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 |
REPOSITORIES: biostudies-literature
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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.
| S-EPMC4444802 | biostudies-literature
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.
| S-EPMC6830440 | biostudies-literature
Project description:BackgroundAdverse family experiences in early life are associated with subsequent psychopathology. This study adds to the growing body of work exploring the nature and associations between adverse experiences over the childhood years.MethodsPrimary carers of 1143 randomly recruited 14-year olds in Cambridgeshire and Suffolk, UK were interviewed using the Cambridge Early Experiences Interview (CAMEEI) to assess family-focused adversities. Adversities were recorded retrospectively in three time periods (early and later childhood and early adolescence). Latent Class Analysis (LCA) grouped individuals into adversity classes for each time period and longitudinally. Adolescents were interviewed to generate lifetime DSM-IV diagnoses using the K-SADS-PL. The associations between adversity class and diagnoses were explored.ResultsLCA generated a 4-class model for each time period and longitudinally. In early childhood 69% were allocated to a low adversity class; a moderate adversity class (19%) showed elevated rates of family loss, mild or moderate family discord, financial difficulties, maternal psychiatric illness and higher risk for paternal atypical parenting; a severe class (6%) experienced higher rates on all indicators and almost exclusively accounted for incidents of child abuse; a fourth class, characterised by atypical parenting from both parents, accounted for the remaining 7%. Class membership was fairly stable (~ 55%) over time with escape from any adversity by 14 years being uncommon. Compared to those in the low class, the odds ratio for reported psychopathology in adolescents in the severe class ranged from 8 for disruptive behaviour disorders through to 4.8 for depressions and 2.0 for anxiety disorders. Only in the low adversity class did significantly more females than males report psychopathology.ConclusionsFamily adversities in the early years occur as multiple rather than single experiences. Although some children escape adversity, for many this negative family environment persists over the first 15 years of life. Different profiles of family risk may be associated with specific mental disorders in young people. Sex differences in psychopathologies may be most pronounced in those exposed to low levels of family adversities.
| S-EPMC3199756 | biostudies-literature
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.
| S-EPMC6339359 | biostudies-literature
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
| 2737649 | ecrin-mdr-crc
Project description:Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. We assessed whether the timing of psychosocial risk from infancy through adolescence predicts cardiometabolic outcomes in young adulthood. Young adults and their mothers participated in a longitudinal study beginning in infancy in Santiago, Chile (N = 1040). At infancy, 5 years, 10 years, and adolescence, mothers reported on depressive symptoms, stressful experiences, support for child development in the home, father absence, parental education, and socioeconomic status (SES) to create a psychosocial risk composite at each time point. Young adults (52.1% female; 21-27 years) provided fasting serum samples and participated in anthropometric and blood pressure (BP) assessments, including a dual-energy X-ray absorptiometry (DXA) scan for measuring body fat. Greater infant psychosocial risk was associated with a greater young adult metabolic syndrome score (β = 0.07, 95% confidence intervals (CI): 0.01 to 0.13, p = 0.02), a higher body mass index and waist circumference composite (β = 0.08, 95% CI: 0.03 to 0.13, p = 0.002), and a higher body fat (DXA) composite (β = 0.07, 95% CI: 0.01 to 0.12, p = 0.02). No psychosocial risk measure from any time point was associated with BP. Infant psychosocial risk predicted cardiometabolic outcomes in young adulthood better than psychosocial risk at 5 years, 10 years, or adolescence, mean of psychosocial risk from infancy through adolescence, and maximum of psychosocial risk at any one time. Consistent with the Developmental Origins of Health and Disease model, findings suggest that infancy is a sensitive period for psychosocial risk leading to poorer cardiometabolic outcomes in young adulthood.
| S-EPMC8107042 | biostudies-literature
Project description:OBJECTIVE:With an emphasis on betrayal trauma, this study used latent profile analysis to examine how childhood traumas co-occur and whether trauma patterns differentially predicted psychological distress. METHOD:A community sample of 806 adolescents and young adults participated. Youths reported their trauma histories, and lifetime DSM-IV disorders were assessed using a structured diagnostic interview. RESULTS:Latent profile analysis yielded 5 profiles: high betrayal trauma physical violence and emotional abuse (HBTPE), high betrayal trauma sexual and emotional abuse (HBTSE), low betrayal trauma (LBT), parent death (PD), and a no/low trauma profile. Logistic regression analyses compared youths in the no/low trauma profile to those in the trauma profiles. Youths in the HBTPE profile were more likely to have moderate/severe major depressive disorder (odds ratio [OR] = 2.92, 95% CI [1.16, 7.32]), posttraumatic stress disorder (OR = 4.33, 95% CI [1.34, 14.03]), and hallucinations (OR = 5.03, 95% CI [2.00, 12.67]); youths in the HBTSE and LBT profiles were more likely to experience hallucinations (OR = 3.19, 95% CI [1.21, 8.39] and OR = 3.20, 95% CI [1.01, 10.19], respectively); and youths in the PD profile were more likely to have moderate/severe depression (OR = 2.42, 95% CI [1.07, 5.43]). CONCLUSIONS:Specific trauma types co-occurred when considering type, level of betrayal, and frequency. The emergence of the 2 high betrayal trauma profiles, with differing symptom presentations, suggests that experiences of high betrayal traumas are not homogenous and specific trauma-focused interventions may be more appropriate for differing trauma profiles.
