Behavioral Sleep Medicine

ISSN: 1540-2002 (Print) 1540-2010 (Online) Journal homepage: http://www.tandfonline.com/loi/hbsm20

Stress Reactivity in Insomnia Philip R. Gehrman, Martica Hall, Holly Barilla, Daniel Buysse, Michael Perlis, Nalaka Gooneratne & Richard J. Ross To cite this article: Philip R. Gehrman, Martica Hall, Holly Barilla, Daniel Buysse, Michael Perlis, Nalaka Gooneratne & Richard J. Ross (2014): Stress Reactivity in Insomnia, Behavioral Sleep Medicine, DOI: 10.1080/15402002.2014.940112 To link to this article: http://dx.doi.org/10.1080/15402002.2014.940112

Published online: 15 Aug 2014.

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Date: 05 November 2015, At: 20:56

Behavioral Sleep Medicine, 00:1–11, 0000 Copyright © Taylor & Francis Group, LLC ISSN: 1540-2002 print/1540-2010 online DOI: 10.1080/15402002.2014.940112

Stress Reactivity in Insomnia Downloaded by [University of Florida] at 20:56 05 November 2015

Philip R. Gehrman Department of Psychiatry Perelman School of Medicine at the University of Pennsylvania; Philadelphia Veterans Administration Medical Center

Martica Hall Sleep Medicine Institute and Department of Psychiatry University of Pittsburgh School of Medicine

Holly Barilla Department of Psychiatry Perelman School of Medicine at the University of Pennsylvania

Daniel Buysse Sleep Medicine Institute and Department of Psychiatry University of Pittsburgh School of Medicine

Michael Perlis Department of Psychiatry Perelman School of Medicine at the University of Pennsylvania

Nalaka Gooneratne Division of Geriatric Medicine Perelman School of Medicine at the University of Pennsylvania

Richard J. Ross Philadelphia Veterans Administration Medical Center; Department of Psychiatry Perelman School of Medicine at the University of Pennsylvania

This study examined whether individuals with primary insomnia (PI) are more reactive to stress than good sleepers (GS). PI and GS (n D 20 per group), matched on gender and age, completed Address correspondence to Philip Gehrman, PhD, CBSM, Department of Psychiatry, University of Pennsylvania, 3535 Market Street, Suite 670, Philadelphia, PA 19104. [email protected]

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three nights of polysomnography. On the stress night, participants received a mild electric shock and were told they could receive additional shocks during the night. Saliva samples were obtained for analysis of cortisol and alpha amylase along with self-report and visual analog scales (VAS). There was very little evidence of increased stress on the stress night, compared to the baseline night. There was also no evidence of greater stress reactivity in the PI group for any sleep or for salivary measures. In the GS group, stress reactivity measured by VAS scales was positively associated with an increase in sleep latency in the experimental night on exploratory analyses. Individuals with PI did not show greater stress reactivity compared to GS.

