Gut Microbiota Regulates the Diet-Anxiety Relationship

• A new conceptual paper published in Frontiers in Nutrition examined the relationship between gut microbiota, diet, and anxiety
• It suggests that gut microbiota mediate the relationship between dietary intake and anxiety
• The paper also critically examined research methodologies employed in the nutritional field to investigate the interactions between diet and anxiety

Many of us have experienced situations where we’re under stress and feel some kind of strong negative emotions. We roam around thinking about what we can do about these intense emotions. Then, we might decide to eat something. Or, after experiencing stress about some aspect of our relationship with others or something we can’t resolve, we may suddenly feel the need to eat. This is called stress-induced eating. It’s an example of emotional eating, a behavior where we eat not because our body needs nutrients but because food intake would make us feel better (Konttinen, 2020; Zeeck et al., 2011).

Stress-induced eating involves eating not because our body needs nutrients but because eating makes us feel better emotionally.

 

What is anxiety?

Anxiety is an emotion we experience when we anticipate danger, but that danger has not yet materialized. In such a situation, we experience a sense of uncertainty as we prepare for what might happen, even if the threat is not immediate or we aren’t even sure what the nature of the threat might be. Sometimes, the threat might not even (objectively) exist.  As such, anxiety is different from fear, the emotion we experience when we are faced with a clearly identified threat (Perkins et al., 2007).

The term anxiety is also used to describe a personality trait, one that makes an individual prone to experiencing anxiety. The author of the famous Reinforcement Sensitivity Theory of Personality, Jeffrey Gray, described this trait of anxiety as representing sensitivity to punishment (Pickering et al., 1995), characterizing individuals who react strongly to signals indicating that they might be punished (punishment sensitivity). The opposite pole of this trait is occupied by individuals whose reactions are stronger to signals indicating that they might receive a reward (reward sensitivity).

The term anxiety is also used to describe a personality trait, one that makes an individual prone to experiencing anxiety.

 

There are also clinical conditions related to experiencing anxiety called anxiety disorders. These are mental health conditions characterized by excessive and persistent feelings of worry and anxiety that are disproportionate to the actual situation and interfere with daily functioning. There are various types of anxiety disorders, including generalized anxiety disorder, panic disorder, and different phobias, each with distinct symptoms and triggers.

Anxiety disorders are one of the most prevalent types of mental health disorders, affecting up to 34% of the population. Females are affected twice as often as men. The prevalence of anxiety disorders seems to have markedly increased during the 2021-2022 COVID-19 pandemic (Basso et al., 2024)

Anxiety disorders are one of the most prevalent types of mental health disorders, affecting up to 34% of the population.

 

The current study

Having in mind this very high prevalence of anxiety disorders, study author Melissa Basso and her colleagues wanted to help integrate the available evidence between anxiety and diet (Basso et al., 2024). Several previous studies explored the associations between dietary intake and anxiety. These authors compiled a list of 50 such studies. The studies in the list explored the association between anxiety and specific nutrients, foods, dietary patterns, and dietary quality indices, very often reporting that specific aspects of dietary intake are associated with anxiety.

The enteric nervous system (ENS) is the part of the autonomic nervous system that governs the activities of the gastrointestinal tract independently
of the brain and the spinal cord.

 

Diet, anxiety, and gut microbiota

Study authors note that there is a cyclical feedback loop between emotions, including anxiety, and behavioral responses that can be reinforced by dietary content. On the one hand, food components can act on the brain and mental health by modulating brain chemistry.

There is a cyclical feedback loop between emotions, including anxiety, and behavioral responses that can be reinforced by dietary content.

 

This can also happen through various mechanisms that depend on the activity of the gut microbiome. These include the modulation of the autonomic and enteric nervous system (the part of the autonomic nervous system that governs the activities of the gastrointestinal tract independently of the brain and the spinal cord), the modulation of the mechanism that controls the release of hormones by gut cells (enteroendocrine signaling) and the one controlling the stress response (the hypothalamic-pituitary-adrenal (HPA) axis signaling). Potential mechanisms also include changes in the production of bacterial by-products, such as short-chain fatty acids, systemic and low-grade inflammation, and damage to the intestinal mucosal barrier, which would, in turn, change the composition of the gut microbiota (see Figure 1).

