BACKGROUND: While heritability has been shown for daytime sleepiness, the heritability of daytime capillary oxygen saturation (SpO(2)) 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 SpO(2). 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)]. SpO(2) 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: SpO(2) 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 SpO(2), and the unshared environmental component explained the remaining 74 % (95 % CI 59, 89 %). No shared environmental influence on SpO(2) was detected. The heritability of SpO(2) was not different between smokers and nonsmokers. CONCLUSION: In summary, individual differences in daytime SpO(2) are explained by genetic and unshared environmental effects. The strong unshared environmental influence highlights the role of prevention of known environmental risk factors.
BACKGROUND: While heritability has been shown for daytime sleepiness, the heritability of daytime capillary oxygen saturation (SpO(2)) 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 SpO(2). 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)]. SpO(2) 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: SpO(2) 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 SpO(2), and the unshared environmental component explained the remaining 74 % (95 % CI 59, 89 %). No shared environmental influence on SpO(2) was detected. The heritability of SpO(2) was not different between smokers and nonsmokers. CONCLUSION: In summary, individual differences in daytime SpO(2) are explained by genetic and unshared environmental effects. The strong unshared environmental influence highlights the role of prevention of known environmental risk factors.
Authors: Madeleine Verhovsek; Matthew P A Henderson; Gerard Cox; Hong-yuan Luo; Martin H Steinberg; David H K Chui Journal: Am J Hematol Date: 2010-11 Impact factor: 10.047
Authors: L Ferini-Strambi; G Calori; A Oldani; G Della Marca; M Zucconi; V Castronovo; G Gallus; S Smirne Journal: Respir Med Date: 1995-05 Impact factor: 3.415
Authors: Brian E Cade; Han Chen; Adrienne M Stilp; Tin Louie; Sonia Ancoli-Israel; Raanan Arens; Richard Barfield; Jennifer E Below; Jianwen Cai; Matthew P Conomos; Daniel S Evans; Alexis C Frazier-Wood; Sina A Gharib; Kevin J Gleason; Daniel J Gottlieb; David R Hillman; W Craig Johnson; David J Lederer; Jiwon Lee; Jose S Loredo; Hao Mei; Sutapa Mukherjee; Sanjay R Patel; Wendy S Post; Shaun M Purcell; Alberto R Ramos; Kathryn J Reid; Ken Rice; Neomi A Shah; Tamar Sofer; Kent D Taylor; Timothy A Thornton; Heming Wang; Kristine Yaffe; Phyllis C Zee; Craig L Hanis; Lyle J Palmer; Jerome I Rotter; Katie L Stone; Gregory J Tranah; James G Wilson; Shamil R Sunyaev; Cathy C Laurie; Xiaofeng Zhu; Richa Saxena; Xihong Lin; Susan Redline Journal: PLoS Genet Date: 2019-04-16 Impact factor: 5.917