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Botanical Name: Zingiber officinale Roscoe.
Pharmacopoeial Name: Zingeribis rhizoma.
Synonym: Amomum zingiber L.
Common Names: Ginger, zingiber.

Summary Table
herb description



Habitat and Cultivation

Perennial, with tuberous rhizomes, native to Southeast Asia, and cultivated in tropical regions, including India, West Indies, Jamaica, Africa, and China.

Parts Used


Common Forms

  • Fresh or Dried Rhizome:   considered different agents in Chinese practice.

Dried Powdered Rhizome.

Tincture (1:5), Fluid Extract (1:1), 90% ethanol, fresh or dried rhizome.

  • Standardized Extracts:   Various, including EV.EXT 33 (Ferrosan) standardized to hydroxy-methoxy phenols; Zintona standardized to 1.4% volatiles and minimum of 2.0 mg gingerols and shogoals per 250-mg capsule.

herb in clinical practice


Best known as a pungent spice and dietary ingredient, ginger is among the top-20 dietary supplements in retail sales in the United States. Primarily viewed by conventional medicine as an antiemetic for motion sickness, the nausea of pregnancy, and postoperative nausea, the herb has many more, diverse therapeutic applications in both Western and Asian botanical medicine. It has potent anti-inflammatory effects on eicosanoid metabolism, circulatory and digestive tonic actions, and metabolic, endocrine, antimicrobial, antipyretic, antioxidant, and antineoplastic activities. Toxicity is minimal, and ginger is free of adverse effects at therapeutic doses.

Therapeutic monographs for ginger generally limit the indications to recent clinical trial–driven applications. Ginger was approved by the German Commission E in 1988 for dyspepsia and motion sickness, although not for morning sickness. 1 The European Scientific Cooperative on Phytotherapy (ESCOP) 2 recently reviewed much of the research but also suggested only motion sickness and postoperative nausea prevention as clinical uses. Broader authoritative surveys of the herb can be found in literature reviews by Mills and Bone 3 and McKenna et al. 4 Recent interest in the cancer chemopreventive properties has provided a new emphasis in pharmacological research into ginger and its constituent compounds. 5,6

Historical/Ethnomedicine Precedent

Ginger has been used for centuries in Ayurvedic and Chinese medicine, where it is a major ingredient in innumerable formulae for many treatment indications. In India, ginger is not only widely used as a spice and meat preservative and antimicrobial digestive tonic, but also considered to have aphrodisiac and cognitive-enhancing effects, especially on memory, and has also been used as a narcotic antagonist. In classical Chinese medicine, the fresh rhizome (Sheng Jiang) is distinguished from the dried and processed rhizome (Gan Jiang) . In light of modern precautions suggesting elevated risk of bleeding with ginger consumption, an interesting Chinese medical use of dried ginger is to arrest bleeding, especially bleeding associated with “Deficiency” and “Cold.” 7 Doses of the herb in Chinese practice are considerably higher than in modern phytotherapy, maximum dosage for Sheng Jiang is 30 g. 7 Traditional Western botanical medicine considers ginger to be a “diffusive stimulant,” to be added to formulae to enhance the bioavailability of other herbs, as well to support diffusive physiological processes (e.g., expectoration, diaphoresis). 3

Known or Potential Therapeutic Uses

Appetite stimulation, dyspepsia, flatulence, digestive/choleretic secretory stimulation, increasing bioavailability of foods and medicines, ulceroprotection, circulatory stimulation, thermogenesis, menstrual flow irregularities, colds, influenza, fevers, atherosclerosis, hypercholesterolemia, hyperviscosity, hepatic protection, pain relief in osteoarthritis and rheumatoid arthritis, Kawasaki's disease, antiemesis in nausea of motion, pregnancy, drug withdrawal, and chemotherapy; antineoplastic adjuvant.

Key Constituents

Pungent oleoresin containing phenolic gingerols and their dehydration derivatives, shogoals (formed by drying); volatile oil (variable composition of monoterpenes and sesquiterpenes depending on botanical chemotypes and physical methods of preparation).

