Predictive Validity of Bulimia Nervosa as a Diagnostic Category

Department of Psychology, University of Minnesota, Minneapolis, USA.
American Journal of Psychiatry (Impact Factor: 12.3). 01/2000; 157(1):136-8. DOI: 10.1176/ajp.157.1.136
Source: PubMed


The authors sought to investigate the predictive validity of bulimia nervosa as a diagnostic category.
More than 10 years after they appeared as patients with bulimia nervosa, 177 women (participation rate=79.7%) completed follow-up assessments.
Among the women with a current eating pathology, most engaged in recurrent binge eating and purging. Anorexia nervosa and binge eating disorder were relatively uncommon. Eating disorder outcome was significantly related to the presence of mood, substance use, and impulse control disorders but not to the presence of anxiety disorders.
These results support the validity of bulimia nervosa as a diagnostic category that is distinct from anorexia nervosa. Furthermore, these results suggest that bulimic symptoms are associated with disorders involving distress and disinhibition.

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    • "Furthermore, our findings may in part reflect an interaction effect with the consequences of possible substance abuse, which is quite common in BN [9]. Prolonged substance abuse may cause inattention, which would not be a comorbidity of BN and ADHS [25], [41]. However, as we used ADHD in childhood to separate the subgroups, long-standing substance abuse seems less likely as a primary cause; it might, however, contribute to symptom severity. "
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    ABSTRACT: Little is known about the contribution of impulsivity, inattention and comorbid attention deficit/hyperactivity disorder (ADHD) in the development and maintenance of bulimia nervosa (BN). In particular, their specific contribution to disordered eating symptoms and whether they have additive effects to the general psychopathological burden remains unclear. Fifty-seven female patients seeking treatment for BN and 40 healthy controls completed diagnostic questionnaires and interviews that investigated: a) ADHD, b) impulsivity, c) eating disorders and d) general psychopathology. Attentional processes and impulsivity were assessed by a comprehensive computer-based neuropsychological battery. Twenty-one percent of patients with BN met the clinical cut-off for previous childhood ADHD compared to 2.5% of healthy controls. Adult ADHD according to DSM IV was also more prevalent in patients with BN, with an odds ratio of 4.2. Patients with BN and previous childhood ADHD were more impulsive and inattentive than patients with BN alone. These patients also displayed more severely disordered eating patterns and more general psychopathological symptoms compared with those without ADHD. Severity of eating disorder symptoms was better explained by inattentiveness than by either impulsivity or hyperactivity. Our data suggest an elevated rate of former childhood and current ADHD-symptoms in treatment-seeking patients with BN. Stronger impulsivity and inattention associated with more severe neuropsychological deficits and eating disorder symptoms indicate an additive risk that is clinically relevant for these patients. Thus, clinicians should identify comorbid patients who might profit from additional ADHD-specific treatments.
    PLoS ONE 05/2013; 8(5):e63891. DOI:10.1371/journal.pone.0063891 · 3.23 Impact Factor
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    • "Consistent with these observations is the evidence that in anorexia nervosa (AN) the presence of binge eating is similarly associated with an elevated risk of greater familial morbidity for substance use disorders, and a higher risk for future alcohol-related problems (Casper et al., 1980; Garfinkel et al., 1980; Toner et al., 1986; Da Costa and Halmi, 1992; Strober et al., 1995). Although the underlying psychosocial and biological variables contributing to deficient impulse control are not entirely known, substantial data exist to assert that impulsivity is a comorbid psychiatric trait that negatively affects the course and prognosis of eating disorders (Keel et al., 2000; Fichter and Quadflieg, 2004; Fichter et al., 2006). "
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    ABSTRACT: We compared symptom patterns, severity of illness, and comorbidity in individuals with eating disorders with and without impulse control disorders (ICD), and documented the temporal pattern of illness onset. Lifetime ICD were present in 16.6% of 709 women with a history of eating disorders. The most common syndromes were compulsive buying disorder and kleptomania. ICD occurred more in individuals with binge eating subtypes, and were associated with significantly greater use of laxatives, diuretics, appetite suppressants and fasting, and with greater body image disturbance, higher harm avoidance, neuroticism, cognitive impulsivity, and lower self-directedness. In addition, individuals with ICD were more likely to have obsessive-compulsive disorder, any anxiety disorder, specific phobia, depression, cluster B personality disorder, avoidant personality disorder, and to use psychoactive substances. Among those with ICD, 62% reported the ICD predated the eating disorder and 45% reported the onset of both disorders within the same 3-year window. The presence of a lifetime ICD appears to be limited to eating disorders marked by binge eating and to be associated with worse eating-related psychopathology, more pathological personality traits, and more frequent comorbid Axis I and II conditions. Untreated ICD may complicate recovery from eating disorders.
    Psychiatry Research 02/2008; 157(1-3):147-57. DOI:10.1016/j.psychres.2007.02.011 · 2.47 Impact Factor
