Childhood Body Mass Index Trajectories Research Articles

Prospective prediction of childhood body mass index trajectories using multi-task Gaussian processes.

Body mass index (BMI) trajectories have been used to assess the growth of children with respect to their peers, and to anticipate future obesity and disease risk. While retrospective BMI trajectories have been actively studied, models to prospectively predict continuous BMI trajectories have not been investigated. Using longitudinal BMI measurements between birth and age 10 y from a mother-offspring cohort, we leveraged a multi-task Gaussian process approach to develop and evaluate a unified framework for modeling, clustering, and prospective prediction of BMI trajectories. We compared its sensitivity to missing values in the longitudinal follow-up of children, compared its prediction performance to cubic B-spline and multilevel Jenss-Bayley models, and used prospectively predicted BMI trajectories to assess the probability of future BMIs crossing the clinical cutoffs for obesity. MagmaClust identified 5 distinct patterns of BMI trajectories between 0 to 10 y. The method outperformed both cubic B-spline and multilevel Jenss-Bayley models in the accuracy of retrospective BMI trajectories while being more robust to missing data (up to 90%). It was also better at prospectively forecasting BMI trajectories of children for periods ranging from 2 to 8 years into the future, using historic BMI data. Given BMI data between birth and age 2 years, prediction of overweight/obesity status at age 10 years, as computed from MagmaClust's predictions exhibited high specificity (0.94), negative predictive value (0.89), and accuracy (0.86). The accuracy, sensitivity, and positive predictive value of predictions increased as BMI data from additional time points were utilized for prediction. MagmaClust provides a unified, probabilistic, non-parametric framework to model, cluster, and prospectively predict childhood BMI trajectories and overweight/obesity risk. The proposed method offers a convenient tool for clinicians to monitor BMI growth in children, allowing them to prospectively identify children with high predicted overweight/obesity risk and implement timely interventions.

Association of maternal pre-pregnancy BMI, gestational weight gain, and gestational diabetes mellitus with BMI trajectory in early childhood: a prospective cohort study

Objective: To examine the associations of pre-pregnancy body mass index (BMI), gestational weight gain, and gestational diabetes mellitus (GDM) with early childhood BMI trajectories. Methods: A total of 1 227 mother-child pairs from the Peking University Birth Cohort in Tongzhou were included in this study. In the cohort, maternal pre-pregnancy weight, height, gestational weight gain, and GDM diagnosis were collected. The children were followed up at birth and at 1, 3, 6, 9, 12, 18, 24, 30, and 36 months of age to obtain height/length and weight data. The longitudinal data-based k-means clustering algorithm was used to identify early childhood BMI trajectory groups. The associations of maternal pre-pregnancy BMI, gestational weight gain, and GDM with early childhood BMI trajectories were analyzed using the logistic regression model. We further explored whether there is an interaction effect between pre-pregnancy overweight/obesity and excessive gestational weight gain on the risk of the high BMI trajectory in early childhood through multiplicative and additive interaction analyses. Results: The prevalence rates of overweight and obesity before pregnancy were 21.2% (260 cases) and 6.6% (81 cases) respectively. The prevalence of excessive gestational weight gain and GDM was 57.7% (708 cases) and 30.9% (379 cases). The early childhood BMI trajectories were named low, medium, and high trajectories, accounting for 30.5%, 45.4% and 24.1%, respectively. After controlling potential confounding factors, it was found that pre-pregnancy overweight (OR=1.54, 95%CI: 1.12-2.12), obesity (OR=2.33, 95%CI: 1.41-3.85), and excessive gestational weight gain (OR=1.47, 95%CI: 1.10-1.97) were risk factors for being in the high BMI trajectory in early childhood. GDM was not significantly associated with early childhood BMI trajectories (P>0.05). Compared with the independent effects of pre-pregnancy overweight/obesity (OR=1.90, 95%CI: 1.17-3.09) and excessive gestational weight gain (OR=1.45, 95%CI: 1.03-2.04), the risk of being in the high BMI trajectory in early childhood was greater when the two factors coexisted (OR=2.38, 95%CI: 1.60-3.54). However, both the multiplicative and additive models showed no interaction effect between pre-pregnancy overweight/obesity and excessive gestational weight gain. Conclusions: Maternal pre-pregnancy overweight/obesity and excessive gestational weight gain are independent risk factors for children being in the high BMI trajectory in early childhood, providing scientific evidence for obesity prevention.

