A Genetic Epidemiological Mega Analysis of Smoking Initiation in Adolescents

Introduction. Previous studies in adolescents were not adequately powered to accurately disentangle genetic and environmental influences on smoking initiation across adolescence. Methods. Mega-analysis of pooled genetically informative data on smoking initiation was performed, with structural equation modeling, to test equality of prevalence and correlations across cultural backgrounds, and to estimate the significance and effect size of genetic and environmental effects according to the classical twin study, in adolescent male and female twins from same-sex and opposite-sex twin pairs (N=19 313 pairs) between age 10 and 19, with 76 358 longitudinal assessments between 1983 and 2007, from 11 population-based twin samples from the US, Europe and Australia. Results. Although prevalences differed between samples, twin correlations did not, suggesting similar etiology of smoking initiation across developed countries. The estimate of additive genetic contributions to liability of smoking initiation increased from approximately 15% to 45% from age 13 to 19. Correspondingly, shared environmental factors accounted for a substantial proportion of variance in liability to smoking initiation at age 13 (70%) and gradually less by age 19 (40%). Conclusions. Both additive genetic and shared environmental factors significantly contribute to variance in smoking initiation throughout adolescence. The present study, the largest genetic epidemiological study on smoking initiation to date, found consistent results across 11 studies for the etiology of smoking initiation. Environmental factors, especially those shared by siblings in a family, primarily influence smoking initiation variance in early adolescence, while an increasing role of genetic factors is seen at later ages, which has important implications for prevention strategies. IMPLICATIONS: This is the first study to find evidence of genetic factors in liability to smoking initiation at ages as young as 12. It also shows the strongest evidence to date for decay of effects of the shared environment from early adolescence to young adulthood. We found remarkable consistency of twin correlations across studies reflecting similar etiology of liability to initiate smoking across different cultures and time periods. Thus familial factors strongly contribute to individual differences in who starts to smoke with a gradual increase in the impact of genetic factors and a corresponding decrease in that of the shared environment

Impact of adiposity on cardiac structure in adult life: the Childhood Determinants of Adult Health (CDAH) study.

BACKGROUND: We have examined the association between adiposity and cardiac structure in adulthood, using a life course approach that takes account of the contribution of adiposity in both childhood and adulthood. METHODS: The Childhood Determinants of Adult Health study (CDAH) is a follow-up study of 8,498 children who participated in the 1985 Australian Schools Health and Fitness Survey (ASHFS). The CDAH follow-up study included 2,410 participants who attended a clinic examination. Of these, 181 underwent cardiac imaging and provided complete data. The measures were taken once when the children were aged 9 to 15 years, and once in adult life, aged 26 to 36 years. RESULTS: There was a positive association between adult left ventricular mass (LVM) and childhood body mass index (BMI) in males (regression coefficient (β) 0.41; 95% confidence interval (CI): 0.14 to 0.67; p = 0.003), and females (β = 0.53; 95% CI: 0.34 to 0.72; p < 0.001), and with change in BMI from childhood to adulthood (males: β = 0.27; 95% CI: 0.04 to 0.51; p < 0.001, females: β = 0.39; 95% CI: 0.20 to 0.58; p < 0.001), after adjustment for confounding factors (age, fitness, triglyceride levels and total cholesterol in adulthood). After further adjustment for known potential mediating factors (systolic BP and fasting plasma glucose in adulthood) the relationship of LVM with childhood BMI (males: β = 0.45; 95% CI: 0.19 to 0.71; p = 0.001, females: β = 0.49; 95% CI: 0.29 to 0.68; p < 0.001) and change in BMI (males: β = 0.26; 95% CI: 0.04 to 0.49; p = 0.02, females: β = 0.40; 95% CI: 0.20 to 0.59; p < 0.001) did not change markedly. CONCLUSIONS: Adiposity and increased adiposity from childhood to adulthood appear to have a detrimental effect on cardiac structure

Genetic Regulation of Hemodynamic Variables During Dynamic Exercise

BACKGROUND: Both resting and exercise levels of blood pressure in individuals have been used as predictors of adult hypertension. One possible mechanism underlying the relation between childhood resting and exercise blood pressure and future blood pressure is a set of genes expressed in childhood that persists to regulate adult blood pressure. METHODS AND RESULTS: To investigate the genetic relation of blood pressure and heart rate during both rest and exercise, we asked: (1) Are the genes that regulate resting hemodynamic variables the same genes that regulate these variables during exercise? (2) How much of the variance in exercise hemodynamic variables is genetic and how much is environmental? (3) Do the genetic and environmental influences on hemodynamic responses change with increasing levels of exercise? To determine how genetic and environmental effects expressed at rest influenced responses during dynamic exercise, a genetic analysis was conducted by fitting a series of models to the covariance matrices with the use of the LISREL VII program. CONCLUSIONS: We found that all the genetic effects expressed at the later stages of exercise can be explained by genetic effects expressed at rest and at the first stage of exercise. The environmental effects appear to be workload specific and include errors of measurement

Genetic regulation of hemodynamic variables during dynamic exercise. The MCV twin study

BACKGROUND: Both resting and exercise levels of blood pressure in individuals have been used as predictors of adult hypertension. One possible mechanism underlying the relation between childhood resting and exercise blood pressure and future blood pressure is a set of genes expressed in childhood that persists to regulate adult blood pressure. METHODS AND RESULTS: To investigate the genetic relation of blood pressure and heart rate during both rest and exercise, we asked: (1) Are the genes that regulate resting hemodynamic variables the same genes that regulate these variables during exercise? (2) How much of the variance in exercise hemodynamic variables is genetic and how much is environmental? (3) Do the genetic and environmental influences on hemodynamic responses change with increasing levels of exercise? To determine how genetic and environmental effects expressed at rest influenced responses during dynamic exercise, a genetic analysis was conducted by fitting a series of models to the covariance matrices with the use of the LISREL VII program. CONCLUSIONS: We found that all the genetic effects expressed at the later stages of exercise can be explained by genetic effects expressed at rest and at the first stage of exercise. The environmental effects appear to be workload specific and include errors of measurement

Age changes in the causes of individual differences in conservatism

Age-related changes are analyzed in the correlation of 3416 monozygotic and 3780 dizygotic U.S. twin pairs aged between 9 and 75+ years for conservatism scores derived from a 28-item social attitude inventory. The effects of the shared environment are overwhelming in twins aged 20 years or younger. In older twins, genetic effects appear to play a larger role. A more dynamic conception of the interaction between genes and environment in the development of complex human differences is needed