Kvalitatiivne uurimustöö Emotsioonide regulatsioon ja stress (0)

2
Emotion regulation in relation..
Emotion regulation in relation to
physiological stress response.
University Name
Research Project
Module Code : xx
2007-2008
Supervised by xxx
Word count: 7261
Abstract
The aim of this study was to investigate the association between psychological and the biological stress response. It is known that humans , interacting with each other or their environment, have emotional reactions that are individually regulated. These emotional responses are linked to changes in autonomic and neuroendocrine systems, which are essential for metabolic support when preparing the body for action . Since emotion can influence such important processes like learning , decision - making , memory and consequently health and welfare of the individual then dysfunctional regulation of emotions can lead to psychopathology. A total of 26 healthy, non smoking male participants, age group 18-42 years were recruited into the study. Based on the theory of Cybernetic 3-Dimensional Model on Emotion Regulation (CMER), three dimensions of emotion regulation was measured. Participants were stressed using the TSST test, and the salivary cortisol and plasma IL-6 was measured as endocrinological markers of the stress response. Multiple regression and correlation analysis were conducted investigating the main hypothesis. The results show that hedonistic emotion regulation (HER) and the distress - augmentative emotion regulation (DAR) were the predictors and AUCg (area under the curve in respect to ground ) and AUCi (area under the curve in respect to increase ) were the dependent variables. Participants, who scored high in HER showed lower cortisol responses, whereas, individuals who scored high in DAR showed a trend towards higher cortisol responses. These results indicate that HER is related to a lower cortisol response to psychosocial stress. In conclusion these results suggest that HER and DAR have an impact on the cortisol response.
Acknowledgements
Firstly I would like to thank my supervisor xxx for his help and advice throughout this research and also xxx is gratefully acknowledged for his support and advice on blood markers of stress.
Table of Contents
1 Introduction 5

The effects of emotion regulation (ER) strategies
in response to psychological stress 6
Figure 1. A process model of emotionregulation 8
Figure 2. Cybernetic 3-Dimentional Model on ER 10
1.3 Stress and physiological factors 11
Figure 3. The hypothalamic-Pituarity- Adrenocortical Axis (HPA) 11
2 Method 14
2.1 Participants 14
2.2 The psychological measurements 14
2.3 Psychological stress response measures 15
2.3.1 Detection of plasma IL-6 15
2.3.2 Detection of salivary cortisol 16
2.4 Psychological procedure 16
2.5 Statistical analysis 17
3 Results 18
3.1 Cortisol response in relation to TSST test 18
Table 1. Mean and Standard Deviation of salivary cortisol 18
Figure 4. Cortisol reactivity 18
3.2 Descriptive statistics for the items of HER and DAR 19
Table 2. Descriptives for HER 19
Table 3. Descriptives for DAR 20
3.3 Emotion regulation (HER and DAR) in relation to cortisol
response as measured by AUCg and AUCi calculations 21
Figure 5. Cortisol reactivity as a function of high and low HER 21
3.4 HER as predictor for cortisol response 22
Figure 6. AUCg as function of HER 22
Figure 7. AUCi as function of HER 22
3.5 Plasma Interleukin- 6 (IL-6) 23
4 Discussion 24
References 29
Appendixes
1 Introduction
The relationship between psychology and the stress response has been studied for many years. Hans Selye (1956) defined stress as the psycho -physiological response to demands that influence the endocrine system and the autonomic nervous system. He conceptually defined stress as a General Adaptation Syndrome (G.A.S) comprising three phases. Firstly an alarm reaction phase accumulated from an arousing external stimuli, followed by a period of adaptation to the stressor or so called resistance stage, until finally the body expresses exhaustion. More recently the effects of exercise -induced stress has been extensively studied in relation to the immune response (Brydon et al 2005,Morita et al., 2005).
