Prather Sleep Protects Again Common Cold
Sleep. 2015 Sep 1; 38(ix): 1353–1359.
Behaviorally Assessed Slumber and Susceptibility to the Cold
Aric A. Prather
oneDepartment of Psychiatry, Academy of California, San Francisco, CA
Denise Janicki-Deverts
iiDepartment of Psychology, Carnegie Mellon University, Pittsburgh, PA
Martica H. Hall
threeDepartment of Psychiatry, University of Pittsburgh Medical Heart, Pittsburgh, PA
Sheldon Cohen
2Department of Psychology, Carnegie Mellon University, Pittsburgh, PA
Received 2014 Oct; Revised 2014 Dec; Accustomed 2015 Jan.
Abstruse
Written report Objectives:
Short slumber duration and poor sleep continuity have been implicated in the susceptibility to infectious illness. However, prior inquiry has relied on subjective measures of slumber, which are bailiwick to call up bias. The aim of this study was to determine whether slumber, measured behaviorally using wrist actigraphy, predicted cold incidence following experimental viral exposure.
Design, Measurements, and Results:
A total of 164 healthy men and women (age range, 18 to 55 y) volunteered for this study. Wrist actigraphy and sleep diaries assessed sleep duration and sleep continuity over 7 consecutive days. Participants were and then quarantined and administered nasal drops containing the rhinovirus, and monitored over five days for the development of a clinical cold (defined by infection in the presence of objective signs of affliction). Logistic regression analysis revealed that actigraphy- assessed shorter sleep duration was associated with an increased likelihood of development of a clinical common cold. Specifically, those sleeping < 5 h (odds ratio [OR] = 4.50, 95% confidence interval [CI], one.08–18.69) or sleeping between v to 6 h (OR = 4.24, 95% CI, one.08–xvi.71) were at greater risk of developing the cold compared to those sleeping > seven h per night; those sleeping vi.01 to seven h were at no greater risk (OR = 1.66; 95% CI 0.40–6.95). This clan was independent of prechallenge antibiotic levels, demographics, season of the year, body mass index, psychological variables, and wellness practices. Sleep fragmentation was unrelated to cold susceptibility. Other sleep variables obtained using diary and actigraphy were non strong predictors of cold susceptibility.
Conclusions:
Shorter slumber duration, measured behaviorally using actigraphy prior to viral exposure, was associated with increased susceptibility to the common cold.
Citation:
Prather AA, Janicki-Deverts D, Hall MH, Cohen South. Behaviorally assessed slumber and susceptibility to the common cold. SLEEP 2015;38(ix):1353–1359.
Keywords: common cold, immunity, rhinovirus, sleep continuity, sleep duration
INTRODUCTION
Growing evidence demonstrates that short sleep duration (< 6 or vii h/night) and poor slumber continuity are associated with the onset and development of a number of chronic illnesses,i–4 susceptibility to astute infectious illness,5–7 and premature mortality.8–11 Experimental prove in animals and humans suggests that the immune system serves as a key biological pathway.12–14 For instance, total and partial slumber impecuniousness in humans results in modulation of immune parameters disquisitional to host resistance, including macerated T cell proliferation,15 shifts in T helper prison cell cytokine responses,sixteen,17 decreases in natural killer (NK) prison cell cytotoxicity,18,19 and increased activation of proinflammatory pathways.xx–23
Slumber related modulation of the immune system is besides observed when slumber is measured in the natural environment, with implications for clinical outcomes.6,24 We recently reported that short sleep duration and poor sleep continuity, measured past sleep diary over xiv sequent days, predicted the incidence of developing a biologically verified common cold following viral exposure.six I of the limitations of this prior written report was a reliance on self-reported sleep, which is subject to call up bias leading to inaccurate sleep estimates. Indeed, individuals often overestimate duration and underestimate minutes awake across the dark.25 Whether objectively measured sleep indices represent significant predictors of acute infectious affliction post-obit viral exposure remains unknown.
