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Volume 14, Issue 2, Pages 176-182 (February 2010)


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Effects of anger and anger regulation styles on pain in daily life of women with fibromyalgia: A diary study

Henriët van MiddendorpaCorresponding Author Informationemail address, Mark A. Lumleyb, Mirjam Moerbeekc, Johannes W.G. Jacobsd, Johannes W.J. Bijlsmad, Rinie Geenenad

Received 23 September 2008; received in revised form 6 February 2009; accepted 17 March 2009. published online 20 April 2009.

Abstract 

Background

Fibromyalgia is characterized by an amplified pain response to various physical stimuli. Through biological and behavioural mechanisms, patients with fibromyalgia may also show an increase of pain in response to emotions. Anger, and how it is regulated, may be particularly important in chronic pain.

Aim

To examine, among patients with fibromyalgia, whether anger during everyday life amplifies pain and whether general and situational anger inhibition and anger expression modulate the anger–pain link.

Methods

For 28 consecutive days, 333 women with fibromyalgia (mean age 47±12years) reported their transient anger and state anger inhibition (anger-in) and expression (anger-out) responses regarding a significant emotional event during the day as well as end-of-day pain. Trait anger inhibition and expression were assessed by questionnaire. Multilevel regression analyses were performed.

Results

State anger predicted higher end-of-day pain (p<.001) in half of the patients, but lower pain in one-quarter of patients. State anger inhibition was unrelated to pain. Trait anger inhibition was related to more pain (p=.02). The lowest pain level was observed among patients with high trait anger expression who actually expressed their anger in an anger-arousing situation (p=.02).

Conclusions

Our study suggests that anger and a general tendency to inhibit anger predicts heightened pain in the everyday life of female patients with fibromyalgia. Psychological intervention could focus on healthy anger expression to try to mitigate the symptoms of fibromyalgia.

Article Outline

Abstract

1. Introduction

2. Methods

2.1. Participants

2.2. Procedures

2.3. Measures

2.3.1. Trait anger regulation

2.3.2. Daily anger

2.3.3. State anger regulation

2.3.4. Pain

2.4. Statistical analyses

3. Results

3.1. Descriptive statistics

3.2. Multilevel structure

3.3. Impact of demographic characteristics and time on pain

3.4. Impact of daily anger on end-of-day pain

3.5. Impact of trait and state anger inhibition and expression on end-of-day pain

3.6. Post-hoc analyses on the role of anger frequency and neuroticism in explaining the associations found between anger-related variables and pain

4. Discussion

Acknowledgment

References

Copyright

1. Introduction 

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Fibromyalgia is characterized by an amplified pain response to various physical stimuli, including pressure and temperature (McDermid et al., 1996, Berglund et al., 2002). Through various biological and behavioural mechanisms (Greenwood et al., 2003), patients with fibromyalgia may also show an increase of pain in response to emotions (Keefe et al., 2001, Zautra et al., 2001, Turk and Okifuji, 2002, Staud et al., 2004, Geenen et al., 2009). Anger may be particularly harmful in chronic pain. Anger is more common in patients with chronic pain than in the general population (Van Middendorp et al., 2008) and it amplifies pain to a greater degree than, and independently from, anxiety and depression (Fernandez and Turk, 1995, Rainville et al., 2005, Burns, 2006).

The effects of emotions, however, are influenced by how they are regulated. Two anger regulation strategies have shown to affect physiological arousal and pain: anger inhibition (anger-in) and anger expression (anger-out) (Bruehl et al., 2006, Burns et al., 2008). Anger inhibition represents the suppression or non-expression of anger (Spielberger et al., 1995). Inhibited anger is rather common in patients with fibromyalgia (Sayar et al., 2004, Van Middendorp et al., 2008) and it has been associated with more intense pain than uninhibited anger (Quartana and Burns, 2007, Quartana et al., 2007). Mechanisms proposed to underlie this effect include physiological arousal due to effortful suppression, and the paradoxical increased accessibility of angry thoughts and feelings after suppression (Burns et al., 2008).

