| 1. |
- Palmer, Nicholette D, et al.
(författare)
-
A genome-wide association search for type 2 diabetes genes in African Americans.
- 2012
-
Ingår i: PloS one. - San Francisco : Public Library of Science (PLoS). - 1932-6203. ; 7:1, s. e29202-
-
Tidskriftsartikel (refereegranskat)abstract
- African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5×10(-8)). SNP rs7560163 (P = 7.0×10(-9), OR (95% CI) = 0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5×10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations.
|
|
| 2. |
- Saxena, Richa, et al.
(författare)
-
Genetic variation in GIPR influences the glucose and insulin responses to an oral glucose challenge
- 2010
-
Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 42:2, s. 142-148
-
Tidskriftsartikel (refereegranskat)abstract
- Glucose levels 2 h after an oral glucose challenge are a clinical measure of glucose tolerance used in the diagnosis of type 2 diabetes. We report a meta-analysis of nine genome-wide association studies (n = 15,234 nondiabetic individuals) and a follow-up of 29 independent loci (n = 6,958–30,620). We identify variants at the GIPR locus associated with 2-h glucose level (rs10423928, β (s.e.m.) = 0.09 (0.01) mmol/l per A allele, P = 2.0 × 10−15). The GIPR A-allele carriers also showed decreased insulin secretion (n = 22,492; insulinogenic index, P = 1.0 × 10−17; ratio of insulin to glucose area under the curve, P = 1.3 × 10−16) and diminished incretin effect (n = 804; P = 4.3 × 10−4). We also identified variants at ADCY5 (rs2877716, P = 4.2 × 10−16), VPS13C (rs17271305, P = 4.1 × 10−8), GCKR (rs1260326, P = 7.1 × 10−11) and TCF7L2 (rs7903146, P = 4.2 × 10−10) associated with 2-h glucose. Of the three newly implicated loci (GIPR, ADCY5 and VPS13C), only ADCY5 was found to be associated with type 2 diabetes in collaborating studies (n = 35,869 cases, 89,798 controls, OR = 1.12, 95% CI 1.09–1.15, P = 4.8 × 10−18).
|
|
| 3. |
- Scott, Robert A, et al.
(författare)
-
No interactions between previously associated 2-hour glucose gene variants and physical activity or BMI on 2-hour glucose levels
- 2012
-
Ingår i: Diabetes. - Alexandria, VA : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 61:5, s. 1291-1296
-
Tidskriftsartikel (refereegranskat)abstract
- Gene-lifestyle interactions have been suggested to contribute to the development of type 2 diabetes. Glucose levels 2 h after a standard 75-g glucose challenge are used to diagnose diabetes and are associated with both genetic and lifestyle factors. However, whether these factors interact to determine 2-h glucose levels is unknown. We meta-analyzed single nucleotide polymorphism (SNP) × BMI and SNP × physical activity (PA) interaction regression models for five SNPs previously associated with 2-h glucose levels from up to 22 studies comprising 54,884 individuals without diabetes. PA levels were dichotomized, with individuals below the first quintile classified as inactive (20%) and the remainder as active (80%). BMI was considered a continuous trait. Inactive individuals had higher 2-h glucose levels than active individuals (β = 0.22 mmol/L [95% CI 0.13-0.31], P = 1.63 × 10(-6)). All SNPs were associated with 2-h glucose (β = 0.06-0.12 mmol/allele, P ≤ 1.53 × 10(-7)), but no significant interactions were found with PA (P > 0.18) or BMI (P ≥ 0.04). In this large study of gene-lifestyle interaction, we observed no interactions between genetic and lifestyle factors, both of which were associated with 2-h glucose. It is perhaps unlikely that top loci from genome-wide association studies will exhibit strong subgroup-specific effects, and may not, therefore, make the best candidates for the study of interactions.
|
|
| 4. |
|
|
| 5. |
- Kilpeläinen, Tuomas O, et al.
(författare)
-
Physical activity attenuates the influence of FTO variants on obesity risk: a meta-analysis of 218,166 adults and 19,268 children.
- 2011
-
Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676 .- 1549-1277. ; 8:11
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n=218,166) and nine studies of children and adolescents (n=19,268). METHODS AND FINDINGS: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r(2)>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTO×PA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (p(interaction) =0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio =1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio =1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents. CONCLUSIONS: The association of the FTO risk allele with the odds of obesity is attenuated by 27% in physically active adults, highlighting the importance of PA in particular in those genetically predisposed to obesity.
|
|
| 6. |
- Wood, Angela M., et al.
