J Behav Med (2007) 30:187–197 DOI 10.1007/s10865-007-9097-4
Depression History, Stress, and Pain in Rheumatoid Arthritis Patients Alex J. Zautra Æ Brendt P. Parrish Æ Christina M. Van Puymbroeck Æ Howard Tennen Æ Mary C. Davis Æ John W. Reich Æ Mike Irwin
Accepted: February 13, 2007 / Published online: April 5, 2007 Springer Science+Business Media, LLC 2007
Abstract This study examined the role of past episodes of depression on pain reports for patients with rheumatoid arthritis (RA) before and during stress induction. A history of major depressive episodes was assessed by diagnostic interviews for 138 RA patients, 74 who later participated in a set of laboratory procedures designed to induce interpersonal stress. Patients were evaluated by a rheumatologist and then asked to report joint and bodily pain throughout the laboratory study. We found that RA patients with a history of two or more episodes of major depression had more pain at baseline, and exhibited higher pain in response to the stress induction than did RA patients with either only one episode or no history of depression. Such findings provide new insight in the dynamic relationships between depression, stress, and pain. Keywords Pain Stress Depression history Rheumatoid arthritis
A. J. Zautra (&) B. P. Parrish M. C. Davis J. W. Reich Department of Psychology, Arizona State University, P.O. Box 871104, Tempe, AZ 85287-1104, USA e-mail:
[email protected] C. M. Van Puymbroeck Estrella Mountain Community College, Avondale, AZ, USA H. Tennen University of Connecticut Health Center, Farmington, CT, USA M. Irwin University of California, Los Angeles, CA, USA
Introduction Depression has been associated with onset and course of a number of illnesses, (Steptoe 2006), and nowhere has this relationship received more support than in the study of chronic pain (Blackburn-Munro and Blackburn-Munro 2001; Romano and Turner 1985). Recent studies have also found considerable evidence that interpersonal stressors can increase vulnerability to episodes of pain and mood disturbance among patients with chronic conditions such as rheumatoid arthritis (RA); (Affleck et al. 1994; Stone et al. 1997; Zautra and Smith 2001). In this study we examine how clinical history of depression and stress separately and in combination influence perceptions of pain among RA patients. Many studies of depression and pain (Katz and Yelin 1993; Zautra and Smith 2001) have shown a strong and stable association between chronic pain and current depressive symptoms in RA as well as other chronic pain disorders (Brown 1990; Creed and Ash 1992; Dickens and Creed 2001). Few studies have relied on diagnostic interviews to reliably identify those patients with a history of depressive disorder (Fifield et al. 1998), an important step in distinguishing between patients simply reporting ongoing psychological distress and those with sufficient symptoms to warrant a diagnosis of a psychiatric illness such as major depression. Tennen et al. (2006) found evidence that a history of major depression lowered the capacity of RA patients to cope effectively with pain, leading to greater negative mood and lower positive mood. These affective disturbances could influence the severity of the pain episode itself, though that question was not addressed in their study. One of the most damaging characteristics of major depressive disorder is its tendency to recur and for its course to become chronic (Judd et al. 2000; Keller et al.
