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Genetic and Environmental Influences on the Relative Timing of Pubertal Change

Published online by Cambridge University Press:  21 February 2012

Lindon Eaves*
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States of America. eaves@mail2.vcu.edu
Judy Silberg
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States of America.
Debra Foley
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States of America.
Cynthia Bulik
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States of America.
Hermine Maes
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States of America.
Alaattin Erkanli
Affiliation:
Epidemiology Program, Department of Psychiatry, Duke University, Durham, North Carolina, United States of America.
Adrian Angold
Affiliation:
Epidemiology Program, Department of Psychiatry, Duke University, Durham, North Carolina, United States of America.
E. Jane Costello
Affiliation:
Epidemiology Program, Department of Psychiatry, Duke University, Durham, North Carolina, United States of America.
Carol Worthman
Affiliation:
Department of Anthropology, Emory University, Atlanta, Georgia, United States of America.
*
*Address for correspondence: Lindon Eaves, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University School of Medicine, PO Box 980003, Richmond VA 23298-0003, USA.

Abstract

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Amulticategory item-response theory model was developed to characterize developmental changes in three items relating to the assessment of puberty in adolescent twin girls and boys. The model allowed for the fixed effects of age on probability of endorsing the responses and for the random effects of individual differences on the timing of pubertal changes relative to chronological age. In girls, the model was applied three-wave data on twin pairs (N = 414 female monozygotic [MZ] and 197 female dizygotic [DZ] pairs) and female twins from boy–girl pairs (N = 300 twins) from the Virginia Twin Study of Adolescent Behavioral Development. In boys, the data comprised 318 MZ and 185 DZ pairs and 297 male twins from boy–girl pairs. A total of 3172 and 2790 individual twin assessments were available in girls and boys, respectively, spanning ages 8–17 years. The availability of twin data allows the contributions of genes, the shared environment and individual unique environmental experiences to be resolved in the relative timing of pubertal changes. Parameters of the mixed model including fixed effects of age and random effects of genes and environment were estimated by Markov Chain Monte Carlo simulations using the BUGS algorithm for Gibbs sampling. The estimated standard deviation of random differences in the timing of puberty relative to age was 0.96 years in girls and 1.01 years in boys. The estimated intraclass correlations for the relative timing of pubertal changes were 0.99 +/−0.01 in MZ girls, 0.52 +/−0.02 in DZ girls, 0.88 +/−0.04 in MZ boys and 0.44+/−0.02 in DZ boys, indicating a very large contribution of genetic factors to the relative timing of pubertal change in both sexes. Additive genetic factors account for an estimated 96.3+/−3.3% of the total variance in random effects in girls and 88.0+/−3.6% in boys. Shared environmental influences account for 3.6+/−3.4% in girls and 0% in boys. In girls, nonshared environmental effects explain 0.1+/−0.1% of the total residual variance. The comparable figure in boys is 12.0+/−;3.6%.

Type
Articles
Copyright
Copyright © Cambridge University Press 2004