Anger expression refers to outwardly revealing the experience of anger (Spielberger et al., 1995). Patients with fibromyalgia tend to express anger as often as the general population (Sayar et al., 2004, Van Middendorp et al., 2008). Both enhanced (Sayar et al., 2004, Bruehl et al., 2006) and reduced (Burns et al., 2003, Burns et al., 2006) pain has been observed after anger expression. This inconsistency might be explained by a trait-by-state matching model (Engebretson et al., 1989). This model suggests that matching a general style to express anger with actual anger-expressive behaviour leads to a reduction of anger and its negative consequences such as pain, whereas not expressing anger in high trait anger-out individuals increases anger and pain (Burns et al., 2006). Because social constraints discourage anger expression, especially in women (Porter et al., 1999), frequent mismatches between an urge to express anger and actual expression are expected (Brosschot and Thayer, 1998).

Knowledge on the association of pain with anger and anger regulation is based solely on cross-sectional and experimental studies. The present study extends this knowledge by applying a daily diary design to examine the pain-modulating role of transient (state) anger experiences in everyday life of female patients with fibromyalgia, as well as the (combined) effects of trait and state anger regulation. It is hypothesized that inhibiting anger generally, or in specific anger-arousing situations, will amplify pain, and that a general tendency to express anger (high trait anger-out) will be related to less pain when anger is expressed (state anger-out; match) than when anger is not expressed (mismatch).

2. Methods 

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2.1. Participants 

Participants were adult women with a rheumatologist-classified diagnosis of fibromyalgia according to established classification criteria (Wolfe et al., 1990) who were recruited at three hospitals in Utrecht and Almere, The Netherlands. To enhance generalizability of the findings, and because comorbid psychological and medical problems and treatments are so common among patients with fibromyalgia, no patients were excluded from participation. Of 403 women who participated in our earlier questionnaire study (Van Middendorp et al., 2008), 83% (n=333) filled out at least 14 daily diaries during a period of 28 consecutive days and comprise the sample described here. Participants had a mean age of 47 (SD=12, range 18–85) years. Demographic and health-related characteristics of the participants can be found in Table 1. The 70 patients who did not complete at least 14 diaries did not differ significantly from the 333 participants in this sample with respect to mean age, marital status, duration of fibromyalgia symptoms, years since diagnosis, medication use, non-medical treatment, and medical or psychological comorbidity.

Table 1.

Demographic and health-related characteristics of female patients with fibromyalgia (n=333).

Characteristics
Demographic
Age (years) [mean (SD)]47.0 (12.1)
Marital status [n (%)]
Single37 (11)
With partner247 (74)
Divorced37 (11)
Widowed12 (4)
Educational level [n (%)]
Primary15 (5)
Secondary256 (77)
Tertiary62 (19)
Health-related
Fibromyalgia complaints (years) [mean (SD)]11.0 (8.8)
Fibromyalgia diagnosis (years) [mean (SD)]3.5 (4.5)
Work status [n (%)]
Employed full time43 (13)
Employed part time113 (34)
Disability pension93 (28)
Sick leave10 (3)
Comorbidity [n (%)]
Rheumatic condition (besides fibromyalgia; e.g., rheumatoid arthritis)46 (14)
Lung disease (e.g., asthma)34 (10)
Diabetes7 (2)
Cancer11 (3)
Cardiovascular condition (e.g., hypertension)17 (5)
Psychological or psychiatric problems (e.g., depression, post-traumatic stress symptoms)57 (17)
Other comorbidity (e.g., endocrine, dermatological, internal, medically unexplained syndromes)139 (42)

