Prediction of low body weight at long-term follow-up in acute anorexia nervosa by low body weight at referral

Himmelmann, G. W.; Herzog, Wolfgang; Herpertz‐Dahlmann, Beate; Steinhausen, Hans-Christoph; Amstein, Margit; Seidel, R.; Deter, Hans‐Christian; Remschmidt, Helmut; Schäfer, Helmut

doi:10.1176/ajp.154.4.566

Cited by 117 publications

(18 citation statements)

References 15 publications

(18 reference statements)

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“…It is also of interest that all risk alleles were directionally consistent for AN risk and higher BMI. This is especially unexpected as (a) patients with AN do not have an elevated premorbid BMI 33 ; (b) BMI-values of followed up patients only infrequently exceed the cutoff for overweight (BMI ≥ 25 kg/m 2 ) 36 and (c) LD-score regression analyses revealed a negative genetic correlation between AN and obesity 30 . It is unlikely that the overlap between the AN (controls) and GIANT GWAMAs explains our results.…”

Section: Discussionmentioning

confidence: 99%

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Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

et al. 2016

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The maintenance of normal body weight is disrupted in patients with anorexia nervosa (AN) for prolonged periods of time. Prior to the onset of AN, premorbid body mass index (BMI) spans the entire range from underweight to obese. After recovery, patients have reduced rates of overweight and obesity. As such, loci involved in body weight regulation may also be relevant for AN and vice versa. Our primary analysis comprised a cross-trait analysis of the 1000 single nucleotide polymorphisms (SNPs) with the lowest p-values in a genome-wide association meta-analysis (GWAMA) of AN (GCAN) for evidence of association in the largest published GWAMA for BMI (GIANT). Subsequently we performed sex-stratified analyses for these 1000 SNPs. Functional ex vivo studies on four genes ensued. Lastly, a look-up of GWAMA-derived BMI related loci was performed in the AN GWAMA. We detected significant associations (p-values < 5×10−5, Bonferroni corrected p < 0.05) for 9 SNP alleles at 3 independent loci. Interestingly, all AN susceptibility alleles were consistently associated with increased BMI. None of the genes (chr. 10: CTBP2, chr. 19: CCNE1, chr. 2: CARF and NBEAL1; the latter is a region with high linkage disequilibrium) nearest to these SNPs has previously been associated with AN or obesity. Sex-stratified analyses revealed that the strongest BMI signal originated predominantly from females (chr. 10 rs1561589; poverall: 2.47 × 10−06/pfemales: 3.45 × 10−07/pmales: 0.043). Functional ex vivo studies in mice revealed reduced hypothalamic expression of Ctbp2 and Nbeal1 after fasting. Hypothalamic expression of Ctbp2 was increased in diet induced obese (DIO) mice as compared to age-matched lean controls. We observed no evidence for associations for the look-up of BMI related loci in the AN GWAMA. A cross-trait analysis of AN and BMI loci revealed variants at three chromosomal loci with potential joint impact. The chromosome 10 locus is particularly promising given that the association with obesity was primarily driven by females. In addition, the detected altered hypothalamic expression patterns of Ctbp2 and Nbeal1 as a result of fasting and DIO implicate these genes in weight regulation.

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Section: Discussionmentioning

confidence: 99%

“…The BMI range of patients at medium term (five to ten years) follow-ups is shifted to the left (lower BMI); in recovered patients overweight occurs with a substantially lower probability than in the general population 36,37 .…”

Section: Introductionmentioning

confidence: 95%

Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

et al. 2016

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“…Such disorders can also have long-term implications for body weight. For example, individuals with anorexia nervosa whose pre-morbid body weight is normally distributed (Coners et al, 1999) only infrequently become overweight or obese after recovery (Hebebrand et al, 1997). …”

Section: The Set Point Regulation Modelmentioning

confidence: 99%

Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity

Speakman

Levitsky

Allison

et al. 2011

Disease Models &Amp; Mechanisms

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The close correspondence between energy intake and expenditure over prolonged time periods, coupled with an apparent protection of the level of body adiposity in the face of perturbations of energy balance, has led to the idea that body fatness is regulated via mechanisms that control intake and energy expenditure. Two models have dominated the discussion of how this regulation might take place. The set point model is rooted in physiology, genetics and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain. This model is consistent with many of the biological aspects of energy balance, but struggles to explain the many significant environmental and social influences on obesity, food intake and physical activity. More importantly, the set point model does not effectively explain the ‘obesity epidemic’ – the large increase in body weight and adiposity of a large proportion of individuals in many countries since the 1980s. An alternative model, called the settling point model, is based on the idea that there is passive feedback between the size of the body stores and aspects of expenditure. This model accommodates many of the social and environmental characteristics of energy balance, but struggles to explain some of the biological and genetic aspects. The shortcomings of these two models reflect their failure to address the gene-by-environment interactions that dominate the regulation of body weight. We discuss two additional models – the general intake model and the dual intervention point model – that address this issue and might offer better ways to understand how body fatness is controlled.

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“…For AN in general, early age at onset of illness, young age, and short duration of illness have been associated with a good outcome, and low body weight, vomiting, bulimia, purgative abuse, and psychiatric comorbidities with a poor outcome [1-3]. It was reported that the prognosis of the AN group with BMI less than 13 kg/m 2 at referral was poor [7,19]. Low BMI would seem to be a strong contributor to the poor outcome of patients who require urgent hospitalization.…”

Section: Discussionmentioning

confidence: 99%

The outcome of treatment for anorexia nervosa inpatients who required urgent hospitalization

Kawai

Yamashita

Kobashi

et al. 2014

BioPsychoSocial Med

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BackgroundThis study was done to determine which psychosocial factors are related to the urgent hospitalization of anorexia nervosa patients (AN) due to extremely poor physical condition and to evaluate their outcome after inpatient treatment.Methods133 hospitalized AN patients were classified into an urgent hospitalization (n = 24) or a planned hospitalization (n = 109) group. Multiple regression analysis was done of clinical features, body mass index (BMI), psychological tests [The Minnesota Multiphasic Personality Inventory (MMPI), alexithymia, relationship with parents, and the Eating Disorder Inventory (EDI)]. The effectiveness of treatment was prospectively determined two years after discharge by the Global Clinical Score (GCS). The hospitalized weight gain and the frequency of outpatient visits were evaluated.ResultsOf the factors assessed, only BMI at admission was related to the necessity of urgent hospitalization (β = − 1.063, P = 0.00). The urgent group had significantly more weight loss after discharge and poorer social adaptation on the GCS, even when the patient had a sufficient increase in body weight during inpatient treatment and an equivalent number of outpatient consultations.ConclusionNone of the parameters of the psychosocial tests studied were significantly different between the groups. The outcome of the urgent group was poor. Two years after discharge they had difficulty maintaining weight and continued to have poor social adaptation.

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Prediction of low body weight at long-term follow-up in acute anorexia nervosa by low body weight at referral

Cited by 117 publications

References 15 publications

Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity

The outcome of treatment for anorexia nervosa inpatients who required urgent hospitalization

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