(författare)
-
Risk thresholds for alcohol consumption : combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies
- 2018
-
Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 391:10129, s. 1513-1523
-
Tidskriftsartikel (refereegranskat)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.
|
|
| 7. |
- Chandola, Tarani, et al.
(författare)
-
The effect of short sleep duration on coronary heart disease risk is greatest among those with sleep disturbance : a prospective study from the Whitehall II cohort.
- 2010
-
Ingår i: Sleep. - 0161-8105 .- 1550-9109. ; 33:6, s. 739-44
-
Tidskriftsartikel (refereegranskat)abstract
- STUDY OBJECTIVES: Short sleep duration is associated with increased CHD (coronary heart disease) mortality and morbidity, although some evidence suggests that sleep disturbance is just as important. We investigated whether a combination of short sleep duration and sleep disturbance is associated with a higher risk of CHD than their additive effects. SETTING: The Whitehall II study. PATIENTS OR PARTICIPANTS: The Whitehall II study recruited 10,308 participants from 20 civil service departments in London, England. Participants were between the ages of 35 and 55 years at baseline (1985-1988) and were followed up for an average of 15 years. INTERVENTIONS: N/A. MEASUREMENTS: Sleep hours and sleep disturbance (from the General Heath Questionnaire-30) were obtained from the baseline survey. CHD events included fatal CHD deaths or incident nonfatal myocardial infarction or angina (ICD-9 codes 410-414 or ICD-10 120-25). RESULTS: Short sleep duration and sleep disturbance were both associated with increased hazards for CHD in women as well as in men, although, after we adjusted for confounders, only those reporting sleep disturbance had a raised risk. There was some evidence for an interaction between sleep duration and sleep disturbance. Participants with short sleep duration and restless disturbed nights had the highest hazard ratios (HR) of CHD (relative risk:1.55, 95% confidence interval:1.33-1.81). Among participants who did not report any sleep disturbance, there was little evidence that short sleep hours increased CHD risk. CONCLUSION: The effect of short sleep (< or = 6 hours) on increasing CHD risk is greatest among those who reported some sleep disturbance. However, among participants who did not report any sleep disturbance, there was little evidence that short sleep hours increased CHD risk.
|
|
| 8. |
|
|
| 9. |
- Fransson, Eleonor, 1971-, et al.
(författare)
-
Job strain as a risk factor for leisure-time physical inactivity : an individual-participant meta-analysis of up to 170,000 men and women
- 2012
-
Ingår i: American Journal of Epidemiology. - Cary : Oxford University Press. - 0002-9262 .- 1476-6256. ; 176:12, s. 1078-1089
-
Forskningsöversikt (refereegranskat)abstract
- Unfavorable work characteristics, such as low job control and too high or too low job demands, have been suggested to increase the likelihood of physical inactivity during leisure time, but this has not been verified in large-scale studies. The authors combined individual-level data from 14 European cohort studies (baseline years from 19851988 to 20062008) to examine the association between unfavorable work characteristics and leisure-time physical inactivity in a total of 170,162 employees (50 women; mean age, 43.5 years). Of these employees, 56,735 were reexamined after 29 years. In cross-sectional analyses, the odds for physical inactivity were 26 higher (odds ratio 1.26, 95 confidence interval: 1.15, 1.38) for employees with high-strain jobs (low control/high demands) and 21 higher (odds ratio 1.21, 95 confidence interval: 1.11, 1.31) for those with passive jobs (low control/low demands) compared with employees in low-strain jobs (high control/low demands). In prospective analyses restricted to physically active participants, the odds of becoming physically inactive during follow-up were 21 and 20 higher for those with high-strain (odds ratio 1.21, 95 confidence interval: 1.11, 1.32) and passive (odds ratio 1.20, 95 confidence interval: 1.11, 1.30) jobs at baseline. These data suggest that unfavorable work characteristics may have a spillover effect on leisure-time physical activity.
|
|
| 10. |
- Friel, Sharon, et al.
(författare)
-
Global health equity and climate stabilisation: a common agenda
- 2008
-
Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 372:9650, s. 1677-1683
-
Tidskriftsartikel (refereegranskat)abstract
- Although health has improved for many people, the extent of health inequities between and within countries is growing. Meanwhile, humankind is disrupting the global climate and other life-supporting environmental systems, thereby creating serious risks for health and wellbeing, especially in vulnerable populations but ultimately for everybody. Underlying determinants of health inequity and environmental change overlap substantially; they are signs of an economic system predicated on asymmetric growth and competition, shaped by market forces that mostly disregard health and environmental consequences rather than by values of fairness and support. A shift is needed in priorities in economic development towards healthy forms of urbanisation, more efficient and renewable energy sources, and a sustainable and fairer food system. Global interconnectedness and interdependence enable the social and environmental determinants of health to be addressed in ways that will increase health equity, reduce poverty, and build societies that live within environmental limits.
|
|
| 11. |
- Heikkila, Katriina, et al.
