Lipoprotein(a) in Youth and Prediction of Major Cardiovascular Outcomes in Adulthood.

BACKGROUND: Elevated lipoprotein(a) [Lp(a)] is a common risk factor for cardiovascular disease outcomes with unknown mechanisms. We examined its potential role in identifying youths who are at increased risk of developing adult atherosclerotic cardiovascular disease (ASCVD). METHODS: Lp(a) levels measured in youth 9 to 24 years of age were linked to adult ASCVD and carotid intima-media thickness in the YFS (Cardiovascular Risk in Young Finns Study), in which 95 of the original 3596 participants (2.7%) recruited as children have been diagnosed with ASCVD at a median of 47 years of age. Results observed in YFS were replicated with the use of data for White participants from the BHS (Bogalusa Heart Study). In BHS, 587 White individuals had data on youth Lp(a) (measured at 8-17 years of age) and information on adult events, including 15 cases and 572 noncases. Analyses were performed with the use of Cox proportional hazard regression. RESULTS: In YFS, those who had been exposed to high Lp(a) level in youth [defined as Lp(a) ≥30 mg/dL] had ≈2 times greater risk of developing adult ASCVD compared with nonexposed individuals (hazard ratio, 2.0 [95% CI, 1.4-2.6]). Youth risk factors, including Lp(a), low-density lipoprotein cholesterol, body mass index, and smoking, were all independently associated with higher risk. In BHS, in an age- and sex-adjusted model, White individuals who had been exposed to high Lp(a) had 2.5 times greater risk (95% CI, 0.9-6.8) of developing adult ASCVD compared with nonexposed individuals. When also adjusted for low-density lipoprotein cholesterol and body mass index, the risk associated with high Lp(a) remained unchanged (hazard ratio, 2.4 [95% CI, 0.8-7.3]). In a multivariable model for pooled data, individuals exposed to high Lp(a) had 2.0 times greater risk (95% CI, 1.0-3.7) of developing adult ASCVD compared with nonexposed individuals. No association was detected between youth Lp(a) and adult carotid artery thickness in either cohort or pooled data. CONCLUSIONS: Elevated Lp(a) level identified in youth is a risk factor for adult atherosclerotic cardiovascular outcomes but not for increased carotid intima-media thickness.

Mitochondrial genome-wide analysis of nuclear DNA methylation quantitative trait loci.

Mitochondria have a complex communication network with the surrounding cell and can alter nuclear DNA methylation (DNAm). Variation in the mitochondrial DNA (mtDNA) has also been linked to differential DNAm. Genome-wide association studies have identified numerous DNAm quantitative trait loci, but these studies have not examined the mitochondrial genome. Herein, we quantified nuclear DNAm from blood and conducted a mitochondrial genome-wide association study of DNAm, with an additional emphasis on sex- and prediabetes-specific heterogeneity. We used the Young Finns Study (n = 926) with sequenced mtDNA genotypes as a discovery sample and sought replication in the Ludwigshafen Risk and Cardiovascular Health study (n = 2317). We identified numerous significant associations in the discovery phase (P < 10-9), but they were not replicated when accounting for multiple testing. In total, 27 associations were nominally replicated with a P < 0.05. The replication analysis presented no evidence of sex- or prediabetes-specific heterogeneity. The 27 associations were included in a joint meta-analysis of the two cohorts, and 19 DNAm sites associated with mtDNA variants, while four other sites showed haplogroup associations. An expression quantitative trait methylation analysis was performed for the identified DNAm sites, pinpointing two statistically significant associations. This study provides evidence of a mitochondrial genetic control of nuclear DNAm with little evidence found for sex- and prediabetes-specific effects. The lack of a comparable mtDNA data set for replication is a limitation in our study and further studies are needed to validate our results.

Neighbourhood deprivation in childhood and adulthood and risk of arterial stiffness: the Cardiovascular Risk in Young Finns study.

Purpose: Individual socioeconomic status is associated with increased arterial stiffness, but limited data are available on the relations of neighbourhood deprivation with this vascular measure. We prospectively examined whether neighbourhood deprivation in childhood and adulthood predicts arterial stiffness indicated by pulse wave velocity (PWV).Materials and methods: The study population comprised 1,761 participants aged 3-18 years at baseline (1980) from the longitudinal Cardiovascular Risk in Young Finns cohort study. PWV was measured in 2007 by whole-body impedance cardiography at ages 30-45 years. Cumulative lifetime neighbourhood deprivation was assessed using data from socioeconomic circumstances in participants' lifetime residential neighbourhoods, categorised as low versus high deprivation.Results: High deprivation in childhood and adulthood was associated with higher PWV in adulthood after adjustment for age, sex, and place of birth (mean difference = 0.57 m/s, 95%CI = 0.26-0.88, P for trend = 0.0004). This association was attenuated but remained statistically significant after further adjustment for childhood parental socioeconomic status and adulthood individual socioeconomic status (mean difference = 0.37 m/s, 95%CI = 0.05-0.70, P for trend 0.048). Also, low individual socioeconomic status in adulthood was associated with higher PWV when adjusted for age, sex, place of birth, parental socioeconomic status in childhood, and lifetime neighbourhood deprivation (mean difference = 0.54 m/s, 95%CI = 0.23-0.84, P for trend 0.0001).Conclusion: These findings suggest that lifetime neighbourhood deprivation and low adulthood socioeconomic status are independent risk factors for increased arterial stiffness in adulthood.

