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Published online before print October 17, 2007, 10.1097/PSY.0b013e318157b12e
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Psychosomatic Medicine 69:807-815 (2007)
© 2007 American Psychosomatic Society

ORIGINAL ARTICLES

Stress, Social Support, and Delayed Skin Barrier Recovery

Theodore F. Robles, PhD

From the Department of Psychology, University of California, Los Angeles, Los Angeles, California.

Address correspondence and reprint requests to Theodore F. Robles, Assistant Professor UCLA Department of Psychology, Box 951563, 1285 Franz Hall, Los Angeles, CA 90095-1563. E-mail: robles{at}psych.ucla.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: To examine the effect of a brief laboratory stressor and social support before the stressor on cardiovascular and cortisol responses, and skin barrier recovery after skin disruption.

Methods: Eighty-five healthy participants (mean age 22.9 ± 4.4 years) underwent a "tape-stripping" procedure that disrupts normal skin barrier function, and were randomly assigned to a No Stress (reading task), Stress (Trier Social Stress Test), or Stress + Social Support condition (support from a confederate before the stressor). Skin barrier recovery was assessed by measuring transepidermal water loss from up to 2 hours after skin disruption.

Results: Compared with the No Stress condition, the stressor delayed skin barrier recovery by 10% at 2 hours after skin disruption (effect size, r = .29), and increased anxiety (r = .24), negative affect (r = .22), cardiovascular activity (r values from .4–.6), and among male participants, cortisol levels (r = .40). Social support did not influence psychological or physiological responses or skin barrier recovery. Larger physiological responses to the tasks did not predict slower skin barrier recovery. Instead, larger systolic blood pressure responses predicted faster skin barrier recovery (r = .26).

Conclusions: This study replicated the effects of short-term laboratory stressors on skin barrier recovery, further establishing the relevance of skin barrier recovery for future research. The support manipulation did not influence physiological responses or skin barrier recovery, suggesting that future research on social support, physiology, and objective health outcomes should focus on naturalistic social interactions, relationships, and stressors.

Key Words: acute stress • social support • wound healing • cardiovascular reactivity • cortisol • skin barrier recovery

Abbreviations: AUCI = area under the curve with respect to increase; BMI = body mass index; DBP = diastolic blood pressure; GCRC = General Clinical Research Center; HR = heart rate; MAP = mean arterial pressure; SBP = systolic blood pressure; TSST = Trier Social Stress Test; TEWL = transepidermal water loss.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
The prevailing theories of how stress affects health emphasize the role of cardiovascular, neuroendocrine, and immune responses to stressors (1,2), and their contribution to the onset or progression of disease (3–6). Similarly, theories of how social support benefits health also emphasize the influence of social support on physiological responses to stress. The empirical basis for the effects of stress and social support on physiological responses comes from laboratory studies involving two key elements: brief laboratory stressors such as public speaking, which reliably increase cardiovascular and cortisol responses (7,8); and a social support manipulation, where a supportive individual is present before or during the brief stressor (9). Two meta-analytic reviews suggest that social support manipulations decrease cardiovascular and cortisol responses to acute stressors (1,10), including social support provided by friends or strangers (11,12), although results vary across individual studies (13,14).

Unfortunately, there is little evidence linking stress-related physiological responses in the laboratory to prospectively measured health outcomes, particularly in healthy adults free of any chronic disease. For instance, although changes in immune function during acute stress are reliable and replicable across a number of studies, the clinical relevance of these short-term changes is still unclear (15). Due to the difficulty in finding clinically relevant health outcomes that change within a few hours, no laboratory-based studies of physiological changes have directly evaluated a measurable health outcome after the brief stressor.