In psychology stress is studied in terms of psychosocial factors, which in turn are thought to affect physiological and immunological responses. In addition to questionnaires that are largely used to measure mood, emotions, the steroid hormone cortisol has been widely measured in experimental psychology to explore physiological stress responses. In addition to physiological responses to external stressors the stress response to emotions has also attracted the interest of researchers. Investigations of how emotions are regulated has mainly looked at emotional states focusing on duration, frequency and intensity, neglecting the emotion regulation processes (Mohiyeddini, 2005). Nevertheless it is known that emotion regulation has an effect on human welfare (Gross, 1999) and positive emotions are associated with a smaller risk of physical disease and a longer healthy life expectancy (Huppert et al., 2004).
1.2 The effect of emotion regulation strategies in response to psychological stress.
Humans, whether interacting with each other or their environment have emotional reactions that are individually regulated. Emotion is a response to a situation that one considers to be relevant to his or her goals (Gross & Thomson , 2007). Gross and Thomson (2007) have presented a modal model of emotion, that illustrates the process; situation→ attention → appraisal → response. Situation can be either external or an internal mental presentation that is attended to on the basis of an individual appraisal that leads to emotional response. This emotional response can influence the situation and can change behaviour. These emotional responses are linked to changes in autonomic and neuroendocrine systems, which are essential for metabolic support when preparing the body for action. Since emotion can influence important processes like learning, decision-making, memory and consequently health and welfare of the individual ( Wolf , 2007; Gross, 2002; Richards & Gross, 2000; Gross and Levenson, 1993) then dysfunctional regulation of emotions can lead to psychopathology (Segerstrom et al., 2000; Nolen-Hoeksema, 2000). There are many different strategies employed to regulate emotions. Gross (2007) has described ER strategies as social - cognitive traditions that are dynamic and ubiquitous in trait . ER can be viewed as trait-like, that is individual tendencies and differences towards certain ER strategies. Individuals are regulating their emotions in communication in order to socially benefit and achieve the ambitions, as well as maintaining a balanced mental state. Also emotions are regulated in order to deal with extraordinary, special or unexpected situations. Although , the regulation of emotions has always been a crucial part of human existence, however , research into emotion regulation (ER) is relatively recent . Nonetheless the research interest in processes involved in ER has grown rapidly. Increasingly attention has been directed to unintentional regulation of emotions and the ways of measuring the biological responses in ER (Wirtz et al., 2006, Rimmele et al, 2007). Previous research interest in ER was largely focused on intentional-responsive regulation, (Muraven et al 1998; Gross & Levenson 1997; Wegner, Erber & Zanakos 1993) where only intentional responses where recorded, and the data was based mainly on self-reports. Consequently LeDoux (2000) pointed out the need to discover new approaches in emotional research. Furthermore , while some field strategies measured ER, there was less attention given to automatic regulatory processes such as physiological responses and taught behaviour patterns in childhood (Fitzsimons & Bargh, 2004; Gollwitzer, 1999; Cohen , 1997). Davidson (2000) argued that there are regulatory processes in emotion that occur automatically which modulate the onset and recovery function of emotion. He suggested that these regulatory processes influence the emotional information processing at the conscious level, however not themselves being in conscious experience. In other words there are operating regulatory processes that are automatic and therefore cannot be controlled intentionally. It is known that people use a range of different strategies to regulate their emotions (Ochsner & Gross, 2004; Gross, 1998b). Gross (2001) has proposed a “process model of ER”, with underlying conception of emotion-generative process that distinguishes between antecendent-focused and response-focused ER strategies. Antecedent-focused strategies include actions before the full activation of emotion response tendencies that endorse changes in behaviour and peripheral physiological responses (cognitive change e.g reappraisal; see figure 1). Response-focused strategies include the actions after response tendencies have been generated and emotion is already in progress (response modulation e.g suppression). In comparison to suppressive emotion expressive behaviour, reappraisal seems effectively to change the outcome in aversive events (Gross, 2002; Richards & Gross, 2000; Gross & Levenson, 1993). However, based on present knowledge it is known that reappraisal can be used not only to alter bad situations, mentally for the better, but is also used to exacerbate bad situations in the mind, which in turn could lead to depression and anxiety ( Segerstrom et al., 2000; Nolen-Hoeksema, 2000; Connor & Leonard, 1998) or ill health (Janine , 2007). Thus, it has become clearer that emotions influence not only our mood but also physiological functions . Sculkin (2003) noted that the appraisal systems, particularly the unconscious mechanisms, are pervasive throughout the nervous system therefore it is crucial to expand the methods of measuring it.
