Midlife Risk Factors Research Articles

Lifetime Risk and Risk Factors for Abdominal Aortic Aneurysm in a 24-Year Prospective Study: The ARIC Study (Atherosclerosis Risk in Communities).

Abdominal aortic aneurysm (AAA) is an important vascular disease in older adults, but data on lifetime risk of AAA are sparse. We examined lifetime risk of AAA in a community-based cohort and prospectively assessed the association between midlife cardiovascular risk factors and AAAs. In ARIC study (Atherosclerosis Risk in Communities), 15 792 participants were recruited at visit 1 in 1987 to 1989 and followed up through 2013. Longitudinal smoking status was defined using smoking behavior ascertained from visit 1 (1987-1989) to visit 4 (1996-1998). We followed up participants for incident, clinical AAAs using hospital discharge diagnoses, Medicare outpatient diagnoses, or death certificates through 2011 and identified 590 incident AAAs. An abdominal ultrasound was conducted in 2011 to 2013 in 5911 surviving participants, and 75 asymptomatic AAAs were identified. We estimated the lifetime risk of AAA from the index age 45 years through 85 years of age. At age 45, the lifetime risk for AAA was 5.6% (95% confidence interval, 4.8-6.1) and was higher in men (8.2%) and current smokers (10.5%). Smokers who quit smoking between visit 1 and visit 4 had a 29% lower AAA lifetime risk compared with continuous smokers but had a higher risk than pre-visit 1 quitters. The lifetime risk of rupture or medical intervention was 1.6% (95% confidence interval, 1.2-1.8). Smoking, white race, male sex, greater height, and greater low-density lipoprotein or total cholesterol were associated with an increased risk of clinical AAA and asymptomatic AAA. At least 1 in 9 middle-aged current smokers developed AAA in their lifetime. Smoking cessation reduced the lifetime risk of AAA.

Educational differences in cardiovascular mortality: The role of shared family factors and cardiovascular risk factors.

To explore the confounding effects of early family factors shared by siblings and cardiovascular risk factors in midlife on the educational differences in mortality from cardiovascular disease (CVD). Data from national and regional health surveys in Norway (1974-2003) were linked with data from the Norwegian Family Based Life Course Study, the National Educational Registry and the Cause of Death Registry. The study population consisted of participants with at least one full sibling among the health survey participants ( n=271,310). Data were available on CVD risk factors, including weight, height, blood pressure, total cholesterol and smoking. The hazards ratio (HR) of CVD mortality was 3.44 (95% confidence interval (CI) 2.98-3.96) in the lowest educational group relative to the highest. The HRs were little altered in the within-sibship analyses. Adjusted for risk factors, the HR for CVD mortality in the cohort analyses was 2.05 (CI 1.77-2.37) in the lowest educational group relative to the highest. The respective HR in the within-sibship analyses was 2.46 (CI 1.48-2.24). Using a sibling design, we did not find that the association between education and CVD mortality was confounded by early life factors shared by siblings, but it was explained to a large extent by CVD risk factors. These results suggest that reducing levels of CVD risk factors could have the greatest effect on mortality in less well-educated people.

Risk of dementia hospitalisation associated with cardiovascular risk factors in midlife and older age: The atherosclerosis risk in communities (ARIC) STUDY

Risk of dementia hospitalisation associated with cardiovascular risk factors in midlife and older age: The atherosclerosis risk in communities (ARIC) STUDY

Operationalizing Frailty in the Atherosclerosis Risk in Communities Study Cohort.

Factors that may contribute to the development of frailty in late life have not been widely investigated. The Atherosclerosis Risk in Communities (ARIC) Study cohort presents an opportunity to examine relationships of midlife risk factors with frailty in late life. However, we first present findings on the validation of an established frailty phenotype in this predominantly biracial population of older adults. Among 6,080 participants, we defined frailty based upon the Cardiovascular Health Study (CHS) criteria incorporating measures of weight loss, exhaustion, slow walking speed, low physical activity, and low grip strength. Criterion and predictive validity of the frailty phenotype were estimated from associations between frailty status and participants' physical and mental health status, physiologic markers, and incident clinical outcomes. A total of 393 (6.5%) participants were classified as frail and 50.4% pre-frail, similar to CHS (6.9% frail, 46.6% pre-frail). In age-adjusted analyses, frailty was concurrently associated with depressive symptoms, low self-rated health, low medication adherence, and clinical biomarker levels (ie, cholesterol, hemoglobin A1c, white blood cell count, C-reactive protein, and hemoglobin). During 1-year follow-up, frailty was associated with falls, low physical ability, fatigue, and mortality. These findings support the validity of the CHS frailty phenotype in the ARIC Study cohort. Future studies in ARIC may elucidate early-life exposures that contribute to late-life frailty.