A better performing algorithm for identification of implausible growth data from longitudinal pediatric medical records

Tracking trajectories of body size in children provides insight into chronic disease risk. One measure of pediatric body size is body mass index (BMI), a function of height and weight. Errors in measuring height or weight may lead to incorrect assessment of BMI. Yet childhood measures of height and weight extracted from electronic medical records often include values which seem biologically implausible in the context of a growth trajectory. Removing biologically implausible values reduces noise in the data, and thus increases the ease of modeling associations between exposures and childhood BMI trajectories, or between childhood BMI trajectories and subsequent health conditions. We developed open-source algorithms (available on github) for detecting and removing biologically implausible values in pediatric trajectories of height and weight. A Monte Carlo simulation experiment compared the sensitivity, specificity and speed of our algorithms to three published algorithms. The comparator algorithms were selected because they used trajectory information, had open-source code, and had published verification studies. Simulation inputs were derived from longitudinal epidemiological cohorts. Our algorithms had higher specificity, with similar sensitivity and speed, when compared to the three published algorithms. The results suggest that our algorithms should be adopted for cleaning longitudinal pediatric growth data.

Associations of early childhood body mass index trajectories with body composition and cardiometabolic markers at age 10 years: the Ethiopian infant anthropometry and body composition (iABC) birth cohort study

BackgroundVariability in body mass index (BMI) (kg/m2) trajectories is associated with body composition and cardiometabolic markers in early childhood, but it is unknown how these associations track to later childhood. ObjectivesWe aimed to assess associations of BMI trajectories from 0 to 5 y with body composition and cardiometabolic markers at 10 y. MethodsIn the Ethiopian infant anthropometry and body composition (iABC) birth cohort, we previously identified 4 distinct BMI trajectories from 0 to 5 y: stable low BMI (19.2%), normal BMI (48.8%), rapid growth to high BMI (17.9%), and slow growth to high BMI (14.1%). At 10 y, we obtained data from 320 children on anthropometry, body composition, abdominal subcutaneous and visceral fat, and cardiometabolic markers. Associations of BMI trajectories and 10-y outcomes were analyzed using multiple linear regression. ResultsCompared with children with the normal BMI trajectory, those with rapid growth to high BMI had 1.7 cm (95% CI: 0.1, 3.3) larger waist circumference and those with slow growth to high had 0.63 kg/m2 (95% CI: 0.09, 1.17) greater fat mass index and 0.19 cm (95% CI: 0.02, 0.37) greater abdominal subcutaneous fat, whereas those with stable low BMI had −0.28 kg/m2 (95% CI: −0.59, 0.03) lower fat-free mass at 10 y. Although the confidence bands were wide and included the null value, children with rapid growth to high BMI trajectory had 48.6% (95% CI: −1.4, 123.8) higher C-peptide concentration and those with slow growth to high BMI had 29.8% (95% CI: −0.8, 69.8) higher insulin and 30.3% (95% CI: −1.1, 71.6) higher homeostasis model assessment of insulin resistance, whereas those with rapid growth to high BMI had −0.23 mmol/L (95% CI: −0.47, 0.02) lower total cholesterol concentration. The trajectories were not associated with abdominal visceral fat, blood pressure, glucose, and other lipids at 10 y. ConclusionsChildren with rapid and slow growth to high BMI trajectories before 5 y tend to show higher measures of adiposity and higher concentrations of markers related to glucose metabolism at 10 y. Clinical Trial RegistryISRCTN46718296 (https://www.isrctn.com/ISRCTN46718296).

Associations of childhood BMI traits with blood pressure and glycated haemoglobin in 6-9-year-old Samoan children.

Prevalence and risk factors for elevated glycated haemoglobin (HbA1c) and blood pressure (BP) are poorly understood among Pacific children. We examined associations of HbA1c and BP in 6-9 year-olds with body mass index (BMI) at ages 2, 5, and BMI velocity between 2-9 years in Samoa. HbA1c (capillary blood) and BP were measured in n = 410 Samoan children who were part of an ongoing cohort study. Multilevel models predicted BMI trajectory characteristics. Generalized linear regressions assessed associations of childhood characteristics and BMI trajectories with HbA1c and BP treated as both continuous and categorical outcomes. Primary caregiver-reported childhood characteristics were used as covariates. Overall, 12.90% (n = 53) of children had high HbA1c (≥5.7%) and 33.17% (n = 136) had elevated BP. BMI at 5-years and BMI velocity were positively associated with high HbA1c prevalence in males. A 1 kg/m2 per year higher velocity was associated with a 1.71 (95% CI: 1.07, 2.75) times higher prevalence of high HbA1c. In females, higher BMI at 5-years and greater BMI velocity were associated with higher BP at 6-9 years (95% CI: 1.12, 1.40, and 1.42, 2.74, respectively). Monitoring childhood BMI trajectories may inform cardiometabolic disease screening and prevention efforts in this at-risk population.

