TY - JOUR
T1 - Genetic influence on capillary oxygen saturation
T2 - A twin study
AU - Tarnoki, David Laszlo
AU - Medda, Emanuela
AU - Tarnoki, Adam Domonkos
AU - Lazar, Zsofia
AU - Fagnani, Corrado
AU - Stazi, Maria Antonietta
AU - Karlinger, Kinga
AU - Torzsa, Peter
AU - Kalabay, Laszlo
AU - Garami, Zsolt
AU - Berczi, Viktor
AU - Horvath, Ildiko
PY - 2014/1/1
Y1 - 2014/1/1
N2 - Background: While heritability has been shown for daytime sleepiness, the heritability of daytime capillary oxygen saturation (SpO2) has not been described in detail. Our aim was to estimate the role of genes and environmental factors-both shared and unshared-in the variation of daytime SpO2. Methods: A total of 193 adult healthy twin pairs (138 monozygotic, 55 dizygotic) were recruited in Hungary and in the United States [age = 43.6 ± 15.6 years (mean ± SD)]. SpO2 was measured by pulse oximetry. Univariate quantitative genetic modeling was performed to decompose the phenotypic variance of the considered parameter into heritability (A), shared (C), and unshared (E) environmental effects. Results: SpO2 twin correlation in monozygotic twins was stronger than in dizygotic twins (0.30 and -0.15, respectively, p < 0.05). Age-, sex-, country-, and body mass index-adjusted genetic effects accounted for 26 % (95 % CI 10, 45 %) of the variance of SpO2, and the unshared environmental component explained the remaining 74 % (95 % CI 59, 89 %). No shared environmental influence on SpO2 was detected. The heritability of SpO2 was not different between smokers and nonsmokers. Conclusion: In summary, individual differences in daytime SpO2 are explained by genetic and unshared environmental effects. The strong unshared environmental influence highlights the role of prevention of known environmental risk factors.
AB - Background: While heritability has been shown for daytime sleepiness, the heritability of daytime capillary oxygen saturation (SpO2) has not been described in detail. Our aim was to estimate the role of genes and environmental factors-both shared and unshared-in the variation of daytime SpO2. Methods: A total of 193 adult healthy twin pairs (138 monozygotic, 55 dizygotic) were recruited in Hungary and in the United States [age = 43.6 ± 15.6 years (mean ± SD)]. SpO2 was measured by pulse oximetry. Univariate quantitative genetic modeling was performed to decompose the phenotypic variance of the considered parameter into heritability (A), shared (C), and unshared (E) environmental effects. Results: SpO2 twin correlation in monozygotic twins was stronger than in dizygotic twins (0.30 and -0.15, respectively, p < 0.05). Age-, sex-, country-, and body mass index-adjusted genetic effects accounted for 26 % (95 % CI 10, 45 %) of the variance of SpO2, and the unshared environmental component explained the remaining 74 % (95 % CI 59, 89 %). No shared environmental influence on SpO2 was detected. The heritability of SpO2 was not different between smokers and nonsmokers. Conclusion: In summary, individual differences in daytime SpO2 are explained by genetic and unshared environmental effects. The strong unshared environmental influence highlights the role of prevention of known environmental risk factors.
KW - Environment
KW - Genetics
KW - Heritability
KW - Oximetry
UR - http://www.scopus.com/inward/record.url?scp=84901267878&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84901267878&partnerID=8YFLogxK
U2 - 10.1007/s00408-014-9563-z
DO - 10.1007/s00408-014-9563-z
M3 - Article
C2 - 24584632
AN - SCOPUS:84901267878
SN - 0341-2040
VL - 192
SP - 429
EP - 434
JO - Lung
JF - Lung
IS - 3
ER -