دانلود مقاله ISI انگلیسی شماره 39085
عنوان فارسی مقاله

نشانه های افسردگی و واکنش پذیری های فیزیولوژیکی ضعیف به عوامل استرس زای آزمایشگاهی

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
39085 2011 9 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.
عنوان انگلیسی
Depressive symptoms and attenuated physiological reactivity to laboratory stressors
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Biological Psychology, Volume 87, Issue 3, July 2011, Pages 430–438

کلمات کلیدی
واکنش پذیری قلب و عروق - نشانه های افسردگی - واکنش پذیری الکترودرمال - نقصان انگیزشی - عوامل استرس زا خود مرتبط
پیش نمایش مقاله
پیش نمایش مقاله نشانه های افسردگی و واکنش پذیری های فیزیولوژیکی ضعیف به عوامل استرس زای آزمایشگاهی

چکیده انگلیسی

Abstract There is evidence that depressive symptoms are associated with attenuated physiological reactivity to active stressors. However, it is not known whether blunted reactivity in depressed individuals is stressor-specific. We examined cardiovascular and electrodermal reactivity in non-clinical participants with varying levels of depressive symptoms to different active and passive stressors. Depressive symptoms were inversely related to both blood pressure and skin conductance reactivity during a public speaking task and the viewing of the speech video. However, no effects were found during a cold pressor task. Together these findings suggest that depressive symptoms are related to attenuated sympathetic nervous system reactivity in response to self-relevant stressors.

مقدمه انگلیسی

Introduction Depression has been discussed to constitute a robust psychosocial risk factor for cardiovascular diseases (CVD; Barth et al., 2004, Rugulies, 2002 and Wulsin and Singal, 2003). In particular, individuals with depressive symptoms are at higher risk for developing coronary artery disease, myocardial infarction, and complications following heart surgery. It has been suggested that the relationship between depression and CVD is mediated by behavioral factors on the one hand (e.g., substance abuse, diminished physical activity), and dysregulations in various physiological systems on the other hand [including the endocrine, immune, and autonomic nervous systems (Joynt et al., 2003 and Lett et al., 2004)]. With respect to autonomic nervous system (ANS) dysregulation there is evidence to suggest that depressive symptoms are related to higher sympathetic nervous system (SNS) activation (Joynt et al., 2003), attenuated vagal tone (Carney et al., 2001, Hughes and Stoney, 2001, Rottenberg, 2007, Schwerdtfeger and Friedrich-Mai, 2009 and Udupa et al., 2007), attenuated baroreceptorreflex-sensitivity (Watkins and Grossman, 1999), and elevated blood pressure (e.g., Grewen et al., 2004, Hamer et al., 2007 and Light et al., 1998). These various effects may impose elevated load on the cardiovascular system, thus fostering the development of CVD. Of note, depressive symptoms have also been related to cardiovascular reactivity (CVR). According to the reactivity hypothesis, repeated stress-related increases in cardiovascular function are assumed to accelerate a wear and tear on the artery walls, leading to endothelial dysfunction and, ultimately, CVD (Chida and Steptoe, 2010, Harris and Matthews, 2004 and Schwartz et al., 2003). Hence, it seems reasonable to assume that elevated CVR constitutes one path through which depression could affect cardiovascular health. A considerable number of studies has been devoted to the relationship between depressive symptoms and CVR. Whereas some studies could observe elevated CVR to laboratory stressors in depressed individuals (e.g., Light et al., 1998 and Matthews et al., 2005), other studies found that this effect was dependent on other psychological variables (e.g., aggression; Betensky and Contrada, 2010) or even failed to support this relationship (Taylor et al., 2006). Of note, a meta-analysis of 11 studies published until 2001 (Kibler and Ma, 2004) report positive, however, not reliable associations between depression and CVR, thus