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1995). An individual who is experiencing a depressive episode has a 50–85% chance of having another episode at some time in the future (Angst 1988; Charney and Weissman 1988). Residual symptoms are common, occur in approximately one-third of all previously depressed patients and are associated with poor outcomes such as increased medical visits, rates of disability, suicide attempts, coronary events and stroke (Tranter et al. 2002). Symptoms also include social and personal maladjustment, dysfunctional attributions, anxiety and irritability (Fava et al. 2002) and greater interpersonal stress (Joiner 2000). Researchers have invoked two related metaphors to capture the dynamic themes that have emerged from analyses of patients with recurrent depression: Episodes as ‘‘kindling’’, and episode as ‘‘scar.’’ The kindling hypothesis suggests that episodes of depression increase the likelihood of future episodes by conferring greater sensitization to the stress of affective disturbance (Kendler et al. 2000). The scar hypothesis proposes that a depressive episode leaves lasting changes in personality and selfconcept that lead the person to be more vulnerable to affective disturbance in the future (Shahar and Davidson 2003; Tranter et al. 2002). We were particularly interested in comparing RA patients who experienced two or more lifetime depressive episodes with those who either reported one or no prior episodes. When compared to individuals with a single prior depressive episode, those with recurrent depression have manifested greater sleep disturbance (Jindal et al. 2002; Thase et al. 1995) and memory deficits (Basso and Bornstein 1999), lower levels of perceived social support (Wilhelm et al. 1999), and less response to placebos (Bialik et al. 1995). Individuals with two or more depressive episodes also have been shown to generate more stressful life events than their single-episode or never-depressed counterparts (Harkness et al. 1999). Together, these findings are consistent with the hypothesis that recurrent depression is associated with more biopsychosocial upset than those with similar single episode cases (Thase et al. 1995). In this study, we sought to determine if these differences extended to joint pain. Overview of the Study Most prior studies relating stress to pain have relied on observational methods to assess stress, leaving unresolved whether pain was the source of stress or whether stress was the source of pain. Interpersonal stress was induced in the present study to provide a more careful test of the combined influences of both depressive illness and stress on pain in RA patients. Three hypotheses were tested in this laboratory study: The first hypothesis was that a history of multiple episodes of depression would be related to greater pain among
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patients with RA. Second, RA patients with a history of multiple episodes of depression were expected to show greater perceived stress and lower positive affect during laboratory stress induction than those with only one episode or no history of depression. Lastly, RA patients with a history of multiple episodes of depression were expected to show higher levels of stress-reactive pain than those with only one episode or no history of depression.
Method Participants A total of 163 patients were screened into the study; 69.6% were women. Participants were recruited from the Phoenix, AZ region via solicitations at health fairs, Arthritis Foundation members, and local physician offices as well as the Veterans Administration (VA) Hospital. Written confirmation of RA from the participant’s rheumatologist was required. Excluded from the study were those RA patients taking cyclical estrogen replacement, and who had Lupus. The average duration of their RA was 11.5 years for the female participants and 13.6 for the males. The mean age was 51.7 for women and 60 for men. Seventy-seven percent of the women and 81% of the men were Caucasian. Both men and women had an average yearly family incomes falling in the $25,000 to $29,000 range. There were missing data on 25 participants reducing the n to 138 for analyses. Procedure After being screened into the study, participants returned an IRB approved informed consent form by mail along with documents authorizing the researchers to contact their rheumatologist to confirm their diagnosis of RA. Upon confirmation of their diagnosis, participants were sent, and returned by mail, an initial packet of questionnaires containing questions on demographic information. At this time, participants were administered the Structured Clinical Interview for DSM IV (First et al. 2002) through phone interview. A second packet of questionnaires containing two measures of pain used in this investigation and a selfreport measure of current depressive symptoms were then mailed to the participants. Following random assignment to lab assessment,1 half of these participants (n = 74) were asked to come to a 1 Participants in this study later participated in an intervention and were given post-tests involving a second laboratory assessment. Only half of the participants were randomly selected to receive a pre-lab to examine and control for the effects of pre-intervention exposure to the laboratory stressor on post-intervention responses.
