Scientists have just discovered a new way our brains govern hunger making a new drug that can ‘switch off’ our food cravings possible.
Researchers identified the mechanism that makes us feel hungry and then chooses whether or not to reach for the bag of chips.
They made the discovery because of a pioneering new use of a tiny periscope allowing them to see the neurons that are in a previously unobservable part of the brain.
Their findings could help people with ‘faulty’ hard wiring in their brain that does not allow them to stop eating when full.
‘To put it simply, when you’re hungry, the picture of a cheeseburger may be incredibly appealing and efficient in influencing your behavior,’ explained the lead author of the study, Yoav Livneh, a postdoctoral fellow at Beth Israel Deaconess Medical Center at Harvard University.
‘But if your belly is full after eating a big meal, the same cheeseburger picture will be unappealing.
‘We think that the pathway we discovered from hunger-promoting neurons to a region of the brain called the insular cortex plays an important role here.’
Obese people’s over-sensitivity to food cues
Brain imaging data supports the idea that the insular cortex – part of the brain – is involved in choosing if a source of food is worth pursuing.
In people with a healthy weight, the insular cortex increases its activity in response to food cues – the sight of a cheeseburger for instance – during hunger but not after a meal.
Studies suggest that the process often goes awry in people with obesity or other eating disorders that involve excessive food cravings.
The findings indicate that specific changes in a brain’s activity, including an increased sensitivity to food cues, may trigger these disorders – rather than a ‘lack of willpower.’
And so the researchers wanted to find out more about how this happens, testing on, mice which are biologically similar to humans.
They used a periscope to track and monitor individual neurons in mice as they responded to food cues in both a satiated and hungry physiological states.
The experiments showed that when they were presented with food, a particular group of neurons in the insular cortex were activated, which were responsible for mice choosing whether or not to eat.
After they had eaten until they were full, this brain response to food cues in the insular cortex was no longer present.
While the mice were still full, the researchers used genetic techniques to artificially trigger them wanting more food by ‘turning on’ specific neurons in the hypothalamus, a part of the brain that has a vital role the regulation and control of hunger.
By activating these neurons, called AgRP, the team caused mice that were full to seek more food once again.
As a result, the hope therapies could dial down this neuron behavior and reduce excessive cravings.
‘These AgRP neurons cause hunger – they are the quintessential hunger neuron,’ explained co-author Bradford Lowell.
‘It’s a major advance to learn that we can artificially turn them on and cause full mice to work to get food and to eat as if they hadn’t eaten in a long time.
‘We’re still trying to understand how this process works.
‘Huge questions remain, but they are now addressable thanks to these new imaging methods.’