Midlife Risk Factors for Impaired Physical and Cognitive Functioning at Older Ages: A Cohort Study.

Background: Previous studies examined midlife risk factors separately for old-age impaired physical and cognitive functioning. We determined the overlap of risk factors for both domains of functioning within the same setting.Methods: Biological and behavioral risk factors at age 50 years and cognitive and physical functioning were assessed 18 (SD = 5) years later in the Whitehall II study (N = 6,316). Impaired physical functioning was defined as ≥1 limitation on the activities of daily living scale. Impaired cognitive functioning was defined as Mini-Mental State Examination score <27. Two statistical analyses were employed: minimally adjusted analysis (for age, sex, and ethnicity) and mutually adjusted analysis (including all risk factors). Missing data on risk factors were imputed.Results: After confounder adjustment, impaired physical and cognitive functioning at older ages were predicted by hypertension (odds ratios [ORs] 1.80 95% confidence interval [CI] 1.39–2.33 and 1.57 95% CI 1.07–2.31, respectively), poor lung function (1.51 95% CI 1.28–1.78 and 1.31 95% CI 1.08–1.59), and physical inactivity, marginally in the case of cognitive function (1.50 95% CI 1.19–1.90 and 1.27 95% CI 0.99–1.62) at age 50 years. Impaired physical functioning but not cognitive functioning was additionally predicted by depression and higher body mass index (1.72 95% CI 1.46–2.03 and 1.29 95% CI 1.16–1.44, respectively).Conclusions: Several midlife risk factors are associated with impaired physical and cognitive functioning in old age, supporting a unified prevention policy. Analysis of 12 risk factors at age 50 suggests that strategies targeting physical inactivity, hypertension, and poor lung function will reduce impairments in both cognitive and physical functioning in old age.

From Heart Health to Brain Health: Legacy of the North Karelia Project for Dementia Research.

Cognitive impairment is very common in advanced age, with dementia representing the main cause of disability in older adults. Over the past 20 years, several modifiable risk factors have been identified for dementia and Alzheimer's disease (AD), and many of them are shared with cardiovascular diseases. Given that the pathologic changes leading to dementia may start decades before dementia is diagnosed, it is crucial to adopt a life course approach when investigating risk factors for dementia. The CAIDE (Cardiovascular Risk Factors, Aging and Dementia) study is one of the first and still very few existing observational studies to have investigated the role of midlife risk factors for the subsequent development of dementia and AD in late life. The CAIDE study is built on the North Karelia Project, enabling risk factor assessment 20 to 30 years before the dementia diagnosis. The CAIDE study has revealed that late-life dementia and AD are heterogeneous and multifactorial disorders, suggesting that multidomain interventions targeting several risk factors simultaneously may be needed for optimal preventive effects. The FINGER (Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability) study is the first large long-term multidomain lifestyle intervention showing effect on prevention of cognitive impairment in at-risk elderly people. The study is conducted within the existing framework and builds on multidisciplinary prevention expertise following the North Karelia Project and CAIDE study. The FINGER study will, together with the ongoing multinational preventive initiatives, pave the way for pragmatic prevention programs and integrated interventions to facilitate healthy brain aging. This paper summarizes major findings on risk and protective factors for dementia and AD, and reviews key aspects and future directions in preventative strategies.

