Major interaction on record — check this product against your medications before combining. Based on 14 of 19 ingredients. Check your meds →
Dietary supplement

Prime Factor (Human Growth Factor Formula) For Men Ingredients & Drug Interactions

by Prime

Prime Factor (Human Growth Factor Formula) For Men label
See full label image
Tablet Or Pill Category: Other Combinations
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 16, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Prime Factor (Human Growth Factor Formula) For Men against your medications. The heart of this page is the interaction checker and the full interaction report — how this product’s ingredients may interact with prescription and over-the-counter medicines you may be taking.

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

The interaction bottom line Most serious interaction: Major

Prime Factor (Human Growth Factor Formula) For Men is a dietary supplement by Prime with 19 active ingredients. Its ingredients are commonly taken for general nutrition and energy, skin and hair health, acne (topical and oral).Based on those ingredients, 1,664 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ashwagandha root extract, Fo Ti root extract, Panax ginseng. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Prime Factor (Human Growth Factor Formula) For Men by Prime

Ask about any prescription or over-the-counter medication and we check it for interactions with Prime Factor (Human Growth Factor Formula) For Men by Prime — and tell you which ingredient is responsible.

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Computed from our clinical databases

HelloPharmacist Scorecard of Prime Factor (Human Growth Factor Formula) For Men by Prime

Four independent checks of what is known — a summary of the available information, not a grade of the product itself.

Evidence for Intended Use
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 assessable

The stated purpose hasn't been mapped to our evidence data yet.

Why this rating?
  • We haven't mapped this product's purpose to our evidence data yet — it'll be graded on the next content refresh.
Ingredient Transparency
Low

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

Why this rating?
  • The label discloses an exact amount for 4 of its 19 active ingredients.
  • “Proprietary Blend” is a proprietary blend — the label gives one combined amount (1,564 mg) without saying how much of each component you get.
Known Interaction Concern
Major identified

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

Why this rating?
  • 13 of the 14 matched ingredients can interact with medications — Iodine, Dhea, Schisandra, Gamma-aminobutyric Acid (gaba), Fo-ti, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 1,665 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.
Safety Information
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 14 of the 14 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 14 of 14.
  • General safety write-ups exist for 14 of 14.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

HelloPharmacist summaryFormula with limited ingredient disclosure with no assessable stated purpose. Major medication interactions have been identified, and safety information is well characterized.

Assessment coverage: 14 of 19 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Feb 23, 2012.

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 Prime Factor (Human Growth Factor Formula) For Men, straight from the product label.

Brand Prime
Net contents 63 Tablet(s)
Market status Off market
Date entered into DSLD Feb 23, 2012
DSLD ID 6182
Product type Other Combinations
Supplement form Tablet Or Pill
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult Male (18-50 Years), Seniors/Mature (>50 Years) - Men ONLY
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 Prime Factor (Human Growth Factor Formula) For Men by Prime, 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:
3 Tablet(s)
Maximum serving Sizes:
3 Tablet(s)
Servings per container
21
IngredientAmount% DV
Pantothenic Acid100 mg1000%
Iodine75 mcg50%
Dehydroepiandrosterone0 NP--
Zinc10 mg67%
Schizandra berry extract0 NP--
Ashwagandha root extract0 NP--
Fo Ti root extract0 NP--
Proprietary Blend1564 mg--
Astragalus root extract0 NP--
Silymarin0 NP--
Chromium50 mcg42%
Lycium berry extract0 NP--
Gamma-Aminobutyric Acid0 NP--
Coleus forskohlii tuber extract0 NP--
L-Alpha-Glycerylphosphorylcholine Hydrate0 NP--
DNA0 NP--
RNA0 NP--
Panax ginseng0 NP--
Ornithine-Alpha-Ketogluterate0 NP--
Red Date fruit extract0 NP--

Other ingredients: Dicalcium Phosphate, Guar Gum, Microcrystalline Cellulose, Calcium Carbonate, Stearic Acid, Vegetable Stearin, citrus pectin, Magnesium Stearate, Silica, Film Coat Ingredients

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.
FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Directions for use: Men over the age of 30, take 3 tablets daily, either with Ultra Prime(TM) of after the first meal of the day. Take for 3 consecutive weeks, skip the fourth week, and repeat.

Precautions

KEEP OUT OF THE REACH OF CHILDREN.

Do not purchase if safety seal is broken or missing.

If you are under the care of a physician or taking any prescription medication, consult a physician before using this product.

Warning: For use only by men 30 years of age or older. Do not exceed recommended daily serving. Do not use this product while you are suffering from a cold or flu.

FDA Disclaimer Statement

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

Storage

Protect from heat, light and moisture. Store at 15-30°C (59-86°F).

Formula

Contains: Fish (Salmon)

General Statements

Made in the USA

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General

REV 308

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See for yourself

Prime Factor (Human Growth Factor Formula) For Men by Prime label

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

Prime Factor (Human Growth Factor Formula) For Men label

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

View the full label (PDF)
What’s inside

The Ingredients in Prime Factor (Human Growth Factor Formula) For Men by Prime

These are the 19 active ingredients this product is made of. Select any to open its full monograph.

Serving size3 Tablet(s) Dosage formTablet Or Pill Servings per container21 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.

Pantothenic Acid

No known
interactions
100 mg per serving Form: D-Calcium Pantothenate

Pantothenic acid is vitamin B5, an essential nutrient your body uses to turn food into energy. True deficiency is very rare because it is found in nea...

Pantothenic Acid monograph & interactions

Iodine

Interacts with
7 drugs
75 mcg per serving Form: Kelp

Iodine is an essential mineral your body needs to make thyroid hormones, and most people get enough from iodized salt, dairy, and seafood. Supplements...

Iodine monograph & interactions

Zinc

Interacts with
67 drugs
10 mg per serving Form: Zinc Arginate

Zinc is an essential mineral that your body needs for immune function, wound healing, taste, and smell. Most people get enough from food, but suppleme...

Zinc monograph & interactions

Proprietary Blend

1564 mg per serving

Chromium

Interacts with
178 drugs
50 mcg per serving Form: Chromium Dinicotinate Glycinate

Chromium is an essential trace mineral involved in how the body handles sugar and fat. Some studies suggest it may modestly help blood sugar control i...

Chromium monograph & interactions

Other (inactive) ingredients: Dicalcium Phosphate, Guar Gum, Microcrystalline Cellulose, Calcium Carbonate, Stearic Acid, Vegetable Stearin, Citrus pectin, Magnesium Stearate, Silica, Film Coat Ingredients. These complete the product’s ingredient list but are not active constituents.

Interaction report

Prime Factor (Human Growth Factor Formula) For Men by Prime Drug Interactions

Prime Factor (Human Growth Factor Formula) For Men contains 19 ingredients, and 13 of them have known drug interactions. Altogether they interact with 1,664 medications. Here’s the picture, then you can look up your own drug.

Want to check YOUR meds against Prime Factor (Human Growth Factor Formula) For Men?

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
1,664Drugs
31 Major 1,591 Moderate 42 Minor

Ingredients driving the most interactions

Ashwagandha root extract 1,372
Fo Ti root extract 1,257
Panax ginseng 1,130
Lycium berry extract 1,000
Coleus forskohlii tuber extract 915

Individual Drug Interactions

The ingredients in Prime Factor (Human Growth Factor Formula) For Men interact with 1,664 drugs. Click any drug to see the details.

13 of the 19 ingredients in Prime Factor (Human Growth Factor Formula) For Men interact with drugs. Each result below shows which ingredient is responsible. Ashwagandha root extract Fo Ti root extract Panax ginseng Lycium berry extract Coleus forskohlii tuber extract Schizandra berry extract Dehydroepiandrosterone Gamma-Aminobutyric Acid Astragalus root extract Chromium Zinc L-Alpha-Glycerylphosphorylcholine Hydrate Iodine

Each ingredient & the kinds of drugs it affects

For each ingredient in Prime Factor (Human Growth Factor Formula) For Men with known interactions, here are the types of medications they can affect. Open any type for the detail — or search your exact drug in the checker above.

Ashwagandha root extract10 drug types · 1,372 drugs

Antidiabetes Drugs

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

Likelihood Possible Evidence B
Antihypertensive Drugs

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

Likelihood Possible Evidence D
Benzodiazepines

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

Likelihood Possible Evidence D
Cns Depressants

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

Likelihood Possible Evidence D
Hepatotoxic Drugs

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

Likelihood Possible Evidence D
Immunosuppressants

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

Likelihood Possible Evidence D
Thyroid Hormone

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

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

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

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

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

Likelihood Possible Evidence D
Serotonergic Drugs

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

Likelihood Possible Evidence C
Ashwagandha root extract full monograph & interactions

Fo Ti root extract17 drug types · 1,257 drugs

Anticoagulant/Antiplatelet Drugs

Fo-ti has been linked to cases of acute liver failure which can decrease clotting factor production and increase the effects of anticoagulants. In one case, a patient who had been stable on warfarin presented with acute hepatitis and an INR elevated to 14.98. The patient had been taking fo-ti for 90 days prior to admission. Discontinuation of warfarin and fo-ti lead to a decrease in the INR and full recovery. Theoretically, concomitant use of fo-ti with anticoagulant or antiplatelet drugs may increase the risk of bleeding in some patients. Until more is known, monitor patients taking fo-ti and drugs that affect bleeding.
Some of these drugs include aspirin, clopidogrel (Plavix), dalteparin (Fragmin), dipyridamole (Persantine), enoxaparin (Lovenox), heparin, ticlopidine (Ticlid), warfarin (Coumadin), and others.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, fo-ti might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Fo-ti reportedly has hypoglycemic effects.

