Advances in the neurobiology of eating disorders

Elburg, Annemarie van; Treasure, Janet

doi:10.1097/yco.0b013e328365a2e7

Cited by 18 publications

(8 citation statements)

References 65 publications

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“…Many of the observed neurocognitive deficits implicated in EDs occur in the area of executive function (EF; Kanakam & Treasure, 2013; van Elburg & Treasure, 2013; Van den Eynde et al, 2011). EF is an umbrella term that refers to a set of neuropsychological processes (primarily centered in prefrontal regions) that govern higher-level, goal-directed behavior (Miyake et al, 2000).…”

Section: Neurocognitive Deficits In Eating Disordersmentioning

confidence: 99%

Could training executive function improve treatment outcomes for eating disorders?

et al. 2015

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Current gold standard treatments for eating disorders (EDs) lack satisfactory efficacy, and traditional psychological treatments do not directly address executive functioning deficits underpinning ED pathology. The goal of this paper is to explore the potential for enhancing ED treatment outcomes by improving executive functioning deficits that have been demonstrated to underlie eating pathology. To achieve our objective, we (1) review existing evidence for executive functioning deficits that underpin EDs and consider the extent to which these deficits could be targeted in neurocognitive training programs, (2) present the evidence for the one ED neurocognitive training program well-studied to date (Cognitive Remediation Therapy), (3) discuss the utility of neurocognitive training programs that have been developed for other psychiatric disorders with similar deficits, and (4) provide suggestions for the future development and research of neurocognitive training programs for EDs. Despite the fact that the body of empirical work on neurocognitive training programs for eating disorders is very small, we conclude that their potential is high given the combined evidence for the role of deficits in executive functioning in EDs, the initial promise of Cognitive Remediation Training, and the success in treating related conditions with neurocognitive training. Based on the evidence to date, it appears that the development and empirical evaluation of neurocognitive training programs for EDs is warranted.

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Section: Neurocognitive Deficits In Eating Disordersmentioning

confidence: 99%

Could training executive function improve treatment outcomes for eating disorders?

et al. 2015

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“…Anorexia nervosa (AN), bulimia nervosa (BN) and binge-eating disorder (BED) are the main forms of eating disorders (EDs) with a combined prevalence of up to 5% of women and 2% of men. 1 Although significant advances in understanding the neurobiological changes of ED have been achieved, 2 , 3 , 4 the molecular mechanisms triggering the onset and maintenance of ED still remain unknown, and the specific genetic influence is uncertain. 5 Accordingly, the unknown pathophysiology of ED explains the absence of specific pharmacological treatment.…”

Section: Introductionmentioning

confidence: 99%

Bacterial ClpB heat-shock protein, an antigen-mimetic of the anorexigenic peptide α-MSH, at the origin of eating disorders

et al. 2014

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The molecular mechanisms at the origin of eating disorders (EDs), including anorexia nervosa (AN), bulimia and binge-eating disorder (BED), are currently unknown. Previous data indicated that immunoglobulins (Igs) or autoantibodies (auto-Abs) reactive with α-melanocyte-stimulating hormone (α-MSH) are involved in regulation of feeding and emotion; however, the origin of such auto-Abs is unknown. Here, using proteomics, we identified ClpB heat-shock disaggregation chaperone protein of commensal gut bacteria Escherichia coli as a conformational antigen mimetic of α-MSH. We show that ClpB-immunized mice produce anti-ClpB IgG crossreactive with α-MSH, influencing food intake, body weight, anxiety and melanocortin receptor 4 signaling. Furthermore, chronic intragastric delivery of E. coli in mice decreased food intake and stimulated formation of ClpB- and α-MSH-reactive antibodies, while ClpB-deficient E. coli did not affect food intake or antibody levels. Finally, we show that plasma levels of anti-ClpB IgG crossreactive with α-MSH are increased in patients with AN, bulimia and BED, and that the ED Inventory-2 scores in ED patients correlate with anti-ClpB IgG and IgM, which is similar to our previous findings for α-MSH auto-Abs. In conclusion, this work shows that the bacterial ClpB protein, which is present in several commensal and pathogenic microorganisms, can be responsible for the production of auto-Abs crossreactive with α-MSH, associated with altered feeding and emotion in humans with ED. Our data suggest that ClpB-expressing gut microorganisms might be involved in the etiology of EDs.

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“…The associated mental health concerns of obesity are well established as an indirect connection with using food as a reward; however, some research now cites the direct physiological changes to the brain and neurological reward systems in relation to eating behaviors . Especially for individuals with eating disorders, as well as those who meet the classification for obesity, the brain's food and reward neural circuitry is potentially altered in ways in which food becomes more rewarding . Researchers also have found that study participants with bulimia nervosa worked harder for food rewards as compared with controls without an eating disorder .…”

Section: Resultsmentioning

confidence: 99%

How Food as a Reward Is Detrimental to Children's Health, Learning, and Behavior

Fedewa

Davis

2015

Journal of School Health

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Advances in the neurobiology of eating disorders

Abstract: New biological models are being developed which explain causal and maintaining factors. The RDoC construct may be used to systematize these findings.

Cited by 18 publications

References 65 publications

Could training executive function improve treatment outcomes for eating disorders?

Could training executive function improve treatment outcomes for eating disorders?

Bacterial ClpB heat-shock protein, an antigen-mimetic of the anorexigenic peptide α-MSH, at the origin of eating disorders

How Food as a Reward Is Detrimental to Children's Health, Learning, and Behavior

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