Abstract 14: Midlife Cardiorespiratory Fitness is Associated with Lower Incidence of Depression and Cardiovascular Death with or without Incident Depression in Later Life

Introduction: Depression disorders are common and debilitating conditions which can affect older individuals, especially those with cardiovascular disease (CVD). The association of midlife cardiorespiratory fitness (fitness), an objective measure of habitual physical activity, with later-life depression is not fully understood. Furthermore, although depression is associated with incident CVD, little is known about the long term association of midlife fitness with CVD death following the onset of depression decades later. Hypothesis: Fitness measured in midlife will be inversely associated with depression in later life and risk of CVD death with or without intercurrent depression. Methods: Linking participant data from the Cooper Center Longitudinal Study with Medicare claims files, we studied 16,728 participants (19% women, mean age 51) without prior history of depression or CVD, who received Medicare coverage from 1999-2009. Midlife fitness was estimated by Balke protocol treadmill time in metabolic equivalents and grouped into age and sex-specific categories: low, moderate, and high fitness. Other midlife risk factors were measured using standard protocols. Depression diagnosis was defined from Medicare claims files according to established algorithms and CVD mortality was determined from National Death Index records. Multivariate survival modeling was used to assess the associations between midlife fitness and time to any of three later life events: incident depression, CVD death without incident depression, and CVD death following incident depression. The model was adjusted for midlife age, gender, year of examination, smoking, systolic blood pressure, cholesterol, BMI, and fasting glucose. Results: After 109,143 person years of Medicare follow-up, we observed 2379 cases of incident depression, 570 CVD deaths without incident depression and 218 CVD deaths following incident depression. High fitness in midlife was associated with a 24% lower risk of depression (hazards ratio [HR] 0.76, 95% CI 0.67-0.86 compared to low fit). High fitness was also associated with a 63% lower risk of CVD death without incident depression (HR 0.37, 95% CI 0.30-0.47 compared to low fit) and 50% lower risk of CVD death (HR 0.50, 95% CI 0.34-0.72 compared to low fit) following incident depression. Conclusion: Midlife fitness, a modifiable CVD risk factor, is associated with lower risk of depression in later life, lower risk of CVD death without incident depression, and lower risk of CVD death following incident depression decades later. These findings suggest the importance of fitness in primary prevention of depression and mortality in older age.

Late-life brain volume: a life-course approach. The AGES-Reykjavik study

The “fetal-origins-of-adult-disease” hypothesis proposes that an unfavorable intrauterine environment, estimated from small birth size, may induce permanent changes in fetal organs, including the brain. These changes in combination with effects of (cardiovascular) exposures during adult life may condition the later risk of brain atrophy. We investigated the combined effect of small birth size and mid-life cardiovascular risk on late-life brain volumes. Archived birth records of weight and height were abstracted for 1348 participants of the age, gene/environment susceptibility-Reykjavik study (RS; 2002–2006) population-based cohort, who participated in the original cohort of the RS (baseline 1967). Mid-life cardiovascular risk factors (CVRF) were collected in the RS. As a part of the late-life age, gene/environment susceptibility-RS examination, a brain magnetic resonance imaging was acquired and from it, volumes of total brain, gray matter, white matter, and white matter lesions were estimated. Adjusting for intracranial volume, demographics, and education showed small birth size (low ponderal index [PI]) and increased mid-life cardiovascular risk had an additive effect on having smaller late-life brain volumes. Compared with the reference group (high PI/absence of mid-life CVRF), participants with lower PI/presence of mid-life CVRF (body mass index >25 kg/m2, hypertension, diabetes, “ever smokers”) had smaller total brain volume later in life; B (95% confidence interval) were −10.9 mL (−21.0 to −0.9), −10.9 mL (−20.4 to −1.4), −20.9 mL (−46.9 to 5.2), and −10.8 mL (−19.3 to −2.2), respectively. These results suggest that exposure to an unfavorable intrauterine environment contributes to the trajectory toward smaller brain volume, adding to the atrophy that may be associated with mid-life cardiovascular risk.

Midlife Cardiovascular Risk Factors and Late-Life Unrecognized and Recognized Myocardial Infarction Detect by Cardiac Magnetic Resonance: ICELAND-MI, the AGES-Reykjavik Study.