2.2. Procedures 

The diary study directly followed the completion of a questionnaire booklet on general emotional functioning, processing, and regulation. The booklet and four paper journals, each containing seven daily diaries, were mailed to participants, who completed the diaries around the same time each evening, starting on the Monday after completing the questionnaire booklet. The booklet was mailed back to the researchers before the start of the diary study, and the completed diaries were mailed back at the end of each week. To increase daily compliance, participants had to write down time-specific weather information, derived from a specified text page on television, at the time of reporting. In total, the 333 participants completed 8341 of the possible 9324 (333×28) diaries (89%). More than half (n=174, 52%) of participants completed all 28 diaries, 22% (n=73) missed less than 7days overall, 18% (n=59) missed one week, and 8% (n=27) missed between 7 and 14days. Missing more diary entries showed a small correlation with a younger age (r=−.14, p=.01) and a higher mean anger level (r=.12, p=.03), but was not associated with other demographic (e.g., marital status, educational status, work status) or health-related characteristics (e.g., disease duration, pain average, comorbidity, medication use).

2.3. Measures 

Trait anger regulation (anger-in and anger-out) was assessed in the baseline questionnaire booklet. Subsequently, a diary assessment with daily end-of-day reporting was applied to capture patient’s experiences in everyday life, reducing retrospection bias and maximizing ecological validity (Porter et al., 1999, Stone and Shiffman, 2002). The diary contained questions on emotions experienced during a significant emotional event of that day and on how these emotions were regulated, as well as on pain at the end of the day. Each sampling occasion took 3–5min to complete.

2.3.1. Trait anger regulation 

The tendency to generally inhibit or express anger was assessed by two scales of the Self-Expression and Control Scale (SECS) (Van Elderen et al., 1996), a validated Dutch questionnaire based on the State-Trait Anger Expression Inventory (Spielberger et al., 1995). Both the anger-in (e.g., “When angry or furious, I’m angrier than I appear to be”, α=.91) and anger-out (e.g., “When angry or furious, I say nasty things to others”, α=.86) scale were measured with 10 items ranging from 1 (almost never) to 4 (almost always).

2.3.2. Daily anger 

To focus participants on a specific situation, they were asked to think about a significant occurrence of that day and briefly write down some key words describing that event. The event could be negative or positive. They were then asked to rate how much they experienced “anger” and “irritability” during that specific event on a scale of 1 (very slightly or not at all) to 5 (extremely). These two items were selected from the hostility scale of the Positive and Negative Affect Schedule – Expanded Form (PANAS-X) (Watson and Clark, 1999). The highly correlated ratings on the two items were averaged into a state anger composite score (Cronbach’s α=.85).

2.3.3. State anger regulation 

To assess whether anger was inhibited or expressed, we asked individuals who rated either of the anger items as 3 or higher whether or not (yes or no) each of 4 anger regulation strategies derived from the SECS applied to them when thinking back at the event. The specific SECS items chosen had large correlations with the total anger-in or anger-out scales and had low correlations with the alternative scale, suggesting that these items adequately differentiate between the constructs. To assess state anger-in, the items were: “I was angrier than I appeared to be” and “I was much angrier than others could see”. For state anger-out, the items were: “I said nasty things” and “I showed my anger”. When at least one of the two anger regulation items was applicable, a score of 1 (present) was assigned, whereas when neither item was applicable, a score of 0 (absent) was assigned.

2.3.4. Pain 

Immediate pain was assessed on a 1 (no pain) to 5 (pain) scale by the item ‘How much pain do you experience at this moment?’.

2.4. Statistical analyses 

Data were screened for deviations from a normal distribution. Anger was positively skewed because most people did not experience anger on a daily basis. According to the assumptions of multilevel analysis, dependent variables do not need to be normally distributed, as long as the residuals (at each level of the data structure) are. When predicting pain from anger, the residuals were normally distributed, allowing us to leave anger ratings as a continuous variable in the analyses. Means and standard deviations of continuous variables and numbers and percentages of dichotomous variables were calculated by aggregating data across all days and patients.

