Correction: Accelerated weight gain, prematurity, and the risk of childhood obesity: A meta-analysis and systematic review.
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ABSTRACT:
SUBMITTER: Ou-Yang MC
PROVIDER: S-EPMC10843033 | biostudies-literature | 2024
REPOSITORIES: biostudies-literature
Publications
Correction: Accelerated weight gain, prematurity, and the risk of childhood obesity: A meta-analysis and systematic review.
Ou-Yang Mei-Chen MC Sun Yao Y Liebowitz Melissa M Chen Chih-Cheng CC Fang Min-Lin ML Dai Weiwei W Chuang Tang-Wei TW Chen Jyu-Lin JL
PloS one 20240205 2
[This corrects the article DOI: 10.1371/journal.pone.0232238.]. ...[more]
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Project description:The purpose of this systematic review and meta-analysis of the literature was to analyze and evaluate the impact of prematurity and accelerated weight gain on the risk of childhood and adolescent obesity. CINAHL, Embase, PubMed, and Web of Science databases were searched until December 2019 which yielded 19 studies with a total of 169,439 children enrolled were systematically reviewed. The results revealed that preterm infants had a greater likelihood of childhood obesity (defined as BMI ≥95th percentile for age-sex), than term infants (OR = 1.19, 95% CI [1.13, 1.26]). However, no difference of childhood obesity was found between "small for gestational age"(SGA) and "appropriate for gestational age"(AGA) among preterms. Accelerated weight gain (defined as weight gain velocity during first two years after birth) significantly increased the likelihood of subsequent childhood obesity among preterms (aOR = 1.87, 95% CI [1.57, 2.231]). In conclusion, accelerated weight gain at infancy among preterm children may be a critical contributor to obesity in later life. Establishing optimal growth trajectories and timely referral to health care providers may be of clinical importance.
| S-EPMC7199955 | biostudies-literature
Project description:Dynamic changes in body weight have long been recognized as important indicators of risk for human health. Many population-based observational studies have shown that rapid weight gain during infancy, including a catch-up growth phenomenon or adiposity rebound in early childhood, predisposes a person to the development of obesity, type 2 diabetes, and cardiovascular diseases later in life. However, a consensus has not been established regarding which period of weight gain contributes to future risks. This review evaluates recent evidence on the relationship between early rapid growth and future obesity and cardiometabolic risk, with a focus on the differential significance of rapid weight gain in infancy and early childhood. Although there is a need for attention to childhood growth during early infancy before 1 yr of age as it may be related to future obesity, emerging evidence strongly suggests that toddlers showing an increase in body mass index (BMI) before 3 yr of age, a period normally characterized by decreased BMI, are prone to developing later cardiometabolic risk.
| S-EPMC7534524 | biostudies-literature
Project description:Background and objectiveEnvironmental or lifestyle exposures in utero may influence the development of childhood asthma. In this meta-analysis, we aimed to assess whether maternal obesity in pregnancy (MOP) or increased maternal gestational weight gain (GWG) increased the risk of asthma in offspring.MethodsWe included all observational studies published until October 2013 in PubMed, Embase, CINAHL, Scopus, The Cochrane Database, and Ovid. Random effects models with inverse variance weights were used to calculate pooled risk estimates.ResultsFourteen studies were included (N = 108 321 mother-child pairs). Twelve studies reported maternal obesity, and 5 reported GWG. Age of children was 14 months to 16 years. MOP was associated with higher odds of asthma or wheeze ever (OR = 1.31; 95% confidence interval [CI], 1.16-1.49) or current (OR = 1.21; 95% CI, 1.07-1.37); each 1-kg/m(2) increase in maternal BMI was associated with a 2% to 3% increase in the odds of childhood asthma. High GWG was associated with higher odds of asthma or wheeze ever (OR = 1.16; 95% CI, 1.001-1.34). Maternal underweight and low GWG were not associated with childhood asthma or wheeze. Meta-regression showed a negative association of borderline significance for maternal asthma history (P = .07). The significant heterogeneity among existing studies indicates a need for standardized approaches to future studies on the topic.ConclusionsMOP and high GWG are associated with an elevated risk of childhood asthma; this finding may be particularly significant for mothers without asthma history. Prospective randomized trials of maternal weight management are needed.
