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No description available.

Obesity is one of the major risk factors for neonate low birthweight among reproductive women. The purpose of this quantitative study was to examine the association between 3 categories of obese status (moderate, severe, and very severe) and low neonate birthweight and preterm birth among women ages 18 to 39 years at all socioeconomic levels. Secondary data were obtained from 141,859 women ages 18-39 years living in the United States who had participated in the 2012-2015 Pregnancy Risk Assessment Monitoring System. Social-ecological theory was used to guide the study, and binary logistic regression was used for the analyses adjusting for age, education, ethnicity, income, marital status, and race confounders. Without accounting for the confounders, moderate, severe, and very severe obesity were associated with preterm birth. However, after adjusting for confounders, the obese categories were no longer associated with preterm birth. The estimated prevalence of preterm birth was higher among moderate, severe, and very severe obesity categories combined (56 preterm births per 1,000 live births) than among normal weight women (43 preterm births per 1,000 live births). Women of moderate obesity had a 10% statistically significant higher odds (p = .046, OR = 1.095) of neonate low birthweight when compared with very severely obese women. Severely obese women were not associated with neonate low birthweight when compared to women with very severe obese status (p = 0.159, OR = 1.056). Findings may be used to promote healthy lifestyle changes that could reduce the prevalence of preterm birth among obese women.

No description available.

No description available.

Obesity is the most common antenatal comorbidity, affecting one in five of the antenatal population in the UK. It is associated with adverse outcomes for mother and baby in both the short and long term. Increasing data suggest that maternal obesity may programme offspring later life obesity and premature mortality, with high birth weight being a marker for increased risk. The mechanism by which maternal obesity causes excessive neonatal birth weight is incompletely understood but considerable evidence implicates insulin resistance and/or hyperglycaemia. There are currently no effective interventions to mitigate the effects of obesity during pregnancy. In this thesis, we present the findings from a randomised, double blind, placebo controlled trial designed to examine the efficacy of metformin, an insulin-sensitising agent, in obese pregnant women. The aim of the trial was to determine whether giving metformin to obese pregnant women from between 12 and 16 weeks’ gestation until birth, would improve maternal and fetal outcomes. The primary outcome measure was birth weight of the baby, using this as a surrogate marker for the future life risk of the child developing obesity. Nested within this large clinical trial were a series of mechanistic sub-studies. To examine the effect of metformin on maternal insulin resistance at 36 weeks’ gestation, we used the hyperinsulinaemic euglycaemic clamp with concomitant use of stable isotope tracers. This enabled us to characterise in greater detail insulin sensitivity, endogenous glucose production and lipolysis. To determine the effect of metformin on maternal and fetal body composition we used magnetic resonance imaging and spectroscopy. This allowed us to quantify subcutaneous and intra-abdominal adipose tissue deposition and hepatic and skeletal muscle ectopic lipid deposition in the mother; and to measure subcutaneous adipose tissue deposition, hepatic lipid and hepatic volume in the fetus. To determine the effect of metformin on maternal endothelial function, we measured endothelium-dependent flow-mediated dilatation at the beginning and end of pregnancy. Change in diameter of the brachial artery in response to a flow stimulus created by arterial occlusion was measured using ultrasound imaging. We found no significant effect of metformin on birth weight. Mean birth weight was 3463 g (SD 660) in the placebo group and 3462 g (SD 548) in the metformin group (adjusted mean difference in z score –0·029, 95% CI –0·217 to 0·158; p=0·7597). Subjects taking metformin did demonstrate increased insulin sensitivity (M/I difference between means during high dose insulin of 0.02 [95% CI 0.001 to 0.03] milligrams per kilogram fat free mass per minute per pmol/L, p=0.04) but also enhanced endogenous glucose production (difference between means 0.54 [95% CI 0.08 to 1.00] milligrams per kilogram fat free mass per minute, p=0.02), compared with those taking placebo. We did not demonstrate any differences between treatment groups in maternal subcutaneous and intra-abdominal adipose tissue, or ectopic lipid deposition, or in fetal body fat distribution and liver volume. Participants in both treatment groups demonstrated a decline in endothelium-dependent flow-mediated dilatation between early and late pregnancy but there were no differences in the magnitude of that decline between the treatment groups. In conclusion, metformin, administered to obese, non-diabetic pregnant women, does not have any significant effect on birth weight of the baby. Our clamp studies demonstrated that subjects taking metformin were indeed more insulin-sensitive than those taking placebo, but the higher endogenous glucose production in this group suggests a reduced ability to suppress hepatic glucose production in response to insulin. This increased glucose flux may in part explain the lack of effect of metformin on fetal nutrition and growth. We can conclude that metformin, should not be used as an intervention in obese pregnant women to prevent excess birth weight. The global obesity epidemic is one of the greatest public health challenges we face and the cycle of disadvantage continues to be perpetuated to the next generation. The lack of any effective interventions for this high-risk group remains a significant concern and an important area for further research.

