@article{35311,
  author       = {{Jansen, K and Tempes, J and Drozdowska, A and Gutmann, M and Falkenstein, M and Buyken, Anette and Libuda, Lars and Rudolf, H and Lücke, T and Kersting, M}},
  issn         = {{0954-3007}},
  journal      = {{Eur J Clin Nutr}},
  number       = {{5}},
  pages        = {{779}},
  title        = {{{Correction: Short-term effects of carbohydrates differing in glycemic index (GI) consumed at lunch on children's cognitive function in a randomized crossover study.}}},
  volume       = {{76}},
  year         = {{2022}},
}

@article{26420,
  author       = {{Hirtz, Raphael and Focker, Manuel and Libuda, Lars and Antel, Jochen and Ozturk, Dana and Kiewert, Cordula and Munteanu, Martin and Peters, Triinu and Fuhrer, Dagmar and Zwanziger, Denise and Thamm, Michael and Hebebrand, Johannes and Grasemann, Corinna}},
  issn         = {{1555-2101}},
  journal      = {{The Journal of Clinical Psychiatry}},
  title        = {{{Increased Prevalence of Subclinical Hypothyroidism and Thyroid Autoimmunity in Depressed Adolescents}}},
  doi          = {{10.4088/jcp.20m13511}},
  year         = {{2021}},
}

@article{26523,
  abstract     = {{<jats:title>Abstract</jats:title><jats:p>With this case report we support our medical hypothesis that metreleptin treatment ameliorates starvation related emotional, cognitive and behavioral symptomatology of anorexia nervosa (AN) and show for the first time strong effects in a male patient with AN. A 15.9 year old adolescent with severe AN of eight-month duration was treated off-label with metreleptin. Hyperactivity was assessed with accelerometry. Visual analogue scales (VAS), validated self- and clinician rating scales and lab results tracked changes from baseline to end of the 24-day dosing period and a five-month follow-up. Substantial improvements of mood and eating disorder related cognitions and hyperactivity set in after two days of treatment. During dosing, sub-physiological testosterone and TT3 levels normalized; clinically libido reemerged. Weight did not increase substantially during the dosing period. During follow-up target weight was attained; mood did not deteriorate; hyperactivity ceased. The results substantiate the strong effects seen in female cases and underscore the need for a double-blind placebo-controlled trial to confirm the observed strong, multiple and rapid onset beneficial effects of metreleptin in AN.</jats:p>}},
  author       = {{Antel, Jochen and Tan, Susanne and Grabler, Marvin and Ludwig, Christine and Lohkemper, Dominik and Brandenburg, Tim and Barth, Nikolaus and Hinney, Anke and Libuda, Lars and Remy, Miriam and Milos, Gabriella and Hebebrand, Johannes}},
  issn         = {{1018-8827}},
  journal      = {{European Child & Adolescent Psychiatry}},
  title        = {{{Rapid amelioration of anorexia nervosa in a male adolescent during metreleptin treatment including recovery from hypogonadotropic hypogonadism}}},
  doi          = {{10.1007/s00787-021-01778-7}},
  year         = {{2021}},
}

@article{27572,
  abstract     = {{<jats:p> Zusammenfassung. Genetische Varianten beeinflussen die Gewichtsregulation und die Entwicklung von Essstörungen. Zunächst haben familienbasierte, sogenannte formalgenetische Studien den erblichen Anteil an der Gewichtsregulation und an der Ätiologie von Essstörungen beleuchtet. In einer Vielzahl von Studien zeigten sich sowohl für die Varianz des Körpergewichts als auch für die Entstehung von Essstörungen Erblichkeitsschätzer (Heritabilitätsraten) von über 50 %. Mit diesem Wissen begab man sich in den 90er-Jahren des letzten Jahrhunderts auf die Suche nach den zugrundeliegenden Genen (genauer: genetischen Varianten), die das Körpergewicht, das Essverhalten oder beide Phänotypen auf Grundlage geteilter Mechanismen beeinflussen. Zunächst wurden Kandidatengenstudien durchgeführt. Dabei untersuchte man auf Grundlage unterschiedlicher, v. a. aber pathophysiologisch plausibler Überlegungen Gene mit hoher Relevanz für die untersuchten Phänotypen. Dieser Ansatz war für Essstörungen nicht sehr erfolgreich, für die Gewichtsregulation konnte eine Handvoll Gene identifiziert werden. Verbunden mit großen methodischen Fortschritten in der genetischen Forschung und v. a. der Etablierung sogenannter genomweiter Assoziationsstudien (GWAS) Anfang der 2000er-Jahre konnten bislang über 1000 Varianten/Genorte detektiert werden, die das Körpergewicht beeinflussen. Für die Essstörung Anorexia nervosa (AN) sind aktuell acht solcher Genorte beschrieben. Diese Ergebnisse, aber auch aktuelle Ansätze zu phänotypübergreifenden Analysen lassen Einblicke in die komplexe Regulation des Körpergewichtes zu und haben zudem unerwartete Pathomechanismen für AN aufgezeigt. </jats:p>}},
  author       = {{Hirtz, Raphael and Zheng, Yiran and Rajcsanyi, Luisa S. and Libuda, Lars and Antel, Jochen and Peters, Triinu and Hebebrand, Johannes and Hinney, Anke}},
  issn         = {{1422-4917}},
  journal      = {{Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie}},
  title        = {{{Ebenen der genetischen Analyse komplexer Phänotypen am Beispiel                     der Anorexia nervosa und der Varianz des Körpergewichts}}},
  doi          = {{10.1024/1422-4917/a000829}},
  year         = {{2021}},
}

