Current practice behaviors for obesity management have remained refractory. Research has shown that lack of time and poor training/skills by primary care providers has led to poor or absent obesity counseling in practice. The purpose of this intervention was to facilitate obesity counseling in a pediatric office by using an evidence-based model called the 5As model of behavioral change. Lewin's change theory was the framework for this project to help clinicians transition their practice to include the 5As model in practice. The project consisted of a 30-minute power point presentation that included 2 case samples demonstrating how the 5As would be applied to each scenario. A physician and two family nurse practitioners evaluated the program via an open-ended survey on their obesity approach and thoughts on the 5As model. The results showed 100% support for the 5As model. All 3 participants stated they would implement the 5As model into practice and had positive remarks on the simplicity of its application. To help prevent clinical inertia and combat childhood obesity providers' must be made aware of the latest evidence and recommendations available to them. Project such as this one serve to merge research into clinical practice. The long-term social implications of getting the 5As into practice can help the United States meet Healthy People 2020 objectives and promote preventive care.

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1.5 million Ontarians, representing 10.2% the population, lived with diabetes in 2015. Treating this number of people with diabetes cost the public healthcare system approximately $6 billion. A staggering 2.3 million Ontarians, representing 13.5% of the population, are projected to have diabetes in the year 2025. This will raise public spending on diabetes to approximately $7.7 billion. Current therapies for Type 2 diabetes only focus on controlling glucose levels and do not target or reverse disease progression and complications, which allows the prevalence of diabetes to continue to rise unchecked. Targeting the source of insulin resistance, as opposed to attempting to control the symptoms of insulin resistance, represents a better strategy for the discovery of novel therapies. We have recently reported that loss of T-Cell Death-Associated Gene 51 (TDAG51) is associated with mature-onset obesity, Type 2 diabetes, and fatty liver. TDAG51 expression is significantly diminished in mice fed a high fat diet, which leads to insulin resistance and obesity, as well as in the leptin-deficient mouse model, a well-established genetic model of Type 2 diabetes and obesity. We have now discovered that restoring TDAG51 protein expression in the livers of TDAG51-null and leptin-deficient mouse models improves response to insulin and reduces total weight gain. We have shown that exogenous TDAG51 protein expression is significantly reduced in two mouse models of insulin resistance compared to healthy controls. The potential for post-translational degradation of TDAG51 protein in insulin-resistant livers is supported by five independent models of fatty liver in which TDAG51 protein expression is diminished while TDAG51 mRNA expression remained unchanged. We have also explored a number of mechanisms by which TDAG51 protein may be regulated post-translationally, and have provided suggestions of how TDAG51 protein may be modified in a fatty liver that would impact its stability. Collectively, we have highlighted the therapeutic potential of increasing liver TDAG51 expression in Type 2 diabetic conditions, and have laid a strong foundation for discovering how TDAG51 expression is regulated. / Thesis / Master of Science (MSc) / 1.5 million Ontarians, representing 10.2% the population, lived with diabetes in 2015. Treating this number of people with diabetes cost the public healthcare system a staggering $6 billion. Current therapies for Type 2 diabetes do not target or reverse disease progression and its complications, which allows the prevalence of diabetes to continue to rise unchecked. We have recently reported that loss of the protein T-Cell Death-Associated Gene 51 (TDAG51) is associated with mature-onset obesity, Type 2 diabetes, and fatty liver. Additionally, TDAG51 protein expression is nearly diminished in three different mouse models of insulin resistance and hepatic steatosis, though the mechanism by which the protein is reduced is unknown. We have now discovered that restoring TDAG51 expression in two mouse models of Type 2 diabetes can reduce weight gain and improve insulin signalling. We have also explored a number of mechanisms by which TDAG51 protein is regulated, and have devised a method for determining how TDAG51 protein might be regulated in normal versus fatty liver. Collectively, we have highlighted the therapeutic potential of increasing liver TDAG51 expression in Type 2 diabetic conditions, and have laid a strong foundation for discovering how TDAG51 expression is regulated.

