scispace - formally typeset

Institution

University of Otago

EducationDunedin, New Zealand
About: University of Otago is a(n) education organization based out in Dunedin, New Zealand. It is known for research contribution in the topic(s): Population & Poison control. The organization has 21668 authors who have published 53810 publication(s) receiving 1835189 citation(s). The organization is also known as: Otago University & otago.ac.nz.


Papers
More filters
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.
Abstract: Summary Background Reliable and timely information on the leading causes of death in populations, and how these are changing, is a crucial input into health policy debates. In the Global Burden of Diseases, Injuries, and Risk Factors Study 2010 (GBD 2010), we 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. Methods We attempted to identify all available data on causes of death for 187 countries from 1980 to 2010 from vital registration, verbal autopsy, mortality surveillance, censuses, surveys, hospitals, police records, and mortuaries. We assessed data quality for completeness, diagnostic accuracy, missing data, stochastic variations, and probable causes of death. We applied six different modelling strategies to estimate cause-specific mortality trends depending on the strength of the data. For 133 causes and three special aggregates we used the Cause of Death Ensemble model (CODEm) approach, which uses four families of statistical models testing a large set of different models using different permutations of covariates. Model ensembles were developed from these component models. We assessed model performance with rigorous out-of-sample testing of prediction error and the validity of 95% UIs. For 13 causes with low observed numbers of deaths, we developed negative binomial models with plausible covariates. For 27 causes for which death is rare, we modelled the higher level cause in the cause hierarchy of the GBD 2010 and then allocated deaths across component causes proportionately, estimated from all available data in the database. For selected causes (African trypanosomiasis, congenital syphilis, whooping cough, measles, typhoid and parathyroid, leishmaniasis, acute hepatitis E, and HIV/AIDS), we used natural history models based on information on incidence, prevalence, and case-fatality. We separately estimated cause fractions by aetiology for diarrhoea, lower respiratory infections, and meningitis, as well as disaggregations by subcause for chronic kidney disease, maternal disorders, cirrhosis, and liver cancer. For deaths due to collective violence and natural disasters, we used mortality shock regressions. For every cause, we estimated 95% UIs that captured both parameter estimation uncertainty and uncertainty due to model specification where CODEm was used. We constrained cause-specific fractions within every age-sex group to sum to total mortality based on draws from the uncertainty distributions. Findings In 2010, there were 52·8 million deaths globally. At the most aggregate level, communicable, maternal, neonatal, and nutritional causes were 24·9% of deaths worldwide in 2010, down from 15·9 million (34·1%) of 46·5 million in 1990. This decrease was largely due to decreases in mortality from diarrhoeal disease (from 2·5 to 1·4 million), lower respiratory infections (from 3·4 to 2·8 million), neonatal disorders (from 3·1 to 2·2 million), measles (from 0·63 to 0·13 million), and tetanus (from 0·27 to 0·06 million). Deaths from HIV/AIDS increased from 0·30 million in 1990 to 1·5 million in 2010, reaching a peak of 1·7 million in 2006. Malaria mortality also rose by an estimated 19·9% since 1990 to 1·17 million deaths in 2010. Tuberculosis killed 1·2 million people in 2010. Deaths from non-communicable diseases rose by just under 8 million between 1990 and 2010, accounting for two of every three deaths (34·5 million) worldwide by 2010. 8 million people died from cancer in 2010, 38% more than two decades ago; of these, 1·5 million (19%) were from trachea, bronchus, and lung cancer. Ischaemic heart disease and stroke collectively killed 12·9 million people in 2010, or one in four deaths worldwide, compared with one in five in 1990; 1·3 million deaths were due to diabetes, twice as many as in 1990. The fraction of global deaths due to injuries (5·1 million deaths) was marginally higher in 2010 (9·6%) compared with two decades earlier (8·8%). This was driven by a 46% rise in deaths worldwide due to road traffic accidents (1·3 million in 2010) and a rise in deaths from falls. Ischaemic heart disease, stroke, chronic obstructive pulmonary disease (COPD), lower respiratory infections, lung cancer, and HIV/AIDS were the leading causes of death in 2010. Ischaemic heart disease, lower respiratory infections, stroke, diarrhoeal disease, malaria, and HIV/AIDS were the leading causes of years of life lost due to premature mortality (YLLs) in 2010, similar to what was estimated for 1990, except for HIV/AIDS and preterm birth complications. YLLs from lower respiratory infections and diarrhoea decreased by 45–54% since 1990; ischaemic heart disease and stroke YLLs increased by 17–28%. Regional variations in leading causes of death were substantial. Communicable, maternal, neonatal, and nutritional causes still accounted for 76% of premature mortality in sub-Saharan Africa in 2010. Age standardised death rates from some key disorders rose (HIV/AIDS, Alzheimer's disease, diabetes mellitus, and chronic kidney disease in particular), but for most diseases, death rates fell in the past two decades; including major vascular diseases, COPD, most forms of cancer, liver cirrhosis, and maternal disorders. For other conditions, notably malaria, prostate cancer, and injuries, little change was noted. Interpretation Population growth, increased average age of the world's population, and largely decreasing age-specific, sex-specific, and cause-specific death rates combine to drive a broad shift from communicable, maternal, neonatal, and nutritional causes towards non-communicable diseases. Nevertheless, communicable, maternal, neonatal, and nutritional causes remain the dominant causes of YLLs in sub-Saharan Africa. Overlaid on this general pattern of the epidemiological transition, marked regional variation exists in many causes, such as interpersonal violence, suicide, liver cancer, diabetes, cirrhosis, Chagas disease, African trypanosomiasis, melanoma, and others. Regional heterogeneity highlights the importance of sound epidemiological assessments of the causes of death on a regular basis. Funding Bill & Melinda Gates Foundation.