Prenatal Exposure to Multiple Endocrine-Disrupting Chemicals and Childhood BMI Trajectories in the INMA Cohort Study.

Prenatal exposure to endocrine-disrupting chemicals (EDCs) may disrupt normal fetal and postnatal growth. Studies have mainly focused on individual aspects of growth at specific time points using single chemical exposure models. However, humans are exposed to multiple EDCs simultaneously, and growth is a dynamic process. The objective of this study was to evaluate the associations between prenatal exposure to EDCs and children's body mass index (BMI) growth trajectories using single exposure and mixture modeling approaches. Using data from the INfancia y Medio Ambiente (INMA) Spanish birth cohort (), prenatal exposure to persistent chemicals [hexachlorobenzene (HCB), 4-4'-dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCB-138, -150, and -180), 4 perfluoroalkyl substances (PFAS)] and nonpersistent chemicals (8 phthalate metabolites, 7 phenols) was assessed using blood and spot urine concentrations. BMI growth trajectories were calculated from birth to 9 years of age using latent class growth analysis. Multinomial regression was used to assess associations for single exposures, and Bayesian weighted quantile sum (BWQS) regression was used to evaluate the EDC mixture's association with child growth trajectories. In single exposure models exposure to HCB, DDE, PCBs, and perfluorononanoic acid (PFNA) were associated with increased risk of belonging to a trajectory of lower birth size followed by accelerated BMI gain by 19%-32%, compared with a trajectory of average birth size and subsequent slower BMI gain [e.g., relative risk ratio (RRR) per doubling in DDE (95% CI: 1.05, 1.35); RRR for (95% CI: 1.05, 1.66)]. HCB and DDE exposure were also associated with higher probability of belonging to a trajectory of higher birth size and accelerated BMI gain. Results from the BWQS regression showed the mixture was positively associated with increased odds of belonging to a BMI trajectory of lower birth size and accelerated BMI gain (odds ratio per 1-quantile increase of the ; credible interval: 1.03, 2.61), with HCB, DDE, and PCBs contributing the most. This study provides evidence that prenatal EDC exposure, particularly persistent EDCs, may lead to BMI trajectories in childhood characterized by accelerated BMI gain. Given that accelerated growth is linked to a higher disease risk in later life, continued research is important. https://doi.org/10.1289/EHP11103.

Childhood body mass index trajectories and asthma and allergies: A systematic review.

Previous systematic reviews have focused on associations between single time point measures of Body Mass Index (BMI) and asthma and allergic diseases. As BMI changes dynamically during childhood, examination of associations between longitudinal trajectories in BMI and allergic diseases is needed to fully understand the nature of these relationships. To systematically synthesise the association between BMI trajectories in childhood (0-18 years) and allergic diseases (asthma, eczema, allergic rhinitis, or food allergies outcomes). We conducted a systematic review following the PRISMA guidelines, and two independent reviewers assessed the study quality using the ROBINS-E and GRADE tools. A narrative synthesis was performed as the statistical heterogeneity did not allow a meta-analysis. A search was performed on PubMed and EMBASE databases on 4th January 2023. Longitudinal cohort studies assessing the associations between childhood BMI trajectories and allergic diseases were included. Eleven studies met the inclusion criteria with a total of 37,690 participants between 0 and 53 years of age. Ten studies examined asthma outcomes, three assessed association with allergic rhinitis, two assessed eczema, and one assessed food allergy. High heterogeneity and high risk of bias were observed. Overall, the quality of evidence was very low. Nevertheless, two consistent findings were identified: (1) a persistently high BMI between 6 and 10 years of age may be associated with an increased risk of asthma at 18 years and (2) a rapid increase in BMI in the first 2 years of life may be associated with subsequent asthma. Maintaining a normal BMI trajectory during childhood may reduce the risk of asthma. Future research that adequately addresses confounding and includes longer-term follow-up is needed. Moreover, additional studies examining potential associations with eczema, food allergies, and allergic rhinitis outcomes are needed.

Maternal weight and its association with risk of overweight in offspring: a trajectory analysis from a birth cohort in China.

