Thesis (Ph. D.)--University of California, San Diego, and San Diego State University, 2005. / Vita. Includes bibliographical references.

The aim of the study was to determine the Body Mass Index with regards to overweight and obesity of Black African children between the ages of six and nine years who were enrolled in three rural public schools within Mpumalanga Province, South Africa. The researcher used a quantitative descriptive research design. Each child’s weight and height was measured and their BMI and BMI percentile for gender and age calculated. According to the BMI percentile calculations for gender and age for the sample which consisted of 902 children, three percent were defined as being underweight, 79 percent as being normal weight, 11 percent as being overweight, and seven percent as being obese. In the sample there were also 21.3 percent children who were at risk of becoming overweight (3.5 percent) and obese (17.8 percent). Without intervention these at risk learners may in their adolescent and adult years be adversely affected by the physiological and psychosocial consequences related to their condition. Suggestion is made to utilise a Forum through which various stakeholders can pool their expertise and resources to develop a programme of intervention with the aim to prevent escalation of overweight and obesity, as well as reversing the current prevalence as identified within the research population.

published_or_final_version / Sports Science / Master / Master of Science in Sports Science

published_or_final_version / Community Medicine / Master / Master of Public Health

Childhood obesity disproportionately affects low-income families and those of Hispanic origin. Obesity is prevalent even among preschool children, and effective preventive interventions remain to be developed. Mothers, through their food choices and modeling behaviors, exert powerful influence over children’s diets and may therefore be ideal targets for such interventions. The purpose of this study was to assess the association between maternal diet quality and children’s body size. Data came from a study of Endotoxin, Obesity, and Asthma in NYC Head Start, to which African American and Hispanic families were recruited. Mothers answered a food frequency questionnaire (FFQ) and a questionnaire about maternal and child characteristics. Children’s body size was measured by child’s BMI z-score and percentile, child’s Waist-to-Height Ratio (WHtR), and child’s triceps and subscapular skinfold thicknesses. For the dissertation, we assessed maternal diet quality measured by HEI-2015 Total Score, and children’s adiposity at baseline and at one- and two-year follow-ups. This secondary analysis used data from 380 mother-child dyads with complete exposure and outcome data at baseline and, of those dyads, 167 mothers and 235 children who provided data at one-year follow-up, and 73 mothers and 110 children who did so at two-year follow-up. Mean HEI-2015 total score at baseline was 64.3±8.7 of 100, but 69.8±8.6 for Dominican and 60.2±6.5 for Mexican mothers. HEI scores were also associated with mothers’ marital status. Of the children, 44% were considered overweight or obese and 75% had WHtR > 0.5. Children of Mexican descent had higher WHtR than other groups. Maternal diet quality was not associated with any of the adiposity variables (BMI z-score, Triceps nor Subscapular z-score, or WHtR) at baseline or one-year follow-up. In regression models, Mexican ethnicity and younger age were associated with greater WHtR at baseline, but not one year later. Although HEI-2015 score was not related to child adiposity, it was related to national origin, which was related to adiposity. Maternal diet quality needs further study and consideration as a target for intervention; it may be an important indicator of family health.

Due to the high childhood obesity rates within the United States, it is necessary to develop efficacious strategies to combat childhood obesity. To explore whether early intervention can produce lasting metabolic improvements, we used a mouse model of genetically-induced hypothalamic leptin resistance (LeprNkx2.1knockout, hereby known as KO) that exhibits early-onset hyperphagia and obesity. We found that KO mice exhibit reduced capacity of the brown adipose tissue (as seen by disorganized mitochondrial structure). Brown adipose tissue capacity can be restored by paired-feeding in the peri-weaning period, leading to persistent improvements in later adiposity even after restriction ends. These studies lead us to investigate the maturation process of brown adipose tissue in the peri-weaning period. We found that brown adipose tissue expansion between 2 to 3 weeks of age is accompanied by a reduced thermogenic capacity in control mice, as determined by protein levels of uncoupling protein 1 and disorganization of the mitochondrial cristae. Thermogenic function was restored by 5 weeks of age, as demonstrated by a peak of uncoupling protein 1, in control mice but not KO mice. Paired-feeding of KO mice in the peri-weaning period rescued this peak at 5 weeks of age. These studies elucidate a critical period when brown adipose tissue expansion is followed by activation. The magnitude of brown adipose tissue activation at this time might be predictive of future obesity and metabolic rate, highlighting a potential therapeutic time window in which to intervene in pediatric obesity.