Likelihood Possible Evidence D
Contraceptive Drugs

Theoretically, taking large amounts of fo-ti might interfere with contraceptive drugs due to competition for estrogen receptors.
In vitro research suggests that fo-ti extract has estrogenic activity.

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

Theoretically, fo-ti might increase or decrease the levels and clinical effects of drugs metabolized by CYP1A2.
In vitro research suggests that fo-ti might inhibit CYP1A2. Additionally, in vitro research suggests that the degree of CYP1A2 inhibition depends on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, in an animal study, an aqueous extract of fo-ti inhibited CYP1A2 while an alcoholic extract of fo-ti induced CYP1A2. Induction or inhibition of CYP1A2 by fo-ti has not been reported in humans.

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

Theoretically, fo-ti might increase the levels and clinical effects of drugs metabolized by CYP2B6.
Animal research suggests that fo-ti might inhibit CYP2B6. One in vitro study suggests that the degree of CYP2B6 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this interaction has not been reported in humans.

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

Theoretically, fo-ti may increase the levels and clinical effects of drugs metabolized by CYP2C19.
Animal and in vitro research suggests that fo-ti may inhibit CYP2C19. An in vitro study suggests that the degree of CYP2C19 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this interaction has not been reported in humans.

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

Theoretically, fo-ti might increase the levels and clinical effects of drugs metabolized by CYP2C8.
In vitro research suggests that fo-ti might inhibit CYP2C8. However, this interaction has not been reported in humans.

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

Theoretically, fo-ti may increase the levels and clinical effects of drugs metabolized by CYP2C9.
Animal and in vitro research suggests that fo-ti may inhibit CYP2C9. However, this interaction has not been reported in humans.

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

Theoretically, fo-ti may increase the levels and clinical effects of drugs metabolized by CYP2D6.
Animal research suggests that fo-ti might inhibit CYP2D6. Additionally, an in vitro study suggests that the degree of CYP2D6 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this interaction has not been reported in humans.

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

Theoretically, fo-ti might increase the levels and clinical effects of drugs metabolized by CYP3A4.
In vitro research suggests that fo-ti might inhibit CYP3A4. One in vitro study suggests that the degree of CYP3A4 inhibition may depend on the type of fo-ti extract (i.e., the raw plant leads to greater inhibition than extensively processed extracts). However, this evidence conflicts with animal research suggesting that fo-ti does not inhibit CYP3A4. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Digoxin (Lanoxin)

Theoretically, fo-ti, particularly raw fo-ti root, might increase the risk of hypokalemia and cardiotoxicity when taken with digoxin.
Raw fo-ti root contains anthraquinone derivatives, which might have stimulant laxative effects. In vitro research shows that fermented and processed fo-ti root have reduced laxative effects compared with raw fo-ti root.

Likelihood Possible Evidence D
Diuretic Drugs

Theoretically, fo-ti, particularly raw fo-ti root, might increase the risk of hypokalemia when taken with diuretic drugs.
Raw fo-ti root contains anthraquinone derivatives, which might have stimulant laxative effects and compound diuretic-induced potassium loss. In vitro research shows that fermented and processed fo-ti root have reduced laxative effects compared with raw fo-ti root.

Likelihood Possible Evidence D
Estrogens

Theoretically, taking large amounts of fo-ti might interfere with hormone replacement therapy through competition for estrogen receptors.
In vitro research suggests that fo-ti extract has estrogenic activity.

Likelihood Probable Evidence D
Hepatotoxic Drugs

Theoretically, fo-ti might increase the risk of liver damage when taken with hepatotoxic drugs.
Fo-ti has been linked to liver damage in many reports.

Likelihood Possible Evidence D
Stimulant Laxatives

Theoretically, fo-ti, particularly raw fo-ti root, might increase the risk of fluid and electrolyte depletion when taken with stimulant laxatives.
Raw fo-ti root contains anthraquinone derivatives, which might have stimulant laxative effects. However, in vitro research shows that fermented and processed fo-ti root have reduced laxative effects compared with raw fo-ti root.

Likelihood Possible Evidence D
Sulindac (Clinoril)

Theoretically, fo-ti might increase or decrease the levels and clinical effects of sulindac.
Animal research suggests that the type of fo-ti extract might affect the levels of sulindac differently; the raw plant may increase levels, but processed parts may decrease levels. Induction or inhibition of CYP1A2 by fo-ti has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, fo-ti might increase the effects and adverse effects of warfarin.
Fo-ti may have stimulant laxative effects and cause diarrhea, especially when the raw or unprocessed fo-ti root is used. Diarrhea can increase the effects of warfarin, increase international normalized ratio (INR), and increase the risk of bleeding. Also, fo-ti has been linked to cases of acute liver failure which can decrease clotting factor production and increase the effects of warfarin. In one case, a patient who had been stable on warfarin presented with acute hepatitis and an INR elevated to 14.98. The patient had been taking fo-ti for 90 days prior to admission. Discontinuation of warfarin and fo-ti lead to a decrease in the INR and full recovery.

Likelihood Possible Evidence D
Fo Ti root extract full monograph & interactions

Panax ginseng20 drug types · 1,130 drugs

Anticoagulant/Antiplatelet Drugs

Although Panax ginseng has shown antiplatelet effects in the laboratory, it is unlikely to increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that ginsenoside constituents in Panax ginseng might decrease platelet aggregation. However, research in humans suggests that ginseng does not affect platelet aggregation. Animal research indicates low oral bioavailability of Rb1 and rapid elimination of Rg1, which might explain the discrepancy between in vitro and human research. Until more is known, use with caution in patients concurrently taking anticoagulant or antiplatelet drugs.

Likelihood Unlikely Evidence B
Antidiabetes Drugs

Theoretically, taking Panax ginseng with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Monitor blood glucose levels closely.

Likelihood Probable Evidence B
Caffeine

Theoretically, taking Panax ginseng with caffeine might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects. Theoretically, caffeine might have an additive effect on the stimulant effects of Panax ginseng.

Likelihood Probable Evidence B
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, Panax ginseng might increase levels of drugs metabolized by CYP2D6. However, research is conflicting.
There is some evidence that Panax ginseng can inhibit the CYP2D6 enzyme by approximately 6%. In addition, in animal research, Panax ginseng inhibits the metabolism of dextromethorphan, a drug metabolized by CYP2D6, by a small amount. However, contradictory research suggests Panax ginseng might not inhibit CYP2D6. Until more is known, use Panax ginseng cautiously in patients taking drugs metabolized by these enzymes.

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

Theoretically, Panax ginseng might increase or decrease levels of drugs metabolized by CYP3A4.
Panax ginseng may affect the clearance of drugs metabolized by CYP3A4. One such drug is imatinib. Inhibition of CYP3A4 was believed to be responsible for a case of imatinib-induced hepatotoxicity. In contrast, Panax ginseng has been shown to increase the clearance of midazolam, another drug metabolized by CYP3A4. Clinical research shows that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng. Until more is known, use Panax ginseng cautiously in combination with CYP3A4 substrates.

Likelihood Possible Evidence B
Estrogens

Theoretically, concomitant use of large amounts of Panax ginseng might interfere with hormone replacement therapy.
Laboratory research and some case reports suggest that Panax ginseng can have estrogenic effects due to competition for estrogen receptors. The estrogenic activity is attributed to the ginsenoside constituents of Panax ginseng.

Likelihood Possible Evidence D
Furosemide (Lasix)

Theoretically, Panax ginseng might reduce the effects of furosemide.
There is some concern that Panax ginseng might contribute to furosemide resistance. There is one case of resistance to furosemide diuresis in a patient taking a germanium-containing ginseng product.

Likelihood Possible Evidence D
Imatinib (Gleevec)

Theoretically, Panax ginseng might increase the effects and adverse effects of imatinib.
A case of imatinib-induced hepatotoxicity has been reported for a 26-year-old male with chronic myelogenous leukemia stabilized on imatinib for 7 years. The patient took imatinib 400 mg along with a Panax ginseng-containing energy drink daily for 3 months. Since imatinib-associated hepatotoxicity typically occurs within 2 years of initiating therapy, it is believed that Panax ginseng affected imatinib toxicity though inhibition of cytochrome P450 3A4. CYP3A4 is the primary enzyme involved in imatinib metabolism.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, Panax ginseng use might interfere with immunosuppressive therapy.
Panax ginseng might have immune system stimulating properties.

Likelihood Possible Evidence B
Insulin

Theoretically, taking Panax ginseng with insulin might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Insulin dose adjustments might be necessary in patients taking Panax ginseng; use with caution.

Likelihood Probable Evidence B
Midazolam (Versed)

Theoretically, Panax ginseng may increase the clearance of midazolam.
Midazolam is metabolized by cytochrome P450 3A4 (CYP3A4). Clinical research suggests that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng.

Likelihood Probable Evidence B
Monoamine Oxidase Inhibitors (Maois)

Theoretically, Panax ginseng can interfere with MAOI therapy.
Concomitant use of Panax ginseng with phenelzine (Nardil) is associated with insomnia, headache, tremors, and hypomania.

Likelihood Probable Evidence D
Nifedipine (Procardia)

Theoretically, taking Panax ginseng with nifedipine might increase serum levels of nifedipine and the risk of hypotension.
Preliminary clinical research shows that concomitant use can increase serum levels of nifedipine in healthy volunteers. This might cause the blood pressure lowering effects of nifedipine to be increased when taken concomitantly with Panax ginseng.

Likelihood Possible Evidence B
Qt Interval-Prolonging Drugs

Theoretically, Panax ginseng has an additive effect with drugs that prolong the QT interval and potentially increase the risk of ventricular arrhythmias. However, research is conflicting.
Clinical research shows that short-term use of Panax ginseng can increase the QT interval. However, no changes in QT interval have been identified with prolonged use.

