Blame the gut-brain connection for your greasy food cravings
Blame the gut-brain connection for your greasy food cravings Now if you’re blaming your tongue for fatty foods causing obesity, diabetes and heart disease, don’t! Researchers have found that the gut-brain connection is the culprit that creates our cravings for high-fat unhealthy foods. The health pioneer shared the results of the study published in Nature.
At the Zuckerman Institute in Columbia, scientists studying mice found that fat entering the gut triggers a signal. Conducted along the nerves to the brain, this signal causes the craving for fatty foods. The study raises the possibility of interfering with this gutbrain connection to helpprevent unhealthy choices and address the growing global health crisis caused by overeating.“We are living in unprecedented times, where excessive consumption of fat and sugar is causing an epidemic of obesity and metabolic disorders,” he first said.author Mengtong Li, PhD, postdoctoral researcher in the laboratory of Charles Zuker, PhD at the Zuckerman Institute, supported by the Howard Hughes Medical Institute.“If we want to control our insatiable cravings for fat, science shows us that the key channel that fuels these cravings is a connection between the gut and the brain.
Researchers have found that glucose activates a specific gut brain circuit that communicates with the brain in the presence of gut sugar.Calorie-free artificial sweeteners, on the other hand, don’t have this effect, which is perhaps why diet sodas can leave us feeling unsatisfied.”Our research shows that the tongue tells our brain what we like, such as things that taste sweet, salty or fatty,” said Dr.Zuker, who is also a professor of molecular biochemistry, biophysics and neuroscience at Columbia’s Vagelos College of Physicians and Surgeons.”The gut, however, tells our brain what we want, what we need.” dr.He wanted them to explore how mice respond to dietary fat – the lipids and fatty acids that every animal must consume to provide the building blocks of life.He offered the mice bottles of water with dissolved fat, including a component of soybean oil, andwater bottles containing sugary substances known not to affect the intestine but which are initially attractive.Rodents developed a strong preference, within days, for oily water.
They also formed this preference when scientists genetically modified mice to suppress the animals’ ability to taste fat using their tongues.”Even though the animals didn’t taste the fat, they were still driven to consume it,” says Dr.Zuker, according to the paper, titled “GutBrain Circuits for Fat Preference,” available on the Eurekalert news site.The researchers reasoned that fat must activate specific brain circuits that determine the animals’ behavioral response to fat.To research this circuit, Dr.Li measured brain activity in mice while feeding the animals fat.Neurons in one particular region of the brainstem, the caudal nucleus of the solitary tract (cNST), fired up.
This was intriguing because the cNST was also implicated in the lab’s earlier discovery of the neural basis of sugar preference. dr.Li then found the communication lines that carried the message to the cNST.Neurons in the vagus nerve, which connects the gut to the brain, also chirped with activity when the mice had gut fat.After identifying the biological mechanism behind a mouse’s preference for fat, Dr.Li then took a close look at the intestine itself:
specifically the endothelial cells that line the intestine.He found two groups of cells that sent signals to vagal neurons in response to fat.“A group of cells functions as a general sensor for essential nutrients, responding not only to fats, but also to sugars and amino acids,” Dr. There said.”The other group only responds to fat, potentially helping the brain distinguish fat from other substances in the gut.” dr.Li then took a big step forward by blocking the activity of these cells with a drug.
Disrupting signaling from both groups of cells prevented vagal neurons from responding to fat in the gut.He then used genetic techniques to inactivate the vagal neurons themselves or the cNST neurons.Either way, a mouse lost its appetite for fat.”These interventions verified that each of these biological pathways from the gut to the brain is critical to an animal’s response to fat,” Dr. There said.”These experiments also provide new strategies for altering the brain’s response to fat and possibly its behavior towards food.” The stakes are high.Obesity rates have nearly doubled worldwide since 1980.Today, nearly half a billion people suffer from diabetes.
Among Indians, the prevalence of obesity increased in 201921 compared to 201516, according to the latest data from the National Family Health Survey (NFHS5).Nearly one in four people are overweight compared to one in five previously.India is already on the verge of becoming the diabetes capital of the world.Obesity is calculated on the basis of a body mass index (BMI).
Anyone with a BMI over 30 is considered obese; a person whose BMI is between 25 and 29.9 is considered overweight.”Excessive consumption of cheap, highly processed foods high in sugar and fat has a devastating impacton human health, especially in low-income people and communities of color,” Dr. Zuker said.”The better we understand how these foods hijack the underlying biological machinery of taste and the gut-brain axis, the more opportunities we will have to intervene.”
The relationship between weight gain and bacteria in the gut is similar to the chicken-and-egg debate.Are weight gain and obesity responsible for an unhealthy gut microbiome, or does our gut microbiome contribute to the rate at which we gain weight?The simple answer is that they influence each other.If the diet disrupts the gut microbiome, the gut microbiome will suffer and therefore cannot help the body digest and metabolize properly.
It is also possible that a damaged gut microbiota (due to illness, stress, intolerance and medications such as antibiotics)it can weaken the gut bacteria population and create imbalances, leading to interrupted hunger cues and poor nutrient utilization.
Several studies in mice have reported that the transfer of intestinal bacteria from an obese subject to a lean subject can lead to weight gain in the lean subject. Although no human studies replicating the methods of these mouse studies have been conducted, the researchersthey were able to distinguish between the microbial composition of obese and lean individuals.
This could mean that if obese people work to change the makeup of their gut microbiome, they might as well beable to alter their ability to break down fiber-rich foods and be more aware of their cues for satiety and hunger. As you can see, there is still much to learn about the relationship and different jobs of bacteria in food metabolism and utilization.But what is indisputable is the importance of maintaining a healthy lifestyleand the stability of our gut bacteria when setting weight loss goals or starting a new health plan.
