Major interaction on record — check this product against your medications before combining. Based on 20 of 23 ingredients. Check your meds →
Dietary supplement

ReversAge Lemon-Lime Flavor Ingredients & Drug Interactions

by Reliv

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

ReversAge Lemon-Lime Flavor is a dietary supplement by Reliv with 23 active ingredients. Its ingredients are commonly taken for replacing fluids and electrolytes, preventing dehydration during exercise or illness, treating low blood sodium (under medical care).Based on those ingredients, 1,769 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo, Quercetin Dihydrate, Diosmin. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of ReversAge Lemon-Lime Flavor by Reliv

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

From our pharmacy team — supplement deep dive

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 1 of its 28 active ingredients.
  • “Proprietary Herbal Blend” is a proprietary blend — the label gives one combined amount (250 mg) without saying how much of each component you get.
  • “Proprietary Longevity Complex” is a proprietary blend — the label gives one combined amount (1.42 Gram(s)) without saying how much of each component you get.
  • “Symbiotropin” is listed as a grouped ingredient — the label doesn't break down how much of each component you get.

ReversAge contains 28 active ingredients including amino acids (L-glutamine, glycine, acetyl L-carnitine, L-lysine, L-arginine), vitamins and cofactors (coenzyme Q10, glutathione), minerals and electrolytes (sodium, potassium citrate, dipotassium phosphate), herbal extracts (ginkgo, Japanese knotweed, stinging nettle, wild yam, maca), probiotics (Lactobacillus acidophilus, Bifidobacterium bifidum), algae (spirulina, chlorella), and other compounds (alpha-lipoic acid, quercetin, diosmin, GABA). It also contains omega-3 fatty acid and anterior pituitary peptides.

The product is formulated as a powder with inactive ingredients including maltodextrin, fructose, citric acid, soy lecithin, xanthan gum, natural and artificial flavors, rebiana (a stevia extract), and potassium citrate.

Does it work?

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

Some clinical evidence supports this product's ingredients for its stated purpose, but it isn't conclusive.

Why this rating?
  • The label markets this product for: promote longevity and slow aging process.
  • We looked for evidence on: Aging, Aging skin, Age-related cognitive decline, Alzheimer disease, Cellular aging, Oxidative stress — and 1 related terms.
  • The strongest evidence on file: Acetyl-l-carnitine is rated "Possibly Effective" for Age-related cognitive decline (Natural Medicines).
  • Also on file: Acetyl-l-carnitine is rated "Possibly Effective" for Alzheimer disease.
  • Also on file: Alpha-gpc is rated "Possibly Effective" for Alzheimer disease.

The evidence for effectiveness varies widely across ingredients and conditions. L-glutamine is effective for sickle cell disease and possibly effective for HIV/AIDS-related wasting and postoperative recovery.

Acetyl L-carnitine is possibly effective for age-related cognitive decline, Alzheimer disease, and depression. Ginkgo is possibly effective for dementia, anxiety, and premenstrual syndrome.

Coenzyme Q10 is likely effective for CoQ10 deficiency and possibly effective for heart failure and migraines. Stinging nettle is possibly effective for diabetes management.

For most other ingredients and conditions, the evidence in our data is insufficient to establish benefit, or the evidence suggests they are ineffective—such as maca for sexual dysfunction and quercetin for most conditions listed. The product as a whole has no single defined indication, so effectiveness depends on your personal health goals and which ingredients matter to you.

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

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

Why this rating?
  • We hold adverse-effect (side-effect) data for 25 of the 26 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 26 of 26.
  • General safety write-ups exist for 26 of 26.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Most individual ingredients are generally well tolerated at typical doses, but several carry important cautions. L-glutamine should be used only under medical supervision in people with kidney or liver disease.

Alpha-lipoic acid can lower blood sugar and is best used under medical guidance; it is not advised during pregnancy or breastfeeding. Acetyl L-carnitine is generally well tolerated short-term, but long-term safety is not fully established, and it should be avoided during pregnancy and breastfeeding.

N-Acetyl Cysteine is generally well tolerated at typical doses but is best used under healthcare guidance. Ginkgo may increase bleeding risk and should be avoided in pregnancy and breastfeeding.

Stinging nettle may cause drug-induced liver injury (rare) and should be avoided during pregnancy; safety while breastfeeding is not established. Chlorella and spirulina quality varies widely—some products can be contaminated with toxins or heavy metals, and both should be avoided in pregnancy and breastfeeding due to insufficient safety data.

Sodium, while essential in small amounts, is linked to high blood pressure and heart strain when taken in excess; the product contains sodium and should not be used as a sodium supplement without medical advice. Common side effects across ingredients include gastrointestinal upset (nausea, diarrhea, bloating), headache, and dizziness.

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

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

Why this rating?
  • 23 of the 26 matched ingredients can interact with medications — Lysine, Quercetin, Ginkgo, Gamma-aminobutyric Acid (gaba), Stinging Nettle, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; seizure medications; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; lithium; Parkinson's medications.
  • For scale: 1,770 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.

Do not use this product if you take nitroglycerin (Major interaction with N-Acetyl Cysteine, causing severe low blood pressure and headaches). Check with your pharmacist if you take blood thinners (warfarin, other anticoagulants, or antiplatelet drugs)—multiple ingredients increase bleeding risk.

Blood pressure medications may be less effective or cause excessive lowering of blood pressure. Diabetes medications may have increased effect; blood sugar monitoring is important.

Lithium levels may rise to toxic levels. Antibiotics taken at the same time may be less effective.

Chemotherapy drugs may have altered effects. Run any prescription medication through the checker on this page before use.

Check your own medication Run your meds through the checker above

The bottom line

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

ReversAge is a complex multi-ingredient supplement with a mix of amino acids, herbs, and probiotics. It is not designed for a single health condition but rather as a general wellness product.

Before taking it, you must check every medication you use against our interaction tool—this product interacts with a very large number of drugs, some at serious levels, and nitroglycerin users should avoid it entirely. If you take blood pressure medications, blood thinners, diabetes drugs, or lithium, talk to your pharmacist before starting.

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

Assessment coverage: 26 of 28 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Oct 22, 2021.

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

At a glance

General information

Key facts about ReversAge Lemon-Lime Flavor, straight from the product label.

Brand Reliv
Barcode (UPC) 91027
Net contents 16.93 oz
Market status On market
Date entered into DSLD Oct 22, 2021
DSLD ID 255798
Product type Other Combinations
Supplement form Powder
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years), Gluten Free
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for ReversAge Lemon-Lime Flavor by Reliv, 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:
16 Gram(s)
Maximum serving Sizes:
16 Gram(s)
Servings per container
30
UPC/BARCODE
91027
IngredientAmount% DV
Calories60 Calorie(s)--
Total Carbohydrates13 Gram(s)5%
L-Glutamine0 NP--
Sodium5 mg1%
Alpha Lipoic Acid0 NP--
Total Fat0 Gram(s)--
Glycine0 NP--
Acetyl L-Carnitine0 NP--
L-Lysine Hydrochloride0 NP--
Maca0 NP--
Protein1 Gram(s)--
Added Sugars6 Gram(s)12%
Total Sugars6 Gram(s)--
Lactobacillus acidophilus0 NP--
Omega-3 Fatty Acid0 NP--
Coenzyme Q100 NP--
Quercetin Dihydrate0 NP--
Japanese Knotweed (root) extract0 NP--
Bifidobacterium bifidum0 NP--
Wild Yam0 NP--
Proprietary Herbal Blend250 mg--
N-Acetyl Cysteine0 NP--
Ginkgo0 NP--
Stinging Nettle0 NP--
Spirulina0 NP--
Chlorella0 NP--
Gamma Aminobutryic Acid0 NP--
Diosmin0 NP--
L-Arginine L-Pyroglutamate0 NP--
Setria Glutathione0 NP--
Anterior Pituitary Peptides0 NP--
Proprietary Longevity Complex1.42 Gram(s)--
Symbiotropin0 NP--
Alpha Glyceryl Phosphorylcholine0 NP--
7-Keto-DHEA0 NP--
S-Adenosyl-L-Methionine0 NP--
Proprietary Antioxidant Complex297.5 mg--
Trimethyl Glycine0 NP--

Other ingredients: Maltodextrin, Fructose, Citric Acid, non-GMO Soy Lecithin, Xanthan Gum, Natural & Artificial flavors, Rebiana, Potassium Citrate, Dipotassium Phosphate

Tap any ingredient to jump to its full detail below.

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

With ReversAge I feel younger! I love that it tastes amazing, gives me energy and keeps me youthful! Sandy S.

For more information or to order, call 800 RELIV US (735.4887).

30 day customer money back guarantee

Formulation

Exclusive blend of herbs and antioxidants to promote longevity from the inside out Antioxidants CoQ10 and resveratrol fight free radicals to slow down the aging process Longevity complex battles hormonal decline to help you look and feel younger, and promote mental focus Herbal complex, containing ginkgo, maca and chlorella, for energy, and cognitive health benefits

Our Targeted Solutions are designed to work with any of our daily Core Nutrition shakes to help you thrive. Visit reliv.com/core-nutrition. This product is approved for use with the Fit3 program.

Gluten Free

Anti-Aging

Fight free radicals to slow down aging

Suggested/Recommended/Usage/Directions

directions Add 1 scoop of ReversAge to 8 oz. of water, juice or milk and shake or blend.

FDA Disclaimer Statement

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

Precautions

Caution: If you are currently pregnant, breast feeding, or planning on becoming pregnant, please discuss this product with your physician before beginning use.

Contains: soy, milk, and fish (anchovy and sardine)

Brand IP Statement(s)

ReversAge has been issued U.S. patent #6,368,617.

Symbiotropin is a registered trademark of Nutraceutics Corporation. 7-Keto is a registered trademark of Humanetics Corporation. Setria is a registered trademark of KYOKA HAKKO BIO CO., LTD.

