Evidence of behavioral, biological similarities between compulsive overeating and addiction
October 17, 2019
Science Daily/Boston University School of Medicine
Does yo-yo dieting drive compulsive eating? There may be a connection.
According to Boston University School of Medicine (BUSM) researchers the chronic cyclic pattern of overeating followed by undereating, reduces the brain's ability to feel reward and may drive compulsive eating. This finding suggests that future research into treatment of compulsive eating behavior should focus on rebalancing the mesolimbic dopamine system -- the part of the brain responsible for feeling reward or pleasure.
An estimated 15 million people compulsively eat in the U.S. It is a common feature of obesity and eating disorders, most notably, binge eating disorder. People often overeat because it is pleasurable in the short term, but then attempt to compensate by dieting, reducing calorie intake and limiting themselves to "safe," less palatable food. However, diets often fail, causing frequent "relapse" to overeating of foods high in fat and sugar (palatable foods).
"We are just now beginning to understand the addictive-like properties of food and how repeated overconsumption of high sugar -- similar to taking drugs -- may affect our brains and cause compulsive behaviors," said corresponding author Pietro Cottone, PhD, associate professor of pharmacology & experimental therapeutics at BUSM and co-director of the Laboratory of Addictive Disorders.
In order to better understand compulsive and uncontrollable eating, Cottone and his team performed a series of experiments on two experimental models: one group received a high sugar chocolate-flavored diet for two days each week and a standard control diet the remaining days of the week (cycled group), while the other group, received the control diet all of the time (control group).
The group that cycled between the palatable food and the less palatable, spontaneously developed compulsive, binge eating on the sweet food and refused to eat regular food. Both groups were then injected with a psychostimulant amphetamine, a drug that releases dopamine and produces reward, and their behavior in a battery of behavioral tests was then observed.
While the control group predictably became very hyperactive after receiving amphetamine, the cycled group did not. Furthermore, in a test of the conditioning properties of amphetamine, the control group was attracted to environments where they previously received amphetamine, whereas the cycled group were not. Finally, when measuring the effects of amphetamine while directly stimulating the brain reward circuit, the control group was responsive to amphetamine, while the cycled group was not.
After investigating the biochemical and molecular properties of the mesolimbic dopamine system of both groups, the researchers determined that the cycled group had less dopamine overall, released less dopamine in response to amphetamine and had dysfunctional dopamine transporters (protein that carries dopamine back into brain cells) due to deficits in their mesolimbic dopamine system.
"We found that the cycled group display similar behavioral and neurobiological changes observed in drug addiction: specifically, a "crash" in the brain reward system," explained Cottone. "This study adds to our understanding of the neurobiology of compulsive eating behavior. Compulsive eating may derive from the reduced ability to feel reward. These findings also provide support to the theory that compulsive eating has similarities to drug addiction."
"Our data suggest that a chronic cyclic pattern of overeating will reduce the brain's ability to feel reward -- feeling satiated. This results in a vicious circle, where diminished reward sensitivity may in turn be driving further compulsive eating," said lead author Catherine (Cassie) Moore, PhD, former graduate student in the Laboratory of Addictive Disorders at BUSM.
The researchers hope these findings spark new avenues of research into compulsive eating that will lead to more effective treatments for obesity and eating disorders.
https://www.sciencedaily.com/releases/2019/10/191017125240.htm
Brain circuit connects feeding and mood in response to stress
September 4, 2019
Science Daily/Baylor College of Medicine
An international team has looked into the possibility of crosstalk between eating and mood and discovered a brain circuit in mouse models that connects the feeding and the mood centers of the brain.
Many people have experienced stressful situations that trigger a particular mood and also change certain feelings toward food. An international team led by researchers at Baylor College of Medicine looked into the possibility of crosstalk between eating and mood and discovered a brain circuit in mouse models that connects the feeding and the mood centers of the brain. Published in the journal Molecular Psychiatry, these findings may help explain some of the observations between changes in mood and metabolism and provide insights into future solutions to these problems by targeting this circuit.
"This study was initiated by first author Dr. Na Qu, a psychiatrist of Wuhan Mental Health Center, China, when she was visiting my lab," said corresponding author Dr. Yong Xu, associate professor of pediatrics and of molecular and cellular biology at Baylor College of Medicine.
Qu, a practicing psychiatrist who also conducts basic brain research, was interested in investigating whether there was a neurological basis for the association between depression and other psychiatric disorders and alterations in metabolism, such as obesity or lack of appetite, she had observed in a number of her patients.
Xu, Qu and their colleagues worked with a mouse model of depression induced by chronic stress and observed that depressed animals ate less and lost weight. Then, they applied a number of experimental techniques to identify the neuronal circuits that changed activity when the animals were depressed.
"We found that POMC neurons in the hypothalamus, which are essential for regulating body weight and feeding behavior, extend physical connections into another region of the brain that has numerous dopamine neurons that are implicated in the regulation of mood," said Xu, who also is a researcher at the USDA/ARS Children's Nutrition Research Center at Baylor and Texas Children's Hospital. "We know that a decrease in dopamine may trigger depression."
In addition to the physical connection between the feeding and the mood centers of the brain, the researchers also discovered that when they triggered depression in mice, the POMC neurons were activated and this led to inhibition of the dopamine neurons. Interestingly, when the researchers inhibited the neuronal circuit connecting the feeding and the mood centers, the animals ate more, gained weight and looked less depressed.
"We have discovered that a form of chronic stress triggered a neuronal circuit that starts in a population of cells that are known to regulate metabolism and feeding behavior and ends in a group of neurons that are famous for their regulation of mood," Xu said. "Stress-triggered activation of the feeding center led to inhibition of dopamine-producing neurons in the mood center."
Although more research is needed, Xu, Qu and their colleagues propose that their findings provide a new biological basis that may explain some of the connections between mood alterations and changes in metabolism observed in people, and may provide solutions in the future.
"Our findings only explain one scenario, when depression is associated with poor appetite. But in other cases depression has been linked to overeating. We are interested in investigating this second association between mood and eating behavior to identify the neuronal circuits that may explain that response," Xu said.
https://www.sciencedaily.com/releases/2019/09/190904213722.htm