HANK YOU FOR forwarding to us the letter fromPressman and colleagues (2015) and for inviting ourresponse.The role of alcohol and its impact on sleep has been stud-ied for more than a century, and a substantial knowledgebase has been created. The studies, like most scientific stud-ies, are dependent on the technology available at the timeandtheavailabilityofdata.Thisissomethingwetookintoconsiderationwhenprepar-ing our qualitative review on the impact of alcohol on nor-malsleep.Theissuesraisedcanbesummarizedasfollows:1. The use of percentages to represent the difference inthe mean values of sleep architecture variables in ourtables,2. Our results and conclusions as they pertain to the impactofalcohol onslowwavesleep(SWS),3. Ourinclusion–exclusioncriteriaforstudies,and4. Alcohol, N3, sleepwalking, and medico-legal conse-quences.1. The use of the mean value as a percentage to representsleeparchitecturevariables:1.1. In our article, we made clear how we have presentedthedata:Valuesforsleep architecturevariablesareprovidedinper-centage terms only. Where the researchers have reportedsleep stage data in minutes we have converted these intopercentages. Some variables, such as sleep onset latencyand rapid eye movement onset latency are reported inminutes only. Only the mean value is displayed for allvariables in the tables to enable a uniform approachthroughout(Ebrahimet al.,2013).1.2. This was accepted by the Journal and the peerreviewers as this review was based on highlighting 2specificareas:1.2.1. The impact of various alcohol doses and their tim-ing on nocturnal sleep in healthy controls and nor-mal populations.1.2.2. The impact of these alcohol doses on various sleepstages.1.3. Asthis was a qualitative reviewand not a quantitativemeta-analysis, it was our aim to provide a broadunderstanding to the “nonsleep specialist”readershipoftheimpactofalcoholonsleep.1.4. Furthermore, in routine clinical practice, sleepstages are reported both in actual time and as apercentage of total sleep, a simple difference in themeans between alcohol and placebo nights wasthought to be the best way to demonstrate theeffect.2. Alcohol andSWS:2.1. Alcohol andfirsthalfofnightSWS(N3):2.1.1. Low dose alcohol studies—Of the 4 studiesreported, 2 showed a significant increase in SWS(MacLean and Cairns, 1982; Van Reen et al., 2011)and the other 2 studies failed to find a significantdifference;2.1.2. Moderatedose studies—Ofthe 5 studies reported,2studies demonstrated a significant increase in SWS(Roehrs et al., 1999; Williams et al., 1983). Theother3 studiesfailedtodemonstrateany significantfindings;2.1.3. High dose studies—Five of the 9 studies reported astatistically significant increase in SWS with alco-hol (Arnedt et al., 2011; Feige et al., 2006;MacLean and Cairns, 1982; Prinz et al., 1980; Wil-liams et al., 1983) and 4 studies did not show anysignificantdifferences.The direction of evidence confirms that at low and moder-ate doses alcohol is not clearly associated with increased
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