Jane E Ferrie

Uppsala University, Uppsala, Uppsala, Sweden

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Publications (200)1165.48 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The status of psychosocial stress at work as a risk factor for type 2 diabetes is unclear because existing evidence is based on small studies and is subject to confounding by lifestyle factors, such as obesity and physical inactivity. This collaborative study examined whether stress at work, defined as "job strain," is associated with incident type 2 diabetes independent of lifestyle factors.
    Diabetes care. 08/2014; 37(8):2268-75.
  • Jane E Ferrie, Shah Ebrahim
    International Journal of Epidemiology 06/2014; 43(3):639-44. · 6.98 Impact Factor
  • Epidemiology (Cambridge, Mass.) 05/2014; 25(3):464-5. · 5.51 Impact Factor
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    ABSTRACT: OBJECTIVE We examined whether psychological distress predicts incident type 2 diabetes and if the association differs between populations at higher or lower risk of type 2 diabetes.RESEARCH DESIGN AND METHODS Prospective cohort of 5,932 diabetes-free adults (4,189 men and 1,743 women, mean age 54.6 years) with three 5-year data cycles (1991-2009), a total of 13,207 person-observations. Participants were classified into four groups according to their prediabetes status and Framingham Offspring Type 2 Diabetes Risk Score: normoglycemia with a risk score of 0-9, normoglycemia with a risk score of 10-19, prediabetes with a risk score of 10-19, and prediabetes with a risk score of >19. Psychological distress was assessed by the General Health Questionnaire. Incident type 2 diabetes was ascertained by 2-h oral glucose tolerance test, doctor diagnosis, or use of antihyperglycemic medication at the 5-year follow-up for each data cycle. Adjustments were made for age, sex, ethnicity, socioeconomic status, antidepressant use, smoking, and physical activity.RESULTSAmong participants with normoglycemia and among those with prediabetes combined with a low risk score, psychological distress did not predict type 2 diabetes. Diabetes incidence in these groups varied between 1.6 and 15.6%. Among participants with prediabetes and a high risk score, 40.9% of those with psychological distress compared with 28.5% of those without distress developed diabetes during the follow-up. The corresponding adjusted odds ratio for psychological distress was 2.07 (95% CI 1.19-3.62).CONCLUSIONS These data suggest that psychological distress is associated with an accelerated progression to manifest diabetes in a subpopulation with advanced prediabetes.
    Diabetes care 05/2014; · 7.74 Impact Factor
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    ABSTRACT: Many patients and healthcare professionals believe that work-related psychosocial stress, such as job strain, can make asthma worse, but this is not corroborated by empirical evidence. We investigated the associations between job strain and the incidence of severe asthma exacerbations in working-age European men and women. We analysed individual-level data, collected between 1985 and 2010, from 102 175 working-age men and women in 11 prospective European studies. Job strain (a combination of high demands and low control at work) was self-reported at baseline. Incident severe asthma exacerbations were ascertained from national hospitalization and death registries. Associations between job strain and asthma exacerbations were modelled using Cox regression and the study-specific findings combined using random-effects meta-analyses. During a median follow-up of 10 years, 1 109 individuals experienced a severe asthma exacerbation (430 with asthma as the primary diagnostic code). In the age- and sex-adjusted analyses, job strain was associated with an increased risk of severe asthma exacerbations defined using the primary diagnostic code (hazard ratio, HR: 1.27, 95% confidence interval, CI: 1.00, 1.61). This association attenuated towards the null after adjustment for potential confounders (HR: 1.22, 95% CI: 0.96, 1.55). No association was observed in the analyses with asthma defined using any diagnostic code (HR: 1.01, 95% CI: 0.86, 1.19). Our findings suggest that job strain is probably not an important risk factor for severe asthma exacerbations leading to hospitalization or death.
