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Coresh, J., Heerspink, H. J., Sang, Y., Matsushita, K., Ärnlöv, J., Astor, B. C., . . . Gansevoort, R. T. (2019). Change in albuminuria and subsequent risk of end-stage kidney disease: an individual participant-level consortium meta-analysis of observational studies.. The Lancet Diabetes and Endocrinology, 7(2), 115-127
Open this publication in new window or tab >>Change in albuminuria and subsequent risk of end-stage kidney disease: an individual participant-level consortium meta-analysis of observational studies.
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2019 (English)In: The Lancet Diabetes and Endocrinology, ISSN 2213-8587, E-ISSN 2213-8595, Vol. 7, no 2, p. 115-127Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Change in albuminuria as a surrogate endpoint for progression of chronic kidney disease is strongly supported by biological plausibility, but empirical evidence to support its validity in epidemiological studies is lacking. We aimed to assess the consistency of the association between change in albuminuria and risk of end-stage kidney disease in a large individual participant-level meta-analysis of observational studies.

METHODS: In this meta-analysis, we collected individual-level data from eligible cohorts in the Chronic Kidney Disease Prognosis Consortium (CKD-PC) with data on serum creatinine and change in albuminuria and more than 50 events on outcomes of interest. Cohort data were eligible if participants were aged 18 years or older, they had a repeated measure of albuminuria during an elapsed period of 8 months to 4 years, subsequent end-stage kidney disease or mortality follow-up data, and the cohort was active during this consortium phase. We extracted participant-level data and quantified percentage change in albuminuria, measured as change in urine albumin-to-creatinine ratio (ACR) or urine protein-to-creatinine ratio (PCR), during baseline periods of 1, 2, and 3 years. Our primary outcome of interest was development of end-stage kidney disease after a baseline period of 2 years. We defined an end-stage kidney disease event as initiation of kidney replacement therapy. We quantified associations of percentage change in albuminuria with subsequent end-stage kidney disease using Cox regression in each cohort, followed by random-effects meta-analysis. We further adjusted for regression dilution to account for imprecision in the estimation of albuminuria at the participant level. We did multiple subgroup analyses, and also repeated our analyses using participant-level data from 14 clinical trials, including nine clinical trials not in CKD-PC.

FINDINGS: Between July, 2015, and June, 2018, we transferred and analysed data from 28 cohorts in the CKD-PC, which included 693 816 individuals (557 583 [80%] with diabetes). Data for 675 904 individuals and 7461 end-stage kidney disease events were available for our primary outcome analysis. Change in ACR was consistently associated with subsequent risk of end-stage kidney disease. The adjusted hazard ratio (HR) for end-stage kidney disease after a 30% decrease in ACR during a baseline period of 2 years was 0·83 (95% CI 0·74-0·94), decreasing to 0·78 (0·66-0·92) after further adjustment for regression dilution. Adjusted HRs were fairly consistent across cohorts and subgroups (ie, estimated glomerular filtration rate, diabetes, and sex), but the association was somewhat stronger among participants with higher baseline ACR than among those with lower baseline ACR (pinteraction<0·0001). In individuals with baseline ACR of 300 mg/g or higher, a 30% decrease in ACR over 2 years was estimated to confer a more than 1% absolute reduction in 10-year risk of end-stage kidney disease, even at early stages of chronic kidney disease. Results were generally similar when we used change in PCR and when study populations from clinical trials were assessed.

INTERPRETATION: Change in albuminuria was consistently associated with subsequent risk of end-stage kidney disease across a range of cohorts, lending support to the use of change in albuminuria as a surrogate endpoint for end-stage kidney disease in clinical trials of progression of chronic kidney disease in the setting of increased albuminuria.

FUNDING: US National Kidney Foundation and US National Institute of Diabetes and Digestive and Kidney Diseases.