Figure 1
Figure 1. A process model of emotion regulation (Gross, 2001).
Much of ER is measured by self-reports, although some current research in to ER has used physiological measurements such as blood pressure in emotion suppression ( Butler et al., 2002) and repression (Giese- Davis et al., 2007) where elevated blood pressure has been observed . Additionally, some functional magnetic resonance imaging (fMRI) studies have shown amygdala activity in accordance with the goal (Schaefer et al., 2002; Ochsner et al., 2002, 2004b). This suggests that whichever particular prefrontal system regulates the amygdala depends on the strategy and the goal. Yet again , these studies are intentional –responsive studies, showing the physiological- neurological difference in functions when intentionally regulating emotions. Only recently researchers have started to apply knowledge to automatic processes by measuring psychobiological responses in relation to emotion regulation. There is evidence that elevated cortisol is associated with negative emotion (Polk et al. 2005). Hostility and trait negative affect (NA) are positively associated with higher levels of systemic inflammation as measured by the pro-inflammatory cytokine Interleukin-6 (IL-6) (Marsland et al., 2008). However, a disadvantage of these studies is the neglect of the immediate ER process. Reading the average account of emotional experience that is measured over the duration of 1 to 2 weeks, demonstrates the results of emotion regulation rather than emotion regulation itself. Despite the currently poor assortment of applicable studies there is nevertheless evidence of elevated stress hormone reactivity to psychosocial stress in relation to poor emotion regulation (Wirtz et al., 2006). Emotional regulation itself has been measured in many different ways and the Cybernetic 3-dimensional Model on Emotion Regulation (CMER) has been recently developed by Mohyeddini (2005). CMER is combined from existing ideas of mood repair ( Singer & Salovey, 1988), motivational approach (Parrott, 1993) and mood congruency effect (Bower, 1981). The CMER consists of 3 dimensions. These are, first the hedonistic regulation (HER) that measures the buffering of emotions, as a result people who score high in HER, use positive reappraisal in order to alleviate the stress and be predominantly positive. In contrast to positive reappraisal a second dimension is distress-augmenting regulation (DAR), which is a measure of intensifying of negative emotions e.g. people who score high in DAR tend to mentally alter stressful situations with exacerbating the negative emotions. Thirdly, moderating regulation (MR), people who score high in MR tend to moderate emotions e.g. using suppression to moderate emotions (Mohiyeddini 1998, 2005; see figure 2).
Figure 2
Figure 2. Cybernetic 3-Dimensional Model on emotion Regulation (Mohiyeddini 1998, 2005)
Although little research to-date has examined the specific effects of ER as measured by e.g. HER and DAR on the physiological stress response, Mohiyeddini and colleagues have reported that hedonistic emotional states link to lower cortisol, epinephrine and nor-epinephrine levels after stress (Wirtz et al., 2006) . Thus further studies in this area would increase our understanding of the emotional regulation of the physiological response and lead to better psychotherapeutic interventions and / or management of the damaging stress response.
1.3 Stress and physiological factors.
Organisms respond to stress with secretion of neuroendocrine mediators. These hormones interact with physical, cognitive and emotional processes. (Steptoe et al., 2007; Herbert et al., 2006; De Kloet et al., 2005; Kiecolt- Glaser et al., 2003; Rohleder et al., 2002,). Psychological and other forms of stress influence the sympathetic nervous system, hypothalamus–pituitary– adrenal (HPA) - axis, and immune system; the interaction between these systems is complex (Raison et al., 2003, Pariante & Miller , 2001; Adler , Felten & Cohen, 2001). Activation of the HPA axis by physical or psychological stress begins with corticotrophin-releasing hormone (CRH) secretion from the Hypothalamus, CRH then signals the Anterior Pituitary gland to secrete Adrenocorticotropic hormone ( ACTH ), ACTH then acts on the Adrenal gland which then produces glucocorticoids such as corticosterone and cortisol (Figure 3) which have important metabolic and immunological effects (Arzt, 2001; Hoffman -Goetz & Pederson, 1994; Fitzgerald , 1998).
