Bulimia nervosa (BN) is a serious and complex disorder, marked by significant over-eating and actions to rid the body of food or perceived weight gain. As a result, BN can have many health and psychological consequences. It affects 2-4% of adolescents and adults, with about 90% of patients being female. Researchers are now looking at chemicals created in the brain, known as neurotransmitters, to better understand bulimia and neurotransmitters and how to more effectively treat BN.
A Cycle of Binging and Purging
Bulimia is characterized by episodes of binging and purging. Binge episodes are described as eating a larger amount of food than what is typical given similar time periods and circumstances. Binge eating episodes are characterized by feeling out of control when eating and not stopping when full.
Often, immediately after binge episodes, patients feel disgust, shame, and guilt. In response to those feelings, they purge or try to remove the effects of binge eating. Purging behaviors include:
- Self-induced vomiting
- Restricting food
- Taking laxatives or diuretics
There are often psychiatric comorbidities present in BN as well, including mood disorders and substance abuse.1
The Causes of Bulimia Nervosa
Bulimia nervosa is a complex disorder with likely many causes, including genetic and environmental factors. The nervosa part of its name refers to faulty thinking that is part of the disorder. Patients with BN put undue emphasis on their body shape and size, seeing it as determining self-worth. They often have a distorted body image and deal with stressors through eating disorder behaviors.
Researchers have been looking at changes in neurotransmitters in the brains of people with BN. Neurotransmitters are pockets of chemicals that are released between two brain cells to help them communicate with each other.
The Role of Serotonin
Serotonin, a neurotransmitter thought to play a key role in mood, feeding, and impulse regulation, may influence BN. Medicines known as serotonin reuptake inhibitors increase the amount of serotonin available in the brain. One such medicine, fluoxetine, is FDA-approved to treat BN. It has been shown to decrease the frequency of binging and purging episodes.
The clinical efficacy of fluoxetine for BN led researchers to study the role of serotonin in BN. In one study, researchers matched 15 women with BN who were normal weight with 14 women without BN. A drug was administered to increase serotonin in the brain. The study results showed:
- Women with BN, when compared to healthy women, had a much smaller increase in serotonin
- The frequency of binge episodes in the 4 weeks prior to the study was inversely related to the amount of serotonin released
- This supported the hypothesis that serotonin may be lower in patients with BN.2
The Role of Tryptophan Depletion
Tryptophan is the amino acid that is the building block for serotonin. A double-blind crossover study related to tryptophan depletion and BN compared a group of 10 women who were in recovery from BN and 12 healthy women with no past history of BN. Researchers gave the women an amino acid mixture that did not contain tryptophan as well as a mixture that was balanced containing tryptophan. Both mixtures were given to all participants at different times.
When the women with a history of BN took the mixture without tryptophan, they experienced:
- Lowered mood
- Increased body image difficulties
- A feeling of loss of control when eating
Although this study was small, it demonstrated the possibility that diminished serotonin may contribute to the cognitive and mood disturbances associated with BN. This provides a mechanism of action to explain how dieting, which could deplete tryptophan and thus lower serotonin, could lead to the development of eating disorders in predisposed individuals.3
The Role of Other Neurotransmitters
Researchers have also looked at other neurotransmitters that could be involved in BN, including dopamine and norepinephrine. Both of these neurotransmitters are known to be associated with other psychiatric conditions.
It is often difficult to directly measure levels of neurotransmitters, so researchers look at the metabolite products of neurotransmitters in the spinal fluid for easier access. One small study looked at the levels of metabolites from dopamine, serotonin, and norepinephrine in 11 women with BN and 17 healthy controls. The results found that the women with BN had significantly lower spinal cord concentrations of the metabolites.
One hypothesis about the relationship to BN was that low serotonin levels in the brain may contribute to decreased satiety, or feeling full, and low levels of dopamine in the brain may contribute to abnormal pleasurable responses to food.4
There are likely many causes of BN, but investigating neurotransmitters appears promising. While the above studies are small, they indicate that abnormalities in neurotransmitters may contribute to developing and maintaining BN. More studies should be conducted.
About the author:
Nicole Garber, M.D., is Chief of Pediatric and Adolescent Eating Disorders at Rosewood Centers for Eating Disorders. Dr. Nicole Garber is one of the few pediatric and adolescent eating disorders experts who is also a Board Certified Psychiatrist and a Board Certified Child and Adolescent Psychiatrist. Because of this dual board certification, Dr. Nicole Garber provides a comprehensive developmental perspective that enhances her work with patients of all ages.
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders Fifth Edition. 2015. 345-350.
- Jimerson, D., Wolfe, B., Metzger, E., Finkelstein, D., Cooper, .T, &Levine J. (1997). “Decreased Serotonin Function in Bulimia Nervosa. Arch of Gen Psych. 54(6), 529-534.
- Smith, K., Fairburn, C., &Cowen P. (1999). Symptomatic Relapse in Bulimia Nervosa Following Acute Tryptophan Depletion. JAMA Psychiatry. 56(2), 171-176.
- Jimerson, D., Lesem, M., Kaye, W., & Brewerton T. (1992). Low Serotonin and Dopamine Metabolite Concentrations in Cerebrospinal Fluid from Bulimic Patients with Frequent Binge Episodes. Arch Gen Psychiatry. 49(2). 132-138.
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Last Updated & Reviewed By: Jacquelyn Ekern, MS, LPC on August 28, 2015. Published on EatingDisorderHope.com