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laboratory session at the cooperating VA hospital. To ensure the accuracy of the random assignment to the lab, ttests were conducted on the study variables showing no significant differences between those who attended lab and those who did not. Upon arrival, participants were given detailed instructions regarding the laboratory procedures, submitted a second informed consent, and one of three VA rheumatologists performed a joint examination. After a 10min resting period to establish baseline measures, stress was induced by two methods, a standard speech task (Davis et al. 2001) and a discussion of an interpersonal conflict used in our prior research to induce stress (Davis 1999; Davis et al. 1999). A 20-min recovery period followed the stress inductions. Self-report measures of joint and bodily pain, positive affect, and perceived stress were taken after baseline, after each stress induction and after recovery: four assessments in all. First Stress Induction Each participant was informed that for the next 10 min they would need to prepare a 5-min speech describing their best and worst personal qualities (Davis et al. 2001). The participant was told that there would be two research assistants present to evaluate the speech for content, clarity and style. To enhance the stressfulness of this experience, the participant was also informed that the speech would be tape recorded for evaluation by a team of psychologists. If the participant stopped before the 5 min were up, he/she was asked to continue. If the participant was unable to continue speaking, the research assistants evaluating them remained in the room without speaking for the full 5 min. Second Stress Induction Participants were first asked to think about a recent conflict with someone close to them (Davis 1999; Davis et al. 2001). They were cued to recall the event and visualize it with as much detail as possible (such as where the conflict took place, the things they could see, hear, and smell, etc.). Next, they were asked to think about the person involved, how the person entered the scene, as well as specifics about how he/she looked, acted and what was said. Then the participant was asked to reflect on his/ her own thoughts, actions, and bodily reactions such as heart rate, tears or muscle tension during this time. The participant was then asked to describe the event to the research assistant and describe his/her emotions, thoughts, how they coped, whether they spoke with another person about the event, if they would have done anything different, and if they had similar experiences with that person.
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Recovery Period Headphones were placed over the participant’s ears and relaxing music was played. The research assistant also suggested that they take a mental vacation such as go to their favorite place or any other place they find peaceful and relaxing and to allow their body and mind to rest. After the experiment was over, the participant was debriefed on their experience, thanked and given $90 for their participation. Assessment Instruments Structured Clinical Interview for DSM IV (SCID) Depression history was measured by the mood disorders modules of the Structured Clinical Interview for DSM IV (SCID-I) (First et al. 2002). Interviews were conducted by advanced clinical psychology graduate or post-doctoral students who were trained in the administration and coding of the SCID-I under the supervision of a clinical psychologist (HT). Interviewers initially completed 11 h of SCID-I training tapes followed by reliability assessment of 10 additional SCID interviews. In the 10 interviews, interviewers obtained 100% agreement for diagnosis decisions as compared to those made by their clinical supervisor and another master’s level SCID evaluator. Furthermore, the supervisor and interviewers held biweekly meetings during data collection to discuss interview protocol. Interviews were conducted over the phone and audio taped with participants’ knowledge and consent. Telephone interviews have been shown to be equivalent with face-to-face interviews for the measurement of Axis I depressive disorders (Rohde et al. 1997; Simon et al. 1993). To qualify for a diagnosis of history of major depression, a participant needed to endorse a time in which he or she experienced depressed mood or loss of interest every day or nearly every day for at least 2 weeks and that these changes in mood/interest significantly impaired his or her functioning at that time. During this period, the individual also needed to experience at least four of the following symptoms (or three if s/he endorsed both depressed mood and loss of interest): Changes in appetite or weight; sleep disturbance; fatigue or lack of energy; diminished self-worth; motor agitation or slowing; and suicidal thoughts. The depressive episode could not be due to normal bereavement, injury, illness, alcohol/drugs, or medication. In necessary cases, SCID evaluators sought consultation from an advising consulting liaison psychiatrist who assisted in determining whether prior depressive symptoms could have been due to medication and/or drug usage. In order to examine the effects of both a history of depression and recurrent depression, we decided to distinguish three groups: RA participants with no depression
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history, those with only one episode, and those with two or more episodes of depression. Initial analyses led to a focus on the contrast between those RA participants with two or more episodes of depression and the remaining sample with either no history or a single episode. Although date of first episode of major depression was sought, less than half of the participants could provide a reliable date; this precluded analyses of time since first episode. Depressive Symptoms Pro-rated raw scores from the Hamilton Depression Inventory (Reynolds and Kobak 1995) were used to assess levels of depression. Depression scores were computed according to standard instructions with a possible score range of 0–73 where a higher score is more depressed. Cronbach’s alpha on the 23-item scale yielded .90. WOMAC Pain and SF-36 Pain Initial pain scores were assessed for the full sample using the pain subscales from the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) (Bellamy et al. 1988) and the MOS 36-Item Short-Form Health Survey (SF-36) (Ware and Sherbourne 1992). The WOMAC pain scale items ranged from 1 (no pain) to 5 (extreme pain). Scores from the 5-item subscale were averaged and had a Cronbach’s alpha of .89. Cronbach’s alpha for the 2-item SF-36 pain subscale was .88. Bodily Pain Laboratory participants were shown a body diagram with areas marked out in zones covering the major quadrants of the body (Affleck et al. 1996) and instructed to rate their soft tissue pain in areas of their neck, shoulders, chest, upper and lower arms, upper and lower legs, back, and buttocks on a scale of zero-to-three where zero was ‘‘No pain’’ and a three meant ‘‘Severe pain’’. Sum scores were computed from the 15 items to create an overall score of their bodily pain. Reliability analyses revealed a Cronbach’s alpha of .89.