Therapeutic Dosing Range

  • Fresh or Dried Rhizome: 2 to 4 g daily.
  • Tincture 1:5 (90% ethanol): 1.25 to 3.0 mL three times daily.
  • Fluid Extract 1:1 (90% ethanol): 0.25 to 0.75 mL three times daily.
  • Standardized Extract: Dose equivalent to 2 to 4 g dried rhizome daily.

interactions review

Strategic Considerations

The available therapeutic monographs on ginger minimize suggestions of herb-drug interactivity. The German Commission E listed ginger interactions under “none known,” 1 ESCOP 2 mentions only the possible increase in bioavailability of sulfaguanide, and the World Health Organization (WHO) 8 monograph suggests an “enhancement” of pharmaceutical anticoagulant therapy, adding that the clinical significance of the possible interaction has not been evaluated. By contrast, secondary literature and commentators in both professional and popular press emphasize potential anticoagulant effects of ginger and freely extrapolate to hypothetical interactions with drugs affecting hemostasis.

The presumed mechanism of interference with normal hemostasis by ginger is based on in vitro studies that suggest the herb may affect platelet aggregation, primarily through inhibition of eicosanoid metabolism and specifically reduction of thromboxane levels. 9 However, the experimental support is inconclusive, and to date the balance of in vivo studies suggest a lack of effect of ginger on thromboxane-induced platelet aggregation in humans. 10-15Until recently, clinical reports were based only on a questionable single case report of platelet aggregation inhibition apparently attributed to the consumption of ginger marmalade. 16 A recent single report of elevated international normalized ratio (INR) and epistaxis in a patient previously stable on phenprocoumon anticoagulant therapy is discussed later. 17 However, no pharmacological data show that ginger affects the coagulation pathways reflected by the INR, so this case remains an isolated and unexplained interaction, its significance unclear. The existence of only two somewhat controversial reports in a quarter century suggests that portentous warnings about risks of combining ginger with anticoagulants may be overstated.

The activity of the herb as an anti-inflammatory, analgesic, and circulatory stimulant has led to its incorporation in protocols for arthritis. Coadministration of ginger in combination regimens with nonsteroidal anti-inflammatory drugs (NSAIDs) or analgesics for arthritis has been examined indirectly in trials that permitted NSAID/analgesic rescue or in one trial where patients added ginger to an existing NSAID regimen. 18-20Although further investigations are warranted, there may be neither significant additive effect between NSAIDs and ginger alone in arthritis nor any significant difference between NSAIDs and ginger alone for arthritic symptom relief. However, ginger's adverse effect profile is superior to conventional NSAID drugs, and ginger could be incorporated into combination protocols for botanical cyclooxygenase-2 (COX-2) inhibition in arthritis and related inflammatory conditions to maintain integrity of the protective, constitutive gastric cyclooxygenase and prostaglandin E2(PGE2). Common compound formulations with ginger include herbs such as rosemary, Boswellia, and the plant-derived compound resveratrol, which act as COX-2 inhibitors at the receptor level and also downregulate inducible COX-2 transcription. Ginger extracts have been shown to exert an ulceroprotective effect against aspirin and indomethacin, implying the pharmacology of ginger-containing combination protocols targeting COX-2 could be applied to a variety of inflammatory conditions, including malignancy. 21

The established antiemetic effects of ginger, well proven for motion sickness and morning sickness of pregnancy, have also been found to be helpful in drug-induced nausea and vomiting. The strong association of certain antineoplastic chemotherapies (e.g., cisplatin) with acute nausea, as well as postoperative nausea and vomiting (PONV) associated with emetogenic anesthetics, constitute beneficial interactions with ginger (see anesthetics and chemotherapies later). Ginger may well find application in the treatment of other cases of drug-induced nausea when symptom occurrence is not inevitable; one report suggests that it can be used for nausea relating to symptoms of disequilibrium after discontinuation of serotonin-inhibiting drugs. 22