    Allergy 04/2014; · 5.88 Impact Factor
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    ABSTRACT: We examined whether socioeconomic and psychosocial adversity in midlife predicts post-retirement depressive symptoms. A prospective cohort study of British civil servants who responded to a self-administered questionnaire in middle-age and at older ages, 21 years later. The study sample consisted of 3,939 Whitehall II Study participants (2,789 men, 1,150 women; mean age 67.6 years at follow-up) who were employed at baseline and retired at follow-up. Midlife adversity was assessed by self-reported socioeconomic adversity (low occupational position; poor standard of living) and psychosocial adversity (high job strain; few close relationships). Symptoms of depression post-retirement were measured by the Center for Epidemiologic Studies Depression scale. After adjustment for sociodemographic and health-related covariates at baseline and follow-up, there were strong associations between midlife adversities and post-retirement depressive symptoms: low occupational position (odds ratio [OR]: 1.70, 95% confidence interval [CI]: 1.15-2.51), poor standard of living (OR: 2.37, 95% CI: 1.66-3.39), high job strain (OR: 1.52, 95% CI: 1.09-2.14), and few close relationships (OR: 1.51, 95% CI: 1.12-2.03). The strength of the associations between socioeconomic, psychosocial, work-related, or non-work related exposures and depressive symptoms was similar. Robust associations from observational data suggest that several socioeconomic and psychosocial risk factors for symptoms of depression post-retirement can be detected already in midlife.
    The American journal of geriatric psychiatry: official journal of the American Association for Geriatric Psychiatry 04/2014; · 3.35 Impact Factor
  • Occupational and environmental medicine 02/2014; · 3.64 Impact Factor
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    ABSTRACT: Background Working long hours might have adverse health effects, but whether this is true for all socioeconomic status groups is unclear. In this meta-analysis stratified by socioeconomic status, we investigated the role of long working hours as a risk factor for type 2 diabetes. Methods We identified four published studies through a systematic literature search of PubMed and Embase up to April 30, 2014. Study inclusion criteria were English-language publication; prospective design (cohort study); investigation of the effect of working hours or overtime work; incident diabetes as an outcome; and relative risks, odds ratios, or hazard ratios (HRs) with 95% CIs, or sufficient information to calculate these estimates. Additionally, we used unpublished individual-level data from 19 cohort studies from the Individual-Participant-Data Meta-analysis in Working-Populations Consortium and international open-access data archives. Effect estimates from published and unpublished data from 222 120 men and women from the USA, Europe, Japan, and Australia were pooled with random-effects meta-analysis. Findings During 1·7 million person-years at risk, 4963 individuals developed diabetes (incidence 29 per 10 000 person-years). The minimally adjusted summary risk ratio for long (≥55 h per week) compared with standard working hours (35–40 h) was 1·07 (95% CI 0·89–1·27, difference in incidence three cases per 10 000 person-years) with significant heterogeneity in study-specific estimates (I2=53%, p=0·0016). In an analysis stratified by socioeconomic status, the association between long working hours and diabetes was evident in the low socioeconomic status group (risk ratio 1·29, 95% CI 1·06–1·57, difference in incidence 13 per 10 000 person-years, I2=0%, p=0·4662), but was null in the high socioeconomic status group (1·00, 95% CI 0·80–1·25, incidence difference zero per 10 000 person-years, I2=15%, p=0·2464). The association in the low socioeconomic status group was robust to adjustment for age, sex, obesity, and physical activity, and remained after exclusion of shift workers. Interpretation In this meta-analysis, the link between longer working hours and type 2 diabetes was apparent only in individuals in the low socioeconomic status groups. Funding Medical Research Council, European Union New and Emerging Risks in Occupational Safety and Health research programme, Finnish Work Environment Fund, Swedish Research Council for Working Life and Social Research, German Social Accident Insurance, Danish National Research Centre for the Working Environment, Academy of Finland, Ministry of Social Affairs and Employment (Netherlands), Economic and Social Research Council, US National Institutes of Health, and British Heart Foundation.
    The Lancet Diabetes & Endocrinology. 01/2014;
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    ABSTRACT: Both sleep duration and sleep quality are related to future health, but their combined effects on mortality are unsettled. We aimed to examine the individual and joint effects of sleep duration and sleep disturbances on cause-specific mortality in a large prospective cohort study. We included 9,098 men and women free of pre-existing disease from the Whitehall II study, UK. Sleep measures were self-reported at baseline (1985-1988). Participants were followed until 2010 in a nationwide death register for total and cause-specific (cardiovascular disease, cancer and other) mortality. There were 804 deaths over a mean 22 year follow-up period. In men, short sleep (≤6 hrs/night) and disturbed sleep were not independently associated with CVD mortality, but there was an indication of higher risk among men who experienced both (HR = 1.57; 95% CI: 0.96-2.58). In women, short sleep and disturbed sleep were independently associated with CVD mortality, and women with both short and disturbed sleep experienced a much higher risk of CVD mortality (3.19; 1.52-6.72) compared to those who slept 7-8 hours with no sleep disturbances; equivalent to approximately 90 additional deaths per 100,000 person years. Sleep was not associated with death due to cancer or other causes. Both short sleep and disturbed sleep are independent risk factors for CVD mortality in women and future studies on sleep may benefit from assessing disturbed sleep in addition to sleep duration in order to capture health-relevant features of inadequate sleep.