(författare)
-
Job Strain and Alcohol Intake : A Collaborative Meta-Analysis of Individual-Participant Data from 140 000 Men and Women
- 2012
-
Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:7, s. Art. no. e40101-
-
Tidskriftsartikel (refereegranskat)abstract
- Background: The relationship between work-related stress and alcohol intake is uncertain. In order to add to the thus far inconsistent evidence from relatively small studies, we conducted individual-participant meta-analyses of the association between work-related stress (operationalised as self-reported job strain) and alcohol intake. Methodology and Principal Findings: We analysed cross-sectional data from 12 European studies (n = 142 140) and longitudinal data from four studies (n = 48 646). Job strain and alcohol intake were self-reported. Job strain was analysed as a binary variable (strain vs. no strain). Alcohol intake was harmonised into the following categories: none, moderate (women: 1-14, men: 1-21 drinks/week), intermediate (women: 15-20, men: 22-27 drinks/week) and heavy (women: > 20, men: > 27 drinks/week). Cross-sectional associations were modelled using logistic regression and the results pooled in random effects meta-analyses. Longitudinal associations were examined using mixed effects logistic and modified Poisson regression. Compared to moderate drinkers, non-drinkers and (random effects odds ratio (OR): 1.10, 95% CI: 1.05, 1.14) and heavy drinkers (OR: 1.12, 95% CI: 1.00, 1.26) had higher odds of job strain. Intermediate drinkers, on the other hand, had lower odds of job strain (OR: 0.92, 95% CI: 0.86, 0.99). We found no clear evidence for longitudinal associations between job strain and alcohol intake. Conclusions: Our findings suggest that compared to moderate drinkers, non-drinkers and heavy drinkers are more likely and intermediate drinkers less likely to report work-related stress.
|
|
| 12. |
- Heikkila, Katriina, et al.
(författare)
-
Job Strain and Tobacco Smoking : An Individual-Participant Data Meta-Analysis of 166 130 Adults in 15 European Studies
- 2012
-
Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:7
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Tobacco smoking is a major contributor to the public health burden and healthcare costs worldwide, but the determinants of smoking behaviours are poorly understood. We conducted a large individual-participant meta-analysis to examine the extent to which work-related stress, operationalised as job strain, is associated with tobacco smoking in working adults. Methodology and Principal Findings: We analysed cross-sectional data from 15 European studies comprising 166 130 participants. Longitudinal data from six studies were used. Job strain and smoking were self-reported. Smoking was harmonised into three categories never, ex- and current. We modelled the cross-sectional associations using logistic regression and the results pooled in random effects meta-analyses. Mixed effects logistic regression was used to examine longitudinal associations. Of the 166 130 participants, 17% reported job strain, 42% were never smokers, 33% ex-smokers and 25% current smokers. In the analyses of the cross-sectional data, current smokers had higher odds of job strain than never-smokers (age, sex and socioeconomic position-adjusted odds ratio: 1.11, 95% confidence interval: 1.03, 1.18). Current smokers with job strain smoked, on average, three cigarettes per week more than current smokers without job strain. In the analyses of longitudinal data (1 to 9 years of follow-up), there was no clear evidence for longitudinal associations between job strain and taking up or quitting smoking. Conclusions: Our findings show that smokers are slightly more likely than non-smokers to report work-related stress. In addition, smokers who reported work stress smoked, on average, slightly more cigarettes than stress-free smokers.
|
|
| 13. |
- Heikkilä, Katriina, et al.
