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In children, the mechanisms implicated in deterioration of glucose homeostasis versus reversion to normal glucose tolerance (NGT) remain uncertain. We aimed to describe the natural history of dysglycemia from childhood to late adolescence and to identify its early determinants. We used baseline (8–10 years, n = 630), 1st follow‐up (10–12 years, n = 564) and 2nd follow‐up (15–17 years, n = 377) data from the QUALITY cohort of White Canadian children with parental obesity. Children underwent a 2‐h oral glucose tolerance test at each cycle with plasma glucose and insulin measured at 0/30/60/90/120 min. American Diabetes Association criteria defined dysglycemia (impaired fasting glucose, impaired glucose tolerance or type 2 diabetes). Longitudinal patterns of insulin sensitivity and beta‐cell function were estimated using generalized additive mixed models. Model averaging identified biological, sociodemographic and lifestyle‐related determinants of dysglycemia. Of the children NGT at baseline, 66 (21%) developed dysglycemia without reverting to NGT. Among children with dysglycemia at baseline, 24 (73%) reverted to NGT. In children with dysglycemia at 1st follow‐up, 18 (53%) later reverted to NGT. Among biological, sociodemographic and lifestyle determinants at 8–10 years, only fasting and 2‐h glucose were associated with developing dysglycemia (odds ratio [95% CI] per 1 mmol/L increase: 4.50 [1.06; 19.02] and 1.74 [1.11; 2.73], respectively). Beta‐cell function decreased by 40% in children with overweight or obesity. In conclusion, up to 75% of children with dysglycemia reverted to NGT during puberty. Children with higher fasting and 2‐h glucose were at higher risk for progression to dysglycemia, while no demographic/lifestyle determinants were identified. [ABSTRACT FROM AUTHOR]

Background: Uncertainty remains regarding the causal effect of physical activity and sedentary behaviours on the development of type 2 diabetes in children. We aimed to estimate average treatment effects of physical activity and sedentary behaviours on risk of type 2 diabetes in individuals who are at risk during childhood and adolescence., Methods: We used data from the Quebec Adipose and Lifestyle Investigation in Youth (QUALITY) cohort of children of western European descent (white non-Hispanic race or ethnicity) with a parental history of obesity (defined as a BMI of 30 kg/m 2 or more, or a waist circumference of more than 102 cm in men and 88 cm in women) evaluated at the ages of 8-10 years (baseline), 10-12 years (first follow-up cycle), and 15-17 years (second follow-up cycle) in Québec, Canada. We measured moderate-to-vigorous physical activity (MVPA) and sedentary time by accelerometry, and leisure screen time by questionnaire at each cycle. Outcomes included fasting and 2 h post-load glycaemia and validated indices of insulin sensitivity and insulin secretion. We estimated average treatment effects of MVPA, sedentary time, and screen time on markers of type 2 diabetes using longitudinal marginal structural models with time-varying exposures, outcomes, and confounders from the ages of 8-10 to 15-17 years and inverse probability of treatment and censoring weighting. We considered both the current and cumulative effects of exposures on outcomes., Findings: 630 children were evaluated at baseline (age 8-10 years) between July, 2005, and December, 2008, 564 were evaluated at the first follow-up (age 10-12 years) between July, 2007, and March, 2011, and 377 were evaluated at the second follow-up (age 15-17 years) between September, 2012, and May, 2016. Based on cumulative exposure results, estimated average treatment effects for MVPA were 5·6% (95% CI 2·8 to 8·5) on insulin sensitivity and -3·8% (-7·1 to -0·5) on second-phase insulin secretion per 10 min daily increment from the ages of 8-10 years to age 15-17 years. Average treatment effects for sedentary time and reported screen time resulted in reduced insulin sensitivity (-8·2% [-12·3 to -3·9] and -6·4% [-10·1 to -2·5], respectively), increased second-phase insulin secretion (5·9% [1·9 to 10·1] and 7·0% [-0·1 to 14·7], respectively), and higher fasting glycaemia (0·03 mmol/L [0·003 to 0·05] and 0·02 mmol/L [0·01 to 0·03], respectively) per additional daily hour from the ages of 8-10 years to 15-17 years., Interpretation: Using modern causal inference approaches strengthened the evidence of MVPA and sedentary behaviours as key drivers of development of type 2 diabetes in at-risk children and adolescents, and should be considered as key targets for prevention., Funding: Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, and Fonds de Recherche du Québec-Santé., Translation: For the French translation of the abstract see Supplementary Materials section., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Objective: Robust evidence exists for the health-enhancing benefits of social support in adults. Inflammatory processes are thought to be an important mechanism linking social support and health risk. Less is known about the relation between social support and chronic inflammation during childhood and adolescence, or when the association emerges during the lifespan., Method: Data from the population-representative 1999 Quebec Child and Adolescent Health and Social (QCAHS) survey were analyzed. Youth aged 9, 13, and 16 years (N = 3613) and their parents answered questions about social support. A subsample (n = 2186) completed a fasting blood draw that was assayed for C-reactive protein (CRP)., Findings: Higher social support was significantly associated with lower hs-CRPlog, after controlling for age, sex, body mass index (BMI Z-score), medication use, puberty, ethnoracial status (French-Canadian), smoking, household income, and parental education (F = 25.88, p = < .001, Total R2adj = 10.2%). The association was largely similar for boys and girls, and strengthened with age., Conclusion: Greater social support was linked to lower chronic low-grade inflammation in a large sample of children and adolescents. Effect sizes were small and consistent with prior findings in the adult literature. Importantly, these findings provide evidence that the relation between social support and inflammation emerges early in the lifespan. Future work should consider broader, more encompassing conceptualizations of social support, the role of social media, and prospective trajectories of social support and inflammatory markers., Competing Interests: The authors have declared that no competing interests exist.