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Psychosomatic Medicine 64:793-802 (2002)
© 2002 American Psychosomatic Society

ORIGINAL ARTICLES

Stress Exposure, Psychological Distress, and Physiological Stress Activation in Midlife Women With Insomnia

Joan L. F. Shaver, PhD, RN, FAAN, Sandra K. Johnston, MS, RN, Martha J. Lentz, PhD, RN and Carol A. Landis, DNSc, RN

From the Department of Medical Surgical Nursing (J.L.F.S.), University of Illinois at Chicago, Chicago, IL and Department of Biobehavioral Nursing and Health Systems (S.K.J., M.J.L., C.A.L.), University of Washington, Seattle, WA.

Address reprint requests to: J. L. Shaver, Professor and Dean, University of Illinois at Chicago, College of Nursing M/C 802, 845 South Damen Avenue, Chicago, IL 60612-7350. Email: jshaver{at}uic.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: The objective of this study was to describe perceived and polysomnograhic (PSG) sleep patterns and determine whether stress exposure, psychological distress, and physiological stress activation differed among midlife women with psychophysiologic-type (PP-type) or subjective only-type (SO-type) insomnia or no insomnia.

METHODS: Women had their sleep monitored, collected urine samples, and completed questionnaires in a week-long field study, and 53 women met criteria for insomnia types or no insomnia based on reported sleep quality and PSG sleep efficiency.

RESULTS: As expected, women with PP-type insomnia were found to have the lowest sleep efficiency, took longer to fall asleep, had more wakefulness after sleep onset, and had more fragmented sleep. Perceptions of stress exposure, either for major or minor events, did not differ among groups. Despite there being no differences in perceived stress exposure, women with both types of insomnia scored higher on psychological distress (SCL-90R), especially on the somatization subscale, than women with no insomnia. Of the physiological stress activation indicators tested, a morning-to-evening difference in urinary cortisol statistically differed across the groups (p < .005). Women in the PP-type insomnia group had the highest levels of urinary cortisol in an early morning urine sample.

CONCLUSIONS: These data provide support for the hypothesis that, in midlife women, cognitive or emotional arousal with chronic stress neuroendocrine activation underlies chronic insomnia, particularly the PP-type.

Key Words: insomnia, • stress exposure, • psychological distress, • stress hormones.

Abbreviations: PSG = polysomnograph/polysomnography;; PP-type = psychophysiologic type;; PTSD = posttraumatic stress disorder;; MMPI = Minnesota Multiphasic Personality Inventory;; SO-type = subjective-only type;; SCL = Symptom Checklist;; REM = rapid eye movements;; NREM = nonrapid eye movements;; SWS = slow-wave sleep;; SPT = sleep-period time,; TIB = time in bed;; SCL-90R = Symptoms Checklist—90 items, revised;; WASO = wake after sleep onset;; TST = total sleep time;; SEI = sleep efficiency index;; BMI = body mass index.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Explanatory ideas about chronic insomnia (perceived poor quality or insufficient sleep) incorporate concepts of psychological arousal or distress, including a propensity to internalize anxiety. In an epidemiologic survey, people with insomnia reported symptoms consistent with anxiety and depression (1). People with chronic insomnia have shown more dysphoria than those without insomnia (2, 3). They have scored above the norm on the rumination, anxiety, inhibition of emotion, and inability to discharge anger outwardly and have tended toward high neuroticism and introversion scores on the subscales of the MMPI (4). People with chronic insomnia have been characterized by a pattern of internalization of problems combined with an anxious-depressive reaction style (5). Bedtime state anxiety has been positively related to perceived sleep latency (6), and negative emotions, stress responsiveness, and attention factors were found to influence particular types of insomnia, ie, sleep-onset vs. maintenance insomnia (7). Chronic insomnia appears to be a function of heightened emotional distress, but whether or not the distress emanates from the extent of perceived stress exposure or to ongoing stressful circumstances remains unclear.

Stressful conditions, especially emotionally profound ones, have been consistently linked to evidence of disturbed sleep patterns, either perceived or corroborated by PSG. Often, this is short term and is labeled acute or transient insomnia. Perceptions of poor sleep quality have been reported in people coping with the Three Mile Island nuclear incident (8), in parents coping with malignant disease in their children (9), and in victims after Hurricane Andrew (10). Increased PSG sleep fragmentation was observed in subjects after Hurricane Andrew (10). Women undergoing divorce, depressed or not, displayed shorter REM latency, more REM percent time, and lower delta wave (slow-wave) sleep patterns compared with control women as long as the divorce status remained unresolved (11).

Enduring or everyday stress, often studied in relation to occupational demands, has been linked with insomnia. For example, female construction workers with perceived job uncertainty and need to overcompensate at work had high reports of insomnia (12).

