Weight Gain In Early Life Research Articles

Early adulthood weight change, midlife “Life’s essential 8” health status and risk of cardiometabolic diseases: a chinese nationwide cohort study

BackgroundThe association between weight change during early adulthood and cardiometabolic diseases remains uncertain in Chinese population. Whether the association varies with comprehensive cardiovascular health (CVH) in midlife assessed by “Life’s Essential 8” has not been characterized. We aim to examine the associations of early adulthood weight change and midlife “Life’s Essential 8” CVH status with cardiometabolic outcomes in a Chinese cohort.MethodsThe study participants were from the China Cardiometabolic Disease and Cancer Cohort (4 C) Study. This analysis included 72,610 middle-aged and older participants followed for a median of 3.6 years. At baseline, the participants recalled body weight at age 20 and 40 years, and we calculated change in weight and BMI between 20 and 40 years of age. Health behaviors information in “Life’s Essential 8” was collected by questionnaire, and health factors were measured in the study center. During follow-up, we ascertained incident cardiovascular events based on medical records, and diagnosed incident diabetes according to the American Diabetes Association 2010 criteria.Results72,610 study participants were included with a mean age of 56.0 ± 8.8 years and 29% of them were males. Weight gain of more than 10 kg between 20 and 40 years of age was associated with 22% increased risk of incident cardiovascular events (HR: 1.22; 95%CI: 1.04–1.43) and 38% increased risk of diabetes (HR: 1.38; 95%CI: 1.25–1.53) compared to stable weight. Besides, the association of weight gain more than 10 kg in early adulthood with cardiometabolic risk was even stronger in those with low CVH score in midlife (HR: 2.44; 95%CI: 2.01–2.97 for incident cardiovascular events; HR: 2.20; 95%CI: 1.90–2.55 for incident diabetes) or with few ideal cardiovascular health metrics in midlife.ConclusionsOur study indicated that weight gain in early adulthood was associated with significantly increased risk of cardiometabolic diseases. And the association could be stronger in those with poor CVH profiles in midlife. These findings confirmed the significance of weight management during early adulthood and suggested that individuals who experienced substantial weight gain in early life should be encouraged to maintain good CVH status in Chinese population.

Rapid weight gain in early life is associated with central precocious puberty in girls, not in boys - a nationwide population-based study in Korea.

This study aimed to investigate the effect of rapid weight gain (RWG) on the incidence of central precocious puberty (CPP) using nationwide population-based data. A total of 253,967 children (101,841 boys and 152,126 girls) who underwent regular health consultations under the National Health Insurance Service from 2007 to 2010 were followed up until the age of 10 years for boys and 9 years for girls. We calculated differences in the weight Z-scores from 4-6 months to 9-12 months (infancy) and from 9-12 months to 18-24 months or 30-36 months (toddlerhood) using the lambda-mu-sigma method. The population was subdivided into four groups: RWGinf/tod (infancy > + 0.67 standard deviation score [SDS], toddlerhood > 0 SDS), RWGinf (infancy > + 0.67 SDS, toddlerhood < 0 SDS), RWGtod (toddlerhood > + 0.67 SDS), and control (no RWG). The diagnosis of CPP was based on the diagnostic codes of the International Classification of Diseases 10th revision and the prescription of gonadotropin-releasing hormone agonists. The cumulative risk of CPP based on age was analyzed using Kaplan-Meier survival curves, and the association between the RWG groups and CPP was assessed using multivariate logistic regression analysis. CPP was diagnosed in 268 boys and 9,225 girls. For the girls, the CPP-free probability was the highest in the control group, followed by the RWGtod, RWGinf, and RWGinf/tod groups (log-rank p < 0.001). However, the incidence of CPP did not vary significantly for the boys. Compared to the control group, the other groups had a higher risk of CPP in girls (RWGinf/tod: adjusted odds ratio [aOR] 1.35, 95%, confidence interval [95% CI] 1.13-1.62; RWGinf: aOR 1.25, 95% CI 1.13-1.38; and RWGtod: aOR 1.18, 95% CI 1.09-1.28). This nationwide population-based study demonstrated that any RWG from birth to 3 years of age contributed to an increased risk of CPP in girls but not in boys. Girls who experienced RWG during both infancy and toddlerhood had the highest risk of developing CPP. These findings suggest that early detection and appropriate management of excessive weight gain in early life may be important for preventing CPP in girls.