To address this gap in the literature, the current study measured sleep behavior objectively using wrist actigraphy and subjectively using slumber diaries over 7 consecutive days and investigated whether measures of sleep duration and continuity predicted susceptibility to the common cold in participants afterward exposed to a virus (rhinovirus) that causes the common cold. Following exposure to the common cold virus, participants were quarantined and monitored for cold symptoms and evolution of clinical affliction. We hypothesized that shorter sleep duration and poorer sleep continuity would be associated with increased incidence of a biologically verified cold and that these associations would be independent of sociodemographic, psychological, and behavioral factors previously shown to predict common cold incidence using this paradigm.six,7,26–28
METHODS
Participants
Data were nerveless between 2007 and 2011. Study participants for these analyses included 94 men and 70 women, anile between 18 and 55 y (mean age = 29.9, standard deviation [SD] = 10.9) from the Pittsburgh, Pennsylvania metropolitan expanse who responded to study advertisements and were judged to be in good health. Volunteers were excluded if they had a history of nasal surgery or whatever other chronic disease (e.m., asthma, coronary heart disease, or obstructive sleep apnea); abnormal findings based on urinalysis, complete claret count, or claret enzyme levels; were meaning or currently lactating; were positive for the human immunodeficiency virus; or taking medications regularly, including sleep medications and oral contraceptives. They were too excluded if they had been hospitalized in the by 5 y or were currently taking medications for psychiatric atmospheric condition. In social club to maximize the rate of infection by the virus, specific levels of serum antibody to the challenge virus were obtained at screening and participants were excluded with titers higher than four. Each participant was paid $1,000 for their participation at the conclusion of the study. This study received institutional review lath approval, and written, informed consent was obtained for each report participant.
Procedures
Volunteers presenting for possible enrollment underwent medical screening, including a blood draw to appraise specific serum neutralizing antibody titer for rhinovirus 39 (RV39). Qualifying participants were enrolled and during the approximately 2 mo that preceded viral claiming they completed questionnaire batteries, ii w of daily interviews to assess positive emotions, and a subsequent 1 w of wrist actigraphy and concurrent slumber diary to considerately and subjectively measure sleep beliefs. Another sample of claret was collected to assess antibody level just before (three–5 days) viral exposure, which provided an estimate of prechallenge antibody titers.
Participants were and so isolated in a local hotel for a 6-solar day flow. During the first 24 h of the quarantine, prior to viral exposure, participants underwent a nasal examination and nasal lavage; baseline nasal mucociliary and nasal mucus product were assessed at this time. Those showing signs or symptoms of a cold on this day were dismissed. Then, participants received nasal drops containing approximately 150 tissue culture infectious dose (TCID50)/mL of RV39. Volunteers were subsequently quarantined for 5 days. On each twenty-four hour period, nasal lavage samples were collected to assess infection (virus civilization). Additionally, daily nasal mucociliary clearance function and nasal mucus production were assessed as objective markers of illness. Approximately 28 days after viral exposure, blood was nerveless for serological testing.
Slumber Measures
Participants wore an Actiwatch-(64) (Philips Respironics Inc, McMurray, PA) on their nondominant wrists for 7 consecutive nights. Data were stored in 1-min epochs and validated software algorithms (Philips Respironics Inc) were used to approximate sleep parameters. The two actigraphy variables included in these analyses were full sleep fourth dimension and fragmentation index. Total slumber time, which was used to estimate sleep duration, was divers as the total amount of minutes scored every bit sleep by the software algorithm in a given defined sleep interval. Fragmentation index is a measure of restlessness during sleep every bit measured past sleep epochs associated with motility (range 0 to 150, with higher values indicating poorer sleep continuity). Equally expected, actigraphy-assessed sleep efficiency, defined every bit the percentage of the slumber interval scored as sleep, was inversely correlated with fragmentation index in this sample (r = −0.59, P < 0.001). We chose fragmentation alphabetize instead of sleep efficiency given the documented poor specificity associated with actigraphy-assessed sleep efficiency.29
Self-written report sleep diaries were obtained concurrently with actigraphy collection. Each morn, participants reported in their sleep diary what fourth dimension they went to sleep, what time they woke upwardly, and the min it took to autumn asleep. Sleep time was calculated as the time a participant reported waking up minus the time the participant went to sleep. Self-reported sleep duration was computed by sleep fourth dimension minus the minutes required to fall comatose. Sleep efficiency was calculated equally sleep duration divided by sleep time multiplied past 100. Actigraphy and diary estimates for sleep (actigraphy: sleep duration and fragmentation; sleep diary: sleep elapsing and slumber efficiency) were obtained by averaging over the collection period for all participants with data for at least 5 of the 7 days.