FDA Statement of Identity

Antioxidant rich dietary supplement

Formula

Natural & artificial lemon-lime flavor

See for yourself

ReversAge Lemon-Lime Flavor by Reliv label

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

What’s inside

The Ingredients in ReversAge Lemon-Lime Flavor by Reliv

These are the 23 active ingredients this product is made of. Select any to open its full monograph.

Serving size16 Gram(s) Dosage formPowder Servings per container30 Amounts shown are per serving.

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

Sodium

Interacts with
205 drugs
5 mg per serving

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

Sodium monograph & interactions

Protein

1 Gram(s) per serving

Proprietary Herbal Blend

250 mg per serving

Proprietary Longevity Complex

1.42 Gram(s) per serving

Proprietary Antioxidant Complex

297.5 mg per serving

Other (inactive) ingredients: Maltodextrin, Fructose, Citric Acid, Non-GMO Soy Lecithin, Xanthan Gum, Natural & Artificial flavors, Rebiana, Potassium Citrate, Dipotassium Phosphate. These complete the product’s ingredient list but are not active constituents.

Interaction report

ReversAge Lemon-Lime Flavor by Reliv Drug Interactions

Want to check YOUR meds against ReversAge Lemon-Lime Flavor?

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
1,769Drugs
2 Major 1,715 Moderate 52 Minor

Ingredients driving the most interactions

Ginkgo 1,266
Diosmin 884

Each ingredient & the kinds of drugs it affects

For each ingredient in ReversAge Lemon-Lime Flavor 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.

Ginkgo23 drug types · 1,266 drugs

Talinolol

Taking ginkgo with talinolol seems to increase blood levels of talinolol.
There is some evidence that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of talinolol by 36% in healthy male individuals. However, single doses of ginkgo do not seem to affect talinolol pharmacokinetics.

Likelihood Probable Evidence B
Alprazolam (Xanax)

Theoretically, ginkgo might decrease the levels and clinical effects of alprazolam.
In clinical research, ginkgo extract (Ginkgold) 120 mg twice daily seems to decrease alprazolam levels by about 17%. However, ginkgo does not appear to decrease the elimination half-life of alprazolam. This suggests that ginkgo is more likely to decrease absorption of alprazolam rather than induce hepatic metabolism of alprazolam.

Likelihood Probable Evidence B
Anticoagulant/Antiplatelet Drugs

Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin. Theoretically, ginkgo might increase the risk of bleeding if used with other anticoagulant or antiplatelet drugs.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. However, population and clinical studies have produced mixed results. Some evidence shows that short-term use of ginkgo leaf does not significantly reduce platelet aggregation and blood clotting. A study in healthy males who took a specific ginkgo leaf extract (EGb 761) 160 mg twice daily for 7 days found no change in prothrombin time. An analysis of a large medical record database suggests that ginkgo increases the risk of a bleeding adverse event by 38% when taken concurrently with warfarin. It has been suggested that ginkgo has to be taken for at least 2-3 weeks to have a significant effect on platelet aggregation. However, a meta-analysis of 18 studies using standardized ginkgo extracts, 80-480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. In addition, a single dose of ginkgo plus clopidogrel or ticlopidine does not seem to significantly increase bleeding time or platelet aggregation. Also, taking ginkgo leaf extract daily for 8 days in conjunction with rivaroxaban does not affect anti-factor Xa activity; however, this study did not evaluate bleeding time.

Likelihood Possible Evidence A
Anticonvulsants

Theoretically, ginkgo might reduce the effectiveness of anticonvulsants.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking ginkgo with antidiabetes drugs might alter the response to antidiabetes drugs.
Ginkgo leaf extract seems to alter insulin secretion and metabolism, and might affect blood glucose levels in people with type 2 diabetes. The effect of ginkgo seems to differ depending on the insulin and treatment status of the patient. In diet-controlled diabetes patients with hyperinsulinemia, taking ginkgo does not seem to significantly affect insulin or blood glucose levels. In patients with hyperinsulinemia who are treated with oral hypoglycemic agents, taking ginkgo seems to decrease insulin levels and increase blood glucose following an oral glucose tolerance test. Researchers speculate that this could be due to ginkgo-enhanced hepatic metabolism of insulin. In patients with pancreatic exhaustion, taking ginkgo seems to stimulate pancreatic beta-cells, resulting in increased insulin and C-peptide levels, but with no significant change in blood glucose levels in response to an oral glucose tolerance test.

Likelihood Possible Evidence B
Atorvastatin (Lipitor)

Theoretically, ginkgo might decrease the levels and clinical effects of atorvastatin.
In humans, intake of ginkgo extract appears to increase atorvastatin clearance, reducing the area under the curve of atorvastatin by 10% to 14% and the maximum concentration by 29%. However, this interaction does not appear to affect cholesterol synthesis and absorption. Further, a model in rats with hyperlipidemia suggests that administering ginkgo extract does not impact blood levels of atorvastatin and leads to lower total cholesterol, low-density lipoprotein cholesterol, and triglycerides when compared with rats given atorvastatin alone.

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

Theoretically, ginkgo might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that ginkgo leaf extract can mildly inhibit CYP1A2 enzymes. However, clinical research suggests ginkgo might not affect CYP1A2. Until more is known, use ginkgo cautiously in patients taking drugs metabolized by these enzymes.

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

Theoretically, ginkgo might decrease levels of drugs metabolized by CYP2C19.
Some clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce CYP2C19 enzymes and potentially decrease levels of drugs metabolized by these enzymes. However, other clinical research shows that taking ginkgo 120 mg twice daily for 12 days has no effect on levels of drugs metabolized by CYP2C19.

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

Theoretically, ginkgo might increase levels of drugs metabolized by CYP2C9.
In vitro, a specific standardized extract of ginkgo leaf (EGb 761) inhibits CYP2C9 activity . The terpenoid (ginkgolides) and flavonoid (quercetin, kaempferol, etc.) constituents seem to be responsible for this effect. Most ginkgo extracts contain some amount of these constituents. Therefore, other ginkgo leaf extracts might also inhibit the CYP2C9 enzyme. However, clinical research suggests that ginkgo might not have a significant effect on CYP2C9 in humans. Ginkgo does not seem to significantly affect the pharmacokinetics of CYP2C9 substrates diclofenac or tolbutamide.

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

Theoretically, ginkgo might decrease levels of drugs metabolized by CYP3A4.
There is conflicting evidence about whether ginkgo induces or inhibits CYP3A4. Ginkgo does not appear to affect hepatic CYP3A4. However, it is not known if ginkgo affects intestinal CYP3A4. Preliminary clinical research suggests that taking ginkgo does not significantly affect levels of donepezil, lopinavir, or ritonavir, which are all CYP3A4 substrates. Other clinical research also suggests ginkgo does not significantly affect CYP3A4 activity. However, there are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4).

Likelihood Possible Evidence B
Efavirenz (Sustiva)

Theoretically, ginkgo might decrease the levels and clinical effects of efavirenz.
There are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. In one case, an HIV-positive male experienced over a 50% decrease in efavirenz levels over the course of 14 months while taking ginkgo extract. HIV-1 RNA copies also increased substantially, from less than 50 to more than 1500. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4). In another case report, a patient stable on antiviral therapy including efavirenz for 10 years, had an increase in viral load from <50 copies/mL to 1350 copies/mL after 2 months of taking a combination of supplements including ginkgo. After stopping ginkgo, the viral load was again controlled with the same antiviral therapy regimen.

Likelihood Possible Evidence D
Ibuprofen (Advil, Others)

Theoretically, ginkgo might increase the risk of bleeding when used with ibuprofen.
Ginkgo might have antiplatelet effects and has been associated with several case reports of spontaneous bleeding. In one case, a 71-year-old male had taken a specific ginkgo extract (Gingium, Biocur) 40 mg twice daily for 2.5 years. About 4 weeks after starting ibuprofen 600 mg daily he experienced a fatal intracerebral hemorrhage. However, the antiplatelet effects of ginkgo have been questioned. A meta-analysis and other studies have not found a significant antiplatelet effect with standardized ginkgo extracts, 80 mg to 480 mg taken daily for up to 32 weeks.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, taking ginkgo with P-glycoprotein substrates might increase the levels and adverse effects of these substrates.
A small clinical study in healthy volunteers shows that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of the P-glycoprotein substrate, talinolol, by 36% in healthy male individuals. However, single doses of ginkgo do not have the same effect.

Likelihood Possible Evidence B
Risperidone (Risperdal)

Theoretically, taking ginkgo with risperidone might increase the levels and adverse effects of risperidone.
A single case of priapism has been reported for a 26-year-old male with schizophrenia who used risperidone 3 mg daily along with ginkgo extract 160 mg daily. Risperidone is metabolized by cytochrome P450 (CYP) 2D6 and CYP3A4. CYP3A4 activity might be affected by ginkgo. Theoretically, ginkgo may inhibit the metabolism of risperidone and increase the risk of adverse effects.

Likelihood Possible Evidence D
Rosiglitazone (Avandia)

Theoretically, ginkgo might decrease the levels and clinical effects of rosiglitazone.
Animal research shows that ginkgo leaf extract orally 100 or 200 mg/kg daily for 10 days alters the pharmacodynamics of rosiglitazone in a dose-dependent manner. The 100 mg/kg and 200 mg/kg doses reduce the area under the concentration time curve (AUC) of rosiglitazone by 39% and 52%, respectively, and the half-life by 28% and 39%, respectively. It is hypothesized that these changes may be due to induction of cytochrome P450 2C8 by ginkgo.

Likelihood Possible Evidence D
Seizure Threshold Lowering Drugs

Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.

Likelihood Possible Evidence D
Simvastatin (Zocor)

Theoretically, ginkgo might decrease the levels and clinical effects of simvastatin.
Clinical research shows that taking ginkgo extract can reduce the area under the curve and maximum concentration of simvastatin by 32% to 39%. However, ginkgo extract does not seem to affect the cholesterol-lowering ability of simvastatin.

