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-EPMC7199955 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:[This corrects the article DOI: 10.1371/journal.pone.0232238.].
| S-EPMC10843033 | 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: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: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
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: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:This meta-analysis summarizes the evidence of a prospective association between the intake of foods [whole grains, refined grains, vegetables, fruit, nuts, legumes, eggs, dairy, fish, red meat, processed meat, and sugar-sweetened beverages (SSBs)] and risk of general overweight/obesity, abdominal obesity, and weight gain. PubMed and Web of Science were searched for prospective observational studies until August 2018. Summary RRs and 95% CIs were estimated from 43 reports for the highest compared with the lowest intake categories, as well as for linear and nonlinear relations focusing on each outcome separately: overweight/obesity, abdominal obesity, and weight gain. The quality of evidence was evaluated with use of the NutriGrade tool. In the dose-response meta-analysis, inverse associations were found for whole-grain (RRoverweight/obesity: 0.93; 95% CI: 0.89, 0.96), fruit (RRoverweight/obesity: 0.93; 95% CI: 0.86, 1.00; RRweight gain: 0.91; 95% CI: 0.86, 0.97), nut (RRabdominal obesity: 0.42; 95% CI: 0.31, 0.57), legume (RRoverweight/obesity: 0.88; 95% CI: 0.84, 0.93), and fish (RRabdominal obesity: 0.83; 95% CI: 0.71, 0.97) consumption and positive associations were found for refined grains (RRoverweight/obesity: 1.05; 95% CI: 1.00, 1.10), red meat (RRabdominal obesity: 1.10; 95% CI: 1.04, 1.16; RRweight gain: 1.14; 95% CI: 1.03, 1.26), and SSBs (RRoverweight/obesity: 1.05; 95% CI: 1.00, 1.11; RRabdominal obesity: 1.12; 95% CI: 1.04, 1.20). The dose-response meta-analytical findings provided very low to low quality of evidence that certain food groups have an impact on different measurements of adiposity risk. To improve the quality of evidence, better-designed observational studies, inclusion of intervention trials, and use of novel statistical methods (e.g., substitution analyses or network meta-analyses) are needed.
| S-EPMC6416048 | biostudies-literature
Project description:A number of studies have previously assessed the impact of antibiotic exposure in early life on the risk of childhood obesity, but no systematic assessment is currently available. A systematic review and meta-analysis was performed to comprehensively and quantitatively elucidate the risk of childhood obesity caused by antibiotic exposure in early life. Literature search was performed in PubMed, Embase, and Web of Science. Random-effect meta-analysis was used to pool the statistical estimates. Fifteen cohort studies involving 445,880 participants were finally included, and all those studies were performed in developed countries. Antibiotic exposure in early life significantly increased risk of childhood overweight [relative risk (RR) = 1.23, 95% confidence interval (CI) 1.13-1.35, P < 0.001] and childhood obesity (RR = 1.21, 95% CI 1.13-1.30, P < 0.001). Antibiotic exposure in early life also significantly increased the z-score of childhood body mass index (mean difference: 0.07, 95% CI 0.05-0.09, P < 0.00001). Importantly, there was an obvious dose-response relationship between antibiotic exposure in early life and childhood adiposity, with a 7% increment in the risk of overweight (RR = 1.07, 95% CI 1.01-1.15, P = 0.03) and a 6% increment in the risk of obesity (RR = 1.06, 95% CI 1.02-1.09, P < 0.001) for each additional course of antibiotic exposure. In conclusion, antibiotic exposure in early life significantly increases risk of childhood obesity. Moreover, current analyses are mainly taken from developed countries, and therefore the impact of antibiotic exposure on risk of childhood obesity in vulnerable populations or developing countries still needs to be evaluated in future studies.
| S-EPMC5517403 | biostudies-other
Project description:BackgroundObesity is one of the most significant causes of morbidity and mortality worldwide. Current studies suggest a new type of obesity, normal weight obesity (NWO), which is defined as having a normal body mass index (BMI), but a high-fat percentage increases the risk of cardiometabolic risk factors (CMRFs). This systematic review and meta-analysis aimed to pool the association between NWO with CMRFs.MethodsA systematic search of the literature in all available electronic databases, including Scopus, Web of Science, EMBASE, and PubMed, was performed until October 2021. All English studies that assessed the association of NWOs [compared to normal weight non-obese (NWNO)] and the CMRFs were included. Two investigators extracted data and performed a quality assessment. The heterogeneity between studies was assessed with I-squared and Cochran's Q tests. Odds ratio (OR) was used as an effect size to pool the association of NWO with CMRFs.ResultsTwenty-five articles that met the inclusion criteria entered the study. The total number of participants was 177,792, with an age range of 13 to 75 years. Most studies were conducted on the general population (adults) and were from China. The result of fixed-effect model meta-analysis indicated an increased odds of hyperglycemia (OR:1.50, 95%:1.23, 1.76), high TG (OR:1.90, 95% CH:1.44, 2.35), low HDL (OR: 1.28, 95% CI:1.06, 1.49) and diabetes (OR:1.39, 95% CI:1.30, 1.49). Moreover, the random effect meta-analysis showed that NWO increased the odds of dyslipidemia (OR:1.83, 95% CI:1.61, 20.4), HTN (OR:1.40, 95% CI:1.28, 1.51) and metabolic syndrome (OR:1.92, 95% CI:1.58, 2.26). Moreover, the mean of all CMRFs except plasma glucose in NWO subjects was statistically higher than NWNO subjects (p-value<0.05).ConclusionThe present study showed that NWO increased the odds of CMRFs. These findings indicate the inadequacy of the BMI measurement and the need for body fat assessment for a better obesity risk assessment.
| S-EPMC8987277 | 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