کورتیزول بزاقی و واکنش پذیری DHEA به استرس روانی در مردان با اضطراب اجتماعی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|39053||2009||6 صفحه PDF||سفارش دهید||5758 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : International Journal of Psychophysiology, Volume 72, Issue 2, May 2009, Pages 198–203
Abstract The purpose of the present study was to examine Hypothalamus–Pituitary–Adrenal (HPA) axis reactivity in social anxiety. The present study used a standardized psychosocial stress protocol (the Trier Social Stress Test; TSST; [Kirschbaum, C., Pirke, K.M., Hellhammer, D.H., 1993. The ‘Trier Social Stress Test’—a tool for investigating psychobiological stress responses in a laboratory setting. Neuropsychobiology 28, 76–81.]) with 11 higher-social-anxiety and 11 lower-social-anxiety male college students. Psychological responses and salivary cortisol and dehydroepiandrosterone (DHEA) reactivity and cortisol/DHEA ratio were assessed at seven different times. The results showed that there was a significantly lower cortisol responsiveness in the higher social anxiety group but there was no significant difference of DHEA responsiveness. Further analyses showed lower responses for the cortisol/DHEA ratio in the higher-social-anxiety group to the TSST. These results suggest that there may be reduced HPA axis reactivity to psychosocial stress in socially anxious people.
. Introduction Social anxiety is a highly prevalent condition in both clinical and non-clinical populations. Social Anxiety Disorder (SAD), or Social Phobia is the commonest of the anxiety disorders, and it has a high rate of lifetime prevalence (Kessler et al., 1994, Magee et al., 1998 and Pellisso et al., 2000). Social anxiety is characterized by a fear of negative evaluation by others (Clark and Wells, 1995 and Rapee and Heimberg, 1997). One of the most fearful situations for SAD patients and for individuals with social anxiety is public speaking (Stein et al., 1996). SAD patients and individuals with high social anxiety have a number of similar psychological and physiological features that differ only in the degree of intensity (Turner et al., 1986 and Turner et al., 1990), therefore, it has been suggested that there is an overlap between shyness, social anxiety and SAD (Rapee, 1995). It is possible that there are common features and a continuum from low to high social anxiety and SAD. Many previous studies have examined the specific psychological and physiological features of SAD patients, as well as of individuals with high social anxiety. These studies have clarified the psychopathology and the pathophysiology of SAD. Recently, an abnormality of the Hypothalamic–Pituitary–Adrenal (HPA) axis has been implicated in major depressive and anxiety disorders (Marshall et al., 2002, Peeters et al., 2004 and Stones et al., 1999). Cortisol is the glucocorticoid hormone that is secreted by the adrenal gland and it has been suggested that cortisol secretion is stimulated by psychological distress and social evaluative threats (Dickerson and Kemeny, 2004). As a result abnormalities and the reactivity of the HPA axis have been the focus of many investigations on psychiatric disorders. Furthermore, cortisol is considered to be the endocrine hormone modulating mental and physical states that are associated with psychosocial stressors. Uhde et al. (1994) found no difference in basal cortisol values between SAD patients and normal controls. Furlan et al. (2001) examined differences in HPA axis reactivity between high and low responding SAD patients and healthy controls using speech and physical tasks and found specific HPA axis responses to speech tasks, but not for physical tasks. Condren et al. (2003) found significantly greater delta max cortisol values (the difference between baseline and maximum cortisol level during stress) in SAD patients in comparison to healthy controls, when a serial subtraction test and a digit span test were conducted. Martel et al. (1999) reported that both social phobia patients and controls had a significantly elevated level of cortisol prior to the Trier Social Stress Test (TSST: Kirschbaum et al., 1993). However, this study did not find a difference in HPA axis reactivity resulting from psychosocial stressors between SAD adolescents and the control group. On the other hand, Beaton et al. (2006) reported lower salivary cortisol levels in a clinically diagnosed social phobia group, compared to a non-clinical control group, in a speech task. Tops et al. (2008) suggested that the fear of negative evaluation, which is core cognition in SAD, was related to a low cortisol mobilization response. The above studies suggest two patterns of HPA axis reactivity to situations causing social anxiety: high and low cortisol responses, and as such, have been inconsistent. Such differences may arise from differences in psychosocial stressors, or from the protocols that have been used in different studies. It is suggested that cortisol response to standardized psychosocial stressors should be evaluated to clarify the role of endocrine reactivity to social anxiety. It is meaningful to examine the salivary dehydroepiandrosterone (DHEA) response to situations causing social anxiety. DHEA, in addition to cortisol, is a major steroid produced by the zona reticularis of the adrenal cortex. Some studies have suggested that lower DHEA levels are associated with lower psychological wellbeing (van Niekerk et al., 2001). One study has shown that DHEA was negatively correlated with depression (Michael et al., 2000). Another investigation has indicated that the administration of DHEA improved mood of healthy young men (Alhaj et al., 2006). Conversely, other studies have reported that the administration of DHEA has little effect on the mood of healthy elderly people (Kudielka et al., 1998 and Wolf and Krischbaum, 1999). In conclusion, these findings have implicated DHEA in the regulation of mental states. However, the mechanism of stress-induced DHEA secretion (Oberbeck et al., 1998) and DHEA reactivity in SAD to psychosocial stressors has not been sufficiently understood. Moreover, a difference in the ratio of cortisol to DHEA has been found in individuals with mental disorders. Blauer et al. (1991) indicated that DHEA could antagonize cortisol activity. Therefore, it is considered that the cortisol to DHEA ratio may be a marker of endocrine imbalance. For example, Goodyer et al. (2003) showed that persistently depressed individuals had a higher cortisol to DHEA ratio than non-depressed and remitted individuals. Goodyer et al. suggested that the high ratio might be a marker of persistent psychiatric disorders. Other studies have found that a higher morning cortisol to DHEA ratio is associated with higher anxiety (van Niekerk et al., 2001). Young et al. (2002) showed that the cortisol to DHEA ratio from saliva samples correlated with the length of the current depressive episode and suggested that the cortisol to DHEA ratio could be a marker of depressive states. Thus, it has been speculated that the cortisol to DHEA ratio would represent an endocrine imbalance of the HPA axis function and may be a marker of the state of other psychiatric disorders. However, no studies have investigated the cortisol to DHEA ratio in social anxiety and SAD. Above-discussed findings suggest that there might be an abnormality of the HPA axis function in individuals with high social anxiety and in SAD patients. Furthermore, this abnormality may influence the regulation of their mental states. Therefore, investigating the HPA axis reactivity in relation to social anxiety, including the roles of cortisol, DHEA and cortisol to DHEA ratio, may be important for understanding the psychopathology of SAD and social anxiety. The present study investigated HPA axis and psychological reactivity to standardized psychosocial stresses as measured by the Trier Social Stress Test in male college students with high and low social anxieties.
