| 1. |
- Madsen, I. E. H., et al.
(författare)
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Job strain as a risk factor for clinical depression : systematic review and meta-analysis with additional individual participant data
- 2017
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Ingår i: Psychological Medicine. - : Cambridge University Press. - 0033-2917 .- 1469-8978. ; 47:8, s. 1342-1356
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Forskningsöversikt (refereegranskat)abstract
- Background. Adverse psychosocial working environments characterized by job strain (the combination of high demands and low control at work) are associated with an increased risk of depressive symptoms among employees, but evidence on clinically diagnosed depression is scarce. We examined job strain as a risk factor for clinical depression. Method. We identified published cohort studies from a systematic literature search in PubMed and PsycNET and obtained 14 cohort studies with unpublished individual-level data from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium. Summary estimates of the association were obtained using random-effects models. Individual-level data analyses were based on a pre-published study protocol. Results. We included six published studies with a total of 27 461 individuals and 914 incident cases of clinical depression. From unpublished datasets we included 120 221 individuals and 982 first episodes of hospital-treated clinical depression. Job strain was associated with an increased risk of clinical depression in both published [relative risk (RR) = 1.77, 95% confidence interval (CI) 1.47-2.13] and unpublished datasets (RR = 1.27, 95% CI 1.04-1.55). Further individual participant analyses showed a similar association across sociodemographic subgroups and after excluding individuals with baseline somatic disease. The association was unchanged when excluding individuals with baseline depressive symptoms (RR = 1.25, 95% CI 0.94-1.65), but attenuated on adjustment for a continuous depressive symptoms score (RR = 1.03, 95% CI 0.81-1.32). Conclusions. Job strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.
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| 2. |
- Kivimäki, M., et al.
(författare)
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Job strain as a risk factor for coronary heart disease : A collaborative meta-analysis of individual participant data
- 2012
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Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 380:9852, s. 1491-1497
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Tidskriftsartikel (refereegranskat)abstract
- Background Published work assessing psychosocial stress (job strain) as a risk factor for coronary heart disease is inconsistent and subject to publication bias and reverse causation bias. We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies. Methods We used individual records from 13 European cohort studies (1985-2006) of men and women without coronary heart disease who were employed at time of baseline assessment. We measured job strain with questions from validated job-content and demand-control questionnaires. We extracted data in two stages such that acquisition and harmonisation of job strain measure and covariables occurred before linkage to records for coronary heart disease. We defined incident coronary heart disease as the first non-fatal myocardial infarction or coronary death. Findings 30 214 (15%) of 197 473 participants reported job strain. In 1•49 million person-years at risk (mean follow-up 7•5 years [SD 1•7]), we recorded 2358 events of incident coronary heart disease. After adjustment for sex and age, the hazard ratio for job strain versus no job strain was 1•23 (95% CI 1•10-1•37). This effect estimate was higher in published (1•43, 1•15-1•77) than unpublished (1•16, 1•02-1•32) studies. Hazard ratios were likewise raised in analyses addressing reverse causality by exclusion of events of coronary heart disease that occurred in the first 3 years (1•31, 1•15-1•48) and 5 years (1•30, 1•13-1•50) of follow-up. We noted an association between job strain and coronary heart disease for sex, age groups, socioeconomic strata, and region, and after adjustments for socioeconomic status, and lifestyle and conventional risk factors. The population attributable risk for job strain was 3•4%. Interpretation Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking. Funding Finnish Work Environment Fund, the Academy of Finland, the Swedish Research Council for Working Life and Social Research, the German Social Accident Insurance, the Danish National Research Centre for the Working Environment, the BUPA Foundation, the Ministry of Social Affairs and Employment, the Medical Research Council, the Wellcome Trust, and the US National Institutes of Health.
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| 3. |
- Virtanen, Marianna, et al.
