Search

Background There is a growing interest in generating precise predictions of survival to improve the assessment of health and life-improving interventions. We aimed to (a) test if observable characteristics may provide a survival prediction independent of chronological age; (b) identify the most relevant predictors of survival; and (c) build a metric of multidimensional age. Methods Data from 3 095 individuals aged ≥60 from the Swedish National Study on Aging and Care in Kungsholmen. Eighty-three variables covering 5 domains (diseases, risk factors, sociodemographics, functional status, and blood tests) were tested in penalized Cox regressions to predict 18-year mortality. Results The best prediction of mortality at different follow-ups (area under the receiver operating characteristic curves [AUROCs] 0.878–0.909) was obtained when 15 variables from all 5 domains were tested simultaneously in a penalized Cox regression. Significant prediction improvements were observed when chronological age was included as a covariate for 15- but not for 5- and 10-year survival. When comparing individual domains, we find that a combination of functional characteristics (ie, gait speed, cognition) gave the most accurate prediction, with estimates similar to chronological age for 5- (AUROC 0.836) and 10-year (AUROC 0.830) survival. Finally, we built a multidimensional measure of age by regressing the predicted mortality risk on chronological age, which displayed a stronger correlation with time to death (R = −0.760) than chronological age (R = −0.660) and predicted mortality better than widely used geriatric indices. Conclusions Combining easily accessible characteristics can help in building highly accurate survival models and multidimensional age metrics with potentially broad geriatric and biomedical applications.

Background To identify brain magnetic resonance imaging (MRI) signatures characterizing people with different patterns of decline in cognition and motor function. Methods In the Swedish National Study on Aging and Care in Kungsholmen, Stockholm, 385 participants had available repeated brain MRI examinations, where markers of brain volumes and white matter integrity were assessed. The speed of cognitive and motor decline was estimated as the rate of a Mini-Mental State Examination and gait speed decline over 12 years (linear mixed models), and further dichotomized into the upper (25% fastest rate of decline) versus the lower quartiles. Participants were grouped in slow/no decliners (reference), isolated motor decliners, isolated cognitive decliners, and cognitive and motor decliners. We estimated the associations between changes in brain markers (linear mixed models) and baseline diffusion tensor imaging measures (linear regression model) and the 4 decline patterns. Results Individuals with concurrent cognitive and motor decline (n = 51) experienced the greatest loss in the total brain (β: −12.3; 95% confidence interval [CI]: −18.2; −6.38) and hippocampal (β: −0.25; 95% CI: −0.34; −0.16) volumes, the steepest accumulation of white matter hyperintensities (β: 1.61; 95% CI: 0.54; 2.68), and the greatest ventricular enlargement (β: 2.07; 95% CI: 0.67; 3.47). Compared to the reference, those only experiencing cognitive decline presented with steeper hippocampal volume loss, whereas those exhibiting only motor decline displayed a greater white matter hyperintensities burden. Lower microstructural white matter integrity was associated with concurrent cognitive and motor decline. Conclusion Concurrent cognitive and motor decline is accompanied by rapidly evolving and complex brain pathology involving both gray and white matter. Isolated cognitive and motor declines seem to exhibit brain damage with different qualitative features.

BACKGROUND: Orthostatic hypotension (OH) has been associated with elevated risk of cardiovascular diseases (CVDs) and dementia risk. To better understand the OH-dementia association, we assessed the associations of OH with CVD and subsequent dementia in older adults and considered the temporality of CVD and dementia onset. METHODS: This 15-year population-based cohort study included, at baseline, 2703 dementia-free participants (mean age, 73.7 years) who were divided into a CVD-free cohort (n=1986) and a CVD cohort (n=717). OH was defined as a systolic/diastolic blood pressure decline of ≥20/10 mm Hg after standing up from a supine position. CVDs and dementia were ascertained by physicians or identified from registers. Multistate Cox regressions were applied to assess the associations of OH with CVD and subsequent dementia in the CVD-free and dementia-free cohort. The OH-dementia association in the CVD cohort was examined with Cox regressions. RESULTS: OH was present in 434 (21.9%) individuals in the CVD-free cohort and 180 (25.1%) individuals in the CVD cohort. OH was associated with a hazard ratio of 1.33 (95% CI, 1.12–1.59) for CVD. OH was not significantly associated with incident dementia in the absence of CVD occurring before dementia diagnosis (hazard ratio, 1.22 [95% CI, 0.83–1.81]). In the CVD cohort, individuals with OH had a higher dementia risk than those without OH (hazard ratio, 1.54 [95% CI, 1.06–2.23]). CONCLUSIONS: The association between OH and dementia may partly be explained by the intermediate development of CVD. In addition, in people with CVD, those with OH may have a poorer cognitive prognosis.

Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99–1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98–1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.

Background Some studies have linked late-life overweight to a reduced mortality risk compared to normal body mass index (BMI). However, the impact of late-life overweight and its combination with mid-life BMI status on healthy survival remains unclear. We aimed to investigate whether and to what extent mid- and/or late-life overweight are associated with chronic disease-free survival. Methods Within the Swedish Twin Registry, 11 597 chronic disease-free twins aged 60−79 years at baseline were followed up for 18 years. BMI (kg/m2) was recorded at baseline and 25−35 years before baseline (ie, midlife) and divided as underweight ( Results Of all participants, 5 640 (48.6%) were overweight/obese at baseline. During the follow-up, 8 772 (75.6%) participants developed at least 1 chronic disease or died. Compared to normal BMI, late-life overweight and obesity were associated with 1.1 (95% CI, 0.3, 2.0) and 2.6 (1.6, 3.5) years shorter chronic disease-free survival. Compared to normal BMI through mid- to late life, consistent overweight/obesity and overweight/obesity only in mid-life led to 2.2 (1.0, 3.4) and 2.6 (0.7, 4.4) years shorter disease-free survival, respectively. Conclusions Late-life overweight and obesity may shorten disease-free survival. Further research is needed to determine whether preventing overweight/obesity from mid- to late life might favor longer and healthier survival.

ObjectivesTo investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND).MethodsWe pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (LAeq8h): ResultsExposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75–79, 80–84 and ≥85 dB(A) exposure groups, compared with ConclusionsWe found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation.

BACKGROUND: Transportation noise may induce cardiovascular disease, but the public health implications are unclear.OBJECTIVES: The study aimed to assess exposure-response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes.METHODS: Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted long-term exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors.RESULTS: A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB L den for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB L den for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure-response relations. A threshold at around 55 dB L den was suggested in the exposure-response relation for road traffic noise and IHD. DISCUSSION: Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. https://doi.org/10.1289/EHP10745.

Background Acute clinical events, such as pneumonia, may impact physical functionality but their effect on cognition and the possible duration of this effect remains to be quantified. This study investigated the impact of pneumonia on cognitive trajectories and dementia development in older people. Methods Data were obtained from 60+ years old individuals, who were assessed from 2001 to 2018 in the population-based SNAC-K study (Sweden). Participants were eligible if they were not institutionalized, had no dementia, and did not experience pneumonia 5 years prior to baseline (N = 2 063). A propensity score was derived to match 1:3 participants hospitalized with a diagnosis of pneumonia (N = 178), to nonexposed participants (N = 534). Mixed linear models were used to model cognitive decline. The hazard of dementia, clinically diagnosed by physicians following Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV, was estimated using Cox regression models. Results We found a transient impact of pneumonia on cognitive decline in the first 2.5 years (B = −0.94, 95% confidence interval [CI] −1.75, −0.15). The hazard ratio (HR) for dementia was not statistically significantly increased in pneumonia participants (HR = 1.17, 95%CI 0.82, 1.66). Conclusions The transient impact of pneumonia on cognitive function suggests an increased need of health care for patients after a pneumonia-related hospitalization and reinforces the relevance of pneumonia prevention.