If acute or chronic insomnia coincides with emotional distress, negative affect, and dysphoria, then this should result in transient or enduring activation of the stress neuroendocrine system. A variety of indicators, including stress hormones or their metabolites, core body temperature, metabolic rate, heart rate, and heart-rate variability, have been used as indices of physiological activation. Generally, they have indicated increased activation in the context of stress exposure and acute or chronic insomnia. Urinary catecholamines were increased for days or weeks in adults living in the vicinity of the Three Mile Island nuclear incident (8), but sleep patterns and stress indicators were only modestly related. However, patients with PTSD had high nocturnal levels of MHPG (a metabolite of norepinephrine derived from the central nervous system) compared with those without PTSD, and night-to-day differences were associated with less PSG total sleep time (13). Twenty-four hour urinary cortisol levels were found to be positively correlated with PSG total wake time, and levels of catecholamine metabolites were directly related to the amount of NREM stage 1 (transitional sleep) and wake after sleep onset in insomnia among young adults (14). Higher core body temperatures in adult ‘poor’ as compared with ‘good’ sleepers were observed in early studies and interpreted as evidence of higher physiological arousal (15, 16), and higher metabolic rates have been observed subsequently in people with insomnia, even in those with no PSG evidence of insomnia (17, 18). Furthermore, nighttime heart rates were significantly higher in people with PSG-documented insomnia compared with controls (19). As well, a heart rate variability pattern indicative of increased sympathetic nervous system activity (ie, increased low frequency with decreased high frequency power density) has been observed in individuals with PSG-documented insomnia (20).

In our previous work on sleep and menopausal status with midlife women recruited from the community and selected for age but not for necessarily sleep problems, 23% of the women reported insomnia. The majority of the women with insomnia (12/19) did not show PSG evidence of insomnia (ie, they had a SEI >85%) based on a single night in the sleep laboratory after a night of adaptation. These women were classified as having SO-type insomnia. The remainder of the women (7/19) did have a low SEI and were classified as having PP-type insomnia (3). The women with SO-type compared with those with PP-type insomnia scored higher in psychological distress as assessed by the revised SCL-90 (SCL-90R). We have continued our studies by specifically selecting midlife women with insomnia and comparing their subjective and objective sleep patterns from a week-long field study with a control group of women with no sleep problems. The purpose of this study was to describe perceived and PSG sleep patterns and determine whether stress exposure, psychological distress, and physiological stress activation differed among women with PP-type or SO-type insomnia or without insomnia. Insomnia types were classified according to their reported sleep quality and PSG sleep efficiency.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Sample
Midlife women with self-reported (N = 101) insomnia of at least 3 months duration and with no insomnia (N = 30) participated in a week-long field study of sleep. They were recruited from community advertisements and initial eligibility determined from a telephone-screening interview. Women were excluded for any known sleep disorder diagnosis other than insomnia; any current or past major medical or mental illness, the routine use of all medications (except for hormone replacement therapy), and night shift work. Women without insomnia served as controls and had no sleep problems. Women with insomnia completed a 14-day sleep log. Logs were scored to assure that women met the criterion of self-reported overall "poor" or "very poor" sleep quality at least 3 nights/week. Additionally, they had to have at least one of the following: a) a sleep latency more than 20 minutes three times/week, b) at least two nighttime awakenings three times/week, or c) early morning awakenings at least two times/week. After human subjects’ approval and thorough explanation of and consent for participation were obtained, the women completed life events, psychological distress, sleep history, and demographic questionnaires at the orientation laboratory visit. Instructions for the home sleep recordings, completion of the daily diaries, and obtaining morning and evening urine samples were explained in detail.

Home Sleep PSG Recordings
On each of six sequential nights, a research assistant applied electrodes and set up the portable sleep recording equipment about 2 hours before the women’s usual bedtime in the home. Electrodes for recording the PSG electroencephalogram, electrooculogram, and electromyogram were placed according to established standards (21), and physiological signals were recorded with a portable sleep-data acquisition system (Oxford Instruments Sleep Analyzing Computer System, Clearwater, FL). An additional ground lead was placed on the forehead, and women were requested to avoid the use of electrical equipment near the bed, especially electric alarm clocks and electric blankets, to reduce electrical noise interference. The women were instructed on initiating and terminating the recordings, disconnecting and connecting from the junction box, and removing skin electrodes in the morning. Night 1 of sleep was considered adaptation, with data from nights 2 through 6 considered for analysis.

PSG Sleep Variables
Sleep stages were initially identified through an automatic scoring algorithm for each 30-second epoch and scored into NREM stage 1, 2, 3, or 4 and REM sleep. Records were then reviewed by trained sleep technicians and overscored visually according to standard criteria (21). Summary sleep variables were calculated for each night and averaged for at least 3 nights of data for each subject. Summary PSG sleep variables included time in bed (TIB; time from beginning to end of recording) and the SPT (first epoch of sleep scored as NREM stage 2 to the last epoch of sleep on the record). WASO and time spent in NREM (stages 1, 2, 3, and 4) and REM sleep stages were calculated as percent of SPT. NREM stages 3 and 4 were combined and reported as percent of slow-wave sleep (SWS). Total sleep time (TST = total time spent in stages 1–4 and REM), sleep efficiency index (SEI = TST/TIB), sleep latency (time from record start to first epoch of NREM stage 2), and REM latency (time from first epoch of NREM stage 2 until first REM epoch) also were calculated. Sleep continuity variables included total fragmentation (number of times stage moved from any NREM stage and REM to stage awake) and fragmentation index (total number of stage changes/hour).