The dynamics of skin repair and wound healing offer a promising model for studying clinically relevant health outcomes that can change in a brief period of time. The skin is the largest organ of the body, and is composed of two major layers, the inner dermis layer and the outer epidermis layer (16). The skin has many functions, including serving as a barrier preventing evaporative water loss and blocking against pathogens. The outermost layer of skin cells, known as the stratum corneum, serves as the primary layer involved in preserving skin barrier function. Any damage to the skin such as dry skin, lacerations, solvents, detergents, and removal of skin cells in the stratum corneum will disrupt and reduce skin barrier function.

Several studies now show that short- and long-term psychological stress delays wound healing (17,18) and that psychological stress may exacerbate certain dermatological conditions (19). Psychological stress also has similar negative effects on skin barrier recovery after disruption. In a medical student sample, approximately 30% skin barrier recovery was achieved at 3 hours after skin disruption during academic examinations, compared with 45% barrier recovery during the end of winter and spring vacation (20). In another study in healthy adults, skin barrier recovery was slowed by an interview stressor (approximately 55% 3 hours after disruption), similar to the laboratory stressor used in this study, compared with skin barrier recovery during a nonstressful baseline the previous day (approximately 69%) (21). Notably, these studies used the same dermatological procedure employed in this study. Currently unknown is whether social support speeds skin barrier recovery and the relationship between stress-related physiological changes and skin barrier recovery.

This study examined the effect of a brief laboratory stressor on a health outcome that is clinically relevant for wound healing and a number of skin disorders, and could be measured within the timeframe of a laboratory stress study: skin barrier recovery post skin disruption. Based on previous work (20,21), it was predicted that exposure to a brief laboratory stressor would delay skin barrier recovery compared with no exposure to a laboratory stressor.

Another aim of the study was to determine whether the moderate-to-large effects of social support on reducing physiological responses to stress would extend to speeding skin barrier recovery. Thus, this study included a social support manipulation before the stressor, which was predicted to speed skin barrier recovery compared with no social support before the laboratory stressor.

A final aim of this study was to examine the relationship between physiological responses during stress and skin barrier recovery. Most researchers suggest that stress-related changes in the endocrine and immune systems mediate the relationship between stress and wound healing (20,22). The initial phases of the response to skin barrier disruption involve lipid synthesis and cytokine expression (23,24) and stress-related biological changes may directly or indirectly affect either or both processes. Garg and colleagues speculated that three potential mechanisms may explain stress-related alterations in skin barrier recovery: stress-related activation of immune and inflammatory processes in deeper skin layers, neuropeptide release from afferent nerves in the peripheral nervous system, and systemic glucocorticoid levels (20). Several lines of evidence in animals support the role of glucocorticoid (25,26) and ß-adrenergic agonists in delaying skin barrier recovery (27). Thus, it was predicted that individuals with larger autonomic (as indexed by cardiovascular measures) and cortisol changes during the laboratory stressor would show delayed skin barrier recovery.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
Healthy individuals aged 18 to 44 years were recruited from the local community surrounding a large Midwest university using fliers posted in public places. Exclusion criteria included pregnancy; medical conditions or medications with obvious immunological, dermatological, or endocrinological consequences; allergies to tape or other adhesives; smoking; and excessive caffeine or alcohol use. Individuals taking hormone-based contraception were excluded because of effects on cortisol responses to stress (28). Female participants were not scheduled around their menstrual cycle stage. A total of 99 individuals participated in the study, of whom 12 women did not report taking hormonal-based contraception on our initial screening form, but reported it during the experimental session. Two individuals were unable to complete the entire protocol. Therefore, data from those 14 individuals were not included in the data analyses that follow, leaving a sample of 85 individuals for the data analyses. The final sample included 44 female and 41 male participants, 66% white, 20% Asian, 11% black, and 3% of other ethnicities. Most participants (69%) had some college education, and the remainder (31%) had completed college.