Current perspectives on insomnia regard the disorder as one of hyperarousal (Riemann et al., 2009). Multiple forms of hyperarousal have been investigated, including emotional hyperarousal as manifested in personality traits such as neuroticism (Kales, Caldwell, Preston, Healey, & Kales, 1976), and cognitive arousal in the form of increased cognitive activity at night that interferes with sleep initiation and maintenance (Harvey, 2002). Some studies have found increased somatic, or physiological, arousal, and found evidence of elevated body temperature and heart rate (Monroe, 1967), 24-hr metabolic rate (Bonnet & Arand, 1996), and decreased heart rate variability measures of parasympathetic activity (Bonnet & Arand, 1998) in patients with insomnia compared to good sleepers, although findings are mixed or of small magnitude. Several studies have found an increase in high-frequency EEG activity, primarily in the beta range, during non-REM (NREM) sleep in patients with insomnia; most reliably observed in female patients (Buysse et al., 2008; Perlis, Merica, Smith, & Giles, 2001). Beta activity is thought to indicate greater cognitive activation and information processing and indicate increased cortical arousal during NREM sleep, compared to controls (Perlis, Giles, Mendelson, Bootzin, & Wyatt, 1997). While the mechanisms underlying these various manifestations of hyperarousal are unknown, there are a number of reasons to suspect involvement of the stress response system. Observational studies have reported associations between poor sleep and stressful life events such as work stress (Linton, 2004), spousal bereavement (Hall et al., 1997), and living near the site of an industrial accident (Davidson, Fleming, & Baum, 1987). In a retrospective study, poor sleepers reported that their sleep difficulties began during periods of significant life stress (Healey et al., 1981). A few experimental studies have used acute stress paradigms to quantify the impact of psychological stress on sleep. Sleep latency was prolonged in participants told that they would have to give a public speech after a daytime nap (Gross & Borkovec, 1982). Exposure to an acute stressor (threat of electric shock) resulted in elevated skin conductance in patients with insomnia but not in good sleepers, although effects on sleep were not reported (Lichstein & Fanning, 1990). Hall et al. had healthy undergraduates with no history of insomnia give a public speech (Hall et al., 2004). Compared to participants randomly assigned to the control condition, stress group participants exhibited vagal withdrawal and increased sympathetic nervous system activity on heart rate variability during both NREM and rapid eye movement (REM) sleep. Increased physiological arousal during sleep, in turn, was associated with decreased sleep continuity as measured by difficulty maintaining sleep. Lastly, investigations of the hypothalamic-pituitary-adrenal (HPA) axis further support the relationship between stress and insomnia. Administration of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) during sleep to good sleepers led to sleep

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disruption (Steiger, 2002). Vgontzas and colleagues measured circulating levels of ACTH and cortisol in participants with insomnia and good sleepers via blood draws obtained every 30 min for 24 hr (Vgontzas et al., 2001). The insomnia group had significantly higher ACTH and cortisol levels in the afternoon, late evening and early night; evening and nighttime cortisol were correlated with greater severity of sleep disturbance in the insomnia group only. Higher circulating levels of cortisol in insomnia has been confirmed by a second group of investigators (Rodenbeck & Hajak, 2001; Rodenbeck, Huether, Rüther, & Hajak, 2002). Overall, these data are consistent with the hypothesis that patients with insomnia experience more stress activation than good sleepers. Further, past studies on the effects of experimental stress on sleep have utilized acute stress paradigms that may not mirror the extended state of anticipatory anxiety associated with insomnia. The present study was designed to test the hypothesis that individuals with insomnia exhibit increased reactivity to stressors, including disrupted sleep, compared to good sleepers.

METHODS Participants Subjects with primary insomnia (PI; n D 20) and age/gender matched good sleeper (GS) controls .n D 20/ were recruited for the study. Eligibility was determined based on selfreport measures and clinical interview, including the SCID. Participants in the PI group met the following Research Diagnostic Criteria for primary insomnia (Edinger et al., 2004): subjective complaint of difficulty initiating or maintaining sleep, waking up too early or having nonrestorative sleep; daytime consequences of the poor sleep; duration of at least six months; no evidence that the sleep disturbance is secondary to a medical or psychiatric condition, including substance use. The insomnia had to occur three or more nights per week. Subjects had to report taking 30 min or longer to fall asleep and/or spend D 30 min awake during the night (Lichstein, Durrence, Taylor, Bush, & Riedel, 2003). Good sleepers had to report consistently getting a good night of sleep and not report any evidence of insomnia on clinical history. Exclusion criteria for both groups were: significant medical or psychiatric illness; evidence of any sleep disorders other than insomnia, including current or recent (past 6 months) shift work; use of any psychoactive or sleep-altering medications; and regular use of tobacco products. The participants (24 females, 16 males) had a mean age of 36.3 .SD D 8:4/ years. Twentyeight (70.0%) were Caucasian American, 10 (25.0%) were African American, and one (2.5%) did not report race. Of these participants, 1 (2.5%) did not complete high school, 3 (7.5%) completed high school, 2 (5.0%) completed trade school after high school, 7 (17.5%) had some college education, 15 (37.5%) completed college, and 11 (27.5%) had a postgraduate degree. Eighteen participants (45.0%) reported being employed full-time, 12 (30.0%) reported working part-time, 3 (7.5%) were unemployed, 4 (10.3) were students, and 2 (5%) reported other. There were no significant differences between groups on any demographic variables. One participant from each group withdrew during the study due either to medical reasons .n D 1/ or scheduling difficulties .n D 1/, leaving 19 participants per group with complete data. The study was approved by the University of Pennsylvania’s Institutional Review Board, and all participants provided written, informed consent.

