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A debate on current eating disorder diagnoses in light of neurobiological findings: is it time for a spectrum model?

Brooks SJ, Rask-Andersen M, Benedict C, Schiöth HB - BMC Psychiatry (2012)

Bottom Line: Sixty percent of eating disorders do not meet criteria for anorexia- or bulimia nervosa, as defined by the Diagnostic and Statistical Manual version 4 (DSM-IV).Instead they are diagnosed as 'eating disorders not otherwise specified' (EDNOS).Here we debate the classification issues, and discuss how brain imaging and genetic discoveries might be interwoven into a model of eating disorders to provide better classification and treatment.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neuroscience, University of Uppsala, Box 593, Uppsala, Sweden. samantha.brooks@neuro.uu.se

ABSTRACT

Background: Sixty percent of eating disorders do not meet criteria for anorexia- or bulimia nervosa, as defined by the Diagnostic and Statistical Manual version 4 (DSM-IV). Instead they are diagnosed as 'eating disorders not otherwise specified' (EDNOS). Discrepancies between criteria and clinical reality currently hampering eating disorder diagnoses in the DSM-IV will be addressed by the forthcoming DSM-V. However, future diagnoses for eating disorders will rely on current advances in the fields of neuroimaging and genetics for classification of symptoms that will ultimately improve treatment.

Discussion: Here we debate the classification issues, and discuss how brain imaging and genetic discoveries might be interwoven into a model of eating disorders to provide better classification and treatment. The debate concerns: a) current issues in the classification of eating disorders in the DSM-IV, b) changes proposed for DSM-V, c) neuroimaging eating disorder research and d) genetic eating disorder research.

Summary: We outline a novel evidence-based 'impulse control' spectrum model of eating disorders. A model of eating disorders is proposed that will aid future diagnosis of symptoms, coinciding with contemporary suggestions by clinicians and the proposed changes due to be published in the DSM-V.

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Neurobiological impulse-control model of temperamental dominance in ED.
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Figure 3: Neurobiological impulse-control model of temperamental dominance in ED.

Mentions: The Val158Met polymorphism in catechol-o-methyl transferase (COMT), which was originally observed to be associated with AN in a Transmission Disequilibrium Test (TDT) performed on 51 Israeli family trios [74], and later observed to also be associated to BN [75], is of particular interest as it leads to a thermodynamically more unstable protein, which in turn leads to a lower rate of dopamine (DA) turnover in the synaptic cleft, particularly in the PFC. Subsequently, a higher DA activity in COMT-regulated neurons could be a predisposing risk factor for developing EDs. Alterations in COMT activity due to the Val158Met polymorphism is likely to have implications for DA signaling in the PFC, as clearance of DA from the synaptic cleft has been shown to be regulated via COMT in the PFC [76]. However, a recent meta-analysis of the COMT polymorphism alone and its link to AN has not shown significant results [77]. Additionally, despite set-shifting being potentially the most robust endophenotype for ED pathology [78] the COMT polymorphism alone does not relate to set-shifting impairments observed in AN and BN [79]. Both these findings suggest, as we imply in our model, that it is an interaction between genotypes (e.g. COMT vs. BDNF) that might lead to a specific ED cognitive and appetitive phenotypes (See Figure 3).


A debate on current eating disorder diagnoses in light of neurobiological findings: is it time for a spectrum model?

Brooks SJ, Rask-Andersen M, Benedict C, Schiöth HB - BMC Psychiatry (2012)

Neurobiological impulse-control model of temperamental dominance in ED.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475111&req=5

Figure 3: Neurobiological impulse-control model of temperamental dominance in ED.
Mentions: The Val158Met polymorphism in catechol-o-methyl transferase (COMT), which was originally observed to be associated with AN in a Transmission Disequilibrium Test (TDT) performed on 51 Israeli family trios [74], and later observed to also be associated to BN [75], is of particular interest as it leads to a thermodynamically more unstable protein, which in turn leads to a lower rate of dopamine (DA) turnover in the synaptic cleft, particularly in the PFC. Subsequently, a higher DA activity in COMT-regulated neurons could be a predisposing risk factor for developing EDs. Alterations in COMT activity due to the Val158Met polymorphism is likely to have implications for DA signaling in the PFC, as clearance of DA from the synaptic cleft has been shown to be regulated via COMT in the PFC [76]. However, a recent meta-analysis of the COMT polymorphism alone and its link to AN has not shown significant results [77]. Additionally, despite set-shifting being potentially the most robust endophenotype for ED pathology [78] the COMT polymorphism alone does not relate to set-shifting impairments observed in AN and BN [79]. Both these findings suggest, as we imply in our model, that it is an interaction between genotypes (e.g. COMT vs. BDNF) that might lead to a specific ED cognitive and appetitive phenotypes (See Figure 3).

Bottom Line: Sixty percent of eating disorders do not meet criteria for anorexia- or bulimia nervosa, as defined by the Diagnostic and Statistical Manual version 4 (DSM-IV).Instead they are diagnosed as 'eating disorders not otherwise specified' (EDNOS).Here we debate the classification issues, and discuss how brain imaging and genetic discoveries might be interwoven into a model of eating disorders to provide better classification and treatment.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neuroscience, University of Uppsala, Box 593, Uppsala, Sweden. samantha.brooks@neuro.uu.se

ABSTRACT

Background: Sixty percent of eating disorders do not meet criteria for anorexia- or bulimia nervosa, as defined by the Diagnostic and Statistical Manual version 4 (DSM-IV). Instead they are diagnosed as 'eating disorders not otherwise specified' (EDNOS). Discrepancies between criteria and clinical reality currently hampering eating disorder diagnoses in the DSM-IV will be addressed by the forthcoming DSM-V. However, future diagnoses for eating disorders will rely on current advances in the fields of neuroimaging and genetics for classification of symptoms that will ultimately improve treatment.

Discussion: Here we debate the classification issues, and discuss how brain imaging and genetic discoveries might be interwoven into a model of eating disorders to provide better classification and treatment. The debate concerns: a) current issues in the classification of eating disorders in the DSM-IV, b) changes proposed for DSM-V, c) neuroimaging eating disorder research and d) genetic eating disorder research.

Summary: We outline a novel evidence-based 'impulse control' spectrum model of eating disorders. A model of eating disorders is proposed that will aid future diagnosis of symptoms, coinciding with contemporary suggestions by clinicians and the proposed changes due to be published in the DSM-V.

Show MeSH
Related in: MedlinePlus