A Vicious Cycle Between Memory and Food Intake Regulation Likely Maintains Obesity

• A paper published in Neuroscience and Biobehavioral Reviews shows that humans have a bidirectional relationship between memory and eating
• Memory of recent meals limits subsequent food intake, and this memory is impaired in obese individuals
• Excessive food intake likely disrupts the functioning of the part of the hippocampus that plays a role in food-related memory, forming a vicious cycle that promotes further increased food intake

Many factors influence our decisions about when and what to eat. To a degree, these decisions depend on our subjective feelings of hunger and fullness. Still, they also depend on whether food is available and what kind, our eating habits, desires and plans, food cues, and many other things.

One often overlooked but also important factor is the memory of recent meals. In the most basic scenario, if we remember that we just had lunch, we will not have it again. However, these decisions are part of a complex behavioral pattern regulating our food intake behaviors.

How do we regulate food intake?

Scientists believe that our food intake behaviors are primarily regulated by the activities of neurons located in the hypothalamus region of the brain. For example, studies on rodents identified a set of neurons called agouti-related protein neurons that, when artificially triggered, make a rodent start eating (Hedrih, 2024; Sternson & Atasoy, 2014). These neurons are part of a complex system that involves hormones like leptin and ghrelin and various neural pathways that react to the presence or absence of nutrients in our body.

Our food intake decisions do not depend solely on the presence or absence of specific nutrients. Most individuals living in organized societies with sufficient food availability have established habits of having meals at specific times of day. Studies indicate that our bodies anticipate those times and prepare for food intake, e.g., by modifying glucose levels in the blood (Isherwood et al., 2023). We also tend to feel hungry when our usual meal time arrives (see Figure 1). For example, food anticipation can trigger a preparatory response in the body, leading to a mild increase in glucose levels as the brain signals the pancreas to release insulin. This response helps the body manage the expected influx of nutrients from the upcoming meal (Teff, 2011).

 

Figure 1. Body changes in anticipation and preparation of food intake 

 

Often, we can develop a desire to eat if we see, smell, or taste delicious food. Sometimes, even thinking about food can make us want to eat it. In scientific terms – food cues can motivate us to eat (Hedrih, 2023). People also tend to eat when they feel bad. This is called emotional eating (Dakanalis et al., 2023; Ljubičić et al., 2023).

 

We can develop a desire to eat if we see, smell, or taste delicious food

 

Memory and food intake regulation

One of the factors important for regulating food intake is memory. Classic studies of patients with amnesia revealed that their memory dysfunction also affects appetite (Parent et al., 2022). In simple words, individuals who are unable to remember whether they had their regular meal or not might decide to have it again.

More recent studies indicate that impaired memory might play a role in the development of obesity and that specific diets known to lead to obesity also tend to produce memory impairments (Hayes et al., 2024; Hsu et al., 2015).

 

One of the most important factors for regulating food intake is memory

The current review

Marise B. Parent and her colleagues reviewed a series of studies on humans and rodents examining the links between memory and eating behaviors (Parent et al., 2022). They aimed to demonstrate a bidirectional relationship between memory functions and eating behaviors. Bidirectional, in this case, means that memory affects eating behaviors and that eating habits affect memory.

Disrupted memory and food intake

They start by reiterating the findings of classic case studies of patients with amnesia. For example, in the 1980s, a group of researchers conducted an experiment on a patient, H.M., who suffered from memory loss after undergoing brain surgery to treat epilepsy. This patient hardly ever mentioned being hungry or thirsty, even after not eating or drinking anything for quite some time. At one point, researchers offered him a meal 1 minute after he had just eaten and forgotten the previous meal. He readily accepted it and ate it. Twenty minutes after this, he could not remember having eaten anything.

However, this one patient might have been specific. His hunger ratings did not seem to depend on whether he had just eaten. In studies by these same researchers, 3 out of 4 patients with similar amnesia would report lower hunger levels after a meal. On the other hand, a different experiment a decade later reported about a patient with amnesia who would refuse an additional meal only after eating two 3-course meals one after another. Other researchers reported similar findings in later years, indicating that this link between memory of the previous meal and eating might be a somewhat general occurrence.

Studies in the 21st century tested the link between memory and food intake by diverting participants’ attention from the meal with a secondary activity while eating (e.g., playing games or watching TV) in the hope that this will prevent them from memorizing the food eaten. Results showed that after eating while being distracted, participants tended to take more snacks in a later test. On the other hand, studies that had participants focus on the food they eat showed that they take less food later (see Figure 2).

