What Is the Economic Case for Treating Obesity?

From both societal and payer perspectives, the economic effect of obesity in the United States is substantial, estimated at approximately 6% of our national health expenditure and cost of care in a major health maintenance organization. The number of physician visits related to obesity has increased 88% in a 6-year period. The morbidity cost (lost productivity) and functional capability of the patient with obesity is increasing rapidly (50% increase in lost productivity, 36% increase in restricted activity, and 28% increase in number of bed-days). Cost savings of treating obesity are comparable to those of treating other chronic diseases such as coronary heart disease and diabetes. Most studies indicate that most of the direct health care costs of obesity are from type 2 diabetes, coronary heart disease and hypertension. To date, however, there have been no published reports of the cost effectiveness of the medical management of obesity treatment. In conclusion, the cost of obesity is comparable to that of other chronic diseases, yet it receives disproportionately less attention. Cost effectiveness studies need to be initiated promptly.     

AMPK ��1 Deletion Reduces Appetite, Preventing Obesity and Hepatic Insulin Resistance

The AMP-activated protein kinase (AMPK) is an αβγ heterotrimer that regulates appetite and fuel metabolism. We have generated AMPK β1^−/− mice on a C57Bl/6 background that are viable, fertile, survived greater than 2 years, and display no visible brain developmental defects. These mice have a 90% reduction in hepatic AMPK activity due to loss of the catalytic α subunits, with modest reductions of activity detected in the hypothalamus and white adipose tissue and no change in skeletal muscle or heart. On a low fat or an obesity-inducing high fat diet, β1^−/− mice had reduced food intake, reduced adiposity, and reduced total body mass. Metabolic rate, physical activity, adipose tissue lipolysis, and lipogenesis were similar to wild type littermates. The reduced appetite and body mass of β1^−/− mice were associated with protection from high fat diet-induced hyperinsulinemia, hepatic steatosis, and insulin resistance. We demonstrate that the loss of β1 reduces food intake and protects against the deleterious effects of an obesity-inducing diet.     

What Is the Future for Zoos and Aquariums?

ABSTRACT

Animal welfare concerns have plagued the professional zoo and aquarium field for decades. Societal differences remain concerning the well-being of animals, but it appears a shift is emerging. Scientific studies of animal welfare have dramatically increased, establishing that many previous concerns were not misguided public empathy or anthropomorphism. As a result, both zoo and aquarium animal welfare policy and science are now at the center of attention within the world’s professional zoos and aquariums. It is now possible to view a future that embraces the well-being of individual captive exotic animals, as well as that of their species, and one in which professional zoos and aquariums are dedicated equally to advancing both. Though the ethics of keeping exotic animals and animals from the wild in captivity are still a contentious subject both outside and even within the profession, this study argues. We argue that this path forward will substantially improve most zoo and aquarium animals' welfare and could significantly reduce societal concerns. If animal welfare science and policy are strongly rooted in compassion and embedded in robust accreditation systems, the basic zoo/aquarium paradigm will move toward a more thoughtful approach to the interface between visitors and animals. It starts with a fundamental commitment to the welfare of individual animals.     

Is Predisposition to NAFLD and Obesity Communicable?

A forthcoming article in Nature reveals that inflammasome deficiency disturbs gut microbiota and predisposes to diet-induced obesity and liver disease. The aberrant microbiota and its consequences could be transferred by cohousing mutant and wild-type mice, suggesting that some aspects of metabolic syndrome can be communicable (Henao-Mejia et?al., 2012).     

Sleep Related Breathing Disorders and Inflammation — The Missing Link? A Cohort Study Evaluating the Interaction of Inflammation and Sleep Related Breathing Disorders and Effects of Treatment

Introduction

Sleep related breathing disorders (SRBD) are associated with both obesity and systemic inflammation. While the relationship between obesity and SRBD is established, the causality between inflammation and SRBD remains unclear. In this study we investigated the relation between SRBD and C-reactive protein (CRP) as a parameter of inflammation and the influence of SRBD treatment on CRP with additional regard to changes in metabolic and cardiovascular parameters.

Methods

Polysomnography (PSG) and laboratory data of patients diagnosed with SRBD over a period of 5 years were prospectively collected in a database and retrospectively analysed regarding the association of SRBD (according to apnoea-hypopnoea- index (AHI), duration of events and extent of desaturation) to CRP, blood pressure, cholesterol, fasting plasma glucose, HbA1c, quality of life measured via a visual analogue scale (VAS 0–100%), and the effects of SRBD therapy on these parameters.

Results

716 patients were included in the study, 171 with mild SRBD (AHI ≥5 to <15/h), 209 with moderate SRBD (AHI 15 to <30/h), 336 with severe SRBD (AHI ≥30/h). Results according to severity of SRBD. Severe SRBD was significantly associated with elevated levels of CRP (3.7 [1.8–7.0] mg/l, vs. moderate (p = 0.001), and mild SRBD (p<0.001), and higher prevalence of hypertension as compared to moderate and mild SRBD (p<0.001, respectively). Results in highly successful treatment. If SRBD treatment was highly successful (AHI <5/h), CRP and quality of life improved significantly (p = 0.001 and p = 0.002), as did blood pressure (p<0.001 for systolic and diastolic values), although BMI increased (p<0.001). Results in partially successful treatment. If success was defined as reduction of AHI of ≥50%, CRP also decreased (p<0.001), as did blood pressure (p<0.001). Again, BMI increased (p<0.001).

Conclusion

This is the first study to show an association of SRBD and CRP independently of BMI in a large cohort. The SRBD therapy-induced CRP decrease was not associated with BMI changes or metabolic changes but rather with the magnitude of AHI improvement.     