Most studies on the association of maternal pregnancy weight with offspring weight trajectory have a short follow-up time. This study aimed to explore the associations of maternal prepregnancy body mass index (BMI) and gestational weight gain (GWG) with childhood weight trajectories in a 7-year birth cohort. A total of 946 mother-child pairs (467 boys and 479 girls) from a longitudinal birth cohort in TianjinCity, China, were included in this study, ranging from pregnancy to offspring at 7years. The outcome variable was defined as overweight or not overweight in offspring at the last round. A group-based trajectory model was applied to identify childhood BMI trajectory groups. Five discrete BMI trajectory groups were identified and characterized as constant underweight (25.2%), constant normal weight (42.8%), and high or increasing trajectory [at risk of overweight (16.9%), progressive overweight (11.0%) and progressive obesity (4.1%)]. Maternal prepregnancy overweight was associated with 1.72 (95% CI 1.14-2.60, P = 0.01) to 4.02 (95% CI 1.94-8.36, P < 0.001) times the risk of all high or increasing trajectory groups, and excessive GWG was related to groups at risk of overweight [relative risk ratio (RRR) 2.09, 95% CI 1.27-3.46, P = 0.004] and progressive obesity (RRR 3.33, 95% CI 1.13-9.79, P = 0.029). Children in all high or increasing trajectory groups were associated with greater overweight risk at the last round [risk ratios (RRs) ranged from 3.54 (95% CI 2.53-4.95, P < 0.001) to 6.18 (95% CI 4.05-9.42, P < 0.001)]. Maternal prepregnancy overweight and excessive gestational weight gain were associated with increasing or high-level childhood body mass index trajectories as well as a greater risk of overweight at 7 years.

Synergistic effect of serum uric acid and body mass index trajectories during middle to late childhood on elevation of liver enzymes in early adolescence: Findings from the Ewha Birth and Growth Study.

We aimed to determine whether serum uric acid (SUA) and body mass index (BMI) trajectories in childhood have longitudinal association with liver enzymes in adolescence. We conducted a study using data from the Ewha Birth and Growth Cohort. Individual trajectories of SUA (n = 203) and BMI (n = 206) from 5, 7, and 9 years were defined by group-based trajectory modeling. Also, liver function enzymes were collected at 11 to 12 year of age (Aspartate Aminotransferase [AST], Alanine transaminase [ALT], and Gamma-glutamyl transferase [γ-GTP]) (n = 206). Using a generalized linear model, the effects of SUA trajectory and BMI trajectory on liver function enzymes were assessed. We also assessed the interaction effect of SUA and BMI trajectories on liver enzymes. For trajectory patterns, both SUA and BMI were classified into two distinct groups (High or Low). Both trajectory of SUA and BMI in childhood were positively associated with levels of liver enzymes at 11-12 years of age. The results showed that the combined effect of SUA and BMI trajectories on liver enzymes had a higher means in high-risk group (high SUA-high BMI trajectories group) than in low-risk group (low SUA-low BMI trajectories group) for ALT and γ-GTP, respectively. It remained significant association when adjusted for covariates. In addition, the interaction of BMI and SUA trajectories showed a significant synergistic effect. Elevated childhood SUA and BMI trajectories are associated with increased liver enzymes in beginning of adolescent. This finding suggesting that early interventions in SUA and BMI may need for optimization of liver enzymes as potential marker for development of related disease in later life.

In utero exposure to perfluoroalkyl substances and early childhood BMI trajectories: A mediation analysis with neonatal metabolic profiles

BackgroundIn utero perfluoroalkyl substances (PFAS) exposure has been associated with childhood adiposity, but the mechanisms are poorly known. ObjectiveTo investigate the potential mediating role of neonatal metabolites in the relationship between prenatal PFAS exposure and childhood adiposity trajectories in the first four years of life. MethodsWe analyzed the data for 1671 mother-child pairs from the Shanghai Birth Cohort study. We included those with PFAS exposure information in early pregnancy, neonatal metabolites data and at least three child anthropometric measurements at 6, 12, 24 and/or 48 months. Body mass index (BMI) z-score trajectories were identified using latent class growth mixture modeling. The associations between PFAS concentrations and trajectory classes were assessed using multinomial logistic regression. Screening and penalization-based selection was used to identify neonatal amino acids and acylcarnitines with significant mediation effects. ResultsThree BMI z-score trajectories in early childhood were identified: a persistent increase trajectory (Class 1, 2.2 %), a stable trajectory (Class 2, 66 %), and a transient increase trajectory (Class 3, 32 %). Increased odds of being in Class 1 were observed in association with one log-unit increase in concentrations of perfluorooctane sulfonate (odds ratio [OR], 1.76 [95 % CI, 0.96–3.23], Class 2 as reference; OR, 2.36 [95 % CI, 1.27–4.40], Class 3 as reference), perfluorononanoic acid (OR, 1.90 [95 % CI, 0.97–3.72], Class 2 as reference; OR, 2.23 [95 % CI, 1.12–4.42], Class 3 as reference) and perfluorodecanoic acid (OR, 1.95 [95 % CI, 1.12–3.38], Class 2 as reference; OR, 2.14 [95 % CI, 1.22–3.76], Class 3 as reference). The effect of prenatal PFAS exposure on being in Class 1 was significantly but partly mediated by octanoylcarnitine (2.64 % for perfluorononanoic acid and 3.70 % for sum of 10 PFAS). ConclusionsIn utero PFAS exposure is a risk factor for persistent growth in BMI z-score in early childhood. The alteration of neonatal acylcarnitines suggests a potential molecular pathway.

