. 1999.
  3. Koutkia P, Chen TC, Holick MF. Vitamin D intoxication associated with an over-the-counter supplement. N Engl J Med 2001;345:66-7. PubMed
  4. Bar-Or D, Yoel G. Calcium and calciferol antagonize effect of verapamil in atrial fibrillation. Br Med J 1981;282:1585-6.
  5. Demontis R, Leflon A, Fournier A, et al. 1 alpha(OH) vitamin D3 increases plasma aluminum in hemodialyzed patients taking AI(OH)3. Clin Nephrol 1986;26:146-9.
  6. Crowe M, Wollner L, Griffiths RA. Hypercalcemia following vitamin D and thiazide therapy in the elderly. Practitioner 1984;228:312-3.
  7. Parfitt AM. Thiazide-induced hypercalcemia in vitamin D-treated hypoparathyroidism. Ann Intern Med 1972;77:557-63. PubMed
  8. Thiazide diuretics and the risk of osteoporosis. Pharmacist's Letter/Prescriber's Letter 2003;19(11):191105.
  9. Moon J. The role of vitamin D in toxic metal absorption. J Am Coll Nutr 1994;13:559-64.
  10. Demontis R, Reissi D, Noel C, et al. Indirect clinical evidence that 1alphaOH vitamin D<SUB>3</SUB> increases the intestinal absorption of aluminum. Clin Nephrol 1989;31:123-7.
  11. Adler AJ, Berlyne GM. Duodenal aluminum absorption in the rat: effect of vitamin D. Am J Physiol 1985;249:G209-13. PubMed
  12. Schwartz JB. Effects of vitamin D supplementation in atorvastatin-treated patients: A new drug interaction with an unexpected consequence. Clin Pharmacol Ther 2009;85:198-203. PubMed
  13. Dietary reference intakes for calcium and vitamin D. Institute of Medicine, November 30, 2010. Available at: http://www.iom.edu/~/media/Files/Report%20Files/2010/Dietary-Reference-Intakes-for-Calcium-and-Vitamin-D/Vitamin%20D%20and%20Calcium%202010%20Repo
  14. Cox KA, Dunn MA. Aluminum toxicity alters the regulation of calbindin-D28k protein and mRNA expression in chick intestine. J Nutr 2001;131:2007-13. PubMed
  15. Escribano, J., Balaguer, A., Pagone, F., Feliu, A., and Roque, I. Figuls. Pharmacological interventions for preventing complications in idiopathic hypercalciuria. Cochrane.Database.Syst.Rev. 2009;(1):CD004754. PubMed
  16. Carlton, S., Clopton, D., and Cappuzzo, K. A. Vitamin D deficiency: appropriate replenishment therapies and the effects of vitamin D toxicity. Consult Pharm 2010;25(3):171-177. PubMed
  17. Wang, H., Xia, N., Yang, Y., and Peng, D. Q. Influence of vitamin D supplementation on plasma lipid profiles: a meta-analysis of randomized controlled trials. Lipids Health Dis. 2012;11:42. PubMed
  18. Turner AN, Carr Reese P, Fields KS, Anderson J, Ervin M, Davis JA, Fichorova RN, Roberts MW, Klebanoff MA, Jackson RD. A blinded, randomized controlled trial of high-dose vitamin D supplementation to reduce recurrence of bacterial vaginosis. Am J Obstet G PubMed
  19. Weiner M, Epstein FH. Signs and symptoms of electrolyte disorders. Yale J Biol Med. 1970;43(2):76-109.
  20. Lappe J, Watson P, Travers-Gustafson D, Recker R, Garland C, Gorham E, Baggerly K, McDonnell SL. Effect of Vitamin D and Calcium Supplementation on Cancer Incidence in Older Women: A Randomized Clinical Trial. JAMA. 2017 Mar 28;317(12):1234-1243. PubMed
  21. Roth DE, Leung M, Mesfin E, Qamar H, Watterworth J, Papp E. Vitamin D supplementation during pregnancy: state of the evidence from a systematic review of randomised trials. BMJ. 2017;359:j5237. PubMed
  22. Murai IH, Fernandes AL, Sales LP, et al. Effect of a single high dose of vitamin D3 on hospital length of stay in patients with moderate to severe COVID-19: A randomized clinical trial. JAMA. 2021.
  23. Wang Z, Schuetz EG, Xu Y, Thummel KE. Interplay between vitamin D and the drug metabolizing enzyme CYP3A4. J Steroid Biochem Mol Biol 2013;136:54-8. PubMed
  24. Doyle D, Browne U, Brickley A, Murphy D. Vitamin D-induced hypercalcaemia and acute kidney injury in sarcoidosis. BMJ Case Rep 2023;16(1):e250580. PubMed
  25. Williamson A, Martineau AR, Sheikh A, Jolliffe D, Griffiths CJ. Vitamin D for the management of asthma. Cochrane Database Syst Rev 2023;2(2):CD011511. PubMed
  26. Kinesya E, Santoso D, Gde Arya N, et al. Vitamin D as adjuvant therapy for diabetic foot ulcers: Systematic review and meta-analysis approach. Clin Nutr ESPEN 2023;54:137-143. PubMed