Daily Diary
Each woman completed a daily diary for the 6 days of sleep recordings related to overall health, perceived stress, daily habits, self-reported sleep (duration, quality, number of nighttime awakenings), medication use, and nap history. All reliabilities for the variables derived from the diaries were calculated as test-retest measures over the 5 days (22). Perceived sleep quality was assessed from a single item on the daily diary that asked subjects to rate their sleep on a five-point scale with 1 = very good to 5 = very poor. The reliability for self-reported sleep quality was .55.

Insomnia Subtypes Group Assignment
From perceived and PSG sleep quality scores, women were classed as having PP-type insomnia based on having at least 3 nights of PSG data with a SEI <85%. Thirty-three of the 101 women with insomnia met this criterion. Their sleep records were scored for sleep apnea (index of >=5 events/hour) and periodic leg movements (four or more movements of 0.5 and 5-second duration separated by not <4 and not >90 seconds) (23), which excluded 10 women. Two other records were excluded because technical difficulties prevented the scoring of leg movement recordings, leaving 21 women in this category. Eighteen women of the 101 women with insomnia met our SO-type insomnia criteria of at least 3 nights of PSG SEI >=88% and no nights with PSG SEI <85%. Fourteen women of the 30 women reporting good sleep demonstrated at least 3 nights of PSG data with a SEI >=88% and were chosen for controls, while the remainder had fewer than 3 nights with SEI >=88% and were excluded.

Stress Exposure
Responses to four items (how stressed do you feel and how stressful are your relationship with your closest friend(s), your family life, and your work) in the diary were averaged per day to create a daily stress exposure score. Each item was rated as 1 = not at all to 6 = very much. The reliability for stress exposure using this measure was .75.

The hassles portion of the Hassles and Uplift Scale was used as another measure of stress exposure (24) and was completed on evenings 3, 4, and 5 in the home. This is a 117-item questionnaire, with each item rated on a four-point scale with 0 = none to 3 = extremely in response to a standard question "How much of a hassle was ___ for you?" Three scores were derived for each evening—total number of hassles per day, hassle severity per day, and an index of hassle severity (total severity divided by the number of hassles). A mean for the three measurement times was calculated. Reliability coefficients were .91 for the total number of hassles per day (range 0–117), .93 for total hassle severity per day (range 0–351), and .94 for the index of severity (0–3).

The Inventory of Small Life Events (ISLE) is a 176-item questionnaire designed to measure the impact of mild stress exposure over the last year in the areas of school, recreation, religion, money and finance, transportation, children, residence, relations with family, love and marriage, social life, health and illness, and work (25).

The Stressful Life Events (SLE) instrument was derived from the Sarason Life Events Survey (LES) as modified by Norbeck to enhance relevance for women (26, 27). This is a 91-item scale that describes events related to health, personal and social life, finances, criminal and legal matters, and parenting. Women rated whether the event occurred during the past year, whether the event was perceived as desirable or undesirable, and the magnitude of effect from 1 (no effect) to 4 (great effect) (27).

For each item on the ISLE and on the SLE, responses were divided into five categories (occurrence [yes or no, 0–1], desirability [desirable, neutral, undesirable, 1–3], expectancy [expected, unexpected, 1–2], control [total, some, none, 1–3], and effect [none, some, great, 1–3]). For the ISLE and for the SLE, the total number of negative events and the total number of positive events were calculated for each woman.

Psychological Distress
The SCL-90R is a 90-item questionnaire used to report psychological distress for the 2 weeks before the sleep study (28). Women rated the degree of distress related to each item on a five-point scale, with 1 = not at all to 5 = extremely, for each item. Mean scores were calculated for nine subscales—somatization, depression, anxiety, hostility, obsessive-compulsive, phobic anxiety, paranoid ideation, interpersonal sensitivity, and psychoticism—and for the global scales of severity index (GSI), total number of positive symptoms (PST), and positive symptom distress index (PSDI). Cronbach’s alpha scores for the nine subscales ranged between .92 (depression) and .76 (somatization and paranoid ideation), and the score was .97 for the GSI.

Physiological Stress Activation Indicators
Mean arterial blood pressure (MAP) and heart rate (HR) (Dinamap, Critikon Co., Tampa, FL) (average of two repeated measures) were obtained after women had been seated quietly for a minimum of 30 minutes after arriving at the laboratory.

Urinary catecholamines and cortisol were measured from specimens collected on the third, fourth, and fifth sleep recording days. Women collected a urine specimen in the evening that represented a 3-hour time span before their usual bedtime and a first-voided urine specimen each morning that represented the overnight filtration into the urine. Urine samples were kept on ice and preserved with disodium EDTA/sodium metabisulfite until they were stored at -70°C and later assayed. Urine catecholamines (CA) were measured in duplicate by high-performance liquid chromatography/electrochemical detection after extraction on Bio-Rex cation exchange resin (BioRad Laboratories, Hercules, CA) followed by acid alumina aluminum oxide (Bio-Rad Laboratories) precipitation using a standard protocol from the core biochemical laboratory in the School of Nursing. Coefficients of variability ranged from 0.4 to 10%. Urine cortisol was assayed in duplicate as per directions of a solid-phase radioimmunoassay (RIA) kit (Diagnostic Products, Los Angeles, CA) after extraction. 125I-labeled cortisol was measured in a gamma counter. The detection limit for cortisol is 0.3 µg/dl. There was an intraassay variation of 8%. Urine concentrations were standardized against the urine creatinine concentration and expressed per unit of creatinine. Concentrations for the hormones from all 3 days were averaged for each subject.

