A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial.
Modifiable vascular and lifestyle-related risk factors have been associated with dementia risk in observational studies. In the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER), a proof-of-concept randomised controlled trial, we aimed to assess a multidomain approach to prevent cognitive decline in at-risk elderly people from the general population.
In a double-blind randomised controlled trial we enrolled individuals aged 60-77 years recruited from previous national surveys. Inclusion criteria were CAIDE (Cardiovascular Risk Factors, Aging and Dementia) Dementia Risk Score of at least 6 points and cognition at mean level or slightly lower than expected for age. We randomly assigned participants in a 1:1 ratio to a 2 year multidomain intervention (diet, exercise, cognitive training, vascular risk monitoring), or a control group (general health advice). Computer-generated allocation was done in blocks of four (two individuals randomly allocated to each group) at each site. Group allocation was not actively disclosed to participants and outcome assessors were masked to group allocation. The primary outcome was change in cognition as measured through comprehensive neuropsychological test battery (NTB) Z score. Analysis was by modified intention to treat (all participants with at least one post-baseline observation). This trial is registered at ClinicalTrials.gov, number NCT01041989.
Between Sept 7, 2009, and Nov 24, 2011, we screened 2654 individuals and randomly assigned 1260 to the intervention group (n=631) or control group (n=629). 591 (94%) participants in the intervention group and 599 (95%) in the control group had at least one post-baseline assessment and were included in the modified intention-to-treat analysis. Estimated mean change in NTB total Z score at 2 years was 0·20 (SE 0·02, SD 0·51) in the intervention group and 0·16 (0·01, 0·51) in the control group. Between-group difference in the change of NTB total score per year was 0·022 (95% CI 0·002-0·042, p=0·030). 153 (12%) individuals dropped out overall. Adverse events occurred in 46 (7%) participants in the intervention group compared with six (1%) participants in the control group; the most common adverse event was musculoskeletal pain (32 [5%] individuals for intervention vs no individuals for control).
Findings from this large, long-term, randomised controlled trial suggest that a multidomain intervention could improve or maintain cognitive functioning in at-risk elderly people from the general population.
Academy of Finland, La Carita Foundation, Alzheimer Association, Alzheimer's Research and Prevention Foundation, Juho Vainio Foundation, Novo Nordisk Foundation, Finnish Social Insurance Institution, Ministry of Education and Culture, Salama bint Hamdan Al Nahyan Foundation, Axa Research Fund, EVO funding for University Hospitals of Kuopio, Oulu, and Turku and for Seinäjoki Central Hospital and Oulu City Hospital, Swedish Research Council, Swedish Research Council for Health, Working Life and Welfare, and af Jochnick Foundation.
The aim of this study was to assess the less studied interrelationships and pathways between parental BMI, socioeconomic factors, family structure and childhood overweight.
The cross-sectional LATE-study was carried out in Finland in 2007-2009. The data for the analyses was classified into four categories: younger boys and girls (ca 3-8 years) (n?=?2573) and older boys and girls (ca 11-16 years) (n?=?1836). Associations between parental BMI, education, labor market status, self-perceived income sufficiency, family structure and childhood overweight were first examined by logistic regression analyses. As parental BMI and education had the most consistent associations with childhood overweight, the direct and indirect (mediated by parental BMI) associations of maternal and paternal education with childhood overweight were further assessed using a path model.
Parental BMI and education were the strongest determinants of childhood overweight. Children of overweight parents had an increased risk of being overweight. In younger boys, maternal and paternal education had both direct (b-coefficient paternal -0.21, 95% CI -0.34 to -0.09; maternal -0.17, 95% CI -0.28 to -0.07) and indirect (b-coefficient paternal -0.04, 95% CI -0.07 to -0.02; maternal -0.04, 95% CI -0.06 to -0.02) inverse associations with overweight. Among the older boys, paternal education had both direct (b-coefficient -0.12, 95% CI -0.24 to -0.01) and indirect (b-coefficient -0.03, 95% CI -0.06 to -0.01) inverse associations with overweight, but maternal education had only an indirect association (b-coefficient -0.04, 95% CI -0.07 to -0.02). Among older girls, only an indirect association of maternal education with childhood overweight was found (b-coefficient -0.03, 95% CI -0.06 to -0.01). In younger girls, parental education was not associated with childhood overweight.
The observed pathways between parental BMI and education and childhood overweight emphasize a need for evidence-based health promotion interventions tailored for families identified with parental overweight and low level of education.
CAIDE Dementia Risk Score is the first validated tool for estimating dementia risk based on a midlife risk profile.
This observational study investigated longitudinal associations of CAIDE Dementia Risk Score with brain MRI, amyloid burden evaluated with PIB-PET, and detailed cognition measures.
FINGER participants were at-risk elderly without dementia. CAIDE Risk Score was calculated using data from previous national surveys (mean age 52.4 years). In connection to baseline FINGER visit (on average 17.6 years later, mean age 70.1 years), 132 participants underwent MRI scans, and 48 underwent PIB-PET scans. All 1,260 participants were cognitively assessed (Neuropsychological Test Battery, NTB). Neuroimaging assessments included brain cortical thickness and volumes (Freesurfer 5.0.3), visually rated medial temporal atrophy (MTA), white matter lesions (WML), and amyloid accumulation.