Procedures
All participants were run individually during a single 3.5 hours session at The Ohio State University General Clinical Research Center (GCRC) beginning at 1:30 PM. Data collection took place between October 2003 and July 2005. Participants refrained from eating, engaging in vigorous exercise, and smoking for 1 hour before the appointment. After providing informed consent, participants were fitted with a blood pressure cuff and sat quietly for 40 minutes. Baseline cardiovascular recordings and a saliva sample were then collected. Next, baseline skin measurements were obtained, the skin was disrupted, and another saliva sample was collected. Participants were randomly assigned to one of three groups: No Stress, Stress, or Stress + Support. Each group received task instructions, prepared for the task for 10 minutes, and then performed the 10-minute task. All participants were seated throughout the tasks.

Participants in the No Stress group were instructed to read an article silently and alone during the preparation period, followed by reading the article and an additional article out loud into a tape recorder. Participants in the No Stress group were told that they were not being evaluated, and they performed the task alone. Video recording equipment was present, but the video camera was turned off and pointed toward a wall. Participants in the two Stress groups were provided instructions for the Trier Social Stress Test (TSST), a 5-minute speech, and a 5-minute mental arithmetic task (29). Participants in the Stress group prepared for their tasks alone. Participants in the Stress + Support group were greeted by the supportive confederate. After preparation, the two Stress groups began the TSST in front of an evaluative and harassing audience and were videotaped throughout. After the task, saliva and skin barrier recovery measures were collected over the next 2 hours. Participants were debriefed by the experimenter at the end of the session. All procedures were approved by The Ohio State University Biomedical Sciences Institutional Review Board.

Social Support Manipulation
The Stress + Support group received support from a same-gender confederate during the 10-minute preparation period. After the confederate entered the room, the experimenter stated: "He/she is going to time the 10-minute preparation period. In addition, he/she will be available if you need help with your speech." The confederate enthusiastically greeted the participant, stating: "I'm here to time the 10-minute preparation period. I'm also available if you need any help with your speech. I need to finish some stuff for a couple of minutes, but if you have any questions about the speech or need help, just let me know." The confederate sat quietly, appearing to read and write at a table for 5 minutes, constituting passive support used in previous studies of social support and cardiovascular reactivity (30). At the end of 5 minutes, or once support was solicited from the confederate, the confederate provided active support patterned after prior work (12,31), including verbal comments and questions followed by empathic comments consisting of emotional (e.g., "How do you feel?" or "It's okay to feel anxious about this,"), instrumental (e.g., "Would you like to rehearse your speech?"), informational (e.g., "It sometimes helps to take a deep breath before you start"), and validation support (e.g., "What you're feeling is quite normal") (32–34). At the end of the 10 minutes, the confederate enthusiastically wished the participant luck, provided additional encouragement, and left the room.

Psychological Measures
A background questionnaire collected a variety of demographic and health information including age, weight, height, medical comorbidity, and for female participants, self-reported menstrual phase (35). Health-related behaviors assessed included medication use, current weight and weight changes in the last two weeks, and physical activity (36). The state version of the Spielberger State-Trait Anxiety Inventory (37) and the Positive and Negative Affect Schedule (38) were administered after skin barrier disruption and immediately after the tasks to assess state anxiety and positive and negative affect. Simple change scores for anxiety and affect were computed by subtracting values after skin barrier disruption from values immediately after the tasks. Cognitive appraisals, including perceptions of threat and coping, were measured after the task instructions, and again after the preparation period (39). Perceived stress, control, and helplessness (40) experienced during reading or the speech and during mental arithmetic were assessed with single items after the task.

Physiological Measures
Cardiovascular Measures
Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were assessed with an automated monitor (Dinamap Critikon 1846SX/P, Tampa, Florida) every 2 minutes during two 10-minute measurement periods: immediately after the 40-minute rest period, and during the task. Values were averaged within each measurement period to increase reliability (41), and change scores were computed by subtracting baseline measures from measures during the task. Baseline values were not significantly correlated with change scores (r values ranged from –0.16–0.10); therefore, simple change scores were used in subsequent analyses (42).