Limited data is available about the association between neighbourhood deprivation and arterial stiffening.We prospectively examined whether neighbourhood deprivation in childhood and adulthood predicts arterial stiffness indicated by pulse wave velocity (PWV) in 1,761 participants aged 3-18 years at baseline (1980) from the longitudinal Cardiovascular Risk in Young Finns cohort study.PWV was measured by whole-body impedance cardiography at ages 30-45 years. Cumulative lifetime neighbourhood deprivation was assessed using data from socioeconomic circumstances in participants' lifetime residential neighbourhoods, categorised as low versus high deprivation.high lifetime neighbourhood deprivation was associated with high PWV in adulthood independently of childhood parental SES and adulthood individual SES.Low individual SES in adulthood was also associated with higher PWV in adulthood and this association was robust to adjustment for parental SES in childhood and lifetime neighbourhood deprivation.These findings suggest that neighbourhood deprivation and low adulthood socioeconomic status are independent risk factors for increased arterial stiffness in adulthood.

Cardiovascular Risk Factor Trajectories Since Childhood and Cognitive Performance in Midlife: The Cardiovascular Risk in Young Finns Study.

BACKGROUND: Cardiovascular risk factors, such as high blood pressure, adverse serum lipids, and elevated body mass index in midlife, may harm cognitive performance. It is important to note that longitudinal accumulation of cardiovascular risk factors since childhood may be associated with cognitive performance already since childhood, but the previous evidence is scarce. We studied the associations of cardiovascular risk factors from childhood to midlife, their accumulation, and midlife cognitive performance. METHODS: From 1980, a population-based cohort of 3596 children (3-18 years of age) have been repeatedly followed up for 31 years. Blood pressure, serum lipids, and body mass index were assessed in all follow-ups. Cardiovascular risk factor trajectories from childhood to midlife were identified using latent class growth mixture modeling. Cognitive testing was performed in 2026 participants 34 to 49 years of age using a computerized test. The associations of the cardiovascular risk factor trajectories and cognitive performance were studied for individual cardiovascular risk factors and cardiovascular risk factor accumulation. RESULTS: Consistently high systolic blood pressure (ß=-0.262 SD [95% CI, -0.520 to -0.005]) and serum total cholesterol (ß=-0.214 SD [95% CI, -0.365 to -0.064]) were associated with worse midlife episodic memory and associative learning compared with consistently low values. Obesity since childhood was associated with worse visual processing and sustained attention (ß=-0.407 SD [95% CI, -0.708 to -0.105]) compared with normal weight. An inverse association was observed for the cardiovascular risk factor accumulation with episodic memory and associative learning (P for trend=0.008; 3 cardiovascular risk factors: ß=-0.390 SD [95% CI, -0.691 to -0.088]), with visual processing and sustained attention (P for trend<0.0001; 3 cardiovascular risk factors: ß=-0.443 SD [95% CI, -0.730 to -0.157]), and with reaction and movement time (P for trend=0.048; 2 cardiovascular risk factors: ß=-0.164 SD [95% CI, -0.318 to -0.010]). CONCLUSIONS: Longitudinal elevated systolic blood pressure, high serum total cholesterol, and obesity from childhood to midlife were inversely associated with midlife cognitive performance. It is important to note that the higher the number of cardiovascular risk factors, the worse was the observed cognitive performance. Therefore, launching preventive strategies against cardiovascular risk factors beginning from childhood might benefit primordial promotion of cognitive health in adulthood.

Obesity during childhood is associated with higher cancer mortality rate during adulthood: the i3C Consortium.

