Too much alcohol is bad for you: We all know this. But even in moderation, it can cause health problems. It can change mood and behavior, cause liver and heart damage, contribute to various types of cancer, and weaken the immune system.
In the United States, alcohol is linked to about 88,000 deaths a year, making it the fourth leading preventable cause of death. It can also cause deaths indirectly—in 2014, almost a third of overall driving-related deaths were due to drunk driving. The National Institutes of Health estimates that 15.1 million people in the U.S. over the age of 18 have an alcohol use disorder (AUD), which makes up more than 6 percent of the age group.
Even though alcohol is bad for us, our bodies are primed to like it; it activates the reward pathway in our brains, which is responsible for the feeling of pleasure, motivation, and craving. The reward pathway is usually used to reinforce a certain behavior to help with an organism's survival and reproduction. Some natural stimuli that activate the reward pathway are food, water, sex, and parental care (which all clearly help with an organism's survival and reproduction). Alcohol, on the other hand, doesn't have any immediately apparent benefits beyond being a great way to decompress after a long day at the office.
This discrepancy might be traced to the fact that, millions of years ago, being able to consume alcohol was likely vital to survival: Our ancestors evolved to metabolize booze right around the time we grew more likely to encounter it. It is possible that the same reward pathway that might have helped our ancestors forage for food is contributing to our society's public-health problem with alcohol today.
A team of researchers led by biologist Matthew Carrigan from the Foundation for Applied Molecular Evolution found in 2015 that, around 10 million years ago, our primate ancestors gained a mutation in alcohol dehydrogenase (ADH4), an enzyme that changes alcohol into safe compounds that cells can use as food. This mutation, which was absent in more distant primates, allowed for a metabolism of alcohol that was 40 times more efficient.
This mutation arose around the time when our primate ancestors became more land-based rather than living in trees, Carrigan and his team wrote. Being more terrestrial might have given our ancestors more access to fruits that fell from trees, which tend to be more fermented than fresh fruits. To ensure that they did not get too sick from eating fruits higher in alcohol content, our ancestors may have adapted by gaining the mutation that metabolizes alcohol more efficiently. First proposed by Robert Dudley from the University of California–Berkeley, the "drunken monkey argument" is the idea that our liking for alcohol is an evolutionary remnant of fermented fruit consumption.
The drunken monkey argument reveals an interesting implication for AUDs. Our craving for alcohol might have resulted from the fact that our early food sources, like fermented fruits, were more likely to contain alcohol. Since food is one of the natural stimuli for the reward pathway, perhaps the association of alcohol and food drove the evolution. The argument is similar to the "thrifty gene hypothesis," which posits that the genes that once helped our ancestors survive by efficiently processing food are now responsible for diabetes and obesity.
The drunken monkey argument does not completely explain alcoholism: If we carry the ADH4 mutation, we would expect most of us to have an AUD, or at least far more than 6 percent. One of the counterarguments for the thrifty gene hypothesis is the same: Why aren't most of us diabetic or obese if these disease were solely driven by genetics?
We now know that, for AUD, diabetes, and obesity, our environment, not just our genetics, has a role. Perhaps this is what we can learn from the drunken monkey argument: There are many people who are potentially at risk for developing an AUD, but since not all of them have an AUD, there has to be other players.
The complex interaction of genetics and environment (nature vs. nurture) for AUDs emphasizes the need for studying both genetic and environmental factors, not just one or the other. Seeing AUDs as purely (or even mostly) genetic could make us think that, if you have a family history of an AUD, there is little hope of evading it. On the other hand, knowing that environment can enhance or mitigate the risk can lead to a better understanding of the disorder and better care.