| 1. |
- Pan, Kuan-Yu, et al.
(författare)
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Psychosocial working conditions, trajectories of disability, and the mediating role of cognitive decline and chronic diseases : A population-based cohort study
- 2019
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Ingår i: PLoS Medicine. - : Public Library of Science (PLoS). - 1549-1277 .- 1549-1676. ; 16:9
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Tidskriftsartikel (refereegranskat)abstract
- Background Unfavorable psychosocial working conditions have been associated with cognitive decline and chronic diseases, both of which may subsequently accelerate functional dependence. This study aimed to investigate the association between job demand-control-support combinations and trajectories of disability in later life and to further explore the role of cognitive decline and the co-occurrence of chronic diseases in mediating this association. Methods and findings In this cohort study, 2,937 community dwellers aged 60+ years (mean age 73 +/- 10.6; 62.9% female) residing in the Kungsholmen District of Stockholm, Sweden, participated in the baseline survey (2001-2004) and were followed up to 12 years. Lifelong occupational history was obtained through a standardized interview; job demands, job control, and social support at work in the longest-held occupation were graded with a psychosocial job-exposure matrix. Job control, demands, and social support were dichotomized using the median values from the matrix, respectively, to further generate demand-control-support combinations. Disability was measured by summing the number of impaired basic and instrumental activities of daily living. Global cognitive function was assessed by Mini-Mental State Examination. Chronic conditions were ascertained by clinical examinations, medical history, and patient clinical records; the total number of chronic diseases was summed. Data were analyzed using linear mixed-effects models and mediation analysis. Age, sex, education, alcohol consumption, smoking, leisure activity engagement, early-life socioeconomic status, occupational characteristic and physical demands, and baseline cognitive function and number of chronic diseases were adjusted for in the analyses. Compared with active jobs (high control/high demands; n = 1,807), high strain (low control/high demands; n = 328), low strain (high control/low demands; n = 495), and passive jobs (low control/low demands; n = 307) were all associated with a faster rate of disability progression (beta = 0.07, 95% CI 0.02-0.13, p = 0.01; beta = 0.10, 95% CI 0.06-0.15, p < 0.001; beta = 0.11, 95% CI 0.05-0.18, p < 0.001). The association between high strain and disability progression was only shown in people with low social support at work (beta = 0.13, 95% CI 0.07-0.19, p < 0.001), but not in those with high social support (beta = 0.004, 95% CI -0.09 to 0.10, p = 0.93). Moreover, we estimated that the association between demand-control status and disability trajectories was mediated 38.5% by cognitive decline and 18.4% by accumulation of chronic diseases during the follow-up period. The limitations of this study include unmeasured confounding, self-reported work experience, and the reliance on a psychosocial job-exposure matrix that does not consider variabilities in individuals' perception on working conditions or job characteristics within occupations. Conclusions Our findings suggest that negative psychosocial working conditions during working life may accelerate disability progression in later life. Notably, social support at work may buffer the detrimental effect of high strain on disability progression. Cognitive decline and chronic-disease accumulation, and especially the former, partially mediate the association of psychosocial working conditions with trajectories of disability. Further studies are required to explore more mechanisms that underlie the association between psychosocial working conditions and disability trajectories. Author summaryWhy was this study done? Work is one of the activities that take up a considerable amount of time in our adult lives, thus potentially making it an important determinant of health, even in later life. Inability to independently carry out daily tasks (defined as disability) can affect older people's quality of life and pose a burden on caregivers and societies. A better understanding of the pathway between midlife working conditions and late-life disability may help the development of preventive strategies. What did the researchers do and find? We studied the association of psychosocial working conditions with the rate of disability progression over 12 years in a cohort of 2,937 individuals aged 60 years and older. We found that unfavorable psychosocial working conditions, including high-strain, low-strain, and passive jobs, were related to a faster rate of disability progression. The association of high-strain jobs with accelerated disability accumulation was only present among people with low social support at work. The decrement in cognitive function and increase in chronic-disease burden, and especially the former, partially explained the relationship between unfavorable working conditions and disability progression in later life. What do these findings mean? Unfavorable psychosocial working conditions during working life are related to the progression of disability in later life. Public health authorities, employers, and employees should all be aware of that. Social support at work is especially important in a high-strain work environment given its capacity to attenuate the impact of high-strain jobs on disability accumulation. Monitoring cognitive function and medical conditions of people with unfavorable working conditions is endorsed by the role of both dimensions, and especially of cognitive dysfunction, in accelerating disability progression in older age.
