| 1. |
- Bokenberger, Kathleen, et al.
(författare)
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Shift work and risk of incident dementia : a study of two population-based cohorts
- 2018
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Ingår i: European Journal of Epidemiology. - : Springer. - 0393-2990 .- 1573-7284. ; 33:10, s. 977-987
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Tidskriftsartikel (refereegranskat)abstract
- This study aimed to investigate the association between shift work and incident dementia in two population-based cohorts from the Swedish Twin Registry (STR). The STR-1973 sample included 13,283 participants born 1926–1943 who received a mailed questionnaire in 1973 that asked about status (ever/never) and duration (years) of shift work employment. The Screening Across the Lifespan Twin (SALT) sample included 41,199 participants born 1900–1958 who participated in a telephone interview in 1998–2002 that asked about night work status and duration. Dementia diagnoses came from Swedish patient registers. Cox proportional-hazards regression was used to estimate hazard ratios (HR) with 95% confidence intervals (CI). Potential confounders such as age, sex, education, diabetes, cardiovascular disease and stroke were included in adjusted models. In genotyped subsamples (n = 2977 in STR-1973; n = 10,366 in SALT), APOE ε4 status was considered in models. A total of 983 (7.4%) and 1979 (4.8%) dementia cases were identified after a median of 41.2 and 14.1 years follow-up in the STR-1973 and SALT sample, respectively. Ever shift work (HR 1.36, 95% CI 1.15–1.60) and night work (HR 1.12, 95% CI 1.01–1.23) were associated with higher dementia incidence. Modest dose-response associations were observed, where longer duration shift work and night work predicted increased dementia risk. Among APOE ε4 carriers, individuals exposed to ≥ 20 years of shift work and night work had increased dementia risk compared to day workers. Findings indicate that shift work, including night shift work, compared to non-shift jobs is associated with increased dementia incidence. Confirmation of findings is needed.
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| 2. |
- Cabrera-Moksnes, Claudia, 1966, et al.
(författare)
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Can the relation between tooth loss and chronic disease be explained by socio-economic status? A 24-year follow-up from the population study of women in Gothenburg, Sweden.
- 2005
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Ingår i: European journal of epidemiology. - : Springer Science and Business Media LLC. - 0393-2990 .- 1573-7284. ; 20:3, s. 229-36
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Tidskriftsartikel (refereegranskat)abstract
- The objective of this study was to evaluate the association between number of missing teeth and all cause, cardiovascular, and cancer mortality as well as morbidity and to explore whether socio-economic factors mediate this association. An ongoing prospective cohort study of 1462 Swedish women included a dental survey in 1968/69 with follow-up until 1992/93. The dental examination included a panoramic radiographic survey and a questionnaire. Number of missing teeth at baseline was analysed in a Cox proportional hazards model to estimate time to mortality and morbidity. Number of missing teeth, independently of socio-economic status variables (the husband's occupational category, combined income, and education) was associated with increased all cause mortality and cardiovascular disease mortality respectively (relative risk (RR): 1.36; 95% confidence interval (95% CI): 1.18-1.58) and (RR: 1.46; 95% CI: 1.15-1.85 per 10 missing teeth), but no associations were found for cancer mortality (RR: 1.18; 95% CI: 0.91-1.52). The relation between poor oral health and future cardiovascular disease could not be explained by measures of socio-economic status in this study.
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| 3. |
- Karlsson, Ida K., et al.
(författare)
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Adiposity and the risk of dementia : mediating effects from inflammation and lipid levels
- 2022
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Ingår i: European Journal of Epidemiology. - : Springer Nature Switzerland AG.. - 0393-2990 .- 1573-7284. ; 37:12, s. 1261-1271
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Tidskriftsartikel (refereegranskat)abstract
- While midlife adiposity is a risk factor for dementia, adiposity in late-life appears to be associated with lower risk. What drives the associations is poorly understood, especially the inverse association in late-life. Using results from genome-wide association studies, we identified inflammation and lipid metabolism as biological pathways involved in both adiposity and dementia. To test if these factors mediate the effect of midlife and/or late-life adiposity on dementia, we then used cohort data from the Swedish Twin Registry, with measures of adiposity and potential mediators taken in midlife (age 40–64, n = 5999) or late-life (age 65–90, n = 7257). Associations between body-mass index (BMI), waist-hip ratio (WHR), C-reactive protein (CRP), lipid levels, and dementia were tested in survival and mediation analyses. Age was used as the underlying time scale, and sex and education included as covariates in all models. Fasting status was included as a covariate in models of lipids. One standard deviation (SD) higher WHR in midlife was associated with 25% (95% CI 2–52%) higher dementia risk, with slight attenuation when adjusting for BMI. No evidence of mediation through CRP or lipid levels was present. After age 65, one SD higher BMI, but not WHR, was associated with 8% (95% CI 1–14%) lower dementia risk. The association was partly mediated by higher CRP, and suppressed when high-density lipoprotein levels were low. In conclusion, the negative effects of midlife adiposity on dementia risk were driven directly by factors associated with body fat distribution, with no evidence of mediation through inflammation or lipid levels. There was an inverse association between late-life adiposity and dementia risk, especially where the body’s inflammatory response and lipid homeostasis is intact.
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