Figure 3. The Hypothalamic-Pituitary-Adrenocortical Axis (HPA)
Cortisol has been widely used in psychology to measure stress. Cortisol has metabolic effects on liver glucose sythnesis, breakdown of skeletal muscle protein to amino acids and in adipose tissue mobilizes fat. It can also have anti-inflammatory and immunosuppressive actions depending on concentration (Rhoades & Pflanzer, 1989). Most of these physiological effects prepare the body for hostile conditions. Cells of the immune system respond to stress or injury in many of ways ( Benoy & Heels, 1998; Mayer & Watkins, 1998; Brines et al, 1996). They secrete a number of cytokines (signalling protein) such as interleukin-6 (IL-6) which is a pro-inflammatory cytokine that mediates the acute phase response to stress. The cytokine IL-6 is also involved in the regulation of the immune system. It is a sensitive immune response marker for stress in laboratory settings and there is now evidence that psychological stressors and hostile behaviour may increase the production of IL-6 (Maes et.al 1998, Morita et al., 2005, Marsland et al 2008). Elliot and Eisdorfer (1982) distinguished two important dimensions in psychological stressors - duration and course (e.g. discrete vs continuous ) and five categories of psychological stress. Amongst these five categories acute stressors such as laboratory challenges (e.g. public speaking, mental arithmetic tests or benji jump ), are the most validated and practical to study stress in psychology. Meta -analyses of 300 empirical studies, conducted by Segerstrom and Miller 2004, implicated that acute stressors were linked with increase in some parameters of natural immunity e.g. natural killer cells and the pro-inflammatory cytokine interleukin-6 (IL-6) and down regulation of some functions of specific immunity (e .g. lymphocyte responses).
Although the steroid hormone cortisol has often been used as a psychological measure of stress however, many studies have failed to find changes in cortisol (Manuck et al, 1991), and there has been inconsistency in the effects of psychological stressors on cortisol activity ( Biondi & Picardi, 1999). Despite these reports, Dikerson and Kemery (2004) in a meta-analysis of acute psychological stressors and various laboratory tests, did show variations in the cortisol response. The public speaking/cognitive task combination was associated with significantly greater cortisol responses than other types of psychological stressors. The combination of social-evaluative threat (being judged negatively by others when performing arithmetic or speaking task) and uncontrollability (time constriction and possible outcome) was the strongest predictor for the cortisol response.
Detecting an association between repeated measures combining several time points , for cortisol the most widely used formulas are the area under the curve (AUCg and AUCi), where AUCg is ´area under curve with respect to ground` and AUCi is `area under the curve with respect to increase´. The calculation of the AUC is used to simplify the statistical analysis with increasing the power of the testing without loosing any information enclosed in repeated measurements (Pruessner et al, 2003). The aim of this study was to investigate any association between psychological variables and the biological stress response. We measured salivary cortisol and IL-6 as markers of the biological stress response. We wished to test the hypothesis that low secreation of cortisol and IL-6, as biological indicators of stress reactivity are associated with a high level of hedonistic regulation (HER) and with a low level of distress augumentative regulation (DAR).
2 Method
2.1 Participants.
A total of 26 healthy, non smoking male participants, who was in age range 18-42 yrs (Mean 27 +- 7,27 SD) and responded to advertisement on ´gumtree´ website ( appendix 1), were recruited for the study. 17 participant data was used for this analysis. All participants were asked to complete a consent form (appendix 1) and general health questionnaire (appendix 1) for exclusion of any mental or chronic illness , the use of medication, abuse of alcohol and/or drugs, or with poor sleeping patterns. Also, participants having regular heavy exercise were excluded. Additionally, a verbal explanation of all procedures was given (including blood being taken by a trained phlebotomist) as well as the option for withdrawal at any time. The approval for the study was given by the Roehampton University ethics committee (appendix 5).

