Genetic and Environmental Influences on Daytime and Nighttime Sleep Duration in Early Childhood

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DOI: 10.1542/peds.2012-2284 ; originally published online May 27, 2013; 2013;131;e1874 Pediatrics Montplaisir Pérusse, Bruno Falissard, Richard E. Tremblay, Michel Boivin and Jacques Y. Evelyne Touchette, Ginette Dionne, Nadine Forget-Dubois, Dominique Petit, Daniel Duration in Early Childhood Genetic and Environmental Influences on Daytime and Nighttime Sleep http://pediatrics.aappublications.org/content/131/6/e1874.full.html located on the World Wide Web at: The online version of this article, along with updated information and services, is of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275. Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2013 by the American Academy published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point publication, it has been published continuously since 1948. PEDIATRICS is owned, PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly at Univ De Montreal on July 2, 2013 pediatrics.aappublications.org Downloaded from

Transcript of Genetic and Environmental Influences on Daytime and Nighttime Sleep Duration in Early Childhood

DOI: 10.1542/peds.2012-2284; originally published online May 27, 2013; 2013;131;e1874Pediatrics

MontplaisirPérusse, Bruno Falissard, Richard E. Tremblay, Michel Boivin and Jacques Y.

Evelyne Touchette, Ginette Dionne, Nadine Forget-Dubois, Dominique Petit, DanielDuration in Early Childhood

Genetic and Environmental Influences on Daytime and Nighttime Sleep  

  http://pediatrics.aappublications.org/content/131/6/e1874.full.html

located on the World Wide Web at: The online version of this article, along with updated information and services, is

 

of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2013 by the American Academy published, and trademarked by the American Academy of Pediatrics, 141 Northwest Pointpublication, it has been published continuously since 1948. PEDIATRICS is owned, PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

at Univ De Montreal on July 2, 2013pediatrics.aappublications.orgDownloaded from

Genetic and Environmental Influences on Daytimeand Nighttime Sleep Duration in Early Childhood

WHAT’S KNOWN ON THIS SUBJECT: Sleep patterns of adultmonozygotic twins are more similar than those of dizygotic twins,showing moderate heritability and little effects of environmentalinfluences. There have been very few genetically informativestudies of sleep in preschool children and results appearinconsistent.

WHAT THIS STUDY ADDS: From previous studies, we investigateddaytime and nighttime continuous sleep duration longitudinally.This is the first time that the etiologies of daytime and nighttimecontinuous sleep duration trajectories were studied in earlychildhood.

abstractOBJECTIVES: To determine the relative contributions of genetic andenvironmental factors on daytime and nighttime continuous sleepduration at 6, 18, 30, and 48 months of age, and to identify differentsubgroups of children who followed different daytime and nighttimesleep duration trajectories and to investigate their etiology.

METHODS: The current study included 995 twins (405 monozygotic and586 dizygotic) of the Quebec Newborn Twin Study recruited from thebirth records of the Quebec Statistics Institute. Daytime and nighttimesleep was assessed through maternal reports at 6, 18, 30, and 48months of age. A semiparametric modeling strategy was used to es-timate daytime and nighttime sleep duration trajectories. Quantitativegenetic models were used to examine to what extent genetic and en-vironmental factors influenced daytime and nighttime continuoussleep duration.

RESULTS: Genetic modeling analyses revealed environmental influen-ces for all daytime sleep duration trajectories. In contrast, strong ge-netic influences were found for consolidated nighttime sleep duration(except at 18 months and for the short-increasing sleep durationtrajectory).

CONCLUSIONS: This is the first indication that early childhood daytimesleep duration may be driven by environmental settings, whereas thevariance in consolidated nighttime sleep duration is largely influencedby genetic factors with a critical environmental time-window influenceat ∼18 months. Pediatrics 2013;131:e1874–e1880

