The social patterning of mortality in a cohort of elderly Swedes

Social class differences in mortality among the elderly have received only limited interest. In this paper we analyze the impact of social class on mortality from mid-life onwards. In 1968 1,860 persons born between 1892 and 1915 were interviewed and followed in the national cause of death registry for the period 1968-1991. In addition. 537 of the 563 survivors were fe-interviewed in 1992. We employ proportional hazard regressions to analyze the impact of social class on death risks over time. There are fairly small class differences in the probability of reaching old age. However, it appears that mortality differentials were steeper before retirement age than after. Still, the size of class differences in mortality seem smaller than expected on the basis of other studies. At the same time steep class gradients in illness and functional abilities exist among survivors. Some possible explanations for these somewhat contradictory findings are discussed

Reducing the risks to health: the role of social protection: report of the Social Protection Task Group for the Strategic Review of Health Inequalities in England post 2010.

We demonstrate that the introduction of social protection systems as well as their generosity and coverage have significant impacts on health. Who receives the benefits within the household affects the health outcomes for the family. The eligibility for and administration of benefits matters. We examine the growth of means testing in the UK and its recent modifications. We find serious difficulties facing those with long term medical conditions who are on the margins of the labour force. Collaboration between the health and social protection systems is poor. We give particular attention to gender and health and the implications this has for the social protection system. We also consider the fate of groups like asylum seekers who are excluded from its normal working.

The contribution of alcohol consumption and smoking to educational inequalities in life expectancy among Swedish men and women during 1991-2008

To assess the level and changes in contribution of smoking and alcohol-related mortality to educational differences in life expectancy in Sweden. We used register data on the Swedish population at ages 30-74 during 1991-2008. Cause of death was used to identify alcohol-related deaths, while smoking-related mortality was estimated using lung cancer mortality to indirectly assess the impact of smoking on all-cause mortality. Alcohol consumption and smoking contributed to educational differences in life expectancy. Alcohol-related mortality was higher among men and contributed substantially to inequalities among men and made a small (but increasing) contribution to inequalities among women. Smoking-related mortality decreased among men but increased among women, primarily among the low educated. At the end of the follow-up, smoking-related mortality were at similar levels among men and women. The widening gap in life expectancy among women could largely be attributed to smoking. Smoking and alcohol consumption contribute to educational differences in life expectancy among men and women. The majority of the widening in the educational gap in mortality among women can be attributed to alcohol and smoking-related mortality.Peer reviewe

Insulitis in human diabetes: a histological evaluation of donor pancreases

Aims/hypothesis According to the consensus criteria developed for type 1 diabetes, an individual can be diagnosed with insulitis when >= 15 CD45(+) cells are found within the parenchyma or in the islet-exocrine interface in >= 3 islets. The aim of this study was to determine the frequency of individuals with type 2 diabetes fulfilling these criteria with reference to non-diabetic and type 1 diabetic individuals. Methods Insulitis was determined by examining CD45(+) cells in the pancreases of 50, 13 and 44 organ donors with type 2 diabetes, type 1 diabetes and no diabetes, respectively. CD3(+) cells (T cells) infiltrating the islets were evaluated in insulitic donors. In insulitic donors with type 2 diabetes, the pancreases were characterised according to the presence of CD68 (macrophages), myeloperoxidase (MPO; neutrophils), CD3, CD20 (B cells) and HLA class I hyperstained islets. In all type 2 diabetic donors, potential correlations of insulitis with dynamic glucose-stimulated insulin secretion in vitro or age, BMI, HbA(1c) or autoantibody positivity were examined. Results Overall, 28% of the type 2 diabetic donors fulfilled the consensus criteria for insulitis developed for type 1 diabetes. Of the type 1 diabetic donors, 31% fulfilled the criteria. None of the non-diabetic donors met the criteria. Only type 1 diabetic donors had >= 15 CD3(+) cells in >= 3 islets. Type 2 diabetic donors with insulitis also had a substantial number of CD45(+) cells in the exocrine parenchyma. Macrophages constituted the largest fraction of CD45(+) cells, followed by neutrophils and T cells. Of type 2 diabetic pancreases with insulitis, 36% contained islets that hyperstained for HLA class I. Isolated islets from type 2 diabetic donors secreted less insulin than controls, although with preserved dynamics. Insulitis in the type 2 diabetic donors did not correlate with glucose-stimulated insulin secretion, the presence of autoantibodies, BMI or HbA(1c). Conclusions/interpretation The current definition of insulitis cannot be used to distinguish pancreases retrieved from individuals with type 1 diabetes from those with type 2 diabetes. On the basis of our findings, we propose a revised definition of insulitis, with a positive diagnosis when >= 15 CD3(+) cells, not CD45(+) cells, are found in >= 3 islets

Changes in life expectancy and lifespan variability by income quartiles in four Nordic countries : a study based on nationwide register data