See these in context on the Vitamin D monograph →

Chrysin 23 references
  1. Galijatovic A, Otake Y, Walle UK, Walle T. Extensive metabolism of the flavonoid chrysin by human Caco-2 and Hep G2 cells. Xenobiotica 1999;29:1241-56. PubMed
  2. Lee H, Yeom H, Kim YG, et al. Structure-related inhibition of human hepatic caffeine N3-demethylation by naturally occurring flavonoids. Biochem Pharmacol 1998;55:1369-75. PubMed
  3. Galijatovic A, Walle UK, Walle T. Induction of UDP-glucuronosyltransferase by the flavonoids chrysin and quercetin in Caco-2 cells. Pharm Res 2000;17:21-6.
  4. Walle UK, Galijatovic A, Walle T. Transport of the flavonoid chrysin and its conjugated metabolites by the human intestinal cell line Caco-2. Biochem Pharmacol 1999;58:431-8. PubMed
  5. Kao YC, Zhou C, Sherman M, et al. Molecular basis of the inhibition of human aromatase (estrogen synthetase) by flavone and isoflavone phytoestrogens: A site-directed mutagenesis study. Environ Health Perspect 1998;106:85-92. PubMed
  6. Jeong HJ, Shin YG, Kim IH, Pezzuto JM. Inhibition of aromatase activity by flavonoids. Arch Pharm Res 1999;22:309-12. PubMed
  7. Walle T, Otake Y, Galijatovic A, et al. Induction of UDP-glucuronosyltransferase UGT1A1 by the flavonoid chrysin in the human hepatoma cell line hep G2. Drug Metab Dispos 2000;28:1077-82. DOI
  8. Walle T, Otake Y, Brubaker JA, et al. Disposition and metabolism of the flavonoid chrysin in normal volunteers. Br J Clin Pharmacol 2001;51:143-6. DOI
  9. Galijatovic A, Otake Y, Walle UK, Walle T. Induction of UDP-glucuronosyltransferase UGT1A1 by the flavonoid chrysin in Caco-2 cells--potential role in carcinogen bioinactivation. Pharm Res 2001;18:374-9. PubMed
  10. Lautraite S, Musonda AC, Doehmer J, et al. Flavonoids inhibit genetic toxicity produced by carcinogens in cells expressing CYP1A2 and CYP1A1. Mutagenesis 2002;17:45-53. PubMed
  11. Han, D. H., Denison, M. S., Tachibana, H., and Yamada, K. Relationship between estrogen receptor-binding and estrogenic activities of environmental estrogens and suppression by flavonoids. Biosci.Biotechnol.Biochem 2002;66(7):1479-1487. PubMed
  12. O'Leary, K. A., de Pascual-Tereasa, S., Needs, P. W., Bao, Y. P., O'Brien, N. M., and Williamson, G. Effect of flavonoids and vitamin E on cyclooxygenase-2 (COX-2) transcription. Mutat.Res 7-13-2004;551(1-2):245-254. PubMed
  13. Woodman, O. L. and Chan, E. C. Vascular and anti-oxidant actions of flavonols and flavones. Clin Exp Pharmacol Physiol 2004;31(11):786-790. PubMed
  14. Simons, A. L., Renouf, M., Hendrich, S., and Murphy, P. A. Human gut microbial degradation of flavonoids: structure-function relationships. J Agric.Food Chem 5-18-2005;53(10):4258-4263. PubMed
  15. Kim, H. J., Lee, S. B., Park, S. K., Kim, H. M., Park, Y. I., and Dong, M. S. Effects of hydroxyl group numbers on the B-ring of 5,7-dihydroxyflavones on the differential inhibition of human CYP 1A and CYP1B1 enzymes. Arch Pharm Res 2005;28(10):1114-1121 PubMed
  16. Moon, Y. J., Wang, X., and Morris, M. E. Dietary flavonoids: effects on xenobiotic and carcinogen metabolism. Toxicol In Vitro 2006;20(2):187-210. PubMed
  17. Landolfi, R., Mower, R. L., and Steiner, M. Modification of platelet function and arachidonic acid metabolism by bioflavonoids. Structure-activity relations. Biochem Pharmacol 5-1-1984;33(9):1525-1530. PubMed
  18. Tsyrlov, I. B., Mikhailenko, V. M., and Gelboin, H. V. Isozyme- and species-specific susceptibility of cDNA-expressed CYP1A P-450s to different flavonoids. Biochim.Biophys Acta 4-13-1994;1205(2):325-335. PubMed
  19. Collins, B. M., McLachlan, J. A., and Arnold, S. F. The estrogenic and antiestrogenic activities of phytochemicals with the human estrogen receptor expressed in yeast. Steroids 1997;62(4):365-372. PubMed
  20. Kuiper, G. G., Lemmen, J. G., Carlsson, B., Corton, J. C., Safe, S. H., van der Saag, P. T., van der Burg, B., and Gustafsson, J. A. Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta. Endocrinology 1998;139(10):4252-4263. PubMed
  21. Liu G, Xie W, He AD, et al. Antiplatelet activity of chrysin via inhibiting platelet aIIbß3-mediated signaling pathway. Mol Nutr Food Res 2016;60(9):1984-93.
  22. Noh K, Oh do G, Nepal MR, et al. Pharmacokinetic interaction of chrysin with caffeine in rats. Biomol Ther (Seoul) 2016;24(4):446-52. PubMed
  23. Mohos V, Fliszár-Nyúl E, Ungvári O, et al. Effects of Chrysin and Its Major Conjugated Metabolites Chrysin-7-Sulfate and Chrysin-7-Glucuronide on Cytochrome P450 Enzymes and on OATP, P-gp, BCRP, and MRP2 Transporters. Drug Metab Dispos 2020;48(10):1064-10 PubMed

