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Journal ArticleDOI

Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study

17 May 1997-The Lancet (Elsevier)-Vol. 349, Iss: 9063, pp 1436-1442
TL;DR: The three leading contributors to the burden of disease are communicable and perinatal disorders affecting children, and the substantial burdens of neuropsychiatric disorders and injuries are under-recognised.
About: This article is published in The Lancet.The article was published on 1997-05-17. It has received 4425 citations till now. The article focuses on the topics: Poison control & Injury prevention.
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Journal ArticleDOI
19 Dec 2002-Nature
TL;DR: The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.
Abstract: Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for myocardial infarctions and most strokes. The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.

7,858 citations


Cites background from "Global mortality, disability, and t..."

  • ...jpg" NDATA ITEM> ]> Cardiovascular disease, currently the leading cause of death and illness in developed countries, will soon become the pre-eminent health problem worldwid...

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Journal ArticleDOI
TL;DR: The evidence is recounted that atherosclerosis, the main cause of CAD, is an inflammatory disease in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree.
Abstract: ecent research has shown that inflammation plays a key role in coronary artery disease (CAD) and other manifestations of atherosclerosis. Immune cells dominate early atherosclerotic lesions, their effector molecules accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes. This review highlights the role of inflammation in the pathogenesis of atherosclerotic CAD. It will recount the evidence that atherosclerosis, the main cause of CAD, is an inflammatory disease in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree. A decade ago, the treatment of hypercholesterolemia and hypertension was expected to eliminate CAD by the end of the 20th century. Lately, however, that optimistic prediction has needed revision. Cardiovascular diseases are expected to be the main cause of death globally within the next 15 years owing to a rapidly increasing prevalence in developing countries and eastern Europe and the rising incidence of obesity and diabetes in the Western world. 1 Cardiovascular diseases cause 38 percent of all deaths in North America and are the most common cause of death in European men under 65 years of age and the second most common cause in women. These facts force us to revisit cardiovascular disease and consider new strategies for prediction, prevention, and treatment.

7,551 citations

Journal Article
TL;DR: In this article, a comprehensive update of disease burden worldwide incorporating a systematic reassessment of disease and injury-specific epidemiology has been done since the 1990 study, and the authors aimed to calculate disease burden globally and for 21 regions for 1990, 2005, and 2010 with methods to enable meaningful comparisons over time.

7,020 citations

Journal ArticleDOI
Christopher J L Murray1, Theo Vos2, Rafael Lozano1, Mohsen Naghavi1  +366 moreInstitutions (141)
TL;DR: The results for 1990 and 2010 supersede all previously published Global Burden of Disease results and highlight the importance of understanding local burden of disease and setting goals and targets for the post-2015 agenda taking such patterns into account.

6,861 citations

Journal ArticleDOI
TL;DR: The discovery of the immune basis of allograft arteriosclerosis demonstrated that inflammation per se can drive arterial hyperplasia, even in the absence of traditional risk factors.
Abstract: Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis. Unraveling the roles of cytokines as inflammatory messengers provided a mechanism whereby risk factors for atherosclerosis can alter arterial biology, and produce a systemic milieu that favors atherothrombotic events. The discovery of the immune basis of allograft arteriosclerosis demonstrated that inflammation per se can drive arterial hyperplasia, even in the absence of traditional risk factors. Inflammation regulates aspects of plaque biology that trigger the thrombotic complications of atherosclerosis. Translation of these discoveries to humans has enabled both novel mechanistic insights and practical clinical advances.

4,307 citations

References
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Book
01 Jan 1996
TL;DR: This is the first in a planned series of 10 volumes that will attempt to "summarize epidemiological knowledge about all major conditions and most risk factors" and use historical trends in main determinants to project mortality and disease burden forward to 2020.
Abstract: This is the first in a planned series of 10 volumes that will attempt to "summarize epidemiological knowledge about all major conditions and most risk factors;...generate assessments of numbers of deaths by cause that are consistent with the total numbers of deaths by age sex and region provided by demographers;...provide methodologies for and assessments of aggregate disease burden that combine--into the Disability-Adjusted Life Year or DALY measure--burden from premature mortality with that from living with disability; and...use historical trends in main determinants to project mortality and disease burden forward to 2020." This first volume includes chapters summarizing results from the project as a whole. (EXCERPT)

