Gestational diabetes mellitus (GDM) negatively affects the health of both mothers and babies, and is the most common pregnancy complication in the United States. Many dietary modification programs for pregnant women diagnosed with GDM rely on a one-size-fits-all approach to menu planning. The purpose of this project was to develop a diet modification program for GDM management using a patient-centered approach. The project objective was to develop the policies, procedures, and supporting documents needed to implement a successful GDM management program for pregnant women receiving antenatal care at an obstetrical clinic. The developed program incorporated strategies for clinic nursing staff to involve pregnant patients and their family members in the planning of individualized daily menus addressing social, motivational, and economic factors. Patient understanding of diet management will be evaluated through the administration of written pre and post-tests, which were included with the program materials. Long term program evaluation will be determined through the tracking of maternal weight gain and infant birth weights. This program has the potential to contribute to positive social change through the reduction of complications resulting from inadequately managed gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) is the most common metabolic complication in pregnancy and is associated with substantial maternal and neonatal morbidity. The standard of care for GDM in most developed countries is universal mid- to late- pregnancy (24-28 weeks gestation) glucose testing. While earlier diagnosis and treatment could improve pregnancy outcomes, tools for early identification of risk for GDM are not commonly used in practice. Existing models for predicting GDM risk within the first trimester of pregnancy based on maternal risk factors perform only modestly in the clinical setting. Heavy reliance on history of GDM to predict GDM development in the current pregnancy prevents these tools from being applicable to nulliparous women (i.e., women who have never given birth). In order to offer timely preventive intervention and enhanced antenatal care to nulliparous women, we need to be able to accurately identify those at high risk for GDM early in pregnancy. Data from the California Office of Statewide Health Planning and Development Linked Birth File was used to address three aims: 1) improve early pregnancy prediction of GDM risk in nulliparous women through development of a risk factor-based model, 2) conduct a systematic review and meta-analysis assessing the relationship between first trimester prenatal screening biomarker levels and development of GDM, and 3) determine if the addition of first and second trimester prenatal screening biomarkers to risk factor-based models will improve early prediction of GDM in nulliparous women. We developed a clinical prediction model including five well-established risk factors for GDM (race/ethnicity, age at delivery, pre-pregnancy body mass index, family history of diabetes, and pre-existing hypertension). Our model had moderate predictive performance among all nulliparous women, and performed particularly well among Hispanic and Black women when assessed within specific racial/ethnic groups. Our risk prediction model also showed superior performance over the commonly used American College of Obstetricians and Gynecologists (ACOG) screening guidelines, encouraging the prompt incorporation of this tool into preconception and prenatal care. Biomarkers commonly assessed in prenatal screening have been associated with a number of adverse perinatal and birth outcomes. However, reports on the relationship between first trimester measurements of prenatal screening biomarkers and GDM development are inconsistent. Our meta-analysis demonstrated that women who are diagnosed with GDM have lower first trimester multiple of the median (MoM) levels of both pregnancy associated plasma protein-A (PAPP-A) and free β-human chorionic gonadotropin (free β-hCG) than women who remain normoglycemic throughout pregnancy. Findings from our meta-analysis suggested that incorporation of prenatal screening biomarkers in clinical risk prediction models could aid in earlier identification of women at risk of developing GDM. Upon linkage of California Office of Statewide Health Planning and Development Linked Birth File and California Prenatal Screening Program records, we found that decreased levels of first trimester PAPP-A, increased second trimester unconjugated estriol, and increased second trimester dimeric inhibin A were associated with GDM development in nulliparous women. However, the addition of these biomarkers in clinical models did not offer improvements to the clinical utility (i.e., risk stratification) of models including maternal risk factors alone. Our findings demonstrate that incorporation of maternal risk factors in a clinical risk prediction model can more accurately identify nulliparous women at high risk for GDM early in pregnancy compared to current standard practice. The maternal characteristics model we developed is based on clinical history and demographic variables that are already routinely collected by clinicians in the United States so that it may be easily adapted into existing prenatal care practice and screening programs. Future work should focus on evaluating the clinical impact of model implementation on maternal and infant outcomes as well as financial costs to the health care system.

