Blame Your Brain If You Can't Stop Eating

Remember how we told you that scientists had potentially discovered the reason why marijuana gives you the munchies?

Nah, of course you don't. Cough, cough.

Well, let us remind you. In addition to the cerebral sludge, weed resin, and other grey-ish matter that takes up space in your head, your brain contains sets of neurons in the hypothalamus known as proopiomelanocortin cells, or POMCs, which are believed to regulate feelings of fullness.

Yale researchers initially hypothesized that exposure to cannabis would turn off the POMC neurons, leading you to gorge yourself on chips and fried shrimp grilled cheese sandwiches. What they found, however, is that cannabinoids essentially turn your POMCs inside out, temporarily make them a neurotransmitter than makes you hungrier.

At the time, neurobiology professor Tomas Horvath told MUNCHIES that further research into POMCs could provide some insight into non-stoned patterns of overeating. Now, a group of scientists at the University of Michigan have potentially completed another part of the I-can't-stop-shoving-these-snacks-in-my-face puzzle.

Neuroscientists already know that a POMC deficiency, although rare, can cause severe obesity in children due to ceaseless hunger. In two recent studies—one published last week in the Proceedings of the National Academy of Sciences, and the other in PLoS Genetics—the University of Michigan researchers focused on the gene within the POMC cells that regulates appetite, as well as biochemical triggers that help to tell your POMCs to remind your body that it's full.

One such trigger is a protein called a transcription factor; the others are two small stretches of DNA called gene enhancers. The transcription factor, named Islet 1, helps your brain to develop POMC neurons while you're still in utero; when your brain is full size, it gets ferried along to be read by the POMCs with the help of the two gene enhancers—likened by the researchers to "signal lights that show pilots the path to an airport runway."

These triggers are, in the words of the University of Michigan, responsible for the "little voice inside your head that tells you to eat, or stop eating." Mice engineered to be born without these triggers developed extreme hunger and became obese.

Therein lies the limitation of the research, however: As with the Yale study, these studies were carried out on mice and fish. While they are useful neurological models, the human brain is more complex and will require further study.

Still, these new studies provide yet more clues to the elusive workings of the brain, and could potentially aid pharmaceutical research into the treatment of some forms of obesity. "In theory, it could be possible to find drugs to increase the production of POMC gene products, or to grow replacement cells for malfunctioning POMC cells," the university notes in a press release. At the very least, research like this could shed light on eating issues that are often considered behavioral, not biological.