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were computed from the 20 joints listed. Cronbach’s alpha was .92. Physician Assessment A rheumatologist palpated 28 joints taken from the DAS28 arthritis measure (Prevoo et al. 1995) to evaluate both joint swelling and tenderness. To rate tenderness, they asked participants to rate their pain on a 0-to-3 scale where 0 meant ‘‘No pain’’ and 3 meant ‘‘Severe pain’’ for each joint. Swelling was assessed on a 0-to-3 scale where 0 meant ‘‘No swelling’’, and a 3 meant ‘‘Severe swelling’’. Sum scores were computed and yielded a Cronbach’s alpha of .94 for tenderness and .81 for swelling. Disease Severity was measured using a single 10 cm visual analogue scale (Felson et al. 1993) by the rheumatologist after the joint exam to provide an overall rating of the participant’s RA disease severity. A 0 rating meant ‘‘No arthritis activity’’ and a 10 would mean ‘‘Worst arthritis’’. Perceived Stress Prior to stress induction, after each stress procedure, and following recovery, each participant was asked to rate the level of stress he/she felt at the time using the following instruction: ‘‘What number between 0 and 100 best describes your average level of stress right now? A zero (0) would mean ‘‘No stress’’ and a one hundred (100) would mean, ‘‘Stress as bad as it can be.’’ This variable was used to assess level of perceived stress throughout the experimental session. Positive Affect (PA) PA was measured using the Positive and Negative Affect Schedule. (Watson et al. 1988) Participants where shown the list of 10 positive mood adjectives and asked to rate the extent to which they had experienced them on a 5-point scale from 1 ‘‘Very slightly or not at all’’ to 5 ‘‘Extremely’’. A final score for the scale was computed by computing means yielding a Cronbach’s alpha of .89. Analytic Strategy
Joint Pain Laboratory participants were shown another body diagram with 20 joints designated and asked to rate their joint pain on a scale of a 0-to-3 where 0 was ‘‘No pain’’ and a 3 meant ‘‘Severe pain’’. This list of joints was taken from the Rapid Assessment of Disease Activity in Rheumatoid Arthritis (RADAR) (Mason et al. 1992). The RADAR is recognized as a valid measure sensitive to disease activity with well-established validity (Fuchs 1995). Sum scores
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In this study there were four sets of analyses, and statistical methods were selected that were the most appropriate for each. To begin, One-way ANOVAs with Tukey HSD Post Hoc comparisons were used to examine whether individual differences in history of depression were associated with differences on variables that were possible sources of confounding. Variables that showed differences in mean level for those with versus without depression history were then retained as covariates in subsequent analyses. Second,
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to test differences in pain reports for the whole sample as a function of depression history, analyses of covariance were performed for the two pain outcomes. The third set of analyses involved tests of differences in several baseline measures of pain and joint tenderness for participants randomly selected for the laboratory portion of the study. For this set of analyses, multivariate analysis of covariance was employed to guard against alpha inflation with multiple dependent variables. The fourth set of analyses was conducted on reports of pain elevations during and after laboratory stress induction procedures. Multilevel modeling was used as the primary data-analytic tool to analyze these data. This method is particularly useful for the linear analysis of data that have a nested hierarchical structure with both between-subject and within-subject predictors, some of which are continuous variables. All multilevel analyses were conducted using the SAS PROC MIXED software (Littell 1996). In these analyses, we asked whether a history of recurrent episodes of major depression influenced stress-reactivity of the RA patients. A measure of perceived stress was taken three times following a baseline assessment: After the initial stress induction, after the second stress induction, and lastly, after the recovery period. A change score on perceived stress was created by subtracting baseline stress scores from all subsequent ratings of stress. In the fixed effects equations predicting pain levels following stress induction, baseline