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| 2. |
- Vetrano, Davide L., et al.
(författare)
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Trajectories of functional decline in older adults with neuropsychiatric and cardiovascular multimorbidity : A Swedish cohort study
- 2018
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Ingår i: PLoS Medicine. - : Public Library of Science (PLoS). - 1549-1277 .- 1549-1676. ; 15:3
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundFunctional decline is a strong health determinant in older adults, and chronic diseases play a major role in this age-related phenomenon. In this study, we explored possible clinical pathways underlying functional heterogeneity in older adults by quantifying the impact of cardiovascular (CV) and neuropsychiatric (NP) chronic diseases and their co-occurrence on trajectories of functional decline.Methods and findingsWe studied 2,385 people >= 60 years (range 60-101 years) participating in the Swedish National study of Aging and Care in Kungsholmen (SNAC-K). Participants underwent clinical examination at baseline (2001-2004) and every 3 or 6 years for up to 9 years. We grouped participants on the basis of 7 mutually exclusive clinical patterns of 0, 1, or more CV and NP diseases and their co-occurrence, from a group without any CV and NP disease to a group characterised by the presence of CV or NP multimorbidity, accompanied by at least 1 other CV or NP disorder. The group with no CV and/or NP diseases served as the reference group. Functional decline was estimated over 9 years of follow-up by measuring mobility (walking speed, m/s) and independence (ability to carry out six activities of daily living [ADL]). Mixed-effect linear regression models were used (1) to explore the individual-level prognostic predictivity of the different CV and NP clinical patterns at baseline and (2) to quantify the association between the clinical patterns and functional decline at the group level by entering the clinical patterns as time-varying measures. During the 9-year follow-up, participants with multiple CV and NP diseases had the steepest decline in walking speed (up to 0.7 m/s; p < 0.001) and ADL independence (up to three impairments in ADL, p < 0.001) (reference group: participants without any CV and NP disease). When the clinical patterns were analyzed as time varying, isolated CV multimorbidity impacted only walking speed (beta -0.1; p < 0.001). Conversely, all the clinical patterns that included at least 1 NP disease were significantly associated with decline in both walking speed (beta -0.21--0.08; p < 0.001) and ADL independence (beta -0.27--0.06; p < 0.05). Groups with the most complex clinical patterns had 5%-20% lower functioning at follow-up than the reference group. Key limitations of the study include that we did not take into account the specific weight of single diseases and their severity and that the exclusion of participants with less than 2 assessments may have led to an underestimation of the tested associations.ConclusionsIn older adults, different patterns of CV and NP morbidity lead to different trajectories of functional decline over time, a finding that explains part of the heterogeneity observed in older adults' functionality. NP diseases, alone or in association, are prevalent and major determinants of functional decline, whereas isolated CV multimorbidity is associated only with declines in mobility.
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| 3. |
- Wang, Hui-Xin, et al.
(författare)
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Association of lifelong exposure to cognitive reserve-enhancing factors with dementia risk : A community-based cohort study
- 2017
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Ingår i: PLoS Medicine. - : Public Library of Science (PLoS). - 1549-1277 .- 1549-1676. ; 14:3
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Variation in the clinical manifestation of dementia has been associated with differences in cognitive reserve, although less is known about the cumulative effects of exposure to cognitive reserve factors over the life course. We examined the association of cognitive reserve-related factors over the lifespan with the risk of dementia in a community-based cohort of older adults.METHODS AND FINDINGS: Information on early-life education, socioeconomic status, work complexity at age 20, midlife occupation attainment, and late-life leisure activities was collected in a cohort of dementia-free community dwellers aged 75+ y residing in the Kungsholmen district of Stockholm, Sweden, in 1987-1989. The cohort was followed up to 9 y (until 1996) to detect incident dementia cases. To exclude preclinical phases of disease, participants who developed dementia at the first follow-up examination 3 y after the baseline were excluded (n = 602 after exclusions). Structural equation modelling was used to generate latent factors of cognitive reserve from three periods