    PLoS ONE 01/2014; 9(4):e91965. · 3.53 Impact Factor
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    ABSTRACT: Context Given the current size and projected growth in the older population globally, it is important to identify early risk factors for depression in this group. Objective We examined whether socioeconomic and psychosocial adversity in midlife predicts post-retirement depressive symptoms. Design and Setting: A prospective cohort study of British civil servants who responded to a self-administered questionnaire in middle-age and at older ages, 21 years later. Participants The study sample consisted of 3,939 Whitehall II Study participants (2,789 men, 1,150 women; mean age 67.6 years at follow-up) who were employed at baseline and retired at follow-up. Measure ments: Midlife adversity was assessed by self-reported socioeconomic adversity (low occupational position; poor standard of living) and psychosocial adversity (high job strain; few close relationships). Symptoms of depression post-retirement were measured by the Center for Epidemiologic Studies Depression (CES-D) scale. Results After adjustment for socio-demographic and health-related covariates at baseline and follow-up, there were strong associations between midlife adversities and post-retirement depressive symptoms: odds ratio of low occupational position 1.70, 95% confidence interval (1.15- 2.51), poor standard of living 2.37 (1.66-3.39), high job strain 1.52 (1.09-2.14), and few close relationships 1.51 (1.12- 2.03). The strength of the associations between socioeconomic, psychosocial, work-related, or non-work related exposures and depressive symptoms was similar. Conclusions Robust associations from observational data suggest that several socioeconomic and psychosocial risk factors for symptoms of depression post-retirement can be detected already in midlife.
    The American Journal of Geriatric Psychiatry. 01/2014;
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    ABSTRACT: BACKGROUND AND AIMS: Many clinicians, patients and patient advocacy groups believe stress to have a causal role in inflammatory bowel diseases, such as Crohn's disease and ulcerative colitis. However, this is not corroborated by clear epidemiological research evidence. We investigated the association between work-related stress and incident Crohn's disease and ulcerative colitis using individual-level data from 95 000 European adults. METHODS: We conducted individual-participant data meta-analyses in a set of pooled data from 11 prospective European studies. All studies are a part of the IPD-Work Consortium. Work-related psychosocial stress was operationalised as job strain (a combination of high demands and low control at work) and was self-reported at baseline. Crohn's disease and ulcerative colitis were ascertained from national hospitalisation and drug reimbursement registers. The associations between job strain and inflammatory bowel disease outcomes were modelled using Cox proportional hazards regression. The study-specific results were combined in random effects meta-analyses. RESULTS: Of the 95 379 participants who were free of inflammatory bowel disease at baseline, 111 men and women developed Crohn's disease and 414 developed ulcerative colitis during follow-up. Job strain at baseline was not associated with incident Crohn's disease (multivariable-adjusted random effects hazard ratio: 0.83, 95% confidence interval: 0.48, 1.43) or ulcerative colitis (hazard ratio: 1.06, 95% CI: 0.76, 1.48). There was negligible heterogeneity among the study-specific associations. CONCLUSIONS: Our findings suggest that job strain, an indicator of work-related stress, is not a major risk factor for Crohn's disease or ulcerative colitis.
