Chronic Stress Disrupts Brain’s Satiety Signals in Mice, Driving Overeating—Human Relevance Unclear

Key Takeaways

  • Chronic stress in mice deactivates the lateral habenula, a brain region that regulates reward responses, leading to unchecked consumption of high-fat/sweet foods.
  • Chronically stressed mice on high-fat diets gained twice as much weight as non-stressed peers, driven by a lack of satiety signaling.
  •  While mice showed stress-induced cravings, human applicability remains unproven, necessitating further research on brain pathways and behaviors.

A recent mouse study investigated how chronic stress influences the brain’s regulation of food intake, leading to increased consumption of high-fat, sugary foods. While the findings offer insight into neural mechanisms, further research is required to determine if the same effects occur in humans. Conducted by researchers at the Garvan Institute of Medical Research in Sydney, Australia, the study was published in Neuron.

Obese Woman

Obese Woman

How Stress Fuels Cravings for Comfort Foods?

In this study, scientists initiated their experiments to understand the impact of chronic stress on eating behaviors in mice. They discovered the critical role of the lateral habenula, a brain area involved in the homeostatic regulation of the reward response in driving the eating behaviors of the mice.

In mice that experienced short-term stress, the lateral habenula remained active and switched off the reward response in the brain. The mice consumed high-fat foods but didn’t overeat. The lateral habenula activation led to a feeling of satiety in these mice. However, in chronically stressed mice, this area of the brain (lateral habenula) didn’t get activated. The mice didn’t develop a feeling of satiety and consumed more high-fat foods in the absence of reward response regulation. Consequently, the stressed mice on a high-fat diet gained twice the weight compared to mice that were not chronically stressed.

Sucralose preference test

Scientists took the next step of analyzing if chronic stress leads to increased consumption of sweet, palatable foods. They provided the mice with water and sweetened water. Stressed mice that were consuming high-fat foods drank the artificially sweetened water three times more than the mice that were consuming high-fat foods but were not stressed. The researchers also observed that mice that were stressed but were on a regular diet didn’t exhibit this preference for sweetened drinks.

What did the study reveal?

Scientists observed that in mice chronic stress disrupted the brain’s reward regulation, leading to overeating. While this study helps explain potential mechanisms, further research is needed to see if human brains respond similarly. In humans, stress is also linked to cravings for high-fat, sugary foods, but the reasons are not fully understood. It is suggested that cortisol, the body’s main stress hormone, may increase cravings for calorie-dense foods, though its connection to the lateral habenula remains unclear.

Research on human eating behaviors aligns with these findings. The comfort food theory suggests that during times of stress, people gravitate toward high-fat, high-sugar foods because they provide temporary emotional relief. Studies show that stress-induced cravings activate the brain’s reward system, much like in the mice study. However, in humans, emotional and cultural factors also play a role. Comfort foods trigger dopamine release, briefly reducing stress, but unlike mice, human eating habits are shaped by emotions and culture. This may explain why stressed individuals tend to seek out foods like ice cream, fast food, and sweets even when not physically hungry.

Limitations of this study

Mentioning the limitations of this study, the scientists emphasized that this study was done in mice so its results may not be generalizable to humans. They also encouraged further research to explore the role of other brain areas that are involved in these mechanisms.

Significance

Chronic stress is already linked to emotional eating and weight gain in humans. This study provides new insights into possible brain mechanisms behind this effect. However, further research is needed to determine whether the same pathways function the same way in people. It provides insights into how a brain region and specific molecules drive these changes. Moreover, it highlights how the reward regulatory mechanisms remain unactivated during chronic stress to enhance the unchecked consumption of fatty and sweet foods. In addition, this study sheds light on the possible prevention strategies to alleviate adverse events associated with chronic stress. These strategies can help prevent weight gain, metabolic diseases, and cardiac and endocrine diseases. Managing stress with exercise, mindfulness, or balanced meals may help reduce emotional eating and prevent weight gain. By learning about the mechanisms learned through this study, many people can manage their stress better and keep their mental health and the associated adverse behaviors in check.

FAQs

How does chronic stress lead to overeating in mice?
Chronic stress silences the lateral habenula, disabling the brain’s ability to signal fullness. This caused stressed mice to overeat high-fat/sweet foods despite caloric needs.

Do these findings apply to humans?
A: Not directly. While stress is linked to emotional eating in humans, mouse brain pathways may differ. Studies on human habenula function are needed.

What practical steps can people take now?
Manage stress through mindfulness, exercise, or therapy to reduce emotional eating risks. Avoid keeping hyper-palatable foods accessible during high-stress periods.

Related Reading:

Obesity: A Deficiency of the CRTC1 Gene Can Lead to Cravings for Fatty and Sweet Foods

Tackling the Underlying Factors of Non-Communicable Diseases: The Weight of Chronic Illness

Coffee Reduces the Risk of Developing Non-alcoholic Fatty Liver Disease in Obese Diabetics

Bottom Line: Real-World Implications

This study clarifies how chronic stress hijacks brain circuits in mice to promote overeating, but is this actionable for humans? While compelling, critical gaps remain:

  • Feasibility: Can human lateral habenula manipulation reduce stress eating? Current tools (e.g., deep brain stimulation) are invasive and unproven for this purpose.
  • Complexity: Human eating behaviors involve social, psychological, and genetic factors absent in mice.
  • Prevention Strategies: Stress management and dietary mindfulness are safer bets until human-specific mechanisms are mapped.

These findings provide insight, but applying them to human behavior requires more research.

References

Ip, C. K., Rezitis, J., Qi, Y., Bajaj, N., Koller, J., Farzi, A., Shi, Y., Tasan, R., Zhang, L., & Herzog, H. (2023). Critical role of lateral habenula circuits in the control of stress-induced palatable food consumption. Neuron. https://doi.org/10.1016/j.neuron.2023.05.010

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