AUTHORS: Evelyne Touchette, PhD,a,b Ginette Dionne, PhD,a

Nadine Forget-Dubois, PhD,a Dominique Petit, PhD,c DanielPérusse, PhD,d Bruno Falissard, MD, PhD,b Richard E.Tremblay, PhD,e,f,g,h Michel Boivin, PhD,a and Jacques Y.Montplaisir, MD, PhDc,i

aResearch Unit on Children’s Psychosocial Maladjustment, LavalUniversity, Québec, Canada; bINSERM U669, Université Paris-Sudand Université Paris-Descartes UMR-S0669, Paris, France; cCenterfor Advanced Research in Sleep Medicine, Sacré-Coeur Hospital,Montreal, Canada; eResearch Unit on Children’s PsychosocialMaladjustment, Departments of dAnthropology, gPediatrics andPsychology, and iPsychiatry, University of Montreal, Montréal,Canada; fResearch Centre, Ste-Justine Hospital, Montreal,Canada; and hSchools of Public Health, Physiotherapy, andPopulation Science, University College Dublin, Dublin, Ireland

KEY WORDSsleep duration, genetic and environmental interplay, earlychildhood, twin study

ABBREVIATIONSBIC—Bayesian information criterionDZ—dizygoticMZ—monozygotic

Dr Touchette conceptualized the paper, analyzed/interpreted thedata, and drafted the initial manuscript; Dr Dionneconceptualized and designed the study, interpreted the data,and drafted the initial manuscript; Dr Forget-Dubois carried outthe genetic analyses and critically reviewed the manuscript; DrsPetit, Falissard, and Tremblay critically reviewed the manuscript;Dr Pérusse conceptualized and designed the study; Dr Boivincoordinated and supervised data collection and criticallyreviewed the manuscript; Dr Montplaisir elaborated the sleepmeasures and critically reviewed the manuscript; and allauthors approved the final manuscript as submitted.

www.pediatrics.org/cgi/doi/10.1542/peds.2012-2284

doi:10.1542/peds.2012-2284

Accepted for publication Feb 11, 2013

Address correspondence to Jacques Y. Montplaisir, MD, PhD,Center for Advanced Research in Sleep Medicine, Sacré-CoeurHospital, 5400 Gouin Blvd West, Montreal, Quebec, Canada, H4J1C5. E-mail: [email protected]

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright © 2013 by the American Academy of Pediatrics

FINANCIAL DISCLOSURE: The authors have indicated they haveno financial relationships relevant to this article to disclose.

FUNDING: The Quebec Newborn Twin Study was supported bygrants from the Canadian Institutes of Health Research, SocialSciences and Humanities Research Council of Canada, CanadaResearch Chair Program, Canadian Institute of AdvancedResearch, National Health Research and Development Program,Quebec Research Funds (FCAR, FQRSC, and FRSQ), QuebecMinistries of Health, Social Services and Families, Lucie andAndré Chagnon Foundation, Ste-Justine Hospital, University ofMontreal, and Laval University.

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Although environmental factors caninfluence sleep duration and quality, itis now known that differences in sleepbehaviors depend largely on geneticvariance among individuals. First, thefindings of stronggenetic contributionsto many sleep-related disorders (eg,narcolepsy, idiopathic hypersomnia,insomnia, restless legs syndrome,sleepwalking, sleep terrors, sleepbruxism,enuresis, sleepapnea,delayedsleep phase syndrome) (for review, seeref 1) provided convincing indications.Then, the discovery of clock genes thatregulate the circadian timing of sleepand wakefulness (for review, see ref 2)and of genes that account for the ho-meostatic process of sleep (forreviews, see refs 3 and 4) dramaticallychanged the backdrop for the study ofsleep.

A review of the relative contributions ofgenetics and environmental factors tosleep patterns and sleep behaviors inadults, obtained through twin studies,demonstrated a moderate heritability(∼30% to 44%) for sleep duration andlittle effect of shared environmentalinfluences (for review, see ref 1). Ininfants, however, our group found thatheritability explained the greater pro-portion of the variance on a day/nightsleep ratio at 6 months (64%), whereasthe variance was mainly explained byshared environment influences at 18months (58%).5 Another study of 18-month-old twins found a strong con-tribution of shared environmentalfactors for both nighttime sleep dura-tion (64%) and daytime sleep (61%),with a moderate contribution of addi-tive genetic effects (31% and 36%, re-spectively).6 This was supported bya recent and very large study of 15-month-old twins; the shared environ-ment influence was predominant forboth nocturnal (66%) and diurnal(57%) sleep and the genetic effect wasmodest (26% and 37%, respectively).7