Prenatal metabolomic profiles mediate the effect of maternal obesity on early childhood growth trajectories and obesity risk: the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) Study

Maternal prepregnancy obesity is an important risk factor for offspring obesity, which may partially operate through prenatal programming mechanisms. The study aimed to systematically identify prenatal metabolomic profiles mediating the intergenerational transmission of obesity. We included 450 African American mother-child pairs from the Conditions Affecting Neurocognitive Development and Learning in Early Childhood Study (CANDLE) pregnancy cohort. Liquid chromatography-mass spectrometry was used to conduct metabolomic profiling on the maternal plasma samples of the second trimester. The childhood growth outcomes of interest included body mass index (BMI) trajectories from birth to age 4 (rising-high-, moderate-, and low-BMI trajectories) as well as overweight/obesity (OWO) risk at age 4. Mediation analysis was conducted to identify metabolite mediators linking maternal OWO and childhood growth outcomes. The potential causal effects of maternal OWO on metabolite mediators were examined using the Mendelian Randomization (MR) method. Among 880 metabolites detected in the maternal plasma during pregnancy, 14 and 11 metabolites significantly mediated the effects of maternal prepregnancy OWO on childhood BMI trajectories and the OWO risk at age 4, respectively, and five of those mediated both outcomes. The MR analysis suggested six of the 20 prenatal metabolite mediators might be causally influenced by maternal prepregnancy OWO, most of which are from the pathways related to the metabolism of amino acids (hydroxyasparagine, glutamate, and homocitrulline), sterols (campesterol), and nucleotides (N2, N2-dimethylguanosine). Our study provided further evidence that prenatal metabolomic profiles might mediate the effect of maternal OWO on early childhood growth trajectories and OWO risk in offspring. The metabolic pathways including identified metabolite mediators might provide novel intervention targets for preventing the intrauterine development of obesity in offspring of mothers with obesity.

Childhood body mass index trajectories, adult-onset type 2 diabetes, and obesity-related cancers.

Elevated childhood body mass index (BMI), commonly examined as a "once-only" value, increases the risk of cancer and type 2 diabetes (T2D) in adulthood. Continuous exposure to adiposity during childhood may further increase cancer risk. We examined whether longitudinal childhood BMI trajectories were associated with adult obesity-related cancer and the role of adult-onset T2D in these associations. Five sex-specific latent class BMI trajectories were generated for 301 927 children (149 325 girls) aged 6-15 years from the Copenhagen School Health Records Register. Information on obesity-related cancers and T2D was obtained from national health registers. Incidence rate ratios (IRR), cumulative incidences, and confidence intervals (CI) were estimated using Poisson regressions. Compared with the average childhood BMI trajectory (containing approximately 40% of individuals), the rate of obesity-related cancer (excluding breast cancer) increased with higher childhood BMI trajectories among women. The highest rates occurred in the overweight (IRR = 1.27, 95% CI = 1.17 to 1.38) and obesity (IRR = 1.79, 95% CI = 1.53 to 2.08) BMI trajectories. Similar patterns were observed among men. In contrast, women with the obesity childhood BMI trajectory had the lowest rate of pre- and postmenopausal breast cancer (IRR = 0.59, 95% CI = 0.43 to 0.80, and IRR = 0.41, 95% CI = 0.30 to 0.57, respectively). For all trajectories, the cumulative risk of obesity-related cancer increased with adult-onset T2D. Consistent childhood overweight or obesity may increase the rates of adult obesity-related cancer and decrease the rates of breast cancer. Adult-onset T2D conferred additional risk for obesity-related cancer, but the effect did not differ across childhood BMI trajectories.

Childhood body mass index trajectories and associations with adult-onset chronic kidney disease in Denmark: A population-based cohort study.

