The present study assessed the prevalence of asthma and allergy, and estimated the importance of genetic and environmental influences on asthma and allergy liability and their association. Longitudinal data on self-reported, doctor-diagnosed asthma and allergy were collected in over 14,000 individuals registered with the Netherlands Twin Register. Structural equation modeling was used for univariate and bivariate genetic analyses on data from twins, their siblings, and parents. Results showed no sex, age, and minimal birth cohort effects for asthma prevalence (11.8%). For allergy, prevalence was higher in women (19.8%) than in men (13.9%). Allergy prevalence at ages 22, 23, and 24 years increased from the 1970 to the 1980 birth cohort. The prevalence of allergy, but not of asthma, was higher in nontwin siblings than in twins. No assortative mating was observed. High (broad-sense) heritabilities were found for asthma (75%) and allergy (66%), with evidence for nonadditive genetic effects in asthma. The association between asthma and allergy (correlation = .65) was largely due to common genes (70%). No sex differences in genetic architecture were found. In conclusion, the prevalence of allergy but not of asthma increased in recent years. Individual differences in the liability to asthma, allergy and their co-occurrence are for a large part accounted for by differences in genetic background. Nonadditive gene action is important, which may have consequences for gene hunting strategies.
In this study aspects of selective attention and working memory were tested in a large sample of nearly 6-year old monozygotic and dizygotic twin pairs, using a computerized test battery (Amsterdam Neuropsychological tasks). In the selective attention task the presence of a foil signal (target signal at an irrelevant location) resulted in more false alarms than a non-target signal. In the working memory task an increase in memory load lead to an increase in response times and errors. We analyzed variations in absolute performance parameters (overall speed and accuracy) and relative performance parameters (increase in errors and/or reaction time). The results showed clear familial resemblances on performance. It proved difficult to ascribe these effects to shared genes or to shared environment. An exception was memory search rate, which was clearly heritable.KEY WORDS: Attention-deficit hyperactivity disorder; endophenotypes; selective attention; twin study; working memory.In order to study the genetics of childhood psychopathologies such as ADHD it is of great importance to identify endophenotypes that predict the liability of the pathology of interest. The advantage of an endophenotypic approach to study complex disorders (or complex traits, such as IQ) is that it allows the identification of genes that by themselves make only a small contribution to the trait under study. A minimal requirement for suitable endophenotypes is that they yield continuously quantifiable measures; another requirement is that endophenotypes are anchored in neuroscience (e.g., Castellanos andTannock, 2002, andBoomsma, 2001). Indeed, researchers of psychopathologies often make use of neurocognitive tasks that are known to activate particular brain systems, and that yield quantitative performance measures, usually reaction times and percentage of errors. For example, Bush et al., (1999), using a counting Stroop task, found that children with ADHD showed underactivation in the anterior cingulate cognitive division (ACcd), and a concurrent increase in distractor interference, relative to controls. Stroop performance may thus qualify as a suitable (cognitive) endophenotype, indicative of ADHD. However, the search for endophenotypes should also be guided by the fact that many psychopathologies are highly heritable, and a recent line of inquiry has started to focus on the heritabilities of the endophenotypes themselves.Twin, adoption and family studies have shown that many psychopathologies are highly heritable (for review, see Acosta et al., 2004). For example, the heritability of ADHD is estimated to be around between 50% and 90% (e.g., Thapar et al., 1999). In a similar vein, the heritability of attention problems as
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