scispace - formally typeset
Search or ask a question
Journal Article•DOI•

A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010

Stephen S Lim1, Theo Vos, Abraham D. Flaxman1, Goodarz Danaei2  +207 more•Institutions (92)
15 Dec 2012-The Lancet (Elsevier)-Vol. 380, Iss: 9859, pp 2224-2260
TL;DR: In this paper, the authors estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010.
About: This article is published in The Lancet.The article was published on 2012-12-15 and is currently open access. It has received 9324 citations till now. The article focuses on the topics: Disease burden & Risk factor.

Summary (1 min read)

Jump to: [Convincing evidence] – [Probable evidence] – [Possible evidence] and [Insufficient evidence]

Convincing evidence

  • Evidence based on epidemiological studies showing consistent associations between exposure and disease, with little or no evidence to the contrary.
  • The available evidence is based on a substantial number of studies including prospective observational studies and where relevant, randomised controlled trials of sufficient size, duration, and quality showing consistent effects.

Probable evidence

  • Evidence based on epidemiological studies showing fairly consistent associations between exposure and disease, but for which there are perceived shortcomings in the available evidence or some evidence to the contrary, which precludes a more definite judgment.
  • Shortcomings in the evidence may be any of the following: insufficient duration of trials (or studies); insufficient trials (or studies) available; inadequate sample sizes; or incomplete follow-up.

Possible evidence

  • Evidence based mainly on findings from case-control and cross-sectional studies.
  • Insufficient randomised controlled trials, observational studies, or non-randomised controlled trials are available.
  • Evidence based on non-epidemiological studies, such as clinical and laboratory investigations, is supportive.
  • More trials are needed to support the tentative associations, which should be biologically plausible.

Insufficient evidence

  • Evidence based on findings of a few studies which are suggestive, but insufficient to establish an association between exposure and disease.
  • Burden of disease attributable to individual risk factors are shown sequentially for ease of presentation.

Did you find this useful? Give us your feedback

Figures (8)
Citations
More filters
This article can be found in the following collections: Global Health; Public Health; Cardiology & Vascular Medicine (Cardiology & vascular-other); Endocrinology (Diabetes); Neurology (Cerebrovascular disease); Nutrition & Metabolism (Nutrition & metabolism-other); Respiratory Medicine (Respiratory medicine-other) Profits and pandemics: prevention of harmful effects of tobacco, alcohol, and ultra-processed food and drink industries

[...]

Rob Moodie Mbbs, David Stuckler, Carlos Augusto Monteiro, Nick Sheron, Bruce Neal, Thaksaphon Thamarangsi, Paul Lincoln, Sally Casswell 
01 Jan 2013
TL;DR: It is concluded that unhealthy commodity industries should have no role in the formation of national or international NCD policy and public regulation and market intervention are the only evidence-based mechanisms to prevent harm caused by the unhealthy commodity industry.
Abstract: The 2011 UN high-level meeting on non-communicable diseases (NCDs) called for multisectoral action including with the private sector and industry. However, through the sale and promotion of tobacco, alcohol, and ultra-processed food and drink (unhealthy commodities), transnational corporations are major drivers of global epidemics of NCDs. What role then should these industries have in NCD prevention and control? We emphasise the rise in sales of these unhealthy commodities in low-income and middle-income countries, and consider the common strategies that the transnational corporations use to undermine NCD prevention and control. We assess the effectiveness of self-regulation, public-private partnerships, and public regulation models of interaction with these industries and conclude that unhealthy commodity industries should have no role in the formation of national or international NCD policy. Despite the common reliance on industry self-regulation and public-private partnerships, there is no evidence of their effectiveness or safety. Public regulation and market intervention are the only evidence-based mechanisms to prevent harm caused by the unhealthy commodity industries.

172 citations

Journal Article•DOI•
Spatial Association Between Ambient Fine Particulate Matter and Incident Hypertension

[...]

Hong Chen1, Richard T. Burnett2, Jeffrey C. Kwong1, Paul J. Villeneuve3, Mark S. Goldberg4, Robert D. Brook5, Aaron van Donkelaar6, Michael Jerrett7, Randall V. Martin6, Alexander Kopp, Jeffrey R. Brook8, Ray Copes1 •
University of Toronto1, Health Canada2, Carleton University3, McGill University Health Centre4, University of Michigan5, Dalhousie University6, University of California, Berkeley7, Environment Canada8
04 Feb 2014-Circulation
TL;DR: An association between PM2.5 and incident hypertension is found, supported by various sensitivity analyses, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time.
Abstract: Background—Laboratory studies suggest that exposure to fine particulate matter (≤2.5 μm in diameter) (PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension. Methods and Results—We assembled a cohort of 35 303 nonhypertensive adults from Ontario, Canada, who responded to 1 of 4 population-based health surveys between 1996 and 2005 and were followed up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants’ postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adju...

