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"Anorexia"
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Essstörungen im Sport: Anorexia nervosa, Sportanorexie, inverse Anorexie
Anorexia nervosa ist eine psychiatrisch anerkannte Essstörung mit charakteristischen Kernmerkmalen (u. a. stark reduziertes Körpergewicht wegen Nahrungsrestriktion, Gewichtsphobie, Körperschemastörung), oft begleitet von exzessivem Sport, strengen Diäten, ritualisiertem Essmuster. Sie ist eine diagnostische Kategorie im DSM-5 und ICD-11 (BMI-Grenzwert < 18,5 kg/m2). Sportanorexie ist keine offizielle Diagnose, sondern ein populärwissenschaftlicher bzw. klinisch-deskriptiver Begriff für ein bestimmtes Verhaltensmuster (u. a. exzessiver Sport zur Gewichtsabnahme, häufig restriktives Essverhalten oder weitere anorektische Verhaltensweisen, Sport zur Kontrolle von Körperform und -gewicht). Diese Anorexia athletica findet man vor allem in Sportarten, in denen u. a. ein optimales Kraft-Last-Verhältnis den sportlichen Erfolg verbessert oder aus vorgegebenen ästhetischen Gründen wie zum Beispiel in der Rhythmischen Sportgymnastik. Die Schadenskette aus niedrigem Körpergewicht – Östrogenmangel – Oligo-/Amenorrhoe – Osteopenie – Osteoporose – Ermüdungsfrakturen im Training findet sich auch im Begriff der Sportlerinnen-Triade (Female Athlete Triad) mit Essstörung, Amenorrhoe und Osteoporose. Inverse Anorexie ist ebenfalls keine eigenständige Diagnose, wird aber als Form der Körperdysmorphophobie („Adoniskomplex“) oder Untergruppe der Muskel-Dysmorphie verstanden. Typische Merkmale sind u. a. die Überzeugung, zu schmächtig oder nicht muskulös genug zu sein – trotz objektiv überdurchschnittlicher Muskulatur, zwanghaftes Krafttraining, strenge diätetische Kontrolle (zum Beispiel hohe Proteinzufuhr) sowie häufig eine gesteigerte körperbezogene Unsicherheit.
Journal Article
A genome-wide association study of anorexia nervosa
Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome-wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2907 cases with AN from 14 countries (15 sites) and 14 860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery data sets. Seventy-six (72 independent) single nucleotide polymorphisms were taken forward for
in silico
(two data sets) or
de novo
(13 data sets) replication genotyping in 2677 independent AN cases and 8629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication data sets comprised 5551 AN cases and 21 080 controls. AN subtype analyses (1606 AN restricting; 1445 AN binge–purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (
P
=3.01 × 10
−7
) in
SOX2OT
and rs17030795 (
P
=5.84 × 10
−6
) in
PPP3CA
. Two additional signals were specific to Europeans: rs1523921 (
P
=5.76 × 10
−
6
) between
CUL3
and
FAM124B
and rs1886797 (
P
=8.05 × 10
−
6
) near
SPATA13
. Comparing discovery with replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (
P
=4 × 10
−6
), strongly suggesting that true findings exist but our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field.
Journal Article
Treating severe and enduring anorexia nervosa: a randomized controlled trial
There are no evidence-based treatments for severe and enduring anorexia nervosa (SE-AN). This study evaluated the relative efficacy of cognitive behavioral therapy (CBT-AN) and specialist supportive clinical management (SSCM) for adults with SE-AN.
Sixty-three participants with a diagnosis of AN, who had at least a 7-year illness history, were treated in a multi-site randomized controlled trial (RCT). During 30 out-patient visits spread over 8 months, they received either CBT-AN or SSCM, both modified for SE-AN. Participants were assessed at baseline, end of treatment (EOT), and at 6- and 12-month post-treatment follow-ups. The main outcome measures were quality of life, mood disorder symptoms and social adjustment. Weight, eating disorder (ED) psychopathology, motivation for change and health-care burden were secondary outcomes.
Thirty-one participants were randomized to CBT-AN and 32 to SSCM with a retention rate of 85% achieved at the end of the study. At EOT and follow-up, both groups showed significant improvement. There were no differences between treatment groups at EOT. At the 6-month follow-up, CBT-AN participants had higher scores on the Weissman Social Adjustment Scale (WSAS; p = 0.038) and at 12 months they had lower Eating Disorder Examination (EDE) global scores (p = 0.004) and higher readiness for recovery (p = 0.013) compared to SSCM.
Patients with SE-AN can make meaningful improvements with both therapies. Both treatments were acceptable and high retention rates at follow-up were achieved. Between-group differences at follow-up were consistent with the nature of the treatments given.
Journal Article
Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa
Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness
1
, affecting 0.9–4% of women and 0.3% of men
2
–
4
, with twin-based heritability estimates of 50–60%
5
. Mortality rates are higher than those in other psychiatric disorders
6
, and outcomes are unacceptably poor
7
. Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)
8
,
9
and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes.
Genome-wide analyses identify eight independent loci associated with anorexia nervosa. Genetic correlations implicate both psychiatric and metabolic components in the etiology of this disorder, even after adjusting for the effects of common variants associated with body mass index.
Journal Article
Fluoxetine for anorexia nervosa after weight restoration: moderation of effect by depression
Pharmacological efforts to treat anorexia nervosa (AN) have predominantly repurposed medications that treat conditions with overlapping symptoms and yielded generally disappointing results. Despite limited empirical support, SSRIs are often prescribed to patients with AN. Whether SSRIs are effective in a subgroup of individuals with AN, such as those with depression, is not known.
A secondary analysis of a randomized trial of fluoxetine versus placebo for relapse prevention in AN was conducted. Participants (
= 92) were weight-restored women with AN who completed the Beck Depression Inventory (BDI) at the time of randomization. BDI scores were dichotomized to reflect moderate/severe depression (BDI > 20,
= 26). A Cox Proportional Hazards model estimated the association of the level of depression, medication, and their interaction with time to relapse. Mixed effects models examined the effects of medication on symptom trajectories in high versus low depression groups and whether depression severity modified the effect of the drug on symptom trajectory.
There was a significant interaction between medication and depression severity in time to relapse (hazard ratio = 0.46, 95% CI: [0.25, 0.85],
= .01). Depression severity modified the effect of fluoxetine on the time course of symptoms of depression (
= -0.27, 95% CI: [-0.42,-0.12],
= 0.001) and bulimia (
= -0.15, 95% CI: [-0.25,-0.05],
= 0.004) in the twelve month follow-up period.
Fluoxetine was more effective than placebo in reducing relapse among more depressed, weight-restored individuals with AN. These results require replication but provide support for the use of antidepressant medication for patients with AN who remain depressed following weight restoration.
Journal Article