Salivary Cortisol
Eight saliva samples were obtained: before and after skin disruption, and 10, 30, 45, 60, 75, and 90 minutes after the beginning of the task (Salivettes, Sarstedt 1534, Sarstedt Inc., Newton, North Carolina). The assays were performed in the GCRC laboratory, using chemiluminescent techniques (43). Raw cortisol values were used as they did not demonstrate significant skew. The last seven cortisol values were integrated into a single cortisol response measure by computing area under the curve with respect to increase (AUCI), which was used in subsequent analyses (44).

Skin Measurement and Skin Barrier Disruption
Baseline skin barrier function was measured by obtaining readings of transepidermal water loss (TEWL) using two electrolytic water meter probes (cyberDERM, Cortex DermaLab, Media, Pennsylvania). The probes were touched to skin on the palm side of the dominant forearm at four sites located 4 cm below the inside of the elbow for 1 to 2 minutes (45). TEWL indicates the skin's ability to prevent water loss from the interior layers. Increased TEWL reflects decreased barrier function, and decreasing TEWL post disruption indicates increasing barrier recovery.

Three sites (total area 2.54 x 5.08 cm) were then disrupted using a dermatological procedure known as "tape-stripping" (24). Cellophane tape (4101, Tesa, Inc., Charlotte, North Carolina), was applied repeatedly (6–51 times) to remove superficial layers of skin cells from the disrupted site. Stripping stopped when TEWL was elevated from the basal levels (5–7 g/m2h) to at least 20 g/m2h at the disrupted site, or a maximum of 51 strips (23). A smaller area, 2.54 x 2.54 cm, was left undisturbed for basal TEWL measurements. Skin measurements were repeated at 1 hour, 90 minutes, and 120 minutes after barrier disruption (or 35, 60, and 90 minutes after the tasks). The two disrupted sites that showed TEWL values closest to one another were averaged together, and skin barrier recovery was computed from TEWL averaged as a percentage of baseline based on a formula used in several studies (21,46).

Data Analysis
Throughout the data analyses, SPSS 13 (SPSS, 2004) was used for all descriptive statistics and general linear models. Effect sizes are reported as r values using standard formulas for converting t and F values to r values (47). General linear models included the following independent variables: Group, Gender, and the interaction between Group and Gender. Multilevel modeling (48) was used to model skin barrier recovery and physiological influences on skin barrier recovery (49). In multilevel models, a model of change is specified at the measurement level (level 1), and the parameters that are modeled include initial values (intercepts) and change over time (slopes). Based on visual inspection of the data and fit indices with different models of change, a model with linear and quadratic (U-shaped) slopes provided the best fit to the data. Skin barrier recovery was modeled with measurement occasions (level 1) nested within individuals (level 2), and time as the level 1 predictor of change over measurement occasions. Models were initially specified with intercepts, linear slopes, and quadratic slopes specified as random (varying between individuals, rather than fixed across individuals). Before the analyses, the intercept value was centered at skin barrier recovery 1 hour after disruption, which was preferred over centering skin barrier recovery at the baseline value (equal to 0 across all participants). The time variable was scaled such that 1 unit of time equaled 1 hour of real time. Across all the models, level 1-error variances were specified as homogeneous. Multigroup multilevel modeling, in which parameter estimates of intercepts and slopes are obtained for each group separately and simultaneously, was used to test the primary hypothesis of group differences in skin barrier recovery. This strategy allowed for statistical testing of group differences in intercepts and slopes using univariate and multivariate contrasts (48,50).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Group Comparisons
The groups did not significantly differ on any demographic, health behavior, or baseline physiological measures (Table 1). Group differences in baseline TEWL (F(2,82) = 4.06, p = .02, r = .22) indicated higher baseline TEWL in the Stress + Support group compared with the No Stress group (95% Confidence Interval (CI) = 0.51–2.89). Baseline TEWL did not significantly differ between the Stress and No Stress groups. The groups did not differ in conditions that might explain the differences in baseline TEWL and number of strips to criterion, including TEWL at the disrupted site after disruption (Table 1), and arm length, room temperature, room humidity, site temperature, and site humidity (data not shown).


