February 28th, 2023
Written by: Marissa Maroni
Trigger warning: sensitive content including eating disorders and early life trauma
With the Superbowl only a few weeks ago, you might have found yourself gathered around the television with an array of dips and appetizers to choose from. Maybe you found yourself sticking to that cheesy and warm buffalo chicken dip or maybe instead you took a sampling of each, noting their flavors. Whatever you decided, ultimately you were eating, a daily activity that everyone takes part in. Despite eating being a universal experience, approximately 9% of Americans struggle with eating disorders1 making this daily action a difficult task. One type of eating disorder that accounts for approximately 14% of cases (1.2% of Americans2) is binge eating disorder. Binge eating disorder is characterized by episodes of overeating often accompanied by a feeling of lack of control. Individuals with binge eating disorder often struggle with obesity as well.
Several research studies suggest that trauma puts people at risk of developing eating disorders3, however it is not known how trauma-altered brain signaling leads to disordered eating. In a recent study, researchers from the University of California San Diego began to uncover how trauma changes neuronal signaling and how these changes may underlie binge eating behavior4.
Modeling Binge Eating
To study this, researchers must model, or recreate, binge eating and early life trauma in mice. But why mice over humans? Mice provide scientists a small and genetically similar system that has a vast number of tools that can be used to better understand neuronal changes.
Early life trauma model: To study early life trauma in mice, scientists need to determine what experiences can induce trauma and stress at an early age. For young mice, being taken away from their mother is traumatic, so to model early life trauma the scientists removed three-day old mouse pups from their mother for a day. To confirm that the experience was actually traumatizing for the mice, they measured levels of a stress-related hormone, corticosterone. Levels of corticosterone increase when an animal is stressed. The scientists found that corticosterone levels increased when the pups were taken away from their mothers, confirming that the experience was stressful.
Binge eating model: Pleasant-tasting food is known to contribute to overeating. In a real-world scenario, this could look like a person who has only ever eaten white rice during their life being given a cookie for the first time. Then, after a couple of days, the person is put in a room with a box of cookies and, as one might be able to imagine, it could be tempting to eat as many cookies as possible before the cookies are taken away again (binge-like eating).
Scientist were able to imitate binge-like eating using a similar scenario in mice. First, the researchers introduced a pleasant-tasting high fat diet to mice who previously have only eaten a regular chow diet (like giving a human a cookie after only eating white rice). After the researchers gave the mice this delicious diet, the mice returned to eating their regular chow diet. When the researchers gave this delicious diet after a few days, the mice showed binge-like eating behavior.
Having established ways to imitate both early life trauma and binge-like eating, the scientists then combined them to examine whether trauma impacted disordered eating. Mice with early life trauma continued to have binge-like eating when given a high fight diet in comparison to mice without early life trauma, who overtime stopped binge-like eating. Thinking back to the real-world scenario, the mice with no early life trauma were like an individual that after getting access to a box of cookies a few times, began to lose the desire to consume them all. However, the mice who were taken from their mothers at an early age were like an individual that continued to eat all the cookies, even after being give them several times before. Altogether, the scientists learned that early life trauma can cause binge-like eating in their model mouse system.
What controls eating behavior? Is it impacted during early life stress?
The hypothalamus is a brain region located in the center of your brain that regulates hunger. The hypothalamus uses a hormone called leptin to influence you to eat less. Normally in the hypothalamus, leptin can bind to proteins designed to accept information, or receptors, which cause neurons in the hypothalamus to be less active or inhibited (figure 1). These less active leptin receptor neurons ultimately cause a decrease in food intake.
Given its important role in causing mice/humans to eat less the researchers reasoned that irregular activity of the hypothalamus and release of leptin could be contributing to the binge-like eating. The researchers found that when they removed leptin receptors in mice without early life trauma, they showed binge-like eating behavior similar to the mice who experience an early life trauma. In other words, getting rid of leptin receptors makes mice act like they experienced an early life trauma. This suggests that early life trauma might disrupt leptin release to produce the binge-like eating behaviors.
To put this idea to the test, researchers used calcium imaging, a genetic tool that causes neurons to light up when they are active (see video 1), to visualize the activity of neurons in mice. In early life trauma mice, neurons that have leptin receptors in the hypothalamus were more active during binge-like eating in comparison to mice without early life trauma. Increased activity in the leptin receptor neurons is opposite to how they normally reduce food intake (see figure 1) suggesting that this change in brain activity in the hypothalamus could be causing the binge-like eating.
Can changing neuronal signaling alleviate binge eating?
To bring this work together, scientists tested whether changing neuronal signaling in the hypothalamus in early life trauma mice can alter binge-like eating behavior. Researchers manipulated the leptin receptor neuron activity in the hypothalamus decreasing its activity. Excitingly, they found that by decreasing neuronal activity in early life trauma mice they alleviated binge-like eating!
Scientific discoveries always leave exciting new questions to investigate. Follow-up studies might ask questions like what kind of stressors are sufficient to cause binge-like eating? Are there drugs that could specifically target these neurons? Even though there’s a lot left to learn about what changes in the brain make people who experience early life trauma more likely to develop binge eating disorder, this research begins to illuminate how eating disorders are wired into the brain. Further, it illustrates how environmental stressors can make changes in brain signaling that make an individual more vulnerable to binge-eating.
References
- Deloitte Access Economics. (2020). The social and economic cost of eating disorders in the United States of America: A report for the strategic training initiative for the prevention of eating disorders and the academy for eating disorders. Strategic Training Initiative for the Prevention of Eating Disorders.
- Hudson, J. I., Hiripi, E., Pope Jr, H. G., & Kessler, R. C. (2007). The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biological psychiatry, 61(3), 348-358.
- Guillaume, S., Jaussent, I., Maïmoun, L., Ryst, A., Seneque, M., Villain, L., … & Courtet, P. (2016). Associations between adverse childhood experiences and clinical characteristics of eating disorders. Scientific reports, 6(1), 35761.
- Shin, S., You, I. J., Jeong, M., Bae, Y., Wang, X. Y., Cawley, M. L., … & Lim, B. K. (2022). Early adversity promotes binge-like eating habits by remodeling a leptin-responsive lateral hypothalamus–brainstem pathway. Nature Neuroscience, 1-13.
Figure created with BioRender.com.
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