Obesity alters brain function, hindering weight loss maintenance, study finds

Researchers from Amsterdam UMC and Yale University have recently unveiled a ground-breaking link between obesity and altered brain responses to nutrients. Their study indicates that obesity leads to reduced dopamine release and diminished nutrient-sensing activity in the brain. Worryingly, these changes persist even after weight loss, potentially explaining why maintaining weight loss is so challenging for many.

The research, published in Nature Metabolism, highlights that the brain’s responses to certain nutrients are impaired in individuals with obesity and don’t show improvement even after shedding weight.

Mireille Serlie, the lead researcher and Professor of Endocrinology at Amsterdam UMC, elaborates on the implications of the study, “Our results point toward enduring alterations in the brain among individuals with obesity, which could have a substantial impact on eating behaviour. We observed that, compared to individuals of normal weight, those with obesity exhibited lower dopamine release in a brain region that plays a pivotal role in the motivation associated with food consumption. Dopamine is crucial for the rewarding aspects of eating. Moreover, those with obesity demonstrated diminished brain activity in response to the infusion of nutrients into the stomach. Collectively, these results suggest that the brain’s ability to sense nutrients in the stomach and gut, or to process nutritional signals, is compromised in obesity, which may have significant repercussions on food intake.”

The regulation of food consumption is dependent on a complex interplay of metabolic and neural signals among the brain and various organs, such as the gut, as well as nutritional signals in the blood. This intricate network governs hunger and satiety sensations, regulates food intake, and controls the motivation to seek food. Though advances have been made in understanding these processes in animals, especially regarding metabolic diseases like obesity, less is known about the human mechanisms, mainly due to challenges in creating experimental setups within clinical settings that can elucidate these processes.

Addressing this knowledge gap, Serlie and her team, including colleagues from Yale, conducted a meticulously designed controlled trial. The study involved 30 participants with obesity and 30 of normal weight. It entailed infusing specific nutrients directly into the participants’ stomachs while simultaneously assessing their brain activity using MRI scans and monitoring dopamine release with SPECT scans.

The study discovered that while participants of normal weight showed distinct patterns of brain activity and dopamine release in response to nutrient infusion, these responses were significantly weakened in those with obesity. Furthermore, even after achieving a 10% body weight loss through a 12-week diet, the brain responses in individuals with obesity did not improve. This finding suggests that obesity induces long-term adaptations in the brain that persist even after weight loss.

“The enduring nature of these brain alterations, which do not reverse even after weight loss, might elucidate why so many individuals tend to regain weight following initial successful weight loss,” Serlie concludes.

This discovery brings to light the intricate challenges faced by those striving to lose weight and maintain the loss, suggesting that strategies need to address not only the physical aspects but also the neurological factors entangled with obesity.