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  		TABLE 1. Demographic and Baseline Physiology and Skin Barrier Measures by Group

 

Anxiety, Affect, and Cognitive Appraisals
As shown in Table 2, there were significant main effects of Group on change scores for anxiety, F(2, 77) = 4.74, p = .01, r = .24, and negative affect, F(2,76) = 3.67, p = .03, r = .22. Planned comparisons showed larger increases in anxiety (95% CI = 1.16–11.39) and negative affect (95% CI = 0.30–6.56) in the Stress + Support group compared with the No Stress group. The Stress group did not significantly differ from the other two groups on anxiety and negative affect change scores. The Stress and Stress + Support groups did not differ on changes in anxiety and negative affect. Positive affect change scores did not differ between the three groups, F < 1.


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  		TABLE 2. Anxiety, Mood, and Cognitive Appraisals by Group

 

Change in expectations of threat and control did not differ between the three groups (Table 2). Additional measures of cognitive appraisals during task were administered after the tasks were completed. The Stress and Stress + Support groups reported more perceived stress (F(2,79) = 30.62, p < .001, r = .53), less perceived control (F(2,79) = 13.12, p < .001, r = .38), and greater perceived helplessness during the task compared with the No Stress group (F(2,79) = 24.30, p < .001, r = .49) (Table 2). In planned comparisons, the Stress and Stress + Support groups did not differ on any of these appraisals during the task. Analyses of additional items of cognitive appraisals during the mental arithmetic portion of the TSST showed that the Stress and Stress + Support group did not differ in perceived stress or perceived helplessness during mental arithmetic, F < 1. However, the Stress group reported more perceived control compared with the Stress + Support group during mental arithmetic, F(1, 56) = 4.14, p = .047, r = .26.

Cardiovascular Changes
As seen in Figure 1, there was a significant main effect of Group across all the cardiovascular indices (HR: F(2,72) = 14.67, r = .41; SBP: F(2,73) = 45.81, r = .62; DBP F(2,73) = 19.36, r = .46; MAP F(2,73) = 31.88, r = .55; all p < .001).1 In planned comparisons, the Stress and Stress + Support groups showed greater change compared with the No Stress group. (Stress – No Stress 95% CIs: HR, 7.6–16.7; SBP, 17.8–28.2; DBP, 5.33–10.9; MAP, 10.2–18.01; for Stress + Support – No Stress: HR, 3.7–13.1; SBP, 14.6–25.2; DBP, 3.9–9.5; MAP, 9.0–17.0). Cardiovascular responses did not significantly differ between the Stress group and the Stress + Support group. Across all the analyses, there were no significant main effects of Gender, or Gender x Group interactions.


Figure 115
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  		Figure 1. Mean (±SEM) cardiovascular change as a function of group status.

 

Cortisol Changes
Data screening identified three outliers with AUCI values greater than 3 standard deviation (SD) above the mean, which were removed from these analyses, resulting in No Stress n = 24, Stress n = 28, and Stress + Support n = 22. There were significant main effects of Group, F(2,68) = 10.88, p < .001, r = .37, and Gender, F(1,68) = 10.08, p = .002, r = .36, on cortisol levels (Figure 2). The Group x Gender interaction was significant, F(2,68) = 4.50, p = .02, r = .25. For the Group main effect, planned comparisons indicated that the Stress group showed greater cortisol change compared with the No Stress group (Stress – No Stress 95% CI = 3.62–10.38). The Stress + Support group showed greater cortisol change compared with the No Stress group (Stress + Support – No Stress 95% CI = 3.56–10.88). Cortisol responses did not significantly differ between the Stress and Stress + Support groups. The main effect of Gender indicated that males had larger cortisol responses compared with females (male – female 95% CI = 1.70–7.46). Follow-up main effects tests of the Group x Gender interaction showed that the effects of Group were significant for male participants, F(2,68) = 13.15, p < .001, r = .40, but not female participants, F < 1. In the male participants, the Stress and Stress + Support groups were significantly different from the No Stress group (Stress – No Stress 95% CI = 5.35–16.05; Stress + Support – No Stress 95% CI = 6.22–18.75) but not different from each other.


