Clinical studies have shown a relationship between allergic disorders and depression, panic disorder, attention deficit/hyperactivity disorder, and social anxiety for a significant subset of patients with these disorders. The nature of the relationship, whether due to shared environmental or biologic vulnerabilities or as a result of the stress of chronic illness, has been less clear. By examining the covariance of atopic disorders and depressive symptoms in a community sample of monozygotic (MZ) and dizygotic (DZ) twins, the contribution of genetic and/or shared environmental etiological factors can be established. A Finnish sample of 1337 MZ and 2506 DZ twin pairs, ages 33-60 years, was sent questionnaires inquiring about history of asthma, eczema, and atopic rhinitis, as well as the Beck Depression Inventory (BDI). The nature of the covariation between twins of these symptoms was investigated by fitting competing genetic and environmental models. Within-person correlation between atopic symptoms and BDI was 0.103 (P < 0.001) for the total sample. Using the Mx statistical modeling program to fit the data to competing quantitative genetic models, the best fitting model estimated that 64% of the association between atopy and BDI was due to shared familial vulnerability, primarily additive genetic influences. Although the measures for allergic disorders and depression are crude, this study supports the hypothesis that there is a small shared genetic risk for atopic and depressive symptoms, and if replicated, may open research for common mechanisms between allergic and depressive disorders. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:146-153, 2000.
Gene-environment interactions and inheritance of asthma were studied in 16-yr-old twins and their parents who participated in the nationwide Finnish Twin Cohort Study. Between 1991 and 1994, questionnaires, including a question on physician-diagnosed asthma, were mailed to the members of 2,483 twin families. The individual response rate ranged from 82 to 93%. Information on parental asthma status allowed the genetic modeling of asthma data in two different groups of twins. In families where one of the parents was asthmatic, as much as 87% of the variation in susceptibility to asthma in twins was explained by genetic factors. On the other hand, for twins whose parents were unaffected, a model including environmental effect alone was sufficient to explain the development of asthma. Genetic influences could not be totally excluded, but their role was significantly smaller. These results indicate that the presence of asthma in successive generations is more likely caused by shared genes than shared environmental risk factors; however, substantial heterogeneity among families may exist. Genetic analysis, especially among the families with an obvious familial component in development of asthma, may enhance the chances of revealing the pathogenetic mechanisms
(birth cohorts 1975 to 1979) and their parents through questionnaires mailed when the twins were ages 16 and 18.5 years old. The sample included 702 monozygotic, 724 same-sex dizygotic, and 762 opposite-sex dizygotic sets of twins. The measures used were length, weight, ponderal index (kilograms per cubic meters), and gestational age at birth, and height, weight, and body mass index (kilograms per square meters) at 16 to 18.5 years of age. The changes in genetic and environmental influences on body size from birth to early adulthood were analyzed by quantitative genetic modeling. Results:The twins who had a higher weight or ponderal index at birth were taller and heavier in early adulthood, whereas those who were longer at birth were taller, but not heavier, later in life. Adult height was affected more by the birth size than body mass index. In the genetic modeling analyses, the genetic factors accounting for the variation of body size became more apparent with age, and both genetic and environmental influences on stature had a sizable carryover effect from birth to late adolescence, whereas for relative weight, the influences were more age-specific. Discussion: The genetic and environmental architecture of body size changes from birth to adulthood. Even in monozygotic twins who share their genetic background, the initially larger twin tended to remain larger, demonstrating the longlasting effects of fetal environment on final body size.
Background-Previous studies have suggested that, in addition to genetic liability and environment in early childhood, intrauterine life also influences the risk for asthma beyond childhood. Low birth weight, prematurity, young maternal age, and maternal smoking have all shown an association with asthma. The eVect of perinatal factors on the risk for asthma in relation to familial and social risk factors was studied in a nationwide population-based sample of adolescent twins. In addition to a distribution of birth characteristics among twins which diVers from that of singletons, data on twins enable a distinction to be made between genetic and environmental sources of variation. Methods-Questionnaires were sent to five consecutive birth cohorts of Finnish 16 year old twins born in 1975-9 and to their parents (3065 families). The outcome measure was life time prevalence of doctor-diagnosed asthma in these adolescents. The association between asthma and potential risk factors was assessed by multiple logistic regression and discordant twin pair analysis. Results-Risk for asthma increased with increasing ponderal index (p for trend <0.01) and decreasing maternal age (p for trend <0.05). Among the 25% of twins with the highest ponderal index, the odds ratio for asthma was 1.82 (95% confidence interval 1.18 to 2.79) compared with those in the lowest 25%. Neither birth weight, gestational age, nor Apgar score was associated with asthma. When perinatal risk factors were combined with familial and social risk factors, ponderal index, maternal smoking, parental asthma, and sibship size were all significant independent determinants of asthma in these adolescents. Conclusions-The risk for asthma in adolescent twins increases with increasing ponderal index when adjusted for familial and social factors. (Thorax 2000;55:25-31)
Large number of older siblings appears to be protective against the development of hay fever.
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