Binge Drinking Tells the Brain to Binge Eat
May 17, 2017
When I first started college, one aspect of campus nightlife completely mystified me. Every Saturday night, a run-down, silver food truck called Uncle Dickie’s set up shop on the edge of the campus frat quad, party central, and at around 12:30 a.m., shambling students would drift towards the truck in search of greasy fries drenched in fake cheese.
I had never seen Uncle Dickie's anywhere else around the city and I could not understand how peddling low-grade, midnight grease bombs to inebriated college students could sustain a business. As I learned more about alcohol, however, I noticed that heavy drinking tended to correspond with cravings for that same greasy food, be it soggy cheese fries, jumbo-slice pizza or fried chicken from the shop that stayed open until 3 a.m.
There’s something about having a little too much to drink that brings out an appetite, which makes no sense biologically. Our appetite is partially driven on a negative feedback loop, where high calorie foods signal the brain that it is time to stop eating. Alcohol is among the most calorically dense molecules in the human diet. It contains enough energy, in fact, that cars can at least partially run off it.
So eating while intoxicated is a scientifically observed and recorded phenomenon, and for years, the reigning theory was that alcohol lowers inhibitions to the point where we don’t notice the signal that tells us we’re full. Researchers from the United Kingdom, however, have found that alcohol stimulates a part of the brain that makes us think we’re starving.
Researchers soaked mouse brain tissue in ethanol (the alcohol found in drinks), both in petri dishes and in live mice by injecting the alcohol into the lining around their internal organs. The live mice ate between 15 and 20 percent more food when they were heavily intoxicated, and the brain cells responsible for creating starvation signals began firing. The research was published in the journal Nature Communications.
You may be wondering what purpose getting a bunch of mice drunk could possibly serve. Studies have shown that alcohol consumption, especially in large doses, leads to binge eating and is correlated with obesity. This issue is also very prevalent as one in four American adults say they binge drink at least four times per month. By understanding the biological mechanisms by which drinking plays into eating, health scientists and doctors could devise new ways to fight obesity.
Alcohol and food have been enjoyed together for almost as long as humans have been drinking alcohol. Specific types of wine pair well with different foods while sports bars wouldn’t be sports bars without beer and chicken wings. Alcohol has even been used to stimulate appetite for hundreds of years in the form of apertifs. Low-alcohol, low-sugar drinks like dry wine or vermouth were supposed to whet the appetite while sweet drinks like port wine and high-proof drinks like whiskey were supposed to aid in the digestion.
This study examines something closer to a 12-pack as the researchers boosted the alcohol content in the mice brains to 50 millimolar, which would translate to about 0.23 percent (almost three times the legal driving limit) in a 170 pound man.
The researchers focused specifically on a group of neurons in the hypothalamus—a small brain segment important in the production of hormones and signaling the rest of the endocrine system—called agouti-related protein neurons (AgRP neurons). AgRP neurons release a protein called AGRP that controls body weight by telling the brain when it is time to eat. Studies have shown that obese men tend to have much more AGRP in their blood than non-obese men and that excess AGRP in the blood is correlated with more belly fat, total fat and blood insulin levels.
In petri dish studies, AgRP neurons fired when they were subjected to heavy doses of alcohol. Ion pumps rapidly swap sodium for calcium and an electrical current runs through the neurons.
The researchers also blocked AgRP neurons in the live mice and found that when the AgRP neurons were blocked, AgRP neuron firing fell to zero and the mice ate half as much as when the AgRP neurons work at full capacity, whether alcohol was present or not. The mechanisms that drive satiety and hunger in the human brain are multitude and complex, but what these results show is that even though AgRP neurons are not solely responsible for human hunger, they do explain the drunken boost in appetite.
The authors of the study do not suggest a need for an AgRP inhibitor to stop people from eating when they are drunk. Instead, the best option to start with is to avoid the heavy drinking that triggers AgRP neurons in the first place, especially as previous studies show that alcohol triggers cravings for greasy, fatty foods. Still, in that moment where the pizza or the chips, or Uncle Dickie’s cheese fries, start calling, keep in mind that that hunger could be one of alcohol’s tricks.
Daniel Lane covers science, medicine, engineering and the environment in North Carolina.