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Dietary supplement

De-Stress + Relax Ingredients & Drug Interactions

by Stressballs

Gummy Or Jelly Category: Botanical
Most serious interaction: Moderate
The interaction bottom line Most serious interaction: Moderate

De-Stress + Relax is a dietary supplement by Stressballs with 4 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, 1,536 medications have a known interaction with it, the most serious rated moderate. The ingredients most likely to interact are Ashwagandha (Withania somnifera) root and leaf extract, Ginseng (Panax ginseng C.A. Meyer) root extract, Lemon Balm (Melissa officinalis L.) leaf extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of De-Stress + Relax by Stressballs

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 4 active ingredients.
  • “Stressballs Relax Herbal Blend” is a proprietary blend — the label gives one combined amount (230 mg) without saying how much of each component you get.

De-Stress + Relax contains four active ingredients. Sodium is an essential mineral, though in supplement form it must be used carefully.

Ashwagandha root and leaf extract, lemon balm leaf extract, and ginseng root extract are all herbal ingredients traditionally used to support relaxation and stress response. The product also contains inactive ingredients like corn syrup, sugar, pectin, and several food colorings and stabilizers to form the gummy.

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: stress and anxiety relief support.
  • We looked for evidence on: Anxiety, Generalized anxiety disorder (GAD), stress management, mental relaxation, nervousness.
  • The strongest evidence on file: Lemon Balm is rated "Possibly Effective" for Stress (Natural Medicines).
  • Also on file: Ashwagandha is rated "Possibly Effective" for Anxiety, Generalized anxiety disorder (GAD), Stress.
  • Also on file: Lemon Balm is rated "Insufficient Reliable Evidence To Rate" for Anxiety.

Ashwagandha is possibly effective for insomnia, anxiety, stress, and generalized anxiety disorder—the conditions this product targets. Lemon balm is also possibly effective for stress and depression.

Ginseng has some evidence for cognitive function and fatigue, though not specifically for stress or anxiety in the data we hold. The evidence for sodium's role here isn't established in our data.

The evidence, ingredient by ingredient Sodium Ashwagandha Lemon Balm Panax Ginseng

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 4 of the 4 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 4 of 4.
  • General safety write-ups exist for 4 of 4.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Ashwagandha and ginseng are generally well tolerated short-term in healthy adults, though long-term safety data are limited. Lemon balm is also generally well tolerated for short-term use.

However, all three herbs carry pregnancy warnings: ashwagandha is likely unsafe in pregnancy due to miscarriage risk; ginseng and lemon balm have insufficient safety data and should be avoided in pregnancy unless your doctor advises otherwise. The same caution applies to breastfeeding.

Sodium in typical dietary amounts is fine, but supplements shouldn't be used without medical advice, especially if you have high blood pressure or kidney disease. Rare but serious adverse effects with ashwagandha include liver damage; lemon balm and ginseng have rare reports of arrhythmias and other cardiovascular events.

Side effects, ingredient by ingredient Sodium Ashwagandha Lemon Balm Panax Ginseng

Meds to double-check

Moderate interaction found
Known Interaction Concern · database check
Moderate identified

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

Why this rating?
  • 4 of the 4 matched ingredients can interact with medications — Lemon Balm, Ashwagandha, Panax Ginseng, Sodium.
  • The most serious interaction on file is rated Moderate.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; diabetes medications; heart-rhythm medications; lithium.
  • For scale: 1,537 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

Check with your doctor or pharmacist before taking this product if you use blood pressure medications (antihypertensives), diabetes medications, sedating drugs, benzodiazepines, corticosteroids, lithium, thyroid hormones, blood thinners like warfarin, or MAOIs. Ginseng also affects medications metabolized in the liver (CYP2D6 and CYP3A4 substrates), furosemide, selegiline, insulin, and raltegravir.

Because of the many possible interactions, checking your exact medications with the search tool on this page is important.

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. Moderate medication interactions have been identified, and safety information is well characterized.