Bisphenol A (BPA) is a common component in plastic consumer products and epoxy resin linings. Initially developed in the 1930s-40s as a synthetic hormone treatment, it is now widely considered an endocrine disrupting chemical (EDC). A growing body of epidemiological literature suggests that ubiquitous exposures to BPA may be contributing to the global epidemic of obesity, with children a particularly vulnerable population. Obesity in children, defined by a body mass index (BMI) greater than or equal to the 95th percentile for age and sex, is an epidemic of great concern in the United States. As with other chemicals, the prenatal and early life period are critical windows of exposure to BPA; however, the mechanism by which BPA may influence the development of body size in children remains unclear. Experimental studies have found that BPA influences adipogenesis in both murine and adult human preadipocyte cell lines and BPA is hypothesized to play a role in enhancing adipogenic regulation by nuclear receptors such as peroxisome proliferator-activated receptor gamma (PPARγ). While the timeline of the processes involved in adipogenesis in humans is not universally agreed upon, it is accepted that PPARγ is highly expressed in adipose tissue and considered to be the master regulator of adipogenesis. To answer the question of both timing and developmental origin of BPA effects on adipogensis, we employed both an epidemiological approach, and experimental methodologies using primordial cell lines, mesenchymal stem cells (MSCs). Our study characterizes early life exposures to BPA, explores the adipogenic mechanism of BPA in human MSCs via cellular morphometrics and PPARγ gene expression, and identifies associations between early life exposure to BPA and childhood obesity and adiposity. For our epidemiological assessments, we studied a birth cohort of African American and Dominican mother and child dyads in New York City. BPA was measured in spot urine samples collected during pregnancy and at child ages 3, 5, and 7 years, from mothers and children (n=568 dyads) in the Columbia Center for Children’s Environmental Health (CCCEH). We compared BPA concentrations across paired samples. We explored relationships between BPA and the class of phthalate chemicals, another common plasticizer. BPA was detected in nearly all urine samples from prenatal third trimester and childhood ages 3 years, 5 years and 7 years. Prenatal urinary BPA concentrations were significantly lower than postnatal urinary BPA concentrations (p<0.001). BPA and phthalate metabolites were correlated prenatally and at 3, 5, and 7 years (all p-values < 0.02). BPA concentrations were correlated with phthalate metabolite concentrations prenatally, and at 3, 5 and 7 years(all p-values < 0.05). Geometric means of BPA were higher among African Americans than among Dominicans in prenatal (p<0.01), 5 year (p<0.001) and 7 year (p=0.02) samples. Postnatal BPA concentrations were significantly higher among children with mothers who had never marrried marital status and were significantly higher in summer than in all other seasons (all p-values < 0.05). These findings reveal widespread BPA exposure in an inner-city minority population. Our in vitro experiment was a feasibility study which sought to determine whether exposure to BPA by human umbilical cord mesenchymal stem cells (HUMSC) induces morphological changes and PPARγ gene expression during adipogenesis. An anonymous sample of n=18 umbilical cords was collected at delivery from mothers registered at New York-Presbyterian Sloane Hospital for Women and New York-Presbyterian Allen Hospital in New York City. HUMSCs were harvested from umbilical cords using an adhesion technique. HUMSCs were then induced in culture to differentiate into adipocytes using: a standard differentiation induction mix medium, a negative vehicle control medium, a positive control medium and experimental control media. Differences in cell surface area and cell count in all cultures were assessed using ImageJ software (version 1.49n, 2014). Gene expression of PPARγ in all cultures was evaluated by RT-PCR. Cell morphometric results were based on 11,676 cells from 3 umbilical cord samples. PPARγ1 and PPARγ2 gene expression was assessed during differntiation phase and early terminal phase adipogenesis (0 to 72 hours). Cell morphometrics were assessed during middle to late terminal phase adipogenesis (days 14 and 21). No differences in cell count were observed for experimental conditions compared to standard induction medium. A significant decrease in surface area was seen in cells exposed to 100 μM concentration of BPA as compared to exposure to standard induction medium at day 14 (t=-37.02 p=0.001). Differences in cell surface area were not observed at day 21. A twofold increased expression of PPARγ1 was observed in cells exposed to 10 μM concentration of BPA by 72 hours of adipogenic induction which was higher than the increase in expression observed for cells exposed to the positive control induction medium containing 10 μM concentration of rosiglitazone. All induction media conditions had negligible effects on PPARγ2 expression. As BPA increases expression of PPARγ1 in HUMSCs during the transition into the early terminal differentiation phase of adipogenesis, HUMSCs may be an approximate target tissue for evaluating BPA effects in adipogenesis. Finally, using a longitudinal research design, we analyzed the possible effect of prenatal and postnatal BPA exposures, measured in urine, on childhood anthropometric outcome measures. Participants in the CCCEH have been followed since the third trimester of pregnancy, providing us with anthropometric data on children from birth through the age of seven years. Available anthropometric outcome measures include body mass index z-scores (BMIZ) at 5 and 7 years, as well as fat mass index (FMI), percent body fat (%BF), and waist circumference (WC) at 7 years. Prenatal urinary BPA concentrations were positively associated with child age 7 FMI (beta=0.31 kg/m2, p-value=0.04, [95%CI 0.01, 0.60]), %BF (beta=0.79, p-value=0.04, [95%CI 0.03, 1.55]), and WC (beta=1.29 cm, p-value=0.01, [95%CI 0.29, 2.30]). Child urinary BPA concentrations were not associated with childhood BMI or other anthropometric outcomes. As the prenatal exposures were associated with childhood measures of adiposity, prenatal BPA exposure may have an effect on adiposity as children age that cannot be determined by the use of BMI alone. Our results suggest BPA may contribute to the developmental origins of obesity and adiposity.

