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Middeldorp, C. M., Mahajan, A., Horikoshi, M., Robertson, N. R., Beaumont, R. N., Bradfield, J. P., . . . Tiemeier, H.-N. (2019). The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia: design, results and future prospects. European Journal of Epidemiology, 34(3), 279-300
Open this publication in new window or tab >>The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia: design, results and future prospects
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2019 (English)In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 34, no 3, p. 279-300Article in journal (Refereed) Published
Abstract [en]

The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.

Keywords
Genetics, Consortium, Childhood traits and disorders, Longitudinal
National Category
Health Sciences
Identifiers
urn:nbn:se:miun:diva-36187 (URN)10.1007/s10654-019-00502-9 (DOI)000463834200009 ()30887376 (PubMedID)
Available from: 2019-05-22 Created: 2019-05-22 Last updated: 2019-05-22Bibliographically approved
Nordström, T., Hurtig, T., Rodriguez, A., Savolainen, J., Rautio, A., Moilanen, I., . . . Ebeling, H. (2017). Different Risk Factors Between Disruptive Behavior Disorders and ADHD in Northern Finland Birth Cohort 1986. Journal of Attention Disorders, 21(11), 904-912
Open this publication in new window or tab >>Different Risk Factors Between Disruptive Behavior Disorders and ADHD in Northern Finland Birth Cohort 1986
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2017 (English)In: Journal of Attention Disorders, ISSN 1087-0547, E-ISSN 1557-1246, Vol. 21, no 11, p. 904-912Article in journal (Refereed) Published
Abstract [en]

Objective: To examine different risk factors between disruptive behavior disorders (DBD) and ADHD or combined DBD and ADHD. Method: The study population was derived from the Northern Finland Birth Cohort 1986. Psychiatric diagnoses were defined from the Schedule for Affective Disorders and Schizophrenia for School-Age Children–Present and Lifetime Version (K-SADS-PL) interview. The study sample was divided into four groups—people with DBD (n = 44), with ADHD (n = 91), with both (n = 72), and without either (n = 250)—to evaluate the different risk factors behind these disorders. Results: After adjusting with possible confounding factors, female gender and paternal admittance to inpatient psychiatric care increased the odds that an adolescent was having DBD. Childhood hyperactivity symptoms increased the odds of having ADHD and childhood hyperactivity symptoms and scholastic impairment increased the odds of having both disorders. Conclusion: Our study indicates DBD and ADHD have clearly different risk factors, and the impact of the paternal factors on DBD should be noted more than has been before.

Keywords
disruptive behavioral disorder, ADHD, conduct disorder, oppositional defiant disorder, comorbidity
National Category
Medical and Health Sciences Psychology
Identifiers
urn:nbn:se:miun:diva-23358 (URN)10.1177/1087054714538654 (DOI)000407802400003 ()25001369 (PubMedID)2-s2.0-85027549766 (Scopus ID)
Note

First Published July 7, 2014

Available from: 2014-11-06 Created: 2014-11-06 Last updated: 2019-05-28Bibliographically approved
Pappa, I., St Pourcain, B., Benke, K., Cavadino, A., Hakulinen, C., Nivard, M. G., . . . Tiemeier, H. (2016). A genome-wide approach to children's aggressive behavior: The EAGLE consortium.. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 171(5), 562-572
Open this publication in new window or tab >>A genome-wide approach to children's aggressive behavior: The EAGLE consortium.
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2016 (English)In: American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, ISSN 1552-4841, E-ISSN 1552-485X, Vol. 171, no 5, p. 562-572Article in journal (Refereed) Published
Abstract [en]