This product may help with short-term stress and anxiety if you're a healthy adult not pregnant or breastfeeding and not taking any of the medications listed in the Med Watch section below. Because of the number and variety of interactions—especially with blood pressure drugs, diabetes medications, sedatives, thyroid hormones, and blood thinners—talk with your doctor or pharmacist before starting, even if you think your medications are "safe." If you're pregnant, planning pregnancy, or breastfeeding, discuss this product with your healthcare provider first.

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

Assessment coverage: 4 of 4 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Nov 22, 2022.

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 De-Stress + Relax, straight from the product label.

Brand Stressballs
Barcode (UPC) 037000516064
Net contents 46 Gummy(ies)
Market status On market
Date entered into DSLD Nov 22, 2022
DSLD ID 278086
Product type Botanical
Supplement form Gummy Or Jelly
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 De-Stress + Relax by Stressballs, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
2 Gummy(ies)
Maximum serving Sizes:
2 Gummy(ies)
Servings per container
23
UPC/BARCODE
037000516064
IngredientAmount% DV
Calories25 Calorie(s)--
Total Carbohydrates6 Gram(s)2%
Sodium15 mg1%
Added Sugars5 Gram(s)9%
Total Sugars5 Gram(s)--
Stressballs Relax Herbal Blend230 mg--
Ashwagandha (Withania somnifera) root and leaf extract0 NP--
Lemon Balm (Melissa officinalis L.) leaf extract0 NP--
Ginseng (Panax ginseng C.A. Meyer) root extract0 NP--

Other ingredients: Corn Syrup, Water, Sugar, hydrogenated Coconut Oil, Natural Flavors, Pectin, Citric Acid, Maltodextrin, Sodium Potassium Tartrate, Soy Lecithin, Sodium Citrate, Sodium Polyphosphate, Yellow 6

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.
Brand IP Statement(s)

P&G www.pg.com Patents: www.pg.com/patents

Formulation

Non-habit forming Non-drowsy

Drug free, gluten free, lactose free, & gelatin free

FDA Disclaimer Statement

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

Formula

Ashwagandha Ginseng Lemon balm

FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Directions: Take two gummies as needed, up to twice a day. Use daily for stronger effect, as results improve over time.

Storage

Store in a cool, dry place.

Precautions

Warnings: Consult a healthcare professional: Before use if below 18 yrs in age; before use if pregnant, attempting to become pregnant or nursing; those with a medical condition including hypertension and diabetes, those taking medication, and those who have chronic diseases

Warnings: Consult a healthcare professional: Before use if below 18 yrs in age; before use if pregnant, attempting to become pregnant or nursing; those with a medical condition including hypertension and diabetes, those taking medication, and those who have chronic diseases; Do not use when consuming alcohol

Warnings: Consult a healthcare professional: Before use if below 18 yrs in age; before use if pregnant, attempting to become pregnant or nursing; those with a medical condition including hypertension and diabetes, those taking medication, and those who have chronic diseases; Do not use when consuming alcohol Keep out of reach of children

Contains: Soy, tree nuts (coconut)

See for yourself

De-Stress + Relax by Stressballs label

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

What’s inside

The Ingredients in De-Stress + Relax by Stressballs

These are the 4 active ingredients this product is made of. Select any to open its full monograph.

Serving size2 Gummy(ies) Dosage formGummy Or Jelly Servings per container23 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
15 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

Other (inactive) ingredients: Corn Syrup, Water, Sugar, Hydrogenated Coconut Oil, Natural Flavors, Pectin, Citric Acid, Maltodextrin, Sodium Potassium Tartrate, Soy Lecithin, Sodium Citrate, Sodium Polyphosphate, Yellow 6. These complete the product’s ingredient list but are not active constituents.

Interaction report

De-Stress + Relax by Stressballs Drug Interactions

Want to check YOUR meds against De-Stress + Relax?

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

Each ingredient & the kinds of drugs it affects

For each ingredient in De-Stress + Relax with known interactions, here are the types of medications they can affect. Open any type for the detail — or search your exact drug in the checker above.