Finally, 2 twin studies concluded that

the genetic contributions to sleep pat-terns and sleep problems of pre-adolescents and adolescents wereclose to those found in adults8,9

The etiology of daytime and nighttimesleep duration in early childhood differfrom that of adults for many reasons.First, sleep consolidation goes throughmajor changes in childhood beforereaching adult sleep patterns. New-borns follow a mostly ultradian cycle,with periods of 3 to 4 hours of sleepspread out across day and night. By 2 to4 months, a circadian rhythm starts toemerge, with most sleep occurringduring the night. Daytime sleepbecomes well-defined naps: 2 to 3 napsper day until age 6 months (3.5 hourstotal), followed by 2 naps per day at∼9to 12 months, and finally, 1 nap in theafternoon after 18 months (2.5 hours)up to age 3.10 Approximately 68% ofchildren have stopped taking a nap byage 4.10 Consolidated nighttime sleepduration increases considerably frombirth to adolescence, when it reachesadult sleep patterns, but substantialindividual variability remains at allages.11,12 Second, sleep-wake periodsare regulated by 2 processes that ma-ture from birth: (1) sleep homeostasis(Process S), by which sleep pressureincreases during wakefulness anddissipates during sleep and (2) circa-dian rhythmicity (Process C), whichshows a wakefulness propensity asa sinus function over a 24-hour pe-riod.13 The progressive development ofthese sleep processes could explainwhy childhood sleep patterns differfrom adult ones.14 Third, there areindications that parental practicesaround the sleep periods of youngchildren affect the latter. Putting chil-dren to bed while they are dozy butstill awake was found conducive todeveloping appropriate sleep-onsetassociations.15,16 Conversely, the needfor parental presence until sleep onsetis considered as a protodyssomnia,

a potential precursor of later sleepproblems.17 Variations in sleep con-solidation during early childhood couldthus be the result of family-basedroutines.

Because the maturation of daytime andnighttime sleep changes throughoutearly childhood, we first aimed to de-termine the relative contributions ofgenetic and environmental factors onthese sleep phenotypes at 6, 18, 30, and48 months of age in a sample of twins.Rather than assume that all childrenfollow the samedevelopmental daytimeand nighttime patterns of sleep overtime, the second objective of this studywas to identify different subgroups ofchildrenwho followeddifferentdaytimeand nighttime sleep duration trajecto-ries and to investigate their etiology.

METHODS

Study Design

Data were collected as part of theQuebec Newborn Twin Study18 ona population-based sample of 1392twins (696 families) born betweenNovember 1995 and July 1998 in thegreater Montreal Area (Canada).Infants had to be born without majormedical conditions, had to have avail-able birth records at the Quebec Sta-tistics Institute, and their mother hadto be fluent in either French or English.A 2-week interval separated the twins’assessments to minimize the homog-enization of answers as much aspossible. Families received detailedinformation by mail on the aims andprocedures of the research programand signed a consent form beforeeach data collection.

Participants

The analyses presented here are basedon data gathered during 4 times ofassessments (at 6, 18, 30, and 48months of age) of daytime and night-time continuous sleep duration. Data

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were available for 983 individual chil-dren (397 monozygotic [MZ], 582 di-zygotic [DZ], and 4 children whosezygositywasmissing; boys=478, girls =505) for both daytime and nighttimecontinuous sleep trajectories. Cor-rected age (for gestational age) at thetargeted 6-, 18-, 30-, and 48-monthassessments were as follows: 5.41months (SD = 0.52), 18.64 months (SD =0.60), 30.96 months (SD = 0.79), and49.31 months (SD = 1.76). The meangestation duration of the presentsample (n = 983) was 36.14 weeks(SD = 2.52). Based on a full-term cri-terion of 37 weeks, 484 twins (49.2%)were born premature. Mean birthweight was 2459 g (SD = 543 g), mean 1minute Apgar scores were 8/10 (SD =1.6), and mean number of days spent inthe hospital after birth was 9.4 (SD =12.9); 47.2% of twins were born by ce-sarean delivery. Mean age of mothersat delivery was 30.7 years (SD = 4.7),15.4% had no high school diploma, av-erage family income was between CAD$40 000 and CAD$50 000 per year, and∼5% of the twins were born to singlemothers. The first language of themother was French for 78.6% ofinfants, English for 10.0%, both for4.9%, and other than French or Englishfor 6.5%.