Likelihood Probable Evidence B
Sofosbuvir (Sovaldi)

Theoretically, ginkgo might increase the levels and clinical effects of sofosbuvir.
Animal research in rats shows that giving a ginkgo extract 25 mg/kg orally daily for 14 days increases the area under the concentration time curve (AUC) after a single sofosbuvir dose of 40 mg/kg by 11%, increases the half-life by 60%, and increases the plasma concentration at 4 hours by 38%. This interaction appears to be related to the inhibition of intestinal P-glycoprotein by ginkgo.

Likelihood Possible Evidence D
Tacrolimus (Prograf)

Theoretically, ginkgo might increase the blood levels of tacrolimus.
In vitro evidence suggests that certain biflavonoids in ginkgo leaves (i.e. amentoflavone, ginkgetin, bilobetin) may inhibit the metabolism of tacrolimus by up to 50%. This interaction appears to be time-dependent and due to inhibition of cytochrome P450 (CYP) 3A4 by these bioflavonoids. In rats given tacrolimus 1 mg/kg orally, amentoflavone was shown to increase the area under the concentration time curve (AUC) of tacrolimus by 3.8-fold.

Likelihood Possible Evidence D
Trazodone (Desyrel)

Theoretically, ginkgo might increase the levels and clinical effects of trazodone.
In a case report, an Alzheimer patient taking trazodone 20 mg twice daily and ginkgo leaf extract 80 mg twice daily for four doses became comatose. The coma was reversed by administration of flumazenil (Romazicon). Coma might have been induced by excessive GABA-ergic activity. Ginkgo flavonoids are thought to have GABA-ergic activity and act directly on benzodiazepine receptors. Ginkgo might also increase metabolism of trazodone to active GABA-ergic metabolites, possibly by inducing cytochrome P450 3A4 (CYP3A4) metabolism.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. Information from a medical database suggests that when taken concurrently with warfarin, ginkgo increases the risk of a bleeding adverse event by 38%. There is also some evidence that ginkgo leaf extract can inhibit cytochrome P450 2C9, an enzyme that metabolizes warfarin. This could result in increased warfarin levels. However, population and clinical research has produced mixed results. Clinical research in healthy people suggests that ginkgo has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. A meta-analysis of 18 studies using standardized ginkgo extracts, 80 mg to 480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. There is also some preliminary clinical research that suggests ginkgo might not significantly increase the effects of warfarin in patients that have a stable INR.

Likelihood Possible Evidence B
Nifedipine (Procardia)

Theoretically, taking ginkgo with oral, but not intravenous, nifedipine might increase levels and adverse effects of nifedipine.
Animal research and some clinical evidence suggests that taking ginkgo leaf extract orally in combination with oral nifedipine might increase nifedipine levels and cause increased side effects, such as headaches, dizziness, and hot flushes. However, taking ginkgo orally does not seem to affect the pharmacokinetics of intravenous nifedipine.

Likelihood Possible Evidence B
Omeprazole (Prilosec)

Theoretically, taking ginkgo with omeprazole might decrease the levels and clinical effects of omeprazole.
Clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce cytochrome P450 (CYP) 2C19 enzymes and decrease levels of omeprazole by about 27% to 42%.

Likelihood Possible Evidence B

Quercetin Dihydrate21 drug types · 1,169 drugs

Antidiabetes Drugs

Theoretically, concomitant use of quercetin and antidiabetes drugs might increase the risk of hypoglycemia.

Clinical research suggests that a combination of quercetin, myricetin, and chlorogenic acid reduce levels of fasting glucose in patients with type 2 diabetes, including those already taking antidiabetes agents. The effect of quercetin alone is unknown.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking quercetin with antihypertensive drugs might increase the risk of hypotension.

Quercetin can modestly decrease blood pressure in people with mild hypertension. Theoretically, it might have additive blood pressure lowering effects when used with antihypertensive drugs.

Likelihood Possible Evidence B
Cyclosporine (Neoral, Sandimmune)

Theoretically, concomitant use might increase the levels and adverse effects of cyclosporine.

A small study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine, possibly due to inhibition of p-glycoprotein or cytochrome P450 3A4 (CYP3A4), which metabolizes cyclosporin.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2C8 substrates.

In vitro research shows that quercetin inhibits CYP2C8. Inhibition of paclitaxel (Taxol) metabolism via CYP2C8 has been reported in vitro. However, a small study in humans found no effect of quercetin on rosiglitazone (Avandia), which is also a CYP2C8 substrate.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2C9 substrates.

A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac, a CYP2C9 substrate, increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar), a substrate of CYP2C9. Furthermore, laboratory research shows that quercetin inhibits CYP2C9.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2D6 substrates.

In vitro research show that quercetin inhibits CYP2D6. This effect has not been reported in humans.

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

Theoretically, concomitant use might alter the effects and adverse effects of CYP3A4 substrates.
A small clinical study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine (Neoral, Sandimmune), a substrate of CYP3A4. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) and quetiapine (Seroquel), substrates of CYP3A4. Other laboratory research also shows that quercetin inhibits CYP3A4. However, one clinical study shows that quercetin can increase the metabolism of midazolam, a substrate of CYP3A4, and decrease serum concentrations of midazolam by about 24% in some healthy individuals, suggesting possible induction of CYP3A4.

Likelihood Possible Evidence D
Diclofenac (Voltaren, Others)

Theoretically, concomitant use might increase the levels and adverse effects of diclofenac.

A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. This is thought to be due to inhibition of CYP2C9 by quercetin.

Likelihood Probable Evidence B
Losartan (Cozaar)

Theoretically, concomitant use might increase the effects and adverse effects of losartan and decrease the effects of its active metabolite.

Animal research shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) while decreasing plasma levels of losartan's active metabolite. This metabolite, which is around 10-fold more potent than losartan, is the result of cytochrome P450 (CYP) 2C9- and CYP3A4-mediated transformation of losartan. Additionally, in vitro research shows that quercetin may inhibit P-glycoprotein-mediated efflux of losartan from the intestines, resulting in increased absorption of losartan. These results suggest that concomitant use of quercetin and losartan might increase systemic exposure to losartan while also decreasing plasma concentrations of losartan's active and more potent metabolite.

Likelihood Possible Evidence D
Midazolam (Versed)

Theoretically, concomitant use might decrease the levels and effects of midazolam.

A small clinical study in healthy volunteers shows that quercetin can increase the metabolism of midazolam, with a decrease in AUC of about 24%.

Likelihood Possible Evidence B
Mitoxantrone

Theoretically, quercetin might increase the effects and adverse effects of mitoxantrone.
In vitro research shows that quercetin increases the intracellular accumulation and cytotoxicity of mitoxantrone, possibly through inhibition of breast cancer resistance protein (BCRP), of which mitoxantrone is a substrate. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Organic Anion Transporter 1 (Oat1) Substrates

Theoretically, concomitant use might increase the effects and adverse effects of OAT1 substrates.

In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT1, with half-maximal inhibitory concentration (IC50) values less than 10 mcM. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Organic Anion Transporter 3 (Oat3) Substrates

Theoretically, concomitant use might increase the effects and adverse effects of OAT3 substrates.

In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT3, with half-maximal inhibitory concentration (IC50) values as low as 0.75 mcM. So far, this interaction has not been reported in humans.

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

Theoretically, concomitant use might increase the effects and adverse effects of OATP substrates.

In vitro evidence shows that quercetin can inhibit organic anion-transporting peptide (OATP) 1B1-mediated uptake of estrone-3-sulfate and pravastatin. Furthermore, clinical research in healthy males shows that intake of quercetin along with pravastatin increases the AUC of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Theoretically, concomitant use might alter the effects and adverse effects of P-glycoprotein substrates.

There is preliminary evidence that quercetin inhibits the gastrointestinal P-glycoprotein efflux pump, which might increase the bioavailability and serum levels of drugs transported by the pump. A small study in healthy volunteers reported that pretreatment with quercetin increased bioavailability and plasma levels after a single dose of cyclosporine (Neoral, Sandimmune). Also, two small studies have shown that quercetin might decrease the absorption of talinolol, a substrate transported by the gastrointestinal P-glycoprotein efflux pump. However, in another small study, several days of quercetin treatment did not significantly affect the pharmacokinetics of saquinavir (Invirase). The reason for these discrepancies is not entirely clear. Until more is known, use quercetin cautiously in combination with P-glycoprotein substrates.

Likelihood Possible Evidence B
Pravastatin (Pravachol)

Theoretically, concomitant use might increase the effects and adverse effects of pravastatin.
In vitro evidence shows that quercetin can inhibit OATP 1B1-mediated uptake of pravastatin. Also, preliminary clinical research in healthy males shows that intake of quercetin along with pravastatin increases the maximum concentration of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.

Likelihood Possible Evidence B
Prazosin (Minipress)

Theoretically, quercetin might increase the effects and adverse effects of prazosin.
In vitro research shows that quercetin inhibits the transcellular efflux of prazosin, possibly through inhibition of breast cancer resistance protein (BCRP), of which prazosin is a substrate. BCRP is an ATP-binding cassette efflux transporter in the intestines, kidneys, and liver. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Quetiapine (Seroquel)

Theoretically, concomitant use might increase the effects and adverse effects of quetiapine.
Animal research shows that pretreatment with quercetin can increase plasma levels of quetiapine and prolong its clearance, possibly due to inhibition of cytochrome P450 3A4 (CYP3A4) by quercetin. Additionally, the brain-to-plasma ratio of quetiapine concentrations increased, possibly due to inhibition of P-glycoprotein at the blood-brain barrier. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, concomitant use might inhibit the effects of quinolone antibiotics.
In vitro, quercetin binds to the DNA gyrase site on bacteria, which may interfere with the activity of quinolone antibiotics.

