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Models for the longitudinal genetic analysis of same-age twins: application to HDL cholesterol

Published online by Cambridge University Press:  21 February 2012

WE Nance*
Affiliation:
Department of Human Genetics. [email protected]
J Bodurtha
Affiliation:
Department of Human Genetics.
LJ Eaves
Affiliation:
Department of Human Genetics.
J Hewitt
Affiliation:
Institute of Behavioral Genetics, University of Colorado, Boulder, Colorado.
H Maes
Affiliation:
Department of Human Genetics.
J Segrest
Affiliation:
Department of Medicine, University of Alabama Medical School, Birmingham, Alabama.
J Meyer
Affiliation:
Millenium Pharmaceuticals Inc., Cambridge, Massachusetts, USA.
M Neale
Affiliation:
Department of Human Genetics.
R Schieken
Affiliation:
Department of Pediatrics, Medical College of Virginia of Virginia Commonwealth University, Richmond, Virginia.
*
*Correspondence: Walter E Nance, MD, PhD, Department of Human Genetics, Medical College of Virginia of Virginia Commonwealth University, PO Box 980033, Richmond, Virginia 23298, USA. Fax: 001 804 828 3760.

Abstract

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Models are presented for the analysis of longitudinal data from same-age twins which permit the exploration of a remarkably diverse array of alternative explanations for continuity and change during development. Data of this type permit the detection of new sources of genetic or environmental covariation during development that are not expressed at earlier ages and, because they include the effects of age-specific genes, the resulting heritability estimates are more reliable than those obtained from relatives who differ in age. The proposed models were applied to measurements of HDL cholesterol obtained on 81 pairs of monozygotic (MZ) twins and 69 dizygotic (DZ) pairs at 11, 12.5 and 14 years of age. All three MZ co-twin correlations were substantially higher than the self correlations across occasions, suggesting that new sources of genetic or environmental covariation must be expressed during early adolescence. This interpretation was confirmed by analysis of the full covariance matrices which showed that only models which assumed the expression of new or age-specific genes could explain the observed pattern of covariation. Because they include the effects of age-specific genes, the resulting heritabilities (0.80–0.83) were substantially higher than many previous estimates.

Type
Articles
Copyright
Copyright © Cambridge University Press 1998