Relationship Between Race and Gestational Weight Gain in Pregnancy and Early Life in the South Birth-Cohort Study.

The goal of this study was to evaluate whether differences in gestational weight gain (GWG) and adverse perinatal outcomes exist for Black and White women who are overweight or have obesity (OW/OB) at entry to prenatal care. We enrolled 183 pregnant women with BMI 25-45kg/m2 (71% black, 29% white) prior to 14 weeks gestation. Data were collected on demographic, medical history, diet and physical activity during pregnancy. Relationships between race and maternal outcomes and infant outcomes were assessed using multivariable logistic regression models. The average age of pregnant women were 26 years (±4.8), with a mean BMI of 32.1 (±5.1) kg/m2 at the time of enrollment. At delivery, 60 women (33%) had GWG within Institute of Medicine recommendations and 69% had at least one comorbidity. No significant differences by race were found in GWG (in lbs) (11±7.5 vs. 11.4±7.3, p=0.2006) as well as other perinatal outcomes including maternal morbidity, LBW and PTB. Race differences were noted for gestational diabetes, total energy expenditure and average daily calorie intake, but these differences did not result in significant differences in GWG or maternal morbidity. The lack of racial differences in GWG and perinatal outcomes demonstrated in this study differs from prior literature and could potentially be attributed to small sample size. Findings suggest that race differences in GWG and perinatal outcomes may diminish for women with a BMI in the overweight or obese range at conception.

Early-life weight gain patterns of term small-for-gestational-age infants and the predictive ability for later childhood overweight/obesity: A prospective cohort study.

We aimed to identify the weight gain patterns of small-for-gestational age (SGA) infants in early life and to explore the predictive value for later overweight/obesity in childhood. We obtained data from a prospective cohort including term SGA infants born between January 2006 and November 2015 who received regular health care from birth to 5 years in West China Second University Hospital, Chengdu, China. A latent class growth analysis (LCGA) was applied to group children with similar growth trajectory patterns. Multiple logistic regression was performed to examine the association between weight gain patterns and later overweight/obesity. A total of 296 term SGA infants were finally included. Five weight gain trajectories were identified, including excessive rapid catch-up growth (ERCG) (class 1, 10.9%), rapid catch-up growth (RCG) (class 2, 17.9%), appropriate catch-up growth (ACG) (class 3, 53.0%), slow catch-up growth (SCG) (class 4, 13.4%) and almost no catch growth (NCG) (class 5, 4.8%). SGA infants in class 1 and class 2 had a higher BMI according to age- and sex-specific Z scores from 2-5 years of age. In addition, 25% of SGA infants in class 1 and 13.2% of SGA infants in class 2 were found to be overweight/obese at 2-5 years of age. After adjusting for confounders, we found that extremely rapid weight gain (class 1) in the first 2 years of life increased the risk of overweight/obesity by 2.1 times at 2 to 5 years of age (aOR=2.1, 95% CI: 1.3~4.8; P<0.05). Furthermore, the increment of ΔWAZ between 0 and 4 mo was prominently related to the risk of overweight/obesity at 2 to 5 years for term SGA infants (aOR=3.2, 95% CI: 1.7~8.1; P<0.001). A receiver operating characteristic (ROC) curve showed the area under curve (AUC) was 0.7, with a 95% confidence interval (CI) from 0.6 to 0.8 (P<0.001). The extremely rapid weight gain pattern of term SGA infants in the first 2 years of life increased the risk of overweight/obesity at 2 to 5 years of age. It suggests monitoring weight gain across the infant period represents a first step towards primary prevention of childhood obesity.