Objectives Levels, trends or changes in socioeconomic mortality differentials are typically described in terms of means, for example, life expectancies, but studies have suggested that there also are systematic social disparities in the dispersion around those means, in other words there are inequalities in lifespan variation. This study investigates changes in income inequalities in mean and distributional measures of mortality in Denmark, Finland, Norway, and Sweden over two decades. Design Nationwide register-based study. Setting The Danish, Finnish, Norwegian and Swedish populations aged 30 years or over in 1997 and 2017. Main outcome measures Income-specific changes in life expectancy, lifespan variation and the contribution of 'early' and 'late' deaths to increasing life expectancy. Results Increases in life expectancy has taken place in all four countries, but there are systematic differences across income groups. In general, the largest gains in life expectancy were observed in Denmark, and the smallest increase among low-income women in Sweden and Norway. Overall, life expectancy increased and lifespan variation decreased with increasing income level. These differences grew larger over time. In all countries, a marked postponement of early deaths led to a compression of mortality in the top three income quartiles for both genders. This did not occur for the lowest income quartile. Conclusion Increasing life expectancy is typically accompanied by postponement of early deaths and reduction of lifespan inequality in the higher-income groups. However, Nordic welfare societies are challenged by the fact that postponing premature deaths among people in the lowest-income groups is not taking place.Peer reviewe

The contribution of educational inequalities to lifespan variation

Peer reviewe

Altered expression of autoimmune regulator in infant down syndrome thymus, a possible contributor to an autoimmune phenotype.

To access publisher's full text version of this article click on the hyperlink at the bottom of the pageDown syndrome (DS), caused by trisomy of chromosome 21, is associated with immunological dysfunctions such as increased frequency of infections and autoimmune diseases. Patients with DS share clinical features, such as autoimmune manifestations and specific autoantibodies, with patients affected by autoimmune polyendocrine syndrome type 1. Autoimmune polyendocrine syndrome type 1 is caused by mutations in the autoimmune regulator (AIRE) gene, located on chromosome 21, which regulates the expression of tissue-restricted Ags (TRAs) in thymic epithelial cells. We investigated the expression of AIRE and TRAs in DS and control thymic tissue using quantitative PCR. AIRE mRNA levels were elevated in thymic tissue from DS patients, and trends toward increased expression of the AIRE-controlled genes INSULIN and CHRNA1 were found. Immunohistochemical stainings showed altered cell composition and architecture of the thymic medulla in DS individuals with increased frequencies of AIRE-positive medullary epithelial cells and CD11c-positive dendritic cells as well as enlarged Hassall's corpuscles. In addition, we evaluated the proteomic profile of thymic exosomes in DS individuals and controls. DS exosomes carried a broader protein pool and also a larger pool of unique TRAs compared with control exosomes. In conclusion, the increased AIRE gene dose in DS could contribute to an autoimmune phenotype through multiple AIRE-mediated effects on homeostasis and function of thymic epithelial cells that affect thymic selection processes.Swedish Research Council 80409601 Marianne and Marcus Wallenberg Foundation Region Vastra Gotaland ALFGBG-771712 Arbetsmarknadens Forsakringsaktiebolag 100258 IngaBritt and Arne Lundbergs Research Foundation AnnMari and Per Ahlqvists Foundation Gothenburg Medical Society Wilhelm and Martina Lundgrens Research Foundatio

Smoking and inequalities in mortality in 11 European countries : a birth cohort analysis

Altres ajuts: Netspar (Network for Studies on Pensions, Aging and Retirement).Purpose: To study the trends of smoking-attributable mortality among the low and high educated in consecutive birth cohorts in 11 European countries. Methods: Register-based mortality data were collected among adults aged 30 to 79 years in 11 European countries between 1971 and 2012. Smoking-attributable deaths were estimated indirectly from lung cancer mortality rates using the Preston-Glei-Wilmoth method. Rate ratios and rate differences among the low and high-educated were estimated and used to estimate the contribution of inequality in smoking-attributable mortality to inequality in total mortality. Results: In most countries, smoking-attributable mortality decreased in consecutive birth cohorts born between 1906 and 1961 among low- and high-educated men and high-educated women, but not among low-educated women among whom it increased. Relative educational inequalities in smoking-attributable mortality increased among both men and women with no signs of turning points. Absolute inequalities were stable among men but slightly increased among women. The contribution of inequality in smoking-attributable mortality to inequality in total mortality decreased in consecutive generations among men but increased among women. Conclusions: Smoking might become less important as a driver of inequalities in total mortality among men in the future. However, among women, smoking threatens to further widen inequalities in total mortality

Educational expansion and inequalities in mortality-A fixed-effects analysis using longitudinal data from 18 European populations

Objective The aim of this paper is to empirically evaluate whether widening educational inequalities in mortality are related to the substantive shifts that have occurred in the educational distribution. Materials and methods Data on education and mortality from 18 European populations across several decades were collected and harmonized as part of the Demetriq project. Using a fixed-effects approach to account for time trends and national variation in mortality, we formally test whether the magnitude of relative inequalities in mortality by education is associated with the gender and age-group specific proportion of high and low educated respectively. Results The results suggest that in populations with larger proportions of high educated and smaller proportions of low educated, the excess mortality among intermediate and low educated is larger, all other things being equal. Conclusion We conclude that the widening educational inequalities in mortality being observed in recent decades may in part be attributed to educational expansion.Peer reviewe