B Herpertz-Dahlmann

RWTH Aachen University, Aachen, North Rhine-Westphalia, Germany

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Publications (127)314.26 Total impact

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    ABSTRACT: Serotonin (5-HT) and the hormone leptin have been linked to the underlying neurobiology of appetite regulation with evidence coming from animal and cellular research, but direct evidence linking these two pathways in humans is lacking. We examined the effects of reduced brain 5-HT synthesis due to acute tryptophan depletion (ATD) on levels of soluble leptin receptor (sOb-R), the main high-affinity leptin binding protein, in healthy adults using an exploratory approach. Women, but not men, showed reduced sOb-R concentrations after ATD administration. With females showing reduced baseline levels of central 5-HT synthesis compared to males diminished brain 5-HT synthesis affected the leptin axis through the sOb-R in females, thereby potentially influencing their vulnerability to dysfunctional appetite regulation and co-morbid mood symptoms.
    Journal of Neural Transmission 09/2014; · 2.87 Impact Factor
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    ABSTRACT: The Wellcome Trust Case Control Consortium 3 anorexia nervosa genome-wide association scan includes 2907 cases from 15 different populations of European origin genotyped on the Illumina 670K chip. We compared methods for identifying population stratification, and suggest list of markers that may help to counter this problem. It is usual to identify population structure in such studies using only common variants with minor allele frequency (MAF) >5%; we find that this may result in highly informative SNPs being discarded, and suggest that instead all SNPs with MAF >1% may be used. We established informative axes of variation identified via principal component analysis and highlight important features of the genetic structure of diverse European-descent populations, some studied for the first time at this scale. Finally, we investigated the substructure within each of these 15 populations and identified SNPs that help capture hidden stratification. This work can provide information regarding the designing and interpretation of association results in the International Consortia
    European Journal of HumanGenetics 02/2014; · 4.23 Impact Factor
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    ABSTRACT: 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.
    Molecular Psychiatry 02/2014; · 15.15 Impact Factor
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    ABSTRACT: Diminished synthesis of the neurotransmitter serotonin (5-HT) in the brain has been linked to disturbed memory processes. The present study investigated the effects of diminished central nervous 5-HT synthesis as achieved by an acute dietary tryptophan depletion (ATD) on verbal declarative episodic memory in young women while controlling for the effects of female sex hormones. Eighteen healthy females (aged 20-31 years) participated in a within-subject repeated measures study, with two separate days of assessment spaced at least one individual menstrual cycle apart. On one day, participants were subjected to ATD, thus lowering central nervous 5-HT synthesis. The other day participants received a tryptophan-balanced amino acid load (BAL = control condition). The study was randomized, counterbalanced and double blind in terms of ATD/BAL administration. Measurements took place in the early follicular phase of the participants' menstrual cycle. Estrogen, FSH and LH levels were assessed at baseline. Verbal declarative episodic memory was assessed using a structured word-learning task. Short-term memory, as indexed by immediate recall, was reduced after ATD intake, whereas delayed recall and recognition after a 25-min delay did not show any differences after intake of ATD or BAL. In young women, verbal short-term memory function was more vulnerable to ATD than consolidation processes. In light of the possible interplay between female sex hormones and 5-HT, further studies comparing different menstrual cycle phases are needed.
    Amino Acids 09/2013; · 3.65 Impact Factor
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    ABSTRACT: Patients with anorexia nervosa (AN) exhibit high rates of psychiatric comorbidity. To disentangle the effects of duration of illness on comorbid psychiatric symptoms, we investigated the rates of comorbid psychiatric disorders, suicidality and self-harm behaviour in adolescent patients with a first onset of AN. In adolescent females (n = 148) with a first onset of AN, body mass index, psychiatric comorbidity (according to DSM-IV), depressive symptoms, suicidality and self-injurious behaviour were assessed. Seventy patients (47.3%) met the criteria for at least one comorbid psychiatric disorder. The binge-purging subtype was associated with increased rates of psychiatric comorbidity, suicidality and self-injurious behaviour. The severity of eating disorder-specific psychopathology influenced current psychiatric comorbidity and suicidal ideation. Prevalence rates of comorbid psychiatric disorders and suicidal ideation are considerably lower among adolescents with AN compared with adults. An early and careful assessment, along with adequate treatment of the eating disorder, might prevent the development of severe psychiatric comorbidities. Copyright © 2013 John Wiley & Sons, Ltd and Eating Disorders Association.