(författare)
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Long working hours and change in body weight : analysis of individual-participant data from 19 cohort studies
- 2020
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Ingår i: International Journal of Obesity. - : Nature Publishing Group. - 0307-0565 .- 1476-5497. ; 44:6, s. 1368-1375
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To examine the relation between long working hours and change in body mass index (BMI). Methods: We performed random effects meta-analyses using individual-participant data from 19 cohort studies from Europe, US and Australia (n = 122,078), with a mean of 4.4-year follow-up. Working hours were measured at baseline and categorised as part time (<35 h/week), standard weekly hours (35–40 h, reference), 41–48 h, 49–54 h and ≥55 h/week (long working hours). There were four outcomes at follow-up: (1) overweight/obesity (BMI ≥ 25 kg/m2) or (2) overweight (BMI 25–29.9 kg/m2) among participants without overweight/obesity at baseline; (3) obesity (BMI ≥ 30 kg/m2) among participants with overweight at baseline, and (4) weight loss among participants with obesity at baseline. Results: Of the 61,143 participants without overweight/obesity at baseline, 20.2% had overweight/obesity at follow-up. Compared with standard weekly working hours, the age-, sex- and socioeconomic status-adjusted relative risk (RR) of overweight/obesity was 0.95 (95% CI 0.90–1.00) for part-time work, 1.07 (1.02–1.12) for 41–48 weekly working hours, 1.09 (1.03–1.16) for 49–54 h and 1.17 (1.08–1.27) for long working hours (P for trend <0.0001). The findings were similar after multivariable adjustment and in subgroup analyses. Long working hours were associated with an excess risk of shift from normal weight to overweight rather than from overweight to obesity. Long working hours were not associated with weight loss among participants with obesity. Conclusions: This analysis of large individual-participant data suggests a small excess risk of overweight among the healthy-weight people who work long hours.
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| 4. |
- Bruder, CEG, et al.
(författare)
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High resolution deletion analysis of constitutional DNA from neurofibromatosis type 2 (NF2) patients using microarray-CGH
- 2001
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Ingår i: Human Molecular Genetics. - Oxford, United Kingdom : Oxford University Press. - 0964-6906 .- 1460-2083. ; 1, s. 271-
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Tidskriftsartikel (refereegranskat)abstract
- Neurofibromatosis type 2 (NF2) is an autosomal dominant disorder whose hallmark is bilateral vestibular schwannoma. It displays a pronounced clinical heterogeneity with mild to severe forms. The NF2 tumor suppressor (merlin/schwannomin) has been cloned and extensively analyzed for mutations in patients with different clinical variants of the disease. Correlation between the type of the NF2 gene mutation and the patient phenotype has been suggested to exist. However, several independent studies have shown that a fraction of NF2 patients with various phenotypes have constitutional deletions that partly or entirely remove one copy of the NF2 gene. The purpose of this study was to examine a 7 Mb interval in the vicinity of the NF2 gene in a large series of NF2 patients in order to determine the frequency and extent of deletions. A total of 116 NF2 patients were analyzed using high-resolution array-comparative genomic hybridization (CGH) on an array covering at least 90% of this region of 22q around the NF2 locus. Deletions, which remove one copy of the entire gene or are predicted to truncate the schwannomin protein, were detected in 8 severe, 10 moderate and 6 mild patients. This result does not support the correlation between the type of mutation affecting the NF2 gene and the disease phenotype. This work also demonstrates the general usefulness of the array-CON methodology for rapid and comprehensive detection of small (down to 40 kb) heterozygous and/or homozygous deletions occurring in constitutional or tumor-derived DNA.
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| 5. |
- Kedra, D, et al.
(författare)
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Characterization of the human synaptogyrin gene family.
- 1998
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Ingår i: Human Genetics. - : Springer Science and Business Media LLC. - 0340-6717 .- 1432-1203. ; 103:2, s. 131-41
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Tidskriftsartikel (refereegranskat)abstract
- Genomic sequencing was combined with searches of databases for identification of active genes on human chromosome 22. A cosmid from 22q13, located in the telomeric vicinity of the PDGFB (platelet-derived growth factor B-chain) gene, was fully sequenced. Using an expressed sequence tag-based approach we characterized human (SYNGR1) and mouse (Syngr1) orthologs of the previously cloned rat synaptogyrin gene (RATSYNGR1). The human SYNGR1 gene reveals three (SYNGR1a, SYNGR1b, SYNGR1c) alternative transcript forms of 4.5, 1.3 and 0.9 kb, respectively. The transcription of SYNGR1 starts from two different promoters, and leads to predicted proteins with different N- and C-terminal ends. The most abundant SYNGR1 a transcript, the 4.5-kb form, which corresponds to RATSYNGR1, is highly expressed in neurons of the central nervous system and at much lower levels in other tissues, as determined by in situ hybridization histochemistry. The levels of SYNGR1b and SYNGR1c transcripts are low and limited to heart, skeletal muscle, ovary and fetal liver. We also characterized two additional members of this novel synaptogyrin gene family in human (SYNGR2 and SYNGR3), and one in mouse (Syngr2). The human SYNGR2 gene transcript of 1.6 kb is expressed at high levels in all tissues, except brain. The 2.2-kb SYNGR3 transcript was detected in brain and placenta only. The human SYNGR2 and SYNGR3 genes were mapped by fluorescence in situ hybridization to 17qtel and 16ptel, respectively. The human SYNGR2 gene has a processed pseudogene localized in 15q11. All predicted synaptogyrin proteins contain four strongly conserved transmembrane domains, which is consistent with the M-shaped topology. The C-terminal polypeptide ends are variable in length, display a low degree of sequence similarity between family members, and are therefore likely to convey the functional specificity of each protein.
