I am a scientist who finds the interplay between genes and environment fascinating.
This board describes how genetics influence the fast growing trend in childhood obesity.
In 10 seconds? The underlying cause of childhood obesity does not depend solely on environmental factors, as it seems there is also a significant genetic component for susceptibility to weight gain as well.
Don’t believe it? Obesity is a highly inheritable trait. Although there are cases of single gene mutations causing severe obesity in children, commonly obesity is more likely to be affected by variances in multiple genes having a more modest effect on weight. Numerous mutations have been found in fat mass- and obesity – associated (FTO) genes and multiple other genes which were associated with increased risk of obesity during childhood (read more).
How do these genetic changes lead to increased weight? Carrying “obesity genes” may lead to higher consumption of fat and total food intake in children. This may be caused by increased circulating levels of the “hunger hormone” ghrelin, which drives your appetite after eating a meal. Children that posses the gene variations are also more likely to experience a diminished reward following food intake, leading to a propensity to opt for more calorie dense meals (read more).
What other factors can affect childhood obesity?
Influences during pregnancy – new evidence is emerging that children weight can be affected by altered early gene expression. Mothers that were obese during pregnancy or were exposed to certain air pollutants or antibiotics, had children that were more likely to be overweight.
Breastfeeding – multiple studies suggest that breastfeeding has a protective effect on obesity.
Environmental factors – while genetics play an important role in weight regulation, the choices we make regarding our diet and levels of physical activity are even more important. There are many people who have “obesity genes” but do not become overweight. These children may have a pre-disposition to weight gain, however, they can avoid obesity through maintenance of a healthy lifestyle and balanced diet (read more).
Abstract: Current studies suggest that the beneficial effect of breastfeeding on overweight and obesity may have been largely overestimated. We examined the relationship between >4 months of full breastfeeding and overweight/obesity in children living in Germany.We analyzed retrospectively collected data on breastfeeding from children aged 3-17 years who participated in the German Health Interview and Examination Survey for Children and Adolescents (KiGGS baseline study) between 2003 and 2006 (n = 13163). To minimize confounding, we applied propensity score matching and multivariate logistic regression analyses to estimate the effect of breastfeeding on childhood overweight and obesity.Adjusted analyses of the matched dataset (n = 8034) indicated that children who were breastfed for >4 months had a significant reduction in the odds of overweight (OR 0.81 [95% CI 0.71–0.92]) and obesity (OR 0.75 [95% CI 0.61–0.92]) compared to children who were not breastfed or who were breastfed for a shorter duration [corrected].Further analyses stratified by age group showed that the association was strongest in children aged 7-10 years (OR 0.67 [95% CI 0.53-0.84] for overweight and OR 0.56 [95% CI 0.39-0.81] for obesity), while no significant effect could be seen in other age groups.Our findings support the hypothesis that breastfeeding does have a beneficial effect on childhood overweight and obesity, although the effect seems to be strongest in children of primary school age.
Pub.: 27 Mar '15, Pinned: 11 May '17
Abstract: Although breastfeeding is associated with improving numerous health outcomes for the child, its role in reducing childhood obesity is contested. Despite this controversy, both the CDC and the US Department of Health and Human Services promote breastfeeding as one of the strategies for reducing childhood obesity. Rural Appalachia has one of the highest rates of childhood obesity and low rates of breastfeeding, compared to rest of the nation. The aim of this study was to examine the association between breastfeeding and childhood obesity at 11 years in the rural Appalachian state of West Virginia (WV).The study used linked data from two cross-sectional data sets to examine this relationship longitudinally in fifth-grade WV children. The main outcome variable was BMI adjusted percent (BMI%) and the main exposure was defined as occurrence of breastfeeding. Mean BMI% of children who were not breastfed was significantly higher, compared to children who were breastfed.The result of the multiple regression analysis showed that breastfeeding significantly predicted BMI% of children after controlling for maternal education, health insurance, family history of hypercholesterolemia and diabetes, child's asthma status, and birth weight of the infant.Our results are consistent with other studies that have shown a significant, but small, inverse association between breastfeeding and childhood obesity. Findings from this study suggest the need to improve breastfeeding rates in the rural Appalachian state of WV as one of the potential strategies to prevent obesity during childhood and adolescence.