(författare)
-
Work stress and risk of cancer: meta-analysis of 5700 incident cancer events in 116 000 European men and women
- 2013
-
Ingår i: The BMJ. - : BMJ. - 1756-1833. ; 345:f165
-
Tidskriftsartikel (refereegranskat)abstract
- Objective To investigate whether work related stress, measured and defined as job strain, is associated with the overall risk of cancer and the risk of colorectal, lung, breast, or prostate cancers.Design Meta-analysis of pooled prospective individual participant data from 12 European cohort studies including 116 056 men and women aged 17-70 who were free from cancer at study baseline and were followed-up for a median of 12 years. Work stress was measured and defined as job strain, which was self reported at baseline. Incident cancers (all n=5765, colorectal cancer n=522, lung cancer n=374, breast cancer n=1010, prostate cancer n=865) were ascertained from cancer, hospital admission, and death registers. Data were analysed in each study with Cox regression and the study specific estimates pooled in meta-analyses. Models were adjusted for age, sex, socioeconomic position, body mass index (BMI), smoking, and alcohol intakeResults A harmonised measure of work stress, high job strain, was not associated with overall risk of cancer (hazard ratio 0.97, 95% confidence interval 0.90 to 1.04) in the multivariable adjusted analyses. Similarly, no association was observed between job strain and the risk of colorectal (1.16, 0.90 to 1.48), lung (1.17, 0.88 to 1.54), breast (0.97, 0.82 to 1.14), or prostate (0.86, 0.68 to 1.09) cancers. There was no clear evidence for an association between the categories of job strain and the risk of cancer.Conclusions These findings suggest that work related stress, measured and defined as job strain, at baseline is unlikely to be an important risk factor for colorectal, lung, breast, or prostate cancers.
|
|
| 14. |
- Jokela, Markus, et al.
(författare)
-
From midlife to early old age : health trajectories associated with retirement.
- 2010
-
Ingår i: Epidemiology. - 1044-3983 .- 1531-5487. ; 21:3, s. 284-90
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Previous studies report contradictory findings regarding health effects of retirement. This study examines longitudinally the associations of retirement with mental health and physical functioning. METHODS: The participants were 7584 civil servants from the Whitehall II cohort study aged 39-64 years at baseline and 54-76 years at the last follow-up. Self-reported mental health and physical functioning were assessed using the Short Form Medical Outcomes Survey questionnaire, and the scales were scored as T-scores (mean [SD] = 50 [10]). Retirement status and health were assessed with 6 repeated measurements over a 15-year period. RESULTS: The associations between retirement and health were dependent on age at retirement, reason for retirement, and length of time spent in retirement. Compared with continued employment, statutory retirement at age 60 and early voluntary retirement, respectively, were associated with 2.2 (95% confidence interval = 1.7 to 2.8) and 2.2 (1.7 to 2.7) points higher mental health and with 1.0 (0.6 to 1.5) and 1.1 (0.8 to 1.4) points higher physical functioning. Retirement due to ill health was associated with poorer mental health (-0.7 points [-1.62 to 0.2]) and physical functioning (-4.5 points [-5.1 to -3.9]). Within-subject analyses suggested a causal interpretation for statutory and voluntary retirement, but health selection for retirement due to ill health. CONCLUSIONS: Longitudinal analyses of repeat data suggest that health status improves after statutory and voluntarily retirement, although the improvement seems to attenuate over time. By contrast, the association between retirement due to ill health and subsequent poor health seems to reflect selection rather than causation.
|
|
| 15. |
- Kivimäki, Mika, et al.
(författare)
-
Association between socioeconomic status and the development of mental and physical health conditions in adulthood : a multi-cohort study
- 2020
-
Ingår i: The Lancet Public Health. - : Elsevier. - 2468-2667. ; 5:3, s. e140-e149
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Socioeconomic disadvantage is a risk factor for many diseases. We characterised cascades of these conditions by using a data-driven approach to examine the association between socioeconomic status and temporal sequences in the development of 56 common diseases and health conditions. Methods: In this multi-cohort study, we used data from two Finnish prospective cohort studies: the Health and Social Support study and the Finnish Public Sector study. Our pooled prospective primary analysis data comprised 109 246 Finnish adults aged 17–77 years at study entry. We captured socioeconomic status using area deprivation and education at baseline (1998–2013). Participants were followed up for health conditions diagnosed according to the WHO International Classification of Diseases until 2016 using linkage to national health records. We tested the generalisability of our findings with an independent UK cohort study—the Whitehall II study (9838 people, baseline in 1997, follow-up to 2017)—using a further socioeconomic status indicator, occupational position. Findings: During 1 110 831 person-years at risk, we recorded 245 573 hospitalisations in the Finnish cohorts; the corresponding numbers in the UK study were 60 946 hospitalisations in 186 572 person-years. Across the three socioeconomic position indicators and after adjustment for lifestyle factors, compared with more advantaged groups, low socioeconomic status was associated with increased risk for 18 (32·1%) of the 56 conditions. 16 diseases formed a cascade of inter-related health conditions with a hazard ratio greater than 5. This sequence began with psychiatric disorders, substance abuse, and self-harm, which were associated with later liver and renal diseases, ischaemic heart disease, cerebral infarction, chronic obstructive bronchitis, lung cancer, and dementia. Interpretation: Our findings highlight the importance of mental health and behavioural problems in setting in motion the development of a range of socioeconomically patterned physical illnesses. Policy and health-care practice addressing psychological health issues in social context and early in the life course could be effective strategies for reducing health inequalities. Funding: UK Medical Research Council, US National Institute on Aging, NordForsk, British Heart Foundation, Academy of Finland, and Helsinki Institute of Life Science.
