Childhood overeating is associated with adverse cardiometabolic and inflammatory profiles in adolescence.
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ABSTRACT:
SUBMITTER: Hubel C
PROVIDER: S-EPMC8203659 | biostudies-literature | 2021 Jun
REPOSITORIES: biostudies-literature
Publications
Childhood overeating is associated with adverse cardiometabolic and inflammatory profiles in adolescence.
Hübel Christopher C Herle Moritz M Santos Ferreira Diana L DL Abdulkadir Mohamed M Bryant-Waugh Rachel R Loos Ruth J F RJF Bulik Cynthia M CM Lawlor Deborah A DA Micali Nadia N
Scientific reports 20210614 1
Childhood eating behaviour contributes to the rise of obesity and related noncommunicable disease worldwide. However, we lack a deep understanding of biochemical alterations that can arise from aberrant eating behaviour. In this study, we prospectively associate longitudinal trajectories of childhood overeating, undereating, and fussy eating with metabolic markers at age 16 years to explore adolescent metabolic alterations related to specific eating patterns in the first 10 years of life. Data a ...[more]
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Project description:Fetal overnutrition predisposes offspring to increased metabolic risk. The current study used metabolomics to assess sustained differences in serum metabolites across childhood and adolescence among youth exposed to three typologies of fetal overnutrition: maternal obesity only, gestational diabetes mellitus (GDM) only, and obesity + GDM. We included youth exposed in utero to obesity only (BMI ≥ 30; n = 66), GDM only (n = 56), obesity + GDM (n = 25), or unexposed (n = 297), with untargeted metabolomics measured at ages 10 and 16 years. We used linear mixed models to identify metabolites across both time-points associated with exposure to any overnutrition, using a false-discovery-rate correction (FDR) <0.20. These metabolites were included in a principal component analysis (PCA) to generate profiles and assess metabolite profile differences with respect to overnutrition typology (adjusted for prenatal smoking, offspring age, sex, and race/ethnicity). Fetal overnutrition was associated with 52 metabolites. PCA yielded four factors accounting for 17-27% of the variance, depending on age of measurement. We observed differences in three factor patterns with respect to overnutrition typology: sphingomyelin-mannose (8-13% variance), skeletal muscle metabolism (6-10% variance), and 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF; 3-4% variance). The sphingomyelin-mannose factor score was higher among offspring exposed to obesity vs. GDM. Exposure to obesity + GDM (vs. GDM or obesity only) was associated with higher skeletal muscle metabolism and CMPF scores. Fetal overnutrition is associated with metabolic changes in the offspring, but differences between typologies of overnutrition account for a small amount of variation in the metabolome, suggesting there is likely greater pathophysiological overlap than difference.
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Project description:PurposeThis study examined the association between a Dietary Inflammatory Score adapted for children (cDIS) and Cardiometabolic Risk (CMR) score in adolescence/early adulthood in the Avon Longitudinal Study of Parents and Children (ALSPAC).MethodsThe cDIS was calculated at 7, 10 and 13 years using diet diary data. Anthropometric and biochemical data at 17 (N = 1937) and 24 (N = 1957) years were used to calculate CMR scores at each age [mean sex-specific z-scores from triacylglycerol, HDL-cholesterol, LDL-cholesterol, mean arterial blood pressure (MAP), homeostatic model assessment of insulin resistance (HOMA-IR) and fat-mass index (FMI)]. Multivariable linear regression models examined associations between cDIS at 7, 10 and 13 years and a continuous CMR z-score and individual CMR markers at 17 and 24 years.ResultsIn fully adjusted models, a higher cDIS (more pro-inflammatory diet) at 7 years was associated with an increase in CMR z-score at 17 years (β 0.19; 95% CI 0.03-0.35 for third versus first cDIS tertile) and at 24 years (β 0.28; 95% CI 0.11,0.44 for third versus first cDIS tertile). There was a weak association between a higher cDIS at 10 years and an increase in CMR z-score at 17 years (β 0.16; 95% CI - 0.003, 0.32 for third versus first cDIS tertile). No other clear associations were evident. FMI, MAP and HOMA-IR were the main CMR factors contributing to these associations.ConclusionA more pro-inflammatory diet during childhood was associated with a worse cardiometabolic profile in late adolescence/early adulthood. A childhood diet abundant in nutrients with anti-inflammatory properties could help reduce development of CMR factors.