Data Analysis
Descriptive statistics were calculated for all variables and the data distributions were examined for normality and equal variance. The Kruskal-Wallis one-way analysis of variance with the chi-square statistic was used to test group differences for the subject characteristic variables of age, income, education, sleep variables, psychological distress, and physiological activation indicators because the data distributions were skewed. The chi-square statistic was used to test differences in ethnicity and marital status between the groups. A one-way analysis of variance (ANOVA) with posthoc least squares was used to test group differences for the data from the ISLE, SLE, and Daily Hassles because these distributions were not skewed. A Pearson product moment correlation test was used to examine relationships among perceived stress exposure, selected PSG sleep variables (fragmentation index, minutes awake, latency to stage 2, and sleep efficiency index), self-reported sleep quality, and the morning urinary cortisol concentration.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Sample Characteristics
Characteristics of the women in the sample are listed in Table 1. Women in all three groups were predominately white, college educated, on average in their mid-40s, and with mean family incomes between $25,000 and $35,000. There were significant differences across the groups only for BMI (p < .03), with the SO-type insomnia group having the highest BMI. Women in both insomnia groups had a higher mean BMI than women in the control group. Very few women in the sample (6%) used nicotine (smoked cigarettes). Fewer women in the insomnia group drank three or more servings of caffeine each day (roughly one third), while about one half of the control women reported this level of caffeine intake. For the women with insomnia, it was chronic, with a mean duration of 89.29 ± 146.41 months and a median of 36 months.


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  		Table 1. Group Characteristics of Women by Psychophysiological-Type (PP-type) Insomnia, Subjective Only-Type (SO-Type) Insomnia, and Without Insomnia (Control)a
 
Sleep Patterns
As anticipated, differences in self-reported sleep quality were evident across the groups (p = .001). Reported sleep quality was poorer for women in the PP-type (mean = 3.1 ± 0.7 SD) and SO-type insomnia (2.7 ± 0.8) groups than for women in the control group (2 ± 0.6). PSG sleep variables by group are summarized in Table 2. As expected on the basis of group classification, PSG SEI differed across the groups (p < .000) and was lowest in women with PP-type insomnia compared with women with SO-type insomnia or no insomnia. Furthermore, the women with PP-type insomnia took longer to fall asleep (p < .002) and had more wakefulness after sleep onset (as a percentage of SPT and in minutes) (p < .000), and the fragmentation index as a measure of sleep continuity was higher compared with the women in the other two groups (p < .02). Women in the SO-type insomnia group had more NREM stage 2 sleep than did women in the other two groups (p < .002).


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  		Table 2. Polysomnographic Sleep Variables by Psychophysiological-Type (PP-type) Insomnia, Subjective Only-Type (SO-type) Insomnia, and Without Insomnia (Control) Groups with Kruskal-Wallis (K-W) One-Way Analysis of Variance Test of Differencesa
 
Stress Exposure
Self-reported indicators of daily stress exposure, daily hassles, and high- and low-impact stressful life events over the past year (ISLE and SLE, respectively) are summarized in Table 3. There were no significant differences across the three groups in any of the stress exposure indicators. The raw scores indicate that the control women tended to report more positive events than the insomnia groups but the scores did not statistically differ.


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  		Table 3. Stress Exposure Indicator Scores by Psychophysiological-Type (PP-Type) Insomnia, Subjective Only-Type (SO-Type) Insomnia, and Without Insomnia (Control)a
 
Psychological Distress
Psychological distress scores for the subscales of the SCL-90R are summarized in Table 4. The somatization subscale score and the total scores for the global severity and symptom distress scales were significantly different across the three groups. Women with insomnia had higher scores on the scales compared with women without insomnia.


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  		Table 4. Psychological Distress Scores (SCL-90R) by Psychophysiological-Type (PP-Type) Insomnia, Subjective Only-Type (SO-Type) Insomnia, and Without Insomnia (Control) with Kruskal-Wallis (K-W) One-Way Analysis of Variance Test of Differences
 
Physiological Stress Activation Indicators
Indicators of physiological stress activation are summarized in Table 5. There were no group differences in mean blood pressure, HR, and urine catecholamines. A trend toward differences across the groups in morning (AM) urine cortisol levels (p < .06) was observed. The raw data indicate that women with insomnia and particularly women classed as having PP-type insomnia had early morning levels that were higher than women with no insomnia. However, the statistically strongest difference across the groups was in the morning-to-evening or AM-to-PM difference scores for cortisol (p < .005). Both of the insomnia groups had a greater AM-to-PM difference for cortisol than the control group.