    PLoS ONE 01/2014; 9(2):e88711. · 3.53 Impact Factor
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    ABSTRACT: BACKGROUND:The importance of chronic inflammation as a determinant of aging phenotypes may have been underestimated in previous studies that used a single measurement of inflammatory markers. We assessed inflammatory markers twice over a 5-year exposure period to examine the association between chronic inflammation and future aging phenotypes in a large population of men and women. METHODS:We obtained data for 3044 middle-aged adults (28.2% women) who were participating in the Whitehall II study and had no history of stroke, myocardial infarction or cancer at our study's baseline (1997-1999). Interleukin-6 was measured at baseline and 5 years earlier. Cause-specific mortality, chronic disease and functioning were ascertained from hospital data, register linkage and clinical examinations. We used these data to create 4 aging phenotypes at the 10-year follow-up (2007-2009): successful aging (free of major chronic disease and with optimal physical, mental and cognitive functioning), incident fatal or nonfatal cardiovascular disease, death from noncardiovascular causes and normal aging (all other participants). RESULTS:Of the 3044 participants, 721 (23.7%) met the criteria for successful aging at the 10-year follow-up, 321 (10.6%) had cardiovascular disease events, 147 (4.8%) died from noncardiovascular causes, and the remaining 1855 (60.9%) were included in the normal aging phenotype. After adjustment for potential confounders, having a high interleukin- 6 level (> 2.0 ng/L) twice over the 5-year exposure period nearly halved the odds of successful aging at the 10-year follow-up (odds ratio [OR] 0.53, 95% confidence interval [CI] 0.38-0.74) and increased the risk of future cardiovascular events (OR 1.64, 95% CI 1.15-2.33) and noncardiovascular death (OR 2.43, 95% CI 1.58-3.80). INTERPRETATION:Chronic inflammation, as ascertained by repeat measurements, was associated with a range of unhealthy aging phenotypes and a decreased likelihood of successful aging. Our results suggest that assessing longterm chronic inflammation by repeat measurement of interleukin-6 has the potential to guide clinical practice.
    Canadian Medical Association Journal 09/2013; · 6.47 Impact Factor
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    BMJ British medical journal 08/2013; 347. · 16.30 Impact Factor
  • Jane E Ferrie, Shah Ebrahim
    International Journal of Epidemiology 08/2013; 42(4):930-1. · 6.98 Impact Factor
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    ABSTRACT: Depressive symptoms are associated with an increased risk of death, but most of this association remains unexplained. Our aim was to explore the contribution of sleep duration and disturbances to the association between depressive symptoms, all-cause and cardiovascular disease mortality. A total of 5813 (4220 men and 1593 women) aged 50-74 years at baseline, participants of the British Whitehall II prospective cohort study, were included. Depressive symptoms, sleep duration and disturbances were assessed in 2003-04. Mortality was ascertained through linkage to the national mortality register until August 2012, with a mean follow-up of 8.8 years. Depressive symptoms were associated with an increased risk of mortality from all causes [hazard ratio (HR) = 1.51; 95% confidence interval (CI): 1.16-1.97)] and cardiovascular diseases (HR = 1.63; 95% CI: 1.01-2.64) after adjustment for sociodemographic characteristics. Further adjustment for sleep duration and disturbances reduced the association between depressive symptoms and cardiovascular mortality by 21% (HR = 1.53; 95% CI: 0.91-2.57). Sleep seems to have a role, as a mediator or confounder, in explaining the association between depressive symptoms and cardiovascular mortality. These findings need replication in larger studies with longer follow-up.
    Journal of Sleep Research 07/2013; · 3.04 Impact Factor
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    ABSTRACT: Cross-sectional evidence suggests associations between sleep duration and levels of the inflammatory markers, C-reactive protein and interleukin-6. This longitudinal study uses data from the London-based Whitehall II study to examine whether changes in sleep duration are associated with average levels of inflammation from 2 measures 5 years apart. Sleep duration (≤5, 6, 7, 8, ≥9 hours on an average week night) was assessed in 5,003 middle-aged women and men in 1991/1994 and 1997/1999. Fasting levels of C-reactive protein and interleukin-6 were measured in 1997/1999 and 2002/2004. Cross-sectional analyses indicated that shorter sleep is associated with higher levels of inflammatory markers. Longitudinal analyses showed that each hour per night decrease in sleep duration between 1991/1994 and 1997/1999 was associated with higher levels of C-reactive protein (8.1%) and interleukin-6 (4.5%) averaged across measures in 1997/1999 and 2002/2004. Adjustment for longstanding illness and major cardiometabolic risk factors indicated that disease processes may partially underlie these associations. An increase in sleep duration was not associated with average levels of inflammatory markers. These results suggest that both short sleep and reductions in sleep are associated with average levels of inflammation over a 5-year period.
