Body Mass Index Rebound Research Articles

Relationship between short stature at 3 years old and height, weight, and body mass index changes for 6 years after birth: a retrospective, nationwide, population-based study of children born 2011-2014 in Korea.

Height at 3 years of age, when catch-up growth based on birth history is completed, is considered a major prognostic factor for predicting short stature, underweight, and growth faltering. However, too few large-scale studies have followed and analyzed height, weight, and body mass index (BMI) changes in children whose stature was short at 3 years of age. This study followed and compared the growth parameters (height, weight, and BMI) of children with short stature at 3 years of age and children with nonshort stature at 3 years of age for 6 years after birth using nationwide, population-based data. We retrospectively analyzed physical measurement data from the National Health Screening Program for Infants and Children for people born in 2011-2014 in Korea and followed to 2020. The data were provided by the National Health Insurance Service's customized data service. Growth parameters were compared using chi-square tests, Student t-tests, analyses of variance, and linear regressions. Among 210,902 enrolled participants, 759 (0.4%) and 210,143 (99.6%) were in the short stature at 3 years group and the nonshort stature at 3 years group, respectively. In both sexes, height, weight, and BMI for 6 years after birth were significantly higher in the nonshort stature at 3 years group than in the short stature at 3 years group (P<0.0001). The BMI rebound was observed later than the standard period in the short stature at 3 years group. Early intervention and close follow-up are necessary to prevent persistent short stature and growth faltering in children with short stature at 3 years of age.

Associations of cord blood leukocyte telomere length with adiposity growth from infancy to adolescence.

Leukocyte telomere length (LTL) may be a biomarker for chronic disease susceptibility, but no work has tested this hypothesis directly. Our study investigated associations of LTL at birth with markers of adiposity growth that are linked with cardiometabolic health later in life. Participants were 375 children in Project Viva (48% female, 71% White). Body mass index (BMI) trajectories from birth to 18 years were tracked using repeated measures of BMI collected in physical examinations and via medical records, then used to predict age (months) and magnitude (kg/m2 ) of BMI peak and rebound. LTL was measured from cord blood via duplex quantitative PCR. A binary variable indicating LTL shorter than the reference population average was the primary exposure. LTL was unrelated to BMI at peak or rebound, but associations were apparent with the timing of BMI growth milestones. Short LTL was related to a later age of peak for females (β=0.99, 95% CI=0.16, 1.82; psex interaction =0.015) and an earlier age of rebound for both males and females (βcombined =-5.26, 95% CI=-9.44, -1.08). LTL at birth may be an early biomarker of altered adiposity growth. Newborn telomere biology may shed new insight into the developmental origins of health and disease.

Exenatide for weight-loss maintenance in adolescents with severe obesity: A randomized, placebo-controlled trial.

This study sought to evaluate the effect of 52 weeks of exenatide extended release (XR) on the maintenance of meal replacement therapy (MRT)-induced BMI reduction in adolescents with severe obesity. In this randomized, double-blind, placebo-controlled trial, 100 participants aged 12 to 18 years with BMI≥1.2 × 95th percentile were enrolled in a short-term MRT run-in phase. Those who achieved ≥5% BMI reduction during the run-in were then randomized to 52 weeks of exenatide XR 2.0 mg or placebo weekly. Both groups also received lifestyle therapy. The prespecified primary end point was mean percent change in BMI from randomization (post run-in) to 52 weeks in the intention-to-treat population. A total of 100 participants were enrolled, and 66 (mean age 16 = [SD 1.5] years; 47% female) achieved ≥5% BMI reduction with MRT and were randomized (33 to exenatide XR and 33 to placebo). From randomization (post run-in) to 52 weeks, mean BMI increased 4.6% and 10.1% in the exenatide XR and placebo groups, respectively. The placebo-subtracted exenatide XR treatment effect was -4.1% (95% CI: -8.6% to 0.5%, p = 0.078). Although not achieving statistical significance, exenatide XR, compared with placebo, may partly mitigate the propensity toward BMI rebound in adolescents who achieved initial weight loss with dietary intervention.

Early Childhood Growth and Risk of Adult Cerebrovascular Disease: The NFBC1966.

