"They all work...when you stick to them" : a qualitative investigation of dieting, weight loss, and physical exercise, in obese individuals

Background
To explore the extent to which people living with obesity have attempted to lose weight, their attitudes towards dieting, physical exercise and weight loss solutions, why their weight loss attempts have failed, and their opinions about what would be most beneficial to them in their struggle with their weight.

Method
Qualitative study, using open-ended interviews, of 76 people living with obesity in Victoria, Australia in 2006/7. Individuals with a BMI of 30 or over were recruited using articles in local newspapers, convenience sampling, and at a later stage purposive sampling techniques to diversify the sample. Data analysis was conducted by hand using a constant, comparative method to develop and test analytical categories. Data were interpreted both within team meetings and through providing research participants the chance to comment on the study findings.

Results
Whilst participants repeatedly turned to commercial diets in their weight loss attempts, few had used, or were motivated to participate in physical activity. Friends or family members had introduced most individuals to weight loss techniques. Those who took part in interventions with members of their social network were more likely to report feeling accepted and supported. Participants blamed themselves for being unable to maintain their weight loss or 'stick' to diets. Whilst diets did not result in sustained weight loss, two thirds of participants felt that dieting was an effective way to lose weight.

Conclusion
Individuals with obesity receive numerous instructions about what to do to address their weight, but very few are given appropriate long term guidance or support with which to follow through those instructions. Understanding the positive role of social networks may be particularly important in engaging individuals in physical activity. Public health approaches to obesity must engage and consult with those currently living with obesity, if patterns of social change are to occur.

Fine-scale effects of habitat loss and fragmentation despite large-scale gene flow for some regionally declining woodland bird species

Habitat loss and associated fragmentation effects are well-recognised threats to biodiversity. Loss of functional connectivity (mobility, gene flow and demographic continuity) could result in population decline in altered habitat, because smaller, isolated populations are more vulnerable to extinction. We tested whether substantial habitat reduction plus fragmentation is associated with reduced gene flow in three 'decliner' woodland-dependent bird species (eastern yellow robin, weebill and spotted pardalote) identified in earlier work to have declined disproportionately in heavily fragmented landscapes in the Box-Ironbark forest region in north-central Victoria, Australia. For these three decliners, and one 'tolerant' species (striated pardalote), we compared patterns of genetic diversity, relatedness, effective population size, sex-ratios and genic (allele frequency) differentiation among landscapes of different total tree cover, identified population subdivision at the regional scale, and explored fine-scale genotypic (individual-based genetic signature) structure. Unexpectedly high genetic connectivity across the study region was detected for 'decliner' and 'tolerant' species. Power analysis simulations suggest that moderate reductions in gene flow should have been detectable. However, there was evidence of local negative effects of reduced habitat extent and structural connectivity: slightly lower effective population sizes, lower genetic diversity, higher within-site relatedness and altered sex-ratios (for weebill and eastern yellow robin) in 10 x 10 km 'landscapes' with low vegetation cover. We conclude that reduced structural connectivity in the Box-Ironbark ecosystem may still allow sufficient gene flow to avoid the harmful effects of inbreeding in our study species. Although there may still be negative consequences of fragmentation for demographic connectivity, the high genetic connectivity of mobile bird species in this system suggests that reconnecting isolated habitat patches may be less important than increasing habitat extent and/or quality if these need to be traded off.

B-cell loss and B-cell apoptosis in human type 2 diabetes are related to islet amyloid deposition

Amyloid deposition and reduced β-cell mass are pathological hallmarks of the pancreatic islet in type 2 diabetes; however, whether the extent of amyloid deposition is associated with decreased β-cell mass is debated. We investigated the possible relationship and, for the first time, determined whether increased islet amyloid and/or decreased β-cell area quantified on histological sections is correlated with increased β-cell apoptosis. Formalin-fixed, paraffin-embedded human pancreas sections from subjects with (n = 29) and without (n = 39) diabetes were obtained at autopsy (64 ± 2 and 70 ± 4 islets/subject, respectively). Amyloid and β cells were visualized by thioflavin S and insulin immunolabeling. Apoptotic β cells were detected by colabeling for insulin and by TUNEL. Diabetes was associated with increased amyloid deposition, decreased -cell area, and increased β-cell βapoptosis, as expected. There was a strong inverse correlation between β-cell area and amyloid deposition (r=0.42, P < 0.001). β-Cell area was selectively reduced in individual amyloid-containing islets from diabetic subjects, compared with control subjects, but amyloid-free islets had β-cell area equivalent to islets from control subjects. Increased amyloid deposition was associated with β-cell apoptosis (r= 0.56, P < 0.01). Thus, islet amyloid is associated with decreased β-cell area and increased β-cell apoptosis, suggesting that islet myloid deposition contributes to the decreased β-cell mass that characterizes type 2 diabetes.

