Increased food energy supply is more than sufficient to explain the US epidemic of obesity

Background: The major drivers of the obesity epidemic are much debated and have considerable policy importance for the population-wide prevention of obesity.

Objective: The objective was to determine the relative contributions of increased energy intake and reduced physical activity to the US obesity epidemic.

Design: We predicted the changes in weight from the changes in estimated energy intakes in US children and adults between the 1970s and 2000s. The increased US food energy supply (adjusted for wastage and assumed to be proportional to energy intake) was apportioned to children and adults and inserted into equations that relate energy intake to body weight derived from doubly labeled water studies. The weight increases predicted from the equations were compared with weight increases measured in representative US surveys over the same period.

Results: For children, the measured weight gain was 4.0 kg, and the predicted weight gain for the increased energy intake was identical at 4.0 kg. For adults, the measured weight gain was 8.6 kg, whereas the predicted weight gain was somewhat higher (10.8 kg).

Conclusions: Increased energy intake appears to be more than sufficient to explain weight gain in the US population. A reversal of the increase in energy intake of 2000 kJ/d (500 kcal/d) for adults and of 1500 kJ/d (350 kcal/d) for children would be needed for a reversal to the mean body weights of the 1970s. Alternatively, large compensatory increases in physical activity (eg, 110–150 min of walking/d), or a combination of both, would achieve the same outcome. Population approaches to reducing obesity should emphasize a reduction in the drivers of increased energy intake.

Glucose indices, health behaviors, and incidence of diabetes in Australia: the Australian diabetes, obesity and lifestyle study (AusDiab)

OBJECTIVE--We examined the associations of objectively measured sedentary time and physical activity with continuous indexes of metabolic risk in Australian adults without known diabetes.

RESEARCH DESIGN AND METHODS--An accelerometer was used to derive the percentage of monitoring time spent sedentary and in light-intensity and moderate-to-vigorous-intensity activity, as well as mean activity intensity, in 169 Australian Diabetes, Obesity and Lifestyle Study (AusDiab) participants (mean age 53.4 years). Associations with waist circumference, triglycerides, HDL cholesterol, resting blood pressure, fasting plasma glucose, and a clustered metabolic risk score were examined.

RESULTS--Independent of time spent in moderate-to-vigorous-intensity activity, there were significant associations of sedentary time, light-intensity time, and mean activity intensity with waist circumference and clustered metabolic risk. Independent of waist circumference, moderate-to-vigorous-intensity activity time was significantly beneficially associated with triglycerides.

CONCLUSIONS--These findings highlight the importance of decreasing sedentary time, as well as increasing time spent in physical activity, for metabolic health.

The Pacific OPIC Project (Obesity Prevention In Communities) : action plans and interventions

Background: The Pacific OPIC Project (Obesity Prevention In Communities) includes whole-of-community intervention programs in four countries (Fiji, Tonga, New Zealand, Australia) aimed at reducing the prevalence of overweight and  obesity in youth.

Development of Action Plans: At each intervention site, preliminary interviews  were conducted with youth to identify the potential socio-cultural barriers and  facilitators to healthy eating and regular physical activity in order to attain and sustain a healthy body size. This and other information was presented at a 2-day workshop with community stakeholders, including youth. The participants then prioritised the components for a draft action plan which was later consolidated through further community consultation.

Action Plan objectives: Each action plan had two overall aims: to build  community capacity and to promote healthy weight. The first three objectives in each action plan were on capacity building, social marketing messages, and evaluation. Next were a set of four to five behavioural objectives with associated strategies involving programs, events, social marketing and environmental  change. Lastly, each site had one or two innovative or developmental objectives.

Progress: Interventions began in all sites from 2005, with the action plans guiding implementation priorities. The initial behavioural objective for targeting in Fiji was eating regular breakfast and meals throughout the day, for Tonga it was physical activity, and for Australia and New Zealand it was increasing water consumption and decreasing consumption of sweet drinks.

