@article{27803, author = {{Schwingshackl, Lukas and Neuenschwander, Manuela and Hoffmann, Georg and Buyken, Anette and Schlesinger, Sabrina}}, issn = {{0002-9165}}, journal = {{The American Journal of Clinical Nutrition}}, pages = {{917--918}}, title = {{{Reply to Khan et al.}}}, doi = {{10.1093/ajcn/nqaa006}}, year = {{2020}}, } @article{27806, abstract = {{AbstractTrend analyses based on dietary records suggest decreases in the intakes of total sugar (TS), added and free sugar since 2005 among children and adolescents in Germany. In terms of age trends, TS intake decreased with increasing age. However, self-reported sugar intake in epidemiological studies is criticised, as it may be prone to bias due to selective underreporting. Furthermore, adolescents are more susceptible to underreporting than children. We thus analysed time and age trends in urinary fructose excretion (FE), sucrose excretion (SE) and the sum of both (FE + SE) as biomarkers for sugar intake among 8·5–16·5-year-old adolescents. Urinary sugar excretion was measured by UPLC-MS/MS in 997 24-h urine samples collected from 239 boys and 253 girls participating in the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) study cohort between 1990 and 2016. Time and age trends of log-transformed FE, SE and FE + SE were analysed using polynomial mixed-effects regression models. Between 1990 and 2016, FE as well as FE + SE decreased (linear time trend: P = 0·0272 and P < 0·0001, respectively). A minor increase in excretion during adolescence was confined to FE (linear age trend: P = 0·0017). The present 24-h excretion measurements support a previously reported dietary record-based decline in sugar intake since 2005. However, the previously seen dietary record-based decrease in TS from childhood to late adolescence was not confirmed by our biomarker analysis, suggesting a constant sugar intake for the period of adolescence.}}, author = {{Perrar, Ines and Gray, Nicola and Kuhnle, Gunter G. and Remer, Thomas and Buyken, Anette and Alexy, Ute}}, issn = {{0007-1145}}, journal = {{British Journal of Nutrition}}, pages = {{164--172}}, title = {{{Sugar intake among German adolescents: trends from 1990 to 2016 based on biomarker excretion in 24-h urine samples}}}, doi = {{10.1017/s0007114520000665}}, year = {{2020}}, } @article{27807, abstract = {{There is no question that elevated postprandial glycemia is a significant driver of common chronic diseases globally [...]}}, author = {{Brand-Miller, Jennie and Buyken, Anette}}, issn = {{2072-6643}}, journal = {{Nutrients}}, title = {{{The Relationship between Glycemic Index and Health}}}, doi = {{10.3390/nu12020536}}, year = {{2020}}, } @article{27022, abstract = {{Abstract Purpose 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 D3 supplementation on depression scores in children and adolescents during standard day and in-patient psychiatric treatment. Methods Patients with vitamin D deficiency [25(OH)D ≤ 30 nmol/l] and at least mild depression [Beck Depression Inventory II (BDI-II) > 13] (n = 113) were 1:1 randomized into verum (VG; 2640 IU vitamin D3/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. Results At admission, 49.3% of the screened patients (n = 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; p = 0.003), the change in BDI-II scores did not differ (+ 1.3; 95% CI − 2.22 to 4.81; p = 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; p = 0.016). Conclusion 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. Trial registration “German Clinical Trials Register” (https://www.drks.de), registration number: DRKS00009758 }}, 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 = {{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.}}, 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{27003, author = {{Perrar, Ines and Schmitting, Sarah and Della Corte, Karen W. and Buyken, Anette and Alexy, Ute}}, issn = {{1436-6207}}, journal = {{European Journal of Nutrition}}, pages = {{1043--1054}}, title = {{{Age and time trends in sugar intake among children and adolescents: results from the DONALD study}}}, doi = {{10.1007/s00394-019-01965-y}}, year = {{2019}}, } @article{27004, author = {{Wong, Tommy H. T. and Buyken, Anette and Brand-Miller, Jennie C. and Louie, Jimmy Chun Yu}}, issn = {{1436-6207}}, journal = {{European Journal of Nutrition}}, pages = {{2357--2367}}, title = {{{Is there a soft drink vs. alcohol seesaw? A cross-sectional analysis of dietary data in the Australian Health Survey 2011–12}}}, doi = {{10.1007/s00394-019-02084-4}}, year = {{2019}}, } @article{27005, abstract = {{ABSTRACT Background There is controversy on the relevance of dietary sugar intake for cardiometabolic health. Objective The aim of this network meta-analysis (NMA) was to assess how isocaloric substitutions of dietary sugar with other carbohydrates affect cardiometabolic risk factors, comparing different intervention studies. Methods We included randomized controlled trials (RCTs) investigating the isocaloric effect of substituting dietary sugars (fructose, glucose, sucrose) with other sugars or starch on cardiometabolic risk markers, including LDL cholesterol, triacylglycerol (TG), fasting glucose (FG), glycated hemoglobin (HbA1c), insulin resistance (HOMA-IR), uric acid, C-reactive protein (CRP), alanine transaminase (ALT), aspartate transaminase (AST), and liver fat content. To identify the most beneficial intervention for each outcome, random-effects NMA was conducted by calculating pooled mean differences (MDs) with 95% CIs, and by ranking the surface under the cumulative ranking curves (SUCRAs). The certainty of evidence was evaluated using the Confidence In Network Meta-Analysis tool. Results Thirty-eight RCTs, including 1383 participants, were identified. A reduction in LDL-cholesterol concentrations was shown for the exchange of sucrose with starch (MD: −0.23 mmol/L; 95% CI: −0.38, −0.07 mmol/L) or fructose with starch (MD: −0.22 mmol/L; 95% CI: −0.39, −0.05 mmol/L; SUCRAstarch: 98%). FG concentrations were also lower for the exchange of sucrose with starch (MD: −0.14 mmol/L; 95% CI: −0.29, 0.01 mmol/L; SUCRAstarch: 91%). Replacing fructose with an equivalent energy amount of glucose reduced HOMA-IR (MD: −0.36; 95% CI: −0.71, −0.02; SUCRAglucose: 74%) and uric acid (MD: −23.77 µmol/L; 95% CI: −44.21, −3.32 µmol/L; SUCRAglucose: 93%). The certainty of evidence was rated very low to moderate. No significant effects were observed for TG, HbA1c, CRP, ALT, and AST. Conclusions Our findings indicate that substitution of sucrose and fructose with starch yielded lower LDL cholesterol. Insulin resistance and uric acid concentrations were beneficially affected by replacement of fructose with glucose. Our findings are limited by the very low to moderate certainty of evidence. This review was registered at www.crd.york.ac.uk/prospero as CRD42018080297. }}, author = {{Schwingshackl, Lukas and Neuenschwander, Manuela and Hoffmann, Georg and Buyken, Anette and Schlesinger, Sabrina}}, issn = {{0002-9165}}, journal = {{The American Journal of Clinical Nutrition}}, title = {{{Dietary sugars and cardiometabolic risk factors: a network meta-analysis on isocaloric substitution interventions}}}, doi = {{10.1093/ajcn/nqz273}}, year = {{2019}}, } @article{27006, abstract = {{Trend analyses suggest that free sugar (FS) intake—while still exceeding 10%E—has decreased among German children and adolescents since 2005, yet that intakes may shift from sugars naturally occurring in foods to added sugars as children age. Thus, we analysed time and age trends in FS intake (%E) from food groups among 3–18 year-olds (1985–2016) using 10,761 3-day dietary records from 1312 DONALD participants (660 boys, 652 girls) by use of polynomial mixed-effects regression models. Among girls, FS from sugar & sweets decreased from 1985 to 2016 (linear trend p < 0.0001), but not among boys (p > 0.05). In the total sample, FS intake from juices increased until 2000 and decreased since 2005 (linear, quadratic trend p < 0.0001). FS from sugar sweetened beverages (SSB) decreased non-linearly from 1985 to 2016 (girls: linear, quadratic, cubic trend p < 0.0001; boys: linear, quadratic, cubic trend p < 0.02). Younger children consumed more FS from juices than older ones, who had a higher FS intake from SSB. FS intake from sugar & sweets increased until early adolescence and decreased afterwards. Since sugar & sweets represent the main source of FS intake and the source with the least pronounced decline in intake, public health measures should focus on these products.