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7/21/2019 Predicting Early Morning Cortisol Via the Interplay of Neural and Phenomenological Life Engagement
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Engagement and Morning Cortisol 1
Running head: NEURAL AND PHENOMENOLOGICAL ENGAGEMENT
Predicting Early Morning Cortisol Via the Interplay
of Neural and Phenomenological Life Engagement
First Year Project of
Owen R. Temple
University of Wisconsin-Madison
Correspondence should be addressed to Owen R. Temple, 1300 University Avenue, 2245 MSC,
Madison, WI 53706 (email: otemple@wisc.edu).
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Engagement and Morning Cortisol 2
Abstract
Regulated release of cortisol (CORT) by the hypothalamic-pituitary-adrenocortical
(HPA) axis is an important factor in healthy aging. The present investigation focuses on the
cortisol awakening response, a reliable biological response that has been associated with
psychosocial variables, stress, and health, and links it to approach-related engagement with life,
indicated neurally in terms of greater relative left frontal EEG asymmetry (Davidson, 1995;
2004; Sutton & Davidson, 1997) and phenomenologically in terms of psychological well-being
(Ryff, 1989). Both forms of engagement were hypothesized to predict lower levels of early
morning cortisol rise. The sample consisted of 135 older women (mean = 74.0, SD = 7.08) on
whom all of the above assessments were available. Although neither measure of engagement
was found to predict levels of early morning rise in cortisol, the interaction between the two was
a significant predictor for 4 of six scales of well-being. Among those who showing high
phenomenological engagement, the magnitude of the CORT morning rise was lower among
those who were more left frontally activated; thus, illustrating an enhancement effect linked with
having both forms of life engagement. However, among those with low self-reported
engagement, the direction of the effect was reversed (i.e., CORT levels were lower among those
showing the absence both forms of engagement). The latter pattern was considered in light of
the prior literature linking a blunted morning rise to hypocortisolism and chronic stress.
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Engagement and Morning Cortisol 3
Predicting Early Morning Cortisol via the Interplay
of Neural and Phenomenological Life Engagement
Dysregulated release of cortisol (CORT) by the hypothalamic-pituitary-adrenocortical
(HPA) axis is a common feature of aging (Deuschle, Gotthardt, Schweiger, Weber, Korner,
Schmider et al., 1997; Ice, Katz-Stein, Himes & Kane, 2004; Wilkinson, Petrie, Murray,
Colasurdo, Raskind, & Peskind, 2001), and this dysregulation in the neuroendocrine system
plays an important role in the etiology of multiple health outcomes such as rheumatoid arthritis,
diabetes, osteoporosis, atherosclerosis, and coronary heart disease (Raff, Raff, Duthie, Wilson,
Sasse, Rudman et al., 1999; Sapolsky, Romero, & Munck, 2005). Despite accumulating
evidence on the importance of regulation of the HPA axis for health in later life, little is currently
known about how positive neurobiological predispositions and positive psychosocial factors
influence these systems and possibly buffer the human organism from disease processes. This
investigation focuses on approach-related engagement with life, indicated neurally in terms of
greater relative left frontal EEG asymmetry (Davidson, 1995; 2004; Sutton & Davidson, 1997)
and phenomenologically in terms of psychological well-being (Ryff, 1989), as possible
protective factors for healthy neuroendocrine function in the course of human aging. We also
examine the extent to which withdrawal-related disengagement, indicated by greater relative
right frontal EEG asymmetry and reported lack of psychological well-being contribute to
dysregulation in neuroendocrine systems and resultant disease.
One window on neuroendocrine function is the morning rise in CORT in response to
waking, which has been found to be a reliable, adrenocortical secretory pattern when measured
with strict reference to waking (Clow, Thorn, Evans, & Hucklebridge, 2004; J. C. Pruessner et
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al., 1997). In the cortisol awakening response, levels of cortisol typically increase 50% to 100%
in the first 30 to 45 minutes after waking to a peak level and then decline rapidly as a part of the
typical diurnal rhythm (Kirschbaum & Hellhammer, 2000). The physiological purpose of this
rise remains unclear, but researchers have suggested metabolic or immunoregulatory roles
(Hucklebridge, Clow, Abeyguneratne, Huezo-Diaz, & Evans, 1999; J. C. Pruessner et al., 1997).