Command Variables
Nosotros controlled for a number of covariates previously associated with susceptibility to the common common cold, including pre-challenge viral-specific antibody levels to RV; age; sex; race; torso mass index (BMI); the flavor in which the trial occurred; years of instruction; household income, health habits including current smoking status, physical activity, and booze consumption; and psychological variables including perceived socioeconomic status, perceived stress, extraversion, conjuration, and positive emotional way. These covariates were assessed either during eligibility screening or in the interval between screening and the viral challenge.
Participants self-reported their age, sex, and race. They described their primary racial and ethnic grouping past choosing from half-dozen categories (white, Caucasian; black, African American; Native American, Eskimo, Aleut; Asian or Pacific Islander; Hispanic, Latino; Other). For the analyses, the racial or ethnic groups were dummy coded, with all simply whites and blacks collapsed into a single "other" category. BMI (weight in kg/superlative in mii) was computed based on measurements of participants' weight and height.
Income was assessed by having participants endorse i of 13 household income categories (before taxes) that best represented them. These categories ranged from less than $5,000 to $150,000 or more; income was defined as the median income for the identified category and treated as a continuous variable. Participants' teaching was assessed past asking them to study on their highest educational attainment. Nine response items were provided, ranging from "didn't stop high school" to "doctoral degree." Answers were converted into number of years of didactics based on their responses (e.g., high school, 12 y; PhD, 20 y). Perceived socioeconomic rank was assessed by participants placing themselves on a nine-rung of a ladder in terms of where they stand up in their state based on income, educational activity, and occupation.26
Health habits were obtained through cocky-report questionnaires. Participants were deemed current smokers if they answered "aye" to beingness asked whether they currently smoked cigarettes, cigars, or pipes on a daily footing. Physical activeness was assessed past asking participants whether they engaged in regular activeness at to the lowest degree once per calendar week (1, yes; 0, no). Alcohol consumption was obtained by request participants the average number of drinks they consumed per day (one drink = one glass of wine, 12 oz of beer, or one shot of hard liquor).
Psychological variables that were assessed by questionnaire included a 10-item perception of stress over the past month30; extraversion and conjuration were assessed using the 10-item versions from the International Personality Particular Pool (IPIP) Big Five Cistron Markers.31 Finally, positive emotional style was measured as part of an evening interview assessment that was conducted over 14 sequent days. During each of the fourteen daily interviews participants reported the extent to which they felt happy, calm, lively, total of pep, and cheerful throughout the preceding twenty-four hour period; ratings for each item were averaged to create a daily total positive touch score across the interview catamenia.27
Virus Culture and Antibiotic Response
Virus-specific neutralizing antibody titers were measured in serum samples obtained before and approximately 28 days afterward viral exposure. The results were expressed as reciprocals of the final dilution of serum.32 Daily nasal lavage samples were frozen at −80°C and after cultured for RV using standard techniques.32
Signs of Disease
Daily fungus production was obtained by collecting used tissues in sealed plastic bags.33 The bags were weighed and the weights of the tissues and bags were subtracted. Nasal mucociliary clearance part was measured by administering a dye into the anterior expanse of the nose and computing the time taken for the dye to reach the nasopharynx.33
Clinical Cold Criteria
Study participants were considered to have a clinical cold if they were both infected and met illness criteria. Infection was divers as the recovery of the challenge virus on whatever of the postchallenge days or a fourfold or greater increase in the virus-specific serum neutralizing antibody titer measured pre-exposure to 28 days post-exposure.33 Affliction criterion for an objective cold required a total adapted fungus weight of ≥ 10 g or a total adjusted nasal clearance time of ≥ 35 min.seven
Statistical Analysis
All analyses were carried out using SPSS version 22 (SPSS Inc., Chicago, IL). Data were drawn from 212 volunteers who participated in this study. Of those, actigraphy measures were collected from 165 participants. Ane participant was identified as a clear outlier (> nine standard deviations in a higher place the mean on sleep duration) and excluded, yielding 164 participants for these analyses. Cocky-study sleep measures obtained by sleep diary were available on 159 participants. Income, BMI, and alcohol consumption were log (base of operations-10) transformed to better approximate a normal distribution. Logistic regression was used to predict colds (one, yes; 0, no). Sleep measures were treated as continuous variables with the exception of self-reported sleep efficiency, which was negatively skewed, and was modeled equally a chiselled (quartile) predictor. We reported regression coefficients with standard errors and probability values.