National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-29275 (URN)10.1016/S2213-8587(18)30313-9 (DOI)30635225 (PubMedID)2-s2.0-85060314551 (Scopus ID)
Available from: 2019-01-14 Created: 2019-01-14 Last updated: 2019-02-04Bibliographically approved
Wändell, P., Carlsson, A. C., Li, X., Gasevic, D., Ärnlöv, J., Sundquist, J. & Sundquist, K. (2019). End-stage kidney diseases in immigrant groups: a nationwide cohort study in Sweden. American Journal of Nephrology, 49(3), 186-192
Open this publication in new window or tab >>End-stage kidney diseases in immigrant groups: a nationwide cohort study in Sweden
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2019 (English)In: American Journal of Nephrology, ISSN 0250-8095, E-ISSN 1421-9670, Vol. 49, no 3, p. 186-192Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Our aim was to study the association between the country of birth and incident end-stage kidney disease (ESKD) in several immigrant groups in Sweden, using individuals born in Sweden or with Swedish-born parents as referents.

METHODS: A cohort study of first- and second-generation immigrants residing in Sweden between January 1, 1998 and December 31, 2012 was performed. Outcomes were defined as having at least one registered diagnosis of ESKD in the National Patient Register. The incidence of ESKD in different immigrant groups was used in the Cox regression models to estimate hazard ratios (HRs) and 95% CIs. All models were stratified by sex and adjusted for age, geographical residence, educational level, marital status, and neighbourhood socioeconomic status.

RESULTS: Compared to their referents, higher incidence rates and HRs of ESKD (HR; 95% CI) were observed in general among foreign-born men (1.10; 1.04-1.16) and women (1.12; 1.04-1.21) but not among second-generation immigrants (persons born in Sweden with foreign-born parents). A particularly high -incidence was noted among men and women from -East-European countries, as well as from non-European regions. A lower incidence of ESKD was noted among men from Finland.

CONCLUSIONS: We observed substantial differences in incidence of ESKD between immigrant groups and the Swedish-born population, which may be clinically relevant when monitoring preventive measures in patient subgroups with a higher risk of deteriorating kidney disease, and suggest higher attention to hypertension and diabetes control in immigrants. Mechanisms attributable to the migration process or ethnic differences may lead to an increased risk of ESKD.

Keywords
End-stage kidney disease, First generation immigrants, Gender, Neighbourhood, Socioeconomic status
National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-29422 (URN)10.1159/000497063 (DOI)30712037 (PubMedID)2-s2.0-85061304574 (Scopus ID)
Available from: 2019-02-05 Created: 2019-02-05 Last updated: 2019-02-25Bibliographically approved
Xu, H., Matsushita, K., Su, G., Trevisan, M., Ärnlöv, J., Barany, P., . . . Carrero, J.-J. (2019). Estimated glomerular filtration rate and the risk of cancer. American Society of Nephrology. Clinical Journal
Open this publication in new window or tab >>Estimated glomerular filtration rate and the risk of cancer
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2019 (English)In: American Society of Nephrology. Clinical Journal, ISSN 1555-9041, E-ISSN 1555-905XArticle in journal (Refereed) Epub ahead of print
Abstract [en]

BACKGROUND AND OBJECTIVES: Community-based reports regarding eGFR and the risk of cancer are conflicting. We here explore plausible links between kidney function and cancer incidence in a large Scandinavian population-based cohort.

DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In the Stockholm Creatinine Measurements project, we quantified the associations of baseline eGFR with the incidence of cancer among 719,033 Swedes ages ≥40 years old with no prior history of cancer. Study outcomes were any type and site-specific cancer incidence rates on the basis of International Classification of Diseases-10 codes over a median follow-up of 5 years. To explore the possibility of detection bias and reverse causation, we divided the follow-up time into different time periods (≤12 and >12 months) and estimated risks for each of these intervals.

