Sex-Specific Associations of Gestational Glucose Tolerance With Childhood Body Composition

OBJECTIVE To examine the associations of maternal gestational glucose tolerance with offspring body composition in late childhood. RESEARCH DESIGN AND METHODS Among 958 women in the prebirth cohort Project Viva, glucose tolerance was assessed in the second trimester by nonfasting 50-g 1-h glucose challenge test (GCT), followed if abnormal by fasting 100-g 3-h oral glucose tolerance test (OGTT). We categorized women as normoglycemic (83.3%) if GCT was ≤140 mg/dL, isolated hyperglycemia (9.1%) if GCT was abnormal but OGTT normal, intermediate glucose intolerance (IGI) (3.3%) if there was one abnormal value on OGTT, or gestational diabetes mellitus (GDM) (4.5%) if there were two or more abnormal OGTT values. Using multivariable linear regression, we examined adjusted associations of glucose tolerance with offspring overall (N = 958) and central (N = 760) adiposity and body composition using dual X-ray absorptiometry (DXA) measured at the school-age visit (95 ± 10 months). RESULTS Compared with that in the male offspring of normoglycemic mothers, DXA fat mass was higher in male offspring of GDM mothers (1.89 kg [95% CI 0.33–3.45]) but not in male offspring of mothers with IGI (0.06 kg [−1.45 to 1.57]). DXA trunk-to-peripheral fat mass, a measure of central adiposity, was also somewhat higher in male offspring of GDM mothers (0.04 [−0.01 to 0.09]). In girls, DXA fat mass was higher in offspring of mothers with IGI (2.23 kg [0.12–4.34]) but not GDM (−1.25 kg [−3.13 to 0.63]). We showed no association of gestational glucose tolerance with DXA lean mass. CONCLUSIONS In this study, only male offspring of GDM mothers manifested increased adiposity, whereas only female offspring of mothers with IGI did so. Sex differences in glycemic sensitivity may explain these findings

Which Fish Should I Eat? Perspectives Influencing Fish Consumption Choices

Background: Diverse perspectives have influenced fish consumption choices

Inflammation and weight gain in reproductive-aged women

To investigate whether mid-pregnancy inflammation predicts rate of subsequent gestational weight gain (GWG), and whether inflammation at 3 years postpartum is associated with weight and waist circumference (WC) gain during a median of 4.4 years follow-up

Correlations among adiposity measures in school-aged children

BACKGROUND: Given that it is not feasible to use dual x-ray absorptiometry (DXA) or other reference methods to measure adiposity in all pediatric clinical and research settings, it is important to identify reasonable alternatives. Therefore, we sought to determine the extent to which other adiposity measures were correlated with DXA fat mass in school-aged children. METHODS: In 1110 children aged 6.5-10.9 years in the pre-birth cohort Project Viva, we calculated Spearman correlation coefficients between DXA (n=875) and other adiposity measures including body mass index (BMI), skinfold thickness, circumferences, and bioimpedance. We also computed correlations between lean body mass measures. RESULTS: 50.0% of the children were female and 36.5% were non-white. Mean (SD) BMI was 17.2 (3.1) and total fat mass by DXA was 7.5 (3.9) kg. DXA total fat mass was highly correlated with BMI (r(s)=0.83), bioimpedance total fat (r(s)=0.87), and sum of skinfolds (r(s)=0.90), and DXA trunk fat was highly correlated with waist circumference (r(s)=0.79). Correlations of BMI with other adiposity indices were high, e.g., with waist circumference (r(s)=0.86) and sum of subscapular plus triceps skinfolds (r(s)=0.79). DXA fat-free mass and bioimpedance fat-free mass were highly correlated (r(s)=0.94). CONCLUSIONS: In school-aged children, BMI, sum of skinfolds, and other adiposity measures were strongly correlated with DXA fat mass. Although these measurement methods have limitations, BMI and skinfolds are adequate surrogate measures of relative adiposity in children when DXA is not practical

Association of Vitamin E Intake at Early Childhood with Alanine Aminotransferase Levels at Mid-Childhood

