https://www.thelancet.com/pdfs/journals/lanpsy/PIIS2215-0366(15)00356-9.pdf

Anorexia nervosa: aetiology, assessment, and treatment

Aim
To examine the evidence to support using a staging heuristic for eating disorders, suggesting that the diagnosis of an eating disorder follows a trajectory across the life course. Specifically, to examine whether high-risk markers and prodromal features presenting in childhood and adolescence can later transition to the full manifestation of the illness in early adulthood, and whether over time, the illness can be described as becoming severe and enduring, often resistant to treatment.

Methods
We conducted a comprehensive literature search on the MEDLINE, PubMed, PsycINFO, EMBASE and Cochrane databases from using the following terms: staging, duration of illness, early intervention, developmental epidemiology, neurobiological marker, phenotype, partial syndrome, severe enduring, chronic, prospective, longitudinal, cohort, epidemiology, adolescent, adult with anorexia nervosa, bulimia nervosa, binge eating disorder, eating disorder. The evidence was organized according to the staging heuristic defined by McGorry.

Results
Evidence from epidemiological studies, neuropsychological findings, treatment responsivity and prognosis, support a specific staging trajectory for anorexia nervosa in that there is a longitudinal trajectory with evidence of neurobiological progression and evidence that interventions matched to stage of illness may optimize the benefit. There is less data at the moment to support such a model for bulimia nervosa and binge eating disorder.

Conclusion
The staging heuristic is a useful model for anorexia nervosa in terms of providing prognostic information and stage matched interventions. Although the evidence is encouraging, further research is needed before a similar model could be applied for bulimia nervosa and binge eating disorder.

Has the time come for a staging model to map the course of eating disorders from high risk to severe enduring illness? An examination of the evidence.

Objective
Attachment insecurity may confer risk for developing an eating disorder. We describe domains of attachment functioning that are relevant to eating disorders including: affect regulation, interpersonal style, coherence of mind, and reflective functioning. Research since 2000 on attachment and eating disorders related to these domains is reviewed.

Method
We searched MedLine/Pubmed and PsycINFO from January 2000 to February 2014 and kept articles that: were empirical, included adults with a diagnosed eating disorder, and used a standard attachment measure. We retained 50 relevant studies.

Results
Compared to controls, those with eating disorders had higher levels of attachment insecurity and disorganized mental states. Lower reflective functioning was specifically associated with anorexia nervosa. Attachment anxiety was associated with eating disorder symptom severity, and this relationship may be mediated by perfectionism and affect regulation strategies. Type of attachment insecurity had specific negative impacts on psychotherapy processes and outcomes, such that higher attachment avoidance may lead to dropping out and higher attachment anxiety may lead to poorer treatment outcomes.

Discussion
Research to date suggests a possible relationship between attachment insecurity and risk for an eating disorder. More research is needed that uses attachment interviews, and longitudinal and case control designs. Clinicians can assess attachment insecurity to help inform therapeutic stances and interventions. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2014; 47:710–717)

Attachment and eating disorders: A review of current research

https://research-information.bris.ac.uk/files/139396229/Full_text_PDF_final_published_version_.pdf

Social cognitive dysfunction as a clinical marker: A systematic review of meta-analyses across 30 clinical conditions

Categorically distinct basic drives (for example, for social versus feeding behaviour1–3) can exert potent influences on each other; such interactions are likely to have important adaptive consequences (such as appropriate regulation of feeding in the context of social hierarchies) and can become maladaptive (such as in clinical settings involving anorexia). It is known that neural systems regulating natural and adaptive caloric intake, and those regulating social behaviours, involve related circuitry4–7, but the causal circuit mechanisms of these drive adjudications are not clear. Here we investigate the causal role in behaviour of cellular-resolution experience-specific neuronal populations in the orbitofrontal cortex, a major reward-processing hub that contains diverse activity-specific neuronal populations that respond differentially to various aspects of caloric intake8–13 and social stimuli14,15. We coupled genetically encoded activity imaging with the development and application of methods for optogenetic control of multiple individually defined cells, to both optically monitor and manipulate the activity of many orbitofrontal cortex neurons at the single-cell level in real time during rewarding experiences (caloric consumption and social interaction). We identified distinct populations within the orbitofrontal cortex that selectively responded to either caloric rewards or social stimuli, and found that activity of individually specified naturally feeding-responsive neurons was causally linked to increased feeding behaviour; this effect was selective as, by contrast, single-cell resolution activation of naturally social-responsive neurons inhibited feeding, and activation of neurons responsive to neither feeding nor social stimuli did not alter feeding behaviour. These results reveal the presence of potent cellular-level subnetworks within the orbitofrontal cortex that can be precisely engaged to bidirectionally control feeding behaviours subject to, for example, social influences. Distinct but partially overlapping subsets of neurons in the orbitofrontal cortex of mice respond to feeding and/or social stimuli and, when optogenetically stimulated at single-cell resolution, specifically regulate reward-seeking behaviours.

H Pinar Caglar-Nazali

Papers

A systematic review and meta-analysis of ‘Systems for Social Processes’ in eating disorders