Pub.: 18 Jul '15, Pinned: 11 May '17
Abstract: The current study investigated the association between breastfeeding and adult weight distribution using an emerging indicator of weight distribution, the waist-to-height ratio (WHtR).The study sample consisted of two subsamples of individuals that were part of the National Longitudinal Study of Adolescent Health. One sample (n = 1,179) consisted of individuals from the sibling pair data. A second sample (n = 4,648) consisted of individuals that were not part of the paired data. Regression models were constructed to establish if there was a relationship between breastfeeding and two measures of weight distribution: WHtR and body mass index (BMI). Controls for parental socioeconomic status, maternal smoking, race, sex, age, birth weight, maternal BMI, genetic ancestry, and a genetic risk score (GRS) for obesity were included. In addition, a behavioral risk score (BRS) was constructed to control for other residual confounding factors.A significant, inverse relationship between breastfeeding and adult WHtR persisted in models constructed from the sibling pair sample (P = 0.002) and unrelated sample (P < 0.0001). This association remained significant with the inclusion of ancestry principal components, GRS, and a measure of maternal obesity.The moderate association between breastfeeding and weight distribution persists into adulthood while controlling for potential confounders. This paper also provides evidence that the WHtR may be a superior outcome measure to BMI in studies investigating breastfeeding and obesity.
Pub.: 25 Dec '15, Pinned: 11 May '17
Abstract: To investigate the association between gestational weight gain (GWG) and total adiposity, body fat distribution, blood pressure (BP), and metabolic profile in offspring.Cross-sectional study.Body mass index (BMI), waist, subscapular and tricipital skinfolds, and BP were measured and blood samples drawn in 12 775 children (aged 2-9 years) from the IDEFICS cohort. Overweight/obesity was defined by IOTF criteria. Parents filled in a questionnaire investigating child and familiar medical history and lifestyle. A section was dedicated to pregnancy history (including GWG).Anthropometric indices linearly and significantly increased across GWG tertiles (BMI z-score: tertile I =0.08, 0.03-0.13; tertile II =0.16, 0.12-0.21; tertile III =0.34, 0.28-0.40, P<0.01, mean, 95% CI) by analysis of covariance (ANCOVA) adjusted by child sex, age and practice of sport, birth weight, current maternal BMI, parental education, gestational age, age at delivery, alcohol and smoking during pregnancy, maternal diabetes mellitus, gestational hypertension, and breastfeeding duration. After inclusion of BMI z-score among covariates, HbA1c significantly increased across tertiles (P=0.009) while no differences were observed for BP, serum insulin, HOMA index, blood glucose and lipids. The adjusted risk of overweight/obesity significantly increased by 14 and 22% in tertiles II and III respectively, in comparison with tertile I by logistic regression analysis controlling for covariates.Maternal GWG is an independent predictor of total adiposity and body fat distribution in offspring during infancy. Exposure to perinatal factors should be taken into account for early prevention of overweight and obesity.
Pub.: 10 Apr '13, Pinned: 21 Apr '17
Abstract: To examine the association of maternal pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) with anthropometry in the offspring of mothers with gestational diabetes mellitus (GDM).We performed a retrospective cohort study in 1263 GDM mother-child pairs. General linear models and Logistic regression models were used to assess the single and joint associations of maternal pre-pregnancy BMI (normal weight, overweight, and obesity) and GWG (inadequate, adequate and excessive GWG) with anthropometry and overweight status in the offspring from birth to 1-5 years old.Maternal pre-pregnancy BMI and GWG were positively associated with birth weight for gestational age Z score and birth weight for length for gestational age Z score at birth, and weight for age Z score, length/height for age Z score, and weight for length/height Z score at of 1-5 years old offspring. Maternal pre-pregnancy overweight, obesity, and excessive GWG were associated with increased risks of large for gestational age [ORs 95% CIs = 1.87 (1.37-2.55), 2.98 (1.89-4.69), and 2.93 (2.07-4.13), respectively] and macrosomia [ORs 95% CIs = 2.06 (1.50-2.84), 2.89 (1.78-4.70), and 2.84 (1.98-4.06), respectively] at birth and childhood overweight at 1-5 years old [ORs 95% CIs = 1.26 (0.92-1.73), 1.96 (1.24-3.09), and 1.59 (1.15-2.21), respectively].Offspring born to GDM mothers with pre-pregnancy overweight/obesity or excessive GWG were associated with increased risks of large for gestational age and macrosomia at birth, and childhood overweight at 1-5 years old, compared with those born to GDM mothers with pre-pregnancy normal weight and adequate GWG.
