Latin name: Zingiber officinale
Pharmacopoeial name Zingiberis rhizome
Other names: Ginger rhizome
About Ginger root
The dried rhizome of Zingiberis officinale Roscoe, with the cork removed, is used as a ‘‘broad spectrum antiemetic’’. Oral doses of up to 2 g of powdered material daily in single or divided doses are recommended over an unlimited period. But other preparations have also been investigated in human studies. These include various extracts of ginger (solvents methanol, ethanol, acetone, liquid carbon-dioxide). All of these have different spectral patterns of coactive constituents compared to crude ginger powder (the more lipophilic the solvent, the higher the content of lipophilic constituents).
Crude ginger contains up to 9% lipids or glycolipids and about 5–8% oleoresin. The pungent principle, accounting for 25% of the oleoresin, consists mainly of gingerols. -Gingerol (the main gingerol) is more pungent than -gingerol or -gingerol. Other gingerols include methylgingerol and gingerdiol, dehydrogingerdione, -dehydrogingerdione, gingerdiones, diarylheptanoids (equivalent to curcuminoids, e.g., hexahydrocurcumin), diterpenlactones and galanolactone (in some species). Ginger contains up to 3% essential oil, accounting for 20–25% of the oleoresin. The oil also contains sesquiterpenes and sesquiterpene alcohols, the latter having an impact on the smell of ginger
Ginger contains a number of coactive constituents, which per se (or after structural modification) might be potentially useful in the treatment of various diseases including hypercholesterolemia, gastric ulcer, irritable bowel syndrome, pain, cancer, microbial infections or cardiovascular diseases (1).
Uses of Ginger root
In a randomized double-blind study 22 healthy humans underwent fasting electrogastrography during hyperglycemic clamping after 1 g of ginger, placebo or the prostaglandin E1 analog misoprostol. Acute hyperglycemia-induced gastric slow wave dysrhythmias were prevented by ginger root; however, dysrhythmias elicited by misoprostol did not show a similar effect, indicating that ginger likely acts to blunt production of prostaglandins rather than inhibit their action (2). Repeated oral stimulation found that the sensations produced by zingerone were predominantly burning and warmth, making it qualitatively similar to capsaicin (3).
Postoperative nausea and vomiting
Ginger was shown to be as effective as metoclopramide as a postoperative antiemetic for minor day-case surgical procedures (4,5). However, metoclopramide is a weak postoperative antiemetic. For metoclopramide, the numbers needed to treat to prevent early and late vomiting were calculated to be 9 and 10, respectively (6). The pooled risk reduction of three studies investigating ginger in the early postoperative period did not show a beneficial effect of 1 g of powdered ginger compared with placebo, both taken before surgery (7). If two further studies (8,9) were included in the meta-analysis, the pooled relative risk to suffer from postoperative nausea and vomiting was 0.91 and the numbers needed to treat to prevent one additional patient from complaints was 25 (10). In summary, there is currently no evidence beyond reasonable doubt that ginger is effective as a postoperative antiemetic. The exploratory study by Pongrojpaw and Chiamchanya showing that 1 g of ginger prevented nausea but not vomiting after outpatient gynecological laparoscopy is unlikely to substantially change the overall pooled result. (11).
Nausea and/or emesis during pregnancy
Three confirmatory studies – two vs. placebo (12,13) and one vs. vitamin B12 (14) –demonstrated that 0.5 or 1 g of ginger powder or an extract (solvent not stated) may be effective in treating nausea and/or emesis during pregnancy. Three exploratory studies back this result (15-17).
Lien et al. investigated 13 volunteers with a history of motion sickness who underwent circular vection (18). Pretreatment with ginger (1000 and 2000 mg) significantly reduced nausea, tachygastria and plasma vasopressin. Ginger also prolonged latency before nausea onset and shortened recovery time after vection cessation. Intravenous vasopressin infusion at 0.1 and 0.2 U/min induced nausea and increased bradygastric activity; ginger pretreatment (2000 mg) affected neither.
Only three of the seven exploratory experimental studies on motion sickness had a positive outcome (19-21). In the remaining four studies – most of them investigated powder of the plant material – ginger was ineffective compared to comparators (22-25). The stimuli might have been too strong and the intrinsic antiemetic potency of ginger weaker than that of conventional antiemetics.
Four exploratory studies (26-29) investigating the incidence of nausea and vomiting caused by traveling, showed that powdered ginger was as effective as other antiemetics and possibly better than placebo in reducing motion sickness.
Other causes of nausea and emesis
Three exploratory clinical studies investigating the effect of ginger on nausea/emesis resulting from other causes (acetonemia (30) or cytostatics (31) showed a trend of effectiveness, which needs to be confirmed in further studies.
There are some very encouraging results showing pain decreasing effects of particular ginger preparations. Unfortunately, important details of the preparations were not declared in the manuscripts, so that the results are difficult to interpret. In the confirmatory study by (32) moderate effectiveness was achieved. Neither the validated WOMAC score nor its component pain showed improvement. But pain while standing up (one of the five WOMAC component pain items) showed significant improvement after 6 weeks of treatment with the proprietary extract. The other two exploratory studies with ginger extracts (33,34) show a trend towards pain relieving effects and are backed by three uncontrolled studies in which up to 50 g ginger/day for musculoskeletal pain were administered (35-36). Further studies are necessary to prove the efficacy of proprietary ginger preparations in the treatment of osteoarthritic pain and to find the optimum daily dosage.
