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127 Copyright 2004 John Wiley & Sons, Ltd.

St r e s s - i nduc e d i nc r e a s e i n
mor ni ng c or t i s ol va r i a nc e
Frank A. Kaspers

and O. Berndt Scholz


Department of Clinical and Applied Psychology, University of Bonn, Germany
*Correspondence to: Dr Frank Kaspers, Abteilung fr
Klinische und Angewandte Psychologie, Universitt
Bonn, Rmerstr. 164, D-53117 Bonn, Germany.

E-mail: f.kaspers@uni-bonn.de
S t r e s s a n d He a l t h
Stress and Health 20: 127139 (2004)
Published online 25 May 2004 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/smi.1004
Received 13 August 2003
Accepted 27 January 2004
on only one of these possibilities: i.e. rising cor-
tisol in the tradition of Selyes general adapta-
tion syndrome (Selye, 1950), and reduced cortisol
levels as examined in more recent studies (Heim,
Ehlert, & Hellhammer, 2000). Comprehensive
psychophysiological models which explain both,
hyper- and hypocortisolism in chronic stress,
or which can be falsied by the third possible
outcome (no change at all) are rare.
Henry (1986, 1993; Henry & Stephens, 1977)
designed a psychophysiological stress theory,
which ascribes physiological processes to specic
reactions to stress. Helplessness under stress is
assumed to go along with HPA activation while
ght-ight behavior results in neurosympathetic
adrenomedullary activation. In subsequent for-
Summary
Empirical evidence for the role of the hypothalamo-pituitary-adrenal axis in chronic stress is con-
tradictory. Findings of enhanced cortisol concentrations conict with hypocortisolism in chronic
stress. Both, high and low cortisol levels, have been reported to go along with psychological and
somatic complaints. To integrate conicting empirical results and theoretical assumptions it is
hypothesized, that (1) the cortisol distribution becomes broader under the inuence of persisting
stress. Because of the association between extreme cortisol values and stress related complaints it
is supposed, that (2) stress related complaints will increase in prevalence in chronic stress. A high
level of chronic stress was assured by recruiting a sample of nursing staff; a waiting list controlled
cognitive-behavioral stress management intervention was implemented to vary stress systemati-
cally. As expected a high level of stress was accompanied by a broader morning cortisol distrib-
ution. After the intervention the distribution was less broad and corresponded with representative
normative values. However, subjects grouped on basis of (extreme) cortisol values did not differ
in the amount of stress, coping or psychophysiological complaints. The results suggest a stress-
induced variation of basal cortisol concentrations. The assumption of specic complaints depend-
ing on cortisol status could not be conrmed. Copyright 2004 John Wiley & Sons, Ltd.
Key Words
chronic stress; saliva cortisol; humans; cognitive-behavioral stress management; distribution
characteristics
Introduction
An investigation of cortisol levels under chronic
stress conditions would be expected to return
three possible results: no change in, enhanced,
and reduced concentrations of cortisol. Empirical
evidence supports each of those outcomes
(Ockenfels, 1995). Theories examining the role of
chronic stress on the hypothalamic-pituitary-
adrenal (HPA) axis (dys)regulation usually focus
mulations of this model Henry integrated aspects
of alexithymia and hemispheric lateralization. He
assumed that the cortisol reaction is particularly
guided righthemispheric. A combination of psy-
chological and physiological models of stress was
proposed by Ursin (1980, 1987, 1998; Levine
& Ursin, 1991). Two basic principles underpin
this approach: (i) activation, and (ii) expectancy.
Activation, the outcome in cases of homeostatic
imbalance, is understood as a process which tends
to re-establish balance by initiating a series of
central nervous-, vegetative-, skeletomuscular-,
endocrine- and immune-system changes. Activa-
tion is therefore an adaptive principle, because its
function is to prepare the organism to respond
to a stressor. Ursin, in agreement with Henry,
postulates a psychoneuroendocrine reaction
specicity, that distinguishes between active
(catecholaminergic), and passive (cortisol),
defense. The connecting link between stressor
and activation is expectancy. Expectancy includes
stimulus-expectancy and outcome-expectancy,
both of which are differentiated by the possible
inuence of coping. There are some meaningful
parallels in Ursins model: stimulus-expectancy
and outcome-expectancy can easily be identied
as Lazarus primary and secondary appraisal
(Lazarus & Folkman, 1984). The concept of
activation reects Selyes physiological view of
the stress process without his problematical
assumption of unspecicity (Mason, 1968). The
cybernetic view of the organism suits modern
psychosomatic thinking (Weiner, 1998).
At rst sight, these theoretical assumptions
satisfactorily explain hypercortisolism but not
hypocortisolism: hypercortisolism occurs when
chronic stress or sustained activation meets help-
lessness, or passive coping. However, it is also
possible to explain hypocortisolism using this
model as being merely necessary to differentiate
at least two ways of passive coping: e.g. helpless-
ness, and denial, to do so. Helplessness, or hope-
lessness, arises from a behavioral (withdrawal)
and physiological (higher cortisol) activation
which differs in kind from that found in denial or
refusal to believe stress (Henry, 1993). In the
latter case neither coping, nor elevated cortisol,
would be expected. Extraordinarily intense levels
of stress may however, evoke activation which
due to this coping-dependent reduced reagibility
of the HPA-axisoccurs more pronouncedly in
the later activation systems, for example in a
higher reagibility of the immune system (Buske-
Kirschbaum, Jobst, & Hellhammer, 1998). This
becomes even more likely, when a physiological
diathesis in the form of a dispositional reagibility
of the HPA-axis is presupposed. In the light of
genetic inuences on cortisol (Kirschbaum, Wst,
Faig, & Hellhammer, 1992) which in interaction
with lower birth weight (Wst, Wolf,
Hellhammer, & Kirschbaum, 1999) or early
stress experiences (King & Edwards, 1999) can
contribute to such a dispositional hypoactivity
this supposition seems appropriate.
The following conclusions can be drawn up to
this point: chronic psychosocial stress results in
activation as described by Ursin. This activation
triggers the described physiological and behav-
ioral dispositions. Under their impact the fre-
quencies of high and low cortisol levels rise and
the distribution of cortisol becomes broader.
(Cortisol is assumed to be normally distributed.
Empirical evidence for this supposition is rare,
occasional veterinary studies (Popot et al., 1997)
as well as singular human publications (Smyth
et al., 1996) favor a decadic logarithmic normal
distribution).
Extreme cortisol-concentrations are assumed
to be physiologically disadvantageous since they
have been linked to diverse psychophysiological
complaints: extremely high cortisol in depression
(e.g. Carroll, Curtis, & Mendels, 1976) and infec-
tious diseases (Dillman & Ostroumova, 1984),
extremely low cortisol in somatoform (Ehlert,
Gaab, & Heinrichs, 2001) and atopic diseases
(Buske-Kirschbaum et al., 1998) or in burnout
syndrome (Prner, 1998; overview in Heim et
al., 2000). The frequency of these complaints is
considered to increase in step with stress-induced
changes in cortisol distribution.
