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Background: Personalized interventions aiming to increase physical activity in individuals are effective. However, from a public health perspective, it would be important to stimulate physical activity in larger groups of people who share the vulnerability to be physically inactive throughout adulthood. To find these high-risk groups, we identified 36-year leisure-time physical activity profiles from young adulthood to late midlife in females and males. Moreover, we uncovered which anthropometric-, demographic-, lifestyle-, and health-related characteristics were associated with these physical activity profiles. Methods: We included 2,778 females and 1,938 males from the population-based older Finnish Twin Cohort Study, who responded to health and behavior surveys at the mean ages of 24, 30, 40 and 60. Latent profile analysis was used to identify longitudinal leisure-time physical activity profiles. Results: We found five longitudinal leisure-time physical activity profiles for both females and males. Females' profiles were: 1) Low increasing moderate (29%), 2) Moderate stable (23%), 3) Very low increasing low (20%), 4) Low stable (20%) and 5) High increasing high (9%). Males' profiles were: 1) Low increasing moderate (29%), 2) Low stable very low (26%), 3) Moderate decreasing low (21%), 4) High fluctuating high (17%) and 5) Very low stable (8%). In both females and males, lower leisure-time physical activity profiles were associated with lower education, higher body mass index, smoking, poorer perceived health, higher sedentary time, high blood pressure, and a higher risk for type 2 diabetes. Furthermore, lower leisure-time physical activity was linked to a higher risk of depression in females. Conclusions: We found several longitudinal leisure-time physical activity profiles with unique changes in both sexes. Fewer profiles in females than in males remained or became low physically active during the 36-year follow-up. We observed that lower education, higher body mass index, and more smoking already in young adulthood were associated with low leisure-time physical activity profiles. However, the fact that several longitudinal profiles demonstrated a change in their physical activity behavior over time implies the potential for public health interventions to improve leisure-time physical activity levels. [ABSTRACT FROM AUTHOR]

Background We used a polygenic score for hand grip strength (PGS HGS) to investigate whether genetic predisposition for higher muscle strength predicts age-related noncommunicable diseases, survival from acute adverse health events, and mortality. Methods This study consisted of 342 443 Finnish biobank participants from FinnGen Data Freeze 10 (53% women) aged 40–108 with combined genotype and health registry data. Associations between PGS HGS and a total of 27 clinical endpoints were explored with linear or Cox regression models. Results A higher PGS HGS was associated with a reduced risk of selected common noncommunicable diseases and mortality by 2%–10%. The risk for these medical conditions decreased by 5%–23% for participants in the highest PGS HGS quintile compared to those in the lowest PGS HGS quintile. A 1 standard deviation (SD) increase in the PGS HGS predicted a lower body mass index (β = −0.112 kg/m2, standard error [ SE ] = 0.017, p  = 1.69E-11) in women but not in men (β = 0.004 kg/m2, p  = .768). PGS HGS was not associated with better survival after acute adverse health events compared to the nondiseased period. Conclusions The genotype that supports higher muscle strength appears to protect against future health adversities, albeit with modest effect sizes. Further research is needed to investigate whether or how a favorable lifestyle modifies this intrinsic capacity to resist diseases, and if the impacts of lifestyle behavior on health differs due to genetic predisposition for muscle strength. [ABSTRACT FROM AUTHOR]

Background: The association of sleep bruxism with mortality has not been studied. Objectives: Altogether 12 040 subjects from the nationwide Finnish twin cohort were included in the analyses. We examined whether self‐reported sleep bruxism is associated with increased risk of mortality, and if so, whether the effect is independent of known common risk factors. The time span of the follow‐up was 30 years. Methods: Cox proportional hazards regression models (Hazard Ratios and their 95% Confidence Intervals) adjusted by age, sex and covariates were used to assess the effect of baseline bruxism status in 1990 on future mortality in 1990–2020. Results: The risk of mortality among all participants (n = 12 040), independent of missing covariates and adjusted by age and sex, was 40% higher in weekly bruxers than in never bruxers (HR 1.40, 95% CI 1.16–1.68, p <.001). However, when adjusted by all studied covariates, (n = 11 427) the risk was no longer observed (HR 1.04, 95% CI 0.86–1.25, p =.717). Despite the overall lack of between bruxism and mortality after adjustment for covariates, we examined the cause‐specific risks for major cause‐of‐death groups. There were no substantial associations of weekly bruxism with major disease outcomes by the fully adjusted hazard ratios for them. Conclusion: Bruxism does not kill—in line with its definition of being rather a behaviour (with all its phenotypes) than a disease. [ABSTRACT FROM AUTHOR]