BackgroundAssociations of atherosclerosis risk factors with unrecognized myocardial infarction (UMI) are unclear. We investigated associations of midlife risk factors with UMI and recognized MI (RMI) detected 31 years later by cardiac magnetic resonance.Methods and ResultsThe Reykjavik Study (1967–1991) collected serial risk factors in subjects, mean (SD) age 48 (7) years. In ICELAND‐MI (2004–2007), 936 survivors (76 (5) years) were evaluated by cardiac magnetic resonance. Analysis included logistic regression and random effects modeling. Comparisons are relative to subjects without MI. At baseline midlife evaluation, a modified Framingham risk score was significantly higher in RMI and in UMI versus no MI (7.4 (6.3)%; 7.1 (6.2)% versus 5.4 (5.8)%, P<0.001). RMI and UMI were more frequent in men (65%, 64% versus 43%; P<0.0001). Baseline systolic and diastolic blood pressure were significantly higher in UMI (138 (17) mm Hg versus 133 (17) mm Hg; P<0.006; 87 (10) mm Hg versus 84 (10) mm Hg; P<0.02). Diastolic BP was significantly higher in RMI (88 (10) mm Hg versus 84 (10) mm Hg; P<0.02). Cholesterol and triglycerides were significantly higher in RMI (6.7 (1.1) mmol/L versus 6.2 (1.1) mmol/L; P=0.0005; and 1.4 (0.7) mmol/L versus 1.1 (0.7) mmol/L; P<0.003). Cholesterol trended higher in UMI (P=0.08). Serial midlife systolic BP was significantly higher in UMI versus no MI (β [SE] = 2.69 [1.28] mm Hg, P=0.04). Serial systolic and diastolic BP were significantly higher in RMI versus no MI (4.12 [1.60] mm Hg, P=0.01 and 2.05 [0.91] mm Hg, P=0.03) as were cholesterol (0.43 [0.11] mmol/L, P=0.0001) and triglycerides (0.3 [0.06] mmol/L, P<0.0001).ConclusionsMidlife vascular risk factors are associated with UMI and RMI detected by cardiac magnetic resonance 31 years later. Systolic blood pressure was the most significant modifiable risk factor associated with later UMI.

Mid‐adulthood cardiometabolic risk factor profiles of sarcopenic obesity

Midlife and contemporaneous cardiometabolic risk factors associated with sarcopenic obesity were examined. Utilizing BMI and sex-specific 24-h urinary creatinine excretion, 1,019 participants from the Framingham cohorts were categorized as non-sarcopenia non-obese (NSNO), non-obese sarcopenia, non-sarcopenic obesity, and sarcopenic obesity. Cardiometabolic risk factors were quantified by standard laboratory assessment cross-sectionally and 10, 20, and 30 years before sarcopenic obesity assessment. NSNO, sarcopenia, obesity, and sarcopenic obesity accounted for 30.0%, 39.6%, 20.0%, and 10.4% of study participants, respectively. Cross-sectionally, participants with sarcopenic obesity had a higher proportion of hypertension, metabolic syndrome, and type 2 diabetes than those with NSNO or sarcopenia (all P < 0.03). Similar patterns were observed retrospectively at 10, 20, and 30 years. Compared with NSNO or sarcopenia, sarcopenic obesity was associated with a higher prevalence of type 2 diabetes at 10 years and hypertension and metabolic syndrome at all three time points before baseline (all P < 0.03). Individuals with sarcopenic obesity had more type 2 diabetes than those with obesity alone at baseline and 10 years prior (all P < 0.001). Older adults with sarcopenic obesity had more adverse midlife cardiometabolic risks, particularly diabetes 10 years earlier, which suggests the importance of early identification of risk factors associated with sarcopenic obesity.

Associations of mid-life cardiovascular risk factors with later life cognitive function

Associations of mid-life cardiovascular risk factors with later life cognitive function

Abstract 11917: Midlife Cardiovascular Risk Factors and Late-Life Unrecognized and Recognized Myocardial Infarction Detected by Cardiac Magnetic Resonance (ICELAND-MI, the AGES-Reykjavik Study)