@article{27573,
  abstract     = {{<jats:p> Zusammenfassung. Einleitung: Klassische ernährungsepidemiologische Studien (Beobachtungsstudien und randomisierte Interventionsstudien) zeigen, dass die Ernährung ein wichtiger Ansatzpunkt für die Prävention und Therapie psychischer Störungen sein könnte. Diese Studientypen haben allerdings Limitationen, die bei der Ergebnisinterpretation berücksichtigt werden müssen. In dieser narrativen übersichtsarbeit wird beschrieben, wie genetische Studien ein Bindeglied darstellen können, um einen Zusammenhang zwischen Ernährung und psychischen Störungen herzustellen. Methodik: Im Artikel werden verschiedene Ansätze genetischer phänotypübergreifender Analysen sowie Beispiele für deren Anwendungen in der ernährungspsychiatrischen Forschung beschrieben. Darüber hinaus werden spezifische Voraussetzungen sowie Stärken und Schwächen diskutiert. Ergebnisse: Als Methoden genetischer phänotypübergreifender Analysen sind im Rahmen ernährungspsychiatrischer Forschung bislang genetische Korrelationsanalysen, Look-up-Analysen sowie Mendelsche Randomisierungsstudien (MR-Studien) eingesetzt worden. Genetische Korrelationsanalysen und Look-up-Analysen geben erste Hinweise auf mögliche genetische überlappungen zwischen einer psychischen Störung und einem Stoffwechselweg und/oder der Versorgung mit einem spezifischen Nährstoff. MR-Studien sind weitergehende Detailanalysen mit dem Ziel, Kausalzusammenhänge zu identifizieren, beinhalten allerdings sehr spezifische Grundvoraussetzungen für ihre Durchführung. Schlussfolgerung: Genetische phänotypübergreifende Analysen sind eine sinnvolle Ergänzung der klassischen Ernährungsepidemiologie. Insbesondere signifikante Ergebnisse von MR-Studien sind eine wichtige Grundlage zur Entwicklung geeigneter Ernährungsinterventionen, die in nachfolgenden randomisiert kontrollierten Interventionsstudien mit deutlich erhöhter Erfolgsaussicht getestet werden können. Sie sind somit wichtige Instrumente einer effizienten ernährungspsychiatrischen Forschung. </jats:p>}},
  author       = {{Libuda, Lars and Hebebrand, Johannes and Föcker, Manuel and Peters, Triinu and Hinney, Anke}},
  issn         = {{1422-4917}},
  journal      = {{Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie}},
  pages        = {{1--10}},
  title        = {{{Ernährungseffekten auf der Spur – Wie die Genetik helfen kann,                     Zusammenhänge zwischen Ernährung und seelischer Gesundheit                     aufzudecken}}},
  doi          = {{10.1024/1422-4917/a000807}},
  year         = {{2021}},
}

