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sleep deprived, others demonstrate remarkable levels of neurobehavioral
resistance to sleep loss, and others show intermediate responses. 171,174 Thus
far, studies from our laboratory and others indicate these phenotypic
responses occur as a normal distribution, 170,175 which suggests the pheno-
type, like chronotype, may be polygenetic.
It remains unclear, however, whether the same individuals vulnerable to
the adverse neurobehavioral effects of chronic sleep restriction are also vul-
nerable to acute total sleep deprivation. Some studies have reported differ-
ences in behavioral, sleep homeostatic and/or physiological responses to
both types of deprivation. 32,176,177 Moreover, only a few experiments
have systematically examined the same subjects in both types of depriva-
tion. 167,175,178-180 These studies reported inconsistent results, likely due
to small sample sizes, different populations, varying doses of sleep restriction,
and different outcome measures.
The reasons for differential neurobehavioral vulnerabilities to sleep loss
are unknown, and thus far have not been accounted for by demographic
factors, IQ, or sleep need. Moreover, psychometric scales have not reliably
identified cognitively vulnerable individuals. 181 The stable, trait-like inter-
individual differences observed in response to acute total sleep deprivation—
with intraclass correlation coefficients accounting for 50-90% of the
variance in neurobehavioral measures 170,171 —point to underlying genetic
components. In support of this statement, a recent study by Kuna et al.
182
conducted in monozygotic and dizygotic twin pairs, found substantial dif-
ferences in individual neurobehavioral responses to total sleep deprivation—
56.2% of the total variance in the monozygotic twins was due to variance
between pairs whereas only 14.5% of the total variance in dizygotic twins
was due to variance between pairs ( Fig. 7.3 ) , indicating that the response
to acute total sleep deprivation is a highly stable, genetically determined trait.
Indeed, data from unrelated individuals further indicate that common
genetic polymorphisms involved in sleep-wake, circadian, and cognitive
regulation may underlie these large interindividual differences in neuro-
behavioral vulnerability to sleep deprivation in healthy adults. 164,181,183
Because of reported differences in behavioral, sleep homeostatic, and
physiological responses to chronic sleep restriction and acute total sleep dep-
rivation, specific candidate genes may play different roles in the degree of
vulnerability and/or resilience to the neurobehavioral and homeostatic
effects of acute total sleep deprivation and chronic sleep restriction. Two
examples—one from a genetic variation involved in circadian regulation
and one from a genetic variation involved in a cognitive regulation—
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