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Protocol Participants underwent an initial screening visit, at which time they provided informed consent, baseline questionnaires, and a psychiatric interview (SCID) administered by a clinical psychologist to rule out comorbid psychiatric disorders. An actigraph (Actiwatch; Philips, Inc.) was worn for two weeks to determine participants’ habitual bedtime and to ensure regular sleeping patterns (i.e., bedtimes and waking times do not vary by more than 1 hr on most nights). Participants then completed three overnight sleep laboratory studies within a two-week period (Figure 1). They were asked to refrain from napping during the day preceding each study night and to avoid caffeine after lunchtime. They were not allowed to eat, drink, or smoke starting at 8:00 p.m. and ending following collection of the final saliva samples the next morning to avoid contamination of these samples. Bedtimes and wake-up times were set to habitual times as determined by the sleep diary and actigraph records. The first night in the sleep laboratory was an adaptation night in order to allow subjects to acclimate to sleeping in the laboratory and to the sleep-recording equipment and to rule out the presence of sleep disorders other than insomnia. The second night was used as a baseline, and the third night as a stress night. The baseline night always preceded the stress night in order to avoid contamination by potential persistent effects of anticipation of the stressor. During the baseline night, 1 hr before their habitual bedtime participants were reminded that nothing unusual would happen during that night of sleep. Ten minutes prior to their habitual bedtime, subjective stress ratings, consisting of the state version of the State-Trait Anxiety Inventory and three visual analog scales, were collected as well as saliva samples. On the third night, the stressor was administered 40 min prior to the participant’s habitual bedtime. One saliva sample, for alpha amylase, was collected 5 min after the stressor, and a second sample, for cortisol, was collected 30 min after the stressor (i.e., 10 min before bedtime).

FIGURE 1

Study protocol diagram.

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Self-Report and Interview Measures The Structured Clinical Interview (SCID-IV-P; First, Spitzer, Gibbon, & Williams, 2001) is a structured interview to assess for the presence of DSM-IV Axis I disorders (APA, 2000), including mood, anxiety, psychotic, and substance use disorders. The SCID was used to screen out any participants with evidence of psychopathology. The Insomnia Severity Index (ISI) (Bastien, Vallieres, & Morin, 2001) is a 7-item (0–4 Likert scale) measure with a maximum total score of 28. The scale provides a measure of overall severity of insomnia. It has good internal consistency .˛ D :74/ and is routinely used in insomnia research. The State-Trait Anxiety Inventory (STAI) was used as a measure of both trait and state anxiety (Spielberger, 1983). The trait subscale (STAI-T) was administered at baseline as a measure of overall anxiety, and the state subscale (STAI-S) was administered on each of the nights in the sleep laboratory as a measure of subjective stress. The 16-item version of the Quick Inventory of Depressive Symptomatology, Self-Report version (QIDS-SR), was used as a measure of depressive symptoms (Rush et al., 2003). While individuals with clinical depression were excluded from the study, the QIDS-SR was used to quantify subclinical symptoms. The Ford Insomnia Response to Stress Test (FIRST) is a questionnaire designed to assess stress-related vulnerability to experience insomnia (Drake, Richardson, Roehrs, Scofield, & Roth, 2004). It contains nine items for which respondents rate the likelihood of experiencing disturbed sleep in association with different stressful events and situations. The FIRST has been shown to have strong test-retest reliability (0.92) and to be predictive of objectively assessed sleep disturbance under stressful conditions. Three visual analog scales (VAS), anchored at each end with the words “relaxed vs. anxious,” “calm vs. nervous,” and “tense vs. peaceful” were created. Consistent with other investigators (e.g., Monk, 1989) the format was such that each item asked the participant, “How __ do you feel?” with the words anxious, nervous, and peaceful inserted. The scales were then anchored at each end with opposing descriptors with respondents asked to mark where on the line best described their current state.