[Truncated abstract] Introduction: Childhood obesity is currently a serious worldwide public health issue associated with many medical and psychosocial complications. The increasing disease burden with the potential for the development of medical co-morbidities has implications for future health care provision. This thesis adds to the understanding of the medical complications of overweight and obesity in childhood. Design and Aims: Two different, but related, research studies are reported. The first study is a cross-sectional study, designed to quantify the medical complications of childhood obesity in primary school-aged children in Western Australia. This study aims to identify the medical complications of primary school children with overweight/obesity. The study also aims to compare the medical complications of obesity in a community sample who have never sought treatment with a clinical sample who are actively seeking treatment for overweight/obesity. Finally, this study also aims to examine the relationship between the medical complications of childhood obesity and a continuum of children's Body Mass Index z-scores, including those in the normal range. The second study is an exercise intervention study to investigate the effect of exercise on one specific medical complication of obesity, namely insulin resistance. This study aims to determine if a structured eight-week exercise program significantly changes insulin resistance in obese children, and to determine if this decrease in insulin resistance is associated with changes in body composition and inflammatory markers. ... Conclusion: The prevalence of the medical complications of overweight and obesity in primary school children indicates that all children should have body mass index regularly checked from a young age. Children who are overweight/obese should be screened for the presence of co-morbidities despite a young age. Parents and health professionals needs to be educated that childhood obesity is associated with medical co-morbidities and is not simply a social or cosmetic concern. The continuous nature of the BMI z-score/co-morbidities relationship suggests that public health and health education strategies should include adopting a populationbased approach to weight management. This continuous relationship means that even in the normal BMI spectrum, the risk of developing co-morbidities rises with increasing BMI. Such an approach would encourage maintenance of normal weight for all children, rather than targeting overweight/obese children only. Increased activity and decreased sedentary behaviours should be recommended for all children in line with the population-based public health approach suggested above. However, exercise has a specific role in weight management strategies for overweight/obese children, and in management strategies for adiposityrelated co-morbidities. Significant metabolic benefits of exercise occur in the absence of changes in body shape and weight. After an exercise program, simple blood investigations (such as lipid profiles, fasting insulin and OGTTs) are likely to miss important metabolic improvements and anthropometry (BMI calculation, waist circumference) may be more indicative of potential metabolic improvement and decreased co-morbidity risk.