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Project description:IntroductionAdolescence is marked by physiological and social changes, such as puberty, increased responsibilities and earlier school start times. This often leads to insufficient sleep on school nights and the need to compensate for lost sleep on weekends, causing a misalignment between biological and social times, which has been termed social jetlag (SJL). SJL triggers stress responses and is associated with several negative health outcomes, including higher cardiometabolic risk in adults. In adolescence, however, SJL has only been consistently related to increases in adiposity but its association with other cardiometabolic indicators are unclear.MethodIn a sample of 278 healthy early adolescents (9-15 years of age; 168 girls) we investigated: 1) whether self-reported SJL is associated (using path analyses) with a cardiometabolic status latent factor obtained by testing the best fitting model via confirmatory factor analyses from an initial set of eight indicators [body mass index (BMI), waist/height ratio, triglyceride concentration, diastolic and systolic blood pressure, glycated hemoglobin, total cholesterol/high-density lipoprotein ratio (chol/HDL), and % body fat]; and 2) whether age and/or pubertal status influence the association between SJL and cardiometabolic status.ResultWe found that, for girls, higher SJL was associated with more adverse cardiometabolic latent scores (the shared variance of BMI, waist/height ratio, chol/HDL and systolic blood pressure, which had acceptable model fit indices). However, the role of age and pubertal status in this association was unclear for both sexes.DiscussionSJL was associated with adverse cardiometabolic latent traits beyond increases in adiposity in this observational study in early female adolescents. Because disruptions of circadian rhythms are believed to lead to dysregulated energy homeostasis and not vice-versa, our findings highlight the need for sleep interventions in adolescence to help reduce the global burden of cardiometabolic ill health, especially in girls.
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Project description:Background and objectiveThere is a paucity of prospective evidence examining the links between sedentary time (ST) and cardiometabolic outcomes in youth. We examined the associations between objectively assessed ST and moderate to vigorous physical activity (MVPA) in childhood with cardiometabolic risk in adolescence.MethodsThe study included 4639 children (47% male) aged 11 to 12 years at baseline whose mothers were enrolled in ALSPAC (Avon Longitudinal Study of Parents and Children) during their pregnancy in the early 1990s. A total of 2963 children had valid blood samples at age 15 to 16 years. Associations with baseline ST and MVPA were examined for BMI, waist circumference, body fat mass, lean body mass, systolic and diastolic blood pressure, fasting triglycerides, total cholesterol, low-density lipoprotein and high-density lipoprotein (HDL) cholesterol, glucose, insulin, C-reactive protein, and a clustered standardized cardiometabolic risk score (CMscore).ResultsBaseline ST was not associated deleteriously with any cardiometabolic markers. MVPA was beneficially associated with the 3 adiposity indicators, lean body mass, systolic blood pressure, triglycerides, C-reactive protein, insulin, HDL cholesterol, and CMscore; once the models were adjusted for baseline levels of these markers, these associations remained for body fat mass (mean difference per 10 minutes of MVPA: -0.320 [95% confidence interval (CI): -0.438 to -0.203]; P < .001), HDL cholesterol (0.006 logged mmol/L [95% CI: 0.001 to 0.011]; P = .028), insulin (-0.024 logged IU/L [95% CI: -0.036 to -0.013]; P < .001), and CMscore (-0.014 [95% CI: -0.025 to -0.004]; P = .009).ConclusionsWe found no evidence linking ST in late childhood with adverse cardiometabolic outcomes in adolescence. Baseline MVPA was beneficially linked to broad cardiometabolic health in adolescence.