Catastrophic loss and the law : a comparison between 2009 Victorian Black Saturday fires and 2011 Queensland floods and Cyclone Yasi

This article explores insurability relating to loss occasioned by catastrophic events in Australia in the context of the current legal regulatory regime. The analysis includes two case studies, in which we juxtapose the Victorian Black Saturday fires in February 2--9 with the Queensland flooding and Cyclone Yasi (December 2010 - February 2011). We argue that the different responses to, and economic losses stemming from, these events illustrate the urgent need for a national regulatory and insurance regime for the prevention and alleviation of disasters and the management of their consequences.

Loss and grief in the workplace. What can we learn from the literature?

Purpose – The purpose of this paper is to determine how Australian workplaces, their managers and employees respond to those who are grieving at work, as a result of chronic or terminal illness, or caring for those with chronic or terminal illness. The review draws on Australian and relevant international literature and seeks to answer this question.
Design/methodology/approach – A literature review was undertaken in preparation for an Australian study examining workplace supports for people who are grieving – because they are carers, have experienced a death, or are balancing their own illness with their work. Using a range of search terms, the literature was searched for relevant work between 1980 and 2010. The search found examples of workplace supports throughout the world and some developing Australian literature.
Findings – Despite illness and death occurring at any stage of a person's life, there is little research that identifies workplace issues associated with grief and loss. And while workplace legislation allows for minimal supports, there was evidence that some workplaces have begun to offer flexibility for work life balance.
Practical implications – Effective workplace supports will involve individual and workplace responses, but also require legislative approaches in order to effect broad-based system change.
Originality/value – The paper compares Australian and international literature about workplace supports and provides an overview of the issues arising.

One year of sitagliptin treatment protects against islet amyloid-associated β-cell loss and does not induce pancreatitis or pancreatic neoplasia in mice

The dipeptidyl peptidase-4 (DPP-4) inhibitor sitagliptin is an attractive therapy for diabetes, as it increases insulin release and may preserve β-cell mass. However, sitagliptin also increases β-cell release of human islet amyloid polypeptide (hIAPP), the peptide component of islet amyloid, which is cosecreted with insulin. Thus, sitagliptin treatment may promote islet amyloid formation and its associated β-cell toxicity. Conversely, metformin treatment decreases islet amyloid formation by decreasing β-cell secretory demand and could therefore offset sitagliptin's potential proamyloidogenic effects. Sitagliptin treatment has also been reported to be detrimental to the exocrine pancreas. We investigated whether long-term sitagliptin treatment, alone or with metformin, increased islet amyloid deposition and β-cell toxicity and induced pancreatic ductal proliferation, pancreatitis, and/or pancreatic metaplasia/neoplasia. hIAPP transgenic and nontransgenic littermates were followed for 1 yr on no treatment, sitagliptin, metformin, or the combination. Islet amyloid deposition, β-cell mass, insulin release, and measures of exocrine pancreas pathology were determined. Relative to untreated mice, sitagliptin treatment did not increase amyloid deposition, despite increasing hIAPP release, and prevented amyloid-induced β-cell loss. Metformin treatment alone or with sitagliptin decreased islet amyloid deposition to a similar extent vs untreated mice. Ductal proliferation was not altered among treatment groups, and no evidence of pancreatitis, ductal metaplasia, or neoplasia were observed. Therefore, long-term sitagliptin treatment stimulates β-cell secretion without increasing amyloid formation and protects against amyloid-induced β-cell loss. This suggests a novel effect of sitagliptin to protect the β-cell in type 2 diabetes that appears to occur without adverse effects on the exocrine pancreas.

Effect of diet versus diet and exercise on weight loss and body composition in class II and III obesity: A systematic review

Class II and III obesity (BMI >35 kg·m2) have increased dramatically in recent years. Current clinical guidelines suggest diet and exercise as first line treatment for adults throughout the spectrum of overweight and obesity. However, to date there is no systematic review that examines the effects of diet and exercise on this high risk population. This systematic review will examine the combined effects of diet versus diet and exercise on body composition in severe obesity. Medline and Cinahl were searched for randomised controlled trials comparing diet and exercise to diet alone. Studies published until July 2013 were included if they used reliable methods for analysing body composition in adults with BMI ≥ 35 kg·m2. Five of 459 studies met the inclusion criteria. Two studies, both in older adults, reported that exercise reduced lean mass loss during weight loss. Two studies showed that exercise facilitated (greater) fat mass loss. The remaining study reported no differences in body composition when exercise is added to energy restriction. Exercise training during energy restriction for individuals with BMI ≥35 kg.m2 may influence body composition outcomes but the evidence is limited. Further studies should focus on the efficacy of different exercise protocols during energy restriction for this population in order to better inform decision making for the treatment of severe obesity in respect to favourable body composition outcomes.