Figure 1. Mechanisms of the diet-anxiety relationship

Short-chain fatty acids produced by gut bacteria are particularly important as they promote the integrity of the intestinal barrier and support the health of the gut lining cells. However, these molecules also influence the activity of immune cells, reducing systemic inflammation. They can affect glucose metabolism and even impact the production of neurotransmitters in the brain.

Short-chain fatty acids influence the activity of immune cells, reducing systemic inflammation. They can affect glucose metabolism and even
impact the production of neurotransmitters in the brain.

 

On the other hand, anxiety promotes unhealthy eating habits through stimulating emotional eating behavior. While engaged in emotional eating, individuals tend to choose unhealthy products, often rich in sugars, trans-fatty acids, and various additives.

High sugar intake, in turn, activates a system in the brain involved in reward processing, motivation, and emotion regulation (the mesocorticolimbic system) in a way that is similar to what happens in substance abuse/addiction. In this way, high sugar consumption creates changes in brain function that alter emotional states (Jacques et al., 2019) (see Figure 2).

Figure 2. High sugar intake and emotional states

Trans-fatty acids (also known as artificial trans fats or industrial trans fats) contribute to low-grade chronic inflammation and gut flora alteration, changes found to increase anxiety in rats.

High sugar intake activates a system in the brain involved in reward processing, motivation, and emotion regulation in a way that is similar
to what happens in substance abuse and addiction.

 

Furthermore, stress, which accompanies anxiety, can cause alterations to the gut microbiome composition but also act on the integrity of the blood-brain barrier and the intestinal barrier, making it easier for molecules produced by gut microbiota to reach and affect the brain. All these mechanisms can create a feedback loop that maintains both increased anxiety and unhealthy dietary patterns associated with it, making treatment of anxiety difficult.

These authors also note that studies indicate that the intake of certain bacterial cultures in probiotics might affect anxiety, but the studies still yield mixed results.

 

Conclusion

Overall, reviewing the existing evidence, the authors of this paper argue that gut microbiota mediates the link between diet and anxiety in both directions. They propose a new theoretical model of this relationship listing different mechanisms through which diet-gut microbiota-anxiety influences are achieved.

Gut microbiota mediates the link between diet and anxiety in both directions.

 

Studies of the interactions between diet, gut microbiota, and the brain are still in their infancy. Still, they do hold promise that a new avenue for treating anxiety and other mental health disorders by influencing gut microbiota might open in the future. This is a very positive development given the less-than-perfect record of existing treatments.

Learn more about the relationship between the microbiome and psychology in CNP’s Continuing Education courses.

The paper “Diet quality and anxiety: a critical overview with focus on the gut microbiome” was authored by Melissa Basso, Irene Zorzan, Nicola Johnstone, Matteo Barberis, and Kathrin Cohen Kadosh.

 

References

Basso, M., Zorzan, I., Johnstone, N., Barberis, M., & Cohen Kadosh, K. (2024). Diet quality and anxiety: A critical overview with focus on the gut microbiome. Frontiers in Nutrition, 11, 1346483. https://doi.org/10.3389/fnut.2024.1346483

Jacques, A., Chaaya, N., Beecher, K., Ali, S. A., Belmer, A., & Bartlett, S. (2019). The impact of sugar consumption on stress driven, emotional and addictive behaviors. Neuroscience & Biobehavioral Reviews, 103, 178–199. https://doi.org/10.1016/j.neubiorev.2019.05.021

Konttinen, H. (2020). Emotional eating and obesity in adults: The role of depression, sleep and genes. Proceedings of the Nutrition Society, 79(3), 283–289. https://doi.org/10.1017/S0029665120000166

Perkins, A. M., Kemp, S. E., & Corr, P. J. (2007). Fear and anxiety as separable emotions: An investigation of the revised reinforcement sensitivity theory of personality. Emotion, 7(2), 252–261. https://doi.org/10.1037/1528-3542.7.2.252

Pickering, A. D., Díaz, A., & Gray, J. A. (1995). Personality and reinforcement: An exploration using a maze-learning task. Personality and Individual Differences, 18(4), 541–558. https://doi.org/10.1016/0191-8869(94)00182-R

The Center for Nutritional Psychology. (2024). Encyclopedia of Nutritional Psychology. https://www.nutritional-psychology.org/encyclopedia/anxiety/

Zeeck, A., Stelzer, N., Linster, H. W., Joos, A., & Hartmann, A. (2011). Emotion and eating in binge eating disorder and obesity. European Eating Disorders Review, 19(5), 426–437. https://doi.org/10.1002/erv.1066