Early-life weight gain is associated with non-atopic asthma in childhood

BackgroundPrevious studies suggest the association between early-life weight gain and asthma. It remains unclear whether early-life weight gain is associated with atopic or non-atopic asthma. This study aimed to investigate whether early-life weight gain is associated with atopic or non-atopic asthma. MethodsIncluded in this study were 1343 singleton-birth children (761 boys, 57%) born between January 2010 and December 2011 participating in the Longitudinal Investigation of Global Health in Taiwanese Schoolchildren (LIGHTS) cohort were evaluated by a modified International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire and interviewed by pediatricians between July 1, 2016 and May 31, 2018 at the mean age of 6.4 years. Weight gain z-scores during the first 6, 12, and 18 months of life were classified into 4 groups: slow (below −0.67), on track (−0.67 to 0.67), rapid (0.67 to 1.28), and extremely rapid (above 1.28). The main outcomes were atopic and non-atopic asthma. Asthma was defined as having physician-diagnosed asthma and the presence of wheeze or asthma exacerbations in the last 12 months. Atopy was determined by Phadiatop Infant. ResultsThe extremely rapid weight gain group of children during the first 6, 12, and 18 months of life was significantly associated with an increased risk of non-atopic asthma (adjusted odd ratio [AOR], 2.14, 95% confidence interval [CI], 1.01–4.53 for the first 6 months; AOR, 2.86, 95% CI, 1.34–6.14 for the first 12 months; AOR, 3.26, 95% CI 1.49–7.15 for the first 18 months) compared with the on track group. No significant association was found in atopic asthma. A sex-stratified analysis revealed the association of early-life weight gain with non-atopic asthma was statistically significant only in boys (AOR, 4.24, 95% CI, 1.44–12.50). ConclusionExtremely rapid weight gain during the first 6–18 months of life was significantly associated with 2.1- to 3.3-fold increased risk of non-atopic asthma, with a more pronounced risk found in boys.

The Relative Body Weight Gain From Early to Middle Life Adulthood Associated With Later Life Risk of Diabetes: A Nationwide Cohort Study.

AimTo determine the effect of decade-based body weight gain from 20 to 50 years of age on later life diabetes risk.Methods35,611 non-diabetic participants aged ≥ 50 years from a well-defined nationwide cohort were followed up for average of 3.6 years, with cardiovascular diseases and cancers at baseline were excluded. Body weight at 20, 30, 40, and 50 years was reported. The overall 30 years and each 10-year weight gain were calculated from the early and middle life. Cox regression models were used to estimate risks of incident diabetes.ResultsAfter 127,745.26 person-years of follow-up, 2,789 incident diabetes were identified (incidence rate, 2.18%) in 25,289 women (mean weight gain 20-50 years, 7.60 kg) and 10,322 men (7.93 kg). Each 10-kg weight gain over the 30 years was significantly associated with a 39.7% increased risk of incident diabetes (95% confidence interval [CI], 1.33-1.47); weight gain from 20-30 years showed a more prominent effect on the risk of developing diabetes before 60 years than that of after 60 years (Hazard ratio, HR = 1.084, 95% CI [1.049-1.121], P <0.0001 vs. 1.015 [0.975-1.056], P = 0.4643; P Interaction=0.0293). It showed a stable effect of the three 10-year intervals weight gain on risk of diabetes after 60 years (HR=1.055, 1.038, 1.043, respectively, all P < 0.0036).ConclusionsThe early life weight gain showed a more prominent effect on developing diabetes before 60 years than after 60 years; however, each-decade weight gain from 20 to 50 years showed a similar effect on risk developing diabetes after 60 years.

Patterns of Early Life Weight Gain and Female Onset of Puberty.

ContextPrepubertal obesity is a well-established predictor of earlier pubertal onset, which is itself a risk factor for poor health and well-being. Identifying specific patterns of weight gain in early life may help explain differential risk for earlier pubertal onset.ObjectiveThe objective of the study was to examine patterns of weight gain across infancy and early childhood in relation to pubertal onset outcomes.Design, Setting, and ParticipantsParticipants were 426 girls in the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development, a longitudinal birth cohort of children and their families followed between birth and adolescence.Main Outcome MeasuresThree pubertal onset outcomes were examined, including age at menarche and ages at Tanner stage II for dimensions of breast and pubic hair development.ResultsIn infancy (birth to 15 months), greater percent weight gain and higher birthweight predicted earlier pubertal onset for all outcomes (Ps < 0.05). In early childhood (24 months to grade 1), body mass index (BMI) trajectories reflecting BMI values that were persistently high or changed from low to high over time (vs BMI values that were stable at median or low levels), predicted younger ages at menarche and the onset of breast (Ps < 0.05), but not pubic hair (Ps > 0.05), development. All associations were independent of breastfeeding, maternal menarcheal age, and race/ethnicity.ConclusionsDistinct patterns of early life weight gain predict differential risk for earlier onset puberty. Focusing on these patterns for earlier and more targeted intervention may help lessen life course linkages between prepubertal obesity, accelerated pubertal development, and negative postpubertal outcomes.