RESULTS: In total, 64,319 cases of cancer (affecting 9% of participants) were detected throughout 3,338,226 person-years. The relationship between eGFR and cancer incidence was U shaped. Compared with eGFR of 90-104 ml/min, lower eGFR strata associated with higher cancer risk (adjusted hazard ratio, 1.08; 95% confidence interval, 1.05 to 1.11 for eGFR=30-59 ml/min and adjusted hazard ratio, 1.24; 95% confidence interval, 1.15 to 1.35 for eGFR<30 ml/min). Lower eGFR strata were significantly associated with higher risk of skin, urogenital, prostate, and hematologic cancers. Any cancer risk as well as skin (nonmelanoma) and urogenital cancer risks were significantly elevated throughout follow-up time, but they were higher in the first 12 months postregistration. Associations with hematologic and prostate cancers abrogated after the first 12 months of observation, suggesting the presence of detection bias and/or reverse causation.

CONCLUSIONS: There is a modestly higher cancer risk in individuals with mild to severe CKD driven primarily by skin and urogenital cancers, and this is only partially explained by bias.

Keywords
Bias, Cancer, Confidence Intervals, Follow-Up Studies, Hematologic Neoplasms, Incidence, International Classification of Diseases, Proportional Hazards Models, Prostatic Neoplasms, Renal Insufficiency, Chronic, Risk, Urogenital Neoplasms, chronic kidney disease, detection bias, estimated glomerular filtration rate, glomerular filtration rate, reverse causation
National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-29666 (URN)10.2215/CJN.10820918 (DOI)30872279 (PubMedID)
Available from: 2019-03-18 Created: 2019-03-18 Last updated: 2019-03-19Bibliographically approved
Lind, L., Sundström, J., Larsson, A., Lampa, E., Ärnlöv, J. & Ingelsson, E. (2019). Longitudinal effects of aging on plasma proteins levels in older adults: associations with kidney function and hemoglobin levels. PLoS ONE, 14(2), Article ID e0212060.
Open this publication in new window or tab >>Longitudinal effects of aging on plasma proteins levels in older adults: associations with kidney function and hemoglobin levels
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2019 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, no 2, article id e0212060Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: A targeted proteomics chip has been shown to be useful to discover novel associations of proteins with cardiovascular disease. We investigated how these proteins change with aging, and whether this change is related to a decline in kidney function, or to a change in hemoglobin levels.

MATERIAL AND METHODS: In the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study, including 1,016 participants from the general population aged 70 at baseline, 84 proteins were measured at ages 70, 75, 80. At these occasions, glomerular filtration rate (eGFR) was estimated and the hemoglobin levels were measured.

RESULTS: Sixty-one of the 84 evaluated proteins changed significantly during the 10-year follow-up (multiple testing-adjusted alpha = 0.00059), most showing an increase. The change in eGFR was inversely related to changes of protein levels for the vast majority of proteins (74%). The change in hemoglobin was significantly related to the change in 40% of the evaluated proteins, with no obvious preference of the direction of these relationships.

CONCLUSION: The majority of evaluated proteins increased with aging in adults. Therefore, normal ranges for proteins might be given in age-strata. The increase in protein levels was associated with the degree of reduction in eGFR for the majority of proteins, while no clear pattern was seen for the relationships between the proteins and the change in hemoglobin levels. Studies on changes in urinary proteins are warranted to understand the association between the reduction in eGFR and increase in plasma protein levels.

National Category
Clinical Laboratory Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-29617 (URN)10.1371/journal.pone.0212060 (DOI)000459710700009 ()30802263 (PubMedID)2-s2.0-85062001083 (Scopus ID)
Available from: 2019-03-05 Created: 2019-03-05 Last updated: 2019-03-14Bibliographically approved
Lind, L., Sundström, J., Ärnlöv, J. & Ingelsson, E. (2019). Proteomic profiling of endothelium-dependent vasodilation. Journal of Hypertension, 37(1), 216-222
Open this publication in new window or tab >>Proteomic profiling of endothelium-dependent vasodilation
2019 (English)In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 37, no 1, p. 216-222Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: As endothelial dysfunction is an early event in atherosclerosis formation, we investigated if proteins previously related to cardiovascular disease also were related to endothelial function using a novel targeted proteomics approach.

