Ginger has long been used as an alternative medication to prevent motion sickness. The mechanism of its action, however, is unknown. We hypothesize that ginger ameliorates the nausea associated with motion sickness by preventing the development of gastric dysrhythmias and the elevation of plasma vasopressin. Thirteen volunteers with a history of motion sickness underwent circular vection, during which nausea (scored 0-3, i.e., none to severe), electrogastrographic recordings, and plasma vasopressin levels were assessed with or without ginger pretreatment in a crossover-design, double-blind, randomized placebo-controlled study. Circular vection induced a maximal nausea score of 2.5 +/- 0.2 and increased tachygastric activity and plasma vasopressin. Pretreatment with ginger (1,000 and 2,000 mg) reduced the nausea, tachygastria, and plasma vasopressin. Ginger also prolonged the latency before nausea onset and shortened the recovery time after vection cessation. Intravenous vasopressin infusion at 0.1 and 0.2 U/min induced nausea and increased bradygastric activity; ginger pretreatment (2,000 mg) affected neither. Ginger effectively reduces nausea, tachygastric activity, and vasopressin release induced by circular vection. In this manner, ginger may act as a novel agent in the prevention and treatment of motion sickness.

Acute hyperglycemia evokes gastric slow wave dysrhythmias via endogenous prostaglandin generation. Ginger exhibits slow wave antiarrhythmic effects in other models, but its actions on hyperglycemia-evoked gastric dysrhythmias are unexplored. We hypothesized that ginger prevents disruption of slow wave rhythm by acute hyperglycemia via inhibition of prostaglandin production but not its actions. Twenty-two healthy humans underwent fasting electrogastrography during hyperglycemic clamping to 250 to 290 mg/dl after double-blind placebo or ginger root (1 g). Responses were compared with the prostaglandin E 1 analog misoprostol (400 g). Dominant frequencies (DF) and the percentage of recording times in the bradygastric [0.5-2 cycles/min (cpm)], normal (2-4 cpm), and tachygastric (4 -9 cpm) frequency ranges were analyzed. After placebo, hyperglycemia reduced normal 2 to 4 cpm activity from 94.4 Ϯ 2.6 to 66.0 Ϯ 10.4%, increased the DF from 2.96 Ϯ 0.04 to 4.09 Ϯ 0.45 cpm, and increased tachygastria from 2.0 Ϯ 1.4 to 29.3 Ϯ 10.7% (P Ͻ 0.05). Hyperglycemia effects on normal activity (77.3 Ϯ 8.3%), DF (3.46 Ϯ 0.37 cpm), and tachygastria (15.6 Ϯ 8.6%) were significantly reduced by ginger (P Ͻ 0.05). Misoprostol evoked decreases in normal activity from 95.4 Ϯ 2.0 to 81.7 Ϯ 3.0% and increases in tachygastria from 3.1 Ϯ 1.6 to 11.2 Ϯ 2.4% (P Ͻ 0.05). However, ginger did not correct these abnormalities versus placebo (P ϭ N.S.). In conclusion, acute hyperglycemia evokes gastric slow wave dysrhythmias that are prevented by ginger root. Conversely, the compound has no effect on dysrhythmias elicited by a prostaglandin E 1 analog, indicating that ginger likely acts to blunt production of prostaglandins rather than inhibiting their action. These findings suggest novel mechanisms for the traditional Chinese herbal remedy ginger.