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Advances in medical technology have provided the mechanisms for sustaining life in premature and low-birthweight infants, resulting in the survival of more of these infants. Low-birthweight (LBW) and preterm infants are placed at risk by a number of medical complications, including intraventricular hemorrhage (IVH). The outcome of low-birthweight infants with intraventricular hemorrhage has been the subject of a great deal of research and continues to be a much-discussed topic in the medical and psychological communities. As more data become available, it appears that more questions arise concerning the later neuodevelopmental and neuropsychological outcome of these infants. For this reason, research concerning the later status of infants born with intraventricular hemorrhage is needed. The purpose of this study was to determine if there are differences in cognitive and motor functioning among infants with intraventricular hemorrhage (IVH), infants who were low birthweight (LBW), and normal-birthweight (NBW) infants. Forty-four subjects (10 with mild IVH, 9 with severe IVH, 12 LBW, and 13 NBW), who were born between January 1, 1984, and June 1, 1985, and were either patients in the neonatal intensive care unit at University of Utah Medical Center (the IVH and LBW infants) or were residents of the well-baby nursery (the NBW infants) at University of Utah Medical Center, served as the sample population. The subjects were tested at 3 to 4.5 years of age using the Stanford-Binet Intelligence Scales (Fourth Edition) and the motor section of the McCarthy Scales of Children's Abilities. In addition, infant medical data were obtained from medical records, and demographic data were collected including mother's age at time of birth, family income, mother's and father's education level, and birth order of the infant. The MIVH, SIVH, and LBW groups had significantly lower gestational ages and birthweights and significantly more medical complications than did the NBW group. The MIVH and SIVH groups also had significantly lower birthweight and gestational ages than did the LBW group, but approximately equivalent numbers of medical complications. Significant group differences were found only between the MIVH and NBW groups on the McCarthy motor score, with the MIVH group appearing to outperform the NBW group following statistical manipulation with analysis of covariance. No other significant group differences were found. Further research with a larger sample is recommended in order to more fully understand the later outcome following LBW and IVH.

Current ACOG guidelines recommend exercise during a low-risk pregnancy for 30 minutes on most, if not all days of the week. However, little is known about how the volume of exercise performed during pregnancy affects fetoplacental size. In addition, the confounding effects of maternal nutrient intake and weight gain, and how they interact with exercise volume to influence fetoplacental size have not been appropriately addressed. Therefore, the purpose of this study was to examine the effects of varying maternal exercise volumes on neonatal birthweight and placental volume, while addressing the influence of maternal nutrient intake and weight gain. Subjects evaluated for this study included pregnant women who walked during gestation (n=26), performed non-walking aerobic exercise during gestation (n=30), or remained as sedentary controls (n=32). At 16, 20, 24, 28, 32, 36 weeks gestation, women recorded their nutrient intake for 3 consecutive days. Additionally, they kept monthly exercise logs indicating the type and duration of their exercise. Nutrient variables calculated included average daily Calorie intake, average daily carbohydrate intake, average daily protein intake, average daily fat intake, and average daily fiber intake. Exercise volume was calculated as the average number of minutes per week spent performing exercise. Latent growth modeling was the statistical procedure used to analyze how change in maternal exercise volume and nutrient intake throughout gestation affects neonatal outcomes. Neonatal outcomes measured were birthweight, corrected birthweight for gestational age, sex, race, and socioeconomic status, and placental volume at delivery. Maternal walking volume had no effect on newborn birthweight or corrected birthweight, while it was inversely related to placental size at birth. Maternal non-walking aerobic exercise volume was inversely related with newborn birthweight, while there was a trend toward an inverse relationship with corrected birthweight and placental volume. Controlling for Calorie intake strengthened the relationship between any form of exercise volume and infant birthweight. Calorie intake, carbohydrate intake, and protein intake were all positively related to infant birthweight. Fiber intake was significantly inversely related to placental volume. Finally, maternal exercise volume and nutrient intake were not related to maternal weight gain. This data suggests that neonatal outcome will be affected by variations in exercise protocol. In addition, nutrient intake is a potentially confounding variable that should be examined when undertaking studies addressing the role of maternal exercise on neonatal outcome.

Birthweight is one of the most important health indicators for a newborn infant. Birthweight at either the lower or higher end is associated with adverse health outcomes in later life. In recent years, birthweight distribution in the United States has shifted to the lower end. This dissertation uses US vital statistics data from 1989 to 2007 to document recent birthweight trends in the US and examines the possible causes behind the trends. Results are reported for all births and by race/ethnicity/nativity. Descriptive analysis suggests that the lowering birthweight trend is the result of the rapid increase of lower-birthweight multiple births and decreasing birthweight among singleton births. The lowering birthweight is reflected in all birthweight measures. Low-birthweight rate is rising, mean birthweight is declining, and the proportion of macrosomic infants is decreasing. While this trend is most pronounced among US-born non-Hispanic whites and least among non-Hispanic blacks, it is prevalent among all race/ethnicity/nativity groups. Regression results suggest that much of the birthweight trend can be explained by shortened gestational age but common maternal socio-demographic, health and behavioral, and health care and medical intervention factors cannot fully explain the birthweight trend. Regression decomposition concludes that both the trends in maternal factors and the changes in the effects of these factors on birthweight contribute to the birthweight trend. Trend in gestational age is the biggest contributor, contributing more than 100% to the birthweight trend, while improvement in education, reduction of smoking during pregnancy and improvement in prenatal care have slowed down the birthweight decrease. Further research needs to be done to identify factors leading to the recent birthweight trend that are not available from the vital statistics. / text