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Project description:ImportanceChildhood stress exposure is associated with inflammation as measured by C-reactive protein (CRP) and interleukin 6 (IL-6). However, findings are inconsistent and effect sizes are small. The addition of soluble urokinase plasminogen activator receptor (suPAR), a new biomarker of chronic inflammation, may improve measurement of stress-related inflammatory burden.ObjectivesTo assess whether exposure to adverse experiences, stress, and violence is associated with an increase in suPAR levels in young people and to test the hypothesis that measuring suPAR in addition to CRP or IL-6 levels improves the assessment of the inflammatory burden associated with early-life stress.Design, setting, and participantsThis cohort study included 1391 participants from a 1994 to 1995 birth cohort of twins from the nationally representative Environmental Risk Longitudinal Twin Study in the United Kingdom. Participants were followed up until 18 years of age (93% retention). Plasma samples were analyzed in July 2018, and statistical analysis was performed from October 1, 2018, to May 31, 2019.ExposuresAdverse childhood experiences and childhood and adolescent experience of stress and violence exposure.Main outcomes and measuresPlasma CRP, IL-6, and suPAR levels at 18 years of age.ResultsAmong 1391 young people (mean [SD] age, 18.4 [0.36] years; 733 [52.7%] female), those who had been exposed to stressful experiences had elevated suPAR levels by 18 years of age after controlling for sex, body mass index, and smoking: 0.03-ng/mL (95% CI, 0.01-0.05 ng/mL) increase in suPAR per each additional adverse childhood experience, 0.09-ng/mL (95% CI, 0.01-0.17 ng/mL) increase in suPAR per each additional severe childhood experience of stress or violence, and 0.04-ng/mL (95% CI, -0.02 to 0.10 ng/mL) increase in suPAR per each additional severe adolescent experience of stress or violence. Individuals exposed to multiple types of violence in both childhood and adolescence had 0.26-ng/mL (95% CI, 0.07-0.45 ng/mL) higher suPAR levels compared with children who did not experience stress or violence. These stress-exposed young people were significantly more likely to have elevated suPAR levels at 18 years of age even if they did not have elevated CRP or IL-6 levels. Measuring suPAR in addition to CRP or IL-6 increased the association between stress exposure and inflammatory burden. For example, after adjusting for CRP and IL-6 levels, each additional adverse childhood experience was associated with a 0.05-mL (95% CI, 0.03-0.07 ng/mL) increase in suPAR, each additional severe childhood experience of stress or violence was associated with a 0.14-ng/mL (95% CI, 0.06-0.22 ng/mL) increase in suPAR, and each additional severe adolescent experience of stress or violence was associated with a 0.10-ng/mL (95% CI, 0.04-0.16 ng/mL) increase in suPAR.Conclusions and relevanceThe results suggest that adult inflammation is associated with childhood exposure to stress. Adding information about suPAR to traditional biomarkers of inflammation may improve the measurement of inflammatory burden associated with exposure to stress and violence.
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Project description:Early identification and interventions are imperative for mitigating the harmful effects of adverse childhood experiences (ACEs). Nonetheless, a substantial barrier persists in identifying adolescents experiencing ACEs. One understudied avenue for early identification of ACEs is through the examination of somatic symptoms endorsed by adolescents. Understanding the relationship between recent ACEs exposure and somatic symptoms may serve as a useful indicator for identifying adolescents affected by ACEs. This study examines the relationships between recent exposure to ACEs (within the past one to two years) and somatic symptoms across adolescence (ages 12-16 years). Longitudinal prospective data of 1354 child and caregiver dyads from the Longitudinal Studies of Child Abuse and Neglect were used in this study. Data from three time points, when adolescents were 12, 14, and 16, were used to conduct longitudinal path analyses. Somatic symptoms- defined as physical symptoms without known medical causes- were measured using the caregiver-report subscale of the Child Behavior Checklist. Recent ACEs in the past one to two years were measured using an index score summing exposure to nine ACE variables. The results indicated a significant association between recent ACEs and increased somatic symptoms at age 12. However, there were no significant associations between recent ACEs and somatic symptoms at ages 14 and 16. The findings indicate a notably stronger relationship between recent ACEs exposure and the presence of increased somatic symptoms at the age of 12, in contrast to what is observed at ages 14 and 16. This finding suggests that somatic symptoms during early adolescence may suggest underlying issues, potentially stemming from stressors such as ACEs.