Introduction: The association of midlife atherosclerosis risk factors (RF) with later unrecognized myocardial infarction (UMI) is unclear. We investigated associations of midlife RF with UMI and recognized MI (RMI) detected 31 years later by cardiac magnetic resonance (CMR). Methods: The Reykjavik Study (1967-91) collected serial measures of RF in subjects born 1907-35, mean (SD) age 48 ± 7 years. In ICELAND-MI (2004-07), 936 randomly selected survivors (76 ± 5 years) were evaluated by CMR. Analysis included logistic regression and random effects modeling adjusted for age, sex, and covariates. All comparisons are relative to the no MI group. Results: At baseline midlife evaluation, atherosclerotic risk assessed by a modified Framingham risk score was significantly higher in RMI and UMI than in no MI (7.4 ± 6.3%; 7.1 ± 6.2% vs 5.4 ± 5.8% respectively, p&lt;0.001). RMI and UMI were more common in men (65%, 64% vs 43%; p&lt;0.0001). Compared with no MI, baseline systolic BP was significantly higher in UMI (138 ± 17 mm Hg vs 133 ± 17 mm Hg; p=0.006), and trended higher in RMI (p=0.06). Likewise, baseline diastolic BP was significantly elevated in both RMI and UMI (88 ± 10 mm Hg and 87 ± 10 mm Hg vs 84 ± 10 mm Hg; p&lt;0.02). Serum cholesterol was significantly higher in RMI (6.7 ± 1.1 mmol/L vs 6.2 ± 1.1 mmol/L; p=0.005), as were serum triglycerides (1.4 ± 0.7 mmol/L vs 1.3 ± 0.7 mmol/L; p&lt;0.03). Serum cholesterol trended higher in UMI (p=0.08). Compared to no MI, serial midlife systolic and diastolic BP were significantly higher in RMI [beta=4.03 ± 1.64 (SE) mm Hg, p=0.014 and 2.05 ± 0.94 mm Hg, p=0.025, respectively] as were cholesterol and triglycerides [0.43 ± 0.11 mmol/L, p=0.001 and 0.31 ± 0.07 mmol/L, p&lt;0.0001, respectively]. Systolic BP was significantly higher in UMI [beta=2.76 ±1.31 mm Hg, p=0.036, figure]. Conclusions: Midlife vascular risk factors are associated with UMI and RMI detected by CMR 31 years later. Systolic BP was the most important individual risk factor associated with later UMI.

Abstract 12233: Low Cardiovascular Risk in Midlife Predicts Active and Healthy Aging

Introduction and hypothesis: Low cardiovascular disease (CVD) risk in midlife predicts survival and fewer CVD events up to old age. But do they also predict a broad concept of “active and healthy aging” (“successful aging”)? We studied this in our long-term cohort. Methods: The Helsinki Businessmen Study is a follow-up study of socioeconomically homogenous cohort of men born 1919-1934 (n=3293). Midlife (average age 42 years) risk factors included BMI, smoking, cholesterol, blood pressure, and one-hour glucose. Total CVD risk was also assessed with Keys’ risk score including age, BMI, smoking, cholesterol, and systolic blood pressure. Mortality follow-up was through 2010 whereupon mailed questionnaire data, including lifestyle, diseases, and quality of life was obtained from survivors. As there is no consensus criteria on active and healthy aging, our definition included the following 6 criteria which in general could be considered important: survival to an average age of 82 years, and 5 dimensions related to health, wellbeing, and physical, cognitive, and social functioning. In the analyses we divided the cohort into 3 age groups: men born 1919-1924 (n=969), 1925-1929 (n=1481), and 1930-1934 (n=843). Results: By 2010, 1788 of the midlife cohort had died and 894 (59% of survivors) responded to mailed questionnaire survey. According to our definition, only 154 men (4.8%) of the whole cohort experienced active and healthy aging fulfilling all 6 criteria. Of the individual midlife CVD risk factors only higher systolic blood pressure reduced odds of active and healthy aging (OR per SD 0.65. 95% CI 0.52 to 0.82, P&lt;0.001) in adjusted analyses. Keys’ score was a powerful predictor of active and healthy aging overall (OR per SD of log value: 0.49, 95% CI 0.41-0.60, P&lt;0.001), and in all age groups. ORs were: 0.52, 95% CI 0.29-0.95 (P=0.03); 0.52, 95% CI 0.38-0.72 (P&lt;0.001), and 0.65, 95% CI 0.46-0.92 (P=0.01) in the oldest, middle and youngest age group, respectively. Conclusions: From a life-course viewpoint, active and healthy aging was relatively infrequent among men of higher social class. Lower systolic blood pressure and CVD risk overall in early midlife strongly predicted active and healthy aging giving impetus to controlling CVD risk in time in aging societies.