نتیجه گیری انگلیسی
Results 3.1. Physiological measures The mean AUCI of cortisol and DHEA were calculated to assess the responsiveness to the TSST. The results show that there was a significantly lower cortisol response in the HS group (t(20) = 2.75, p < .01). However, no significant difference was found for DHEA (t(20) =1.06, p = .30). All variables of the HPA axis (cortisol, DHEA, and cortisol/DHEA ratio) were examined in two-way ANOVAs. The results of the ANOVAs (2 groups × 7 times) showed significant group × time interactions for cortisol and cortisol/DHEA ratio, shown (F(2.11, 42.26) = 4.53, p < .05, Fig. 1; F(2.07, 41.40) = 3.72, p < .05, Fig. 2, respectively), but not for DHEA (F(3.56, 71.10) = 1.10, p = .36). For cortisol, DHEA, and cortisol/DHEA, a significant main effect of time was found (F(2.11, 42.26) =13.44, p < .01; F(3.56, 71.10) = 6.28, p < .01, Fig. 3; F(2.07, 41.40) = 7.77, p < .05, respectively). However, there was no significant main group effect in all values (F(1, 20) = 2.00, p = .17; F(1, 20) = .01, p = .97; F(1, 20) = .59, p = .45, respectively). Cortisol responses at different times. BL: 10 min before the start of the stress ... Fig. 1. Cortisol responses at different times. BL: 10 min before the start of the stress task, PR; just before the start of the stress task, SP: just after the stress task, SS: just after the serial subtraction task, R1: 20 min after the start of the stress task, R2: 30 min after the start of the stress task, R3: 40 min after the start of the stress task. Error bars show ± standard error of the mean. Figure options Cortisol/DHEA ratios at different times. BL: 10 min before the start of the ... Fig. 2. Cortisol/DHEA ratios at different times. BL: 10 min before the start of the stress task, PR; just before the start of the stress task, SP: just after the stress task, SS: just after the serial subtraction task, R1: 20 min after the start of the stress task, R2: 30 min after the start of the stress task, R3: 40 min after the start of the stress task. Error bars show ± standard error of the mean. Figure options DHEA responses at different times. BL: 10 min before the start of the stress ... Fig. 3. DHEA responses at different times. BL: 10 min before the start of the stress task, PR; just before the start of the stress task, SP: just after the stress task, SS: just after the serial subtraction task, R1: 20 min after the start of the stress task, R2: 30 min after the start of the stress task, R3: 40 min after the start of the stress task. Error bars show ± standard error of the mean. Figure options Post hoc tests for the cortisol values showed lower cortisol secretions at SS (p = .10), R1 (p < .05) and R2 (p < .05) in the HS group compared with the LS group. For the LS group, the cortisol secretion at SP, SS, R1 and R2 was higher than at BL (ps < .05). For the cortisol/DHEA ratio in the LS group, the ratio at R1 was higher than at BL (p < .05) and the ratios at SS, R1, and R2 were higher than at PR (p < .05). For the HS group, the ratio at BL was higher than at SP (p = .07). Furthermore, the ratio at BL for the HS group was marginally higher than for the LS group (p = .10). 3.2. Psychological measures Two-way ANOVAs were used to compare all values. There were no significant interactions with all values (Fs(2.82, 62.14) = 1.74, ps > .17). For tension-anxiety, significant main effects for time and group were found (time, F(3.76, 75.19) = 38.62, p < .01; group, F(1, 20) =5.31, p < .05). For other factors, main effects of time were found for perceived stress (F(3.04, 60.70) = 39.07, p < .01), depression (F(4.08, 81.53) = 4.89, p < .01), anger (F(2.86, 57.28) = 7.00, p < .01), fatigue (F(3.22, 64.29) = 4.29, p < .01), and confusion (F(3.57, 71.41) = 15.78, p < .01). There was not a significant difference for vigor (F(3.21, 64.22) =2.08, p = .11). These results suggest that both groups showed psychological reactivity to the TSST, and the HS group reported more tension-anxiety in the experiments.