Age and prechallenge viral-specific antibody titers were included as covariates in all analyses. Next, we conducted a series of regressions entering ane of the fourteen separate covariates, along with age and prechallenge antibody titers. The arroyo reduces the risks of "overfitting" the regression models34,35; however, we likewise computed unmarried models that included all report covariates simultaneously. In addition, to better elucidate the independent and interactive contributions of duration and continuity measures on cold susceptibility, we fit models that included both actigraphy assessed sleep duration and fragmentation simultaneously as predictors too as tested the interaction between them (slumber duration × fragmentation).
Finally, to meliorate clarify associations between actigraphy assessed sleep elapsing and cold incidence and to provide an estimate upshot size, sleep duration was categorized based on hours of slumber (< 5 h, due north = 36; v to 6 h, n = 54; six.01 to seven h, northward = 52; > 7 h, n = 22). We fitted a logistic regression using this chiselled slumber variable and reported odds ratios (OR) with 95% confidence intervals (CIs).
RESULTS
Sample Characteristics and Slumber Scores
Table 1 presents descriptive information for all variables involved in the analyses. Of the 164 participants, 124 (75.6%) were infected and 48 (29.3%) developed a biologically verified cold, which was defined as infection and objective cold criterion. As expected, sleep measures were intercorrelated (actigraphy slumber elapsing and fragmentation, r = −0.37, P < 0.001; actigraphy sleep duration and self-reported sleep duration, r = 0.49, P < 0.001; actigraphy sleep duration and self-reported slumber efficiency, r = 0.27, P < 0.001; actigraphy fragmentation and self-reported slumber efficiency, r = −0.12, P = 0.xiv).
Table i
Sample characteristics (n = 164).
Sleep and Susceptibility to the Common Common cold
Adjusting for age and prechallenge antibiotic titers, shorter sleep duration, assessed using actigraphy, was associated with increased risk for the development of the common cold (b = −0.44, standard error [SE] = 0.17, P = 0.011). In contrast, sleep fragmentation and self-reported sleep duration were non significant predictors of cold susceptibility (fragmentation: b = −0.01, SE = 0.01, P = 0.715; self-reported sleep duration: b = −0.xv, SE = 0.16, P = 0.325). Similarly, participants reporting slumber efficiency in the bottom quartile were no more likely to develop the cold than individuals in the top quartile (b = 0.57, SE = 0.51, P = 0.258).
To follow up on the meaning association between actigraphy-assessed sleep duration and the likelihood of developing a biologically verified cold, boosted models were computed adjusting for written report covariates. Here, nosotros carried out a fix of regressions that entered each covariate one by 1 in divide models (14 carve up models). As displayed in Tabular array 2, shorter sleep elapsing connected to be associated with increased rates of developing a cold (all Ps < 0.015). Furthermore, shorter sleep duration predicted increased odds of developing a cold when all covariates were included in a single model (b = −0.49, SE = 0.20, P = 0.012). Sleep fragmentation was non significantly related to cold incidence when all covariates were included in a single model (b = −0.01, SE = 0.02, P = 0.755). This was similarly the instance for self-reported sleep duration and efficiency (information non shown).