Midlife adiposity predicts earlier onset of Alzheimer's dementia, neuropathology and presymptomatic cerebral amyloid accumulation.

Understanding how midlife risk factors influence age at onset (AAO) of Alzheimer's disease (AD) may provide clues to delay disease expression. Although midlife adiposity predicts increased incidence of AD, it is unclear whether it affects AAO and severity of Alzheimer's neuropathology. Using a prospective population-based cohort, Baltimore Longitudinal Study of Aging (BLSA), this study aims to examine the relationships between midlife body mass index (BMI) and (1) AAO of AD (2) severity of Alzheimer's neuropathology and (3) fibrillar brain amyloid deposition during aging. We analyzed data on 1394 cognitively normal individuals at baseline (8643 visits; average follow-up interval 13.9 years), among whom 142 participants developed incident AD. In two subsamples of BLSA, 191 participants underwent autopsy and neuropathological assessment, and 75 non-demented individuals underwent brain amyloid imaging. Midlife adiposity was derived from BMI data at 50 years of age. We find that each unit increase in midlife BMI predicts earlier onset of AD by 6.7 months (P=0.013). Higher midlife BMI was associated with greater Braak neurofibrillary but not CERAD (Consortium to Establish a Registry for Alzheimer's Disease) neuritic plaque scores at autopsy overall. Associations between midlife BMI and brain amyloid burden approached statistical significance. Thus, higher midlife BMI was also associated with greater fibrillar amyloid measured by global mean cortical distribution volume ratio (P=0.075) and within the precuneus (left, P=0.061; right, P=0.079). In conclusion, midlife overweight predicts earlier onset of AD and greater burden of Alzheimer's neuropathology. A healthy BMI at midlife may delay the onset of AD.

Association of cognitive function with glucose tolerance and trajectories of glucose tolerance over 12 years in the AusDiab study.

IntroductionWe investigated the association between glucose tolerance status and trajectories of change in blood glucose, and cognitive function in adults aged 25 to 85.MethodsThe sample (n = 4547) was drawn from a national, population-based cohort study in Australia (AusDiab). Fasting plasma glucose (FPG), glycated haemoglobin (HbA1c) and general health were assessed at 0, 5 and 12 years. Covariates included age, education, body mass index, blood pressure and physical activity. At 12 years, participants completed assessments of memory, processing speed and verbal ability.ResultsKnown diabetes at baseline was associated with slower processing speed at 12 years in both younger (25–59 years) and older (>60 years) age-groups. After 12 years of follow-up, adults aged < 60 with diabetes at baseline had a mean speed score of 49.17 (SE = 1.09) compared with 52.39 (SE = 0.20) in normals. Among younger males without diagnosed diabetes, reduced memory at 12 years was associated with higher HbA1c at 5 years (β = −0.91, SE = 0.26, p < 0.001). No effects were apparent for females or older males. Adjusting for insulin sensitivity (HOMA-%S) and hs-C reactive protein attenuated these associations, but depression and CVD risk did not. Latent class analysis was used to analyse the associations between trajectories of HbA1C and glucose over 12 years, and cognition. Identified classes were described as 1) normal and stable blood glucose over time (reference), 2) high intercept but stable blood glucose over time, and 3) increasing blood glucose over time. In both young males and females, high stable glucose measures were associated with poorer cognitive function after 12 years.ConclusionThose with type 2 diabetes, younger males with high non-diabetic HbA1c, and adults with high stable blood glucose are at increased risk of poorer cognition. The findings reinforce the need for management of diabetes risk factors in midlife.Electronic supplementary materialThe online version of this article (doi:10.1186/s13195-015-0131-4) contains supplementary material, which is available to authorized users.