Obesity has more than doubled worldwide since 1980 and it has become the focus of public health due to a wide range of serious complications. It is believed to be a complex disorder triggered by multiple genes, environmental factors and their interactions. The total number of single nucleotide polymorphisms (SNPs) associated with adult body mass index (BMI) at genome-wide significance level (P<5×10-8) has recently increased to 136. However, these genome-wide association studies (GWAS) have been conducted primarily in populations of European ancestry. This thesis aims to: 1) investigate whether these BMI SNPs are also associated with BMI in other ethnicities (South Asian, East Asian, African, Latino American and Native American) using a multi-ethnic prospective EpiDREAM cohort study; 2) explore the parental and child genetic contributions to obesity-related traits in children from birth to 5 years in the FAMILY cohort; 3) examine the maternal and child genetic contribution of BMI SNPs to maternal gestational weight gain (GWG) and postpartum weight retention in the FAMILY cohort. The major findings are: 1) most BMI susceptibility genes identified in Europeans are also associated with BMI in other five ethnicities. The effects of some SNPs and BMI genetic risk score (GRS) were modified by ethnicity; 2) SNPs contributing to adult BMI start to exert their effect at birth and in early childhood. Parent-of-origin effects may occur in a limited subset of obesity predisposing SNPs; and 3) there is no association between maternal and child GRS and GWG. But there is a genetic link between pre-pregnancy BMI variation and offspring birth weight and maternal postpartum weight retention. Taken together, these findings indicate that GWAS of specific ethnic group, children, birth weight and GWG are necessary to look for novel variants and alternative pathways influencing the development of obesity. / Thesis / Doctor of Philosophy (PhD) / Obesity is a chronic disorder triggered by multiple genes, environmental factors and their interactions. Currently most of the common genetic alterations, called single nucleotide polymorphisms (SNPs), associated with adult body mass index (BMI) were identified in populations of European ancestry. This thesis aims to: 1) investigate whether these BMI-associated SNPs are also associated with BMI in other ethnic groups; 2) explore the parental and child genetic contributions in children from birth to 5 years; 3) examine the maternal and child genetic contribution to maternal gestational weight gain (GWG) and postpartum weight retention. The major findings are: 1) BMI SNPs identified in Europeans are partially generalizable to other five ethnicities; 2) The collective SNPs contributing to adult BMI start to exert their effect at birth and in early childhood; and 3) There is a genetic link between pre-pregnancy BMI and offspring birth weight and maternal postpartum weight retention.

The purpose of this paper is to provide a review of current approaches to the treatment of obesity and to review literature on the effectiveness of the various treatments. Chapter 1 will present methods for measuring and diagnosing obesity. Some negative effects of obesity including physical and psychological factors will be specified briefly to stress the importance of treatment. The second chapter will provide a summary of medical, tradional psychological, and behavioral treatments including the underlying assumptions of each strategy, specific techniques used, and a summary of typical research results. Chapter 3 focuses on behavioral variables and techniques used in the treatment of obesity. Although behavioral treatments have been the most successful approach to weight control, the results have demonstrated wide inter-subject variability. therefore, attempts to explain this variability and predict success in behavorial weight control programs will be reviewed. An integrative summary and conclusion will be provided emphasizied recommendations for the treatment of obesity and for future research.

Obesity remains one of the greatest public health concerns in the United States due to both its cost and complexity. To effectively identify the potential causes and evaluate the effectiveness of interventions to reduce obesity requires multiple dimensions of analysis to ensure the goals of analysis are being adequately addressed. This paper contains three papers that span the spectrum of obesity research, from potential causes in the local food environment, to potential programs to address obesity in the worksite. The first chapter addresses the effectiveness evaluation of weight loss programs, which usually focuses on significant changes in weight. However, the underlying goal of weight loss is to reduce weight to reduce health risks. This requires a second dimension in the effectiveness evaluation, since the relationship between body mass index (BMI) and obesity health risks is non-linear. Severity can be used to address this dimension by using the squared depth of obesity, which can better detect changes in BMI that indicate changes in obesity risks. When used in the time-effect analysis it can identify important heterogeneous responses to the treatment, which can be used to direct future research. The second chapter addresses the missing data dimension of the cost-effectiveness analysis (CEA) of weight loss programs. Most previous studies ignore missingness in the CEA of weight loss programs, but this could result in biased results. Comparing two sample selections reveals that the analysis is sensitive not only to the missingness mechanism, but also which outcome is considered, and the experimental design. Finally, the third chapter considers potential causes of obesity in the local food environment. Although the spatial dimension of access is often overlooked, it could help better explain previous mixed findings. Access hypothesizes that living further from a supermarket increases the probability of obesity, which would result in spatial variation in the distribution of the outcomes relative to supermarkets. Spatial scanning statistics can detect this specific type of variation, which can then be formally tested for in conditional regression analysis. / Ph. D.

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Diss. (sammanfattning) Linköping : Linköpings universitet, 2009. / Härtill 4 uppsatser.

Thesis (Ph.D.)--Drexel University, 2010. / Includes abstract and vita. Includes bibliographical references (leaves 80-92).

Source: Masters Abstracts International, Volume: 47-01, page: 0346. Adviser: Asha S. Kapadia. Includes bibliographical references.