BACKGROUND: In high-income countries, cancer is the leading cause of death among middle-aged adults. Prospective data on the effects of childhood risk exposures on subsequent cancer mortality are scarce. METHODS: We examined whether childhood body mass index (BMI), blood pressure, glucose and lipid levels were associated with adult cancer mortality, using data from 21,012 children enrolled aged 3-19 years in seven prospective cohort studies from the U.S., Australia, and Finland that have followed participants from childhood into adulthood. Cancer mortality (cancer as a primary or secondary cause of death) was captured using registries. RESULTS: 354 cancer deaths occurred over the follow-up. In age-, sex, and cohort-adjusted analyses, childhood BMI (Hazard ratio [HR], 1.13; 95% confidence interval [CI] 1.03-1.24 per 1-SD increase) and childhood glucose (HR 1.22; 95%CI 1.01-1.47 per 1-SD increase), were associated with subsequent cancer mortality. In a multivariable analysis adjusted for age, sex, cohort, and childhood measures of fasting glucose, total cholesterol, triglycerides, and systolic blood pressure, childhood BMI remained as an independent predictor of subsequent cancer mortality (HR, 1.24; 95%CI, 1.03-1.49). The association of childhood BMI and subsequent cancer mortality persisted after adjustment for adulthood BMI (HR for childhood BMI, 1.35; 95%CI 1.12-1.63). CONCLUSIONS: Higher childhood BMI was independently associated with increased overall cancer mortality.

Risk Factor Profile in Youth, Genetic Risk, and Adulthood Cognitive Function: The Cardiovascular Risk in Young Finns Study.

INTRODUCTION: The role of risk factor profile in childhood and adolescence on adulthood cognitive function and whether it differs by genetic risk is still obscure. To bring this evidence, we determined cognitive domain-specific youth risk factor profiles leveraging the childhood/adolescence data from the Cardiovascular Risk in Young Finns Study and examined whether genetic propensity for poor cognitive function modifies the association between the risk profiles and adulthood cognitive function. METHODS: From 1980, a population-based cohort of 3,596 children (age 3-18 years) has been repeatedly followed up for 31 years. Computerized cognitive test measuring (1) memory and learning, (2) short-term working memory, (3) reaction time, and (4) information processing was performed for 2,026 participants (age 34-49 years). Cognitive domain-specific youth risk profile scores, including physical and environmental factors, were assessed from the data collected at baseline and categorized into favourable, intermediate, and unfavourable. A polygenic risk score for a poor cognitive function was categorized into low, intermediate, and high risk. RESULTS: At all genetic risk levels, a favourable youth risk factor profile is associated with better learning and memory, short-term working memory, and information processing compared to unfavourable risk profile (e.g., ß = 0.501 SD, 95% CI: 0.043-0.959 for memory and learning among participants with high genetic risk). However, no significant interactions were observed between the youth risk factor profile score and genetic propensity for any cognitive domain (p > 0.299 for all). CONCLUSION: A favourable youth risk factor profile may be beneficial for cognitive function in adulthood, irrespective of genetic propensity for poor cognitive function.

Associations of parental physical activity trajectories with offspring's physical activity patterns from childhood to middle adulthood: The Young Finns Study.

We investigated the association of parental physical activity (PA) trajectories with offspring's youth and adult PA. Self-reported PA data were extracted from the Young Finns Study with three follow-ups for parents between 1980 and 1986 and nine follow-ups for their offspring in youth between 1980 and 2011 (aged 9-39 years, n = 2402) and in adulthood in 2018. Accelerometer-derived PA was quantified in 2018-2020 (aged 43-58 years, n = 1134). Data were analyzed using mixture models and conducted in 2022. We identified three trajectories for fathers and mothers (high-stable activity, 20.2%/16.6%; moderate-stable activity, 50.5%/49.6%; and low-stable activity, 29.4%/33.7%) and four for youth male and female offspring (persistently active, 13.4%/5.1%; increasingly active, 32.1%/43.1%; decreasingly active, 14.4%/12.6%; and persistently low-active, 40.1%/39.1%). Compared to low-stable active parents, high-stable active fathers had a higher probability of having their sons and daughters classified as persistently active, increasingly active, and decreasingly active in youth (Brange = 0.50-1.79, all p < 0.008), while high- and moderate-stable active mothers had significantly increased likelihood of having their daughters classified as persistently active and decreasingly active in youth (Brange = 0.63-1.16, all p < 0.009). Fathers' and mothers' high-stable activity was associated with higher self-reported PA of adult offspring than parental low-stable activity. Persistently active and increasingly active offspring in youth accumulated more adult total PA, moderate-to-vigorous PA, step counts, and self-reported PA than persistently low-active ones (all p < 0.036). Parental persistent PA, particularly paternal persistent PA, predicts offspring's PA concurrently and prospectively. Increasing and maintaining PA in youth predicts higher PA levels in midlife.

Use of antibiotics and risk of type 2 diabetes, overweight and obesity: the Cardiovascular Risk in Young Finns Study and the national FINRISK study.