See these in context on the Chrysin monograph →

Diindolylmethane 14 references
  1. Natl Inst Health, Natl Inst Environmental Health Sci. Indole-3-carbinol. Available at: http://ntp-server.niehs.nih.gov.
  2. Balk JL. Indole-3-carbinol for cancer prevention. Altern Med Alert 2000; 3:105-7.
  3. Riby JE, Chang GHF, Firestone GL, Bjeldanes LF. Ligand-independent activation of estrogen receptor function by 3,3'-diindolylmethane in human breast cancer cells. Biochem Pharmacol 2000;60:167-77. PubMed
  4. Lake BG, Tredger JM, Renwick AB, et al. 3'3-diindolylmethane induces CYP1A2 in cultured precision-cut human liver slices. Xenobiotica 1998;28:803-11. PubMed
  5. Dalessandri, K. M., Firestone, G. L., Fitch, M. D., Bradlow, H. L., and Bjeldanes, L. F. Pilot study: effect of 3,3'-diindolylmethane supplements on urinary hormone metabolites in postmenopausal women with a history of early-stage breast cancer. Nutr Canc PubMed
  6. Reed, G. A., Arneson, D. W., Putnam, W. C., Smith, H. J., Gray, J. C., Sullivan, D. K., Mayo, M. S., Crowell, J. A., and Hurwitz, A. Single-dose and multiple-dose administration of indole-3-carbinol to women: pharmacokinetics based on 3,3'-diindolylmetha
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DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.

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