7,154 citations

Journal ArticleDOI
TL;DR: A theory of epidemiologic transition, sensitive to the formulations of population theorists who have stressed the demographic, biologic, sociologic, economic and psychologic ramifications of transitional processes, was conceived by this author less than four years ago.
Abstract: Although demography continues to be the most prominent discipline concerned with population dynamics, involvement of other disciplines is highly desirable. The case for a multidisciplinary approach to population theory has been aptly stated by Kurt Mayer: “Any meaningful interpretation of the cause and effects of population changes must … extend beyond formal statistical measurement of the components of change, i.e. fertility, mortality and migration, and draw on the theoretical framework of several other disciplines for assistance (Mayer 1962).” In noting that the “analysis of the causal determinants and consequences of population change forms the subject matter of population theory,” Mayer inferentially acknowledges the epidemiologic character of population phenomena, for as its etymology indicates, (epi, upon; demos, people; logos, study), epidemiology is the study of what “comes upon” groups of people. More specifically, epidemiology is concerned with the distribution of disease and death, and with their determinants and consequences in population groups. Inasmuch as patterns of health and disease are integral components of population change, epidemiology's reservoir of knowledge about these patterns and their determinants in population groups serves not only as a basis for prediction of population change but also as a source of hypotheses that can be further tested to correct, refine and build population theory. Furthermore, many epidemiologic techniques that have heretofore been limited to the examination of health and disease patterns can be profitably applied as well to the exploration of other mass phenomena, such as fertility control. A theory of epidemiologic transition, sensitive to the formulations of population theorists who have stressed the demographic, biologic, sociologic, economic and psychologic ramifications of transitional processes, was conceived by this author less than four years ago. Recognition of the limitations of demographic transition theory and of the need for comprehensive approaches to population dynamics stimulated the development of this theory (Van Nort and Karon 1955; Micklin 1968).

2,043 citations

Journal Article
TL;DR: Detailed assumptions used in constructing a new indicator of the burden of disease, the disability-adjusted life year (DALY), are presented and the formula for calculating DALYs based on these assumptions is provided.
Abstract: Detailed assumptions used in constructing a new indicator of the burden of disease, the disability-adjusted life year (DALY), are presented. Four key social choices in any indicator of the burden of disease are carefully reviewed. First, the advantages and disadvantages of various methods of calculating the duration of life lost due to a death at each age are discussed. DALYs use a standard expected-life lost based on model life-table West Level 26. Second, the value of time lived at different ages is captured in DALYs using an exponential function which reflects the dependence of the young and the elderly on adults. Third, the time lived with a disability is made comparable with the time lost due to premature mortality by defining six classes of disability severity. Assigned to each class is a severity weight between 0 and 1. Finally, a three percent discount rate is used in the calculation of DALYs. The formula for calculating DALYs based on these assumptions is provided.