172 citations

Journal Article•DOI•
Health impacts of anthropogenic biomass burning in the developed world

[...]

Torben Sigsgaard1, Bertil Forsberg2, Isabella Annesi-Maesano3, Anders Blomberg2, Anette Kocbach Bølling4, Christoffer Boman2, Jakob Hjort Bønløkke1, Michael Brauer5, Nigel Bruce, Marie Eve Héroux, Maija-Riitta Hirvonen6, Frank J. Kelly7, Nino Künzli8, Bo Lundbäck9, Hanns Moshammer10, Curtis W. Noonan11, Joachim Pagels12, Gerd Sallsten9, Jean-Paul Sculier, Bert Brunekreef13 •
Aarhus University1, Umeå University2, French Institute of Health and Medical Research3, Norwegian Institute of Public Health4, University of British Columbia5, University of Eastern Finland6, King's College London7, Swiss Tropical and Public Health Institute8, University of Gothenburg9, Medical University of Vienna10, University of Montana11, Lund University12, Utrecht University13
24 Sep 2015-European Respiratory Journal
TL;DR: It is concluded that emissions from current biomass combustion products negatively affect respiratory and, possibly, cardiovascular health in Europe and emissions need to reduce to protect public health.
Abstract: Climate change policies have stimulated a shift towards renewable energy sources such as biomass. The economic crisis of 2008 has also increased the practice of household biomass burning as it is often cheaper than using oil, gas or electricity for heating. As a result, household biomass combustion is becoming an important source of air pollutants in the European Union.This position paper discusses the contribution of biomass combustion to pollution levels in Europe, and the emerging evidence on the adverse health effects of biomass combustion products.Epidemiological studies in the developed world have documented associations between indoor and outdoor exposure to biomass combustion products and a range of adverse health effects. A conservative estimate of the current contribution of biomass smoke to premature mortality in Europe amounts to at least 40 000 deaths per year.We conclude that emissions from current biomass combustion products negatively affect respiratory and, possibly, cardiovascular health in Europe. Biomass combustion emissions, in contrast to emissions from most other sources of air pollution, are increasing. More needs to be done to further document the health effects of biomass combustion in Europe, and to reduce emissions of harmful biomass combustion products to protect public health.

172 citations

Posted Content•DOI•
Mutational signatures associated with tobacco smoking in human cancer

[...]

Ludmil B. Alexandrov1, Young Seok Ju2, Kerstin Haase3, Peter Van Loo3, Inigo Martincorena4, Serena Nik-Zainal4, Yasushi Totoki, Akihiro Fujimoto5, Hidewaki Nakagawa, Tatsuhiro Shibata6, Peter J. Campbell4, Paolo Vineis7, David H. Phillips8, Michael R. Stratton4 •
Los Alamos National Laboratory1, KAIST2, Francis Crick Institute3, Wellcome Trust Sanger Institute4, Kyoto University5, University of Tokyo6, Medical Research Council7, King's College London8
03 May 2016-bioRxiv
TL;DR: The results are consistent with the proposition that smoking increases cancer risk by increasing the somatic mutation load, although direct evidence for this mechanism is lacking in some smoking-related cancer types.
Abstract: Tobacco smoking increases the risk of at least 15 classes of cancer. We analyzed somatic mutations and DNA methylation in 5,243 cancers of types for which tobacco smoking confers an elevated risk. Smoking is associated with increased mutation burdens of multiple distinct mutational signatures, which contribute to different extents in different cancers. One of these signatures, mainly found in cancers derived from tissues directly exposed to tobacco smoke, is attributable to misreplication of DNA damage caused by tobacco carcinogens. Others likely reflect indirect activation of DNA editing by APOBEC cytidine deaminases and of an endogenous clock-like mutational process. The results are consistent with the proposition that smoking increases cancer risk by increasing the somatic mutation load, although direct evidence for this mechanism is lacking in some smoking-related cancer types.