providing only limited support for the assumption that CVR links depression with adverse health outcomes. On the contrary, an increasing number of recently published studies found evidence for attenuated – and not elevated – CVR with increasing depression scores (e.g., Carroll et al., 2007, Phillips, 2011, Salomon et al., 2009 and York et al., 2007). For example, using a mental arithmetic task as a laboratory stressor Carroll et al. (2007) found in a population study that individuals with elevated depressive symptoms showed lower systolic blood pressure (SBP) and heart rate (HR) responses. Essentially the same finding was reported by Phillips (2011). Similarly, York et al. (2007) could observe that depressed individuals with coronary artery disease exhibited smaller increases in HR and SBP during a public speaking task than their counterparts with comparably low depression scores. Hence, it appears that depression might be associated with diminished CVR during certain aversive encounters. However, the role of stressor type in studies on depression and CVR is not well understood. Generally, two types of laboratory stressors can be distinguished, namely active stressors (e.g., public speaking tasks, mental arithmetics) and passive stressors [e.g., the cold pressor task (CP) or mirror tracing; Hurwitz et al., 1993 and Obrist, 1981]. Whereas active stressors are associated with a cardiovascular response pattern, which can be characterized by blood pressure increase, elevated cardiac contractility and cardiac output, as well as decreased peripheral resistance (indicating a beta-adrenergic response profile), the blood pressure increase to passive stressors is accompanied by attenuated cardiac output, and elevated peripheral resistance (indicating an alpha-adrenergic response profile; Brownley et al., 2000 and Hurwitz et al., 1993). It is interesting to note here that attenuated CVR in depressed individuals was mainly found when beta-adrenergic stressors were applied (Carroll et al., 2007, Phillips, 2011 and York et al., 2007), but there is little support for this finding for alpha-adrenergic stressors. In particular, Salomon et al. (2009) examined CVR to a public speaking task and a mirror tracing task in individuals diagnosed with major depressive disorder and healthy controls, thus allowing to contrast the effects of stressor type within the same study. In line with recent evidence, depressed individuals showed significantly lower SBP, HR, and cardiac output during the speech stressor, whereas the evidence for attenuated CVR was less clear for the mirror tracing task, which is an alpha-adrenergic stressor. Hence, blunted CVR in depressed individuals seems to depend on the type of stressor. Importantly, the finding of blunted CVR to active, beta-adrenergic stressors in depressed individuals is entirely consistent with the phenomenon of a motivational deficit in depression. Depressed individuals show a deficit in approach-related behavior. For example, McFarland and Klein (2009) recently found that depressed individuals exhibited attenuated emotional reactivity to anticipated monetary rewards, but did not differ from non-depressed when they anticipated non-reward or punishment. In line with this evidence, Brinkmann and Gendolla (2008) could observe that depressive symptoms among otherwise healthy participants were associated with attenuated SBP reactivity in response to a difficult stress task but not in response to an easy task. The authors argued that individuals mobilize resources as long as success is possible and worthwhile. In the case of depression, negative mood functions as information for high task demand, resulting in effort deterioration and, correspondingly, lower SBP reactivity. Taken together, depressed individuals show an appetitive deficit in laboratory tasks and, consequently, may not invest much effort during active tasks, resulting in lower CVR. 1.1. Aim of the study The aim of this study was to examine CVR in non-clinical individuals with varying depression scores to