Associations of 1.5- and 3-year Phthalate Exposure Levels with Early Adiposity Rebound and Overweight/Obesity in Japanese Children: An Adjunct Study of the Japan Environment and Children's Study.

The relationship between early childhood phthalate exposure and early adiposity rebound is unclear. This study aimed to investigate the association between 1.5- and 3-year phthalate exposure and EAR and overweight/obesity in 7.5-year-old Japanese children. A total of 452 mother-child pairs were enrolled from the Aichi Regional Cohort of the Japan Environment and Children's Study. The children were followed up at birth and at 1.5, 2, 3, 4, 5, 6, and 7.5 years of age for physical examination. Human biomonitoring of 16 urinary metabolites of eight phthalates was performed at 1.5 and 3 years of age. Latent class mixed models, binary logistic regression, and quantile g-computation were performed to identify body mass index (BMI) trajectories and investigate the relationships of single or mixed phthalate exposure with EAR and overweight/obesity. A one-unit increase in log10-transformed 3-year-old Σdi(2-ethylhexyl) phthalate (ΣDEHP) exposure levels was significantly associated with 6-year-old BMI in girls. The 1.5-year mono-iso-butyl phthalate and 3-year Σdi-isodecyl phthalate exposure levels were significantly associated with the repeated measures of longitudinal BMIs in girls. Single phthalate exposure showed null associations with EAR or overweight/obesity in the 7.5-year-old children. Σdi-isononyl phthalate, ΣDEHP, and mono-n-butyl phthalate exhibited the highest proportion of partial positive weights of being in the EAR trajectory after confounder adjustment. Phthalate mixture exposure in 1.5- and 3-year-old children was not significantly associated with EAR. Early childhood phthalate exposure was not related to EAR or overweight/obesity in 7.5-year-old Japanese children. However, few phthalates were positively associated with longitudinal BMIs in girls.

Exclusive human milk feeding and prevalence of early adiposity rebound in ELBW infants: a retrospective cohort study.

The purpose of the present study was to evaluate the prevalence of early adiposity rebound (EAR) and factors associated with its occurrence in a cohort of extremely low birth weight infants (ELBW). We conducted a retrospective longitudinal study including ELBW infants followed-up for up to 10 years after discharge. EAR was defined as occurring before 5 years of age. A multivariate binary logistic regression analysis was performed to evaluate maternal and perinatal variables independently associated with EAR. Out of 212 ELBW infants included in the analysis, 40.6% developed EAR and 21.5% showed it before 4 years of age. Only formula milk feeding at discharge was independently associated with a higher risk of EAR. The mean BMI of children with EAR was higher than that of children without EAR. Furthermore, the prevalence of overweight and obesity was higher in the EAR group than in the timely AR group.  Conclusions: ELBW infants in our cohort developed EAR in a relatively high percentage of cases. In this already at-risk population, EAR may represent a further risk factor for an adverse metabolic outcome. Monitoring preterm infants' growth within a long-term follow-up program and promoting and supporting human milk feeding is advisable. What is Known: • Preterm-born infants are at high risk for long-term adverse health outcomes, especially cardiovascular and metabolic. • The occurrence of early adiposity rebound (EAR) is associated with the risk of later obesity and metabolic syndrome. What is New: • The occurrence of EAR in ELBW infants may represent an additional risk factor for later adverse metabolic outcomes in an already vulnerable population. • Future preventive strategies should include a long-term follow-up and the promotion of exclusive breastfeeding.

Comparison between type A and type B early adiposity rebound in predicting overweight and obesity in children: a longitudinal study.

Early adiposity rebound (EAR) predicts paediatric overweight/obesity, but current approaches do not consider both the starting point of EAR and the BMI trajectory. We compared the clinical characteristics at birth, age 3-5 and 6-8 years of children, according to the EAR and to its type (type A/type B-EAR). We assessed the children's odds of being classified as overweight/obese at age 6-8 years, according to the type of EAR as defined at age 3-5 years. As part of this two-wave observational study, 1055 children were recruited and examined at age 3-5 years. Antenatal and postnatal information was collected through interviews with parents, and weight and height from the health records. Type A and type B-EAR were defined in wave 1 according to the BMI nadir and the variation of BMI z-score between the starting point of the adiposity rebound and the last point on the curve. At 6-8 years (wave 2), 867 children were followed up; 426 (40·4 %) children demonstrated EAR. Among them, 172 had type A-EAR, higher rates of parental obesity (P < 0·05) and greater birth weight compared with other children (P < 0·001). Odds for overweight/obesity at 6-8 years, when adjusting for antenatal and postnatal factors, was 21·35 (95 % CI 10·94, 41·66) in type A-EAR children and not significant in type B-EAR children (OR 1·76; 95 % CI 0·84, 3·68) compared with children without EAR. Classification of EAR into two subtypes provides physicians with a reliable approach to identify children at risk for overweight/obesity before the age of 5 years.

Determinants of Adiposity Rebound Timing in Children.