By design, the data had a hierarchical structure. The 28 repeated assessments of pain, anger, and state anger regulation (level 1) were nested within the 333 patients at the between-subjects level (level 2). Multilevel regression analysis was performed because it accounts for within- and between-person variance. The program MLWin was used (Rasbash et al., 2002). Continuous predictor variables were centred on their grand mean (i.e., the overall mean was subtracted from all individual values). Dichotomous variables were not transformed. The intercept was allowed to vary randomly across patients, allowing the course of pain over time to differ between persons. Because the study contained 28 repeated measures, we included as many polynomial terms (i.e., linear, quadratic, cubic etc.) of ‘day since start of study’ (0–27) as significantly contributed to the model to represent unexplained differences between individuals (Snijders and Bosker, 1999). Nested models were compared by calculating the decrease in deviance (−2 log likelihood) of the model including new variables and examining the significance of the resulting value with a χ2-test. The significance of the effects of included variables was determined with the Wald test: Z=(estimate/SE of estimate), where Z refers to the standard normal distribution (Hox, 2002). An alpha level of .05 was used for all statistical tests.

To examine whether there was significant variation in pain fluctuations between persons (level 2), the ‘empty’ two-level model (without any predictor variables) was compared with an empty one-level model, which does not account for nesting of measurements within persons, also without any predictor variables. The empty two-level model provides insight into the proportion of the total variance in pain accounted for by individual differences (intra-class correlation) and by variance of repeated measures within persons.

In the second step, the impact of potential covariates on pain was examined. Age, marital status, and education level did not predict pain levels, and therefore were not controlled. Week day (Monday to Sunday) and week of study (week 1–4) significantly contributed to explaining the variance in pain and were entered as covariates in all subsequent analyses.

In the third step, the contribution of the experience of anger during the day on end-of-day pain was examined by adding anger to the equation. When the random slope of anger was found to be significant, this would indicate that the association between anger and pain differed between persons. To examine that further, post hoc analyses were performed in SPSS by calculating separate correlation coefficients for each person. Correlation coefficients above .10, .30, and .50 are considered to be small, moderate, and large, respectively (Cohen, 1992). Demographic and emotion variables that might be responsible for the individual differences in correlations were examined by performing independent samples t-tests (for continuous variables) or χ2-tests (in case of categorical data) comparing people with a negative correlation (r−.10) to people with a positive correlation (r.10).

In step four, whether anger management contributed to pain was examined by separately entering trait and state anger-in and anger-out to the equations with pain as the dependent variable.

Finally, the trait-by-state matching hypothesis of anger-out was examined by means of a multilevel hierarchical regression analysis. Pain was the dependent variable. The predictors included were anger, trait anger-out, state anger-out, and the interaction between trait anger-out and state anger-out. In case of a significant interaction effect, the regression equation was computed for low (−1 SD) and high (+1 SD) values on trait anger-out in combination with the occurrence of state anger-out (0 for no, 1 for yes), according to general procedures (Aiken and West, 1991). Although we only expected main effects of trait and state anger-in, we also examined the trait-by-state matching hypothesis for anger-in according to the same procedure.

3. Results 

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3.1. Descriptive statistics 

With aggregation of the data across the 333 patients and the 28days of the study, a moderate overall pain level was reported (mean=3.35, SD=0.68 on a scale from 1 to 5) and a relatively low level of anger (mean=1.62, SD=1.05 on a scale from 1 to 5). On average, on 6 of the 28days (SD=4.6, range=0–27) a moderate-to-high anger level (at least one anger item scored 3 or higher) was reported. The use of state anger-in was related to a lower use of state anger-out (r=−.23, p<.001). A higher number of days in which anger was inhibited was strongly related to a higher number of days in which anger was expressed (r=.58, p<.001).

Trait anger-in (mean=2.36, SD=0.70 on a scale of 1–4) and trait anger-out (mean=1.94, SD=0.55 on a scale of 1–4) were negatively related (r=−.29, p<.001). Trait anger-in was related to more use of state anger-in (r=.22, p<.001) and less use of state anger-out (r=−.16, p<.001). The opposite pattern was found for trait anger-out that was related to more use of state anger-out (r=.19, p<.001) and less use of state anger-in (r=−.13, p<.001).