Pub.: 23 Jun '15, Pinned: 21 Apr '17
Abstract: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n = 218,166) and nine studies of children and adolescents (n = 19,268).All studies identified to have data on the FTO rs9939609 variant (or any proxy [r(2)>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTO×PA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (p(interaction) = 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents.The association of the FTO risk allele with the odds of obesity is attenuated by 27% in physically active adults, highlighting the importance of PA in particular in those genetically predisposed to obesity.
Pub.: 10 Nov '11, Pinned: 21 Apr '17
Abstract: The fat mass and obesity associated gene (FTO) polymorphisms have been implicated in the susceptibility of overweight/obesity in children and adolescents. However, the results have been inconsistent. In this study, we performed a meta-analysis to clarify the association of FTO gene polymorphisms with overweight/obesity risk among children and adolescents.PubMed and Embase were used to search for eligible published literatures. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using random- or fixed-effect models.A total of 21 articles containing 23 studies (11208cases and 35015controls) were included in our analysis. The results indicated that variant in FTO gene was significantly associated with increased risk of overweight/obesity in children and adolescents (OR=1.35; 95%CI: 1.27-1.44; P<0.001). The overall pooled ORs for risk obesity and overweight were 1.34 (95%CI: 1.21-1.48) and 1.35 (95%CI: 1.25-1.47), respectively. Subgroup analyses also showed similar trends in most subgroups of adjustment for covariates and unadjustment, different ethnicities (Caucasians, Asians, and Amerindians), and each of three investigated polymorphisms (rs9939609, rs1421085, and rs1558902).The present meta-analysis suggested a positive association between FTO gene polymorphism and overweight/obesity risk among children and adolescents. Further prospective studies should be recommended to confirm the observed association, and underlying mechanism should be investigated to clarify the association of FTO gene polymorphism with overweight/obesity.
Pub.: 28 Nov '13, Pinned: 21 Apr '17
Abstract: To evaluate the associations between candidate FTO single nucleotide polymorphisms (SNPs) and obesity, a case-control study was conducted among Chinese school-age children, which included 500 obese cases and 500 matched controls (age, gender and location). We selected 24 candidate FTO tag-SNPs via bio-informatics analysis and performed genotyping using SNPScan technology. Results indicated that rs7206790 and rs11644943 were significantly associated with obesity among school-age children in both additive and recessive models (P<0.05) after adjusting confounders. Comparing rs7206790 CC and CG genotype of carriers, those carrying the GG genotype had an increased risk of obesity (adjusted odds ratio [OR], 3.76; 95% Confidence interval [CI], 1.24-11.43). Carriers of the AA allele of rs11644943 had a lower risk of obesity (adjusted OR, 0.16; 95% CI, 0.04-0.72) compared with those of the T allele (TT and TA). These two SNPs (rs7206790 and rs11644943) were not Linkage Disequilibrium (LD) with previous reported obesity-associated SNPs. Under the recessive model adjusted for age and gender and location, rs7206790 GG allele carriers had significantly increased BMIs (P = 0.012), weight (P = 0.012), waist circumferences (WC) (P = 0.045) and hip circumferences (HC) (P = 0.033). Conversely, rs11644943 AA allele carriers had significantly decreased BMIs (P = 0.006), WC (P = 0.037) and Waist-to-height ratios (WHtR) (P = 0.012). A dose-response relationship was found between the number of risk alleles in rs7206790, rs11644943 and rs9939609 and the risk of obesity. The Genetic Risk Score (GRS) of the reference group was 3; in comparison, those of 2, 4, and ≥5 had ORs for obesity of 0.24 (95%CI, 0.05-1.13), 1.49 (95%CI, 1.10-2.01), and 5.20 (95%CI, 1.75-15.44), respectively. This study confirmed the role of FTO variation on genetic susceptibility to obesity. We reported two new obesity-related FTO SNPs (rs7206790 and rs11644943) among Chinese school-age children.