Environmental Determinants of Type 1 Diabetes: From Association to Proving Causality.

The rising incidence of type 1 diabetes (T1D) cannot be ascribed to genetics alone, and causative environmental triggers and drivers must also be contributing. The prospective TEDDY study has provided the greatest contributions in modern time, by addressing misconceptions and refining the search strategy for the future. This review outlines the evidence to date to support the pathways from association to causality, across all stages of T1D (seroconversion to beta cell failure). We focus on infections and vaccinations; infant growth and childhood obesity; the gut microbiome and the lifestyle factors which cultivate it. Of these, the environmental determinants which have the most supporting evidence are enterovirus infection, rapid weight gain in early life, and the microbiome. We provide an infographic illustrating the key environmental determinants in T1D and their likelihood of effect. The next steps are to investigate these environmental triggers, ideally though gold-standard randomised controlled trials and further prospective studies, to help explore public health prevention strategies.

Infant weight gain and DXA-measured adolescent adiposity: data from the Japan Kids Body-composition Study

BackgroundRapid weight gain in early life is associated with adiposity later in life. However, there is limited information on the association between weight gain and body fat mass measured using precise methods. This study aimed to investigate whether weight gain is associated with body fat mass measured by dual-energy X-ray absorptiometry (DXA) in adolescents.MethodsParticipants of this retrospective cohort study were 423 adolescents born at full-term who were enrolled in the Japan Kids Body-composition Study. Anthropometric measurements related to pregnancy, delivery, and child health were obtained from the Japanese Maternal and Child Health Handbook. Fat mass in adolescents was measured with a DXA scanner. Weight gain was defined as the change in body weight from birth to age 1.5 years. Associations between birthweight and fat mass, and between weight gain and fat mass, were evaluated using multiple regression analysis.ResultsThere was a significant positive association between weight gain from birth to age 1.5 years and fat mass in adolescents (boys: standardized regression coefficient (β) = 0.253, p < 0.01; girls: β = 0.246, p < 0.01), but not between birthweight standardized for gestational age and fat mass.ConclusionChildren with a greater change in weight from birth to age 1.5 years tended to have increased fat mass in adolescence. Weight gain in early life has a greater impact on fat mass in adolescents than birthweight.

Associations between KCNQ1 and ITIH4 gene polymorphisms and infant weight gain in early life.

An earlier meta-analysis of genome-wide association studies in Asian populations detected five novel body mass index-associated single-nucleotide polymorphisms (SNPs), including potassium voltage-gated channel subfamily Q member 1 (KCNQ1) (rs2237892), ALDH2/MYL2 (rs671, rs12229654), ITIH4 (rs2535633), and NT5C2 (rs11191580). Whether these SNPs take effect in early life, for example, affect infant rapid weight gain (RWG), is unclear. We obtained genomic DNA from 460 term infants with normal birth weight. RWG was defined as the change of weight-for-age standardized Z-score, calculated according to the Children Growth Standard released by the World Health Organization, from birth to 3 months of age >0.67. Using genetic models, associations between the candidate SNPs and infant RWG were examined, along with the interaction between the SNPs and the potential risk factors. RWG was presented in 225 of 460 infants. SNP rs2535633 and rs2237892 were associated with the risk of RWG. Both additive and multiplicative interaction effects were found between infant delivery mode and rs2237892. The negative association between the rs2237892 T allele and infant RWG was only observed in vaginally delivered infants. Obesity-related loci rs2535633 and rs2237892 are associated with infant RWG in the first 3 months of infancy. The relationship between rs2237892 and infant RGW might be moderated by cesarean delivery. Genetic predisposition is an essential aspect to understand infant weight gain. Obesity-related SNPs, rs2535633 and rs2237892, are associated with RWG in very early years of life. The negative association between rs2237892 T allele and RWG is only observed in infants delivered vaginally instead of cesarean section.