@article{27574,
  abstract     = {{<jats:p>In adults with major depressive disorder (MDD), a dysfunction between the hypothalamus-pituitary-adrenal (HPA) and the hypothalamus-pituitary-thyroid (HPT) axis has been shown, but the interaction of both axes has not yet been studied in adolescent major depressive disorder (MDD). Data from 273 adolescents diagnosed with MDD from two single center cross-sectional studies were used for analysis. Serum levels of thyrotropin (TSH), free levothyroxine (fT4), and cortisol were determined as indicators of basal HPT and HPA axis functioning and compared to that of adolescent controls by t-tests. Quantile regression was employed in the sample of adolescents with MDD to investigate the relationship between both axes in the normal as well as the pathological range of cortisol levels, considering confounders of both axes. In adolescent MDD, cortisol levels and TSH levels were significantly elevated in comparison to controls (<jats:italic>p</jats:italic> = &amp;lt;.001, <jats:italic>d</jats:italic> = 1.35, large effect size, and <jats:italic>p</jats:italic> = &amp;lt;.001, <jats:italic>d</jats:italic> = 0.79, moderate effect size, respectively). There was a positive linear relationship between TSH and cortisol (<jats:italic>p</jats:italic> = .003, <jats:italic>d</jats:italic> = 0.25, small effect size) at the median of cortisol levels (50<jats:sup>th</jats:sup> percentile). However, no relationship between TSH and cortisol was found in hypercortisolemia (cortisol levels at the 97.5<jats:sup>th</jats:sup> percentile). These findings imply that HPT and HPA axis dysfunction is common in adolescents with MDD and that function of both axes is only loosely related. Moreover, the regulation of the HPA and HPT axis are likely subjected to age-related maturational adjustments since findings of this study differ from those reported in adults.</jats:p>}},
  author       = {{Hirtz, Raphael and Libuda, Lars and Hinney, Anke and Föcker, Manuel and Bühlmeier, Judith and Antel, Jochen and Holterhus, Paul-Martin and Kulle, Alexandra and Kiewert, Cordula and Hebebrand, Johannes and Grasemann, Corinna}},
  issn         = {{1664-2392}},
  journal      = {{Frontiers in Endocrinology}},
  title        = {{{Lack of Evidence for a Relationship Between the Hypothalamus-Pituitary-Adrenal and the Hypothalamus-Pituitary-Thyroid Axis in Adolescent Depression}}},
  doi          = {{10.3389/fendo.2021.662243}},
  year         = {{2021}},
}

@article{27575,
  abstract     = {{<jats:p>There is a distinct increase in the prevalence of depression with the onset of puberty. The role of peripubertal testosterone levels in boys in this context is insufficiently understood and may be modulated by a functional polymorphism of the androgen receptor gene (AR), a variable number of CAG repeats. Moreover, there is preliminary evidence that the relationship between testosterone, CAG repeat length, and the severity of depressive symptoms may differ between subclinical and overt depression, but this has neither been studied in a clinical sample of adolescents with depression nor compared between subclinical and overt depression in an adequately powered study. To investigate the relationship between free testosterone, CAG repeat length of the AR, depression status (subclinical vs. overt), and the severity of depressive symptoms, 118 boys treated as in- or daycare patients at a single psychiatric hospital were studied. Of these, 73 boys had at least mild depressive symptoms according to the Beck Depression Inventory-II (BDI-II &amp;gt; 13). Higher-order moderation analysis in the multiple regression framework revealed a constant relationship between free testosterone and depression severity irrespective of the number of CAG repeats in adolescents with a BDI-II score ≤ 13. In adolescents with a BDI-II score &amp;gt; 13, however, there was a significant negative relationship between free testosterone and BDI-II score in patients with &amp;lt;19 CAG repeats and a significant positive relationship regarding free testosterone and BDI-II score in those with more than 28 CAG repeats, even when considering important covariates. These results suggest that the effects of testosterone on mood in male adolescents with depression depend on the genetic make-up of the AR as well as on depression status. This complex relationship should be considered by future studies addressing mental health issues against an endocrine background and may, moreover, contribute to tailored treatment concepts in psychiatric medicine, especially in adults.</jats:p>}},
  author       = {{Hirtz, Raphael and Libuda, Lars and Hinney, Anke and Föcker, Manuel and Bühlmeier, Judith and Holterhus, Paul-Martin and Kulle, Alexandra and Kiewert, Cordula and Hebebrand, Johannes and Grasemann, Corinna}},
  issn         = {{1664-0640}},
  journal      = {{Frontiers in Psychiatry}},
  title        = {{{Size Matters: The CAG Repeat Length of the Androgen Receptor Gene, Testosterone, and Male Adolescent Depression Severity}}},
  doi          = {{10.3389/fpsyt.2021.732759}},
  year         = {{2021}},
}