Likelihood Possible Evidence B
Sulfasalazine (Azulfidine)

Theoretically, quercetin might increase the effects and adverse effects of sulfasalazine.
Animal research shows that quercetin increases the maximum serum concentration (Cmax) and area under the curve (AUC) of sulfasalazine, possibly through inhibition of breast cancer resistance protein (BCRP), of which sulfasalazine is a substrate. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, quercetin may increase the risk of bleeding if used with warfarin.
Animal and in vitro studies show that quercetin might increase serum levels of warfarin. Quercetin and warfarin have the same human serum albumin (HSA) binding site, and in vitro research shows that quercetin has stronger affinity for the HSA binding site and can theoretically displace warfarin, causing higher serum levels of warfarin. Animal research shows that taking quercetin for 2 weeks before initiating warfarin increases the maximum serum level of warfarin by 30%, the half-life by 10%, and the overall exposure by 63% when compared with control. Concomitant administration of quercetin and warfarin, without quercetin pre-treatment, also increased these measures, but to a lesser degree. Researchers theorize that inhibition of CYP3A4 by quercetin may explain these effects. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D

Diosmin9 drug types · 884 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, diosmin may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
A case of spontaneous intraventricular hemorrhage has been reported for a 77-year-old female after 6 weeks of warfarin therapy, despite an international normalized ratio (INR) of only 1.8. The patient had also been taking aspirin and diosmin for several years. Experts speculate that chronic intake of diosmin predisposed the patient to spontaneous intraventricular hemorrhage by inducing chronic microcirculatory hypertension and inhibiting platelet aggregation. The presence of aspirin was also thought to play a role in this event.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, diosmin might reduce the effects of carbamazepine and increase the risk for convulsions.
A pharmacokinetic study in humans shows that taking diosmin (Venex) 500 mg daily for 10 days prior to oral administration of carbamazepine 200 mg increases blood levels of carbamazepine by approximately 58% and decreases carbamazepine clearance by 42%. It also decreases the formation of carbamazepine's active metabolite. It is speculated that diosmin reduces the metabolism of carbamazepine by inhibiting cytochrome P450 3A4 (CYP3A4).

Likelihood Probable Evidence B
Chlorzoxazone (Parafon Forte, Paraflex)

Theoretically, diosmin might increase the levels and clinical effects of chlorzoxazone.
A pharmacokinetic study in humans shows that taking diosmin (Venex 500) 500 mg daily for 9 days prior to oral administration of chlorzoxazone 250 mg increases blood levels of chlorzoxazone by 53% and decreases chlorzoxazone clearance by 40%. It is speculated that diosmin reduces the metabolism of chlorzoxazone by inhibiting cytochrome P450 2E1 (CYP2E1).

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

Theoretically, diosmin might inhibit the metabolism of CYP2C9 substrates.
Diclofenac is metabolized by CYP2C9 enzymes. Clinical and laboratory research shows that diosmin inhibits the metabolism of diclofenac. A pharmacokinetic study in humans shows that taking diosmin (Venex 500) 500 mg daily for 9 days prior to oral administration of diclofenac 100 mg increases blood levels of diclofenac and decreases diclofenac clearance.

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

Theoretically, diosmin might inhibit the metabolism of CYP2E1 substrates.
Chlorzoxazone is metabolized by CYP2E1 enzymes. A pharmacokinetic study in humans shows that taking diosmin (Venex 500) 500 mg daily for 9 days prior to oral administration of chlorzoxazone (Paraflex 250) 250 mg increases blood levels of chlorzoxazone by 34% and decreases chlorzoxazone clearance by 40%. It is speculated that diosmin reduces the metabolism of chlorzoxazone by inhibiting CYP2E1.

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

Theoretically, diosmin might inhibit the metabolism of CYP3A4 substrates.
Laboratory research is conflicting with respect to the effects of diosmin on CYP3A4. Some research suggests that diosmin does not affect CYP3A4 activity. However, other research suggests that diosmin alters the metabolism of carbamazepine, a CYP3A4 substrate. Laboratory and animal research show that oral administration of diosmin for 7 days prior to oral administration of carbamazepine increases plasma concentrations of carbamazepine, decreases the clearance of carbamazepine, and decreases the formation of carbamazepine's active metabolite. Additionally, pharmacokinetic research in healthy male subjects shows that taking diosmin (Venex) 500 mg daily for 10 days prior to oral administration of carbamazepine 200 mg increases blood levels of carbamazepine by approximately 58% and decreases carbamazepine clearance by 42%. It is speculated that diosmin reduces the metabolism of carbamazepine by inhibiting CYP3A4. Diosmetin, a metabolite of diosmin, may also inhibit CYP3A4.

Likelihood Possible Evidence B
Diclofenac (Voltaren, Others)

Theoretically, diosmin might increase the levels and clinical effects of diclofenac.
Clinical and laboratory research shows that diosmin inhibits the metabolism of diclofenac. A pharmacokinetic study in humans shows that taking diosmin (Venex 500) 500 mg daily for 9 days prior to oral administration of diclofenac 100 mg increases blood levels of diclofenac and decreases diclofenac clearance. It is speculated that diosmin reduces the metabolism of diclofenac by inhibiting cytochrome P450 2C9 (CYP2C9).

Likelihood Probable Evidence B
Fexofenadine (Allegra)

Theoretically, diosmin might increase the levels and clinical effects of fexofenadine.
A pharmacokinetic study in humans shows that taking diosmin (Venex) 500 mg daily for 10 days prior to oral administration of fexofenadine 120 mg increases blood levels of fexofenadine by approximately 49% and decreases the apparent oral clearance of fexofenadine by 41%. The time taken to reach maximum plasma concentration, the half-life, and the apparent renal clearance of fexofenadine are not affected. For this reason, it is speculated that diosmin alters the pharmacokinetics of fexofenadine via inhibition of P-glycoprotein in the intestine, but not in the kidney or liver.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Theoretically, diosmin might increase levels of drugs that are substrates of P-glycoprotein (P-gp).
Preliminary laboratory research suggests that diosmin inhibits P-gp. Additionally, pharmacokinetic research in healthy male subjects shows that taking diosmin (Venex) 500 mg daily for 10 days prior to oral administration of fexofenadine 120 mg increases blood levels of fexofenadine, a P-gp substrate, by approximately 49% and decreases the apparent oral clearance of fexofenadine by 41%. The time taken to reach maximum plasma concentration, the half-life, and the apparent renal clearance of fexofenadine are not affected. For this reason, it is speculated that diosmin inhibits P-gp in the intestine, but not in the kidney or liver.

Likelihood Possible Evidence D

Japanese Knotweed (root) extract7 drug types · 826 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, hu zhang might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
Hu zhang contains the constituent resveratrol. Resveratrol seems to have antiplatelet effects.

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

Theoretically, hu zhang might increase levels of drugs metabolized by CYP1A2.
Hu zhang contains the constituent resveratrol. In vitro research shows that resveratrol might inhibit the CYP1A2 enzyme. This interaction has not been reported in humans.

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

Theoretically, hu zhang might increase levels of drugs metabolized by CYP2C19.
Hu zhang contains the constituent resveratrol. In vitro research shows that resveratrol might inhibit the CYP2C19 enzyme. This interaction has not been reported in humans.

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

Theoretically, hu zhang might increase levels of drugs metabolized by CYP2E1.
Hu zhang contains the constituent resveratrol. In vitro research shows that resveratrol might inhibit the CYP2E1 enzyme. Also, a pharmacokinetic study shows that taking resveratrol 500 mg daily for 10 days prior to taking a single dose of chlorzoxazone 250 mg increases the maximum concentration of chlorzoxazone by about 54%, the area under the curve of chlorzoxazone by about 72%, and the half-life of chlorzoxazone by about 35%. Chlorzoxazone is used as a probe drug for CYP2E1.

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

Theoretically, hu zhang might increase levels of drugs metabolized by CYP3A4.
Hu zhang contains the constituent resveratrol. In vitro research shows that resveratrol might inhibit the CYP3A4 enzyme. However, a clinical study in adults with NAFLD found that adding resveratrol 3000 mg daily for 8 weeks did not necessitate dose adjustments to any established medications metabolized by CYP3A4.

Likelihood Possible Evidence D
Estrogens

Theoretically, hu zhang might competitively inhibit the effects of estrogen replacement therapy.
In vitro research shows that hu zhang might have estrogenic activity.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, hu zhang might increase the effects and adverse effects of carbamazepine.
In animals, blood and tissue levels of carbamazepine were increased when given in combination with hu zhang. It is thought that increased levels of carbamazepine are due to cytochrome P450 3A4 (CYP3A4) inhibition. This interaction has not been reported in humans.

Likelihood Possible Evidence D

Omega-3 Fatty Acid3 drug types · 375 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, DHA may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Although some clinical evidence suggests that DHA might reduce collagen-stimulated platelet aggregation and thromboxane release, most clinical evidence suggests that DHA alone does not affect blood clotting. However, theoretically, when given in combination with EPA as fish oil, concomitant use with anticoagulant or antiplatelet drugs (including aspirin) might increase risk of bleeding.

Likelihood Unlikely Evidence B
Antidiabetes Drugs

Theoretically, taking DHA with antidiabetes drugs might reduce the effects of these medications.
In people with type 2 diabetes, including those taking oral hypoglycemic medications, DHA seems to increase fasting blood glucose levels.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking DHA with antihypertensive drugs might increase the risk of hypotension.
Fish oils containing DHA can lower blood pressure and might have additive effects in patients treated with antihypertensives; use with caution.

Likelihood Probable Evidence B

Chlorella2 drug types · 337 drugs

Photosensitizing Drugs

Theoretically, chlorella might have additive effects with photosensitizing drugs.
Chlorella has been reported to cause photosensitization. In five case reports, patients who had ingested chlorella exhibited swelling followed by erythematopurpuric lesions on sun-exposed areas of the body. Theoretically, concomitant use with photosensitizing drugs may exacerbate effects.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, chlorella might reduce the clinical effects of warfarin.
Chlorella contains significant amounts of vitamin K. There is at least one case report of warfarin therapy becoming sub-therapeutic after initiation of chlorella supplements.