levels of stress was added in the prediction equation along with current depressive symptoms and age (which served as controls for confounding with depression history) along with measures of change in stress, depression history, and the interaction between recurrent depression history and changes in perceived stress. This equation allowed us to examine mixed effects of a between-person variable (depression history) with a within-person variable (change in perceived stress) to address the question: Do RA patients who have a history of recurrent depression show greater pain when faced with an interpersonal stressor. The basic equation that was initially specified was as follows for joint pain: Joint pain = b0 + b1covariants + b2 stress change þ b3 recurrent depression history þ b4baseline stress + b5 stress change recurrent depression history + r b0 yields an estimate of the intercept for joint pain, b1 is used here to stand in for one or more covariates added to the prediction equation (and multiple Betas); b2–b5 provide slope estimates of the effects of predictor variables. In this equation the slope (b2) designates the estimated relation-
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ship between pain and change in stress from baseline for each participant, b3 provides the slope coefficient for main effects due to recurrent depression history, b4 yields estimates of the effects of between-person differences in baseline stress levels, and b5 tests the interaction of change in stress with depression history as a means of examining evidence of differences in stress reactivity for RA patients differing in depression history. The remaining specifications for this model were selected following Singer (Singer 1998) to identify the best fitting model of the variances and covariances of the variables under study. The dependent variables were modeled as random variables, and the effect of changes in stress was modeled as a random effect. A first-order autoregressive variance-covariance matrix was chosen to model the within-subjects variance on the dependent variables. This autoregressive function assumes a linear relationship between adjacent scores and an exponential decay in that relationship, with increasing time between measures. To test for heterogeneity in variances across repeated measures (e.g., violations of sphericity), autoregressive models were also employed that did not assume homogeneity of variance across the repeated measures (arh models in SAS PROC MIXED, (Littell 1996)). These models provided a poorer fit for the data so were not retained. Results In Table 1, the means and standard deviations of the study variables are shown for three groups: Participants with no history of depression, those with one major depressive episode, and those with two or more episodes of major depression. In addition, the distributional properties of all predictor variables were examined; all were found to be within accepted range (skew < 2.00 kurtosis < 2.00). As this table shows, there were no differences between groups in education, physician ratings of disease severity, or disease duration. Although there were differences in income and gender distribution between those with no history of depression and those with two or more episodes, these demographic variables were unrelated to pain reports, and when included as covariates in subsequent analyses, proved inconsequential. Differences in age were related to SF-36 and WOMAC pain in the full sample but not for the more comprehensive laboratory pain measures. Table 1 also provides results of tests of Hypothesis 1 providing evidence that participants with multiple episodes of major depression also reported more pain than those with no history or one past episode. These tests were conducted first on two measures of pain collected from the whole sample (n = 138): Bodily pain from the SF-36 and the pain subscale from the WOMAC. Both SF-36 Pain and
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Table 1 Descriptive statistics for demographic and study variables Past episodes of depression
0 (n = 71) Mean(SD)
1 (n = 30) Mean(SD)
Age
58.08(12.5)a
2 + (n = 37) Mean(SD)
50.90(14.4)b a
50.38(12.1)b 83.8% Womenb
Gender
59.2% Women
Income
21% < 25 k
44% < 25 k
Mean 30–40 k
Mean 21–25 k
Mean 25–30 k
Education: Highest level
9.9% H.S.a
13.8% H.S.a
8.6% H.S.a
Completed
84.5% College
75.9% College
88.6% College
Depression Disease duration SF36 Pain
9.66(6.5)
a
12.53(12.2)
76.7% Women