@article{27571,
  abstract     = {{<jats:p>(1) Background: Evidence has accumulated that patients with anorexia nervosa (AN) are at higher risk for vitamin D deficiency than healthy controls. In epidemiologic studies, low 25(OH) vitamin D (25(OH)D) levels were associated with depression. This study analyzed the relationship between 25(OH)D serum levels in adolescent patients and AN and depressive symptoms over the course of treatment. (2) Methods: 25(OH)D levels and depressive symptoms were analyzed in 93 adolescent (in-)patients with AN from the Anorexia Nervosa Day patient versus Inpatient (ANDI) multicenter trial at clinic admission, discharge, and 1 year follow up. Mixed regression models were used to analyze the relationship between 25(OH)D levels and depressive symptoms assessed by the Beck Depression Inventory (BDI-II). (3) Results: Although mean 25(OH)D levels constantly remained in recommended ranges (≥50 nmol/L) during AN treatment, levels decreased from (in)patient admission to 1 year follow up. Levels of 25(OH)D were neither cross-sectionally, prospectively, nor longitudinally associated with the BDI-II score. (4) Conclusions: This study did not confirm that 25(OH)D levels are associated with depressive symptoms in patients with AN. However, increasing risks of vitamin D deficiency over the course of AN treatment indicate that clinicians should monitor 25(OH)D levels.</jats:p>}},
  author       = {{Föcker, Manuel and Timmesfeld, Nina and Bühlmeier, Judith and Zwanziger, Denise and Führer, Dagmar and Grasemann, Corinna and Ehrlich, Stefan and Egberts, Karin and Fleischhaker, Christian and Wewetzer, Christoph and Wessing, Ida and Seitz, Jochen and Herpertz-Dahlmann, Beate and Hebebrand, Johannes and Libuda, Lars}},
  issn         = {{2072-6643}},
  journal      = {{Nutrients}},
  title        = {{{Vitamin D Level Trajectories of Adolescent Patients with Anorexia Nervosa at Inpatient Admission, during Treatment, and at One Year Follow Up: Association with Depressive Symptoms}}},
  doi          = {{10.3390/nu13072356}},
  year         = {{2021}},
}

@article{26632,
  abstract     = {{<jats:title>Abstract</jats:title><jats:p>Anorexia nervosa (AN) is a severe eating disorder and often associated with altered humoral immune responses. However, distinct B cell maturation stages in peripheral blood in adolescents with AN have not been characterized. Treatment effects and the relationship between clinical and B cell parameters are also not fully understood. Here we investigated the phenotype of circulating B cell subsets and the relationship with body composition in adolescents with AN before (T0, n = 24) and after 6 weeks (T1, n = 20) of treatment. Using multi-parameter flow cytometry, we found increased percentages of antigen-experienced B cells and plasmablasts in patients with AN compared to healthy controls (n = 20). In contrast, percentages of CD1d<jats:sup>+</jats:sup>CD5<jats:sup>+</jats:sup> B cells and transitional B cells with immunoregulatory roles were reduced at T0 and T1. These B cell frequencies correlated positively with fat mass, fat mass index (FMI), free fat mass index, and body mass index standard deviation score. In addition, scavenger-like receptor CD5 expression levels were downregulated on transitional B cells and correlated with fat mass and FMI in AN. Our findings that regulatory B cell subgroups were reduced in AN and their strong relationship with body composition parameters point toward an impact of immunoregulatory B cells in the pathogenesis of AN.</jats:p>}},
  author       = {{Freff, Jana and Schwarte, Kathrin and Bröker, Lisa and Bühlmeier, Judith and Kraft, Isabelle and Öztürk, Dana and Hinney, Anke and Arolt, Volker and Dannlowski, Udo and Romer, Georg and Baune, Bernhard T. and Hebebrand, Johannes and Föcker, Manuel and Alferink, Judith}},
  issn         = {{2045-2322}},
  journal      = {{Scientific Reports}},
  title        = {{{Alterations in B cell subsets correlate with body composition parameters in female adolescents with anorexia nervosa}}},
  doi          = {{10.1038/s41598-020-80693-4}},
  year         = {{2021}},
}