PURPOSE: To investigate whether exposure to systemic antibiotics influences the risk of developing type 2 diabetes and overweight/obesity. METHODS: The study sample comprised 2209 (110 with incident diabetes) participants from the population-based Cardiovascular Risk in Young Finns Study (YFS) aged 24-39 years in 2001. The exposure was national linked register data on purchased antibiotic courses between 1993 and 2001. Clinical examinations including BMI were conducted in 2001, 2007 and 2011. Participants with prevalent diabetes in 2001 were excluded. Data on type 2 diabetes was also obtained from two national registers until 2017. Data from four population-based National FINRISK studies were used for replication (N = 24,674, 1866 with incident diabetes). RESULTS: Prior antibiotic exposure (> 5 versus 0-1 antibiotic courses) was associated with subsequent type 2 diabetes in both YFS (OR 2.29; 95%CI 1.33-3.96) and FINRISK (HR 1.73; 95%CI 1.51-1.99). An increased risk for type 2 diabetes was observed in YFS (OR 1.043; 95%CI 1.013-1.074) and FINRISK (HR 1.022; 95%CI 1.016-1.029) per course. Exposure to antibiotics increased the risk of overweight/obesity (BMI > 25 kg/m2) after a 10-year follow-up in YFS (OR 1.043; 95%CI 1.019-1.068) and in FINRISK (OR 1.023; 95%CI 1.018-1.029) at baseline per antibiotic course. Adjustments for confounders from early life in YFS and at baseline in FINRISK, including BMI, socioeconomic status, smoking, insulin, blood pressure, and physical activity, did not appreciably alter the findings. CONCLUSION: Our results show that exposure to antibiotics was associated with increased risk for future type 2 diabetes and overweight/obesity and support judicious antibiotic prescribing.

Longitudinal associations between parental and offspring's leisure-time physical activity: The Young Finns Study.

PURPOSE: The longitudinal influence of parental leisure-time physical activity (LTPA) on their offspring's LTPA is poorly understood. This study examined the longitudinal associations between parental LTPA and offspring's LTPA at two-time intervals. METHOD: Child (offspring) participants (N = 3596) were enrolled from the Cardiovascular Risk in Young Finns Study in 1980. Their LTPA was self-rated through nine phases from baseline to 2018 and categorized by year into youth (1980-1986) and adult (1992-2018) LTPA. Parental LTPA was assessed with a single self-reported question at three phases from 1980 to 1986. Latent growth curve modeling stratified by gender was fitted to estimate the potential pathways between parental LTPA and offspring's youth and adult LTPA. RESULTS: Higher initial levels of paternal and maternal LTPA were independently associated with greater initial levels of youth and adult LTPA of offspring in both genders, respectively, except maternal LTPA, which did not associate with male offspring's adult LTPA. The initial levels of paternal LTPA were directly related to changes in male offspring's youth LTPA after adjusting for age, residential place, paternal education and occupation, having siblings, and offspring's body mass index. CONCLUSION: Our study demonstrates that the initial levels of parental LTPA are directly linked to the initial levels of offspring's LTPA during youth and adulthood, while changes in parental LTPA are unrelated to changes in offspring's youth and adult LTPA for either gender over time. These results imply that higher initial levels of LTPA in parents may serve as a predictor of offspring's LTPA across life stages.

Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study.

BACKGROUND AND AIMS: The relationship between childhood tobacco smoke exposure and cardiac structure and function in midlife is unclear. We investigated the association between parental smoking with cardiac structure and function in adulthood. METHODS: 1250 participants (56.5% female) from the Cardiovascular Risk in Young Finns Study who had data on parental smoking and/or serum cotinine, a biomarker of exposure to tobacco smoke, at baseline 1980 (age 3-18 years) and echocardiography performed in 2011. Parental smoking hygiene (i.e., smoking in the vicinity of children) was categorized by parental smoking and serum cotinine levels in offspring. Dimensions of the left ventricle, diastolic and systolic function, and cardiac remodeling were used as outcomes. Analyses were adjusted for sex, age, and covariates (blood pressure (BP), serum lipids, body mass index, socioeconomic status, smoking (only in adulthood)) in childhood and adulthood. RESULTS: Parental smoking was not associated with systolic or diastolic function in adulthood. Participants exposed to parental smoking (odds ratio (OR) 1.90, 95%CI 1.23-2.92), hygienic parental smoking (OR 1.74, 95%CI 1.12-2.71), and non-hygienic parental smoking (OR 1.88, 95%CI 1.02-3.45) had higher odds of concentric remodeling (relative wall thickness >85th sex-specific percentile without left ventricular hypertrophy). These associations were attenuated after adjustment for child and adult covariates in the non-hygienic parental smoking group. CONCLUSIONS: Exposure to parental smoking in childhood was associated with a higher likelihood of concentric remodeling and thicker left ventricular and interventricular septal walls in midlife, which was not improved by parents who smoked hygienically. Parental smoking was not related to systolic or diastolic function in this relatively young population.