The question of if and how chronic stress may
cause long-term HPA-axis dysregulation, may be
answered, if at all, by controlled prospective lon-
gitudinal studies. At the same time however, in
view of the many likely determinants of HPA-axis
activity such as genetic makeup (Kirschbaum
et al., 1992), age (Heuser et al., 1994), sex
(Reinberg et al., 1996), smoking (Kirschbaum,
Strasburger, & Scherer, 1994), nyctohemeral
changes (Hakola, Hrm, & Laitinen, 1996),
physical activity (Opstad, 1991), physical illness
(Geiss, Varadi, Steinbach, Bauer, & Anton, 1997),
psychopathology (Caroll et al., 1976) or acute
stress (Kirschbaum et al., 1991), it is questionable
whether all potential inuences may be able to be
controlled. An alternative strategy and one which
places lower demands upon the experimenter, is
presented in this article, i.e. the acquisition of
F. A. Kaspers and O. B. Scholz
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 128
subjects from a population with high pre-existing
stress levels. A systematic variation of the hypoth-
esized inuence factor, stress, was then applied.
Nursing staff have been identied in many studies
as a profession with high levels of chronic job
stress (Addey, 1987; Cherniss, 1980; Gentry,
Forster, & Froehling, 1982; Maslach, 1978).
Hence, for this study subjects were recruited from
nursing staff.
The aims of this study may be summarized as
follows:
(a) sustained psychophysiological activation
and (habitual) dysfunctional coping interact
in such a way as to make constitutionally
extreme cortisol levels become even more
extreme in response to chronic stress. Conse-
quently, populations who suffer from chronic
stress should show a greater cortisol variation
and an increased frequency of extreme corti-
sol values.
(b) Extreme cortisol values are assumed to be dis-
advantagous, having been shown to co-occur
with diverse psychophysiological complaints.
Hence, it is expected that along with changes
in cortisol distribution such complaints
should increase in frequency.
(c) A cognitive behavioral stress management
(CBSM) intervention would be expected to
improve coping and reduce stress, as well as
normalize HPA-axis functioning and decrease
the frequency of stress/cortisol-related
complaints.
Materials and methods
Subjects
Thirty-six hospital nurses were recruited from
local hospitals in Bonn, Germany. Eleven of them
were excluded from the study for a number of
reasons: four dropped out of the intervention,
four were unable to deliver the post-intervention
measurement though taking part in the interven-
tion regularly, two moved out of Bonn, one
subjects set of saliva-samples contained no saliva.
The nal sample comprised 25 subjects (23
female, 2 male). The mean age was 39.1 8.2
years (2354 years). Subjects who received med-
ication that could affect HPA-axis activity were
excluded from analysis. The participants had
worked as nurses for 127 years (mean and
standard deviation: 13.6 8.3). Most worked in
orthopedic (seven) or psychiatric wards (eight),
four worked in neurosurgery, three in oncology
and the remainder in various other wards. Only
six subjects were on shift work (two early, four
late, no night shift workers). Nearly 73% worked
full-time (38.5 hours per week) whilst the remain-
der worked part-time on a 5075 per cent time
schedule. Those subjects who were working part-
time did not have any other jobs. Subjects were
recruited by offering the nursing services the
opportunity for their staff to take part in a free-
of-charge stress management intervention. The
nursing services were contacted via mail, tele-
phone and personal contact. Three hospitals par-
ticipated in the study. The present sample is not
representative and was not intended to be so,
since the primary aim was to select a population
representative of high stress levels.
To evaluate the efcacy of the CBSM two
versions of the interventiona full and a blocked
version (described later in this article)were
compared with a waiting-list control group. Sub-
jects were not randomly allocated to the experi-
mental conditions because the primary aim was
to have three equivalent experimental groups of
similar size comprised of individuals with similar
stress levels. However, this strategy failed due to
the dropout rate. Subjects were allocated to the
experimental conditions as follows: full version,
n = 10; blocked version, n = 7; waiting-list, n =
8.
Saliva sampling and cortisol analysis
For later cortisol analysis four saliva samples
were obtained at home from each subject at
20-minute intervals after awakening by means
of the Salivette device (Sarstedt, Rommelsdorf,
Germany). Recent studies suggest that multiple
morning cortisol measures to be a more reliable
marker for basal HPA-axis activity than single
assessments at xed times, e.g. at 8 a.m. (Prner
et al., 1997). Subjects were instructed neither to
brush their teeth in the sampling period nor to eat
or drink coffee, tea or carbonated soft drinks. All
saliva samples were stored at -20C until bio-
chemical analysis. For analysis of change in HPA-
axis activity, cortisol was measured before (t
1
)
and after (t
2
) the stress management intervention.
For controls the second measurement was taken
at the same time as that for the intervention
groups. While subjects were told not to disrupt
their awakening routines at t
1
they were
Stress-induced increase in morning cortisol variance
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 129
instructed to wake up at the same time on t
2
.
Salivary cortisol analysis was performed using
uorescence immunoassay according to
Dressendrfer, Kirschbaum, Rohde, Stahl, &
Strasburger (1992). Intra- and inter-assay vari-
ability of the assays was less than 10 and 12 per
cent, respectively. The analysis was carried out at
the biochemical laboratory of the Center for Psy-
chobiological and Psychosomatic Research at the
University of Trier, Germany. Two strategies were
used to analyze divergence in the distribution of
cortisol in this chronically stressed sample: the
count of extreme values, and a comparison of
variances. In both cases the sample values were
also compared with the normative values from
Wst et al. (2000) (n = 509).
Psychological variables
Three features of perceived stress were examined:
chronic stress, nursing-stress, and everyday stress.
Chronic stress was assessed using the Trier
Inventory for the Assessment of Chronic Stress
(TICS; Schulz & Schlotz, 1999). This Inventory
aims especially to assess the impact of stress upon
health. The TICS consists of 39 items which
record retrospective stress experiences over a 1
year period, using a ve-step frequency rating.
The test items constitute six scales: work over-
load, work discontent, social stress, lack of
social recognition, worries and intrusive mem-
ories. Internal consistency (Cronbachs a) ranges
between 0.76 and 0.91, split-half-reliability
(Guttman) between 0.79 and 0.90. Individual
test-scores were aggregated to a sum score of
chronic stress. Nursing stress was assessed using
the Nursing Stress Questionnaire (KP-SF;
Widmer, 1988). This test was developed in a
Swiss study and assesses seven dimensions of job
stress in nursing: workload, relationship to the
superior, insecurity, patient & ethics, lack of
independence, staff conicts and relationship
to the doctor. These scales comprise 50 items
describing job stress situations which can be rated
with respect to the extent of perceived stress on
a ve-stage Likert scale. Internal consistency
ranges between 0.68 and 0.84 (Cronbachs a).
