What part of the brain causes weight loss?
What part of the brain causes weight loss?
The hypothalamus is a tiny part of the brain that manages hunger. It pulls together the signals from the gut, fat cells and the brain. It tells us when we are hungry and when we have had enough to eat.
Hypothalamic obesity (HyOb) is a complicated medical condition. It can happen from the growth of rare brain tumors. It can also happen from other types of injury to the hypothalamus. Craniopharyngioma (krā’nē-ō-fə-rĭn’jē-ō’ma) is one of the tumors that can cause HyOb.
What Happens in Hypothalamic Obesity?
When the hypothalamus is injured, the brain and the gut have a hard time understanding each other’s signals. The brain cannot “hear” the messages from the body fat, trying to tell the brain to turn off hunger. This mix up in the brain leaves the person always feeling hungry. Because the person is hungry they will eat more and more. The body will store the extra energy from the food as fat. This can cause 1-2 pounds of weight gain a week.
As more and more weight is gained, the body begins to store fat in places that it usually does not, like muscles, the liver and in and around other important organs in the belly. This can make it hard for these important organs to work right and it can harm the person’s health.
Hypothalamic Obesity Symptoms
Besides the feeling of non-stop hunger, the person may feel short tempered or grouchy because the body makes more insulin.
Insulin is a hormone the body makes to help handle food.
Hypothalamic Obesity Treatment
Some medications have been used with some measures of success with hypothalamic obesity.
Gastric bypass surgery has also been found to help with weight loss and managing hunger in people with hypothalamic obesity.
After surgery, the person loses weight. The body makes less insulin. The constant feelings of hunger are under better control.
Weight loss surgery is not the best option for everyone. It is recommended only after all other weight-loss plans have failed.
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Obesity and the Brain
Some mice are naturally obese due to an inherited genetic mutation that causes them to eat excessively. Although the mutant mice are normal-sized when born, they may eventually weigh as much as three times more than unaffected mice. Researchers’ studies of these animals led to the discovery of the hormone leptin, which helps control appetite.
Courtesy of Oak Ridge National Laboratory, U.S. Department of Energy.
Brain scans show that when people view images of appetizing foods (right), there is more activity in the striatum — a brain region associated with reward — than when the foods are distasteful (left). This image shows brain activity in a teenager with deficiencies in the hormone leptin, which helps control appetite. After taking leptin supplements, his brain responses show this normal pattern of activation (above).
Published with permission of Paul C. Fletcher and Sadaf Farooqi, University of Cambridge. © 2007.
Fat cells produce a hormone called leptin, which travels through the body’s blood stream and acts on a brain region called the hypothalamus. Leptin helps to regulate appetite and metabolism. A lack of leptin, or its receptor in the brain, can lead to uncontrolled food intake and obesity.
©1997 Society for Neuroscience, Illustration by Lydia Kibiuk
Studies show that rates of obesity are increasing rapidly. About two-thirds of adults in the United States are now overweight, obese, or extremely obese, according to data from the Centers for Disease Control and Prevention.
Courtesy of the National Center for Health Statistics Health E-Stats, December 2008.
Brain research is helping to identify what causes obesity, as well as how to curb an epidemic and promote wellness.
Studies of feeding behavior in animals and people have led neuroscientists to discover that complex systems in the brain, not just the intestine, determine food intake. More research about how genes, chemicals, and the environment interact and control our urge to eat could help curb an obesity epidemic.
In the last 30 years, the prevalence of obesity has doubled in children and quadrupled in adolescents.. The human body is so devoted to warding off potential starvation that in a society of plenty, innate weight-control mechanisms may harm more than they help. With excessive body weight comes a host of medical dangers, at a price of more than $140 billion a year in U.S. health-care costs.
Fat mice and the first insights into obesity
Weight control used to be considered a simple matter of willpower: you versus food. Researchers now know that controlling body weight is a complex process influenced by genes and regulated by the brain.
A Tale of Two Mice
In the early 1900s, doctors noticed that patients of normal weight who suffered damage in a brain region called the hypothalamus often became obese or gaunt after injury. This observation led researchers to suspect that the brain controls weight gain and loss.
Solid evidence that specific brain chemicals regulate weight came many years later, in the 1970s. Researchers thought a molecule that travels through the blood to the brain might determine whether an animal feels stuffed or ravenous. To find out, they studied mice that were naturally obese because of a rare genetic mutation. When these mice were exposed to chemicals in the blood of other types of mice, the obese mice ate less and lost weight. These findings suggested that unlike normal mice, the obese mice lacked a hormone that made them feel full.