    European Eating Disorders Review 09/2013; · 1.38 Impact Factor
  • A Maier, J-P Ernst, S Müller, D Gross, F D Zepf, B Herpertz-Dahlmann, U Hagenah
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    ABSTRACT: Background: The stigma of mental illness has been identified as an important barrier to treatment and recovery. Previous research reported the stigmatization of individuals with eating disorders by both health professionals and the general public. The aim of this pilot study was to empirically assess the previous stigmatization and discrimination experiences of young female patients with anorexia nervosa (AN) using a retrospective explorative approach. Methods: An in-house questionnaire that was developed to survey experiences of stigmatization was mailed to 75 former adolescent patients with AN. The mean time of assessment after discharge was 5.6 ± 1.2 years. The patients were asked to respond anonymously. The response rate was approximately 48% (n = 36). Results: Feelings that society held negative stereotypes of individuals with AN, concrete experiences of stigmatization and discrimination, and rejection by peers were reported. A remarkable degree of self-stigmatization, as indexed by high rates of agreement to stigmatizing statements, was detected. Approximately one third of the participants reported delayed initiation of treatment due to fear of stigmatization and discrimination. Conclusion: Stigmatization plays a decisive role in young patients with AN and impacts their motivation to seek professional help and engage in treatment. Clinicians should be aware of the stigmatization related to eating disorders and its burden for affected patients.
    Psychopathology 07/2013; · 1.56 Impact Factor
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    ABSTRACT: Bipolar disorder (BD) and attention deficit/hyperactivity disorder (ADHD) may share common genetic risk factors as indicated by the high co-morbidity of BD and ADHD, their phenotypic overlap especially in pediatric populations, the high heritability of both disorders, and the co-occurrence in families. We therefore examined whether known polygenic BD risk alleles are associated with ADHD. We chose the eight best SNPs of the recent genome-wide association study (GWAS) of BD patients of German ancestry and the nine SNPs from international GWAS meeting a 'genome-wide significance' level of α = 5 × 10(-8). A GWAS was performed in 495 ADHD children and 1,300 population-based controls using HumanHap550v3 and Human660 W-Quadv1 BeadArrays. We found no significant association of childhood ADHD with single BD risk alleles surviving adjustment for multiple testing. Yet, risk alleles for BD and ADHD were directionally consistent at eight of nine loci with the strongest support for three SNPs in or near NCAN, BRE, and LMAN2L. The polygene analysis for the BP risk alleles at all 14 loci indicated a higher probability of being a BD risk allele carrier in the ADHD cases as compared to the controls. At a moderate power to detect association with ADHD, if true effects were close to estimates from GWAS for BD, our results suggest that the possible contribution of BD risk variants to childhood ADHD risk is considerably lower than for BD. Yet, our findings should encourage researchers to search for common genetic risk factors in BD and childhood ADHD in future studies.
    Journal of Neural Transmission 05/2013; · 2.87 Impact Factor
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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency 1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P=2.8 × 10(-4) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P=1.2 × 10(-3) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P=4.3 × 10(-2)). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.Molecular Psychiatry advance online publication, 20 November 2012; doi:10.1038/mp.2012.161.
    Molecular Psychiatry 11/2012; · 15.15 Impact Factor
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    ABSTRACT: Starvation represents an extreme physiological state and entails numerous endocrine and metabolic adaptations. The large-scale application of metabolomics to patients with acute anorexia nervosa (AN) should lead to the identification of state markers characteristic of starvation in general and of the starvation specifically associated with this eating disorder. Novel metabolomics technology has not yet been applied to this disorder. Using a targeted metabolomics approach, we analysed 163 metabolite concentrations in 29 patients with AN in the acute stage of starvation (T0) and after short-term weight recovery (T1). Of the 163 metabolites of the respective kit, 112 metabolites were quantified within restrictive quality control limits. We hypothesized that concentrations are different in patients in the acute stage of starvation (T0) and after weight gain (T1). Furthermore, we compared all 112 metabolite concentrations of patients at the two time points (T0, T1) with those of 16 age and gender matched healthy controls. Thirty-three of the metabolite serum levels were found significantly different between T0 and T1. At the acute stage of starvation (T0) serum concentrations of 90 metabolites differed significantly from those of healthy controls. Concentrations of controls mostly differed even more strongly from those of AN patients after short-term weight recovery than at the acute stage of starvation. We conclude that AN entails profound and longer lasting alterations of a large number of serum metabolites. Further studies are warranted to distinguish between state and trait related alterations and to establish diagnostic sensitivity and specificity of the thus altered metabolites.