    American journal of epidemiology 06/2013; · 5.59 Impact Factor
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    ABSTRACT: Job strain is associated with an increased coronary heart disease risk, but few large-scale studies have examined the relationship of this psychosocial characteristic with the biological risk factors that potentially mediate the job strain - heart disease association. We pooled cross-sectional, individual-level data from eight studies comprising 47,045 participants to investigate the association between job strain and the following cardiovascular disease risk factors: diabetes, blood pressure, pulse pressure, lipid fractions, smoking, alcohol consumption, physical inactivity, obesity, and overall cardiovascular disease risk as indexed by the Framingham Risk Score. In age-, sex-, and socioeconomic status-adjusted analyses, compared to those without job strain, people with job strain were more likely to have diabetes (odds ratio 1.29; 95% CI: 1.11-1.51), to smoke (1.14; 1.08-1.20), to be physically inactive (1.34; 1.26-1.41), and to be obese (1.12; 1.04-1.20). The association between job strain and elevated Framingham risk score (1.13; 1.03-1.25) was attributable to the higher prevalence of diabetes, smoking and physical inactivity among those reporting job strain. In this meta-analysis of work-related stress and cardiovascular disease risk factors, job strain was linked to adverse lifestyle and diabetes. No association was observed between job strain, clinic blood pressure or blood lipids.
    PLoS ONE 06/2013; 8(6):e67323. · 3.53 Impact Factor
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    ABSTRACT: Objectives. We examined the associations of job strain, an indicator of work-related stress, with overall unhealthy and healthy lifestyles. Methods. We conducted a meta-analysis of individual-level data from 11 European studies (cross-sectional data: n = 118 701; longitudinal data: n = 43 971). We analyzed job strain as a set of binary (job strain vs no job strain) and categorical (high job strain, active job, passive job, and low job strain) variables. Factors used to define healthy and unhealthy lifestyles were body mass index, smoking, alcohol intake, and leisure-time physical activity. Results. Individuals with job strain were more likely than those with no job strain to have 4 unhealthy lifestyle factors (odds ratio [OR] = 1.25; 95% confidence interval [CI] = 1.12, 1.39) and less likely to have 4 healthy lifestyle factors (OR = 0.89; 95% CI = 0.80, 0.99). The odds of adopting a healthy lifestyle during study follow-up were lower among individuals with high job strain than among those with low job strain (OR = 0.88; 95% CI = 0.81, 0.96). Conclusions. Work-related stress is associated with unhealthy lifestyles and the absence of stress is associated with healthy lifestyles, but longitudinal analyses suggest no straightforward cause-effect relationship between work-related stress and lifestyle. (Am J Public Health. Published online ahead of print May 16, 2013: e1-e8. doi:10.2105/AJPH.2012.301090).
    American Journal of Public Health 05/2013; · 3.93 Impact Factor
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    ABSTRACT: BACKGROUND:It is unclear whether a healthy lifestyle mitigates the adverse effects of job strain on coronary artery disease. We examined the associations of job strain and lifestyle risk factors with the risk of coronary artery disease. METHODS:We pooled individual-level data from 7 cohort studies comprising 102 128 men and women who were free of existing coronary artery disease at baseline (1985-2000). Questionnaires were used to measure job strain (yes v. no) and 4 lifestyle risk factors: current smoking, physical inactivity, heavy drinking and obesity. We grouped participants into 3 lifestyle categories: healthy (no lifestyle risk factors), moderately unhealthy (1 risk factor) and unhealthy (2-4 risk factors). The primary outcome was incident coronary artery disease (defined as first nonfatal myocardial infarction or cardiac-related death). RESULTS:There were 1086 incident events in 743 948 person-years at risk during a mean follow-up of 7.3 years. The risk of coronary artery disease among people who had an unhealthy lifestyle compared with those who had a healthy lifestyle (hazard ratio [HR] 2.55, 95% confidence interval [CI] 2.18-2.98; population attributable risk 26.4%) was higher than the risk among participants who had job strain compared with those who had no job strain (HR 1.25, 95% CI 1.06-1.47; population attributable risk 3.8%). The 10-year incidence of coronary artery disease among participants with job strain and a healthy lifestyle (14.7 per 1000) was 53% lower than the incidence among those with job strain and an unhealthy lifestyle (31.2 per 1000). INTERPRETATION:The risk of coronary artery disease was highest among participants who reported job strain and an unhealthy lifestyle; those with job strain and a healthy lifestyle had half the rate of disease. A healthy lifestyle may substantially reduce disease risk among people with job strain.