Table 2
Logistic regression models with actigraphy-based sleep duration predicting incidence of the cold, adjusting for each study covariate separately.
To amend narrate the effect of sleep elapsing on odds of developing a cold, sleep categories were created. As illustrated in Figure i, the predictive influence of sleep duration on common cold susceptibility indicates a threshold effect at 6 or fewer hours of sleep (< five h, OR = four.50; 95% CI 1.08–18.69; 5–half dozen h, OR = 4.24; 95% CI 1.08–16.71; six.01–7 h, OR = 1.66; 95% CI 0.40–6.95; > seven h, ane [reference]).
Sleep elapsing (measured by wrist actigraphy) averaged over a seven-day menses before virus exposure is associated with percentage of participants who subsequently adult a cold. The percentage of colds is based on predicted values (adjusted for age and prechallenge viral-specific antibody levels).
The observed elevated risk of developing the cold in participants experiencing shorter slumber duration may have been due to increased susceptibility to infection and/or increased affliction expression among those infected. In this regard, in adjusted analyses, actigraphy assessed slumber duration was unrelated to rates of infection (b = −0.eleven, SE = 0.17, P = 0.543). Similarly, among those who were infected (n = 124), shorter sleep duration was not significantly related to increased odds of meeting illness criteria for mucus product or nasal clearance time (b = −0.32, SE = 0.19, P = 0.090). Although there were no significant relationships of actigraphy-assessed sleep elapsing with either infection or expression of disease, the association with cold incidence appears to be primarily driven by illness expression.
Because measures of actigraphy assessed sleep duration and fragmentation capture dissimilar aspects of an individual's slumber, nosotros tested whether the effects of duration operated independent of fragmentation in predicting adventure for a biologically verified cold. To this end, we fit a regression model with both measures entered together. Analyses revealed that sleep elapsing continued to predict cold incidence adjusting for age and prechallenge antibody levels (b = −0.53, SE = 0.nineteen, P = 0.005) also every bit in the fully adjusted (16 covariates and fragmentation) model (b = −0.56, SE = 0.21, P = 0.006). There was no evidence that sleep elapsing and fragmentation interacted to predict cold incidence (P = 0.92).
Discussion
Shorter sleep duration, measured past wrist actigraphy over a 7-day catamenia, was prospectively associated with increased incidence of the common common cold following experimental viral challenge. This association was independent of a core of covariates, including historic period, prechallenge antibody levels, sex, body mass index, race, season of trial, income, education, perceived socioeconomic status, smoking, physical activeness, alcohol consumption, perceived stress, agreeableness, extraversion, and positive emotional style. This study provides the commencement prospective evidence that behaviorally assessed sleep duration serves as a predictor of cold susceptibility.
Analyses revealed a linear association betwixt slumber elapsing and cold susceptibility; however, when categorized based on hours of sleep, a threshold effect was observed such that individuals sleeping fewer than 6 h of sleep per night were at elevated run a risk whereas those sleeping more than 6 h were non. This is consequent with some epidemiologic bear witness that find strong effects on morbidity and mortality in brusque sleepers compared to normal sleepers.1,11,36 For instance, Patel and colleagues establish that in a sample of nearly 57,000 women, those who reported sleeping ≤ 6 h per night were at significantly greater risk of developing pneumonia compared to those sleeping 8 h per night.v Those sleeping 7 h were at no greater risk than viii-h sleepers. Emerging bear witness also suggests that long sleepers (≥ 9 h per night) are at increased risk of illness.10,11,37 The underlying mechanisms linking negative health and long sleep are poorly understood38–40; however, depression and medical comorbidities take been implicated.38 Very few participants in this study reported sleeping more than 9 h per dark (11.iii% by sleep diary, 0.half-dozen% by actigraphy), making information technology difficult to make up one's mind whether long sleep was a risk cistron of common cold incidence. The modest sample of long sleepers in this written report may be due to the fact that the study sample was carefully screened to meet proficient wellness standards, including being free from psychiatric illness.