    Journal of Psychiatric Research 09/2012; · 4.09 Impact Factor
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    Beate Herpertz-Dahlmann
    Journal of Neural Transmission 08/2012; 119(9):987-8. · 2.87 Impact Factor
  • Neuropsychiatrie de l Enfance et de l Adolescence 07/2012; 60(5):S156.
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    ABSTRACT: Background: In addition to the triad of impairments observed in autism, sensory processing abnormalities have also been reported. Recent studies have suggested that abnormal electroencephalography (EEG) frequency oscillations may indicate impaired sensory processing in psychiatric disorders, including Autism Spectrum Disorders (ASD). Specifically, abnormal oscillations in the gamma frequency band have been found in ASD and proposed as a potential biomarker; however, these findings have been mixed depending on whether evoked versus resting gamma oscillations were examined. While many studies have investigated gamma oscillations in ASD, none have reported an association between gamma and ASD symptom severity. Examining the relationship between the degree of ASD symptomatology and gamma abnormalities may be a first step towards better understanding the extent to which gamma oscillations function as a potential biomarker in ASD. Objectives: 1) To investigate resting gamma power in high functioning males with ASD compared to age and IQ matched typically developing controls (TDC) using EEG and 2) to explore associations between the gamma frequency band and ASD symptom severity as measured by the Social Responsiveness Scale (SRS). Methods: Resting scalp EEG was recorded from 15 boys diagnosed with ASD and 18 typically developing boys (TDC) ranging in age from 9 to 18 years (M=14.5 years, SD=2.8 years). Total gamma power was calculated for 9 electrodes, averaged across frontal (F5, Fz, F6), central (C5, Cz, C6) and parietal (P5, Pz, P6) regions and a repeated measures ANOVA was used to determine significant differences by group and brain region. Groups were matched on age and IQ. Exploratory analyses included Pearson correlations to examine associations between resting gamma power and SRS total across all subjects. Results: In the gamma frequency band, significant main effects of topography (p<0.001) and a topography by subject group (diagnosis) interaction (p=0.012) were found. A t-test confirmed that at central electrodes, resting gamma power was reduced in ASD compared to TDC (p =0.014). Exploratory analyses yielded a significant negative correlation between gamma power at central electrodes and the SRS total (Pearson r = -0.4; p = 0.021). Conclusions: To our knowledge, this is the first study to report an association between abnormal power oscillations in the gamma frequency band and ASD symptom severity. Our findings provide a foundation for future studies to investigate the relationships between physiological measures and ASD symptomatology in order to increase our understanding of the fundamental neural deficits observed in ASD and provide further support of gamma oscillations as a possible biomarker. Future studies should include males and females with lower-functioning ASD relative to other clinical comparison groups (e.g., ADHD) to further elucidate this finding.
    2012 International Meeting for Autism Research; 05/2012
  • G G von Polier, T D Vloet, B Herpertz-Dahlmann
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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is one of the most prevalent psychiatric disorders of childhood and adolescence. Until now, it has been unclear whether ADHD by itself constitutes a risk factor for later delinquency or does so only in combination with other disruptive symptoms. This article seeks to give a comprehensive account of the literature to shed light on the developmental pathway from childhood ADHD to adult criminality. Comorbid ADHD and conduct disorder (CD) are significantly related to a range of biological and environmental risk factors such as neurocognitive impairment, high parental psychopathology, poor social functioning, and other comorbid mental disorders, particularly substance abuse, that are described in this review. In addition, the results of treatment studies are presented, with a special focus on the results of the Multimodal Treatment Study of Children with ADHD (MTA). Although treatment programs, including medication and psychosocial treatment, can be very effective in improving the functioning of children with ADHD in the social and academic domains in the short term, there is no conclusive evidence that such treatments lower the risk for developing delinquency in adulthood.
    Behavioral Sciences & the Law 02/2012; 30(2):121-39. · 0.96 Impact Factor
  • B Herpertz-Dahlmann, K Holtkamp, K Konrad
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    ABSTRACT: Eating disorders have morbidity and mortality rates that are among the highest of any mental disorders. This chapter covers diagnoses, epidemiology, course, and outcome of anorexia and bulimia nervosa, presents several factors that are probably important for their etiology, and gives a short overview on intervention. Emphasis is laid on biological contributions to illness onset and maintenance. Genetic predisposition may be an essential risk factor triggered by cultural or social influences and/or personal adversities. The starvation process itself leads to neural circuit dysfunction, probably mediated by altered neurotransmitter metabolism and endocrinological changes. Neuroimaging and neuropsychological studies give insight into disorder-associated alterations of brain structure and function. Starvation-related changes in neuropeptide secretion or function may contribute to maintain typical psychopathology. It is important to understand the neurobiological mechanism underlying these disorders, to develop more effective evidence-based therapeutic strategies.
