Genetic Influences Contribute To Neurobehavioral Response To Acute Sleep Deprivation

1191 Editorial—Barclay and Ellis Sleep deprivation as an experimental protocol allows for the investigation of the underlying processes of sleep as well as characterising potential functional impairments during and following prolonged wakefulness. Numerous studies have investigated the consequent neurobehavioral impairments in performance on tasks of sustained attention, typically using the psychomotor vigilance task (PVT). Performance deterioration on the PVT is considered to represent impaired behavioral alertness and sleep tendency,1 and hence can be considered an indicator of sleep-homeostatic drive. The impact of sleep deprivation is considered to be in part dependent on sleep/circadian influences, arousal system influences, and individual characteristics,2 suggesting that resulting neurobehavioral impairments are likely to show vast interindividual differences. One factor considered to influence interindividual response to sleep deprivation is genetics. In this issue of SLEEP, Kuna and colleagues3 present the first twin study to assess the heritability of response to experimentally induced total sleep deprivation. The authors assessed the accumulation of performance deficits on the PVT (defined as lapses > 500 msec per trial, at regular 2-hour intervals) following 38 hours of total sleep deprivation. The accumulation of “sleep drive” demonstrated substantial genetic influence, with broad-sense heritability estimated at 83%. One of the main strengths of the paper by Kuna et al.3 is the use of three complimentary methods of analysis to assess heritability. First, heritability was assessed using classical methods comparing intra-class correlation coefficients between monozygotic (MZ) and dizygotic (DZ) twin pairs. Second, ANOVA based methods were used to test the validity of the twin model (testing the assumption that the phenotype of interest does not differ as a function of zygosity). Finally, standard biometrical model-fitting approaches of maximum likelihood estimation were used to allow for the examination of possible modes of genetic transmission (i.e., allowing variance to be parsed into additive and non-additive [dominance] genetic influences). Additionally, the stability of the trait in question was assessed by comparison of the grand mean of performance lapses in the final 24 hours of the deprivation protocol within MZ twin pairs. This method of analysis allows EDITORIAL