Independent effect of gestational weight gain and prepregnancy obesity on pregnancy outcomes among Saudi women: A sub-cohort analysis from Riyadh mother and baby cohort study (RAHMA)

Background Gestational weight gain (GWG) and prepregnancy obesity are garnering more attention as determining factors of pregnancy outcomes when it comes to the wellbeing of both the mother and her baby. This study was conducted to describe the pattern of GWG among participants of Riyadh Mother and Baby Multicenter Cohort Study (RAHMA) and to investigate the detrimental effects of excessive GWG and prepregnancy obesity on pregnancy outcomes. Methods RAHMA is a multicentre cohort study conducted in three hospitals in Riyadh, Saudi Arabia. Participants were categorized according to the Institute of Medicine into inadequate, adequate, and excessive GWG, and stratified by body mass index (BMI) into under/normal weight, overweight, and obese. To examine the independent effect of maternal prepregnancy obesity and GWG, a multivariate regression model was used and adjusted odds ratio (AOR) and 95% Confidence Interval (CI) for each outcome were calculated. Results A total of 7029 participants were included in this study; 31.8% had adequate GWG, 25.9% had excessive GWG and 42.3% had inadequate GWG, while 29.7% had normal BMI, 33.3% were overweight, 34.8% were obese, and 2.2% were underweight. Excessive GWG was independently associated with increased risk of hypertensive events, (AOR = 1.77, 95% CI 1.20–2.63). Obesity was associated with higher risk of gestational diabetes (AOR 2.11, 95% CI 1.76–2.53), hypertensive events (AOR 2.06, 95% CI 1.48–3.01), and delivery by emergency caesarean section (AOR = 1.63, 95% CI 1.35–1.97). Infants of obese women had increased odds of macrosomia (AOR 3.11, 95% CI 1.94–4.99) and lower odds of low birth weight (AOR = 0.68, 95% CI 0.53–0.88). Conclusion In comparison to excessive GWG, which increases the risk of hypertensive events during pregnancy, prepregnancy obesity is associated with more adverse outcomes including GDM, hypertensive events in pregnancy and emergency CS.

The effect of prepregnancy body mass index on maternal micronutrient status: a meta-analysis

The relationship between prepregnancy body mass index (BMI) and maternal micronutrient status is inconsistent and has not received sufficient attention. This meta-analysis aimed to evaluate the effect of prepregnancy BMI on micronutrient levels in pregnant women. PubMed, Embase, Web of Science, and the Cochrane Library were searched for articles that contained information on micronutrient levels and prepregnancy BMI. A random-effects model was used to determine the association between prepregnancy BMI and maternal micronutrient status. Sixty-one eligible articles were eventually included, with 83,554 participants. Vitamin B12, folate, vitamin D, iron and ferritin were the main micronutrients evaluated in our meta-analysis. Prepregnancy obesity and overweight may lead to an increased risk of micronutrient deficiency, including vitamin B12, folate and vitamin D deficiency, while prepregnancy obesity or overweight may have no significant association with ferritin deficiency. Additionally, the results of the dose–response analyses demonstrated a possible significant inverse correlation between prepregnancy BMI and levels of micronutrient, except for iron and ferritin. Compared with women with normal weight, women who were overweight or obese prepregnancy have lower micronutrient concentrations and are more likely to exhibit micronutrient deficiency during pregnancy, which is harmful to both mothers and neonates.

Trends in Prepregnancy Obesity and Association With Adverse Pregnancy Outcomes in the United States, 2013 to 2018

Background The prevalence of obesity in the population has increased in parallel with increasing rates of adverse pregnancy outcomes (APOs). Quantifying contemporary trends in prepregnancy obesity and associations with interrelated APOs (preterm birth, low birth weight, and pregnancy‐associated hypertension) together and individually can inform prevention strategies to optimize cardiometabolic health in women and offspring. Methods and Results We performed a serial, cross‐sectional study using National Center for Health Statistics birth certificate data including women aged 15 to 44 years with live singleton births between 2013 and 2018, stratified by race/ethnicity (non‐Hispanic White, non‐Hispanic Black, Hispanic, and non‐Hispanic Asian). We quantified the annual prevalence of prepregnancy obesity (body mass index ≥30.0 kg/m 2 ; body mass index ≥27.5 kg/m 2 if non‐Hispanic Asian). We then estimated adjusted associations using multivariable logistic regression (odds ratios and population attributable fractions) for obesity‐related APOs compared with normal body mass index (18.5–24.9 kg/m 2 ; 18.5–22.9 kg/m 2 if non‐Hispanic Asian). Among 20 139 891 women, the prevalence of prepregnancy obesity increased between 2013 and 2018: non‐Hispanic White (21.6%–24.8%), non‐Hispanic Black (32.5%–36.2%), Hispanic (26.0%–30.5%), and non‐Hispanic Asian (15.3%–18.6%) women ( P ‐trend < 0.001 for all). Adjusted odds ratios (95% CI) for APOs associated with obesity increased between 2013 and 2018, and by 2018, ranged from 1.27 (1.25–1.29) in non‐Hispanic Black to 1.94 (1.92–1.96) in non‐Hispanic White women. Obesity was most strongly associated with pregnancy‐associated hypertension and inconsistently associated with preterm birth and low birth weight. Population attributable fractions of obesity‐related APOs increased over the study period: non‐Hispanic White (10.6%–14.7%), non‐Hispanic Black (3.7%–6.9%), Hispanic (7.0%–10.4%), and non‐Hispanic Asian (7.4%–9.7%) women ( P ‐trend < 0.01 for all). Conclusions The prevalence of prepregnancy obesity and burden of obesity‐related APOs have increased, driven primarily by pregnancy‐associated hypertension, and vary across racial/ethnic subgroups.