@article{35303,
  abstract     = {{<jats:title>Abstract</jats:title><jats:sec>
                <jats:title>Purpose</jats:title>
                <jats:p>Studies about effects of lunch dietary Glycemic Index (GI) on cognition of schoolchildren are scarce. Our previous CogniDo GI study found no changes of cognition in the early postprandial phase after consumption of two rice types with medium vs. high dietary GI for lunch (i.e., 45 min after starting lunch). This study investigated whether the dietary GI of lunch has an impact on cognition of schoolchildren in the late postprandial phase, 90 min after lunch.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Methods</jats:title>
                <jats:p>A randomized, 2 × 2 crossover intervention study was conducted at a comprehensive school with 5th and 6th grade students. Participants (<jats:italic>n</jats:italic> = 212) were randomly assigned to either sequence 1 or 2. In the first period, participants of sequence 1 received a dish with high GI rice (GI: 79), those of sequence 2 with medium GI rice (GI: 64)—in the second period, 1 week later, vice versa. Computer-based cognitive testing was performed 90 min after lunch examining tonic alertness, visual search and task switching, and working memory. Treatment effects and treatment effects adjusted for estimated lunch glycemic load (GL) were analyzed using a linear mixed model.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Results</jats:title>
                <jats:p>The selected cognitive parameters were not affected by the GI of lunch 90 min after lunch, neither after intention-to-treat nor in the per-protocol analysis. Adjustment for GL also did not change results.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Conclusion</jats:title>
                <jats:p>The present study revealed no notable differences after the consumption of two rice types with medium vs. high dietary GI for lunch in children’s cognitive function in the late postprandial phase, 90 min after lunch.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Clinical trial registration</jats:title>
                <jats:p>German Clinical Trials Register (DRKS00013597); date of registration: 16/04/2018, retrospectively registered.</jats:p>
              </jats:sec>}},
  author       = {{Drozdowska, Alina and Sinningen, Kathrin and Falkenstein, Michael and Rudolf, Henrik and Libuda, Lars and Buyken, Anette and Lücke, Thomas and Kersting, Mathilde}},
  issn         = {{1436-6207}},
  journal      = {{European Journal of Nutrition}},
  keywords     = {{Nutrition and Dietetics, Medicine (miscellaneous)}},
  number       = {{3}},
  pages        = {{1637--1647}},
  publisher    = {{Springer Science and Business Media LLC}},
  title        = {{{Impact of lunch with carbohydrates differing in glycemic index on children's cognitive functioning in the late postprandial phase: a randomized crossover study}}},
  doi          = {{10.1007/s00394-021-02766-y}},
  volume       = {{61}},
  year         = {{2021}},
}

@article{26526,
  author       = {{Gappa, Monika and Filipiak‐Pittroff, Birgit and Libuda, Lars and Berg, Andrea and Koletzko, Sibylle and Bauer, Carl‐Peter and Heinrich, Joachim and Schikowski, Tamara and Berdel, Dietrich and Standl, Marie}},
  issn         = {{0105-4538}},
  journal      = {{Allergy}},
  pages        = {{1903--1907}},
  title        = {{{Long‐term effects of hydrolyzed formulae on atopic diseases in the GINI study}}},
  doi          = {{10.1111/all.14709}},
  year         = {{2020}},
}

@article{26527,
  abstract     = {{<jats:title>Abstract</jats:title><jats:sec>
                <jats:title>Background</jats:title>
                <jats:p>While observational studies revealed an inverse association between serum 25(OH)vitamin D (25(OH)D) and the risk of attention deficit/hyperactivity disorder (ADHD), the causality of this relationship remains unclear.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Methods</jats:title>
                <jats:p>We conducted a bidirectional two-sample Mendelian Randomization (MR) study to examine whether 25(OH)D has an effect on the risk to develop ADHD or vice versa. Information on single nucleotide polymorphisms (SNP) associated with serum 25(OH)D was obtained from a genome-wide association study (GWAS) considering phenotype data from 79,366 individuals of European ancestry. Data on risk for ADHD were derived from a GWAS analysis with 20,183 individuals diagnosed with ADHD and 35,191 controls. For our analysis, we considered effect sizes based on the European participants (19,099 cases and 34,194 controls).</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Results</jats:title>
                <jats:p>Single SNP analyses showed a causal effect of vitamin D on ADHD risk for only one SNP (rs12785878, <jats:italic>p</jats:italic> = 0.024). The overall MR estimates did not reveal a causal effect of 25(OH)D on risk for ADHD. In the reverse analysis, neither any single nor the multi-SNP MR analyses showed a causal effect of ADHD on 25(OH)D.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Conclusion</jats:title>
                <jats:p>Results from this two-sample MR study did not confirm a causal effect of 25(OH)D on ADHD or vice versa. Accordingly, our study does not provide evidence that improving 25(OH)D via supplementation could reduce the risk of developing ADHD.</jats:p>
              </jats:sec>}},
  author       = {{Libuda, Lars and Naaresh, Roaa and Ludwig, Christine and Laabs, Björn-Hergen and Antel, Jochen and Föcker, Manuel and Hebebrand, Johannes and Hinney, Anke and Peters, Triinu}},
  issn         = {{1436-6207}},
  journal      = {{European Journal of Nutrition}},
  pages        = {{2581--2591}},
  title        = {{{A mendelian randomization study on causal effects of 25(OH)vitamin D levels on attention deficit/hyperactivity disorder}}},
  doi          = {{10.1007/s00394-020-02439-2}},
  year         = {{2020}},
}