|
|
| 16. |
- Kristenson, Margareta, 1950-
(författare)
-
The LiVcordia Study : Possible causes for the differences in coronary heart disease mortality between Lithuania and Sweden
- 1998
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background: In recent decades coronary heart disease (CHD) mortality has declined in Western Europe and increased in Central and Eastern Europe. A large difference in CHD mortality has developed and the causes are not known. Lithuania and Sweden had similar CHD mortality rates for middle-aged men twenty years ago but in 1994 this mortality was four times higher in Lithuania than in Sweden. Also within countries CHD mortality is higher in low socioeconomic groups.Aim of the study: The LiVicordia (Linköping-Vilnius-coronary-artery-disease-risk-assessment) study aimed at identifying possible explanations for the different CHD mortality rates in the two countries.Method: This cross-sectional study concomitantly compared 150 randomly sampled 50-year-old men in each of the cities Vilnius, Lithuania and Linköping, Sweden from October 1993 nntil March 1995 using identical, standardised methodology. Investigations included a broad range of traditional and psychosocial risk factors for CHD, measures of oxidative stress, a standardised laboratory stress test and ultrasound measures of Peripheral atherosclerosis.Results: The differences found in traditional risk factors for CHD were small. Systolic blood pressure (SBP) was higher in Vilnius men, smoking was similar and plasma LDL cholesterol levels higher in Linköping men. Lower serum levels of the lipid soluble antioxidant vitamins carotene, lycopene and ytocopherol were found in Vilnius men, and also a higher susceptibility of LDL to oxidation in vitro. An unfavourable pattern of psychosocial risk factors for CHD: job strain, social isolation, depression and vital exhaustion characterised Vilnins men, who also showed an attenuated cortisol response to the laboratory stress test. This stress response has earlier been shown in states of chronic stress; loss of dynamic capacity to respond to new demands may be a predisposing factor for disease. Vilnius men had more peripheral atherosclerosis; thicker intima media, more and larger plaques and greater stiffness. Measures of atherosclerosis related to SBP, smoking, LDL cholesterol arrl P-carotene. The same unfavourable profile of risk factors for CHD, which characterised Vilnius men, was also found in underprivileged groups withip the cities. There were few differences in traditional risk factors.Conclusions: Thus, based on our survey on risk factors for CHD, it can be stated that traditional risk factors seem not to explain the different CHD mortality rates between Lithuania and Sweden. Possible alternative explanations are psychosocial strain and oxidative stress. These factors were also found among men in underprivileged groups within the cities. Therfore the influence of the risk factors studied may be relevant also for socioeconomic inequalities in CHD mortality within countries.
|
|
| 17. |
- Kumari, Meena, et al.
(författare)
-
Self-reported sleep duration and sleep disturbance are independently associated with cortisol secretion in the Whitehall II study.
- 2009
-
Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 94:12, s. 4801-9
-
Tidskriftsartikel (refereegranskat)abstract
- CONTEXT: The association of short sleep duration with cortisol secretion has not been thoroughly examined in large community dwelling populations and the relative importance of short sleep duration and sleep disturbance is unclear. OBJECTIVE: The objective of the study was to assess the relationships between self-reported sleep duration, sleep disturbance, and salivary cortisol secretion. DESIGN: This was a cross-sectional analysis using data from phase 7 (2002-2004) of the Whitehall II study. Sleep disturbances were assessed using a modified version of the Jenkins Scale. SETTING: The occupational cohort was originally recruited in 1985-1989. PARTICIPANTS: Analyses included 2751 participants with complete cortisol measures and who collected their first sample within 15 min of waking, were not on medication affecting cortisol secretion, and had complete information for all covariates. OUTCOME MEASURE: Six saliva samples were taken on waking, waking + 0.5, 2.5, 8, and 12 h and bedtime for the assessment of the cortisol awakening response and the slope in cortisol secretion across the day. RESULTS: In mutually adjusted analyses, both sleep duration and disturbances were independently associated with a flatter diurnal slope in cortisol secretion, such that evening cortisol secretion was raised in those reporting short sleep duration and high sleep disturbance. Short sleep duration was also associated with the cortisol awakening response. These effects were independent of a number of covariates, including waking time on day of sampling and stress on the day of cortisol assessment. CONCLUSION: Short sleep duration and increased sleep disturbances are independently associated with diurnal slope in cortisol secretion of a large community-based cohort of middle-aged men and women.
|
|
| 18. |
- Lewis, Kate Marie, et al.