State dependent asymmetric loss and the consensus forecast of real U.S. GDP growth

It has been well documented that the consensus forecast from surveys of professional forecasters shows a bias that varies over time. In this paper, we examine whether this bias may be due to forecasters having an asymmetric loss function. In contrast to previous research, we account for the time variation in the bias by making the loss function depend on the state of the economy. The asymmetry parameter in the loss function is specified to depend on set state variables which may cause forecaster to intentionally bias their forecasts. We consider both the Lin–Ex and asymmetric power loss functions. For the commonly used Lin–Ex and Lin–Lin loss functions, we show the model can be easily estimated by least squares. We apply our methodology to the consensus forecast of real U.S. GDP growth from the Survey of Professional Forecasters. We find that forecast uncertainty has an asymmetric effect on the asymmetry parameter in the loss function dependent upon whether the economy is in expansion or contraction. When the economy is in expansion, forecaster uncertainty is related to an overprediction in the median forecast of real GDP growth. In contrast, when the economy is in contraction, forecaster uncertainty is related to an underprediction in the median forecast of real GDP growth. Our results are robust to the particular loss function that is employed in the analysis.

Australia’s unknown soldier: a powerful symbol of loss and faith

The tomb of the unknown soldier in the Hall of Memory at the Australian War Memorial might seem to the casual visitor the timeless and natural symbolic centre of the memorial. But it was not always so: it was only in 1993 that the body of an unknown Australian soldier was repatriated and entombed here.

Loss and re-adaptation of lumbar intervertebral disc water signal intensity after prolonged bedrest

© 2015, International Society of Musculoskeletal and Neuronal Interactions. All right reserved. The adaptation and re-adaptation process of the intervertebral disc (IVD) to prolonged bedrest is important for understanding IVD physiology and IVD herniations in astronauts. Little information is available on changes in IVD composition. In this study, 24 male subjects underwent 60-day bedrest and In/Out Phase magnetic resonance imaging sequences were performed to evaluate IVD shape and water signal intensity. Scanning was performed before bedrest (baseline), twice during bedrest, and three, six and twenty-four months after bedrest. Area, signal intensity, average height, and anteroposterior diameter of the lumbar L3/4 and L4/5 IVDs were measured. At the end of bedrest, disc height and area were significantly increased with no change in water signal intensity. After bedrest, we observed reduced IVD signal intensity three months (p=0.004 versus baseline), six months (p=0.003 versus baseline), but not twenty-four months (p=0.25 versus baseline) post-bedrest. At these same time points post-bedrest, IVD height and area remained increased. The reduced lumbar IVD water signal intensity in the first months after bedrest implies a reduction of glycosaminoglycans and/or free water in the IVD. Subsequently, at two years after bedrest, IVD hydration status returned towards pre-bedrest levels, suggesting a gradual, but slow, re-adaptation process of the IVD after prolonged bedrest.

Short-term differences in animal assemblages in patches formed by loss and growth of habitat

Ecological theory predicts that habitat growth and loss will have different effects on community structure, even if they produce patches of the same size. Despite this, studies on the effects of patchiness are often performed without prior knowledge of the processes responsible for the patchiness. We manipulated artificial seagrass habitat in temperate Australia to test whether fish and crustacean assemblages differed between habitats that formed via habitat loss and habitat growth. Habitat loss treatments (originally 16 m2) and habitat growth treatments (originally 0 m2) were manipulated over 1 week until each reached a final patch size of 4 m2. At this size, each was compared through time (0-14 days after manipulation) with control patches (4 m2 throughout the experiment). Assemblages differed significantly among treatments at 0 and 1 day after manipulation, with differences between growth and loss treatments contributing to most of the dissimilarity. Immediately after the final manipulation, total abundance in habitat loss treatments was 46% and 62% higher than controls and habitat growth treatments, respectively, which suggests that animals crowded into patches after habitat loss. In contrast to terrestrial systems, crowding effects were brief (≤1 day), signifying high connectivity in marine systems. Growth treatments were no different to controls, despite the lower probability of animals encountering patches during the growth phase. Our study shows that habitat growth and loss can cause short-term differences in animal abundance and assemblage structure, even if they produce patches of the same size.