Of Mice and Men
Researchers identified this hormone 20 years later by isolating the gene that was mutated in the obese mice. The gene produced a protein called leptin that is made in fat cells. Because of the mutation, the mice could not make functional leptin. When treated with leptin, their appetites decreased and metabolism increased, causing them to lose weight.
Because humans also produce leptin, researchers hoped giving the hormone to obese people would result in weight loss. However, leptin did not turn out to be the amazing cure-all for which scientists, physicians, and patients had hoped. In a clinical trial, it did help three obese children lose weight, but they had an extremely rare form of obesity: like the mice studied in the lab, these children had a leptin deficiency caused by a rare mutation.
Although these findings did not result in an obesity treatment, they indicated the importance of the brain in regulating weight and formed a platform for further understanding of weight mechanisms in people.
Connecting chemical and genetic contributors to obesity
Hoping to understand obesity, brain researchers continued to hunt for molecules that, like leptin, control food intake. What they found was a complex system of chemicals and genes that tightly control appetite and weight.
Circulating Chemicals: Triggering Hunger or Fullness
Researchers soon found that in addition to leptin, a whole host of chemicals signal the brain to trigger hunger or fullness. Many of these hormones act at a brain region in the hypothalamus called the arcuate nucleus. In turn, this region secretes molecules that affect appetite. One type of brain cell in the arcuate produces chemicals that activate the appetite. Another type makes appetite-quashing molecules. Together, the neurons alternately encourage and discourage feeding.
Additional compounds made elsewhere in the hypothalamus, such as orexin, and in the stomach, such as ghrelin, also promote eating. What emerges is a complex system of interacting chemical messengers that regulate weight.
Inherited Obesity
Disturbing this chemical system can have dire effects — brain researchers have found that in rare instances, gene mutations that affect these very chemicals can cause obesity in people. Studies have shown that some people are more prone to weight gain than others due to their genetic makeup. In fact, obesity researchers estimate that 40 to 70 percent of the differences between body types are genetic. The answers now pursued in the lab are not whether a genetic component for obesity exists, but which genes are responsible.
However, so far, geneticists have found only rare gene mutations that contribute to isolated cases of obesity. More sophisticated genetics research will help explain the combination of genetic factors contributing to the vast majority of the obese population.
Stemming an obesity epidemic
Thanks to decades of systematic research, scientists now better understand how the brain tightly regulates body weight. Why, then, do obesity rates continue to climb? New research is investigating how complex environments — including the increased availability of highly palatable but nutritionally poor foods in developed countries — affect brain chemistry. The findings indicate the importance of healthy choices in maintaining weight and suggest new avenues of treatment.
Food as an Addiction
Neuroscientists have recently learned that fatty food taps the pleasure centers of the brain, the same areas that are associated with heroin and cocaine habits. For addicted individuals, eating becomes compulsive, regardless of negative health or societal consequences.
Research shows that after extended periods of excessive eating, brain connections are permanently altered on a molecular level. In rats fed a high-fat, high-calorie diet, the brain pleasure centers become less responsive over time, just as they do following drug use. Moreover, when the rats were offered healthy food after weeks of junk food, they were less likely to eat it than rats fed healthy food only. These findings suggest the difficulty in changing established eating habits and highlight the importance of obesity prevention.
New Treatments
With more than 78 million obese people in the United States, the need for weight-control treatments is acute. Therapeutic solutions that target the behavioral, chemical, and genetic components of the disease are all in development. For example, an appetite-reducing drug now in clinical trials activates natural hunger-dampening chemicals and at the same time blocks hunger-stimulating ones. Another treatment is intended to prevent brain cells from responding to noradrenaline and serotonin, brain chemicals linked to addiction.
Because obesity is a complex condition affected by genes, chemicals, behavior, and the environment, explaining it will likely require a comprehensive approach. The coordination and funding of this research, by institutions such as the U. S. National Institutes of Health and Food and Drug Administration, will be vital to stem the epidemic. So too will be research on healthy habits that can encourage wellness, especially in the young.
Obesity can cause changes in the brain similar to Alzheimer’s, study suggests
Brain scans show patterns of shrinkage in regions involved in learning, memory and judgment. Experts hope losing weight could reverse some of the damage.
Scan of the brain of a patient affected by Alzheimer’s. BSIP / Universal Images Group via Getty Images
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Jan. 31, 2023, 2:05 PM UTC
By Linda Carroll
Being overweight in midlife has been linked to greater risk of developing Alzheimer’s disease or dementia, and a new study shows that brain changes in obese people mirror some of those with Alzheimer’s.