over the life course: early (before 20 y), adulthood (around 30-55 y), and late life (75 y and older). The correlation between early- and adult-life latent factors was strong (γ = 0.9), whereas early-late (γ = 0.27) and adult-late (γ = 0.16) latent factor correlations were weak. One hundred forty-eight participants developed dementia during follow-up, and 454 remained dementia-free. The relative risk (RR) of dementia was estimated using Cox models with life-course cognitive reserve-enhancing factors modelled separately and simultaneously to assess direct and indirect effects. The analysis was repeated among carriers and noncarriers of the apolipoprotein E (APOE) ε4 allele. A reduced risk of dementia was associated with early- (RR 0.57; 95% CI 0.36-0.90), adult- (RR 0.60; 95% CI 0.42-0.87), and late-life (RR 0.52; 95% CI 0.37-0.73) reserve-enhancing latent factors in separate multivariable Cox models. In a mutually adjusted model, which may have been imprecisely estimated because of strong correlation between early- and adult-life factors, the late-life factor preserved its association (RR 0.65; 95% CI 0.45-0.94), whereas the effect of midlife (RR 0.73; 95% CI 0.50-1.06) and early-life factors (RR 0.76; 95% CI 0.47-1.23) on the risk of dementia was attenuated. The risk declined progressively with cumulative exposure to reserve-enhancing latent factors, and having high scores on cognitive reserve-enhancing composite factors in all three periods over the life course was associated with the lowest risk of dementia (RR 0.40; 95% CI 0.20-0.81). Similar associations were detected among APOE ε4 allele carriers and noncarriers. Limitations include measurement error and nonresponse, with both biases likely favouring the null. Strong correlation between early- and adult-life latent factors may have led to a loss in precision when estimating mutually adjusted effects of all periods.CONCLUSIONS: In this study, cumulative exposure to reserve-enhancing factors over the lifespan was associated with reduced risk of dementia in late life, even among individuals with genetic predisposition.
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| 4. |
- Xu, Wei-Li, et al.
(författare)
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HHEX_23 AA Genotype Exacerbates Effect of Diabetes on Dementia and Alzheimer Disease : A Population-Based Longitudinal Study
- 2015
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Ingår i: PLoS Medicine. - : Public Library of Science (PLoS). - 1549-1277 .- 1549-1676. ; 12:7
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Tidskriftsartikel (refereegranskat)abstract
- Background Research has suggested that variations within the IDE/HHEX gene region may underlie the association of type 2 diabetes with Alzheimer disease (AD). We sought to explore whether IDE genes play a role in the association of diabetes with dementia, AD, and structural brain changes using data from two community-based cohorts of older adults and a subsample with structural MRI. Methods and Findings The first cohort, which included dementia-free adults aged >= 75 y (n = 970) at baseline, was followed for 9 y to detect incident dementia (n = 358) and AD (n = 271) cases. The second cohort (for replication), which included 2,060 dementia-free participants aged >= 60 y at baseline, was followed for 6 y to identify incident dementia (n = 166) and AD (n = 121) cases. A subsample (n = 338) of dementia-free participants from the second cohort underwent MRI. HHEX_23 and IDE_9 were genotyped, and diabetes (here including type 2 diabetes and prediabetes) was assessed. In the first cohort, diabetes led to an adjusted hazard ratio (HR) of 1.73 (95% CI 1.19-2.32) and 1.66 (95% CI 1.06-2.40) for dementia and AD, respectively, among all participants. Compared to people carrying the GG genotype without diabetes, AA genotype carriers with diabetes had an adjusted HR of 5.54 (95% CI 2.407.18) and 4.81 (95% CI 1.88-8.50) for dementia and AD, respectively. There was a significant interaction between HHEX_23-AA and diabetes on dementia (HR 4.79, 95% CI 1.63-8.90, p = 0.013) and AD (HR 3.55, 95% CI 1.45-9.91, p = 0.025) compared to the GG genotype without diabetes. In the second cohort, the HRs were 1.68 (95% CI 1.04-2.99) and 1.64 (1.02-2.33) for the diabetes-AD and dementia-AD associations, respectively, and 4.06 (95% CI 1.06-7.58, p = 0.039) and 3.29 (95% CI 1.02-8.33, p = 0.044) for the interactions, respectively. MRI data showed that HHEX_23-AA carriers with diabetes had significant structural brain changes compared to HHEX_23-GG carriers without diabetes. No joint effects of IDE_9 and diabetes on dementia were shown. As a limitation, the sample sizes were small for certain subgroups. Conclusions A variant in the HHEX_23 gene interacts with diabetes to be associated with a substantially increased risk of dementia and AD, and with structural brain changes among dementia-free elderly people.
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