Likelihood Possible Evidence B
Raltegravir (Isentress)

Theoretically, taking Panax ginseng with raltegravir might increase the risk of liver toxicity.
A case report suggests that concomitant use of Panax ginseng with raltegravir can increase serum levels of raltegravir, resulting in elevated liver enzymes levels.

Likelihood Possible Evidence D
Selegiline (Eldepryl)

Theoretically, Panax ginseng might increase or decrease levels of selegiline, possibly altering the effects and side effects of selegiline.
Animal research shows that taking selegiline with a low dose of Panax ginseng extract (1 gram/kg) reduces selegiline bioavailability, while taking a high dose of Panax ginseng extract (3 grams/kg) increases selegiline bioavailability. More research is needed to confirm these effects.

Likelihood Possible Evidence D
Stimulant Drugs

Theoretically, taking Panax ginseng with stimulant drugs might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Panax ginseng might affect the clearance of warfarin. However, this interaction appears to be unlikely.
There has been a single case report of decreased effectiveness of warfarin in a patient who also took Panax ginseng. However, it is questionable whether Panax ginseng was the cause of this decrease in warfarin effectiveness. Some research in humans and animals suggests that Panax ginseng does not affect the pharmacokinetics of warfarin. However, other research in humans suggests that Panax ginseng might modestly increase the clearance of the S-warfarin isomer. More evidence is needed to determine whether Panax ginseng causes a significant interaction with warfarin.

Likelihood Unlikely Evidence B
Fexofenadine (Allegra)

Theoretically, Panax ginseng might decrease blood levels of oral or intravenous fexofenadine.
Animal research suggests that taking Panax ginseng in combination with oral or intravenous fexofenadine may reduce the bioavailability of fexofenadine. Some scientists have attributed this effect to the ability of Panax ginseng to increase the expression of P-glycoprotein.

Likelihood Possible Evidence D
Lopinavir/Ritonavir (Kaletra)

Although Panax ginseng has demonstrated variable effects on cytochrome P450 3A4 (CYP3A4), which metabolizes lopinavir, Panax ginseng is unlikely to alter levels of lopinavir/ritonavir.
Lopinavir is metabolized by CYP3A4 and is administered with the CYP3A4 inhibitor ritonavir to increase its plasma concentrations. Panax ginseng has shown variable effects on CYP3A4 activity in humans. However, taking Panax ginseng (Vitamer Laboratories) 500 mg twice daily for 14 days did not alter the pharmacokinetics of lopinavir/ritonavir in 12 healthy volunteers.

Likelihood Unlikely Evidence B
Panax ginseng full monograph & interactions

Lycium berry extract8 drug types · 1,000 drugs

Warfarin (Coumadin)

Goji can increase the effects of warfarin and possibly increase the risk of bleeding.
There are at least 5 case reports of increased international normalized ratio (INR) in patients stabilized on warfarin who began drinking goji juice, concentrated goji tea, or goji wine. Goji may inhibit the metabolism of warfarin by cytochrome P450 2C9 (CYP2C9).

Likelihood Probable Evidence D
Antihypertensive Drugs

Theoretically, concomitant use of goji root bark, but not goji fruit, with antihypertensive drugs might have additive effects.
Animal and in vitro research suggest that goji root bark has hypotensive effects. However, goji fruit juice does not appear to reduce systolic or diastolic blood pressure in humans.

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

Theoretically, goji berry might inhibit CYP2C19 and reduce metabolism of CYP2C19 substrates.
In vitro research shows that goji berry tincture and juice inhibit CYP2C19 enzymes. Concomitant use with goji may decrease metabolism and increase levels of CYP2C19 substrates. However, this has not been reported in humans.

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

Theoretically, goji berry might inhibit CYP2C9 and reduce metabolism of CYP2C9 substrates.
In vitro research shows that goji berry tincture and juice inhibit CYP2C9 enzymes. Additionally, multiple case reports suggest that goji berry concentrated tea and juice inhibit the metabolism of warfarin, a CYP2C9 substrate. Concomitant use with goji may decrease metabolism and increase levels of CYP2C9 substrates.

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

Theoretically, goji berry might inhibit CYP2D6 and reduce metabolism of CYP2D6 substrates.
In vitro research shows that goji berry juice inhibits CYP2D6 enzymes. Concomitant use with goji may decrease metabolism and increase levels of CYP2D6 substrates. However, this has not been reported in humans.

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

Theoretically, goji berry might inhibit CYP3A4 and reduce metabolism of CYP3A4 substrates.
In vitro research shows that goji berry juice inhibits CYP3A4 enzymes. Concomitant use with goji may decrease metabolism and increase levels of CYP3A4 substrates. However, this has not been reported in humans.

Likelihood Possible Evidence D
Flecainide (Tambocor)

Theoretically, goji berry might increase the levels and clinical effects of flecainide.
In one case report, a 75-year-old patient stable on flecainide and warfarin presented to the emergency room with fainting and pleomorphic arrhythmia caused by flecainide toxicity. Flecainide toxicity was attributed to drinking 1-2 glasses of concentrated goji tea daily for 2 weeks. Theoretically, goji may have inhibited the cytochrome P450 2D6 (CYP2D6) metabolism of flecainide.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, concomitant use of goji fruit polysaccharides or goji root bark with antidiabetes drugs might have additive effects.
Animal and in vitro research show that goji root bark and fruit polysaccharides might have hypoglycemic effects. However, clinical research has only shown that taking goji fruit polysaccharides with or without antidiabetes drugs modestly reduces postprandial glucose when compared with control, with no reports of hypoglycemia.

Likelihood Possible Evidence B
Lycium berry extract full monograph & interactions

Coleus forskohlii tuber extract7 drug types · 915 drugs

Calcium Channel Blockers

Theoretically, combining coleus with calcium channel blockers might increase the coronary vasodilatory effects.
Forskolin, a constituent of coleus, and calcium channel blockers both cause coronary vasodilatory effects.

Likelihood Probable Evidence B
Nitrates

Theoretically, combining coleus with nitrates might increase the coronary vasodilatory effects.
Forskolin, a constituent of coleus, and nitrates both cause coronary vasodilatory effects.

Likelihood Probable Evidence B
Anticoagulant/Antiplatelet Drugs

Theoretically, concomitant use of coleus and anticoagulant or antiplatelet drugs might increase the risk of bruising and bleeding.
In vitro and animal research shows that forskolin, a constituent of coleus, can inhibit platelet aggregation and adhesion.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, combining coleus with antihypertensive drugs might cause additive blood pressure lowering effects and increase the risk of hypotension.
Animal research shows that forskolin, a constituent of coleus, may lower blood pressure.

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

Theoretically, taking coleus may affect drugs metabolized by CYP2C9 and increase the risk of adverse effects or reduce the effectiveness.
Research on the effect of coleus on CYP2C9 is conflicting. Some animal research shows that coleus extract can induce CYP2C9, while in vitro research shows that coleus can inhibit CYP2C9. Until more is known, advise patients that taking coleus might increase or decrease levels of drugs metabolized by CYP2C9.

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

Theoretically, taking coleus might decrease serum levels of drugs metabolized by CYP3A4.
In vitro research shows that coleus can activate 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 coleus and other drugs affected by these enzymes.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, taking coleus may affect the metabolism of warfarin and increase the risk of adverse effects or reduce the effectiveness.
Some animal research shows that coleus extract can induce cytochrome P450 2C9 (CYP2C9), an enzyme that metabolizes warfarin. However, other in vitro research shows that coleus can inhibit CYP2C9. Theoretically, taking coleus with drugs metabolized by CYP2C9 might affect drug levels and the risk of adverse effects. Until more is known, advise patients that taking coleus might increase or decrease levels of warfarin.

Likelihood Possible Evidence D
Coleus forskohlii tuber extract full monograph & interactions

Schizandra berry extract12 drug types · 803 drugs

Cyclophosphamide

Theoretically, schisandra might increase the levels and clinical effects of cyclophosphamide.
In vitro research shows that schisandra increases the concentration of cyclophosphamide, likely through inhibition of cytochrome P450 3A4. After multiple doses of the schisandra constituents schisandrin A and schisantherin A, the maximum concentration of cyclophosphamide was increased by 7% and 75%, respectively, while the overall exposure to cyclophosphamide was increased by 29% and 301%, respectively.

Likelihood Probable Evidence D
Cyclosporine (Neoral, Sandimmune)

Schisandra can increase the levels and clinical effects of cyclosporine.
A small observational study in children with aplastic anemia found that taking schisandra with cyclosporine increased cyclosporine trough levels by 93% without increasing the risk of adverse events. However, the dose of cyclosporine was reduced in 9% of children to maintain appropriate cyclosporine blood concentrations.

Likelihood Probable Evidence B
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, schisandra might increase the levels and clinical effects of CYP2C19 substrates.
In vitro research shows that schisandra inhibits CYP2C19, and animal research shows that schisandra increases the concentration of voriconazole, a CYP2C19 substrate. Theoretically, schisandra may also inhibit the metabolism of other CYP2C19 substrates. This effect has not been reported in humans.

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

Theoretically, schisandra might decrease the levels and clinical effects of CYP2C9 substrates.
In vitro and animal research suggests that schisandra induces CYP2C9 enzymes. This effect has not been reported in humans.

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

Schisandra can increase the levels and clinical effects of drugs metabolized by CYP3A4.
Most clinical and laboratory research shows that schisandra, administered either as a single dose or up to twice daily for 14 days, inhibits CYP3A4 and increases the concentration of CYP3A4 substrates such as cyclophosphamide, midazolam, tacrolimus, and talinolol. Although one in vitro and animal study shows that schisandra may induce CYP3A4 metabolism, this effect appears to be overpowered by schisandra's CYP3A4 inhibitory activity and has not been reported in humans.