Background: Due to different assessment modes employed, a clear picture of the prevalence of sleep bruxism across time cannot be formed. Moreover, studies on the persistent or fluctuating nature of sleep bruxism have yielded divergent and even contradictory results. The aim of the present study was to evaluate in a nationwide twin cohort whether self‐reported sleep bruxism was correlated longitudinally, pairwise and cross‐twin over a 20‐year period. Objectives: Self‐reported bruxism was assessed in 1990 and 2011 by mailed questionnaires in the Finnish Twin Cohort study of same‐sex twins born 1945–1957. Methods: We assessed the phenotypic stability over time for all participating individuals (n = 4992). Among zygosity verified pairs (n = 516 MZ and n = 837 DZ), we estimated the cross‐sectional zygosity correlations and the zygosity‐specific cross‐twin cross‐time correlations. Results: Reported bruxism appeared rather persistent over time without significant difference regarding zygosity. The overall phenotypic longitudinal correlation was 0.540 and somewhat higher in men (0.596) than in women (0.507). Pairwise trait correlations in 1990 and 2011 were higher in MZ than in DZ pairs. The cross‐twin cross‐time correlations were higher in MZ twins than in DZ twins, but less than the cross‐sectional MZ and DZ pairwise correlations. Conclusions: The higher correlation of reported sleep bruxism in the cross‐twin cross‐time analyses in MZ than in DZ pairs implies a genetic background for bruxism persistence. Also, bruxism over time in individual twins appears to be fairly persistent and somewhat higher in men than women. [ABSTRACT FROM AUTHOR]

Objective: This study investigated 36‐year BMI trajectories in twins whose BMI in young adulthood was below, within, or above their genetically predicted BMI, with a focus on twin pairs with large intrapair BMI differences (within‐pair ΔBMI ≥ 3 kg/m2). Methods: Together, 3227 like‐sexed twin pairs (34% monozygotic) were examined at age ~30 years in 1975 and followed up in 1981, 1990, and 2011. An individual's observed BMI in 1975 was considered within (±2.0), below (<−2.0), or above (>+2.0) genetically predicted BMI, measured by a polygenic risk score of 996,919 single nucleotide polymorphisms. Results: In monozygotic and dizygotic twin pairs with large intrapair BMI differences, the co‐twin with a higher observed BMI in 1975 deviated above predicted BMI more frequently (~2/3) than the co‐twin with a lower BMI deviated below prediction (~1/3). Individuals below, within, and above prediction in 1975 reached, respectively, normal weight, overweight, and obesity by 2011, with a mean BMI increase of 4.5 (95% CI: 4.3–4.8). Conclusions: Categorizing BMI as below, within, or above polygenic risk score‐predicted BMI helps identifying individuals who have been resistant or susceptible to weight gain. This may provide new insights into determinants and consequences of obesity. [ABSTRACT FROM AUTHOR]

Although we found no genetic correlation between baseline BMI and alcohol consumption, a genetic correlation associating baseline BMI with a change in alcohol consumption was observed in both men and women. The aims of the current study were therefore (1) to study the relationship between BMI and alcohol consumption trajectories, (2) to highlight the genetic and environmental components underlying changes in BMI and alcohol consumption, and (3) to investigate possible genetic and environmental correlations between BMI and alcohol consumption trajectories. Obesity and heavy alcohol consumption are major public health issues worldwide due to their high and increasing prevalence in recent decades [[1]]. These results support the existence of complex genetic architectures influencing (1) alcohol consumption and changes in alcohol consumption, (2) BMI with changes in BMI, and (3) BMI intercept with alcohol-related behavior over time. [Extracted from the article]

