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The authors review the many adverse effects of obesity on pregnancy, including hypertension, diabetes, insulin resistance, subfertility, miscarriage, and congenital abnormalities.

Long-chain omega 3 fatty acids, eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3) exert potent anti-inflammatory properties in humans. This study characterized the effects of omega-3 ω-3 fatty acids supplements (ω-3 FA) on the inflammatory status in the placenta and adipose tissue of overweight/obese pregnant women. A randomized, double-masked controlled trial was conducted in overweight/obese pregnant women that were randomly assigned to receive DHA plus EPA (2 g/day) or the equivalent of a placebo twice a day from week 10-16 to term. Inflammatory pathways were characterized in: 1) adipose tissue and placenta of treated vs. untreated women; and 2) adipose and trophoblast cells cultured with long chain FAs. The sum of plasma DHA and EPA increased by 5.8 fold and ω-3 FA/ω-6 FA ratio was 1.5 in treated vs. untreated women (p< 0.005). Plasma CRP concentrations were reduced (p<0.001). The adipose tissue and placenta of treated women exhibited a significant decrease in TLR4 adipose and placental expression as well as IL6, IL8, and TNFα In vitro, EPA and DHA suppressed the activation of TLR4, IL6, IL8 induced by palmitate in culture of adipose and trophoblast cells. Supplementation of overweight/obese pregnant women with dietary ω-3 FAs for >25 weeks reduced inflammation in maternal adipose and the placental tissue. TLR4 appears as a central target of the anti-inflammatory effects at the cellular level. ClinicalTrials.gov NCT00957476.

OBJECTIVE: Offspring of obese mothers have an increased risk for obesity and diabetes. The purpose of this study was to determine whether fetuses of obese women have increased obesity, insulin resistance, and markers of inflammation, supporting the concept of fetal programming. RESEARCH DESIGN AND METHODS: Fifty-three lean and 68 obese women with singleton term pregnancies were evaluated at elective cesarean delivery. Maternal and umbilical cord blood was obtained for measures of insulin resistance and cytokines. Neonatal body composition was estimated using anthropometric measurements within 24 h of delivery. RESULTS: The fetuses of obese mothers had greater percent body fat (13.1 ± 3.4 vs. 11.6 ± 2.9%, P = 0.02), homeostasis model assessment of insulin resistance (1.51 ± 0.86 vs. 1.06 ± 0.70, P = 0.003), cord leptin (14.5 ± 13.5 vs. 8.2 ± 4.7 ng/ml, P = 0.001), and interleukin-6 (3.5 ± 2.3 vs. 2.4 ± 1.4 pg/ml, P = 0.02) than fetuses of lean women. There was a strong positive correlation between fetal adiposity and insulin resistance (r = 0.32, P = 0.0008) as well as maternal pregravid BMI and fetal insulin resistance (r = 0.31, P = 0.007) even with adjustment for potential confounders. Cord leptin had a significant correlation with fetal insulin resistance (r = 0.30, P = 0.001), but there was no significant correlation between any other umbilical cord cytokines and fetal insulin resistance. CONCLUSIONS: These data suggest that maternal obesity creates a significant risk for the next generations with metabolic compromise already apparent at birth. Therefore, if prevention of obesity is the goal rather than treatment, the perinatal period may be an important focus of future research.

Aims/hypothesisThis study aimed to examine changes in the insulin secretory response in early pregnancy, while accounting for changes in insulin sensitivity.MethodsThis is a secondary analysis of a previously conducted longitudinal physiological study. In 34 women, insulin secretory response (by IVGTT) and insulin sensitivity (by euglycaemic clamp) were assessed prior to pregnancy, in early pregnancy (12–14 weeks gestation) and in late pregnancy (34–36 weeks gestation). Using mixed-effects models, we compared insulin secretory response and sensitivity in early pregnancy to the same variables prior to pregnancy and in late pregnancy, with adjustment for age, obesity status and gestational diabetes mellitus (GDM). We examined changes in insulin secretory response after adjustment for insulin sensitivity using both multivariate modelling and the disposition index (DI). We explored the relationship between insulin secretory response and circulating hormones.ResultsThe insulin secretory response increased from prior to pregnancy to early pregnancy (unadjusted mean [SD] first-phase insulin response 465.1 [268.5] to 720 [358.2], p < 0.0001) and from early pregnancy to late pregnancy (to 924 [494.6], p = 0.01). Insulin sensitivity increased from prior to pregnancy to early pregnancy (insulin sensitivity index 0.10 [0.04] to 0.12 [0.05], p = 0.001) and decreased in late pregnancy (to 0.06 [0.03], p < 0.0001). Accounting for changes in insulin sensitivity, using either multivariate modelling or the DI, did not attenuate the early-pregnancy augmentation of insulin secretory response. Leptin was positively associated with insulin secretory response, independent of insulin sensitivity and adiposity (p = 0.004). Adjustment for leptin attenuated the observed augmentation of insulin secretory response in early pregnancy (adjusted mean change 121.5, p = 0.13).Conclusions/interpretationThe insulin secretory response increases markedly in early pregnancy, prior to and independent of changes in insulin sensitivity. Circulating hormones may mediate this metabolic adaptation. Identifying mediators of this physiological effect could have therapeutic implications for treating hyperglycaemia during and outside of pregnancy.