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    ABSTRACT: Söömishäirete keskmeks on pealetungivad mõtted oma kehakaalust ja –kujust ning tugev hirm kehakaalu tõusu ees, mistõttu tehakse äärmuslikke katseid seda vältida. On näidatud, et suurenenud serotoniini süsteemi aktiivsus viib söömise piiramiseni ja alanenud serotoniini süsteemi aktiivsus kutsub esile liigsöömist. Samas on söömishäiretega patsientidel läbiviidud uurimused andnud vastuolulisi tulemusi, kuna raske on eristada toidu piiramisega kaasnenud serotonergilise aktiivsuse muutusi püsiomadustega kaasnevatest serotoniinisüsteemi eripäradest. Väitekiri püüab vastata küsimusele, kas serotoniinisüsteemi funktsioon seostub otseselt häirunud söömiskäitumisega või pigem nende püsivate omaduste kaudu, mis söömissümptomaatikat mõjutavad. Serotoniini transporteri (5-HTT) geen on üks kindlamaid kandidaate seletamaks bioloogilist haavatavust söömishäiretele. Selle lühikest alleeli (s-alleel) seostatakse võrreldes pika alleeliga (l-alleel) pärsitud serotoniini tagasihaardemehhanismiga ning afektiivse ebastabiilsuse ja impulsiivse käitumisega. Käesolevates uurimustes ilmnes, et söömishäirega naised, kellele on iseloomulikud kontrollimatud ülesöömishood ja kes on s-alleeli kandjad, kogevad enam tungi üle süüa ja kontrollimatuid ülesöömishooge, ning neil esineb rohkem emotsiooni ja käitumise regulatsiooni raskusi. Lühikese alleeli kandlus seostus ka suurenenud ülesöömisega varases täiskasvanueas, kui lapsepõlves kogeti keskmisest enam negatiivseid elusündmusi Uurides kahe serotoniinisüsteemi markeri, monoamiinide oksüdaasi (MAO) aktiivsuse ja 5-HTT geeni polümorfismi koosmõju söömishäirete sümptomaatikale, ilmnes, et l/l genotüübiga tüdrukud, kel on kõrge MAO aktiivsus, on oluliselt rohkem hõivatud dieedimõtetest. Sarnased tulemused leiti ka söömishäiretega patsientide valimil. Sõltumata söömishäire alatüübist seostus 5-HTT geeni l/l genotüüp suurema hõivatusega kehakaalust ja välimusest, ning eksimuste pärast muretsemisega. Kuna mõlemaid kognitiivseid nähtusi seostatakse suurenenud kognitiivse rigiidsusega, siis võivad need tulemused selgitada, miks l/l genotüübiga indiviididel kehakaaluga seonduvad mõtted ei taha taanduda, hoides alal probleemset söömiskäitumist. Toitumise piiramise ja ülesöömise vaheliste seoste uurimiseks vaadati aju kasvufaktori (BDNF) geeni Val66Met polümorfismi mõju. Tulemustest nähtub, et met-alleeli kandjatel, kes oma toitumist piiravad, esineb rohkem ülesöömishooge, mis võib selgitada, miks dieedi pidamine viib mõnedel inimestel ülesöömishoogudeni ja teistel mitte. Söömishäiretega patsientide seisund kujuneb mitmest vastastikku mõjutavast protsessist: toitumise piiramisest, impulsiivsete ja kompulsiivsete joonte mõjudest ning keskkonnategurite toimest. Käesoleva väitekirja tulemustest nähtub, et serotoniinisüsteemi markerid mõjutavad eelmainitud protsesside toimet söömissümptomitele, mis võib selgitada söömishäirete sümptomaatikas ja kaasuvates joontes ilmnevat märkimisväärset heterogeensust. Eating disorders are characterized by intense fear of weight gain and preoccupation with body image and body weight, which leads to extreme food restriction, and other dysfunctional weight control behaviours. Although it has been shown that alterations in serotonergic activity contribute to various expressions of eating pathology it is not clear which changes in serotonin function observed in eating disorders patients represent effects induced by food restriction vs. effects related to traits. The aim of the present thesis was to explore whether the markers of the serotonin system may explain the heterogeneity in eating disorder symptoms and related traits. The serotonin transporter (5-HTT) gene is a firm candidate to explain biological vulnerability to eating disorders. The short or s-allele is associated to inhibited serotonin reuptake as compared to the homozygousity for the long or l-allele, and has been associated to affective instability and impulse control deficiencies. In the present study it was found that in women screened positively for binge-type eating disorders, the s-allele carriers show more severe binge eating and higher levels of impulsivity and emotional instability. Moreover, the s-allele carriers were observed to be more sensitive to adverse life events and to show elevated binge eating in response to chronic stress. Examining the effect of two markers of the serotonergic system, platelet monoamine oxidase (MAO) activity and the 5-HTT gene polymorphism on symptoms of eating disorders, it was found that the preoccupation with dieting and weight gain was the highest in girls with the l/l genotype and high MAO activity. Similarly, in women with eating disorders the l/l genotype was related to preoccupation with dieting and body image, and concern over mistakes. These results may refer to the cognitive inflexibility in eating disorders patients with l/l genotype, thus maintaining the preoccupation with body image and the disturbed eating behaviour. The results of the present thesis also show that brain-derived neurotrophic factor Val66Met genotype moderates the effect of food restriction on binge eating and suggest that the met-allele carriers are especially vulnerable to this effect. This finding may explain why some people develop binge eating in response to dieting and others do not. To conclude, studies indicate that the momentary status of the eating disorder patients represents diverse contributing processes: transient effects of food restriction, effects related to impulsive and compulsive traits, and the effects precipitated by environmental stimuli. In the present thesis it was found that the markers of the serotonin system moderate these effects and may explain the heterogenity in eating disorder symptoms and related traits. Väitekirja elektrooniline versioon ei sisalda publikatsioone
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