3 Simple Neurons Might Be Behind Driving You To Want To Eat
Our appetites may be regulated by a circuit in our brains that is made up of three types of neurons, according to a new study involving mice. In the mice, just three types of brain cells drove them to eat more or less food.
The three-part circuit works by first having specialized neurons sense certain hormones that signal hunger. They communicate whether an animal is hungry or full.
Then, the neurons control neural activity in another part of the brain, which, in turn, controls a third set of neurons located in the jaw. They direct the movements that are required for chewing.
No conscious thought is needed for the three-part circuit to function—it is like a reflex. It was detected in mice but has yet to be identified in humans. If humans are found to have it, the discovery could change the way we as a society view obesity.
“The control of how much we eat and when we eat is not so much based on your decision process, it just happens—it’s a simple circuit,” said Christin Kosse, a lead author of the study and a research associate at the Rockefeller University in New York.
Obesity has been deemed a chronic disease with various causes, such as genetics. Previously, it was regarded as the result of personal decisions related to eating.
However, the new study further supports the idea that physiological differences are a major contributor to obesity. It also helps connect several theories about hunger.
One of them is called “set point theory,” which argues that people have a set point in body weight determined by their genetics and their environment.
According to the theory, the body tries to keep a consistent weight, even if a person eats more or less food than they need.
Olga Krivokoneva – stock.adobe.com – illustrative purposes only, not the actual person – pictured above is a woman eating yogurt in her kitchen
Multiple physiological mechanisms maintain a caloric balance. But if these mechanisms fail to do their job, people may gain or lose significant amounts of weight.
Usually, fat cells and cells in the gut will release hunger-controlling hormones that signal to the brain that you’re full.
But if the hormone signaling is somehow disrupted, people can still feel really hungry even when they’ve eaten enough, leading them to overeat and become obese in some cases.
In the past, research has shown that neurons in the hypothalamus aid in appetite regulation. They are targeted by weight loss drugs like Ozempic.
Additionally, reductions in a protein known as brain-derived neurotrophic factor (BDNF) are linked to obesity in both humans and animals.
In the new study, neurons in the hypothalamus that produce BDNF are activated in the brains of mice who were fed a diet high in fats and became obese. This indicates that these neurons respond to weight gain and work to suppress the rodents’ appetites.
The team switched the BDNF neurons on and off to test their hypothesis. When the neurons were inactive, the mice ate approximately 1200 percent more food than normal.
They also made chewing movements even when no food was present. At times, they tried to eat objects like wooden blocks.
When the neurons were active, the mice stopped eating so much and did not make chewing movements.
It is possible that humans may have a similar circuit system for hunger in our brains. The team plans to investigate whether the circuit changes depending on emotional states, such as anxiety.
The study was published in the journal Nature.
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