Polysomnography Standard polysomnographic procedures were used to record the EEG, EOG, EMG, and EKG using the Sandman system. Electrode placements of FpZ , CZ , and OZ were placed according to the International 10/20 system. The Cz placement was the primary one used for scoring purposes. Two EOG electrodes were placed, positioned 1 cm below and lateral to the outer canthus of the left eye and 1 cm above and lateral to the outer canthus of the right eye. Two EMG electrodes were taped onto the chin 2 cm apart. On the first night of recording, additional leads were used to measure leg movements and breathing in order to rule out the presence of occult sleep disorders. Two electrodes were taped over the anterior tibialis muscle of each leg to detect leg movements. Flexible Resp-EZ belts were placed to measure breathing-related movements, a nasal cannula was used to detect pressure, and a finger oximeter probe measured blood oxygen saturation. Individuals with an apnea-hypopnea index greater than 15 events per hr or a periodic limb movement index greater than 15 events per hr were excluded (Silber et al., 2007). Records were scored in 30-s epochs according to established R&K criteria (Rechtschaffen & Kales, 1968). Standard sleep architecture variables were computed. The following sleep

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continuity variables were computed: sleep onset latency (SOL; time from lights out to the first epoch of stage 2 or higher), wake after sleep onset (WASO; number of minutes spent awake between lights out and lights on), total sleep time (TST), and sleep efficiency (SE; total sleep time divided by the total recording period). SOL was the primary outcome measure for the study, as it was hypothesized that temporal proximity to the stressor would make this period of the night the most vulnerable.

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Stress Procedure The threat of electric shock was used as an experimental stressor. A study staff member first self-administered a shock in order to demonstrate the tolerability of the stimulus to the subjects. Participants were then administered one electric shock (1.5 mA, 50 msec). The surface of the skin was cleaned with an alcohol wipe to remove excess oils that could interfere with the current. The electric shock was delivered by two pure tin disk electrodes placed 1 cm apart over the median nerve of the left wrist (Grass S48 Square Pulse Stimulator and SIU5 transformer isolation unit). A shock of this intensity was generally described by participants as “moderately painful and less intense than expected” and similar in intensity to snapping a rubber band on one’s wrist. Participants were told that they would receive up to three electric shocks during the night, although no shocks were actually administered. In the morning after the stress night, participants were debriefed by the study investigator due to the use of deception. Several factors were considered in choosing threat of electric shock as the stressor, which could impact subsequent sleep by creating a state of anticipation of a negative event. Other commonly used laboratory stressors, such as difficult mental arithmetic, were not used as their effects are often transient and return to baseline levels during the recovery period (Mezick, Matthews, Hall, Richard Jennings, & Kamarck, 2013). Anticipatory stress was also thought to represent an analog of the experience of insomnia. Patients with insomnia often report anticipating another night of tossing and turning in bed, unable to sleep.

Salivary Assays Saliva samples were used to measure activation of the HPA and sympathetic components of the stress response. Compared to urine and plasma samples, saliva samples are noninvasive, easy to collect, and able to provide hormone levels that correspond to a specific point in time (Kirschbaum & Hellhammer, 1989). All saliva samples were collected at the same times within participants in order to reduce the impact of circadian variation, with the exact timing determined by their habitual bedtime (Kirschbaum & Hellhammer, 1989). As described above, one saliva sample, for alpha amylase, was collected 5 min after the stressor, and a second sample, for cortisol, was collected 30 min after the stressor. The differing timing of the alpha amylase and cortisol samples was based on past studies demonstrating the time course to peak levels in saliva following exposure to a stressor for each marker (Gallacher & Petersen, 1983; Kirschbaum & Hellhammer, 1989). Saliva was collected with a Salivette sampling device (Salimetrics, State College, PA). Subjects were instructed not to eat or brush their teeth for at least 60 min prior to the first sample. Salivettes were stored in a 20ı C freezer for later analysis.

