| 1. |
- Wormser, David, et al.
(author)
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Adult height and the risk of cause-specific death and vascular morbidity in 1 million people : individual participant meta-analysis
- 2012
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In: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 41:5, s. 1419-1433
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Journal article (peer-reviewed)abstract
- BackgroundThe extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain.MethodsWe calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual-participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies.ResultsFor people born between 1900 and 1960, mean adult height increased 0.5-1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96-0.99) for death from any cause, 0.94 (0.93-0.96) for death from vascular causes, 1.04 (1.03-1.06) for death from cancer and 0.92 (0.90-0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12-1.42) for risk of melanoma death to 0.84 (0.80-0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators.ConclusionAdult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases.
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| 2. |
- Agardh, Emilie E., et al.
(author)
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Alcohol-attributed disease burden in four Nordic countries between 2000 and 2017 : Are the gender gaps narrowing? A comparison using the Global Burden of Disease, Injury and Risk Factor 2017 study
- 2021
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In: Drug and Alcohol Review. - : Wiley. - 0959-5236 .- 1465-3362. ; 40:3, s. 431-442
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Journal article (peer-reviewed)abstract
- Introduction and Aims. The gender difference in alcohol use seems to have narrowed in the Nordic countries, but it is not clear to what extent this may have affected differences in levels of harm. We compared gender differences in all-cause and cause-specific alcohol-attributed disease burden, as measured by disability-adjusted life-years (DALY), in four Nordic countries in 2000-2017, to find out if gender gaps in DALYs had narrowed. Design and Methods. Alcohol-attributed disease burden by DALYs per 100 000 population with 95% uncertainty intervals were extracted from the Global Burden of Disease database. Results. In 2017, all-cause DALYs in males varied between 2531 in Finland and 976 in Norway, and in females between 620 in Denmark and 270 in Norway. Finland had the largest gender differences and Norway the smallest, closely followed by Sweden. During 2000-2017, absolute gender differences in all-cause DALYs declined by 31% in Denmark, 26% in Finland, 19% in Sweden and 18% in Norway. In Finland, this was driven by a larger relative decline in males than females; in Norway, it was due to increased burden in females. In Denmark, the burden in females declined slightly more than in males, in relative terms, while in Sweden the relative decline was similar in males and females. Discussion and Conclusions. The gender gaps in harm narrowed to a different extent in the Nordic countries, with the differences driven by different conditions. Findings are informative about how inequality, policy and sociocultural differences affect levels of harm by gender.
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| 3. |
- Agardh, Emilie E., et al.
(author)
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Disease Burden Attributed to Drug use in the Nordic Countries : a Systematic Analysis for the Global Burden of Diseases, Injuries, and Risk Factors Study 2019
- 2023
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In: International Journal of Mental Health and Addiction. - 1557-1874 .- 1557-1882.
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Journal article (peer-reviewed)abstract
- The Nordic countries share similarities in many social and welfare domains, but drug policies have varied over time and between countries. We wanted to compare differences in mortality and disease burden attributed to drug use over time. Using results from the Global Burden of Disease (GBD) study, we extracted age-standardized estimates of deaths, DALYs, YLLs and YLDs per 100 000 population for Denmark, Finland, Iceland, Norway, and Sweden during the years 1990 to 2019. Among males, DALY rates in 2019 were highest in Finland and lowest in Iceland. Among females, DALY rates in 2019 were highest in Iceland and lowest in Sweden. Sweden have had the highest increase in burden since 1990, from 252 DALYs to 694 among males, and from 111 to 193 among females. Norway had a peak with highest level of all countries in 2001-2004 and thereafter a strong decline. Denmark have had the most constant burden over time, 566-600 DALYs among males from 1990 to 2010 and 210-240 DALYs among females. Strict drug policies in Nordic countries have not prevented an increase in some countries, so policies need to be reviewed.
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| 4. |
- Franco, Irene, et al.