Individual differences in aggressive behavior emerge in early childhood and predict persisting behavioral problems and disorders. Studies of antisocial and severe aggression in adulthood indicate substantial underlying biology. However, little attention has been given to genome-wide approaches of aggressive behavior in children. We analyzed data from nine population-based studies and assessed aggressive behavior using well-validated parent-reported questionnaires. This is the largest sample exploring children's aggressive behavior to date (N = 18,988), with measures in two developmental stages (N = 15,668 early childhood and N = 16,311 middle childhood/early adolescence). First, we estimated the additive genetic variance of children's aggressive behavior based on genome-wide SNP information, using genome-wide complex trait analysis (GCTA). Second, genetic associations within each study were assessed using a quasi-Poisson regression approach, capturing the highly right-skewed distribution of aggressive behavior. Third, we performed meta-analyses of genome-wide associations for both the total age-mixed sample and the two developmental stages. Finally, we performed a gene-based test using the summary statistics of the total sample. GCTA quantified variance tagged by common SNPs (10-54%). The meta-analysis of the total sample identified one region in chromosome 2 (2p12) at near genome-wide significance (top SNP rs11126630, P = 5.30 × 10(-8) ). The separate meta-analyses of the two developmental stages revealed suggestive evidence of association at the same locus. The gene-based analysis indicated association of variation within AVPR1A with aggressive behavior. We conclude that common variants at 2p12 show suggestive evidence for association with childhood aggression. Replication of these initial findings is needed, and further studies should clarify its biological meaning. © 2015 Wiley Periodicals, Inc.

National Category
Psychology Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:miun:diva-27327 (URN)10.1002/ajmg.b.32333 (DOI)26087016 (PubMedID)
Available from: 2016-03-23 Created: 2016-03-23 Last updated: 2017-12-13Bibliographically approved
Kyu, H. H., Pinho, C., Wagner, J. A., Brown, J. C., Bertozzi-Villa, A., Charlson, F. J., . . . Vos, T. (2016). Global and National Burden of Diseases and Injuries Among Children and Adolescents Between 1990 and 2013: Findings From the Global Burden of Disease 2013 Study.. JAMA pediatrics, 170(3), 267-287
Open this publication in new window or tab >>Global and National Burden of Diseases and Injuries Among Children and Adolescents Between 1990 and 2013: Findings From the Global Burden of Disease 2013 Study.
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2016 (English)In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 3, p. 267-287Article in journal (Refereed) Published
Abstract [en]

IMPORTANCE: The literature focuses on mortality among children younger than 5 years. Comparable information on nonfatal health outcomes among these children and the fatal and nonfatal burden of diseases and injuries among older children and adolescents is scarce.

OBJECTIVE: To determine levels and trends in the fatal and nonfatal burden of diseases and injuries among younger children (aged <5 years), older children (aged 5-9 years), and adolescents (aged 10-19 years) between 1990 and 2013 in 188 countries from the Global Burden of Disease (GBD) 2013 study.

EVIDENCE REVIEW: Data from vital registration, verbal autopsy studies, maternal and child death surveillance, and other sources covering 14 244 site-years (ie, years of cause of death data by geography) from 1980 through 2013 were used to estimate cause-specific mortality. Data from 35 620 epidemiological sources were used to estimate the prevalence of the diseases and sequelae in the GBD 2013 study. Cause-specific mortality for most causes was estimated using the Cause of Death Ensemble Model strategy. For some infectious diseases (eg, HIV infection/AIDS, measles, hepatitis B) where the disease process is complex or the cause of death data were insufficient or unavailable, we used natural history models. For most nonfatal health outcomes, DisMod-MR 2.0, a Bayesian metaregression tool, was used to meta-analyze the epidemiological data to generate prevalence estimates.

FINDINGS: Of the 7.7 (95% uncertainty interval [UI], 7.4-8.1) million deaths among children and adolescents globally in 2013, 6.28 million occurred among younger children, 0.48 million among older children, and 0.97 million among adolescents. In 2013, the leading causes of death were lower respiratory tract infections among younger children (905 059 deaths; 95% UI, 810 304-998 125), diarrheal diseases among older children (38 325 deaths; 95% UI, 30 365-47 678), and road injuries among adolescents (115 186 deaths; 95% UI, 105 185-124 870). Iron deficiency anemia was the leading cause of years lived with disability among children and adolescents, affecting 619 (95% UI, 618-621) million in 2013. Large between-country variations exist in mortality from leading causes among children and adolescents. Countries with rapid declines in all-cause mortality between 1990 and 2013 also experienced large declines in most leading causes of death, whereas countries with the slowest declines had stagnant or increasing trends in the leading causes of death. In 2013, Nigeria had a 12% global share of deaths from lower respiratory tract infections and a 38% global share of deaths from malaria. India had 33% of the world's deaths from neonatal encephalopathy. Half of the world's diarrheal deaths among children and adolescents occurred in just 5 countries: India, Democratic Republic of the Congo, Pakistan, Nigeria, and Ethiopia.

