CURRENT OBESITY REPORTS

This review aims to examine (i) the aetiology of obesity; (ii) how and why a perception of personal responsibility for obesity so dominantly frames this condition and how this mindset leads to stigma; (iii) the consequences of obesity stigma for people living with obesity, and for the public support for interventions to prevent and manage this condition; and (iv) potential strategies to diminish our focus on personal responsibility for the development of obesity, to enable a reduction of obesity stigma, and to move towards effective interventions to prevent and manage obesity within the population. We summarise literature which shows that obesity stems from a complex interplay of genetic and environment factors most of which are outside an individual’s control. Despite this, evidence of obesity stigmatisation remains abundant throughout areas of media, entertainment, social media and the internet, advertising, news outlets, and the political and public health landscape. This has damaging consequences including psychological, physical, and socioeconomic harm. Obesity stigma does not prevent obesity. A combined, concerted, and sustained effort from multiple stakeholders and key decision-makers within society is required to dispel myths around personal responsibility for body weight, and to foster more empathy for people living in larger bodies. This also sets the scene for more effective policies and interventions, targeting the social and environmental drivers of health, to ultimately improve population health.

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This paper describes the epidemiologic evidence linking parent–child relationships, self-regulation, and weight status with a focus on early childhood. The emotional quality of parent–child interactions may influence children’s risk for obesity through multiple pathways. Prospective studies linking observer ratings of young children’s self-regulation, particularly inhibitory control, to future weight status are discussed. Although findings are preliminary, promoting positive relationships between parents/caregivers and young children holds promise as a component of efforts to prevent childhood obesity. Multi-disciplinary collaborations between researchers with training in developmental science and child health should be encouraged.

Clinical registries systematically collect prospective information about patients with a particular medical condition, who have had a medical device implanted or who have undergone a particular procedure. When these variables are collected with pre-defined quality indices included, the benched-marked risk-adjusted data may be a valuable resource for providing feedback on outcomes, including performance, to practitioners, patients, health services and device manufacturers. There are examples of feedback from clinical registries positively influencing patient care. The Australian National Joint Registry identified a poorly performing hip prosthesis which was ultimately withdrawn from the market. Feedback from the Victorian State Prostate Cancer Registry has contributed to improved patient care and fewer positive surgical margins noted over a 5-year reporting period. There are several national and regional registries collecting information on patients undergoing bariatric surgery, however, few currently focus on quality outcome measures. Whilst, current bariatric registries have contributed to improved understanding of some of the clinical situations relating to bariatric surgery, as well as developing composite risk scores and measuring quality cultures, they have not as yet demonstrably directly influenced patient care. This may reflect the fact that many of the registries do not hold data that are mature enough for proper analysis, but may also reflect problems with systematic data collection, bias from missing results and lack of appropriate funding. It will be important in the future that bariatric surgery registries actively seek to measure and validate their contribution to patient outcomes.

Sepsis has become a global health problem with rising incidence and high mortality, creating a substantial social and economic burden. Early diagnosis and treatment can improve outcome, but reliable sepsis biomarkers are lacking. This review summarizes current evidence of the pathophysiological mechanisms linking adipose tissue to sepsis and presents experimental and clinical data on adipokines and sepsis along with important insights into the obesity paradox in sepsis survival. Sepsis is characterized by significant alterations in circulating cytokines and adipokines, biologically active molecules produced by the adipose tissue, being implicated in metabolic and inflammatory processes. Although data are inconclusive regarding classic adipokines such as leptin and adiponectin, recent evidence have highlighted the striking elevation of resistin and visfatin in critical illness and sepsis as well as their association with sepsis severity and outcomes. Given that inflammatory and metabolic pathways are involved in sepsis, studying adipokines presents an attractive, innovative, and promising research field that may provide more powerful diagnostic and prognostic biomarkers as well as novel therapeutic targets, empowering the therapeutic armamentarium for sepsis management in order to improve survival.

Australia, like other developed countries, has a high prevalence of overweight and obesity, in both adults and children. This review examines progress in food policy in Australia, particularly at a national level, around key policy domains as well as in relation to public education. Australia lacks a national nutrition strategy or an obesity prevention strategy, incorporating best practice recommendations to improve diets. Examination of current progress shows patchy implementation of key food policy initiatives and significant gaps, particularly at the federal level. In the absence of a long-term strategic approach, the response of the federal government has been ad hoc around the adoption of key policies and funding for programs to improve what Australians eat. Consensus around a platform for obesity prevention for national action, including food policy, is building from public health, academic and consumer groups.

Obesity is a chronic illness and its prevalence is growing worldwide and numerous factors play a role in the regulation of food intake. The prefrontal cortex (PFC) is involved in high-order executive function, regulation of limbic reward regions, and the inhibition of impulsive behaviors. Understanding the role of the PFC in the control of appetite regulation may contribute to a greater understanding of the etiology of obesity and could improve weight loss outcomes. Neuroimaging studies have identified lower activation in the left dorsolateral PFC (DLPFC) in obese compared to lean individuals and others have focused on efforts to improve cognitive control in this area of the brain. The DLPFC is a critical brain area associated with appetitive control, food craving, and executive functioning, indicating a candidate target area for treatment. Further studies are needed to advance our understanding of the relationship between obesity, appetite, and the DLPFC and provide validation for the effectiveness of novel treatments in clinical populations.

In this review, we summarize current evidence on the association between antibiotics and the subsequent development of obesity through modulation of the gut microbiome. Particular emphasis is given on (i) animal and human studies and their limitations; (ii) the reservoir of antibiotics in animal feed, emerging antibiotic resistance, gut dysbiosis, and obesity; (iii) the role of infections, specifically viral infections, as a cause of obesity; and (iv) the potential therapeutic approaches other than antibiotics to modulate gut microbiome. Overall, the majority of animal studies and meta-analyses of human studies on the association between antibiotics and subsequent development of obesity are suggestive of a link between exposure to antibiotics, particularly early exposure in life, and the development of subsequent obesity as a result of alterations in the diversity of gut microbiota. The evidence is strong in animal models whereas evidence in humans is inconclusive requiring well-designed, long-term longitudinal studies to examine this association. Based on recent meta-analyses and epidemiologic studies in healthy children, factors, such as the administration of antibiotics during the first 6 months of life, repeated exposure to antibiotics for ≥ 3 courses, treatment with broad-spectrum antibiotics, and male gender have been associated with increased odds of overweight/obesity. Early antibiotic exposure in animal models has shown that reductions in the population size of specific microbiota, such as Lactobacillus, Allobaculum, Rikenellaceae, and Candidatus Arthromitus, are related to subsequent adiposity. These data suggest that the loss of diversity of the gut microbiome, especially early in life, may have potential long-term detrimental effects on the adult host gut microbiome and metabolic health. Genetic, environmental, and age-related factors influence the gut microbiome throughout the lifetime. More large-scale, longer-term, longitudinal studies are needed to determine whether changes that occur in the microbiome after exposure to antibiotics, particularly early exposure, are causal of subsequent weight gain or consequent of weight gain in humans. Further well-designed, large-scale RCTs in humans are required to evaluate the effects of administration of antibiotics, particularly early administration, and the subsequent development of overweight/obesity. Therapeutic interventions, such as bacteriophage treatment or the use of probiotics, especially genetically engineered ones, need to be evaluated in terms of prevention and management of obesity.