171 citations

Journal Article•DOI•
Smoking as a Risk Factor for Stroke in Women Compared With Men A Systematic Review and Meta-Analysis of 81 Cohorts, Including 3 980 359 Individuals and 42 401 Strokes

[...]

Sanne A.E. Peters1, Rachel R. Huxley2, Mark Woodward3•
The George Institute for Global Health1, Utrecht University2, University of Minnesota3
01 Oct 2013-Stroke
TL;DR: Compared with nonsmokers, the excess risk of stroke is at least as great among women who smoke compared with men who smoke.
Abstract: Background and Purpose—It is currently unknown whether the excess risk of stroke by smoking is the same for women and men. We performed a systematic review and meta-analysis to estimate the effect of smoking on stroke in women compared with men. Methods—PubMed MEDLINE was systematically searched for prospective population-based cohort studies published between January 1, 1966, and January 26, 2013. Studies that presented sex-specific estimates of the relative risk of stroke comparing current smoking with nonsmoking and its associated variability were selected. The sex-specific relative risks and their ratio (RRR), comparing women with men, were pooled using random-effects meta-analysis with inverse variance weighting. Similarly, the RRR for former versus never smoking was pooled. Results—Data from 81 prospective cohort studies that included 3 980 359 individuals and 42 401 strokes were available. Smoking was an independent risk factor for stroke in both sexes. Overall, the pooled multiple-adjusted RRR ind...

171 citations

References
More filters
Journal Article•DOI•
Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.

[...]

William C. Knowler1, Elizabeth Barrett-Connor1, Sarah E. Fowler1, Richard F. Hamman1, John M. Lachin1, Elizabeth A. Walker, David M. Nathan1 •
George Washington University1
07 Feb 2002-The New England Journal of Medicine
TL;DR: In this paper, the authors compared a lifestyle intervention with metformin to prevent or delay the development of Type 2 diabetes in nondiabetic individuals. And they found that the lifestyle intervention was significantly more effective than the medication.
Abstract: Background Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors — elevated plasma glucose concentrations in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle — are potentially reversible. We hypothesized that modifying these factors with a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes. Methods We randomly assigned 3234 nondiabetic persons with elevated fasting and post-load plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle modification program with the goals of at least a 7 percent weight loss and at least 150 minutes of physical activity per week. The mean age of the participants was 51 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 34.0; 68 percent were women, and 45 percent were members of minority groups. Results The average follow-up was 2.8 years. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence by 58 percent (95 percent confidence interval, 48 to 66 percent) and metformin by 31 percent (95 percent confidence interval, 17 to 43 percent), as compared with placebo; the lifestyle intervention was significantly more effective than metformin. To prevent one case of diabetes during a period of three years, 6.9 persons would have to participate in the lifestyle-intervention program, and 13.9 would have to receive metformin. Conclusions Lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. The lifestyle intervention was more effective than metformin.

17,333 citations

Journal Article•DOI•
Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010

[...]

Rafael Lozano1, Mohsen Naghavi1, Kyle J Foreman2, Stephen S Lim1  +192 more•Institutions (95)
15 Dec 2012-The Lancet
TL;DR: The Global Burden of Diseases, Injuries, and Risk Factors Study 2010 aimed to estimate annual deaths for the world and 21 regions between 1980 and 2010 for 235 causes, with uncertainty intervals (UIs), separately by age and sex, using the Cause of Death Ensemble model.

11,809 citations

Journal Article•DOI•
Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies.

[...]

Sarah Lewington, Robert Clarke, Nawab Qizilbash, Richard Peto, Rory Collins 
14 Dec 2002-The Lancet
TL;DR: Throughout middle and old age, usual blood pressure is strongly and directly related to vascular (and overall) mortality, without any evidence of a threshold down to at least 115/75 mm Hg.

9,101 citations

Book•
The global burden of disease: a comprehensive assessment of mortality and disability from diseases injuries and risk factors in 1990 and projected to 2020.

[...]

Christopher J L Murray, Alan D. Lopez
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 Article•DOI•
Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010

[...]

Theo Vos, Abraham D. Flaxman1, Mohsen Naghavi1, Rafael Lozano1  +360 more•Institutions (143)
15 Dec 2012-The Lancet
TL;DR: Prevalence and severity of health loss were weakly correlated and age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010, but population growth and ageing have increased YLD numbers and crude rates over the past two decades.