The psychological measurements
The 34-item Emotional Regulation Inventory (ERI; Mohiyeddini, 1998; see appendix 2) is specially suited for assessment of behavioral regulation of emotions. It comprises a hedonistic way of emotional regulation, i.e. hedonistic regulation (HER), buffering of emotions, i.e. emotional moderation (EM), and intensifying of negative emotions, i.e. distress-augmenting regulation (DAR). Using a 6-point rating scale ranging from 1 (almost never ) to 6 (almost always), participants were asked to rate how often they use specific strategies (e.g. listen to cheerful music, go out with friends) to regulate their emotions. Higher scores mean higher HER, stronger buffering of emotions in EM, and higher distress augmenting regulation in DAR.

Physiological stress response measures.
Participants collected their saliva by chewing plain (non-citric acid) cotton Salivettes and the samples (8 time points as described in section 2.4 on p 15) were frozen at – 20oC prior to assaying for cortisol. Peripheral venous blood (2 ml anticoagulant with heparin) was obtained by a trained phlebotomist 10 min before the TSST and again 50 min after the TSST. The whole blood was centrifuged (250g for 10 mins) and the resulting plasma layer was removed, aliquoted and stored at – 70oC for cytokine analysis. All samples were numerically coded (known to the principal investigator) and laboratory measurements (see below ) undertaken blind .

Detection of Plasma IL-6
Plasma IL-6 was detected using commercially available paired antibodies enabling cytokine detection in an ELISA ( Enzyme Linked ImmunoAssay) format (R & D systems Ltd, Abingdon, UK). The sensitivity for the IL-6 ELISA was 9 – 1000 pg/ml. There was no reported cross-reactivity with other cytokines (R & D systems Ltd, Abingdon, UK).

Detection of Salivary Cortisol
Salivary cortisol was dectected using a commercially available ELISA (Salimetrics, LCC, USA). Briefly , a 96-well microtitre plate coated with monoclonal antibodies to cortisol was used. Cortisol standards (3.000, 1.000, 0.333, 0.111, 0.037, and 0.012 μg/ml) and the unknown compete with cortisol linked to horseradish perxidase for the antibody binding sites . Following incubation (55 mins) the plate was washed to remove unbound material. Bound cortisol peroxidase was measured by the reaction of the peroxidase enzyme on the substrate tetramethylbenzidine (TMB). After incubation for 25 mins this reaction was stopped with 50 μl per well of stop solution (H2SO4). The colour change was measured on a plate reader at 450 nm. The cortisol peroxidase detected is inversely proportional to the amount of cortisol present.

Psychosocial procedure
Two rooms were used in the procedure, one room for resting and the other for Trier Social Stress Test (TSST; see appendix 3). All experimental sessions took place in Roehampton University between 1300 and 1700 h and lasted approximately 2h (see timetable appendix 3). To cause acute psychosocial stress, the Trier Social Stress Test (TSST) was used (Kirschbaum et al., 1993) consisting of 5 min preparation , a 5 min mock interview and mental arithmetic ( serial subtraction, 5 min) in front of a mixed gender audience. On arrival at the laboratory participants where asked to undertake a 45 min resting period before TSST (seated and listening to calming music in a resting room). Participants were asked to provide a saliva samples (chew cotton salvettes). Samples of saliva for cortisol analysis were collected by participants themselves in the resting room in two time points 10 min before introduction to the TSST (30 and 40 min after arrival) to assess resting levels. Additionally blood was taken by a phlebotomist 10 min before the TSST. After the TSST, participants were sent to the other resting room, where the saliva was collected just after the test and then at 10, 20, 30, 40 and 50 min. Additionally a second blood sample was taken 50 min after TSST. Throughout the procedure the participants were asked to complete questionnaires designed to assess their emotional regulation type (e.g. DAR, MR, HER; Mohiyeddini, 2005).