Likelihood Probable Evidence D
Midazolam (Versed)

Schisandra can increase the levels and clinical effects of midazolam.
A small pharmacokinetic study in healthy adults shows that taking schisandra extract (Hezheng Pharmaceutical Co.) containing deoxyschizandrin 33.75 mg twice daily for 8 days and a single dose of midazolam 15 mg on day 8 increases the overall exposure to midazolam by about 119%, increases the peak plasma level of midazolam by 86%, and decreases midazolam clearance by about 52%. This effect has been attributed to inhibition of CYP3A4 by schisandra.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Schisandra might increase the levels and clinical effects of P-glycoprotein substrates.
In vitro research shows that schisandra extracts and constituents such as schisandrin B inhibit P-glycoprotein mediated efflux in intestinal cells and in P-glycoprotein over-expressing cell lines. Additionally, a small clinical study shows that schisandra increases the peak concentration and overall exposure to talinolol, a P-glycoprotein probe substrate. Theoretically, schisandra might inhibit the efflux of other P-glycoprotein substrates.

Likelihood Possible Evidence D
Sirolimus (Rapamune)

Schisandra can increase the levels and clinical effects of sirolimus.
A small pharmacokinetic study in healthy volunteers shows that taking 3 capsules of schisandra (Hezheng Pharmaceutical Company) containing a total of 33.75 mg deoxyschizandrin twice daily for 13 days and then taking a single dose of sirolimus 2 mg increases the overall exposure and peak level of sirolimus by two-fold. This effect is thought to be due to inhibition of cytochrome P450 3A4 by schisandra, as well as possible inhibition of the P-glycoprotein drug transporter.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Schisandra can increase the levels and clinical effects of tacrolimus.
Clinical research in healthy children and adults, transplant patients, and patients with nephrotic syndrome and various rheumatic immunologic disorders shows that taking schisandra with tacrolimus increases tacrolimus peak levels by 183% to 268%, prolongs or delays time to peak tacrolimus concentrations, increases overall exposure to tacrolimus by 126% to 343%, and decreases tacrolimus clearance by 19% to 73%. This effect is thought to be due to inhibition of P-glycoprotein drug transporter and CYP3A4 and CYP3A5 by schisandra. Some clinical and observational studies suggest that schisandra increases tacrolimus levels similarly in both expressors and non-expressors of CYP3A5, while other studies suggest it does so to a greater degree in CYP3A5 expressors than non-expressors. Animal research suggests that the greatest increase in tacrolimus levels occurs when schisandra is taken either concomitantly or up to 2 hours before tacrolimus, and clinical and observational research in humans suggests that schisandra may increase whole blood levels of tacrolimus and decrease clearance of tacrolimus in a dose-dependent manner.

Likelihood Probable Evidence B
Talinolol

Schisandra can increase the levels and clinical effects of talinolol.
A small pharmacokinetic study in healthy volunteers shows that taking schisandra extract 300 mg twice daily for 14 days with a single dose of talinolol 100 mg on day 14 increases the peak talinolol level by 51% and the overall exposure to talinolol by 47%. This effect is thought to be due to the possible inhibition of cytochrome P450 3A4 and P-glycoprotein by schisandra. tly.

Likelihood Probable Evidence B
Voriconazole (Vfend)

Theoretically, schisandra might increase the levels and clinical effects of voriconazole.
Animal research shows that oral schisandra given daily for 1 or 14 days increases levels of intravenously administered voriconazole, a cytochrome P450 (CYP) 2C19 substrate. This effect is thought to be due to inhibition of CYP2C19 by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, schisandra might decrease the levels and clinical effects of warfarin.
Animal research suggests that oral schisandra extract, given daily for 6 days, reduces levels of intravenously administered warfarin. This effect might be due to the induction of cytochrome P450 (CYP) 2C9 metabolism by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Schizandra berry extract full monograph & interactions

Dehydroepiandrosterone10 drug types · 776 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, DHEA might increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Human and laboratory research show that DHEA and DHEA-S can inhibit platelet aggregation.

Likelihood Possible Evidence D
Antidepressant Drugs

Theoretically, DHEA might increase the risk of psychiatric adverse events when used with antidepressants.
In a human case report, the use of a selective serotonin reuptake inhibitor (SSRI) with DHEA caused a manic episode. Concern for this interaction may be greater in younger individuals with higher baseline DHEA levels.

Likelihood Possible Evidence D
Aromatase Inhibitors

Theoretically, DHEA might interfere with the clinical effects of aromatase inhibitors.
DHEA is a potent estrogen agonist, which may antagonize the anti-estrogen activity of aromatase inhibitors.

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

Theoretically, DHEA might increase the levels of drugs metabolized by CYP3A4.
Some preliminary evidence shows that DHEA may inhibit CYP3A4; however, the clinical significance of this potential interaction is not known.

Likelihood Possible Evidence D
Fulvestrant (Faslodex)

Theoretically, DHEA might interfere with the anti-estrogen effects of fulvestrant.
DHEA is a potent estrogen agonist. Some research shows that it can overcome the estrogen receptor antagonist action of fulvestrant in estrogen-receptor positive cancer cells.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, DHEA might interfere with the anti-estrogen effects of tamoxifen.
DHEA is a potent estrogen agonist. Some research shows that it can overcome the estrogen receptor antagonist activity of tamoxifen in estrogen-receptor positive cancer cells.

Likelihood Possible Evidence D
Triazolam (Halcion)

DHEA can increase blood levels of triazolam.
Administration of DHEA 200 mg daily for two weeks was shown to inhibit the cytochrome P450 3A4 (CYP3A4) metabolism of triazolam. This inhibition appears to be due to DHEA-S, rather than DHEA.

Likelihood Probable Evidence D
Tuberculosis Vaccine

DHEA might reduce the effectiveness of the tuberculosis vaccine.
Animal research shows that high doses of DHEA can reduce the efficacy of the Bacillus Calmette-Guérin (BCG) tuberculosis vaccine.

Likelihood Possible Evidence D
Estrogens

Theoretically, DHEA might increase the effects and adverse effects of estrogen therapy.
DHEA is a precursor to estrogen and androgen and is metabolized into those substances. In clinical research, DHEA supplements increase the levels of these hormones. Also, in clinical research, estrogen-progestin oral contraceptives and conjugated estrogens reduce blood levels of DHEA and DHEA-S. The clinical significance of these findings is unclear.

Likelihood Possible Evidence D
Testosterone

Theoretically, DHEA might increase the effects and side effects of testosterone therapy.
DHEA is a precursor to estrogen and androgen and is metabolized into those substances. In clinical research, DHEA supplements increase the levels of these hormones. The clinical significance of these findings is unclear.

Likelihood Possible Evidence D
Dehydroepiandrosterone full monograph & interactions

Gamma-Aminobutyric Acid2 drug types · 419 drugs

Antihypertensive Drugs

Theoretically, taking GABA with antihypertensive drugs might increase the risk of hypotension.
Some clinical research shows that GABA can decrease blood pressure in patients with hypertension.

Likelihood Possible Evidence B
Cns Depressants

Theoretically, GABA might have additive sedative effects when used in conjunction with CNS depressants. However, it is unclear if this concern is clinically relevant.
Endogenous GABA has well-established relaxant effects and GABA(A) receptors have an established physiological role in sleep. However, the effects of GABA supplements are unclear, as it is unknown whether exogenous GABA crosses the blood-brain barrier. Although there have been limited reports of drowsiness or tiredness with GABA supplements, these effects have not been widely reported in clinical studies. Additionally, intravenous GABA 0.1-1 mg/kg has been shown to induce anxiety in a dose-dependent manner.

Likelihood Unlikely Evidence D
Gamma-Aminobutyric Acid full monograph & interactions

Astragalus root extract4 drug types · 208 drugs

Antidiabetes Drugs

Theoretically, taking astragalus with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research in humans shows that astragalus might have hypoglycemic effects. Theoretically, taking astragalus, especially in combination with other hypoglycemic agents, might increase the risk of hypoglycemia.

Likelihood Probable Evidence A
Cyclophosphamide

Theoretically, astragalus might interfere with cyclophosphamide therapy.
Evidence regarding the effect of astragalus on immunosuppression caused by cyclophosphamide is conflicting. Some animal research suggests that astragalus reverses cyclophosphamide-induced immunosuppression. However, other animal research shows no effect.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, astragalus might interfere with immunosuppressive therapy.
Astragalus seems to stimulate immune function. Theoretically, taking astragalus might decrease the effects of immunosuppressive therapy.

Likelihood Possible Evidence D
Lithium

Theoretically, astragalus might increase levels and adverse effects of lithium.
Animal research suggests that astragalus has diuretic properties. Theoretically, due to this diuretic effect, astragalus might reduce excretion and increase levels of lithium.

Likelihood Probable Evidence D
Astragalus root extract full monograph & interactions

Chromium5 drug types · 178 drugs

Antidiabetes Drugs

Theoretically, chromium may have additive effects with antidiabetic agents and increase the risk of hypoglycemia.
Some research shows that taking chromium might lower blood glucose levels, especially in patients with poorly controlled type 2 diabetes.

Likelihood Possible Evidence A
Insulin

Theoretically, concomitant use of chromium and insulin might increase the risk of hypoglycemia.
In clinical research, chromium has been shown to increase insulin sensitivity,

Likelihood Possible Evidence B
Levothyroxine (Synthroid, Others)

Chromium might bind levothyroxine in the intestinal tract and decrease levothyroxine absorption.
Clinical research in healthy volunteers shows that taking chromium picolinate 1000 mcg with levothyroxine 1 mg decreases serum levels of levothyroxine by 17% when compared to taking levothyroxine alone. Advise patients to take levothyroxine at least 30 minutes before or 3-4 hours after taking chromium.