| S-EPMC4767667 | biostudies-literature
Project description:ObjectiveMaternal adiposity is associated with poor offspring cardiometabolic health. We aimed to evaluate the relationship of maternal pre-pregnancy body mass index (BMI) on the BMI, body composition and cardiometabolic characteristics of the offspring.MethodsForty offspring of overweight/obese mothers (O-OW) and 28 offspring of normal weight mothers (O-NW) underwent evaluation of body composition, abdominal fat distribution, blood pressure measurement, fasting lipids and an oral glucose tolerance test. The anthropometric and cardiometabolic characteristics of O-OW were compared with those of O-NW, and the relationship to maternal BMI was evaluated.ResultsSubjects (mean age: 12.6 ± 0.4, female: 52.9%) had similar gestational age, birth weight, age, gender, and Tanner stage. However, O-OW had a significantly higher BMI (24.4 ± 1.2 vs. 19.7 ± 0.8 kg/m(2) , p = 0.001), % body fat (31.7 ± 1.6 vs. 24.6 ± 1.1%, p < 0.001), visceral fat (41.9 ± 4.7 vs. 26.1 ± 3.9 cm(2) , p = 0.012) with no difference in lean body mass compared with O-NW. O-OW had lower whole body insulin sensitivity index (WBISI) with an adverse cardiovascular disease risk profile [higher blood pressure (BP), triglycerides to high-density lipoprotein (HDL) ratio, hs-C-reactive protein (CRP) and lower HDL]. In addition to offspring's %body fat (β = -0.60, p < 0.001), maternal pre-pregnancy BMI (β = -0.19, p = 0.046) contributed significantly and independently to the offspring's WBISI (R(2) =0.55, p < 0.001).ConclusionsHigh pre-pregnancy BMI is an important contributor to excess adiposity, insulin resistance, and cardiometabolic disease risk in the offspring during childhood.
| S-EPMC4534350 | biostudies-literature
Project description:Background and aimsEnergy dense, high fat, low fibre diets may contribute to obesity in young people, however their relationships with other cardiometabolic risk factors are unclear. We examined associations between an 'energy-dense, high-fat and low-fibre' dietary pattern (DP) and cardiometabolic risk factors, and the tracking of this DP in adolescence.Methods and resultsData was sourced from participants in the Western Australian Pregnancy (Raine) Cohort Study. At 14 and 17 y, dietary intake, anthropometric and biochemical data were measured and z-scores for an 'energy dense, high fat and low fibre' DP were estimated using reduced rank regression (RRR). Associations between DP z-scores and cardiometabolic risk factors were examined using regression models. Tracking of DP z-scores was assessed using Pearson's correlation coefficient. A 1 SD unit increase in DP z-score between 14 and 17 y was associated with a 20% greater odds of high metabolic risk (95% CI: 1.01, 1.41) and a 0.04 mmol/L higher fasting glucose in boys (95% CI: 0.01, 0.08); a 28% greater odds of a high-waist circumference (95% CI: 1.00, 1.63) in girls. An increase of 3% and 4% was observed for insulin and HOMA (95% CI: 1%, 7%), respectively, in boys and girls, for every 1 SD increase in DP z-score and independently of BMI. The DP showed moderate tracking between 14 and 17 y of age (r = 0.51 for boys, r = 0.45 for girls).ConclusionAn 'energy dense, high fat, low fibre' DP is positively associated with cardiometabolic risk factors and tends to persist throughout adolescence.
| S-EPMC4510146 | biostudies-literature
Project description:Background Gastric Helicobacter pylori colonization leads to iron deficiency anemia (IDA), especially in children and adolescents. However the pathogenesis is poorly understood. Objective We sought to identify specific H. pylori genes involved in IDA development, by comparing bacterial genome-wide expression profiling in patients affected or not. Methods H. pylori were isolated from four children with IDA and four from matched controls without IDA. Based on these isolates, cDNA microarrays under iron-replete or depleted conditions were systematically performed to compare gene expression profiles at the whole genome level. Real-time reverse-transcription (RT-) PCR and protein assays were performed for further assessing the profile differentiation of the identified H. pylori IDA-associated genes. Results We identified 29 and 11 genes with significantly higher or lower expression in the IDA isolates compared to non-IDA isolates, respectively. Especially notable were higher expression of sabA gene encoding sialic acid-binding adhesin in the IDA isolates, which was confirmed by real-time RT-PCR study. Moreover, iron-depletion in vitro led to up-regulation of fecA1 and frpB1 genes and down-regulation of pfr, as predicted. Known iron-regulated genes such as fur, pfr, fecA, and feoB did not significantly differ between both groups. The IDA isolates had significantly higher expression of vacuolating cytotoxin gene vacA than non-IDA isolates, consistent with the results of VacA protein assays. There were no significant differences in bacterial growth value between IDA and non-IDA isolates. Conclusions It is likely that H. pylori carrying high expression of sabA causes IDA, especially in children and adolescents who have increased daily iron demand. In addition, it is possible that several host-interactive genes, including vacA, may play a synergistic role for sabA in IDA development.
2017-07-25 | GSE101807 | GEO