Scientists at McGill University in Montreal analyzed brain scans of more than 1,300 people in the first research to directly compare the patterns of brain shrinkage in obese people and in Alzheimer’s patients.
The scans revealed similar brain thinning in regions involved in learning, memory and judgment in both groups, according to the report published Tuesday in the Journal of Alzheimer’s Disease.
Obesity can cause changes in the body that are associated with raising the risk of Alzheimer’s, including damage to the brain’s blood vessels and the accumulation of abnormal proteins, earlier studies have found. The new research takes it a step further.
“We showed that there is a similarity between the brains of people who are obese and those with Alzheimer’s,” said the study’s first author, Filip Morys, a postdoctoral neuroscience researcher at McGill University. “And it boils down to the thickness of the cerebral cortex.”
The cerebral cortex, which in humans is responsible for higher brain functions such as speech, perception, long-term memory and judgment, is the outer layer of the brain.
Thinning in that brain region might reflect a decrease in the number of brain cells, Morys said.
The McGill researchers suspect that obese people, and possibly those who are overweight — a BMI of 25 to 25.9 — might be able to slow cognitive decline if they can get closer to a healthy weight.
Morys wasn’t able to identify a target weight.
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Why is obesity hazardous to the brain?
The science isn’t clear. Other conditions that are bad for the brain — including high blood pressure, high cholesterol and type 2 diabetes — are also connected to obesity, Morys notes.
To take a closer look at the impact of obesity on brain structure, Morys and his colleagues scrutinized brain scans from 341 Alzheimer’s patients and 341 obese individuals with a BMI of 30 or more, along with scans from 682 healthy individuals.
All of the brain scans and other information came from two large health databases: the U.K. Biobank and the Alzheimer’s Disease Neuroimaging Initiative, a program that recruits participants across North America and is funded in part by the National Institutes of Health.
Cognitive tests taken by the obese individuals in the study did not reveal obvious mental deficits, but it’s possible that subtle changes in cognition related to the thinning seen on the brain scans might not be picked up on the types of tests used to evaluate mental status, Morys said.
The new research “showed us something we didn’t know before,” said metabolism researcher Sabrina Diano, director of the Institute of Human Nutrition at the Columbia Irving Medical Center.
“The study showed that obese individuals and those with Alzheimer’s disease have common areas of the brain that are smaller in size, possibly due to a neurodegenerative process,” meaning that the nerve cells in these regions may be experiencing damage and could be dying, Diano said.
The scans can’t show that obesity is causing the thinning of these areas, but it makes sense that controlling body weight might be a way to reduce the risks, she said.
“We know that if you take a mouse that has a genetic predisposition to develop Alzheimer’s and you put that mouse on a diet rich in carbohydrates and fat —similar to the Western diet — you can induce increases in body weight in the animal and as they gain weight cognitive impairment and the brain degeneration is accelerated,» Diano said.
Could weight loss reverse the damage?
The study opens the door to further exploration of whether weight loss might reverse some of the brain changes, said Dr. Joseph Malone, an assistant professor of neurology in the cognitive disorders division at the University of Pittsburgh. Malone was not involved with the study.
“We do know that obesity is associated with other diseases that can affect the blood vessels in the brain, such as type 2 diabetes, high blood pressure, high cholesterol and inflammation, all of which could lead to the breakdown of blood vessels in the brain and thus contribute to brain cell death,” Malone said.
While the obese individuals in the study did not show memory declines, it’s possible that what the researchers are seeing is an early stage in the development of Alzheimer’s, Malone suggested.
One limitation in the research is that it doesn’t directly report on what people are eating, just that they’re obese, said Linda Van Horn, chief of nutrition at the Northwestern University Feinberg School of Medicine, who was not involved with the study.
“Given that, it leaves a lot of room for speculation and hypothesis generation,» Van Horn said. «Intuitively, you would think it would have an impact on various organs including the brain.”
While the hope is that weight loss could stop or reduce the brain degeneration, «we, unfortunately, are discovering more and more that there are certain points of no return,» Van Horn said.
«I believe, based on examples like osteoporosis, that the chances of reversing the disease are lower than that of preserving what’s there,” she said.
Linda Carroll
Linda Carroll is a regular health contributor to NBC News. She is coauthor of «The Concussion Crisis: Anatomy of a Silent Epidemic» and «Out of the Clouds: The Unlikely Horseman and the Unwanted Colt Who Conquered the Sport of Kings.»