Patients who generally tend to inhibit their anger (top third on trait anger-in; n=100) actually used both anger inhibition and expression in 33% (n=144) of anger days, only anger inhibition strategies in 47% (n=202), only anger-expressive strategies in 13% (n=57), and no anger inhibition or expression in 6% (n=27) of anger days. Those relatively high on trait anger-out (n=119) used both anger inhibition and expression in 38% (n=178) of anger days, only anger-expressive strategies in 25% (n=114), only anger inhibition strategies in 28% (n=130), and neither anger expression nor inhibition in 9% (n=41) of anger days.

3.2. Multilevel structure 

Of the total variance in pain across the 28days, 42% could be attributed to differences between patients and 58% to differences within patients between days, indicating the appropriateness of a multilevel analysis of between- and within-subjects variance.

3.3. Impact of demographic characteristics and time on pain 

Pain varied as a function of day of the week (p<.001); it was highest at the end of the week (Thursdays and Fridays) and lowest on Sundays. The average pain varied from 3.24 on Sundays to 3.40 on Fridays. Pain reports also varied as a function of weeks (p<.001), with a lower level in the first as compared to the other three weeks; the other three weeks did not significantly differ among each other (average pain week 1=3.27, week 2=3.40, week 3=3.37, week 4=3.36). Including the interactions between days and weeks did not significantly improve the model.

3.4. Impact of daily anger on end-of-day pain 

A higher level of anger in response to a specific event during the day predicted more severe pain at the end of that day (β=.09, p<.001). Significance of the random slope of the association between anger and pain (p<.001) indicated significant variability between persons in the association between anger and pain. Listing the individual correlations, which varied from −.48 to .70, showed that 52% (n=168) of patients showed at least a small positive correlation (r.10) between daily anger and end-of-day pain, with 33% of patients showing a small correlation (.10r<.30), 17% a moderate correlation (.30r<.50), and 3% a large correlation (r.50). Further, 28% (n=91) had a non-relevant association (−.10<r<.10) and 19% (n=63) had a negative correlation between anger during the day and end-of-day pain (15% small, 4% moderate, 0% large). Fig. 1 illustrates the level of pain as a function of the occurrence of moderate-to-high anger (at least one anger item scored 3 or higher) vs. none-to-low anger (both anger items scored below 3) during the day.


View full-size image.

Fig. 1. Average end-of-day pain (and standard error of the mean) as a function of experiencing moderate-to-high anger (at least one of the anger items scored 3 or higher) vs. none-to-low anger (both anger items scored below 3). Note: day 1, 8, 15, and 22 are Mondays.


We next explored which demographic and medical history variables predicted which patients would have positive rather than negative correlations between daily anger and pain. Post-hoc analyses showed that patients reporting high end-of-day pain when angry during the day (positive correlation) had a longer duration since diagnosed with fibromyalgia (3.8±5.2years vs. 2.5±2.6years, p=.02) and experienced a higher average level of anger during the study (1.7±0.5 vs. 1.5±0.4, p=.02) than patients showing low end-of-day pain when angry (negative correlation). No significant differences were found for age (p=.60), marital status (p=.46), or education level (p=.35) between patients showing a positive vs. a negative anger–pain association.

3.5. Impact of trait and state anger inhibition and expression on end-of-day pain 

Trait anger-in showed a positive relationship with end-of-day pain (β=.07, p=.02), whereas state anger-in was unrelated to end-of-day pain level (β=.02, p=.20).

For anger-out, the association of trait anger-out with less pain (β=−.07, p=.03) became non-significant (p=.19) after including the interaction between trait and state anger expression (p=.02), whereas the association of state anger-out with less pain (β=−.06, p=.02) remained significant (p=.03). The interaction is illustrated in Fig. 2. In case of a high tendency to express anger (high trait anger-out), actual anger expression (match) was associated with a lower pain level than not expressing anger (mismatch), whereas actual anger expression did not impact pain level in case of a low general tendency to express anger, i.e., low trait anger-out. As anticipated, no significant interaction was found between trait and state anger inhibition (p=.16).