The CORT morning rise has been found to be associated with a growing list of psychological
and physical conditions. Exaggerated, or excessive secretion of CORT in response to waking
has been associated with depression (Bhagwagar, Hafizi, & Cowen, 2005; M. Pruessner,
Hellhammer, Pruessner, & Lupien, 2003), perceived stress (J. C. Pruessner, Hellhammer, &
Kirschbaum, 1999), loneliness (Steptoe, Owen, Kunz-Ebrecht, & Brydon, 2004), neuroticism
(Portella, Harmer, Flint, Cowen, & Goodwin, 2005), and work overload (Lundberg & Hellström,
2002), and feelings of loneliness, threat, dysphoria, and of being overwhelmed on the previous
day (Adam, Hawkley, Kudielka, & Cacioppo, 2006). Alternatively, hyposecretion of CORT in
response to waking has also been associated with atypical depression (Stetler & Miller, 2005),
marital strain (Barnett, Steptoe, & Gareis, 2005), material hardship (Ranjit, Young, & Kaplan,
2005), high fatigue and physical symptoms (Adam, Hawkley, Kudielka, & Cacioppo, 2006), and
burnout (J. C. Pruessner, Hellhammer, & Kirschbaum, 1999). This pattern of findings reflects
previous work suggesting that challenge or stress may result in either increases (Melamed et al.,
1999; Schaeffer & Baum, 1984) or decreases (J. C. Pruessner et al., 1999; Yehuda, Giller,
Levengood, Southwick, & Siever, 1995) in morning cortisol levels.
Continuing with the focus on maladaptive linkages, those with lower approach-related
engagement with life (i.e., low PWB) and hypoactivity of the left PFC (i.e., lower relative left
frontal EEG asymmetry) may be vulnerable to adverse HPA outcomes. Normally, activation of
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the left PFC is believed to inhibit signaling by the amygdala (Davidson, 2004). However, with
the absence or suspension of approach-related engagement and reduced activity of the left PFC,
day-to-day challenges may result in increased and persistent release of CRH by the amygdala to
its connections in the paraventricular nucleus (PVN) of the hypothalamus, the key initiating
region of the HPA axis (Plotsky, Owens, & Nemeroff, 1998). Persistent hyperactivation of the
HPA axis may eventually disrupt the glucocorticoid-mediated negative feedback normally
imposed on the HPA axis by the hippocampus and other brain regions, resulting in either
continued excessive cortisol release (hypercortisolism) or, after compensatory downregulation by
these initiating regions of the HPA axis, too little cortisol release by the HPA axis
(hypocortisolism) (Fries, Hesse, J. Hellhammer, & D. H. Hellhammer, 2005; Jacobson &
Sapolsky, 1991; Parker, Schatzberg, & Lyons, 2003; Sapolsky, Romero, & Munck, 2000). As
noted earlier, hyposecretion of CORT has been reported in other groups experiencing prolonged
stress (J. C. Pruessner et al., 1999; Yehuda et al., 1995).
Our emphasis, however, is not just how these related systems go awry, but also on what
constitutes adaptive neurobiological processes. Thus, we emphasize approach-related
engagement in life -- the ongoing, active pursuit of goals, a vitally important aspect of human
functioning that our physiological and psychological systems evolved to perform. We assess
such engagement in an individual’s life both at the cognitive level as consciously accessible
memory for previous approach-related engagement communicated via self-report inventories;
and, at the neurobiological level as a neural predisposition for approach-related
electroencephalograph activation.
Engagement with life can be represented in the brain as the activation of the approach
system, or greater left- than right-sided prefrontal EEG activation (Davidson, 1995). Greater
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relative left frontal (GRLF) EEG asymmetry is hypothesized to be reflective of asymmetrical
frontal systems and to indicate greater approach activation relative to withdrawal activation
(Davidson, 1995; 2004; Harmon-Jones & Allen, 1997; Sutton & Davidson, 1997). To explain the
approach-withdrawal system in terms of known PFC function, activation of the left hemisphere
PFC is argued to implement processes that promote the temporal continuity of approach
motivation, suppression of interference by competing motivational tendencies, and shifts in
motivational priorities toward approach-related goals (Tomarken & Keener, 1998). Continued
approach-related engagement and activation of left PFC at the level of neural substrates thus
represents vitality vis-à-vis ongoing challenge, and, therefore, predicts regular inhibition of the
amygdala and concomitant release of CORT within healthy ranges (i.e., adaptive neuroendocrine
regulation).
To date, no prior work has documented a direct relation between greater relative left
frontal EEG asymmetry and lower cortisol in adults, yet previous studies show the plausibility of
such relationships. Greater relative left frontal EEG activation has been linked to higher scores
on PWB (Urry et al., 2004), and higher reported PWB has been related to lower cortisol levels
(Lindfors & Lundberg, 2002; Ryff, Singer, and Love, 2004). Additionally, greater relative right
prefrontal EEG activation has been associated with depression (Henriques and Davidson, 1991),
and symptoms of depression have been frequently linked to higher cortisol levels (e.g., Parker,
Schatzberg and Lyons, 2003). In a study in non-human primates, a direct link between greater
relative left frontal EEG asymmetry and lower cortisol levels has been demonstrated (Kalin et
al., 1998).
Taken together, the previous literature indicates that integrated self-reported measures of
engagement and neurophysiological measures of engagement may contribute to richer
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understanding of aspects of neuroendocrine regulation and dysregulation. In terms of main
effect hypotheses, we predict that those showing higher levels of phenomenological life
engagement, measured by self-reported well-being, will show lower levels of morning CORT.
