Study Preview
Study Title and Description
Stress-related sleep disturbance and polysomnographic response to caffeine.
Key Questions Addressed
| 1 | For [population], is caffeine intake above [exposure dose], compared to intakes [exposure dose] or less, associated with adverse effects on behavior*? |
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Primary Publication Information
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| Title | Stress-related sleep disturbance and polysomnographic response to caffeine. |
| Author | CL Drake,C Jefferson,T Roehrs,T Roth, |
| Country | |
| Year | 2006 |
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Secondary Publication Information
There are currently no secondary publications defined for this study.
Extraction Form: Behavior - Design Details - INCLUDED Studies
Arms
No arms have been defined in this extraction form.
| Question... Follow Up | Answer | Follow-up Answer | |
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| Refid | 16996309 |
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| What outcome is being evaluated in this paper? | Behavior |
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| What is the objective of the study (as reported by the authors)? | To determine the sleep response to caffeine in individuals vulnerable to stress-related sleep disturbance as measured by polysomnography. |
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| Provide a general description of the methods as reported by the authors. Information should be extracted based on relevance to the SR (i.e., caffeine related methods) | 2.1. Subjects Participants were recruited from individuals who had participated in previous sleep center protocols as well as from media advertisements (newspaper and television). The study sample included two groups of individuals, none of whom met diagnostic criteria for insomnia. Thus, individuals in each group were healthy normal volunteers without significant illnesses. A total of 30 individuals met initial screening criteria, but nine individuals did not complete the study for a variety of reasons. Specifically, one subject dropped out due to pregnancy, one could not swallow the caffeine pills, five were discontinued due to noncompliance with some aspect of the protocol, one subject did not feel comfortable sleeping in the laboratory, and one subject had unreadable PSG screening data. Using a median split on FIRST scores, individuals were separated into two groups: those scoring low (≤ 18) on the FIRST scale (n = 11, 4 women, mean age = 32.64 ± 15.46 years) and those scoring high (> 18) on this measure (n = 10, 6 women, mean age = 34.20 ± 13.73 years). There were no significant differences in age or gender distribution between the groups (P>0.05). There are no questions on the FIRST addressing an individual’s sleep-response to caffeine. All procedures were approved by the institutional review board and informed consent was obtained from all participants. Individuals were paid for study participation. 2.2. Procedures Prior to the experimental nights, participants completed an adaptation night in the laboratory, during which they were evaluated for any signs of periodic limb movements or sleep-disordered breathing using a nasal–oral thermister and leg electromyogram (EMG). Participants were then scheduled for two overnight visits, each separated by 1 week. In several cases, screening PSG bedtimes were allowed to vary according to each participant’s habitually reported bedtime although most subjects were recruited from a previous protocol with screening PSGs offset to 8.5 h time in bed. In order to standardize the experimental nights, PSGs were set to 8 h beginning at 11 p.m. (lights-out) and ending at 7 a.m. (lights-on). Caffeine was administered 60 min prior to bedtime at 10 p.m. Each recording included electroencephalograms (EEG) (C3, C4, O1, O2 referenced to contralateral ear electrodes), two electro-oculograms (EOG) (bilateral horizontal), submental EMG and electrocardiogram (ECG) (V5 lead) and were scored in 30- s epochs according to standard procedures [26]. In addition, leg movements were monitored using a bilateral tibialis EMG, and respiration was monitored using a nasal/oral thermistor. All recordings were made using Grass Heritage or Aurora digital polygraphs (Grass-Telefactor, Astromed, Inc, West Warwick, RI). Participants were administered 3 mg/kg of caffeine in pill form on one of the two overnight laboratory visits. This dose was chosen as it has been shown to produce small to moderate disruptions of sleep initiation in healthy normal individuals [27]. Counterbalancing was incomplete due to scheduling conflicts and attrition. Overall, 12 subjects were studied with the control night as the first experimental night, while nine participants were studied with caffeine administration as the first experimental night. Subjects were instructed to eat a meal prior to coming into the laboratory at 8 p.m., and subjects did not consume any food thereafter on the laboratory nights. Subjects were given breakfast at approximately 7 a.m. Subjects were instructed to refrain from consuming any alcohol or caffeine after 5 p.m. on any laboratory night. 2.3. Statistics The primary outcome measure for the present study was latency to persistent sleep (20 continuous epochs of PSG sleep). This selection was based on its frequent use as an outcome measure of sleep onset in the clinical insomnia literature, sleep latency as a component in the diagnosis of chronic primary insomnia, and the documented effect of caffeine on sleep latency [27]. Furthermore, the moderate dose of caffeine utilized as the sleep-related challenge (3 mg/kg caffeine) has not been shown to produce significant sleep disturbance beyond a latency effect when administered prior to bedtime. Nonetheless, sleep efficiency was also tested as a secondary measure in order to facilitate comparisons with other clinical insomnia literature [28]. A two-factor mixed (Group X Caffeine) repeated measures analysis of variance (ANOVA) was used to test for differences in the sleep-related response to caffeine for latency to persistent sleep and sleep efficiency. Follow-up post-hoc t-tests were performed if an interaction was present. An alpha criterion of 0.05 was used to determine statistical significance. Potential differences in demographic variables were tested using the Student’s ttest and χ2 analysis, respectively. |
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| How many outcome-specific endpoints are evaluated? | 1 |
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| What is the (or one of the) endpoint(s) evaluated? (Each endpoint listed separately) | sleep |
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| List additional health endpoints (separately). |
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| List additional health endpoints (separately) |