Low birth weight is associated with an increased risk of adulthood cerebrovascular disease (CVD). Not much is known about effects of early childhood growth. We studied whether the risk of adult CVD is associated with growth or nutritional factors during early childhood. Within the Northern Finland Birth Cohort 1966, 11 991 persons were followed from birth to 52 years of age. CVD diagnoses were extracted from national hospital and death registers with diagnostic coding based on the World Health Organization recommendations. Cox proportional hazard models were used to estimate associations of childhood growth variables, growth trajectories (by Latent Class Growth Modeling), and nutritional factors with adult CVD, for example, ischemic and hemorrhagic strokes. The analyses were adjusted for childhood socioeconomic status and birth weight. A total of 453 (3.8%) CVDs were recorded during follow-up. Among females, groups with low early childhood weight and height had an increased risk for adulthood ischemic CVDs, with an adjusted hazard ratio of 1.97 (95% CI, 1.21-3.20) and 2.05 (CI, 1.11-3.81), respectively. In addition, females with body mass index over 1 SD at body mass index rebound had an increased risk for ischemic CVDs (adjusted hazard ratio, 1.90 [CI, 1.19-3.04]) compared with females with body mass index -1 to +1 SD. These associations were not found among males. The findings suggest that timing of weight gain during childhood is of significance for development of CVD risk among females.

Timing of Adiposity Rebound and Determinants of Early Adiposity Rebound in Korean Infants and Children Based on Data from the National Health Insurance Service.

Adiposity rebound (AR) is defined as the second rise in the body mass index (BMI) usually occurring in early childhood. This study aimed to investigate the timing of AR and the factors determining early AR (EAR) by tracking BMI patterns using large-scale longitudinal nationwide data (n = 142,668; 73,389 boys and 69,279 girls) over seven time periods (4–6, 9–12, 18–24, 30–36, 42–48, 54–60, and 66–71 months). The average BMI rebound indicating AR was found before the age of 5 years (6th time period, 54–60 months). Interestingly, children experiencing BMI rebound during the 4th to 6th time periods showed a small increase in the proportion of underweight in the 2nd time period, but a dramatically higher proportion of underweight during the corresponding time period, similar to M-shaped patterns. In contrast, overweight or obese children in the above group showed opposite W-shaped patterns. The parameters predicting the risk of EAR are diverse for each time period by sex. Adequate breastfeeding before the age of 1 year, adequate diet, and reduced sugar-sweetened beverage consumption after the age of 1 year were important for reducing EAR. This study presents for the first time, the timing of AR and the major determinants of EAR among Korean infants and children based on large-scale nationwide data.

Body mass index rebound and pubertal timing in girls with and without a family history of breast cancer: the LEGACY girls study.

Heavier body mass index (BMI) is the most established predictor of earlier age at puberty. However, it is unknown whether the timing of the childhood switch to heavier BMI (age at BMI rebound) also matters for puberty. In the LEGACY Girls Study (n = 1040), a longitudinal cohort enriched with girls with a family history of breast cancer, we collected paediatric growth chart data from 852 girls and assessed pubertal development every 6 months. Using constrained splines, we interpolated individual growth curves and then predicted BMI at ages 2, 4, 6, 8 and 9 years for 591 girls. We defined age at BMI rebound as the age at the lowest BMI between ages 2 and 8 years and assessed its association with onset of thelarche, pubarche and menarche using Weibull survival models. The median age at BMI rebound was 5.3 years (interquartile range: 3.6-6.7 years). A 1-year increase in age at BMI rebound was associated with delayed thelarche (HR = 0.90; 95% CI = 0.83-0.97) and menarche (HR = 0.86; 95% CI = 0.79-0.94). The magnitude of these associations remained after adjusting for weight between birth and 2 years, was stronger after adjusting for BMI at age 9, and was stronger in a subset of girls with clinically assessed breast development. Earlier BMI rebound is associated with earlier pubertal timing. Our observation that BMI rebound may be a driver of pubertal timing in girls with and without a family history of breast cancer provides insight into how growth and pubertal timing are associated with breast cancer risk.

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.

Separating Algorithms From Questions and Causal Inference With Unmeasured Exposures: An Application to Birth Cohort Studies of Early Body Mass Index Rebound.