| S-EPMC4187236 | biostudies-literature
Project description:Gaining excessive gestational weight may increase obesity risk in the offspring, while breastfeeding lowers that risk. Using data from the Special Supplemental Nutrition Programme for Women, Infants and Children (WIC) in Southern California, we examined the associations between gestational weight gain (GWG), breastfeeding during infancy and childhood obesity at 2-4 years, and determined whether breastfeeding moderated the association between GWG and childhood obesity. GWG was based on weight measurements collected during the first trimester and within a month before delivery. GWG values were standardized by gestational age (GWG z-scores), per maternal prepregnancy body mass index (BMI) and categorized into tertiles. Fully breastfeeding duration was determined by WIC infant package data indicating the amount of infant formula received monthly. Children's length (or height) and weight measurements were used to calculate BMI-for-age z-scores and identify obesity (z-score ≥ 95th percentile). Multivariable linear and modified Poisson regression analyses were conducted. Fully breastfeeding moderated the association between GWG z-scores tertile and obesity in the offspring. Each additional month of fully breastfeeding was associated with 3%-5% obesity risk reduction for each age group and GWG z-scores tertile, except at age 4 years for children whose mothers had low GWG z-scores (tertile 1). Shorter fully breastfeeding duration was associated with greater obesity risk among children of mothers with high GWG z-scores (tertile 3), but not for those whose mothers had low GWG z-scores. Longer fully breastfeeding duration may provide greater protection against obesity among children at higher risk due to intrauterine exposure to high gestational weight gain.
| S-EPMC10483944 | biostudies-literature
Project description:ImportanceEarly slow postnatal weight gain, a surrogate for low insulinlike growth factor 1 (IGF-1) levels, is predictive of retinopathy of prematurity (ROP). While low IGF-1 levels inhibit retinal vessel growth, a later rise theoretically activates vascular endothelial growth factor, causing neovascularization. Rate of rise of IGF-1 level is represented by weight gain acceleration (WGA) and may be used to evaluate risk of ROP.ObjectiveTo evaluate whether faster WGA during a later postnatal period is associated with a higher, rather than lower, risk of severe ROP.Design, setting, and participantsThis secondary analysis of data from the Postnatal Growth and Retinopathy of Prematurity (G-ROP) study included 6835 infants undergoing ROP examinations from 29 hospitals in North America from January 2006 to June 2012. Data were analyzed from September to December 2016.Main outcomes and measuresEarly weight gain rate (WGR) during 29 to 33 weeks' postmenstrual age and late WGA during 34 to 38 weeks' postmenstrual age were determined using linear regression of daily weight measurements and changes in daily weight measurements, respectively. The primary outcome was the association of late WGA with severe ROP.ResultsOf the 6835 included infants, the mean (SD) birth weight was 1086 (357) g, and the mean (SD) gestational age was 27.9 (2.5) weeks. Risk of severe ROP increased with increasing late WGA up to about the 80th percentile of WGA. After adjusting for birth weight and gestational age, among infants in the lowest early WGR tertile, there was no association of late WGA with severe ROP, and among infants in the moderate and highest early WGR tertiles, the moderate WGA tertiles had the highest risk of ROP (moderate early WGR tertile: adjusted odds ratio, 1.38; 95% CI, 0.98-1.94; highest early WGR tertile: adjusted odds ratio, 1.63; 95% CI, 1.02-2.60).Conclusions and relevanceAlthough much attention has been paid to the association of slow weight gain with ROP, the association may be more complex than appreciated. These findings suggest that low early WGR is associated with severe ROP regardless of subsequent WGA, but if early WGR is moderate or high, subsequent rapid rises in WGR are associated with increasing risk of severe ROP. If validated in additional cohorts, this finding may affect potential therapies, such as the timing of IGF-1 supplementation.