Ashwagandha (Withania somnifera) root and leaf extract10 drug types · 1,372 drugs

Antidiabetes Drugs

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

Likelihood Possible Evidence B
Antihypertensive Drugs

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

Likelihood Possible Evidence D
Benzodiazepines

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

Likelihood Possible Evidence D
Cns Depressants

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

Likelihood Possible Evidence D
Hepatotoxic Drugs

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

Likelihood Possible Evidence D
Immunosuppressants

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

Likelihood Possible Evidence D
Thyroid Hormone

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

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

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

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

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

Likelihood Possible Evidence D
Serotonergic Drugs

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

Likelihood Possible Evidence C

Ginseng (Panax ginseng C.A. Meyer) root extract20 drug types · 1,130 drugs

Anticoagulant/Antiplatelet Drugs

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

Likelihood Unlikely Evidence B
Antidiabetes Drugs

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

Likelihood Probable Evidence B
Caffeine

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

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

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

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

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

Likelihood Possible Evidence B
Estrogens

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

Likelihood Possible Evidence D
Furosemide (Lasix)

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

Likelihood Possible Evidence D
Imatinib (Gleevec)

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

Likelihood Possible Evidence D
Immunosuppressants

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

Likelihood Possible Evidence B
Insulin

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

Likelihood Probable Evidence B
Midazolam (Versed)

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

Likelihood Probable Evidence B
Monoamine Oxidase Inhibitors (Maois)

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

Likelihood Probable Evidence D
Nifedipine (Procardia)

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

Likelihood Possible Evidence B
Qt Interval-Prolonging Drugs

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

Likelihood Possible Evidence B
Raltegravir (Isentress)

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

Likelihood Possible Evidence D
Selegiline (Eldepryl)

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

Likelihood Possible Evidence D
Stimulant Drugs

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

Likelihood Possible Evidence D
Warfarin (Coumadin)

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

Likelihood Unlikely Evidence B
Fexofenadine (Allegra)

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

Likelihood Possible Evidence D
Lopinavir/Ritonavir (Kaletra)

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

Likelihood Unlikely Evidence B

Lemon Balm (Melissa officinalis L.) leaf extract2 drug types · 264 drugs

Cns Depressants

Theoretically, concomitant use of lemon balm might have additive effects with CNS depressant drugs.
Lemon balm seems to have CNS depressant activity in animals and in humans.

Likelihood Possible Evidence B
Thyroid Hormone

Theoretically, lemon balm might interfere with thyroid hormone replacement therapy.
In vitro, constituents of lemon balm extract bind to thyroid stimulating hormone (TSH), preventing TSH receptor-binding and leading to the inhibition of TSH-stimulated adenylate cyclase activity. In animals, lemon balm extract has been shown to decrease levels of circulating TSH and inhibit thyroid secretion.

Likelihood Possible Evidence D

Sodium7 drug types · 205 drugs

Antihypertensive Drugs

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

Likelihood Probable Evidence A
Corticosteroids

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

Likelihood Possible Evidence D
Didanosine (Videx)

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

Likelihood Probable Evidence C
Lithium

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

Likelihood Probable Evidence B
Sodium Phosphates

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

Likelihood Possible Evidence D
Sodium-Containing Drugs

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

Likelihood Possible Evidence D
Tolvaptan (Samsca)

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

Likelihood Probable Evidence C
The maker

Brand information

Manufacturer and brand details for De-Stress + Relax, from the product label.

Stressballs

See all Stressballs products
Phone Number
(855) 236-3323
Web Address
Mystressballs.com
Pharmacist Counseling Corner