METHODS: In the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study (n = 850-970, all aged 70 years), endothelium-dependent vasodilation (EDV) in the forearm was assessed by intra-arterial infusion of acetylcholine. Flow-mediated vasodilation (FMD) was investigated in the brachial artery by ultrasound. The same investigations were carried out in the Prospective investigation of Obesity, Energy and Metabolism (POEM) study (n = 375-461, all aged 50 years). After strict quality control, 84 cardiovascular-related proteins measured by the proximity extension assay were studied in relation to EDV and FMD in PIVUS (discovery sample) and POEM (validation sample).

RESULTS: Of the 15 proteins being significantly related to EDV in PIVUS (false discovery rate <0.025), seven could be replicated in POEM at nominal significance and same effect direction when adjusted for sex and storage time. Of those, only cathepsin D remained significant following further adjustment for traditional cardiovascular risk factors (beta, -0.08; 95% confidence interval, -0.16, -0.01; P = 0.033; change in ln-transformed EDV per 1-SD increase in protein level). No protein was significantly related to FMD.

CONCLUSION: Using a discovery/validation approach in two samples, our results indicate an inverse association between plasma cathepsin D levels and endothelial-dependent vasodilation.

National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-28816 (URN)10.1097/HJH.0000000000001863 (DOI)30339551 (PubMedID)2-s2.0-85057537816 (Scopus ID)
Available from: 2018-10-23 Created: 2018-10-23 Last updated: 2018-12-17Bibliographically approved
Morris, A. P., Le, T. H., Wu, H., Akbarov, A., van der Most, P. J., Hemani, G., . . . Franceshini, N. (2019). Trans-ethnic kidney function association study reveals putative causal genes and effects on kidney-specific disease aetiologies. Nature Communications, 10(1), Article ID 29.
Open this publication in new window or tab >>Trans-ethnic kidney function association study reveals putative causal genes and effects on kidney-specific disease aetiologies
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2019 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 10, no 1, article id 29Article in journal (Refereed) Published
Abstract [en]

Chronic kidney disease (CKD) affects ~10% of the global population, with considerable ethnic differences in prevalence and aetiology. We assemble genome-wide association studies of estimated glomerular filtration rate (eGFR), a measure of kidney function that defines CKD, in 312,468 individuals of diverse ancestry. We identify 127 distinct association signals with homogeneous effects on eGFR across ancestries and enrichment in genomic annotations including kidney-specific histone modifications. Fine-mapping reveals 40 high-confidence variants driving eGFR associations and highlights putative causal genes with cell-type specific expression in glomerulus, and in proximal and distal nephron. Mendelian randomisation supports causal effects of eGFR on overall and cause-specific CKD, kidney stone formation, diastolic blood pressure and hypertension. These results define novel molecular mechanisms and putative causal genes for eGFR, offering insight into clinical outcomes and routes to CKD treatment development.

National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-29255 (URN)10.1038/s41467-018-07867-7 (DOI)000454756900006 ()30604766 (PubMedID)2-s2.0-85059496132 (Scopus ID)
Available from: 2019-01-07 Created: 2019-01-07 Last updated: 2019-01-21Bibliographically approved
Carlsson, A. C., Ruge, T., Kjøller, E., Hilden, J., Kolmos, H. J., Sajadieh, A., . . . Ärnlöv, J. (2018). 10-year associations between tumor necrosis factor receptors 1 and 2 and cardiovascular events in patients with stable coronary heart disease: a CLARICOR (effect of clarithromycin on mortality and morbidity in patients with ischemic heart disease) trial substudy. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 7(9), Article ID e008299.
Open this publication in new window or tab >>10-year associations between tumor necrosis factor receptors 1 and 2 and cardiovascular events in patients with stable coronary heart disease: a CLARICOR (effect of clarithromycin on mortality and morbidity in patients with ischemic heart disease) trial substudy
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2018 (English)In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 7, no 9, article id e008299Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: We aimed to assess the associations and predictive powers between the soluble receptors for tumor necrosis factor (TNF)-α (TNFR1 and TNFR2) and cardiovascular outcomes in patients with stable coronary heart disease.