Discovery of mitochondrial DNA variants associated with genome-wide blood cell gene expression: a population-based mtDNA sequencing study.

The effect of mitochondrial DNA (mtDNA) variation on peripheral blood transcriptomics in health and disease is not fully known. Sex-specific mitochondrially controlled gene expression patterns have been shown in Drosophila melanogaster but in humans, evidence is lacking. Functional variation in mtDNA may also have a role in the development of type 2 diabetes and its precursor state, i.e. prediabetes. We examined the associations between mitochondrial single-nucleotide polymorphisms (mtSNPs) and peripheral blood transcriptomics with a focus on sex- and prediabetes-specific effects. The genome-wide blood cell expression data of 19 637 probes, 199 deep-sequenced mtSNPs and nine haplogroups of 955 individuals from a population-based Young Finns Study cohort were used. Significant associations were identified with linear regression and analysis of covariance. The effects of sex and prediabetes on the associations between gene expression and mtSNPs were studied using random-effect meta-analysis. Our analysis identified 53 significant expression probe-mtSNP associations after Bonferroni correction, involving 7 genes and 31 mtSNPs. Eight probe-mtSNP signals remained independent after conditional analysis. In addition, five genes showed differential expression between haplogroups. The meta-analysis did not show any significant differences in linear model effect sizes between males and females but identified the association between the OASL gene and mtSNP C16294T to show prediabetes-specific effects. This study pinpoints new independent mtSNPs associated with peripheral blood transcriptomics and replicates six previously reported associations, providing further evidence of the mitochondrial genetic control of blood cell gene expression. In addition, we present evidence that prediabetes might lead to perturbations in mitochondrial control.

Childhood and Adulthood Passive Smoking and Nonalcoholic Fatty Liver in Midlife: A 31-year Cohort Study.

INTRODUCTION: Identifying early life risk factors remains key to the prevention of nonalcoholic fatty liver (hereinafter "fatty liver") in adulthood. However, the longitudinal association of childhood passive smoking with adult fatty liver is not studied. We examined the association of childhood and adulthood passive smoking with fatty liver in midlife. METHODS: This was a 31-year prospective cohort study of 1,315 participants. Information on childhood passive smoking (parental smoking) was collected in 1980 (aged 3-18 years) and 1983 and adulthood passive smoking in 2001, 2007, and 2011. Fatty liver was determined by ultrasound in 2011 (aged 34-49 years). RESULTS: The prevalence of fatty liver was 16.3%. Both childhood and adulthood passive smoking were associated with higher risk of fatty liver, adjusting for potential confounders such as age, sex, childhood socioeconomic status, and adulthood physical activity and alcohol consumption (relative risk = 1.41, 95% confidence interval: 1.01-1.97 for childhood; 1.35, 1.01-1.82 for adulthood). Individuals with persistent exposure to passive smoking between childhood and adulthood had the highest risk (relative risk = 1.99, 95% confidence interval: 1.14-3.45) compared with those without passive smoking in either childhood or adulthood. DISCUSSION: Passive smoking in both child and adult lives are associated with increased risk of adult fatty liver, suggesting that the prevention of passive smoking should start as early as possible and maintain throughout lifetime.

Association between Number of Siblings and Cardiovascular Risk Factors in Childhood and in Adulthood: The Cardiovascular Risk in Young Finns Study.

OBJECTIVE: To determine the association of number of siblings on cardiovascular risk factors in childhood and in adulthood. STUDY DESIGN: In total, 3554 participants (51% female) from the Cardiovascular Risk in Young Finns Study with cardiovascular disease risk factor data at baseline 1980 (age 3-18 years) and 2491 participants with longitudinal risk factor data at the 2011 follow-up. Participants were categorized by number of siblings at baseline (0, 1, or more than 1). Risk factors (body mass index, physical activity, hypertension, dyslipidemia, and overweight, and metabolic syndrome) in childhood and in adulthood were used as outcomes. Analyses were adjusted for age and sex. RESULTS: In childhood, participants without siblings had higher body mass index (18.2 kg/m2, 95% CI 18.0-18.3) than those with 1 sibling (17.9 kg/m2, 95% CI 17.8-18.0) or more than 1 sibling (17.8 kg/m2, 95% CI 17.7-17.9). Childhood physical activity index was lower among participants without siblings (SD -0.08, 95% CI -0.16-0.00) compared with participants with 1 sibling (SD 0.06, 95%CI 0.01-0.11) or more than 1 sibling (SD -0.02, 95% CI -0.07-0.03). OR for adulthood hypertension was lower among participants with 1 sibling (OR 0.73, 95% CI 0.54-0.98) and more than 1 sibling (OR 0.71, 95% CI 0.52-0.97) compared with participants with no siblings. OR for obesity was lower among participants with 1 sibling (OR 0.72, 95% CI 0.54-0.95) and more than 1 sibling (OR 0.75, 95% CI 0.56-1.01) compared with those with no siblings. CONCLUSIONS: Children without siblings had poorer cardiovascular risk factor levels in childhood and in adulthood. The number of siblings could help identify individuals at increased risk that might benefit from early intervention.