De-Stress + Relax by Stressballs: Common Questions

Does De-Stress + Relax by Stressballs interact with any medications?
Yes. Based on its ingredients, De-Stress + Relax has a known interaction with 1,536 medications. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
De-Stress + Relax contains 4 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.
Can I take this while pregnant or breastfeeding?
No. Ashwagandha is likely unsafe in pregnancy due to miscarriage risk. Ginseng and lemon balm have insufficient safety data, so they're best avoided during pregnancy and breastfeeding unless your doctor advises otherwise. Talk with your healthcare provider about whether this product is right for you.
Is this safe if I take blood pressure or diabetes medication?
Not without checking first. Ashwagandha, ginseng, and sodium all interact with blood pressure and diabetes drugs in ways that could reduce the drug's effect or increase your risk of low blood pressure or low blood sugar. Check your exact medications with your doctor or pharmacist before starting.
What does ashwagandha do in this product?
Ashwagandha is a traditional herb that has some evidence it may help with insomnia, anxiety, stress, and generalized anxiety disorder—the main conditions this product aims to address.
Does this product have fillers?
Yes. Inactive ingredients include corn syrup, sugar, pectin, food colorings like Yellow 6, citric acid, and other stabilizers to form the gummy.
What are the most common side effects?
Ashwagandha and ginseng can cause diarrhea, nausea, insomnia, and headache in some people—though these don't occur commonly at typical doses. Lemon balm may cause dizziness. Serious adverse effects are rare but have been reported and include liver damage with ashwagandha and heart rhythm problems with ginseng.
How long is it safe to take this?
The safety data we hold are strongest for short-term use—up to a few months—in healthy adults. Long-term safety hasn't been well studied for any of these herbal ingredients, so talk with your doctor about how long it's appropriate for you to use it.

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.

De-Stress + Relax label
Sources

Sources & How We Checked

De-Stress + Relax'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.

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The 148 references behind this product’s interaction data

Every citation that drives the interaction findings for this product’s ingredients, from the evidence-graded Natural Medicines (TRC Healthcare) database. Open an ingredient to browse its citations — links open the study on PubMed or the publisher’s site.