BackgroundAlthough excess adult adiposity is a strong risk factor for chronic kidney disease (CKD), evidence for associations with early life body size is limited. We investigated whether childhood body mass index (BMI) trajectories are associated with adult-onset CKD and end-stage kidney disease (ESKD) using a population-based cohort. Further, we examined the role of adult-onset type 2 diabetes (T2D) in these associations.Methods and findingsWe included 151,506 boys and 148,590 girls from the Copenhagen School Health Records Register, born 1930 to 1987 with information on measured weights and heights at ages 6 to 15 years. Five sex-specific childhood BMI trajectories were analyzed. Information on the main outcomes CKD and ESKD, as well as T2D, came from national health registers. Incidence rate ratios (IRRs) and 95% confidence intervals (CIs) were estimated using Poisson regression adjusted for year of birth. During a median of 30.8 person-years of follow-up, 5,968 men and 3,903 women developed CKD and 977 men and 543 women developed ESKD. For both sexes, the rates of CKD and ESKD increased significantly with higher child BMI trajectories in comparison with the average BMI trajectory (40% to 43% of individuals) and the below-average BMI trajectory (21% to 23% of individuals) had the lowest rates. When including T2D, most associations were significant and men (IRR = 1.39, 95% CI: 1.13 to 1.72) and women (IRR = 1.54, 95% CI: 1.28 to 1.86) with the obese childhood BMI trajectory (2% of individuals) had significantly higher CKD rates than the average BMI trajectory, whereas for ESKD, the associations were positive, but nonsignificant, for men (IRR = 1.38, 95% CI: 0.83 to 2.31) but significant for women (IRR = 1.97, 95% CI: 1.25 to 3.11) with the obese BMI trajectory. A main study limitation is the use of only hospital-based CKD diagnoses.ConclusionsIndividuals with childhood BMI trajectories above average had higher rates of CKD and ESKD than those with an average childhood BMI trajectory. When including T2D, most associations were significant, particularly with CKD, emphasizing the potential information that the early appearance of above-average BMI growth patterns provide in relation to adult-onset CKD beyond the information provided by T2D development.

Neighborhood Socioeconomic Disadvantage and Childhood Body Mass Index Trajectories From Birth to 7 Years of Age.

The epidemic of increasing childhood overweight and obesity is a major global health concern, with local contextual factors identified as possible contributors. Robust research is needed to establish an evidence base supporting health policy decisions to reverse the trend. We aimed to examine the association between neighborhood socioeconomic disadvantage and trajectories of body mass index (BMI) from birth to age 7. The present study included 11,023 children born within the Southwest Finland Birth Cohort who were free of severe conditions affecting growth with adequate exposure and growth data. We obtained child growth data until school age from municipal follow-up clinics. We based cumulative childhood neighborhood socioeconomic disadvantage on the average annual income, unemployment, and level of education in a residential area defined using a geographic grid at a spatial resolution of 250 m by 250 m. Cumulative neighborhood socioeconomic disadvantage was associated with distinct childhood BMI z score trajectories from birth to age 7. Despite being born in the lowest BMI z scores, children growing up in disadvantaged neighborhoods subsequently exhibited a trajectory of increasing BMI z scores starting at 4 years of age, ending up with a higher risk of overweight at the end of the follow-up (30%) as compared with children living in more affluent neighborhoods (22%). The corresponding risk of obesity was 5 % for those in affluent neighborhoods and 9 % and those in disadvantaged neighborhoods. Cumulative exposure to neighborhood socioeconomic disadvantage is independently associated with unfavorable BMI development and obesity in childhood.

Early childhood body mass index trajectory and overweight/obesity risk differed by maternal weight status.

To evaluate the associations of maternal prepregnancy body mass index (pp-BMI) and gestational weight gain (GWG) with the childhood BMI z-score (BMI-z) trajectories from birth to 2 years old and the risk of overweight/obesity (OWO) at 2 years of age. Mother-child dyads (23,617) were involved in the analysis. They were followed up from early pregnancy to 2 years postpartum with their healthcare data recorded in the Wuhan Maternal and Child Health Management Information System (WMCHMIS). The OWO in children was defined as BMI-z > 1. Linear mixed models (LMM) and unconditional logistic regression were used to evaluate the independent and joint associations of pp-BMI and GWG with the BMI-z trajectory of children per their anthropometric measurements at 0, 1, 3, 6, 9, 12, 18, and 24 months old and the risk of OWO at 2 years of age. Maternal overweight/obesity and excessive GWG independently and jointly increased the risks of their offspring falling into high BMI-z trajectories of birth to 2 years (p < 0.001). In addition, the children whose mothers were overweight/obese before pregnancy and gained excessive weight during pregnancy independently and jointly increased the OWO risk in children at age 2, with adjusted odds ratios (adjOR) of 1.36 (95% CI, 1.22-1.53), 1.28 (95% CI, 1.18-1.39), and 1.76 (95% CI: 1.52-2.03), respectively. Maternal prepregnancy overweight/obesity and excessive GWG can independently and jointly increase the risks of their children falling into high BMI-z trajectories from birth to 2 years of age and becoming overweight/obese at age 2. Maternal overweight/obesity and excessive gestational weight should be the prime targets for early obese prevention efforts.