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Project description:BackgroundReports on body mass index (BMI) trajectories from childhood into late adolescence, their determinants, and subsequent cardiometabolic risk markers, particularly among European populations have been few. Moreover, sex-specific investigation is necessary considering the sex difference in BMI, and the sex-specific association between BMI and some cardiometabolic risk markers.MethodsUsing a sample from the DOrtmund Nutritional and Anthropometric Longitudinally Designed study, we explored sex-specific trajectories of the BMI standard deviation score (SDS) from 4 to 18 years of age in 354 males and 335 females by latent (class) growth models. The determinants of trajectory were assessed by logistic regression. We identified cardiometabolic risk markers that were highly associated with BMI SDS trajectory by random forest regression, and finally we used generalized linear models to investigate differences in the identified cardiometabolic risk markers between pairs of trajectories.ResultsWe observed four: 'low-normal weight', 'mid-normal weight', 'high-normal weight', and 'overweight', and three: ''low-normal weight', 'mid-normal weight', and 'high-normal weight' trajectories in males and females, respectively. Higher maternal prepregnancy BMI was associated with the 'overweight' trajectory, and with 'high-normal weight' trajectory in both sexes. In addition, employed mothers and first-born status were associated with 'high-normal weight' trajectory in females. BMI SDS trajectory was associated with high-density lipoprotein-cholesterol and interleukin-18 (IL-18) in males, and diastolic blood pressure and interleukin-6 (IL-6) in females. However, only males following the 'overweight' trajectory had significantly higher IL-18 when compared to their 'low-normal weight' counterpart.ConclusionsWe identified sex-specific distinct trajectories of BMI SDS from childhood into late adolescence, higher maternal prepregnancy BMI as a common determinant of the 'high-normal weight' and 'overweight' trajectories, and 'overweight' trajectory being associated with elevated IL-18 in late adolescence-young adulthood. This study emphasizes the role of maternal prepregnancy BMI in overweight, and highlights IL-18 as a cardiometabolic signature of overweight across life.
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Project description:Interventions: Group 1: Patients with a malignant disease are initially reported to the German Childhood Cancer Registry (DKKR) by the pediatric oncology centers treating them. This generates a PatID (patient identifier) ??and a MaligID (malignant identifier). If there is a malignant endocrine tumor that is recorded in our registry, the DKKR sends a notification form with these two IDs to the MET registry center. The registry center then contacts the reporting pediatric oncology department and sends the patient information and declarations of consent.
The treating physicians initially check the existence of inclusion and exclusion criteria. Insofar as inclusion criteria are met but exclusion criteria are not present, there is detailed medical information and written information about the content, risks and benefits of the MET registry. If the patient and the legal guardian agree, the patient can be included in the MET registry. In some cases, pediatric oncology centers contact the MET Help Desk for clinical advice. Patient data in German-speaking countries is recorded via the GPOH platform MARVIN (XClinical) in so-called electronic Case Report Forms” (eCRFs).
The patient information and declarations of consent are then sent in this way.
Primary outcome(s): The primary objectives of the MET Registry include:
1. The prospective registration of all children and adolescents with an initial diagnosis of a malignant endocrine tumor between the ages of 0 and 18 years
2. The scientific evaluation with the aim of optimizing the therapy of affected patients
Study Design: Allocation: ; Masking: ; Control: ; Assignment: ; Study design purpose: Prognosis
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Project description:Metabolic syndrome is a cluster of risk factors for cardiovascular disease afflicting more than 1 billion people worldwide and is increasingly being identified in younger age groups and in socioeconomically disadvantaged settings in the global south. Enteropathogen exposure and environmental enteropathy in infancy may contribute to metabolic syndrome by disrupting the metabolic profile in a way that is detectable in cardiometabolic markers later in childhood. A total of 217 subjects previously enrolled in a birth cohort in Amazonian Peru were monitored annually from ages 2 to 5 years. A total of 197 blood samples collected in later childhood were analyzed for 37 cardiometabolic biomarkers, including adipokines, apolipoproteins, cytokines, which were matched to extant early-life markers of enteropathy ascertained between birth and 2 years. Multivariate and multivariable regression models were fitted to test for associations, adjusting for confounders. Fecal and urinary markers of intestinal permeability and inflammation (myeloperoxidase, lactulose, and mannitol) measured in infancy were associated with later serum concentrations of soluble CD40-ligand, a proinflammatory cytokine correlated with adverse metabolic outcomes. Fecal myeloperoxidase was also associated with later levels of omentin-1. Enteric protozoa exposure showed stronger associations with later cardiometabolic markers than viruses, bacteria, and overall diarrheal episodes. Early-life enteropathy markers were associated with altered adipokine, apolipoprotein, and cytokine profiles later in childhood consistent with an adverse cardiometabolic disease risk profile in this cohort. Markers of intestinal permeability and inflammation measured in urine (lactulose, mannitol) and stool (myeloperoxidase, protozoal infections) during infancy may predict metabolic syndrome in adulthood.
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