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  		Table 5. Physiological Stress Activation Variables by Psychophysiological-Type (PP-Type) Insomnia, Subjective Only-Type (SO-Type) Insomnia and Without Insomnia (Control) with Kruskal-Wallis (K-W) One-Way Analysis of Variance Test of Differences
 
Correlations Among Perceived Stress Exposure Indicators and PSG Sleep Variables
Women in the control group demonstrated an inverse correlation (r = -.61, p = .02) between perceived stress exposure and PSG WASO and tended to have a positive correlation between perceived stress exposure and PSG sleep onset latency (r = .50, p = .07). Therefore, higher stress exposure was associated with a longer time to fall asleep but with less wakefulness after sleep did ensue. Women in the SO-type insomnia group also showed a trend toward a positive relationship between stress exposure and sleep efficiency (r = .43, p = .07). No other significant associations became evident.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
In this study, we used PSG data across multiple days to classify women more purely into those with PP-type insomnia and those with SO-only insomnia patterns and compared with women demonstrating high sleep efficiency. We found no evidence that women with either type of chronic insomnia compared with women with good sleep perceived more major or everyday stress exposure. This could be due to a small sample size and lack of power, in particular for number of daily hassles. However, the results across all three groups were remarkably similar and also similar to those reported in a study of older adults with good and poor sleep whereby the groups were indistinguishable in levels of perceived stress (29). In college students, not selected for insomnia, life events had only a weak association with recalled sleep quality (30). These observations would imply that insomnia is more a function of individuals’ styles, traits, or genetic propensities than of perceived features in the external environment. This is in concert with the idea that insomnia can persist in people with an anxious/tense style that overwhelms the dynamics that induce sleep. Moreover, the inability to sleep serves to reinforce the anxiety and perpetuate wakefulness such that these dynamics create a ‘vicious cycle’ (31). Of note in one study is that people with chronic insomnia compared with people with good sleep were found to experience more stressful life events in the year that their insomnia began (32). In our study, subjects endorsed mild- or high-stress exposure items relative to the past year, but we did not assess recall within the insomnia onset time frame. Perceptions of higher life stress have been associated with perceptions of more difficulty falling asleep but less early morning awakening in poor sleepers but not in good sleepers (29). Higher perceived stress exposure tended to be related to longer PSG sleep onset latency in our data also but, in contrast, only in the control group.

We found no strong associations between perceived stress exposure and PSG sleep variables. Similarly, Dagan et al. (33) found no actigraphic sleep differences between people with insomnia associated with the stress-related condition of PTSD and healthy gender and age-matched controls. However, other studies have revealed PSG changes in association with PTSD and other stress-related conditions. For example, PTSD patients were found to have lower sleep efficiency and higher REM density than control subjects (13). Comparing normal and depressed adolescents, stressful life events were associated with reduced REM latency and increased total REM time in the nondepressed, healthy adolescents (34). In another study of adults, subjective stress burden (interaction between stress-related intrusive thought tendency and the number of recent stressful events) was associated with decreased delta power as determined by spectral analysis of the sleep electroencephalogram (EEG). As well, there was a tendency for subjects to report stress-related intrusive thoughts and these were associated with a trend toward higher beta power (35). For our study, we calculated traditional PSG sleep variables and have not completed power spectral analysis on the EEG data. More refined data reduction and analysis might uncover relationships between perceived exposure to stress and sleep patterns.

It is conceivable that a propensity to be emotionally or cognitively aroused is not tightly linked to perceived stress exposure. In spite of perceived stress exposure, our results support the view of increased psychological distress in women with insomnia, as is evident in several other studies. Other researchers have noted that individuals with PP-type insomnia reported frequent cognitive activity and negative thoughts (36). Our earlier studies in midlife women (not recruited specifically for insomnia) indicated that distress scores using the SCL-90R were significantly higher in women reporting insomnia compared with women reporting no insomnia. As well, women with SO-type insomnia had the highest psychological distress scores compared with women with PP-type insomnia (37). This difference in psychological distress between insomnia subtypes was not confirmed in this study. In most studies, including our study, subjects were not screened for coexisting psychiatric diagnosis. However, the scores on the SCL-90R for this and our previous studies do not fall in the range of published psychiatric outpatient mean scores. In this study, the GSI total mean scores were 0.60 and 0.50 for the PP-type and SO-type insomnia groups, respectively, and 0.28 for the control group. These scores are lower than those reported for a mixed-gender psychiatric outpatient group (mean of 1.26) and, for the control women, are about equal to those reported for a nonpatient group (mean score of 0.31) (28). Enhanced psychological or emotional arousal, at a level subclinical to psychiatric disorder, is seen as a factor in women with chronic insomnia, regardless of whether there is objective evidence of PSG sleep changes. Whether psychological distress contributes disproportionately more to insomnia in women with SO-type than in women with PP-type insomnia deserves further study. The relatively high scores on the SCL-90R that we observed in the women with insomnia, particularly for the somatization subscale, might be indicative of a propensity to negative affectivity. Negative affectivity represents a pervasive mood disposition manifested as generalized and enduring distress and dissatisfaction that negatively skews self-reports of personal health and well being of any type (38). Negative affectivity has been profiled to involve feelings of nervousness, tension, worry, and vulnerability (39). It has been measured numerous ways, including Tellegen’s Negative Emotionality Scale of the Multidimensional Personality Questionnaire, the Eysenck Personality Neuroticism Scale, the Spielberger State-Trait Anxiety Inventory, and Byrne Repression-Sensitization Scale (40–43). People with chronic insomnia have been reported to have anxious worrying traits, as indicated by high scores on the Taylor Manifest Anxiety Scale, the Eysenck Neuroticism Scale, and the Byrne’s Repression-Sensitization Scale (44). Further, negative affectivity has been shown to be strongly and positively associated with somatic symptoms and affect the reporting of life events (45). Brett et al. (46) have urged that caution be used in the interpretation of life events and well-being (eg, sleep quality) relationships in the absence of negative affectivity assessment (46).