Early-childhood BMI trajectories in relation to preclinical cardiovascular measurements in adolescence.

Cardiovascular diseases are the leading causes of morbidity and mortality. Overweight, obesity, and accelerated growth during early childhood have been associated with adverse cardiovascular outcomes in later life. Few studies have assessed whether trajectories of accelerated growth in early childhood are associated with preclinical cardiovascular measurements. We aimed to evaluate the associations between childhood body mass index (BMI) growth trajectories and measures of macro- and microvascular function in early adolescence. Measurements of macrovascular function (systolic and diastolic blood pressure (SBP and DBP), pulse wave velocity (PWV), and microvascular function (central retinal arteriolar/veinular equivalent) were assessed at 11 years old in a Spanish birth cohort study (n = 489). BMI trajectories from birth to 9 years were identified using latent class growth analysis. Multiple linear regression assessed the associations between the BMI trajectories and macro- and microvascular function. Compared to children with average birth size and slower BMI gain (reference), children with a lower birth size and accelerated BMI gain had increased SBP [β = 6.57; (95% CI 4.00, 9.15)], DBP [β = 3.65; (95% CI 1.45, 5.86)], and PWV [β = 0.14; (95% CI 0.01, 0.27)]. Children with higher birth size and accelerated BMI gain had increased SBP [β = 4.75; (95% CI 1.79, 7.71) compared to the reference. No significant associations between BMI trajectories and the microvascular measurements were observed. In conclusion, we found that childhood BMI trajectories characterized by accelerated growth are associated with preclinical macrovascular measurements in young adolescents.

Association of Early Antibiotic Exposure With Childhood Body Mass Index Trajectory Milestones

Past studies have showed associations between antibiotic exposure and child weight outcomes. Few, however, have documented alterations to body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) trajectory milestone patterns during childhood after early-life antibiotic exposure. To examine the association of antibiotic use during the first 48 months of life with BMI trajectory milestones during childhood in a large cohort of children. This retrospective cohort study used electronic health record data from 26 institutions participating in the National Patient-Centered Clinical Research Network from January 1, 2009, to December 31, 2016. Participant inclusion required at least 1 valid set of same-day height and weight measurements at each of the following age periods: 0 to 5, 6 to 11, 12 to 23, 24 to 59, and 60 to 131 months (183 444 children). Data were analyzed from June 1, 2019, to June 30, 2020. Antibiotic use at 0 to 5, 6 to 11, 12 to 23, 24 to 35, and 36 to 47 months of age. Age and magnitude of BMI peak and BMI rebound. Of 183 444 children in the study (mean age, 3.3 years [range, 0-10.9 years]; 95 228 [51.9%] were boys; 80 043 [43.6%] were White individuals), 78.1% received any antibiotic, 51.0% had at least 1 episode of broad-spectrum antibiotic exposure, and 65.0% had at least 1 episode of narrow-spectrum antibiotic exposure at any time before 48 months of age. Exposure to any antibiotics at 0 to 5 months of age (vs no exposure) was associated with later age (β coefficient, 0.05 months [95% CI, 0.02-0.08 months]) and higher BMI (β coefficient, 0.09 [95% CI, 0.07-0.11]) at peak. Exposure to any antibiotics at 0 to 47 months of age (vs no exposure) was associated with an earlier age (-0.60 months [95% CI, -0.81 to -0.39 months]) and higher BMI at rebound (β coefficient, 0.02 [95% CI, 0.01-0.03]). These associations were strongest for children with at least 4 episodes of antibiotic exposure. Effect estimates for associations with age at BMI rebound were larger for those exposed to antibiotics at 24 to 35 months of age (β coefficient, -0.63 [95% CI, -0.83 to -0.43] months) or 36 to 47 (β coefficient, -0.52 [95% CI, -0.72 to -0.31] months) than for those exposed at 0 to 5 months of age (β coefficient, 0.26 [95% CI, 0.01-0.51] months) or 6 to 11 (β coefficient, 0.00 [95% CI, -0.20 to 0.20] months). In this cohort study, antibiotic exposure was associated with statistically significant, but small, differences in BMI trajectory milestones in infancy and early childhood. The small risk of an altered BMI trajectory milestone pattern associated with early-life antibiotic exposure is unlikely to be a key factor during prescription decisions for children.

Joint effects of ambient air pollution and maternal smoking on neonatal adiposity and childhood BMI trajectories in the Healthy Start study.