Background this article investigates the association between life satisfaction and disability-free survival, and explores the roles of chronic diseases and healthy lifestyle in this association. Method a cohort of 2,116 functionally independent adults aged ≥60 was followed up to 12 years. At baseline, life satisfaction was assessed with the Life Satisfaction Index A (LSI-A). Disability-free survival was defined as the survival till the first occurrence of either death, dementia or physical disability. Information on lifestyle factors was collected via questionnaire. Chronic diseases were ascertained through clinical examinations at baseline and each follow-up. Data were analysed using Cox proportional hazard regression models and Laplace regression. Results over follow-up, 1,121 participants died, developed dementia, or became disabled. High LSI-A versus Low LSI-A had a lower risk of death, dementia and physical disability (hazard ratio [HR] 0.79, 95% confidence intervals [CI] 0.67–0.94), and had a longer disability-free period by 1.73 (95% CI 0.18–3.32) years. In mediation analysis, accumulation of chronic diseases mediated 17.8% of the association between LSI-A and disability-free survival. In joint effect analysis, participants with high LSI-A and a favourable lifestyle profile had a HR of 0.53 (95% CI 0.41–0.69) for the composite endpoint, and lived 3.2 (95% CI 1.35–5.11) disability-free years longer than those with low life satisfaction and an unfavourable lifestyle profile. Discussion high life satisfaction is independently associated with longer disability-free survival. This association is partially mediated by a lower burden of chronic diseases and is reinforced by healthy lifestyle.

Summary Background & aims Healthy diet has been associated with decreased mortality, but its impact on survival without disability is less clear. We aimed to investigate the association between the Nordic Prudent Diet Pattern (NPDP) and dementia- and disability-free survival, and to assess its interaction with other healthy lifestyle behaviors. Methods Within the Swedish National Study on Aging and Care-Kungsholmen, 2290 dementia- and disability-free adults aged ≥60 were followed up to 12 years to detect survival free from dementia (standard criteria) and disability (Katz's Activities of Daily Living). NPDP index was assessed at baseline with a 98-item food frequency questionnaire (characterized mainly by more frequent intakes of vegetable, fruit, cooking, cereals, whole grains, fish, and water) and was further categorized into tertiles (low, moderate, or high). Information on lifestyle factors was collected via baseline questionnaire. A favorable (vs unfavorable) lifestyle profile was determined based on smoking status, social network and physical activity. Data were analyzed using Cox proportional hazard regression models and Laplace regression. Results During the follow-up, 1074 participants survived without dementia and disability (614 died, 518 became disabled, and 84 developed dementia). Compared to low NPDP adherence, the hazard ratio (HR) of high NPDP adherence was 1.19 (95% CI 1.04–1.34) for dementia- and disability-free survival. High NPDP adherence prolonged lifespan without mental and physical disability by an average of 1.24 years (95% CI 0.11–2.37). Further, among participants with high NPDP adherence, a favorable lifestyle profile was associated with an even higher HR (1.96, 95% CI 1.52–2.42) of dementia- and disability-free survival, corresponding to an average of 3.80 (95% CI 2.25–5.35) years longer life compared to those with low NPDP adherence and an unfavorable lifestyle profile. Conclusion High adherence to NPDP prolongs survival with good mental and physical function for more than one year, and this could increase to almost four years with a favorable lifestyle.

Background the aim of this study was to examine the cross-sectional and longitudinal associations of different multimorbidity patterns with physical frailty in older adults. Methods we used data from the Swedish National study on Aging and Care in Kungsholmen to generate a physical frailty measure, and clusters of participants with similar multimorbidity patterns were identified through fuzzy c-means cluster analyses. The cross-sectional association (n = 2,534) between multimorbidity clusters and physical frailty was measured through logistic regression analyses. Six- (n = 2,122) and 12-year (n = 2,140) longitudinal associations were determined through multinomial logistic regression analyses. Results six multimorbidity patterns were identified at baseline: psychiatric diseases; cardiovascular diseases, anaemia and dementia; sensory impairments and cancer; metabolic and sleep disorders; musculoskeletal, respiratory and gastrointestinal diseases; and an unspecific pattern lacking any overrepresented diseases. Cross-sectionally, each pattern was associated with physical frailty compared with the unspecific pattern. Over 6 years, the psychiatric diseases (relative risk ratio [RRR]: 3.04; 95% confidence intervals [CI]: 1.59–5.79); cardiovascular diseases, anaemia and dementia (RRR 2.25; 95% CI: 1.13–4.49) and metabolic and sleep disorders (RRR 1.99; 95% CI: 1.25–3.16) patterns were associated with incident physical frailty. The cardiovascular diseases, anaemia and dementia (RRR: 4.81; 95% CI: 1.59–14.60); psychiatric diseases (RRR 2.62; 95% CI: 1.45–4.72) and sensory impairments and cancer (RRR 1.87; 95% CI: 1.05–3.35) patterns were more associated with physical frailty, compared with the unspecific pattern, over 12 years. Conclusions we found that older adults with multimorbidity characterised by cardiovascular and neuropsychiatric disease patterns are most susceptible to developing physical frailty.