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| 6. |
- Theorell, Töres, et al.
(författare)
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Job strain in relation to body mass index : pooled analysis of 160 000 adults from 13 cohort studies
- 2012
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Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 272:1, s. 65-73
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Tidskriftsartikel (refereegranskat)abstract
- Job strain in relation to body mass index: pooled analysis of 160 000 adults from 13 cohort studies. J Intern Med 2012; 272: 6573. Background. Evidence of an association between job strain and obesity is inconsistent, mostly limited to small-scale studies, and does not distinguish between categories of underweight or obesity subclasses. Objectives. To examine the association between job strain and body mass index (BMI) in a large adult population. Methods. We performed a pooled cross-sectional analysis based on individual-level data from 13 European studies resulting in a total of 161 746 participants (49% men, mean age, 43.7 years). Longitudinal analysis with a median follow-up of 4 years was possible for four cohort studies (n = 42 222). Results. A total of 86 429 participants were of normal weight (BMI 18.524.9 kg m-2), 2149 were underweight (BMI < 18.5 kg m-2), 56 572 overweight (BMI 25.029.9 kg m-2) and 13 523 class I (BMI 3034.9 kg m-2) and 3073 classes II/III (BMI = 35 kg m-2) obese. In addition, 27 010 (17%) participants reported job strain. In cross-sectional analyses, we found increased odds of job strain amongst underweight [odds ratio 1.12, 95% confidence interval (CI) 1.001.25], obese class I (odds ratio 1.07, 95% CI 1.021.12) and obese classes II/III participants (odds ratio 1.14, 95% CI 1.011.28) as compared with participants of normal weight. In longitudinal analysis, both weight gain and weight loss were related to the onset of job strain during follow-up. Conclusions. In an analysis of European data, we found both weight gain and weight loss to be associated with the onset of job strain, consistent with a U-shaped cross-sectional association between job strain and BMI. These associations were relatively modest; therefore, it is unlikely that intervention to reduce job strain would be effective in combating obesity at a population level.
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| 7. |
- Heikkilä, Katriina, et al.
(författare)
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Job strain and COPD exacerbations: an individual-participant meta-analysis
- 2014
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 44:1, s. 247-251
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Tidskriftsartikel (refereegranskat)abstract
- To the Editor:Chronic obstructive pulmonary disease (COPD) is a major cause of mortality and disability worldwide (1). The clinical course of COPD is characterised by exacerbations, which can be minor and manageable at home or in primary care, or severe, leading to hospitalisation or even death. Known causes of exacerbations include tobacco smoke, air pollution, dusts and fumes, and respiratory infections (1, 2). One less well understood risk factor is stress, which could plausibly lead to COPD exacerbations as it can trigger inflammation (3, 4) and is associated with increased smoking (5), which are both implicated in COPD pathology (2). Work is an important source of stress in the age groups in which COPD is typically diagnosed (1, 6). However, we are not aware of previous investigations of work-related stress and the risk of COPD exacerbations.In this study, we examined the associations between job strain (the most widely studied conceptualisation of work-related stress) and severe COPD exacerbations using individual-level data from 10 prospective cohort studies from the Individual Participant Data Meta-analysis in Working Populations (IPD-Work) Consortium (7). Job strain is defined as a combination of high demands (excessive amounts of work) and low control (having little influence on what tasks to.
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| 8. |
- Möllerberg, Marie-Louise, et al.
