Table 1.

Predictions of the “drunken monkey” hypothesis and supporting empirical evidence.

Prediction	Supporting Evidence	References
Ethanol occurs naturally at low levels within many fruits and nectars.	A variety of tropical fruits, as well as some nectars, contain ethanol at low concentrations.	[12,13,14,15]
Olfaction can be used to localize and preferentially select ethanol-containing nutritional resources.	Fruits consumed by primates produce numerous volatiles, including ethanol. Olfactory abilities are well-developed in primates, but have not been explicitly tested relative to use in fruit localization or selection.	[16,17]
Ethanol at low concentrations is not aversive to frugivores and nectarivores.	Diverse vertebrates consume food items containing low-concentration ethanol.	[18,19,20,21,22,23,24,25]
Ethanol acts as a feeding stimulant.	Modern humans increase caloric ingestion following consumption of an aperitif. Effects of dietary ethanol on ingestion rates for free-ranging primates have not yet been evaluated.	[3]
Genetic variation in the ability to metabolize ethanol is correlated with the extent of dietary exposure.	Substantial variation in ADH tracks dietary inclusion of fruit and nectar among mammals. Ethanol catabolism was up-regulated in African apes ~10 Mya ago, in parallel with terrestrialization.	[26,27]
Hormetic advantage derives from chronic consumption of ethanol.	Mortality is reduced at low levels of ethanol ingestion in modern humans and rodents, and also in Drosophila flies exposed to low-concentration ethanol vapor.	[28,29,30,31,32,33]