(författare)
-
Mothers education and offspring asthma risk in 10 European cohort studies
- 2017
-
Ingår i: European Journal of Epidemiology. - : SPRINGER. - 0393-2990 .- 1573-7284. ; 32:9, s. 797-805
-
Tidskriftsartikel (refereegranskat)abstract
- Highly prevalent and typically beginning in childhood, asthma is a burdensome disease, yet the risk factors for this condition are not clarified. To enhance understanding, this study assessed the cohort-specific and pooled risk of maternal education on asthma in children aged 3-8 across 10 European countries. Data on 47,099 children were obtained from prospective birth cohort studies across 10 European countries. We calculated cohort-specific prevalence difference in asthma outcomes using the relative index of inequality (RII) and slope index of inequality (SII). Results from all countries were pooled using random-effects meta-analysis procedures to obtain mean RII and SII scores at the European level. Final models were adjusted for child sex, smoking during pregnancy, parity, mothers age and ethnicity. The higher the score the greater the magnitude of relative (RII, reference 1) and absolute (SII, reference 0) inequity. The pooled RII estimate for asthma risk across all cohorts was 1.46 (95% CI 1.26, 1.71) and the pooled SII estimate was 1.90 (95% CI 0.26, 3.54). Of the countries examined, France, the United Kingdom and the Netherlands had the highest prevalences of childhood asthma and the largest inequity in asthma risk. Smaller inverse associations were noted for all other countries except Italy, which presented contradictory scores, but with small effect sizes. Tests for heterogeneity yielded significant results for SII scores. Overall, offspring of mothers with a low level of education had an increased relative and absolute risk of asthma compared to offspring of high-educated mothers.
|
|
| 19. |
- Ruiz, Milagros, et al.
(författare)
-
Impact of Low Maternal Education on Early Childhood Overweight and Obesity in Europe
- 2016
-
Ingår i: Paediatric and Perinatal Epidemiology. - : WILEY-BLACKWELL. - 0269-5022 .- 1365-3016. ; 30:3, s. 274-284
-
Tidskriftsartikel (refereegranskat)abstract
- BackgroundComparable evidence on adiposity inequalities in early life is lacking across a range of European countries. This study investigates whether low maternal education is associated with overweight and obesity risk in children from distinct European settings during early childhood. MethodsProspective data of 45 413 children from 11 European cohorts were used. Childrens height and weight obtained at ages 4-7 years were used to assess prevalent overweight and obesity according to the International Obesity Task Force definition. The Relative/Slope Indices of Inequality (RII/SII) were estimated within each cohort and by gender to investigate adiposity risk among children born to mothers with low education as compared to counterparts born to mothers with high education. Individual-data meta-analyses were conducted to obtain aggregate estimates and to assess heterogeneity between cohorts. ResultsLow maternal education yielded a substantial risk of early childhood adiposity across 11 European countries. Low maternal education yielded a mean risk ratio of 1.58 (95% confidence interval (CI) 1.34, 1.85) and a mean risk difference of 7.78% (5.34, 10.22) in early childhood overweight, respectively, measured by the RII and SII. Early childhood obesity risk by low maternal education was as substantial for all cohorts combined (RII = 2.61 (2.10, 3.23)) and (SII = 4.01% (3.14, 4.88)). Inequalities in early childhood adiposity were consistent among boys, but varied among girls in a few cohorts. ConclusionsConsiderable inequalities in overweight and obesity are evident among European children in early life. Tackling early childhood adiposity is necessary to promote childrens immediate health and well-being and throughout the life course.
|
|
| 20. |
- Ruiz, Milagros, et al.