Likelihood Probable Evidence B
Aspirin

Theoretically, aspirin might increase chromium absorption.
Animal research suggests that aspirin may increase chromium absorption and chromium levels in the blood.

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

NSAIDs might increase chromium levels in the body.
Drugs that are prostaglandin inhibitors, such as NSAIDs, seem to increase chromium absorption and retention.

Likelihood Possible Evidence D
Chromium full monograph & interactions

Zinc10 drug types · 67 drugs

Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)

Theoretically, zinc 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 zinc containing products.

Likelihood Probable Evidence D
Cephalexin (Keflex)

Zinc might decrease cephalexin levels by chelating with cephalexin in the gut and preventing its absorption.
A pharmacokinetic study shows that zinc sulfate 250 mg taken concomitantly with cephalexin 500 mg decreases peak levels of cephalexin by 31% and reduces the exposure to cephalexin by 27%. Also, taking zinc sulfate 3 hours before cephalexin decreases peak levels of cephalexin by 11% and reduces the exposure to cephalexin by 18%. By decreasing cephalexin levels, zinc might increase the risk of treatment failure. This effect does not occur when zinc is taken 3 hours after the cephalexin dose. To avoid an interaction, advise patients take zinc sulfate 3 hours after taking cephalexin.

Likelihood Probable Evidence B
Cisplatin (Platinol-Aq)

Theoretically, zinc might interfere with the therapeutic effects of cisplatin.
Animal research suggests that zinc stimulates tumor cell production of the protein metallothionein, which binds and inactivates cisplatin. It is not known whether zinc supplements or high dietary zinc intake can cause clinically significant interference with cisplatin therapy. Cisplatin might also increase zinc excretion.

Likelihood Possible Evidence D
Integrase Inhibitors

Theoretically, taking zinc along with integrase inhibitors might decrease the levels and clinical effects of these drugs.
Zinc is a divalent cation. Pharmacokinetic studies have shown that other divalent cations such as calcium and iron can decrease blood levels of the integrase inhibitor dolutegravir through chelation.

Likelihood Possible Evidence D
Penicillamine (Cuprimine, Depen)

Zinc might reduce the levels and clinical effects of penicillamine.
By forming an insoluble complex with penicillamine, zinc interferes with penicillamine absorption and activity. Zinc supplements reduce the efficacy of low-dose penicillamine (0.5-1 gram/day), but do not seem to affect higher doses (1-2.75 gram/day), provided dosing times are separated. Advise patients to take zinc and penicillamine at least 2 hours apart.

Likelihood Probable Evidence B
Quinolone Antibiotics

Zinc can decrease the levels and clinical effects of quinolones antibiotics.
Quinolones form complexes with zinc in the gastrointestinal tract, reducing absorption of both the quinolone and zinc if taken at the same time. Advise patients to take these drugs at least 2 hours before, or 4-6 hours after, zinc supplements.

Likelihood Probable Evidence B
Ritonavir (Norvir)

Zinc modestly reduces levels of ritonavir.
Clinical research shows that zinc might reduce serum ritonavir levels by chelating with ritonavir in the gut and preventing its absorption. In patients with HIV, ritonavir is taken with atazanavir to prevent the metabolism and increase the effects of atazanavir. A pharmacokinetic study shows that, in patients being treated with atazanavir/ritonavir, co-administration of zinc sulfate (Solvazinc tablets) 125 mg as a single dose or as multiple daily doses for 2 weeks reduces plasma levels of ritonavir by about 16%. However, atazanavir levels still remains high enough to prevent HIV virus replication. Therefore, the decrease in ritonavir levels is not likely to be clinically significant.

Likelihood Probable Evidence B
Tetracycline Antibiotics

Zinc might reduce levels of tetracycline antibiotics.
Tetracyclines form complexes with zinc in the gastrointestinal tract, which can reduce absorption of both the tetracycline and zinc when taken at the same time. Taking zinc sulfate 200 mg with tetracycline reduces absorption of the antibiotic by 30% to 40%. Demeclocycline and minocycline cause a similar interaction. However, doxycycline does not seem to interact significantly with zinc. Advise patients to take tetracyclines at least 2 hours before, or 4-6 hours after, zinc supplements to avoid any interactions.

Likelihood Probable Evidence B
Amiloride (Midamor)

Amiloride can modestly reduce zinc excretion and increase zinc levels.
Clinical research shows that amiloride can reduce urinary zinc excretion, especially at doses of 10 mg per day or more. This zinc-sparing effect can help to counteract zinc losses caused by thiazide diuretics, but it is unlikely to cause zinc toxicity at usual amiloride doses. The other potassium-sparing diuretics, spironolactone (Aldactone) and triamterene (Dyrenium), do not seem to have a zinc-sparing effect.

Likelihood Probable Evidence B
Atazanavir (Reyataz)

Zinc modestly reduces levels of atazanavir, although this effect does not seem to be clinically significant.
Clinical research shows that zinc might decrease serum atazanavir levels by chelating with atazanavir in the gut and preventing its absorption. Although a single dose of zinc sulfate (Solvazinc tablets) 125 mg orally does not affect atazanavir concentrations in patients being treated with atazanavir/ritonavir, co-administration of zinc sulfate 125 mg daily for 2 weeks reduces plasma levels of atazanavir by about 22% in these patients. However, despite this decrease, atazanavir levels still remain at high enough concentrations for the prevention of HIV virus replication.

Likelihood Probable Evidence B
Zinc full monograph & interactions

L-Alpha-Glycerylphosphorylcholine Hydrate1 drug type · 16 drugs

Scopolamine (Transderm Scop)

Theoretically, alpha-GPC might decrease the effects of scopolamine.
A small clinical study shows that alpha-GPC can partially counteract the attention and memory impairment effects caused by scopolamine given intramuscularly. Whether alpha-GPC can decrease the beneficial anti-motion sickness effects of the scopolamine patch (Transderm Scop) is unclear.

Likelihood Possible Evidence B
L-Alpha-Glycerylphosphorylcholine Hydrate full monograph & interactions

Iodine3 drug types · 7 drugs

Amiodarone (Cordarone)

Combining iodine with amiodarone might cause excessively high iodine levels.
Amiodarone contains 37.3% iodine and can increase iodine levels. Concomitant use with iodine might increase the risk of having excessive iodine levels and adversely affecting thyroid function. Monitor thyroid function.

Likelihood Probable Evidence D
Antithyroid Drugs

Iodine might alter the effects of antithyroid drugs.
Iodine in high doses has been reported to cause both hyperthyroidism and hypothyroidism, depending on the individual's past medical history. Taking iodine while using antithyroid drugs could alter the effects of the antithyroid drugs.

Likelihood Probable Evidence D
Lithium

Combining iodine with lithium might have additive hypothyroid effects.
Lithium can inhibit thyroid function. Several case reports suggest that concomitant use of lithium and potassium iodide can reduce thyroid function in otherwise healthy adults. Monitor thyroid function.

Likelihood Probable Evidence D
Iodine full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Prime Factor (Human Growth Factor Formula) For Men, from the product label.

Prime

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Name
Market America, Inc.
Street Address
1302 Pleasant Ridge Road
City
Greensboro
State
NC
ZipCode
27409
Pharmacist Counseling Corner

Prime Factor (Human Growth Factor Formula) For Men by Prime: Common Questions

Does Prime Factor (Human Growth Factor Formula) For Men by Prime interact with any medications?
Yes. Based on its ingredients, Prime Factor (Human Growth Factor Formula) For Men has a known interaction with 1,664 medications, including 31 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Prime Factor (Human Growth Factor Formula) For Men contains 19 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.

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.

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The Full Monographs Behind Prime Factor (Human Growth Factor Formula) For Men’s Ingredients

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

Herb & supplement monograph

Pantothenic Acid

Pantothenic acid is vitamin B5, an essential nutrient your body uses to turn food into energy. True deficiency is very rare because it is found in nearly all foods, and most people meet thei...

Read the full Pantothenic Acid monograph → Herb & supplement monograph

Iodine

Interacts with 7 drugs

Iodine is an essential mineral your body needs to make thyroid hormones, and most people get enough from iodized salt, dairy, and seafood. Supplements help when you are truly deficient, but...

Read the full Iodine monograph → Herb & supplement monograph

Zinc

Interacts with 67 drugs

Zinc is an essential mineral that your body needs for immune function, wound healing, taste, and smell. Most people get enough from food, but supplements can help correct or prevent a defici...

Read the full Zinc monograph → Herb & supplement monograph

Dhea

Interacts with 776 drugs

DHEA is a natural hormone that the body makes and that declines with age, and it is sold as a supplement claiming many benefits. The evidence is mixed and limited for most uses, and because...

Read the full Dhea monograph → Herb & supplement monograph

Schisandra

Interacts with 803 drugs

Schisandra is a traditional Chinese medicine berry used as an adaptogen for stress, fatigue, and liver support. Human evidence is limited and most claims are not well proven, but it appears...

Read the full Schisandra monograph → Herb & supplement monograph

Ashwagandha

Interacts with 1,372 drugs

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

Read the full Ashwagandha monograph → Herb & supplement monograph

Fo-ti

Interacts with 1,257 drugs

Fo-ti (He Shou Wu) is a root used in traditional Chinese medicine, often promoted for healthy aging and hair. High-quality human evidence for these benefits is limited, and processed Fo-ti h...

Read the full Fo-ti monograph → Herb & supplement monograph

Astragalus

Interacts with 208 drugs

Astragalus is a root used for centuries in traditional Chinese medicine, mainly to support the immune system and help the body cope with stress. While early studies are interesting, strong h...

Read the full Astragalus monograph → Herb & supplement monograph

Goji

Interacts with 1,000 drugs

Goji berries are a nutritious fruit rich in antioxidants, vitamins, and plant polysaccharides, and they are safe for most people as a food. While they are popular for eye health, immune supp...