Figure 215
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  		Figure 2. Mean (±SEM) cortisol change assessed by area under the curve with respect to increase (AUCI), group, and gender.

 

Skin Barrier Recovery
The first step in modeling skin barrier recovery was examining the level 1-parameter estimates for each group in an initial model. There were no significant slope variances, therefore, in the final model linear and quadratic slope parameters were specified as fixed. Intercepts continued to be specified as a random parameter. The fixed parameter estimates in the initial model (intercepts and slopes specified as random) and the final model (intercepts specified as random and slopes specified as fixed) were very similar and did not change the interpretation of the results. Thus, data from the initial model are not shown, and data from the final model are shown in Table 3. Multivariate and univariate contrasts comparing parameters between the three groups indicated that parameter estimates in the No Stress group significantly differed from the Stress and Stress + Support groups combined (p = .007) (Table 3), and from the Stress and Stress + Support groups separately (p = .03). The Stress and Stress + Support groups did not significantly differ on intercepts or slopes. As shown in Figure 3, the No Stress group showed significantly steeper linear slopes (i.e., faster healing) compared with the Stress and Stress + Support groups combined (r = .29), and compared with the Stress and Stress + Support group separately (Table 3). By 2 hours after disruption, the No Stress group on average showed 47% recovery, whereas the two Stress groups showed 37% recovery. There were no group differences in changes in intercepts or slopes for TEWL at the undisturbed control site (data not shown). Thus, the effect of stress on skin barrier recovery was not due to general changes in TEWL in undisturbed skin.


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  		TABLE 3. Final Multigroup Multilevel Modeling Parameter Estimates for Percent Skin Barrier Recovery With Slope Variances Fixed

 

Figure 315
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  		Figure 3. Predicted percent skin barrier recovery over the course of the session, by group.

 

Physiology and Wound Healing
Rather than conducting separate multilevel models for each group and comparing parameters with univariate and multivariate contrasts, simple change in SBP, DBP, and HR, and cortisol AUCI were included as level-2 predictors of intercepts and slopes in one model. Only 66 participants had all cardiovascular and cortisol measures intact for the subsequent analyses. In these analyses, only SBP change was related to skin barrier recovery, predicting quadratic slopes (Table 4). As shown in Figure 4, larger increases in SBP during the tasks were significantly related to faster recovery (r = .26). No other physiological variables were significantly related to recovery. Including physiological variables accounted for an additional 3% of the variance in intercepts, 6% of the variance in linear change, and 12% of the variance in quadratic change.


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  		TABLE 4. Multilevel Modeling Parameter Estimates for Percent Skin Barrier Recovery, Including Cardiovascular and Cortisol Changes as Level-2 Predictors of Intercepts and Slopes

 

Figure 415
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  		Figure 4. Predicted percent skin barrier recovery during the session as a function of increasing systolic blood pressure changes.

 


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
This study provided further evidence that acute stress in the laboratory delays skin barrier recovery after disruption, replicating previous work by other laboratories which showed that public speaking or academic examination stress delayed skin barrier recovery by 10% to 15% after 3 hours (20,21). Moreover, this study extends prior work on the relationship between stress and skin barrier recovery by demonstrating effects in a between-subjects design, rather than a within-subjects design where participants serve as their own controls. Similar to other work, stress-related delays in skin barrier recovery could not be accounted for by group differences in basal skin barrier function at the undisturbed site.