Nutrition during pregnancy is a critical dimension not only for women's health but also for the lifelong health of the offspring. Very limited national data exist on the usual dietary intakes of pregnant women. To estimate total usual nutrient intakes (from foods and dietary supplements) and the population prevalence of meeting or exceeding the National Academies of Sciences, Engineering, and Medicine Dietary Reference Intake recommendations among pregnant US women. A cross-sectional analysis was performed of a nationally representative sample of 1003 pregnant US women aged 20 to 40 years from the 2001-2014 National Health and Nutrition Examination Survey. Usual dietary intakes assessed by two 24-hour dietary recalls (including dietary supplements) adjusted for within-person variation using the National Cancer Institute method. The proportion of women at risk of inadequate dietary intake as determined by the Estimated Average Requirement, the proportion of women assumed to have adequate dietary intake as determined by the Adequate Intake, and the proportion of women at risk of excess dietary intake as determined by the Tolerable Upper Intake Level. Demographic differences between pregnant and nonpregnant women were compared with t tests. As representative of the US population, this sample of 1003 pregnant women had a mean (SE) age of 28.0 (0.3) years, was predominantly non-Hispanic white (mean [SE], 54.5% [3.1%]), and was at above 185% of the income to poverty ratio (mean [SE], 56.8% [3.0%]). Most pregnant women used a dietary supplement (mean [SE], 69.8% [2.3%]). A total of 10% or more of pregnant women had a total usual intake that is less than the Estimated Average Requirement for magnesium (mean [SE], 47.5% [2.8%]), vitamin D (mean [SE], 46.4% [2.7%]), vitamin E (mean [SE], 43.3% [2.7%]), iron (mean [SE], 36.2% [2.8%]), vitamin A (mean [SE], 15.5% [2.1%]), folate (mean [SE], 16.4% [1.6%]), calcium (mean [SE], 12.9% [2.4%]), vitamin C (mean [SE], 11.5% [1.9%]), vitamin B6 (mean [SE], 11.5% [1.5%]), and zinc (mean [SE], 10.9% [1.9%]). Some pregnant women exceeded the Adequate Intake for potassium (mean [SE], 41.7% [2.9%]), choline (mean [SE], 7.9% [3.2%]), and vitamin K (mean [SE], 47.9% [4.3%]). Most women exceeded the Tolerable Upper Intake Level for sodium (mean [SE], 95.0% [2.2%]), and some women exceeded the Tolerable Upper Intake Level of folic acid (mean [SE], 33.4% [2.8%]), iron (mean [SE], 27.9% [2.8%]), calcium (mean [SE], 3.0% [0.8%]), and zinc (mean [SE], 7.1% [1.6%]). For iron, the prevalence of an at-risk intake from foods alone was lower among women who used supplements (mean [SE], 80.3% [4.3%]) than those who did not use supplements (mean [SE], 95.3% [7.3%]); however, supplement use increased the risk of excessive iron and folic acid intakes given the amounts that are being consumed from supplemental products. This study suggests that a significant number of pregnant women are not meeting recommendations for vitamins D, C, A, B6, K, and E, as well as folate, choline, iron, calcium, potassium, magnesium, and zinc even with the use of dietary supplements. Almost all pregnant women in this study were at risk of excessive consumption of sodium, and many were at risk of excessive consumption of folic acid and iron. Improved dietary guidance to help pregnant women meet but not exceed dietary recommendations is warranted.

Infusion of TNF-α results in increased insulin resistance in rat and human skeletal muscle cells incubated in culture (21), although TNF-α neutralization over a period of 4 weeks had no effect on insulin sensitivity in obese type 2 diabetic subjects (22). The role of excess lipid turnover and cytokine production from adipose tissue, especially in obese patients, could potentially be very important in the overall insulin resistance and excess substrate supply that drives maternal-fetal energy transfer and increased neonatal adiposity.