}}, author = {{Perrar, Ines and Schadow, Alena M. and Schmitting, Sarah and Buyken, Anette and Alexy, Ute}}, issn = {{2072-6643}}, journal = {{Nutrients}}, title = {{{Time and Age Trends in Free Sugar Intake from Food Groups among Children and Adolescents between 1985 and 2016}}}, doi = {{10.3390/nu12010020}}, year = {{2019}}, } @article{27023, abstract = {{Abstract Background 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. Methods 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). Results 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. Conclusions 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. }}, 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}}, } @article{27758, abstract = {{Published meta-analyses indicate significant but inconsistent incident type-2 diabetes (T2D)-dietary glycemic index (GI) and glycemic load (GL) risk ratios or risk relations (RR). It is now over a decade ago that a published meta-analysis used a predefined standard to identify valid studies. Considering valid studies only, and using random effects dose–response meta-analysis (DRM) while withdrawing spurious results (p < 0.05), we ascertained whether these relations would support nutrition guidance, specifically for an RR > 1.20 with a lower 95% confidence limit >1.10 across typical intakes (approximately 10th to 90th percentiles of population intakes). The combined T2D–GI RR was 1.27 (1.15–1.40) (p < 0.001, n = 10 studies) per 10 units GI, while that for the T2D–GL RR was 1.26 (1.15–1.37) (p < 0.001, n = 15) per 80 g/d GL in a 2000 kcal (8400 kJ) diet. The corresponding global DRM using restricted cubic splines were 1.87 (1.56–2.25) (p < 0.001, n = 10) and 1.89 (1.66–2.16) (p < 0.001, n = 15) from 47.6 to 76.1 units GI and 73 to 257 g/d GL in a 2000 kcal diet, respectively. In conclusion, among adults initially in good health, diets higher in GI or GL were robustly associated with incident T2D. Together with mechanistic and other data, this supports that consideration should be given to these dietary risk factors in nutrition advice. Concerning the public health relevance at the global level, our evidence indicates that GI and GL are substantial food markers predicting the development of T2D worldwide, for persons of European ancestry and of East Asian ancestry.}}, author = {{Livesey, Geoffrey and Taylor, Richard and Livesey, Helen F. and Buyken, Anette and Jenkins, David J. A. and Augustin, Livia S. A. and Sievenpiper, John L. and Barclay, Alan W. and Liu, Simin and Wolever, Thomas M. S. and Willett, Walter C. and Brighenti, Furio and Salas-Salvadó, Jordi and Björck, Inger and Rizkalla, Salwa W. and Riccardi, Gabriele and Vecchia, Carlo La and Ceriello, Antonio and Trichopoulou, Antonia and Poli, Andrea and Astrup, Arne and Kendall, Cyril W. C. and Ha, Marie-Ann and Baer-Sinnott, Sara and Brand-Miller, Jennie C.}}, issn = {{2072-6643}}, journal = {{Nutrients}}, title = {{{Dietary Glycemic Index and Load and the Risk of Type 2 Diabetes: A Systematic Review and Updated Meta-Analyses of Prospective Cohort Studies}}}, doi = {{10.3390/nu11061280}}, year = {{2019}}, } @article{27759, abstract = {{While dietary factors are important modifiable risk factors for type 2 diabetes (T2D), the causal role of carbohydrate quality in nutrition remains controversial. Dietary glycemic index (GI) and glycemic load (GL) have been examined in relation to the risk of T2D in multiple prospective cohort studies. Previous meta-analyses indicate significant relations but consideration of causality has been minimal. Here, the results of our recent meta-analyses of prospective cohort studies of 4 to 26-y follow-up are interpreted in the context of the nine Bradford-Hill criteria for causality, that is: (1) Strength of Association, (2) Consistency, (3) Specificity, (4) Temporality, (5) Biological Gradient, (6) Plausibility, (7) Experimental evidence, (8) Analogy, and (9) Coherence. These criteria necessitated referral to a body of literature wider than prospective cohort studies alone, especially in criteria 6 to 9. In this analysis, all nine of the Hill’s criteria were met for GI and GL indicating that we can be confident of a role for GI and GL as causal factors contributing to incident T2D. In addition, neither dietary fiber nor cereal fiber nor wholegrain were found to be reliable or effective surrogate measures of GI or GL. Finally, our cost–benefit analysis suggests food and nutrition advice favors lower GI or GL and would produce significant potential cost savings in national healthcare budgets. The high confidence in causal associations for incident T2D is sufficient to consider inclusion of GI and GL in food and nutrient-based recommendations.}}, author = {{Livesey, Geoffrey and Taylor, Richard and Livesey, Helen F. and Buyken, Anette and Jenkins, David J. A. and Augustin, Livia S. A. and Sievenpiper, John L. and Barclay, Alan W. and Liu, Simin and Wolever, Thomas M. S. and Willett, Walter C. and Brighenti, Furio and Salas-Salvadó, Jordi and Björck, Inger and Rizkalla, Salwa W. and Riccardi, Gabriele and Vecchia, Carlo La and Ceriello, Antonio and Trichopoulou, Antonia and Poli, Andrea and Astrup, Arne and Kendall, Cyril W. C. and Ha, Marie-Ann and Baer-Sinnott, Sara and Brand-Miller, Jennie C.