Original ArticleHow smoking affects sleep: A polysomnographical analysis
Introduction
Studies of large cohorts have shown that smokers have subjectively reduced quality of sleep compared with non-smokers and more insomnia-like symptoms (reduced sleep quality, longer time to fall asleep, less restorative sleep) [1], [2], [3]. Besides a craving for tobacco, nicotine withdrawal can induce not only dysphoria, fear, anhedonia, irritability, restlessness, and increased appetite, but often also remarkable sleep disturbances [4], [5]. Insomnia complaints during nicotine withdrawal are reported in up to 39% of cases [4], [6]. Sleep disturbances in general constitute a risk factor for depressed mood [7], [8], [9] and addiction [10]. Depression in turn is associated with more severe withdrawal symptoms and an increased relapse risk during periods of smoking cessation [11], [12]. It has been assumed that chronic smokers try to control depressive symptoms by smoking. Among other mechanisms this anti-depressive effect could be done by affecting sleep architecture [13], [14].
Sleep is characterized by the dynamic interaction between two states, i.e. non-REM and REM (rapid eye movement) sleep. According to the reciprocal interaction model of McCarley and Hobson [15], REM sleep results from cholinergic stimulation of neurons in the gigantocellular tegmental field, and their activity inhibits non-REM sleep. Nicotine stimulates nicotinic acetylcholine receptors in the brain and results in the release of a variety of neurotransmitters in the brain, most importantly dopamine [16]. Based on these effects nicotine could interact with sleep regulating mechanisms and may affect, for example, sleep efficiency or REM sleep.
Few studies have used PSG methods to investigate sleep changes in smokers. Soldatos et al. [17] found that smokers had longer sleep latency and spent more time awake during the night than non-smokers. These findings were confirmed in a large longitudinal cohort study [18], in which unattended polysomnograms were conducted at home; smokers showed longer sleep latency and REM sleep latency (REM periods occurred later after sleep onset), shorter total sleep time (TST; amount of actual sleep time in a sleep period, i.e. the total sleep period less awake time), and less short wave sleep (SWS) than non-smokers, and reduced sleep efficiency (TST as a percentage of total time spent in bed). A spectral analysis of sleep electroencephalograms (EEGs), which allows a more detailed assessment of the spectral power of several EEG frequencies, showed an increase in α-frequencies (8–12 Hz) and a reduction in δ-frequencies (4–7 Hz) in smokers [19], indicating a reduction of the deeper sleep stages. Methodological differences such as unattended polysomnography (PSG) at home rather than in a sleep laboratory, differences in age and the handling of (psychotropic) medication intake between investigated groups as sleep-influencing parameters make the results of the previous PSG studies hard to compare. Furthermore sleep may also be disturbed by sleep-related breathing disorders such the sleep apnea syndrome, which is found more frequently in smokers [20], [21], and by the restless legs syndrome (RLS), a neurological disorder with periodic leg movements (PLMs) [22] that is also more prevalent in smokers [23]. Only one PSG study has investigated PLMs in smokers and found no differences in RLS and PLMs compared with non-smokers [24].
In the present study, we used PSG to investigate sleep in smokers and non-smokers in a sleep laboratory setting to detect changes in sleep architecture as well as leg movements and breathing abnormalities. We investigated the participants after an adaptation night to minimize first-night effect. We aimed to avoid differences between control and experimental groups by matching by age and sex, and to control most sleep-influencing parameters other than smoking by a careful screening process. Our primary hypothesis was that the sleep of smokers is characterized by an increased frequency of symptoms of insomnia (longer sleep latency, increased number of awakenings, less SWS, shorter TST, worse sleep efficiency), higher REM pressure (measured by REM latency and density), more arousals, more apneas and more leg movements. Therefore subjective sleep quality should be reduced in smokers.
Section snippets
Methods
This comparative, observational study was performed in 2007 and 2008 at the Sleep Center of the Department of Psychiatry and Psychotherapy, Freiburg University Hospital, Germany. We included 44 participants recruited via postings and advertisements who smoked cigarettes daily and had a high level of tobacco dependence, indicated by a Fagerström score (FTND [25]) of ⩾5. An additional diagnosis of tobacco dependence was made according to the DSM-IV criteria [26]. We recruited study subjects aged
Sample characteristics
We screened 55 smokers and identified 44 subjects (29 men and 15 women) who met the inclusion criteria. Eleven smokers were excluded for the following reasons: iron deficiency (two subjects), elevated liver enzymes in laboratory testing (one subject), use of psychotropic medication (two), FTND score <5 (two), withdrawal of consent (three), and working variable shifts (one). More men were recruited than women (29 versus 15). From our database of control subjects, we matched a non-smoking person
Discussion
This study investigated whether cigarette smoking is associated with sleep impairments in an otherwise young and healthy sample of smoking individuals. Other sleep-influencing parameters were controlled for in a standardized way and smokers were compared with age- and sex-matched controls. Insomnia-like sleep changes (increased sleep latency and shorter SPT) were found in smokers. These findings confirm previous polysomnographic studies [17], [18], [19] and reports of subjectively reduced sleep
Funding
This work was supported by the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG; Grant No. RI1565/9-1), within the framework of the national priority program (Schwerpunktprogramm) SPP1226 Nicotine: (www.nicotine-research.com).
Conflicts of interest
The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: doi: 10.1016/j.sleep.2012.06.026.
Acknowledgements
The authors thank Jacquie Klesing, ELS, and James Balmford, PhD for editing assistance with the manuscript.
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