CONCLUSIONS AND RELEVANCE: Understanding the levels and trends of the leading causes of death and disability among children and adolescents is critical to guide investment and inform policies. Monitoring these trends over time is also key to understanding where interventions are having an impact. Proven interventions exist to prevent or treat the leading causes of unnecessary death and disability among children and adolescents. The findings presented here show that these are underused and give guidance to policy makers in countries where more attention is needed.

National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:miun:diva-27324 (URN)10.1001/jamapediatrics.2015.4276 (DOI)000372304700018 ()26810619 (PubMedID)2-s2.0-84962415067 (Scopus ID)
Note

Group author: Global Burden of Disease Pediatrics Collaboration

Available from: 2016-03-23 Created: 2016-03-23 Last updated: 2021-01-25Bibliographically approved
Young, S., Absoud, M., Blackburn, C., Branney, P., Colley, B., Farrag, E., . . . Mukherjee, R. (2016). Guidelines for identification and treatment of individuals with attention deficit/hyperactivity disorder and associated fetal alcohol spectrum disorders based upon expert consensus. BMC Psychiatry, 16(1), Article ID 324.
Open this publication in new window or tab >>Guidelines for identification and treatment of individuals with attention deficit/hyperactivity disorder and associated fetal alcohol spectrum disorders based upon expert consensus
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2016 (English)In: BMC Psychiatry, E-ISSN 1471-244X, Vol. 16, no 1, article id 324Article in journal (Refereed) Published
Abstract [en]

Background: The association of attention deficit/hyperactivity disorder (ADHD) and fetal alcohol spectrum disorders (FASD) results in a complex constellation of symptoms that complicates the successful diagnosis and treatment of the affected individual. Current literature lacks formal guidelines, randomized control trials, and evidence-based treatment plans for individuals with ADHD and associated FASD. Therefore, a meeting of professional experts was organized with the aim of producing a consensus on identification and treatment guidelines that will aid clinicians in caring for this unique patient population. Methods: Experts from multiple disciplines in the fields of ADHD and FASD convened in London, United Kingdom, for a meeting hosted by the United Kingdom ADHD Partnership (UKAP; www.UKADHD.com) in June 2015. The meeting provided the opportunity to address the complexities of ADHD and FASD from different perspectives and included presentations, discussions, and group work. The attendees worked towards producing a consensus for a unified approach to ADHD and associated FASD. Results: The authors successfully came to consensus and produced recommended guidelines with specific regards to identification and assessment, interventions and treatments, and multiagency liaisons and care management, highlighting that a lifespan approach to treatment needs to be adopted by all involved. Included in the guidelines are: 1) unique 'red flags', which when identified in the ADHD population can lead to an accurate associated FASD diagnosis, 2) a treatment decision tree, and 3) recommendations for multiagency care management. Conclusions: While clinically useful guidelines were achieved, more research is still needed to contribute to the knowledge base about the diagnosis, treatment, and management of those with ADHD and associated FASD.

Keywords
Attention deficit/hyperactivity disorder (ADHD), Co-morbid or associated FASD, Consensus, Fetal alcohol spectrum disorders (FASD), Interventions, Treatment guidelines
National Category
Psychology
Identifiers
urn:nbn:se:miun:diva-29137 (URN)10.1186/s12888-016-1027-y (DOI)000384343900001 ()2-s2.0-84988499041 (Scopus ID)
Available from: 2016-10-27 Created: 2016-10-27 Last updated: 2024-01-17Bibliographically approved
van der Valk, R. J., Kreiner-Møller, E., Kooijman, M. N., Guxens, M., Stergiakouli, E., Sääf, A., . . . Jaddoe, V. W. (2015). A novel common variant in DCST2 is associated with length in early life and height in adulthood. Human Molecular Genetics, 24(4), 1155-68, Article ID ddu510.
Open this publication in new window or tab >>A novel common variant in DCST2 is associated with length in early life and height in adulthood
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2015 (English)In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 24, no 4, p. 1155-68, article id ddu510Article in journal (Refereed) Published
Abstract [en]

