Do we really have free will when it comes to eating? It is an irritating question that is in the heart of why so many people are so concealed to adhere to a diet.
To obtain answers, a neuroscientist, Harvey J. Grill of the University of Pennsylvania, turned to rats and asked what would happen if he removed all his brains, except his encephalic trunk. The brain 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 enough calories?
To find out, Dr. Grill dripped liquid food in his mouth.
“When they reached a stop point, they allowed the food to drain from the mouth,” he said.
Those studies, initiated decades ago, were a starting point for a research body that has continually surprised scientists and has taken home that how complete animals feel has nothing to do with consciousness. The work has gained more relevance as scientists disconnect how exactly the new drugs that cause weight loss, commonly called and including Ozempic, affect brain food control systems.
The story that is emerging does not explain why some people become obese and others do not. Instead, sacrifices clues about what makes us start eating and when we stop.
Although most of the studies were in rodents, belief defies that humans are somewhat different, said Dr. Jeffrey Friedman, an obesity researcher at Rockefeller University in New York. Humans, he said, are subject to billions of years of evolution, which leads to elaborate neuronal roads that control when eating and when to stop eating.
As they have tried how food is controlled, researchers learned that the brain is obtaining signals that hint how calorically dense is a meal. There is a certain amount of calories that the body needs, and these signs make sure the body obtains them.
The process begins before a laboratory animal takes a single bite. Only food view causes neurons to anticipate whether many calories will be packaged in that meal. Neurons respond more strongly to a food such as peanut butter loaded with calories, than to a calorie decline like the mouse.
The next control point occurs when the animal knows the food: neurons calculate caloric density again from the signs sent from the mouth to the brain trunk.
Finally, when the food reaches the intestine, a new set of signals to the brain allows neurons to determine the caloric content.
And the calorie content that the intestine evaluates is real, as Zachary Knight learned, a neuroscientist from the University of California in San Francisco.
He saw this when he directly infused three types of foods in the stomach of the mice. An infusion was of fatty food, another carbohydrates and the third of the protein. Each infusion had the same number of calories.
In each case, the message to the brain, the same: neurons were pointing out the amount of energy, in the form of calories and not the source of calories.
When the brain determines that sufficient calories were consumed, neurons send a signal to stop eating.
Dr. Knight said the thesis discoveries surprised him. He had always thought that the sign of stopping 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 that reference, some people who diet try to drink a large glass or water before a meal, or fill with low -calorie foods, such as celery.
But those tricks have not worked for most people because they do not take into account how the brain controls food. In fact, Dr. Knight discovered that mice not only send satiety signals to the brain when everything they are getting is water.
It is true that people can decide to eat even when they are taken out, or they can decide not to eat when they try to lose weight. And, said Dr. Grill, in an intact brain, not only in an encephalic log, other areas of the brain also exert control.
But, said Dr. Friedman, in the end the brain controls generally cancel a person’s conscious decisions about whether they feel the need to eat. He said, by analogy, you can contain your breathing, but just for so long. And you can suppress a cough, but only to some extent.
Scott Sternson, a neuroscientist from the University of California in San Diego and the Howard Hughes Medical Institute, agreed.
“There is a great proportion of appetite control that is automatic,” said Dr. Sternson, who is also co -founder of a starting company, Penguin Bio, which is developing obesity treatments. People can decide to eat or not at a given time. But, he added, coining that type of control uses a lot of mental resources.
“Possible, attention goes to other things and the automatic process will end up dominating,” said Hey.
As the brain food control systems advanced, researchers were continually surprised.
They learned, for example, about the rapid response of the brain in view of food.
The neuroscientists found in mice a few thousand neurons in the hypothalamus, in the depths of the brain, which responded to hunger. But how do they regulate? They knew for previous studies that the hunger neurons quickly turned and that neurons were less active when an animal was well fed.
His theory was that neurons responded to the fat stores on the body. When fat stores were low, as is the case when an animal fasts, for example, leptin levels, a hormone released from fat, are also low. That would turn on their hunger neurons. As an ATS animal, its fat stores rejoiced, leptin levels go and the neurons were supposed to shut up.
However, the entire system responded slowly to the energy storage state in the body.
But then, three groups of researchers, directed independently by Dr. Knight, Dr. Sternson and Mark Andermann or Beth Israel Diacononess Medical Center, examined the activity moment from the neurons of hunger.
They met hungry mice. Their hunger neurons were firing quickly, a sign that animals needed food.
The surprise happened when the researchers showed the food of the animals.
“Even before the first food bite, the activity of those neurons went out,” said Dr. Knight. “The neurons were making a prediction. The mouse looks at the food. The mouse predicts how many calories will eat.”
The richer in calories the food is, the more neurons go out.
“The three laboratories were surprised,” said Dr. Bradford B. Lowell, who worked with Dr. Andermann at Beth Israel Deaconess. “It was very unexpected.”
Dr. Lowell then asked what could happen if he deliberately turned off the neurons of hunger, even thought the mice had had much to eat. Researchers can do this with genetic manipulations that mark neurons so that they can turn them on and turn them off with a medicine or with a blue light.
These mice would not eat for hours, even with food right in front of them.
Dr. Lowell and Dr. Sternson made the opposite experiment independent, lighting neurons in mice that had just had a great meal, the mouse equivalent of a Thanksgiving dinner. The animals were reclined, feeling filling.
But, said Dr. Andermann, who repeated the experiment, when hunger neurons lit, “the mouse rises and eats another 10 to 15 percent of their body weight.” He added: “The neurons say,” just concentrate on food. “”
Continuous researchers are surprised by what they are finding: layers of brain controls that ensure that eating is rigorously regulated. And indications of new ways to develop drugs to control food.
Amber Alhadeff discovered a line of evidence, a neuroscientist at the Monell Chemical Sensions Center and the University of Pennsylvania. Recently he found two separate groups of neurons in the brain trunk that respond to GLP-1 obesity medications.
A group of neurons said animals have had enough to eat. The other group caused the equivalent of the nausea rodent. Current obesity drugs hit both groups of neurons, reports, which can be a factor in the side effects that many feel. She proposes that it is possible to develop drugs that hit Satty neurons but not nausea.
Alexander Nectow, or Columbia University, has another surprise discovery. He identified a group of neurons in the brainstem that regulate how large a meal is desired, tracking each bite of food. “We don’t know how they do,” he said.
“I have been studying this region of the brain trunk for a decade and a half,” Dr. Ir. Nectow said: “But when we got used to and used all our elegant tools, we found that this population of neurons never had a study.”
Now ask if neurons could be objective for a drug class to lose weight that could eclipse the LPG-1.
“That would be really surprising,” said Dr. Nectow.
