Adjustment For Pre-pregnancy Body Mass Index Research Articles

Endotoxin Biomarkers Are Associated With Adiposity and Cardiometabolic Risk Across 6 Years of Follow-up in Youth.

Metabolic endotoxemia may be a shared mechanism underlying childhood obesity and early-onset metabolic diseases (eg, type 2 diabetes, nonalcoholic fatty liver disease). Examine prospective associations of serum endotoxin biomarkers lipopolysaccharide (LPS) and its binding protein, LPS binding protein (LBP), and anti-endotoxin core immunoglobulin G (EndoCab IgG) with adiposity and cardiometabolic risk in youth. This prospective study included 393 youth in the Exploring Perinatal Outcomes Among Children cohort in Colorado. Participants were recruited from 2006 to 2009 at age 10 years (baseline) and followed for 6 years (follow-up). We examined associations of endotoxin biomarkers at baseline with adiposity [body mass index (BMI) z-score, visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), skinfolds, waist circumference] and cardiometabolic risk (insulin, glucose, adipokines, lipid profile, blood pressure) across both visits using mixed-effects regression, and with hepatic fat fraction (HFF) at follow-up using linear regression. Higher LPS and LBP predicted greater adiposity across follow-up. Each 1-unit log-transformed LPS corresponded with 0.23 (95% CI 0.03, 0.43) units BMI z-score, 5.66 (95% CI 1.99, 9.33) mm3 VAT, 30.7 (95% CI 8.0, 53.3) mm3 SAT, and 8.26 (95% CI 4.13, 12.40) mm skinfold sum. EndoCab IgG was associated with VAT only [3.03 (95% CI 0.34, 5.71) mm3]. LPS was associated with higher insulin [1.93 (95% CI 0.08, 3.70) µU/mL] and leptin [2.28 (95% CI 0.66, 3.90) ng/mL] and an adverse lipid profile. No association was observed with HFF. Accounting for pubertal status and lifestyle behaviors did not change findings. However, adjustment for prepregnancy BMI and gestational diabetes attenuated most associations. Serum endotoxin may be a marker of pathophysiological processes underlying development of childhood obesity and cardiometabolic conditions associated with exposure to fetal overnutrition.

Breastfeeding Initiation as Related to the Interaction of Race/Ethnicity and Maternal Diabetes.

Introduction: The health benefits of breastfeeding for both the mother and her offspring are well established, and breastfeeding may be especially important for mitigating negative health effects of pregnancy complicated by diabetes. Objective: This study sought to examine the association between race/ethnicity, maternal diabetes, and breastfeeding initiation in South Carolina (SC). Materials and Methods: Our study population is comprised of all live, singleton, full-term births in SC delivered January 2004 to December 2016 (292,468 non-Hispanic Whites, 173,158 non-Hispanic Blacks, and 52,174 Hispanics). Generalized estimating equations and an interaction term between race/ethnicity and maternal diabetes status were used to estimate the race/ethnic-specific odds ratio (OR) and 95% confidence intervals (CIs) that a mother with diabetes versus without diabetes initiated breastfeeding. Models were adjusted for maternal and infant sociodemographics (Model 1), additionally for clinical variables and birth outcomes (Model 2), and also for maternal prepregnancy body mass index (BMI) (Model 3). Results: We found statistically significant differences in breastfeeding initiation by race/ethnicity and diabetes status in Model 1. These associations were attenuated and lost significance upon additional adjustment. Non-Hispanic Black mothers with gestational diabetes were significantly more likely to initiate breastfeeding than nondiabetic non-Hispanic Black mothers, even after adjustment for prepregnancy BMI (OR: 1.07 [95% CI 1.02-1.12]). Conclusion: This large, population-based study of all live, singleton, full-term births in SC improves our understanding of how race/ethnicity and maternal metabolic disorders impact breastfeeding initiation, and may inform future hospital-based breastfeeding interventions in populations with the most need.

Pregnancy as a Window to Racial Disparities in Hypertension.