In contrast to prior research on social support and physiological responses (10,12,51), support provided by a confederate in this study did not reduce physiological responses or speed skin barrier recovery after disruption. The social support manipulation did not significantly affect self-reported anxiety, positive and negative affect, and cognitive appraisals of the task. Thus, the support manipulation was not an effective manipulation in terms of subjective experience or physiology. The finding that the Stress + Support group reported less perceived control during the arithmetic task compared with the Stress group suggests that the support manipulation actually resulted in a more uncontrollable experience. Most studies of social support and cardiovascular reactivity that found positive results included supportive audiences during the stressor (10), rather than support before the stressor used in this study. Previous studies of social support and cortisol responses to stress used opposite-gender rather than same-gender confederates (12) or familiar sources of support (12,51). Whereas participants in the Stress + Support group were explicitly told by the experimenter that they were not being evaluated by the confederate, confederates did complete unrelated tasks (e.g., crosswords, other reading) during the passive support, and also completed a questionnaire to track their use of supportive statements during the active support. Thus, participants may have perceived the confederates' activities as evaluative. However, the fact that both the Stress and Stress + Support groups had similar cortisol responses also suggests that they experienced similar levels of perceived social-evaluative threat.

Although social support from a confederate did not speed wound healing in this study, this does not discount the role of social interactions in skin barrier recovery and wound healing more generally. For instance, mice or hamsters housed in pairs showed faster wound healing compared with being housed alone (52, 53). A recent study demonstrated that socially supportive interactions in married couples are related to faster wound healing relative to conflict interactions (54).

Similar to previous studies, this study showed low cortisol responses to stress among female participants (28). The blunted cortisol responses among women could not be explained by menstrual phase, as the groups did not systematically differ in distribution of menstrual phase, or self-reported affective and cognitive responses to the tasks, which were similar across men and women. A prior study showed that a stressor involving social rejection uniquely elevated cortisol responses in women compared with an achievement-oriented stressor (55). Thus, the task may have been perceived as more achievement-oriented rather than involving social rejection. However, the TSST is typically considered capable of eliciting social rejection (7).

Elevated cardiovascular and cortisol levels were not related to slower skin barrier recovery. Instead, greater SBP change was related to faster recovery, which may be due to changes in skin blood flow. Elevated SBP is generally related to increased cardiac output. Although the relationship between cardiac output and local skin blood flow is not clear, increased skin blood flow after removing occlusion corresponds with decreased TEWL and faster skin barrier recovery after disruption (56). However, the effect of increased SBP on skin barrier recovery was similar across groups, and the groups that showed an increase in SBP on average also demonstrated delayed skin barrier recovery. Therefore, other stress-related mechanisms may have larger effects on skin barrier recovery compared with skin blood flow alone.

Several studies in animals and humans suggest that elevated glucocorticoids mediate stress-related delays in skin barrier recovery (25,57). In mice, the effects of externally administered corticosterone, social disruption, and restraint stress on delaying skin barrier recovery can be blocked by the glucocorticoid receptor antagonist RU-486 (25). Topical administration of glucocorticoids also results in delayed skin barrier recovery, with similar effects observed in mice (26).

In contrast to prior work, this study found no association between cortisol responses and skin barrier recovery. Similarly, a previous study found a negative but nonsignificant relationship between cortisol levels during stress and subsequent skin barrier recovery (21). Evidence for glucocorticoid mediation of skin barrier recovery comes from studies involving prolonged stressors, such as 2 weeks of restraint stress (25,58) or general perceived stress (57); wounding after rather than before stressors; and among studies using exogenous administration of glucocorticoids, pharmacological dosages of high potency corticosteroids (e.g., dexamethasone, clobetasol) (26,59). Additional candidate mechanisms that explain stress-related delays in skin barrier recovery but have received less attention in the literature include stress-related activation of inflammatory processes in the skin and neuropeptide release from afferent nerves in the peripheral nervous system (20,60). A key issue for future research on mechanisms explaining stress-related delays in skin barrier recovery will be measuring the activity of glucocorticoids, neuropeptides, and other mediators in the epidermis.