Childhood Socioeconomic Disadvantage and Risk of Fatty Liver in Adulthood: The Cardiovascular Risk in Young Finns Study.

Fatty liver is a preventable cause of liver failure, but early risk factors for adulthood fatty liver are poorly understood. We examined the association of childhood socioeconomic disadvantage with adulthood fatty liver and tested adulthood risk factors of fatty liver as possible mediators of this link. The study population comprised 2,042 participants aged 3-18 years at baseline (1980) from the longitudinal Cardiovascular Risk in Young Finns Study. Follow-up with repeated clinical examinations was 31 years. Childhood socioeconomic disadvantage was assessed using data from parents' socioeconomic position and socioeconomic circumstances in participants' residential neighborhoods, categorized as high versus low socioeconomic disadvantage. Fatty liver was determined by ultrasound during the last follow-up (2011) at ages 34-49 years. Childhood and adulthood risk factors, including metabolic biomarkers and lifestyle variables, were assessed in clinical examinations. A total of 18.9% of the participants had fatty liver in adulthood. High childhood socioeconomic disadvantage was associated with an increased risk of fatty liver (risk ratio [95% confidence interval], 1.42 [1.18-1.70]; P = 0.0002). This association was robust to adjustment for age, sex, and childhood risk factors of fatty liver, including high body mass index, elevated insulin, and low birth weight (1.33 [1.09-1.62]; P = 0.005). High childhood socioeconomic disadvantage was also associated with the development of risk factors of fatty liver in adulthood. Adulthood risk factors linking childhood socioeconomic disadvantage with fatty liver included waist circumference (proportion mediated of the total effect of childhood socioeconomic disadvantage, 45%), body mass index (40%), systolic blood pressure (29%), insulin (20%), physical activity (15%), triglycerides (14%), and red meat consumption (7%). Conclusion: Childhood socioeconomic disadvantage was associated with multiple risk factors of fatty liver and increased likelihood of fatty liver in adulthood.

Associations of Serum Fatty Acid Proportions with Obesity, Insulin Resistance, Blood Pressure, and Fatty Liver: The Cardiovascular Risk in Young Finns Study.

BACKGROUND: The links between fatty acids (FAs) and cardiometabolic outcomes are topics of debate. OBJECTIVE: Our aim was to investigate the associations between serum standardized FA percentages and cardiometabolic outcomes. METHODS: We used cross-sectional (n = 2187-2200 subjects, age 24-39 y, women 54%) and 10-year prospective data (n = 975-1414 subjects) from the Young Finns Study. Outcomes included prevalent and incident obesity, insulin resistance (HOMA-IR index in the upper quintile), elevated blood pressure (BP; taking medication, or diastolic or systolic BP in the upper quintile), and incident nonalcoholic fatty liver. Logistic regression models were used to calculate ORs per SD increase in fatty acids (FAs). The models were adjusted for age and sex, and additionally for other potential confounders. RESULTS: Several cross-sectional findings were also statistically significant in prospective models (Bonferroni corrected P < 0.003). In fully-adjusted models for obesity, these consisted of SFAs (OR: 1.28) and MUFAs (OR: 1.38), including palmitoleic (OR: 1.39) and oleic acids (OR: 1.37). Furthermore, PUFAs (OR: 0.70), including linoleic (OR: 0.67) and docosahexaenoic acids (OR: 0.75), were inversely related with obesity, whereas γ-linolenic acid (OR: 1.32) was positively associated with obesity. In age- and sex-adjusted models for insulin resistance, MUFAs (OR: 1.26) and oleic acid (OR: 1.25) were positively, and PUFAs (OR: 0.81), particularly linoleic acid (OR: 0.78), were inversely associated with HOMA-IR. Similarly with elevated BP, palmitic acid (OR: 1.22), MUFAs (OR: 1.28), and oleic acid (OR: 1.28) were positively associated with elevated BP, whereas PUFAs (OR: 0.77), n-6 (omega-6) PUFAs (OR: 0.79), and linoleic acid (OR: 0.77) were inversely associated. In fully-adjusted models for incident fatty liver, the most consistent predictors were high palmitic (OR: 1.61) and low linoleic acid (OR: 0.63) percentages. The n-6/n-3 (omega-3) PUFA ratio was not linked with any adverse outcomes. CONCLUSIONS: High serum percentages of total SFAs and MUFAs and low PUFAs, but also several specific FAs, predict future unfavorable cardiometabolic outcomes in Finnish adults.

