Ginger has demonstrated anti-emetic activity in both experimental models and human studies, the exact mechanism of which is still unknown although both shogaols and gingerols have been shown to have anti-emetic activity (Kawai et al 1994).

It appears that several key constituents and several different mechanisms are responsible. According to both animal and human studies, ginger reduces emesis due to a peripherally acting mechanism, acting on the gastrointestinal tract alone (Holtmann et al 1989). One constituent found in ginger, galanolactone, is a serotonin receptor antagonist, which may partly explain the anti-emetic effect (Huang et al 1991a, Mustafa et al 1993, Yamahara et al 1990). It also explains the inhibitory effect of ginger on serotonin-induced diarrhoea and antispasmodic effects on visceral and vascular smooth muscle.

Ginger has been shown to blunt gastric dysrhythmias and nausea evoked by acute hyperglycaemia in humans. The anti-arrhythmic and anti-emetic effects are thought to be due to a blockade of prostaglandins rather than inhibition of their release (Gonlachanvit 2001). Ginger has also been shown to reduce radiation-induced gastrointestinal distress and emesis in rat models, which is thought to be due at least in part to its antioxidant properties and the ability to scavenge free radicals and inhibit lipid peroxidation (Sharma et al 2005).

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