A recent study suggests that obesity might have a lasting impact on the brain’s ability to process signals related to satiety and fullness, particularly after eating foods rich in sugars and fats.
This research, published in the journal Nature Metabolism, highlights a potential link between obesity and impaired brain responses to signals originating from the gut, which normally inform the brain about the presence of nutrients and play a crucial role in regulating eating behavior.
The study aimed to investigate how the brain responds to two types of nutrients – sugars and fats – in individuals with varying body mass indexes (BMI). Participants were divided into two groups: those with a BMI of 25 or lower, considered to have a healthy weight, and those with a BMI of 30 or higher, classified as obese.
To directly assess brain responses, researchers administered sugars and fats through feeding tubes. Afterwards, they used functional magnetic resonance imaging (fMRI) to analyze the brain’s chemical reactions to these nutrients.
Among those with lower BMIs, the infusion of sugars and fats led to reduced activity in various brain regions associated with hunger regulation. However, no discernable brain response to these nutrients was observed in individuals with obesity. This stark contrast in brain activity suggested that the brains of obese individuals might have a significantly diminished capacity to react to signals of fullness and satiety triggered by nutrient intake.
Senior study author Mireille Serlie, MD, PhD, of the Yale School of Medicine in New Haven, Connecticut, said in a statement, “This was surprising.”
“We thought there would be different responses between lean people and people with obesity, but we didn’t expect this lack of changes in brain activity in people with obesity,” Dr. Serlie added.
Brain Signals for Fullness and Satiety Didn’t Return Even After Weight Loss
To further explore if the lack of brain response could still be reversed, researchers asked participants with obesity to engage in a 12-week weight loss program. But, despite some participants successfully losing at least 10 percent of their body weight during the program, their brain’s unresponsiveness to sugars and fats stayed unchanged.
“None of the diminished responses were recovered,” said Dr. Serlie.
While this study provides valuable insights into the relationship between obesity and impaired brain signaling related to nutrient intake, it has its limitations. The brain imaging was done within a pretty short timeframe of approximately 30 minutes after nutrient infusion, possibly missing delayed or less pronounced brain responses in obese individuals.
Additionally, the study exclusively focused on individuals aged 40 years and above, raising the possibility of different results for younger participants.
Lack of Brain Signaling May Contribute to High-Caloric Intake
However, one notable strength of the study was its method of directly administering nutrients into the stomach, which minimized the potential influence of taste and sensory factors on brain responses.
Professor and director of the Center for Human Nutrition at the Washington University School of Medicine in St. Louis, Dr. Samuel Klein, MD, emphasized the significance of this approach. He highlighted its capacity to provide insights into the purely physiological aspects of brain signaling.
Notably, Dr. Klein was not involved in the study.
He said, “These results suggest alterations in how the brain responds to ingested nutrients in people with obesity could contribute to high calorie intake that causes obesity and to weight regain after diet-induced weight loss.”
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