10,602 citations

Journal ArticleDOI
Stephen S Lim1, Theo Vos, Abraham D. Flaxman1, Goodarz Danaei2  +207 moreInstitutions (92)
Abstract: Methods We 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 eff ects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. W e estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specifi c deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden. Findings In 2010, the three leading risk factors for global disease burden were high blood pressure (7·0% [95% uncertainty interval 6·2–7·7] of global DALYs), tobacco smoking including second-hand smoke (6·3% [5·5–7·0]), and alcohol use (5·5% [5·0–5·9]). In 1990, the leading risks were childhood underweight (7·9% [6·8–9·4]), household air pollution from solid fuels (HAP; 7·0% [5·6–8·3]), and tobacco smoking including second-hand smoke (6·1% [5·4–6·8]). Dietary risk factors and physical inactivity collectively accounted for 10·0% (95% UI 9·2–10·8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily aff ect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient defi ciencies, fell in rank between 1990 and 2010, with unimproved water

8,301 citations

Journal ArticleDOI
Marie Ng1, Tom P Fleming1, Margaret Robinson1, Blake Thomson1, Nicholas Graetz1, Christopher Margono1, Erin C Mullany1, Stan Biryukov1, Cristiana Abbafati2, Semaw Ferede Abera3, Jerry Abraham4, Niveen M E Abu-Rmeileh, Tom Achoki1, Fadia AlBuhairan5, Zewdie Aderaw Alemu6, Rafael Alfonso1, Mohammed K. Ali7, Raghib Ali8, Nelson Alvis Guzmán9, Walid Ammar, Palwasha Anwari10, Amitava Banerjee11, Simón Barquera, Sanjay Basu12, Derrick A Bennett8, Zulfiqar A Bhutta13, Jed D. Blore14, N Cabral, Ismael Ricardo Campos Nonato, Jung-Chen Chang15, Rajiv Chowdhury16, Karen J. Courville, Michael H. Criqui17, David K. Cundiff, Kaustubh Dabhadkar7, Lalit Dandona18, Lalit Dandona1, Adrian Davis19, Anand Dayama7, Samath D Dharmaratne20, Eric L. Ding21, Adnan M. Durrani22, Alireza Esteghamati23, Farshad Farzadfar23, Derek F J Fay19, Valery L. Feigin24, Abraham D. Flaxman1, Mohammad H. Forouzanfar1, Atsushi Goto, Mark A. Green25, Rajeev Gupta, Nima Hafezi-Nejad23, Graeme J. Hankey26, Heather Harewood, Rasmus Havmoeller27, Simon I. Hay8, Lucia Hernandez, Abdullatif Husseini28, Bulat Idrisov29, Nayu Ikeda, Farhad Islami30, Eiman Jahangir31, Simerjot K. Jassal17, Sun Ha Jee32, Mona Jeffreys33, Jost B. Jonas34, Edmond K. Kabagambe35, Shams Eldin Ali Hassan Khalifa, Andre Pascal Kengne36, Yousef Khader37, Young-Ho Khang38, Daniel Kim39, Ruth W Kimokoti40, Jonas Minet Kinge41, Yoshihiro Kokubo, Soewarta Kosen, Gene F. Kwan42, Taavi Lai, Mall Leinsalu22, Yichong Li, Xiaofeng Liang43, Shiwei Liu43, Giancarlo Logroscino44, Paulo A. Lotufo45, Yuan Qiang Lu21, Jixiang Ma43, Nana Kwaku Mainoo, George A. Mensah22, Tony R. Merriman46, Ali H. Mokdad1, Joanna Moschandreas47, Mohsen Naghavi1, Aliya Naheed48, Devina Nand, K.M. Venkat Narayan7, Erica Leigh Nelson1, Marian L. Neuhouser49, Muhammad Imran Nisar13, Takayoshi Ohkubo50, Samuel Oti, Andrea Pedroza, Dorairaj Prabhakaran, Nobhojit Roy51, Uchechukwu K.A. Sampson35, Hyeyoung Seo, Sadaf G. Sepanlou23, Kenji Shibuya52, Rahman Shiri53, Ivy Shiue54, Gitanjali M Singh21, Jasvinder A. Singh55, Vegard Skirbekk41, Nicolas J. C. Stapelberg56, Lela Sturua57, Bryan L. Sykes58, Martin Tobias1, Bach Xuan Tran59, Leonardo Trasande60, Hideaki Toyoshima, Steven van de Vijver, Tommi Vasankari, J. Lennert Veerman61, Gustavo Velasquez-Melendez62, Vasiliy Victorovich Vlassov63, Stein Emil Vollset41, Stein Emil Vollset64, Theo Vos1, Claire L. Wang65, Xiao Rong Wang66, Elisabete Weiderpass, Andrea Werdecker, Jonathan L. Wright1, Y Claire Yang67, Hiroshi Yatsuya68, Jihyun Yoon, Seok Jun Yoon69, Yong Zhao70, Maigeng Zhou, Shankuan Zhu71, Alan D. Lopez14, Christopher J L Murray1, Emmanuela Gakidou1 
