The Pleasure Circuit Interrupted
An international research team, comprising scientists from China, the United States, and Switzerland, discovered a brain mechanism that may explain why individuals with obesity enjoy food less. The study, recently published in the journal Nature, observed that obese mice fed a high-fat diet displayed an alteration in the physiological circuit from the lateral nucleus accumbens, a brain region associated with reward, to the area responsible for processing motivation, known as the ventral tegmental area.
The key appears to be a decrease in neurotensin, a molecule that modulates signals between these brain regions. Despite preferring fatty foods in their cages, the overweight mice showed little interest in consuming them without effort, a behavior comparable to unlimited food access in modern human environments.
Interestingly, after resuming a regular diet for two weeks, the animals regained both neurotensin signaling and pleasurable food response, suggesting that the system might be reversible with potential therapeutic implications.
Food as Reward: Between Hunger and Pleasure
The new study’s findings align with a review published in Neuron about the neurobiology of overeating. This review described how food behavior is governed by two interconnected systems: the homeostatic system, which regulates hunger and satiety, and the hedonic system that favors consumption for pleasure. The latter is driven by a brain network releasing the neurotransmitter dopamine – highlighted in the Nature article’s circuit – that can encourage eating even when the body no longer needs energy.
The issue arises from chronic exposure to ultra-processed, high-fat, and high-sugar foods that can alter this system, generating a sort of “tolerance” to pleasure, similar to addictive drugs.
In humans, scientists have observed reduced availability of dopamine D2 receptors in individuals with excess body fat, which has been linked to decreased sensitivity to the pleasure of food. This phenomenon might explain why some obese individuals need to consume more or more intensely palatable foods to achieve the same level of satisfaction.
Neurotensin as a Therapeutic Target
On the other hand, a study by American researchers Katie D. Thompson and Gina M. Leinninger delves into the multifunctional role of neurotensin in the human body. This molecule, produced both in the central nervous system and peripheral tissues, can either increase or decrease appetite depending on its location and the type of receptor it binds to.
While promoting fat absorption in the intestine – which can favor weight gain – in the brain, neurotensin participates in regulating satiety and reward control. The loss of neurotensin signaling in obese individuals might be a key mechanism to understand the loss of food pleasure and maintenance of excess weight.
The significance of the Nature study lies in its proactive approach: by artificially restoring neurotensin expression in obese mice’s brains, researchers managed to restore their hedonic feeding behavior and moderate weight gain. This suggests that manipulating this pathway could be an effective strategy for treating certain types of obesity.
Food Without Pleasure: A Difficult Cycle to Break
Losing interest in food not only affects emotional well-being but also reinforces a vicious cycle: without satisfaction, more quantity or intense flavor is sought, leading to consuming more calories without resolving the pleasure deficit. This pattern contributes to obesity maintenance and can hinder adherence to healthy diets.
The reversibility of this phenomenon observed in animals offers hope, as it suggests that a dietary change can restore normal pleasure circuit functioning. However, this process might require time and appropriate conditions.
Current studies indicate that obesity is not merely a matter of willpower or personal choices but also a condition where the brain and body respond differently to food stimuli. Understanding the biological mechanisms that reduce pleasure can achieve two goals: reduce stigma and, simultaneously, design more effective interventions.
The future of obesity treatment may lie not only in controlling how much we eat but also in understanding and modifying what we feel when we put food in our mouths.