To determine associations of gestational diabetes mellitus (GDM) and obesity with adverse pregnancy outcomes in the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study. Participants underwent a 75-g oral glucose tolerance test (OGTT) between 24 and 32 weeks. GDM was diagnosed post hoc using International Association of Diabetes and Pregnancy Study Groups criteria. Neonatal anthropometrics and cord serum C-peptide were measured. Adverse pregnancy outcomes included birth weight, newborn percent body fat, and cord C-peptide >90th percentiles, primary cesarean delivery, preeclampsia, and shoulder dystocia/birth injury. BMI was determined at the OGTT. Multiple logistic regression was used to examine associations of GDM and obesity with outcomes. Mean maternal BMI was 27.7, 13.7% were obese (BMI ≥33.0 kg/m(2)), and GDM was diagnosed in 16.1%. Relative to non-GDM and nonobese women, odds ratio for birth weight >90th percentile for GDM alone was 2.19 (1.93-2.47), for obesity alone 1.73 (1.50-2.00), and for both GDM and obesity 3.62 (3.04-4.32). Results for primary cesarean delivery and preeclampsia and for cord C-peptide and newborn percent body fat >90th percentiles were similar. Odds for birth weight >90th percentile were progressively greater with both higher OGTT glucose and higher maternal BMI. There was a 339-g difference in birth weight for babies of obese GDM women, compared with babies of normal/underweight women (64.2% of all women) with normal glucose based on a composite OGTT measure of fasting plasma glucose and 1- and 2-h plasma glucose values (61.8% of all women). Both maternal GDM and obesity are independently associated with adverse pregnancy outcomes. Their combination has a greater impact than either one alone.

Abstract Context An obesogenic perinatal environment contributes to adverse offspring metabolic health. Previous studies have been limited by lack of direct adiposity measurements and failure to account for potential confounders. Objective Examine the joint associations of maternal midpregnancy body mass index (BMI) and glycemia with direct adiposity measures in 10-14 year old offspring. Design and Setting International, epidemiological study: Hyperglycemia and Adverse Pregnancy Outcome (HAPO) and HAPO Follow-up Study, conducted between 2000-2006 and 2013-2016, respectively. Participants and Main Outcome Measures In 4832 children, adiposity measures for body mass index (BMI), body fat with air displacement plethysmography, skinfold thickness, and waist circumference were obtained at mean age 11.4 years. Results Maternal BMI and glucose, as continuous and categorical variables, were the primary predictors. In fully adjusted models controlling for child age, sex, field center, and maternal characteristics, maternal BMI had significant, positive associations with all childhood adiposity outcomes, while maternal glycemia had significant, positive associations with childhood adiposity outcomes except BMI. In joint analyses, and compared with a nonobese, nongestational diabetes mellitus (GDM) reference group, maternal obesity and GDM were associated with higher odds (maternal obesity odds ratio; OR [95% confidence interval; CI], GDM OR [95% CI]; combined OR [95% CI]) of childhood overweight/obese BMI (3.00 [2.42-3.74], 1.39 [1.14-1.71], 3.55 [2.49-5.05]), obese BMI (3.54 [2.70-4.64], 1.73 [1.29-2.30], 6.10 [4.14-8.99]), percent body fat >85th percentile (2.15 [1.68-2.75], 1.33 [1.03-1.72], 3.88 [2.72-5.55]), sum of skinfolds >85th percentile (2.35 [1.83-3.00], 1.75 [1.37-2.24], 3.66 [2.55-5.27]), and waist circumference >85th percentile (2.52 [1.99-3.21], 1.39 [1.07-1.80], 4.18 [2.93-5.96]). Conclusions Midpregnancy maternal BMI and glycemia are independently and additively associated with direct adiposity measures in 10-14 year old children. The combination of maternal obesity and GDM is associated with the highest odds of childhood adiposity.

Some have attributed risks of adverse outcomes associated with GDM, such as birth weight that is large for gestational age (LGA), excess fetal adiposity, and higher rate of cesarean section, to confounding characteristics, such as obesity, more advanced maternal age, or other medical complications, rather than glucose intolerance (7-9). [...] it is likely that additional well-designed randomized controlled trials and other clinical studies will be needed to determine 1 cost-effective therapeutic strategies for treatment of GDM diagnosed by the IADPSG Consensus Panel-recommended criteria; 2 optimal glycemic treatment targets; 3 appropriate follow-up of mothers to determine risks for later development of diabetes, other metabolic disorders, or CVD risk factors; and 4 follow-up of children to assess potential associations of maternal glycemia with long-term risks of obesity, altered glucose metabolism, and CVD risk factors.