METHODS AND RESULTS: <0.001 for TNFR2). The associations were similar in the replication sample. The associations with the composite outcome were mainly driven by acute myocardial infarction, cardiovascular mortality, and noncardiovascular mortality. The addition of TNFR1 and TNFR2 to established cardiovascular risk factors improved prediction only modestly (<1%).

CONCLUSIONS: Increased concentrations of circulating TNFR1 and TNFR2 were associated with increased risks of cardiovascular events and mortality in patients with stable coronary heart disease. Yet, the utility of measuring TNFR1 and TNFR2 to improve risk prediction in these patients appears limited.

CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT00121550.

Keywords
cohort study, coronary atherosclerosis, tumor necrosis factor‐α
National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-27534 (URN)10.1161/JAHA.117.008299 (DOI)000432332800014 ()29686027 (PubMedID)2-s2.0-85046402672 (Scopus ID)
Available from: 2018-04-26 Created: 2018-04-26 Last updated: 2018-06-05Bibliographically approved
Nowak, C. & Ärnlöv, J. (2018). A Mendelian randomization study of the effects of blood lipids on breast cancer risk. Nature Communications, 9(1), Article ID 3957.
Open this publication in new window or tab >>A Mendelian randomization study of the effects of blood lipids on breast cancer risk
2018 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 9, no 1, article id 3957Article in journal (Refereed) Published
Abstract [en]

Observational studies have reported inconsistent associations between circulating lipids and breast cancer risk. Using results from >400,000 participants in two-sample Mendelian randomization, we show that genetically raised LDL-cholesterol is associated with higher risk of breast cancer (odds ratio, OR, per standard deviation, 1.09, 95% confidence interval, 1.02-1.18, P = 0.020) and estrogen receptor (ER)-positive breast cancer (OR 1.14 [1.05-1.24] P = 0.004). Genetically raised HDL-cholesterol is associated with higher risk of ER-positive breast cancer (OR 1.13 [1.01-1.26] P = 0.037). HDL-cholesterol-raising variants in the gene encoding the target of CETP inhibitors are associated with higher risk of breast cancer (OR 1.07 [1.03-1.11] P = 0.001) and ER-positive breast cancer (OR 1.08 [1.03-1.13] P = 0.001). LDL-cholesterol-lowering variants mimicking PCSK9 inhibitors are associated (P = 0.014) with lower breast cancer risk. We find no effects related to the statin and ezetimibe target genes. The possible risk-promoting effects of raised LDL-cholesterol and CETP-mediated raised HDL-cholesterol have implications for breast cancer prevention and clinical trials.

National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-28660 (URN)10.1038/s41467-018-06467-9 (DOI)000445819400008 ()30262900 (PubMedID)2-s2.0-85054088248 (Scopus ID)
Available from: 2018-10-05 Created: 2018-10-05 Last updated: 2018-10-16Bibliographically approved
Mokdad, A., Azzopardi, P., Cini, K., Kennedy, E., Sawyer, S., El Bcheraoui, C., . . . Murray, C. J. L. (2018). Adolescent health in the Eastern Mediterranean Region: findings from the global burden of disease 2015 study. International Journal of Public Health, 63(S1), 79-96
Open this publication in new window or tab >>Adolescent health in the Eastern Mediterranean Region: findings from the global burden of disease 2015 study
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2018 (English)In: International Journal of Public Health, ISSN 1661-8556, E-ISSN 1661-8564, Vol. 63, no S1, p. 79-96Article in journal (Refereed) Published
Abstract [en]

The 22 countries of the East Mediterranean Region (EMR) have large populations of adolescents aged 10-24 years. These adolescents are central to assuring the health, development, and peace of this region. We described their health needs. Using data from the Global Burden of Disease Study 2015 (GBD 2015), we report the leading causes of mortality and morbidity for adolescents in the EMR from 1990 to 2015. We also report the prevalence of key health risk behaviors and determinants. Communicable diseases and the health consequences of natural disasters reduced substantially between 1990 and 2015. However, these gains have largely been offset by the health impacts of war and the emergence of non-communicable diseases (including mental health disorders), unintentional injury, and self-harm. Tobacco smoking and high body mass were common health risks amongst adolescents. Additionally, many EMR countries had high rates of adolescent pregnancy and unmet need for contraception. Even with the return of peace and security, adolescents will have a persisting poor health profile that will pose a barrier to socioeconomic growth and development of the EMR