Observational studies reporting on adjusted associations between childhood body mass index (BMI; weight (kg)/height (m)2) rebound and subsequent cardiometabolic outcomes have often not paid explicit attention to causal inference, including definition of a target causal effect and assumptions for unbiased estimation of that effect. Using data from 649 children in a Boston, Massachusetts-area cohort recruited in 1999-2002, we considered effects of stochastic interventions on a chosen subset of modifiable yet unmeasured exposures expected to be associated with early (<age 4 years) BMI rebound (a proxy measure) on adolescent cardiometabolic outcomes. We considered assumptions under which these effects might be identified with available data. This leads to an analysis where the proxy, rather than the exposure, acts as the exposure in the algorithm. We applied targeted maximum likelihood estimation, a doubly robust approach that naturally incorporates machine learning for nuisance parameters (e.g., propensity score). We found a protective effect of an intervention that assigns modifiable exposures according to the distribution in the observational study of persons without (vs. with) early BMI rebound for fat mass index (fat mass (kg)/ height (m)2; -1.39 units, 95% confidence interval: -1.63, -0.72) but weaker or no effects for other cardiometabolic outcomes. Our results clarify distinctions between algorithms and causal questions, encouraging explicit thinking in causal inference with complex exposures.

Diagnosis of obesity based on body composition-associated health risks-Time for a change in paradigm.

Traditional diagnosis and understanding of the pathophysiology of obesity are based on excessive fat storage due to a chronically positive energy balance characterized by body mass index (BMI). Quantitative and qualitative analysis of lean and adipose tissue compartments by body composition analysis reveals that characterization of obesity as "overfat" does not facilitate a comprehensive understanding of obesity-associated health risk. Instead of being related to fat mass, body composition characteristics underlying BMI-associated prognosis may depend (i) on accelerated growth by a gain in lean mass or fat-free mass (FFM) in children with early BMI rebound or adolescents with early puberty; (ii) on a low muscle mass in aging, associated chronic disease, or severe illness; and (iii) on impaired adipose tissue expandability with respect to cardiometabolic risk. It is therefore time to call the adipocentric paradigm of obesity into question and to avoid the use of BMI and body fat percentage. By contrast, obesity should be seen in face of a limited FFM/muscle mass together with a limited capacity of fat storage.

The Relation of Adiposity Rebound to Subsequent BMI in a Large Electronic Health Record Database.

Objective: The beginning of postinfancy increase in BMI has been termed the adiposity rebound, and an early rebound increases the risk for obesity in adolescence and adulthood. We examined whether the relation of the age at BMI rebound (agerebound) to subsequent BMI is independent of childhood BMI. Design: From the electronic health records of 2.8 million children, we selected 17,077 children examined at least once each year between ages 2 and <8 years, and who were reexamined between age 10 and <16 years. The mean age at the last visit was 12 years (SD = 1). We identified agerebound for each child using lowess, a smoothing technique. Results: Children who had an agerebound <3 years were, on average, 6.8 kg/m2 heavier after age 10 years than were children with an agerebound >7 years. However, BMI after age 10 years was more strongly associated with BMI at the rebound (BMIrebound) than with agerebound (r = 0.63 vs. -0.49). Although the relation of agerebound to BMI at the last visit was mostly independent of the BMIrebound, adjustment for age-5 BMI reduced the association's magnitude by about 55%. Conclusions: Both agerebound and the BMIrebound are independently related to BMI and obesity after age 10 years. However, a child's BMIrebound and at ages 5 and 7 years accounts for more of the variability in BMI levels after age 10 years than does agerebound.

The timing of adrenarche in Maya girls, Merida, Mexico.

BackgroundAdrenarche involves maturation of the hypothalamic‐pituitary‐adrenal axis and increased production of dehydroepiandrosterone and its sulfate ester, dehydroepiandrosterone‐sulfate (DHEA‐S). It occurs at ages 6 to 8 in industrialized populations, marking the transition from childhood to juvenility and cognitive development at middle childhood. Studies in subsistence level populations indicate a later age (8‐9) for adrenarche, but only two such studies currently exist for comparison.AimsTo investigate adrenarcheal age among Maya girls and its association with body composition and dietary variables. We hypothesized adrenarche would occur earlier given the current dual burden of nutrition in Mexico.Materials and Methods25 Maya girls aged 7 to 9 from Merida, Mexico using ELISAs to measure salivary DHEA‐S, standard anthropometry for height, weight, and skinfolds, bioelectrical impedance for body composition variables, as well as a food frequency questionnaire for dietary information.ResultsOur hypothesis was rejected—adrenarche occurred close to 9 years. While no measures of body composition were significantly associated with adrenarcheal status, girls eating meat and dairy products more frequently had significantly higher DHEA‐S levels.DiscussionLike other populations living in ecologically challenging environments, adrenarche occurred relatively late among Maya girls. Adrenarche has been linked to measures of body composition, particularly, the adiposity or body mass index rebound, but no relevant anthropometric measures were associated, possibly because of the small sample.ConclusionFurther studies are required to illuminate how adrenarcheal variation relates to developmental plasticity, body composition, pubertal progression, and animal product consumption in other transitional populations.