Effects on Drug Metabolism and Bioavailability

An experimental study found that ginger enhanced the absorption of sulfaguanidine across the small intestine in rodents. 23 Secretory increases by the pancreas and bile are also associated with ginger administration. 24 An early study suggests glucuronide conjugation and renal and biliary excretion are involved in elimination of the volatile component zingerone. 25 In rats, [6]-gingerol was eliminated partly by hepatic metabolism, and the gingerol was more than 90% bound to serum protein. 26

Traditionally, ginger has been used to promote the absorption of herbs in multiherb botanical prescriptions. The Ayurvedic Trikatu formula is a mixture of ginger with long-pepper and black pepper that has been shown to increase the bioavailability of several pharmaceuticals. 27 A more recent study of the effect of Trikatu on the kinetics of sodium diclofenac found the opposite effect: a significant reduction of bioavailability. 28 These studies are not applicable directly to ginger alone, and the piperine ingredient of the other herbs in the formula are known to have modulating effects on several cytochrome P450 isoforms. 29

Data on potential effects of ginger and its constituents on drug-metabolizing enzymes are largely unavailable at this time. Although traditional botanical prescribing conventions may use ginger for increasing bioavailability of other herbs, the effects on pharmaceutical drug absorption are not predictable on the basis of the current data. One study has documented an inhibitory effect on P-glycoprotein (P-gp). Accumulation of daunorubicin was increased in a multidrug-resistant cell line in the presence of [6]-gingerol, which also appeared to increase the cytotoxicity of vinblastine, suggesting an inhibition of P-gp–mediated efflux of the cytotoxic drug from the cells. 30 Until further data are available, the prediction of P-gp–mediated drug-ginger interactions remains speculative, if theoretically possible.

herb-drug interactions
Anesthesia, General
Antiplatelet Agents
Antiplatelet thromboprophylactics:Acetylsalicylic acid (acetosal, acetyl salicylic acid, ASA, salicylsalicylic acid; Arthritis Foundation Pain Reliever, Ascriptin, Aspergum, Asprimox, Bayer Aspirin, Bayer Buffered Aspirin, Bayer Low Adult Strength, Bufferin, Buffex, Cama Arthritis Pain Reliever, Easprin, Ecotrin, Ecotrin Low Adult Strength, Empirin, Extra Strength Adprin-B, Extra Strength Bayer Enteric 500 Aspirin, Extra Strength Bayer Plus, Halfprin 81, Heartline, Regular Strength Bayer Enteric 500 Aspirin, St. Joseph Adult Chewable Aspirin, ZORprin); combination drugs: ASA and caffeine (Anacin), ASA, caffeine, and propoxyphene (Darvon Compound); ASA and carisoprodol (Soma Compound); ASA, codeine, and carisoprodol (Soma Compound with Codeine); ASA and codeine (Empirin with Codeine); ASA, codeine, butalbital, and caffeine (Fiorinal); cilostazol (Pletal), clopidogrel (Plavix), dipyridamole (Permole, Persantine), ticlopidine (Ticlid); combination drug: ASA and extended-release dipyridamole (Aggrenox, Asasantin). Monoclonal antibody antiplatelet agents:Abciximab (ReoPro), eptifibatide (Integrelin), tirofiban (Aggrastat).
Potential or Theoretical Adverse Interaction of Uncertain Severity

Probability: 6. Unknown
Evidence Base: Mixed

Effect and Mechanism of Action

A theoretical interaction extrapolated from the “NSAID-like” activity of ginger and its active compounds through inhibition of thromboxane-evoked platelet aggregation, creating an assumed additive disabling of platelets. The interaction has not been clinically demonstrated to date.