(författare)
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Evaluation of skin reactions during proton beam radiotherapy : patient-reported versus clinician-reporte
- 2021
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Ingår i: Technical innovations & patient support in radiation oncology. - : Elsevier. - 2405-6324. ; 19, s. 11-17
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Tidskriftsartikel (refereegranskat)abstract
- Background: Skin reaction is a common side-effect of radiotherapy and often only assessed as clinician-reported outcome (CRO). The aim was to examine and compare patient-reported outcome (PRO) of skin reactions with CRO for signs of acute skin reactions for patients with primary brain tumour receiving proton beam radiotherapy (PBT). A further aim was to explore patients' experiences of the skin reactions.Methods: Acute skin reactions were assessed one week after start of treatment, mid-treatment and end of treatment among 253 patients with primary brain tumour who underwent PBT. PRO skin reactions were assessed with the RSAS and CRO according to the RTOG scale. Fleiss' kappa was performed to measure the inter-rater agreement of the assessments of skin reactions.Results: The results showed a discrepancy between PRO and CRO acute skin reactions. Radiation dose was associated with increased skin reactions, but no correlations were seen for age, gender, education, occupation, other treatment or smoking. There was a poor agreement between patients and clinicians (κ = -0.016) one week after the start of PBT, poor (κ = -0.045) to (κ = 0.396) moderate agreement at mid treatment and poor (κ = -0.010) to (κ = 0.296) moderate agreement at end of treatment. Generally, patients' symptom distress toward skin reactions was low at all time points.Conclusion: The poor agreement between PRO and CRO shows that the patient needs to be involved in assessments of skin reactions for a more complete understanding of skin reactions due to PBT. This may also improve patient experience regarding involvement in their own care.
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| 9. |
- Johnsen, Anna M., et al.
(författare)
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Association between occupational physical activity and myocardial infarction : A prospective cohort study
- 2016
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Ingår i: BMJ Open. - : BMJ. - 2044-6055. ; 6:10
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Tidskriftsartikel (refereegranskat)abstract
- Objective Recommendations regarding physical activity typically include both leisure time and occupational physical activity. However, the results from previous studies on occupational physical activity and the association with myocardial infarction have been inconsistent. The aim of this study was to investigate if occupational physical activity is associated with the risk of myocardial infarction. Design Prospective cohort study. Participants Data from the Swedish Work, Lipids and Fibrinogen (WOLF) study was used, comprising 9961 employees (6849 men, 3112 women, mean age 42.7 years) having no history of myocardial infarction. The participants were categorised into 3 groups according to their level of occupational physical activity. Outcome Data regarding incident myocardial infarction were obtained from the Swedish National Patient Register and the Cause of Death Register. Cox proportional hazard regression was used for estimation of HRs for different levels of occupational physical activity in relation to the risk of myocardial infarction. Results During a mean follow-up of 13.1 years, 249 cases of incident myocardial infarction were identified. In analyses adjusted for age, sex and socioeconomic status, participants standing and walking more than 50% of their working day had an HR of 1.13 (95% CI 0.83 to 1.54), compared with participants seated more than 50% of their working day. The corresponding HR for participants whose work included lifting or carrying was 0.86 (95% CI 0.59 to 1.24). Further adjustment did not alter the results. Stratified analyses resulted in a significantly decreased risk for young people whose work included lifting or carrying, HR 0.37 (95% CI 0.17 to 0.84), compared with younger persons who sat most of their working day. Conclusions No significant association between occupational physical activity and the risk of myocardial infarction was observed in the total group of employees in this study. Based on the results from this study, occupational physical activity in general does not seem to be enough for reducing the risk of myocardial infarction.
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| 10. |
- Kivimäki, Mika, et al.
(författare)
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Long working hours as a risk factor for atrial fibrillation : a multi-cohort study
- 2017
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Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 38:34, s. 2621-2628
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Tidskriftsartikel (refereegranskat)abstract
- Aims Studies suggest that people who work long hours are at increased risk of stroke, but the association of long working hours with atrial fibrillation, the most common cardiac arrhythmia and a risk factor for stroke, is unknown. We examined the risk of atrial fibrillation in individuals working long hours (>= 55 per week) and those working standard 35-40 h/week. Methods and results In this prospective multi-cohort study from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium, the study population was 85 494 working men and women (mean age 43.4 years) with no recorded atrial fibrillation. Working hours were assessed at study baseline (1991-2004). Mean follow-up for incident atrial fibrillation was 10 years and cases were defined using data on electrocardiograms, hospital records, drug reimbursement registers, and death certificates. We identified 1061 new cases of atrial fibrillation (10-year cumulative incidence 12.4 per 1000). After adjustment for age, sex and socioeconomic status, individuals working long hours had a 1.4-fold increased risk of atrial fibrillation compared with those working standard hours (hazard ratio = 1.42, 95% CI= 1.13-1.80, P= 0.003). There was no significant heterogeneity between the cohort-specific effect estimates (I-2= 0%, P = 0.66) and the finding remained after excluding participants with coronary heart disease or stroke at baseline or during the follow-up (N= 2006, hazard ratio= 1.36, 95% CI= 1.05-1.76, P = 0.0180). Adjustment for potential confounding factors, such as obesity, risky alcohol use and high blood pressure, had little impact on this association. Conclusion Individuals who worked long hours were more likely to develop atrial fibrillation than those working standard hours.
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