Department of Cardiology, Tays Heart Hospital, Tampere University Hospital and Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland.
Aortic sinus dilatation can lead to aortic valve regurgitation or even aortic dissection. Our objective was to examine the association between body surface area (BSA) measures from childhood to middle age and aortic sinus diameter in middle age. Understanding the relation of these two clarifies how aortic size is normally determined.
Cardiovascular Risk in Young Finns Study is a longitudinal study with follow-up of over 31 years (1980-2011). The study comprises information of body composition from multiple time points of 1950 subjects with cardiac ultrasound measurements made in 2011. The association between BSA in different ages and aortic sinus diameter in middle age was analysed by linear regression modelling adjusted with age, sex and diastolic blood pressure. Missing BSA values were derived for each life year (ages 3-33 years) from subject-specific curves for body weight and height estimated from longitudinal measurements using mixed model regression splines.
BSA estimates in early 20s are most strongly associated with aortic sinus diameter in middle age. Top association was observed at age 23 years with one SD increase in estimated BSA corresponding to 1.04?mm (0.87-1.21?mm) increase in aortic diameter. Increase in body weight beyond early 20s does not associate with aortic sinus diameter, and the association between middle age BSA and aortic size is substantially weaker (0.74?mm increase (0.58-0.89?mm)). These results were confirmed in a subpopulation using only measured data.
The association between aortic sinus diameter and BSA is stronger when considering BSA in young adulthood compared with BSA in middle age.
Cardiovascular risk factor levels in 2011 and 4-year changes between 2007 and 2011 were examined using data collected in follow-ups of the Cardiovascular Risk in Young Finns Study.
The study population comprised 2063 Finnish adults aged 34-49 years (45% male). Lipid and blood pressure levels, glucose and anthropometry were measured and life style risk factors examined with questionnaires.
Mean total cholesterol level in 2011 was 5.19 mmol/l, low density lipoprotein (LDL)-cholesterol 3.27 mmol/l, high density lipoprotein (HDL)-cholesterol 1.33 mmol/l, and triglycerides 1.34 mmol/l. Using American Diabetes Association criteria, Type 2 diabetes (T2D) was observed in 4.1% and prediabetes (fasting glucose 5.6-6.9 mmol/l or glycated hemoglobin 5.7-6.4%) diagnosed for 33.8% of the participants. Significant changes (P
We studied whether exposure to parental smoking in childhood/adolescence is associated with midlife cognitive function, leveraging data from the Cardiovascular Risk in Young Finns Study. A population-based cohort of 3,596 children/adolescents aged 3-18 years was followed between 1980 and 2011. In 2011, cognitive testing was performed on 2,026 participants aged 34-49 years using computerized testing. Measures of secondhand smoke exposure in childhood/adolescence consisted of parental self-reports of smoking and participants' serum cotinine levels. Participants were classified into 3 exposure groups: 1) no exposure (nonsmoking parents, cotinine
Fatty liver is a potentially preventable cause of serious liver diseases. This longitudinal study aimed to identify childhood risk factors of fatty liver in adulthood in a population-based group of Finnish adults.
Study cohort included 2,042 individuals from the Cardiovascular Risk in Young Finns Study aged 3-18years at baseline in 1980. During the latest follow-up in 2011, the liver was scanned by ultrasound. In addition to physical and environmental factors related to fatty liver, we examined whether the genetic risk posed by a single nucleotide polymorphism in the patatin-like phospholipase domain-containing protein 3 gene (PNPLA3) (rs738409) strengthens prediction of adult fatty liver.
Independent childhood predictors of adult fatty liver were small for gestational age, (odds ratio=1.71, 95% confidence interval=1.07-2.72), variant in PNPLA3 (1.63, 1.29-2.07 per one risk allele), variant in the transmembrane 6 superfamily 2 gene (TM6SF2) (1.57, 1.08-2.30), BMI (1.30, 1.07-1.59 per standard deviation) and insulin (1.25, 1.05-1.49 per standard deviation). Childhood blood pressure, physical activity, C-reactive protein, smoking, serum lipid levels or parental lifestyle factors did not predict fatty liver. Risk assessment based on childhood age, sex, BMI, insulin levels, birth weight, TM6SF2 and PNPLA3 was superior in predicting fatty liver compared with the approach using only age, sex, BMI and insulin levels (C statistics, 0.725 vs. 0.749; p=0.002).