ab
13.28(8.3) a
45.15(19.74)
9.26(8.5) a
a
32% < 25 k
ab
16.38(8.0)b
a
14.94(15.9)a
48.60(24.34)
55.56(22.0)b 13.47(3.96)b
WOMAC pain
11.03(3.76)
Laboratory measures Disease activity
(n = 47) 2.6(1.3)a
(n = 10) 3.4(1.4)a
(n = 17) 2.4(1.4)a
Baseline joint pain
5.1(5.9)a
5.2(3.3)a
12(9.9)b
4.2(5.0)
a
3.6(3.0)
a
11.4(9.2)b
7.2(9.7)
a
9.9(9.4)
ab
16.7(15.0)b
DAS28 Swelling
7.6(4.9)
a
9.9(6.9)
a
5.07(5.7)a
Average perceived stress
18.4(16.2)a
Baseline bodily pain DAS28 Tenderness
Average positive affect
2.9(0.7)
a
11.16(4.32)
a
ab
19.7(12.4)a 2.2(0.5)
b
32.4(18.3)b 2.2(0.6)b
Note: Different superscripts within a row represent significantly different groups in Tukey HSD Post Hoc comparisons at p < .05 for all variables except gender for which a v2 test was conducted. Scores with the same superscript do not differ by group, statistically
WOMAC pain were higher in the group with multiple episodes of depression than those with only one episode, or no history. Two covariates were also significant predictors of pain for the whole sample. Older participants reported more pain than younger participants (SF-36 Pain: (F(1,133) = 8.24, p < .01, Eta-squared = .06;WOMAC Pain: (F(1,133) = 12.52, p < .01, Eta-squared = .09), and those with higher scores on current depression also reported more pain (Sf-36 Pain: F(1,133) = 31.32, p < .01, Eta-squared = .18; WOMAC Pain: F(1,136) = 37.67; p < .01, Eta-squared = .221). Current depression accounted for the differences in pain on the SF-36 Pain but the WOMAC Pain, an arthritis specific pain measure, was significantly elevated for those participants with two or more episodes of depression (F(1,136) = 4.36, p < .05; Eta-squared = .03) even when covarying current depression. Next, we examined differences in pain between groups among the 74 participants randomly selected for lab stress procedures. Three additional pain measures were available for this sample taken during a baseline period at the lab; each measure demonstrated a similar pattern: Significantly higher pain reports for those with a history of multiple episodes of depression compared with the other two groups. To examine these relationships further, we conducted a multivariate analysis of covariance of pain data gathered in the laboratory. Current levels of disease
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severity as measured by physician’s global rating, age and estimates of depressive symptoms recorded prior to the lab session were included as covariates to control for these potential confounds in the prediction of pain. These analyses yielded significant differences between groups on measures of joint pain, F(1, 56) = 5.48, p < .05, Etasquared = .09, bodily pain, F(1, 56) = 7.64, p < .01, Eta-squared = .12, and physician’s ratings on the DAS28 measure of tenderness, F(1, 56) = 4.86, p < .05, Etasquared = .08. No effects were found for depression history on physician ratings of joint swelling. Neither disease severity nor current depression was related to the three pain measures. Follow-up contrast analyses revealed that those with no history of major depression were significantly different from those with two or more episodes for bodily pain (p < .01) and joint pain (p < .01), and DAS28 assessment of tenderness (p < .05). Those with one episode had significantly less pain than those with two or more depressive episodes for measures of joint pain (p < .01) and bodily pain (p < .01). Finally, there were no significant differences between those with no past history compared to those with one episode on all three measures of pain. Figure 1 below displays the findings for the lab and the whole sample. Table 1 also provides data on tests of Hypothesis 2. Perceived stress was significantly higher across the laboratory session for participants with a history of multiple
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18 0 Episodes
16
1 Episode 2+ Episodes
14 12 10 8 6 4 2 0 WOMAC Pain
Sf-36 Pain*
Full Sample
Joint Pain
Body Pain
DAS28 Tenderness
Lab Sample
Fig. 1 Means for outcome pain measures across groups. *Rescaled by 1/10 to fit graph