Individual test-scores were aggregated to a sum
score of nursing stress. To control the inuence
of acute stress, daily hassles were measured by
using the Hassles and Uplifts Scale (DeLongis,
Folkman, & Lazarus, 1988) in an own translated
version which was also modied for German
conditions. It was employed on three consecutive
days at t
1
and two days at t
2
.
Coping was assessed by the Coping with Stress
Questionnaire (SVF 120-S, Janke & Erdmann,
1997). The SVF 120-S constitutes 20 subscales
which measure individual coping preferences. A
situation-specic version of the questionnaire was
used to examine coping under job-stress condi-
tions. Two kinds of passive coping were identied
by combining subscales and secondary scales:
passive coping due to helplessness/hopelessness
appeared to be linked with the subscales: ight,
social withdrawal, cognitive rumination, res-
ignation, self-pity and self-blame; avoid-
ance/denial of stress appeared to be linked with
the strategies of minimization, playing down
and blame-defence.
Several aspects of strain in terms of complaints
were considered: burnout, depression and bodily
complaints. Burnout was measured using the
Maslach Burnout Inventory (MBI; Maslach &
Jackson, 1986) in a German version (Barth, 1992;
Bssing & Perrar, 1992). The Allgemeine
Depressions Skala (ADS; Hautzinger & Bailer,
1993) is a screening instrument for depression
based on the Center for Epidemiological Studies
Depression Scale (CES-D; Radloff, 1977). Bodily
complaints were assessed by means of self report
using the Freiburg Complaint List (FBL-W;
Fahrenberg, 1986). Forty items, grouped into
ve scalesgeneral condition, cardiovascular,
gastrointestinal, tenseness and painwhose
scores can be combined to give a total score.
Cognitive-behavioral stress management
(CBSM) intervention
The specic content of the training is described
elsewhere in more detail (Kaspers, 2001). The
treatment consisted of a standardized group
training program, based on the intervention by
Kaluza (1996). The aim of this health interven-
tion program is to teach participants more exi-
ble ways of coping with individual stress. The
intervention consists of training in progressive
muscle relaxation, problem solving, and pleasure-
enhancement. The originally nonspecic pre-
ventive intervention was adapted so as to
better address nursing stress, and to facilitate the
reduction of stress-specic complaints. This was
achieved by tailoring the therapeutic materials
(e.g. in psychoeducation) to nursing-stress
demands, and by adding a number of other spe-
F. A. Kaspers and O. B. Scholz
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 130
cic elements to the intervention (e.g. the demon-
stration of psychophysiological interconnec-
tions in stress and relaxation, via biofeedback
(Dimsdale, Stern, & Dillon, 1988)). Table I lists
the original and additional elements of the
intervention.
The CBSM intervention was drawn up as a
series of 12 weekly meetings of 120 minutes.
Because of shift work it was anticipated that par-
ticipants may not be able to regularly visit every
session. Hence, a second version was provided, to
avoid this problem by combining the meetings
into four weekly blocks of 360 minutes (plus
break-time).
Statistical analysis
According to Curio (1989) two procedures were
used to calculate indices of morning cortisol:
deviation from the normative progression, and
calculation of the area under the curve (AUC).
The normative data of Wst et al. (2000) were
used to construct a model curve of morning cor-
tisol progression. This model makes it possible to
identify deviations from the norm. Albeit the
values from Wst et al. were gathered at differ-
ent time intervals (+0, +30, +45 and +60 minutes
after awakening) they can easily be extrapolated
(mathematically or graphically) for the time inter-
vals of the present study (+0, +20, +40 and +60
minutes after awakening). The AUC values were
calculated according to Prner (1998) with the
following formula for identical time intervals:
AUC = C
1
+ C
2
+ C
3
+ (C
4
- C
1
)/2 (with C
i
for
the single measures).
The statistical comparison of sample means
with normative values was made using t-values,
differences between the sample variances at t
1
with those at t
2
were tested with F-tests, differ-
ences between sample variances with normative
variances with c
2
tests. The latter were also used
to compare expected and observed frequencies.
Because of the rather small group sizes, group
differences were tested with KruskalWallis test
and MannWhitney-U-test to account for possi-
bly violated test conditions regarding analysis
of variance. The data analysis was performed
on a personal computer using Statistica

for
Windows.
Results
Stress: plausibility check and
manipulation check
The selection of subjects from nursing staff
should have served to provide a sample with
above-average stress levels. Table II contains the
comparisons of the sample means in the two
stress questionnaires (TICS, KP-SF) with the
normative values of the test-scales.
With the exception of the subscales work
discontent and intrusive memories all aspects of
chronic stress as measured with the TICS are
more strongly delineated in the present sample,
with work overload and lack of social recogni-
tion reaching statistical signicance. The extent
of nursing stress does not differ from the expected
values in Widmer (1988) though workload is
even higher in the present sample. These ndings
conrm that, as previously hypothesized, this
sample of nursing staff does indeed experience
stress at a high level.
The purpose of the CBSM intervention was to
systematically vary the level of subjective stress.
Compared to t
1
it was expected that at t
2
subjects
would show improved coping and reduced levels
of perceived stress. While the KruskalWallis test
Stress-induced increase in morning cortisol variance
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 131
Table I. Specication of the intervention components under aspects of bodily complaint reduction.
Problem solving Relaxation Pleasure enhancement
Focusing on bodily effects of Progressive muscle relaxation Promotion of exercise and
stress in the modules education, as a method which sensitizes activity
behavior analysis and coping for psychosomatic
interconnections in
Additional module: tension/relaxation
demonstration of
psychophysiological processes Additional modules:
via biofeedback (Dimsdale et al., imaginative strategies of
1988) pain management
was unable to detect signicant time or group
effects in coping effectiveness (apart from a ten-
dency to relax more under stress in the two inter-
vention groups at t
2
) there was a signicant time
effect in stress over all three groups, which was
due to reductions in nursing stress but not in
chronic stress. Table III shows the result of the
statistical analysis.
The data suggest that stress is reduced at t
2
, and
that the hypothesized changes in cortisol con-
centrations may be expected under all three
experimental conditions. While the data fail to
demonstrate a signicant treatment effect which
exceeds the effect of the waiting control condi-
tion, they prove a signicant stress reduction in
treatment and control subjects. Due to the under-
lying group differences in regard to stress levels
it seemed advisable to subject these differences
to further analysis, for example by using change
measures unaffected by the initial values.
Cortisol
Analysis of morning cortisol shows the typical
rise immediately after awakening. Table IV illus-
trates the cortisol concentrations before and after
the CBSM intervention.