Childhood risk factors on the development of fatty liver were small for gestational age, high insulin and high BMI. Prediction of adult fatty liver was enhanced by taking into account genetic variants in PNPLA3 and TM6SF2 genes.
The increase in pediatric obesity emphasizes the importance of identification of children and adolescents at high risk of fatty liver in adulthood. We used data from the longitudinal Cardiovascular Risk in Young Finns Study to examine the associations of childhood (3-18years) risk variables with fatty liver assessed in adulthood at the age of 34-49years. The findings suggest that a multifactorial approach with both lifestyle and genetic factors included would improve early identification of children with a high risk of adult fatty liver.
Research Center of Applied and Preventive Cardiovascular Medicine, University of Turku, Kiinamyllynkatu 10, 20520, Turku, Finland; Division of Medicine, Turku University Hospital, Kiinamyllynkatu 4-8, 20521, Turku, Finland; Department of Medicine, Satakunta Central Hospital, Sairaalantie 3, 28500, Pori, Finland. Electronic address: jskosk@utu.fi.
Carotid plaque is a specific sign of atherosclerosis and adults with carotid plaque are at increased risk for cardiovascular outcomes. Atherosclerosis has roots in childhood and pediatric guidelines provide cut-off values for cardiovascular risk factors. However, it is unknown whether these cut-offs predict adulthood advanced atherosclerosis.
The Cardiovascular Risk in Young Finns Study is a follow-up of children that begun in 1980 when 2653 participants with data for the present analyses were aged 3-18 years. In 2001 and 2007 follow-ups, in addition to adulthood cardiovascular risk factors, carotid ultrasound data was collected. Long-term burden, as the area under the curve, was evaluated for childhood (6-18 years) risk factors. To study the associations of guideline-based cut-offs with carotid plaque, both childhood and adult risk factors were classified according to clinical practice guidelines.
Carotid plaque, defined as a focal structure of the arterial wall protruding into lumen >50% compared to adjacent intima-media thickness, was present in 88 (3.3%) participants. Relative risk for carotid plaque, when adjusted for age and sex, was 3.03 (95% CI, 1.76-5.21) for childhood dyslipidemia, 1.51 (95% CI, 0.99-2.32) for childhood elevated systolic blood pressure, and 1.93 (95% CI, 1.26-2.94) for childhood smoking. Childhood dyslipidemia and smoking remained independent predictors of carotid plaque in models additionally adjusted for adult risk factors and family history of coronary heart disease. Carotid plaque was present in less than 1% of adults with no childhood risk factors.
Findings reinforce childhood prevention efforts and demonstrate the utility of guideline-based cut-offs in identifying children at increased risk for adulthood atherosclerosis.
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.
Increasing evidence supports the importance of socioeconomic factors in the development of atherosclerotic cardiovascular disease. However, the association of childhood socioeconomic status (SES) with arterial stiffness in adulthood has not been reported. Our aim was to determine whether higher childhood family-level SES is associated with lower arterial stiffness in adulthood. The analyses were performed using data gathered within the longitudinal Young Finns Study. The sample comprised 2566 participants who had data concerning family SES at ages 3 to 18 years in 1980 and arterial pulse wave velocity and carotid artery distensibility measured 21 or 27 years later in adulthood. Higher family SES in childhood was associated with lower arterial stiffness in adulthood; carotid artery distensibility being higher (ß value±SE, 0.029±0.0089%/10 mm Hg; P=0.001) and pulse wave velocity lower (ß value±SE, -0.062±0.022 m/s; P=0.006) among those with higher family SES in a multivariable analysis adjusted with age, sex, and conventional childhood cardiometabolic risk factors. The association remained significant after further adjustment for participant's SES in adulthood (ß value±SE, 0.026±0.010%/10 mm Hg; P=0.01 for carotid artery distensibility and ß value±SE, -0.048±0.023 m/s; P=0.04 for pulse wave velocity) but attenuated after adjustment for adulthood cardiometabolic risk factors (ß value±SE, 0.015±0.008%/10 mm Hg; P=0.08 for carotid artery distensibility and ß value±SE, -0.019±0.02 m/s; P=0.38 for pulse wave velocity). In conclusion, we observed an association between higher family SES in childhood and lower arterial stiffness in adulthood. Our findings suggest that special attention could be paid to children from low SES families to prevent cardiometabolic diseases primordially.
