Fetal growth does not modify the relationship of infant weight gain with childhood adiposity and blood pressure in the Southampton women's survey.
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SUBMITTER: Norris T
PROVIDER: S-EPMC7261399 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Obesity and asthma have increased in westernised countries. Maternal obesity may increase childhood asthma risk. If this relation is causal, it may be mediated through factors associated with maternal adiposity, such as fetal development, pregnancy complications or infant adiposity. We investigated the relationships of maternal body mass index (BMI) and fat mass with childhood wheeze, and examined the influences of infant weight gain and childhood obesity.Maternal prepregnancy BMI and estimated fat mass (from skinfold thicknesses) were related to asthma, wheeze and atopy in 940 children. Transient or persistent/late wheeze was classified using questionnaire data collected at ages 6, 12, 24 and 36 months and 6 years. At 6 years, skin-prick testing was conducted and exhaled nitric oxide and spirometry measured. Infant adiposity gain was calculated from skinfold thickness at birth and 6 months.Greater maternal BMI and fat mass were associated with increased childhood wheeze (relative risk (RR) 1.08 per 5 kg/m(2), p=0.006; RR 1.09 per 10 kg, p=0.003); these reflected associations with transient wheeze (RR 1.11, p=0.003; RR 1.13, p=0.002, respectively), but not with persistent wheeze or asthma. Infant adiposity gain was associated with persistent wheeze, but not significantly. Adjusting for infant adiposity gain or BMI at 3 or 6 years did not reduce the association between maternal adiposity and transient wheeze. Maternal adiposity was not associated with offspring atopy, exhaled nitric oxide, or spirometry.Greater maternal adiposity is associated with transient wheeze but not asthma or atopy, suggesting effects upon airway structure/function but not allergic predisposition.
| S-EPMC3661999 | biostudies-literature
Project description:BackgroundPoor diet quality in early childhood is inconsistently linked to obesity risk. Understanding may be limited by the use of cross-sectional data and the use of body mass index (BMI) to define adiposity in childhood.ObjectiveThe objective of this study is to examine the effects of continued exposure to diets of varying quality across early childhood in relation to adiposity at 6 years.MethodsOne thousand and eighteen children from a prospective UK birth cohort were studied. Diet was assessed using food frequency questionnaires when the children were aged 6 and 12 months, and 3 and 6 years; diet quality was determined according to scores for a principal component analysis-defined dietary pattern at each age (characterized by frequent consumption of fruits, vegetables and fish). At each age, children were allocated a value of 0/1/2 according to third of the distribution (bottom/middle/top) their diet quality score was in; values were summed to calculate an overall diet quality index (DQI) for early childhood (range 0-8). Obesity outcomes considered at 6 years were dual-energy X-ray absorptiometry-assessed fat mass and BMI.ResultsOne hundred and seven (11%) children had a DQI=0, indicating a consistently low diet quality, 339 (33%) had a DQI=1-3, 378 (37%) had a DQI=4-6 and 194 (19%) had a DQI=7-8. There was a strong association between lower DQI and higher fat mass z-score at 6 years that was robust to adjustment for confounders (fat mass s.d. per 1-unit DQI increase: β=-0.05 (95% confidence interval (CI): -0.09, -0.01), P=0.01). In comparison with children who had the highest diet quality (DQI=7-8), this amounted to a difference in fat mass of 14% (95% CI: 2%, 28%) at 6 years for children with the poorest diets (DQI=0). In contrast, no independent associations were observed between DQI and BMI.ConclusionsContinued exposure to diets of low quality across early childhood is linked to adiposity at the age of 6 years.
