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Background: Due to the pandemic of child and adolescent overweight and obesity, improvements in overweight and obesity treatment availability and accessibility are needed., Methods: In this prospective study, we investigated if reductions in body mass index (BMI) standard deviation scores (SDS) and waist circumference (WC) would occur during 1.5 years of community-based overweight and obesity treatment based upon an effective hospital-based overweight and obesity treatment protocol, The Children's Obesity Clinics' Treatment protocol. Height, weight, and WC were measured at all consultations. Changes in BMI SDS and WC were analyzed using linear mixed models based upon the repeated measures in each child., Results: From June 2012 to January 2015, 1,001 children (455 boys) were consecutively enrolled in the community-based treatment program. Upon entry, the median age was 11 years (range: 3-18), and the median BMI SDS was 2.85 (range: 1.26-8.96) in boys and 2.48 (range: 1.08-4.41) in girls. After 1.5 years of treatment BMI SDS was reduced in 74% of the children. BMI SDS was reduced by a mean of 0.38 (95% confidence interval (CI): 0.30-0.45, p<0.0001) in boys and 0.18 (95% CI: 0.12-0.25, p<0.0001) in girls after 1.5 years of treatment, independently of baseline age, BMI SDS, and Tanner stage (all p>0.08). WC was reduced by a mean of 3.8 cm (95% CI: 2.7-4.9, p>0.0001) in boys and 5.1 cm (95% CI: 4.0-6.2, p>0.0001) in girls. The dropout rate was 31% after 1.5 years. A median of 4.5 consultation hours was invested per child per year., Conclusion: BMI SDS and WC were reduced after 1.5 years of treatment. Hence, this community-based overweight and obesity treatment program may help accommodate the need for improvements in treatment availability and accessibility.

Objective: The aim of this study was to investigate the prevalence of overweight/obesity among parents of children entering childhood obesity treatment and to evaluate changes in the parents' weight statuses during their child's treatment., Methods: The study included parents of 1,125 children and adolescents aged 3-22 years, who were enrolled in a multidisciplinary childhood obesity treatment program. At baseline, weight and height of the parents were obtained by self-reported information and parental body mass index (BMI) was calculated. Weight and height of the children were measured in the clinic and BMI standard deviation scores were calculated. Furthermore, anthropometric data from parents of 664 children were obtained by telephone interview after a mean of 2.5 years of treatment (ranging 16 days to 7 years), and changes in parental BMI were analyzed., Results: Data on changes in BMI were available in 606 mothers and 479 fathers. At baseline, the median BMI of the mothers was 28.1 kg/m2 (range: 16.9-66.6), and the median BMI of the fathers was 28.9 kg/m2 (range: 17.2-48.1). Seventy percent of the mothers and 80% of the fathers were overweight or obese at the time of their child's treatment initiation. Both the mothers and fathers lost weight during their child's treatment with a mean decrease in BMI in the mothers of 0.5 (95% CI: 0.2-0.8, p = 0.0006) and in the fathers of 0.4 (95% CI: 0.2-0.6, p = 0.0007). Of the overweight/obese parents, 60% of the mothers and 58% of the fathers lost weight during their child's treatment., Conclusion: There is a high prevalence of overweight/obesity among parents of children entering childhood obesity treatment. Family-based childhood obesity treatment with a focus on the child has a positive effect on parental BMI with both mothers and fathers losing weight., Trial Registration: ClinicalTrials.gov NCT00928473., Competing Interests: The authors have declared that no competing interests exist.

Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P

Background: Long‐time survivors of pediatric liver transplantation have an increased incidence of the metabolic syndrome. Adult recipients have an increased risk of post‐transplantation obesity; however, pediatric data are limited. Methods: The study included 42 recipients of pediatric liver transplantation in Denmark, transplanted between 1990 and 2014. The study participants were examined with anthropometric measures, dual‐energy X‐ray scans and blood samples. From the anthropometric measures, body mass index (BMI) and BMI standard deviation score (SDS) were calculated. From the dual‐energy X‐ray scans, fat percent was assessed, and body fat mass index (BFMI) was calculated. Results: The median age was 17.4 years (range 4.1–38.9) at the time of the study, and the median time since transplantation was 8.5 years (range 0.4–23.9). The prevalence of overweight and obesity was 31.0% based on BMI SDS (age below 18) and BMI (age 18 and above). When compared to the participants with normal weight, the participants with overweight and obesity had a higher BFMI (9.29 vs 5.57 kg/m2, p <.001) and fat percent (38.35% vs 29.50%, p =.006). They had higher levels of total cholesterol (4.3 vs 3.6 mmol/L, p =.023) and low‐density lipoprotein (2.5 vs 1.7, p =.015), and had had longer time since transplantation (15.6 vs 8.5 years respectively, p =.045). Conclusions: Long‐time survivors of pediatric liver transplantation have a higher BMI or BMI SDS than the general pediatric population. The obesity is characterized by a higher BFMI, fat percent, and cholesterols levels, when compared to recipients without overweight or obesity. [ABSTRACT FROM AUTHOR]