Summary: Background: Living in single parent and blended families or as an only child—compared to living in two‐parent biological families or with siblings, respectively—is associated with a higher body mass index (BMI) in cross‐sectional studies. However, longitudinal research addressing the children's BMI in this context is scarce. Further, little is known about the association between family structure and metabolic health. Objectives: This study aimed at investigating the association between both aspects of family structure with BMI and a metabolic score (MetS). Methods: Cross‐sectional data from 7804 children participating in the European multi‐center I.Family study (2013/2014) and longitudinal data from 5621 children who also participated previously in the IDEFICS study (2007–2010) were used. Family structure was assessed by a detailed interview. BMI z‐score and the MetS were based on measured anthropometry, blood pressure, high‐density lipoprotein, blood glucose, and triglycerides. Linear regressions were performed to model associations between family structure with BMI and MetS. Results: Children from single‐parent families had higher BMI z‐scores in the cross‐sectional (β = 0.09, 95% confidence interval [CI]: 0.001 to 0.18) and longitudinal analyses compared to those from two‐parent families. Cross‐sectionally, the number of siblings was associated with lower BMI z‐scores (β = −0.07, 95% CI: −0.10 to −0.03) and lower MetS (β = −0.14, 95% CI: −0.26 to −0.01). Longitudinally, only children between baseline and follow‐up had higher BMI z‐scores at follow‐up (β = 0.07, 95% CI: 0.01 to 0.14) compared to stable siblings. Conclusion: Obesity prevention measures should focus on single‐parent households and families with an only child. [ABSTRACT FROM AUTHOR]

Genetic and early environmental differences including early health habits associate with future health. To provide insight on the causal nature of these associations, monozygotic (MZ) twin pairs discordant for health habits provide an interesting natural experiment. Twin pairs discordant for leisure‐time physical activity (LTPA) in early adult life is thus a powerful study design to investigate the associations between long‐term LTPA and indicators of health and wellbeing. We have identified 17 LTPA discordant twin pairs from two Finnish twin cohorts and summarize key findings of these studies in this paper. The carefully characterized rare long‐term LTPA discordant MZ twin pairs have participated in multi‐dimensional clinical examinations. Key findings highlight that compared with less active twins in such MZ twin pairs, the twins with higher long‐term LTPA have higher physical fitness, reduced body fat, reduced visceral fat, reduced liver fat, increased lumen diameters of conduit arteries to the lower limbs, increased bone mineral density in loaded bone areas, and an increased number of large high‐density lipoprotein particles. The findings increase our understanding on the possible site‐specific and system‐level effects of long‐term LTPA. [ABSTRACT FROM AUTHOR]

Background: Do drinking patterns in late adolescence/early adulthood predict lifetime childlessness and number of children? Research on this question has been only tangentially relevant and the results inconsistent. The designs used to date have been compromised by genetic and environmental confounds that are poorly controlled; covariate effects of smoking and education that are often ignored; males being understudied; population‐based sampling rare, and long‐term prospective studies with genetically informative designs yet to be reported. Method: In a 33‐year follow‐up, we linked the drinking patterns of >3500 Finnish twin pairs, assessed at ages 18–25, to registry data on their eventual number of children. Analyses distinguished associations of early drinking patterns with lifetime childlessness from those predictive of family size. Within‐twin pair analyses used fixed‐effects regression models to account for shared familial confounds and genetic liabilities. Childlessness was analyzed with Cox proportional hazards models and family size with Poisson regression. Analyses within‐pairs and of twins as individuals were run before and after adjustment for smoking and education, and for oral contraceptive (OC) use in individual‐level analyses of female twins. Results: Baseline abstinence and heavier drinking both significantly predicted lifetime childlessness in individual‐level analyses. Few abstinent women used OCs, but they were nonetheless more often eventually childless; adjusting for smoking and education did not affect this finding. Excluding childless twins, Poisson models of family size showed heavier drinking at 18–25 to be predictive of fewer children in both men and women. Those associations were replicated in within‐pair analyses of dizygotic twins, each level of heavier drinking being associated with smaller families. Among monozygotic twins, associations of drinking with completed family size yielded effects of similar magnitude, reaching significance at the highest levels of consumption, ruling out familial confounds. Conclusions: Compared to moderate levels of drinking, both abstinence and heavier drinking in late adolescence/early adulthood predicted a greater likelihood of lifetime childlessness and eventual number of children. Familial confounds do not fully explain these associations. [ABSTRACT FROM AUTHOR]