OBJECTIVE: Adiposity rebound (AR) or BMI (body mass index) rebound refers to the increase in BMI following the minimum BMI in early childhood. Early AR (before age 5) is predictive of adult obesity. To determine how 4 domains - demographics, maternal BMI, food security, and behavioral characteristics - may affect timing of AR. STUDY DESIGN: A total of 248 children, ages 2.5-3.5 years, in Latino farmworker families in North Carolina were examined at baseline and every 3 months for 2 years. BMI was plotted serially for each child and the onset of BMI rebound was determined by visual inspection of the graphs. Given the ages of the children, all rebounds were detected before age 5 years and were deemed "early," whereas other children were classified as "nonrebounders." Classes were then compared in terms of the 4 domains with the use of bivariate analyses and linear mixed models. RESULTS: A total of 131 children demonstrated early rebound, 59 children were nonrebounders, and a further 35 had inconclusive data. Parents of early rebounders were less likely to have documentation permitting legal residence in the US. Mothers of early rebounders were on average 3 BMI units heavier. Sex, household food security, diet quality, caloric intake, and daily activity did not differ between classes. In multivariable analysis, female sex, limited maternal education, increased maternal BMI, and increased caloric intake were significant predictors of early rebound. CONCLUSION: High maternal BMI was the strongest predictor of early BMI rebound, but increased caloric intake also was significant. Limiting excess calories could delay premature AR and lower the risk of future obesity.

Adiposity rebound from three to six years of age was associated with a higher insulin resistance risk at eight-and-a-half years in a birth cohort study.

AIM: The association between adiposity rebound and insulin resistance in middle childhood has seldom been studied. We examined the effect of body mass index (BMI) velocity and early adiposity rebound on the insulin resistance of prepubertal children. METHODS: BMI data from a longitudinal follow-up of a birth cohort in Thailand were used. The homoeostatic model assessment of insulin resistance (HOMA-IR) was calculated from 12-hour fasting plasma glucose and serum insulin at eight-and-a-half years of age. BMI velocity was calculated from four periods: zero to one, one to three, three to six and six to eight-and-a-half years of age. A multiple linear regression model was used to assess the association of BMI velocity during these four periods and insulin resistance at the age of eight-and-a-half years. RESULTS: In 814 children - 76.7% of the initial cohort - BMI velocities between years one to three, three to six and six to eight-and-a-half years were positively associated with HOMA-IR levels after adjusting for demographic, behavioural and socio-economic factors. Children who had BMI gains between three and six years had mean HOMA-IR values that were 43% higher than those who did not. CONCLUSION: BMI velocity during early and middle childhood, and early adiposity rebound between three and six years, was associated with a higher insulin resistance risk at eight-and-a-half years.

Early adiposity rebound: predictors and outcomes.

Adiposity rebound (AR) refers to the second rise of the body mass index (BMI) curve that usually occurs between six and eight years of age. AR timing has a significant impact on patients' health: early AR (EAR), usually before the age of five, is considered to be the earliest indicator of obesity and its related health conditions later in life. Many studies have evaluated factors that can be predictors of EAR, and identified low birth weight and gestational weight gain as novel predictors of EAR, highlighting the role of the intrauterine environment in the kinetics of adiposity. Furthermore, children with breastfeeding longer than 4 months have been found to be less likely to have an EAR, whereas children born to advanced-age mothers, high maternal BMI had a higher risk of having an EAR. Some differences were found in the timing of AR in boys and girls, with girls being more likely to have EAR. The aim of this review is to answer the following three questions: 1) Which are the prenatal and perinatal factors associated with increased risk of EAR? Is gender one of these? 2) Which are the outcomes of EAR in childhood and in adulthood? 3) Which measures can be taken in order to prevent premature AR?

LIMIT: LIfestyle and Microbiome InTeraction Early Adiposity Rebound in Children, a Study Protocol.

Childhood obesity is a strong predictor of adult obesity with health and economic consequences for individuals and society. Adiposity rebound (AR) is a rise in the Body Mass Index occurring between 3 and 7 years. Early adiposity rebound (EAR) occurs at a median age of 2 years and predisposes to a later onset of obesity. Since obesity has been associated with intestinal dysbiosis, we hypothesize that EAR could be related to early microbiome changes due to maternal/lifestyle changes and environmental exposures, which can increase the unhealthy consequences of childhood obesity. LIMIT is a prospective cohort study that aims at identifying the longitudinal interplay between infant gut microbiome, infant/maternal lifestyle, and environmental variables, in children with EAR vs. AR. Methods. The study evaluated 272 mother-infant pairs, enrolled at an Italian neonatal unit, at different time points (T0, at delivery; T1, 1 month; T2, 6 months; T3, 12 months; T4, 24 months; T5, 36 months after birth). The variables that were collected include maternal/infant anthropometric measurements, lifestyle habits, maternal environmental endocrine disruptor exposure, as well as infant AR. The LIMIT results will provide the basis for early identification of those maternal and infant modifiable factors on which to act for an effective and personalized prevention of childhood obesity.

Early adiposity rebound in patients with Prader-Willi syndrome.

Background Prader-Willi syndrome (PWS) is associated with marked obesity that can lead to severe complications such as diabetes mellitus. Early adiposity rebound (AR) is associated with future obesity and an increased risk of diabetes mellitus and metabolic syndrome. Previous reports have shown that the onset of AR occurred earlier in diseases that cause obesity. However, there have been no studies focusing on the timing of AR in PWS, or on the effect of growth hormone (GH) treatment on AR. The aim of this study was to explore AR in PWS patients and to analyze the effect of GH treatment on AR. Methods This retrospective study evaluated 48 patients, with 16 of the patients found to have AR prior to GH treatment. AR was constructed for each patient using Microsoft Excel, and the exact point of the nadir of body mass index (BMI) following the initial peak was determined. We additionally analyzed the relationship between GH treatment and the timing of AR onset. Results AR onset for patients found to have AR before starting GH treatment was 16.0 (13.0-21.0) months. In contrast, AR onset for patients found to have AR after starting GH treatment was 27.5 (23.8-36.3) months. The difference between the two groups was statistically significant (p=0.0001). A positive correlation was found between the GH treatment period and AR (p=0.00013). Conclusion The median age of AR onset in PWS patients was 16.0 (13.0-21.0) months, and GH treatment might delay the early AR onset.