| 1. |
- Baker, Laura, et al.
(författare)
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Resting heart rate and the development of antisocial behavior from age 9 to 14 : genetic and environmental influences
- 2009
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Ingår i: Development and psychopathology (Print). - 0954-5794 .- 1469-2198. ; 21:3, s. 939-960
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Tidskriftsartikel (refereegranskat)abstract
- The genetic and environmental basis of a well-replicated association between antisocial behavior (ASB) and resting heart rate was investigated in a longitudinal twin study, based on two measurements between the ages of 9 and 14 years. ASB was defined as a broad continuum of externalizing behavior problems, assessed at each occasion through a composite measure based on parent ratings of trait aggression, delinquent behaviors, and psychopathic traits in their children. Parent ratings of ASB significantly decreased across age from childhood to early adolescence, although latent growth models indicated significant variation and twin similarity in the growth patterns, which were explained almost entirely by genetic influences. Resting heart rate at age 9-10 years old was inversely related to levels of ASB but not change patterns of ASB across age or occasions. Biometrical analyses indicated significant genetic influences on heart rate during childhood, as well as ASB throughout development from age 9 to 14. Both level and slope variation were significantly influenced by genetic factors. Of importance, the low resting heart rate and ASB association was significantly and entirely explained by their genetic covariation, although the heritable component of heart rate explained only a small portion (1-4%) of the substantial genetic variance in ASB. Although the effect size is small, children with low resting heart rate appear to be genetically predisposed toward externalizing behavior problems as early as age 9 years old.
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| 2. |
- Gao, Yu, et al.
(författare)
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Genetic and environmental influences on frontal EEG asymmetry and alpha power in 9–10 -year-old twins
- 2009
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Ingår i: Psychophysiology. - : Wiley. - 0048-5772 .- 1469-8986. ; 46:4, s. 787-796
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Tidskriftsartikel (refereegranskat)abstract
- Modest genetic influences on frontal EEG asymmetry have been found in adults, but little is known about its genetic origins in children. Resting frontal asymmetry and alpha power were examined in 951 9-10-year-old twins. Results showed that in both males and females: (1) a modest but significant amount of variance in frontal asymmetry was accounted for by genetic factors (11-28%) with the remainder accounted for by non-shared environmental influences, and (2) alpha power were highly heritable, with 71-85% of the variance accounted for by genetic factors. Results suggest that the genetic architecture of frontal asymmetry and alpha power in late childhood are similar to that in adulthood and that the high non-shared environmental influences on frontal asymmetry may reflect environmentally influenced individual differences in the maturation of frontal cortex as well as state-dependent influences on specific measurements.
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| 3. |
- Tuvblad, Catherine, 1968-, et al.
(författare)
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The genetic and environmental etiology of sympathetic and parasympathetic activity in children
- 2010
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Ingår i: Behavior Genetics. - : Springer Science and Business Media LLC. - 0001-8244 .- 1573-3297. ; 40:4, s. 452-466
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Tidskriftsartikel (refereegranskat)abstract
- The present study examines the genetic and environmental etiology of the associations among respiratory sinus arrhythmia (RSA), heart rate (HR), skin conductance level (SCL), and non-specific skin conductance responses (NS-SCR)-measures that purportedly index the parasympathetic and sympathetic branches of the autonomic nervous system. The sample was drawn from a cohort of 1,219 preadolescent twins (aged 9-10). Multivariate analyses of the data were conducted using structural equation modeling. Almost all genetic and environmental influences on the measures acted through two latent factors. The first latent factor was largely responsible for the variance in heart rate, SCL and NS-SCR, reflecting sympathetic activity, and its proportions of variance due to genetic and shared environmental influences were 27 and 28% in males, and 31 and 41% in females, respectively. The second latent factor accounted for the variance in RSA and heart rate, reflecting parasympathetic activity; genetic and shared environmental factors explained 27 and 23% of the variance in males, respectively, and 35 and 18% of the variance in females. Measurement-specific genetic effects accounted for 14-27% of the total variance in RSA and SCL, and measurement- specific shared environmental effects accounted for 10-12% in SCL. In general, the validity of separate sympathetic and parasympathetic constructs was supported.
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