Background: Epigenetic clocks are composite markers developed to predict chronological age or mortality risk from DNA methylation (DNAm) data. The present study investigated the associations between 4 epigenetic clocks (Horvath's and Hannum's DNAmAge and DNAm GrimAge and PhenoAge) and physical functioning during a 3-year follow-up.Method: We studied 63- to 76-year-old women (N = 413) from the Finnish Twin Study on Aging. DNAm was measured from blood samples at baseline. Age acceleration (AgeAccel), that is, discrepancy between chronological age and DNAm age, was determined as residuals from linear model. Physical functioning was assessed under standardized laboratory conditions at baseline and at follow-up. A cross-sectional analysis was performed with path models, and a longitudinal analysis was conducted with repeated measures linear models. A nonrandom missing data analysis was performed.Results: In comparison to the other clocks, GrimAgeAccel was more strongly associated with physical functioning. At baseline, GrimAgeAccel was associated with lower performance in the Timed Up and Go (TUG) test and the 6-minute walk test. At follow-up, significant associations were observed between GrimAgeAccel and lowered performance in the TUG, 6-minute and 10-m walk tests, and knee extension and ankle plantar flexion strength tests.Conclusions: The DNAm GrimAge, a novel estimate of biological aging, associated with decline in physical functioning over the 3-year follow-up in older women. However, associations between chronological age and physical function phenotypes followed similar pattern. Current epigenetic clocks do not provide strong benefits in predicting the decline of physical functioning at least during a rather short follow-up period and restricted age range. [ABSTRACT FROM AUTHOR]

Living in the same household exposes family members to shared environments and may be reflected in estimates of shared environment in twin analyses. The age at the separation of cotwins in a twin pair marks the end of such shared exposure, and the age of separation is commonly self-reported in studies. The objective of the study was to summarize the age at separation from residential records and use it to validate with self-reported separation status and age at the third and fourth wave of data collection in the FinnTwin12 cohort. Age at separation was generated from the address information, linking it to the Finnish Population information system since birth. Descriptive statistics by sex and zygosity are presented. The mean age at separation from residential records was 20.36 years old. Women separated earlier than men and dizygotic pairs earlier than monozygotic pairs. We also calculated the sensitivity and specificity with the self-reported separation status at waves 3 and 4, and interrater reliability with the self-reported separation age at wave 4. Age at separation from residential records had a relatively poor agreement with the self-report. This work enables us to use a more precise and objective measure for the shared environment in future twin studies. [ABSTRACT FROM AUTHOR]

Study Objectives: Poor sleep is one of the multiple health issues associated with heavy alcohol consumption. While acute effects of alcohol intake on sleep have been widely investigated, the longitudinal associations remain relatively underexplored. The objective of our research was to shed light on cross-sectional and longitudinal associations between alcohol use and poor sleep quality over time, and to elucidate the role of familial confounding factors in such associations. Methods: Using self-report questionnaire data from the Older Finnish Twin Cohort (N = 13 851), we examined how alcohol consumption and binge drinking are associated with sleep quality during a period of 36 years. Results: Cross-sectional logistic regression analyses revealed significant associations between poor sleep and alcohol misuse, including heavy and binge drinking, at all four time points (OR range = 1.61-3.37, p < .05), suggesting that higher alcohol intake is associated with poor sleep quality over the years. Longitudinal cross-lagged analyses indicated that moderate, heavy and binge drinking predict poor sleep quality (OR range = 1.25-1.76, p < .05), but not the reverse. Withinpair analyses suggested that the associations between heavy drinking and poor sleep quality were not fully explained by genetic and environmental influences shared by the co-twins. Conclusions: In conclusion, our findings support previous literature in that alcohol use is associated with poor sleep quality, such that alcohol use predicts poor sleep quality later in life, but not vice versa, and that the association is not fully explained by familial factors. [ABSTRACT FROM AUTHOR]