The prevalence of childhood obesity is escalating rapidly and it considered to be a major public health problem. Diet is a recognised precursor of fatness, and current evidence supports the premise that in Westernised countries, the dietary intakes of children are likely to be important in obesity genesis. However, we have a relatively poor understanding of the environments in which a child’s eating is learnt and maintained. Much of the existing work in this area is based on small-scale or experimental studies, or has been derived from homogeneous populations within the USA. Despite these limitations, there is evidence that aspects of the child’s family environment are likely to be important in determining obesity risk in children. This thesis examines the impact of the family food environment on a child’s eating through two related studies. The first study, titled the Children and Family Eating (CAFÉ) study comprised three phases. Phase one involved qualitative interviews with 17 parents of 5-6 year-old children to explore parental perceptions regarding those factors in a child’s environment believed to influence the development of their child’s eating habits. These interviews were used to inform the development of quantitative measures of the family food environment. The second phase involved the development of a Food Frequency Questionnaire (FFQ) to assess dietary intake in 5-6 year-olds. The FFQ was informed by analysis of 1995 Australian National Nutrition Survey data. In the final phase the relationships between dietary intakes of 5-6 year-old children, and potential predictors of dietary intake were examined in a cross-sectional study of 560 families. Predictors included measures of: parental perceptions of the adequacy of their child’s diet; food availability and accessibility; child-feeding; the opportunities for parental modelling of food intake; a child’s television exposure; maternal Body Mass Index; and maternal education. Analysis of the CAFÉ data provides unique information regarding the relationships between a child’s family food environment and their food consumption. Models developed for a range of dietary outcomes considered to be predictive of increased risk for obesity, including total energy and fat intakes, vegetable variety, vegetable consumption, and high-energy (non-dairy) fluid consumption, explained between 11 and 20 percent of the variance in dietary intake. Two aspects of the family food environment, parental perception of a child’s dietary adequacy, and the total minutes of television viewed per day, were frequently found to be predictive of dietary outcomes likely to promote fatness in these children. The second study, titled the Parent Education and Support (PEAS) Feeding Intervention Study, was a prospective pre/post non-randomised intervention trial that assessed the impact of a feeding intervention to 240 first-time mothers of one-year-old children. This intervention focused on one aspect of the family food environment, child-feeding, which has been proposed as influential in the development of obesogenic eating behaviours. In this study, Maternal and Child Health Nurses (MCHNs), using a ‘Division of Responsibility’ model of feeding, taught parents to provide nutritious food at regular intervals and to let children decide if to eat and how much to eat. Thus parents were encourages to food their child without exerting pressure, or employing coercion or rewards (controlling behaviours). The aim was to influence parental attitudes and beliefs regarding child-feeding. Through the use of these feeding techniques, this intervention also aimed to increase the variety of fruits and vegetables a child consumed by teaching parents to persist with offering these foods, over the year of the intervention, in non-emotive environments. Fruits and vegetables were chosen in this intervention because they are likely to be protective in the development of obesity. Analysis of the PEAS data suggests that this low-level feeding intervention, delivered through existing Maternal and Child Health services, was modestly effective in changing parental attitudes and beliefs regarding the feeding of young children. Further, the validity of fruits offered to intervention group children increased. This thesis expands the existing knowledge base by providing a comprehensive analysis of the relative impact of aspects of the family environment on dietary intakes of 5-6 year-olds. Further, the analysis of a feeding intervention in first-time parents provides important insights regarding the potential to influence child-feeding and the impact this may have on the promotion of eating behaviours protective against obesity.

Thesis (Ph. D.)--University of Texas at Austin, 2004. / Vita. Includes bibliographical references.