What Is the Tree of Life?

A universal Tree of Life (TOL) has long been a goal of molecular phylogeneticists, but reticulation at the level of genes and possibly at the levels of cells and species renders any simple interpretation of such a TOL, especially as applied to prokaryotes, problematic.One of the several ways in which microbiology puts the neo-Darwinian synthesis in jeopardy is by the threatening to “uproot the Tree of Life (TOL)” [1]. Lateral gene transfer (LGT) is much more frequent than most biologists would have imagined up until about 20 years ago, so phylogenetic trees based on sequences of different prokaryotic genes are often different. How to tease out from such conflicting data something that might correspond to a single, universal Tree of Life becomes problematic. Moreover, since many important evolutionary transitions involve lineage fusions at one level or another, the aptness of a tree (a pattern of successive bifurcations) as a summary of life’s history is uncertain [2–4].     

Optimal Sleep Duration in the Subarctic with Respect to Obesity Risk Is 8–9 Hours

Introduction

Sleep duration, chronotype and social jetlag have been associated with body mass index (BMI) and abdominal obesity. The optimal sleep duration regarding BMI has previously been found to be 7–8 hours, but these studies have not been carried out in the subarctic or have lacked some central variables. The aims of our study were to examine the associations between sleep variables and body composition for people living in the subarctic, taking a range of variables into consideration, including lifestyle variables, health variables and biological factors.

Methods

The cross sectional population Tromsø Study was conducted in northern Norway, above the Arctic Circle. 6413 persons aged 30–65 years completed questionnaires including self-reported sleep times, lifestyle and health. They also measured height, weight, waist and hip circumference, and biological factors (non-fasting serum level of cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides and glucose). The study period was from 1 October 2007 to 19 December 2008.

Results

The optimal sleep length regarding BMI and waist circumference was found to be 8–9 hours. Short sleepers (<6 h) had about 80% increased risk of being in the BMI≥25 kg/m2 group and male short sleepers had doubled risk of having waist circumference ≥102 cm compared to 8–9 hours sleepers. We found no impact of chronotype or social jetlag on BMI or abdominal obesity after controlling for health, lifestyle, and biological parameters.

Conclusions

In our subarctic population, the optimal sleep duration time regarding risk of overweight and abdominal obesity was 8–9 hours, which is one hour longer compared to findings from other studies. Short sleepers had 80% increased risk of being overweight, and men had a doubled risk of having abdominal obesity. We found no associations between chronotype or social jetlag and BMI or abdominal obesity, when we took a range of life-style, health and biological variables into consideration.     

What Is the Accurate Prevalence of Obesity in Sweden in the 21st Century? Methodological Experiences From the Skaraborg Project

Objective: To examine the impact of non‐response to self‐reported body weight and height in health questionnaires for the estimation of obesity prevalence. Methods and Procedures: A cross‐sectional population‐based health survey in the community of Vara with 16,009 residents (in year 2002) in South‐western Sweden. Participants randomly selected in strata by sex and age among residents being 30–74 years old were consecutively invited to the local health care center for a health examination, including two visits. Self‐reported information on body weight and height were obtained by health questionnaires at the first visit, and measured information on both variables at the second visit. For this study 1,809 subjects (904 men and 905 women) completed both visits (participation rate 81%), and a nurse measured body weight and height of all at visit two. Participants not self‐reporting body weight and/or height at the first visit were defined as non‐responders. Results: Both male and female non‐responders were significantly older than responders. Female non‐responders had significantly higher BMI (29.8 ± 5.8 kg/m²) than female responders (26.6 ± 5.3 kg/m²), (P < 0.001). No similar findings were seen in men. Non‐responders were more likely to be obese than responders both in men (odds ratio (OR) 2.06, 95% confidence interval (CI) 1.03–4.11) and in women (OR 2.24, 95% CI 1.25–4.02). Discussion: Non‐responders to self‐reported body weight and height in health questionnaires contribute to the underestimation of obesity. Measured body weight and height are to prefer when describing the accurate prevalence of obesity in populations.     

Is Obstructive Sleep Apnea Associated with Cardiovascular and All-Cause Mortality?

Background

Studies have reported inconsistent findings regarding the association between obstructive sleep apnea (OSA) and future risks of cardiovascular and all-cause mortality. We conducted a meta-analysis to investigate whether OSA is an independent predictor for future cardiovascular and all-cause mortality using prospective observational studies.

Methods

Electronic literature databases (Medline and Embase) were searched for prospective observational studies published prior to December 2012. Only observational studies that assessed baseline OSA and future risk of cardiovascular and all-cause mortality were selected. Pooled hazard risk (HR) and corresponding 95% confidence intervals (CI) were calculated for categorical risk estimates. Subgroup analyses were based on the severity of OSA.

Results

Six studies with 11932 patients were identified and analyzed, with 239 reporting cardiovascular mortality, and 1397 all-cause mortality. Pooled HR of all-cause mortality was 1.19 (95% CI, 1.00 to 1.41) for moderate OSA and 1.90 (95% CI, 1.29 to 2.81) for severe OSA. Pooled HR of cardiovascular mortality was 1.40 (95% CI, 0.77 to 2.53) for moderate OSA and 2.65 (95% CI, 1.82 to 3.85) for severe OSA. There were no differences in cardiovascular mortality in continuous positive airway pressure (CPAP) treatment compared with healthy subjects (HR 0.82; 95% CI, 0.50 to 1.33).

Conclusions

Severe OSA is a strong independent predictor for future cardiovascular and all-cause mortality. CPAP treatment was associated with decrease cardiovascular mortality.