The comparison of means (analysis of variance,
two factors, repeated measurement on both)
show a signicant main effect within (F = 21.01,
df = 3, p = 0.000), not between the days (F = 0.00,
df = 1, p = 0.953), the interaction effect is also
not signicant (F = 0.28, df = 3, p = 0.840). Pair-
wise comparisons of means (t-tests) show signi-
cant (p < 0.05) differences between the rst and
the third and the fourth value. The characteristic
pattern of rising morning cortisol was shown by
18 (72 per cent) subjects, which is little less than
the responder rate (77 per cent) found by Wst
et al. (2000). Correlations (product-moment)
between the morning cortisol concentrations on
two consecutive days range between 0.61 to 0.83
with a correlation for AUC of 0.70 (all correla-
tions statistically signicant with p < 0.001). This
is a stronger relationship than that found for
normal values over two consecutive days reported
by Wst et al.
Firstly the variances at t
1
were compared with
those at t
2
. It was expected that the higher stress
levels at t
1
would go along with higher variances,
while the variances should be smaller at t
2
when
F. A. Kaspers and O. B. Scholz
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 132
Table II. Plausibility check: comparison of the sample means at t
1
with the normative values in the two stress
questionnaires concerning chronic stress (TICS, normative values according to Schulz & Schlotz, 1999) and
nursing stress (KP-SF, normative values according to Widmer, 1988). As expected, nurses show higher levels of
chronic stress; nursing stress is comparable to values reported in literature (variables with values which were
signicantly different are marked with an asterisk).
Subscale Normative Standard Sample t
empir.
t
crit.,a=5 per cent
value deviation mean
Work overload (TICS)* 21.0 5.33 24.88 3.64 1.71
Social stress (TICS) 14.9 4.69 16.12 1.30 1.71
Worries (TICS) 16.7 3.19 17.52 1.29 1.71
Work discontent (TICS) 12.7 4.09 12.52 -0.22 1.71
Lack of social 16.9 3.30 18.28 2.09 1.71
recognition (TICS)*
Intrusive memories 16.1 4.40 15.80 -0.34 1.71
(TICS)
Relationship to the 2.46 0.93 2.63 0.91 2.06
superior (KP-SF)
Workload (KP-SF)* 2.78 0.70 3.04 4.14 2.06
Insecurity (KP-SF) 2.96 0.75 2.87 -0.60 2.06
Patient & ethics (KP-SF) 3.65 0.66 3.45 -1.52 2.06
Lack of independence 2.51 0.85 2.66 0.88 2.06
(KP-SF)
Staff conicts (KP-SF) 3.09 0.82 3.22 0.79 2.06
Relationship to the 2.38 0.90 2.57 1.06 2.06
doctor (KP-SF)
Total score (KP-SF) 2.88 0.56 2.96 0.71 2.06
stress was found to be reduced. As Table IV
shows, three of the four variances are signicantly
smaller at t
2
.
Secondly, the sample variances of the four
morning cortisol measures were compared with
the normal values. Table V shows the result
of this analysis. At t
1
, the variance for all four
morning cortisol measures in the present sample
is greater than the critical variances reported by
Wst et al., whereas only one of the variances in
Stress-induced increase in morning cortisol variance
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 133
Table III. Manipulation check: pre-post-comparison of means (MN) in the
stress measures (chronic stress reects a weighted mean from the TICS
subscales as a total score; nursing stress reects the total score of the KP-
SF). Changes are analyzed separately for the two training groups (full, full
version; block, blocked version) and control group. The analysis of
variance (two factorized MANOVA with repeated measurement on the
time factor) only results in a signicant time effect (F
2,21
= 5.625, p =
0.001).
Training
full,n=10
Training
block,n=7
Controls
n=8
MN
Pre
MN
Post
MN
Pre
MN
Post
MN
Pre
MN
Post
Chronic stress 2.595 2.552 2.438 2.586 3.029 3.030
Nursing stress 2.964 2.868 2.609 2.329 3.268 3.003
Table IV. Morning cortisol concentration means (MN, nmol/l) and
variances (s
2
) before (t
1
) and after (t
2
) the CBSM intervention. The
variances are compared using F-tests. Except for the fourth value (+60
minutes) all variances at t
2
are signicantly smaller than the corresponding
ones at t
1
.
MN
t
1
MN
t
2
s
2
t
1
s
2
t
2
F-value p-value
+0 minutes* 15.083 14.237 98.823 23.602 4.187 0.001
+20 minutes 20.995 19.237 149.170 56.103 2.659 0.010
+40 minutes 24.461 24.527 201.419 92.432 2.179 0.031
+60 minutes 21.652 22.283 127.657 116.609 1.095 0.413
*Because of missing data in two cases (the awakening saliva sample at t
2
contained
no saliva) the sample size differs in the awakening condition (n = 23).
Table V. Comparison of variances of the present sample (empir. s
2
) with
those according to Wst et al. (2000, crit. s
2
) before (t
1
) and after (t
2
) the
CBSM intervention. At t
1
all variances differ signicantly from the
normative distribution. While the fourth value (+60 minutes) at t
1
and t
2
reaches signicance at 5 per cent-level (respectively 2.5 per cent, bilateral
test), the rst three values also stand the test, when a = 0.001.
empir. s
2
crit. s
2
empir. c
2
crit. c
2
a=2.5 per cent
+0 minutes t
1
98.82 39.06 55.66 (p = 0.000) 36.78*
t
2
23.60 13.29 (p = 0.925)
+20 minutes t
1
149.17 65.61 54.57 (p = 0.000) 39.36
t
2
56.10 20.52 (p = 0.667)
+40 minutes t
1
201.42 88.36 54.71 (p = 0.000) 39.36
t
2
92.43 25.11 (p = 0.400)
+60 minutes t
1
127.66 68.06 45.02 (p = 0.006) 39.36
t
2
116.16 41.12 (p = 0.016)
*Because of missing data in two cases (the awakening saliva sample at t
2
contained
no saliva) the expected value differs in the awakening condition.
condition t
2
showed a signicant difference from
the normative variance.
Thirdly, extreme values were counted. Values
were judged as extreme when they differed by
more than one standard deviation from the
sample mean. In a normal distribution 68.26 per
cent of all values lie inside, and 31.74 per cent
outside, the interval of one standard deviation on
both sides of the distribution mean. It is therefore
possible to postulate the expected frequency of
values for given sample sizes. These expected fre-
quencies can then be compared with the observed
count before (t
1
) and after (t
2
) treatment. Table VI
shows the results of these calculations.
At t
1
three of the four frequencies of observed
extreme values exceed the expected frequencies.
For the third value (+40 minutes) even an inver-
sion of expected frequencies can be shown with
56 per cent of the observed values lying outside
the aforementioned one-standard-deviation inter-
val. At t
2
none of the comparisons between
observed and expected frequencies show any sig-
nicant difference.