Statistical Analysis
Multiple regression and correlation analysis were used. Hedonistic emotion regulation and the distress- augmentative emotion regulation were the predictors and AUCg and AUCi were the dependent variables. Furthermore, a one factorial analysis of variance (ANOVA) was conducted to explore the differences between individuals with high vs. low tendency to hedonistic emotion regulation (see appendix 4). Additionally, the reliability of hedonistic and distress-augmentative regulation was investigated using Cronbach’s Alpha . The ‘Area under the curve with respect to ground’ (AUCg) and the ‘Area under the curve with respect to increase’ (AUCi) was calculated using the following formulas:
Note . t = time difference between two cortisol sample, mi = cortisol sample at time I
Note. t = time, mi = cortisol sample at time I
All data set analysis was undertaken anonymously using the coded laboratory sample results.

Results
3.1 Cortisol response in relation to TSST test
Table 1 represent the descriptive statistics for the cortisol samples. As expected , the salivary cortisol level showed an increase at points 3 and 4 (see table 1 & figure 4). This corresponded to the TSST test being applied at points 2 and 3 and the stress response as measured by salivary cortisol increasing at points 3 and 4 ( maximum ) with the recovery response observed from 6 to 8.
Table 1
timeMean
Std. Deviation
Minimum
Maximum
10.16
0.15
0.03
0.61
20.16
0.16
0.02
0.64
30.23
0.24
0.03
0.81
40.41
0.42
0.04
10.32
50.35
0.40
0.03
10.51
60.23
0.22
0.03
0.70
70.22
0.23
0.04
0.82
80.12
0.10
0.03
0.37
Table1. Mean and standard deviation of salivary cortisol (μg/ml) over 8 time points, n=17. TSST was applied between time points 2 and 3.
Figure 4. Cortisol reactivity over time. n=17

Descriptive statistics for the items of HER and DAR
Table 2 shows the descriptive statistics for the items of HER. And table 3 shows the descriptive statistics for the items of DAR.
Table 2 Descriptive Statistics
Mean
Std. Deviation
Corrected Item-Total Correlation
Cronbach's Alpha if Item Deleted
HED1
3.20
1.38
.41
.86
HED2
3.00
1.00
.33
.86
HED3
3.12
1.05
.45
.86
HED4
3.68
1.22
.63
.85
HED5
2.80
1.41
.33
.86
HED6
3.00
1.50
.62
.85
HED7
2.96
1.37
.50
.86
HED8
3.52
1.05
.09
.87
HED9
4.60
1.19
.04
.87
HED10
4.16
1.21
.07
.87
HED11
3.27
1.48
.71
.85
HED12
3.62
1.44
.63
.85
HED13
4.58
1.10
.36
.86
HED14
3.31
1.12
.64
.85
HED15
3.50
1.42
.59
.85
HED16
3.31
1.46
.42
.86
HED17
3.62
1.13
.21
.86
HED18
3.23
1.21
.70
.85
HED19
2.69
1.29
.51
.86
HED20
2.69
1.26
.49
.86
HED21
2.72
1.24
.30
.86
HED22
3.38
1.68
.05
.87
HED23
3.04
1.37
.60
.85
HED24
3.04
1.22
.34
.86
HED25
2.96
1.46
.57
.85
Note. N = 26.
