Metagenomics analysis of gut microbiota in response to diet intervention and gestational diabetes in overweight and obese women: a randomised, double-blind, placebo-controlled clinical trial.

OBJECTIVE: Gut microbiota and diet are known to contribute to human metabolism. We investigated whether the metagenomic gut microbiota composition and function changes over pregnancy are related to gestational diabetes mellitus (GDM) and can be modified by dietary supplements, fish oil and/or probiotics. DESIGN: The gut microbiota of 270 overweight/obese women participating in a mother-infant clinical study were analysed with metagenomics approach in early (mean gestational weeks 13.9) and late (gestational weeks 35.2) pregnancy. GDM was diagnosed with a 2 hour 75 g oral glucose tolerance test. RESULTS: Unlike women with GDM, women without GDM manifested changes in relative abundance of bacterial species over the pregnancy, particularly those receiving the fish oil + probiotics combination. The specific bacterial species or function did not predict the onset of GDM nor did it differ according to GDM status, except for the higher abundance of Ruminococcus obeum in late pregnancy in the combination group in women with GDM compared with women without GDM. In the combination group, weak decreases over the pregnancy were observed in basic bacterial housekeeping functions. CONCLUSIONS: The specific gut microbiota species do not contribute to GDM in overweight/obese women. Nevertheless, the GDM status may disturb maternal gut microbiota flexibility and thus limit the capacity of women with GDM to respond to diet, as evidenced by alterations in gut microbiota observed only in women without GDM. These findings may be important when considering the metabolic complications during pregnancy, but further studies with larger populations are called for to verify the findings.

Maternal obesity and the risk of group B streptococcal colonisation in pregnant women.

The aim of the study was to test if maternal obesity and being overweight are independent risk factors for rectovaginal Group B Streptococcus (GBS) colonisation in pregnancy and for early onset GBS disease in the neonate. A case-control study of 9877 deliveries was conducted. The obese gravidas were significantly more likely to be colonised by GBS when compared with non-obese gravidas (22.7% versus 17.5%, P < .001). Obese gravidas were still 33% more likely than non-obese women to test positive for GBS after adjusting for the perinatal factors (adjusted OR 1.33 [95% CI 1.12-1.56]). The risk of early onset GBS disease was not calculated due to its very low incidence. The conclusion is that maternal obesity is a significant risk factor for GBS colonisation at term. Impact statement What is already known on this subject? Group B Streptococcus (GBS) is as an important cause of perinatal mortality and morbidity if prophylaxis is not performed. Intrapartum antibiotics are given if the carrier status is positive or unknown, provided that the risk factors are present. What do the results of this study add? Maternal obesity is a significant and independent risk factor for GBS colonisation at term. What are the implications of these findings for clinical practice and/or further research? Maternal obesity may be considered as a risk factor that should be taken into account in strategies for reducing GBS disease in neonates.

Association Between Maternal Obesity and Group B Streptococcus Colonization in a National U.S. Cohort.

Objective: To investigate the association between maternal obesity as measured by prepregnancy body mass index (BMI) and group B streptococcus (GBS) colonization. Methods: We conducted a secondary analysis from the Consortium on Safe Labor Study (CSL) in the United States cohort study (2002-2008). Pregnant women with deliveries at ≥37 weeks of gestation who attempted labor were included (115,070 assessed deliveries). The association between maternal prepregnancy BMI, categorized as normal weight or below (<25 kg/m2), overweight (25 to <30 kg/m2), class I obesity (30 to <35 kg/m2), class II obesity (35 to <40 kg/m2), and class III obesity (≥40 kg/m2), and GBS colonization was modeled using logistic regression with generalized estimating equations. Models adjusted for maternal age, parity, race, pregestational diabetes, insurance status, study site/region, and year of delivery. Results: The overall prevalence of GBS colonization was 20.5% (23,625/115,070), which increased with rising maternal BMI, normal weight 19.3% (13,543/70,098), overweight 20.8% (5,353/25,733), class I obesity 23.0% (2,596/11,275), class II obesity 26.1% (1,270/4,850), and class III obesity 27.7% (863/3,114). In multivariable analysis, increasing maternal obesity severity was associated with higher odds of GBS colonization, namely overweight (adjusted odds ratio [AOR]: 1.09, 95% confidence interval [CI]: 1.05-1.13), class I obesity (AOR: 1.20, 95% CI: 1.15-1.26), class II obesity (AOR: 1.42, 95% CI: 1.33-1.51), and class III obesity (AOR: 1.50; 95% CI: 1.38-1.62) compared with normal weight. In secondary analyses, these associations persisted when stratified by maternal race. Conclusions: In a national U.S. sample, increasing maternal obesity severity as assessed by prepregnancy BMI was associated with a higher likelihood of maternal GBS colonization during pregnancy.