To test the second hypothesis, that extreme cor-
tisol concentrations occur together with diverse
complaints (results of this hypothesis testing are
presented later), subjects were divided into three
groups, representing the two extremes and the
undeviating values in the middle of the distribu-
tion. In order to get comparable sample sizes, a
weaker criterion for classifying values as extreme
was applied here. By using the normative data of
Wst et al. mean values 2/3 standard deviation
were set as the cut-off criteria. In a normal dis-
tribution this should divide the distribution into
two nearly equal parts (hither versus beyond the
mean range). Values were labelled as hypo-
cortisolism if at least three of the four morning
cortisol values lay below the criterion of mean -
2/3 standard deviation; they were labelled as
hyper-cortisolism when they lay above mean
+2/3 standard deviation. Applying these criteria,
21 of the data sets at t
2
could unambiguously be
classied as hypo- (n = 7), hyper- (n = 6) or
normo-cortisolism (n = 8), while the curves of
the remainder were nontypical. When these crite-
ria were applied to t
2
a different picture emerged:
only one data set could be classied as hypo-
and only four as hyper-cortisolism whilst the
larger proportion of curve shapes (16) were
within the normal range. Figure 1 shows the
movements of group memberships from t
1
to t
2
.
To further illustrate the breadth of morning
cortisol distribution in t
1
and the changes in t
2
,
equidistant categories of AUCs were established.
Then the category frequencies for the AUCs were
computed. The results are presented in Figure 2.
It shows that at t
1
only 13 subjects (56.5 per cent)
lay within the range of mean 1 standard devia-
tion. At t
2
this number rises up to 17 subjects (74
per cent).
Strain
As mentioned earlier, subjects were divided into
three groups, classifying them as hyper-, hypo-
and normo-cortisolism group in order to test
the second hypothesis. This hypothesis assumes
a higher frequency of psychophysiological com-
F. A. Kaspers and O. B. Scholz
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 134
Table VI. Comparison of expected and observed frequencies of extreme
cortisol values before (t
1
) and after (t
2
) the CBSM intervention (values
outside mean 1 standard deviation; expected frequencies were calculated
according to the normative values of Wst et al. (2000) (n = 509). Three
of the four values differ from the expected frequencies at t
1
, none at t
2
(c
2
crit.,a=5 per cent
= 2.71, c
2
crit.,a=1 per cent
= 6.63).
Expected value Observed value c
2
empir.
+0 minutes 7.3* t
1
10 1.46 (p = 0.114)
t
2
6 0.34 (p = 0.280)
+20 minutes 7.9 t
1
12 3.10 (p = 0.039)
t
2
7 0.16 (p = 0.345)
+40 minutes 7.9 t
1
14 6.87 (p = 0.004)
t
2
8 0.00 (p > 0.90)
+60 minutes 7.9 t
1
13 4.80 (p = 0.014)
t
2
9 0.21 (p = 0.325)
*Because of missing data in two cases (the awakening saliva sample at t
2
contained
no saliva) the expected value differs in the awakening condition.
plaints or strain in the extreme groups. Group
membership was allocated using the mean values
2/3 standard deviationcriterion as described
earlier. Because of reduced number of extreme
values at t
2
a statistical comparison is only possi-
ble for t
1
. The means of the strain variables are
presented in Table VII.
With group membership at t
1
as the indepen-
dent variable, no identiable differences were seen
either between extreme groups and the normo-
cortisolism group, or between the hypo-
and hyper-cortisolism group in any of the
self report measures (F
14,22
= 1.092, p = 0.415).
This meant that the groups did not differ in the
amount of stress, coping quality (helplessness/
hopelessness versus avoidance/denial) or quan-
tity (extent of ineffective coping), in strain
quality (depression versus burnout) or quantity,
or in the amount or prole of physical
complaints.
Discussion
A high level of stress at t
1
and a reduced stress
level at t
2
were the conditions to test causal
hypotheses about the role of chronic stress in the
chosen quasi-experimental design. The rst ques-
tion was whether chronic stress caused a broader
distribution of basal cortisol levels. This could
be shown for the concentrations at t
1
, compared
to those at t
2
, indicated by sample variances and
extreme values count. As construct validity is
critical in quasi-experimental designs, some
efforts can be made in order to enhance it and
broaden the basis of data generalization (Cook &
Stress-induced increase in morning cortisol variance
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 135
Hypo Hyper
42 1
11 40 2 8
24 25 5
9 28
4 34
6 12
14
Normo 20 26 27
39
43
Figure 1. Movements in group-membership regarding
hypocortisolism or hypercortisolism respectively
normocortisolism from t
1
to t
2
. Subjects were classied
as extreme, when at least three of the four morning cor-
tisol levels lay outside mean 2/3 standard deviation.
Movements are illustrated by arrows.
m-2s m-s m m+s m+2s m-2s m-s m m+s m+2s
0
1
2
3
4
5
6
7
8
0
-
1
2
1
2
-
2
4
2
4
-
3
6
3
6
-
4
8
4
8
-
6
0
6
0
-
7
2
7
2
-
8
4
8
4
-
9
6
9
6
-
1
0
8
>
1
0
8
0
1
2
3
4
5
6
7
8
0
-
1
2
1
2
-
2
4
2
4
-
3
6
3
6
-
4
8
4
8
-
6
0
6
0
-
7
2
7
2
-
8
4
8
4
-
9
6
9
6
-
1
0
8
>
1
0
8
Figure 2. Distribution of morning cortisol areas under the curve (AUC) at t
1
(left) and t
2
(right). The abscissa con-
tains 10 equidistant categories of AUCs, represented by the category borders. The ordinate shows the categorial
frequencies. Vertical dotted lines indicate means (m) and standard deviations (s) as benchmarks of the distribution
of the normative control sample. They were computed from the data reported by Wst et al. (2000). Because
of missing data in two cases (the awakening saliva sample at t
2
contained no saliva) the comparison was only
performed for complete samples (n = 23).
Campbell, 1979). This was intended when the
data obtained from subjects in this study were
compared with normative data. In the present
sample morning cortisol concentrations showed a
broader distribution than predicted by studies
which provided normative values for morning
cortisol (Wst et al., 2000). This broader distrib-
ution was found in all morning cortisol measures,
with each group of four showing greater vari-
ability and with three measures out of the four
having more extreme values. Only the measure
taken on awakening value the comparison
between observed and expected frequencies
missed statistical signicance. One possible con-
clusion may be that interindividual differences
in morning cortisol are primarily differences of
increase rather than differences in baseline level.
This is consistent with the results of Buske-
Kirschbaum et al. (1998) who reported that
attenuated cortisol concentrations in atopic der-
matitis were found for the HPA-axis reactiviy, but
not for the baselines. The nding of a broader dis-
tribution of cortisol in chronic stress integrates
contrary ndings of rising versus falling cortisol
levels (Ockenfels, 1995).
