EEG sleep patterns in man: a twin study

Linkowski, Paul; Kerkhofs, Myriam; Hauspie, Roland; Susanne, Charles; Mendlewicz, Julien

doi:10.1016/0013-4694(89)90106-5

Cited by 78 publications

(54 citation statements)

References 10 publications

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“…Zung and Wilson (1967) reported concordance of sleeping patterns together with REM (rapid eye movement) pattern in four MZ and dissimilar patterns in two DZ twin pairs. This was confirmed by Linkowski et al (1989). EEG was recorded during three consecutive nights in 14 MZ and 12 DZ pairs.…”

Section: Genetics Of Eeg Powers As Defined By Spectral Analysis Technmentioning

confidence: 57%

Genetics of the human electroencephalogram (EEG) and event-related brain potentials (ERPs): a review

1994

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Twin and family studies of normal variation in the human electroencephalogram (EEG) and event related potentials (ERPs) are reviewed. Most of these studies are characterized by small sample sizes. However, by summarizing these studies in one paper, we may be able to gain some insight into the genetic influences on individual differences in central nervous system functioning that may mediate genetically determined differences in behavior. It is clear that most EEG parameters are to a large extent genetically determined. The results for ERPs are based on a much smaller number of studies and suggest medium to large heritability.

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Section: Genetics Of Eeg Powers As Defined By Spectral Analysis Technmentioning

confidence: 57%

Genetics of the human electroencephalogram (EEG) and event-related brain potentials (ERPs): a review

1994

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“…2c). Because the amount of SWS as well as the amount of delta power are stable individual traits that are highly heritable (23)(24)(25)(26), our findings suggest that there may be a genetic predisposition to develop diabetes when SWS deteriorates.…”

Section: Discussionmentioning

confidence: 80%

“…bolus. Blood samples were then taken at times 2,3,4,5,6,8,10,12,15,19,21,22,24,26,28,30,40,50,60,70,90, 100, 120, 140, 180, 210, and 240 min. At time 20 min, i.v.…”

Section: (A) Baseline Night (B1) (B) First Night Of Sws Suppression mentioning

confidence: 99%

Slow-wave sleep and the risk of type 2 diabetes in humans

Tasali

Leproult²,

Ehrmann³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

800

617

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There is convincing evidence that, in humans, discrete sleep stages are important for daytime brain function, but whether any particular sleep stage has functional significance for the rest of the body is not known. Deep non-rapid eye movement (NREM) sleep, also known as slow-wave sleep (SWS), is thought to be the most ''restorative'' sleep stage, but beneficial effects of SWS for physical well being have not been demonstrated. The initiation of SWS coincides with hormonal changes that affect glucose regulation, suggesting that SWS may be important for normal glucose tolerance. If this were so, selective suppression of SWS should adversely affect glucose homeostasis and increase the risk of type 2 diabetes. Here we show that, in young healthy adults, all-night selective suppression of SWS, without any change in total sleep time, results in marked decreases in insulin sensitivity without adequate compensatory increase in insulin release, leading to reduced glucose tolerance and increased diabetes risk. SWS suppression reduced delta spectral power, the dominant EEG frequency range in SWS, and left other EEG frequency bands unchanged. Importantly, the magnitude of the decrease in insulin sensitivity was strongly correlated with the magnitude of the reduction in SWS. These findings demonstrate a clear role for SWS in the maintenance of normal glucose homeostasis. Furthermore, our data suggest that reduced sleep quality with low levels of SWS, as occurs in aging and in many obese individuals, may contribute to increase the risk of type 2 diabetes.aging ͉ sleep quality ͉ sleep disordered breathing ͉ delta waves ͉ insulin resistance H uman sleep is composed of rapid-eye-movement (REM) sleep and stages 1, 2, 3, and 4 of non-REM (NREM) sleep. The deeper stages of NREM sleep, i.e., stages 3 and 4, also known as slow-wave sleep (SWS), are thought to be the most ''restorative.'' There is indeed evidence that SWS plays a role in waking neurobehavioral function (1), particularly in memory consolidation (2, 3), but whether SWS is also important for peripheral physiological function is not known. The initiation of SWS is temporally associated with transient metabolic, hormonal, and neurophysiologic changes, all of which could potentially affect glucose homeostasis. These include decreased brain glucose utilization, stimulation of growth hormone release, inhibition of corticotropic activity, decreased sympathetic nervous activity, and increased vagal tone. We therefore hypothesized that SWS plays a role in glucose regulation and that suppression of SWS may adversely affect glucose homeostasis.To test this hypothesis, we developed an experimental model in young healthy lean individuals that was designed to selectively suppress SWS and assessed the impact of this intervention on glucose homeostasis. The EEG was continuously monitored, and SWS was suppressed by delivering acoustic stimuli of varying frequencies and intensities. The intervention was designed to substitute deep NREM sleep, i.e., stages 3 and 4, with shallow NREM slee...

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“…From a quantitative genetic viewpoint, twin studies in adults have determined that objectively measured sleep characteristics such as the overall EEG spectral composition of non-REM sleep (Ambrosius et al 2008;De Gennaro et al 2008), the proportion of time spent in sleep stage 2 and slow-wave sleep (stages 3 and 4), and the density of REM (rapid eye movement) sleep (Linkowski et al 1991;Linkowski et al 1989) have a strong genetic component. In addition, studies using selfreport data have estimated that around 30-50% of the variance in subjective sleep quality is accounted for by genetic influence Heath et al 1990;Partinen et al 1983).…”

Section: Introductionmentioning

confidence: 99%

Nonshared Environmental Influences on Sleep Quality: A Study of Monozygotic Twin Differences

et al. 2011

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Research has consistently demonstrated that environmental influences are important for explaining the variability in sleep quality observed in the general population. Although there is substantial evidence assessing associations between sleep quality and a host of environmental variables, it is possible that their effects are mediated by genetic influence. A monozygotic twin differences design was used to assess the specific contribution of nonshared environmental influences on sleep quality, whilst controlling for genetic and shared environmental effects in a sample of 380 monozygotic twins (mean age 19.8 years, SD=1.26, range=18-22 years). Participants completed the Pittsburgh Sleep Quality Index and questionnaires assessing several candidate "environmental" measures. When controlling for genetic and shared environmental effects, within monozygotic twin-pair differences in sleep quality were associated with within monozygotic twin-pair differences in general health for males (β=1.56, p<.001) and relationship satisfaction for females (β=1.01, p<.05). For the remaining environmental measures the results suggest that these seemingly "environmental" influences are actually in part dependent on genetics and/or the shared environment. These findings give insight into how specific environments affect sleep and the possible mechanisms behind these associations.

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EEG sleep patterns in man: a twin study

Cited by 78 publications

References 10 publications

Genetics of the human electroencephalogram (EEG) and event-related brain potentials (ERPs): a review

Genetics of the human electroencephalogram (EEG) and event-related brain potentials (ERPs): a review

Slow-wave sleep and the risk of type 2 diabetes in humans

Nonshared Environmental Influences on Sleep Quality: A Study of Monozygotic Twin Differences

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