scispace - formally typeset
Search or ask a question
Journal ArticleDOI

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 moreInstitutions (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)

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
Proceedings ArticleDOI
04 Mar 2018
TL;DR: In this article, a deep recurrent neural network (RNN) consisting of multilayered Long Short-Term Memory (LSTM) networks was proposed for arterial blood pressure (BP) estimation.
Abstract: Existing methods for arterial blood pressure (BP) estimation directly map the input physiological signals to output BP values without explicitly modeling the underlying temporal dependencies in BP dynamics. As a result, these models suffer from accuracy decay over a long time and thus require frequent calibration. In this work, we address this issue by formulating BP estimation as a sequence prediction problem in which both the input and target are temporal sequences. We propose a novel deep recurrent neural network (RNN) consisting of multilayered Long Short-Term Memory (LSTM) networks, which are incorporated with (1) a bidirectional structure to access larger-scale context information of input sequence, and (2) residual connections to allow gradients in deep RNN to propagate more effectively. The proposed deep RNN model was tested on a static BP dataset, and it achieved root mean square error (RMSE) of 3.90 and 2.66 mmHg for systolic BP (SBP) and diastolic BP (DBP) prediction respectively, surpassing the accuracy of traditional BP prediction models. On a multi-day BP dataset, the deep RNN achieved RMSE of 3.84, 5.25, 5.80 and 5.81 mmHg for the 1st day, 2nd day, 4th day and 6th month after the 1st day SBP prediction, and 1.80, 4.78, 5.0, 5.21 mmHg for corresponding DBP prediction, respectively, which outperforms all previous models with notable improvement. The experimental results suggest that modeling the temporal dependencies in BP dynamics significantly improves the long-term BP prediction accuracy.

116 citations

Journal ArticleDOI
15 Feb 2015-Heart
TL;DR: The components of air pollution, an overview of the cardiovascular effects ofAir pollution exposure, and a review of the basic mechanisms that are activated by exposure to promote CVD are provided.
Abstract: Air pollution is a significant cause of cardiovascular morbidity and mortality worldwide. Although the epidemiologic association between air pollution exposures and exacerbation of cardiovascular disease (CVD) is well established, the mechanisms by which these exposures promote CVD are incompletely understood. This review provides an overview of the components of air pollution, an overview of the cardiovascular effects of air pollution exposure, and a review of the basic mechanisms that are activated by exposure to promote CVD.

116 citations

Journal ArticleDOI
TL;DR: Polygenic score analysis suggests pleiotropy between psychiatric disorders and suicidal ideation whereas the tendency to act on such thoughts may have a partially independent genetic diathesis.
Abstract: Epidemiological studies have recognized a genetic diathesis for suicidal behavior, which is independent of other psychiatric disorders. Genome-wide association studies (GWAS) on suicide attempt (SA) and ideation have failed to identify specific genetic variants. Here, we conduct further GWAS and for the first time, use polygenic score analysis in cohorts of patients with mood disorders, to test for common genetic variants for mood disorders and suicide phenotypes. Genome-wide studies for SA were conducted in the RADIANT and GSK-Munich recurrent depression samples and London Bipolar Affective Disorder Case-Control Study (BACCs) then meta-analysis was performed. A GWAS on suicidal ideation during antidepressant treatment had previously been conducted in the Genome Based Therapeutic Drugs for Depression (GENDEP) study. We derived polygenic scores from each sample and tested their ability to predict SA in the mood disorder cohorts or ideation status in the GENDEP study. Polygenic scores for major depressive disorder, bipolar disorder and schizophrenia from the Psychiatric Genomics Consortium were used to investigate pleiotropy between psychiatric disorders and suicide phenotypes. No significant evidence for association was detected at any SNP in GWAS or meta-analysis. Polygenic scores for major depressive disorder significantly predicted suicidal ideation in the GENDEP pharmacogenetics study and also predicted SA in a combined validation dataset. Polygenic scores for SA showed no predictive ability for suicidal ideation. Polygenic score analysis suggests pleiotropy between psychiatric disorders and suicidal ideation whereas the tendency to act on such thoughts may have a partially independent genetic diathesis.

115 citations

Journal ArticleDOI
Siqi Zhang1, Guoxing Li1, Lin Tian1, Qun Guo1, Xiaochuan Pan1 
TL;DR: Evidence was found that short-term exposure to air pollution was associated with increasing risk of hospital utilization for COPD and asthma in the whole population, the elderly and children, but not in people aged 15-64.

115 citations

Journal ArticleDOI
TL;DR: Limited, inconclusive evidence for associations between air pollution and COPD incidence is found using a large, nationally representative cohort based on primary care records linked to hospital admissions.
Abstract: Objectives The role of outdoor air pollution in the incidence of chronic obstructive pulmonary disease (COPD) remains unclear. We investigated this question using a large, nationally representative cohort based on primary care records linked to hospital admissions. Methods A cohort of 812 063 patients aged 40– 89 years registered with 205 English general practices in 2002 without a COPD diagnosis was followed from 2003 to 2007. First COPD diagnoses recorded either by a general practitioner (GP) or on admission to hospital were identified. Annual average concentrations in 2002 for particulate matter with an aerodynamic diameter <10 mm (PM10) and <2.5 mm (PM2.5), nitrogen dioxide (NO2), ozone and sulfur dioxide (SO2 )a t 1 km 2 resolution were estimated from emission-based dispersion models. Hazard ratios (HRs) per interquartile range change were estimated from Cox models adjusting for age, sex, smoking, body mass index and area-level deprivation. Results 16 034 participants (1.92%) received a COPD diagnosis from their GP and 2910 participants (0.35%) were admitted to hospital for COPD. After adjustment, HRs for GP recorded COPD and PM10 ,P M2.5 and NO2 were close to unity, positive for SO2 (HR=1.07 (95% CI 1.03 to 1.11) per 2.2 mg/m 3 ) and negative for ozone (HR=0.94 (0.89 to 1.00) per 3 mg/m 3 ). For admissions HRs for PM2.5 and NO2 remained positive (HRs=1.05 (0.98 to 1.13) and 1.06 (0.98 to 1.15) per 1.9 mg/m 3 and 10.7 mg/m 3 , respectively). Conclusions This large population-based cohort study found limited, inconclusive evidence for associations between air pollution and COPD incidence. Further work, utilising improved estimates of air pollution over time and enhanced socioeconomic indicators, is required to clarify the association between air pollution and COPD incidence.

115 citations

References
More filters
Journal ArticleDOI
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 ArticleDOI
Rafael Lozano1, Mohsen Naghavi1, Kyle J Foreman2, Stephen S Lim1  +192 moreInstitutions (95)
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 ArticleDOI
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
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
Theo Vos, Abraham D. Flaxman1, Mohsen Naghavi1, Rafael Lozano1  +360 moreInstitutions (143)
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)
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.