Conclusions: The action plans have provided the basis for community engagement in the project, the guide to the implementation of activities and the template for the evaluation plan.

Obesity prevention in children and adolescents

Childhood and adolescent obesity has been increasing in most middle- and high-income countries, and, as with adult obesity, this has been driven by increasingly obesogenic environments, especially the food environment. This constitutes a “market failure,” signaling the need for government interventions with policies, programs, and social marketing. Population prevention strategies are critical, and children and adolescents should be the priority populations. Food marketing to children is a central policy issue for governments to address, and comprehensive regulations are needed to provide substantive protection for children. Community-based intervention programs show some real promise in reducing childhood obesity, but the 2 big challenges ahead are to ensure that there is substantial ongoing funding so that the community capacity to promote healthy weights can be scaled up to a national level and to ensure that policies are in place to support these efforts. The social and cultural shifts that support healthy eating and physical activity occur differentially, and special efforts are needed to reduce the socioeconomic gradients associated with childhood obesity. A positive public health approach encompassing environmental, regulatory, sociocultural, and educational strategies offer the best chance of reducing obesity without increasing disordered eating patterns.

Creating community action plans for obesity prevention using the ANGELO (Analysis Grid for Elements Linked to Obesity) framework

Community-based interventions are an important component of obesity prevention efforts. The literature provides little guidance on priority-setting for obesity prevention in communities, especially for socially and culturally diverse populations. This paper reports on the process of developing prioritized, community-participatory action plans for obesity prevention projects in children and adolescents using the ANGELO (Analysis Grid for Elements Linked to Obesity) Framework. We combined stakeholder engagement processes, the ANGELO Framework (scans for environmental barriers, targeted behaviours, gaps in skills and knowledge) and workshops with key stakeholders to create action plans for six diverse obesity prevention projects in Australia (n = 3), New Zealand, Fiji and Tonga from 2002 to 2005. Some sites included sociocultural contextual analyses in the environmental scans. Target groups were under-5-year-olds (Australia), 4–12-year-olds (Australia) and 13–18-year-olds (all four countries). Over 120 potential behavioural, knowledge, skill and environmental elements were identified for prioritization leading into each 2-day workshop. Many elements were common across the diverse cultural communities; however, several unique sociocultural elements emerged in some cultural groups which informed their action plans. Youth were actively engaged in adolescent projects, allowing their needs to be incorporated into the action plans initiating the process of ownership. A common structure for the action plan promoted efficiencies in the process while allowing for community creativity and innovation. The ANGELO is a flexible and efficient way of achieving an agreed plan for obesity prevention with diverse communities. It is responsive to community needs, combines local and international knowledge and creates stakeholder ownership of the action plan.

Family food environments as determinants of children's eating : implications for obesity prevention

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.