different laboratory stressors. In order to investigate the specificity of the findings with respect to stressor type in more detail, participants were faced with both active and passive aversive encounters. We implemented three different stressors. There was an active beta-adrenergic stressor (public speaking task), in which participants were instructed to prepare and deliver a speech within a social-evaluative context (similar to the public speaking task used by Salomon et al., 2009), and two different alpha-adrenergic passive stressors (a CP task and a video viewing task). We decided to implement two different passive stressors for the following reasons: first, previous studies largely neglected passive stressors to provoke CVR in non-clinical individuals with depressive symptoms. Hence, there is a need for research applying different passive stressors to gain a broader view of blunted CVR in mildly depressed individuals. Second, passive stressors usually are of little self-relevance, whereas active stressors are much more relevant to the self (e.g., via the evaluation of personal performance). Hence, when contrasting the role of stressor type to examine CVR there is a risk of confounding stressor type with self-relevance. Of note, personal relevance and negative self-views are a central feature of many theories of depression (e.g., Beck et al., 1979 and Wisco, 2009). Thus, self-relevance could be more crucial for CVR as related to depressive symptoms than stressor type. Taken together, we were interested to examine CVR to two passive tasks which differed with respect to self-relevance. The CP was chosen as a physically challenging task with little self-relevance. In order to contrast the CP with a passive self-relevant stressor, we additionally implemented a video viewing task in which participants were asked to watch the videotape of them presenting the speech. Thus, the video viewing task mirrored the speech task, but this time it was a passive task, requiring no effort allocation. In line with previous evidence we expected that depressive symptoms would be associated with blunted CVR to the active task (i.e., less effort allocation and approach behavior in depressives when active task performance is required), but not during the passive non self-relevant task (e.g., Salomon et al., 2009). Moreover, if self-relevance is the key to diminished CVR in depressive individuals, we would predict that depressive symptoms will also be related with attenuated reactivity to the viewing of the speech video, but not to the CP. Importantly, besides the well-studied cardiovascular system we also opted for recording electrodermal reactivity (EDR). Of note, electrodermal hyporeactivity in depressed individuals has been reported in a number of previous studies (e.g., Dawson et al., 1977, Donat and McCullough, 1983, Greenfield et al., 1963, Iacono et al., 1983, Lader and Wing, 1969, McCarron, 1973, Noble and Lader, 1971, Thorell, 2009 and Zuckerman et al., 1968). Similar to blood pressure, electrodermal activity is predominately influenced by sympathetic nerve fibers (e.g., Boucsein, 1992). Hence, these findings might be interpreted in terms of a more generalized sympathetic nervous system dysfunction in individuals with depressive symptoms. Finally, we aimed to exploratively analyze physiological recovery. Of note, recent research suggests that especially cardiovascular recovery may be more important for physical health than peak reactivity to a challenge (Brosschot et al., 2006 and Steptoe and Marmot, 2005). With respect to depression, the so-called perseverative cognition hypothesis (e.g., Brosschot, 2010 and Brosschot et al., 2006) suggests that ruminating thoughts and worry may lead to sustained physiological activation, ultimately imposing risk for disease. However, recent research on diminished CVR in depression largely neglected recovery (e.g., Carroll et al., 2007, Phillips, 2011 and York et al., 2007) or found no consistent association (Salomon et al., 2009), thus necessitating further research.

