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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.

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Citations
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Journal Article•DOI•
Association between hyperinsulinemia and increased risk of cancer death in nonobese and obese people: A population-based observational study.

[...]

Tetsuro Tsujimoto, Hiroshi Kajio, Takehiro Sugiyama
01 Jul 2017-International Journal of Cancer
TL;DR: Improvement of hyperinsulinemia may be an important approach for preventing cancer regardless of the presence or absence of obesity, considering that nonobese people with hyperinsulainemia were at higher risk of cancer mortality than those without hyperinsULinemia.
Abstract: Obesity, metabolic syndrome and type 2 diabetes are associated with cancer-related mortality. We assessed whether hyperinsulinemia is a risk factor for cancer death in nonobese people without diabetes. We conducted a prospective cohort study using data from the National Health and Nutrition Examination Survey 1999-2010 and followed up the participants until December 31, 2011. For the primary analysis of cancer mortality, we used Cox proportional hazard models to estimate hazard ratios (HRs) in the participants with hyperinsulinemia and those without. Hyperinsulinemia was defined as a fasting insulin level of ≥10 μU/mL. To identify causes of deaths, the International Classification of Diseases, Tenth Revision codes were used. This study included 9,778 participants aged 20 years or older without diabetes or a history of cancer: 6,718 nonobese participants (2,057 with hyperinsulinemia [30.6%]) and 3,060 obese participants (2,303 with hyperinsulinemia [75.3%]). A total of 99.9% completed follow-up. Among all study participants, cancer mortality was significantly higher in those with hyperinsulinemia than in those without hyperinsulinemia (adjusted HR 2.04, 95% CI 1.24-3.34, p = 0.005). Similarly, among nonobese participants, multivariable analysis showed that cancer mortality was significantly higher in those with hyperinsulinemia than in those without (adjusted HR 1.89, 95% CI 1.07-3.35, p = 0.02). Considering that nonobese people with hyperinsulinemia were at higher risk of cancer mortality than those without hyperinsulinemia, improvement of hyperinsulinemia may be an important approach for preventing cancer regardless of the presence or absence of obesity.

94 citations

Journal Article•DOI•
Targeted Health Behavior Interventions Promoting Physical Activity: A Conceptual Model

[...]

Philip J. Morgan1, Myles D. Young, Jordan J. Smith, David R. Lubans•
University of Newcastle1
01 Apr 2016-Exercise and Sport Sciences Reviews
TL;DR: It is hypothesize that researchers who enhance the sociocultural relevance of their core intervention components and recognize the unique contributions of both intervention design and delivery will experience greater intervention engagement and improved outcomes.
Abstract: This article presents a conceptual model illustrating a targeted approach to the design and delivery of health behavior interventions that focus on physical activity promotion. We hypothesize that researchers who i) enhance the sociocultural relevance of their core intervention components and ii) recognize the unique contributions of both intervention design and delivery will experience greater intervention engagement and improved outcomes.

94 citations

Journal Article•DOI•
Nutrition and health in women, children, and adolescent girls

[...]

Francesco Branca1, Ellen Piwoz2, Werner Schultink3, Lucy Martinez Sullivan•
World Health Organization1, Bill & Melinda Gates Foundation2, UNICEF3
14 Sep 2015-BMJ
TL;DR: Urgent action is needed to tackle malnutrition in all forms and to help nutrition unlock the potential of investment in the health of women, children, and adolescents, say Francesco Branca and colleagues.
Abstract: Urgent action is needed to tackle malnutrition in all forms and to help nutrition unlock the potential of investment in the health of women, children, and adolescents, say Francesco Branca and colleagues

94 citations

Journal Article•DOI•
Influence of diet and obesity on COPD development and outcomes

[...]