Subjects with extreme morning cortisol con-
centrations did not differ in self-report measures,
whether with respect to each or with respect to a
group whose levels of cortisol were in the average
range. The second hypothesis, which postulated
differences in psychophysiological complaints,
burnout and depression was not conrmed. The
groups did not differ in the amount of perceived
stress or in their locus of control. Nor could dif-
ferences in coping styles be conrmed by the data.
It was postulated that denial of stress would lead
to hypocortisolism, passive coping to hypercorti-
solism. The use of a questionnaire, to measure
avoidance/denial, may be problematic and a
possible reason for this unexpected result. As
this method requires the primary appraisal of an
imagined situation as stressful (as the Coping
with Stress Questionnaire does), future exami-
nation might more appropriately use behavioral
observation.
How may a stress induced increase in morning
cortisol variation be explained? Stress models
are usually dened as diathesis-stress-models. In
Ursins activation theory diatheses could be
located in the habitually-preferred method of
information processing, physiological reaction, or
coping style. The nature of the information
processing in Ursins theory is a state or condition
of expectancy. His neuropsychological model of
expectancy resembles the assumptions of Grays
theory of emotion (1987, 1990). According to
Leplow and Ferstl (1998) Grays theory is likely
to modulate the diathesis in diathesis-stress-
concepts. For psychophysiological disorders they
postulate a hyperactivity in the behavioral inhi-
bition system (BIS), which Gray locates in the
septo-hippocampal region of the brain. Hyperac-
tivity of the BIS results in a behavior blockade
(passive, or no coping), which leads to an empha-
sized HPA-activation under stressful conditions
and an accentuated production of cortisol. From
this, three diatheses can be assumed whichat
rstare quite independent of each other:
(a) Cortisol diathesisgenetics (Kirschbaum
et al., 1992) as well as early stress experiences
(King & Edwards, 1999) or other factors may
contribute to a dispositional HPA-axis level
of activity.
(b) Expectancy diathesisthe denial to believe
stress represents dysfunctional primary
appraisal of objectively sustaining stressors.
Activation skips the HPA-axis and occurs
F. A. Kaspers and O. B. Scholz
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 136
Table VII. Extreme group (cortisol) comparison of means in the strain measures at t
1
(chronic stress reects a
weighted mean from the TICS subscales as a total score; nursing stress reects the total score of the KP-SF).
Subjects were classied as extreme, when at least three of the four morning cortisol levels lay outside mean 2/3
standard deviation.
Hypocortisolism
n=7
Normocortisolism
n=8
Hypercortisolism
n=6
Chronic stress 2.793 2.504 3.019
Nursing stress 2.857 2.889 3.200
Helplessness 10.095 9.286 13.083
Avoidance/denial 12.095 11.048 8.833
Depression 50.143 43.571 48.333
Burnout 2.456 2.360 2.625
Physical complaints 81.429 76.429 87.667
more pronouncedly in the later activation
systems while the protective effects of
cortisol fail (e.g. the mobilization of energy
reserves (Demitrack et al., 1991); or regula-
tion of the immune system (Munck, Guyre,
& Holbrook, 1984)). It may be that this
diathesis emerges more from social learning
processes such as modeling, or the social
reinforcement of toughness (Dienstbier,
1989). From a neurophysiological perspective
it could be speculated that the expectancy
diathesis is accompanied by a hyporeactive
BIS. Empirical evidence for lower cortisol in
impulsivity (King, Jones, Scheuer, Curtis, &
Zarcone, 1990; Moss, Vanyukov, & Martin,
1995) or extraversion (Dabbs & Hopper,
1990; Prner, 1994) supports this
speculation.
(c) Activation diathesisthis diathesis represents
those theoretical assumptions of Henry and
Ursin, which view high cortisol concentra-
tions as a result of passive, helpless coping. In
later formulations Henry (1993) integrated
alexithymia and righthemispheric dominance
in his concept. In doing this he strongly sug-
gested that this reaction specity is a trait
or a diathesis. As described earlier, this
diathesis is accompanied by a hyperreactive
BIS.
The three diatheses interact in a dysfunctional
way which results in a broader cortisol distribu-
tion, as already described. This study, however,
shows that this process is a reversible one. CBSM
can sensitize participants to perceive stress situa-
tions; this improves the adequacy of expectancy.
Training in problem solving enhances active
coping. Both are conditions that operate in a way
that better adapt coping to situational demands.
As expected, the present sample of nursing staff
showed an attenuated level of chronic stress,
particularly in work overload and lack of social
recognition. Job-specic workload was even
higher than in comparable nursing staff studies
(Widmer, 1988). This warrants the assumption
that the choice of subjects did establish a high
level of stress in the present sample. After the
CBSM intervention not only the two experimen-
tal groups but also the waiting-list control group
showed lower levels of stress. The reasons for this
unintended effect are unclear nor is it the purpose
of this present study to seek an explanation for
such an outcome. To fulll the aims of this study
it was necessary to reduce stress at t
2
; that this
effect occurred in the control group as well may
be seen as benecial. It may be that the fact of
taking part in a scientic program which included
procedures aimed at stress reduction (even
though after a time interval) produced a thera-
peutic effect on the control group. This effect
could be described in terms of reframing, which
can be seen as an aspect of cognitive coping. As
another explanation, being allocated to the
waiting-list could have had a positive effect on
motivation in sense of a Now more than ever!
kind of reaction. This would result in a mobi-
lization of coping resources.
Shift work can alter circadian rhythms; altered
circadian rhythms can affect morning cortisol
concentrations (Hakola et al., 1996; Motohashi,
1992). It could be argued, that abnormal morning
cortisol concentrations in nurses are rather the
result of shift work than of anything else. Only
six subjects were on shift work during the period
of investigation. So it seems unlikely that shift
work is responsible for changes in cortisol
concentrations which affect the whole sample. An
alternative theory could explain reduced vari-
ances at t
2
as an effect of learned behavior: it
might be that the actual stress of collecting
cortisol affected the concentrations observed.
However, studies could show, that this is usually
not the case (Prner, 1998; Prner et al., 1997;
Wst et al., 2000).
There are, of course, several limitations in the
present studyone being the small sample size,
another that this was a highly selected non-
representative samplethat call for caution in
discussing the data. Further research would be
required to provide a broader basis for the drawn
conclusions.
Acknowledgment
Very special thanks to: Prof. Dr Dirk H. Hellhammer
for his support.
References
Addey, C. (1987). Who cares? Nursing Times, 83, 5253.
Barth, A.-R. (1992). Burnout bei Lehrern. Gttingen:
Hogrefe.
