The ability of ghrelin receptor antagonists demonstrated by Jerlhag et al. (2009b) and by us to decrease ethanol intake, together with decreased ethanol preference in GHSR 1a knockout mice (Jerlhag et al., 2009b), indicate that endogenous ghrelin promotes alcohol intake. In this sense, our results also concur with studies showing increased plasma ghrelin levels in alcoholic patients at various stages of alcoholism, i.e. active drinking, abstainers and in withdrawal (Kim et al., 2005; Kraus et al., 2005) and with results by Addolorato et al. (2006) showing that ghrelin was linked to craving for alcohol. On the other hand, the fact that peripherally-injected ghrelin did not promote alcohol intake in food-deprived mice (Lyons et al., 2008), while intracerebroventricular ghrelin did (Jerlhag et al., 2009b) suggest the intriguing possibility that the source of the endogenous ghrelin regulating alcohol intake is central and not peripheral. This possibility will be addressed in future studies.