Prevalence of disability according to multimorbidity and disease clustering: a population-based study

Background: The prevalence of chronic diseases has increased with population ageing, and research has attempted to elucidate the correlation between chronic diseases and disability. However, most studies in older populations have focused on the effect of single disabling conditions, even though most older adults have more than one chronic disease (multimorbidity). Objective: The aims of this study were to evaluate the association of disability with disease, in terms of multimorbidity and specified pairs of diseases, in a population-based study of older adults. Materials and Methods: Using the Kungsholmen Project, we estimated the prevalence of disability by the number of chronic diseases, disease status by organ systems, and in specific pairs of chronic conditions, in a Swedish population (n=1,099; ≥77 years). Disability was defined as need of assistance in at least one activity of daily living (Katz index). Results: Functional disability was seen in 17.9% of participants. It increased as the number of chronic diseases increased. The prevalence of disability varied greatly amongst specific pairs of diseases: from 6.7% in persons affected by hypertension and atrial fibrillation to 82.4% in persons affected by dementia and hip fracture. In multivariate logistic regression models, the disease pairs that were significantly associated with the highest increased relative odds of disability contained dementia (dementia–hip fracture, dementia–CVD, and dementia–depression). Conclusions: Our findings suggest specific pairs of diseases are much more highly associated with disability than others, particularly diseases coupled with dementia. This knowledge may improve prevention of disablement and planning of resource distribution.Journal of Comorbidity 2011;1(1):11–1

personality and survival in older age the role of lifestyle behaviors and health status

Objective We intended to assess the relationship between personality and survival in an older population and to explore the role of lifestyle behaviors and health status as potential mediators. Design Population-based cohort study. Setting Swedish National Study of Aging and Care in Kungsholmen, Sweden. Participants 2,298 adults aged 60 or more years, without dementia or depression, followed for 11 years. Measurements Personality (extraversion, neuroticism, and openness) was assessed with a shortened version of the NEO-Five Factor Inventory. We tested whether personality affected mortality and examined the potential mediating effect of health status (body mass index, number of chronic diseases, impairment in instrumental activities of daily living, and C-reactive protein) and lifestyle behaviors (leisure activities, social network, smoking, and alcohol consumption). Results Over 11 years of follow-up, higher levels of extraversion were associated with a 14% reduction in mortality. Examination of different combinations of personality traits showed that independent of levels of neuroticism and openness, high extraversion were associated with up to 65% lower mortality. Decomposing the effect of extraversion on mortality, we found that the majority (44%) of the beneficial effect was mediated by healthy lifestyle behaviors. Health status accounted for 5% of the association. Conclusions Extroverted people, who are characterized by higher optimism and high self-efficacy, are prone to healthier behaviors and better health, which may result in longer survival. These results highlight the importance of a healthy lifestyle in survival

Disease or function? What matters most for self-rated health in older people depends on age

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Measuring gait speed to better identify prodromal dementia

Abstract Slow gait speed has been shown to predict incident dementia and cognitive decline in older individuals. We aimed to summarize the evidence concerning the association of slow gait speed with cognitive decline and dementia, and discuss the possible shared pathways leading to cognitive and motor impairments, under the unifying hypothesis that body and mind are intimately connected. This is a scoping review supported by a systematic search of the literature, performed on PubMed and Web of Science. Longitudinal studies providing information on the role of gait speed in the prediction of cognitive decline and dementia in cognitively intact people and in those with initial cognitive impairment were eligible. Of 39 studies selected, including overall 57,456 participants, 33 reported a significant association between gait speed and cognitive outcomes, including dementia. Neurodegenerative pathology and cerebrovascular burden may damage cerebral areas involved in both cognitive functions and motor control. At the same time, systemic conditions, characterized by higher cardiorespiratory, and metabolic and inflammatory burden, can affect a number of organs and systems involved in motor functions, including the brain, having ultimately an impact on cognition. The interplay of body and mind seems relevant during the development of cognitive decline and dementia. The measurement of gait speed may improve the detection of prodromal dementia and cognitive impairment in individuals with and without initial cognitive deficits. The potential applicability of such a measure in both clinical and research settings points at the importance of expanding our knowledge about the common underlying mechanisms of cognitive and motor decline

social engagement in late life may attenuate the burden of depressive symptoms due to financial strain in childhood