Participants were 526 mother-child pairs, born ≥37 weeks. Cotinine was measured at ~27 weeks gestation. Whole pregnancy and trimester-specific O3 and PM2.5 were estimated via. inverse-distance weighted interpolation from stationary monitors. Neonatal adiposity (fat mass percentage) was measured via. air displacement plethysmography. Child weight and length/height were abstracted from medical records. Interaction was assessed by introducing cotinine (<31.5 vs. ≥31.5 ng/mL [indicating active smoking]), O3/PM2.5 (low [tertiles 1-2] vs. high [tertile 3]), and their product term in linear regression models for birth weight and neonatal adiposity and mixed-effects models for BMI trajectories. The rate of BMI growth among offspring jointly exposed to maternal smoking and high PM2.5 (between 8.1 and 12.7 μg/m3) in the third trimester was more rapid than would be expected due to the individual exposures alone (0.8 kg/m2 per square root year; 95% CI = 0.1, 1.5; P for interaction = 0.03). We did not detect interactions between maternal smoking and O3 or PM2.5 at any other time on birth weight, neonatal adiposity, or BMI trajectories. Although PM2.5 was generally below the EPA annual air quality standards of 12.0 μg/m3, exposure during the third trimester may influence BMI trajectories when combined with maternal smoking.

Prenatal exposure to multiple persistent organic pollutants and childhood BMI trajectories- a comparison of three different methods for exposure mixture analysis in a mixed model framework

Background: Prenatal exposure to organochlorine compounds has been associated with increased risk for pediatric obesity; however, evidence is still inconclusive and most previous studies did not include repeated outcome measures.Aim: To determine the association between prenatal exposure to three organochlorine pesticide and six polychlorinated biphenyl concentrations in 2nd pregnancy trimester maternal serum and childhood body mass index (BMI) trajectories across 4 to 11 years of age in 280 child-mother dyads from the prospective mother-child RHEA study.Methods: We first applied independent linear mixed effect models to evaluate the association between individual compounds and BMI trajectories, using a Bonferroni adjustment to account for multiple comparisons. As an alternative, we applied the Bayesian Weighted Quantile Sum Regression (BWQSR) to model all exposures jointly and to provide an overall association of all compounds on BMI trajectories. We also used the Bayesian varying coefficient kernel machine regression (BVCKMR) to model the exposure mixture jointly while allowing for non-linear and non-additive associations. All results were adjusted for socio-demographic information.Results: From the linear mixed model, a 10-fold increase of HCB and PCB-118 was significantly associated with 0.5 kg/m2 (95%CI: 0.3, 0.7) and 0.3 kg/m2 (95%CI:0.2, 0.6) increase in BMI trajectories across 4-11 years respectively. The BWQSR found that an increase in the chemicals mixture was associated with an increase of 0.12 kg/m2 (95%CI: 0.02, 0.24) in childhood BMI trajectories; HCB, DDE, and PCB-156 were important drivers of this association, as indicated by posterior inclusion probabilities. The BVCKMR identified positive associations of HCB, DDT, and PCB-118 with BMI trajectories and a negative association between DDE and BMI trajectories.Conclusions: Despite some inconsistencies, all three analyses demonstrated a positive association between HCB and BMI trajectories. Novel methods offer new opportunities for assessing exposure mixture effects on outcome trajectories, but results should be interpreted considering each method’s strengths and limitations.

Associations between body mass index trajectories in childhood and cardiovascular risk factors in adulthood

Background and aimsChildren with a growth trajectory of overweight have higher levels of cardiovascular disease (CVD) risk factors than children with a normal-weight trajectory. However, less is known about how trajectories of body mass index (BMI) across the rest of the BMI spectrum relate to CVD risk factors and whether adult BMI affects these associations. Our aim was to examine associations between childhood BMI trajectories and adult CVD risk factors. MethodsWe included 2466 individuals with childhood weights and heights (ages 6–14) from the Copenhagen School Health Records Register and adult CVD risk factors (ages 20–81) from the Copenhagen City Heart Study. Associations between childhood BMI trajectories identified by latent class modelling and CVD risk factors were examined using generalized linear regression analyses with and without adjustment for adult BMI. Normal-weight and overweight were defined by growth references from the Centers for Disease Control and Prevention. ResultsWe identified four childhood trajectories within the normal-weight spectrum and one trajectory of overweight. Compared to the trajectory with the lowest BMI level, several higher BMI trajectories were associated with worse circumference, HDL and glucose homeostasis in adulthood. The highest trajectory was additionally associated with higher total cholesterol and triglycerides. When adjusting for adult BMI, the higher BMI trajectories had lower waist circumference, blood pressure and triglycerides. ConclusionsTrajectories of BMI within the normal-weight range and in the overweight range are associated with a worse CVD risk profile than in the lowest BMI trajectory, and these associations are modifiable by growth after childhood.