Similarly, we predict that those showing greater relative left frontal EEG asymmetry will show
lower levels of early morning CORT. Conversely, we also predict that lack of engagement,
measured by low reported well-being and greater relative right frontal EEG asymmetry are
predicted to be linked with higher early morning CORT.
Where our investigation goes beyond prior inquiry, however, pertains to the interplay
between the two types of engagement. With regard to interaction effects, we envisioned multiple
possibilities. In terms of beneficial patterns, an enhancement effect would be evident if those
showing higher phenomenological and neural engagement had lower levels of early morning
CORT, compared to those who had only one engagement advantage. A compensation effect , in
contrast, would be evident if those engagement vulnerability at one level (phenomenological or
neural) was offset by engagement advantage at the other level, such that those showing this
pattern had lower levels of early morning CORT compared to those lacking either form of
engagement. The latter combination would illustrate a negative amplification effect such that the
absence of both forms of engagement is linked with higher levels of early morning CORT,
compared to those showing only one such vulnerability. A further detrimental possibility
pertains to a compromise effect , in which lack of engagement on one level offsets the benefits of
engagement on another. Given that no prior research has investigated any of these possibilities,
we did not have a basis on which to predict the prominence of one over another. In addition, we
note that the above effects reflect primarily a hypercortisolism perspective, even though previous
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research also addresses the problem of hypocortisolism. We return to these contrasts in
presentation and discussion of the findings.
Method
Participants
The sample consisted of 135 women, all of whom had participated in a prior longitudinal
study built around the transition of community relocation. Additional research support allowed
for the recruitment of approximately half of the prior study’s sample for data collection that
included psychosocial assessments and a comprehensive array of biomarkers. There were no
selection criteria, apart from being able to complete the questionnaires and visit the General
Clinical Research Center (GCRC) for biological assessments. The sample ranged in age from 61
to 91 (mean = 74.0; SD = 7.08). Respondents had moderate incomes (mean = USD 26,360; SD =
USD 18,340) and slightly more than a high school education (mean = 14.1 years of schooling;
SD = 2.8 years). Over half (55.6%) were widowed, with the rest married (17%), never married
(8.9%), or divorced or separated (18.5%).
Measures
Self-administered questionnaires were sent to respondents 3–4 weeks prior to their visit
to the UW-Madison campus for the biomarker assessments. These were completed
independently and returned to investigators at the time of their campus visit.
Neurophysiological Measures. Engagement on the neural level was operationalized as the
activation of the approach system, or greater left- than right-sided prefrontal EEG activation
(Davidson, 1995; Sutton & Davidson, 1997). EEG data collection in both samples consisted of
the collection of scalp-recordings focused on assessment of EEG asymmetry during a resting
baseline and during picture viewing of positive, neutral and negative pictures. EEG asymmetry
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serves as an approach-related engagement independent variable on the neural level,
conceptualized as activation of the approach system, or greater left- than right-sided prefrontal
EEG activation (Davidson, 1995; Sutton & Davidson, 1997). Greater alpha power indicates
lower activation in a given region, and the mean alpha power of artifact-free epochs log
transformed to symmetrize its distribution. The asymmetry metric was calculated (log right – log
left) for alpha power at midfrontal (F4 & F3) leads. Again, because alpha power inversely
correlates with activation, a positive asymmetry score indicates greater left than right activation.
All EEG asymmetry measures were measured according to the following protocol: Following an
overnight stay at a GCRC, in the afternoon, a hearing test was administered, and then EEG
Baselines (4 minutes, 2 with eyes closed, 2 with eyes open) were recorded. After the EEG
session, participants returned home.
Psychological Well-Being. Engagement on the phenomenological level was measured
using the Psychological Well Being (PWB) Inventory (Ryff, 1989) to index self-reports of active
goal pursuit and engagement in multiple life domains (e.g., “I enjoy making plans for the
future…”). The PWB Inventory was developed to provide a measure of eudemonic well-being to
seek to measure psychosocial functioning in important life domains. Items on the instrument
represent challenges individuals encounter as they strive to function positively, and Active
engagement with the existential challenges of living was operationalized with the six subscales
of the PWB Inventory: autonomy, environmental mastery, personal growth, positive relations
with others, purpose in life and self-acceptance. The instrument probably is best conceptualized
as a measure of perceived active goal pursuit (Ryff, 1989; Ryff & Keyes, 1995). These subscales
were based on Ryff’s (1989) theoretical integration of numerous formulations of positive
functioning. The hypothesized 6-factor structure of well-being has been supported by data from a
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national sample of Americans (Ryff & Keyes, 1995). In this study, each well-being dimension
was measured with 14 self-descriptive items (scale range = 14–84). Cronbach’s alpha
coefficients for the six scales ranged from 0.85 to 0.91. In the analysis, all psychological well-
being scales were cubed to symmetrize the distribution of scores.