@article{26529,
  abstract     = {{<jats:title>Abstract</jats:title><jats:sec>
                <jats:title>Purpose</jats:title>
                <jats:p>The influences of nutrition in childhood on puberty onset could have sustained consequences for health and wellbeing later in life. The aim of this study was to investigate the prospective association of diet quality prior to puberty with the timing of puberty onset.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Methods</jats:title>
                <jats:p>We considered data from 3983 SCCNG (Southwest China Childhood Nutrition and Growth) study participants with dietary data, anthropometric measurement, and information on potential confounders at their baseline assessment (mean age: 7.1 years for girls and 7.3 years for boys; mean length of follow-up was 4.2 years). Cox proportional hazard regression estimating hazard ratios (HRs) and 95% confidence intervals (CIs) were used to examine the relationship between diet quality and puberty onset. Dietary intake at baseline was assessed using a validated food frequency questionnaire. Diet quality was determined using the Chinese Children Dietary Index (CCDI) which measures adherence to current dietary recommendations (theoretical range: 0–160 points). Age at Tanner stage 2 for breast/genital development (B2/G2), menarche or voice break (M/VB) were used as pubertal markers.
</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Results</jats:title>
                <jats:p>The CCDI score ranged from 56.2 to 136.3 for girls and 46.1–131.5 for boys. Pubertal markers consistently indicate that girls and boys with higher diet quality were more likely to enter their puberty later than their counterparts with lower CCDI scores (higher vs. lower CCDI tertiles: adjusted HR for age at B2: 0.85 (95% CI, 0.81–0.94), <jats:italic>p</jats:italic> for trend = 0.02; G2: 0.86 (95% CI,0.80–0.96), <jats:italic>p</jats:italic> for trend = 0.02; M: 0.86 (95% CI,0.80–0.95), <jats:italic>p</jats:italic> for trend = 0.02; VB: 0.86 (95% CI,0.79–0.98), <jats:italic>p</jats:italic> for trend = 0.03), after adjustment for paternal education level, baseline energy intake, and pre-pubertal body fat.</jats:p>
              </jats:sec><jats:sec>
                <jats:title>Conclusions</jats:title>
                <jats:p>Our data suggested a later puberty onset and later timing of progressed puberty stages in children with a high diet quality, which were independent of pre-pubertal body fat.</jats:p>
              </jats:sec>}},
  author       = {{Duan, Ruonan and Qiao, Tian and Chen, Yue and Chen, Mengxue and Xue, Hongmei and Zhou, Xue and Yang, Mingzhe and Liu, Yan and Zhao, Li and Libuda, Lars and Cheng, Guo}},
  issn         = {{1436-6207}},
  journal      = {{European Journal of Nutrition}},
  pages        = {{2423--2434}},
  title        = {{{The overall diet quality in childhood is prospectively associated with the timing of puberty}}},
  doi          = {{10.1007/s00394-020-02425-8}},
  year         = {{2020}},
}

@article{27019,
  abstract     = {{<jats:title>Abstract</jats:title><jats:p>To examine the hypothesis that normalization of low circulating leptin levels in patients with anorexia nervosa ameliorates hyperactivity, three seriously ill females with hyperactivity were treated off-label with metreleptin (recombinant human leptin) for up to 14 days. Drive for activity, repetitive thoughts of food, inner restlessness, and weight phobia decreased in two patients. Surprisingly, depression improved rapidly in all patients. No serious adverse events occurred. Due to obvious limitations of uncontrolled case series, placebo-controlled clinical trials are mandatory to confirm the observed rapid onset of beneficial effects. Our findings suggest an important role of hypoleptinemia in the mental and behavioral phenotype of anorexia nervosa.</jats:p>}},
  author       = {{Milos, Gabriella and Antel, Jochen and Kaufmann, Lisa-Katrin and Barth, Nikolaus and Koller, Antonia and Tan, Susanne and Wiesing, Urban and Hinney, Anke and Libuda, Lars and Wabitsch, Martin and von Känel, Roland and Hebebrand, Johannes}},
  issn         = {{2158-3188}},
  journal      = {{Translational Psychiatry}},
  title        = {{{Short-term metreleptin treatment of patients with anorexia nervosa: rapid on-set of beneficial cognitive, emotional, and behavioral effects}}},
  doi          = {{10.1038/s41398-020-00977-1}},
  year         = {{2020}},
}

@article{27020,
  author       = {{Peters, Triinu and Nüllig, Lena and Antel, Jochen and Naaresh, Roaa and Laabs, Björn-Hergen and Tegeler, Lisa and Amhaouach, Chaima and Libuda, Lars and Hinney, Anke and Hebebrand, Johannes}},
  issn         = {{1664-8021}},
  journal      = {{Frontiers in Genetics}},
  title        = {{{The Role of Genetic Variation of BMI, Body Composition, and Fat Distribution for Mental Traits and Disorders: A Look-Up and Mendelian Randomization Study}}},
  doi          = {{10.3389/fgene.2020.00373}},
  year         = {{2020}},
}