(författare)
-
Mother's education and the risk of preterm and small for gestational age birth: a DRIVERS meta-analysis of 12 European cohorts
- 2015
-
Ingår i: Journal of Epidemiology and Community Health. - : BMJ Publishing Group. - 0143-005X .- 1470-2738. ; 69:9, s. 826-833
-
Tidskriftsartikel (refereegranskat)abstract
- Background A healthy start to life is a major priority in efforts to reduce health inequalities across Europe, with important implications for the health of future generations. There is limited combined evidence on inequalities in health among newborns across a range of European countries. Methods Prospective cohort data of 75 296 newborns from 12 European countries were used. Maternal education, preterm and small for gestational age births were determined at baseline along with covariate data. Regression models were estimated within each cohort and meta-analyses were conducted to compare and measure heterogeneity between cohorts. Results Mothers education was linked to an appreciable risk of preterm and small for gestational age (SGA) births across 12 European countries. The excess risk of preterm births associated with low maternal education was 1.48 (1.29 to 1.69) and 1.84 (0.99 to 2.69) in relative and absolute terms (Relative/Slope Index of Inequality, RII/SII) for all cohorts combined. Similar effects were found for SGA births, but absolute inequalities were greater, with an SII score of 3.64 (1.74 to 5.54). Inequalities at birth were strong in the Netherlands, the UK, Sweden and Spain and marginal in other countries studied. Conclusions This study highlights the value of comparative cohort analysis to better understand the relationship between maternal education and markers of fetal growth in different settings across Europe.
|
|
| 21. |
- Talmud, Philippa J., et al.
(författare)
-
Gene-centric Association Signals for Lipids and Apolipoproteins Identified via the HumanCVD BeadChip
- 2009
-
Ingår i: American Journal of Human Genetics. - : Elsevier BV. - 0002-9297. ; 85:5, s. 628-642
-
Tidskriftsartikel (refereegranskat)abstract
- Blood lipids are important cardiovascular disease (CVD) risk factors with both genetic and environmental determinants. The Whitehall II study (n = 5592) was genotyped with the gene-centric HumanCVD BeadChip (Illumina). We identified 195 SNPs in 16 genes/regions associated with 3 major lipid fractions and 2 apolipoprotein components at p < 10(-5), with the associations being broadly concordant with prior genome-wide analysis. SNPs associated with LDL cholesterol and apolipoprotein B were located in LDLR, PCSK9, APOB, CELSR2, HWGCR, CETP, the TOMM40-APOE-C1-C2-C4 cluster, and the APOA5-A4-C3-A1 cluster; SNPs associated with HDL cholesterol and apolipoprotein AI were in CETP, LPL, LIPC, APOA5-A4-C3-A1, and ABCA1; and SNPs associated with triglycerides in GCKR, BAZIB, MLXIPL, LPL, and APOA5-A4-C3-A1. For 48 SNPs in previously unreported loci that were significant at p < 10(-4) in Whitehall II, in silico analysis including the British Women's Heart and Health Study, BRIGHT, ASCOT, and NORDIL studies (total n > 12,500) revealed previously unreported associations of SH2B3 (p < 2.2 x 10(-6)), BMPR2 (p < 2.3 x 10(-7)), BCL3/PVRL2 (flanking APOE; p < 4.4 x 10(-8)), and SMARCA4 (flanking LDLR; p < 2.5 x 10(-7)) with LDL cholesterol. Common alleles in these genes explained 6.1%-14.7% of the variance in the five lipid-related traits, and individuals at opposite tails of the additive allele score exhibited substantial differences in trait levels (e.g., > 1 mmol/L in LDL cholesterol [similar to 1 SD of the trait distribution]). These data suggest that multiple common alleles of small effect can make important contributions to individual differences in blood lipids potentially relevant to the assessment of CVD risk. These genes provide further insights into lipid metabolism and the likely effects of modifying the encoded targets therapeutically.
|
|
| 22. |
- Theorell, Töres, et al.
(författare)
-
Job Strain as a Risk Factor for Type 2 Diabetes : A Pooled Analysis of 124,808 Men and Women
- 2014
-
Ingår i: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 37:8, s. 2268-2275
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE 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. RESEARCH DESIGN AND METHODS We extracted individual-level data for 124,808 diabetes-free adults from 13 European cohort studies participating in the IPD-Work Consortium. We measured job strain with baseline questionnaires. Incident type 2 diabetes at follow-up was ascertained using national health registers, clinical screening, and self-reports. We analyzed data for each study using Cox regression and pooled the study-specific estimates in fixed-effect meta-analyses. RESULTS There were 3,703 cases of incident diabetes during a mean follow-up of 10.3 years. After adjustment for age, sex, and socioeconomic status (SES), the hazard ratio (HR) for job strain compared with no job strain was 1.15 (95% CI 1.06-1.25) with no difference between men and women (1.19 [1.06-1.34] and 1.13 [1.00-1.28], respectively). In stratified analyses, job strain was associated with an increased risk of diabetes among those with healthy and unhealthy lifestyle habits. In a multivariable model adjusted for age, sex, SES, and lifestyle habits, the HR was 1.11 (1.00-1.23). CONCLUSIONS Findings from a large pan-European dataset suggest that job strain is a risk factor for type 2 diabetes in men and women independent of lifestyle factors.
|
|
| 23. |
- Vaccarella, Salvatore, et al.