episodes of depression. Follow-up analyses showed that this difference was non-significant after covarying baseline levels of perceived stress (b = 3.59 t = .93, p > .35). Analyses reported in Table 1 also show differences in positive affect between groups during the laboratory session. In this case, PA deficits were observed for those with one as well as multiple episodes of depression. Even when controlling for baseline levels, positive affect remained lower across the laboratory session for those with any history of depression. To examine whether laboratory stress induction influenced pain differentially depending upon past history of depression, we conducted multilevel analyses of the laboratory stress data using SAS Proc Mixed. (Littell 1996) In a separate regression analysis, we confirmed that the laboratory procedures increased these stress reports. Significant linear (b = 56.03, t = 11.69, p < .01), and quadratic effects (b = –10.97, t = 11.67, p < .01 ) of the lab stress induction were found accounting for 20.8% of the total variance in perceived stress from baseline following the two stress induction procedures, with a decline to baseline levels after the recovery period.2 A stress response score was computed by subtracting baseline scores of perceived stress from each of the subsequent assessments. This score removes variance due to individual differences in perceived stress observed prior to stress induction procedures both at baseline and at subsequent assessments. This measure of stress response was then entered along with baseline stress levels, and history of depression in a mixed model regression equation predicting Joint Pain and Bodily Pain across the four laboratory periods. Depressive symptoms 2
Computation of variance explained performed according to guidelines described in Singer (1998).
and age were also entered to control for these potential confounds. In these analyses (see Tables 2 and 3), we focused on group contrasts between those with 0, 1, vs. 2 or more past episodes. Multiple episodes of major depression, current depressive symptoms, and baseline stress all had significant main effects on both joint pain and bodily pain. Elevations in stress also showed a significant interaction with history of depression in predicting both joint and bodily pain. Those with multiple episodes of major depression reported more Joint and Bodily Pain following the experimental inductions of stress than those with fewer episodes. After testing for contrasts between groups with different depression histories, we found significantly greater pain reports for those RA patients with two or more episodes of depression compared with those with either no history or one episode when stress was elevated through laboratory procedures. An ameliorative role of PA was found qualifying the interaction between depression history and perceived stress. Neither PA at baseline nor changes in PA during stress induction had main effects on pain reports. However, multi-level analyses of depression history (the between-person factor) and two within-person repeated measures factors (PA and perceived stress) revealed a three-way interaction of PA with perceived stress and history of depression predicting Joint Pain (b = –.09, t(206) = –2.12, p < .05), and Bodily Pain (b = –.07, t(208) = –2.21, p < .05). In each case, the presence of PA when stress was high reduced the association between multiple episodes of depression and pain. These results are shown in Tables 2 and 3. Figure 2 displays these relationships for joint pain. A similar picture emerged for bodily pain. Altogether, history of recurrent depression accounted for an additional 4% of the variance in stress related joint pain and an additional 7% of the variance in stress related bodily pain2. Other possible relationships were examined including interaction effects between current depressive symptoms and reports of stress predicting pain. None of these interactions approached significance. Current depressive symptoms were associated with higher pain as shown in Tables 2 and 3, but did not interact with lab stress or positive affect to influence these pain reports.
Discussion In this study, we found consistent evidence that a history of multiple episodes of depression increases risk for pain among RA patients. Two kinds of evidence were examined regarding the role of depression history and both provided support for link between past depression and current pain. First, we examined self-reports of pain as well as physician
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Table 2 Depression history, stress, and positive affect in the prediction of joint pain Covariance parameter estimates Intercept
b
SE
Z
59.42
11.19
P
Table 3 Depression history, stress, and positive affect in the prediction of bodily pain Covariance parameter estimates
b
Z
P
5.31