The groups tended to differ statistically with regard to TIB, although not in TST. The women with PP-type insomnia had the longest time in bed but the least amount of sleep time. This supports the idea that women with PP-type insomnia spend more time in bed to achieve a sleep amount that women with SO-type or no insomnia can achieve more efficiently. Compared with a laboratory study of women selected for midlife age, and regardless of sleep quality, allowed to go to bed and get up at "usual times," the mean TIB for the women with PP-type insomnia in this home study (455.5 ± 54 minutes) was comparable (TIB lab study, 464 ± 69 minutes) (37). Many PSG insomnia studies have controlled the time in bed. In one study, subjects (mean age 46.7 ± 13.8 years) were allowed to remain in bed for 8 hours, and the data were analyzed separately for males and females. Women with insomnia (no insomnia subclassification reported) had a mean TST of 362 minutes (in this study, 362.4 minutes) and control women had a mean TST of 427.5 minutes (in this study, 379.9 minutes) (47). In our study, it seems that the control women in their natural environments might not be getting any more sleep than the insomnia women and potentially are partially sleep deprived.

We acknowledge that the evening 3-hour urine collection period was not an optimum measure for characterizing cortisol as a physiological stress indicator. It was not feasible to obtain 24-hour urine measures or repeated blood samples from subjects at home for this study. Because we were most interested in the AM (postsleep) specimens, we chose to block the collection times and average across three separate nights rather than to obtain one or multiple 24-hour collections. The AM cortisol values tended to be higher in the PP-type insomnia group compared with controls, with the mean values for the SO-type insomnia group in-between. The difference in AM cortisol across groups approached but lacked power to achieve statistical significance. The difference across groups in the mean AM-to-PM diurnal scores was due to a high PM mean level of urinary cortisol in the women with no insomnia. Speculations on the reason for this are difficult. Perhaps the control women for this study in their natural environments had more stressful activity impinging several hours before bedtime than the women with insomnia, creating this pattern of prebedtime cortisol output. Contrary to this pattern, based on half-hourly blood draws for plasma cortisol, investigators showed that a mixed-gender group of young adults with insomnia had a statistically significant higher plasma cortisol concentration compared with those without insomnia during the evening and early sleep (time span = 2100–0030; p = .003) but not during sleep (time span = 2300–0630; p = .49) (48). In general, making inferences from data comparisons across studies is difficult due to differences in measures. Moreover, sex hormone levels and gender differences can create variability. For example, an indwelling intravenous catheter constitutes a mild stress and has been associated with a more pronounced urinary free cortisol and disturbed sleep effect in older women not on estrogen-replacement therapy compared with those on estrogen-replacement therapy (49). In a study of people with recent-onset PTSD symptoms 1 month after a motor vehicle accident, 15-hour urinary cortisol levels were elevated in men and not women (50). Few data about all-night neuroendocrine function in insomnia are available, and more work clearly needs to be done, with attention paid to blood draws as a stressor, gender, sex hormone levels, age, and environmental conditions.

High nighttime cortisol and disturbed PSG sleep patterns have been linked in other studies, although we did not find a positive correlation between average AM cortisol levels and PSG indicators of WASO or sleep fragmentation. Higher 24-hour urinary free cortisol has been associated with more wake time and PSG sleep disturbances in an uncontrolled study of young men with insomnia (N = 15) (14) and in serial blood cortisol samples in healthy young men deprived of sleep (51, 52). Cortisol has been found to vary inversely with the amount of slow-wave sleep (53). In a mixed-gender sample, people with insomnia and a very low sleep efficiency showed higher plasma cortisol than people with insomnia but a somewhat higher sleep efficiency (48). With insomnia, it remains difficult to determine whether a stress-related pattern of elevated nighttime cortisol is influencing sleep depth and continuity or a more fundamentally disturbed sleep pattern is affecting the cortisol rhythm. The effects in either case on daytime cortisol remain unclear.

In summary, this study showed that, in midlife women with insomnia of either the SO-type or PP-type, psychological distress was evident, although not linked to perceived stress exposure. Our observations imply that one’s propensity for experiencing negative affect or emotional distress regardless of circumstances can be a defining element in the perception of sleep quality. It stands to reason that a propensity for negative affect would be embodied in perceptions of poor sleep. However, how much a propensity to experience negative affect contributes to enduring poor PSG sleep quality or the opposite remains unclear. The elevated AM cortisol that we observed in women with insomnia implies that chronic insomnia has elements that conform to a chronic stress model of physiological stress activation. However, much more work needs to be done to characterize the relationships among psychological distress arousal, physiological stress activation, and insomnia according to insomnia subtypes.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This work was supported by National Institutes of Health/National Institute of Nursing Research Grants NR01118 and 5T32NR7039. We are grateful for technical support from James Rothermel and Stacy Ofstad.