| S-EPMC4597330 | biostudies-literature
Project description:Different pathways likely underlie the association between early weight gain and cardiovascular disease risk. We examined whether birth weight for length relationship and weight gain up to 2 years of age are associated with lipid profiles and blood pressure (BP) in early adolescence and determined whether childhood adiposity mediates these associations.Data from QUALITY (Quebec Adipose and Lifestyle Investigation in Youth), a cohort of white children with parental history of obesity, were analyzed (n=395). Sex-specific weight for length z scores from birth to 2 years were computed. Rate of postnatal weight gain was estimated using individual slopes of weight for length z-score measurements. Percentage of body fat was measured at 8 to 10 years. Fasting lipids and BP were measured at 10 to 12 years. Using path analysis, we found indirect effects of postnatal weight gain, through childhood adiposity, on all outcomes: Rate of postnatal weight for length gain was positively associated with childhood adiposity, which in turn was associated with unfavorable lipid and BP levels in early adolescence. In contrast, small beneficial direct effects on diastolic BP z scores, independent of weight at other time points, were found for birth weight for length (?=-0.05, 95% CI, -0.09 to -0.002) and for postnatal weight gain (?=-0.02, 95% CI, -0.03 to -0.002).Among children with at least 1 obese parent, faster postnatal weight gain leads to cardiovascular risk factors in early adolescence through its effect on childhood adiposity. Although heavier newborns may have lower BP in early adolescence, this protective direct effect could be offset by a deleterious indirect effect linking birth weight to later adiposity.
| S-EPMC5586463 | biostudies-other
Project description:BackgroundPotentially driven by the lack of mother-to-infant transmission of microbiota at birth, cesarean delivery has been associated with higher risk of offspring obesity. Yet, no studies have examined when delivery-mode differences in adiposity begin to emerge. In this study, we examine differences in infant weight and adiposity trajectories from birth to 12 months by delivery mode.MethodsFrom 2013 to 2015, we recruited pregnant women into the Nurture Study and followed up their 666 infants. We ascertained maternal delivery method and infant birth weight from medical records. We measured weight, length, and skinfold thicknesses (subscapular, triceps, abdominal) when infants were 3, 6, 9, and 12 months of age. The main outcome, infant weight-for-length z score, was derived based on the WHO Child Growth Standards. We used linear regression models to assess the difference at each time point and used linear mixed models to examine the growth rate for infant weight and adiposity trajectories. We controlled for maternal age, race, marital status, education level, household income, smoking status, maternal pre-pregnancy body mass index, and infant birth weight.ResultsOf the 563 infants in our final sample, 179 (31.8%) were cesarean delivered. From birth to 12 months, the rate of increase in weight-for-length z score was 0.02/month (p = 0.03) greater for cesarean-delivered than vaginally-delivered infants. As a result of more rapid growth, cesarean-delivered infants had higher weight-for-length z score (0.26, 95% CI: 0.05, 0.47) and sum of subscapular and triceps (SS + TR) skinfold thickness (0.95 mm, 95% CI: 0.30, 1.60)-an indicator for overall adiposity-at 12 months, compared to vaginally-delivered infants.ConclusionsCompared to vaginal delivery, cesarean delivery was associated with greater offspring rate of weight gain over the first year and differences in adiposity that appear as early as 3 months of age. Monitoring cesarean-delivered infants closely for excess weight gain may help guide primordial prevention of obesity later in life.
| S-EPMC6476694 | biostudies-literature
Project description:Prenatal air pollution exposure inhibits fetal growth, but implications for postnatal growth are unknown.We assessed weights and lengths of US infants in the Project Viva cohort at birth and 6 months. We estimated 3rd-trimester residential air pollution exposures using spatiotemporal models. We estimated neighborhood traffic density and roadway proximity at birth address using geographic information systems. We performed linear and logistic regression adjusted for sociodemographic variables, fetal growth, and gestational age at birth.Mean birth weight-for-gestational age z-score (fetal growth) was 0.17 (standard deviation [SD] = 0.97; n = 2,114), 0- to 6-month weight-for-length gain was 0.23 z-units (SD = 1.11; n = 689), and 17% had weight-for-length ?95th percentile at 6 months of age. Infants exposed to the highest (vs. lowest) quartile of neighborhood traffic density had lower fetal growth (-0.13 units [95% confidence interval (CI) = -0.25 to -0.01]), more rapid 0- to 6-month weight-for-length gain (0.25 units [95% CI = 0.01 to 0.49]), and higher odds of weight-for-length ?95th percentile at 6 months (1.84 [95% CI = 1.11 to 3.05]). Neighborhood traffic density was additionally associated with an infant being in both the lowest quartile of fetal growth and the highest quartile of 0- to 6-month weight-for-length gain (Q4 vs. Q1, odds ratio = 3.01 [95% CI = 1.08 to 8.44]). Roadway proximity and 3rd-trimester black carbon exposure were similarly associated with growth outcomes. For 3rd-trimester particulate matter (PM2.5), effect estimates were in the same direction, but smaller and imprecise.Infants exposed to higher traffic-related pollution in early life may exhibit more rapid postnatal weight gain in addition to reduced fetal growth.