}}, issn = {{2072-6643}}, journal = {{Nutrients}}, title = {{{Dietary Glycemic Index and Load and the Risk of Type 2 Diabetes: Assessment of Causal Relations}}}, doi = {{10.3390/nu11061436}}, year = {{2019}}, } @article{27772, author = {{Oluwagbemigun, Kolade and Buyken, Anette and Alexy, Ute and Schmid, Matthias and Herder, Christian and Nöthlings, Ute}}, issn = {{1475-2840}}, journal = {{Cardiovascular Diabetology}}, title = {{{Developmental trajectories of body mass index from childhood into late adolescence and subsequent late adolescence–young adulthood cardiometabolic risk markers}}}, doi = {{10.1186/s12933-019-0813-5}}, year = {{2019}}, } @article{27026, abstract = {{While observational studies show an association between 25(OH)vitamin D concentrations and depressive symptoms, intervention studies, which examine the preventive effects of vitamin D supplementation on the development of depression, are lacking. To estimate the role of lowered 25(OH)vitamin D concentrations in the etiology of depressive disorders, we conducted a two-sample Mendelian randomization (MR) study on depression, i.e., “depressive symptoms” (DS, n = 161,460) and “broad depression” (BD, n = 113,769 cases and 208,811 controls). Six single nucleotide polymorphisms (SNPs), which were genome-wide significantly associated with 25(OH)vitamin D concentrations in 79,366 subjects from the SUNLIGHT genome-wide association study (GWAS), were used as an instrumental variable. None of the six SNPs was associated with DS or BD (all p > 0.05). MR analysis revealed no causal effects of 25(OH)vitamin D concentration, either on DS (inverse variance weighted (IVW); b = 0.025, SE = 0.038, p = 0.52) or on BD (IVW; b = 0.020, SE = 0.012, p = 0.10). Sensitivity analyses confirmed that 25(OH)vitamin D concentrations were not significantly associated with DS or BD. The findings from this MR study indicate no causal relationship between vitamin D concentrations and depressive symptoms, or broad depression. Conflicting findings from observational studies might have resulted from residual confounding or reverse causation.}}, author = {{Libuda, Lars and Laabs, Björn-Hergen and Ludwig, Christine and Bühlmeier, Judith and Antel, Jochen and Hinney, Anke and Naaresh, Roaa and Föcker, Manuel and Hebebrand, Johannes and König, Inke R. and Peters, Triinu}}, issn = {{2072-6643}}, journal = {{Nutrients}}, title = {{{Vitamin D and the Risk of Depression: A Causal Relationship? Findings from a Mendelian Randomization Study}}}, doi = {{10.3390/nu11051085}}, year = {{2019}}, } @article{27025, author = {{Knoll-Pientka, Nadja and Bühlmeier, Judith and Peters, Triinu and Albrecht, Muriel and Adams, Frederike and Wustrau, Katharina and Teufel, Martin and Hebebrand, Johannes and Föcker, Manuel and Libuda, Lars}}, issn = {{1590-1262}}, journal = {{Eating and Weight Disorders - Studies on Anorexia, Bulimia and Obesity}}, pages = {{911--919}}, title = {{{Risk factors for a low weight gain in the early stage of adolescent anorexia nervosa inpatient treatment: findings from a pilot study}}}, doi = {{10.1007/s40519-019-00705-9}}, year = {{2019}}, } @article{27521, author = {{Hebebrand, Johannes and Milos, Gabriella and Wabitsch, Martin and Teufel, Martin and Führer, Dagmar and Bühlmeier, Judith and Libuda, Lars and Ludwig, Christine and Antel, Jochen}}, issn = {{1664-1078}}, journal = {{Frontiers in Psychology}}, title = {{{Clinical Trials Required to Assess Potential Benefits and Side Effects of Treatment of Patients With Anorexia Nervosa With Recombinant Human Leptin}}}, doi = {{10.3389/fpsyg.2019.00769}}, year = {{2019}}, } @article{27981, author = {{Weber, KS and Simon, MC and Strassburger, K and Markgraf, DF and Buyken, Anette and Szendroedi, J and Müssig, K and Roden, M and Group, GDS}}, issn = {{2072-6643}}, journal = {{Nutrients}}, number = {{6}}, title = {{{Habitual Fructose Intake Relates to Insulin Sensitivity and Fatty Liver Index in Recent-Onset Type 2 Diabetes Patients and Individuals without Diabetes.}}}, doi = {{10.3390/nu10060774}}, volume = {{10}}, year = {{2018}}, } @article{25929, author = {{Buyken, Anette and Mela, DJ and Dussort, P and Johnson, IT and Macdonald, IA and Stowell, JD and FJPH, Brouns}}, issn = {{0954-3007}}, journal = {{Eur J Clin Nutr}}, number = {{12}}, pages = {{1625--1643}}, title = {{{Dietary carbohydrates: a review of international recommendations and the methods used to derive them.}}}, doi = {{10.1038/s41430-017-0035-4}}, volume = {{72}}, year = {{2018}}, }