Work ability and all cause mortality: A 25-year longitudinal study among Finnish municipal workers

BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e045678
Author(s):  
Marit Müller De Bortoli ◽  
Inger M. Oellingrath ◽  
Anne Kristin Moeller Fell ◽  
Alex Burdorf ◽  
Suzan J. W. Robroek

ObjectivesThe aim of this study is to assess (1) whether lifestyle risk factors are related to work ability and sick leave in a general working population over time, and (2) these associations within specific disease groups (ie, respiratory diseases, cardiovascular disease and diabetes, and mental illness).SettingTelemark county, in the south-eastern part of Norway.DesignLongitudinal study with 5 years follow-up.ParticipantsThe Telemark study is a longitudinal study of the general working population in Telemark county, Norway, aged 16 to 50 years at baseline in 2013 (n=7952) and after 5-year follow-up.Outcome measureSelf-reported information on work ability (moderate and poor) and sick leave (short-term and long-term) was assessed at baseline, and during a 5-year follow-up.ResultsObesity (OR=1.64, 95% CI: 1.32 to 2.05) and smoking (OR=1.62, 95% CI: 1.35 to 1.96) were associated with long-term sick leave and, less strongly, with short-term sick leave. An unhealthy diet (OR=1.57, 95% CI: 1.01 to 2.43), and smoking (OR=1.67, 95% CI: 1.24 to 2.25) were associated with poor work ability and, to a smaller extent, with moderate work ability. A higher lifestyle risk score was associated with both sick leave and reduced work ability. Only few associations were found between unhealthy lifestyle factors and sick leave or reduced work ability within disease groups.ConclusionLifestyle risk factors were associated with sick leave and reduced work ability. To evaluate these associations further, studies assessing the effect of lifestyle interventions on sick leave and work ability are needed.


2014 ◽  
Vol 89 (6) ◽  
pp. 772-780 ◽  
Author(s):  
Stephen W. Farrell ◽  
Carrie E. Finley ◽  
Allen W. Jackson ◽  
Gloria L. Vega ◽  
James R. Morrow

BMJ Open ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. e024563
Author(s):  
Lauren Schofield ◽  
David Walsh ◽  
Zhiqiang Feng ◽  
Duncan Buchanan ◽  
Chris Dibben ◽  
...  

ObjectivesIt has been proposed that part of the explanation for higher mortality in Scotland compared with England and Wales, and Glasgow compared with other UK cities, relates to greater ethnic diversity in England and Wales. We sought to assess the extent to which this excess was attenuated by adjusting for ethnicity. We additionally explored the role of country of birth in any observed differences.SettingScotland and England and Wales; Glasgow and Manchester.ParticipantsWe used the Scottish Longitudinal Study and the Office for National Statistics Longitudinal Study of England and Wales (2001–2010). Participants (362 491 in total) were aged 35–74 years at baseline.Primary outcome measuresRisk of all-cause mortality between 35 and 74 years old in Scotland and England and Wales, and in Glasgow and Manchester, adjusting for age, gender, socioeconomic position (SEP), ethnicity and country of birth.Results18% of the Manchester sample was non-White compared with 3% in Glasgow (England and Wales: 10.4%; Scotland: 1.2%). The mortality incidence rate ratio was 1.33 (95% CI 1.13 to 1.56) in Glasgow compared with Manchester. This reduced to 1.25 (1.07 to 1.47) adjusting for SEP, and to 1.20 (1.02 to 1.42) adjusting for ethnicity and country of birth. For Scotland versus England and Wales, the corresponding figures were 18% higher mortality, reducing to 10%, and then 7%. Non-Whites born outside the UK had lower mortality. In the Scottish samples only, non-Whites born in the UK had significantly higher mortality than Whites born in the UK.ConclusionsThe research supports the hypothesis that ethnic diversity and migration from outside UK play a role in explaining Scottish excess mortality. In Glasgow especially, however, a large excess remains: thus, previously articulated policy implications (addressing poverty, vulnerability and inequality) still apply.


2020 ◽  
Vol 20 (12) ◽  
pp. 1126-1132
Author(s):  
Hai Nguyen ◽  
Yu‐Tzu Wu ◽  
Alexandru Dregan ◽  
Silia Vitoratou ◽  
Kia‐Chong Chua ◽  
...  

Addiction ◽  
2008 ◽  
Vol 103 (7) ◽  
pp. 1149-1159 ◽  
Author(s):  
Lau C. Thygesen ◽  
Christoffer Johansen ◽  
Niels Keiding ◽  
Edward Giovannucci ◽  
Morten Grønbæk

2018 ◽  
Vol 47 (4) ◽  
pp. 220-229 ◽  
Author(s):  
Allan M. Andersen ◽  
Philip T. Ryan ◽  
Fredrick X. Gibbons ◽  
Ronald L. Simons ◽  
Jeffrey D. Long ◽  
...  

Objectives.—Determine whether an epigenetic assay for smoking predicts all-cause mortality in adults participating in a longitudinal study of Iowa adoptees. Background.—Improved biomarkers for smoking are needed given its large public health impact and significant limitations of both self-report and current biomarkers, such as cotinine in detecting smoking. In the past 5 years, multiple epigenome-wide association studies of smoking have identified loci suitable for translation as epigenetic biomarkers for smoking, in particular the CpG cg05575921. Digital polymerase chain reaction methods hold promise for the development of this and other epigenetic biomarkers. Methods.—Participants in the Iowa Adoption Studies were interviewed regarding their smoking habits. DNA was prepared from whole blood and bisulfite-converted for methylation analysis and digital droplet polymerase chain reaction assay of methylation at cg05575921 was performed. National Death Index records were requested for 584 study participants, resulting in 24 complete matches, 210 partial matches and 350 non-matching records. Complete matches were coded as deceased while the remainder were coded as alive (ie, censored). In total, methylation data and vital status information were available for a total of N = 193 subjects, including 15 deceased and 178 non-deceased. Cox regression was used to examine the ability of cg05575921 methylation as a continuous value to predict the timing of mortality with and without the inclusion of age, sex, race, BMI, marital status, educational status, socioeconomic status, cardiovascular risk factors, and a history of cancer as covariates. Results.—Methylation at cg05575921 predicted the hazard of mortality as the sole predictor and after accounting for major demographic and clinical risk factors. The fitted model showed the hazard ratio increased by 3.5% for every 1% decrease in methylation. Conclusions.—Decreased methylation at cg05575921, an emerging epigenetic biomarker for smoking, was associated with early mortality in a longitudinal study of adults after accounting for the impact of major demographic and clinical risk factors for all-cause mortality. This approach may be useful in clinical research or actuarial assessments.


Author(s):  
Cathal McCrory ◽  
Giovanni Fiorito ◽  
Belinda Hernandez ◽  
Silvia Polidoro ◽  
Aisling M. O’Halloran ◽  
...  

ABSTRACTThe aging process is characterized by the presence of high interindividual variation between individuals of the same chronical age prompting a search for biomarkers that capture this heterogeneity. The present study examines the associations of four epigenetic clocks - Horvath, Hannum, PhenoAge, GrimAge - with a wide range of clinical phenotypes, and with all-cause mortality at up to 10-year follow-up in a sample of 490 participants in the Irish Longitudinal Study on Ageing. Results indicate that the GrimAge clock represents a step-improvement in the predictive utility of the epigenetic clocks for identifying age-related decline in an array of clinical phenotypes.


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