Depressive Symptoms. Symptoms of depression were assessed using the CES-D Scale
(Radloff, 1977), a 20-item instrument (scale range = 0–60) that represents a general lack of
engagement (“I could not get going”) and suspension of goal pursuit in multiple life domains.
Respondents answered each item with regard to how much they had experienced each symptom
over the past week. High scores indicate high depressive symptoms. The alpha coefficient for
depressive symptoms was 0.89.
Health Behavior and Physical Measures. Respondents were checked into the GCRC
located within the UW Hospital and Clinics for an overnight stay. A trained nurse or physician
took the respondent’s medical history and conducted a physical health examination.
Neuroendocrine Function. Measurement of the dependent variable salivary CORT was
performed during a stay at a GCRC. Early morning CORT levels were assessed via Salivette
(Sarstedt, Rommelsdorf, Germany) at waking and every ten minutes thereafter for fifty minutes
(6 total samples). With assistance from a GCRC staff, samples were collected promptly at all
intervals, eliminating compliance as a potential confounder, to ascertain CORT levels at fixed
time points with strict reference to waking. Salivary free cortisol levels were measured via
radioimmunoassay (RIA) and enzyme immunoassay (EIA). From these repeated samples, area
under the curve ( AUC I ) with respect to increase was calculated for each participant according to
the method suggested by Pruessner, Kirschbaum, Meinlschmid, & Hellhammer (2002). AUC I
can be conceptualized as the sensitivity of the system, revealing changes over time in response to
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the challenge of waking. AUC I calculated from CORT early morning levels taken every 10 min
for first 50 minutes after waking has been shown to be a dynamic, robust measure total time slept
or alcohol consumption the night before (J. C. Pruessner et al., 1997), though some new evidence
suggests it is sensitive to waking time (Edwards, Evans, Hucklebridge, & Clow, 2001). Thus,
early morning CORT is a reliable biological marker when measured repeatedly with strict
reference to the time of awakening, and importantly, the awakening response dominates the
diurnal cycle for free cortisol (J. C. Pruessner et al., 1997).
Medications. Some respondents reported taking corticosteroid medications to treat
inflammation. Analyses involving salivary cortisol also controlled for whether respondents
reported taking any steroidal medications.
Statistical Analyses
Data analysis was conducted in multiple steps. First, frequency distributions for all
measures (psychological and biological) were examined and symmetrized as needed. Such
normalizing transformations were noted, where appropriate, in the above description of
measures. Second, outliers were Winsorized (Dixon & Tukey, 1968), meaning that extreme
observations (i.e. those above the 97th percentile and below the 3rd percentile) were replaced by
the value of the nearest unaffected observation. Third, all independent variables were
standardized and, finally, hierarchical multiple regression was used to test study hypotheses. In
the multiple regression analyses, a primary model entered age, corticosteroid medication use, and
depressive symptoms. A second and third model tested main effects of baseline resting
midfrontal asymmetry and the PWB subscale. The two independent variables were not entered
simultaneously at this stage but were entered in two steps. To make sure the order of entering
independent variables did not influence main effect results, two versions of this sequence were
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run; one version entered midfrontal asymmetry first and added the PWB subscale second, and
the other version entered the PWB subscale first and then entered midfrontal asymmetry second.
That is, one version entered the PWB subscale alone first to determine whether main effects exist
(without controlling for asymmetry) and then an alternate version of this model was run that
entered midfrontal asymmetry alone first to assess main effects (without controlling for PWB). A
final model tested the moderation hypotheses using interaction terms between midfrontal
asymmetry psychological well-being subscales.
Results
Tables 1-6 provide results from regression analyses for the six separate scales of
psychological well-being (phenomenological engagement). All analyses first controlled for age,
use of corticosteroid medication, and depressive symptoms. What is evident from the tables is
that there were no main effects of midfrontal asymmetry or psychological well-being on the
magnitude of the CORT response to waking across any of these analyses. However, significant
interactions were found between midfrontal asymmetry and four scales of the psychological
well-being measure (i.e., positive relations with others, self acceptance, personal growth, and
purpose in life) on the magnitude of the CORT response to waking. These statistics and posthoc
tests of simple slope are summarized on Table 7. There was a significant interaction between
midfrontal resting baseline asymmetry and positive relations with others on morning rise in
cortisol, ! = -0.37, t (100) = -2.77, p <0.01. A test of simple slopes revealed that the slope of
morning cortisol rise regressed on midfrontal asymmetry at 1 standard deviation (SD) below the
mean of positive relations with others was significantly different than zero, ! = 0.30, t (100) =
1.95, p < 0.05, and the slope at one SD above the mean score on positive relations with others
was also significantly different than zero, ! = -0.24, t (100) = -2.02, p < 0.05. Figure 1 illustrates
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the pattern of this effect and shows that among those who showing high interpersonal
engagement, the magnitude of the CORT morning rise decreases as one becomes evermore left
frontally activated; thus, illustrating the enhancement effect linked with having both forms of life
engagement. However, among those with low positive relations with others, the direction of the
effect is reversed. Here the pattern shows that early morning CORT levels are lower among
those showing the absence both forms of engagement – an effect contrary to the prediction that
this combination would amplify HPA dysregulation.