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

See these in context on the Sodium monograph →

Ashwagandha 32 references
  1. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
  2. Upton R, ed. Ashwagandha Root (Withania somnifera): Analytical, quality control, and therapuetic monograph. Santa Cruz, CA: American Herbal Pharmacopoeia 2000:1-25.
  3. Davis L, Kuttan G. Effect of Withania somnifera on cyclophosphamide-induced urotoxicity. Cancer Lett 2000;148:9-17. PubMed
  4. Davis L, Kuttan G. Suppressive effect of cyclophosphamide-induced toxicity by Withania somnifera extract in mice. J Ethnopharmacol 1998;62:209-14. PubMed
  5. Mishra LC, Singh BB, Dagenais S. Scientific basis for the therapeutic use of Withania somnifera (ashwagandha): a review. Altern Med Rev 2000;5:334-46. DOI
  6. Andallu B, Radhika B. Hypoglycemic, diuretic and hypocholesterolemic effect of winter cherry (Withania somnifera, Dunal) root. Indian J Exp Biol 2000;38:607-9.
  7. Kulkarni RR, Patki PS, Jog VP, et al. Treatment of osteoarthritis with a herbomineral formulation: a double-blind, placebo-controlled, cross-over study. J Ethnopharmacol 1991;33:91-5. PubMed
  8. Ahumada F, Aspee F, Wikman G, Hancke J. Withania somnifera exract. Its effects on arterial blood pressure in anaesthetized dogs. Phytother Res 1991;5:111-14.
  9. Panda S, Kar A. Withania somnifera and Bauhinia purpurea in the regulation of circulating thyroid hormone concentrations in female mice. J Ethnopharmacol 1999;67:233-39. PubMed
  10. Panda S, Kar A. Changes in thyroid hormone concentrations after administration of ashwagandha root extract to adult male mice. J Pharm Pharmacol 1998;50:1065-68. PubMed
  11. Sehgal, V. N., Verma, P., and Bhattacharya, S. N. Fixed-drug eruption caused by ashwagandha (Withania somnifera): a widely used Ayurvedic drug. Skinmed. 2012;10(1):48-49.
  12. Agnihotri AP, Sontakke SD, Thawani VR, Saoji A, Goswami VS. Effects of Withania somnifera in patients of schizophrenia: a randomized, double blind, placebo controlled pilot trial study. Indian J Pharmacol. 2013;45(4):417-8. PubMed
  13. Biswal BM, Sulaiman SA, Ismail HC, Zakaria H, Musa KI. Effect of Withania somnifera (Ashwagandha) on the development of chemotherapy-induced fatigue and quality of life in breast cancer patients. Integr Cancer Ther. 2013;12(4):312-22.
  14. Sharma AK, Basu I, Singh S. Efficacy and safety of Ashwagandha root extract in subclinical hypothyroid patients: a double-blind, randomized placebo-controlled trial. J Altern Complement Med. 2018 Mar;24(3):243-248. PubMed
  15. Durg S, Bavage S, Shivaram SB. Withania somnifera (Indian ginseng) in diabetes mellitus: A systematic review and meta-analysis of scientific evidence from experimental research to clinical application. Phytother Res. 2020;34(5):1041-1059.
  16. Björnsson HK, Björnsson ES, Avula B, et al. Ashwagandha-induced liver injury: A case series from Iceland and the US Drug-Induced Liver Injury Network. Liver Int. 2020;40(4):825-829. PubMed
  17. Tharakan A, Shukla H, Benny IR, Tharakan M, George L, Koshy S. Immunomodulatory Effect of Withania somnifera (Ashwagandha) Extract-A Randomized, Double-Blind, Placebo Controlled Trial with an Open Label Extension on Healthy Participants. J Clin Med 2021;1 PubMed
  18. Ireland PJ, Hardy T, Burt AD, Donnelly MC. Drug-induced hepatocellular injury due to herbal supplement ashwagandha. J R Coll Physicians Edinb. 2021;51(4):363-365. PubMed
  19. Kamal HI, Patel K, Brdak A, Heffernan J, Ahmad N. Ashwagandha as a unique cause of thyrotoxicosis presenting with supraventricular tachycardia. Cureus. 2022 Mar 25;14(3):e23494. PubMed
  20. Suryawanshi G, Abdallah M, Thomson M, Desai N, Chauhan A, Lim N. Ashwagandha-Associated Acute Liver Failure Requiring Liver Transplantation. Am J Ther 2023;30(1):e80-e83. PubMed
  21. Pusec CM, Wolsky R, Llerena C, Sura P. A Case of Supplement-Induced Hepatitis. Cureus 2022;14(10):e30433. PubMed
  22. Ajgaonkar A, Jain M, Debnath K. Efficacy and Safety of Ashwagandha (Withania somnifera) Root Extract for Improvement of Sexual Health in Healthy Women: A Prospective, Randomized, Placebo-Controlled Study. Cureus 2022;14(10):e30787. PubMed
  23. Haron MH, Dale O, Martin K, et al. Evaluation of the Herb-Drug Interaction Potential of Commonly Used Botanicals on the US Market with Regard to PXR- and AhR-Mediated Influences on CYP3A4 and CYP1A2. J Diet Suppl 2022. PubMed
  24. Lubarska M, Halasinski P, Hryhorowicz S, et al. Liver Dangers of Herbal Products: A Case Report of Ashwagandha-Induced Liver Injury. Int J Environ Res Public Health 2023;20(5):3921. PubMed
  25. Tóth M, Benedek AE, Longerich T, Seitz HK. Ashwagandha-induced acute liver injury: A case report. Clin Case Rep 2023;11(3):e7078.
  26. Bokan G, Glamocanin T, Mavija Z, et al. Herb-Induced Liver Injury by Ayurvedic Ashwagandha as Assessed for Causality by the Updated RUCAM: An Emerging Cause. Pharmaceuticals (Basel) 2023;16(8):1129. PubMed
  27. Patel PA, Sanborn E, Then R, Williams DM. Recurrent Reversible Cerebral Vasoconstriction Syndrome: A Report of Two Cases. Cureus 2023;15(8):e42992. PubMed
  28. Majeed M, Nagabhushanam K, Murali A, Vishwanathan DT, Mamidala RV, Mundkur L. A Standardized Withania somniferra (Linn.) Root Extract with Piperine Alleviates the Symptoms of Anxiety and Depression by Increasing Serotonin Levels: A Double-Blind, Randomize
  29. Philips CA, Valsan A, Theruvath AH, et al. Ashwagandha-induced liver injury-A case series from India and literature review. Hepatol Commun 2023;7(10):e0270. PubMed
  30. Hayashi M, Hamada H, Azuma SI, Hayashi K. Painless Thyroiditis by Withania somnifera (Ashwagandha). Cureus 2024;16(3):e55352. PubMed
  31. Vazirani S, Kothari A, Fujimoto J, Gomez M. Supplements Are Not a Synonym for Safe: Suspected Liver Injury From Ashwagandha. Fed Pract 2023;40(9):315-319. PubMed
  32. Patel M, Newell R, Hillier M, Ramalingam R. Herbal remedies as a potential cause of hypoadrenalism. Br J Hosp Med (Lond) 2024;85(6):1-4. PubMed