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The primary outcome measure from saliva was cortisol, which is a standard measure of stress-induced HPA axis activation (Kirschbaum & Hellhammer, 1989). Alpha amylase, a salivary enzyme secreted in response to sympathetic activation (Chatterton, Vogelsong, Lu, Ellman, & Hudgens, 1996; Gallacher & Petersen, 1983), was the secondary outcome measure. A number of studies have consistently found that salivary alpha-amylase levels increase in response to both physiological (e.g., Kivlighan & Granger, 2006) and psychological (e.g., Nater, Rohleder, Schlotz, Ehlert, & Kirschbaum, 2007) stressors. Saliva assays were conducted using standardized kits (Salimetrics, State College, PA). All assays were performed in duplicate, and reliability analyses were computed. Data Analyses Baseline characteristics of the PI and GS groups, as determined using questionnaires, were compared using independent sample t-tests. The only significant deviations from normality were for SOL and WASO, both of which were positively skewed, so log transformations were performed for these variables. To test the main hypotheses, ANOVAs were performed. For each ANOVA, the dependent variable was the outcome of interest, CONDITION (baseline or stress) was treated as a within-subjects factor, and GROUP (PI or GS) was treated as a between-subjects factor. The test of the GROUP  CONDITION interaction effect was the primary effect of interest. First, as manipulation checks, the impact of the experimental stressor on subjective ratings of stress, and concurrently salivary cortisol and alpha amylase, were examined in a mixed effects model. Second, the main hypothesis that the PI group, compared to the GS group, would have a larger increase in sleep latency in response to the stressor was examined. In exploratory analyses, we sought to examine the relationships among changes in symptoms of stress and changes in sleep latency from the baseline to the stress night. Change scores were computed (night 2 to night 3) for SOL, salivary cortisol and amylase, the three VAS scales, and the STAI state ratings. A series of linear regressions were performed using change in SOL as the dependent variable and change in the other measures, GROUP (PI or GS) and interaction effects (change score  group) as the independent variables. RESULTS The PI group, compared to the GS group, had significantly greater insomnia severity (ISI), higher depression scores (QIDS), and higher vulnerability to insomnia (FIRST; see Table 1). There were no significant main or interaction effects for either salivary cortisol or alpha amylase. There was a significant main effect of group for VAS Tense ratings, in which the PI group reported greater tension than the GS group, but this effect did not vary by condition. There were no significant group, condition, or interaction effects for VAS Relaxed or Calm ratings, or for STAI-S ratings. Nighttime self-report ratings and salivary assays are shown in Table 3. Sleep architecture and sleep continuity variables are shown in Table 2. Main and interaction effects were not statistically significant (all p > 0:05). In secondary analyses, each of the other sleep measures was examined as a dependent variable, again with no statistically significant main or interaction effects.

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TABLE 1 Baseline Questionnaires (Mean and SD Provided) Good Sleepers (n D 19)

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Insomnia Severity Index State-Trait Anxiety Inventory, trait version Quick Inventory of Depressive Symptomatology Ford Insomnia Response to Stress Test

3.9 46.7 3.3 16.4

Insomnia (n D 19)

(4.9) (10.3) (2.9) (4.8)

17.6 53.0 6.4 21.9

t-test df D 37 t t t t

(3.6) (10.6) (3.6) (6.2)

D D D D

10:1; p < :0001 1:92; p D :062 3:02; p D :0045 3:15; p D :003

For the VAS scales, there was a significant GROUP  CONDITION interaction effect on sleep latency .p < 0:05/, which was then followed by simple effects. For each VAS item in the GS group, only, larger increases in ratings of stress/tension on the stress night were associated with larger increases in sleep latency.

DISCUSSION The goal of this study was to examine whether individuals with primary insomnia (PI), compared to good sleepers (GS), were more reactive to an experimental stressor as measured by PSG-assessed sleep, subjective ratings, and salivary cortisol and alpha amylase. We hypothesized that the PI group would demonstrate greater stress reactivity than the GS group.