Measures

Zygosity

Zygosity was determined on physicalresemblance using the Zygosity Ques-tionnaire for Young Twins.19 At 18months, zygosity was confirmed withDNA analysis of 8 to 10 highly poly-morphous genetic markers on half thesample (n = 237 pairs) for same-sextwin pairs. This concordance rate(94%) was obtained after a case-by-case assessment of each pair’s physi-cal similarity using a shortenedversion of the Zygosity Questionnairefor Young Twins, which is similar torates in other twin samples.20 Uncertain

zygosity diagnoses were periodicallyreevaluated based on the assessmentof physical similarity by interviewersand genetic markers whenever possi-ble.

Measures of Infant SleepCharacteristics

The Self-Administered Questionnairefor the Mother, which took about 20minutes to complete, provided in-formation on the infant’s sleep char-acteristics, such as the number ofconsecutive hours slept in general perday and per night. As previously de-scribed in the methodology of anotherstudy,21 the number of consecutivehours of sleep during daytime ornighttime was obtained through ma-ternal reports, with the question: “Ingeneral, how many uninterruptedhours does your baby/twin sleep dur-ing the day or at night?” The duration ofcontinuous sleep during nighttime wasassessed in rounded hours rangingfrom ,4 hours to $8 hours at 6months and up to $10 hours (whichwe considered to be 11 hours) at otherages. The duration of the longest con-tinuous sleep period during daytimewas assessed in rounded hours rang-ing from the following: does not nap(0), #1, .1 hour to ,2 hours, .2hours to ,3 hours, .3 hours to ,4hours, and $4 consecutive hours. The“less than” and “more than” categorieswere rounded to the next whole value,as previously done in the same twincohort.5 The terms “consolidated” or“continuous” do not imply the absenceof brief awakening episodes. It simplymeans that the child did not signal anyawakening to the parents, and thuswas able to self-soothe and rapidly goback to sleep. Indeed, it was shownusing video recordings that even the“good sleepers/nonsignalers” woke upon average 3 times per night betweenthe ages of 1 and 3.22 However, it wasalso revealed that signalers were

losing on average 1 hour and 22minutes of sleep per night comparedwith nonsignalers.16

Statistical Analyses

Analyses of Transversal Twin Data

Analyses of twin data are based on thecomparison of the covariance betweenMZ twins and DZ twins, knowing thecoefficient of genetic relatedness,which is 1.0 forMZ twins andonaverage0.5 for DZ pairs. It is hypothesized thata higher within-pair correlation in MZreflects a genetic influence on thevariance of the phenotype under study,assuming that the environment ofboth types of twins is equally similar.The phenotypic variance that is notexplained by genetic variance is at-tributed to the environmental variance,either common (the environmentalinfluences that make twins more alike)or unique (the environmental influen-ces that make twins more different;this portion includes the measurementerror). We analyzed the within-pair co-variance at 6, 18, 30, and 48 months ofage to estimate genetic and environ-mental contributions to the variance indaytime and nighttime continuous sleepduration. We used the Full InformationMaximum Likelihood estimation pro-cedure, which fits the testedmodel to allnonmissingdata forall participants, andis the default estimator in the statisticalpackage Mx. Full Information MaximumLikelihood with missing data at randomhas been shown to produce accurateparameter estimates.23

Sleep Trajectories

Rather than assume that all childrenfollow the same developmental patterndaytime and nighttime sleep durationover time, a semiparametricmodelwasused to identify subgroups of childrenwho followed different developmentalsleep duration trajectories using PROCTRAJ, a package of SAS (SAS InstituteInc, Cary, NC).24 Briefly, trajectory

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methodology uses all available de-velopmental data points and assignsindividuals to trajectories based ona posterior probability rule. We chosethe model that permitted the inclusionof the greater number of subjects (upto 2 missing data points out of 4 areallowed). The best model, with the op-timal number of groups and slopesthat best fit the longitudinal data, wasidentified based on the Bayesian in-formation criterion (BIC).

