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A prospective study of maternal prenatal weight and offspring cardiometabolic health in midchildhood.

ABSTRACT: To examine the relations of maternal prepregnancy body mass index (ppBMI) and gestational weight gain (GWG) with offspring cardiometabolic health.We studied 1090 mother-child pairs in Project Viva, a Boston-area prebirth cohort. We measured overall (dual x-ray absorptiometry total fat; body mass index z-score) and central adiposity (dual x-ray absorptiometry trunk fat), and systolic blood pressure in offspring at 6 to 10 years. Fasting bloods (n = 687) were assayed for insulin and glucose (for calculation of homeostatic model assessment of insulin resistance), triglycerides, leptin, adiponectin, high sensitivity C-reactive protein, and interleukin 6. Using multivariable linear regression, we examined differences in offspring outcomes per 1 SD maternal ppBMI and GWG.After adjustment for confounders, each 5 kg/m² higher ppBMI corresponded with 0.92 kg (95% confidence interval, 0.70-1.14) higher total fat, 0.27 BMI z-score (0.21-0.32), and 0.39 kg (0.29-0.49) trunk fat. ppBMI was also positively associated with homeostatic model assessment of insulin resistance, leptin, high sensitivity C-reactive protein, interleukin 6, and systolic blood pressure; and lower adiponectin. Each 5 kg of GWG predicted greater adiposity (0.33 kg [0.11-0.54] total fat; 0.14 kg [0.04-0.23] trunk fat) and higher leptin (6% [0%-13%]) in offspring after accounting for confounders and ppBMI.Children born to heavier mothers have more overall and central fat and greater cardiometabolic risk. Offspring of women with higher GWG had greater adiposity and higher leptin.

SUBMITTER: Perng W

PROVIDER: S-EPMC4254266 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature

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A prospective study of maternal prenatal weight and offspring cardiometabolic health in midchildhood.

Perng Wei W Gillman Matthew W MW Mantzoros Christos S CS Oken Emily E

Annals of epidemiology 20140903 11

<h4>Purpose</h4>To examine the relations of maternal prepregnancy body mass index (ppBMI) and gestational weight gain (GWG) with offspring cardiometabolic health.<h4>Design</h4>We studied 1090 mother-child pairs in Project Viva, a Boston-area prebirth cohort. We measured overall (dual x-ray absorptiometry total fat; body mass index z-score) and central adiposity (dual x-ray absorptiometry trunk fat), and systolic blood pressure in offspring at 6 to 10 years. Fasting bloods (n = 687) were assayed ...[more]

PMID: 25263237

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Project description:BackgroundNumerous intrauterine factors may affect the offspring's growth during childhood. We aimed to explore if maternal and paternal prenatal lipid, apolipoprotein (apo)B and apoA1 levels are associated with offspring weight, length, and body mass index from 6 weeks to eight years of age. This has previously been studied to a limited extent.MethodsThis parental negative control study is based on the Norwegian Mother, Father and Child Cohort Study and uses data from the Medical Birth Registry of Norway. We included 713 mothers and fathers with or without self-reported hypercholesterolemia and their offspring. Seven parental metabolites were measured by nuclear magnetic resonance spectroscopy, and offspring weight and length were measured at 12 time points. Data were analyzed by linear spline mixed models, and the results are presented as the interaction between parental metabolite levels and offspring spline (age).ResultsHigher maternal total cholesterol (TC) level was associated with a larger increase in offspring body weight up to 8 years of age (0.03 ≤ Pinteraction ≤ 0.04). Paternal TC level was not associated with change in offspring body weight (0.17 ≤ Pinteraction ≤ 0.25). Higher maternal high-density lipoprotein cholesterol (HDL-C) and apoA1 levels were associated with a lower increase in offspring body weight up to 8 years of age (0.001 ≤ Pinteraction ≤ 0.005). Higher paternal HDL-C and apoA1 levels were associated with a lower increase in offspring body weight up to 5 years of age but a larger increase in offspring body weight from 5 to 8 years of age (0.01 ≤ Pinteraction ≤ 0.03). Parental metabolites were not associated with change in offspring height or body mass index up to 8 years of age (0.07 ≤ Pinteraction ≤ 0.99).ConclusionsMaternal compared to paternal TC, HDL-C, and apoA1 levels were more strongly and consistently associated with offspring body weight during childhood, supporting a direct intrauterine effect.