Received for publication November 28, 2000.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA 1989; 262: 1479–84.[Abstract]
  2. Rosa RR, Bonnet MH. Reported chronic insomnia is independent of poor sleep as measured by electroencephalography. Psychosom Med 2000; 62: 474–82.[Abstract/Free Full Text]
  3. Shaver JL, Paulsen VM. Sleep, psychological distress, and somatic symptoms in perimenopausal women. Fam Pract Res J 1993; 13: 373–84.[Medline]
  4. Kales A, Caldwell, A, Soldatos CR, Bixler EO, Kales JD. Biopsychobehavioral correlates of insomnia. II: pattern specificity and consistency with the Minnesota Multiphasic Personality Inventory. Psychosom Med 1983; 45: 341–55.[Abstract/Free Full Text]
  5. Schramm E, Hohagen F, Kappler C, Grasshoff U, Berger M. Mental comorbidity of chronic insomnia in general practice attenders using DSM-III-R. Acta Psychiatr Scand 1995; 91: 10–7.[Medline]
  6. Chambers MJ, Kim JY. The role of state-trait anxiety in insomnia and daytime restedness. Behav Med 1993; 19: 42–6.[Medline]
  7. Waters WF, Adams SGJ, Binks P, Varnado P. Attention, stress and negative emotion in persistent sleep-onset and sleep-maintenance insomnia. Sleep 1993; 16: 128–36.[Medline]
  8. Davidson LM, Fleming R, Baum A. Chronic stress, catecholamines, and sleep disturbance at Three Mile Island. J Hum Stress 1987; 13: 75–83.
  9. Magni G, Carli M, De Leo D, Tshilolo M, Zanesco L. Longitudinal evaluations of psychological distress in parents of children with malignancies. Acta Paediatr Scand 1986; 75: 283–8.[Medline]
  10. David D, Mellman TA, Mendoza LM, Kulick-Bell R, Ironson G, Schneiderman N. Psychiatric morbidity following Hurricane Andrew. J Trauma Stress 1996; 9: 607–12.[CrossRef][Medline]
  11. Cartwright RD, Wood E. Adjustment disorders of sleep: the sleep effects of a major stressful event and its resolution. Psychiatry Res 1991; 39: 199–209.[CrossRef][Medline]
  12. Goldenhar LM, Swanson NG, Hurrell JJ, Ruder A, Deddens J. Stressors and adverse outcomes for female construction workers. J Occup Health Psychol 1998; 3: 19–32.[CrossRef][Medline]
  13. Mellman TA, Kumar A, Kulick-Bell R, Kumar M, Nolan B. Nocturnal/daytime urine noradrenergic measures and sleep in combat-related PTSD. Biol Psychiatry 1995; 38: 174–9.[CrossRef][Medline]
  14. Vgontzas AN, Tsigos C, Bixler EO, Stratakis CA, Zachman K, Kales A, Vela-Bueno A, Chrousos GP. Chronic insomnia and activity of the stress system: a preliminary study. J Psychosom Res 1998; 45: 21–31.[CrossRef][Medline]
  15. Munroe L. Psychological and physiological differences between good and poor sleepers. J Abnorm Psychol 1967; 72: 255–64.[CrossRef][Medline]
  16. Adam K, Tomeny M, Oswald I. Physiological and psychological differences between good and poor sleepers. J Psychiatr Res 1986; 20: 301–16.[CrossRef][Medline]
  17. Bonnet MH, Arand DL. 24-Hour metabolic rate in insomniacs and matched normal sleepers. Sleep 1995; 18: 581–8.[Medline]
  18. Bonnet MH, Arand DL. Physiological activation in patients with sleep state misperception. Psychosom Med 1997; 59: 533–40.[Abstract/Free Full Text]
  19. Stepanski E, Glinn M, Zorick FJ, Roehrs T, Roth T. Heart rate changes in chronic insomnia. Stress Med 1994; 10: 261–6.
  20. Bonnet MH, Arand DL. Heart rate variability in insomniacs and matched normal sleepers. Psychosom Med 1997; 60: 610–5.[Abstract/Free Full Text]
  21. Rechtschaffen A, Kales A. A manual of standardized terminology, techniques, and scoring systems for sleep stages of human subjects. Los Angeles (CA): Brain Information/Brain Research Institute UCLA; 1968.
  22. Heise DR. Separating reliability and stability in test-retest correlation. Am Sociol Rev 1969; 34: 93–101.[CrossRef]
  23. American Sleep Disorders Association and Sleep Research Society. Atlas and scoring rules: recording and scoring leg movements. Sleep 1993; 16: 748–59.[Medline]
  24. Lazarus RS, Folkman S. Manual for the hassles and uplifts scales. Palo Alto (CA): Consulting Psychologists Press; 1989.
  25. Folkman S, Lazarus RS. Relationship between coping and emotions. Soc Sci Med 1988; 26: 309–17.
  26. Sarason IG, Johnson JH, Siegel JM. Assessing the impact of life changes: developing the life experiences survey. Consult Clin Psychol 1978; 4: 932–46.
  27. Norbeck JS. Modification of life event questionnaires for use with female respondents. Res Nurs Health 1984; 7: 61–71.[Medline]
  28. Derogatis L. SCL-90 manual. Baltimore (MD): Johns Hopkins University School of Medicine; 1977.