Gestational diabetes (GDM) is a potentially serious disorder requiring timely diagnosis and management to prevent adverse maternal and fetal outcomes. Of increasing concern today, when treating the woman with GDM, is the need to provide every woman with an intensive management plan to optimise the likelihood of favourable pregnancy outcomes. Early identification of those women with GDM who require insulin therapy in addition to diet therapy would be beneficial in the planning and standardisation of clinical management protocols, to enhance pregnancy outcomes and increase cost benefits with improved allocation of resources. The aim of this study was to evaluate the ability of the fasting plasma glucose level (FPG) at diagnosis to predict an increased risk to the fetus and the need for insulin therapy in a pregnancy complicated by GDM. A prospective longitudinal study design and recruitment by convenience sample was used. Data were obtained from 327 women and their babies. Diagnosis of GDM was made by a 75 gram oral glucose tolerance test (OGTT) using Australasian Diabetes in Pregnancy Society (ADIPS) criteria with the exception of seven women diagnosed on a blood glucose level >11.1mmol/l. Following consent of the women data were collected by a self report questionnaire and the medical record system at three points; at first intervention, following delivery and at the postpartum OGTT. Demographic, social, medical, maternal and neonatal outcome data were collected. The management protocol was similar for all of the women. Following nutritional intervention any woman who could not meet the glycemic targets of <= 5mmol/l fasting and/or <= 6.5mmol/l two hours postprandial was commenced on insulin therapy. The women had a mean age of 32 years, body mass index (BMI) of 25.7 and parity of 2 (range 1-12). Diagnosis was made at an average of 30 weeks and 70 women required insulin therapy with a mean dose of 34 IU per day, commencing at a mean of 31 weeks gestation. Mean birthweight was 3400G. Of the babies 12% were >4000G. Congenital abnormalities occurred in 3%, neonatal morbidities in 2% and there was 1 death in utero. Logistic regression analysis found the following significant associations: Increasing maternal BMI was related to increasing FPG levels at diagnosis and the requirement of higher insulin doses. There was a negative linear relationship to weight gain. Ethnicity was associated with maternal BMI and ethnicity with BMI was associated with birthweight in the specific ethnic group. BMI with insulin therapy as a covariate and the FPG value at OGTT were predictive of persistent glucose intolerance in 14% of women postpartum. Each value of the OGTT was a significant predictor of the need for insulin therapy as a function of the week of gestation. The FPG level was the statistical model of best fit. A 50% probability for requiring insulin was reached with a FPG at diagnosis of 4.0 mmol/l if tested at 10 weeks gestation, 5.1mmol/l at 20 weeks and 6.1 mmol/l at 30 weeks (p<.001). These results support the substantive research aim of the study. The model has the power to predict the probability (risk) of requiring insulin therapy based on the maternal FPG level at the OGTT according to the week of gestation. The study results demonstrate that glucose intolerance is linked to a number of adverse maternal and fetal outcomes in a continuous and graded fashion. The degree of reversibility of maternal and fetal risk through therapeutic interventions such as nutrition therapy, blood glucose monitoring, exercise and active patient participation aimed at improving glucose tolerance is unknown. Therefore, the rationale for, and feasibility of, new treatment strategies such as the application of this statistical model as a management approach require large scale randomised intervention studies, oriented toward measuring maternal and fetal outcomes amongst different populations.