TABLE 2 Polysomnography Data (Untransformed Means and SD Provided)

Group SOL (min) Total sleep time (min) Sleep efficiency (%) WASO (min) Stage 1% Stage 2% Stage 3/4% Stage REM%

GS INS GS INS GS INS GS INS GS INS GS INS GS INS GS INS

Baseline Night 26.2 24.8 393.4 401.7 85.3 86.9 66.8 60.8 6.6 7.4 54.2 58.3 18.0 15.1 21.1 20.1

(24.1) (30.6) (60.4) (61.1) (8.7) (11.1) (40.0) (52.0) (4.0) (6.0) (9.9) (12.4) (10.4) (8.9) (4.8) (4.2)

Stress Night 38.3 (45.2) 20.7 (22.3) 369.8 (79.2) 403.1 (49.2) 82.0 (14.8) 88.3 (7.4) 80.7 (66.3) 54.2 (32.3) 6.6 (4.1) 8.1 (7.1) 54.8 (12.7) 55.8 (12.4) 18.7 (13.5) 15.2 (7.9) 19.9 (4.2) 20.9 (4.3)

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TABLE 3 Nighttime Self-Report Ratings and Salivary Markers (Means and SD Provided)

Cortisol Alpha amylase STAI-State

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VAS-Relaxed (0) to anxious (100) VAS-Calm (0) to nervous (100)

Baseline Night

Stress Night

GS PI GS PI GS PI GS PI GS PI

.044 (.034) .067 (.112) 114.5 (114.6) 90.6 (92.1) 39.3 (5.0) 43.5 (7.3) 10.7 (10.1) 21.5 (18.8) 9.3 (8.7) 21.5 (20.0)

.083 (.129) .112 (.161) 101.5 (100.9) 90.8 (65.6) 40.4 (5.6) 43.3 (7.6) 14.4 (16.8) 22.2 (18.9) 13.6 (16.8) 24.1 (20.5)

GS PI

90.3 (8.6) 69.6 (28.8)

84.8 (15.2) 72.5 (23.7)

VAS-Tense (0) to peaceful (100)

This hypothesis was not confirmed, as there were no significant differences between the groups in stress reactivity. There are at least two explanations for this pattern of results. First, the experimental stressor may not have been of sufficient intensity to reliably produce a stress response in this sample. In support of this perspective is the notable lack of main effect of condition (baseline vs. stress nights) on either subjective or objective markers of the stress response system. Participants in both groups may not have perceived the electric shock paradigm as stressful. Anecdotally, while several participants reported feeling anxious about the electric shock, others were surprised that the test shock was less aversive than they had anticipated. A limitation of this study is that no manipulation check was conducted to verify that the electric shock was perceived as stressful, so it is not possible to determine whether the manipulation was successful or not. The relatively young, healthy nature of the sample may also have buffered them against the stressor. As a result, this study was not able to adequately test the hypotheses of interest. Second, there may in fact be no differences in stress reactivity between individuals with PI and good sleepers. This would seem to contradict the growing literature on stress reactivity as a factor that increases vulnerability to insomnia that is partially attributable to genetic influences (Drake, Friedman, Wright, & Roth, 2011). It may be that only a subset of those with insomnia are highly stress-reactive. The sample in this study may not have included enough of these more stress-reactive individuals to find significant differences compared to GS. Insomnia may also be associated with greater tonic levels of stress system activation or slower recovery rather than greater reactivity. Exploratory analyses were used to further investigate this limitation by examining whether the magnitude of change in sleep, as assessed by SOL, was associated with changes in measures of stress reactivity. For GS only, those who experienced greater increases in tension/anxiety had greater difficulty falling asleep on the stress night. This relationship was not observed in the PI group, suggesting that perceived stress may have different relationships to sleep in PI and GS.

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In summary, this study did not find evidence of greater stress reactivity in individuals with primary insomnia compared to good sleepers. This is not the first study to fail to find differences between PI and GS groups, likely indicating that the class of patients with insomnia is a heterogeneous group. However, the results of this study are limited by the fact that the experimental stressor may have failed to reliably activate self-reported and physiological indices of stress. Future studies should consider other experimental paradigms for eliciting stress that have greater ecological validity, more thoroughly calibrate the stressor for each individual to reliably activate a stress response, and include manipulation checks. It would also be of value to identify good sleepers who are more reactive to stress, such as those who score high on the FIRST, and examine their responses to stress paradigms compared to those of individuals who are less vulnerable.

FUNDING This project was supported by NIH grant 7R21MH079187-02 and the resources of the University of Pennsylvania Institute for Diabetes, Obesity, and Metabolism. Additional support provided by NIH grants R01MH077900 and R01AT003332.