Early Life Risk Factors for Stroke and Cognitive Impairment

Cerebrovascular disease may present in later life with stroke or cognitive impairment and dementia, or may be silent, with changes seen incidentally on imaging or pathology. Midlife vascular risk factors such as hypertension, smoking and diabetes are well recognised. However, factors from much earlier in life may contribute to later vascular risk. In this commentary, we outline the importance of considering the whole life course in the development of cerebrovascular disease. We consider mainly factors from childhood, childhood intelligence test scores, education and socioeconomic status, which have been shown to contribute to stroke and cognitive impairment. Factors from even earlier in life, e.g. birth weight and breastfeeding also influence vascular risk factors. We discuss potential mechanisms for the observed relationships, e.g. whether childhood IQ or access to education may influence availability of social and economic resources and adoption of certain lifestyle choices and behaviours which are beneficial to health. Other possible mechanisms behind the observed relationships include differences in brain resilience and integrity reflected in intelligence which may lead to reduced susceptibility to cerebrovascular disease or the ability to sustain a higher degree of pathology before disease becomes clinically evident. Ongoing epidemiological, data linkage, imaging and translational studies are exploring the interrelationships and underlying mechanisms, but meanwhile, it is important to take a life course perspective when considering risk factors for cerebrovascular disease.

The CAIDE Dementia Risk Score App: The development of an evidence-based mobile application to predict the risk of dementia

BackgroundThe CAIDE (Cardiovascular Risk Factors, Aging, and Incidence of Dementia) Dementia Risk Score is a validated tool to predict late-life dementia risk (20 years later), based on midlife vascular risk factors. The goal was to render this prediction tool widely accessible. MethodsThe CAIDE Risk Score (mobile application) App was developed based on the CAIDE Dementia Risk Score, involving information on age, educational level, hypertension, hypercholesterolemia, obesity, and physical inactivity. ResultsThe CAIDE Risk Score App is an evidence-based practical tool, which allows users to detect their individual risk, provides guidance for risk modification, and suggests consulting a health care practitioner if needed. Moreover, it allows practitioners to discuss preventive measures and monitor risk reduction. ConclusionsThe CAIDE Risk Score App is the first to predict the risk for dementia through an important evidence-based tool. The App can encourage users to actively decrease their modifiable risk factors and postpone cognitive impairment and dementia.

Comparing the impact of personal and parental risk factors, and parental lifespan on all-cause mortality and cardiovascular disease: findings from the Midspan Family cohort study

BackgroundWe aimed to identify which personal and parental factors best explained all-cause mortality and cardiovascular disease (CVD).MethodsIn 1996, data were collected on 2338 adult offspring of the participants in the...

Modifiable midlife risk factors, independent aging, and survival in older men: report on long-term follow-up of the Uppsala Longitudinal Study of Adult Men cohort.

To examine relationships between modifiable midlife factors, aging, and physical and cognitive function (independent aging) and survival in very old age. Prospective cohort. Uppsala Longitudinal Study of Adult Men, Uppsala, Sweden. Swedish men investigated in 1970-74 (aged 48.6-51.1) and followed up for four decades (N=2,293). Conventional cardiovascular risk factors, body mass index (BMI), and dietary biomarkers were measured, and a questionnaire was used to gather information on lifestyle variables at age 50. Four hundred seventy-two men were reinvestigated in 2008-09 (aged 84.8-88.9). Independent aging was defined as survival to age 85, Mini-Mental State Examination score of 25 or greater, not living in an institution, independent in personal care and hygiene, able to walk outdoors without personal help, and no diagnosis of dementia. The National Swedish Death Registry provided survival data. Thirty-eight percent of the cohort survived to age 85. Seventy-four percent of the participants in 2008-09 were aging independently. In univariable analyses, high leisure-time physical activity predicted survival but not independent aging. Low work-time physical activity was associated more strongly with independent aging (odds ratio (OR)=1.84, 95% confidence interval (CI)=1.18-2.88) than with survival (OR=1.27, 95% CI=1.05-1.52). In multivariable analyses, midlife BMI was negatively associated (OR=0.80/SD, 95% CI=0.65-0.99/SD), and never or former smoking was positively associated (OR=1.66, 95% CI=1.07-2.59), with independent aging. As expected, conventional cardiovascular and lifestyle risk factors were associated with mortality. A normal midlife BMI and not smoking were associated with independent aging close to four decades later, indicating that normal weight at midlife has the potential not only to increase survival, but also to preserve independence with aging.

Somatometric and clinical cardiovascular risk factors in midlife and older women. A tale of four European countries

Somatometric and clinical cardiovascular risk factors in midlife and older women. A tale of four European countries