| S-EPMC4285344 | biostudies-literature
Project description:ObjectiveTo examine the importance of timing of gestational weight gain during three time periods: 1: ? 20 weeks gestation), 2: 21-29 weeks) and 3: ? 30 weeks) on fetal growth and infant birth size.MethodsStudy uses secondary data from the PRECONCEPT randomized controlled trial in Thai Nguyen province, Vietnam (n = 1436). Prospective data were collected on women starting pre-pregnancy through delivery. Maternal conditional weight gain (CWG) was defined as window-specific weight gains, uncorrelated with pre-pregnancy body mass index and all prior body weights. Fetal biometry, was assessed by ultrasound measurements of head and abdomen circumferences, biparietal diameter, and femoral length throughout pregnancy. Birth size outcomes included weight and length, and head, abdomen and mid upper arm circumferences as well as small for gestational age (SGA). Adjusted generalized linear and logistic models were used to examine associations.ResultsOverall, three-quarters of women gained below the Institute of Medicine guidelines, and these women were 2.5 times more likely to give birth to a SGA infant. Maternal CWG in the first window (? 20 weeks), followed by 21-29 weeks, had the greatest association on all parameters of fetal growth (except abdomen circumference) and infant size at birth. For birth weight, a 1 SD increase CWG in the first 20 weeks had 3 times the influence compared to later CWG (? 30 weeks) (111 g vs. 39 g) and was associated with a 43% reduction in SGA risk (OR (95% CI): 0.57 (0.46-0.70).ConclusionThere is a need to target women before or early in pregnancy to ensure adequate nutrition to maximize impact on fetal growth and birth size.Trial registrationClinicalTrials.gov, NCT01665378.
| S-EPMC5256875 | biostudies-literature
Project description:ImportanceBoth fetal and infant growth influence obesity later in life. The association of longitudinal fetal and infant growth patterns with organ fat is unknown.ObjectiveTo examine the associations of fetal and infant weight change with general, visceral, and organ adiposity at school age.Design, setting, and participantsThis cohort study was embedded in the Generation R Study, a population-based prospective cohort study in Rotterdam, the Netherlands. Pregnant women with a delivery date between April 2002 and January 2006 were eligible to participate. Follow-up measurements were performed for 3205 children. Data analysis of this population was performed from July 26, 2018, to February 7, 2019.ExposuresFetal weight was estimated in the second and third trimester of pregnancy. Infant weight was measured at 6, 12, and 24 months. Fetal and infant weight acceleration or deceleration were defined as a change in standard deviation scores greater than 0.67 between 2 ages.Main outcomes and measuresVisceral fat index, pericardial fat index, and liver fat fraction were measured by magnetic resonance imaging.ResultsThe sample consisted of 3205 children (1632 girls [50.9%]; mean [SD] age, 9.8 [0.3] years). Children born small for gestational age had the lowest median body mass index compared with children born appropriate for gestational age and large for gestational age (16.4 [90% range, 14.1-23.6] vs 16.9 [90% range, 14.4-22.8] vs 17.4 [90% range, 14.9-22.7]). Compared with children with normal fetal and infant growth (533 of 2370 [22.5%]), those with fetal weight deceleration followed by infant weight acceleration (263 of 2370 [11.1%]) had the highest visceral fat index (standard deviation scores, 0.18; 95% CI, 0.03-0.33; P = .02) and liver fat fraction (standard deviation scores, 0.34; 95% CI, 0.20-0.48; P < .001).Conclusions and relevanceFetal and infant weight change patterns were both associated with childhood body fat, but weight change patterns in infancy tended to have larger effects. Fetal growth restriction followed by infant growth acceleration was associated with increased visceral and liver fat.
