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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Notes
We had an a priori hypothesis that we would find a parasympathetic factor defined by heart rate (HR) and respiratory sinus arrhythmia (RSA). However, there are problems with model identification for factors defined by only two variables. Thus, we added a second heart rate variable (from Rest 2) in order to help identify the parasympathetic factor. The decision to include a second heart rate variable was arbitrary. Importantly, when models were re-run with two measures of RSA (i.e., from Rest 1 and Rest 2) and only HR from Rest 1, we obtained a similar pattern of results. Thus, although the decision to include both HR1 and HR2 may have influenced our estimates of shared versus non-shared measurement error, it did not effect the main results of the study.
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Acknowledgment
This study was funded by NIMH (R01 MH58354). Catherine Tuvblad was supported by post-doctoral stipends from the Swedish Council for Working Life and Social Research (Project 2006-1501) and the Sweden-America Foundation. Adrian Raine was supported by NIMH (Independent Scientist Award K02 MH01114-08). Kristen Jacobson was supported by NIMH (Mentored Scientist Career Development Award K01 MH068484). We thank the Southern California Twin Project staff for their assistance in collecting data, and the twins and their families for their participation.
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Edited by Dorret Boomsma.
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Tuvblad, C., Isen, J., Baker, L.A. et al. The Genetic and Environmental Etiology of Sympathetic and Parasympathetic Activity in Children. Behav Genet 40, 452–466 (2010). https://doi.org/10.1007/s10519-010-9346-0
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DOI: https://doi.org/10.1007/s10519-010-9346-0