Equivocal results have been obtained in experimental and in vitro studies attempting to characterize effects of ginger extracts and isolated ginger compounds on platelet aggregation, although there is evidence for a dual inhibitory effect on eicosanoid synthesis, with lipoxygenase as well as cyclooxygenase subject to inhibition. 14,15,41-43 COX-2 effects may be mediated by the effect of [6]-gingerol on nuclear factor kappa B (NF-κB) activation. Kim et al. 44 used a mouse skin model and found evidence of the ginger compound blocking phosphorylation of I-κBα as well as p65. This was reversed by a p38 mitogen-activating protein (MAP) kinase inhibitor, implicating the p38 MAP kinase signaling pathway of NF-κB as the upstream mediator of COX-2 downregulation. 44

Four human studies have investigated the effects of ginger on platelet aggregation. Verma et al. 45 examined the effects of a fatty diet (100 g butter for 7 days) on platelet aggregation in 20 healthy volunteers. Ten individuals also consumed 5 g dried ginger with the fatty meal. Adenosine diphosphate (ADP) and epinephrine-induced platelet aggregation was significantly lower in the butter-plus-ginger group than in the butter-only group. Lumb 12 conducted a small, double-blind randomized trial with eight healthy volunteers who consumed 2 g ginger or placebo. No effect was found on any parameters of platelet activity (samples taken 3 and 24 hours after ginger administration), including bleed time, aggregometry, and platelet count. Srivastava 10 measured platelet thromboxane in human volunteers before and after 7 days consumption of 5 g/day fresh garlic or 70 g/day raw onion. Thromboxane B 2 (TXB 2 ) levels (measured after sample clotted by incubation for 1 hour) were reduced by approximately one third in the ginger group ( n= 7). The small sample size was statistically underpowered ( p<0.1). The onion-consuming group exhibited a trend to increased TXB 2 after clotting.

Another study investigated the effects of ginger on TXB 2 with higher doses of ginger administered by vanilla custard, with 15 g raw ginger daily or 40 g cooked stem ginger for 2 weeks, in 18 healthy volunteers of both genders. There was no washout period in the crossover design, and when venous blood samples were taken on both day 12 and day 14, no significant change in TXB 2 levels was detected between either form of ginger and placebo. In contrast, an earlier pilot study by the same researchers had detected significant (39%) TXB 2 reduction after only 3 mg/day administration of acetylsalicylic acid (ASA). 13 Bordia et al. 11 used a placebo-controlled trial to examine the effects of powdered ginger administered at 4 g daily for 3 months in 60 patients with a history of coronary artery disease. Blood lipids and glucose, plasma fibrinogen, and fibrinolytic activity, as well as ADP and epinephrine-induced platelet aggregation, were measured at 1½ and 3 months. No significant differences were found between the placebo and ginger groups in any of the parameters measured. However, a single 10-g dose of ginger did produce significant reduction in platelet aggregation evoked by the two test agonists measured 4 hours after ginger administration.

Jiang et al. 46 conducted a small, open-label trial (12 healthy male volunteers) and examined a range of pharmacokinetic and hemostasis parameters after administration of ginger or ginkgo, alone or with warfarin. Aggregation, INR, warfarin enantiomer concentrations in plasma and urine, and warfarin enantiomer binding were all measured at day 1 and day 7. The dose of ginger was three tablets of 0.4 g powdered rhizome three times for 1 week. Neither ginger nor ginkgo produced significant effect on clotting status or the pharmacokinetics and pharmacodynamics of warfarin.

Clinical Implications and Adaptations

The quality of the evidence is variable, partly because of small sample sizes, different forms of ginger tested (or different purified compounds), and differing doses used. However, the balance of available data suggests that the effects of ginger compounds on cyclooxygenase and lipoxygenase inhibition do not appear to have detectable clinical effects on primary hemostasis. By extension, it appears that ginger can be safely utilized at therapeutic doses along with antiplatelet and anticoagulant medications. Theoretically, for certain individuals with unique pharmacogenomic susceptibility or subclinical platelet disorders, ginger preparations might interact adversely with either antiplatelet or anticoagulant agents.

Cisplatin and Emetogenic Antineoplastic Chemotherapies
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) and Analgesic Antiarthritics
Phenprocoumon and Related Oral Vitamin K Antagonist Anticoagulants
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Aminoglycoside Antibiotics
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