REFERENCES American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author. Bastien, C. H., Vallieres, A., & Morin, C. M. (2001). Validation of the Insomnia Severity Index as an outcome measure for insomnia research. Sleep Medicine, 2(4), 297–307. doi:S1389945700000654 Bonnet, M., & Arand, D. (1996). Metabolic rate and the restorative function of sleep. Physiology & Behavior, 59, 777–782. Bonnet, M., & Arand, D. (1998). Heart rate variability in insomniacs and matched normal sleepers. Psychosomatic Medicine, 60, 610–615. Buysse, D. J., Germain, A., Hall, M. L., Moul, D. E., Nofzinger, E. A., Begley, A., : : : Kupfer, D. J. (2008). EEG spectral analysis in primary insomnia: NREM period effects and sex differences. Sleep, 31(12), 1673–1682. Chatterton, R. T., Jr., Vogelsong, K. M., Lu, Y. C., Ellman, A. B., & Hudgens, G. A. (1996). Salivary alpha-amylase as a measure of endogenous adrenergic activity. Clinical Physiology (Oxford, England), 16(4), 433–448. Davidson, L., Fleming, R., & Baum, A. (1987). Chronic stress, catecholamines, and sleep disturbance at Three Mile Island. Journal of Human Stress, 13, 75–83. Drake, C., Richardson, G., Roehrs, T., Scofield, H., & Roth, T. (2004). Vulnerability to stress-related sleep disturbance and hyperarousal. Sleep, 27, 285–291. Drake, C. L., Friedman, N. P., Wright, K. P., Jr., & Roth, T. (2011). Sleep reactivity and insomnia: Genetic and environmental influences. Sleep, 34(9), 1179–1188. doi:10.5665/SLEEP.1234; 10.5665/SLEEP.1234 Edinger, J. D., Bonnet, M. H., Bootzin, R. R., Doghramji, K., Dorsey, C. M., Espie, C. A., : : : American Academy of Sleep Medicine Work, G. (2004). Derivation of research diagnostic criteria for insomnia: Report of an American Academy of Sleep Medicine Work Group. Sleep, 27(8), 1567–1596. First, M., Spitzer, R., Gibbon, M., & Williams, J. (2001). Structured clinical interview for Axis I DSM-IV-TR disorders. New York, NY: New York State Psychiatric Institute. Gallacher, D. V., & Petersen, O. H. (1983). Stimulus-secretion coupling in mammalian salivary glands. International Review of Physiology, 28, 1–52. Gross, R. T., & Borkovec, T. D. (1982). Effects of a cognitive intrusion manipulation on the sleep-onset latency of good sleepers. Behavior Therapy, 13, 112–116.