  29. Friedman L, Brooks JO, Bliwise DL, Yesavage JA, Wicks DS. Perceptions of life stress and chronic insomnia in older adults. Psychol Aging 1995; 10: 352–7.[CrossRef][Medline]
  30. Cernovsky ZZ. Life stress measures and reported frequency of sleep disorders. Percept Mot Skills 1984; 8: 39–49.
  31. Morin CM, Stone J, Trinkle D, Mercer J, Remsberg S. Dysfunctional beliefs and attitudes about sleep among older adults with and without insomnia complaints. Psychol Aging 1993; 8: 463–7.[CrossRef][Medline]
  32. Healey ES. Onset of insomnia: role of life-stress events. Psychosom Med 1981; 43: 439–51.[Abstract/Free Full Text]
  33. Dagan Y, Zinger Y, Lavie P. Actigraphic sleep monitoring in posttraumatic stress disorder (PTSD) patients. J Psychosom Res 1997; 42: 577–81.[CrossRef][Medline]
  34. Williamson DE, Dahl RE, Birmaher B, Goetz RR, Nelson B, Ryan ND. Stressful life events and EEG sleep in depressed and normal control adolescents. Biol Psychiatry 1995; 37: 859–65.[CrossRef][Medline]
  35. Hall M, Buysse DJ, Nowell PD, Prigerson HG, Kupfer DJ, Reynolds CF. Symptoms of stress and depression as correlates of sleep in primary insomnia. Psychosom Med 2000; 62: 227–30.[Abstract/Free Full Text]
  36. Kuisk LA, Bertelsen AD, Walsh JK. Presleep cognitive hyperarousal and affect as factors in objective and subjective insomnia. Percept Mot Skills 1987; 69: 1219–25.
  37. Shaver JLF, Giblin E, Paulsen V. Sleep quality subtypes in mid-life women. Sleep 1991; 14: 18–23.[Medline]
  38. Watson D, Clark LA. Negative affectivity: the disposition to experience aversive emotional states. Psychol Bull 1984; 96: 465–90.[CrossRef][Medline]
  39. Vassend O. Dimensions of negative affectivity, self-reported somatic symptoms, and health-related behaviors. Soc Sci Med 1989; 28: 29–36.
  40. Tellegen H. The Differential Personality Questionnaire. Minneapolis (MN): University of Minnesota; 1982.
  41. Eysenck HJ, Eyenck SGB. Manual of the Eysenck Personality Inventory. London: University of London Press; 1984.
  42. Spielberger CD. Manual for the State-Trait Anxiety Inventory. Palo Alto (CA): Consulting Psychologists Press, Inc.; 1983.
  43. Byrne D. The repression-sensitization scale: rationale, reliability, and validity. J Pers 1961; 29: 334–9.[CrossRef][Medline]
  44. Coursey RD. Personality measures and evoked responses in chronic insomniacs. J Abnorm Psychol 1975; 84: 239–249.[CrossRef][Medline]
  45. Watson D, Pennebaker JW. Health complaints, stress and distress. Exploring the central role of negative affectivity. Psychol Rev 1989; 96: 234–54.[CrossRef][Medline]
  46. Brett JF, Brief AP, Burke MJ, George JM, Webster J. Negative affectivity and the reporting of stressful life events. Health Psychol 1990; 9: 57–68.[CrossRef][Medline]
  47. Stepanski E, Zorick FJ, Roehrs T, Young D, Roth T. Daytime alertness in patients with chronic insomnia compared with asymptomatic control subjects. Sleep 1988; 11: 54–60.[Medline]
  48. Vgontzas AN, Bixler EO, Lin H, Prolo P, Mastorakos G, Vela-Bueno A, Kales A, Chrousos GP. Chronic insomnia is associated with nyctohemeral activation of the hypothalamic-pituitary-adrenal axis: clinical implications. J Clin Endocrinol Metab 2001; 86: 3787–94.[Abstract/Free Full Text]
  49. Prinz P, Bailey S, Moe K, Wilkinson C, Scanlan J. Urinary free cortisol and sleep under baseline and stressed conditions in health senior women: effects of estrogen replacement therapy. J Sleep Res 2001; 10: 19–26.[CrossRef][Medline]
  50. Hawk LW, Dougall LA, Ursano RJ, Baum A. Urinary catecholamines and cortisol in recent-onset posttraumatic stress disorder after motor vehicle accidents. Psychosom Med 2000; 62: 423–34.[Abstract/Free Full Text]
  51. Vgontzas AN, Mastorakos G, Bixler EO, Kales A, Gold PW, Chrousos GP. Sleep deprivation effects on the activity of the hypothalamic-pituitary-adrenal and growth axes: potential clinical implications. Clin Endocrinol (Oxf) 1999; 51: 205–15.[CrossRef][Medline]
  52. Spath-Schwalbe E, Gofferje M, Kern W, Born J, Fehm HL. Sleep disruption alters nocturnal ACTH and cortisol secretory patterns. Biol Psychiatry 1991; 29: 575–84.[CrossRef][Medline]
  53. Gronfier C, Luthringer R, Follenius M, Schaltenbrand N, Macher JP, Muzet A, Brandenberger G. Temporal relationships between pulsatile cortisol secretion and electroencephalographic activity during sleep in man. Electroencephalogr Clin Neurophysiol 2001; 103: 405–8.



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