Higher CAIDE Dementia Risk Score was related to more pronounced deep WML (OR 1.22, 95% CI 1.05-1.43), lower total gray matter (ß-coefficient -0.29, p?=?0.001) and hippocampal volume (ß-coefficient -0.28, p?=?0.003), lower cortical thickness (ß-coefficient -0.19, p?=?0.042), and poorer cognition (ß-coefficients -0.31 for total NTB score, -0.25 for executive functioning, -0.33 for processing speed, and -0.20 for memory, all p?
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The definition of a smoker as someone who smokes daily has been challenged. No consensus exists regarding whether intermittent smoking represents transition toward daily smoking or cessation or whether intermittent smokers consistently maintain their low tobacco use frequency. Although abundant evidence supports the adverse health consequences of daily smoking, less evidence is available on intermittent smoking.
We examined characteristics and health consequences of intermittent cigarette smoking among Finnish adult twins. We used longitudinal data of 21,340 persons with smoking status from questionnaires in 1975 and 1981 and data on lung cancer incidence from 1982 to 2004 from the Finnish Cancer Registry.
We identified 641 consistent intermittent smokers comprising 3% of the study population. Consistent intermittent smokers had higher education, less use of other tobacco products, healthier lifestyles, and partly more favorable mental health profiles compared with lifetime regular smokers. However, in terms of other lifestyle factors, intermittent smokers compared mostly unfavorably with never-smokers, despite being better educated. Intermittent smoking showed substantial heritability. There were 213 incident lung cancer cases among all study subjects; only one case was found among the intermittent smokers. The sex- and age-adjusted hazard ratios of lung cancer were not significantly elevated for the intermittent smokers, but they were increased more than 10-fold for all other smokers.
Although the present study did not find evidence of elevated lung cancer risk among intermittent smokers, compared with never-smokers, further studies should investigate other health consequences of intermittent smoking, such as cardiovascular and nonmalignant pulmonary outcomes.
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The objective was to examine the influences of body anthropometrics, axial disc area, and lifting strength on disc degeneration and to compare these with the effects of lifetime physical demands and age.
Although recent studies have shown that heredity is a dominant factor in disc degeneration, the common notion that occupational physical loading is the major risk factor persists. However, substantial variations in disc degeneration, particularly at the lowest lumbar levels, remain unexplained by heredity or occupational physical demands.
Univariate methods and stepwise multiple regression modeling were used to estimate associations of body height, weight, fat content, axial disc area, isokinetic lifting performance, and lifetime routine physical activities at work and leisure with disc height narrowing and disc signal (in T2 images) based on lumbar MRIs. These data were available from a population sample of 600 men, 35 to 70 years of age.
Lower disc signal, representing disc desiccation, was associated with higher age, lower body mass and lifting strength, and larger axial disc area. Of the variance in disc signal, age explained 8.0% (P
We examined whether externalizing problem behaviors (hyperactivity-impulsivity, aggressiveness, and inattention) predict illicit drug use independently, or whether their associations with drug use are mediated through cigarette smoking. We used a prospective longitudinal design within the FinnTwin12-17 study among Finnish adolescents with baseline at age 12 and follow-up surveys at ages 14 and 17. Path models were conducted with Mplus and included 1992 boys and 2123 girls. The outcome was self-reported ever use of cannabis or other illicit drugs at age 17. The predictors were: externalizing behaviors (hyperactivity-impulsivity, aggressiveness, and inattention) assessed by teachers and parents (age 12) and self-reported cigarette smoking (age 14). The findings differed across behavior studied. The association of hyperactivity-impulsivity with drug use was mostly mediated through earlier cigarette smoking. Concerning aggressiveness and inattention, the results were different among girls than boys. Among girls no significant mediation occurred, whereas among boys more consistent evidence on mediation was seen. Consistently in all models, the direct association of early cigarette smoking on drug use was strong and highly significant. We conclude that the associations of externalizing problem behaviors with illicit drug use are partially mediated through cigarette smoking. Although interventions targeting externalizing problem behaviors may protect adolescents from early onset smoking and subsequently experimenting with drugs, interventions to prevent cigarette smoking initiation are also important in reducing risk of later drug use.
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Finland is known for a sharp decrease in the intake of saturated fat and cardiovascular mortality. Since 2000, however, the consumption of butter-containing spreads - an important source of saturated fats - has increased. We examined social and health-related predictors of the increase among Finnish men and women.
An 11-year population follow-up.
A representative random sample of adult Finns, invited to a health survey in 2000.
Altogether 5414 persons aged 30-64 years at baseline in 2000 were re-invited in 2011. Of men 1529 (59 %) and of women 1853 (66 %) answered the questions on bread spreads at both time points. Respondents reported the use of bread spreads by choosing one of the following alternatives: no fat, soft margarine, butter-vegetable oil mixture and butter, which were later categorized into margarine/no spread and butter/butter-vegetable oil mixture (= butter). The predictors included gender, age, marital status, education, employment status, place of residence, health behaviours, BMI and health. Multinomial regression models were fitted.
