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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.

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Figures (8)
Citations
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Journal ArticleDOI
TL;DR: The results show that these severe haze events were equally affected by biomass combustion in all three regions, whereas the sources of the dominant fossil fuel component was dramatically different between north and south.
Abstract: Thick haze plagued northeastern China in January 2013, strongly affecting both regional climate and human respiratory health. Here, we present dual carbon isotope constrained (Δ14C and δ13C) source apportionment for combustion-derived black carbon aerosol (BC) for three key hotspot regions (megacities): North China Plain (NCP, Beijing), the Yangtze River Delta (YRD, Shanghai), and the Pearl River Delta (PRD, Guangzhou) for January 2013. BC, here quantified as elemental carbon (EC), is one of the most health-detrimental components of PM2.5 and a strong climate warming agent. The results show that these severe haze events were equally affected (∼30%) by biomass combustion in all three regions, whereas the sources of the dominant fossil fuel component was dramatically different between north and south. In the NCP region, coal combustion accounted for 66% (46–74%, 95% C.I.) of the EC, whereas, in the YRD and PRD regions, liquid fossil fuel combustion (e.g., traffic) stood for 46% (18–66%) and 58% (38–68%), re...

223 citations

Journal ArticleDOI
TL;DR: The sources and formation of haze are described, the mitigation measures in force, the relationship between haze pollution and public health is reviewed, the potential policy options for prevention, the need for wider public dialogue and the implications for scientific research are discussed.

222 citations

Journal ArticleDOI
TL;DR: Maternal, fetal, and childhood nutrition are crucial contributors to these programming effects and synergistically act to augment the effects of developmental programming; this observation might explain in part the disproportionate burden of chronic disease in these regions.
Abstract: An adverse intrauterine environment is associated with an increased risk of elevated blood pressure and kidney disease in later life. Many studies have focused on low birth weight, prematurity and growth restriction as surrogate markers of an adverse intrauterine environment; however, high birth weight, exposure to maternal diabetes and rapid growth during early childhood are also emerging as developmental risk factors for chronic diseases. Altered programming of nephron number is an important link between exposure to developmental stressors and subsequent risk of hypertension and kidney disease. Maternal, fetal, and childhood nutrition are crucial contributors to these programming effects. Resource-poor countries experience the sequential burdens of fetal and childhood undernutrition and subsequent overnutrition, which synergistically act to augment the effects of developmental programming; this observation might explain in part the disproportionate burden of chronic disease in these regions. Numerous nutritional interventions have been effective in reducing the short-term risk of low birth weight and prematurity. Understanding the potential long-term benefits of such interventions is crucial to inform policy decisions to interrupt the developmental programming cycle and stem the growing epidemics of hypertension and kidney disease worldwide.

222 citations

Journal ArticleDOI
TL;DR: Modification of gut microbiota via prebiotics, probiotics or other dietary interventions has provided evidence to support a possible beneficial effect of interventions targeting gut microbiota modulation to treat components or complications of metabolic syndrome.
Abstract: The gut microbiome contributes approximately 2kg of the whole body weight, and recent studies suggest that gut microbiota has a profound effect on human metabolism, potentially contributing to several features of the metabolic syndrome. Metabolic syndrome is defined by a clustering of metabolic disorders that include central adiposity with visceral fat accumulation, dyslipidemia, insulin resistance, dysglycemia and non-optimal blood pressure levels. Metabolic syndrome is associated with an increased risk of cardiovascular diseases and type 2 diabetes. It is estimated that around 20-25 percent of the world's adult population has metabolic syndrome. In this manuscript, we have reviewed the existing data linking gut microbiome with metabolic syndrome. Existing evidence from studies both in animals and humans support a link between gut microbiome and various components of metabolic syndrome. Possible pathways include involvement with energy homeostasis and metabolic processes, modulation of inflammatory signaling pathways, interferences with the immune system, and interference with the renin-angiotensin system. Modification of gut microbiota via prebiotics, probiotics or other dietary interventions has provided evidence to support a possible beneficial effect of interventions targeting gut microbiota modulation to treat components or complications of metabolic syndrome.

221 citations

Journal ArticleDOI
TL;DR: Blood pressure-lowering therapy is likely to prevent stroke and death in patients with uncomplicated grade 1 hypertension, and withdrawal from treatment due to adverse effects was more common in the active groups.
Abstract: Background: Effects of blood pressure reduction in persons with grade 1 hypertension are unclear. Purpose: To investigate whether pharmacologic blood pressure reduction prevents cardiovascular even ...

221 citations

References
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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

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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.