@article{27022,
  abstract     = {{<jats:title>Abstract</jats:title><jats:sec>
<jats:title>Purpose</jats:title>
<jats:p>While observational studies revealed inverse associations between serum vitamin D levels [25(OH)D] and depression, randomized controlled trials (RCT) in children and adolescents are lacking. This RCT examined the effect of an untreated vitamin D deficiency compared to an immediate vitamin D<jats:sub>3</jats:sub> supplementation on depression scores in children and adolescents during standard day and in-patient psychiatric treatment.</jats:p>
</jats:sec><jats:sec>
<jats:title>Methods</jats:title>
<jats:p>Patients with vitamin D deficiency [25(OH)D ≤ 30 nmol/l] and at least mild depression [Beck Depression Inventory II (BDI-II) &gt; 13] (<jats:italic>n</jats:italic> = 113) were 1:1 randomized into verum (VG; 2640 IU vitamin D<jats:sub>3</jats:sub>/d) or placebo group (PG) in a double-blind manner. During the intervention period of 28 days, both groups additionally received treatment as usual. BDI-II scores were assessed as primary outcome, DISYPS-II (Diagnostic System for Mental Disorders in Childhood and Adolescence, Self- and Parent Rating) and serum total 25(OH)D were secondary outcomes.</jats:p>
</jats:sec><jats:sec>
<jats:title>Results</jats:title>
<jats:p>At admission, 49.3% of the screened patients (<jats:italic>n</jats:italic> = 280) had vitamin D deficiency. Although the intervention led to a higher increase of 25(OH)D levels in the VG than in the PG (treatment difference: + 14 ng/ml; 95% CI 4.86–23.77; <jats:italic>p</jats:italic> = 0.003), the change in BDI-II scores did not differ (+ 1.3; 95% CI − 2.22 to 4.81; <jats:italic>p</jats:italic> = 0.466). In contrast, DISYPS parental ratings revealed pronounced improvements of depressive symptoms in the VG (− 0.68; 95% CI − 1.23 to − 0.13; <jats:italic>p</jats:italic> = 0.016).</jats:p>
</jats:sec><jats:sec>
<jats:title>Conclusion</jats:title>
<jats:p>Whereas this study failed to show a vitamin D supplementation effect on self-rated depression in adolescent in- or daycare patients, parents reported less depressive symptoms in VG at the end of our study. Future trials should consider clinician-rated depressive symptoms as primary outcome.</jats:p>
</jats:sec><jats:sec>
<jats:title>Trial registration</jats:title>
<jats:p>“German Clinical Trials Register” (<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="https://www.drks.de">https://www.drks.de</jats:ext-link>), registration number: DRKS00009758</jats:p>
</jats:sec>}},
  author       = {{Libuda, Lars and Timmesfeld, Nina and Antel, Jochen and Hirtz, Raphael and Bauer, Jens and Führer, Dagmar and Zwanziger, Denise and Öztürk, Dana and Langenbach, Gina and Hahn, Denise and Ring, Stefanie and Peters, Triinu and Hinney, Anke and Bühlmeier, Judith and Hebebrand, Johannes and Grasemann, Corinna and Föcker, Manuel}},
  issn         = {{1436-6207}},
  journal      = {{European Journal of Nutrition}},
  pages        = {{3415--3424}},
  title        = {{{Effect of vitamin D deficiency on depressive symptoms in child and adolescent psychiatric patients: results of a randomized controlled trial}}},
  doi          = {{10.1007/s00394-020-02176-6}},
  year         = {{2020}},
}

@article{27018,
  abstract     = {{<jats:p>Acute anorexia nervosa (AN) constitutes an extreme physiological state. We aimed to detect state related metabolic alterations during inpatient admission and upon short- and long-term weight regain. In addition, we tested the hypothesis that metabolite concentrations adapt to those of healthy controls (HC) after long-term weight regain. Thirty-five female adolescents with AN and 25 female HC were recruited. Based on a targeted approach 187 metabolite concentrations were detected at inpatient admission (T0), after short-term weight recovery (T1; half of target-weight) and close to target weight (T2). Pattern hunter and time course analysis were performed. The highest number of significant differences in metabolite concentrations (N = 32) were observed between HC and T1. According to the detected main pattern, metabolite concentrations at T2 became more similar to those of HC. The course of single metabolite concentrations (e.g., glutamic acid) revealed different metabolic subtypes within the study sample. Patients with AN after short-term weight regain are in a greater “metabolic imbalance” than at starvation. After long-term weight regain, patients reach a metabolite profile similar to HC. Our results might be confounded by different metabolic subtypes of patients with AN.</jats:p>}},
  author       = {{Föcker, Manuel and Cecil, Alexander and Prehn, Cornelia and Adamski, Jerzy and Albrecht, Muriel and Adams, Frederike and Hinney, Anke and Libuda, Lars and Bühlmeier, Judith and Hebebrand, Johannes and Peters, Triinu and Antel, Jochen}},
  issn         = {{2218-1989}},
  journal      = {{Metabolites}},
  title        = {{{Evaluation of Metabolic Profiles of Patients with Anorexia Nervosa at Inpatient Admission, Short- and Long-Term Weight Regain—Descriptive and Pattern Analysis}}},
  doi          = {{10.3390/metabo11010007}},
  year         = {{2020}},
}