Physical inactivity from youth to adulthood and adult cardiometabolic risk profile.

Adults with a low physical activity (PA) level are at increased risk for cardiometabolic diseases, but little is known on the association between physical inactivity since youth and cardiometabolic health in adulthood. We investigated the association of persistent physical inactivity from youth to adulthood with adult cardiometabolic risk factors. Data were drawn from the ongoing Cardiovascular Risk in Young Finns Study with seven follow-ups between 1980 and 2011 (baseline age 3-18 years, n = 1961). Physical activity data from a standardized questionnaire was expressed as a PA-index. Using the PA-index, four groups were formed: 1)persistently physically inactive (n = 246), 2)decreasingly active (n = 305), 3)increasingly active (n = 328), and 4)persistently active individuals (n = 1082). Adulthood cardiometabolic risk indicators included waist circumference, body mass index (BMI), blood pressure, and fasting lipids, insulin, and glucose. Clustered cardiometabolic risk was defined using established criteria for metabolic syndrome. Persistently physically inactive group was used as a reference. Compared to the persistently physically inactive group, those who were persistently active had lower risk for adult clustered cardiometabolic risk (RR = 0.67;CI95% = 0.53-0.84; Harmonized criteria), obesity (BMI > 30 kg/m2, RR = 0.76;CI95% = 0.59-0.98), high waist circumference (RR = 0.82;CI95% = 0.69-0.98), and high triglyceride (RR = 0.60;CI95% = 0.47-0.75), insulin (RR = 0.58;CI95% = 0.46-0.74) and glucose (RR = 0.77;CI95% = 0.62-0.96) concentrations as well as low high-density lipoprotein cholesterol (HDLC) concentration (RR = 0.78;CI95% = 0.66-0.93). Comparable results were found when persistently physically inactive individuals were compared with those who increased PA. The results remained essentially similar after adjustment for education, diet, smoking, and BMI. Persistently physically inactive lifestyle since youth is associated with an unfavorable cardiometabolic risk profile in adulthood. Importantly, even minor increase in PA lowers the cardiometabolic risk.

Childhood physical activity as a labor market investment.

This study examined the role of physical activity and changes in physical activity levels during childhood in long-term labor market outcomes. To address this important but under-researched theme, the study utilized data drawn from longitudinal research, the Cardiovascular Risk in Young Finns Study (YFS), and from registries compiled by Statistics Finland. The study consisted of children aged 9 (n = 1565) and 15 (n = 2445) at the time their physical activity was measured. Labor market outcomes, including employment status, average employment months, and average unemployment months, were calculated from 1997 to 2010, when the participants were aged 20 to 48 years. Regression models were used to assess the relationship between physical activity and labor market outcomes. The results show that the consequences of childhood physical activity may be far-reaching, as higher childhood physical activity was positively related to the probability of being employed and employment months and was negatively related to unemployment months. On average, a one-unit increase in physical activity index was related to a 1% higher probability of being employed, 0.10 more months of yearly employment, and 0.05 fewer months of yearly unemployment. The results also imply that persistently active individuals had the highest level of employment and the lowest level of unemployment compared with other activity groups. In conclusion, investments in childhood physical activity may not only promote health and well-being but may also correlate with better labor market outcomes later in life, providing both personal and societal benefits.

Life-course leisure-time physical activity trajectories in relation to health-related behaviors in adulthood: the Cardiovascular Risk in Young Finns study.

BACKGROUND: Evidence on whether leisure-time physical activity (LTPA) facilitates individuals' adoption of multiple healthy behaviors remains scarce. This study investigated the associations of diverse longitudinal LTPA trajectories from childhood to adulthood with diet, screen time, smoking, binge drinking, sleep difficulties, and sleep duration in adulthood. METHODS: Data were drawn from the Cardiovascular Risk in Young Finns Study. Participants were aged 9-18 years (N = 3553; 51% females) in 1980 and 33-49 years at the latest follow-up in 2011. The LTPA trajectories were identified using a latent profile analysis. Differences in self-reported health-related behaviors across the LTPA trajectories were studied separately for women and men by using the Bolck-Croon-Hagenaars approach. Models were adjusted for age, body mass index, education level, marital status, total energy intake and previous corresponding behaviors. RESULTS: Persistently active, persistently low-active, decreasingly and increasingly active trajectories were identified in both genders and an additional inactive trajectory for women. After adjusting the models with the above-mentioned covariates, the inactive women had an unhealthier diet than the women in the other trajectories (p <  0.01; effect size (ES) > 0.50). The low-active men followed an unhealthier diet than the persistently and increasingly active men (p <  0.01; ES > 0.50). Compared to their inactive and low-active peers, smoking frequency was lower in the increasingly active women and men (p <  0.01; ES > 0.20) and persistently active men (p <  0.05; ES > 0.20). The increasingly active men reported lower screen time than the low-active (p <  0.001; ES > 0.50) and persistently active (p <  0.05; ES > 0.20) men. The increasingly and persistently active women reported fewer sleep difficulties than the inactive (p <  0.001; ES > 0.80) and low-active (p <  0.05; ES > 0.50 and > 0.80, respectively) women. Sleep duration and binge drinking were not associated with the LTPA trajectories in either gender, nor were sleep difficulties in men and screen time in women. CONCLUSIONS: Not only persistently higher LTPA but also an increasing tendency to engage in LTPA after childhood/adolescence were associated with healthier diet and lower smoking frequency in both genders, having less sleep difficulties in women and lower screen time in increasingly active men. Inactivity and low activity were associated with the accumulation of several unhealthy behaviors in adulthood. Associations were stronger in women.