    Handbook of Clinical Neurology 01/2012; 106:447-62.
  • B. Herpertz-Dahlmann, M. de Zwaan
    Der Nervenarzt 09/2011; 82(9):1091-1092. · 0.86 Impact Factor
  • B Herpertz-Dahlmann, M de Zwaan
    Der Nervenarzt 08/2011; 82(9):1091-2. · 0.86 Impact Factor
  • B Herpertz-Dahlmann, K Bühren, J Seitz
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    ABSTRACT: The estimated prevalence of anorexia nervosa is highest in teenagers and probably increasing in prepubertal girls, while morbidity rates in female adults remain constant. Childhood and adolescent AN often take a chronic and disabling course with severe consequences for somatic and mental health in adulthood and an eventually high mortality. Besides a reduced growth, diminished reproduction rate and an increased risk of osteoporosis a prolonged course of the disorder may impact on the development of the adolescent brain, probably by hormonal dysfunctions such as those of the corticoid and gonadal system and by severe changes in neuropeptides such as leptin. Thus, besides a genetic disposition, longer lasting effects of starvation on brain development might explain the high prevalence of mental disorders in adulthood of former AN patients. Neuropsychological findings resembling those in obsessive-compulsive disorder and autism spectrum disorders are of growing importance because they might contribute to more effective and specific interventions in both adolescent and adult eating disorders.
    Der Nervenarzt 07/2011; 82(9):1093-9. · 0.86 Impact Factor
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    ABSTRACT: Evidence from adults suggests that changes in thyroid function are associated with the development of bipolar disorder (BD) and severe mood dysregulation. A dysregulation profile based on the Child Behavior Checklist (CBCL-DP) describes a phenotype with severe mood problems in youth. The present study investigated whether altered thyroid functioning in youths is associated with the severe mood dysregulation symptoms characterized by the CBCL-DP. We analyzed the thyroid function data from 262 children and adolescents (n = 262 for serum TSH, n = 148 for free triiodothyronine [fT3] and n = 153 for free thyroxine [fT4]) with their CBCL-DP composite score. We created and compared high CBCL-DP and low CBCL-DP subgroups with regard to their serum TSH, fT3 and fT4 concentrations as well as the presence or absence of subclinical hypothyroidism. We did not detect between-group differences in serum TSH, fT3 and fT4 concentrations, nor were there significant correlations between youths' CBCL-DP scores and their serum TSH, fT3 and fT4 concentrations for either the whole sample or any subgroup. Post-hoc power analyses indicated that adequate to moderate power existed to detect between-group differences in fT3 and fT4 concentrations, respectively, but that larger TSH samples would be required to detect the same differences in those concentrations. This study had a retrospective design, fewer females than males, and reduced power with respect to TSH concentrations. The present investigation does not support the association between elevated serum-TSH concentrations and severe mood dysregulation in youths. However, these findings should be confirmed in future large-scale studies.
