title: Heritability of performance deficit accumulation during acute sleep deprivation in twins.
abstract: OBJECTIVE
  To determine if the large and highly reproducible interindividual differences in rates of performance deficit accumulation during sleep deprivation, as determined by the number of lapses on a sustained reaction time test, the Psychomotor Vigilance Task (PVT), arise from a heritable trait.
  
  
  METHODS
  Prospective, observational cohort study.
  
  
  METHODS
  Academic medical center.
  
  
  METHODS
  There were 59 monozygotic (mean age 29.2 ± 6.8 [SD] yr; 15 male and 44 female pairs) and 41 dizygotic (mean age 26.6 ± 7.6 yr; 15 male and 26 female pairs) same-sex twin pairs with a normal polysomnogram.
  
  
  METHODS
  Thirty-eight hr of monitored, continuous sleep deprivation.
  
  
  RESULTS
  Patients performed the 10-min PVT every 2 hr during the sleep deprivation protocol. The primary outcome was change from baseline in square root transformed total lapses (response time ≥ 500 ms) per trial. Patient-specific linear rates of performance deficit accumulation were separated from circadian effects using multiple linear regression. Using the classic approach to assess heritability, the intraclass correlation coefficients for accumulating deficits resulted in a broad sense heritability (h(2)) estimate of 0.834. The mean within-pair and among-pair heritability estimates determined by analysis of variance-based methods was 0.715. When variance components of mixed-effect multilevel models were estimated by maximum likelihood estimation and used to determine the proportions of phenotypic variance explained by genetic and nongenetic factors, 51.1% (standard error = 8.4%, P < 0.0001) of twin variance was attributed to combined additive and dominance genetic effects.
  
  
  CONCLUSIONS
  Genetic factors explain a large fraction of interindividual variance among rates of performance deficit accumulations on PVT during sleep deprivation.
authors.affiliation: Department of Medicine and Center for Sleep and Circadian Neurobiology, University of Pennsylvania, Philadelphia, PA, USA. skuna@mail.med.upenn.edu
authors.forename: Samuel T
authors.initials: ST
authors.lastname: Kuna
authors.forename: Greg
authors.initials: G
authors.lastname: Maislin
authors.forename: Frances M
authors.initials: FM
authors.lastname: Pack
authors.forename: Bethany
authors.initials: B
authors.lastname: Staley
authors.forename: Robert
authors.initials: R
authors.lastname: Hachadoorian
authors.forename: Emil F
authors.initials: EF
authors.lastname: Coccaro
authors.forename: Allan I
authors.initials: AI
authors.lastname: Pack
mesh_terms: D000208:Acute Disease; D000243:Adenosine Deaminase / Q000235:genetics*; D000328:Adult; D000704:Analysis of Variance; D015331:Cohort Studies; D005260:Female; D006801:Humans; D008297:Male; D056950:Period Circadian Proteins / Q000235:genetics*; D011446:Prospective Studies; D011597:Psychomotor Performance; D011930:Reaction Time / Q000235:genetics*; D012892:Sleep Deprivation / Q000235:genetics*; D014429:Twins, Dizygotic / Q000235:genetics; D014430:Twins, Monozygotic / Q000235:genetics
chemical_list: C512644:PER3 protein, human; D056950:Period Circadian Proteins; D000243:Adenosine Deaminase