Insufficient average sleep duration has been inconsistently associated with poor diet and obesity risks in youth. Inconsistencies in findings across studies may be due to a general failure to examine associations in weekday versus weekend sleep. We hypothesized that greater variations in weekday and weekend sleep duration would be associated with more disinhibited eating behaviors, which, in turn, might be involved in the relationship between sleep and weight. We, therefore, examined, among healthy, non-treatment seeking youth, the associations of average weekly, weekend, and weekday sleep duration with eating in the absence of hunger (EAH), a disinhibited eating behavior associated with disordered eating and obesity. Sleep was assessed via actigraphy for 14 days. Participants completed a self-report measure of EAH. Adiposity was measured by dual-energy X-ray absorptiometry. Linear regressions were used to test the associations of sleep duration with EAH and the associations of sleep duration and EAH, with fat mass. Among 123 participants (8–17 years, 52.0% female, and 30.9% with overweight), there was no significant association between average weekly sleep and EAH. Further, there was no significant association among average weekly sleep duration or EAH and fat mass. However, average weekday sleep was negatively associated, and average weekend sleep was positively associated, with EAH (ps < 0.02). Weekend “catch-up” sleep (the difference between weekend and weekday sleep) was positively associated with EAH (p < 0.01). Findings indicate that shorter weekday sleep and greater weekend “catch-up” sleep are associated with EAH, which may place youth at risk for the development of excess weight gain over time.

Background. Prospective data suggest depressive symptoms worsen insulin resistance and accelerate type 2 diabetes (T2D) onset.Purpose. We sought to dete

Interpersonal psychotherapy (IPT) prevents weight gain and reduces loss-of-control (LOC)-eating in adults. However, IPT was not superior to health-education (HE) for preventing excess weight gain and reducing LOC-eating over 1-year in adolescent girls at risk for excess weight gain and eating disorders. Limited data suggest that older and non-White youth may be especially responsive to IPT. In secondary analyses, we examined if age or race moderated weight and LOC-eating outcomes. The 113 participants (12–17 years; 56.6% White) from the original trial were re-contacted 3 years later for assessment. At baseline and follow-up visits through 3 years, we assessed BMI, adiposity by dual energy X-ray absorptiometry, and LOC-eating presence. In linear mixed models, baseline age moderated 3-year BMI outcome; older girls in IPT had the lowest 3-year BMI gain compared to younger girls in IPT and all girls in HE, p = 0.04. A similar pattern was observed for adiposity. Race moderated 3-year LOC-eating; non-White girls in IPT were most likely to abstain from LOC-eating at 3 years compared to all other girls, p = 0.04. This hypothesis-generating analysis suggests future studies should determine if IPT is especially efficacious at reducing LOC-eating in older, non-White adolescents.

Loss of control (LOC) eating in youth is associated with elevated fasting serum leptin, even after accounting for adiposity. Anxiety is closely linked to, and may exacerbate, LOC eating. Yet, it remains unclear how anxiety relates to leptin, or if the relationship is moderated by the presence of LOC eating. We examined whether self-reported trait anxiety interacted with LOC eating in relation to leptin in a convenience sample of youths (n = 592; 13.1 ± 2.7 years; body mass index z-score (BMIz) = 0.9 ± 1.1; 61.8% girls; 53.5% non-Hispanic White; 36.6% with LOC eating). LOC eating was assessed by interview. Leptin was measured after an overnight fast. Exploratory analyses were conducted to examine anxiety and LOC eating in relation to laboratory intake patterns in three sub-samples. In a generalized linear model adjusting for relevant covariates, anxiety significantly interacted with LOC eating in relation to leptin (p = 0.02), such that greater trait anxiety related to higher concentrations of leptin only among youth with LOC eating. Trait anxiety was not significantly related to fasting serum leptin independently in a generalized linear model adjusting for age, race, height, sex, study type, and fat mass (kg). Exploratory mechanistic analyses of food intake patterns did not identify consistent results for participants with both anxiety and LOC eating. Among youth with LOC eating, anxiety may be associated with higher serum leptin. Prospective data are required to elucidate the directionality and mechanisms of these relationships.

Multisystem inflammatory syndrome in children (MIS-C) is a rare but life-threatening hyperinflammatory condition induced by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes pediatric COVID-19 (pCOVID-19). The relationship of the systemic tissue injury to the pathophysiology of MIS-C is poorly defined. We leveraged the high sensitivity of epigenomics analyses of plasma cell-free DNA (cfDNA) and plasma cytokine measurements to identify the spectrum of tissue injury and glean mechanistic insights. Compared with pediatric healthy controls (pHCs) and patients with pCOVID-19, patients with MIS-C had higher levels of cfDNA primarily derived from innate immune cells, megakaryocyte-erythroid precursor cells, and nonhematopoietic tissues such as hepatocytes, cardiac myocytes, and kidney cells. Nonhematopoietic tissue cfDNA levels demonstrated significant interindividual variability, consistent with the heterogenous clinical presentation of MIS-C. In contrast, adaptive immune cell–derived cfDNA levels were comparable in MIS-C and pCOVID-19 patients. Indeed, the cfDNA of innate immune cells in patients with MIS-C correlated with the levels of innate immune inflammatory cytokines and nonhematopoietic tissue–derived cfDNA, suggesting a primarily innate immunity–mediated response to account for the multisystem pathology. These data provide insight into the pathogenesis of MIS-C and support the value of cfDNA as a sensitive biomarker to map tissue injury in MIS-C and likely other multiorgan inflammatory conditions.