P5316Birthweight, childhood growth patterns and left ventricular structure at midlife: Northern Finland 1966 Birth Cohort Study

Abstract Background Higher cardiac left ventricular (LV) mass (LVM) has independently been associated with cardiovascular risk and mortality. Changes in LV structure have been observed in children with obesity. However, information about the long-term influence of early growth on LV structure is limited. Purpose To explore the associations between early growth patterns, specifically birth weight, age and body mass index (BMI) at infant BMI peak and at childhood BMI rebound, and LV structure at midlife. Methods At the age of 46, a sample of the participants of the Northern Finland Birth Cohort 1966 took part in follow-up examinations. A randomly selected subpopulation was enrolled to echocardiographic examinations (n=1124). BMI at various ages in childhood was calculated from frequent anthropometric measurements collected from child welfare clinical records. Age and BMI at BMI peak (n=541, mean age 9.0 months) and at BMI rebound (n=657, mean age 5.8 years) were derived from random effect models. Results Birth weight (n=1124), BMI at BMI peak and at BMI rebound were directly associated with LVM (beta [standardized]: 0.171, 0.186 and 0.223, respectively, p&lt;0.001 for all) and LVM index (LVMI) (beta: 0.146, 0.120 and 0.120, respectively, p&lt;0.01 for all) at midlife. All the associations, except that between BMI at BMI peak and LVMI, remained significant after adjustments for gender, adult blood pressure, heart rate, antihypertensive medications, heart diseases and diabetes (p&lt;0.05 for all). Significant interaction between gender and age at BMI rebound was observed in LVMI. Age at BMI rebound was inversely associated with LVMI in both genders, the association being stronger in males (beta: −0.212, p&lt;0.001) compared to females (beta: −0.117, p=0.025) and independent of potential confounders. There were direct univariate associations of birth weight and BMI at BMI peak and rebound with LV relative wall thickness (p=0.009–0.019), which were largely explained by potential confounders. However, the association of birth weight with LV relative wall thickness retained its significance even after relevant adjustments (beta: 0.097, p=0.001). After additional adjustments for adult BMI, only associations of birth weight and BMI at BMI peak with LVM remained significant, which, however, did not remain significant after additional adjustment for adult height. Conclusions This study shows that birth weight and early growth patterns are associated with LV structure at midlife, which is largely explained by adult BMI. Therefore, the relationship between early growth patterns to LV structure in the adulthood may be largely explained by their strong tracking to obesity and related cardiovascular risk factors at midlife and to some extent by normal somatic growth.

Developmental pathways and programming of diabetes: epidemiological aspects.

Type 2 diabetes (T2D) is a major, rapidly increasing global public health challenge. The major risk factors for T2D include overweight and obesity, lifestyle related factors and genetic factors. Early life exposures shape the developmental trajectories and alter susceptibility to T2D. Based on epidemiological studies it has been suggested that fetal undernutrition plays a role in the etiology of T2D. A low birth weight has been considered a proxy for fetal undernutrition. A meta-analysis reported that a 1 kg increase in birth weight is associated with a roughly 20% lower risk of T2D. Although fetal life is of major importance for future health, the period spanning the first 1 000 days of life, is characterized by great plasticity and largely influencing later health. Different growth trajectories during this time period have also been associated with an increased risk of T2D. Studies assessing the association between age at BMI rebound in childhood and later risk for T2D have reported a 5-fold difference in T2D according to age at BMI rebound. Developmental and epidemiological cohort studies focusing on T2D have major public health implications supporting a paradigm shift; a shift from focusing upon risk factor modification in adult life to adopting a life course perspective when studying T2D. This paradigm shift will not only help us in getting a better understanding of the pathophysiology underlying T2D, but it will also open new possibilities and opportunities in the prevention of T2D and related disorders.