Table 3 Descriptive statistics of DAR-Items
Mean
Std. Deviation
Corrected Item-Total Correlation
Cronbach's Alpha if Item Deleted
DAER1
4.38
1.44
.42
.81
DAER2
4.38
1.66
.47
.80
DAER3
5.00
1.22
.72
.79
DAER4
5.50
0.83
.40
.81
DAER5
3.79
1.61
.57
.80
DAER6
3.92
1.77
.54
.80
DAER7
4.25
1.22
.53
.80
DAER8
3.08
1.25
.17
.82
DAER9
4.17
0.96
.52
.80
DAER10
4.08
1.38
.23
.82
DAER11
4.33
1.34
.21
.82
DAER12
4.58
1.06
.41
.81
DAER13
4.63
1.44
.34
.81
DAER14
4.46
1.38
.53
.80
DAER15
4.58
1.21
.30
.81
DAER16
4.04
1.12
.12
.83
DAER17
4.71
1.23
.64
.79
DAER18
3.71
1.23
.44
.80
DAER19
3.88
0.90
.19
.82
Note. N = 26.

Emotion regulation (HER and DAR) in relation to cortisol response as measured by AUCg and AUCi calculation.
The results show that the correlation between HER and salivary cortisol responses was significant (r (17)= -.525, p The correlation between DAR and cortisol reactivity, was not significant (r(17) = 0.30, p> .05), although there was a trend for positive relationship. Furthermore, the correlation between DAR and AUCi is not significant (r(17) = 0.259, p> .05)
Figure 5 cortisol reactivity as a function of High and low HER .

Hedonistic emotion regulation as predictor for cortisol response.
The results of regression analysis shows (figure 6) that HER can predict the AUCG ( = -0.525, t(17) = 2.32, p explain R² =27.6% of variance of the cortisol reactivity. This amount of variance is significant (F(1,16) = 5.71, p = .03).
Figure 6
Figure 6. AUCG as function of hedonistic emotion regulation.
Furthermore, HER can predict the increase in cortisol response (figure 7) ( = -0.524, t(17) = 2.38, p Figure 7
Figure 7. AUCI as function of hedonistic emotion regulation.

Plasma Interleukin –6 (IL-6)
We were only able to detect plasma IL-6 in 13 out of the 26 participants studied. Plasma IL-6 in these samples ranged from 1.20 to 327 pg/ml. Furthermore, there was no difference in plasma IL-6 concentrations 50 mins after the TSST test compared with the baseline sample (data not shown).
4. Discussion
The aim of this study was to investigate the association between psychological variables and the biological stress response and test the hypothesis that people who score high in HER and/or low in DAR have a lower cortisol response. Emotion regulation was measured based on the theory of Cybernetic 3-Dimensional Model on Emotion Regulation (CMER; Mohiyeddini, 2005) which integrates the previous theories of mood congruency effect (Bower, 1981), mood repair approach (Singer & Salovey, 1988) and motivational approach of emotion regulation (Parrott, 1993).
In conclusion the results of regression analysis show that HER can predict the AUCG ( = -0.525, t(17) = 2.32, p means that people who score highly in HER have a lower salivary cortisol response. In those who score high in DAR in contrast showed a trend towards higher salivary cortisol responses. This means that the findings support the idea that different paterns of emotion regulation could cause long term stress and in turn greater susceptibility to stress related illnesses. In view of these results the role of ER in relation to stress related disorders maybe important.