Leptin and the development of obesity

The focus of this thesis was leptin and its role in the development of obesity and non-insulin-dependent diabetes mellitus (NIDDM). Studies in Psammomys obesus, a polygenic animal model of obesity and NIDDM, showed that ob gene expression and plasma leptin concentration correlated significantly with body weight, percentage body fat and plasma insulin concentration. In addition, plasma leptin concentrations were significantly elevated in insulin resistant Psammomys obesus independent of body weight. Dietary energy restriction from weaning in Psammomys obesus prevented excessive body weight gain, hyperleptinemia and hyperglycemia compared with ad libitum fed animals. Interestingly, 19% of the energy-restricted animals still developed hyperinsulinemia and tended to have increased plasma leplin compared with normoinsulinemic energy-restricted Psammomys obesus. Fasting for 24 hours significantly reduced plasma leptin concentration in lean, insulin-sensitive but not obese, insulin-resistant P. obesus, suggesting a dysregulation in the response of leptin to acute caloric deprivation in these animals. The effects of leptin administration to P. obesus were also investigated. Single daily intraperitoneal injection of 5 mg leptin/kg body weight for 14 days had no significant effect in lean or obese P. obesus. This dose had previously been shown to rapidly and significantly reduce food intake and body weight in ob/ob and wild-type mice, suggesting relative leptin resistance in P. obesus. Acute (8 hour) effects of administration of 5 mg leptin/kg body weight were also investigated. No significant effects on food intake or plasma insulin were detected, however blood glucose concentrations were significantly elevated in obese, glucose intolerant P. obexus, suggesting an exacerbation of insulin resistance in susceptible animals. Treatment of lean, healthy P. obesus with 45 mg leptin/kg body weight/day for 7 days resulted in significant decreases in food intake and percentage body fat, showing that the leptin resistance observed in this species could be overcome by the administration of very large doses of leptin. In another study, leplin was shown to significantly inhibit maximal insulin binding to isolated adipocytes, suggesting that leptin may respresent an important link between obesity and NIDDM. Links between aspects of obesity and NIDDM and polymorphisms in the ob and p3-adrencrgic receptor genes were also investigated in two human populations.

Liver fat metabolism, obesity and diabetes in Psammomys obesis

Defects in fat metabolism are central to the aetiology and pathogenesis of obesity and type II diabetes. The liver plays a central role in these disease states via its regulation of glucose and fat metabolism. In addition, accumulation of fat within the liver has been associated with changes in key pathways of carbohydrate and fat metabolism. However a number of questions remain. It is hypothesised that fat accumulation within the liver is a primary defect in the aetiology and pathogenesis of obesity and type II diabetes. Fat accumulating in the liver is the result of changes in the gene expression of key enzymes and proteins involved with fat uptake, fat transport, fat oxidation, fat re-esterification or storage and export of fat from the liver and these changes are regulated by key lipid responsive transcription factors. To study these questions Psammomys obesus was utilised. This polygenic rodent model of obesity and type II diabetes develops obesity and diabetes in a similar pattern to susceptible human populations. In addition dietary and environmental changes to Psammomys obesus were employed to create different states of energy balance, which allowed the regulation of liver fat gene expression to be examined. These investigations include: 1) Measurement of fat accumulation and fatty acid binding proteins in lean, obese and diabetic Psammomys obesus. 2) Characterisation of hepatic lipid enzymes, transport protein and lipid responsive transcription factor gene expression in lean, obese and diabetic Paammomys obesus. 3) The effect of acute and chronic energy restriction on hepatic lipid metabolism in Psammomys obesus. 4) The effect of sucrose feeding on the development of obesity and type II diabetes in Psammomys obesus. 5) The effect of nicotine treatment in lean and obese Psammomys obesus, 6) The effect of high dose leptin administration on hepatic fat metabolism in Psammomys obesus. The results of these studies demonstrated that fat accumulation within the liver was not a primary defect in the aetiology and pathogenesis of obesity and type II diabetes. Fat accumulating in the liver was not the result of changes in the gene expression of key enzymes and proteins involved in hepatic fat metabolism. However changes in the mRNA level of the transcription factors PPAR∝ and SREBP-1C was associated with the development of diabetes and the gene expression of these two transcription factors was associated with changes in diabetic status.