Abstract MP62: Associations of Timing of Complementary Feeding Introduction and Adiposity Throughout Childhood and Adolescence

Introduction: Complementary feeding includes introducing food or beverages other than breastmilk or formula to infants. We previously showed associations of early complementary feeding (&lt;4 months old) with higher obesity risk at 3 years old in formula-fed children only. Hypothesis: We hypothesized that associations with adiposity would persist into early adolescence. Methods: Among 991 children from Project Viva, a pre-birth prospective cohort, we examined associations of complementary feeding timing with later body mass index (BMI) z-scores, waist circumference, and dual-energy radiograph absorptiometry (DXA) measured adiposity in mid-childhood (mean: 7.8, SD 0.8 years old; N=681) and in early adolescence (mean: 13.2, SD 0.9 years old; N=637). We used linear regression models adjusted for socio-demographic characteristics, parental BMI, and change in weight-for-age z-score from 0 to 4 months (as a marker of early infant growth); the reference group for all analyses was complementary feeding initiation between 4 to &lt;6 months. We ran separate models for infants who were breastfed for ≥4 months (breastfed) and infants who were never breastfed or weaned &lt;4 months of age (formula-fed). As a secondary analysis, we fitted individual BMI trajectories using mixed-effect models with natural cubic spline functions (N=952), and then examined the association of timing of complementary feeding with age at BMI rebound derived from the trajectories, using linear regression models, adjusting for previously listed covariates. Results: At 4 months of life, 66% (654 of 991) of children were breastfed and 34% (337 of 991) were formula-fed. Complementary feeding was introduced &lt;4 months for 19% (188 of 991), between 4 to &lt;6 months for 68% (674 of 991; reference group), and ≥6 months for 13% (129 of 991) of children. Complementary feeding &lt;4 months was associated with higher waist circumference in both formula-fed (β 2.60, 95% CI [0.35, 4.86] cm) and breastfed children (1.98 [0.07, 3.89] cm) in mid-childhood, while in early adolescence, it was associated with higher BMI z-score (0.36 [0.04, 0.68]) in formula-fed children, and with higher waist circumference in both formula-fed (4.99 [1.14, 8.84] cm) and breastfed children (3.12 [0.02, 6.21] cm). Complementary feeding &lt;4 months was additionally associated with an earlier age at BMI rebound (-7.6 [-12.6, -2.5] months) in breastfed children. Complementary feeding initiated ≥6 months was associated with higher BMI z-score (0.50 [0.04, 0.97]) in mid-childhood and with an earlier age at BMI rebound (-11.5 [-20.0, -2.9] months) in formula-fed children only. Conclusions: We found associations of both early and late introduction of complementary feeding with BMI z-score in formula-fed infants and with waist circumference in breastfed and formula-fed infants throughout childhood.

Childhood growth patterns and cardiovascular autonomic modulation in midlife: Northern Finland 1966 Birth Cohort Study.

To test the hypothesis that age and body mass index (BMI) at BMI peak during infancy and at BMI rebound in childhood are related to cardiovascular autonomic modulation in adulthood. At the age of 46 years, a sample (n = 5861) of the participants of the Northern Finland Birth Cohort 1966 took part in follow-up examinations. Heart rate variability (HRV), baroreflex sensitivity (BRS) and low-frequency oscillations of systolic blood pressure (LFSBP) were measured during sympathetic stimulus by standing. BMI at various ages was calculated from frequent anthropometric measurements collected from child welfare clinical records. BRS and LFSBP were available for 1243 participants with BMI peak data and 1524 participants with BMI rebound data, and HRV for 2137 participants with BMI peak data and 2688 participants with BMI rebound data. Age at BMI rebound had a significant inverse association with LFSBP (beta = -0.071, p = 0.006) after all adjustments (p < 0.001) and was also directly associated with BRS (beta = 0.082, p = 0.001) independently of birth and maternal factors (p = 0.023). BMI at BMI peak and at BMI rebound was inversely associated with high-frequency component of HRV (HF) (beta = -0.045, p = 0.036 for BMI at peak; beta = -0.043, p = 0.024 for BMI at rebound) and directly associated with the ratio of low- and high-frequency components of HRV (LF/HF ratio) (beta = 0.084, p = < 0.001 for BMI at peak; beta = 0.069, p < 0.001 for BMI at rebound). These associations remained significant after all adjustments (p < 0.05 for all). This novel study shows that younger age at BMI rebound and higher BMI at BMI peak and at BMI rebound are associated with higher levels in markers suggestive of augmented sympathetic and reduced vagal cardiovascular modulation in midlife.