@article{27021,
  author       = {{Jansen, Kathrin and Tempes, Jana and Drozdowska, Alina and Gutmann, Maike and Falkenstein, Michael and Buyken, Anette and Libuda, Lars and Rudolf, Henrik and Lücke, Thomas and Kersting, Mathilde}},
  issn         = {{0954-3007}},
  journal      = {{European Journal of Clinical Nutrition}},
  pages        = {{757--764}},
  title        = {{{Short-term effects of carbohydrates differing in glycemic index (GI) consumed at lunch on children’s cognitive function in a randomized crossover study}}},
  doi          = {{10.1038/s41430-020-0600-0}},
  year         = {{2020}},
}

@article{27023,
  abstract     = {{<jats:title>Abstract</jats:title>
               <jats:sec>
                  <jats:title>Background</jats:title>
                  <jats:p>Blood immunoreactive biomarkers, such as C-reactive protein (CRP), and metabolic abnormalities have been associated with schizophrenia. Studies comprehensively and bidirectionally probing possible causal links between such blood constituents and liability to schizophrenia are lacking.</jats:p>
               </jats:sec>
               <jats:sec>
                  <jats:title>Methods</jats:title>
                  <jats:p>To disentangle putative causal links between CRP blood levels and schizophrenia in both directions, we conducted multiple univariable Mendelian-randomization (MR) analyses, ranging from fixed-effect to inverse variance-weighted (IVW), weighted-median, MR Egger and generalized summary-data-based Mendelian-randomization (GSMR) models. To prioritize metabolic risk factors for schizophrenia, a novel multivariable approach was applied: multivariable Mendelian-randomization–Bayesian model averaging (MR-BMA).</jats:p>
               </jats:sec>
               <jats:sec>
                  <jats:title>Results</jats:title>
                  <jats:p>All forward univariable MR analyses consistently showed that CRP has a protective effect on schizophrenia, whereas reverse MR analyses consistently suggested absent causal effects of schizophrenia liability on CRP blood levels. Using MR-BMA, as the top protective factors for schizophrenia we prioritized leucine and as the prime risk-factor triglycerides in medium very-low-density lipoprotein (VLDL). The five best-performing MR-BMA models provided one additional risk factor: triglycerides in large VLDL; and two additional protective factors: citrate and lactate.</jats:p>
               </jats:sec>
               <jats:sec>
                  <jats:title>Conclusions</jats:title>
                  <jats:p>Our results add to a growing body of literature hinting at metabolic changes—in particular of triglycerides—independently of medication status in schizophrenia. We also highlight the absent effects of genetic liability to schizophrenia on CRP levels.</jats:p>
               </jats:sec>}},
  author       = {{Lin, Bochao D and Alkema, Anne and Peters, Triinu and Zinkstok, Janneke and Libuda, Lars and Hebebrand, Johannes and Antel, Jochen and Hinney, Anke and Cahn, Wiepke and Adan, Roger and Luykx, Jurjen J}},
  issn         = {{0300-5771}},
  journal      = {{International Journal of Epidemiology}},
  pages        = {{1505--1514}},
  title        = {{{Assessing causal links between metabolic traits, inflammation and schizophrenia: a univariable and multivariable, bidirectional Mendelian-randomization study}}},
  doi          = {{10.1093/ije/dyz176}},
  year         = {{2019}},
}

@article{27024,
  author       = {{Kalhoff, Hermann and Mesch, Christina M. and Stimming, Madlen and Israel, Andreas and Spitzer, Christoph and Beganovic, Latifa and Perez, Rocio Estella and Koletzko, Berthold and Warschburger, Petra and Kersting, Mathilde and Libuda, Lars}},
  issn         = {{0954-3007}},
  journal      = {{European Journal of Clinical Nutrition}},
  pages        = {{682--690}},
  title        = {{{Effects of LC-PUFA supply via complementary food on infant development—a food based intervention (RCT) embedded in a total diet concept}}},
  doi          = {{10.1038/s41430-019-0491-0}},
  year         = {{2019}},
}