Likelihood Possible Evidence D

Spirulina3 drug types · 327 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, spirulina blue-green algae might increase the risk of bleeding if used with other anticoagulant or antiplatelet drugs. However, this is unlikely.
Spirulina blue-green algae have shown antiplatelet and anticoagulant effects in vitro. However, one preliminary study in 24 patients receiving spirulina blue-green algae 2.3 grams daily for 2 weeks showed no effect on platelet activation or measures of clotting time.

Likelihood Unlikely Evidence D
Antidiabetes Drugs

Theoretically, taking blue-green algae with antidiabetes drugs might increase the risk of hypoglycemia.
Human research shows that spirulina blue-green algae can have hypoglycemic effects in patients with diabetes, at least some of whom were using antidiabetes drugs. However, blue-green algae does not seem to improve glycated hemoglobin (HbA1c) levels in patients with diabetes. A meta-analysis of animal studies also suggests that spirulina blue-green algae have hypoglycemic effects.

Likelihood Possible Evidence B
Immunosuppressants

Theoretically, concurrent use of blue-green algae might interfere with immunosuppressive therapy.
Blue-green algae have been shown to stimulate the immune system.

Likelihood Possible Evidence D

N-Acetyl Cysteine5 drug types · 294 drugs

Nitroglycerin

N-acetyl cysteine can increase the risk for hypotension and headaches when taken with intravenous or transdermal nitroglycerin.
Clinical research shows that concomitant administration of N-acetyl cysteine and intravenous or transdermal nitroglycerin can cause severe hypotension and intolerable headaches. Furthermore, in vitro research suggests that N-acetyl cysteine increases the anticoagulant activity of nitroglycerin.

Likelihood Probable Evidence B
Activated Charcoal

N-acetyl cysteine might reduce the effects of activated charcoal, while activated charcoal might reduce the absorption of N-acetyl cysteine.
N-acetyl cysteine appears to reduce the capacity of activated charcoal to adsorb acetaminophen and salicylic acid. Conversely, although clinical research suggests that although activated charcoal can reduce the absorption of N-acetyl cysteine by up to 40%, it does not seem to reduce its clinical effects. Other clinical evidence suggests that activated charcoal does not affect the absorption of N-acetyl cysteine.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, N-acetyl cysteine might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
Clinical research suggests that intravenous N-acetyl cysteine decreases prothrombin time, prolongs coagulation time, decreases platelet aggregation, and increases blood loss in surgical patients. Furthermore, in vitro research suggests that N-acetyl cysteine increases the anticoagulant activity of nitroglycerin.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, N-acetyl cysteine might increase the risk of hypotension when taken with antihypertensive drugs.
Animal research suggests that N-acetyl cysteine potentiates the hypotensive effects of the angiotensin-converting enzyme inhibitors (ACEIs) captopril and enalaprilat. Theoretically, combining N-acetyl cysteine with other antihypertensive drugs might increase the risk of hypotension.

Likelihood Possible Evidence D
Chloroquine (Aralen)

Theoretically, N-acetyl cysteine might interfere with the antimalarial effects of chloroquine.
Animal research suggests that N-acetyl cysteine might reduce the antimalarial effects of chloroquine by increasing cellular levels of glutathione.

Likelihood Possible Evidence D

Alpha Lipoic Acid5 drug types · 263 drugs

Alkylating Agents

Theoretically, the antioxidant effects of alpha-lipoic acid might alter the effectiveness of alkylating agents.
The use of antioxidants like alpha-lipoic acid during chemotherapy is controversial. There are concerns that antioxidants could reduce the activity of chemotherapy drugs that generate free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as alpha-lipoic acid have on chemotherapy. Advise patients to consult their oncologist before using alpha-lipoic acid.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, alpha-lipoic acid may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro, alpha-lipoic acid inhibits platelet aggregation.

Likelihood Possible Evidence D
Antitumor Antibiotics

Theoretically, the antioxidant effects of alpha-lipoic acid might alter the effectiveness of antitumor antibiotics.
The use of antioxidants like alpha-lipoic acid during chemotherapy is controversial. There are concerns that antioxidants could reduce the activity of antitumor antibiotic drugs, which work by generating free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as alpha-lipoic acid have on chemotherapy involving antitumor antibiotics. Advise patients to consult their oncologist before using alpha-lipoic acid.

Likelihood Possible Evidence D
Thyroid Hormone

Theoretically, alpha-lipoic acid might decrease the effects of thyroid hormone drugs.
Animal research suggests that co-administration of thyroxine with alpha-lipoic acid reduces conversion into the active T3 form.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking alpha-lipoic acid with antidiabetes drugs might increase the risk of hypoglycemia.
Although some small clinical studies have suggested that alpha-lipoic acid can lower blood glucose levels, larger clinical studies in patients with diabetes have shown no clinically meaningful effect. Additionally, co-administration of single doses of alpha-lipoic acid and glyburide or acarbose did not cause detectable drug interactions in healthy volunteers.

Likelihood Unlikely Evidence B

Sodium7 drug types · 205 drugs

Antihypertensive Drugs

Theoretically, a high intake of dietary sodium might reduce the effectiveness of antihypertensive drugs.
High intake of dietary sodium can increase systolic and diastolic blood pressure. Also, high intake of sodium may necessitate increased use of antihypertensive medications to achieve blood pressure control in some patients, such as those with chronic kidney disease.

Likelihood Probable Evidence A
Corticosteroids

Concomitant use of mineralocorticoids and some glucocorticoids with sodium supplements might increase the risk of hypernatremia.
Mineralocorticoids and some glucocorticoids (corticosteroids) cause sodium retention. This effect is dose-related and depends on mineralocorticoid potency. It is most common with hydrocortisone, cortisone, and fludrocortisone, followed by prednisone and prednisolone.

Likelihood Possible Evidence D
Didanosine (Videx)

Concomitant use of didanosine with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia.
Didanosine formulations contain a significant amount of sodium.

Likelihood Probable Evidence C
Lithium

Altering dietary intake of sodium might alter the levels and clinical effects of lithium.
High sodium intake can reduce plasma concentrations of lithium by increasing lithium excretion. Reducing sodium intake can significantly increase plasma concentrations of lithium and cause lithium toxicity in patients being treated with lithium carbonate. Stabilizing sodium intake is shown to reduce the percentage of patients with lithium level fluctuations above 0.8 mEq/L. Patients taking lithium should avoid significant alterations in their dietary intake of sodium.

Likelihood Probable Evidence B
Sodium Phosphates

Theoretically, concomitant use of sodium phosphate with sodium supplements might increase the risk of hypernatremia.
Use of high doses (> 45 mL in 24 hours) of sodium phosphate, such as those used for bowel cleansing before surgery, can lead to serious electrolyte disturbances, including hypernatremia. The risk of hypernatremia is highest in the elderly and people with other risk factors for electrolyte disturbances.

Likelihood Possible Evidence D
Sodium-Containing Drugs

Concomitant use of sodium-containing drugs with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia and long-term sodium-related complications.
The Chronic Disease Risk Reduction (CDRR) intake level of 2.3 grams of sodium daily indicates the intake at which it is believed that chronic disease risk increases for the apparently healthy population. Some medications contain high quantities of sodium. When used in conjunction with sodium supplements or high-sodium diets, the CDRR may be exceeded. Additionally, concomitant use may increase the risk for hypernatremia; this risk is highest in the elderly and people with other risk factors for electrolyte disturbances.

Likelihood Possible Evidence D
Tolvaptan (Samsca)

Theoretically, concomitant use of tolvaptan with sodium might increase the risk of hypernatremia.
Tolvaptan is a vasopressin receptor 2 antagonist that is used to increase sodium levels in patients with hyponatremia. Patients taking tolvaptan should use caution with the use of sodium salts such as sodium chloride.

Likelihood Probable Evidence C

Acetyl L-Carnitine4 drug types · 203 drugs

Acenocoumarol (Sintrom)

Theoretically, acetyl-L-carnitine might increase the anticoagulant effects of acenocoumarol.
L-carnitine, the parent compound of acetyl-L-carnitine, might enhance the anticoagulant effects of acenocoumarol, an oral anticoagulant that is similar to warfarin, but shorter-acting. There are at least two case reports of INR elevation when L-carnitine was taken with acenocoumarol. In one case, a 33-year-old male with a previously stable INR had an elevated INR of 4.65 after L-carnitine was started and continued for 10 weeks. INR normalized after discontinuation of the L-carnitine-containing product. It is unclear if such an interaction would also occur with acetyl-L-carnitine.

Likelihood Possible Evidence D
Serotonergic Drugs

Theoretically, acetyl-L-carnitine might increase the risk of serotonergic side effects, including serotonin syndrome and cerebral vasoconstrictive disorders, when taken with serotonergic drugs.
Animal research shows that acetyl-L-carnitine can increase levels of serotonin in the brain.

Likelihood Possible Evidence D
Thyroid Hormone

Theoretically, acetyl-L-carnitine might decrease the effectiveness of thyroid hormone replacement.
L-carnitine appears to act as a peripheral thyroid hormone antagonist by inhibiting entry of thyroid hormone into the nucleus of cells. Taking L-carnitine also seems to diminish some of the symptoms of hyperthyroidism. It is unclear if such an interaction would occur with acetyl-L-carnitine.

Likelihood Probable Evidence B
Warfarin (Coumadin)

Theoretically, acetyl-L-carnitine might increase the anticoagulant effects of warfarin.
L-carnitine, the parent compound of acetyl-L-carnitine, might increase the anticoagulant effects of acenocoumarol, a shorter-acting oral anticoagulant similar to warfarin. There is not enough information to know whether this interaction occurs with acetyl-L-carnitine and warfarin.