At present, there is no evidence that ginger in the doses clinically used interacts with other medications, e.g., with warfarin. Ginger may cause heartburn. In quantities higher than 6 g ginger may act as a gastric irritant. Inhalation of dust from ginger may produce IGE-mediated allergy.
Keywords: Ginger; anti-inflammatory effects; post-operative nausea and vomiting; nausea pregnancy; motion sickness; nausea; osteoarthritis
1. Afzal, M., AlHadidi, D., Menon, M., Pesek, J., Dhami, M.S., 2001. Drug Metab. Drug Interact. 18, 159–190.
2. Gonlachanvit, S., Chen, Y.H., Hasler, W.L., Sun, W.M., Owyang, C., 2003. J. Pharmacol. Exp. Ther. 307, 1098–1103.
3. Prescott, J., Stevenson, R.J., 1996a. Physiol. Behav. 60, 617–624.
4. Bone, M.E., Wilkinson, D.J., Young, J.R., McNeil, J., Charlton, S., 1990. Anaesthesia 45, 669–671.
5. Phillips, S., Ruggier, R., Hutchinson, S.E., 1993 Anaesthesia 48, 715–717.
6. Henzi, I., Walder, B., Tramer, M.R., 1999. Br. J. Anaesth. 83, 761–771
7. Ernst, E., Pittler, M.H., 2000. Br. J. Anaesth. 84, 367–371.
8. Visalyaputra, S., Petchpaisit, N., Somcharoen, K., Choavaratana, R., 1998. Anaesthesia 53, 506–510.
9. Eberhart, L.H., Mayer, R., Betz, O., Tsolakidis, S., Hilpert, W., Morin, A.M., 2003 Anesth. Analg. 96, 995–998.
10. Eberhart, L., 2003 FACT (Focus Alternative Complementary Med.) 8, 418.
11. Pongrojpaw, D., Chiamchanya, C., 2003. J. Med. Assoc. Thai 86, 244–250.
12. Vutyavanich, T., Kraisarin, T., Ruangsri, R., 2001. Obstet. Gynecol. 97, 577–582
13. Willetts, K.E., Ekangaki, A., Eden, J.A., 2003. Aust. N. Z.J. Obstet. Gynaecol. 43, 139–144.
14. Sripramote, M., Lekhyananda, N., 2003. J. Med. Assoc. Thai 86, 846–853
15. Fischer-Rasmussen, W., Kjaer, S.K., Dahl, C., Asping, U., 1990. Eur. J. Obstet. Gynecol. Reprod. Biol. 38, 19–24.
16. Keating, A., Chez, R.A., 2002. Alternative Ther. Health Med. 8, 89–91.
17. Portnoi, G., Chng, L.A., Karimi-Tabesh, L., Koren, G., Tan, M.P., Einarson, A., 2003. Am. J. Obstet. Gynecol. 189, 1374–1377.
18. Lien, H.C., Sun, W.M., Chen, Y.H., Kim, H., Hasler, W.,Owyang, C., 2003. Am. J. Physiol. Gastrointest. Liver Physiol. 284, G481–G489
19. Mowrey, D.B., Clayson, D.E., 1982. Lancet 1 (8273), 655–657.
20. Grontved, A., Hentzer, E., 1986. ORL J. Otorhinolaryngol. Relat. Spec. 48, 282–286.
21. Lien, H.C., Sun, W.M., Chen, Y.H., Kim, H., Hasler, W.,Owyang, C., 2003. Am. J. Physiol. Gastrointest. Liver Physiol. 284, G481–G489
22. Stott, J.R.R., Hubble, M.P., Spencer, M.B., 1984. Advisory Group Aerospace Res. Dev. Conf. Proc. 372 39-1-6.
23. Wood, C.D., Manno, J.E., Wood, M.J., Manno, B.R., Mims, M.E., 1988. Clin. Res. Pr. Drug Regul. Aff. 6, 129–136.
24. Holtmann, S., Clarke, A.H., Scherer, H., Hohn, M., 1989. Acta Otolaryngol. 108, 168–174.
25. Stewart, J.J., Wood, M.J., Wood, C.D., Mims, M.E., 1991. Pharmacology 42, 111–120.
26. Kirchdorfer, A.M., Heister, R., 1983. Unpublished Pharmaton Report.
27. Riebenfeld, D., Borzone, L., 1986. Phytomedicine 12 (2005) 684–701 699
28. Grontved, A., Brask, T., Kambskard, J., Hentzer, E., 1988.Acta Otolaryngol. 105, 45–49.
29. Schmid, R., Schick, T., Steffen, R., Tschopp, A., Wilk, 1994. J. Travel Med. 1, 203–206.
30. Careddu, P., 1986 Unpublished Pharmaton Report.
31. Meyer, K., Schwartz, J., Crater, D., Keyes, B., 1995. Dermatol. Nurs. 7, 242–244.
32. Altman, R.D., Marcussen, K.C., 2001. Arthritis Rheum. 44, 2531–2538.
33. Wigler, I., Grotto, I., Caspi, D., Yaron, M., 2003. Osteoarthritis Cartilage 11, 783–789.
34. Bliddal, H., Rosetzsky, A., Schlichting, P., Weidner, M.S.,Andersen, L.A., Ibfelt, H.H., 2000. Osteoarthritis Cartilage 8, 9–12.
35. Srinivasan, K., Sambaiah, K., 1991. Int. J. Vitam. Nutr. Res. 61, 364–369.
36. Mustafa, T., Srivastava, K.C., 1990. J. Ethnopharmacol. 29, 267–273.