The limitations of this study are worth noting as they provide areas of improvement for future research in studies of acute stress, social support, and skin barrier recovery. This study included greater numbers compared with previous stress and skin barrier recovery studies, particularly the number of participants undergoing acute stress, and had sufficient power to test large effect sizes. However, the study had low-to-moderate power to test small-to-moderate effect sizes, and generally the analyses comparing the Stress and Stress + Support groups were underpowered. The use of confederates rather than actual sources of social support from the participants' social network likely explained the lack of effects of the support manipulation on subjective ratings, physiology, and skin barrier recovery. In addition, this study did not examine individual differences in approach and avoidance orientations to others (e.g., attachment), which can influence physiological responses to stress (61) or the participants' broader context in terms of stressful life events or early-life experiences (62,63).

The clinical implications of stress-related delays in skin barrier recovery are important for populations for whom delayed skin barrier recovery may exacerbate existing disease. For example, stress-related delays in skin barrier recovery may play a role in the "Koebner phenomenon," in which psoriasis patients show lesions in uninvolved skin after skin trauma, including skin barrier disruption (64). Exposure to acute or chronic stress, by exacerbating delays in skin barrier recovery after skin trauma, may prolong inflammatory processes that result in psoriasis symptoms. One prospective study suggests that that stressful life events are related to increased severity of psoriatic symptoms (65). At the same time, several studies comparing prevalence of stressful life events in psoriasis patients compared with other noninflammatory skin disorder patients are equivocal (19,66,67). Among psoriasis patients receiving photochemotherapy treatment, individuals reporting high chronic worry took 1.8 times longer to clear psoriatic lesions compared with individuals reporting low chronic worry (68). Notably, several psychological intervention studies show that mindfulness meditation-based stress reduction (69) and cognitive-behavioral stress management (70) are efficacious adjunctive treatments for psoriasis, improving rates of skin clearing and reducing psoriatic symptoms compared with standard treatment alone.

In general, research in animals and humans suggests that long-term and chronic social conditions such as different lifetime histories of social contact (pair housing versus housed alone) or 48 hours of isolation (52,53) or caregiving (17) and enduring negative aspects of marriage (54) may have more profound effects on skin barrier recovery and wound healing compared with the short-term stressors that delay skin barrier recovery. Taken together, the beneficial effects of social support and the detrimental effects of social disruption and psychological stress on skin barrier recovery may be best observed by examining social interactions in established relationships, and/or prolonged social disruption, over periods of time longer than hours or days. Thus, a key future direction for this work will be incorporating real-life social interactions, relationships, and stressors in understanding stress, social relationships, and skin barrier recovery.

This study is based on a doctoral dissertation by the first author. I wish to thank Janice Kiecolt-Glaser and the Ohio State University Stress and Health Study for their support of this project, my undergraduate research assistants for their work, and my dissertation committee for their valuable input. Portions of this study were presented at the 2004 annual meeting of the American Psychosomatic Society in Vancouver, BC, Canada and the 2007 annual meeting of the Society for Investigative Dermatology in Los Angeles, CA.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
1The analyses for cardiovascular reactivity were conducted using simple change from baseline as the dependent variable. Controlling for initial baseline values in the cardiovascular measures did not alter the pattern of results (heart rate: F(2,71) = 14.29; systolic blood pressure: F(2,72) = 46.98; diastolic blood pressure F(2,72) = 19.36; mean arterial pressure: F(2,72) = 21.83, all p < .001) or differences between groups. Back

Received for publication December 6, 2006; revision received July 23, 2007.

This project was supported by a Graduate Research Award from the American Psychological Association (APA), Division 38; an Alumni Grant for Graduate Research and Scholarship from the Graduate School, The Ohio State University; an APA Dissertation Research Award; the Department of Psychology, The Ohio State University; and MO1-RR-0034 (Ohio State University General Clinical Research Center).

DOI:10.1097/PSY.0b013e318157b12e


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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