The present finding of an increased salivary cortisol in response to the psychosocial stress test TSST is consistent with previous findings (Dikerson and Kemery, 2004 ). Several new and important findings emerge from the present study. Supporting our hypothesis, participants, who score high in HER did show lower cortisol response. . These result indicate that HER is predictive of a lower cortisol response to the psychosocial stress test TSST,. This finding is in agreement with Wirtz et al., (2006) who also reported high HER with a low cortisol response in a clinical sample. In contrast DAR did not show any significant association with the cortisol response, although there was positive correlation with cortisol in this group but which was not significant. Interestingly there is evidence that elevated cortisol is associated with negative emotion (Polk et al., 2005). However, a disadvantage of previous studies is the neglect of the immediate ER process. Reading the average account of emotional experience that is measured over the duration of 1 to 2 weeks, demonstrates the results of emotion regulation rather than emotion regulation itself. This study in addition to Wirtz (2006) provides evidence for physiological response of immediate emotional regulation. This finding validates the psychological questionnaire that was used in this study. Importantly the present findings and those described above support the process model proposed by Gross (2001), suggesting that cognitive change-reappraisal occurs before the emotion response tendencies. Thus these findings support the idea that people who score high in HER, by using automatic reappraisal to positive, can change the perception of the situation before the emotion response tendencies , which in turn could be the reason for lower cortisol release . The present results for IL-6 dose not support the findings of Edwards et al (2006) who found increased plasma IL-6 levels in males following a psychological stress task known as the paced auditory serial addition task (PASAT). However, it is interesting to note that their reported differences were very small and were less than 1 pg/ml. Interestingly, the highest values reported by Edwards et al (2006) were at 30 mins following the stress test. It is possible that our lack of change in plasma IL-6 after the TSST test and inability to detect plasma IL-6 in many of the participants may reflect the late time point we used to obtain plasma samples (50 mins). Moreover , Edwards et al (2006) used a different psychological stress protocol (PASAT) than the one we employed (TSST) and this may also have contributed to the differences in results between the studies. Further research using earlier time points would resolve this problem and provide for a better comparison between the effects of the two psychological stress protocols on plasma IL-6. Moreover, many of the studies using TSST as the psychological stress protocol in relation to an increase in IL-6 have used isolated leucocytes in vitro rather than plasma IL-6 measurements (Steptoe et al 2007).
Despite these findings that show an association between cortisol and ER types, more studies are needed, as there are several limitations to the present study. Firstly the participants were restricted to males and the findings may not be applicable to females. There is evidence of gender differences in response to stress ( Laurent & Powres, 2007). Also women have a different kinetic profile for IL-6 (Edwards et al., 2006), and different stress related disorders, e.g general anxiety disorder (Alonso et al., 2004). Secondly the sample size was relatively small thus increasing the sample size may power the study to produce statistically significant results for e.g correlation between DAR and salivary cortisol. Thirdly, the apparent lack of difference in the plasma IL-6 concentration after the TSST test may be due to using a single time point sample (50 min.) rather than a full time course consisting of e.g. three 15 minutes sampling time points. And lastly, HER and DAR should not be perceived as opposite ends of a spectrum of ER. The balance of HER, DAR within individuals may vary considerably leading to complex interactions which affect physiological stress responses such as cortisol, and it is not known whether variables such as age or testosterone could also have an influential role in determining which ER type and individual scores higher.
It is know that emotion can influence such important processes like learning, decision-making, memory and consequently health and welfare of the individual (Wolf, 2007; Gross, 2002) then dysfunctional regulation of emotions can lead to psychopathology (Segerstrom et al., 2000; Nolen-Hoeksema, 2000). Our findings support the suggestions that there are regulatory processes in emotion that occur automatically and influence the emotional information processing at the conscious level (Davidson, 2000). Additionally to previous findings, the current study investigated automatic strategies through their effects on physiological responses and suggests that the type of ER may affect the physiological stress response, which in turn may impact on an individuals´ health and well-being. The importance of ER type in the development of stress related disorders e.g. hypertension, is unclear thus long term studies in people (men and women) with different ER and their subsequent development of stress related disorders would be of interest. Studies in females may give enhanced information that can lead to better understanding of anxiety related disorders where the majority of diagnosed are females. However, it is believed that social environment may be a factor in the gender difference in relation to the chance of developing anxiety or depression (Maier et al., 1999). The current study draws attention to individual differences in ER that may have a strong influence on the health of the individual. Thus further studies in this area would increase our understanding of the emotional regulation of the physiological response and lead to better psychotherapeutic interventions and / or management of the damaging stress response. It would also be interesting to investigate training effects, as opposed to participants being naïve, of psychological stress tests on the physiological stress response as measured by the salivary cortisol response in relation to ER. Such studies may reveal for example which ER types are better learners. Additionally, the use of more sensitive physiological stress markers of ER such as dehydroepiandrosterone (DHEA) and α- amylase and a panel of specific markers may in the future be predictive in individuals of their longer term response to stress and susceptibly to stress related disorders.
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