Obesity Level and Attrition: Support for Patient-Treatment Matching in Obesity Treatment

Obesity treatment studies report attrition rates front 20% to 45%. To reduce attrition, researchers have proposed matching patients to treatment based upon level of obesity. The current study attempted to validate the commonly held assumption that a mismatch between obesity level and treatment will promote attrition. The level of obesity and attrition rates of 39 adults who enrolled in a 12-session behavior therapy program were examined. As obesity level increased, so did attrition. Sixty-nine percent of subjects with mild obesity, 43% of subjects with moderate obesity and 0% of subjects with severe obesity completed treatment.     

Obesity epidemic: origins and consequences

Obesity is a chronic disease with serious health consequences. Initial weight gain is related to behavioural and environmental factors acting on a biological (mainly genetic) predisposition. The evolution of the disease is characterized by the development of an inflammatory organ disease that involves the adipocytes and other adipose tissue components. These alterations lead to various clinical complications and to a progressive resistance to diet effects. The treatment of obesity must be adapted to the stage of development of the disease and to the prevalent complications.     

Brain Peptides and Obesity: Pharmacologic Treatment

Obesity results from an imbalance between nutrient ingestion and metabolism, with more calories being ingested than utilized. The brain plays an important role in coordinating these complex behavioral and physiological functions, operating through multiple neurochemical systems with distinct properties. This review focuses on two hypothalamic peptide systems, neuropeptide Y (NPY) and galanin (GAL), that illustrate how the brain operates through different mechanisms to control the body's nutrient stores, in different states or conditions. These peptides have different behavioral and physiological effects and are, themselves, differentially responsive to feedback signals from circulating steroids, peptides, and nutrients. They can be distinguished by their relation to natural feeding patterns and endogenous hormones and by their specificity of action in relation to natural biological rhythms. The neuroanatomical substrates involved in these actions of NPY and GAL are also distinct. The neurocircuit mediating NPY's actions originates in the arcuate nucleus and terminates in the medial portion of the paraventricular nucleus; the GAL-containing neurons, in contrast, are concentrated in the lateral portion of the paraventricular nucleus, in addition to the medial preoptic area, which contribute to local GAL innervation as well as projections to the median eminence. Regarding their distinct functions, the evidence suggests that the NPY system is more closely related to patterns of carbohydrate ingestion and carbohydrate utilization, channeling nutrients towards the synthesis of fat. It is most strongly activated at the start of the active feeding cycle or after weaning, in close association with the adrenal steroid, corticosterone. The GAL system, in contrast, is more closely associated with patterns of fat consumption and signals related to fat oxidation. This peptide system is most active during the middle of the feeding cycle or immediately after puberty, in close association with the gonadal steroids. The gene expression and synthesis of these peptides in their respective neuronal cell groups is inhibited by circulating insulin and altered by dietary nutrients. Disturbances in sensitivity to insulin and steroid feedback regulation in the brain are believed to be involved in producing abnormal patterns of peptide function that result in overeating and body weight gain.     

Obesity: overview of pathogenesis and treatment

This paper presents an overview of selected current concepts of the pathogenesis and treatment of obesity. It has been estimated using the 1981 Canada Fitness Survey data that 14.1% of Canadian adult men and 20.6% of women are greater than 20% above reference table weight. Recent advances in adipocyte metabolism and control have shown that hyperplastic obesity can occur at any age and that there are differences in the replicative rate of adipocyte precursor cells from the massively obese. Furthermore, a number of the complications of obesity, including hypertension, have been related to regional body fat distribution, independent of total body fat. It is suggested that some of the controversy on the relationship between body weight/weight loss and hypertension may be due to failure to account for this. There is now suggestive evidence that abnormalities in diet-induced thermogenesis and (or) brown adipose tissue may result in human obesity. The roles of the major treatment modalities (diet, behaviour therapy, and exercise) are reviewed as are the potential hazards of the weight loss process.     