Read the full Goji monograph → Herb & supplement monograph

Gamma-aminobutyric Acid (gaba)

Interacts with 419 drugs

GABA is a calming chemical messenger (neurotransmitter) that your body makes on its own, and it is sold as a supplement for stress, anxiety, and sleep. The science behind oral GABA supplemen...

Read the full Gamma-aminobutyric Acid (gaba) monograph → Herb & supplement monograph

Coleus

Interacts with 915 drugs

Coleus is a plant from the mint family whose root contains a compound called forskolin, often marketed for weight loss, asthma, and heart health. While early lab and small human studies are...

Read the full Coleus monograph → Herb & supplement monograph

Alpha-gpc

Interacts with 16 drugs

Alpha-GPC is a choline-containing compound used mainly for memory, brain health, and as a choline source. There is some evidence it may help cognition in people with dementia, but evidence i...

Read the full Alpha-gpc monograph → Herb & supplement monograph

Panax Ginseng

Interacts with 1,130 drugs

Panax ginseng is a popular traditional herb used to boost energy, ease stress, and support overall wellness, though scientific evidence is mixed and mostly preliminary. It is generally well...

Read the full Panax Ginseng monograph → Herb & supplement monograph

Chromium

Interacts with 178 drugs

Chromium is an essential trace mineral involved in how the body handles sugar and fat. Some studies suggest it may modestly help blood sugar control in certain people with type 2 diabetes, b...

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Sources

Sources & How We Checked

Prime Factor (Human Growth Factor Formula) For Men'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 487 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.

Pantothenic Acid 11 references
  1. McEvoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
  2. Yates AA, Schlicker SA, Suitor CW. Dietary reference intakes: The new basis for recommendations for calcium and related nutrients, B vitamins, and choline. J Am Diet Assoc 1998;98:699-706. PubMed
  3. Debourdeau PM, Djezzar S, Estival JL, et al. Life-threatening eosinophilic pleuropericardial effusion related to vitamins B5 and H. Ann Pharmacother 2001;35:424-6. DOI
  4. Schmuth, M., Wimmer, M. A., Hofer, S., Sztankay, A., Weinlich, G., Linder, D. M., Elias, P. M., Fritsch, P. O., and Fritsch, E. Topical corticosteroid therapy for acute radiation dermatitis: a prospective, randomized, double-blind study. Br.J.Dermatol. 2 PubMed
  5. Schreck, U., Paulsen, F., Bamberg, M., and Budach, W. Intraindividual comparison of two different skin care conceptions in patients undergoing radiotherapy of the head-and-neck region. Creme or powder? Strahlenther.Onkol. 2002;178(6):321-329. PubMed
  6. Herbst, R. A., Uter, W., Pirker, C., Geier, J., and Frosch, P. J. Allergic and non-allergic periorbital dermatitis: patch test results of the Information Network of the Departments of Dermatology during a 5-year period. Contact Dermatitis 2004;51(1):13-1 PubMed
  7. Champault, G. and Patel, J. C. [Treatment of constipation with Bepanthene]. Med.Chir Dig. 1977;6(1):57-59.
  8. Scott LN, Fiume M, Bergfeld WF, et al. Safety Assessment of Panthenol, Pantothenic Acid, and Derivatives as Used in Cosmetics. Int J Toxicol 2022;41(3_suppl):77-128. PubMed
  9. Han J, Warshaw EM. Allergic Contact Dermatitis to Panthenol in "Hypoallergenic" Products. Dermatitis 2023;34(1):62-63. PubMed
  10. Blanchard G, Kerre S, Walker A, et al. Allergic contact dermatitis from pantolactone and dexpanthenol in wound healing creams. Contact Dermatitis 2022;87(5):468-471. PubMed
  11. Peltier E, Trapp S, de Salvo R, et al. A new dexpanthenol-containing liquid cleanser for atopic-prone skin: Results from two prospective clinical studies evaluating cutaneous tolerability, moisturization potential, and effects on barrier function. J Cosme PubMed

See these in context on the Pantothenic Acid monograph →

Iodine 26 references
  1. McEvoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
  2. Goodman GA, Rall TW, Nies AS, Taylor P. The Pharmacological Basis of Therapeutics, 9th ed.
  3. Ghent WR, Eskin BA, Low DA, Hill LP. Iodine replacement in fibrocystic disease of the breast. Can J Surg 1993;36:453-60.
  4. Potassium iodide for nuclear exposure. Pharmacist's Letter/Prescriber's Letter 2001;17(12):171214.
  5. 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.
  6. Cabezas C, Bustamante B, Holgado W, Begue RE. Treatment of cutaneous sporotrichosis with one daily dose of potassium iodide. Pediatr Infect Dis J 1996;15:352-4. PubMed
  7. Sterling JB, Heymann WR. Potassium iodide in dermatology: a 19th century drug for the 21st century-uses, pharmacology, adverse effects, and contraindications. J Am Acad Dermatol 2000;43:691-7. PubMed
  8. Yarrington CD, Pearce EN. Dietary iodine in pregnancy and postpartum. Clin Obstet Gynecol 2011;54:459-70. PubMed
  9. Goel, S., Mandhani, A., Srivastava, A., Kapoor, R., Gogoi, S., Kumar, A., and Bhandari, M. Is povidone iodine an alternative to silver nitrate for renal pelvic instillation sclerotherapy in chyluria? BJU.Int 2004;94(7):1082-1085. PubMed
  10. Teng, W., Shan, Z., Teng, X., Guan, H., Li, Y., Teng, D., Jin, Y., Yu, X., Fan, C., Chong, W., Yang, F., Dai, H., Yu, Y., Li, J., Chen, Y., Zhao, D., Shi, X., Hu, F., Mao, J., Gu, X., Yang, R., Tong, Y., Wang, W., Gao, T., and Li, C. Effect of iodine int
  11. Crawford, B. A., Cowell, C. T., Emder, P. J., Learoyd, D. L., Chua, E. L., Sinn, J., and Jack, M. M. Iodine toxicity from soy milk and seaweed ingestion is associated with serious thyroid dysfunction. Med J Aust. 10-4-2010;193(7):413-415. PubMed
  12. Ohkuma, M. Molluscum contagiosum treated with iodine solution and salicylic acid plaster. Int J Dermatol. 1990;29(6):443-445. PubMed
  13. Connelly KJ, Boston BA, Pearce EN, Sesser D, Snyder D, Braverman LE, Pino S, LaFranchi SH. Congenital hypothyroidism caused by excess prenatal maternal iodine ingestion. J Pediatr. 2012 Oct;161(4):760-2. PubMed
  14. Kasahara T, Narumi S, Okasora K, Takaya R, Tamai H, Hasegawa T. Delayed onset congenital hypothyroidism in a patient with DUOX2 mutations and maternal iodine excess. Am J Med Genet A. 2013 Jan;161A(1):214-7.
  15. Murcia M, Rebagliato M, Iñiguez C, Lopez-Espinosa MJ, Estarlich M, Plaza B, Barona-Vilar C, Espada M, Vioque J, Ballester F. Effect of iodine supplementation during pregnancy on infant neurodevelopment at 1 year of age. Am J Epidemiol. 2011 Apr 1;173(7):8 PubMed
  16. Sang Z, Wang PP, Yao Z, Shen J, Halfyard B, Tan L, Zhao N, Wu Y, Gao S, Tan J, Liu J, Chen Z, Zhang W. Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. Am J Clin Nutr. 2012 Feb;95(2):367-73 PubMed
  17. Speeckaert MM, Speeckaert R, Wierckx K, Delanghe JR, Kaufman JM. Value and pitfalls in iodine fortification and supplementation in the 21st century. Br J Nutr. 2011 Oct;106(7):964-73. PubMed
  18. Yun SE, Kang Y, Bae EJ, Hwang K, Jang HN, Cho HS, Chang SH, Park DJ. Iodine-induced thyrotoxic hypokalemic paralysis after ingestion of Salicornia herbace. Ren Fail. 2014 Apr;36(3):461-3.
  19. Iodine Hypersensitivity. Pharmacist's Letter/Prescriber's Letter 2011; 27(5):270504.
  20. Hammel JA, Selby JC. Pustular eruption in a patient with cancer treated with complementary and alternative medicine. JAMA Dermatology 2017 October; E1. doi: 10.1001/jamadermatol.2017.3749. [Epub ahead of print] PubMed
  21. Gil GS, Smith BW, Guerra JR, Williams WT. Acute Delirium in a Hypothyroid Patient Precipitated by Iodine Supplements Use. Am J Ther. 2018;25(6):e717-e718. PubMed
  22. Hamby T, Kunnel N, Dallas JS, Wilson DP. Maternal iodine excess: an uncommon cause of acquired neonatal hypothyroidism. J Pediatr Endocrinol Metab. 2018;31(9):1061-1064. PubMed
  23. Censi S, Watutantrige-Fernando S, Groccia G, et al. The Effects of Iodine Supplementation in Pregnancy on Iodine Status, Thyroglobulin Levels and Thyroid Function Parameters: Results from a Randomized Controlled Clinical Trial in a Mild-to-Moderate Iodine
  24. Rovner MS, Wolf BJ, Rubin M, et al. Instillation of 5% Povidone-Iodine Ophthalmic Drops Decreases the Respiratory Rate in Children Undergoing Strabismus Surgery: A Randomized Controlled Trial. J Pediatr Ophthalmol Strabismus. 2019;56(6):378-382. PubMed
  25. Guenezan J, Garcia M, Strasters D, et al. Povidone Iodine Mouthwash, Gargle, and Nasal Spray to Reduce Nasopharyngeal Viral Load in Patients With COVID-19: A Randomized Clinical Trial. JAMA Otolaryngol Head Neck Surg. 2021;147(4):400-401. PubMed
  26. Li F, Wan S, Zhang L, et al. A Meta-Analysis of the Effect of Iodine Excess on the Intellectual Development of Children in Areas with High Iodine Levels in their Drinking Water. Biol Trace Elem Res 2022;200(4):1580-1590. PubMed

