A recent study has revealed that obesity may impair the brain’s ability to recognize the sensation of fullness and satisfaction after consuming fats and sugars. Furthermore, these brain changes could persist even after individuals classified as medically obese successfully lose a significant amount of weight, potentially explaining why many individuals experience weight regain after initial weight loss.
According to Dr. Caroline Apovian, a professor of medicine at Harvard Medical School, these findings suggest that individuals with obesity continued to lack the chemical responses in their brains that signal satiety and satisfaction, indicating that reversibility was not observed, per KSL.com. The study’s results shed light on the underlying neurological changes associated with obesity, validating its classification as a disease.
Dr. I. Sadaf Farooqi, a professor of metabolism and medicine at the University of Cambridge, praised the study for its rigorous design and comprehensive approach. The research builds upon previous studies that have already identified various brain alterations caused by obesity.
The study, published in Nature Metabolism, employed a controlled clinical trial involving 30 medically obese individuals and 30 individuals with normal weight. The participants were fed sugar carbohydrates (glucose), fats (lipids), or water (as a control) directly into their stomachs via a feeding tube on separate days. By bypassing the mouth, the researchers aimed to investigate the gut-brain connection and determine how nutrients influence the brain independently of sensory perception.
Using functional magnetic resonance imaging and single-photon emission computed tomography, the researchers examined the brain’s response to the nutrients over a 30-minute period. The scans measured oxygen utilization in specific brain regions and dopamine levels, a hormone associated with the brain’s reward system.
In individuals with normal weight, the brain signals in the striatum, the region involved in motivation and habit formation, decreased when sugars or fats were introduced into the digestive system. This reduction in brain activity corresponded with the recognition of satiety. Additionally, dopamine levels increased, indicating activation of the brain’s reward centers.
However, the same responses were not observed in medically obese individuals. Brain activity did not slow down, and dopamine levels did not rise, particularly when fats were consumed. This discrepancy is significant since foods high in fat content tend to elicit stronger reward responses in the brain.
To assess the impact of weight loss, participants with obesity were asked to lose 10% of their body weight within three months, a substantial amount known to have positive effects on health. Surprisingly, losing weight did not reset the brain’s response in individuals with obesity. The study’s author, Dr. Mireille Serlie, emphasized that the brain continued to exhibit an inability to recognize fullness and satisfaction even after weight loss, suggesting that the neurological impact of obesity may not be as reversible as previously assumed.
The study acknowledged that further research is necessary to fully comprehend the effects of obesity on the brain and to determine whether the changes observed are due to fat tissue, specific food types, or other environmental and genetic factors. Understanding when these brain alterations occur during weight gain and exploring the potential influence of genetics are crucial areas for future investigation.
The study also emphasized the importance of rejecting weight stigma in the fight against obesity. Serlie emphasizes that oversimplifying weight gain as a lack of willpower overlooks the fact that malfunctioning brain mechanisms may contribute to the struggle with food intake. The findings hope to foster greater empathy and understanding for individuals grappling with obesity, recognizing that their challenges may stem from neurological factors beyond their control.