Abstract Background : It remains poorly understood if childhood financial strain is associated with old-age depression and if active social life may mitigate this relationship. Aims : To investigate the association between childhood financial strain and depressive symptoms during aging; to examine whether late-life social engagement modifies this association. Method : 2884 dementia-free individuals (aged 60+) from the Swedish National study of Aging and Care-Kungsholmen were clinically examined over a 15-year follow-up. Presence of childhood financial strain was ascertained at baseline. Depressive symptoms were repeatedly assessed with the Montgomery–Asberg Depression Rating Scale. Social engagement comprised information on baseline social network and leisure activities. Linear, logistic and mixed-effect models estimated baseline and longitudinal associations accounting for sociodemographic, clinical, and lifestyle factors. Results : Childhood financial strain was independently associated with a higher baseline level of depressive symptoms (β = 0.37, 95%CI 0.10-0.65), but not with symptom change over time. Relative to those without financial strain and with active social engagement, depressive burden was increased in those without financial strain but with inactive social engagement (β = 0.43, 95%CI: 0.15-0.71), and in those with both financial strain and inactive engagement (β = 0.99; 95%CI: 0.59-1.40). Individuals with financial strain and active social engagement exhibited similar depressive burden as those without financial strain and with active social engagement. Limitations : Recall bias and reverse causality may affect study results, although sensitivity analyses suggest their limited effect. Conclusions : Early-life financial strain may be of lasting importance for old-age depressive symptoms. Active social engagement in late-life may mitigate this association

effect of the interplay between genetic and behavioral risks on survival after age 75

Objectives To explore the association between genes that may be related to human mortality, taking into account the possible contribution of morbidity, and investigate whether lifestyle behaviors may attenuate genetic risk. Design Twenty-five-year population-based cohort study. Setting Kungsholmen cohort, Stockholm, Sweden. Participants Individuals aged 75 and older (N = 1,229). Measurements The associations between single-nucleotide variations in 14 genes (previously associated with mortality or to diseases linked to mortality), relevant lifestyle risk behaviors (smoking; mental, physical, or social inactivity; moderate or poor social network), and mortality were estimated using Cox regression. Results People with allelic variation in four genes related to cardiovascular diseases and metabolism were more likely to die: apolipoprotein (APO)C1 GG and AG carriers, APOE ɛ4 carriers, insulin-degrading enzyme (IDE) TC carriers, and phosphatidylinositol 3-kinase (PI3KCB) GG carriers. Individuals with multiple adverse alleles had 62% higher mortality rate than those with none. In contrast, people with no risk behaviors (low-risk profile) had 65% lower mortality rate than people with all examined risk behaviors (high-risk profile). Combining the genetic and environmental factors, it was found that, independent of genetic profile, individuals with a low-risk profile had up to 64% lower mortality rate than those with a moderate high– or high-risk profile and at least one genetic risk factor. Conclusion This study supports and expands evidence that genetic variations in APOE, IDE, and PI3KCB are associated with lower mortality rate, although lifestyle behaviors can modulate their effects

Association Between Speed of Multimorbidity Accumulation in Old Age and Life Experiences: A Cohort Study

Abstract Rapidly accumulating multiple chronic conditions (multimorbidity) during aging are associated with many adverse outcomes. We explored the association between 4 experiences throughout life—childhood socioeconomic circumstances, early-adulthood education, midlife occupational stress, and late-life social network—and the speed of chronic disease accumulation. We followed 2,589 individuals aged ≥60 years from the Swedish National Study on Aging and Care in Kungsholmen for 9 years (2001–2013). Information on life experiences was collected from detailed life-history interviews. Speed of disease accumulation was operationalized as the change in the count of chronic conditions obtained from clinical examinations, medical histories, laboratory data, drug use, and register linkages over 9 years. Linear mixed models were used to analyze the data. Speed of disease accumulation was lower in individuals with more than elementary education (for secondary, β × time = −0.065, 95% CI: −0.126, −0.004; for university, β × time = −0.118, 95% CI: −0.185, −0.050); for active occupations compared with high-strain jobs (β × time = −0.078, 95% CI: −0.138, −0.017); and for richer social networks (for moderate tertile, β × time = −0.102, 95% CI: −0.149, −0.055; for highest tertile, β × time = −0.135, 95% CI: −0.182, −0.088). The association between childhood circumstances and speed of disease accumulation was attenuated by later-life experiences. Diverse experiences throughout life might decelerate chronic disease accumulation during aging

walking speed drives the prognosis of older adults with cardiovascular and neuropsychiatric multimorbidity