Obesity and cancer: pathophysiological and biological mechanisms

Excess body weight (overweight and obesity) is characterized by chronic hyperinsulinaemia and insulin resistance, and is implicated both in cancer risk and cancer mortality. The list of cancers at increased risk of development in an "obesogenic" environment include common adult cancers such as endometrium, post-menopausal breast, colon and kidney, but also less common malignancies such as leukaemia, multiple myeloma, and non-Hodgkin's lymphoma. The pathophysiological and biological mechanisms underpinning these associations are only starting to be understood. Insulin resistance is at the heart of many, but there are several other candidate systems including insulin-like growth factors, sex steroids, adipokines, obesity-related inflammatory markers, the nuclear factor kappa beta (NF-kappa B) system and oxidative stresses. With such as diversity of obesity-related cancers, it is unlikely that there is a "one system fits all" mechanism. While public health strategies to curb the spread of the obesity epidemic appear ineffective, there is a need to better understand the processes linking obesity and cancer as a pre-requisite to the development of new approaches to the prevention and treatment of obesity-related cancers.     

Obesity and inflammation

The prevalence of obesity has recently increased dramatically and has contributed to the increasing prevalence of various pathological conditions, including type 2 diabetes mellitus, nonalcoholic fatty liver disease, asthma, various types of cancer, cardiovascular and neurodegenerative diseases, and others. Accumulating evidence points to localized inflammation in adipose tissue, which, in turn, promotes systemic low-grade inflammation as a primary force contributing to the development of these pathologies. A better understanding of the underlying mechanisms behind obesity-induced adipose tissue inflammation is required to develop effective therapeutic or prophylactic strategies. This review is aimed to present the current knowledge of adipose tissue inflammation associated with obesity.     

Exercise and Obesity

This paper reviews succinctly the evidence for a role of regular exercise in the prevention and the treatment of obesity and of its metabolic complications. Seventeen propositions relevant to an understanding of the topic are considered. The evidence suggests that regular exercise can be an important factor in the development of sustained negative energy balance conditions provided the volume of activity is high. This implies a program of low to moderate intensity exercise performed on an almost daily basis for at least one hour per session. To induce significant weight and fat losses and to treat overweight and obese patients, compliance to the program for several years becomes a necessity. Exercise increases lipid substrate oxidation and may favor carbohydrate intake for the same amount of energy intake. The acute effects of exercise on resting metabolic rate are well documented, but the long-term influences of exercise training seem to be small and are rapidly suppressed with the cessation of training. The obese benefits also from a regular exercise regimen in terms of improved insulin sensitivity, lipid and lipoprotein profile, and blood pressure, as well as reduced risk of death. Regular exercise, such as walking, is a healthy course of action for the overweight or the obese patients.     

Redrawing the US Obesity Landscape: Bias-Corrected Estimates of State-Specific Adult Obesity Prevalence

Background

State-level estimates from the Centers for Disease Control and Prevention (CDC) underestimate the obesity epidemic because they use self-reported height and weight. We describe a novel bias-correction method and produce corrected state-level estimates of obesity and severe obesity.

Methods

Using non-parametric statistical matching, we adjusted self-reported data from the Behavioral Risk Factor Surveillance System (BRFSS) 2013 (n = 386,795) using measured data from the National Health and Nutrition Examination Survey (NHANES) (n = 16,924). We validated our national estimates against NHANES and estimated bias-corrected state-specific prevalence of obesity (BMI≥30) and severe obesity (BMI≥35). We compared these results with previous adjustment methods.

Results

Compared to NHANES, self-reported BRFSS data underestimated national prevalence of obesity by 16% (28.67% vs 34.01%), and severe obesity by 23% (11.03% vs 14.26%). Our method was not significantly different from NHANES for obesity or severe obesity, while previous methods underestimated both. Only four states had a corrected obesity prevalence below 30%, with four exceeding 40%–in contrast, most states were below 30% in CDC maps.

Conclusions

Twelve million adults with obesity (including 6.7 million with severe obesity) were misclassified by CDC state-level estimates. Previous bias-correction methods also resulted in underestimates. Accurate state-level estimates are necessary to plan for resources to address the obesity epidemic.