There was also a significant interaction between midfrontal resting baseline asymmetry
and self acceptance on morning rise in cortisol, ! = -0.40, t (101) = -2.91, p <0.01. A test of
simple slopes revealed that the slope of cortisol morning rise regressed on midfrontal asymmetry
at 1 SD below the mean of self acceptance was significantly different than zero, ! = 0.31, t (101)
= 2.06, p < 0.05, and also that the slope at one SD above the mean score on self-acceptance was
significantly different than zero, ! = -0.26, t (101) = -2.11, p < 0.05. The pattern of this effect,
illustrated in Figure 2, also indicates that the magnitude of CORT morning rise becomes smaller
for individuals with high self-acceptance (an enhancement effect) as one becomes increasingly
left frontally activated, and the reverse pattern for those individuals with low self acceptance,
such that early morning CORT rise is lower for those for those with low phenomenological
engagement and low neural engagement as represented by EEG midfrontal asymmetry.
There was also a significant interaction between midfrontal resting baseline asymmetry
and personal growth on morning rise in CORT, ! = -0.31, t (101) = -2.21, p< 0.05. For this
effect, however, neither of the simple slope tests was significantly different from zero, although
the simple slope of CORT morning rise at 1 SD above the mean of personal growth showed a
trend toward significance. Similarly, there was a significant interaction between midfrontal
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resting baseline asymmetry and purpose in life on morning rise in cortisol, ! = -0.36, t ( 100) = -
2.24, p<0.05, and the accompanying simple slope tests were not significantly different from zero,
although tests both 1 SD above and 1 SD below the mean of purpose in life showed trends
toward significance. These latter interactions are illustrated in Figures 3 and 4, which show
pattern of effects consistent with the two preceding effects.
Discussion
The purpose of the present investigation was to assess the extent to which early morning
rise in cortisol could be predicted by two forms of life engagement, one neural and the other
phenomenological. As such, it is the first study to date to assess the combined influences of
approach-oriented engagement, measured both in terms of EEG asymmetry and self-reported
psychological well-being, on CORT levels. A further feature of the study, consistent with
proposed guidelines for assessing links between positive psychological factors and biology
(Pressman & Cohen, 2005; Steptoe & Wardle, 2005), was that the above engagement effects
were examined after controlling for negative affect (assessed here with depressive symptoms).
So doing sharpens the analytic focus on whether hypothesized positive influences have separate
and independent effects beyond what is attributed to negative psychological factors.
Although neither form of engagement was found to significantly predict morning rise in
cortisol, the interaction between the two was a significant predictor, with such an effect
demonstrated across four of six well-being measures. The pattern of these interactions was
consistent, showing the hypothesized enhancement effect, in which lower levels of early morning
cortisol were seen among those who had both forms of engagement – i.e., greater relative left
frontal EEG activation and higher levels of well-being. Thus, although neither aspect of
engagement was a significant predictor in itself, the combination of having high levels of both
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neurological and phenomenological engagement did predict ever lower levels of early morning
cortisol rise. Alternatively, among those who showed high levels of well-being and greater
relative right EEG activation higher levels of early morning cortisol were observed. Such a
pattern illustrates how lack of engagement at the neural level may compromise, or override, the
benefits link with having both types of engagement.
We had also suggested a possible amplification of the negative effect in which ever higher
levels of early morning cortisol would accrue to those who lacked both neural and
phenomenological engagement. The findings showed, however, the opposite directional pattern.
That is, those showing lower levels of engagement, both in terms of self-reported well-being and
greater relative right EEG asymmetry, showed ever lower levels of early morning cortisol rise
compared to those who reported lower well-being and had greater relative left EEG asymmetry.
One possible interpretation of this pattern pertains to hypocortisolism. The difficulty, of course,
is that there is no consensus about actual morning levels of CORT that might constitute either
hypercortisolemia, or hypocortisolemia (Clow et al., 2004). Indeed, definitions of these
conditions are often determined only relative to the mean and variability within study samples,
with few objective criteria available for either. Efforts such as those by Ranjit and colleagues
(Ranjit, Young, Raghunathan, & Kaplan, 2005), and other ongoing studies, such as the Midlife in
the U.S. (MIDUS) national survey, are essential to help define parameters of cortisol rhythms for
different populations so as to assist in the characterization of hyper- and hypo-secretion of
cortisol.