Aim: This study investigates the prevalence of disturbed eating behaviours in children and adolescents initiating obesity treatment, and how the prevalence varies with age, sex and body mass index (BMI) standard deviation score (SDS). Secondly, it examines whether the presence of disturbed eating behaviours at enrolment is associated with the degree of weight loss after 12 months of treatment.Methods: A total of 3621 patients aged 3-18 years enrolled in a multidisciplinary obesity treatment programme were studied. Follow-up data after a median of 12.4 months were available for 2055 patients. Upon entry, patients were assessed for the following disturbed eating behaviours: meal skipping, emotional eating, overeating and rapid eating. Height and weight were measured at baseline and follow-up.Results: At enrolment, median age was 11.4 years, median BMI SDS was 2.87, and 82.2% of patients exhibited one or more disturbed eating behaviours. The prevalence of meal skipping, emotional eating and rapid eating increased with age (P < 0.01). Patients who reported overeating or rapid eating exhibited a 0.06-0.11 higher BMI SDS at enrolment than patients without these disturbed eating behaviours (P < 0.02). After 1 year of treatment, BMI SDS was reduced in 75.7% of patients, and the median reduction was 0.24 (95% confidence interval: 0.22-0.27). Overeating was associated with a higher degree of weight loss, while meal skipping, emotional eating and rapid eating did not associate with the degree of weight loss at follow-up.Conclusions: Disturbed eating behaviours were highly prevalent in children and adolescents with overweight or obesity, and varied with age and sex. After 1 year of treatment, the degree of obesity improved, regardless of the presence of disturbed eating behaviours at treatment initiation. [ABSTRACT FROM AUTHOR]

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Background: Childhood obesity is a highly heritable disorder, for which the underlying genetic architecture is largely unknown. Four common variants involved in inflammatory-adipokine triggering (IL6 rs2069845, LEPR rs1137100, NAMPT rs3801266, and AMD1 rs2796749) have recently been associated with obesity and related traits in Indian children. The current study aimed to examine the effect of these variants on risk of childhood/juvenile onset obesity and on obesity-related quantitative traits in two Danish cohorts. Methods: Genotype information was obtained for 1461 young Caucasian men from the Genetics of Overweight Young Adults (GOYA) study (overweight/obese: 739 and normal weight: 722) and the Danish Childhood Obesity Biobank (TDCOB; overweight/obese: 1022 and normal weight: 650). Overweight/obesity was defined as having a body mass index (BMI) ≥25 kg/m2; among children and youths, this cut-off was defined using age and sex-specific cut-offs corresponding to an adult body mass index ≥25 kg/m2. Risk of obesity was assessed using a logistic regression model whereas obesity-related quantitative measures were analyzed using a general linear model (based on z-scores) stratifying on the case status and adjusting for age and gender. Meta-analyses were performed using the fixed effects model. Results: No statistically significant association with childhood/juvenile obesity was found for any of the four gene variants among the individual or combined analyses (rs2069845 OR: 0.94 CI: 0.85-1.04; rs1137100 OR: 1.01 CI: 0.90-1.14; rs3801266: 0.96 CI: 0.84-1.10; rs2796749 OR: 1.02 CI: 0.90-1.15; p > 0.05). However, among normal weight children and juvenile men, the LEPR rs1137100 A-allele significantly associated with lower BMI (β = -0.12, p = 0.0026). Conclusions: The IL6, LEPR, NAMPT, and AMD1 gene variants previously found to associate among Indian children did not associate with risk of obesity or obesity-related quantitative measures among Caucasian children and juvenile men from Denmark [ABSTRACT FROM AUTHOR]