Pub.: 25 Sep '14, Pinned: 21 Apr '17
Abstract: Genome-wide association studies have identified variants within the FTO (fat mass and obesity associated) locus as the strongest predictors of obesity amongst all obesity-associated gene loci. Recent evidence suggests that variants in FTO directly affect human adipocyte function through targeting IRX3 and IRX5 and thermogenesis regulation.We addressed the relevance of this proposed FTO-IRX pathway in adipose tissue (AT) of children.Expression of IRX3 was higher in adipocytes compared to SVF. We found increased adipocyte-specific expression of IRX3 and IRX5 with the presence of the FTO risk haplotype in lean children, whereas it was unaffected by risk variants in obese peers. We further show that IRX3 expression was elevated in isolated adipocytes and AT of lean compared to obese children, particularly in UCP1-negative adipocytes, and inversely correlated with BMI SDS. Independent of BMI, IRX3 expression in adipocytes was significantly related to adipocyte hypertrophy, and subsequent associations with AT inflammation and HOMA-IR in the children.One interpretation of our observation of FTO risk variants linked to IRX3 expression and adipocyte size restricted to lean children, along with the decreased IRX3 expression in obese compared to lean peers, may reflect a defense mechanism for protecting body-weight, which is pertinent for lean children.
Pub.: 26 Aug '16, Pinned: 21 Apr '17
Abstract: The heritability of obesity and body weight in general is high. A small number of confirmed monogenic forms of obesity-the respective mutations are sufficient by themselves to cause the condition in food abundant societies-have been identified by molecular genetic studies. The elucidation of these genes, mostly based on animal and family studies, has led to the identification of important pathways to the disorder and thus to a deeper understanding of the regulation of body weight. The identification of inborn deficiency of the mostly adipocyte-derived satiety hormone leptin in extremely obese children from consanguineous families paved the way to the first pharmacological therapy for obesity based on a molecular genetic finding. The genetic predisposition to obesity for most individuals, however, has a polygenic basis. A polygenic variant by itself has a small effect on the phenotype; only in combination with other predisposing variants does a sizeable phenotypic effect arise. Common variants in the first intron of the 'fat mass and obesity associated' gene (FTO) result in an elevated body mass index (BMI) equivalent to approximately +0.4 kg/m(2) per risk allele. The FTO variants were originally detected in a genome wide association study (GWAS) pertaining to type 2 diabetes mellitus. Large meta-analyses of GWAS have subsequently identified additional polygenic variants. Up to December 2009, polygenic variants have been confirmed in a total of 17 independent genomic regions. Further study of genetic effects on human body weight regulation should detect variants that will explain a larger proportion of the heritability. The development of new strategies for diagnosis, treatment and prevention of obesity can be anticipated.
Pub.: 04 Feb '10, Pinned: 21 Apr '17
Abstract: The increase in childhood obesity is a serious public health concern. Several studies have indicated that breastfed children have a lower risk of childhood obesity than those who were not breastfed, while other studies have provided conflicting evidence. The objective of this meta-analysis was to investigate the association between breastfeeding and the risk of childhood obesity.The PubMed, EMBASE and CINAHL Plus with Full Text databases were systematically searched from start date to 1st August 2014. Based on the meta-analysis, pooled adjusted odds ratio (AOR) and 95% confidence interval (CI) were calculated. I2 statistic was used to evaluate the between-study heterogeneity. Funnel plots and Fail-safe N were used to assess publication bias and reliability of results, and results from both Egger test and Begg test were reported.Twenty-five studies with a total of 226,508 participants were included in this meta-analysis. The studies' publication dates ranged from 1997 to 2014, and they examined the population of 12 countries. Results showed that breastfeeding was associated with a significantly reduced risk of obesity in children (AOR = 0.78; 95% CI: 0.74, 0.81). Categorical analysis of 17 studies revealed a dose-response effect between breastfeeding duration and reduced risk of childhood obesity.Results of our meta-analysis suggest that breastfeeding is a significant protective factor against obesity in children.