Although HPA axis hypo-function is poorly understood (Antonijevic, 2006), many have
argued that flattening, or hypocortisolism may occur after a prolonged period of hyperactivity of
the HPA axis due to chronic stress (e.g., Fries, Hesse, Hellhammer et al., 2005). With regard to
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hypocortisolism in early morning rise, our finding converge those of Pruessner, Hellhammer, and
Kirschbaum (1999) and Ranjit, Young, & Kaplan (2005) showing a similar pattern among
severely stressed individuals. Other researchers have investigated the pattern of hypocortisolism
and have found it linked to post traumatic stress disorder, chronic fatigue syndrome,
fibromyalgia, and other somatoform disorders (for review, see Heim, Ehlert, & Hellhammer,
1999). Whether any of these conditions, or other forms of chronic stress, or traumatic events are
part of the past experience profiles of the older women in this study is an important future
direction, which would strengthen the plausibility the hypocortisolism interpretation among
those lacking both neural and phenomenological engagement.
From a mechanistic perspective, it is also important to probe how these different levels of
analysis (neural, phenomenological, neuroendocrine) are linked. Our study presumes that
effective functioning of the PFC plays a role in the effective regulation of CORT during the
morning rise. The left prefrontal cortex (PFC), and specifically, the dorsolateral PFC (dlPFC),
mediates working memory and the maintenance of representations of important goals over time
and likely implements key features of these approach-related processes (Tomarken & Keener,
1998). The level of activation of the left dlPFC may have consequences for the release of CORT
such that inhibition of the amygdala by PFC reduces the amygdalae’s excitatory stimulation of
the paraventricular nucleus of the hypothalamus, perhaps resulting, ultimately, in reduced release
of CORT via the HPA axis (Plotsky, P. M., Owens, M. J., & Nemeroff, 1998).
The PFC inhibits the amygdala via GABAergic-mediated projections (Davidson, 2000;
Thayer & Brosschot, 2005), and because the dlPFC plays a role in the maintenance of
representations of goals over time and attention to goal oriented stimuli (Davidson, 2004), and
activation in this region may drive the inhibition of the amygdala via dorsolateral PFC’s
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connectivity to the ventromedial PFC and from ventromedial PFC’s innervation of the amygdala.
Thus, continued approach-oriented engagement and its left dlPFC neural substrates may
represent vitality in the face of ongoing challenge. The PFC’s inhibition of the amygdala’s
stimulatory signaling of PVN of hypothalamus could result in reduced release of CORT at
adrenal cortex.
On the other hand, suspension of approach-oriented engagement and hypoactivity of left
dlPFC, and the resultant lack of inhibition of amygdala may allow increased and persistent
release of cortisol via HPA axis. If hyperactivity of the release of CORT is maintained, the
excessive presence of glucocorticoids may disrupt intercellular regulatory signaling between
glucocorticoids in processed of negative feedback, or the inhibition of further release of cortisol,
that is normally imposed by the hippocampus and other brain regions, and this disruption of
appropriate negative feedback by way of compensatory intercellular processes may result in
either continued excessive release cortisol or too little release of glucorticoids (Sapolsky,
Romero, & Munck, 2000).
Notwithstanding the importance of electrophysiological recordings of patterns of
neurons, it is likely that representations of previous active engagement experience can be
accessed during the working memory function of the dlPFC by individuals and measured via
reliable, valid self-report inventories such as the PWB Inventory. Enhanced attention to these
representations may further enhance activation of left dlPFC. Additionally, the self-reported
information in its interplay with processes measured via neurophysiologic measurements
predicted CORT patterns in the morning rise, while neither self-reported nor
electroencephalogram related independently to CORT morning rise. Therefore, reliable, valid
self-report inventories should continue to be included in similar investigations of engagement on
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Engagement and Morning Cortisol 18
neuroendocrine function. Approach-related engagement assessed via these two methods may
suggest an important common mechanism that helps clinicians predict who will be at risk for
disability and disease caused by dysregulated interaction of glucocorticoids.
Among the limitations of the present work is the cross-sectional design, which precludes
assessment of causal directionality among the three levels of analysis. In addition, the sample
consists of older white women and as such, offers limited generalizability to other
sociodemographic groups. The work could also be strengthened by the use of source localization
techniques (Pizzagalli, 2006; Pizzagalli, Sherwood, Henriques, & Davidson, 2005) in studies of
engagement and aging to elucidate the role of the dlPFC in measures of engagement. Other
studies report that between subject variation is sizable, and in one study, it accounted for 62% of
total variance (Ranjit et al., 2005).
Nonetheless, the investigation does provide a first attempt to integrate different levels of
analysis (e.g., neural via EEG, phenomenological via self-report, biomarkers such as CORT) in
the same participants so as to elucidate combinations of vulnerabilities and protective factors that
influence the course of aging. These findings speak to the benefits of measuring approach-
related engagement in life at the phenomenological level using reliable, valid self-report
inventories that tap conscious impressions of well-being retrieved from long term memory as
well as at the neurobiological level via greater relative left frontal EEG activation. Moreover, it
was the interplay of the two levels of analysis, rather than either type of engagement alone that
predicted levels of early morning cortisol rise. As such, the work points to a possible coherence
in multi-level measures of approach-oriented engagement that may lead to a better understanding
of the role of positive factors in promoting later life health.