Gestational diabetes, a common medical complication in pregnancy, may lead to severe fetal consequences if left untreated. A major concern with the use of antidiabetic drugs in pregnancy is the potential for placental transfer and fetal toxicity. The presence of endocytic pathways and several ABC transporter proteins has been demonstrated in the human placenta and are believed to play an important role in determining fetal exposure to drugs used in pregnancy. The objective of this thesis is to investigate the safety and transfer of the oral hypoglycemic agent, glyburide, and the new long acting insulin analog, insulin glargine, across the human placenta. The oral antidiabetic, glyburide, has been shown to be actively effluxed across the placenta in the fetal to maternal direction. The transport of glyburide in the presence of a breast cancer resistance protein (BCRP) inhibitor was investigated in the dually perfused human placenta model. The results of the perfusion studies indicate that BCRP plays a role in protecting the fetus from the accumulation of glyburide. Subsequently, cellular studies were carried out to determine the effect of the naturally occurring single nucleotide polymorphism within the coding region of BCRP (C421A/Q141K) on glyburide transport. Results suggest that glyburide transport may be reduced in the presence of the Q141K polymorphism. While insulin remains as the gold standard, the potential for maternal hypoglycemia with insulin injection has resulted in the development of insulin analogs. Insulin glargine, a human insulin analog, has a long half life with no pronounced peak when compared to currently used NPH insulin. Human placental perfusion experiments examining the extent and rate of transfer of insulin glargine across the placenta demonstrated that, at therapeutic concentrations, insulin glargine does not cross the placenta to a measurable extent. To further determine the fetal safety of insulin glargine therapy compared with NPH insulin, a systematic review and meta-analysis were performed. No evidence was identified for increased adverse fetal outcomes with the use of insulin glargine during pregnancy. Overall, the results of this research serve to provide improved treatment options for women with diabetes in pregnancy.

Gestational diabetes, a common medical complication in pregnancy, may lead to severe fetal consequences if left untreated. A major concern with the use of antidiabetic drugs in pregnancy is the potential for placental transfer and fetal toxicity. The presence of endocytic pathways and several ABC transporter proteins has been demonstrated in the human placenta and are believed to play an important role in determining fetal exposure to drugs used in pregnancy. The objective of this thesis is to investigate the safety and transfer of the oral hypoglycemic agent, glyburide, and the new long acting insulin analog, insulin glargine, across the human placenta. The oral antidiabetic, glyburide, has been shown to be actively effluxed across the placenta in the fetal to maternal direction. The transport of glyburide in the presence of a breast cancer resistance protein (BCRP) inhibitor was investigated in the dually perfused human placenta model. The results of the perfusion studies indicate that BCRP plays a role in protecting the fetus from the accumulation of glyburide. Subsequently, cellular studies were carried out to determine the effect of the naturally occurring single nucleotide polymorphism within the coding region of BCRP (C421A/Q141K) on glyburide transport. Results suggest that glyburide transport may be reduced in the presence of the Q141K polymorphism. While insulin remains as the gold standard, the potential for maternal hypoglycemia with insulin injection has resulted in the development of insulin analogs. Insulin glargine, a human insulin analog, has a long half life with no pronounced peak when compared to currently used NPH insulin. Human placental perfusion experiments examining the extent and rate of transfer of insulin glargine across the placenta demonstrated that, at therapeutic concentrations, insulin glargine does not cross the placenta to a measurable extent. To further determine the fetal safety of insulin glargine therapy compared with NPH insulin, a systematic review and meta-analysis were performed. No evidence was identified for increased adverse fetal outcomes with the use of insulin glargine during pregnancy. Overall, the results of this research serve to provide improved treatment options for women with diabetes in pregnancy.

Women with gestational diabetes (GD) are at higher risk of developing type 2 diabetes (DM) after delivery compared to those without GD. Numerous studies in the general population have identified that adoption of healthy lifestyles can prevent DM; however limited research has focused on women with GD. The purpose of this randomized pilot study was to determine the effectiveness of an educational intervention of SUGAR (Start Understanding Gestational Diabetes and Risk of Type 2 Diabetes), on women’s perceived risk of developing DM, knowledge of DM, self-efficacy to adopt healthy lifestyle behaviors and adoption of healthy lifestyle behaviors after childbirth among women with GD. A total of 23 women (mean age of 29.7, SD=3.9), 18 in SUGAR group and 5 in control group (CG) completed self-reported standardized questionnaires (Risk Perception Survey for Developing Diabetes adapted for women with GD; Self-Rated Abilities for Health Practices; Health Promotion Lifestyle Profile II; General Sleep Disturbance Scale; and Demographic Questionnaire) at baseline (third trimester) and post-test (postpartum 6-8 weeks). Intervention was given post the baseline data collection with a booster session at 2-4 weeks postpartum. The women in CG received attention control treatment. Study participants were obese (BMI M=33.1, SD=7.7) and a majority had a family history of DM. Findings showed that self-efficacy was the single significant predictor and accounted for 22% of the variance of healthy lifestyle behaviors. Participants had a clinical significant sleep disturbance during both pregnancy and postpartum. At baseline, poor sleepers reported a lower self-efficacy. The intervention significantly increased DM knowledge for women in the SUGAR group; however, not for perceived risk, self-efficacy nor healthy lifestyle behaviors. There was no difference between groups for postpartum glucose screening rates with only 39% receiving recommended testing. Future research needs to focus on prevention programs and center on self-efficacy, postpartum glucose screening, improve sleep, and adoption of healthy lifestyle behaviors. To ensure a better preventive care for GD women, education provided for both patients and health care provider is needed.