Of the 2582 baseline margarine/no spread users, 24.6% shifted to butter. Only a few of the baseline sociodemographic or health-related determinants predicted the change. Finnish women were more likely to change to butter than men. Living with a spouse predicted the change among men.
The change from margarine to butter between 2000 and 2011 seemed not to be a matter of compliance with official nutrition recommendations. Further longitudinal studies on social, behavioural and motivational predictors of dietary changes are needed.
No previous studies on the effect of genetic factors on the liability to disability retirement have been carried out. The main aim of this study was to investigate the contribution of genetic factors on disability retirement due to the most common medical causes, including depressive disorders.
The study sample consisted of 24,043 participants (49.7% women) consisting of 11,186 complete same-sex twin pairs including 3519 monozygotic (MZ) and 7667dizygotic (DZ) pairs. Information on retirement events during 1.1.1975-31.12.2004, including disability pensions (DPs) with diagnoses, was obtained from the Finnish nationwide official pension registers. Correlations in liability for MZ and DZ twins and discrete time correlated frailty model were used to investigate the genetic liability to age at disability retirement.
The 30 year cumulative incidence of disability retirement was 20%. Under the best fitting genetic models, the heritability estimate for DPs due to any medical cause was 0.36 (95% CI 0.32-0.40), due to musculoskeletal disorders 0.37 (0.30-0.43), cardiovascular diseases 0.48 (0.39-0.57), mental disorders 0.42 (0.35-0.49) and all other reasons 0.24 (0.17-0.31). The effect of genetic factors decreased with increasing age of retirement. For DP due to depressive disorders, 28% of the variance was explained by environmental factors shared by family members (95% CI 21-36) and 58% of the variance by the age interval specific environmental factors (95% CI 44-71).
A moderate genetic contribution to the variation of disability retirement due to any medical cause was found. The genetic effects appeared to be stronger at younger ages of disability retirement suggesting the increasing influence of environmental factors not shared with family members with increasing age. Familial aggregation in DPs due to depressive disorders was best explained by the common environmental factors and genetic factors were not needed to account for the pattern of familial aggregation.
Many cardiovascular risk factors are shown to increase the risk of dementia and Alzheimer's disease (AD), but the impact of heart disease on later development of dementia is still unclear.
The aim of the study was to investigate the long-term risk of dementia and Alzheimer's disease (AD) related to midlife and late-life atrial fibrillation (AF), heart failure (HF), and coronary artery disease (CAD) in a population-based study with a follow-up of over 25 years.
Cardiovascular Risk Factors, Aging and Dementia (CAIDE) study includes 2000 participants who were randomly selected from four separate, population-based samples originally studied in midlife (1972, 1977, 1982, or 1987). Re-examinations were carried out in 1998 and 2005-2008. Altogether 1,510 (75.5%) persons participated in at least one re-examination, and 127 (8.4%) persons were diagnosed with dementia (of which 102 had AD).
AF in late-life was an independent risk factor for dementia (HR 2.61, 95% CI 1.05-6.47; p = 0.039) and AD (HR 2.54, 95% CI 1.04-6.16; p = 0.040) in the fully adjusted analyses. The association was even stronger among the apolipoprotein E (APOE) e4 non-carriers. Late-life HF, but not CAD, tended to increase the risks as well. Heart diseases diagnosed at midlife did not increase the risk of later dementia and AD.
Late-life heart diseases increase the subsequent risk of dementia and AD. Prevention and effective treatment of heart diseases may be important also from the perspective of brain health and cognitive functioning.
Twin studies suggest that both disc degeneration and back pain have a genetic component. We were interested in estimating the heritability of low back pain in men and examining whether genetic influences on back pain are mediated through genetic influences on disc degeneration. Thus, we conducted a classic twin study with multivariate quantitative genetic models to estimate the degree to which genetic (or environmental) effects on back pain were correlated with genetic (or environmental) effects on disc degeneration. Subjects included 147 monozygotic and 153 dizygotic male twin pairs (N=600 subjects) from the population-based Finnish Twin Cohort. All subjects underwent lumbar magnetic resonance imaging and completed an extensive interview, including back pain history and exposure to suspected risk factors. Disc height narrowing was the degenerative finding most associated with pain history, and was used to index disc degeneration in the models. Statistically significant genetic correlations were found for disc height narrowing and different definitions of back pain, such as duration of the worst back pain episode (r(g)=0.46) and hospitalization for back problems (r(g)=0.49), as well as disability in the previous year from back pain (r(g)=0.33). The heritability estimates for these back pain variables ranged from 30% to 46%. There also were statistically significant, but weaker, environmental correlations for disc height narrowing with back symptoms over the prior year. A substantial minority of the genetic influences on pain was due to the same genetic influences affecting disc degeneration. This suggests that disc degeneration is one pathway through which genes influence back pain.