    Journal of Affective Disorders 06/2011; 134(1-3):478-82. · 3.76 Impact Factor
  • M. Schulte-Rther, E. Otte, I. Koch, B. Herpertz-Dahlmann, K. Konrad
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    ABSTRACT: Background: It has been suggested that patients with autism spectrum disorders (ASD) have a fundamental impairment of the mirror neuron system (MNS). Several studies have reported deficits for the imitation and the automatic mimicry of facial expressions. Findings for hand- and finger movements are inconsistent. Thus, it remains unclear at which level an impairment in the MNS may occur. Furthermore, the developmental trajectories of these abilities in typically developing controls (TDC) are poorly understood. Objectives: We aimed at investigating the developmental trajectories of automatic mirroring of observed movements (hand movements and facial expressions) using electromyography (EMG) in patients with ASD and TDC. Methods: 39 children and adolescents (aged 6 to 19 years) were investigated using EMG. We employed a paradigm that allowed testing for the effect of automatic mirroring effects (likely mediated by the mirror neuron systems) by using an observation/execution interference task. The participants were asked to execute pre-specified finger movements (lifting of middle or index finger) or facial expressions (smiling or frowning), as indicated by a color cue. Simultaneously, photos were presented that depicted either congruent, incongruent or non-moving/neutral finger movements or facial expressions. EMG signals were acquired at the musculus corrugator supercilii, musculus zygomaticus major (facial expressions), musculus extensor indicis and musculus extensor digitorum (finger movements). For each trial, the latency of muscle activity (as indicated by the EMG-signal) was determined, relative to the onset of the movement cue. Mean error rates and reaction times for congruent, incongruent and neutral conditions were calculated. To avoid a speed/accuracy trade-off effect, only correct trials were used to calculate reaction times. An additional sample comprising 20 adolescents with ASD is currently being collected. Results: Irrespective of age, a significant congruency effect could be observed for the TDC. In congruent conditions (i.e. observed and executed movements were identical) participants had shorter reaction times and made less errors than in incongruent and neutral conditions. Furthermore, we observed that the size of the congruency effect was modulated by age. Both reaction time and error rate effects decreased with age. Further analyses will show whether congruency effects can also be observed in patients with ASD and whether these are similarly modulated by age. Conclusions: The observed congruency effect is likely mediated by the mirror neuron system. Automatic mirroring of observed movements seems to be present from early childhood on and is subject to developmental change. The decrease of congruency effects with age suggests that in TDC, automatic mirroring can be overridden more effectively at older ages due to maturing control processes. In TDC, comparable results were observed for finger movements and emotional facial expressions. The paradigm is thus well designed to investigate differential impairments of the MNS in ASD for both modalities. Observed differences will give important insights into the nature of such impairments, whereas an intact congruency effect and comparable developmental changes would be a strong argument against a core impairment of the MNS in ASD.
    International Meeting for Autism Research 2011; 05/2011
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    ABSTRACT: Due to their sub-normally low fat mass, leptin levels in patients with acute anorexia nervosa (AN) are well below reference levels for age and sex-matched controls. This hypoleptinemia entails endocrinological and behavioral characteristics observed in AN patients during starvation. We aimed to study the appropriateness of hypoleptinemia as a diagnostic marker for AN by assessing sensitivity, specificity and likelihood ratios for different referral serum leptin levels for predicting anorexia nervosa and healthy leanness. For prediction, we additionally generated a score based on a multivariate logistic model including body mass index (BMI; kg/m²) and leptin level. For this purpose, we measured leptin levels in 74 female patients with acute AN upon admission for inpatient or outpatient treatment. Adolescent and adult patients were recruited according to DSM-IV criteria from two multi-center studies. Additionally, leptin levels were measured in 65 female healthy, lean students. Mean serum leptin level was significantly decreased in patients with AN compared to underweight controls (0.87 ± 0.90 vs. 6.43 ± 3.55 μg/L, p < 0.001). Leptin predicted AN independently of BMI; we confirmed a cutoff value in the range of 2 μg/L as having both high specificity and sensitivity. Hypoleptinemia represents a state marker of acute AN and is useful for a laboratory-based diagnostic screening.
    Journal of Neural Transmission 04/2011; 118(4):571-8. · 2.87 Impact Factor

Publication Stats

2k Citations
314.26 Total Impact Points


  • 2000–2013
    • RWTH Aachen University
      • Department of Child and Adolescent Psychiatry and Psychotherapy
      Aachen, North Rhine-Westphalia, Germany
  • 2007–2012
    • University of Duisburg-Essen
      Essen, North Rhine-Westphalia, Germany
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany
  • 1987–2012
    • Philipps University of Marburg
      • Klinik für Kinder- und Jugendpsychiatrie und -psychotherapie (Marburg)
      Marburg, Hesse, Germany
  • 2004–2011
    • University Hospital RWTH Aachen
      • Department of Neurology
      Aachen, North Rhine-Westphalia, Germany
    • University of Wuerzburg
      Würzburg, Bavaria, Germany
  • 2008–2009
    • University of Rostock
      • Zentrum für Nervenheilkunde
      Rostock, Mecklenburg-Vorpommern, Germany
  • 2004–2006
    • Deutschen Gesellschaft für Kinder- und Jugendpsychiatrie, Psychosomatik und Psychotherapie e.V.
      Aachen, North Rhine-Westphalia, Germany
  • 2002–2005
    • Universität Ulm
      • Clinic of Child and Adolescent Psychiatry/ Psychotherapy
      Ulm, Baden-Wuerttemberg, Germany