Common genetic variants have been identified for adult height, but not much is known about the genetics of skeletal growth in early life. To identify common genetic variants that influence fetal skeletal growth, we meta-analyzed 22 genome-wide association studies (Stage 1; N = 28 459). We identified seven independent top single nucleotide polymorphisms (SNPs) (P < 1 × 10(-6)) for birth length, of which three were novel and four were in or near loci known to be associated with adult height (LCORL, PTCH1, GPR126 and HMGA2). The three novel SNPs were followed-up in nine replication studies (Stage 2; N = 11 995), with rs905938 in DC-STAMP domain containing 2 (DCST2) genome-wide significantly associated with birth length in a joint analysis (Stages 1 + 2; β = 0.046, SE = 0.008, P = 2.46 × 10(-8), explained variance = 0.05%). Rs905938 was also associated with infant length (N = 28 228; P = 5.54 × 10(-4)) and adult height (N = 127 513; P = 1.45 × 10(-5)). DCST2 is a DC-STAMP-like protein family member and DC-STAMP is an osteoclast cell-fusion regulator. Polygenic scores based on 180 SNPs previously associated with human adult stature explained 0.13% of variance in birth length. The same SNPs explained 2.95% of the variance of infant length. Of the 180 known adult height loci, 11 were genome-wide significantly associated with infant length (SF3B4, LCORL, SPAG17, C6orf173, PTCH1, GDF5, ZNFX1, HHIP, ACAN, HLA locus and HMGA2). This study highlights that common variation in DCST2 influences variation in early growth and adult height.

National Category
Medical Genetics Psychology
Identifiers
urn:nbn:se:miun:diva-24414 (URN)10.1093/hmg/ddu510 (DOI)000350138300021 ()25281659 (PubMedID)2-s2.0-84985023154 (Scopus ID)
Available from: 2015-02-24 Created: 2015-02-24 Last updated: 2018-01-11Bibliographically approved
Newton, J. N., Briggs, A. D., Murray, C. J., Dicker, D., Foreman, K. J., Wang, H., . . . Davis, A. C. (2015). Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013. The Lancet, 386(10010), 2257-2274
Open this publication in new window or tab >>Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013
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2015 (English)In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 386, no 10010, p. 2257-2274Article in journal (Refereed) Published
Abstract [en]

Background In the Global Burden of Disease Study 2013 (GBD 2013), knowledge about health and its determinants has been integrated into a comparable framework to inform health policy. Outputs of this analysis are relevant to current policy questions in England and elsewhere, particularly on health inequalities. We use GBD 2013 data on mortality and causes of death, and disease and injury incidence and prevalence to analyse the burden of disease and injury in England as a whole, in English regions, and within each English region by deprivation quintile. We also assess disease and injury burden in England attributable to potentially preventable risk factors. England and the English regions are compared with the remaining constituent countries of the UK and with comparable countries in the European Union (EU) and beyond. Methods We extracted data from the GBD 2013 to compare mortality, causes of death, years of life lost (YLLs), years lived with a disability (YLDs), and disability-adjusted life-years (DALYs) in England, the UK, and 18 other countries (the first 15 EU members [apart from the UK] and Australia, Canada, Norway, and the USA [EU15+]). We extended elements of the analysis to English regions, and subregional areas defined by deprivation quintile (deprivation areas). We used data split by the nine English regions (corresponding to the European boundaries of the Nomenclature for Territorial Statistics level 1 [NUTS 1] regions), and by quintile groups within each English region according to deprivation, thereby making 45 regional deprivation areas. Deprivation quintiles were defined by area of residence ranked at national level by Index of Multiple Deprivation score, 2010. Burden due to various risk factors is described for England using new GBD methodology to estimate independent and overlapping attributable risk for five tiers of behavioural, metabolic, and environmental risk factors. We present results for 306 causes and 2337 sequelae, and 79 risks or risk clusters. Findings Between 1990 and 2013, life expectancy from birth in England increased by 5·4 years (95% uncertainty interval 5·0-5·8) from 75·9 years (75·9-76·0) to 81·3 years (80·9-81·7); gains were greater for men than for women. Rates of age-standardised YLLs reduced by 41·1% (38·3-43·6), whereas DALYs were reduced by 23·8% (20·9-27·1), and YLDs by 1·4% (0·1-2·8). For these measures, England ranked better than the UK and the EU15+ means. Between 1990 and 2013, the range in life expectancy among 45 regional deprivation areas remained 8·2 years for men and decreased from 7·2 years in 1990 to 6·9 years in 2013 for women. In 2013, the leading cause of YLLs was ischaemic heart disease, and the leading cause of DALYs was low back and neck pain. Known risk factors accounted for 39·6% (37·7-41·7) of DALYs; leading behavioural risk factors were suboptimal diet (10·8% [9·1-12·7]) and tobacco (10·7% [9·4-12·0]). Interpretation Health in England is improving although substantial opportunities exist for further reductions in the burden of preventable disease. The gap in mortality rates between men and women has reduced, but marked health inequalities between the least deprived and most deprived areas remain. Declines in mortality have not been matched by similar declines in morbidity, resulting in people living longer with diseases. Health policies must therefore address the causes of ill health as well as those of premature mortality. Systematic action locally and nationally is needed to reduce risk exposures, support healthy behaviours, alleviate the severity of chronic disabling disorders, and mitigate the effects of socioeconomic deprivation. Funding Bill & Melinda Gates Foundation and Public Health England. © 2015 Newton et al. Open Access article distributed under the terms of CC BY.