See these in context on the Ashwagandha monograph →

Lemon Balm 12 references
  1. Wolbling RH, Leonhardt K. Local therapy of herpes simplex with dried extract from Melissa officinalis. Phytomedicine 1994;1:25-31.
  2. Akhondzadeh S, Noroozian M, Mohammadi M, et al. Melissa officinalis extract in the treatment of patients with mild to moderate Alzheimer's disease: a double blind, randomised, placebo controlled trial. J Neurol Neurosurg Psychiatry 2003;74:863-6. PubMed
  3. Kennedy DO, Scholey AB, Tildesley NT, et al. Modulation of mood and cognitive performance following acute administration of Melissa officinalis (lemon balm). Pharmacol Biochem Behav 2002;72:953-64. PubMed
  4. Albrecht M, Berger W, Laux P, Schmidt U, et al. Psychopharmaka und Verkehrssicherheit. Der Einfluß von Euvegal® - Dragees forte auf die Fahrtüchtigkeit und Kombinationswirkungen mit Alkohol Z Allg Med 1995;71:1215-25.
  5. Herberg, KW. Nebenwirkungen pflanzlicher Beruhigungsmittel/ Leistung und Befinden nach Einnahme einer Baldrian-Hopfen-Kombination. Z.Allg Med 1996;72:234-240.
  6. Soulimani R, Fleurentin J, Mortier F, et al. Neurotropic action of the hydroalcoholic extract of Melissa officinalis in the mouse. Planta Med. 1991 Apr;57:105-9.
  7. Sourgens H, Winterhoff H, Gumbinger HG, et al. Antihormonal effects of plant extracts. TSH- and prolactin-suppressing properties of Lithospermum officinale and other plants. Planta Med. 1982 Jun;45:78-86. DOI
  8. Auf'mkolk M, Ingbar JC, Amir SM, et al. Inhibition by certain plant extracts of the binding and adenylate cyclase stimulatory effect of bovine thyrotropin in human thyroid membranes. Endocrinology. 1984 Aug;115:527-34. PubMed
  9. Santini F, Vitti P, Ceccarini G, et al. In vitro assay of thyroid disruptors affecting TSH-stimulated adenylate cyclase activity. J Endocrinol Invest. 2003 Oct;26:950-5. PubMed
  10. Alijaniha F, et al. Heart palpitation relief with Melissa officinalis leaf extract: double blind, randomized, placebo controlled trial of efficacy and safety. J Ethnopharmacol. 2015;164:378-384. doi: 10.1016/j.jep.2015.02.007. Epub 2015 Feb 11. PubMed
  11. Araj-Khodaei M, Noorbala AA, Yarani R, et al. A double-blind, randomized pilot study for comparison of Melissa officinalis L. and Lavandula angustifolia Mill. with Fluoxetine for the treatment of depression. BMC Complement Med Ther. 2020;20(1):207. PubMed
  12. Kucuk U, Pham M, Raza Raja MH, Saad Shaukat MH, Clark R. Transient complete atrioventricular block associated with herbal supplement use. S D Med 2023;76(7):311-313.