The black-white disparity in hypertension (HTN) among U.S. women persists after accounting for known risk factors. Pregnancy complications may reveal increased risks for later HTN. We examined the contribution of HTN risk factors measured at both midlife and pregnancy to black-white disparities in midlife HTN. Data came from a Michigan-based longitudinal study beginning in pregnancy. At 7-15 years postpregnancy (n = 615, mean age = 37), women were assessed for cardiovascular health, including blood pressure, and categorized as hypertensive (n = 126), prehypertensive (n = 149), and normotensive (n = 340). Midlife risk factors for HTN were assessed in four domains: socioeconomic status (SES), psychosocial, behavioral, and physiological. We used generalized logit models to assess the degree to which each domain attenuated the black (vs. white) odds ratio (OR) for HTN at midlife. We then added indicators of pregnancy health, that is, preterm delivery, prepregnancy body mass index (BMI), C-reactive protein (CRP) levels, depressive symptoms, smoking, hypertensive disorders, and lipid levels. Black women had 3.3 (95% CI: 2.0-5.5) times the odds of HTN compared to white women after adjusting for age. Following adjustment for midlife SES, and psychosocial, behavioral, and physiological factors, the OR was 2.1 (95% CI: 1.2-4.0). Adjustment for prepregnancy BMI, CRP, and depressive symptoms during pregnancy reduced the OR to 1.9 (95% CI: 1.0-3.7). Known risk factors measured at midlife explained some, but not all, of the race disparity in midlife HTN. Indicators of pregnancy health also contributed to the race disparity in HTN at midlife.

Maternal BMI, gestational diabetes, and weight gain in relation to childhood obesity: The mediation effect of placental weight.

High prepregnancy body mass index (BMI), excessive gestational weight gain (GWG), and gestational diabetes mellitus (GDM) are associated with the risk of childhood obesity. This study aims to examine the extent to which these effects may be mediated through the placenta. Data included 33,893 mothers and their singleton infants from birth to 7 years old (total 154,590 visits) in the Collaborative Perinatal Project, a U.S. multicenter prospective cohort study from 1959 to 1976. The placentas were weighed after removing cord and membranes. We performed sequential generalized estimating equation-linear models excluding and including placental weight to evaluate its mediation effect. In this population, 21.7% of mothers had overweight or obesity, 17.3% had excessive GWG, and 350 (1%) had diagnosed GDM; in addition, 7.2% children had obesity. After adjustment for prepregnancy BMI and other covariates, childhood BMI was 0.23 (95% CI: 0.05, 0.40) kg/m(2) higher for children born to mothers with GDM versus those without GDM. Inclusion of placental weight in the model attenuated the association by 52% to 0.11 (95% CI: -0.06, 0.28) and similarly attenuated the associations with childhood BMI for GWG by 25% and maternal prepregnancy BMI by 17%. Placental weight partly mediates the effects of prepregnancy BMI, excessive GWG, and GDM on childhood BMI.

Gestational Weight Gain, Early Pregnancy Maternal Adiposity Distribution, and Maternal Hyperglycemia

To estimate the effects of gestational weight gain (GWG), central adiposity and subcutaneous fat on maternal post-load glucose concentration, pregnant women [n = 413, 62% black, 57% with pregravid body mass index (BMI) ≥25] enrolled in a cohort study at ≤13 weeks gestation. GWG was abstracted from medical records. In a sub-sample of women (n = 214), waist circumference (WC), and biceps and triceps skinfold thicknesses were measured at enrollment. At 24-28 weeks gestation, post-load glucose concentration was measured using a 50-g 1-h oral glucose tolerance test. After adjustment for pre-pregnancy BMI, age, parity, race/ethnicity, smoking, marital status, annual family income, education, family history of diabetes, and gestational age of GDM screening, each 0.3-kg/week increase in weight in the first trimester was associated with a 2.2 (95% CI 0.1, 4.3)-mg/dl increase in glucose concentration. Each 8.6-mm increase in biceps skinfold thickness and each 11.7-mm increase in triceps skinfold thickness was associated with 4.3 (95% CI 0.2, 8.5)-mg/dl increase in maternal glucose, independent of BMI and other confounders. Neither GWG in the second trimester nor WC at ≤13 weeks was significantly associated with glucose concentration after confounder adjustment. Independent of pre-pregnancy BMI, high early pregnancy GWG and maternal subcutaneous body fat may be positively associated with maternal glucose concentrations at 24-28 weeks.