Few studies have measured the changes of postpartum weight retention (PWR), and none of them have assessed the effect of pregnancy on waist circumference (WC) in Taiwanese women. The primary aims of this longitudinal study were to explore the changes in body weight and WC during the first six months postpartum and to identify the explanatory factors of PWR and of WC. A theoretical framework that incorporated Bandura's social learning theory and the results of a literature review was used to guide this study. Structured questionnaires were used for data collection. Postpartum body weight and WC were measured. Data were collected from May 2011 to January 2013 and analyzed using the SPSS 19.0 and Mplus 6.12. A sample of 200 healthy postpartum women was recruited from three clinics in Tainan City, Taiwan. The mean age of the women was 31.19 years, and the majority of them were married (98.0%), primiparas (56%), had a bachelor's degree (52.5%), and planned to have this pregnancy (62.5%). The mean prepregnancy body weight was 55.84 kg, and the mean GWG was 13.76 kg. About one third of the sample gained weight exceeding the GWG recommendations of the IOM. The mean PWR decreased over time from 9.13 kg at hospitalization to 2.73 kg at 6 months postpartum. Approximately 24% of the participants still retained 5 kg or more at 6 months postpartum, and about 44% of the women had at least one kind of weight-related risk--substantial PWR, overweight, or central obesity. Age, prepregnancy BMI, parity, GWG, and place for doing the month significantly affected PWR. The final latent growth curve (LGC) model of PWR explained 91.5% and 33.9% of the variance in initial status and overall change rate in PWR. Age, prepregnancy BMI, parity, GWG, and cesarean delivery significantly affected WC, which explained 84.1% and 38.1% of the variance in initial status and change rate in WC. GWG was the most influential factor in the change rate of PWR and WC. Establishing tailored recommendations for GWG for Taiwanese women is warranted. / text

The purpose of this biobehavioral study was to explore relationships between psychosocial stressors of acculturation, acculturative stress, and metabolic markers of leptin and adiponectin in Mexican American women with and without gestational diabetes mellitus (GDM). A case control design was used for this secondary analysis which included a sample of 38 pregnant women with GDM and 38 healthy controls without GDM, who were matched on age and BMI status. Subjects completed two surveys—the Multidimensional Acculturation Scale II (MASII) and the Multidimensional Acculturative Stress Inventory (MASI)—which measured acculturation and acculturative stress. Descriptive statistics, Pearson r correlations, and independent sample t-tests were used to analyze the data. The results from this study indicated that significant relationships do exist between some of the variables of interest; however, there were no overall significant differences found between women with and without gestational diabetes. These mixed results may be an indicator of a need to further explore these concepts. / text

Population health data suggests that the development of metabolic disease is influenced by early life events. Gestational diabetes (GDM) is a common complication of pregnancy, but its effects on the offspring are poorly understood. It is hypothesized that a diet high in fat and sucrose will cause excessive weight gain and obesity during pregnancy accompanied by hyperglycemia and hyperinsulinemia that are characteristic of GDM. It is also hypothesized that gestational exposure to GDM will cause obesity, hepatic steatosis and insulin resistance in the offspring when compared to the offspring from metabolically healthy, lean mothers.

Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 73-81).