Do we really have free will when it comes to food? This is an annoying question that is based on why so many people are so hard to stick to their diet.
To get answers, one neurobiologist, Harvey J. Grill of the University of Pennsylvania, turned to the rats and asked what would happen if he removed all their brains except the brain trunk. Brainst controls basic functions such as heart rate and breathing. But the animals did not smell, they could not see, they did not remember.
Would they know when they consumed enough calories?
To find out, Dr. Grill was dripping in his mouth of liquid food.
“When they reached the stopping point, they let the food run out of the mouth,” he said.
These studies, initiated decades ago, were the starting point for research, which constantly surprised scientists and led to the house that how they feel full of animals have nothing to do with consciousness. The work has gained more importance because scientists determine how modern drugs that cause weight loss, commonly called GLP-1 and in this ozempic, affect brain food control systems.
The emerging story does not explain why some people are obese and others do not. Instead, it offers tips on what makes us start eating and when we stop.
While most of the studies concerned rodents, they do not believe that people are different, said Dr. Jeffrey Friedman, an obesity researcher from Rockefeller University in Fresh York. He said that people are subject to billions of years of evolution, which leads to sophisticated neural paths that they control, when to eat and when to stop eating.
When they examined how the food is controlled, scientists learned that the brain is constantly getting signals that indicate how calorie the food is. There is a certain amount of calories that the body needs, and these signals make sure that the body will get it.
The process begins before a laboratory animal wins a single bite. Only the view of food neurons causes whether a lot of calories will be packed in this food. Neurons react more strongly to food such as peanut butter-calorie-low to low calorie, such as mice.
The next checkpoint takes place when the animal tastes food: neurons Calculate the caloric density again based on signals Posted from the mouth to the brain trunk.
Finally, when the food goes to the intestine, a modern set of brain signals allows neurons to re -determine the calorie content.
And it is really a calorie content, which according to Zachary Knight, a neurobiologist at the University of California San Francisco.
He saw it when he directly poured three types of food into the mouse’s stomachs. One infusion had fatty food, the other carbohydrates and a third protein. Each infusion had the same number of calories.
In each case, the message to the brain was the same: neurons signaled the amount of energy in the form of calories, not a source of calories.
When the brain determines enough calories, neurons send a signal to stop eating.
Dr. Knight said that these discoveries surprised him. He always thought that the signal of stopping food would be “communication between the intestine and the brain,” he said. There would be a feeling of full stomach and a deliberate decision to stop food.
Using this reasoning, some dietitians try to drink a enormous glass of water before a meal or fill low -calorie dishes such as celery.
But these tricks did not work for most people, because they do not take into account how the brain controls food. In fact, Dr. Knight said that mice do not even send satiety signals to the brain When everything they get, it’s water.
It is true that people can decide to eat, even when they are formulated or can decide not to eat when they try to lose weight. Dr. Grill said, in the intact brain – not only the brain trunk – other areas of the brain also exert control.
But Dr. Friedman said that in the end brain control usually replaces a person’s conscious decisions about whether they feel the need for food. He said, similarly, you can hold your breath – but only so long. And you can suppress the cough – but only to some extent.
Scott Sternson, a neurobiologist at the University of California in San Diego, agreed.
“There is a very enormous part of the appetite control that is automatic,” said Dr. Sternson, a co -founder of the startup company, Penguin Bio, which develops obesity treatment. People can decide to eat or not at a given moment. He added, however, that maintaining this type of control uses many mental resources.
“After all, attention concerns other things, and the automatic process will end in dominant,” he said.
When they examined brain food control systems, scientists were constantly surprised.
For example, they learned about the rapid brain response to the sight of food.
Neuronauts found several thousand neurons in the hypothalamus, deep in the brain that reacted to hunger. But how are they regulated? From previous studies, they knew that Post included these hunger neurons and that the neurons were less lively when the animal was well fed.
Their theory was that neurons reacted to hefty body stores. When fat stores were low – as it happens, when the animal postutes, for example – leptin levels, a hormone released from fat, are also low. That would include hunger neurons. When the animal eats, its fat stores are complemented, leptin levels boost, and, as assumed, neurons will silence.
It was believed that the whole system slowly reacts only to the state of energy storage in the body.
But then three groups of scientists, independently led by Dr. Knight, dr Sternson and Mark Andermann from Beth Israel Deaconess Medical Center, examined the activity of the moment to the moment of hunger neurons.
They started with hungry mice. Their hunger neurons shot quickly, what animals need food.
The surprise took place when the researchers showed food animals.
“Even before the first bite of food, the activity of these neurons turned off,” said Dr. Knight. “Neurons predicted. The mouse looks at food. The mouse predicts how many calories it will eat.”
The more affluent in calories food, the more neurons turn off.
“All three laboratories were shocked,” said Dr. Bradford B. Lowell, who collaborated with Dr. Andermann in Deaconess Beth Israel. “It was very unexpected.”
Dr. Lowell then asked what could happen if he intentionally turned off the hunger neurons, even though the mice didn’t have much to eat. Scientists can do this with genetic manipulations, which mean neurons so that they can turn them on and off with the drug or blue delicate.
These mice would not eat for many hours, even with food just before them.
Dr. Lowell and Dr. Sternson independently conducted the opposite experiment, including neurons at mice, which had a huge meal, mice equivalent to dinner for thanksgiving. The animals were decaying, they felt stuffed.
But, said Dr. Andermann, who repeated the experiment when they turned on the hunger neurons: “The mouse gets up and eats another 10 to 15 percent body weight.” He added: “Neurons say,” Focus on food. “
Researchers are still surprised by what they find – the layers of brain control, which provide strict adjustable food. And tips on modern drug development ways to control food.
One line of evidence was discovered by Amber Alhadeff, a neuronaut at the Monell Chemical Senses Center and the University of Pennsylvania. She recently found Two separate groups of neurons In the brain trunk, which reacts to GLP-1 obesity drugs.
One group of neurons signaled that the animals had enough to eat. The second group caused the equivalent of rodent nausea. Current obesity drugs hit both groups of neurons, informs what can be a factor of side effects that he feels a lot. He suggests that he can develop drugs that hit the neurons of satiety, but not nausea.
Alexander Nectow from Columbia University has another discovery of a surprise. He identified neuron group In the brain trunk, which regulates how desirable a meal is, following every bite of food. “We don’t know how they are doing it,” he said.
“I’ve been studying this region of the brainstem for a decade for a year and a half,” said Dr. Nectow, “But when we went and used all our fancy tools, we found a population of neurons that we never studied.”
He is now asking if neurons can be a target for the class of slimming drugs that can be at the Mount GLP-1S.
“It would be really amazing,” said Dr. Nectow.