(author)
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Whole genome DNA sequencing provides an atlas of somatic mutagenesis in healthy human cells and identifies a tumor-prone cell type
- 2019
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In: Genome Biology. - : Springer Science and Business Media LLC. - 1465-6906 .- 1474-760X. ; 20:1
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Journal article (peer-reviewed)abstract
- Background: The lifelong accumulation of somatic mutations underlies age-related phenotypes and cancer. Mutagenic forces are thought to shape the genome of aging cells in a tissue-specific way. Whole genome analyses of somatic mutation patterns, based on both types and genomic distribution of variants, can shed light on specific processes active in different human tissues and their effect on the transition to cancer. Results: To analyze somatic mutation patterns, we compile a comprehensive genetic atlas of somatic mutations in healthy human cells. High-confidence variants are obtained from newly generated and publicly available whole genome DNA sequencing data from single non-cancer cells, clonally expanded in vitro. To enable a well-controlled comparison of different cell types, we obtain single genome data (92% mean coverage) from multi-organ biopsies from the same donors. These data show multiple cell types that are protected from mutagens and display a stereotyped mutation profile, despite their origin from different tissues. Conversely, the same tissue harbors cells with distinct mutation profiles associated to different differentiation states. Analyses of mutation rate in the coding and non-coding portions of the genome identify a cell type bearing a unique mutation pattern characterized by mutation enrichment in active chromatin, regulatory, and transcribed regions. Conclusions: Our analysis of normal cells from healthy donors identifies a somatic mutation landscape that enhances the risk of tumor transformation in a specific cell population from the kidney proximal tubule. This unique pattern is characterized by high rate of mutation accumulation during adult life and specific targeting of expressed genes and regulatory regions.
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| 5. |
- Hernandez, Leah, et al.
(author)
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Blood-brain barrier and gut barrier dysfunction in chronic kidney disease with a focus on circulating biomarkers and tight junction proteins
- 2022
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In: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 12:1
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Journal article (peer-reviewed)abstract
- Kidney failure and associated uraemia have implications for the cardiovascular system, brain, and blood-brain barrier (BBB). We aim to examine BBB disruption, by assessing brain-derived neurotropic factor (BDNF), neuron-specific enolase (NSE) levels, and gut-blood barrier (GBB) disruption by trimethylamine N-oxide (TMAO), in chronic kidney disease (CKD) patients. Additionally, endothelial tight-junction protein expressions and modulation via TMAO were assessed. Serum from chronic kidney disease (CKD) female and male haemodialysis (HD) patients, and controls, were used to measure BDNF and NSE by enzyme-linked immunosorbent assays, and TMAO by mass spectrometry. Immunofluorescent staining of subcutaneous fat biopsies from kidney transplant recipients, and controls, were used to measure microvascular expression of tight-junction proteins (claudin-5, occludin, JAM-1), and control microvasculature for TMAO effects. HD patients versus controls, had significantly lower and higher serum levels of BDNF and NSE, respectively. In CKD biopsies versus controls, reduced expression of claudin-5, occludin, and JAM-1 were observed. Incubation with TMAO significantly decreased expression of all tight-junction proteins in the microvasculature. Uraemia affects BBB and GBB resulting in altered levels of circulating NSE, BDNF and TMAO, respectively, and it also reduces expression of tight-junction proteins that confer BBB maintenance. TMAO serves as a potential candidate to alter BBB integrity in CKD.
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| 6. |
- Sarwar, Nadeem, et al.
(author)
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Interleukin-6 receptor pathways in coronary heart disease : a collaborative meta-analysis of 82 studies
- 2012
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In: The Lancet. - New York, NY, USA : Elsevier. - 0140-6736 .- 1474-547X. ; 379:9822, s. 1205-1213
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Journal article (peer-reviewed)abstract
- Background: Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling. Methods: In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6. Findings: The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele >= 0.04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34.3% (95% CI 30.4-38.2) and of interleukin 6 by 14.6% (10.7-18.4), and mean concentration of C-reactive protein was reduced by 7.5% (5.9-9.1) and of fibrinogen by 1.0% (0.7-1.3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3.4% (1.8-5.0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes. Interpretation: Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.
