The Italian Consensus Position Statement on Diagnosis, Treatment and Prevention of Obesity in Children and Adolescents integrates and updates the previous guidelines to deliver an evidence based approach to the disease. The following areas were reviewed: (1) obesity definition and causes of secondary obesity; (2) physical and psychosocial comorbidities; (3) treatment and care settings; (4) prevention. The main novelties deriving from the Italian experience lie in the definition, screening of the cardiometabolic and hepatic risk factors and the endorsement of a staged approach to treatment. The evidence based efficacy of behavioral intervention versus pharmacological or surgical treatments is reported. Lastly, the prevention by promoting healthful diet, physical activity, sleep pattern, and environment is strongly recommended since the intrauterine phase.

The melanocortin-4 receptor (MC4R) gene pathogenic mutations are the most prevalent forms of monogenic obesity, responsible for ∼2% of obesity cases, but its role in common obesity is still elusive. We analyzed the contribution of non-synonymous mutations V103I (rs2229616, c.307G > A) and I251L (no rs, c.751A > C) to obesity in 16 797 individuals of European origin from nine independent case–control, population-based and familial cohorts. We observed a consistent negative association of I251L variant (prevalence ranging 0.41–1.21%) with both childhood and adult class III obesity [odds ratio (OR) ranging from 0.25 to 0.76, 0.001 < P-value < 0.05] and with modulation of body mass index (BMI) in general populations, in eight out of nine studies, whereas only one study showed an association between V103I and BMI. Meta-analyses of previous published data with the current ones provided strong evidence of the protective effect of I251L toward obesity (OR = 0.52, P = 3.58 10-5), together with a modest negative association between V103I and obesity (OR = 0.80, P = 0.002). Taken together, gain-of-function mutations I251L and V103I may be responsible for a preventive fraction of obesity of 2%, which mirrors the prevalence of monogenic obesity due to MC4R haploinsufficiency. These results also emphasize the importance of the MC4R signalling tonus to prevent obesity, even in the context of our current obesogenic environment.

Prevention of obesity should start as early as possible after birth. We aimed to build clinically useful equations estimating the risk of later obesity in newborns, as a first step towards focused early prevention against the global obesity epidemic. We analyzed the lifetime Northern Finland Birth Cohort 1986 (NFBC1986) (N = 4,032) to draw predictive equations for childhood and adolescent obesity from traditional risk factors (parental BMI, birth weight, maternal gestational weight gain, behaviour and social indicators), and a genetic score built from 39 BMI/obesity-associated polymorphisms. We performed validation analyses in a retrospective cohort of 1,503 Italian children and in a prospective cohort of 1,032 U.S. children. In the NFBC1986, the cumulative accuracy of traditional risk factors predicting childhood obesity, adolescent obesity, and childhood obesity persistent into adolescence was good: AUROC = 0·78[0·74–0.82], 0·75[0·71–0·79] and 0·85[0·80–0·90] respectively (all p<0·001). Adding the genetic score produced discrimination improvements ≤1%. The NFBC1986 equation for childhood obesity remained acceptably accurate when applied to the Italian and the U.S. cohort (AUROC = 0·70[0·63–0·77] and 0·73[0·67–0·80] respectively) and the two additional equations for childhood obesity newly drawn from the Italian and the U.S. datasets showed good accuracy in respective cohorts (AUROC = 0·74[0·69–0·79] and 0·79[0·73–0·84]) (all p<0·001). The three equations for childhood obesity were converted into simple Excel risk calculators for potential clinical use. This study provides the first example of handy tools for predicting childhood obesity in newborns by means of easily recorded information, while it shows that currently known genetic variants have very little usefulness for such prediction.

Introduction: To evaluate time in tight range (TITR) 70–140 mg/dL (3.9–7.8 mmol/L), its correlation with standard continuous glucose monitoring (CGM) metrics and the clinical variables that possibly have a substantial impact on its value, in a large cohort of pediatric subjects using different treatment strategies. Materials and Methods: A total of 854 children and adolescents with type 1 diabetes were consecutively recruited in this real world, dual center, cross-sectional study. Participants were categorized into four treatment groups (multiple daily injections [MDI] + real-time CGM, MDI + intermittently scanned CGM, sensor augmented pump, and hybrid closed loop [HCL]). Demographical and clinical data, including CGM data, were collected and analyzed. Results: The overall study population exhibited an average TITR of 36.4% ± 12.8%. HCL users showed higher TITR levels compared to the other treatment groups ( P < 0.001). A time in range (TIR) cut-off value of 71.9% identified subjects achieving a TITR ≥50% (area under curve [AUC] 0.98; 95% confidence interval 0.97–0.99, P < 0.001), and a strong positive correlation between these two metrics was observed ( r = 0.95, P < 0.001). An increase in TIR of 1% was associated with 1.84 ( R ² Nagelkerke = 0.35, P < 0.001) increased likelihood of achieving TITR ≥50%. Use of HCL systems ( B = 7.78; P < 0.001), disease duration ( B = −0.26, P = 0.006), coefficient of variation ( B = −0.30, P = 0.004), and glycated hemoglobin ( B = −8.82; P < 0.001) emerged as significant predictors of TITR levels. Conclusions: Our study highlights that most children and adolescents with type 1 diabetes present TITR levels below 50%, except those using HCL. Tailored interventions and strategies should be implemented to increase TITR.