Pub.: 17 Dec '14, Pinned: 21 Apr '17
Abstract: In animal studies, exposure to multivitamins may be associated with obesity in the offspring; however, data in humans are sparse. We therefore examined the association between prenatal vitamin intake during pregnancy and offspring obesity.We investigated the association between prenatal vitamin intake and obesity among 29,160 mother-daughter dyads in the Nurses' Health Study II. Mothers of participants provided information on prenatal vitamin use during pregnancy with the nurse daughter. Information on body fatness at ages 5 and 10, body mass index (BMI) at age 18, weight in 1989 and 2009, waist circumference, and height was obtained from the daughter. Polytomous logistic regression was used to predict BMI in early adulthood and adulthood, and body fatness in childhood. Linear regression was used to predict waist circumference in adulthood.In utero exposure to prenatal vitamins was not associated with body fatness, either in childhood or in adulthood. Women whose mothers took prenatal vitamins during pregnancy had a covariate-adjusted odds ratio (OR) of being obese in adulthood of 0.99 (95% confidence interval (CI) 0.92-1.05, P-value = 0.68) compared with women whose mothers did not take prenatal vitamins. Women whose mothers took prenatal vitamins during pregnancy had a covariate-adjusted OR of having the largest body shape at age 5 of 1.02 (95% CI 0.90-1.15, P-value = 0.78). In additional analyses, in utero exposure to prenatal vitamins was also unrelated to adult abdominal adiposity.Exposure to prenatal vitamins was not associated with body fatness either in childhood or in adulthood.
Pub.: 20 Jun '14, Pinned: 21 Apr '17
Abstract: Cesarean section (CS) and antibiotic use during pregnancy may alter normal maternal-offspring microbiota exchange, thereby contributing to aberrant microbial colonization of the infant gut and increased susceptibility to obesity later in life. We hypothesized that (i) maternal use of antibiotics in the second or third trimester of pregnancy and (ii) CS are independently associated with higher risk of childhood obesity in the offspring.Of the 727 mothers enrolled in the Northern Manhattan Mothers and Children Study, we analyzed the 436 mother-child dyads followed until 7 years of age with complete data. We ascertained prenatal antibiotic use by a questionnaire administered late in the third trimester, and delivery mode by medical record. We derived age- and sex-specific body mass index (BMI) z-scores using the CDC SAS Macro, and defined obesity as BMI z⩾95th percentile. We used binary regression with robust variance and linear regression models adjusted for maternal age, ethnicity, pre-gravid BMI, maternal receipt of public assistance, birth weight, sex, breastfeeding in the first year and gestational antibiotics or delivery mode.Compared with children not exposed to antibiotics during the second or third trimester, those exposed had 84% (33-154%) higher risk of obesity, after multivariable adjustment. Second or third trimester antibiotic exposure was also positively associated with BMI z-scores, waist circumference and % body fat (all P<0.05). Independent of prenatal antibiotic usage, CS was associated with 46% (8-98%) higher offspring risk of childhood obesity. Associations were similar for elective and non-elective CS.In our cohort, CS and exposure to antibiotics in the second or third trimester were associated with higher offspring risk of childhood obesity. Future studies that address the limitations of our study are warranted to determine if prenatal antibiotic use is associated with offspring obesity. Research is also needed to determine if alterations in neonatal gut microbiota underlie the observed associations.