To estimate the genetic and environ-mental etiology of both daytime andnighttime continuous sleep durationtrajectories, we analyzed the concor-dance of twin pairs in trajectorymembership, represented by thewithin-pair tetrachoric correlation co-efficient. For each model fitted, mem-bership to a given trajectory wasdichotomized into (0) not a member ofthis trajectory and (1) a member of thistrajectory. The genetic analysis of or-dinal data assumes an underlying

normal distribution and estimates thethresholds on the hypothesized normaldistribution corresponding to the pro-portions of participants in the 2 cate-gories (in the trajectoryornot). Equalityof thresholds is assumed between MZand DZ twins. All analyses were con-ducted by using raw data to maximizepower and treat missing data appro-priately.23

RESULTS

Genetic and EnvironmentalInfluences of Daytime andNighttime Sleep Duration

Becauseof thesmallNandresulting lowpower, we reported only the full geneticACE (A, additive genetic component ofvariance; C, shared environmentalcomponent of variance; E, unique en-vironmental component of variance)models anddidnot attempt to testmoreparsimonious nested models. All mod-els showed adequate fit when com-

pared with their respective saturatedmodels, except for the 30-monthnighttime continuous sleep duration.Table 1 shows that as the childbecomes a toddler, shared environ-mental influences explain a largerproportion of variance in daytime sleepduration (18 months = 33%, 30 months= 48%, and 48 months = 79%). In con-trast, strong genetic influences werefound for nighttime sleep duration at 6months (47%), 30 months (58%), and48 months (54%); however, we ob-served a strong shared environmentaleffect (on nighttime sleep duration at18 months (48%).

Sleep Duration Trajectories

Daytime continuous sleep duration wasmoderately stable across ages (r =0.20–0.25; all correlations significant atP , .001). The best-fitting and mostparsimoniousmodel was a 3-trajectorymodel (BIC = –3262.20) in which 2 tra-jectories had a quadratic shape and 1

TABLE 1 Genetic and Environmental Influence on Infant Daytime and Nighttime Sleep in the Quebec Newborn Twin Study

Within-PairCorrelations

Variance Components Model Fit

MZ DZ A (95% CI) C (95% CI) E (95% CI) x2 df P

Daytime continuous sleep duration6 moa 0.67 0.47 0.32 (0.10–0.54) 0.33 (0.14–0.50) 0.35 (0.28–0.44) 4.98 4 .2918 moa 0.55 0.47 0.26 (0.00–0.52) 0.33 (0.11–0.52) 0.41 (0.33–0.52) 6.68 4 .1530 moa 0.63 0.54 0.15 (0.00–0.39) 0.48 (0.27–0.63) 0.37 (0.29–0.48) 1.28 4 .8748 moa 0.94 0.86 0.15 (0.08–0.24) 0.79 (0.70–0.84) 0.06 (0.04–0.08) 1.19 4 .88Trajectoriesb,c

Rapidly decreasing daytime sleepd 0.99 0.99 0.01 (0.00–0.44) 0.98 (0.84–1.00) 0.01 (0.01–0.05) 3.36 3 .34Normally decreasing daytime sleep 0.75 0.72 0.04 (0.00–0.43) 0.70 (0.38–0.82) 0.26 (0.14–0.38) 2.24 3 .52Slowly decreasing daytime sleep 0.71 0.66 0.08 (0.00–0.54) 0.62 (0.24–0.78) 0.29 (0.16–0.44) 1.79 3 .62

Nighttime continuous sleep duration6 moa 0.65 0.47 0.47 (0.25–0.69) 0.22 (0.02–0.39) 0.31 (0.25–0.40) 3.91 4 .4218 moa 0.67 0.58 0.20 (0.00–0.40) 0.48 (0.30–0.64) 0.32 (0.26–0.41) 1.15 4 .8830 moa,e 0.67 0.26 0.58 (0.28–0.69) 0.04 (0.00–0.30) 0.38 (0.31–0.47) 21.23 4 .0048 moa 0.72 0.42 0.54 (0.25–0.77) 0.17 (0.00–0.41) 0.29 (0.22–0.39) 2.76 4 .60Trajectoriesb,c

