Background and objective: Physical activity level and obesity are both partly determined by genes and childhood environment. To determine the associations between long-term leisure-time physical activity, weight gain and waist circumference and whether these are independent of genes and childhood effects. Design and subjects: The study design is a 30-year follow-up twin study in Finland. For this study, 146 twin pairs were comprehensively identified from the large Finnish Twin Cohort. These twin pairs were discordant for both intensity and volume of leisure physical activity in 1975 and 1981 and were healthy in 1981. At follow-up in 2005, both members of 89 pairs were alive and participated in a structured telephone interview. In the interview self-measured weight and waist circumference, and physical activity level for the whole follow-up were assessed. Paired tests were used in the statistical analyses. .9) less in the active compared to inactive co-twins (paired t-test, P ¼ 0.003). In 2005, the mean waist circumference was 8.4 cm (95% CI 4.0-12.7) less in the active compared with inactive co-twins (Po0.001). These trends were similar for both monozygotic and dizygotic twin pairs. Pairwise differences in weight gain and waist circumference were not seen in the 47 twin pairs, who were not consistently discordant for physical activity. Conclusion: Persistent participation in leisure-time physical activity is associated with decreased rate of weight gain and with a smaller waist circumference to a clinically significant extent even after partially controlling for genetic liability and childhood environment.
The older Finnish Twin Cohort (FTC) was established in 1974. The baseline survey was in 1975, with two follow-up health surveys in 1981 and 1990. The fourth wave of assessments was done in three parts, with a questionnaire study of twins born during 1945–1957 in 2011–2012, while older twins were interviewed and screened for dementia in two time periods, between 1999 and 2007 for twins born before 1938 and between 2013 and 2017 for twins born in 1938–1944. The content of these wave 4 assessments is described and some initial results are described. In addition, we have invited twin-pairs, based on response to the cohortwide surveys, to participate in detailed in-person studies; these are described briefly together with key results. We also review other projects based on the older FTC and provide information on the biobanking of biosamples and related phenotypes.
ObjectivePhysical activity (PA) is associated with a decreased incidence of dementia, but much of the evidence comes from short follow-ups prone to reverse causation. This meta-analysis investigates the effect of study length on the association.DesignA systematic review and meta-analysis. Pooled effect sizes, dose–response analysis and funnel plots were used to synthesise the results.Data sourcesCINAHL (last search 19 October 2021), PsycInfo, Scopus, PubMed, Web of Science (21 October 2021) and SPORTDiscus (26 October 2021).Eligibility criteriaStudies of adults with a prospective follow-up of at least 1 year, a valid cognitive measure or cohort in mid-life at baseline and an estimate of the association between baseline PA and follow-up all-cause dementia, Alzheimer’s disease or vascular dementia were included (n=58).ResultsPA was associated with a decreased risk of all-cause dementia (pooled relative risk 0.80, 95% CI 0.77 to 0.84, n=257 983), Alzheimer’s disease (0.86, 95% CI 0.80 to 0.93, n=128 261) and vascular dementia (0.79, 95% CI 0.66 to 0.95, n=33 870), even in longer follow-ups (≥20 years) for all-cause dementia and Alzheimer’s disease. Neither baseline age, follow-up length nor study quality significantly moderated the associations. Dose–response meta-analyses revealed significant linear, spline and quadratic trends within estimates for all-cause dementia incidence, but only a significant spline trend for Alzheimer’s disease. Funnel plots showed possible publication bias for all-cause dementia and Alzheimer’s disease.ConclusionPA was associated with lower incidence of all-cause dementia and Alzheimer’s disease, even in longer follow-ups, supporting PA as a modifiable protective lifestyle factor, even after reducing the effects of reverse causation.
T he physically active lifestyle is associated with low future morbidity and mortality, but the causality between physical activity and health is not always clear. As some inherited biological characteristics and childhood experiences may cause selection bias in observational studies, we sought to take them into account by identifying 16 twin pairs (7 MZ, 9 DZ, mean age 60 years) discordant for leisure time physical activity habits for thirty years. We conducted detailed health-related examinations among these twin pairs. Our main aims were to study the effects of physical activity and genes on fitness and body composition, with special reference to body fat compartments, metabolic syndrome components and related diseases and risk factor levels, status of arteries, structure and function of the heart, bone properties, and muscle and fat tissue-related mechanisms linked to physical activity and chronic disease development. Our physical activity assessments showed that inactive co-twins were on average 8.8 MET hours/day less active than their active co-twins through out their midlife (2.2 ± 2.3 vs. 11.0 ± 4.1 MET h/day, p < .001). Follow-up fitness tests showed that physically inactive co-twins were less fit than their active co-twins (estimated VO 2peak 26.4 ± 4.9 vs. 32.5 ± 5.5 ml/kg/min, p < .001). Similar differences were found in both MZ and DZ pairs. On the basis of earlier epidemiological observations on nonrelated individuals, these physical activity and fitness differences are large enough to cause differences in many mechanisms and risk factors related to the development of chronic diseases and to permit future analyses.
Observational studies report a strong inverse relationship between leisure-time physical activity and all-cause mortality. Despite suggestive evidence from population-based associations, scientists have not been able to show a beneficial effect of physical activity on the risk of death in controlled intervention studies among individuals who have been healthy at baseline. On the other hand, high cardiorespiratory fitness is known to be a strong predictor of reduced mortality, even more robust than physical activity level itself. Here, in both animals and/or human twins, we show that the same genetic factors influence physical activity levels, cardiorespiratory fitness, and risk of death. Previous observational follow-up studies in humans suggest that increasing fitness through physical activity levels could prolong life; however, our controlled interventional study with laboratory rats bred for low and high intrinsic fitness contrast with these findings. Also, we find no evidence for the suggested association using pairwise analysis among monozygotic twin pairs who are discordant in their physical activity levels. Based on both our animal and human findings, we propose that genetic pleiotropy might partly explain the frequently observed associations between high baseline physical activity and later reduced mortality in humans.
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