Differences in health behaviors partly explain the socioeconomic gap in cardiovascular health. We prospectively examined the association between childhood socioeconomic status (SES) and lifestyle factors in adulthood, and the difference of lifestyle factors according to childhood SES in multiple time points from childhood to adulthood.
The sample comprised 3453 participants aged 3-18?years at baseline (1980) from the longitudinal Young Finns Study. The participants were followed up for 31?years (N?=?1675-1930). SES in childhood was characterized as reported annual family income and classified on an 8-point scale. Diet, smoking, alcohol intake and physical activity were used as adult and life course lifestyle factors. Higher childhood SES predicted a healthier diet in adulthood in terms of lower consumption of meat (ß?±?SE -3.6?±?0.99,p?
We prospectively examined whether family socioeconomic status (SES) in childhood is associated with metabolic syndrome (MetS), impaired fasting glucose (IFG), or type 2 diabetes in adulthood.
The sample comprised 2,250 participants from the longitudinal Cardiovascular Risk in Young Finns Study cohort. Participants were 3-18 years old at baseline (mean age 10.6 years), and they were followed for 31 years. SES was characterized as reported annual income of the family and classified on an 8-point scale.
For each 1-unit increase in family SES in childhood, the risk for adult MetS decreased (risk ratio [95% confidence interval] 0.94 [0.90-0.98]; P = 0.003) when adjusted for age, sex, childhood cardiometabolic risk factors (lipids, systolic blood pressure, insulin, and BMI), childhood physical activity, and fruit and vegetable consumption. The association remained after adjustment for participants' own SES in adulthood (0.95 [0.91-0.99]; P = 0.005). A similar association was seen between childhood SES and the risk of having either adult IFG or type 2 diabetes (0.96 [0.92-0.99]; P = 0.01, age and sex adjusted). This association became nonsignificant after adjustment for childhood risk factors (P = 0.08). Of the individual components of MetS, lower SES in childhood predicted large waist circumference (0.96 [0.93-0.99]; P = 0.003) and a high triglycerides concentration (0.96 [0.92-1.00]; P = 0.04) after adjustment for the aforementioned risk factors.
Lower SES in childhood may be associated with an increased risk for MetS, IFG, and type 2 diabetes in adulthood. Special attention could be paid to children of low SES families to decrease the prevalence of MetS in adulthood.
Age, education, and sex associate with cognitive performance. We investigated associations between age, sex, education, and cognitive performance in young or middle-aged adults and evaluated data reduction methods to optimally capture cognitive performance in our population-based data.
This study is part of the Cardiovascular Risk in Young Finns Study. The 3,596 randomly selected subjects (aged 3-18 years in 1980) have been followed up for 30 years. In 2011, a computer-based cognitive testing battery (the Cambridge Neuropsychological Test Automated Battery [CANTAB]) was used to assess several cognitive domains. Principal component analysis, categorical and standardized classifications were applied to the cognitive data.
Among 34- to 49-year-old participants, cognitive performance declined with age, while education associated with better cognitive functions in several cognitive domains. Men had higher performance on all cognitive domains except visual or episodic memory, in which women outperformed men. The results were similar regardless of the data reduction method used.
The associations between sex, age, education, and cognitive performance are already apparent in young adulthood or middle age. Principal component analyses, categorical and standardized classifications are useful tools to analyze CANTAB cognitive data. (PsycINFO Database Record