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| 7. |
- Stamatakis, Emmanuel, et al.
(author)
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Emerging collaborative research platforms for the next generation of physical activity, sleep and exercise medicine guidelines : the Prospective Physical Activity, Sitting, and Sleep consortium (ProPASS)
- 2020
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In: British Journal of Sports Medicine. - : BMJ. - 0306-3674 .- 1473-0480. ; 54:8, s. 435-437
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Journal article (other academic/artistic)abstract
- Galileo Galilei’s quote ‘measure what is measurable, and make measurable what is not so’ has particular relevance to health behaviours, such as physical activity (PA), sitting and sleep, whose measurement during free living is notoriously difficult. To date, much of what we know about how these behaviours affect our health is based on self-report by questionnaires which have limited validity, are prone to bias and inquire about selective aspects of these behaviours. Although self-reported evidence has made great contributions to shaping public health and exercise medicine policy and guidelines until now,1 the ongoing advancements of accelerometry-based measurement and evidence synthesis methods are set to change the landscape. The aim of this editorial is to outline new directions in PA and sleep-related epidemiology that open new horizons for guideline development and improvement; and to describe a new research collaboration platform: the Prospective Physical Activity, Sitting, and Sleep consortium (ProPASS).
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| 8. |
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| 9. |
- Wood, Angela M., et al.
(author)
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Risk thresholds for alcohol consumption : combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies
- 2018
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In: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 391:10129, s. 1513-1523
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Journal article (peer-reviewed)abstract
- Background: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease.Methods: We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12.5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5.6 years [5th-95th percentile 1.04-13.5]) from 71 011 participants from 37 studies.Findings: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5.4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1.14, 95% CI, 1.10-1.17), coronary disease excluding myocardial infarction (1.06, 1.00-1.11), heart failure (1.09, 1.03-1.15), fatal hypertensive disease (1.24, 1.15-1.33); and fatal aortic aneurysm (1.15, 1.03-1.28). By contrast, increased alcohol consumption was loglinearly associated with a lower risk of myocardial infarction (HR 0.94, 0.91-0.97). In comparison to those who reported drinking >0-<= 100 g per week, those who reported drinking >100-<= 200 g per week, >200-<= 350 g per week, or >350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1-2 years, or 4-5 years, respectively.Interpretation: In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines.
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| 10. |
- Anderberg, Mats, 1961-, et al.
(author)
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Adolescents with substance abuse problems in outpatient treatment : a one-year prospective follow-up study
- 2021
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In: Nordic Studies on Alcohol and Drugs. - : Sage Publications. - 1455-0725 .- 1458-6126. ; 38:5, s. 466-479
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Journal article (peer-reviewed)abstract
- Aim: There is a lack of knowledge about how adolescents with substance abuse problems manage after taking part in treatment. It is also difficult to perform traditional follow-up studies with this group. This article presents the outcome of a prospective study of 455 adolescents who underwent outpatient treatment, based on data taken from official registers. It aims to describe and analyse indications of continued use of substance (CUS) and how various risk and protective factors predict outcomes after initiated treatment at a Maria clinic in Sweden. Design: The study is based on structured interviews at intake, and the data that indicated CUS were taken from several different national registers. The analyses included descriptive data and bivariate associations, logistic regressions and a CHAID analysis. Results: Almost two thirds of the adolescents have no indication of CUS at one-year follow-up. The ten studied risk factors independently were weak predictors of CUS and it was instead the accumulation of risk factors that were linked to a negative outcome. Conclusion: The majority of adolescents who start outpatient treatment for substance abuse problems return to a lesser extent in registers that may indicate a continued problem with alcohol and drugs one year later. A concentration of more than five risk factors appears to be associated with a registration. The study also provides an example of an alternative method for following up adolescents with alcohol and drug abuse problems.
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