نتیجه گیری انگلیسی

Results Table 1 shows the descriptive statistics of the physiological variables in the course of this experiment. The mixed-effects analyses of the various physiological reactivity measures are presented in Table 2 (public speaking task), Table 3 (CP), and Table 4 (video viewing task). Table 1. Means and standard deviations (in brackets) of the main variables throughout the experiment. BL Prep. Speech Rec. BL Prep. CP Rec. BL Prep. Video Rec. HR 75.56 (12.74) 88.06 (16.33) 99.91 (16.83) 75.08 (13.01) 74.08 (11.97) 75.48 (12.40) 84.26 (14.58) 73.14 (11.19) 72.80 (11.11) 76.61 (11.95) 75.51 (11.64) 73.00 (11.16) SBP 115.96 (16.48) 131.16 (20.89) 138.35 (27.62) 114.19 (23.10) 114.54 (13.34) 119.91 (18.25) 133.78 (30.29) 116.95 (20.65) 113.26 (14.47) 119.97 (20.21) 125.59 (24.93) 116.92 (20.50) DBP 80.26 (15.18) 88.36 (18.49) 94.32 (21.07) 74.91 (22.73) 81.10 (10.38) 83.88 (14.14) 93.39 (23.83) 82.52 (16.83) 79.98 (10.92) 83.60 (15.08) 88.74 (18.16) 82.70 (17.60) NSSCR 5.65 (4.53) 10.29 (4.92) 12.67 (3.53) 4.91 (3.99) 4.69 (3.80) 6.33 (3.84) 9.48 (5.47) 3.09 (3.37) 4.68 (3.87) 7.46 (4.41) 10.94 (4.52) 3.80 (3.46) Note: BL = baseline, Prep. = preparation period, Speech = speech stressor, Rec. = recovery, CP = cold pressor, Video = video stressor. Table options Table 2. Linear mixed-effects models for predicting heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and the number of skin conductance responses (NSSCR; right side) to the speech task. Variable HR SBP DBP NSSCR/min b a SE T b a SE T b a SE T b a SE T Intercept 73.83 2.92 25.30* 120.59 3.61 33.40* 80.24 3.45 23.23* 5.69 0.84 6.74* Sex (0 = male, 1 = female) 2.44 3.69 0.66 −7.20 4.62 −1.56 0.30 4.42 0.07 0.15 0.93 0.16 Age 0.64 0.55 1.17 −0.51 0.69 −0.74 −0.74 0.66 −1.13 −0.16 0.14 −1.13 BMI −0.33 0.55 −0.59 1.06 0.69 1.53 0.71 0.66 1.07 0.13 0.14 0.90 BDI −0.02 0.11 −0.20 −0.07 0.13 −0.50 −0.18 0.13 −1.46 −0.06 0.04 −1.64 Preparation (vs. BL) 12.42 1.27 9.76* 15.34 1.65 9.31* 8.02 1.29 6.22* 4.60 0.38 12.16* Speech (vs. BL) 23.80 1.60 14.92* 23.32 2.76 8.46* 14.44 1.96 7.39* 6.90 0.49 14.10* Recovery (vs. BL) −0.44 0.64 −0.69 −1.80 2.67 −0.67 −5.58 2.31 −2.42* −0.77 0.33 −2.33* BDI × preparation (vs. BL) −0.15 0.07 −2.02* −0.27 0.09 −2.86* −0.15 0.07 −2.02* −0.05 0.02 −2.35* BDI × speech (vs. BL) −0.15 0.09 −1.61 −0.49 0.16 −3.06* −0.28 0.11 −2.51* −0.01 0.03 −0.51 BDI × recovery (vs. BL) 0.01 0.04 0.21 −0.21 0.15 −1.37 −0.15 0.13 −1.15 −0.004 0.02 −0.22 Note: BDI = Beck Depression Inventory, BL = baseline. a Unstandardized partial regression coefficients. * p < .05. Table options Table 3. Linear mixed-effects models for predicting heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and the number of skin conductance responses (NSSCR; right side) to the cold pressor (CP). Variable HR SBP DBP NSSCR/min b a SE T b a SE T b a SE T b a SE T Intercept 73.90 2.68 27.59* 120.63 2.30 52.37* 84.24 1.89 44.60* 5.32 0.79 6.71* Sex (0 = male, 1 = female) −0.11 3.33 −0.03 −9.62 2.84 −3.39* −5.03 2.28 −2.21* −0.88 0.96 −0.91 Age 0.65 0.50 1.30 0.11 0.42 0.27 0.06 0.34 0.19 −0.04 0.14 −0.25 BMI −0.23 0.50 −0.46 1.33 0.43 3.11* 1.16 0.34 3.39* 0.005 0.14 0.03 BDI 0.01 0.10 0.11 0.10 0.09 1.17 0.06 0.07 0.79 −0.04 0.03 −1.16 Preparation (vs. BL) 1.45 0.37 3.93* 5.39 1.11 4.86* 2.78 0.84 3.30* 1.60 0.37 4.33* CP (vs. BL) 10.24 1.24 8.28* 18.98 3.33 5.70* 12.95 2.78 4.65* 4.73 0.62 7.59* Recovery (vs. BL) −1.02 0.42 −2.40* 2.90 1.64 1.77 1.74 1.41 1.23 −1.65 0.30 −5.56* BDI × preparation (vs. BL) −0.006 0.02 −0.29 0.04 0.06 0.57 0.02 0.05 0.40 0.005 0.02 0.21 BDI × CP (vs. BL) 0.002 0.07 0.02 −0.29 0.19 −1.54 −0.20 0.16 −1.26 −0.05 0.04 −1.49 BDI × recovery (vs. BL) 0.01 0.02 0.54 −0.08 0.09 −0.80 −0.06 0.08 −0.76 0.03 0.02 1.68 Note: BDI = Beck Depression Inventory, BL = baseline. a Unstandardized partial regression coefficients. * p < .05. Table options Table 4. Linear mixed-effects models for predicting heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and the number of skin conductance responses (NSSCR; right side) to the viewing of the speech video. Variable HR SBP DBP NSSCR/min b a SE T b a SE T b a SE T b a SE T Intercept 70.98 2.51 28.27* 118.04 2.99 39.52* 81.01 2.22 36.48* 5.44 0.83 6.53* Sex (0 = male, 1 = female) 2.70 3.16 0.86 −7.98 3.78 −2.11* −1.81 2.79 −0.65 −1.21 1.01 −1.20 Age 0.92 0.47 1.95 0.81 0.56 1.44 0.67 0.41 1.62 −0.09 0.15 −0.59 BMI −0.37 0.47 −0.79 0.32 0.57 0.56 0.20 0.42 0.48 0.04 0.15 0.24 BDI −0.01 0.09 −0.06 −0.04 0.11 −0.40 −0.11 0.08 −1.36 −0.009 0.03 −0.28 Preparation (vs. BL) 3.90 0.61 6.40* 7.29 1.33 5.49* 3.96 0.91 4.37* 2.77 0.39 7.05* Video (vs. BL) 2.52 0.73 3.47* 13.09 2.32 5.64* 8.96 1.53 5.85* 6.26 0.47 13.38* Recovery (vs. BL) −0.11 0.40 −0.28 3.54 1.72 2.06* 2.38 1.37 1.74 −0.85 0.30 −2.81* BDI × preparation (vs. BL) −0.05 0.04 −1.52 −0.17 0.08 −2.28* −0.12 0.05 −2.31* −0.06 0.02 −2.48* BDI × video (vs. BL) −0.03 0.04 −0.72 −0.31 0.13 −2.35* −0.20 0.09 −2.31* −0.06 0.03 −2.20* BDI × recovery (vs. BL) 0.003 0.02 0.15 −0.24 0.10 −2.38* −0.20 0.08 −2.49* 0.002 0.02 0.10 Note: BDI = Beck Depression Inventory, BL = baseline. a Unstandardized partial regression coefficients. * p < .05. Table options 3.1. CVR For the speech task we found significant increases from baseline to preparation and speech delivery for each cardiovascular variable with a subsequent decrease during recovery, suggesting that the stressor was effective. Please note that DBP during recovery was lower than during baseline. Moreover, the interaction of BDI and preparation was significant for HR, SBP, and DBP, documenting negative associations between depressive symptoms and CVR during preparation. The interaction of BDI and speech delivery was also significant for SBP and DBP, but failed to reach significance for HR. To examine these interaction effects further, we calculated simple-slope analyses. Therefore, we rescaled the BDI at the standard deviation, thus allowing us to analyze individuals high (1 SD above the mean) and low (1 SD below the mean) on the BDI, thereby controlling for all other covariates. Specifically, two continuous variables were calculated that were scaled to zero at either 1 SD above (i.e., BDI+) or 1 SD below the mean (i.e., BDI−). Then, two additional analyses were run in which the newly computed high and low BDI variables were separately entered into the equation replacing the original BDI variable. Importantly, this kind of analysis makes use of the whole sample size, thus retaining the same statistical power as the previous models. These analyses suggested that individuals high in depressive symptoms showed approximately 9 mmHG (preparation period) and 17 mmHg (speech) lower SBP reactivity than individuals low in depression. The difference in DBP was 5 mmHG for the preparation period and 10 mmHG for the speech. Further, individuals high in depressive symptoms showed a 5 BPM lower HR during preparation than individuals with comparably few depressive symptoms. For the CP task (Table 3) there were significant increases to both preparation and task performance for each cardiovascular variable. Moreover, CVR returned to baseline levels for SBP and DBP, and decreased below baseline level for HR. Of note, there were no significant interactions of BDI and any of the periods of the CP task (all |T|s < 1.55). Further, there were significant sex effects for blood pressure, indicating 9 mmHg lower SBP and 5 mmHg lower DBP in women as compared to men. Finally, during baseline both SBP and DBP were positively associated with BMI, indicating elevated blood pressure with higher BMI. For the video viewing task (Table 4) there were significant cardiovascular increases to preparation and task performance. Moreover, HR and DBP significantly decreased to baseline levels during recovery, whereas SBP exceeded baseline level during recovery. Importantly, there were significant interactions of BDI and preparation, BDI and video viewing, and BDI and recovery for SBP and DBP, respectively. Again, simple-slope analyses as described above were calculated to examine