The extent to which vitamin E (alpha-tocopherol) intake early in childhood is associated with alanine aminotransferase (ALT) level later in childhood is unknown. The objective of this research is to test the hypothesis that higher alpha-tocopherol intake during early childhood is associated with lower odds of elevated ALT levels during mid-childhood, and to examine how body mass index (BMI) influences these relationships. We studied 528 children in Project Viva. Mothers reported child dietary intake at early childhood visits (median 3.1 years) using a validated food frequency questionnaire. At mid-childhood (median 7.6 years), we collected child blood and anthropometric data. The main outcome was elevated sex-specific mid-childhood ALT level (≥ 22.1 units/liter for females and ≥ 25.8 units/liter for males). In multivariable logistic regression models, we assessed the association of energy-adjusted alpha-tocopherol intake with ALT levels, adjusting for child age, sex, race/ethnicity, diet, and age-adjusted, sex-specific BMIz at mid-childhood. Among children in this study, 48% were female, 63% were non-Hispanic white, 19% were non-Hispanic black, and 4% Hispanic/Latino. Mean alpha-tocopherol intake was 3.7±1.0 mg/day (range 1.4-9.2) at early childhood. At mid-childhood, mean BMIz was 0.41±1.0 units and 22% had an elevated ALT level. In multivariable-adjusted logistic regression models, children with higher early childhood vitamin E intake had lower odds of elevated mid-childhood ALT [adjusted odds ratio (AOR) 0.62 (95% CI: 0.39-0.99)] for quartiles 2-4 compared with the lowest quartile of intake. Findings persisted after accounting for early childhood diet [0.62 (0.36, 1.08)] and were strengthened after additionally accounting for mid-childhood BMIz [0.56 (0.32, 0.99)]. Conclusion: In this cohort, higher early childhood intake of alpha-tocopherol was associated with lower odds of elevated mid-childhood ALT level

Maternal corticotropin-releasing hormone is associated with LEP DNA methylation at birth and in childhood: an epigenome-wide study in Project Viva

BackgroundCorticotropin-releasing hormone (CRH) plays a central role in regulating the secretion of cortisol which controls a wide range of biological processes. Fetuses overexposed to cortisol have increased risks of disease in later life. DNA methylation may be the underlying association between prenatal cortisol exposure and health effects. We investigated associations between maternal CRH levels and epigenome-wide DNA methylation of cord blood in offsprings and evaluated whether these associations persisted into mid-childhood.MethodsWe investigated mother-child pairs enrolled in the prospective Project Viva pre-birth cohort. We measured DNA methylation in 257 umbilical cord blood samples using the HumanMethylation450 Bead Chip. We tested associations of maternal CRH concentration with cord blood cells DNA methylation, adjusting the model for maternal age at enrollment, education, maternal race/ethnicity, maternal smoking status, pre-pregnancy body mass index, parity, gestational age at delivery, child sex, and cell-type composition in cord blood. We further examined the persistence of associations between maternal CRH levels and DNA methylation in children's blood cells collected at mid-childhood (n = 239, age: 6.7-10.3 years) additionally adjusting for the children's age at blood drawn.ResultsMaternal CRH levels are associated with DNA methylation variability in cord blood cells at 96 individual CpG sites (False Discovery Rate <0.05). Among the 96 CpG sites, we identified 3 CpGs located near the LEP gene. Regional analyses confirmed the association between maternal CRH and DNA methylation near LEP. Moreover, higher maternal CRH levels were associated with higher blood-cell DNA methylation of the promoter region of LEP in mid-childhood (P < 0.05, β = 0.64, SE = 0.30).ConclusionIn our cohort, maternal CRH was associated with DNA methylation levels in newborns at multiple loci, notably in the LEP gene promoter. The association between maternal CRH and LEP DNA methylation levels persisted into mid-childhood

Residential Proximity to Major Roadways at Birth, DNA Methylation at Birth and Midchildhood, and Childhood Cognitive Test Scores: Project Viva(Massachusetts, USA).