See these in context on the Lemon Balm monograph →

Panax Ginseng 66 references
  1. Scaglione F, Cattaneo G, Alessandria M, Cogo R. Efficacy and safety of the standardized Ginseng extract G115 for potentiating vaccination against the influenza syndrome and protection against the common cold. Drugs Exp Clin Res 1996;22:65-72.
  2. Palmer BV, Montgomery AC, Monteiro JC, et al. Gin Seng and mastalgia [letter]. BMJ 1978;1:1284. PubMed
  3. Hopkins MP, Androff L, Benninghoff AS. Ginseng face cream and unexplained vaginal bleeding. Am J Obstet Gynecol 1988;159:1121-2. PubMed
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  5. Gonzalez-Seijo JC, Ramos YM, Lastra I. Manic episode and ginseng: Report of a possible case. J Clin Psychopharmacol 1995;15:447-8.
  6. Dega H, Laporte JL, Frances C, et al. Ginseng as a cause of Stevens-Johnson syndrome. Lancet 1996;347:1344.
  7. Hamid S, Rojter S, Vierling J. Protracted cholestatic hepatitis after the use of Prostata. Ann Intern Med 1997;127:169-70.
  8. Shader RI, Greenblatt DJ. Phenelzine and the dream machine-ramblings and reflections. J Clin Psychopharmacol 1985;5:65. PubMed
  9. Jones BD, Runikis AM. Interaction of ginseng with phenelzine. J Clin Psychopharmacol 1987;7:201-2. PubMed
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  11. Becker BN. Ginseng-induced diuretic resistance. JAMA 1996;276:606-7. PubMed
  12. Gurley BJ, Gardner SF, Hubbard MA. Clinical assessment of potential cytochrome P450-mediated herb-drug interactions. AAPS Ann Mtg & Expo Indianapolis, IN: 2000; Oct 29 - Nov 2:presentation #3460.
  13. Park HJ, Lee JH, Song YB, Park KH. Effects of dietary supplementation of lipophilic fraction from Panax ginseng on cGMP and cAMP in rat platelets and on blood coagulation. Biol Pharm Bull 1996;19:1434-9. PubMed
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  15. Choi HK, Jung GW, Moon KH, et al. Clinical study of SS-Cream in patients with lifelong premature ejaculation. Urology 2000;55:257-61. PubMed
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  21. Chan LY, Chiu PY, Lau TK. An in-vitro study of ginsenoside Rb(1)-induced teratogenicity using a whole rat embryo culture model. Hum Reprod 2003;18:2166-8..
  22. Gurley BJ, Gardner SF, Hubbard MA, et al. Cytochrome P450 phenotypic ratios for predicting herb-drug interactions in humans. Clin Pharmacol Ther 2002;72:276-87.. PubMed
  23. Wiklund IK, Mattsson LA, Lindgren R, et al. Effects of a standardized ginseng extract on quality of life and physiological parameters in symptomatic postmenopausal women: a double-blind, placebo-controlled trial. Int J Clin Pharmacol Res 1999;19:89-99..
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  25. Punnonen R, Lukola A. Oestrogen-like effect of ginseng. Br Med J 1980;281:1110.. PubMed
  26. Lee YJ, Jin YR, Lim WC, et al. Ginsenoside-Rb1 acts as a weak phytoestrogen in MCF-7 human breast cancer cells. Arch Pharm Res 2003;26:58-63.. PubMed
  27. Xu QF, Fang XL, Chen DF. Pharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats. J Ethnopharmacol 2003;84:187-92. PubMed
  28. Jiang X, Williams KM, Liauw WS, et al. Effect of St John's wort and ginseng on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Br J Clin Pharmacol 2004;57:592-9. PubMed
  29. Yun YP, Do JH, Ko SR, et al. Effects of Korean red ginseng and its mixed prescription on the high molecular weight dextran-induced blood stasis in rats and human platelet aggregation. J Ethnopharmacol 2001;77:259-64. PubMed
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  31. Kabalak AA, Soyal OB, Urfalioglu A, et al. Menometrorrhagia and tachyarrhythmia after using oral and topical ginseng. J Womens Health (Larchmt) 2004;13:830-3. PubMed
  32. Jiang X, Blair EY, McLachlan AJ. Investigation of the effects of herbal medicines on warfarin response in healthy subjects: a population pharmacokinetic-pharmacodynamic modeling approach. J Clin Pharmacol 2006;46:1370-8. PubMed