| S-EPMC6487630 | biostudies-literature
Project description:INTRODUCTION:Placental function is an important determinant of fetal growth, and fetal growth influences obesity risk in childhood and adult life. Here we investigated how FTO and MC4R gene variants linked with obesity relate to patterns of fetal growth and to placental FTO expression. METHODS:Southampton Women's Survey children (n = 1990) with measurements of fetal growth from 11 to 34 weeks gestation were genotyped for common gene variants in FTO (rs9939609, rs1421085) and MC4R (rs17782313). Linear mixed-effect models were used to analyse relations of gene variants with fetal growth. RESULTS:Fetuses with the rs9939609 A:A FTO genotype had faster biparietal diameter and head circumference growth velocities between 11 and 34 weeks gestation (by 0.012 (95% CI 0.005 to 0.019) and 0.008 (0.002-0.015) standard deviations per week, respectively) compared to fetuses with the T:T FTO genotype; abdominal circumference growth velocity did not differ between genotypes. FTO genotype was not associated with placental FTO expression, but higher placental FTO expression was independently associated with larger fetal size and higher placental ASCT2, EAAT2 and y + LAT2 amino acid transporter expression. Findings were similar for FTO rs1421085, and the MC4R gene variant was associated with the fetal growth velocity of head circumference. DISCUSSION:FTO gene variants are known to associate with obesity but this is the first time that the risk alleles and placental FTO expression have been linked with fetal growth trajectories. The lack of an association between FTO genotype and placental FTO expression adds to emerging evidence of complex biology underlying the association between FTO genotype and obesity.
| S-EPMC4776702 | biostudies-literature
Project description:BACKGROUND:Polymorphic variants within human melanocortin-3 receptor gene (MC3R) gene have been associated with obesity. However, its influence on infancy and early childhood adiposity has not been reported before. OBJECTIVES:We assessed associations between genotype at polymorphic sites within MC3R with early childhood adiposity and interaction with early childhood appetitive traits. METHODS:We studied 1090 singletons in an Asian mother-offspring cohort genotyped for MC3R and in a subgroup (n?=?422) who had completed Child Eating Behaviour Questionnaires (CEBQ) at 12 months. Children were followed from birth to 48 months, and up to 10 measurements of body mass index and five measures of triceps and subscapular skin-folds were obtained. RESULTS:Independent of potential confounders, each additional MC3R minor allele copy was associated with greater body mass index standard deviation score [B{95% confidence interval}: 0.004?units/month {0.001,0.007}; p?=?0.007], triceps [0.009?mm/month {0.001,0.02}; p?=?0.021] and subscapular skin-fold [0.008?mm/month {0.002,0.01}; p?=?0.011] gain velocity in the first 48 months. Each additional MC3R minor allele copy was also associated with increased odds of overweight [odds ratio {95% confidence interval}: 1.48{1.17-1.88}] and obesity [1.58{1.10-2.28}] in the first 48 months. Every additional copy of MC3R minor allele was positively associated with 'slowness-in-eating' appetitive trait [0.24{0.06,0.39}, p?=?0.006]; however, the relationship between 'slowness-in-eating' with adiposity gain was not statistically significant. CONCLUSIONS:Our findings support the role of MC3R genetic variants in adiposity gain during early childhood.
| S-EPMC5111755 | biostudies-literature
Project description:BackgroundRapid weight gain (RWG) by 6 months of life is a significant risk factor of childhood overweight (OW)/obesity. Infant sleep patterns are associated with incident OW in childhood, but few have examined its relationship with RWG.ObjectiveExamine associations between newborn sleep-wake patterns and incident RWG at 6 months of life and OW at 36 months.MethodsLow-income Mexican/Mexican-American women with OW/obesity and their infants (n = 126) enrolled in a 1-year randomized controlled trial designed to prevent incident, infant RWG and toddlerhood OW/obesity. Sleep pattern metrics at 1 month were extracted from the Brief Infant Sleep Questionnaire-Revised. Outcome measures included RWG (>0.67 positive change in weight-for-age Z-score) from birth to 6 months and incident OW (body mass index percentile ≥85) at 36 months.ResultsBy 6 months, 35.7% (n = 45) of infants experienced RWG, and by 36 months 42.3% (n = 41) of toddlers were OW. Napping ≥5x/day at 1-month was significantly associated with decreased odds for RWG compared to napping <5x (OR = 0.11, 95%CI:0.02, 0.63). Each 1-hour increase in nocturnal vs diurnal sleep was associated with greater odds of incident OW at 36 mos (OR = 1.51, 95%CI:1.13, 2.03).ConclusionsEarly-life sleep patterns related to infant nap frequency and nocturnal vs diurnal sleep distribution were associated with obesity outcomes and may be important intervention targets to prevent lasting consequences on infant growth.
| S-EPMC8344177 | biostudies-literature