Short-increasing nighttime sleepd 0.80 0.74 0.00 (0.00–0.69) 0.73 (0.13–0.87) 0.27 (0.09–0.48) 3.96 3 .27Short-persistent nighttime sleepd 0.95 0.57 0.71 (0.09–0.99) 0.22 (0.00–0.76) 0.07 (0.01–0.25) 3.89 3 .2710-h nighttime sleep 0.84 0.56 0.58 (0.24–0.90) 0.27 (0.00–0.55) 0.15 (0.08–0.27) 1.46 3 .6911-h nighttime sleep 0.91 0.67 0.48 (0.21–0.77) 0.43 (0.15–0.66) 0.09 (0.04–0.17) 2.71 3 .44

x2 represents the difference between the –2LL of the ACE model and the saturated model. Nonsignificance indicates a good fit. A, additive genetic component of variance; C, sharedenvironmental component of variance; CI, confidence interval; E, unique environmental component of variance.a Intraclass correlations with 95% CIs.b Concordance rates.c Tetrachoric correlations.d Less than 5% of the sample in this category.e Assumption of equality of variance between MZ and DZ twins not respected.

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had a linear shape. A small proportionof children (4.3%) were in the “rapidlydecreasing daytime sleep duration”trajectory. Most children (75.7%) werein the “normally decreasing daytimesleep duration” trajectory. The remain-ing 20% of the children were in the“slowly decreasing daytime sleep du-ration” trajectory (see Fig 1A).

Nighttime continuous sleep durationwasmoderately stable across ages (r =0.31–0.40; all correlations significant atP , .001). The best-fitting and mostparsimoniousmodel was a 4-trajectorymodel (BIC = –4539.1) in which eachtrajectory had a quadratic shape.Small proportions of children were inthe “short-persistent nighttime sleepduration” trajectory (4.9%) and in the“short-increasing nighttime sleep du-ration” trajectory (4.6%). Most children

were in the “10-hour nighttime sleepduration” trajectory (47.6%) and the“11-hour nighttime sleep duration”trajectory (42.8%) of the sample (seeFig 1B).

Genetic and EnvironmentalInfluences of Sleep DurationTrajectories

All genetic-environmental models ofdaytime and nighttime sleep trajecto-ries showed adequate fit when com-pared with their respective saturatedmodel. The full genetic-environmentalmodels showed strong common andunique environment influences for alldaytime sleep duration trajectories,and no variance was attributed to ge-netic factors. In contrast, the modelsshowed strong heritability for the var-iance in the nighttime short-persistent

sleep and 10-hour sleep trajectories.A combination of genetic and commonenvironment influences was found forthe 11-hour sleep trajectory. Finally,only common and unique environmentaccounted for the variance in the short-increasing sleep trajectory.

DISCUSSION

Toour knowledge, this is thefirst articleto investigate daytime sleep durationlongitudinally. These results illustratea decrease of daytime sleep durationwhen the child grows up. However, wefound a lower prevalence of childrenwho had stopped taking a nap by age 4years (4.3%) compared with thatreported by an Italian study (68.0%)10;this could be explained by differentcultural influences. Indeed, we foundthat all patterns of daytime sleep du-ration are strongly influenced byshared environmental factors, asshown by Brescianini and colleagues6

and by Fisher and colleagues.7

The consolidated nighttime sleep du-ration trajectories of the present twinstudy replicated the number andshapesofothersleep trajectories foundin a sample of singletons from theprovince of Quebec.21 We found thatconsolidated nighttime sleep durationis largely influenced by genetic factors(at 6, 30, and 48 months) with a criticalenvironmental time-window influenceat ∼18 months. To our knowledge, 2other infant twin studies have demon-strated the strongest shared environ-mental influence on nighttime sleepduration at 18 months (64%6 and 66%7

compared with 48% in our study). Thecurrent study corroborates this im-portant consistency. At 18 months, itcould suggest a good timing for pa-rental interventions on nighttimesleep.

A strong heritability (71%) was ob-served for the short-persistent night-time sleep duration trajectory. A studyinvestigating specific genes observed

FIGURE 1A, Daytime continuous sleep duration trajectories at 6, 18, 30, and 48months of age (n=983)::: rapidly-decreasing daytime sleep (n = 42; 4.3%),d: normally decreasing daytime sleep (n = 744; 75.7%), and♦:slowly decreasing daytime sleep (n = 197; 20.0%). B, Nighttime continuous sleep duration trajectoriesat 6, 18, 30, and 48 months of age (n = 995)::: short-persistent nighttime sleep (n = 49; 4.9%), n: short-increasing nighttime sleep (n = 46; 4.6%),d: 10-hour nighttime sleep (n = 474; 47.6%), and ♦: 11-hournighttime sleep (n = 426; 42.8%).