University of Washington1, Sapienza University of Rome2, Mekelle University3, University of Texas at San Antonio4, King Saud bin Abdulaziz University for Health Sciences5, Debre markos University6, Emory University7, University of Oxford8, University of Cartagena9, United Nations Population Fund10, University of Birmingham11, Stanford University12, Aga Khan University13, University of Melbourne14, National Taiwan University15, University of Cambridge16, University of California, San Diego17, Public Health Foundation of India18, Public Health England19, University of Peradeniya20, Harvard University21, National Institutes of Health22, Tehran University of Medical Sciences23, Auckland University of Technology24, University of Sheffield25, University of Western Australia26, Karolinska Institutet27, Birzeit University28, Brandeis University29, American Cancer Society30, Ochsner Medical Center31, Yonsei University32, University of Bristol33, Heidelberg University34, Vanderbilt University35, South African Medical Research Council36, Jordan University of Science and Technology37, New Generation University College38, Northeastern University39, Simmons College40, Norwegian Institute of Public Health41, Boston University42, Chinese Center for Disease Control and Prevention43, University of Bari44, University of São Paulo45, University of Otago46, University of Crete47, International Centre for Diarrhoeal Disease Research, Bangladesh48, Fred Hutchinson Cancer Research Center49, Teikyo University50, Bhabha Atomic Research Centre51, University of Tokyo52, Finnish Institute of Occupational Health53, Heriot-Watt University54, University of Alabama at Birmingham55, Griffith University56, National Center for Disease Control and Public Health57, University of California, Irvine58, Johns Hopkins University59, New York University60, University of Queensland61, Universidade Federal de Minas Gerais62, National Research University – Higher School of Economics63, University of Bergen64, Columbia University65, Shandong University66, University of North Carolina at Chapel Hill67, Fujita Health University68, Korea University69, Chongqing Medical University70, Zhejiang University71
TL;DR: The global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013 is estimated using a spatiotemporal Gaussian process regression model to estimate prevalence with 95% uncertainty intervals (UIs).
Abstract: Summary Background In 2010, overweight and obesity were estimated to cause 3·4 million deaths, 3·9% of years of life lost, and 3·8% of disability-adjusted life-years (DALYs) worldwide. The rise in obesity has led to widespread calls for regular monitoring of changes in overweight and obesity prevalence in all populations. Comparable, up-to-date information about levels and trends is essential to quantify population health effects and to prompt decision makers to prioritise action. We estimate the global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013. Methods We systematically identified surveys, reports, and published studies (n=1769) that included data for height and weight, both through physical measurements and self-reports. We used mixed effects linear regression to correct for bias in self-reports. We obtained data for prevalence of obesity and overweight by age, sex, country, and year (n=19 244) with a spatiotemporal Gaussian process regression model to estimate prevalence with 95% uncertainty intervals (UIs). Findings Worldwide, the proportion of adults with a body-mass index (BMI) of 25 kg/m 2 or greater increased between 1980 and 2013 from 28·8% (95% UI 28·4–29·3) to 36·9% (36·3–37·4) in men, and from 29·8% (29·3–30·2) to 38·0% (37·5–38·5) in women. Prevalence has increased substantially in children and adolescents in developed countries; 23·8% (22·9–24·7) of boys and 22·6% (21·7–23·6) of girls were overweight or obese in 2013. The prevalence of overweight and obesity has also increased in children and adolescents in developing countries, from 8·1% (7·7–8·6) to 12·9% (12·3–13·5) in 2013 for boys and from 8·4% (8·1–8·8) to 13·4% (13·0–13·9) in girls. In adults, estimated prevalence of obesity exceeded 50% in men in Tonga and in women in Kuwait, Kiribati, Federated States of Micronesia, Libya, Qatar, Tonga, and Samoa. Since 2006, the increase in adult obesity in developed countries has slowed down. Interpretation Because of the established health risks and substantial increases in prevalence, obesity has become a major global health challenge. Not only is obesity increasing, but no national success stories have been reported in the past 33 years. Urgent global action and leadership is needed to help countries to more effectively intervene. Funding Bill & Melinda Gates Foundation.