Rationale: Ambient air pollution exposure has been linked to mortality from chronic cardiorespiratory diseases, while evidence on respiratory infections remains more limited. Objectives: We examined the association between long-term exposure to air pollution and pneumonia-related mortality in adults in a pool of eight European cohorts. Methods: Within the multicenter project ELAPSE (Effects of Low-Level Air Pollution: A Study in Europe), we pooled data from eight cohorts among six European countries. Annual mean residential concentrations in 2010 for fine particulate matter, nitrogen dioxide (NO2), black carbon (BC), and ozone were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and pneumonia, influenza, and acute lower respiratory infections (ALRI) mortality. Measurements and Main Results: Of 325,367 participants, 712 died from pneumonia and influenza combined, 682 from pneumonia, and 695 from ALRI during a mean follow-up of 19.5 years. NO2 and BC were associated with 10–12% increases in pneumonia and influenza combined mortality, but 95% confidence intervals included unity (hazard ratios, 1.12 [0.99–1.26] per 10 μg/m3 for NO2; 1.10 [0.97–1.24] per 0.5 1025m21 for BC). Associations with pneumonia and ALRI mortality were almost identical. We detected effect modification suggesting stronger associations with NO2 or BC in overweight, employed, or currently smoking participants compared with normal weight, unemployed, or nonsmoking participants. Conclusions: Long-term exposure to combustion-related air pollutants NO2 and BC may be associated with mortality from lower respiratory infections, but larger studies are needed to estimate these associations more precisely.

Background: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear. Objectives: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association. Methods: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5μm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25%fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model. Results: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2–3.2) per interquartile range difference up to mean PM2.5 level (8.6μg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74–1.06). The presence of cerebrovascular diseases further increased such risk by 6%. Conclusion: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.

Background The functional consequences of injurious falls are well known. However, studies of the factors that can modify trajectories of disability after an injury from a fall are scarce. Aims We aimed to investigate whether sociodemographic and health-related factors may impact this association. Methods The study population consisted of 1426 community-dwelling older adults (≥ 60 years) from the SNAC-K cohort study in Stockholm, Sweden. Functional status over 12 years of follow-up was assessed using the number of limitations in basic and instrumental activities of daily living. Sex, cohabitation status, physical activity, and self-rated health were assessed at baseline. Injurious falls were defined as falls requiring healthcare and were assessed over 3 years starting at baseline. Data were analyzed using linear-mixed effects models. Results The fastest increase in the number of disabilities was observed in those who had endured an injurious fall and were living alone (β coefficient = 0.408; p β coefficient = 0.587; p β coefficient = 0.514; p Discussion Living alone, being physically inactive, and having poor self-rated health magnifies the negative effect of an injurious fall on functional status. Among individuals who endure an injurious fall, the heterogeneity in long-term functional status is substantial, depending on the individuals’ characteristics and behaviors. Conclusions These findings emphasize the need for a person-centered approach in care provision and can guide secondary prevention within health care.

Long-term air pollution exposure increases the risk for cardiovascular disease, but little is known about the temporal relationships between exposure and health outcomes. This study aims to estimate the exposure-lag response between air pollution exposure and risk for ischemic heart disease (IHD) and stroke incidence by applying distributed lag non-linear models (DLNMs). Annual mean concentrations of particles with aerodynamic diameter less than 2.5 µm (PM2.5) and black carbon (BC) were estimated for participants in five Swedish cohorts using dispersion models. Simultaneous estimates of exposure lags 1–10 years using DLNMs were compared with separate year specific (single lag) estimates and estimates for lag 1–5- and 6–10-years using moving average exposure. The DLNM estimated no exposure lag-response between PM2.5 total, BC, and IHD. However, for PM2.5 from local sources, a 20% risk increase per 1 µg/m3 for 1-year lag was estimated. A risk increase for stroke was suggested in relation to lags 2–4-year PM2.5 and BC, and also lags 8–9-years BC. No associations were shown in single lag models. Increased risk estimates for stroke in relation to lag 1–5- and 6–10-years BC moving averages were observed. Estimates generally supported a greater contribution to increased risk from exposure windows closer in time to incident IHD and incident stroke.