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Engagement and Morning Cortisol 19
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Table I. Hierarchical OLS Regression Coefficients for Significant Interactions for Positive Relations with Others
Model 1 Model 2 Model 3 Model 4
Variables b ! " R # b ! " R # b ! " R # b ! " R
Age -.011 -.008 -.033 -.023 -.029 -.020 .016 .011
Corticosteroid Medication -.163 -.122 -.171 -.128 -.170 -.127 -.174 -.130
Depressive Symptoms -.150 -.113 .022 -.059 -.044 -.059 -.044 -.050 -.038
Positive Relations (PR) .265 .193 .032 .263 .192 .203 .148
Midfrontal Asymmetry -.055 -.040 .002 .042 .031
Asymmetry X PR -.376 ** -.275 .067
Age -.011 -.008 -.006 -.004 -.029 -.020 .016 .011
Corticosteroid Medication -.163 -.122 -.161 -.120 -.170 -.127 -.174 -.130
Depressive Symptoms -.150 -.113 .022 -.150 -.113 -.059 -.044 -.050 -.038
Midfrontal Asymmetry -.062 -.045 .002 -.055 -.040 .203 .148
Positive Relations (PR) .263 .192 .002 .042 .031
Asymmetry X PR -.376 ** -.275 .067
* p < .05. ** p < .01. *** p < .001 (two-tailed tests)
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Table II. Hierarchical OLS Regression Coefficients for Significant Interactions for Self Acceptance
Model 1 Model 2 Model 3 Model 4
Variables B ! " R # b ! " R # b ! " R # b ! " R
Age -.030 -.021 -.030 -.021 -.027 -.018 -.026 -.018
Corticosteroid Medication -.187 -.138 -.187 -.139 -.187 -.138 -.179 -.132
Depressive Symptoms -.166 -.124 .028 -.175 -.131 -.180 -.134 -.106 -.079
Self Acceptance (SA) -.014 -.011 .000 -.021 -.016 -.066 -.048
Midfrontal Asymmetry -.045 -.032 .001 .043 .031
Asymmetry X SA -.397 ** -.293 .075
Age -.030 -.021 -.027 -.019 -.027 -.018 -.026 -.018
Corticosteroid Medication -.187 -.138 -.186 -.138 -.187 -.138 -.179 -.132
Depressive Symptoms -.166 -.124 .028 -.166 -.125 -.180 -.134 -.106 -.079
Midfrontal Asymmetry -.043 -.031 .001 -.045 -.032 .043 .031
Self Acceptance (SA) -.021 -.016 .000 -.066 -.048
Asymmetry X SA -.397 ** -.293 .075
* p < .05. ** p < .01. *** p < .001 (two-tailed tests)
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Table III. Hierarchical OLS Regression Coefficients for Significant Interactions for Personal Growth
Model 1 Model 2 Model 3 Model 4
Variables b ! " R # b ! " R # B ! " R # b ! " R
Age -.030 -.021 -.018 -.012 -.015 -.010 -.004 .003
Corticosteroid Medication -.187 -.138 -.187 -.139 -.187 -.138 -.185 -.137
Depressive Symptoms -.166 -.124 .028 -.140 -.105 -.140 -.105 -.067 -.050
Personal Growth (PG) -.060 .044 .001 -.060 .044 .104 .077
Midfrontal Asymmetry -.043 -.031 .001 .008 .006
Asymmetry X PG -.306 * -.220 .045
Age -.030 -.021 -.027 -.019 -.015 -.010 -.004 .003
Corticosteroid Medication -.187 -.138 -.186 -.138 -.187 -.138 -.185 -.137
Depressive Symptoms -.166 -.124 .028 -.166 -.125 -.140 -.105 -.067 -.050
Midfrontal Asymmetry -.043 -.031 .001 -.043 -.031 .008 .006
Personal Growth (PG) -.060 .044 .001 .104 .077
Asymmetry X PG -.306 * -.220 .045
* p < .05. ** p < .01. *** p < .001 (two-tailed tests)
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Table IV. Hierarchical OLS Regression Coefficients for Significant Interactions for Purpose in Life
Model 1 Model 2 Model 3 Model 4
Variables b ! " R # b ! " R # B ! " R # b ! " R
Age -.010 -.007 -.001 -.001 -.001 -.001 -.034 -.023
Corticosteroid Medication -.200 -.148 -.206 -.152 -.206 -.152 -.232 -.172
Depressive Symptoms -.169 -.127 .031 -.086 -.065 -.086 -.065 -.025 -.019
Purpose in Life (PL) .147 .108 .008 .148 .109 .154 .113
Midfrontal Asymmetry .009 .006 .000 .031 .022
Asymmetry X PL -.361 * -.221 .046
Age -.010 -.007 -.000 -.007 -.001 -.001 -.034 -.023
Corticosteroid Medication -.200 -.148 -.200 -.148 -.206 -.152 -.232 -.172
Depressive Symptoms -.169 -.127 .031 -.169 -.127 -.086 -.065 -.025 -.019
Midfrontal Asymmetry -.001 .000 .000 .009 .006 .031 .022