1,391 citations

Journal ArticleDOI
08 Oct 1994-BMJ
TL;DR: The consumption of alcohol appeared to reduce the risk of ischaemic heart disease, largely irrespective of amount, among British men in middle or older age; among regular drinkers mortality from all causes combined increased progressively with amount drunk above 21 units a week.
Abstract: Objective : To assess the risk of death associated20with various patterns of alcohol consumption. Design - Prospective study of mortality in relation to alcohol drinking habits in 1978, with causes of death sought over the next 13 years (to 1991). Subjects : 12 321 British male doctors born between 1900 and 1930 (mean 1916) who replied to a postal questionnaire in 1978. Those written to in 1978 were the survivors of a long running prospective study of the effects of smoking that had begun in 195120and was still continuing. Results - Men were divided on the basis of their response to the 1978 questionnaire into two groups according to whether or not they had ever had any type of vascular disease, diabetes, or “life threatening disease” and into seven groups according to the amount of alcohol they drank. By 1991 almost a third had died. All statistical analyses of mortality were standardised for age, calendar year, and smoking habit. There was a U shaped relation between all cause mortality and the average amount of alcohol reportedly drunk; those who reported drinking 8-14 units of alcohol a week (corresponding to an average of one to two units a day) had the lowest risks. The causes of death were grouped into three main categories: “alcohol augmented” causes (6% of all deaths: cirrhosis, liver cancer, upper aerodigestive (mouth, oesophagus, larynx, and pharynx) cancer, alcoholism, poisoning, or injury), ischaemic heart disease (33% of all deaths), and other causes. The few deaths from alcohol augmented causes showed, at least among regular drinkers, a progressive trend, with the risk increasing with dose. In contrast, the many deaths from ischaemic heart disease showed no significant trend among regular drinkers, but there were significantly lower rates in regular drinkers than in non-drinkers. The aggregate of all other causes showed a U shaped dose-response relation similar to that for all cause mortality. Similar differences persisted irrespective of a history of previous disease, age (under 75 or 75 and older), and period of follow up (first five and last eight years). Some, but apparently not much, of the excess mortality in non-drinkers could be attributed to the inclusion among them of a small proportion of former drinkers. Conclusion : The consumption of alcohol appeared to reduce the risk of ischaemic heart disease, largely irrespective of amount. Among regular drinkers mortality from all causes combined increased progressively with amount drunk above 21 units a week. Among British men in middle or older age the consumption of an average of one or two units of alcohol a day is associated with significantly lower all cause mortality than is the consumption of no alcohol, or the consumption of substantial amounts. Above about three units (two American20units) of alcohol a day, progressively greater levels of consumption are associated with progressively higher all cause mortality.

1,235 citations

Journal ArticleDOI
TL;DR: This book represents an impressively comprehensive report on deaths from tobacco smoking between 1950 and 2000, tracing the smoking epidemic in developed countries over the past four decades and projecting how many more deaths tobacco will cause in the final decade of the century.
Abstract: This book represents an impressively comprehensive report on deaths from tobacco smoking between 1950 and 2000. It is a unique and authoritative record, tracing the smoking epidemic in developed countries over the past four decades and projecting how many more deaths tobacco will cause in the final decade of the century. It contains previously unpublished data for each major developed country (including figures for the individual countries within the former USSR). In addition, there are aggregated statistics for deaths from tobacco in the following groups: all developed countries, the former Socialist economies, the OECD developed countries, the current European Union (EU) (12 countries) and the planned EU (16 countries). It also contains some projections on deaths in developing countries. The work is aimed at clarifying for international governments, health professionals and the public, the real importance of the epidemic. Many of the figures and tables presented are designed for use as visual aids, and so most parts of the book may be reproduced freely without seeking copyright permission from the publisher or authors. Current death rates from smoking are presented for each separate developed country. These demonstrate the rapidly increasing mortality caused by smoking in both sexes which contrasts with the steadily decreasing mortality rates that have been seen among non-smokers in the 'OECD' developed countries. On almost every page, the scale of the numbers of deaths caused by smoking is alarming. The estimated average loss of life for those killed from smoking is about 16 years, and half of all regular smokers are eventually killed by their habit. On present trends, 4-5 million of young people (aged under 20) now living in the UK will eventually become regular smokers and tobacco will kill nearly half of them, with about 1 million of them killed by tobacco in middle age and another million in old age. Tobacco still causes one-third of all cancer deaths in the UK and between 1950 and 2000, tobacco will have killed about 6 million people in the UK. This is not to imply that all the data in this book is discouraging. Mortality from smoking in the UK has declined by about a fifth since 1970 as a result of a decline in cigarette sales and reductions in cigarette tar yields, and is still declining. Internationally, there are some striking differences. Thus in 1965, the UK had the worst mortality rates from smoking in the world whereas Poland had quite low rates. Now, however, the situation is reversed and Poland, like some of the other former socialist economies, is one of the worst-affected countries in the world. The final chapter deals with the spread of the epidemic to developing countires. Over the next few decades worldwide deaths from tobacco are projected to rise from 3 million a year now (including 'only' 1 million in the less-developed countries) to 10 million a year in about 2025 (including 7 million a year in less-developed countries). The contents of this book are overwhelmingly chastening. They also amount to a compelling case for governments everywhere to implement the World Health Organization's plea that children be protected from the advertising and promotion of tobacco. No-one and no organisation with an interest in public health or disease causation should be without this book.

985 citations