    Canadian Medical Association Journal 05/2013; · 6.47 Impact Factor
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    ABSTRACT: OBJECTIVE: The main aims of this longitudinal study were to (i) examine associations between changes in economic difficulties and health functioning among middle-aged employees and (ii) assess whether the associations remained after considering conventional domains of socioeconomic position. The associations were tested in two European welfare state occupational cohorts to strengthen the evidence base and improve generalizability. METHODS: Data came from two cohorts: the Finnish Helsinki Health Study (baseline 2000-2002, follow-up 2007, N=6328) and the British Whitehall II Study (baseline 1997-1999, follow-up 2003-2004, N=4350). Responses to the survey item "finding it hard to afford adequate food and clothes and pay bills" repeated at baseline and follow-up were used to examine persistent, increasing, and decreasing economic difficulties. Poor physical and mental health functioning were denoted as being in the lowest quartile of the Short Form 36 physical and mental component summary. Logistic regression analyses were adjusted for sex, age, childhood economic difficulties, household income at baseline and follow-up, employment status at follow-up, and baseline health functioning. RESULTS: We observed strong sex- and age-adjusted associations between increasing [odds ratio (OR) range 1.69-2.96] and persistent (OR range 2.54-3.21) economic difficulties and poorer physical and mental health functioning in both British and Finnish occupational cohorts. These associations remained after full adjustments. Those reporting decreasing difficulties over follow-up also had poorer functioning (OR range 1.30-1.61) compared to those who did not have difficulties at baseline, possibly reflecting residual effects of economic difficulties at baseline. CONCLUSION: Changes in economic difficulties are associated with poorer physical and mental health functioning independent of income, employment status, and baseline health functioning.
    Scandinavian Journal of Work, Environment & Health 04/2013; · 3.10 Impact Factor

Publication Stats

7k Citations
1,165.48 Total Impact Points

Institutions

  • 2014
    • Uppsala University
      Uppsala, Uppsala, Sweden
  • 2011–2014
    • University of Bristol
      • MRC Centre for Causal Analyses in Translational Epidemiology
      Bristol, England, United Kingdom
    • University of Texas Health Science Center at San Antonio
      • Division of Clinical Epidemiology
      San Antonio, TX, United States
  • 1997–2014
    • University College London
      • Department of Epidemiology and Public Health
      Londinium, England, United Kingdom
  • 2013
    • University of Duisburg-Essen
      Essen, North Rhine-Westphalia, Germany
  • 2003–2013
    • Finnish Institute of Occupational Health
      • Centre of Expertise for Work Organizations
      Helsinki, Southern Finland Province, Finland
  • 2012
    • University Hospital of Lausanne
      Lausanne, Vaud, Switzerland
  • 2004–2012
    • Karolinska Institutet
      • Institutionen för klinisk neurovetenskap
      Solna, Stockholm, Sweden
  • 2000–2012
    • University of Helsinki
      • • Department of Dental Public Health
      • • Department of Psychology
      Helsinki, Province of Southern Finland, Finland
  • 2009–2011
    • National Institute for Health and Welfare, Finland
      Helsinki, Southern Finland Province, Finland
    • National Public Health Institute
      Helsinki, Southern Finland Province, Finland
    • University of Turku
      • Department of Public Health
      Turku, Western Finland, Finland
    • Public Health England
      Londinium, England, United Kingdom
  • 2005–2011
    • French Institute of Health and Medical Research
      • Centre de Recherche en Épidémiologie et Santé des Populations CESP U1018
      Paris, Ile-de-France, France
  • 2009–2010
    • Stockholm University
      • Stress Research Institute
      Stockholm, Stockholm, Sweden
  • 2008
    • The University of Warwick
      • Warwick Medical School (WMS)
      Coventry, ENG, United Kingdom
  • 2007
    • Warwick Business School
      Warwick, England, United Kingdom
  • 2002–2005
    • University of Tampere
      • Medical School
      Tampere, Western Finland, Finland
  • 1992–1993
    • London School of Hygiene and Tropical Medicine
      Londinium, England, United Kingdom
    • Middlesex University, UK
      Londinium, England, United Kingdom