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IJE Advance Access originally published online on April 14, 2005
International Journal of Epidemiology 2005 34(6):1302-1309; doi:10.1093/ije/dyi061
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Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2005; all rights reserved.

Genetic Epidemiology

A comparison of genetic and environmental variance structures for asthma, hay fever and eczema with symptoms of the same diseases: a study of Norwegian twins

Wenche Nystad*, Espen Røysamb, Per Magnus, Kristian Tambs and Jennifer R Harris

Division of Epidemiology, Norwegian Institute of Public Health, Nydalen, Oslo, Norway

* Corresponding author. Division of Epidemiology, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway. E-mail: wenche.nystad{at}fhi.no

Background We compared patterns of genetic and environmental influences on variation in liability for asthma, hay fever and eczema with those for symptoms of the same diseases, and determined how common sets of genes and environmental factors contribute to the relationship between diseases and symptoms among Norwegian twins.

Methods Analyses were based on self-reported asthma, hay fever and eczema and symptoms of the same diseases among 3334 pairs of Norwegian twins aged 18–35 years. Structural equation modelling was conducted to estimate the genetic and environmental variance structures.

Results For all diseases the concordances and the twin correlations were higher among monozygotic than among dizygotic twins. The results of the modelling confirmed that genetic effects were substantial for the diseases, and were more moderate for symptoms. The phenotypic correlation between disease and symptom was 0.67 for asthma and wheeze (a/w), 0.64 for hay fever and sneeze (hf/s), and 0.54 for eczema and itch (e/i). Decomposition of these correlations into genetic (G) and environmental (E) pathways revealed that G = 0.48 and E = 0.19 for a/w, G = 0.40 and E = 0.24 for hf/s, and G = 0.34 and E = 0.20 for e/i. For the diseases, the specific sources of genetic variance accounted for more variation than the specific environmental variance. Variance decomposition revealed that specific sources of variance were primarily explained by genetic effects for diseases and by environmental influences for symptoms.

Conclusions Genetic effects account for greater variation in reported diseases than symptoms. Co-occurrence of diseases and symptoms is mainly explained by genetic effects common to both phenotypes, but non-shared environment is also important.

Keywords Genes, environment, atopic diseases, symptoms

Accepted 1 March 2005


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