Role of leptin receptors in the development of obesity

The focus of this dissertation was leptin and the leptin receptor, and the role of these genes (OB and OB-R) in the development of obesity and type 2 diabetes in humans and Psammomys obesus, a polygenic rodent model of obesity and type 2 diabetes. Studies in humans showed that circulating leptin concentrations were positively associated with adiposity, and independently associated with circulating insulin and triglyceride concentrations. Analysis of two leptin receptor sequence polymorphisms in a Caucasian Australian population and a population of Nauruan males, with very high prevalence rates of obesity, showed no associations between sequence variation within the OB-R gene and obesity- or diabetes-related phenotypic measures. In addition, these two OB-R polymorphisms were not associated with longitudinal changes in body mass or composition in either of the populations examined. A unique analysis of the effects of multiple gene defects in the Nauruan population, demonstrated that the presence of sequence alterations in both the OB and OB-R genes were associated with insulin resistance. Psammomys obesus is regarded as an excellent rodent model in which to study the development of obesity and type 2 diabetes in humans. Examination of circulating leptin concentrations in Psammomys revealed that, as in humans, leptin concentrations were associated with adiposity, and independently associated with circulating insulin concentrations. This animal model was utilised to examine expression of OB-R, and the regulation of expression of this gene after dietary manipulation. OB-R is known to have several isoforms, and in particular, OB-RA and OB-RB gene expression were examined. OB-RB is the main signalling isoform of the leptin receptors. It has a long intracellular domain and has previously been shown to play an important role in energy balance and body weight regulation in rodents and humans. OB-RA is a much shorter isoform of OB-R, and although it lacks the long intracellular domain necessary to activate the JAK/STAT pathway, OB-RA is also capable of signalling, although to a lesser degree than OB-RB. OB-RA is found to be expressed almost ubiquitously throughout the body, and this isoform may be involved in transport of leptin into the cell, although its role remains unclear. OB-RA and OB-RB were both found to be expressed in a large number of tissues in Psammomys obesus. Interestingly, obese Psammomys were found to have lower levels of expression of OB-RA and OB-RB in the hypothalamus, compared to lean animals. This finding raises the possibility that decreased leptin signalling in the brain of obese, hyperleptinemic Psammomys obesus may contribute to the leptin resistance previously described in this animal model. However, the primary defect is unclear, as alternatively, increased circulating leptin concentrations may lead to down-regulation of leptin receptors. The effect of fasting on leptin concentrations and gene expression of OB-RA and OB-RB was also examined. A 24-hour fast resulted in no change in body weight, but a reduction in circulating leptin concentrations, and an increase in hypothalamic OB-RB gene expression in lean Psammomys. In obese animals, fasting again did not alter body weight, but resulted in an increase in both circulating leptin concentrations and hypothalamic OB-RB gene expression. In the liver, fasting resulted in a large increase in OB-RA gene expression in both lean and obese animals. These results highlighted the fact that regulation of leptin receptor gene expression in polygenic models of obesity and type 2 diabetes is complex, and not solely under the control of circulating leptin concentrations. Sucrose-feeding is an established method of inducing obesity and type 2 diabetes in rodents, and this experimental paradigm was utilised to examine the effects of longer term perturbations of energy balance on the leptin signalling pathway in Psammomys obesus. Addition of a 5% sucrose solution to the diet of lean and obese Psammomys resulted in increased body weight in both groups of animals, however only obese Psammomys showed increased fat mass and the development of type 2 diabetes. The changes in body mass and composition with sucrose-feeding were accompanied by decreased circulating leptin concentrations in both groups of animals, as well as a range of changes in leptin receptor gene expression. Sucrose-feeding increased hypothalamic OB-RB gene expression in obese Psammomys only, while in the liver there was evidence of a reduction in OB-RA and OB-RB gene expression in both lean and obese animals. The direct effects of sucrose on the leptin signalling pathway are unclear, however it is possible to speculate that the effect of sucrose to decrease leptin concentrations may have been involved in the exacerbation of obesity and the development of type 2 diabetes in obese Psammomys, From these studies, it appears that sequence variation in the OB and OB-R genes is unlikely to be a major factor in the etiology of obesity in human populations. The ability to examine regulation of expression of these genes in Psammomys obesus, however, has demonstrated that the effects of nutritional modifications on leptin receptor gene expression need closer attention. The role of the OB and OB-R genes in metabolism and the development of type 2 diabetes also warrants further examination, with particular attention on the differential effects of dietary modifications on leptin receptor gene expression across a range of tissues.