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| Notes | includes sleep latency and sleep efficiency |
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| Clinical |
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| Physiological | Physiological |
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| Other |
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| What is the study design? | Controlled Trial |
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| Randomized or Non-Randomized? | NCT |
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| What were the diagnostics or methods used to measure the outcome? | Objective |
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| Optional: Name of Method or short description | polysomnography |
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| Caffeine (general) | Caffeine (general) |
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| Coffee |
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| Chocolate |
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| Energy drinks |
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| Gum |
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| Medicine/Supplement |
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| Soda |
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| Tea |
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| Measured | Measured |
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| Self-report |
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| Children |
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| Adolescents |
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| Adults | Adults |
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| Pregnant Women |
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| What was the reference, comparison, or control group(s)? (e.g. high vs low consumption, number of cups, etc.) | control night where nothing was administered (no placebo) vs 300 mg caffeine |
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| What were the listed confounders or modifying factors as stated by the authors? (e.g. multi-variable components of models. Copy from methods) | N/A |
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| Provide a general description of results (as reported by the authors). | A main effect for caffeine was present (main effect of condition, F(1,19) = 8.97, P = 0.007), illustrating that this dose of caffeine was effective at producing prolonged sleep latency. Importantly, there was a significant interaction (group by condition, F(1,19) = 4.90, P = 0.04) (Fig. 1), suggesting an effect of caffeine at this moderate-low dose only in the vulnerable group (High FIRST). Post-hoc t-tests showed that the High FIRST group responded to caffeine with an increased latency to sleep (P < 0.02), while the Low FIRST group did not (P = 0.46). The effect size calculated for the High FIRST group in terms of the effects of caffeine in standard deviation units (Cohen’s d) was d = 1.21. No differences in sleep efficiency were found between FIRST groups (main effect of group, F(1,19) = 0.28, P = 0.60=n.s.), further supporting the contention that none of the participants in either group were insomniacs. A main effect of caffeine was found (Main effect of condition, F(1,19) = 10.39, P = 0.004), also providing evidence for the impact of caffeine on sleep efficiency, although much of this effect was likely accounted for by the impact of nocturnal caffeine administration on sleep onset latency as described above. No interaction was present for sleep efficiency (Interaction F(1,19) = 0.48, P = 0.50). |
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| Did the authors perform a dose-response analysis (or trend/related analysis)? | No |
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| What were the authors's observations re: trend analysis? |
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| What were the author's conclusions? | Specifically, the current data demonstrate that individuals who report a vulnerability to stress-induced sleep disturbance also show elevated sleep-related reactivity in terms of their polysomnographic response to the effects of a pharmacological challenge (3 mg/kg caffeine). This is an important extension in that it supports, along with our previous work, the possibility that individual vulnerability to sleep disturbance may be mediated by an underlying physiological reactivity to stimuli that cross broad categories of psychological and physiological challenges to the sleep system. An important result of the present study is that following nocturnal caffeine administration, the vulnerable population had a higher sleep latency (~60 min) than is typically reported for chronic insomniacs [30] and longer than that found in studies using similar doses of caffeine in healthy subjects [27]. |
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| What were the sources of funding? | This study was supported by a National Institute of Mental Health Grant: MH68372. This study was supported by a National Institute of Mental Health Grant: MH-068372 |
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| What conflicts of interest were reported? | None reported |
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| Does the exposure (dose) need to be standardized to the SR? | Yes |
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| Provide calculations/conversions for the exposure based on the decision tree in the guide (for all endpoints/exposure levels of interest). | 3 mg/kg caffeine dose, no average weight provided 3 mg/kg x 80 kg adult = 240 mg/day caffeine |
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| List all the endpoint(s) followed by the dose (mg) which will be used in comparison to Nawrot. Characterize value as LOAEL/NOAEL, etc. if possible. | sleep - LOAEL = 240 mg/day caffeine (high susceptibility to sleep disturbance subjects) (increase in the latency to persistent sleep) sleep - NOAEL = 240 mg/day caffeine (low susceptibility to sleep disturbance subjects) |
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| Notes regarding selection/listing of endpoints and exposures/doses to be compared to Nawrot. | single dose the adverse effect of increasing the latency to persistent sleep onset was only significant in the group of subjects that was identified as highly susceptible to stress, but not in the low group. |
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| What is the importance of the study with respect to the adverseness of the outcome? | Important |
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Baseline Characteristics
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Results & Comparisons
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Adverse Events
| Arm or Total | Title | Description | Comments |
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Quality Rating
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