 

Figure 2. Distracted eating vs. focused eating

 

Studies on rodents showed that a group of neurons in the brain’s hippocampus region (dorsal hippocampal glutamatergic neurons) likely mediates the ability of memories about previous meals to stop later intake. Their activity immediately after a meal seems to be critical for this.

Obesity is associated with impaired memory

The authors of this review note that many studies in both rodents and humans report specific aspects of cognition to be impaired in obese individuals. This is particularly the case with certain memory functions. This association is present even in young, otherwise healthy adults. The authors also cite research findings that link obesity with changes in areas of the brain known to play a role in memory processes. There is also a finding that obese individuals tend to have lower global brain volume.

Looking at possible mechanisms through which obesity might lead to changes in the brain and memory impairments, the authors of this review propose that these might be inflammation of the brain and insulin resistance.

Conclusion – the vicious cycle

Based on all the findings, the authors of this review propose that there is a vicious cycle between memory and obesity. Obesity likely leads to memory and other cognitive impairments by stimulating inflammatory processes in the brain and insulin resistance. On the other hand, impaired memory disrupts the food intake regulation mechanism, leading to increased food intake, maintaining or even exacerbating obesity (see Figure 3).

 

Figure 3. Memory-obesity vicious cycle

 

Because of this, future research and obesity prevention programs need to be aware of this bidirectional relationship and devise ways to break the vicious cycle if they are to prevent or treat obesity successfully.

The paper “Memory and eating: A bidirectional relationship implicated in obesity” was authored by Marise B. Parent, Suzanne Higgs, Lucy G. Cheke, and Scott E. Kanoski.

 

References

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Hayes, A. M. R., Lauer, L. T., Kao, A. E., Sun, S., Klug, M. E., Tsan, L., Rea, J. J., Subramanian, K. S., Gu, C., Tanios, N., Ahuja, A., Donohue, K. N., Décarie-Spain, L., Fodor, A. A., & Kanoski, S. E. (2024). Western diet consumption impairs memory function via dysregulated hippocampus acetylcholine signaling. Brain, Behavior, and Immunity, 118, 408–422. https://doi.org/10.1016/j.bbi.2024.03.015

Hedrih, V. (2023). Are Hunger Cues Learned in Childhood? CNP Articles. https://www.nutritional-psychology.org/are-hunger-cues-learned-in-childhood/

Hedrih, V. (2024, March 4). Researchers Identify Neural Pathways Transmitting Anti-Inflammatory Effects of Hunger. CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/researchers-identify-neural-pathways-transmitting-anti-inflammatory-effects-of-hunger/

Hsu, T. M., Konanur, V. R., Taing, L., Usui, R., Kayser, B. D., Goran, M. I., & Kanoski, S. E. (2015). Effects of sucrose and high fructose corn syrup consumption on spatial memory function and hippocampal neuroinflammation in adolescent rats. Hippocampus, 25(2), Article 2. https://doi.org/10.1002/hipo.22368

Isherwood, C. M., van der Veen, D. R., Hassanin, H., Skene, D. J., & Johnston, J. D. (2023). Human glucose rhythms and subjective hunger anticipate meal timing. Current Biology, 33(7), Article 7. https://doi.org/10.1016/j.cub.2023.02.005

Ljubičić, M., Matek Sarić, M., Klarin, I., Rumbak, I., Colić Barić, I., Ranilović, J., Dželalija, B., Sarić, A., Nakić, D., Djekic, I., Korzeniowska, M., Bartkiene, E., Papageorgiou, M., Tarcea, M., Černelič-Bizjak, M., Klava, D., Szűcs, V., Vittadini, E., Bolhuis, D., & Guiné, R. P. F. (2023). Emotions and Food Consumption: Emotional Eating Behavior in a European Population. Foods, 12(4), Article 4. https://doi.org/10.3390/foods12040872

Parent, M. B., Higgs, S., Cheke, L. G., & Kanoski, S. E. (2022). Memory and eating: A bidirectional relationship implicated in obesity. Neuroscience & Biobehavioral Reviews, 132, 110–129. https://doi.org/10.1016/j.neubiorev.2021.10.051

Sternson, S. M., & Atasoy, D. (2014). Agouti-related protein neuron circuits that regulate appetite. Neuroendocrinology, 100, 95–102. https://doi.org/10.1159/000369072

Teff, K. L. (2011). How neural mediation of anticipatory and compensatory insulin release helps us tolerate food. Physiology & Behavior, 103(1), 44. https://doi.org/10.1016/j.physbeh.2011.01.012