Likelihood Possible Evidence D

Coenzyme Q103 drug types · 198 drugs

Alkylating Agents

Coenzyme Q10 has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals.
Theoretically, antioxidants such as coenzyme Q10 might protect tumor cells from chemotherapeutic agents that work by inducing oxidative stress, such as alkylating agents (e.g., cyclophosphamide) and radiation therapy. The clinical importance of this interaction is unknown.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Coenzyme Q10 is chemically similar to menaquinone and might have vitamin K-like procoagulant effects, which could decrease the effects of warfarin.
Concomitant use of coenzyme Q10 and warfarin might reduce the anticoagulant effects of warfarin. Four cases of decreased warfarin efficacy thought to be due to coenzyme Q10 have been reported. However, there is some preliminary clinical research that suggests coenzyme Q10 might not significantly decrease the effects of warfarin in patients who have a stable INR.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, coenzyme Q10 might have additive effects with antihypertensive drugs.
Some clinical research shows that coenzyme Q10 can significantly lower blood pressure, although other studies have shown conflicting results.

Likelihood Possible Evidence B

S-Adenosyl-L-Methionine2 drug types · 189 drugs

Levodopa

SAMe might reduce the effectiveness of levodopa.
SAMe methylates levodopa, which might reduce its effectiveness for treating Parkinson disease.

Likelihood Possible Evidence D
Serotonergic Drugs

Taking SAMe with serotonergic drugs might increase the risk of serotonin syndrome and other serotonergic side effects.
SAMe has serotonergic effects. Theoretically, combining serotonergic drugs with SAMe might increase the risk of serotonergic side effects, including serotonin syndrome and cerebral vasoconstrictive disorders. In one case report, SAMe 100 mg intramuscularly was given daily with clomipramine (Anafranil) 25 mg per day. When the clomipramine dose was increased to 75 mg per day the patient experienced serotonin syndrome about 48-72 hours later, requiring hospitalization.

Likelihood Possible Evidence D

Lactobacillus acidophilus1 drug type · 182 drugs

Antibiotic Drugs

Theoretically, taking Lactobacillus acidophilus with antibiotic drugs might decrease the effectiveness of L. acidophilus.
L. acidophilus preparations usually contain live and active organisms. Therefore, simultaneously taking antibiotics might kill a significant number of the organisms. Tell patients to separate administration of antibiotics and L. acidophilus preparations by at least two hours.

Likelihood Probable Evidence D

Bifidobacterium bifidum1 drug type · 182 drugs

Antibiotic Drugs

Theoretically, taking Bifidobacterium. bifidum with antibiotic drugs might decrease the effectiveness of B. bifidum.
Since B. bifidum preparations usually contain live and active organisms, simultaneously taking antibiotics might kill a significant number of the organisms. Tell patients to separate administration of antibiotics and B. bifidum preparations by at least 2 hours.

Likelihood Probable Evidence D

Stinging Nettle4 drug types · 164 drugs

Antidiabetes Drugs

Theoretically, stinging nettle might have additive effects with antidiabetes drugs.
Clinical research shows that stinging nettle might decrease blood glucose levels in patients with diabetes.

Likelihood Possible Evidence B
Diuretic Drugs

Theoretically, combining stinging nettle with diuretic drugs may have additive effects.
Animal research suggests that the above ground parts and roots of stinging nettle may have a diuretic effect.

Likelihood Possible Evidence D
Lithium

Theoretically, stinging nettle might reduce excretion and increase levels of lithium.
Animal research suggests that stinging nettle has diuretic and natriuretic properties, which could alter the excretion of lithium. The dose of lithium might need to be decreased.

Likelihood Possible Evidence D
Warfarin (Coumadin)

There is some concern that stinging nettle might decrease the effects of anticoagulant drugs such as warfarin.
Stinging nettle contains a significant amount of vitamin K. When taken in large quantities, this might interfere with the activity of warfarin.

Likelihood Possible Evidence D

Wild Yam1 drug type · 41 drugs

Estrogens

Theoretically, wild yam might increase or decrease the effects of estrogen.
Wild yam root shows estrogenic and anti-estrogenic effects in vitro. Theoretically, wild yam might interfere with hormone therapy.

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for ReversAge Lemon-Lime Flavor, from the product label.

Reliv

See all Reliv products
Name
Reliv International, Inc.
City
Chesterfield
State
MO
ZipCode
63005
Phone Number
1-800-735-4887
Pharmacist Counseling Corner

ReversAge Lemon-Lime Flavor by Reliv: Common Questions

Does ReversAge Lemon-Lime Flavor by Reliv interact with any medications?
Yes. Based on its ingredients, ReversAge Lemon-Lime Flavor has a known interaction with 1,769 medications, including 2 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
ReversAge Lemon-Lime Flavor contains 23 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Is this safe to take during pregnancy?
Most ingredients lack sufficient safety data in pregnancy; several are best avoided. L-glutamine is likely safe, but alpha-lipoic acid, acetyl L-carnitine, maca, ginkgo, stinging nettle, spirulina, chlorella, and others are not recommended. Talk with your doctor or pharmacist before use.
Can I take this while breastfeeding?
Safety data for breastfeeding is limited or absent for most ingredients. L-glutamine is likely safe, but alpha-lipoic acid, acetyl L-carnitine, maca, ginkgo, stinging nettle, spirulina, and chlorella should be avoided. Check with your healthcare provider.
Will this lower my blood sugar?
Possibly. Alpha-lipoic acid, stinging nettle, spirulina, and L-arginine may all lower blood glucose. If you take diabetes medications, this could increase your risk of low blood sugar (hypoglycemia). Monitor blood sugar and talk to your doctor before starting.
Does this help with energy or fatigue?
The evidence in our data is insufficient to establish that any ingredient reliably improves energy or fatigue. Several ingredients (like acetyl L-carnitine and glutathione) have been studied for age-related decline and brain health, but effectiveness for general fatigue is not established.
What are the most common side effects?
Gastrointestinal upset—bloating, nausea, diarrhea, constipation, and abdominal pain—is most common across ingredients. Headache and dizziness have also been reported. Most are mild and often resolve with continued use, but nausea or GI pain at high doses may warrant dose reduction.
Does this contain any ingredients we couldn't check for interactions?
Yes. We could not check omega-3 fatty acid or anterior pituitary peptides—we hold no interaction data for them. All other 26 ingredients were reviewed. If you have questions about omega-3, ask your pharmacist.

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.

ReversAge Lemon-Lime Flavor label
Go deeper

The Full Monographs Behind ReversAge Lemon-Lime Flavor’s Ingredients

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

Herb & supplement monograph

Sodium

Interacts with 205 drugs

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

Read the full Sodium monograph →
Herb & supplement monograph

Maca

Maca is a nutrient-rich Andean root often used for energy, libido, and menopause symptoms. Early studies suggest it may modestly help sexual desire and some menopause symptoms, but the evide...

Read the full Maca monograph →
Herb & supplement monograph

Quercetin

Interacts with 1,169 drugs

Quercetin is a plant flavonoid with antioxidant and anti-inflammatory properties found in many common foods and sold as a supplement. While early research is interesting for allergies, blood...

Read the full Quercetin monograph →
Herb & supplement monograph

Wild Yam

Interacts with 41 drugs

Wild yam is a root traditionally used for menopausal symptoms, cramps, and as a so-called 'natural' hormone supplement, but solid human evidence for these uses is lacking. Despite popular cl...

Read the full Wild Yam monograph →
Herb & supplement monograph

Ginkgo

Interacts with 1,266 drugs

Ginkgo is one of the world's most popular herbal supplements, mostly taken to support memory and circulation. The evidence for these uses is mixed and generally weak, and it is not proven to...

Read the full Ginkgo monograph →
Herb & supplement monograph

Stinging Nettle

Interacts with 164 drugs

Stinging nettle is a common plant used as food and in traditional medicine, most often for prostate symptoms, allergies, and joint pain. The evidence is mixed and mostly preliminary, so it i...

Read the full Stinging Nettle monograph →
Herb & supplement monograph

Blue-green Algae

Interacts with 327 drugs

Blue-green algae are nutrient-rich aquatic microorganisms (such as spirulina and Klamath Lake algae) taken as a supplement for energy, nutrition, and general wellness. Evidence for most heal...

Read the full Blue-green Algae monograph →
Herb & supplement monograph

Chlorella

Interacts with 337 drugs

Chlorella is a nutrient-rich freshwater green algae taken as a supplement for general wellness, immune support, and 'detox.' Some small studies suggest possible benefits for cholesterol, blo...

Read the full Chlorella monograph →
Herb & supplement monograph

Diosmin

Interacts with 884 drugs

Diosmin is a citrus-derived flavonoid most often used for vein-related problems such as chronic venous insufficiency and hemorrhoids, and it is usually combined with a related flavonoid call...

Read the full Diosmin monograph →
Herb & supplement monograph

Acetyl-l-carnitine

Interacts with 203 drugs

Acetyl-L-carnitine is a form of the amino acid carnitine that the body uses to help produce energy in cells. It is most studied for nerve pain and memory-related conditions, though the evide...

Read the full Acetyl-l-carnitine monograph →
Herb & supplement monograph

Lactobacillus Acidophilus

Interacts with 182 drugs

Lactobacillus acidophilus is a 'friendly' bacterium used as a probiotic to support gut and vaginal health. It is generally well tolerated in healthy people, and there is reasonable evidence...

Read the full Lactobacillus Acidophilus monograph →
Herb & supplement monograph

Docosahexaenoic Acid (dha)

Interacts with 375 drugs

DHA is an omega-3 fatty acid found in fatty fish and algae that is a building block for the brain, nervous system, and eyes. It is widely used and generally well tolerated, with the stronges...

Read the full Docosahexaenoic Acid (dha) monograph →
Herb & supplement monograph

Bifidobacterium Bifidum

Interacts with 182 drugs

Bifidobacterium bifidum is a 'friendly' bacteria (probiotic) that naturally lives in the human gut and is taken to support digestion and gut balance. Some evidence suggests probiotics may he...

