How your brain cells might be sabotaging your diet
It might be tough to stick to a diet because of the activity of self-cannibalizing neurons in the brain.
That’s according to a report last summer (August 2011) in the journal Cell Metabolism. Researchers at New York’s Albert Einstein College of Medicine say that, when we don’t eat, hunger-causing neurons in the brain start munching on themselves. And that, in turn, can trigger excessive hunger. Researchers at Albert Einstein indicated that understanding the specifics of this neural self-destruction might offer a pathway of intervention for people who struggle to control their appetite.
Rajat Singh, who led the team of researchers at Albert Einstein, examined the brains of fasting mice. They spotted a cellular mechanism known as autophagy (self-eating) in neurons inside the brain’s hypothalamus. The self-cannibalizing action of the neurons was triggered when the mice were hungry. Immediately following that action, lipids within the so-called agouti-related peptide (AgRP) neurons got moving, which triggered the production of fatty acids. In turn, those fatty acids boosted levels of AgRP, aka the body’s hunger signal.
What does all this mean? Simply: if you don’t eat, you get hungry. That’s a no-brainer!
But here’s where the study provides a new insight. It suggests that, if you can interfere with the cascade of chemical reactions that causes hunger, you might be able to prevent appetite from getting extreme. According to medicalxpress:
When autophagy is blocked in AgRP neurons, AgRP levels fail to rise in response to starvation, the researchers show. Meanwhile, levels of another hormone … remain elevated. That change in body chemistry led mice to become lighter and leaner as they ate less after fasting, and burned more energy.
In other words, if you can chemically stop AgRP neurons from eating themselves, the brain doesn’t cause quite as much stomach rumbling. Singh said in a press release:
Chronically high levels of fatty acids in the bloodstream, as happens in those on a high-fat diet, might alter hypothalamic lipid metabolism, ‘setting up a vicious cycle of overfeeding and altered energy balance.’ Treatments aimed at the pathway might ‘make you less hungry and burn more fat,’ a good way to maintain energy balance in a world where calories are cheap and plentiful.
Dr. Singh also indicated that autophagy plays an important role in other parts of the body, in terms of providing energy in times of starvation. Until now, the brain was thought to be relatively resistant to that type of action.
He added that his findings about the action of hunger upon the brain might also help scientists figure out what sorts of appetite and metabolic changes occur, as the body ages.
Bottom line: Researchers at New York’s Albert Einstein College of Medicine say that, when we don’t eat, hunger-causing neurons in the brain start munching on themselves. And that, in turn, can trigger excessive hunger. Their report appears in the August 2011 issue of the journal Cell Metabolism.