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Ginger

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

Summary Table
herb description

Family

Zingiberaceae.

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

Rhizome.

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

Overview

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
Cisplatin and Emetogenic Antineoplastic Chemotherapies
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) and Analgesic Antiarthritics
Phenprocoumon and Related Oral Vitamin K Antagonist Anticoagulants
  • Evidence: Phenprocoumon (Jarsin, Marcumar).
  • Extrapolated, based on similar properties: Anisindione (Miradon), dicumarol, ethyl biscoumacetate (Tromexan), nicoumalone (acenocoumarol; Acitrom, Sintrom), phenindione (Dindevan), warfarin (Coumadin, Marevan, Warfilone).
Potential or Theoretical Adverse Interaction of Uncertain Severity

Probability: 4. Plausible
Evidence Base: Mixed

Effect and Mechanism of Action

A theoretical additive effect between coumarin anticoagulants and ginger on hemostasis is hypothesized to increase INR and risk of bleeding. Unsupported by the currently known pharmacology of the herb, a single report of the possible interaction is available. The clinical significance of the proposed interaction is minimal.

Research

There are no human studies investigating pharmacodynamic effects of ginger on the vitamin K–dependent clotting factors II, VII, IX, and X. Weidener and Sigwart 60 conducted a series of experimental investigations with EV.EXT 33 ginger extracts on Wistar rats, including a study of the effects of oral warfarin (0.25 mg/kg daily) alone and in combination with the ginger extract. Warfarin significantly increased prothrombin time (PT) and activated partial thromboplastin time (APTT) compared with normal controls. Coadministration of ginger extract at 100 mg/kg for 4 days had no effect on warfarin-induced changes in PT and APTT and did not alter these coagulation parameters in a control group receiving no warfarin. 60

In a recent study described earlier under Antiplatelet Agents, Jiang et al. 46 found that ginger and ginkgo had no significant effect on clotting status or the pharmacological profile of warfarin.

Pharmacokinetic data demonstrating any effect of the herb on drug-metabolizing enzymes mediating coumarin drug metabolism (cytochromes P450 1A2 and 2C9) are also unavailable. Further studies are required to establish definitively an absence of effect of ginger on coagulation, but the balance of currently available evidence suggests such effects are unlikely.

Reports

A single German case involving ginger and phenprocoumon was reported by Krüth et al. 17 in 2004. A 76-year-old woman with a history of mitral insufficiency, atrial fibrillation, congestive heart failure, and osteoporosis who was taking concurrent cholecalciferol, captopril, piretanide, digoxin, and a nitrate vasodilator was maintaining a stable INR (range, 2.0 to 3.0) while receiving long-term phenprocoumon therapy. Because of a peripheral bleed incident (epistaxis), she was admitted to hospital, and INR was greater than 10. Phenprocoumon was stopped, and she received three doses of vitamin K 1 (initially 10 mg intravenously, then 5.0 mg and 3.0 mg orally after 3 and 6 days, respectively). By day 6, the INR and PTT normalized and phenprocoumon was resumed, with INR maintained at normal levels by the same dose used before the bleeding episode. A detailed history revealed “a regular ginger intake (pieces of dried ginger and tea from ginger powder)” for several weeks before the bleeding incident occurred. The patient was advised to refrain from ginger use, and no further episodes of bleeding were noted. The authors note that the current pharmacological data on ginger do not provide any obvious mechanism for the observed effects.

The report, although complete in some respects, lacks vital information. The exact form, amount, dose, frequency, and duration of ginger administration are not given, making the incident impossible to evaluate. Further, “Dried ginger pieces” is an unusual form of ingesting the herb given its pungent and acrid taste, and “ginger tea” does not exclude the presence of nonginger ingredients. The ginger was apparently consumed for several weeks before the INR elevation. Case data show a rapid elevation of INR between two measurements 7 days apart. Relating this to an unstated dose of ginger consumed several weeks earlier does not constitute a reasonable association by timing for the INR effect to be causally associated with the herb consumption. The INR plots show values maintained within therapeutic range for more than a week before the bleed episode, presumably during the “several weeks” consumption of ginger. The observed INR increase might be explained by excessive phenprocoumon levels caused by inadvertent drug misadministration, a dietary pharmacokinetic interaction, or sudden decrease in dietary intake of vitamin K–containing foods, none of which was considered by the authors. 17

Clinical Implications and Adaptations

The single available case report is insufficient to confirm the existence of a ginger–oral anticoagulant interaction, especially with the lack of a plausible pharmacological mechanism and inadequacies in the report data. In addition, some controlled trial evidence suggests that ginger has no measurable effect on warfarin pharmacokinetics or pharmacodynamics. Until further data are available, it cannot be assumed that moderate ginger consumption exerts clinically significant effects on the coagulation cascade and INR values. As normally occurs with coumarin-effected anticoagulation, monitoring of INR and alerting patients to report early signs of bleeding (e.g., epistaxis, ecchymoses) remain essential elements of vitamin K antagonist therapy. Possible antiplatelet activity cannot be ruled out completely at this time (see Antiplatelet Agents), but epistaxis or other serious bleeding episode would be expected with an INR higher than 10.

The use of cured ginger in Chinese medicine to arrest bleeding in certain conditions has already been mentioned. Anecdotal clinical experience also suggests that at normal therapeutic dose ranges for appropriate indications, ginger and ginger extracts present no significant risk of bleeding in patients on oral vitamin K antagonist anticoagulation.

theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Aminoglycoside Antibiotics
Sulfaguanidine
Citations
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