Read the full Bifidobacterium Bifidum monograph →
Herb & supplement monograph

7-keto-dhea

7-keto-DHEA is a lab-made metabolite of the hormone DHEA that is marketed mainly for weight loss and a faster metabolism. Unlike DHEA, it is not thought to convert into estrogen or testoster...

Read the full 7-keto-dhea monograph →
Herb & supplement monograph

Same

Interacts with 189 drugs

SAM-e is a compound your body makes naturally that is sold as a supplement, most often for depression and osteoarthritis. Some research suggests it may help with these conditions, but the qu...

Read the full Same monograph →
Herb & supplement monograph

Alpha-lipoic Acid

Interacts with 263 drugs

Alpha-lipoic acid (ALA) is an antioxidant made naturally by the body and found in small amounts in foods. It is most studied for diabetic nerve pain, where some evidence suggests it may help...

Read the full Alpha-lipoic Acid monograph →
Herb & supplement monograph

Coenzyme Q10

Interacts with 198 drugs

CoQ10 is a vitamin-like substance your body makes naturally that helps cells produce energy and acts as an antioxidant. It is generally well tolerated and is most studied for heart condition...

Read the full Coenzyme Q10 monograph →
Herb & supplement monograph

Hu Zhang

Interacts with 826 drugs

Hu Zhang (Japanese knotweed root) is a traditional Chinese herb that is one of the richest natural sources of resveratrol and emodin. Some lab and early human research looks interesting for...

Read the full Hu Zhang monograph →
Herb & supplement monograph

N-acetyl Cysteine (nac)

Interacts with 294 drugs

N-acetyl cysteine (NAC) is a supplement form of the amino acid cysteine and a building block for the antioxidant glutathione. It has well-established prescription uses for acetaminophen over...

Read the full N-acetyl Cysteine (nac) monograph →
Herb & supplement monograph

Glutathione

Glutathione is a powerful antioxidant your body makes naturally, and many people take it as a supplement hoping for skin, detox, or anti-aging benefits. However, strong human evidence is lim...

Read the full Glutathione monograph →
Sources

Sources & How We Checked

ReversAge Lemon-Lime Flavor'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 672 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.

Glutamine 11 references
  1. Miller AL. Therapeutic considerations of L-glutamine: a review of the literature. Altern Med Rev 1999;4:239-48..
  2. Bozzetti F, Biganzoli L, Gavazzi C, et al. Glutamine supplementation in cancer patients receiving chemotherapy: a double-blind randomized study. Nutrition 1997;13:748-51.. PubMed
  3. Mebane AH. L-Glutamine and mania. Am J Psychiatry 984;141:1302-3.
  4. Meldrum BS. Glutamate as a neurotransmitter in the brain: review of physiology and pathology. J Nutr 2000;130:1007S-15S.. PubMed
  5. Garlick PJ. Assessment of the safety of glutamine and other amino acids. J Nutr 2001;131:2556S-61S.. PubMed
  6. Chapman AG. Glutamate and epilepsy. J Nutr 2000;130:1043S-5S.. PubMed
  7. Ziegler TR. Glutamine supplementation in cancer patients receiving bone marrow transplantation and high dose chemotherapy. J Nutr 2001;131:2578S-84S.. PubMed
  8. Laviano A, Molfino A, Lacaria MT, Canelli A, De Leo S, Preziosa I, Rossi Fanelli F. Glutamine supplementation favors weight loss in nondieting obese female patients. A pilot study. Eur J Clin Nutr. 2014 Nov;68(11):1264-6. PubMed
  9. Endari (l-glutamine) [package insert]. Torrance, CA: Emmaus Medical,Inc; 2017.
  10. Niihara Y, Miller ST, Kanter J, et al. A Phase 3 Trial of l-Glutamine in Sickle Cell Disease. N Engl J Med 2018;379(3):226-35. doi: 10.1056/NEJMoa1715971.
  11. Ogden HB, Child RB, Fallowfield JL, et al. Gastrointestinal Tolerance of Low, Medium and High Dose Acute Oral l-Glutamine Supplementation in Healthy Adults: A Pilot Study. Nutrients. 2020;12(10):2953. PubMed

See these in context on the Glutamine monograph →

Sodium 38 references
  1. Garabedian-Ruffalo SM, Ruffalo RL. Drug and nutrient interactions. Am Fam Physician 1986;33:165-74.
  2. Food and Drug Administration Science Background: Safety of Sodium Phosphates Oral Solution. September 17, 2001. Available at: http://www.fda.gov/cder/drug/safety/sodiumphospate.htm
  3. Coton T, Mallaret C, Coilliot C, Carre D, Guisset M. Severe acute ulcerated gastritis induced by salt. Presse Med 2009;38(3):499-500. PubMed
  4. Frings-Meuthen P, Buehlmeier J, Baecker N, et al. High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses. J Appl Physiol 2011;111(2):537-542. PubMed
  5. Frings-Meuthen P, Baecker N, Heer M. Low-grade metabolic acidosis may be the cause of sodium chloride-induced exaggerated bone resorption. J Bone Miner Res 2008;23(4):517-524. PubMed
  6. Alam S, Johnson AG. A meta-analysis of randomised controlled trials (RCT) among healthy normotensive and essential hypertensive elderly patients to determine the effect of high salt (NaCl) diet of blood pressure. J Hum Hypertens 1999;13(6):367-74.
  7. Boudville N, Ward S, Benaroia M, House AA. Increased sodium intake correlates with greater use of antihypertensive agents by subjects with chronic kidney disease. Am J Hypertens 2005;18(10):1300-5. PubMed
  8. Bennett WM. Drug interactions and consequences of sodium restriction. Am J Clin Nutr 1997;65(2 Suppl):678S-681S. PubMed
  9. Okusa MD, Crystal LJ. Clinical manifestations and management of acute lithium intoxication. Am J Med 1994;97(4):383-9. PubMed
  10. Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for water, potassium, sodium, chloride, and sulfate. Washington, DC: National Academy Press, 2005. Available at: http://www.nap.edu/openbook.php?record_id=10925. DOI
  11. D'Elia L, Rossi G, Ippolito R, Cappuccio FP, Strazzullo P. Habitual salt intake and risk of gastric cancer: a meta-analysis of prospective studies. Clin Nutr 2012;31(4):489-98. PubMed
  12. Goldsmith SR. Hyponatremia in heart failure: time for a trial. J Card Fail 2013;19(6):398-400. PubMed
  13. Willocks L, Brettle R, Keen J, Valentine C, Pinching AJ. Formulations of didanosine (ddI) and salt overload. Lancet 1992;339(8786):190.
  14. Chen L, Zhang Z, Chen W, Whelton PK, Appel LJ. Lower Sodium Intake and Risk of Headaches: Results From the Trial of Nonpharmacologic Interventions in the Elderly. Am J Public Health. 2016;106(7):1270-5. PubMed
  15. Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014;129(9):981-9. PubMed
  16. Cook NR, Appel LJ, Whelton PK. Sodium Intake and All-Cause Mortality Over 20 Years in the Trials of Hypertension Prevention. J Am Coll Cardiol. 2016;68(15):1609-1617. PubMed
  17. Mente A, O'Donnell M, Rangarajan S, et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. Lancet. 2016;388(10043):465-75. PubMed
  18. Moosavian SP, Haghighatdoost F, Surkan PJ, Azadbakht L. Salt and obesity: a systematic review and meta-analysis of observational studies. Int J Food Sci Nutr. 2017;68(3):265-277. PubMed
  19. O'Donnell M, Mente A, Rangarajan S, et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014;371(7):612-23. DOI
  20. Poggio R, Gutierrez L, Matta MG, Elorriaga N, Irazola V, Rubinstein A. Daily sodium consumption and CVD mortality in the general population: systematic review and meta-analysis of prospective studies. Public Health Nutr. 2015;18(4):695-704. PubMed
  21. Stallings VA, Harrison M, Oria M; Committee to Review the Dietary Reference Intakes for Sodium and Potassium, Food and Nutrition Board, Health and Medicine Division, National Academies of Sciences, Engineering, and Medicine. Washington (DC): National Acad
  22. Mahtani KR, Heneghan C, Onakpoya I, et al. Reduced Salt Intake for Heart Failure: A Systematic Review. JAMA Intern Med. 2018 Dec 1;178(12):1693-1700. PubMed
  23. Yancy CW. Sodium Restriction in Heart Failure: Too Much Uncertainty-Do the Trials. JAMA Intern Med. 2018 Dec 1;178(12):1700-1701. PubMed
  24. He FJ, Campbell NRC, Ma Y, MacGregor GA, Cogswell ME, Cook NR. Errors in estimating usual sodium intake by the Kawasaki formula alter its relationship with mortality: implications for public health. Int J Epidemiol. 2018;47(6):1784-1795. PubMed
  25. Murthy K, Ondrey GJ, Malkani N, et al. THE EFFECTS OF HYPONATREMIA ON BONE DENSITY AND FRACTURES: A SYSTEMATIC REVIEW AND META-ANALYSIS. Endocr Pract. 2019;25(4):366-378. PubMed
  26. Messerli FH, Hofstetter L, Syrogiannouli L, et al. Sodium intake, life expectancy, and all-cause mortality. Eur Heart J 2021;42(21):2103-2112. PubMed
  27. Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database Syst Rev 2020;12(12):CD004022. PubMed
  28. Giatti S, Santos RB, Aielo AN, et al. Association of sodium with obstructive sleep apnea. The ELSA-Brasil study. Ann Am Thorac Soc 2021;18(3):502-510. PubMed
  29. Nan X, Lu H, Wu J, et al. The interactive association between sodium intake, alcohol consumption and hypertension among elderly in northern China: a cross-sectional study. BMC Geriatr 2021;21(1):135. PubMed
  30. Kyozuka H, Fukusda T, Murata T, et al. Impact of preconception sodium intake on hypertensive disorders of pregnancy: The Japan Environment and Children's study. Pregnancy Hypertens 2021;23:66-72. PubMed
  31. Zhao L, Ogden CL, Yang Q, et al. Association of usual sodium intake with obesity among US children and adolescents, NHANES 2009-2016. Obesity (Silver Spring) 2021;29(3):587-594. PubMed
  32. Ma Y, He FJ, Sun Q, et al. 24-Hour urinary sodium and potassium excretion and cardiovascular risk. N Engl J Med 2022;386(3):252-263. PubMed
  33. Liu J, Yang X, Zhang P, et al. Association of urinary sodium excretion and left ventricular hypertrophy in people with type 2 diabetes mellitus: A cross-sectional study. Front Endocrinol (Lausanne) 2021;12:728493. PubMed
  34. Filippini T, Malavolti M, Whelton PK, Vinceti M. Sodium intake and risk of hypertension: A systematic review and dose-response meta-analysis of observational cohort studies. Curr Hypertens Rep 2022;24(5):133-144. PubMed
  35. Wang DD, Li Y, Nguyen XT, et al. Dietary sodium and potassium intake and risk of non-fatal cardiovascular diseases: The million veteran program. Nutrients 2022;14(5):1121. PubMed
  36. Kwak JH, Park CH, Eun CS, et al. The associations of dietary intake of high sodium and low zinc with gastric cancer mortality: A prospective cohort study in Korea. Nutr Cancer 2022;74(10):3501-3508. PubMed
  37. George S, Maiti R, Mishra BR, Jena M, Mohapatra D. Effect of regulated add-on sodium chloride intake on stabilization of serum lithium concentration in bipolar disorder: A randomized controlled trial. Bipolar Disord 2023;25(1):66-75. PubMed
  38. Zhou TL, Schütten MTJ, Kroon AA, et al. Urinary Sodium Excretion and Salt Intake Are Not Associated With Blood Pressure Variability in a White General Population. J Am Heart Assoc 2023;12(1):e026578. PubMed

