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Review
. 2019 Jul 1:206:185-190.
doi: 10.1016/j.physbeh.2019.04.007. Epub 2019 Apr 10.

Motivation to eat and not to eat - The psycho-biological conflict in anorexia nervosa

Guido K W Frank  1 , Marisa C DeGuzman  2 , Megan E Shott  3
Affiliations
Review

Motivation to eat and not to eat - The psycho-biological conflict in anorexia nervosa

Guido K W Frank et al. Physiol Behav. .

Abstract

Anorexia nervosa is a severe psychiatric illness with high mortality. Brain imaging research has indicated altered reward circuits in the disorder. Here we propose a disease model for anorexia nervosa, supported by recent studies, that integrates psychological and biological factors. In that model, we propose that there is a conflict between the conscious motivation to restrict food, and a body-homeostasis driven motivation to approach food in response to weight loss. These opposing motivations trigger anxiety, which maintains the vicious cycle of ongoing energy restriction and weight loss.

Keywords: Anorexia nervosa; Anxiety; Brain; Conflict; Motivation.

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Figures

Figure 1.
Figure 1.
Previous studies have shown that prediction error brain response (PE) was positively correlated with harm avoidance as a measure for anxious temperament in adolescents with anorexia nervosa (AN), which correlated positively with core AN behaviors drive food thinness and body dissatisfaction, but negatively with weight gain in treatment; PE was also positively related to the dynamic effective connectivity from ventral striatum to hypothalamus (adapted from Frank et al., JAMA Psychiatry, 2018); OFC, orbitofrontal cortex.
Figure 2.
Figure 2.
A schematic model that integrates the empiric findings from Figure 1. with previous research on neuroendocrine function in human studies and animal models for the effects of food restriction. After deciding to change eating behavior and lose weight, endocrine changes occur that signal the need to eat; the dopamine system gets activated to support the motivation to seek out food; perfectionism and high anxiety mediate the transition to developing AN core behaviors while the original conscious motivation is sustained. Weight loss briefly alleviates anxiety and reinforces food restriction. However, gut hormones and dopamine that stimulate food seeking, elevate anxiety and subsequently elevate AN core behaviors. Anxiety triggers a food-control circuitry from ventral striatum to hypothalamus that depends on dopamine D1 receptors, which have been sensitized in the context of food restriction. Anxiety gets further elevated in the illness process due to the possibility of loss of control and weight gain, and this becomes a self-reinforcing process. Ongoing food restriction and weight loss perpetuate the cycle.
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References

    1. Golden NH Eating disorders in adolescence and their sequelae. Best Pract. Res. Clin. Obstet. Gynaecol 2003,17:57–73. - PubMed
    1. Arcelus J, Mitchell AJ, Wales J, Nielsen S Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Arch. Gen. Psychiatry 2011,68:724–31. - PubMed
    1. Sullivan PF Mortality in anorexia nervosa. Am. J. Psychiatry 1995,152:1073–4. - PubMed
    1. American Psychiatric Association. Desk reference to the diagnostic criteria from DSM-5. Washington, DC: American Psychiatric Publishing; 2013.
    1. Bulik CM Exploring the gene-environment nexus in eating disorders. J. Psychiatry Neurosci 2005,30:335–9. - PMC - PubMed

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