7,021 citations

Related Papers (5)
Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010

[...]

15 Dec 2012-The Lancet
Rafael Lozano, Mohsen Naghavi, Kyle J Foreman  +193 more
Global burden of hypertension: analysis of worldwide data

[...]

15 Jan 2005-The Lancet
Patricia M. Kearney, Patricia M. Kearney, Megan Whelton, Kristi Reynolds, Paul Muntner, Paul K. Whelton, Jiang He 
Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies.

[...]

14 Dec 2002-The Lancet
Sarah Lewington, Robert Clarke, Nawab Qizilbash, Richard Peto, Rory Collins 
The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.

[...]

21 May 2003-JAMA
Aram V. Chobanian, George L. Bakris, Henry R. Black, William C. Cushman, Lee A. Green, Joseph L. Izzo, Daniel W. Jones, Barry J. Materson, Suzanne Oparil, Jackson T. Wright, Edward J. Roccella 
2013 ESH/ESC Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).

[...]

21 Jul 2013-European Heart Journal
Giuseppe Mancia, Robert Fagard, Krzysztof Narkiewicz, Josep Redon, Alberto Zanchetti, Michael Böhm, Thierry Christiaens, Renata Cifkova, Guy De Backer, Anna F. Dominiczak, Maurizio Galderisi, Diederick E. Grobbee, Tiny Jaarsma, Paulus Kirchhof, Sverre E. Kjeldsen, Stéphane Laurent, Athanasios J. Manolis, Peter M. Nilsson, Luis M. Ruilope, Roland E. Schmieder, Per Anton Sirnes, Peter Sleight, Margus Viigimaa, Bernard Waeber, Faiez Zannad, Michel Burnier, Ettore Ambrosioni, Mark Caufield, Antonio Coca, Michael H. Olsen, Costas Tsioufis, Philippe van de Borne, José Luis Zamorano, Stephan Achenbach, Helmut Baumgartner, Jeroen J. Bax, Héctor Bueno, Veronica Dean, Christi Deaton, Çetin Erol, Roberto Ferrari, David Hasdai, Arno W. Hoes, Juhani Knuuti, Philippe Kolh, Patrizio Lancellotti, Aleš Linhart, Petros Nihoyannopoulos, Massimo F Piepoli, Piotr Ponikowski, Juan Tamargo, Michal Tendera, Adam Torbicki, William Wijns, Stephan Windecker, Denis Clement, Thierry C. Gillebert, Enrico Agabiti Rosei, Stefan D. Anker, Johann Bauersachs, Jana Brguljan Hitij, Mark J. Caulfield, Marc De Buyzere, Sabina De Geest, Geneviève Derumeaux, Serap Erdine, Csaba Farsang, Christian Funck-Brentano, Vjekoslav Gerc, Giuseppe Germanò, Stephan Gielen, Herman Haller, Jens Jordan, Thomas Kahan, Michel Komajda, Dragan Lovic, Heiko Mahrholdt, Jan Östergren, Gianfranco Parati, Joep Perk, Jorge Polónia, Bogdan A. Popescu, Zeljko Reiner, Lars Rydén, Yuriy Sirenko, Alice Stanton, Harry A.J. Struijker-Boudier, Charalambos Vlachopoulos, Massimo Volpe, David A. Wood 
Frequently Asked Questions (4)
Q1. What are the contributions mentioned in the paper "A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990—2010: a systematic analysis for the global burden of disease study 2010 author" ?

Lim, Stephen S, Vos, Umer, Shibuya, Shibaya, Kenji, AdairRohani, Heather, Amann, Markus, Anderson, H Ross, Andrews, Kathryn G, Aryee, Martin, Gmel, Gerhard, Graham, Kathryn, Grainger, Rebecca, Grant, Bridget, Gunnell, David, Gutierrez, Hialy R, Hall, Wayne, Hoek, Hans W, Hogan, Anne-Charlson, H Dean, this paper, Nolla, Nissim, Nelson, Paul K 

Shortcomings in the evidence may be any of the following: insufficient duration of trials (or studies); insufficient trials (or studies) available; inadequate sample sizes; or incomplete follow-up. 

The available evidence is based on a substantial number of studies including prospective observational studies and where relevant, randomised controlled trials of sufficient size, duration, and quality showing consistent effects. 

In reality, the burden attributable to different risks overlaps because of multicausality and because the effects of some risk factors are partly mediated throughLim et al.