Patterns of body mass index milestones in early life and cardiometabolic risk in early adolescence.

Few studies have examined the independent and combined relationships of body mass index (BMI) peak and rebound with adiposity, insulin resistance and metabolic risk later in life. We used data from Project Viva, a well-characterized birth cohort from Boston with repeated measures of BMI, to help fill this gap. Among 1681 children with BMI data from birth to mid childhood, we fitted individual BMI trajectories using mixed-effects models with natural cubic splines and estimated age, and magnitude of BMI, at peak (in infancy) and rebound (in early childhood). We obtained cardiometabolic measures of the children in early adolescence (median 12.9 years) and analysed their associations with the BMI parameters. After adjusting for potential confounders, age and magnitude at infancy BMI peak were associated with greater adolescent adiposity, and earlier adiposity rebound was strongly associated with greater adiposity, insulin resistance and metabolic risk score independently of BMI peak. Children with a normal timing of BMI peak plus early rebound had an adverse cardiometabolic profile, characterized by higher fat mass index {β 2.2 kg/m2 [95% confidence interval (CI) 1.6, 2.9]}, trunk fat mass index [1.1 kg/m2 (0.8, 1.5)], insulin resistance [0.2 units (0.04, 0.4)] and metabolic risk score [0.4 units (0.2, 0.5)] compared with children with a normal BMI peak and a normal rebound pattern. Children without a BMI peak (no decline in BMI after the rise in infancy) also had adverse adolescent metabolic profiles. Early age at BMI rebound is a strong risk factor for cardiometabolic risk, independent of BMI peak. Children with a normal peak-early rebound pattern, or without any BMI decline following infancy, are at greatest risk of adverse cardiometabolic profile in adolescence. Routine monitoring of BMI may help to identify children who are at greatest risk of developing an adverse cardiometabolic profile in later life and who may be targeted for preventive interventions.

Prenatal Exposure to Traffic Pollution and Childhood Body Mass Index Trajectory.

Background: Limited evidence suggests an association between prenatal exposure to traffic pollution and greater adiposity in childhood, but the time window during which growth may be most affected is not known.Methods: We studied 1,649 children in Project Viva, a Boston-area pre-birth cohort. We used spatiotemporal models to estimate prenatal residential air pollution exposures and geographic information systems to estimate neighborhood traffic density and roadway proximity. We used weight and stature measurements at clinical and research visits to estimate a BMI trajectory for each child with mixed-effects natural cubic spline models. In primary analyses, we examined associations of residential PM2.5 and black carbon (BC) exposures during the third trimester and neighborhood traffic density and home roadway proximity at birth address with (1) estimated BMI at 6 month intervals through 10 years of age, (2) magnitude and timing of BMI peak and rebound, and (3) overall BMI trajectory. In secondary analyses, we examined associations of residential PM2.5 and BC exposures during the first and second trimesters with BMI outcomes.Results: Median (interquartile range; IQR) concentration of residential air pollution during the third trimester was 11.4 (1.7) μg/m3 for PM2.5 and 0.7 (0.3) μg/m3 for BC. Participants had a median (IQR) of 13 (7) clinical or research BMI measures from 0 to 10 years of age. None of the traffic pollution exposures were significantly associated with any of the BMI outcomes in covariate-adjusted models, although effect estimates were in the hypothesized direction for neighborhood traffic density and home roadway proximity. For example, greater neighborhood traffic density [median (IQR) 857 (1,452) vehicles/day x km of road within 100 m of residential address at delivery] was associated with a higher BMI throughout childhood, with the strongest associations in early childhood [e.g., per IQR increment natural log-transformed neighborhood traffic density, BMI at 12 months of age was 0.05 (−0.03, 0.13) kg/m2 higher and infancy peak BMI was 0.05 (−0.03, 0.14) kg/m2 higher].Conclusions: We found no evidence for a persistent effect of prenatal exposure to traffic pollution on BMI trajectory from birth through mid-childhood in a population exposed to modest levels of air pollution.