See these in context on the Iodine monograph →

Dhea 98 references
  1. Frye RF, Kroboth PD, Folan MM, et al. Effect of DHEA on CYP3A-mediated metabolism of triazolam. Clin Pharmacol Ther 2000;67:109 (abstract PI-82).
  2. Kuritzky L. DHEA: Science or wishful thinking? Hosp Pract 1998;33:85-6. PubMed
  3. Van Vollenhoven RF, Morabito LM, Engleman EG, et al. Treatment of systemic lupus erythematosus with dehydroepiandrosterone: 50 patients treated up to 12 months. J Rheumatol 1998;25:285-9.
  4. Van Vollenhoven RF, Engleman EG, McGurie JL. Dehydroepiandrosterone in Systemic Lupus Erythematosus. Arth Rheum 1995;38:1826-31. DOI
  5. Ebeling P, Koivisto VA. Physiological importance of dehydroepiandrosterone. Lancet 1994;343:1479-81. PubMed
  6. Yen SS, Morales AJ, Khorram O. Replacement of DHEA in aging men and women. Potential remedial effects. Ann N Y Acad Sci 1995;774:128-42. PubMed
  7. Labrie F, Diamond P, Cusan L, et al. Effect of 12 month dehydroepiandrosterone replacement therapy on bone, vagina, and endometrium in postmenopausal women. J Clin Endocrinol Metab 1997;82:3498-505. PubMed
  8. Casson PR, Faquin LC, Stentz FB. Replacement of dehydroepiandrosterone enhances T-lymphocyte insulin binding in postmenopausal women. (abstract) Fertil Steril 1995;63:1027-31. DOI
  9. Morales AJ, Haubrich RH, Hwang JY, et al. The effect of six months treatment with a 100 mg daily dose of dehydroepiandrosterone (DHEA) on circulating sex steroids, body composition and muscle strength in age-advanced men and women. Clin Endocrinol (Oxf)1 PubMed
  10. Arlt W, Justl H, Callies F, et al. Oral dehydroepiandrosterone for adrenal androgen replacement: pharmacokinetics and peripheral conversion to androgens and estrogens in young healthy females after dexamethasone suppression. [Abstract] J Clin Endocrinol PubMed
  11. Kline MD, Jaggers ED. Mania onset while using dehydroepiandrosterone (letter). Am J Psychiatry 1999;156:971. PubMed
  12. Callies F, Arlt W, Siekmann L, et al. Influence of oral dehydroepiandrosterone (DHEA) on urinary steroid metabolites in males and females. Steroids 2000;65:98-102. PubMed
  13. Markowitz JS, Carson WH, Jackson CW. Possible dihydroepiandrosterone-induced mania. Biol Psychiatry 1999;45:241-2. PubMed
  14. Stoll BA. Dietary supplements of dehydroepiandrosterone in relation to breast cancer risk. Eur J Clin Nutr 1999;53:771-5. PubMed
  15. Dean CE. Prasterone (DHEA) and mania. Ann Pharmacother 2000;34:1419-22. PubMed
  16. Himmel PB, Seligman TM. A Pilot Study Employing Dehydroepiandrosterone (DHEA) in the Treatment of Chronic Fatigue Syndrome. [Abstract]. J Clin Rheumatol 1999:5:56-9. PubMed
  17. Hunt PJ, Gurnell EM, Huppert FA, et al. Improvement in mood and fatigue after dehydroepiandrosterone replacement in Addison's disease in a randomized, double blind trial. J Clin Endocrinol Metab 2000;85:4650-6.. PubMed
  18. Johannsson G, Burman P, Wiren L, et al. Low dose dehydroepiandrosterone affects behavior in hypopituitary androgen-deficient women: a placebo-controlled trial. J Clin Endocrinol Metab 2002;87:2046-52. PubMed
  19. Calhoun KE, Pommier RF, Muller P, et al. Dehydroepiandrosterone sulfate causes proliferation of estrogen receptor-positive breast cancer cells despite treatment with fulvestrant. Arch Surg 2003;138:879-83.. PubMed
  20. Morris KT, Toth-Fejel S, Schmidt J, et al. High dehydroepiandrosterone-sulfate predicts breast cancer progression during new aromatase inhibitor therapy and stimulates breast cancer cell growth in tissue culture: a renewed role for adrenalectomy. Surgery PubMed
  21. Calhoun K, Pommier R, Cheek J, et al. The effect of high dehydroepiandrosterone sulfate levels on tamoxifen blockade and breast cancer progression. Am J Surg 2003;185:411-5.. PubMed
  22. Stomati M, Monteleone P, Casarosa E, et al. Six-month oral dehydroepiandrosterone supplementation in early and late postmenopause. Gynecol Endocrinol 2000;14:342-63.. PubMed
  23. Petri MA, Mease PJ, Merrill JT, et al. Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus. Arthritis Rheum 2004;50:2858-68. PubMed
  24. Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone mineral density and body composition in elderly women and men. Clin Endocrinol (Oxf) 2000;53:561-8. PubMed
  25. Acacio BD, Stanczyk FZ, Mullin P, et al. Pharmacokinetics of dehydroepiandrosterone and its metabolites after long-term daily oral administration to healthy young men. Fertil Steril 2004;81:595-604. PubMed
  26. Petri MA, Lahita RG, Van Vollenhoven RF, et al. Effects of prasterone on corticosteroid requirements of women with systemic lupus erythematosus: a double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2002;46:1820-9. PubMed
  27. Pino JA, Marbot R. Volatile flavor constituents of acerola (Malpighia emarginata DC.) fruit. J Agric Food Chem 2001;49:5880-2.
  28. Nair KS, Rizza RA, O'Brien P, et al. DHEA in elderly women and DHEA or testosterone in elderly men. N Engl J Med 2006;355:1647-59. PubMed
  29. Alkatib AA, Cosma M, Elamin MB, et al. A systematic review and meta-analysis of randomized placebo-controlled trials of DHEA treatment effects on quality of life in women with adrenal insufficiency. J Clin Endocrinol Metab 2009;94:3676-81. PubMed
  30. Jesse, R. L., Loesser, K., Eich, D. M., Qian, Y. Z., Hess, M. L., Nestler, J. E. Dehydroepiandrosterone inhibits human platelet aggregation in vitro and in vivo. Ann N.Y.Acad Sci 1995;774:281-90.
  31. Bertoni, A., Rastoldo, A., Sarasso, C., Di Vito C., Sampietro, S., Nalin, M., Bagarotti, A., Sinigaglia, F. Dehydroepiandrosterone-sulfate inhibits thrombin-induced platelet aggregation. Steroids 2012;77(3):260-8. PubMed
  32. Cui, Y., Choi, I. S., Koh, Y. A., Lin, X. H., Cho, Y. B., Won, Y. H. Effects of combined BCG and DHEA treatment in preventing the development of asthma. Immunol Invest 2008;37(3):191-202. PubMed
  33. Aisaka, K., Mori, H., Ogawa, T., Kigawa, T. Effects of dehydroepiandrosterone-sulphate (DHEA-S) administration on puerperal lactation and maternal prolactin and estradiol levels. Nippon Sanka Fujinka Gakkai Zasshi 1984;36(10):1935-42.
  34. Lauritzen, C. [Therapeutic attempts with dehydroepiandrosterone sulfate in threatened pregnancies]. Arch Gynakol 1971;211(1):247-9.
  35. Mortola, J. F. Yen, S. S. The effects of oral dehydroepiandrosterone on endocrine-metabolic parameters in postmenopausal women. J Clin Endocrinol Metab 1990;71(3):696-704. PubMed
  36. Rabijewski, M., Zgliczynski, W. [Positive effects of DHEA therapy on insulin resistance and lipids in men with angiographically verified coronary heart disease--preliminary study]. Endokrynol Pol 2005;56(6):904-10.
  37. Weiss, E. P., Shah, K., Fontana, L., Lambert, C. P., Holloszy, J. O., Villareal, D. T. Dehydroepiandrosterone replacement therapy in older adults: 1- and 2-y effects on bone. Am J Clin Nutr 2009;89(5):1459-67. PubMed
  38. Jankowski, C. M., Gozansky, W. S., Kittelson, J. M., Van Pelt, R. E., Schwartz, R. S., Kohrt, W. M. Increases in bone mineral density in response to oral dehydroepiandrosterone replacement in older adults appear to be mediated by serum estrogens. J Clin E PubMed
  39. Poretsky, L., Song, L., Brillon, D. J., Ferrando, S., Chiu, J., McElhiney, M., Ferenczi, A., Sison, C., Haller, I., Rabkin, J. Metabolic and hormonal effects of oral DHEA in premenopausal women with HIV infection: a randomized, prospective, placebo-contro
  40. Libe, R., Barbetta, L., Dall'Asta, C., Salvaggio, F., Gala, C., Beck-Peccoz, P., Ambrosi, B. Effects of dehydroepiandrosterone (DHEA) supplementation on hormonal, metabolic and behavioral status in patients with hypoadrenalism. J Endocrinol Invest 2004;27 PubMed
  41. Genazzani, A. R., Inglese, S., Lombardi, I., Pieri, M., Bernardi, F., Genazzani, A. D., Rovati, L., Luisi, M. Long-term low-dose dehydroepiandrosterone replacement therapy in aging males with partial androgen deficiency. Aging Male 2004;7(2):133-43. PubMed
  42. von Muhlen D., Laughlin, G. A., Kritz-Silverstein, D., Bergstrom, J., Bettencourt, R. Effect of dehydroepiandrosterone supplementation on bone mineral density, bone markers, and body composition in older adults: the DAWN trial. Osteoporos Int 2008;19(5):