Early overnutrition in male mice negates metabolic benefits of a diet high in monounsaturated and omega-3 fats

Overconsumption of saturated fats promotes obesity and type 2 diabetes. Excess weight gain in early life may be particularly detrimental by promoting earlier diabetes onset and potentially by adversely affecting normal development. In the present study we investigated the effects of dietary fat composition on early overnutrition-induced body weight and glucose regulation in Swiss Webster mice, which show susceptibility to high-fat diet-induced diabetes. We compared glucose homeostasis between a high-fat lard-based (HFL) diet, high in saturated fats, and a high-fat olive oil/fish oil-based (HFO) diet, high in monounsaturated and omega-3 fats. We hypothesized that the healthier fat profile of the latter diet would improve early overnutrition-induced glucose dysregulation. However, early overnutrition HFO pups gained more weight and adiposity and had higher diabetes incidence compared to HFL. In contrast, control pups had less weight gain, adiposity, and lower diabetes incidence. Plasma metabolomics revealed reductions in various phosphatidylcholine species in early overnutrition HFO mice as well as with diabetes. These findings suggest that early overnutrition may negate any beneficial effects of a high-fat diet that favours monounsaturated and omega-3 fats over saturated fats. Thus, quantity, quality, and timing of fat intake throughout life should be considered with respect to metabolic health outcomes.

Early growth according to protein content of infant formula: Results from the EDEN and ELFE birth cohorts.

In several systematic reviews, rapid weight gain in early life has been related to increased risk of later obesity. In line with this finding, the "early protein hypothesis" suggests that reducing early protein intake is a potential lever for obesity prevention. To determine whether the variability of protein content of infant formula used in France over the period 2003-2012 is significantly associated with early growth in children. A pooled sample of infants from the EDEN (Etude des Déterminants pré et postnatals de la santé et du développement de l'Enfant) mother-child cohort (born in 2003-2006) and the ELFE (Etude Longitudinale Française depuis l'Enfance) birth cohort (born in 2011) (ntotal =5846) was used. Protein content of the infant formula received at 4months was classified into five groups. Associations between protein content (or breastfed status) at 4 months and weight-, length- and BMI-for-age z-scores at 6, 12 and 18 months were analysed by multivariable linear regression. This analysis showed a positive association between protein content and weight-, length- and BMI-for-age z-scores at 6months and only for weight-for-age at 12 months. At 6months, as compared with the intermediate protein-content group (2.1-2.5g/100 kcal), infants receiving very-high protein content (>2.8g/100 kcal) had higher BMI-for-age z-score and those from the very-low protein-content group (<2.0g/100 kcal) had lower BMI-for-age z-score. Exclusively breastfed infants had lower length and weight z-scores than formula-fed infants at any age. Our findings show a positive association, under real conditions of use, between protein contents in infant formula still on the market and weight-, length- and BMI-for-age z-scores from 6 to 18 months.

Rapid weight gain in early life is associated with severity of respiratory syncytial virus (RSV) bronchiolitis in children.

This study aimed to investigate whether rapid weight gain in early life was associated with the severity of respiratory syncytial virus (RSV) bronchiolitis in children. We retrospectively reviewed 190 patients (1-24 months) hospitalized for RSV bronchiolitis. Parameters of bronchiolitis severity were compared between rapid (change in weight z-score from birth >0.67, n = 65) and normal weight gain groups (n = 125). We assessed for correlations between bronchiolitis severity and weight gain. Linear regression was performed to predict for bronchiolitis severity based on weight gain, controlling for covariates. SPSS was used for statistical analyses. The rapid weight gain group had longer mean durations of tachypnea (2.3±2.0 vs. 1.7±1.8 days, P = 0.027), wheezing (3.2±2.5 vs. 1.6±1.8 days, P < 0.001), and chest retractions (1.5±2.2 vs. 0.6±1.3 days, P = 0.007). Correlations of weight gain with tachypnea (r = 0.146), wheezing (r = 0.279), and chest retractions (r = 0.179) were statistically significant. Weight gain predicted for tachypnea (B = 0.485, P = 0.013) and wheezing (B = 0.846, P = 0.001) durations after adjusting for covariates of severity (age, sex, current weight, RSV type, coinfection, recurrent bronchiolitis, hospital stay, fever, oxygen supplementation, maximal respiratory and heart rates, and laboratory indices). Our findings suggest an association between weight gain and severity of RSV bronchiolitis in young children. Weight gain was significantly associated with the durations of tachypnea and wheezing. The trajectory of weight gain in early life may play a significant role in the clinical course of RSV bronchiolitis.