Keywords
Adolescent health; Burden of disease; Eastern Mediterranean Region
National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-28036 (URN)10.1007/s00038-017-1003-4 (DOI)000433519400010 ()28776253 (PubMedID)
Available from: 2018-06-28 Created: 2018-06-28 Last updated: 2018-06-28Bibliographically approved
Griswald, M. G., Fullman, N., Hawley, C., Arian, N., Zimsen, S. R. M., Tymeson, H. D., . . . Gakidou, E. (2018). Alcohol use and burden for 195 countries and territories, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet, 392(10152), 1015-1035
Open this publication in new window or tab >>Alcohol use and burden for 195 countries and territories, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016
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2018 (English)In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 392, no 10152, p. 1015-1035Article in journal (Refereed) Published
Abstract [en]

Background: Alcohol use is a leading risk factor for death and disability, but its overall association with health remains complex given the possible protective effects of moderate alcohol consumption on some conditions. With our comprehensive approach to health accounting within the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we generated improved estimates of alcohol use and alcohol-attributable deaths and disability-adjusted life-years (DALYs) for 195 locations from 1990 to 2016, for both sexes and for 5-year age groups between the ages of 15 years and 95 years and older. 

Methods: Using 694 data sources of individual and population-level alcohol consumption, along with 592 prospective and retrospective studies on the risk of alcohol use, we produced estimates of the prevalence of current drinking, abstention, the distribution of alcohol consumption among current drinkers in standard drinks daily (defined as 10 g of pure ethyl alcohol), and alcohol-attributable deaths and DALYs. We made several methodological improvements compared with previous estimates: first, we adjusted alcohol sales estimates to take into account tourist and unrecorded consumption; second, we did a new meta-analysis of relative risks for 23 health outcomes associated with alcohol use; and third, we developed a new method to quantify the level of alcohol consumption that minimises the overall risk to individual health. 

Findings: Globally, alcohol use was the seventh leading risk factor for both deaths and DALYs in 2016, accounting for 2.2% (95% uncertainty interval [UI] 1.5-3.0) of age-standardised female deaths and 6.8% (5.8-8.0) of age-standardised male deaths. Among the population aged 15-49 years, alcohol use was the leading risk factor globally in 2016, with 3.8% (95% UI 3.2-4-3) of female deaths and 12.2% (10.8-13-6) of male deaths attributable to alcohol use. For the population aged 15-49 years, female attributable DALYs were 2.3% (95% UI 2.0-2.6) and male attributable DALYs were 8.9% (7.8-9.9). The three leading causes of attributable deaths in this age group were tuberculosis (1.4% [95% UI 1. 0-1. 7] of total deaths), road injuries (1.2% [0.7-1.9]), and self-harm (1.1% [0.6-1.5]). For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27.1% (95% UI 21.2-33.3) of total alcohol-attributable female deaths and 18.9% (15.3-22.6) of male deaths. The level of alcohol consumption that minimised harm across health outcomes was zero (95% UI 0.0-0.8) standard drinks per week. 

Interpretation: Alcohol use is a leading risk factor for global disease burden and causes substantial health loss. We found that the risk of all-cause mortality, and of cancers specifically, rises with increasing levels of consumption, and the level of consumption that minimises health loss is zero. These results suggest that alcohol control policies might need to be revised worldwide, refocusing on efforts to lower overall population-level consumption.

National Category
Clinical Medicine
Research subject
Health and Welfare
Identifiers
urn:nbn:se:du-28664 (URN)10.1016/S0140-6736(18)31310-2 (DOI)000445098800025 ()30146330 (PubMedID)
Available from: 2018-10-08 Created: 2018-10-08 Last updated: 2018-10-08Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-6933-4637

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