  43. Kritz-Silverstein, D., von, Muhlen D., Laughlin, G. A., Bettencourt, R. Effects of dehydroepiandrosterone supplementation on cognitive function and quality of life: the DHEA and Well-Ness (DAWN) Trial. J Am Geriatr Soc 2008;56(7):1292-8. PubMed
  44. Penisson-Besnier, I., Devillers, M., Porcher, R., Orlikowski, D., Doppler, V., Desnuelle, C., Ferrer, X., Bes, M. C., Bouhour, F., Tranchant, C., Lagrange, E., Vershueren, A., Uzenot, D., Cintas, P., Sole, G., Hogrel, J. Y., Laforet, P., Vial, C., Vila, A
  45. Casson, P. R., Santoro, N., Elkind-Hirsch, K., Carson, S. A., Hornsby, P. J., Abraham, G., Buster, J. E. Postmenopausal dehydroepiandrosterone administration increases free insulin-like growth factor-I and decreases high-density lipoprotein: a six-month t
  46. Araneo, B. Daynes, R. Dehydroepiandrosterone functions as more than an antiglucocorticoid in preserving immunocompetence after thermal injury. Endocrinology 1995;136(2):393-401. PubMed
  47. Nordmark, G., Bengtsson, C., Larsson, A., Karlsson, F. A., Sturfelt, G., Ronnblom, L. Effects of dehydroepiandrosterone supplement on health-related quality of life in glucocorticoid treated female patients with systemic lupus erythematosus. Autoimmunity PubMed
  48. Srinivasan, M., Irving, B. A., Frye, R. L., O'Brien, P., Hartman, S. J., McConnell, J. P., Nair, K. S. Effects on lipoprotein particles of long-term dehydroepiandrosterone in elderly men and women and testosterone in elderly men. J Clin Endocrinol Metab 2 PubMed
  49. Srinivasan, M., Irving, B. A., Dhatariya, K., Klaus, K. A., Hartman, S. J., McConnell, J. P., Nair, K. S. Effect of dehydroepiandrosterone replacement on lipoprotein profile in hypoadrenal women. J Clin Endocrinol Metab 2009;94(3):761-4. PubMed
  50. Jankowski, C. M., Gozansky, W. S., Van Pelt, R. E., Wolfe, P., Schwartz, R. S., Kohrt, W. M. Oral dehydroepiandrosterone replacement in older adults: effects on central adiposity, glucose metabolism and blood lipids. Clin Endocrinol (Oxf) 2011;75(4):456-6 PubMed
  51. McHenry, C. M., Bell, P. M., Hunter, S. J., Thompson, C. J., Courtney, C. H., Ennis, C. N., Sheridan, B., McCance, D. R., Mullan, K. R., Atkinson, A. B. Effects of dehydroepiandrosterone sulphate (DHEAS) replacement on insulin action and quality of life i
  52. Jankowski, C. M., Gozansky, W. S., Schwartz, R. S., Dahl, D. J., Kittelson, J. M., Scott, S. M., Van Pelt, R. E., Kohrt, W. M. Effects of dehydroepiandrosterone replacement therapy on bone mineral density in older adults: a randomized, controlled trial. J PubMed
  53. Forsblad-d'Elia, H., Carlsten, H., Labrie, F., Konttinen, Y. T., Ohlsson, C. Low serum levels of sex steroids are associated with disease characteristics in primary Sjogren's syndrome; supplementation with dehydroepiandrosterone restores the concentration
  54. Finckh, A., Berner, I. C., Aubry-Rozier, B., So, A. K. A randomized controlled trial of dehydroepiandrosterone in postmenopausal women with fibromyalgia. J Rheumatol 2005;32(7):1336-40.
  55. Gebre-Medhin, G., Husebye, E. S., Mallmin, H., Helstrom, L., Berne, C., Karlsson, F. A., Kampe, O. Oral dehydroepiandrosterone (DHEA) replacement therapy in women with Addison's disease. Clin Endocrinol (Oxf) 2000;52(6):775-80. PubMed
  56. Lovas, K., Gebre-Medhin, G., Trovik, T. S., Fougner, K. J., Uhlving, S., Nedrebo, B. G., Myking, O. L., Kampe, O., Husebye, E. S. Replacement of dehydroepiandrosterone in adrenal failure: no benefit for subjective health status and sexuality in a 9-month,
  57. Pillemer, S. R., Brennan, M. T., Sankar, V., Leakan, R. A., Smith, J. A., Grisius, M., Ligier, S., Radfar, L., Kok, M. R., Kingman, A., Fox, P. C. Pilot clinical trial of dehydroepiandrosterone (DHEA) versus placebo for Sjogren's syndrome. Arthritis Rheum
  58. Christiansen, J. J., Andersen, N. H., Sorensen, K. E., Pedersen, E. M., Bennett, P., Andersen, M., Christiansen, J. S., Jorgensen, J. O., Gravholt, C. H. Dehydroepiandrosterone substitution in female adrenal failure: no impact on endothelial function and
  59. Panjari, M., Bell, R. J., Jane, F., Wolfe, R., Adams, J., Morrow, C., Davis, S. R. A randomized trial of oral DHEA treatment for sexual function, well-being, and menopausal symptoms in postmenopausal women with low libido. J Sex Med 2009;6(9):2579-90. PubMed
  60. Mamas, L., Mamas, E. Dehydroepiandrosterone supplementation in assisted reproduction: rationale and results. Curr Opin Obstet Gynecol 2009;21(4):306-8. PubMed
  61. Hartkamp, A., Geenen, R., Godaert, G. L., Bootsma, H., Kruize, A. A., Bijlsma, J. W., Derksen, R. H. Effect of dehydroepiandrosterone administration on fatigue, well-being, and functioning in women with primary Sjogren syndrome: a randomised controlled tr
  62. Yeung, T. W., Li, R. H., Lee, V. C., Ho, P. C., Ng, E. H. A randomized double-blinded placebo-controlled trial on the effect of dehydroepiandrosterone for 16 weeks on ovarian response markers in women with primary ovarian insufficiency. J Clin Endocrinol PubMed
  63. Virkki, L. M., Porola, P., Forsblad-d'Elia, H., Valtysdottir, S., Solovieva, S. A., Konttinen, Y. T. Dehydroepiandrosterone (DHEA) substitution treatment for severe fatigue in DHEA-deficient patients with primary Sjogren's syndrome. Arthritis Care Res (Ho
  64. Binder, G., Weber, S., Ehrismann, M., Zaiser, N., Meisner, C., Ranke, M. B., Maier, L., Wudy, S. A., Hartmann, M. F., Heinrich, U., Bettendorf, M., Doerr, H. G., Pfaeffle, R. W., Keller, E. Effects of dehydroepiandrosterone therapy on pubic hair growth an
  65. Klove, K. L., Roy, S., Lobo, R. A. The effect of different contraceptive treatments on the serum concentration of dehydroepiandrosterone sulfate. Contraception 1984;29(4):319-24. PubMed
  66. Cibula, D., Fanta, M., Vrbikova, J., Stanicka, S., Dvorakova, K., Hill, M., Skrha, J., Zivny, J., Skrenkova, J. The effect of combination therapy with metformin and combined oral contraceptives (COC) versus COC alone on insulin sensitivity, hyperandrogena
  67. White, T., Jain, J. K., Stanczyk, F. Z. Effect of oral versus transdermal steroidal contraceptives on androgenic markers. Am J Obstet Gynecol 2005;192(6):2055-9. PubMed
  68. Vacheron-Trystram, M. N., Cheref, S., Gauillard, J., Plas, J. [A case report of mania precipitated by use of DHEA]. Encephale 2002;28(6 Pt 1):563-6.
  69. Gurnell, E. M., Hunt, P. J., Curran, S. E., Conway, C. L., Pullenayegum, E. M., Huppert, F. A., Compston, J. E., Herbert, J., Chatterjee, V. K. Long-term DHEA replacement in primary adrenal insufficiency: a randomized, controlled trial. J Clin Endocrinol PubMed
  70. Christiansen, J. J., Bruun, J. M., Christiansen, J. S., Jorgensen, J. O., Gravholt, C. H. Long-term DHEA substitution in female adrenocortical failure, body composition, muscle function, and bone metabolism: a randomized trial. Eur J Endocrinol 2011;165(2 PubMed
  71. Bloch, M., Ish-Shalom, S., Greenman, Y., Klein, E., Latzer, Y. Dehydroepiandrosterone treatment effects on weight, bone density, bone metabolism and mood in women suffering from anorexia nervosa-a pilot study. Psychiatry Res 2012;200(2-3):544-9. PubMed
  72. Merritt, P., Stangl, B., Hirshman, E., Verbalis, J. Administration of dehydroepiandrosterone (DHEA) increases serum levels of androgens and estrogens but does not enhance short-term memory in post-menopausal women. Brain Res 11-5-2012;1483:54-62. PubMed
  73. Stangl, B., Hirshman, E., and Verbalis, J. Administration of dehydroepiandrosterone (DHEA) enhances visual-spatial performance in postmenopausal women. Behav Neurosci 2011;125(5):742-52. PubMed
  74. Artini, P. G., Simi, G., Ruggiero, M., Pinelli, S., Di Berardino, O. M., Papini, F., Papini, S., Monteleone, P., Cela, V. DHEA supplementation improves follicular microenviroment in poor responder patients. Gynecol Endocrinol 2012;28(9):669-73. PubMed
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Fo-ti 28 references
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Coleus 16 references
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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.

© 2021 Therapeutic Research Center, LLC

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