Objective: We assessed the detection, treatment and outcomes of DSM‐5 eating disorders in a nationwide community setting. Method: The FinnTwin12 cohort comprises twins born in 1983–1987 in Finland (n = 5,600), with follow‐up starting at age 12. We outline treatment and outcomes of the 127 females and 15 males diagnosed with a lifetime DSM‐5 eating disorder in interviews conducted for a subsample (n = 1,347) in their early 20s. Results: Only 45 (32%) of those diagnosed with eating disorder in the interviews had their condition detected in healthcare, and even fewer received treatment (30% of females, 13% of males). Anorexia nervosa (AN), bulimia nervosa, and atypical AN were detected and treated more often than other eating disorders. Five years after disease onset, 41% of those diagnosed had recovered. There were no statistically significant differences in the course of different eating disorders (log‐rank p = 0.66) but the outcome was more favourable among males (log‐rank p = 0.008). The likelihood of 5‐year recovery did not differ between those who had and who had not received treatment (41.1% vs. 40.5%, log‐rank p = 0.66). Conclusion: Although eating disorders are common and symptoms are persistent for many, they remain under‐diagnosed and under‐treated. In real‐world settings, effectiveness of provided treatments may be limited. Key points: Although eating disorders affected one in six females and one in 40 males in the community, only one‐third of these cases were detected by healthcare providers, and even fewer received any treatment. Atypical disorders remain rarely recognized and treated.Eating disorder symptoms can be persistent for many sufferers; 5 years after disease onset, less than two‐fifths of the females and two‐thirds of the males had recovered.Real‐world treatments available in healthcare may have limited effectiveness, as the likelihood of recovery within 5 years was 40 percent in both treated and untreated groups. [ABSTRACT FROM AUTHOR]

Introduction Genetic pleiotropy, in which the same genes affect two or more traits, may partially explain the frequently observed associations between high physical activity (PA) and later reduced morbidity or mortality. This study investigated associations between PA polygenic risk scores (PRS) and cardiometabolic diseases among the Finnish population. Methods PRS for device-measured overall PA were adapted to a FinnGen study cohort of 218,792 individuals with genomewide genotyping and extensive digital longitudinal health register data. Associations between PA PRS and body mass index, diseases, and mortality were analyzed with linear and logistic regression models. Results A high PA PRS predicted a lower body mass index (β = −0.025 kg·m−2 per one SD change in PA PRS, SE = 0.013, P = 1.87 × 10−80). The PA PRS also predicted a lower risk for diseases that typically develop later in life or not at all among highly active individuals. A lower disease risk was systematically observed for cardiovascular diseases (odds ratio [OR] per 1 SD change in PA PRS = 0.95, P = 9.5 × 10−19) and, for example, hypertension [OR = 0.93, P = 2.7 × 10−44), type 2 diabetes (OR = 0.91, P = 4.1 × 10−42), and coronary heart disease (OR = 0.95, P = 1.2 × 10−9). Participants with high PA PRS had also lower mortality risk (OR = 0.97, P = 0.0003). Conclusions Genetically less active persons are at a higher risk of developing cardiometabolic diseases, which may partly explain the previously observed associations between low PA and higher disease and mortality risk. The same inherited physical fitness and metabolism-related mechanisms may be associated both with PA levels and with cardiometabolic disease risk. [ABSTRACT FROM AUTHOR]