Bssing, A., & Perrar, K.-M. (1992). Die Messung von
Burnout. Untersuchung einer deutschen Fassung des
Maslach Burnout Inventory (MBI-D). Diagnostica, 38(4),
328353.
Buske-Kirschbaum, A., Jobst, S., & Hellhammer, D.H.
(1998). Altered reactivity of the hypothalamus-pituitary-
adrenal axis in patients with atopic dermatitis: pathologic
Stress-induced increase in morning cortisol variance
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 137
factor or symptom? Annals of the New York Academy of
Science, 840, 747754.
Carroll, B.J., Curtis, G.C., & Mendels, J. (1976). Neuro-
endocrine regulation in depression. I. Limbic system-
adrenocortical dysfunction. Archives of General Psychiatry,
33, 10391044.
Cherniss, C. (1980). Professional burnout in human service
organizations. New York: Praeger.
Cook, T.D., & Campbell, D.T. (1979). Quasi experimenta-
tion: Design and analysis issues for eld settings. Chicago,
IL: Rand McNally.
Curio, I. (1989). Einzelfall- und Zeitreihenanalyse biochemis-
cher Indikatoren. In F. Petermann (Ed.), Einzelfallanalyse.
2., vllig berarbeitete Auage (pp. 307315). Munich:
Oldenbourg.
Dabbs, J.M., & Hopper, C.H. (1990). Cortisol, arousal, and
personality in two groups of normal men. Personality and
Individual Differences, 11(9), 931935.
DeLongis, A., Folkman, S., & Lazarus, R.S. (1988). The
impact of daily stress on health and mood: Psychological
and social resources as mediators. Journal of Personality
and Social Psychology, 54(3), 486495.
Demitrack, M.A., Dale, J., Straus, S.E., Laue, L., Listwak, S.J.,
Kruesi, M.J.P., Chrousos, G.P., & Gold, P.W. (1991).
Evidence for impaired activation of the hypothalamic-
pituitary-adrenal axis in patients with chronic fatigue
syndrome. Journal of Clinical Endocrinology and Metabo-
lism, 73, 12241234.
Dienstbier, R.A. (1989). Arousal and physiological toughness:
Implications for mental and physical health. Psychological
Reviews, 96, 84100.
Dillman, V.M., & Ostroumova, M.N. (1984). Hypothalamic,
metabolic, and immune mechanisms of the inuence of
stress. In B.H. Fox, & B.H. Newberry (Eds), Impact of psy-
choendocrine systems in cancer and immunity (pp. 5885).
New York: Hogrefe.
Dimsdale, J.E., Stern, M.J., & Dillon, E. (1988). The stress
interview as a tool for examining physiological reactivity.
Psychosomatic Medicine, 50, 6471.
Dressendrfer, R.A., Kirschbaum, C., Rohde, W., Stahl, F., &
Strasburger, C.J. (1992). Synthesis of a cortisol-biotin con-
jugate and evaluation as a tracer in immunoassay for sali-
vary cortisol measurement. Journal of Steroid Biochemistry
and Molecular Biology, 43, 683692.
Ehlert, U., Gaab, J., & Heinrichs, M. (2001). Psychoneu-
roendocrinological contributions to the etiology of depres-
sion, posttraumatic stress disorder and stress-related bodily
disorders: The role of the hypothalamus-pituitary-adrenal
axis. Biological Psychology 57, 141152.
Fahrenberg, J. (1986). Die Freiburger Beschwerdenliste FBL.
Diagnostica, 20, 7996.
Geiss, A., Varadi, E., Steinbach, K., Bauer, H.W., & Anton, F.
(1997). Psychoneuro-immunological correlates of persisting
sciatic pain in patients who underwent discectomy. Neuro-
science Letters, 237, 6568.
Gentry, W.D., Forster, S.B., & Froehling, S. (1982). Psycho-
logic response to situational stress in intensive and nonin-
tensive nursing. In E.A. McConnell (Ed.), Burnout in the
nursing profession (pp. 262266). St. Louis: Mosby.
Gray, J.A. (1987). The neuropsychology of anxiety. Oxford:
Clarendon Press.
Gray, J. (1990). Brain systems that mediate both emotions and
cognition. In J. Gray (Ed.), Psychobiological aspects of rela-
tionships between emotion and cognition (pp. 269288).
East Sussex: Erlbaum.
Hakola, T., Hrm, M.I., & Laitinen, J.T. (1996). Circadian
adjustment of men and women to night work.
Scandinavian Journal of Work and Environmental Health,
22, 133138.
Hautzinger, M., & Bailer, M. (1993). ADS, Allgemeine
Depressions Skala, manual. Weinheim: Beltz.
Heim, C., Ehlert, U., & Hellhammer, D.H. (2000). The poten-
tial role of hypocortisolism in the pathophysiology of stress
related bodily disorders. Psychoneuroendocrinology, 25,
135.
Henry, J.P. (1986). Neuroendocrine patterns of emotional
response. In R. Plutchik, & H. Kellerman (Eds), Emotion:
Theory, research and experiences, vol 3 (pp. 3760). San
Diego, CA: Academic Press.
Henry, J.P. (1993). Psychological and physiological responses
to stress: The right hemisphere and the hypothalamo-
pituitary-adrenal axis. An inquiry into problems of human
bondings. Integrative Physiological and Behavioral Science,
28, 368387.
Henry, J.P., & Stephens, P.M. (1977). Stress, health and the
social environment: A sociobiologic approach to medicine.
New York: Springer.
Heuser, I.J., Gotthardt, U., Schweiger, U., Schmider, J.,
Lammers, C.H., Dettling, M., & Holsboer, F. (1994). Age-
associated changes of pituitary-adrenocortical hormone
regulation in humans: Importance of gender. Neurobiology
of Aging, 15, 227231.
Janke, W., & Erdmann, G. (1997). Streverarbeitungsbogen
(SVF120) nach W. Janke, G. Erdmann, K.W. Kallus und W.
Boucsein. Kurzbeschreibung und grundlegende Kennwerte.
Gttingen: Hogrefe.
Kaluza, G. (1996). Gelassen und sicher im Stre; psycholo-
gisches Programm zur Gesund-heitsfrderung. Berlin:
Springer.
Kaspers, F.A. (2001). Endokrinologische Korrelate krper-
licher Beschwerden bei chronischem Stre. Gttingen:
Cuvillier.
King, J.A., & Edwards, E. (1999). Early stress and genetic
inuences on hypothalamic-pituitary-adrenal axis function-
ing in adulthood. Hormones and Behavior, 36, 7985.
King, R.J., Jones, J., Scheuer, J.W., Curtis, D., & Zarcone, V.P.
(1990). Plasma cortisol correlates of impulsivity and sub-
stance abuse. Personality and Individual Differences, 11(3),
287291.
Kirschbaum, C., Strasburger, C.J., & Scherer, G. (1994). Pitu-
itary and adrenal hormone responses to pharmacological,
physical and psychological stimulation in habitual smokers
and nonsmokers. Clinical Investigation, 72, 804810.