Olfactory impairment is increasingly common with older age, which may be in part explained by cumulative effects of exposure to inhaled toxins. However, population-based studies investigating the relationship between air pollution and olfactory ability are scarce.We aimed to investigate associations between exposure to common air pollutants and longitudinal change in odor identification.Our study of 2,468 participants (Participants showed significant decline in odor identification ability for each year in the study {Our results suggest an association between air pollution exposure and subsequent olfactory decline. We speculate that cumulative effects of airborne pollutants on the olfactory system may be one underlying cause of olfactory impairment in aging. https://doi.org/10.1289/EHP9563.

Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed. Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders. Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93–1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99–1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00–1.16 per 10 ng/m3). Conclusions: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.

Background Olfactory dysfunction is common in aging and associated with dementia and mortality. However, longitudinal studies tracking change in olfactory ability are scarce. We sought to identify predictors of interindividual differences in rate of olfactory identification change in aging. Method Participants were 1780 individuals, without dementia at baseline and with at least 2 olfactory assessments over 12 years of follow-up (mean age = 70.5 years; 61.9% female), from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K). Odor identification was assessed with the Sniffin’ Sticks. We estimated the impact of demographic, health, and genetic factors on rate of olfactory change with linear mixed effect models. Results Advancing age, manufacturing profession, history of cerebrovascular disease, higher cardiovascular disease burden, diabetes, slower walking speed, higher number of medications, and the APOE ε4 allele were associated with accelerated odor identification decline (ps < .014). Multi-adjusted analyses showed unique associations of age, diabetes, and ε4 to olfactory decline (ps < .017). In 1531 participants who remained free of dementia (DSM IV criteria) during follow-up, age, cardiovascular disease burden, and diabetes were associated with accelerated decline (ps < .011). Of these, age and diabetes remained statistically significant in the multi-adjusted model (ps < .001). Conclusion Demographic, vascular, and genetic factors are linked to rate of decline in odor identification in aging. Although some olfactory loss may be an inevitable part of aging, our results highlight the importance of vascular factors for the integrity of the olfactory system, even in the absence of dementia.

Objective:We investigated the extent to which combining cognitive markers increases the predictive value for future dementia, when compared to individual markers. Furthermore, we examined whether predictivity of markers differed depending on a range of modifying factors and time to diagnosis.Method:Neuropsychological assessment was performed for 2357 participants (60+ years) without dementia from the population-based Swedish National Study on Aging and Care in Kungsholmen. In the main sample analyses, the outcome was dementia at 6 years. In the time-to-diagnosis analyses, a subsample of 407 participants underwent cognitive testing 12, 6, and 3 years before diagnosis, with dementia diagnosis at the 12-year follow-up.Results:Category fluency was the strongest individual predictor of dementia 6 years before diagnosis [area under the curve (AUC) = .903]. The final model included tests of verbal fluency, episodic memory, and perceptual speed (AUC = .913); these three domains were found to be the most predictive across a range of different subgroups. Twelve years before diagnosis, pattern comparison (perceptual speed) was the strongest individual predictor (AUC = .686). However, models 12 years before diagnosis did not show significantly increased predictivity above that of the covariates.Conclusions:This study shows that combining markers from different cognitive domains leads to increased accuracy in predicting future dementia 6 years later. Markers from the verbal fluency, episodic memory, and perceptual speed domains consistently showed high predictivity across subgroups stratified by age, sex, education, apolipoprotein E ϵ4 status, and dementia type. Predictivity increased closer to diagnosis and showed highest accuracy up to 6 years before a dementia diagnosis. (JINS, 2020,00, 1–13)

Ambient air pollution is an established risk factor for premature mortality from chronic cardiovascular, respiratory and metabolic diseases, while evidence on neurodegenerative diseases and psychiatric disorders remains limited. We examined the association between long-term exposure to air pollution and mortality from dementia, psychiatric disorders, and suicide in seven European cohorts. Within the multicenter project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from seven European cohorts from six countries. Based on the residential addresses, annual mean levels of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), ozone (O3), and 8 PM2.5 components were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and mortality from dementia, psychiatric disorders, and suicide. Of 271,720 participants, 900 died from dementia, 241 from psychiatric disorders, and 164 from suicide, during a mean follow-up of 19.7 years. In fully adjusted models, we observed positive associations of NO2 (hazard ratio [HR] = 1.38; 95 % confidence interval [CI]: 1.13, 1.70 per 10 µg/m3), PM2.5 (HR = 1.29; 95 % CI: 0.98, 1.71 per 5 µg/m3), and BC (HR = 1.37; 95 % CI: 1.11, 1.69 per 0.5 × 10−5/m) with psychiatric disorders mortality, as well as with suicide (NO2: HR = 1.13 [95 % CI: 0.92, 1.38]; PM2.5: HR = 1.19 [95 % CI: 0.76, 1.87]; BC: HR = 1.08 [95 % CI: 0.87, 1.35]), and no association with dementia mortality. We did not detect any positive associations of O3 and 8 PM2.5 components with any of the three mortality outcomes. Long-term exposure to NO2, PM2.5, and BC may lead to premature mortality from psychiatric disorders and suicide.