Influence of early life risk factors and lifestyle on systemic vascular resistance in later adulthood: the cardiovascular risk in young Finns study.

PURPOSE: There are limited data available concerning the effects of lifetime risk factors and lifestyle on systemic hemodynamics, especially on systemic vascular resistance. The purpose of the study was to evaluate how lifetime cardiovascular risk factors (body mass index (BMI), high-density lipoprotein, low-density lipoprotein, triglycerides, systolic blood pressure, blood glucose) and lifestyle factors (vegetable consumption, fruit consumption, smoking and physical activity) predict systemic vascular resistance index (SVRI) and cardiac index (CI) assessed in adulthood. MATERIALS AND METHODS: Our study cohort comprised 1635 subjects of the Cardiovascular Risk in Young Finns Study followed up for 27 years since baseline (1980; aged 3-18 years, females 54.3%) who had risk factor and lifestyle data available since childhood. Systemic hemodynamics were measured in 2007 (aged 30-45 years) by whole-body impedance cardiography. RESULTS: In the multivariable regression analysis, independent predictors of the adulthood SVRI were childhood BMI, blood glucose, vegetable consumption, smoking, and physical activity (p ≤ .046 for all). Vegetable consumption, smoking, and physical activity remained significant when adjusted for corresponding adult data (p ≤ .036 for all). For the CI, independent predictors in childhood were BMI, systolic blood pressure, vegetable consumption, and physical activity (p ≤ .044 for all), and the findings remained significant after adjusting for corresponding adult data (p ≤ .046 for all). The number of childhood and adulthood risk factors and unfavourable lifestyle factors was directly associated with the SVRI (p < .001) in adulthood. A reduction in the number of risk factors and unfavourable lifestyle factors or a favourable change in BMI status from childhood to adulthood was associated with a lower SVRI in adulthood (p < .001). CONCLUSION: Childhood BMI, blood glucose, vegetable consumption, smoking and physical activity independently predict systemic vascular resistance in adulthood. A favourable change in the number of risk factors or BMI from childhood to adulthood was associated with lower vascular resistance in adulthood.

Association of lifetime blood pressure with adulthood exercise blood pressure response: the cardiovascular risk in young Finns study.

PURPOSE: Elevated blood pressure (BP) in childhood has been associated with increased adulthood BP. However, BP and its change from childhood to adulthood and the risk of exaggerated adulthood exercise BP response are largely unknown. Therefore, we studied the association of childhood and adulthood BP with adulthood exercise BP response. MATERIALS AND METHODS: This investigation consisted of 406 individuals participating in the ongoing Cardiovascular Risk in Young Finns Study (baseline in 1980, at age of 6-18 years; follow-up in adulthood in 27-29 years since baseline). In childhood BP was classified as elevated according to the tables from the International Child Blood Pressure References Establishment Consortium, while in adulthood BP was considered elevated if systolic BP was ≥120 mmHg or diastolic BP was ≥80 mmHg or if use of antihypertensive medications was self-reported. A maximal cardiopulmonary exercise test with BP measurements was performed by participants in 2008-2009, and exercise BP was considered exaggerated (EEBP) if peak systolic blood pressure exceeded 210 mmHg in men and 190 mmHg in women. RESULTS: Participants with consistently high BP from childhood to adulthood and individuals with normal childhood but high adulthood BP had an increased risk of EEBP response in adulthood (relative risk [95% confidence interval], 3.32 [2.05-5.40] and 3.03 [1.77-5.17], respectively) in comparison with individuals with normal BP both in childhood and adulthood. Interestingly, individuals with elevated BP in childhood but not in adulthood also had an increased risk of EEBP [relative risk [95% confidence interval], 2.17 [1.35-3.50]). CONCLUSIONS: These findings reinforce the importance of achieving and sustaining normal blood pressure from childhood through adulthood.