Pre-, Perinatal, and Parental Predictors of Body Mass Index Trajectory Milestones

To assess associations of pre-, perinatal, and parental factors with age and magnitude at body mass index (BMI) peak and rebound. Among 1681 children with BMI data from birth to mid-childhood in Project Viva, we fitted individual BMI trajectories using mixed-effect models with natural cubic spline functions and estimated age and magnitude at peak in infancy and rebound in early childhood. We used stepwise multivariable regression to identify predictors of peak and rebound in the 1354 (63.6%) children with estimable trajectory milestones. The mean (SD) of age at BMI peak was 8.4 (2.7) months and at rebound was 59.8 (19.6) months, and the mean (SD) of magnitude at peak was 18.0 (1.4) kg/m2 and at rebound was 15.9 (1.2) kg/m2. Girls had a later age at peak, earlier age at rebound, and lower magnitudes at peak and rebound than boys. Maternal isolated hyperglycemia (vs normoglycemia: β 0.7 months [95% CI 0.2-1.2]) and pre-eclampsia (vs normal blood pressure: 1.6 months [0.8-2.4]) were associated with a later peak, and impaired glucose tolerance (vs normoglycemia: -0.5 kg/m2 [-0.9, -0.1]) was associated with a lower magnitude at peak. Greater maternal first-trimester weight gain, smoking during pregnancy, no breastfeeding, parental obesity, and no university education were associated with greater BMI at rebound. We have identified modifiable prenatal and parental predictors of BMI peak in infancy and rebound in childhood. Early-life interventions that address these factors may be effective in changing BMI peak and rebound and potentially preventing later obesity.

Earlier BMI rebound and lower pre-rebound BMI as risk of obesity among Japanese preschool children.

Longitudinal growth data of children were analyzed to clarify the relationship between the timing of body mass index (BMI) rebound and obesity risk in later ages. Of 54 558 children born between April 2004 and March 2005 and longitudinally measured in April and October every year in the preschool period, 15 255 children were analyzed wherein no longitudinal measurement is missing after 1 year of age. BMI rebound age was determined as the age with smallest BMI value across longitudinal individual data after 1 year of age. Rebound age was compared between overweight and non-overweight groups. The subjects were divided into groups based on the timing of rebound. The sex- and age-adjusted mean of the BMI, height and weight s.d. scores for age group, along with 6 months weight and height gain, were compared among groups using analysis of covariance. Among those who were overweight at 66-71 months of age, BMI rebound age obtained at approximately 3 years of age was compared with the non-overweight group, whose BMI rebound age was utmost 66 months or later (P<0.001). The comparison among BMI age group showed that earlier BMI rebound results in larger BMI (P<0.001) and larger weight and height gain after the rebound (P<0.001). Among the group with BMI rebound earlier than 30 months of age, low BMI was observed (P<0.001). Slight elevation of height and weight gain was observed before the BMI rebound among groups with rebound age earlier than 60 months of age (P<0.001). Earlier BMI rebound timing with pre-rebound low BMI leads to greater childhood obesity risk; hence, early detection and prevention is necessary for such cases.

Bayesian Piecewise Linear Mixed Models With a Random Change Point: An Application to BMI Rebound in Childhood.

Background:Body mass index (BMI) rebound refers to the beginning of the second rise in BMI during childhood. Accurate estimation of an individual’s timing of BMI rebound is important because it is associated with health outcomes in later life.Methods:We estimated BMI trajectories for 6545 children from the Avon Longitudinal Study of Parents and Children. We used a novel Bayesian two-phase piecewise linear mixed model where the “change point” was an individual-level random effect corresponding to the individual-specific timing of BMI rebound. The model’s individual-level random effects (intercept, prechange slope, postchange slope, change point) were multivariate normally distributed with an unstructured variance–covariance matrix, thereby, allowing for correlation between all random effects.Results:Average age at BMI rebound (mean change point) was 6.5 (95% credible interval: 6.4 to 6.6) years. The standard deviation of the individual-specific timing of BMI rebound (random effects) was 2.0 years for females and 1.6 years for males. Correlation between the prechange slope and change point was 0.57, suggesting that faster rates of decline in BMI prior to rebound were associated with rebound occurring at an earlier age. Simulations showed that estimates from the model were less biased than those from models, assuming a common change point for all individuals or a nonlinear trajectory based on fractional polynomials.Conclusions:Our model flexibly estimated the individual-specific timing of BMI rebound, while retaining parameters that are meaningful and easy to interpret. It is applicable in any situation where one wishes to estimate a change-point process which varies between individuals.