| Popis: |
Humans’ long association with alcohol raises questions about both our biological adaptations to handling ethanol and its origins. Fermented foods have less sugar, and require additional detoxification than unfermented versions of the same food, and are thus are generally inferior food choices. I summarize recent studies which indicate that our ability to exploit ethanol depends on several mutations in alcohol dehydrogenase (ADH) enzymes that allow ethanol to be metabolized rapidly, thereby reducing the likelihood that the blood alcohol concentration reaches intoxicating levels. Genetic and biochemical analyses for a wide range of primate and non-primate species suggest that these mutations are shared primarily with the two African great apes (chimpanzees and gorillas). These mutations thus date back at least 10 million years, to a period when the tropical forests were contracting during a major episode of climate change. Mutations enabling rapid ethanol metabolism may have enabled ancestral apes to exploit otherwise toxic, ethanol-rich fermenting fruits on the forest floor that were metabolically inaccessible to their ecological competitors. These adaptations enabling exploitation of an inferior food suggest that modern proclivities towards ethanol consumption may derive from the utilization of fermented food as a particular type of fallback food. If so, the fermented fallback food hypothesis can be seen as a special case of the drunken monkey hypothesis. |