Lipid ratios representing SCD1, FADS1, and FADS2 activities as candidate biomarkers of early growth and adiposity.

BackgroundAltered lipid metabolism in early life has been associated with subsequent weight gain and predicting this could aid in obesity prevention and risk management. Here, a lipidomic approach was used to identify circulating markers for future obesity risk in translational murine models and validate in a human infant cohort.MethodsLipidomics was performed on the plasma of APOE*3 Leiden, Ldlr-/-.Leiden, and the wild-type C57BL/6J mice to capture candidate biomarkers predicting subsequent obesity parameters after exposure to high-fat diet. The identified candidate biomarkers were mapped onto corresponding lipid metabolism pathways and were investigated in the Cambridge Baby Growth Study. Infants’ growth and adiposity were measured at 0-24 months. Capillary dried blood spots were sampled at 3 months for lipid profiling analysis.FindingsFrom the mouse models, cholesteryl esters were correlated with subsequent weight gain and other obesity parameters after HFD period (Spearman's r≥0.5, FDR p values <0.05) among APOE*3 Leiden and Ldlr-/-.Leiden mice, but not among the wild-type C57BL/6J. Pathway analysis showed that those identified cholesteryl esters were educts or products of desaturases activities: stearoyl-CoA desaturase-1 (SCD1) and fatty acid desaturase (FADS) 1 and 2. In the human cohort, lipid ratios affected by SCD1 at 3 months was inversely associated with 3-12 months weight gain (B±SE=-0.31±0.14, p=0.027), but positively with 12-24 months weight and adiposity gains (0.17±0.07, p=0.02 and 0.17±0.07, 0.53±0.26, p=0.04, respectively). Lipid ratios affected by SCD1 and FADS2 were inversely associated with adiposity gain but positively with height gain between 3-12 months.InterpretationFrom murine models to human setting, the ratios of circulating lipid species indicating key desaturase activities in lipid metabolism were associated with subsequent body size increase, providing a potential tool to predict early life weight gain.

Abstract 16076: Elevated Body Mass Index and Blood Pressure Among Male High-School American Style Football Athletes

Introduction: The impact of American Style Football (ASF) participation on cardiovascular health is unclear. Early-life weight gain among ASF athletes is common and is associated with risk of multiple later-life health afflictions. Despite the popularity of ASF participation among the youth, a rigorous comparison of the cardiovascular health profiles between ASF and non-ASF athletes at the high-school level has not been undertaken. We performed an observational cross-sectional study comparing the body mass index and blood pressures of ASF and non-ASF high-school athletes. Methods: Between October 2012 to November 2018 we performed voluntary cardiac screens including height, weight and blood pressure among predominantly high-school students. Inclusion criteria included the following: male sex; &gt;10 hours of exercise per week; single-sport athlete; age &gt;14 years old. Of the 6973 young individuals who underwent screening, 508 athletes were included in the analyzed data. Results: ASF athletes represented 18% of all high-school athletes. The mean age of ASF and non-ASF athletes was 18.5 and 18.0 years, respectively. BMI was higher in ASF athletes compared to non-ASF participating athletes (26.9 vs 21.2 p&lt;0.0001). There was a higher prevalence of class I and class II obesity among ASF athletes (class I obesity: 15% vs 1%; class II obesity: 10% vs 1%, p&lt;0.0001 for each). ASF athletes had an increased systolic (SBP) and diastolic blood pressure (DBP) compared to non-ASF participating athletes (SBP: 121 vs 114 p&lt;0.0001; DBP: 73 vs 70 p=0.0028). Among all athletes, there was a positive correlation between blood pressure and BMI (SBP: R=0.4149, DBP: R=0.2076, p&lt;0.0001 for each). Conclusions: High-school athletes that participate in ASF have a higher BMI, prevalence of obesity and blood pressure compared to their non-ASF counterparts. It is important to screen young ASF athletes for obesity and hypertension in order to optimize cardiovascular health at an early age.