Corrine Hanson1, Erica P.A. Rutten, Emiel F.M. Wouters2, Stephen I. Rennard1•
University of Nebraska Medical Center1, Maastricht University2
05 Aug 2014-International Journal of Chronic Obstructive Pulmonary Disease
TL;DR: Current evidence regarding the role that Obesity and diet play in the development of COPD, and in COPD-related outcomes suggests that a focus on obesity and diet should be part of public health campaigns to reduce the burden of lung disease.
Abstract: The global increase in the prevalence and incidence of obesity has called serious attention to this issue as a major public health concern. Obesity is associated with many chronic diseases, including cardiovascular disease and diabetes, and recently the role of overweight and obesity in lung disease has received new interest. Independently of obesity, diet also plays a role as a risk factor for many chronic diseases, and evidence is accumulating to support a role for diet in the prevention and management of several lung diseases. Chronic obstructive lung disease is the third-leading cause of death globally, and both obesity and diet appear to play roles in its pathophysiology. Obesity has been associated with decreased lung-function measures in population-based studies, with increased prevalence of several lung diseases and with compromised pulmonary function. In contrast, obesity has a protective effect against mortality in severe chronic obstructive pulmonary disease (COPD). Nutrient intake and dietary patterns have also been associated with lung-function measures and the development and progression of COPD. Taken together, this suggests that a focus on obesity and diet should be part of public health campaigns to reduce the burden of lung disease, and could have important implications for clinicians in the management of their patients. Future research should also focus on elucidating these relationships in diverse populations and age-groups, and on understanding the complex interaction between behavior, environment, and genetics in the development and progression of COPD. The goal of this article is to review current evidence regarding the role that obesity and diet play in the development of COPD, and in COPD-related outcomes.

93 citations

Journal Article•DOI•
Metabolomic Identification of a Novel Pathway of Blood Pressure Regulation Involving Hexadecanedioate

[...]

Cristina Menni1, Delyth Graham2, Gabi Kastenmüller, Nora H J Alharbi2, Safaa Mohammed M. Alsanosi2, Martin W. McBride3, Massimo Mangino2, Philip Titcombe4, So-Youn Shin, Maria Psatha1, Thomas Geisendorfer, Anja Huber, Annette Peters5, Rui Wang-Sattler6, Tao Xu7, M J Brosnan8, Jeff K. Trimmer, Christian Reichel, Robert P. Mohney, Nicole Soranzo9, Mark H. Edwards4, Cyrus Cooper4, Cyrus Cooper5, Alistair C. Church6, Karsten Suhre7, Christian Gieger, Anna F. Dominiczak2, Tim D. Spector1, Sandosh Padmanabhan2, Ana M. Valdes •
King's College London1, University of Glasgow2, University of Bristol3, University of Southampton4, University of Oxford5, Jubilee Hospital6, Cornell University7, University of Nottingham8, Wellcome Trust Sanger Institute9
01 Aug 2015-Hypertension
TL;DR: The findings indicate that hexadecanedioate is causally associated with blood pressure regulation through a novel pathway that merits further investigation.
Abstract: High blood pressure is a major contributor to the global burden of disease and discovering novel causal pathways of blood pressure regulation has been challenging. We tested blood pressure associations with 280 fasting blood metabolites in 3980 TwinsUK females. Survival analysis for all-cause mortality was performed on significant independent metabolites (P<8.9×10−5). Replication was conducted in 2 independent cohorts KORA (n=1494) and Hertfordshire (n=1515). Three independent animal experiments were performed to establish causality: (1) blood pressure change after increasing circulating metabolite levels in Wistar–Kyoto rats; (2) circulating metabolite change after salt-induced blood pressure elevation in spontaneously hypertensive stroke-prone rats; and (3) mesenteric artery response to noradrenaline and carbachol in metabolite treated and control rats. Of the15 metabolites that showed an independent significant association with blood pressure, only hexadecanedioate, a dicarboxylic acid, showed concordant association with blood pressure (systolic BP: β [95% confidence interval], 1.31 [0.83–1.78], P=6.81×10−8; diastolic BP: 0.81 [0.5–1.11], P=2.96×10−7) and mortality (hazard ratio [95% confidence interval], 1.49 [1.08–2.05]; P=0.02) in TwinsUK. The blood pressure association was replicated in KORA and Hertfordshire. In the animal experiments, we showed that oral hexadecanedioate increased both circulating hexadecanedioate and blood pressure in Wistar–Kyoto rats, whereas blood pressure elevation with oral sodium chloride in hypertensive rats did not affect hexadecanedioate levels. Vascular reactivity to noradrenaline was significantly increased in mesenteric resistance arteries from hexadecanedioate-treated rats compared with controls, indicated by the shift to the left of the concentration–response curve (P=0.013). Relaxation to carbachol did not show any difference. Our findings indicate that hexadecanedioate is causally associated with blood pressure regulation through a novel pathway that merits further investigation.

93 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

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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.