Abstract Background We investigated the impact of multiple cardiovascular and neuropsychiatric diseases on all-cause and cause-specific mortality in older adults, considering their functional status. Methods This cohort study included 3241 participants (aged ≥60 years) in the Swedish National study of Aging and Care in Kungsholmen (SNAC-K). Number of cardiovascular and neuropsychiatric diseases was categorized as 0, 1, or ≥2. Functional impairment was defined as walking speed of Results After 3 years, compared with participants with preserved walking speed and without either cardiovascular or neuropsychiatric diseases, the multivariable-adjusted HR (95% confidence interval) of all-cause mortality for people with functional impairment in combination with 0, 1, and ≥2 cardiovascular diseases were 1.88 (1.29-2.74), 3.85 (2.60-5.70), and 5.18 (3.45-7.78), respectively. The corresponding figures for people with 0, 1, and ≥2 neuropsychiatric diseases were, respectively, 2.88 (2.03-4.08), 3.36 (2.31-4.89), and 3.68 (2.43-5.59). Among people with ≥2 cardiovascular or ≥2 neuropsychiatric diseases, those with functional impairment had an excess risk for 3-year all-cause mortality of 18/100 person-years and 17/100 person-years, respectively, than those without functional impairment. At 5 years, the association between the number of cardiovascular diseases and mortality resulted independent of functional impairment. Conclusions Functional impairment magnifies the effect of cardiovascular and neuropsychiatric multimorbidity on mortality among older adults. Walking speed appears to be a simple clinical marker for the prognosis of these two patterns of multimorbidity

Multimorbidity burden and dementia risk in older adults : The role of inflammation and genetics

Funding: Swedish National study on Aging and Care; Ministry of Health and Social Affairs; Swedish Research Council, Grant/Award Number: 2016-00981; Swedish Research Council for Health,Working Life andWelfare, Grant/Award Number: 2017-01764; Italian Ministry of Health, Grant/Award Number: PE-2016-02364885We investigate dementia risk in older adults with different disease patterns and explore the role of inflammation and apolipoprotein E (APOE) genotype. A total of 2,478 dementia-free participants with two or more chronic diseases (ie, multimorbidity) part of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K) were grouped according to their multimorbidity patterns and followed to detect clinical dementia. The potential modifier effect of C-reactive protein (CRP) and apolipoprotein E (APOE) genotype was tested through stratified analyses. People with neuropsychiatric, cardiovascular, and sensory impairment/cancer multimorbidity had increased hazards for dementia compared to the unspecific (Hazard ration (HR) 1.66, 95% confidence interval [CI] 1.13-2.42; 1.61, 95% CI 1.17-2.29; 1.32, 95% CI 1.10-1.71, respectively). Despite the lack of statistically significant interaction, high CRP increased dementia risk within these patterns, and being APOE ε4 carriers heightened dementia risk for neuropsychiatric and cardiovascular multimorbidity. Individuals with neuropsychiatric, cardiovascular, and sensory impairment/cancer patterns are at increased risk for dementia and APOE ε4, and inflammation may further increase the risk. Identifying such high-risk groups might allow tailored interventions for dementia prevention

A self-report risk index to predict occurrence of dementia in three independent cohorts of older adults: The ANU-ADRI

Background and Aims: The Australian National University AD Risk Index (ANU-ADRI, http://anuadri.anu.edu.au) is a self-report risk index developed using an evidence-based medicine approach to measure risk of Alzheimer's disease (AD). We aimed to evaluate the extent to which the ANU-ADRI can predict the risk of AD in older adults and to compare the ANU-ADRI to the dementia risk index developed from the Cardiovascular Risk Factors, Aging and Dementia (CAIDE) study for middle-aged cohorts. Methods: This study included three validation cohorts, i.e., the Rush Memory and Aging Study (MAP) (n = 903, age ≥53 years), the Kungsholmen Project (KP) (n = 905, age ≥75 years), and the Cardiovascular Health Cognition Study (CVHS) (n = 2496, age ≥65 years) that were each followed for dementia. Baseline data were collected on exposure to the 15 risk factors included in the ANU-ADRI of which MAP had 10, KP had 8 and CVHS had 9. Risk scores and C-statistics were computed for individual participants for the ANU-ADRI and the CAIDE index. Results: For the ANU-ADRI using available data, the MAP study c-statistic was 0.637 (95% CI 0.596-0.678), for the KP study it was 0.740 (0.712-0.768) and for the CVHS it was 0.733 (0.691-0.776) for predicting AD. When a common set of risk and protective factors were used c-statistics were 0.689 (95% CI 0.650-0.727), 0.666 (0.628-0.704) and 0.734 (0.707-0.761) for MAP, KP and CVHS respectively. Results for CAIDE ranged from c-statistics of 0.488 (0.427-0.554) to 0.595 (0.565-0.625). Conclusion: A composite risk score derived from the ANU-ADRI weights including 8-10 risk or protective factors is a valid, self-report tool to identify those at risk of AD and dementia. The accuracy can be further improved in studies including more risk factors and younger cohorts with long-term follow-up. © 2014 Anstey et al