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Genetic studies on atopy and asthma in Wessex

Three years ago a research team was formed at the University of Southampton to study genetic determinants of atopy and asthma. The group included S. T. Holgate, R. Beasley (now in New Zealand), B. Begishvih, I. Doull, S. Lawrence, M. Watson (now in Australia), S. Thomas, M. Howell, and J. Harvey. Our research programme spans random and multiplex families and parametric and non-parametric analyses. Results with parametric analyses of random families are described here. The sample consists of 131 nuclear famihes with three or more children, selected through General Practitioner lists without regard to atopy [1]. The observations include total IgE (but not so far specific IgE), skinprick tests to common allergens, bronchial reactivity to histamine challenge, and a standard questionnaire with video. Preliminary analysis of eight quantitative traits showed that the logarithmic of total IgE adjusted for age and sex (IGE) correlates very highly with atopy as a principal component and is more heritable than bronchial response or other measures of asthma: IGE h = 0-587 ± 0053 and BR ĥ = 0-282 ± 0-061. For none of the traits was the mother-child correlation significantly greater than the father-child correlation (Table 1). This argues against maternal effects or paternal imprinting for these traits. Others have obtained similar results [2]. Excess mother-child concordance is sometimes found for anamnestic data, usually provided by the mother, and lower prevalence in women than men assures excess mother-child concordance [3] which, if observed, would therefore be ambiguous. Commingling analysis suggested two or three distributions for each trait. This is consistent with (but does not prove) segregation of major genes. Segregation analysis supports common genes. IGE agrees with the analysis of Gerrard et al. (1978) in favouring recessivity of high titres against a polygenic background, but this evidence is sensitive to leptokurtosis and common environment.