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  34. Smith M, Lin KM, and Zheng YP. PIII-89 an open trial of nifedipine-herb interactions: Nifedipine with St. John's wort, ginseng or ginkgo biloba. Clin Pharm Ther 2001;69:P86.
  35. Mateo-Carrasco, H., Galvez-Contreras, M. C., Fernandez-Gines, F. D., and Nguyen, T. V. Elevated liver enzymes resulting from an interaction between Raltegravir and Panax ginseng: a case report and brief review. Drug Metabol.Drug Interact. 2012;27(3):171-1
  36. Oh, K. J., Chae, M. J., Lee, H. S., Hong, H. D., and Park, K. Effects of Korean red ginseng on sexual arousal in menopausal women: placebo-controlled, double-blind crossover clinical study. J Sex Med 2010;7(4 Pt 1):1469-1477. PubMed
  37. Kim, T. H., Jeon, S. H., Hahn, E. J., Paek, K. Y., Park, J. K., Youn, N. Y., and Lee, H. L. Effects of tissue-cultured mountain ginseng (Panax ginseng CA Meyer) extract on male patients with erectile dysfunction. Asian J Androl 2009;11(3):356-361. PubMed
  38. Hu, Z., Yang, X., Ho, P. C., Chan, S. Y., Heng, P. W., Chan, E., Duan, W., Koh, H. L., and Zhou, S. Herb-drug interactions: a literature review. Drugs 2005;65(9):1239-1282. PubMed
  39. Zhang, R., Jie, J., Zhou, Y., Cao, Z., and Li, W. Long-term effects of Panax ginseng on disposition of fexofenadine in rats in vivo. Am J Chin Med 2009;37(4):657-667.
  40. Lee, Y. H., Lee, B. K., Choi, Y. J., Yoon, I. K., Chang, B. C., and Gwak, H. S. Interaction between warfarin and Korean red ginseng in patients with cardiac valve replacement. Int J Cardiol. 11-19-2010;145(2):275-276. PubMed
  41. Liu, P., Yin, H., Xu, Y., Zhang, Z., Chen, K., and Li, Y. Effects of ginsenoside Rg1 on postimplantation rat and mouse embryos cultured in vitro. Toxicol In Vitro 2006;20(2):234-238. PubMed
  42. Liu, P., Xu, Y., Yin, H., Wang, J., Chen, K., and Li, Y. Developmental toxicity research of ginsenoside Rb1 using a whole mouse embryo culture model. Birth Defects Res B Dev Reprod Toxicol 2005;74(2):207-209. PubMed
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  44. Wesnes KA, Faleni RA, Hefting NR, and et al. The cognitive, subjective, and physical effects of a Ginkgo biloba/Panax ginseng combination in healthy volunteers with neurasthenic complaints. Psychopharmacol Bull 1997;33(4):677-683.
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  46. Kakisaka Y, Ohara T, Tozawa H, Sato S, Katayama S, Suzuki T, Hino-Fukuyo N, Kure S. Panax ginseng: a newly identified cause of gynecomastia. Tohoku J Exp Med 2012;228(2):143-5. PubMed
  47. Malati CY, Robertson SM, Hunt JD, Chairez C, Alfaro RM, Kovacs JA, Penzak SR. Influence of Panax ginseng on cytochrome P450 (CYP)3A and P-glycoprotein (P-gp) activity in healthy participants. J Clin Pharmacol 2012;52(6):932-9.
  48. Sen A. Orobuccolingual dyskinesia after long-term use of black cohosh and ginseng. J Neuropsychiatry Clin Neurosci 2013 Fall;25(4):E50. PubMed
  49. Oh MR, Park SH, Kim SY, Back HI, Kim MG, Jeon JY, Ha KC, Na WT, Cha YS, Park BH, Park TS, Chae SW. Postprandial glucose-lowering effects of fermented red ginseng in subjects with impaired fasting glucose or type 2 diabetes: a randomized, double-blind, pla
  50. Kim HG, Cho JH, Yoo SR, Lee JS, Han JM, Lee NH, Ahn YC, Son CG. Antifatigue effects of Panax ginseng C.A. Meyer: a randomised, double-blind, placebo-controlled trial. PLoS One 2013;8(4):e61271. PubMed
  51. Rhee MY, Kim YS, Bae JH, Nah DY, Kim YK, Lee MM, Kim HY. Effect of Korean red ginseng on arterial stiffness in subjects with hypertension. J Altern Complement Med 2011;17(1):45-9.
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See these in context on the Panax Ginseng monograph →

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

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

© 2021 Therapeutic Research Center, LLC

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