Place, publisher, year, edition, pages
Lancet Publishing Group, 2015
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:miun:diva-26706 (URN)10.1016/S0140-6736(15)00195-6 (DOI)000365993200029 ()2-s2.0-84949529269 (Scopus ID)
Note

Export Date: 21 December 2015 CODEN: LANCA Correspondence Address: Newton, J.N.; Public Health England, Wellington HouseUnited Kingdom; email: john.newton@phe.gov.uk References: Murray C.J.L., Richards M.A., Newton J.N., UK health performance: Findings of the Global Burden of Disease Study 2010 (2013) Lancet, 381, pp. 997-1020; Greer S.L., Devolution and divergence in UK health policies (2008) BMJ, 337, p. a2616; England N.H.S., (2014) Five Year Forward View, , http://www.england.nhs.uk/ourwork/futurenhs/, (accessed Aug 24, 2015); Naghavi M., Wang H., Lozano R., Global, regional and national levels of age-specific mortality and 240 causes of death, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013 (2015) Lancet, 385, pp. 117-171; Global, regional, and national incidence, prevalence, and years lived with disabilities for 301 acute and chronic diseases and injuries for 188 countries, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013 (2015) Lancet, 386, pp. 743-800; Global, regional, and national comparative risk assessment of 76 behavioural, environmental, occupational, and metabolic risks or clusters of risks in 188 countries 1990-2013: A systematic analysis for the Global Burden of Disease study 2013 (2015) Lancet, , http://dx.doi.org/10.1016/S0140-6736(15)00128-2, published online Sept 11; Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990-2013: Quantifying the epidemiological transition (2015) Lancet, , http://dx.doi.org/10.1016/S0140-6736(15)61340-X, published online Aug 27; Vos T., Flaxman A.D., Naghavi M., 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 (2012) Lancet, 380, pp. 2163-2196; Murray C.J.L., Ezzati M., Flaxman A.D., GBD 2010: Design, definitions, and metrics (2012) Lancet, 380, pp. 2063-2066; Statistical Bulletin. 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Available from: 2015-12-21 Created: 2015-12-21 Last updated: 2020-11-03Bibliographically approved
Rodriguez, A., Wang, Y., Khan, A. A., Gissler, M., Cartwright, R. & Jarvelin, M.-R. (2015). Exposure to antenatal corticosteroid therapy is associated with reduced size at birth: Evidence from Finnish Medical Birth Register of 278,508 births. Paper presented at 45th Annual Meeting of the International-Society-of-Psychoneuroendocrinology (ISPNE) on Stress and the Brain - From Fertility to Senility, SEP 08-11, 2015, Edinburgh, SCOTLAND. Psychoneuroendocrinology, 61, 37-37
Open this publication in new window or tab >>Exposure to antenatal corticosteroid therapy is associated with reduced size at birth: Evidence from Finnish Medical Birth Register of 278,508 births
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2015 (English)In: Psychoneuroendocrinology, ISSN 0306-4530, E-ISSN 1873-3360, Vol. 61, p. 37-37Article in journal, Meeting abstract (Refereed) Published
National Category
Pediatrics
Identifiers
urn:nbn:se:miun:diva-25946 (URN)10.1016/j.psyneuen.2015.07.489 (DOI)000360250400105 ()
Conference
45th Annual Meeting of the International-Society-of-Psychoneuroendocrinology (ISPNE) on Stress and the Brain - From Fertility to Senility, SEP 08-11, 2015, Edinburgh, SCOTLAND
Available from: 2015-09-23 Created: 2015-09-23 Last updated: 2017-12-01Bibliographically approved
Rodriguez, A. (2015). Global, regional, and national age–sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. The Lancet, 385(9963), 117-171
Open this publication in new window or tab >>Global, regional, and national age–sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013
2015 (English)In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 385, no 9963, p. 117-171Article in journal (Refereed) Published
Abstract [en]

