UNIVARIATE GENETIC-ANALYSIS OF OXYGEN-TRANSPORT REGULATION IN CHILDREN - THE MEDICAL-COLLEGE-OF-VIRGINIA TWIN STUDY

Citation
Wb. Moskowitz et al., UNIVARIATE GENETIC-ANALYSIS OF OXYGEN-TRANSPORT REGULATION IN CHILDREN - THE MEDICAL-COLLEGE-OF-VIRGINIA TWIN STUDY, Pediatric research, 33(6), 1993, pp. 645-648
Citations number
28
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
33
Issue
6
Year of publication
1993
Pages
645 - 648
Database
ISI
SICI code
0031-3998(1993)33:6<645:UGOORI>2.0.ZU;2-Y
Abstract
We investigated the relative contributions of genetic, individual envi ronmental, and shared environmental effects on 2,3-diphosphoglycerate (DPG) regulation in preadolescent children. In a population of 165 ear ly pubescent boy and girl twin pairs (11.4 y old), of whom 63 were pas sive smokers, we asked: 1) Are there differences in the control of DPG levels between early pubertal boys and girls? 2) If present, are thes e differences influenced by exposure to passive cigarette smoke? Non-p assive-smoking boys and girls had similar DPG levels. With exposure to passive smoke, DPG levels increased in boys (p = 0.02) but not in gir ls. Analysis of variance on DPG demonstrated a parental smoking effect (p = 0.008) and suggested an interactive effect between parental smok ing and sex of the child (p = 0.08). Univariate genetic analyses sugge sted that genes operated at different magnitudes in boys (9%) and girl s (39%) in explaining a significant portion of the variance in DPG. Th e magnitude of shared environmental influences was greater in boys (62 %) than in girls (34%), whereas individual environmental effects were similar in boys (29%) and girls (26%). Early pubertal boys differ from girls in their regulation of DPG. Environmental stressors such as pas sive cigarette smoke may elicit different responses in males and femal es, even at an early age. The use of path analysis may provide importa nt insights into the mechanisms and interactions of genetic and enviro nmental effects that underly the childhood antecedents of atherosclero tic heart disease.