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Hall, M., Buysse, D. J., Dew, M. A., Prigerson, H. G., Kupfer, D. J., & Reynolds, C. F., 3rd. (1997). Intrusive thoughts and avoidance behaviors are associated with sleep disturbances in bereavement-related depression. Depression and Anxiety, 6(3), 106–112. Hall, M., Vasko, R., Buysse, D., Ombao, H., Chen, Q., Cashmere, J., : : : Thayer, J. (2004). Acute stress affects heart rate variability during sleep. Psychosomatic Medicine, 66, 56–62. Harvey, A. (2002). A cognitive model of insomnia. Behaviour Research and Therapy, 40, 869–893. Healey, E. S., Kales, A., Monroe, L., Bixler, E. O., Chamberlin, K., & Soldatos, C. R. (1981). Onset of insomnia: Role of life-stress events. Psychosomatic Medicine, 43, 439–451. Kales, A., Caldwell, A. B., Preston, T. A., Healey, S., & Kales, J. D. (1976). Personality patterns in insomnia. Archives of General Psychiatry, 33, 1128–1134. Kirschbaum, C., & Hellhammer, D. H. (1989). Salivary cortisol in psychobiological research: An overview. Neuropsychobiology, 22, 150–169. Kivlighan, K. T., & Granger, D. A. (2006). Salivary alpha-amylase response to competition: Relation to gender, previous experience, and attitudes. Psychoneuroendocrinology, 31(6), 703–714. doi:10.1016/j.psyneuen.2006.01.007 Lichstein, K., & Fanning, J. (1990). Cognitive anxiety in insomnia: An analogue test. Stress Medicine, 6, 47–51. Lichstein, K. L., Durrence, H. H., Taylor, D. J., Bush, A. J., & Riedel, B. W. (2003). Quantitative criteria for insomnia. Behaviour Research and Therapy, 41(4), 427–445. Linton, S. J. (2004). Does work stress predict insomnia? A prospective study. British Journal of Health Psychology, 9(Pt 2), 127–136. doi:10.1348/135910704773891005 [doi] Mezick, E. J., Matthews, K. A., Hall, M. H., Richard Jennings, J., & Kamarck, T. W. (2013). Sleep duration and cardiovascular responses to stress in undergraduate men. Psychophysiology, 88, 51–96. doi:10.1111/psyp.12144 Monk, T. (1989). A visual analogue scale technique to measure global vigor and affect. Psychiatry Research, 27(1), 89–99. Monroe, L. J. (1967). Psychological and physiological differences between good and poor sleepers. Journal of Abnormal Psychology, 72, 255–264. Nater, U. M., Rohleder, N., Schlotz, W., Ehlert, U., & Kirschbaum, C. (2007). Determinants of the diurnal course of salivary alpha-amylase. Psychoneuroendocrinology, 32(4), 392–401. doi:10.1016/j.psyneuen.2007.02.007 Perlis, M., Giles, D., Mendelson, W., Bootzin, R., & Wyatt, J. (1997). Psychophysiological insomnia: The behavioural model and a neurocognitive perspective. Journal of Sleep Research, 6, 179–188. Perlis, M., Merica, H., Smith, M., & Giles, D. (2001). Beta EEG activity and insomnia. Sleep Medicine Reviews, 5, 365–376. Rechtschaffen, A., & Kales, A. (1968). A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects. Los Angeles. CA: Brain Information Service. Riemann, D., Spiegelhalder, K., Feige, B., Voderholzer, U., Berger, M., Perlis, M., & Nissen, C. (2009). The hyperarousal model of insomnia: A review of the concept and its evidence. Sleep Medicine Reviews, 14(1), 19–31. doi:10.1016/j.smrv.2009.04.002 Rodenbeck, A., & Hajak, G. (2001). Neuroendocrine dysregulation in primary insomnia. Revue Neurologique, 157, S57–S61. Rodenbeck, A., Huether, G., Rüther, E., & Hajak, G. (2002). Interactions between evening and nocturnal cortisol secretion and sleep parameters in patients with severe chronic primary insomnia. Neuroscience Letters, 324, 159– 163. Rush, A. J., Trivedi, M. H., Ibrahim, H. M., Carmody, T. J., Arnow, B., Klein, D. N., : : : Keller, M. B. (2003). The 16-Item Quick Inventory of Depressive Symptomatology (QIDS), clinician rating (QIDS-C), and self-report (QIDS-SR): A psychometric evaluation in patients with chronic major depression. Biological Psychiatry, 54(5), 573–583. Silber, M. H., Ancoli-Israel, S., Bonnet, M. H., Chokroverty, S., Grigg-Damberger, M. M., Hirshkowitz, M., : : : Iber, C. (2007). The visual scoring of sleep in adults. Journal of Clinical Sleep Medicine, 3(2), 121–131. Spielberger, C. D. (1983). Manual for the State-Trait Anxiety Inventory (Form Y). Palo Alto, CA: Consulting Psychologists Press. Steiger, A. (2002). Sleep and the hypothalamo-pituitary-adrenocortical system. Sleep Medicine Reviews, 6, 125–138. Vgontzas, A., Bixler, E., Lin, H., Prolo, P., Mastorakos, G., Vela-Bueno, A., : : : Chrousos, G. (2001). Chronic insomnia is associated with nyctohemeral activation of the hypothalamic-pituitary-adrenal axis: Clinical implications. Journal of Clinical Endocrinology & Metabolism, 86, 3878–3794.

Stress Reactivity in Insomnia.

This study examined whether individuals with primary insomnia (PI) are more reactive to stress than good sleepers (GS). PI and GS (n = 20 per group), ...
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