Adolescent growth and BMI and their associations with early childhood growth in an urban South African cohort.

The timing and magnitude of adolescent growth may be influenced by ethnicity and early life factors. We aimed to (a) characterize ethnic differences in the magnitude, timing, and intensity of adolescent growth in height, weight, and BMI; (b) assess the effect of early childhood growth on adolescent growth in black children. Data were from the Birth to Twenty Plus cohort (Bt20+) in Johannesburg, South Africa (n= 3273). Height, weight, and BMI were modeled with ethnic comparisons using the SuperImposition by Translation and Rotation for 2089 participants who had data from 7 to 23 years. Relative weight gain and relative linear growth between 0 and 24 months and 24 and 60 months were generated. Multiple regression analyses were used to assess associations between childhood and adolescent growth. White children were 5cm (SE: 0.7) taller than black children through adolescence. Black boys had a later timing of adolescent height (0.65 years ±0.12) than white boys, which in black girls was 0.24 years (0.11) earlier than in white girls. Black girls had faster BMI velocity than white girls. Among black children, birth weight and both relative weight gain 0 to 24 and relative linear growth between 3 and 24 months and 24 and 60 months were positively associated with the magnitude of adolescent growth and negatively associated with timing. Sex dimorphism in ethnic differences in timing of adolescent height growth may reflect some yet unexplained drivers for rapid weight gain and obesity in black females but not black males. Rapid weight gain in early life may contribute to faster adiposity accrual in adolescence.

Sex-dependent associations of maternal androgen levels with offspring BMI and weight trajectory from birth to early childhood.

In preclinical studies, high androgen levels during pregnancy are associated with low birth weight and rapid postnatal weight gain in the offspring. However, human data linking prenatal androgens with birth weight and early life weight gain in the offspring are scarce. We evaluated 516 mother-child pairs enrolled in the New England birth cohorts of the Collaborative Perinatal Project (1959-1966). We assayed androgen bioactivity in maternal sera during third-trimester using a receptor-mediated luciferase expression bioassay. Age and sex-specific BMI Z-scores (BMIz), defined using established standards, were assessed at birth, 4 months, 1 year, 4 years, and 7 years. We used linear mixed models to evaluate the relation of maternal androgens with childhood BMIz overall and by sex. We examined the association of maternal androgens with fetal growth restriction. The association of weight trajectories with maternal androgens was examined using multinomial logistic regression. Higher maternal androgen levels associated with lower BMIz at birth (β = -0.39, 95% CI: -0.73, -0.06); this relation was sex-dependent, such that maternal androgens significantly associated with BMIz at birth in girls alone (β = -0.72, 95% CI: -1.40, -0.04). The relation of maternal androgens with fetal growth restriction revealed dose threshold effects that differed by sex. There was no significant association between maternal androgens and weight trajectory overall. However, we found a significant sex interaction (p = 0.01); higher maternal androgen levels associated with accelerated catch-up growth in boys (aOR = 2.14, 95% CI: 1.14, 4.03). Our findings provide evidence that maternal androgens may have differential effects on the programming of intrauterine growth and postnatal weight gain depending on fetal sex.

Association between early weight gain and later adiposity in Sri Lankan adolescents.