these interactions in more detail. We found that elevated BDI scores were accompanied by lower SBP and DBP reactivity throughout different phases of the task. In particular, holding all other variables constant SBP reactivity in individuals with elevated BDI scores (1 SD above the mean) was 6 mmHG (preparation), 11 mmHG (video viewing), and 8 mmHG (recovery) lower as compared to individuals with low BDI scores (1 SD below the mean). For DBP the respective differences were 4 mmHg (preparation), 7 mmHg (video viewing), and 5 mmHg (recovery). The SBP and DBP response curves for high and low depressive individuals throughout the tasks are depicted in Fig. 1. Systolic blood pressure (SBP; upper figure) and diastolic blood pressure (DBP, ... Fig. 1. Systolic blood pressure (SBP; upper figure) and diastolic blood pressure (DBP, lower figure) of high (1 SD above the mean of the BDI; BDI+) and low (1 SD below the mean of the BDI; BDI−) depressive participants throughout the different tasks. Values are derived from the mixed effect models and are adjusted for gender, age, and BMI. Reactivity from baseline in response to the speech and the video viewing task was significantly diminished in individuals with relatively more depressive symptoms. Note: BL = baseline, PREP = preparation, SP = speech task, CP = cold pressor task, VID = video viewing task. Figure options 3.2. EDR As revealed in Table 2, analyses of NSSCR for the speech task revealed significant increases from baseline to preparation and speech delivery, and a subsequent drop below baseline level during recovery. Further, there was a significant interaction of BDI and preparation, indicating lower EDR with increasing BDI scores. Again, simple-slope analyses were calculated to elucidate this effect. Individuals with comparably low BDI scores (1 SD above the mean) showed an excess of 1.8 NSSCRs above those with comparably high BDI scores (1 SD below the mean). The interactions for the speech delivery and recovery periods, respectively, did not reach significance. For the CP task (Table 3) we found significant increases from baseline to both preparation and CP. During recovery, NSSCR was significantly reduced as compared to baseline. No other effects reached significance. In particular, there were no significant interactions of BDI and any of the periods of the task (all |T|s < .1.69). Finally, the analysis of the video viewing task (Table 4) revealed significant NSSCR increases from baseline to preparation and video viewing, with a subsequent drop below baseline level during recovery. Again, there was a significant BDI × preparation interaction, indicating lower EDR to preparation in individuals with elevated BDI scores. Simple-slope analyses were calculated as described earlier. The respective predicted values were 3.74 NSSCRs for individuals scoring low on the BDI (1 SD below the mean) and 1.79 NSSCRs for those scoring high on the BDI (1 SD above the mean). Importantly, the interaction for the video viewing was also significant, thus mirroring the effect of the preparation period. Specifically, for individuals scoring low on the BDI the predicted value was 7.29 NSSCRs and for individuals scoring high on the BDI it was 5.23 NSSCRs. The adjusted NSSCR response curves for high and low depressed individuals are depicted in Fig. 2. Number of non-specific skin conductance responses (NSSCR) of high (1 SD above ... Fig. 2. Number of non-specific skin conductance responses (NSSCR) of high (1 SD above the mean of the BDI; BDI+) and low (1 SD below the mean of the BDI; BDI−) depressive participants throughout the different tasks. Values are derived from the mixed effect models and are adjusted for gender, age, and BMI. Reactivity from baseline in response to the speech and the video viewing task was significantly diminished in individuals with relatively more depressive symptoms. Note: BL = baseline, PREP = preparation, SP = speech task, CP = cold pressor task, VID = video viewing task.

خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.