7,968 citations

Journal ArticleDOI
Abstract: Summary The use of both linear and generalized linear mixed-effects models (LMMs and GLMMs) has become popular not only in social and medical sciences, but also in biological sciences, especially in the field of ecology and evolution. Information criteria, such as Akaike Information Criterion (AIC), are usually presented as model comparison tools for mixed-effects models. The presentation of ‘variance explained’ (R2) as a relevant summarizing statistic of mixed-effects models, however, is rare, even though R2 is routinely reported for linear models (LMs) and also generalized linear models (GLMs). R2 has the extremely useful property of providing an absolute value for the goodness-of-fit of a model, which cannot be given by the information criteria. As a summary statistic that describes the amount of variance explained, R2 can also be a quantity of biological interest. One reason for the under-appreciation of R2 for mixed-effects models lies in the fact that R2 can be defined in a number of ways. Furthermore, most definitions of R2 for mixed-effects have theoretical problems (e.g. decreased or negative R2 values in larger models) and/or their use is hindered by practical difficulties (e.g. implementation). Here, we make a case for the importance of reporting R2 for mixed-effects models. We first provide the common definitions of R2 for LMs and GLMs and discuss the key problems associated with calculating R2 for mixed-effects models. We then recommend a general and simple method for calculating two types of R2 (marginal and conditional R2) for both LMMs and GLMMs, which are less susceptible to common problems. This method is illustrated by examples and can be widely employed by researchers in any fields of research, regardless of software packages used for fitting mixed-effects models. The proposed method has the potential to facilitate the presentation of R2 for a wide range of circumstances.

