B.E.D. is the most common eating disorder among United States adults,*1 more prevalent than anorexia nervosa and bulimia nervosa combined.*1,2 The exact cause of B.E.D. is unknown, but several theories suggest a neurobiological basis, with genetic and environmental influencers. Learn more about the possible causes of B.E.D. in this educational video.

*Estimated 12-month and lifetime prevalence among an eating disorder-assessed subsample (n=2,980) of the National Comorbidity Survey Replication, a nationally representative face-to-face household survey of English-speaking adults aged ≥18 years.

While the exact cause of binge eating disorder (B.E.D.) is unknown,

Research suggests B.E.D. may have a neurobiological basis
with genetic and environmental risk factors

Prevailing theories that may support a neurobiological basis for B.E.D.:

Reward center and impulsivity
dysregulation theory3-7

Adults with B.E.D. have shown reduced activity in impulse
control–related regions of the brain3

Neurotransmitter dysregulation theory7-10

Dopamine signaling converts sensory stimuli into processes that may generate or enhance “wanting” of a particular food8,11,12

Endogenous µ-opioid signaling
dysfunction theory7,8,13,14

  • μ-Opioid receptor polymorphisms are more often found
    in adults with B.E.D.8
  • Opioid receptor involvement in reward processing has been
    demonstrated primarily from animal studies13,14

Research suggests risk factors for B.E.D. may include:

Genetic influences7,8,15,16

  • B.E.D. appears to run in families, which may reflect additive
    genetic influences15
  • Genetic differences in neurobiological components of the
    brain's reward center have been observed8,16

Environmental and social influences17,18

  • In a case-controlled retrospective assessment of 162 women with B.E.D., stressful life events were reported more frequently in the year preceding B.E.D. onset than in non-B.E.D. controls17
  • In a nationally representative survey of 5,702 adults, of the men (n=30) and women (n=75) who reported having B.E.D., 98% and 90%, respectively, reported experiencing some form of trauma*18

*Exposure to events such as combat, life-threatening
accidents, a major disaster, or physical or sexual assault.18

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  2. Kessler RD, Berglund PA, Chiu WT, et al. The prevalence and correlates of binge eating disorder in the world health organization world mental health surveys. Biol Psychiatry. 2013;73(9):904-914.
  3. Balodis IM, Molina ND, Kober H, et al. Obesity (Silver Spring). 2013;21(2):367-377.
  4. Schäfer A, Vaitl D, Schienle A. Neuroimage. 2010;50(2):639-643.
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  9. Wang GJ, Geliebter A, Volkow ND, et al. Obesity (Silver Spring). 2011;19(8):1601-1608.
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  12. Wyvell CL, Berridge KC. J Neurosci. 2000;20(21):8122-8130.
  13. Naleid AM, Grace MK, Chimukangara M, Billington CJ, Levine AS. Am J Physiol Regul Integr Comp Physiol. 2007;293(1):R99-R105.
  14. Boggiano MM, Chandler PC, Viana JB, Oswald KD, Maldonado CR, Wauford PK. Behav Neurosci. 2005;119(5):1207-1214.
  15. American Psychiatric Association. Binge-eating disorder. In: Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013:350-353.
  16. Davis C, Levitan RD, Yilmaz Z, Kaplan AS, Carter JC, Kennedy JL. Prog Neuropsychopharmacol Biol Psychiatry. 2012;38(2):328-335.
  17. Pike KM, Wilfley D, Hilbert A, Fairburn CG, Dohm FA, Striegel-Moore RH. Psychiatry Res. 2006;142(1):19-29.
  18. Mitchell KS, Mazzeo SE, Schlesinger MR, Brewerton TD, Smith BN. Int J Eat Disord. 2012;45(3):307-315.