Prevalence and Social and Built Environmental Determinants of Maternal Prepregnancy Obesity in 68 Major Metropolitan Cities of the United States, 2013–2016

Objective. Maternal prepregnancy obesity is related to increased maternal morbidity and mortality and poor birth outcomes. However, prevalence and risk factors for prepregnancy obesity in US cities are not known. This study examines the prevalence and social and environmental determinants of maternal prepregnancy obesity (BMI ≥30), overweight/obesity (BMI ≥25), and severe obesity (BMI ≥40) in the 68 largest metropolitan cities of the United States. Methods. We fitted logistic and Poisson regression models to the 2013–2016 national vital statistics birth cohort data (N = 3,083,600) to derive unadjusted and adjusted city differentials in maternal obesity and to determine social and environmental determinants. Results. Considerable disparities existed across cities, with the prevalence of prepregnancy obesity ranging from 10.4% in San Francisco to 36.6% in Detroit. Approximately 63.0% of mothers in Detroit were overweight or obese before pregnancy, compared with 29.2% of mothers in San Francisco. Severe obesity ranged from 1.4% in San Francisco to 8.5% in Cleveland. Women in Anchorage, Buffalo, Cleveland, Fresno, Indianapolis, Louisville, Milwaukee, Oklahoma City, Sacramento, St Paul, Toledo, Tulsa, and Wichita had >2 times higher adjusted odds of prepregnancy obesity compared to those in San Francisco. Race/ethnicity, maternal age, parity, marital status, nativity/immigrant status, and maternal education were important individual-level risk factors and accounted for 63%, 39%, and 72% of the city disparities in prepregnancy obesity, overweight/obesity, and severe obesity, respectively. Area deprivation, violent crime rates, physical inactivity rates, public transport use, and access to parkland and green spaces remained significant predictors of prepregnancy obesity even after controlling for individual-level covariates. Conclusions. Substantial disparities in maternal prepregnancy obesity among the major US cities remain despite risk-factor adjustment, with women in several Southern and Midwestern cities experiencing high risks of obesity. Sound urban policies are needed to promote healthier lifestyles and favorable social and built environments for obesity reduction and improved maternal health.

Placental mobilization of free fatty acids contributes to altered materno-fetal transfer in obesity

Background Metabolic changes in obese pregnant women, such as changes of plasma lipids beyond physiological levels, may subsequently affect fetal development in utero. These metabolic derangements may remain in the offspring and continue throughout life. The placenta mediates bidirectional exchange of nutrients between mother and fetus. The impact of prepregnancy obesity on placental transfer of lipids is still unknown. Objective We aimed to examine materno-to-fetal free fatty acid (FFA) transfer by a combined experimental and modeling approach. Flux of 13C-labeled FFA was evaluated by ex vivo perfusion of human placentae as a function of prepregnancy obesity. Mathematical modeling complemented ex vivo results by providing FFA kinetic parameters. Results Obesity was strongly associated with elevated materno-to-fetal transfer of applied 13C-FFA. Clearance of polyunsaturated 13C-docosahexaenoic acid (DHA) was most prominently affected. The use of the mathematical model revealed a lower tissue storage capacity for DHA in obese compared with lean placentae. Conclusion Besides direct materno-to-fetal FFA transfer, placental mobilization accounts for the fetal FA supply. Together, with metabolic changes in the mother and an elevated materno-fetal FFA transfer shown in obesity, these changes suggest that they may be transmitted to the fetus, with yet unknown consequences.

High-fat-diet induced obesity increases the proportion of linoleic acyl residues in dam serum and milk and in suckling neonate circulation

Maternal obesity increases the risk of offspring to become obese and develop related pathologies. Exposure to maternal high-fat diet (HFD) only during lactation increases the risk of obesity-related diseases, suggesting that factors in milk affect long-term health. We hypothesized that prepregnancy obesity induced by HFD alters milk lipidome, and in turn, alterations may affect neonate serum lipidome. The objective of this study was to determine the effect of prepregnancy obesity induced by HFD on circulating lipids in dams and neonates and in milk. Female mice were fed an HFD (60% kcal fat) or control diet (CON, 10% kcal fat) beginning 4 weeks before breeding. On postnatal day 2 (PND2), pups were cross-fostered to create pup groups exposed to HFD during pregnancy, lactation, or both or exposed to CON. On PND12, dams were milked and then euthanized along with pups to collect blood. Serum and milk were processed for multiple reaction monitoring (MRM) lipidomics profiling to quantify the relative expression of lipid classes. Lipidome of HFD dam serum and milk had increased proportion of C18:2 free fatty acid and fatty acyl residues in all lipid classes. Lipidome of serum from pups exposed to maternal HFD during lactation was similarly affected. Thus, maternal HFD induced redistribution of fatty acyl residues in the dam’s circulation, which was associated with modification in milk and suckling neonate’s lipidome. Further studies are needed to determine if increased circulating levels of C18:2 in neonate affects development and predisposes offspring to obesity and metabolic syndrome.