We assessed mortality risks associated with source-specific fine particles (PM2.5) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM2.5identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM2.5components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 μg/m3increase) across five identified sources. On a 1 μg/m3basis, the residual oil-related PM2.5had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM2.5mass, suggesting that past estimates using the generic PM2.5exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.

This study aimed to quantify the relationships between the American Heart Association (AHA) Cardiovascular Health (CVH) metrics, namely AHA Life's Simple 7, and cognitive outcomes. We searched PubMed and Embase (January 1, 2010-August 24, 2022) and finally included 14 longitudinal studies (311654 participants with 8006 incident dementia cases). Random-effects meta-analysis and one-stage linear mixed-effects models were performed. Increased CVH score seemed to associate with decreased risk of incident dementia in a linear manner, but this relationship varied by the measurement age of CVH metrics. That is, midlife CVH tended to have a linear association with late-life dementia risk, whereas a J-shaped association was observed between the late-life CVH score and dementia. In addition, late-life dementia risk was reduced significantly if individuals maintained an ideal level of AHA's CVH guidelines of physical activity, fasting plasma glucose, total cholesterol, and smoking. However, our meta-analysis did not show a significant association between CVH score and global cognitive decline rate. Following AHA's CVH guidelines and maintaining CVH at an optimal level would substantially reduce the late-life dementia risk. More research is required to explore the link between a favorable CVH score and cognitive trajectories among cognitively asymptomatic older populations.

Background & aims: The impact of nutrient patterns on cognitive decline is complex and findings are still inconclusive. We aimed to identify major nutrient patterns and to explore their association with cognitive decline over time among older adults. Methods: In a population-based cohort, 2250 cognitively healthy people aged >=60 years were identified at baseline (2001-2004), and followed-up to 9 years. Global cognitive function was tested with the Mini-Mental State Examination (MMSE) at baseline and follow-ups. Nutrients intake was assessed on the basis of food intake using a 98-semi-quantitative food frequency questionnaire at baseline, and nutrient-based patterns were identified by principal components analysis based on 30 nutrients. Mixed-effects linear regression models were used to determine their association with change in cognitive function taking into account potential confounders. Results: Four major patterns (the plant-, animal-, dairy-derived nutrients and animal/plants-derived fats) were identified. Over the follow-up time, each one unit increment in plant- (? = 0.081, P = 0.002) and animal-derived nutrients pattern scores (? = 0.098, P < 0.001) was associated with slower decline in MMSE score. On the other hand, one-unit higher in dairy-derived nutrients pattern was related to a faster decline in global cognitive function (? = -0.064, P = 0.014). No significant association between animal/plants fats pattern and cognitive decline was observed. In stratified analyses, the association of high scores of plants- and animal-derived nutrient pattern with slower cognitive decline was stronger in APOE ?4 carriers than in ?4 non-carriers. Conclusions: Plant- and animal -derived nutrients are associated with preserved cognitive function, especially among the APOE ?4 carriers, whereas nutrients derived from dairy products may accelerate cognitive decline in older adults.

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the “Effects of low-level air pollution: A study in Europe” (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO 2), particulate matter with diameter 2.5), black carbon (BC), warm-season ozone (O 3), and eight elemental components of PM 2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO 2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 μg/m 3), PM 2.5 (1.12, 0.92-1.36 per 5 μg/m 3), and BC (1.15, 1.00-1.33 per 0.5 10 −5/m) and liver cancer incidence. Associations with NO 2 and BC persisted in two-pollutant models with PM 2.5. Most components of PM 2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM 2.5 or NO 2. Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.