See these in context on the Sodium monograph →

Alpha-lipoic Acid 48 references
  1. Labriola D, Livingston R. Possible interactions between dietary antioxidants and chemotherapy. Oncology 1999;13:1003-8.
  2. Anon. Alpha-lipoic acid. Altern Med Rev 1998;3:308-10.
  3. Konrad T, Vicini P, Kusterer K, et al. Alpha-lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with Type 2 diabetes. Diabetes Care 1999;22:280-7. PubMed
  4. Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the antioxidant alpha-lipoic acid: A 3-week, multicentre randomized controlled trial (ALADIN Study). Diabetologia 1995;38:1425-33.
  5. Gleiter CH, Schreeb KH, Freudenthaler S, et al. Lack of interaction between thioctic acid, glibenclamide and acarbose. Br J Clin Pharmacol 1999;48:819-25. PubMed
  6. Jacob S, Henriksen EJ, Tritschler HJ, et al. Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabet 1996;104:284-8. PubMed
  7. Jacob S, Henriksen EJ, Schiemann AL, et al. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung 1995;45:872-4.
  8. Jacob S, Ruus P, Hermann R, et al. Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled, pilot trial. Free Rad Biol Med 1999;27:309-14.
  9. Segermann J, Hotze A, Ulrich H, Rao GS. Effect of alpha-lipoic acid on the peripheral conversion of thyroxine to triiodothyronine and on serum lipid-, protein- and glucose levels. Arzneimittelforschung 1991;41:1294-8.
  10. Beitner H. Randomized, placebo controlled, double-blind study on the clinical efficacy of a cream containing 5% alpha-lipoic acid related to photoaging of facial skin. Br J Dermatol 2003;149:841-9.
  11. Ziegler D, Nowak H, Kempler P, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: A meta-analysis. Diabet Med 2004;21:114-21.
  12. Prasad KN. Rationale for using high-dose multiple dietary antioxidants as an adjunct to radiation therapy and chemotherapy. J Nutr 2004;134:3182S-3S. PubMed
  13. Conklin KA. Cancer chemotherapy and antioxidants. J Nutr 2004;134:3201S-3204S. PubMed
  14. Vincent HK, Bourguignon CM, Vincent KR, Taylor AG. Effects of alpha-lipoic acid supplementation in peripheral arterial disease: a pilot study. J Alt Complement Med 2007;13:577-84. PubMed
  15. Furukawa N, Miyamura N, Nishida K, et al. Possible relevance of alpha lipoic acid contained in a health supplement in a case of insulin autoimmune syndrome. Diabetes Res Clin Pract 2007;75:366-7. PubMed
  16. Ziegler D., Ametov A., Barinov A., Dyck P. J., Gurieva I., Low P. A., Munzel U., Yakhno N., Raz I., Novosadova M., Maus J., Samigullin, R. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: the SYDNEY 2 trial. Diabetes Car
  17. Gu X. M., Zhang S. S., Wu J. C., Tang Z. Y., Lu Z. Q., Li H., Liu C., Chen L., Ning, G. [Efficacy and safety of high-dose a-lipoic acid in the treatment of diabetic polyneuropathy]. Zhonghua Yi Xue Za Zhi 2010;90(35):2473-2476.
  18. Porasuphatana S., Suddee S., Nartnampong A., Konsil J., Harnwong B., Santaweesuk A. Glycemic and oxidative status of patients with type 2 diabetes mellitus following oral administration of alpha-lipoic acid: a randomized double-blinded placebo-controlled
  19. Ansar H., Mazloom Z., Kazemi F., Hejazi N. Effect of alpha-lipoic acid on blood glucose, insulin resistance and glutathione peroxidase of type 2 diabetic patients. Saudi Med J 2011;32(6):584-588. DOI
  20. de Oliveira A. M., Rondó P. H., Luzia L. A., D'Abronzo F. H., Illison V. K. The effects of lipoic acid and a-tocopherol supplementation on the lipid profile and insulin sensitivity of patients with type 2 diabetes mellitus: a randomized, double-blind, pla
  21. Mazloom Z., Ansar H. The Effect of Alpha-Lipoic Acid on Blood Pressure in Type 2 Diabetics. Iranian Journal of Endocrinology and Metabolism 2009;11(3):245-250.
  22. Volchegorskii I. A., Rassokhina L. M., Koliadich M. I., Alekseev M. I. [Comparative study of alpha-lipoic acid and mexidol effects on affective status, cognitive functions and quality of life in diabetes mellitus patients]. Eksp Klin Farmakol 2011;74(11):
  23. Cavalcanti D. R., da Silveira F. R. Alpha lipoic acid in burning mouth syndrome--a randomized double-blind placebo-controlled trial. J Oral Pathol Med 2009;38(3):254-261. PubMed
  24. Koh E. H., Lee W. J., Lee S. A., Kim E. H., Cho E. H., Jeong E., Kim D. W., Kim M. S., Park J. Y., Park K. G., Lee H. J., Lee I. K., Lim S., Jang H. C., Lee K. H., Lee K. U. Effects of alpha-lipoic Acid on body weight in obese subjects. Am J Med 2011;124( PubMed
  25. Bergqvist-Karlsson, A., Thelin, I., and Bergendorff, O. Contact dermatitis to alpha-lipoic acid in an anti-wrinkle cream. Contact Dermatitis 2006;55(1):56-57.
  26. Tang, J., Wingerchuk, D. M., Crum, B. A., Rubin, D. I., and Demaerschalk, B. M. Alpha-lipoic acid may improve symptomatic diabetic polyneuropathy. Neurologist. 2007;13(3):164-167. PubMed
  27. Hegazy SK, Tolba OA, Mostafa TM, Eid MA, El-Afify DR. Alpha-lipoic acid improves subclinical left ventricular dysfunction in asymptomatic patients with type 1 diabetes. Rev Diabet Stud 2013;10(1):58-67. PubMed
  28. Huang Z, Wan X, Liu J, et al. Short-term continuous subcutaneous insulin infusion combined with insulin sensitizers rosiglitazone, metformin, or antioxidant a-lipoic acid in patients with newly diagnosed type 2 diabetes mellitus. Diabetes Technol Ther 201
  29. Sarezky D, Raquib AR, Dunaief JL, Kim BJ. Tolerability in the elderly population of high-dose alpha lipoic acid: a potential antioxidant therapy for the eye. Clin Ophthalmol. 2016 Sep 29;10:1899-1903. PubMed
  30. Boriani F, Granchi D, Roatti G, Merlini L, Sabattini T, Baldini N. Alpha-lipoic acid after median nerve decompression at the carpal tunnel: a randomized controlled trial. J Hand Surg Am. 2017 Apr;42(4):236-42. PubMed
  31. Karkabounas S, Papadopoulos N, Anastasiadou C, et al. Effects of a-lipoic Acid, carnosine, and thiamine supplementation in obese patients with type 2 diabetes mellitus: A randomized, double-blind study. J Med Food. 2018;21(12):1197-1203.
  32. Murray GL, Colombo J. (r)Alpha lipoic acid is a safe, effective pharmacologic therapy of chronic orthostatic hypotension associated with low sympathetic tone. Int J Angiol. 2019;28(3):188-193. PubMed
  33. Bobe G, Michels AJ, Zhang WJ, et al. A randomized controlled trial of long-term (R)-&alpha;-lipoic acid supplementation promotes weight loss in overweight or obese adults without altering baseline elevated plasma triglyceride concentrations. J Nutr. 2020:
  34. Passiatore M, Perna A, De-Vitis R, Taccardo G. The use of alfa-lipoic acid-R (ALA-R) in patients with mild-moderate carpal tunnel syndrome: A randomised controlled open label prospective study. Malays Orthop J. 2020;14(1):1-6. PubMed
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Acetyl-l-carnitine 22 references
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Lysine 7 references
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Maca 1 reference
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Lactobacillus Acidophilus 15 references
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Docosahexaenoic Acid (dha) 49 references
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See these in context on the N-acetyl Cysteine (nac) monograph →

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Stinging Nettle 23 references
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Blue-green Algae 22 references
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Chlorella 13 references
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Diosmin 20 references
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L-arginine 66 references
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