Temperament and Character in Women with Anorexia Nervosa

Klump, Kelly L.; Bulik, Cynthia M.; Pollice, Christine; Halmi, Katherine A.; Fichter, Manfred M.; Berrettini, Wade H.; Devlin, Bernie; Strober, Michael; Kaplan, Allan S.; Woodside, D. Blake; Treasure, Janet; Shabbout, Mayadah; Lilenfeld, Lisa R.; Plotnicov, Katherine; Kaye, Walter H.

doi:10.1097/00005053-200009000-00001

Cited by 194 publications

(173 citation statements)

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“…[14][15][16] A strong relationship between ED and some personality traits has been described. [24][25][26] We report here that BN patients carrying the NTRK2 high-risk haplotype C-A-insC display high scores in Harm 27,28 These results support the involvement of NTRK2 in the development of ED, not only through a direct participation in food intake and body weight regulation, as suggested by animal models, but also through the modulation of different personality traits that may increase the risk of AN and BN, such as depression or anxiety.…”

Section: Ntrk2 and Eating Disorders M Ribases Et Alsupporting

confidence: 82%

Contribution of NTRK2 to the genetic susceptibility to anorexia nervosa, Harm avoidance and minimum body mass index

et al. 2005

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Anorexia nervosa (AN) and bulimia nervosa (BN) are eating disorders (ED) with complex genetic and environmental components. Genetic studies and animal models support the participation of brain-derived neurotrophic factor (BDNF) in the vulnerability to AN and BN. We investigated the genetic contribution of the BDNF-specific receptor neurotrophic tyrosine kinase receptor type 2 (NTRK2) to the susceptibility to ED. We have screened the entire NTRK2 gene in 91 patients with ED and have identified 14 single-nucleotide polymorphisms (SNPs). A population-based association study with six SNPs from the NTRK2 locus was performed in 164 ED patients and 121 controls. Significant evidence of association for markers -69C4G and IVS13 þ 40G4A was detected. We also observed a strong association between the C-A-insC haplotype (-69/IVS13 þ 40/2784-2785) and binge-eating/purging AN (ANP, P ¼ 0.006; OR ¼ 2.27), and a reduced frequency of haplotype G-A-delCl in BN patients (P ¼ 0.034; OR ¼ 0.6). The analysis of ED-related phenotypes revealed a clear association between NTRK2, high scores of Harm avoidance measured by the temperament and character inventory (TCI-R; P ¼ 0.003) and minimum body mass index (minBMI; Po0.001). Our data support a contribution of NTRK2 to the genetic susceptibility of ED, mainly ANP, and ED-related phenotypic traits, such as Harm avoidance and minBMI. Keywords: anorexia; bulimia; eating disorders; harm avoidance; BDNF; NTRK2 Eating disorders (ED) are complex psychiatric diseases characterized by alterations in eating behaviour, body shape perception and body weight regulation. Different genetic, psychological and environmental factors contribute to the vulnerability to both anorexia nervosa (AN) and bulimia nervosa (BN), but the pathophysiology of these disorders is still largely unknown. 1 Brain-derived neurotrophic factor (BDNF) encodes for a neurotrophic factor expressed in the hypothalamic nuclei that regulate eating behaviour and modulates synaptic efficiency and neuronal plasticity through the control of different neurotransmitter systems previously involved in ED.2,3 Intraventricular administration of Bdnf induces appetite suppression and body weight reduction in rats, while Bdnf knockout mice develop obesity associated to hyperphagia and serotonin dysfunctions.3-5 Moreover, we and others have previously reported a strong association between BDNF and both AN and BN in different populations. [6][7][8][9] Due to the strong association between BDNF and ED, we propose its high-affinity receptor neurotrophic tyrosine kinase receptor type 2 (NTRK2) as a candidate gene to participate in the aetiology of ED and suggest that alterations on its function or expression pattern could contribute to the development of AN and BN. Different lines of evidences support this hypothesis. NTRK2 is expressed in hypothalamic neurons that control food intake and energy expenditure. Infusion of the Ntrk2 specific ligands, Bdnf or Nt4/5, transiently reverse the eating behaviour and obesity of the Bdnf (7) knockout mice and the ...

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Section: Ntrk2 and Eating Disorders M Ribases Et Alsupporting

confidence: 82%

Contribution of NTRK2 to the genetic susceptibility to anorexia nervosa, Harm avoidance and minimum body mass index

et al. 2005

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“…Someone with this diagnosis is frequently constrained, conforming, obsessional, rigid, and perfectionistic" (p. S69). To demonstrate, we present a vignette of an individual with AN ( Figure 2) drawn from an historical account from 1866 (cited in Brumberg, 1988) to highlight features extensively documented in AN both premorbidly and following weight restoration: cognitive and behavioral rigidity (Anderluh et al, 2003;, perfectionism (Bastiani, Rao, Weltzin, & Kaye, 1995;Bulik et al, 2003;Halmi et al, 2000;Woodside et al, 2002), social withdrawal (Diaz-Marsa, Carrasco, & Saiz, 2000; I. C. Gillberg et al, 1995;Godart et al, 2004;Holliday, Uher, Landau, Collier, & Treasure, 2006;Karwautz, Troop, Rabe-Hesketh, Collier, & Treasure, 2003;Kaye et al, 2004), constriction (Geller, Cockell, Hewitt, Goldner, & Flett, 2000), and harm avoidance (Diaz-Marsa et al, 2000;Klump et al, 2000Klump et al, , 2004. In fact, the reliable presentation of this behavioral and personality cluster has been demonstrated to add to the incremental validity of diagnostic accuracy (Westen & Harnden-Fischer, 2001).…”

Section: Overview Of the Phenotypic Expression Of Anmentioning

confidence: 99%

Anorexia nervosa and autism spectrum disorders: Guided investigation of social cognitive endophenotypes.

