Do we really have the free will when it comes to eating? It is an irritating question that is at the center of the reason why so many people find so difficult to stick to a diet.
To obtain answers, a neuroscientist, Harvey J. Grill of the University of Pennsylvania, turned to the mice and asked what would have happened if he had removed the whole brain except their brain trunks. The cerebral trunk controls basic functions such as heart rate and breathing. But the animals could not smell, they could not see, they could not remember.
Would they know when they had consumed quite calories?
To find out, Dr. Grill dried liquid food in the mouth.
“When they reached a parking point, they allowed food to drain from the mouth,” he said.
Those studies, started decades ago, were a starting point for a corpus of research that continually surprised the scientists and the house that feel at home where full animals have nothing to do with consciousness. The work has acquired greater importance since scientists eliminate as exactly the new drugs that cause weight loss, commonly called GLP-1 and including the ozempici, influence the food control systems of the brain.
The story that is emerging does not explain why some people become obese and others do not. Instead, it offers clues to what makes us start eating and when we stop.
While most of the studies were in the rodents, he challenges the belief to think that humans are somehow different, said dr. Jeffrey Friedman, obesity researcher at Rockefeller University in New York. The humans said, are subject to billions of years of evolution that lead to elaborate neural paths they control when to eat and when to stop eating.
Since they were assessed how consumption is controlled, the researchers learned that the brain is constantly obtaining signs that suggest how calorically dense a food is. There are a certain amount of calories that the body needs and these signals ensure that the body obtains them.
The process begins before a laboratory animal takes a single bite. Only the view of food neurons to predict if many calories are packed in that food. The neurons respond more strongly to a food such as the arachid butter of calories-but to a low calorie one like a mouse chow.
The next control point occurs when the animal has the flavor of food: neurons calculate the calorie density from the signals sent from the mouth to the brain trunk.
Finally, when the food heads for the intestine, a new series of brain signals allows neurons again to ascertain the calorie content.
And it is actually the calorie content that the intestine evaluates, as Zachary Knight, neuroscientist of the University of California in San Francisco learned.
He saw this when he directly infused three types of food in the stomach of mice. An infusion was of fatty food, another carbohydrates and the third of the proteins. Each infusion had the same number of calories.
In any case, the message to the brain was the same: the neurons reported the amount of energy, in the form of calories and not the source of calories.
When the brain determines quite calories, neurons send a signal to stop eating.
Dr. Knight said these discoveries surprised him. He had always thought that the signal of stopping eating would be “a communication between the intestine and the brain,” he said. There would be the feeling of having a full stomach and a deliberate decision to stop eating.
Using this reasoning, some people on a diet try to drink a large glass of water before a meal or fill with low calorie foods, such as celery.
But those tricks have not worked for most people because they don't explain the way the brain controls eating. In fact, Dr. Knight discovered that mice does not even send signs of satiety to the brain when everything they are getting is water.
It is true that people can decide to eat even when they are saters or they may decide not to eat when they are trying to lose weight. And, said Dr. Grill, in an intact brain – not only a brain trunk – other areas of the brain also exert control.
But, said Dr. Friedman, in the end the brain checks generally overwrite the aware decisions of a person on the fact that they feel the need to eat. He said, by analogy, you can hold your breath, but only for so long. And you can suppress a cough, but only up to a certain point.
Scott Sternon, neuroscientist of the University of California in San Diego agreed.
“There is a very large percentage of appetite control which is automatic,” said dr. Sternon, co-founder of a startup company, Penguin Bio, who is developing obesity treatments. People can decide to eat or not at a certain moment. But, he added, keeping that type of control uses many mental resources.
“In the end, attention goes to other things and the automatic process will end up dominating,” he said.
While the brain -controlled control systems are outlined, the researchers were continuously surprised.
They learned, for example, on the rapid response of the brain to the view of food.
The neuroscientists had found a few thousand neurons in the mice in the hypothalamus, deep in the brain, which responded to hunger. But how are they regulated? They knew from previous studies that fasting turned on these hunger neurons and that neurons were less active when an animal was well fed.
Their theory was that neurons were responding to body fat deposits. When fat deposits were low – as happens when a digital animal, for example – leptin levels, a hormone released by fat, are also low. This would turn on the neurons of hunger. While an animal eats, its fat stores are supplied, the leptin levels increase and neurons, they presumed, would have calmed down.
It was thought that the entire system only slowly responded to the state of accumulation of energy in the body.
But then three groups of researchers, guided regardless of Dr. Knight, Dr. Sternon and Mark Andermann of the Beth Israel Deaconess Medical Center, have examined the moment moment about the hunger neurons.
They started with hungry mice. Their hunger neurons were shooting quickly, a sign that animals needed food.
The surprise took place when investigators showed food to animals.
“Even before the first food bite, the activity of those neurons goes out,” said dr. Knight. “The neurons were making a forecast. The mouse looks at food. The mouse foresees how many calories he will eat.”
The more the food full of calories, the more neuron goes out.
“All three laboratories were shocked,” said dr. Bradford B. Lowell, who worked with Dr. Andermann to Beth Israel Deaconess. “It was very unexpected.”
Dr. Lowell therefore asked what could happen if he deliberately turned off the hunger neurons even if the mice didn't have much to eat. The researchers can do it with genetic manipulations that mark neurons so that they can turn them on and turn off with a drug or a blue light.
These mice did not eat for hours, even with food right in front of them.
Dr. Lowell and Dr. Sternon made the opposite experiment independently, turning on the neurons in the mice that had just eaten a huge meal, the equivalent of the mouse of a thanksgiving dinner. The animals were reclining, they felt stuffed.
But, said dr. Andermann, who repeated the experiment, when they turned on the neurons of hunger, “the mouse gets up and eats another 10-15 percent of his body weight”. He added: “The neurons say:” focus only on food “.”
The researchers continue to be amazed by what they are finding: layers of checks in the brain that ensure that consumption is rigorously regulated. And hints of new ways to develop drugs to control consumption.
A line of tests was discovered by Amber Alhadeff, a neuroscientist of the Monell Chemical Senses Center and the University of Pennsylvania. He recently found two separate groups of neurons in the brain trunk that respond to the drugs of Obesity GLP-1.
A group of neurons reported that animals have had enough to eat. The other group caused the equivalent of the rodent of nausea. The current drugs of obesity affect both groups of neurons, reports, which can be a factor in the side effects that many feel. It proposes that it could be possible to develop drugs that affect the neurons of satiety but not those of nausea.
Alexander Nectow, Columbia University, has another surprise discovery. He identified a group of neurons in the brain trunk that regulate how much a meal is desired, monitoring every bite of food. “We don't know how they do it,” he said.
“I have studied this region of the brain trunk for a decade and a half,” said dr. Nectow, “But when we went to use all our imaginative tools, we found this population of neurons that we had never studied.”
Now he is asking if neurons could be targeted for a class of weight loss drugs that could exceed the GLP-1.
“It would be truly surprising,” said dr. Nectow.