Background

Up-to-date evidence on levels and trends for age-sex-specific all-cause and cause-specific mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries.

Methods

We estimated age-sex-specific all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specific causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-year group to sum to all-cause mortality based on draws from the uncertainty distributions.

Findings

Global life expectancy for both sexes increased from 65·3 years (UI 65·0–65·6) in 1990, to 71·5 years (UI 71·0–71·9) in 2013, while the number of deaths increased from 47·5 million (UI 46·8–48·2) to 54·9 million (UI 53·6–56·3) over the same interval. Global progress masked variation by age and sex: for children, average absolute differences between countries decreased but relative differences increased. For women aged 25–39 years and older than 75 years and for men aged 20–49 years and 65 years and older, both absolute and relative differences increased. Decomposition of global and regional life expectancy showed the prominent role of reductions in age-standardised death rates for cardiovascular diseases and cancers in high-income regions, and reductions in child deaths from diarrhoea, lower respiratory infections, and neonatal causes in low-income regions. HIV/AIDS reduced life expectancy in southern sub-Saharan Africa. For most communicable causes of death both numbers of deaths and age-standardised death rates fell whereas for most non-communicable causes, demographic shifts have increased numbers of deaths but decreased age-standardised death rates. Global deaths from injury increased by 10·7%, from 4·3 million deaths in 1990 to 4·8 million in 2013; but age-standardised rates declined over the same period by 21%. For some causes of more than 100 000 deaths per year in 2013, age-standardised death rates increased between 1990 and 2013, including HIV/AIDS, pancreatic cancer, atrial fibrillation and flutter, drug use disorders, diabetes, chronic kidney disease, and sickle-cell anaemias. Diarrhoeal diseases, lower respiratory infections, neonatal causes, and malaria are still in the top five causes of death in children younger than 5 years. The most important pathogens are rotavirus for diarrhoea and pneumococcus for lower respiratory infections. Country-specific probabilities of death over three phases of life were substantially varied between and within regions.

Interpretation

For most countries, the general pattern of reductions in age-sex specific mortality has been associated with a progressive shift towards a larger share of the remaining deaths caused by non-communicable disease and injuries. Assessing epidemiological convergence across countries depends on whether an absolute or relative measure of inequality is used. Nevertheless, age-standardised death rates for seven substantial causes are increasing, suggesting the potential for reversals in some countries. Important gaps exist in the empirical data for cause of death estimates for some countries; for example, no national data for India are available for the past decade.

Funding

Bill & Melinda Gates Foundation.

National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:miun:diva-24242 (URN)10.1016/S0140-6736(14)61682-2 (DOI)
Available from: 2015-01-28 Created: 2015-01-28 Last updated: 2020-10-07Bibliographically approved
Forouzanfar, M. H., Alexander, L., Anderson, H. R., Bachman, V. F., Biryukov, S., Brauer, M., . . . Murray, C. J. (2015). Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.. The Lancet, 386(10010), 2287-2323
Open this publication in new window or tab >>Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.
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2015 (English)In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 386, no 10010, p. 2287-2323Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution.

METHODS: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian meta-regression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol.

FINDINGS: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa.

INTERPRETATION: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks.

FUNDING: Bill & Melinda Gates Foundation.

National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:miun:diva-27325 (URN)10.1016/S0140-6736(15)00128-2 (DOI)000365993200031 ()26364544 (PubMedID)2-s2.0-85049491557 (Scopus ID)
Available from: 2016-03-23 Created: 2016-03-23 Last updated: 2020-08-05Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-1209-8802

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