Cocky-reported diary measures of duration and sleep efficiency were unrelated to cold incidence. This is in contrast to our prior piece of work that found that poorer sleep efficiency and shorter sleep duration, measured via a 14-day daily interview, predicted cold susceptibility.vi There are several possible explanations for differences across studies. First, fewer participants became infected in this sample, which may have limited our power to detect effects using self-written report measures. 2d, this written report relied on a shorter seven-mean solar day sleep diary rather than a 14-day daily interview, which may accept produced less stable averages likewise every bit less accurate estimates of sleep. In regard to sleep estimates, employment of a daily interview in the prior study helped ensure timely assessments of self-reported sleep, which potentially decreased recall bias. Third, given that actigraphy has been well correlated with polysomnography,41 the gilt standard of measurement in sleep enquiry, it is also possible that had our prior study included actigraphy assessment concurrently with the daily interview sleep data, those findings would have been even more robust. Future studies incorporating both actigraphy and sleep diaries are needed to sympathize when and why certain sleep measures significantly predict allowed part.
What are the mechanisms that might link sleep and susceptibility to acute infectious illness? Slumber, along with circadian rhythms, exerts substantial regulatory effects on the immune organisation.42,43 Circulating allowed cells, including T and B cells, peak early in the night and and so decline throughout the nocturnal hours moving out of apportionment into lymphoid organs where exposure to virally infected cells occur.43–45 Studies employing experimental sleep loss also support functional changes relevant to host resistance. Sleep deprivation results in down regulation in T prison cell production of interleukin-219,44 and a shift away from T-helper 1 responses, marked by a reduction in the ratio of interferon-γ/IL-4 production.sixteen Sleep loss is associated with macerated proliferative chapters of T cells in vitro fifteen as well as modulation of the function of antigen presenting cells disquisitional to virus uptake.46
Affliction expression in colds is generally attributed to blunted downregulation of local inflammatory responses.47,48 Emerging prove demonstrates bidirectional links between sleep and inflammation.14,42,49 Proinflammatory activity has a role in the homeostatic regulation of slumber.50,51 Besides, some merely not all studies that use partial and total sleep brake detect substantial increases in systemic levels of proinflammatory cytokines52 every bit well as enhanced inflammatory factor expression and transcriptional pathways that support inflammatory processes.20,21 In addition, recent prove suggests that elevated systemic inflammation mediates prospective associations between short slumber elapsing and premature mortality.53 Future studies characterizing the immunologic mediators of cold incidence in the context of sleep duration and our viral challenge image are needed to analyze when in the infection process slumber has the virtually potent furnishings.
Like prior work, we find that infectious risk is strongest in the shortest of sleepers, suggesting that "normal" sleepers (eastward.g., 7 to 9 h per night for adults) would exist protected in this context. Whether sleep interventions aimed at increasing sleep duration would protect individuals from cold incidence remains an open question. In this regard, recent findings that cognitive behavioral therapy for older adults with insomnia resulted in decreased levels of systemic inflammation54 raises the possibility that a similar enhancement in jail cell-mediated immunity could too be observed. Given that infectious illness (i.due east., influenza and pneumonia) remains one of the pinnacle 10 leading causes of expiry in the U.s.,55 the electric current data suggest that a greater focus on sleep duration, as well as sleep wellness more broadly,56 is indicated.
In summary, these novel findings provide the first evidence that sleep duration assessed behaviorally through actigraphy predicts incidence of infectious illness using an experimental viral challenge. Although this report does not provide directly testify of causality, the prospective nature of the viral challenge design does eliminate concerns of reverse causation. It is recognized that actigraphy is a behavioral mensurate of rest/ activeness patterns and is not an objective mensurate of slumber per se. Although actigraphy has been shown to correlate well with polysomnography in salubrious samples,41 actigraphy-assessed indices of sleep duration cannot identify specific dimensions of slumber (e.g., decreased slow wave slumber) that may be contributing to infectious risk. In improver, future studies investigating the immunologic mechanisms underlying these effects as well equally generalizability of these findings to other samples (i.e., older adults; sleep disordered patients) are warranted.
Footnotes
A commentary on this article appears in this issue on page 1341.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531403/
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