Alcohol is the second most calorie-dense nutrient after fat, so why do we tend to reach for munchies while drinking?
A team of scientists from the Francis Crick Institute Mill Hill Laboratory in London set out to answer this paradox using a mouse model.
Previous research has shown that agouti-related protein, or Agrp neurons, are activated when our bodies are in need of calories, and they send out signals like hunger pangs in the stomach to notify us to seek out food.
The researchers focused on Agrp cells for the study.
To confirm that mice would overeat after consuming alcohol like humans do, the team injected alcohol directly into the abdomens of mice once per day for three days, replicating a three-day “alcoholic weekend.”
Each injection correlated to a human’s consumption of a couple bottles of wine, or six to eight pints of beer. The researchers observed that the mice (both male and female) ate significantly more during the three-day binge than sober mice. This was particularly heightened on the second day, the researchers noted.
The mice were housed separately to prevent any social factors that may also contribute to overeating.
For the second phase of the study, mice brains were thinly sliced into sections and calcium in the Agrp neurons was made to glow green under a microscope to demonstrate cell activity. The slices were soaked in different concentrations of alcohol. More alcohol in the bath correlated to an increase in calcium levels, and probes recorded a boost in neural firing.
But these effects were only temporary. Once the alcohol wore off, the mice’s appetites returned to normal. Also, when the Agrp neurons were deactivated before the alcohol injections, the mice did not overeat, further supporting the researcher’s theory.
The link between alcohol intake and overeating has become a recognized clinical concern, and the study results show that there are other biological causes, other than a lack of self-control and other social pressures from drinking.
“Here we show that core elements of the brain’s feeding circuits—the hypothalamic Agrp neurons that are normally activated by starvation and evoke intense hunger—display electrical and biochemical hyperactivity on exposure to dietary doses of ethanol in brain slices,” wrote the researchers. “These data reveal how a widely consumed nutrient can paradoxically sustain brain starvation signals, and identify a biological factor required for appetite evoked by alcohol.”
The findings were published in Nature Communications on Jan. 10.