(författare)
-
Socioeconomic inequalities in cancer mortality between and within countries in Europe : a population-based study
- 2023
-
Ingår i: The Lancet Regional Health. - : Elsevier. - 2666-7762. ; 25
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Reducing socioeconomic inequalities in cancer is a priority for the public health agenda. A systematic assessment and benchmarking of socioeconomic inequalities in cancer across many countries and over time in Europe is not yet available.METHODS: Census-linked, whole-of-population cancer-specific mortality data by socioeconomic position, as measured by education level, and sex were collected, harmonized, analysed, and compared across 18 countries during 1990-2015, in adults aged 40-79. We computed absolute and relative educational inequalities; temporal trends using estimated-annual-percentage-changes; the share of cancer mortality linked to educational inequalities.FINDINGS: Everywhere in Europe, lower-educated individuals have higher mortality rates for nearly all cancer-types relative to their more highly-educated counterparts, particularly for tobacco/infection-related cancers [relative risk of lung cancer mortality for lower- versus higher-educated = 2.4 (95% confidence intervals: 2.1-2.8) among men; = 1.8 (95% confidence intervals: 1.5-2.1) among women]. However, the magnitude of inequalities varies greatly by country and over time, predominantly due to differences in cancer mortality among lower-educated groups, as for many cancer-types higher-educated have more similar (and lower) rates, irrespective of the country. Inequalities were generally greater in Baltic/Central/East-Europe and smaller in South-Europe, although among women large and rising inequalities were found in North-Europe (relative risk of all cancer mortality for lower- versus higher-educated ≥1.4 in Denmark, Norway, Sweden, Finland and the England/Wales). Among men, rate differences (per 100,000 person-years) in total-cancer mortality for lower-vs-higher-educated groups ranged from 110 (Sweden) to 559 (Czech Republic); among women from approximately null (Slovenia, Italy, Spain) to 176 (Denmark). Lung cancer was the largest contributor to inequalities in total-cancer mortality (between-country range: men, 29-61%; women, 10-56%). 32% of cancer deaths in men and 16% in women (but up to 46% and 24%, respectively in Baltic/Central/East-Europe) were associated with educational inequalities.INTERPRETATION: Cancer mortality in Europe is largely driven by levels and trends of cancer mortality rates in lower-education groups. Even Nordic-countries, with a long-established tradition of equitable welfare and social justice policies, witness increases in cancer inequalities among women. These results call for a systematic measurement, monitoring and action upon the remarkable socioeconomic inequalities in cancer existing in Europe.FUNDING: This study was done as part of the LIFEPATH project, which has received financial support from the European Commission (Horizon 2020 grant number 633666), and the DEMETRIQ project, which received support from the European Commission (grant numbers FP7-CP-FP and 278511). SV and WN were supported by the French Institut National du Cancer (INCa) (Grant number 2018-116). PM was supported by the Academy of Finland (#308247, # 345219) and the European Research Council under the European Union's Horizon 2020 research and innovation programme (grant agreement No 101019329). The work by Mall Leinsalu was supported by the Estonian Research Council (grant PRG722).
|
|
| 24. |
- Westerlund, Hugo, et al.
(författare)
-
Does working while ill trigger serious coronary events? The Whitehall II study.
- 2009
-
Ingår i: Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine. - 1536-5948. ; 51:9, s. 1099-104
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Working while ill has been found to predict coronary heart disease. We tested if this association was due to triggering. METHODS: We used a nested case-control study in an occupational cohort to examine sickness absences during a 2-year period immediately before the first coronary event for 133 cases and 928 matched controls without a history of coronary events. Working while ill was defined as no absence despite being unhealthy (suboptimal self-rated health or psychological distress). RESULTS: The odds of a coronary event were not higher for cases who worked while ill than for correspondingly unhealthy controls who took >0 to 14 days of absence per year (OR = 0.62; 95% CI = 0.28 to 1.38). These results were little affected by multiple adjustments. CONCLUSIONS: We found no evidence that working while ill acts as a short-term trigger for coronary events.
|
|
| 25. |
|
|