Purpose in Life (PL) .148 .109 .008 .154 .113
Asymmetry X PL -.361 * -.221 .046
* p < .05. ** p < .01. *** p < .001 (two-tailed tests)
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Table V. Hierarchical OLS Regression Coefficients for Significant Interactions for Environmental Mastery
Model 1 Model 2 Model 3 Model 4
Variables b ! " R # b ! " R # B ! " R # b ! " R
Age -.010 -.007 -.013 -.009 -.013 -.009 -.030 -.021
Corticosteroid Medication -.200 -.148 -.197 -.146 -.197 -.146 -.204 -.151
Depressive Symptoms -.169 -.127 .031 -.072 -.054 -.072 -.054 -.046 -.035
Environmental Mastery (EM) .157 .113 .008 .157 .113 .104 .075
Midfrontal Asymmetry .001 .001 .000 .070 .049
Asymmetry X EM -.265 -.190 .031
Age -.010 -.007 -.001 -.007 -.013 -.009 -.030 -.021
Corticosteroid Medication -.200 -.148 -.200 -.148 -.197 -.146 -.204 -.151
Depressive Symptoms -.169 -.127 .031 -.169 -.127 -.072 -.054 -.046 -.035
Midfrontal Asymmetry -.001 .000 .000 .001 .001 .070 .049
Environmental Mastery (EM) .157 .113 .008 .104 .075
Asymmetry X EM -.265 -.190 .031
* p < .05. ** p < .01. *** p < .001 (two-tailed tests)
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Table VI. Hierarchical OLS Regression Coefficients for Significant Interactions for Autonomy
Model 1 Model 2 Model 3 Model 4
Variables b ! " R # b ! " R # B ! " R # b ! " R
Age -.010 -.007 -.014 -.010 -.014 -.010 -.002 -.002
Corticosteroid Medication -.200 -.148 -.199 -.147 -.199 -.147 -.207 -.153
Depressive Symptoms -.169 -.127 .031 -.189 -.142 -.189 -.142 -.174 -.131
Autonomy (AU) -.070 -.051 .002 -.070 -.051 -.117 -.086
Midfrontal Asymmetry -.003 -.002 .000 .011 .008
Asymmetry X AU -.203 -.161 .024
Age -.010 -.007 -.010 -.007 -.014 -.010 -.002 -.002
Corticosteroid Medication -.200 -.148 -.200 -.148 -.199 -.147 -.207 -.153
Depressive Symptoms -.169 -.127 .031 -.169 -.127 -.189 -.142 -.174 -.131
Midfrontal Asymmetry -.001 .000 .000 -.003 -.002 .011 .008
Autonomy (AU) -.070 -.051 .002 -.117 -.086
Asymmetry X AU -.203 -.161 .024
* p < .05. ** p < .01. *** p < .001 (two-tailed tests)
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Table VII. Tests of Simple Slope for Interactions of EEG Asymmetry with Psychological Well-Being on Early Morning Cortisol
! t p-value Sig.
Positive Relations with Others
1 SD below the mean of psychological well-being scale 0.30 1.93 0.05 p<0.05
1 SD above the mean of psychological well-being scale -0.24 -2.02 0.05 p<0.05
Self Acceptance
1 SD below the mean of psychological well-being scale 0.31 2.06 0.04 p<0.051 SD above the mean of psychological well-being scale -0.26 -2.11 0.04 p<0.05
Personal Growth
1 SD below the mean of psychological well-being scale 0.22 1.49 0.14
1 SD above the mean of psychological well-being scale -0.22 -1.70 0.09 p<0.10
Purpose in Life
1 SD below the mean of psychological well-being scale 0.26 1.75 0.08 p<0.10
1 SD above the mean of psychological well-being scale -0.24 -1.66 0.10 p<0.10
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Figure Captions
Figure 1. Plot of simple slopes for magnitude of cortisol morning rise regressed on midfrontalasymmetry at 1 standard deviation above and below the mean score on positive relations with
others.
Figure 2. Plot of simple slopes for magnitude of cortisol morning rise regressed on midfrontalasymmetry at 1 standard deviation above and below the mean score on self acceptance.
Figure 3. Plot of simple slopes for magnitude of cortisol morning rise regressed on midfrontal
asymmetry at 1 standard deviation above and below the mean score on personal growth.
Figure 4. Plot of simple slopes for magnitude of cortisol morning rise regressed on midfrontalasymmetry at 1 standard deviation above and below the mean score on purpose in life.
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