What Does Serotonin Have to Do With Eating Disorders?

Serotonin is a chemical produced mostly in our digestive tract.¹ Despite its humble beginnings in the gut, serotonin has the important job of deciding which brain cells to "turn off" (inhibit) during cellular conversations.

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By controlling which cells can "speak" during cell conversations, serotonin can influence anything from how hungry we are, to how anxious we feel.

Simply put, serotonin can control the conversations our cells have about many important body functions.

Why Do People have Different Serotonin Levels?

Our bodies require certain amounts of serotonin to run optimally. However, not everyone's body produces the "optimal" amount of serotonin.

One reason people have different serotonin levels is our genes, which determine how much serotonin our bodies produce.²

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Genes are instruction manuals we inherit from our parents that tell our bodies what protein parts are needed for our bodies to run at their best.

For many people, the instruction manual for serotonin produces an efficient number of parts, making these people more resilient to certain disorders, such as depression.

Not everyone inherits the same serotonin instruction manual, though. Rather, some people's instruction manual tells their body to produce more (or less) serotonin-related proteins than necessary, or to create proteins that are misshapen.

These differences in protein production can lead to extreme serotonin increases or decreases, throwing off precise biological (e.g., digestion and stress) and psychological (e.g., anxiety) functions that keep us healthy.

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In addition to our genetics, our environments can also influence how much serotonin our bodies produce. Who we socialize with, what and how much we eat, and how much we sleep can all impact our serotonin levels, as can stress, exercise, age, and sunlight exposure.³

Serotonin and Binge Eating Disorders

While we know that serotonin plays a significant role in eating disorder (ED) development, exactly how remains unclear.

People who binge eat (e.g., binge eating disorder (BED) and bulimia nervosa (BN)) tend to have lower than average serotonin levels.⁴ This makes sense considering that several BED characteristics could be influenced by low serotonin.

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For example, low serotonin levels contribute to depression⁵, which is often co-diagnosed with BED.⁶ It has been found that people who binge eat experience heightened reward from eating⁷, meaning that eating could be one way they relieve depression.

Additionally, low serotonin has been associated with impulsivity and difficulties recognizing fullness⁸, both of which are typical in BED.⁷ One of serotonin’s primary jobs is to tell us when we’re full, and when serotonin levels are too low, the fullness cue becomes quiet. If the fullness cue is too quiet for some people, they might continue eating beyond what would otherwise satisfy them. This is especially true if they act on impulses to reduce depression (e.g., eating).

Serotonin and Food Restriction Disorders

The relationship between restrictive eating (e.g., anorexia nervosa (AN)) and serotonin is a little more confusing.

While some studies have found that people with AN have lower than average serotonin levels, other findings suggest that people with AN have higher than average serotonin levels, and that these unusually high levels are hidden by starvation.⁴ This is because during food restriction our serotonin levels drop.

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High serotonin levels can help explain several AN symptoms.

For example, high levels of serotonin are often associated with anxiety, particularly compulsions.⁹ Obsessive compulsive disorder (OCD) is the most common anxiety disorder in AN, with the two disorders having possible genetic overlap. Anxiety might motivate people with AN to compulsively engage in ED behaviors that reduce anxiety, such as food restriction.

Another AN symptom that high serotonin levels might contribute to is perfectionism.¹⁰ People with AN usually have perfectionistic personality traits, which, when coupled with anxiety and compulsiveness, could explain why these individuals engage in repeated, yet destructive, behaviors. Compulsively pursuing perfection might reduce their anxiety.

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Finally, high serotonin levels are associated with behavioral constraint, or the ability to prevent ourselves from doing something.¹¹ People with AN are often rigid and restrictive, which helps explain why these individuals are able to stick to strict “rules” they set for themselves, such as extreme calorie counting.

Serotonin and Lesser Known Eating Disorders

Unfortunately, we know very little about serotonin's role in avoidant restrictive food intake disorder (ARFID) and pica.

Nonetheless, pharmacology studies have shown that serotonin medications (e.g., SSRIs) reduce ARFID and pica symptoms, possibly by decreasing anxiety about meals and food, as well as compulsiveness.^{12; 13} More research is needed, though, to understand these effects.

The Challenges of Making Conclusions About Serotonin and Eating Disorders

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Despite the promise of these findings, it is too soon to make definitive conclusions about serotonin's role in EDs.

One reason for this is that we lack the technology to analyze specific molecular functions in people with EDs. Animal models of EDs can clarify some of these mysteries, but only to a certain extent. We need more precise technologies to fully understand the molecular aspects of EDs.

Additionally, because most research studies observe serotonin in people currently ill with or recovered from an ED, it is difficult to determine what serotonin levels were like before the ED developed. In other words, did atypical serotonin levels contribute to the development of the ED? Or did having the ED change the person's serotonin levels? Malnutrition and other side effects of an ED (e.g., cardiovascular problems) can also make studying serotonin difficult.

This shouldn't be discouraging, though. While we're still struggling to find the best ways to study serotonin in EDs, the limited evidence we do have has demonstrated that serotonin is likely one of the most important chemicals involved in ED development and its persistence. This alone can help guide future pharmacological treatments for EDs, making the future of ED treatment bright.