Kirschbaum, C., Wst, S., Faig, H.G., & Hellhammer, D.H.
(1992). Heritability of cortisol responses to h-CRH, ergom-
etry and psychosocial stress in humans. Journal of Clinical
Endocrinology and Metabolism, 75, 15261530.
Kirschbaum, C., Steyer, R., Eid, M., Patalla, U.,
Schwenkmezger, P., & Hellhammer, D.H. (1991). Cortisol
and behavior. 2. Application of a latent state-trait model
to salivary cortisol. Psychoneuroendocrinology, 15(4),
297307.
Lazarus, R.S., & Folkman, S. (1984). Stress, appraisal and
coping. New York: Springer.
Leplow, B., & Ferstl, R. (1998). Psychophysiologische Strun-
gen [Psychophysiological disorders]. In H. Reinecker (Ed.),
Lehrbuch der Klinischen Psychologie. 3., berarbeitete und
erweiterte Auage (pp. 539562). Gttingen: Hogrefe.
Levine, S., & Ursin, H. (1991). What is stress? In M.R.
Brown, C. Rivier, & H. Koob (Eds), Neurobiology and neu-
roendocrinology of stress (pp. 321). New York: Marcel
Decker.
Maslach, C. (1978). The client role in staff burn-out. Journal
of Social Issues, 34(4), 111124.
F. A. Kaspers and O. B. Scholz
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 138
Maslach, C., & Jackson, S.E. (1986). Maslach Burnout Inven-
tory (2nd ed.). Palo Alto: Consulting Psychologists Press,
Inc.
Mason, J.W. (1968). A review of psychoendocrine research on
the pituitary-adrenal cortical system. Psychosomatic Medi-
cine, 30, 576607.
Moss, H.B., Vanyukov, M.M., & Martin, C.S. (1995). Sali-
vary cortisol responses and the risk for substance abuse in
prepubertal boys. Biological Psychiatry, 38(8), 546555.
Motohashi, Y. (1992). Alterations of circadian rhythm in
shift-working ambulance personnel. Monitoring of salivary
cortisol rhythm. Ergonomics, 35(11), 11311340.
Munck, A., Guyre, P.M., & Holbrook, N.M. (1984). Physio-
logical functions of glucocorti-coids. Endocrine Reviews, 5,
2544.
Ockenfels, M. (1995). Der Einu von chronischem Stre auf
die Cortisolkonzentration im Speichel: Gesamtkonzentra-
tion, Tagesprol und Cortisolreaktivitt auf alltgliche
Stressoren. Munich/New York: Waxmann.
Opstad, P.K. (1991). Androgenic hormones during prolonged
physical stress, sleep, and energy deciency. Journal of
Clinical Endocrinology and Metabolism, 74, 11761183.
Popot, M.A., Houghton, E., Ginn, A., Jones, M., Teale, P.,
Samuels, T., Lassourd, V., Dunnett, N., Cowan, D.A.,
Bonnaire, Y., & Toutain, P.L. (1997). Cortisol concentra-
tions in post competition horse urine: A French and British
survey. Equine Veterinary Journal, 29(3), 226229.
Prner, J. (1994). Effekte wiederholter psychischer Belastung
auf die Cortisolspiegel unter Bercksichtigung von Persn-
lichkeitsvariablen. Unpublished diploma thesis, University
of Trier, Germany.
Prner, J.C. (1998). Freie Cortisolspiegel am Morgen: Unter-
suchungen zu Anstieg, Stabilitt, soziodemographischen
und psychologischen Variablen. Gttingen: Cuvillier.
Prner, J.C., Wolf, O.T., Hellhammer, D.H., Buske-
Kirschbaum, A., Auer, K., von, Jobst, S., Kaspers, F., &
Kirschbaum, C. (1997). Free cortisol levels after awaken-
ing: A reliable marker for the assessment of adrenocortical
activity. Life Sciences, 61(26), 25392549.
Radloff, L.S. (1977). The CES-D scale: A self-report depres-
sion scale for research in the general population. Applied
Psychological Measurement, 1(3), 385401.
Reinberg, A.E., Touitou, Y., Soudant, E., Bernard, D., Bazin,
R., & Mechkouri, M. (1996). Oral contraceptives alter
circadian rhythm parameters of cortisol, melatonin, blood
pressure, heart rate, skin blood ow, transepidermal water
loss and skin amino acids of healthy young women.
Chronobiology International, 13(3), 199211.
Schulz, P., & Schlotz, W. (1999). Trierer Inventar zur Erfas-
sung von chronischem Stre (TICS): Skalenkonstruktion,
teststatistische berprfung und Validierung der Skala
Arbeitsberlastung. Diagnostica, 45(1), 819.
Selye, H. (1950). Stress. (The physiology and pathology of
exposure to stress). Montreal: Acta, Inc.
Smyth, J.M., Ockenfels, M.C., Gorin, A.A., Catley, D., Porter,
L.S., Kirschbaum, C., Hellhammer, D.H., & Stone, A.A.
(1996). Individual differences in the diurnal cycle of corti-
sol. Psychoneuroendocrinology, 22(2), 89105.
Ursin, H. (1980). Personality, activation and somatic health.
In S. Levine, & H. Ursin (Eds), Coping and health (pp.
259280). New York: Plenum Press.
Ursin, H. (1987). Expectancy and activation: An attempt to
systematize stress theory. In D.H. Hellhammer, I. Florin, &
H. Weiner (Eds), Neurobiological Approaches to Human
Disease (pp. 313343). Bern: Huber.
Ursin, H. (1998). The psychology in psychoneuroendocrinol-
ogy. Psychoneuroendocrinology, 23(6), 555570.
Weiner, H. (1998). Notes on an evolutionary medicine.
Psychosomatic Medicine, 60, 510520.
Widmer, M. (1988). Stress, Stressbewltigung und Arbeit-
szufriedenheit beim Krankenpegepersonal. Aarau:
Schweizerisches Institut fr Gesundheits- und
Krankheitswesen SKI.
Wst, S., Wolf, J.M., Hellhammer, D.H., & Kirschbaum, C.
(1999). Salivary cortisol levels after awakening as a new
index for adrenocortical activity: Normal values and recent
ndings. Poster presented at the XXXth annual ISPNE Con-
gress, July 30August 3, 1999, Orlando, Florida.
Wst, S., Wolf, J.M., Hellhammer, D.H., Federenko, I.,
Schommer, N., & Kirschbaum, C. (2000). The cortisol
awakening responsenormal values and confounds. Noise
& Health, 7, 7988.
Stress-induced increase in morning cortisol variance
Copyright 2004 John Wiley & Sons, Ltd. Stress and Health 20: 127139 (2004) 139

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