6,363 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.
Abstract: Summary Background Measuring disease and injury burden in populations requires a composite metric that captures both premature mortality and the prevalence and severity of ill-health. The 1990 Global Burden of Disease study proposed disability-adjusted life years (DALYs) to measure disease burden. No comprehensive update of disease burden worldwide incorporating a systematic reassessment of disease and injury-specific epidemiology has been done since the 1990 study. We aimed to calculate disease burden worldwide and for 21 regions for 1990, 2005, and 2010 with methods to enable meaningful comparisons over time. Methods We calculated DALYs as the sum of years of life lost (YLLs) and years lived with disability (YLDs). DALYs were calculated for 291 causes, 20 age groups, both sexes, and for 187 countries, and aggregated to regional and global estimates of disease burden for three points in time with strictly comparable definitions and methods. YLLs were calculated from age-sex-country-time-specific estimates of mortality by cause, with death by standardised lost life expectancy at each age. YLDs were calculated as prevalence of 1160 disabling sequelae, by age, sex, and cause, and weighted by new disability weights for each health state. Neither YLLs nor YLDs were age-weighted or discounted. Uncertainty around cause-specific DALYs was calculated incorporating uncertainty in levels of all-cause mortality, cause-specific mortality, prevalence, and disability weights. Findings Global DALYs remained stable from 1990 (2·503 billion) to 2010 (2·490 billion). Crude DALYs per 1000 decreased by 23% (472 per 1000 to 361 per 1000). An important shift has occurred in DALY composition with the contribution of deaths and disability among children (younger than 5 years of age) declining from 41% of global DALYs in 1990 to 25% in 2010. YLLs typically account for about half of disease burden in more developed regions (high-income Asia Pacific, western Europe, high-income North America, and Australasia), rising to over 80% of DALYs in sub-Saharan Africa. In 1990, 47% of DALYs worldwide were from communicable, maternal, neonatal, and nutritional disorders, 43% from non-communicable diseases, and 10% from injuries. By 2010, this had shifted to 35%, 54%, and 11%, respectively. Ischaemic heart disease was the leading cause of DALYs worldwide in 2010 (up from fourth rank in 1990, increasing by 29%), followed by lower respiratory infections (top rank in 1990; 44% decline in DALYs), stroke (fifth in 1990; 19% increase), diarrhoeal diseases (second in 1990; 51% decrease), and HIV/AIDS (33rd in 1990; 351% increase). Major depressive disorder increased from 15th to 11th rank (37% increase) and road injury from 12th to 10th rank (34% increase). Substantial heterogeneity exists in rankings of leading causes of disease burden among regions. Interpretation Global disease burden has continued to shift away from communicable to non-communicable diseases and from premature death to years lived with disability. In sub-Saharan Africa, however, many communicable, maternal, neonatal, and nutritional disorders remain the dominant causes of disease burden. The rising burden from mental and behavioural disorders, musculoskeletal disorders, and diabetes will impose new challenges on health systems. Regional heterogeneity highlights the importance of understanding local burden of disease and setting goals and targets for the post-2015 agenda taking such patterns into account. Because of improved definitions, methods, and data, these results for 1990 and 2010 supersede all previously published Global Burden of Disease results. Funding Bill & Melinda Gates Foundation.

6,252 citations


Authors

Showing all 21668 results

NameH-indexPapersCitations
David Miller2032573204840
Terrie E. Moffitt182594150609
Tien Yin Wong1601880131830
Grant W. Montgomery157926108118
Ichiro Kawachi149121690282
David M. Fergusson12747455992
Carlos A. Camargo125128369143
Philip H Butler12597071999
Francis V. Chisari12332254772
Michael P. Murphy12060153338
Guy S. Salvesen11633775598
Mitch Dowsett11447862453
Valerie Beral11447153729
Gordon Dougan11471555037
Christopher A. Hunter11363352559
Network Information
Related Institutions (5)
University of Melbourne

174.8K papers, 6.3M citations

93% related

University of Queensland

155.7K papers, 5.7M citations

93% related

University of Sydney

187.3K papers, 6.1M citations

92% related

Utrecht University

139.3K papers, 6.2M citations

90% related

University College London

210.6K papers, 9.8M citations

90% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202244
20213,631
20203,481
20192,973
20182,844
20172,932