BackgroundEpigenetic variability is hypothesized as a regulatory pathway through which prenatal exposures may influence child development and health.ObjectiveWe sought to examine the associations of residential proximity to roadways at birth and epigenome-wide DNA methylation. We also assessed associations of differential methylation with child cognitive outcomes.MethodsWe estimated residential proximity to roadways at birth using a geographic information system (GIS) and cord blood methylation using Illumina's HumanMethylation450-array in 482 mother-child pairs in Project Viva. We identified individual CpGs associated with residential-proximity-to-roadways at birth using robust linear regression [[Formula: see text]]. We also estimated association between proximity-to-roadways at birth and methylation of the same sites in blood samples collected at age 7-11 y ([Formula: see text]). We ran the same analyses in the Generation R Study for replication ([Formula: see text]). In Project Viva, we investigated associations of differential methylation at birth with midchildhood cognition using linear regression.ResultsLiving closer to major roadways at birth was associated with higher cord blood (and-more weakly-midchildhood blood) methylation of four sites in LAMB2. For each halving of residential-proximity-to-major-roadways, we observed a 0.82% increase in DNA methylation at cg05654765 [95% confidence interval (CI): (0.54%, 1.10%)], 0.88% at cg14099457 [95% CI: (0.56%, 1.19%)], 0.19% at cg03732535 [95% CI: (0.11%, 0.28)], and 1.08% at cg02954987 [95% CI: (0.65%, 1.51%)]. Higher cord blood methylation of these sites was associated with lower midchildhood nonverbal cognitive scores. Our results did not replicate in the Generation R Study.ConclusionsOur discovery results must be interpreted with caution, given that they were not replicated in a separate cohort. However, living close to major roadways at birth was associated with cord blood methylation of sites in LAMB2-a gene known to be linked to axonal development-in our U.S. cohort. Higher methylation of these sites associated with lower nonverbal cognitive scores at age 7-11 y in the same children. https://doi.org/10.1289/EHP2034

Weight gain in pregnancy and risk of maternal hyperglycemia

OBJECTIVE: The purpose of this study was to examine associations of weight gain from prepregnancy to glycemic screening with glucose tolerance status. STUDY DESIGN: Main outcomes were failed glycemic screening (1-hour glucose result \u3eor= 140 mg/dL) with either 1 high value on 3-hour oral glucose tolerance testing (impaired glucose tolerance in pregnancy) or \u3eor= 2 high values on 3-hour oral glucose tolerance testing (gestational diabetes mellitus). We performed multinomial logistic regression to determine the odds of these glucose intolerance outcomes by quartile of gestational weight gain among 1960 women in Project Viva. RESULTS: Mean gestational weight gain was 10.2 +/- 4.3 (SD) kg. Compared with the lowest quartile of weight gain, participants in the highest quartile had an increased odds of impaired glucose tolerance in pregnancy (adjusted odds ratio, 2.54; 95% confidence interval, 1.25-5.15), but not gestational diabetes mellitus (odds ratio, 0.93; 95% confidence interval, 0.50-1.70). CONCLUSION: Higher weight gain predicted impaired glucose tolerance in pregnancy, but not gestational diabetes mellitus

Misperceived pre-pregnancy body weight status predicts excessive gestational weight gain: findings from a US cohort study

<p>Abstract</p> <p>Background</p> <p>Excessive gestational weight gain promotes poor maternal and child health outcomes. Weight misperception is associated with weight gain in non-pregnant women, but no data exist during pregnancy. The purpose of this study was to examine the association of misperceived pre-pregnancy body weight status with excessive gestational weight gain.</p> <p>Methods</p> <p>At study enrollment, participants in Project Viva reported weight, height, and perceived body weight status by questionnaire. Our study sample comprised 1537 women who had either normal or overweight/obese pre-pregnancy BMI. We created 2 categories of pre-pregnancy body weight status misperception: normal weight women who identified themselves as overweight ('overassessors') and overweight/obese women who identified themselves as average or underweight ('underassessors'). Women who correctly perceived their body weight status were classified as either normal weight or overweight/obese accurate assessors. We performed multivariable logistic regression to determine the odds of excessive gestational weight gain according to 1990 Institute of Medicine guidelines.</p> <p>Results</p> <p>Of the 1029 women with normal pre-pregnancy BMI, 898 (87%) accurately perceived and 131 (13%) overassessed their weight status. 508 women were overweight/obese, of whom 438 (86%) accurately perceived and 70 (14%) underassessed their pre-pregnancy weight status. By the end of pregnancy, 823 women (54%) gained excessively. Compared with normal weight accurate assessors, the adjusted odds of excessive gestational weight gain was 2.0 (95% confidence interval [CI]: 1.3, 3.0) in normal weight overassessors, 2.9 (95% CI: 2.2, 3.9) in overweight/obese accurate assessors, and 7.6 (95% CI: 3.4, 17.0) in overweight/obese underassessors.</p> <p>Conclusion</p> <p>Misperceived pre-pregnancy body weight status was associated with excessive gestational weight gain among both normal weight and overweight/obese women, with the greatest likelihood of excessive gain among overweight/obese underassessors. Future interventions should test the potential benefits of correcting misperception to reduce the likelihood of excessive gestational weight gain.</p