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a –263G/C single nucleotide poly-morphism responsible for the cyclicproduction and secretion of melatoninin 4 of 5 short sleepers, but in only 1 of5 long sleepers.25 By contrast, theshort-increasing nighttime sleep du-ration trajectory did not appear highlyheritable. Children following this tra-jectory may be more likely influencedby environmental factors (73%). Futurestudies should aim at clarifying whichenvironmental factors influence thelikelihood of belonging to this trajec-tory. We could hypothesize that thesechildren were more likely to be influ-enced by transient disruptive environ-mental factors, such as inadequateparental behaviors surrounding sleepperiods, and returned to their bi-ologically determined sleep consolida-tion thereafter. For the 10-hour sleepduration trajectory, we found a stron-ger genetic role (58%) than sharedenvironmental influence (27%). Finally,for the 11-hour sleep duration trajec-tory, we observed a more balancedgenetic role (48%) and environmentalinfluence (43%). Like Fisher et al,7 wefound that a very small proportion ofthe variance was attributable to uniqueenvironment, a term that includesmeasurement error.

This study has a number of strengths,including the use of a relatively largesample of twins and of longitudinalassessments of daytime and nighttimecontinuous sleep in early childhood.

One limitation important to mention isthat the twin similarity may have beeninflated by the recourse to a single in-formant for both twins of each pair,leading, in turn, to inflated heritabilityand shared environment estimates,even though the questionnaire for thesecond twinwas filled out 2weeks afterthat for the first twin. Another impor-tant limitation is the use of ordinalcategories for daytime and nighttimesleep duration. This study needs to bereplicated with quantitative sleep meas-ures (actigraphy or polysomnography)to minimize informant bias and reducethe limitations induced by ordinal cate-gories of daytime and nighttime sleepduration. In addition, one has to keep inmind that sleep is more fragmentedthan parents are aware of; however,brief awakenings are normal and, thus,the analysis of pure sleep consolidationis not what was targeted here. Finally,one of the genetic models, the 30-monthnighttime continuous sleep duration ACEmodel, did not meet the assumption ofequality of variance between MZ and DZtwins and should be interpreted withcaution.

CONCLUSIONS

This study is the first to show thatdaytime sleep duration in early child-hood is strongly influenced by en-vironmental factors. In contrast,consolidated nighttime sleep duration

is largely influenced by genetic factorswith a critical environmental time-window influence at ∼18 months. Therole of genetic factors was especiallyevident for the short-persistent sleepduration trajectory. Results need to bereplicated with objective sleep meas-ures and more studies are needed toidentify the biological mechanismscontributing to short-persistent night-time sleep duration in early childhood.Future studies will be needed to un-derstand which family settings seem toplay a role in daytime sleep durationduring early childhood. Future inves-tigations will also be needed to identifythe genetic mechanisms contributingto short-persistent nighttime sleepduration in early childhood and beyondto promote the development of ade-quate treatment modalities.

ACKNOWLEDGMENTSWe thank the children and familieswhose ongoing participation made thisstudy possible. We acknowledge theconsiderable contribution of the studycoordinator, Jocelyn Malo, and thetireless work of interviewers whoassessed the subjects during thecourse of this study. We are thankfulto Hélène Paradis for her valuablestatistical expertise. The first authorhad full access to all of the data inthe study and takes responsibility forthe integrity of the data and the accu-racy of the data analysis.

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DOI: 10.1542/peds.2012-2284; originally published online May 27, 2013; 2013;131;e1874Pediatrics

MontplaisirPérusse, Bruno Falissard, Richard E. Tremblay, Michel Boivin and Jacques Y.

Evelyne Touchette, Ginette Dionne, Nadine Forget-Dubois, Dominique Petit, DanielDuration in Early Childhood

Genetic and Environmental Influences on Daytime and Nighttime Sleep  

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