Pub.: 10 Oct '14, Pinned: 21 Apr '17
Abstract: Prenatal exposure to antibacterials may permanently dysregulate fetal metabolic patterns via epigenetic pathways or by altering maternal microbiota. We examined the association of prenatal exposure to systemic antibacterials with overweight and obesity in schoolchildren.We conducted a prevalence study among Danish schoolchildren aged 7-16 years using data from routine school anthropometric evaluations conducted during 2002-2013. Prenatal exposure to antibacterials was ascertained by using maternal prescription dispensations and infection-related hospital admissions during pregnancy. We defined overweight and obesity among the children using standard age- and sex-specific cutoffs. We computed sex-specific adjusted prevalence ratios (aPRs) of overweight and obesity associated with exposure to prenatal antibacterials, adjusting for maternal age at delivery, marital status, smoking in pregnancy and multiple gestation; we also stratified the analyses by birth weight.Among 9886 schoolchildren, 3280 (33%) had prenatal exposure to antibacterials. aPRs associated with the exposure were 1.26 (95% confidence interval (CI): 1.10-1.45) for overweight and 1.29 (95% CI: 1.03-1.62) for obesity. Among girls, aPRs were 1.16 (95% CI: 0.95-1.42) for overweight and 1.27 (95% CI: 0.89 to 1.82) for obesity. Among boys, aPRs were 1.37 (95% CI: 1.13-1.66) for overweight and 1.29 (95% CI: 0.96-1.73) for obesity. The aPR for overweight was higher among schoolchildren with birth weight <3500 g (aPR: 1.30, 95% CI: 1.05-1.61) than in schoolchildren with birth weight ⩾3500 g (aPR: 1.18, 95% CI: 0.95-1.46). Inversely, the association for obesity was higher among schoolchildren with birth weight ⩾3500 g (aPR: 1.35, 95% CI: 1.00-1.81) than among those who were <3500 g at birth (aPR: 1.16, 95% CI: 0.82-1.65).Prenatal exposure to systemic antibacterials is associated with an increased risk of overweight and obesity at school age, and this association varies by birth weight.
Pub.: 17 Jul '15, Pinned: 21 Apr '17
Abstract: There are concerns that prenatal exposure to endocrine-disrupting chemicals increases children's risk of obesity. African-American and Hispanic children born in the Bronx or Northern Manhattan, New York (1998-2006), whose mothers underwent personal air monitoring for polycyclic aromatic hydrocarbon (PAH) exposure during pregnancy, were followed up to ages 5 (n = 422) and 7 (n = 341) years. At age 5 years, 21% of the children were obese, as were 25% of those followed to age 7 years. After adjustment for child's sex, age at measurement, ethnicity, and birth weight and maternal receipt of public assistance and prepregnancy obesity, higher prenatal PAH exposures were significantly associated with higher childhood body size. In adjusted analyses, compared with children of mothers in the lowest tertile of PAH exposure, children of mothers in the highest exposure tertile had a 0.39-unit higher body mass index z score (95% confidence interval (CI): 0.08, 0.70) and a relative risk of 1.79 (95% CI: 1.09, 2.96) for obesity at age 5 years, and they had a 0.30-unit higher body mass index z score (95% CI: 0.01, 0.59), a 1.93-unit higher percentage of body fat (95% CI: 0.33, 3.54), and a relative risk of 2.26 (95% CI: 1.28, 4.00) for obesity at age 7 years. The data indicate that prenatal exposure to PAHs is associated with obesity in childhood.
Pub.: 17 Apr '12, Pinned: 21 Apr '17
Abstract: Previous evidence suggests that exposure to outdoor air pollution during pregnancy could alter fetal metabolic function, which could increase the risk of obesity in childhood. However, to our knowledge, no epidemiologic study has investigated the association between prenatal exposure to air pollution and indicators of fetal metabolic function. We investigated the association between maternal exposure to nitrogen dioxide and fine particulate matter (aerodynamic diameter ≤2.5 µm) and umbilical cord blood leptin and adiponectin levels with mixed-effects linear regression models among 1,257 mother-infant pairs from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, conducted in Canada (2008-2011). We observed that an interquartile-range increase in average exposure to fine particulate matter (3.2 µg/m(3)) during pregnancy was associated with an 11% (95% confidence interval: 4, 17) increase in adiponectin levels. We also observed 13% (95% confidence interval: 6, 20) higher adiponectin levels per interquartile-range increase in average exposure to nitrogen dioxide (13.6 parts per billion) during pregnancy. Significant associations were seen between air pollution markers and cord blood leptin levels in models that adjusted for birth weightzscore but not in models that did not adjust for birth weightzscore. The roles of prenatal exposure to air pollution and fetal metabolic function in the potential development of childhood obesity should be further explored.
Pub.: 31 Mar '16, Pinned: 21 Apr '17
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