| S-EPMC6735493 | biostudies-literature
Project description:BackgroundMaternal metabolic abnormalities have been related to offspring obesity especially during childhood.ObjectivesWe analyzed whether the gestational diabetes mellitus (GDM)-associated melatonin receptor 1B (MTNR1B) genotype of mothers modified the relation between maternal gestational weight gain and childhood obesity.MethodsA total of 1114 Chinese mother-child pairs (mothers with or without prior GDM) were included. Mothers' MTNR1B rs10830962 genotype and gestational weight gain were assessed. Indicators of childhood obesity included BMI-for-age z-score, weight-for-age z-score, waist circumference, and body fat. Childhood overweight and obesity were also analyzed.ResultsWe found that the maternal MTNR1B genotype significantly interacted with gestational weight gain on indicators of offspring's obesity (all P for interaction < 0.05). After multivariable adjustment, BMI-for-age z-scores associated with 1-kg gestational weight gain were 0.009 (SE 0.018), 0.026 (SE 0.010), and 0.061 (SE 0.010) in children with the maternal MTNR1B genotype CC, CG, and GG, respectively (P-interaction = 0.012). Similar interactions were observed for weight-for-age z-score, waist circumference, and body fat (P-interaction = 0.001, 0.003, and 0.012, respectively). The associations remained consistently significant in women with and without GDM. We also found significant interactions between the maternal MTNR1B genotype and gestational weight gain on the offspring's childhood overweight and obesity (P-interaction = 0.005 and 0.026, respectively).ConclusionsThe maternal MTNR1B genotype might interact with gestational weight gain on offspring's obesity risk during childhood.
| S-EPMC6997086 | biostudies-literature
Project description:Overweight and obesity is a major public health concern that includes associations with the development of cardiovascular disease (CVD) risk factors during childhood and adolescence as well as premature mortality in adults. Despite the high prevalence of childhood and adolescent obesity as well as adult CVD, individual studies as well as previous systematic reviews examining the relationship between childhood obesity and adult CVD have yielded conflicting results. The purpose of this study was to use the aggregate data meta-analytic approach to address this gap.Studies were included if they met the following criteria: (1) longitudinal and cohort studies (including case-cohort), (2) childhood exposure and adult outcomes collected on the same individual over time, (3) childhood obesity, as defined by the original study authors, (4) English-language articles, (5) studies published up to June, 2015, (6) one or more of the following CVD risk factors [systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), non-high-density lipoprotein cholesterol (non-HDL), and triglycerides (TG)], (7) outcome(s) not self-reported, and (8) exposure measurements (child's adiposity) assessed by health professionals, trained investigators, or self-reported. Studies were retrieved by searching three electronic databases as well as citation tracking. Fisher's r to z score was calculated for each study for each outcome. Pooled effect sizes were calculated using random-effects models while risk of bias was assessed using the STROBE instrument. In order to try and identify sources of heterogeneity, random-effects meta-regression was also performed.Of the 4840 citations reviewed, a total of 23 studies were included in the systematic review and 21 in the meta-analysis. The findings suggested that childhood obesity is significantly and positively associated with adult SBP (Zr = 0.11; 95% CI: 0.07, 0.14), DBP (Zr = 0.11; 95% CI: 0.07, 0.14), and TG (Zr =0.08; 95% CI: 0.03, 0.13), and significantly and inversely associated with adult HDL (Zr = -0.06; 95% CI: -0.10, -0.02). For those studies that adjusted for adult body mass index (BMI), associations were reversed, suggesting that adult BMI may be a potential mediator. Nine studies had more than 33% of items that placed them at an increased risk for bias.The results of this study suggest that childhood obesity may be a risk factor for selected adult CVD risk factors. However, a need exists for additional, higher-quality studies that include, but are not limited to, both unadjusted and adjusted measures such as BMI before any definitive conclusions can be reached.PROSPERO 2015: CRD42015019763 .