Early growth pattern is increasingly recognized as a determinant of later obesity. This study aimed to identify the association between weight gain in early life and anthropometry, adiposity, leptin, and fasting insulin levels in adolescence. A cross-sectional study was conducted in 366 school children aged 11-13 years. Weight, height, and waist circumference (WC) were measured. Fat mass (FM) was assessed using bioelectrical impedance analysis. Blood was drawn after a 12-h fast for insulin and leptin assay. Birth weight and weight at 6 months and at 18 months were extracted from Child Health Development Records. An increase in weight SD score (SDS) by ≥0.67 was defined as accelerated weight gain. Linear mixed-effects modeling was used to predict anthropometry, adiposity, and metabolic outcomes using sex, pubertal status, accelerated weight gain as fixed factors; age, birth weight, and family income as fixed covariates, and school as a random factor. Children with accelerated weight gain between birth and 18 months had significantly higher body mass index (BMI) SDS, WC SDS, height SDS, %FM, fat mass index (FMI), fat free mass index (FFMI), and serum leptin levels in adolescence. Accelerated weight gain between 6 and 18 months was associated with higher BMI SDS, WC SDS, %FM, and FMI, but not with height SDS or FFMI. Accelerated weight gain at 0-6 months, in children with low birth weight, was associated with higher height SDS, BMI SDS, WC SDS, %FM, and FMI; in children with normal birth weight, it was associated with BMI SDS, WC SDS, height SDS, and FFMI, but not with %FM or FMI. Effects of accelerated weight gain in early life on anthropometry and adiposity in adolescence varied in different growth windows. Accelerated weight gain during 6-18 months was associated with higher FM rather than linear growth. Effects of accelerated weight gain between 0 and 6 months varied with birth weight.

Weight Gain and Blood Pressure in Toddlers Born Very Preterm

Preterm birth is a risk factor for elevated blood pressure in childhood and the development of hypertension and cardiometabolic disease in adulthood; however, mechanisms for the development of both are poorly understood. Rapid weight gain early in childhood may serve as a driver directly and indirectly through cortisol levels found to be elevated in early childhood in individuals born preterm. The objective of this pilot study was to examine the effect sizes of the relationships between weight gain and blood pressure in toddlers born very preterm. A secondary aim was to note any mediating effect of cortisol on the relationships between weight gain and blood pressure. A cross-sectional design with a convenience sample of 36 toddlers who were born very preterm was used to examine the relationships between postnatal weight gain, cortisol, and blood pressure at follow-up. Many of the participants experienced rapid weight gain in the first 12 months of life. Mean systolic and diastolic readings were 94 and 56.6, respectively. Diastolic blood pressure readings were obtained from 23 participants and the majority were elevated. Weight gain was associated with diastolic blood pressure with a medium effect size. A mediating role with cortisol was not supported.Although findings need to be validated in a larger sample, the blood pressure elevations in this sample were alarming. If readings continue to amplify as these children age, the fact that elevations are already present during the toddler period could indicate more significant cardiovascular disease in adulthood for this population. Rapid weight gain in early life may be a driver for elevated blood pressure even during early childhood in individuals born preterm.

Breastmilk Lipids and Oligosaccharides Influence Branched Short-Chain Fatty Acid Concentrations in Infants with Excessive Weight Gain.

The aim is to identify breastmilk components associated with fecal concentration of SCFAs and to investigate whether they differ between infants with high weight gain (HW) and normal weight gain (NW). Breastmilk and fecal samples are collected from mother-infant dyads with HW (n=11) and NW (n=15) at 5 and 9 months of age. Breastmilk is profiled on ultra-performance LC-quadrupole TOF-MS platform. Fecal SCFAs are quantified using an isotope-labeled chemical derivatization method. Human milk oligosaccharides (HMOs) are quantified using HPLC after fluorescent derivatization. Lower levels of α-linolenic acid, oleic acid, 3-oxohexadecanoic acid, LPE (P-16:0), LPC (16:0), LPC (18:0), PC (36:2) in breastmilk from mothers from the HW-group at 5 months of age is found. Fecal SCFA concentrations are increased during the transition period from breastfeeding to complementary feeding. Fecal butyrate concentration is higher in the NW-group at 9 months of age. Fecal branched SCFAs are positively associated with breastmilk phospholipid levels, free-fatty acid levels, HMO-diversity, sialylated-HMOs, 6'-sialyllactose, and disialyl-lacto-N-hexaose. Fecal branched SCFA concentrations seem to be affected by breastmilk lipid and HMO composition. These differences in breastmilk metabolites may partially explain the excessive weight gain in early life.