Zucker¹,

Losh²,

Bulik³

et al. 2007

Psychological Bulletin

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Death by suicide occurs in a disproportionate percentage of individuals with anorexia nervosa (AN), with a standardized mortality ratio indicating a 57-fold greater risk of death from suicide relative to an age-matched cohort. Longitudinal studies indicate impaired social functioning increases risk for fatal outcomes, while social impairment persists following recovery. Study of social cognition in AN may elucidate impaired processes that may influence therapeutic efficacy. Symptoms of autism spectrum disorders (ASD) are overrepresented in those who evidence a chronic course. Relative to that in AN, social information processing in ASD is well characterized and may inform systematic study in AN. This article (a) reviews impaired interpersonal processes in AN, (b) compares the phenotype of AN with that of ASD, (c) highlights deficits of social cognitive disturbance in ASD relative to AN, and (d) proposes a new framework to understand the interaction of individuals with AN with their social context.Keywords: anorexia nervosa, social cognition, autism, interpersonal functioning, eating disorders Individuals with anorexia nervosa (AN) have a nearly 12-fold greater risk of death from all causes and a 57-fold greater risk of death from suicide relative to their age-matched peers (Keel et al., 2003). Such troubling statistics speak to the incapacitating, perplexing, and isolating nature of AN, a severe psychiatric illness that negatively impacts the biological, emotional, and psychosocial functioning of both the affected individual and her or his family (Harris & Barraclough, 1998;Treasure, Whitaker, Whitney, & Schmidt, 2005). In fact, AN exacts a toll on the family reported to exceed that experienced by families with a child with a severe psychiatric disorder such as schizophrenia . Although guiding epidemiologic data are currently lacking, there has been increasing concern regarding several notable trends: (a) an upsurge of AN in both younger and older ages than has been previously reported Johnson, Cohen, Kasen, & Brook, 2006;Marcus & Kalarchian, 2003), (b) increased incidence in minority groups hitherto thought protected (Decaluwe, Braet, & Fairburn, 2003;Tanofsky-Kraff et al., 2003), and (c) recent published reports of extensive illness burden among family members Treasure, Whitaker, Whitney, & Schmidt, 2005;Whitney & Eisler, 2005). Such patterns highlight the broad impact of these illnesses and underscore the urgency of alternative approaches to illness management.While advances have been made in the treatment of adolescents with a relatively short duration of illness (Lock & le Grange, 2005), progress in the treatment of adults with AN remains limited, at best (W. S. Agras et al., 2004;Kaplan, 2002). Of note, a report issued by the National Institute of Mental Health (W. S. Agras et al., 2004) emphasized the absence of innovative treatment approaches over the past several decades. This conclusion was recently echoed in an evidence-based review calling for novel intervention strategies that target core biological...

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“…AN and BN are thought to share some common etiologic factors (Klump et al, 2000). Still, a number of factors distinguish the subgroups, such as extremes of eating behavior and impulse control.…”

Section: Only Rec An Have Reduced [mentioning

confidence: 99%

Altered 5-HT2A Receptor Binding after Recovery from Bulimia-Type Anorexia Nervosa: Relationships to Harm Avoidance and Drive for Thinness

Bailer

Price

Meltzer

et al. 2004

Neuropsychopharmacol

153

107

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Several lines of evidence suggest that a disturbance of serotonin neuronal pathways may contribute to the pathogenesis of anorexia nervosa (AN) and bulimia nervosa (BN). This study applied positron emission tomography (PET) to investigate the brain serotonin 2A (5-HT 2A ) receptor, which could contribute to disturbances of appetite and behavior in AN and BN. To avoid the confounding effects of malnutrition, we studied 10 women recovered from bulimia-type AN (REC AN-BN, 41 year normal weight, regular menstrual cycles, no binging, or purging) compared with 16 healthy control women (CW) using PET imaging and a specific 5-HT 2A 18 F]altanserin binding potential and drive for thinness in several cortical regions. In conclusion, this study extends research suggesting that altered 5-HT neuronal system activity persists after recovery from bulimia-type AN, particularly in subgenual cingulate regions. Altered 5-HT neurotransmission after recovery also supports the possibility that this may be a trait-related disturbance that contributes to the pathophysiology of eating disorders. It is possible that subgenual cingulate findings are not specific for AN-BN, but may be related to the high incidence of lifetime major depressive disorder diagnosis in these subjects.

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Temperament and Character in Women with Anorexia Nervosa

Cited by 194 publications

References 35 publications

Contribution of NTRK2 to the genetic susceptibility to anorexia nervosa, Harm avoidance and minimum body mass index

Contribution of NTRK2 to the genetic susceptibility to anorexia nervosa, Harm avoidance and minimum body mass index

Anorexia nervosa and autism spectrum disorders: Guided investigation of social cognitive endophenotypes.

Altered 5-HT2A Receptor Binding after Recovery from Bulimia-Type Anorexia Nervosa: Relationships to Harm Avoidance and Drive for Thinness

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