Project description:ObjectivesQuantifying long-term offspring cardiometabolic health risks associated with maternal prenatal anxiety and depression can guide cardiometabolic risk prevention. This study examines associations between maternal prenatal anxiety and depression, and offspring cardiometabolic risk from birth to 18 years.DesignThis study uses data from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort.ParticipantsParticipants were 526-8606 mother-offspring pairs from the ALSPAC cohort.SettingBritish birth cohort set, Bristol, UK.Primary and secondary outcomesExposures were anxiety (Crown-Crisp Inventory score) and depression (Edinburgh Postnatal Depression Scale score) measured at 18 and 32 weeks gestation. Outcomes were trajectories of offspring body mass index; fat mass; lean mass; pulse rate; glucose, diastolic and systolic blood pressure (SBP); triglycerides, high-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol and insulin from birth/early childhood to 18 years. Exposures were analysed categorically using clinically relevant, cut-offs and continuously to examine associations across the distribution of prenatal anxiety and depression.ResultsWe found no strong evidence of associations between maternal anxiety and depression and offspring trajectories of cardiometabolic risk factors. Depression at 18 weeks was associated with higher SBP at age 18 (1.62 mm Hg (95% CI 0.17 to 3.07). Anxiety at 18 weeks was also associated with higher diastolic blood pressure at 7 years in unadjusted analyses (0.70 mm Hg (95% CI 0.02 to 1.38)); this difference persisted at age 18 years (difference at 18 years; 0.89 mm Hg (95% CI 0.05 to 1.73). No associations were observed for body mass index; fat mass; lean mass; pulse rate; glucose; triglycerides, high-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol and insulin.ConclusionsThis is the first examination of maternal prenatal anxiety and depression and trajectories of offspring cardiometabolic risk. Our findings suggest that prevention of maternal prenatal anxiety and depression may have limited impact on offspring cardiometabolic health across the first two decades of life.

Project description:ObjectiveThe aim of the study was to investigate prospective, longitudinal associations between maternal prenatal cortisol response to an interpersonal stressor and child health for the subsequent 3 years.MethodsOne hundred twenty-three women expecting their first child provided salivary cortisol samples between 12 and 32 weeks of gestation (M (SD) = 22.4 (4.9) weeks) before and after a videotaped couple conflict discussion with their partner. Mothers reported on overall child health and several indicators of child illness (sick doctor visits, fevers, ear, and respiratory infections) when children were 6 months (n = 114), 1 (n = 116), and 3 (n = 105) years old. Associations between maternal prenatal cortisol reactivity and recovery and later child health at each of the three time points were analyzed using longitudinal regression models.ResultsGreater cortisol reactivity in response to the couple conflict discussion was associated with maternal self-report of better overall child health (p = .016, 95% CI = 0.06-1.30, Cohen's f = 0.045) across the study period. Greater cortisol reactivity was also associated with lower incidence rate ratios for maternal reports of sick doctor visits (incidence rate ratio 95% CI = 0.25-0.83, p = .006), fevers (95% CI = 0.25-0.73, p = .002), ear infections (95% CI = 0.25-0.58, p < .001), and respiratory infections (95% CI = 0.08-1.11, p = .073). Cortisol recovery was unrelated to study outcomes (all p's > 0.05). Maternal prenatal depressive symptoms moderated the association between cortisol reactivity and overall child health (p = .034, 95% CI = 0.07-1.87 for interaction term) but no other health outcomes (p's > 0.05). Among women with lower depressive symptoms, cortisol reactivity was not associated with overall child health; among women with higher levels of depressive symptoms, greater cortisol reactivity was associated with better overall child health.ConclusionsThis study provides longitudinal evidence that greater maternal cortisol reactivity to a salient interpersonal stressor during pregnancy is associated with fewer child health problems and better maternal report of overall child health during infancy and into early childhood.Trial registrationClinicaltrials.gov ID NCT01901536.

Project description:Study objectivesThe neurobiological processes involved in establishing sleep regulation are vulnerable to environmental exposures as early as seven weeks of gestation. Studies have linked in utero pesticide exposure to childhood sleep-disordered breathing. However, the impact of in utero pesticide exposure on the sleep health of adolescents remains unexplored.Materials and methodsData from 137 mother-adolescent pairs from a Mexico City cohort were analyzed. We used maternal urinary 3-phenoxybenzoic acid (3-PBA, pyrethroid metabolite) and 3, 5, 6-trichloro-2-pyridinol (TCPy, chlorpyrifos metabolite) from trimester three to estimate in utero pesticide exposure. Among adolescents, we obtained repeated measures of objectively assessed sleep duration, midpoint, and fragmentation using wrist-actigraphy devices for 7 consecutive days in 2015 and 2017. Unstratified and sex-stratified associations between maternal urinary 3-PBA and TCPy and adolescent sleep measures were examined using generalized linear mixed models (GLMMs). We also examined the interactive effects of maternal pesticide exposure and offspring sex on sleep outcomes.Results3-PBA and TCPy were detected in 44.4% and 93% of urine samples, respectively. Adjusted findings demonstrated that higher exposure to maternal TCPy was associated with longer sleep duration and later sleep timing. Findings from interaction tests between maternal pesticide exposure and offspring sex were not statistically significant, although adjusted sex-stratified findings showed that the association between TCPy with duration and midpoint was evident only among female offspring. To illustrate, those in the highest tertile of exposure had a 59 minute (95% CI: 12.2, 104.8) (p, trend = 0.004) longer sleep duration and a 0.6 hour (95% CI: 0.01, 1.3) (p, trend = 0.01) later sleep midpoint. We found no significant associations between 3-PBA and sleep outcomes.ConclusionWithin a cohort of mother-adolescent pairs, we found associations between maternal prenatal pesticide exposure and longer sleep duration and later sleep timing among adolescent offspring. Further, this association may be female-specific.

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A prospective study of maternal prenatal weight and offspring cardiometabolic health in midchildhood.

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A prospective study of maternal prenatal weight and offspring cardiometabolic health in midchildhood.

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