| S-EPMC5575877 | biostudies-other
Project description:BackgroundMaternal obesity and excessive gestational weight gain may have persistent effects on offspring fat development. However, it remains unclear whether these effects differ by severity of obesity, and whether these effects are restricted to the extremes of maternal body mass index (BMI) and gestational weight gain. We aimed to assess the separate and combined associations of maternal BMI and gestational weight gain with the risk of overweight/obesity throughout childhood, and their population impact.Methods and findingsWe conducted an individual participant data meta-analysis of data from 162,129 mothers and their children from 37 pregnancy and birth cohort studies from Europe, North America, and Australia. We assessed the individual and combined associations of maternal pre-pregnancy BMI and gestational weight gain, both in clinical categories and across their full ranges, with the risks of overweight/obesity in early (2.0-5.0 years), mid (5.0-10.0 years) and late childhood (10.0-18.0 years), using multilevel binary logistic regression models with a random intercept at cohort level adjusted for maternal sociodemographic and lifestyle-related characteristics. We observed that higher maternal pre-pregnancy BMI and gestational weight gain both in clinical categories and across their full ranges were associated with higher risks of childhood overweight/obesity, with the strongest effects in late childhood (odds ratios [ORs] for overweight/obesity in early, mid, and late childhood, respectively: OR 1.66 [95% CI: 1.56, 1.78], OR 1.91 [95% CI: 1.85, 1.98], and OR 2.28 [95% CI: 2.08, 2.50] for maternal overweight; OR 2.43 [95% CI: 2.24, 2.64], OR 3.12 [95% CI: 2.98, 3.27], and OR 4.47 [95% CI: 3.99, 5.23] for maternal obesity; and OR 1.39 [95% CI: 1.30, 1.49], OR 1.55 [95% CI: 1.49, 1.60], and OR 1.72 [95% CI: 1.56, 1.91] for excessive gestational weight gain). The proportions of childhood overweight/obesity prevalence attributable to maternal overweight, maternal obesity, and excessive gestational weight gain ranged from 10.2% to 21.6%. Relative to the effect of maternal BMI, excessive gestational weight gain only slightly increased the risk of childhood overweight/obesity within each clinical BMI category (p-values for interactions of maternal BMI with gestational weight gain: p = 0.038, p < 0.001, and p = 0.637 in early, mid, and late childhood, respectively). Limitations of this study include the self-report of maternal BMI and gestational weight gain for some of the cohorts, and the potential of residual confounding. Also, as this study only included participants from Europe, North America, and Australia, results need to be interpreted with caution with respect to other populations.ConclusionsIn this study, higher maternal pre-pregnancy BMI and gestational weight gain were associated with an increased risk of childhood overweight/obesity, with the strongest effects at later ages. The additional effect of gestational weight gain in women who are overweight or obese before pregnancy is small. Given the large population impact, future intervention trials aiming to reduce the prevalence of childhood overweight and obesity should focus on maternal weight status before pregnancy, in addition to weight gain during pregnancy.
| S-EPMC6370184 | biostudies-literature
Project description:BackgroundThe prevalence of obesity is increasing worldwide, and there is growing interest in better delineating the role of the human gut microbiome in this phenomenon. Obesity-specific gut microbiome features have been observed in both human and animal studies, and these variations appear to play a causative role in increasing body weight. There is evidence that antibiotics can modify the composition and diversity of the gut microbiome and that this may contribute to body weight changes. The primary objective of the proposed systematic review is to evaluate and synthesize the existing evidence evaluating the possible association between antibiotic use, weight gain, and obesity.MethodsA comprehensive search of the MEDLINE and EMBASE databases will be performed. Both randomized and non-randomized studies (excluding case reports) in neonates, children, adults, and pregnant women will be included. The exposure of interest is antibiotics of any type, duration, and route given for any indication. All included studies must have a comparator group. The primary outcomes are the development of overweight and obesity. Secondary outcomes are percent weight-change from baseline and change in body mass index or waist circumference. Additional secondary outcomes in pregnant women are gestational weight gain, postpartum weight retention, offspring birth weight, childhood weight, and obesity. Risk of bias of included trials will be performed. Two reviewers will screen and perform data extraction independently.DiscussionThis systematic review will summarize the existing evidence evaluating the association between antibiotic use, weight gain, and obesity and facilitate the identification of important gaps and uncertainties in the literature.Systematic review registrationPROSPERO CRD42017069177.
| S-EPMC5571496 | biostudies-literature
Project description:ObjectivesTo systematically review the evidence from prospective and retrospective cohort studies on the association between gestational weight gain (GWG) and offspring's body weight.MethodsElectronic databases PubMed, Web of Science, CINAHL, and Academic Search Premiere were searched from inception through March 18, 2013. Included studies (n = 23) were English articles that examined the independent associations of GWG with body mass index (BMI) and/or overweight status in the offspring aged 2 to 18.9 years. Two authors independently extracted the data and assessed methodological quality of the included studies.ResultsEvidence from cohort studies supports that total GWG and exceeding the Institute of Medicine maternal weight gain recommendation were associated with higher BMI z-score and elevated risk of overweight or obesity in offspring. The evidence of high rate of GWG during early- and mid-pregnancy is suggestive. Additionally, the evidence on inadequate GWG and net GWG in relation to body weight outcomes in offspring is insufficient to draw conclusions.ConclusionsThese findings suggest that GWG is a potential risk factor for childhood obesity. However, findings should be interpreted with caution due to measurement issues of GWG and potential confounding effects of shared familial characteristics (i.e., genetics and maternal and child's lifestyle factors).
| S-EPMC4202338 | biostudies-literature