View full-size image.

Fig. 2. Associations of state anger expression with end-of-day pain for different levels of trait anger expression.


3.6. Post-hoc analyses on the role of anger frequency and neuroticism in explaining the associations found between anger-related variables and pain 

When number of anger days (at least one anger item scored 3 or higher) and anger during the day were included simultaneously in the model, both variables predicted end-of-day pain (β=.10, p=.002 for anger frequency; β=.09, p<.001 for anger). Re-analyzing the data for 151 patients who reported anger on 6 or more days (above the median) showed that the significant associations between anger variables and pain remained. Somewhat larger regression coefficients were found for anger (β=.11, p<.001), trait anger-out (β=.13, p=.005), and trait anger-in (β=.13, p=.006) than in the total group and in patients with a low anger frequency (β=.06, p<.001, β=−.03, p=.61, and β=.006, p=.45, respectively). State anger inhibition remained a non-significant predictor of pain in both the low (p=.32) and high (p=.29) anger groups.

The effect of anger and anger inhibition on pain was not explained by conceptual overlap with neuroticism. Neuroticism, as assessed with the 25-item version of the Big Five Inventory (Denissen et al., 2008), did not significantly predict end-of-day pain (p=.33), nor did it impact the prediction of end-of-day pain by anger, trait anger-in, or the interaction between trait and state anger-out (after controlling for neuroticism, p-values remained <.001 for anger, .02 for trait anger-in, and .02 for the interaction).

4. Discussion 

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The present study extends knowledge on the pain-modulating effect of anger and its regulation in everyday life situations. In female patients with fibromyalgia, anger triggered by daily life experiences predicted more pain at the end of the day, the general tendency to inhibit anger predicted more pain in daily life, and a general tendency to express anger predicted pain relief when combined with the actual expression of anger in an everyday anger-arousing situation.

In half of the female patients, the experience of anger in response to a significant daily emotional event predicted more pain at the end of that day. This finding supports studies showing the pain-enhancing effects of anger in anger induction experiments and in individuals who generally experience high levels of anger (Fernandez and Turk, 1995, Rainville et al., 2005, Bruehl et al., 2006). It is also in agreement with findings from research on the prediction of daily pain from general negative affect in patients with chronic pain (Zautra et al., 2001, Staud et al., 2003). Our finding that neuroticism did not impact the associations between anger and pain supports the claim that the momentary experience of anger is not simply a proxy for negative affectivity in general. Although the anger–pain association showed large individual differences, five times as many patients had a positive compared to a negative moderate-to-high association between anger and subsequent pain levels. The positive anger–pain link was more pronounced among patients with a longer duration of fibromyalgia and those with higher average anger levels. Overall, our findings suggest that everyday anger can be related to pain fluctuations in the day-to-day life of a significant number of women with fibromyalgia.

Consistent with theories and research on the adverse effects of anger suppression (Burns et al., 2007, Quartana et al., 2007), a general tendency to inhibit anger was associated with more pain. The suggestion that general negative affectivity accounts mainly for the amplified pain perception in high trait anger inhibitors (Burns et al., 2008) was not confirmed in our study; trait anger inhibition remained associated with pain after controlling for neuroticism. Unexpectedly, no effect of the actual inhibition of daily anger on pain was observed. In experimental anger induction studies, individuals instructed to suppress their anger showed larger pain reactivity (Burns et al., 2008). More than spontaneous anger inhibition, specifically asking people to suppress their anger may paradoxically increase accessibility of angry thoughts and feelings, corresponding with the ironic process model of mental control (Burns et al., 2008). Potentially, the inclusion of only women in our study may have limited the size of the effects, since anger suppression may be more detrimental for male than for female patients with chronic pain (Burns et al., 1998). Overall, whether anger inhibition is an appropriate response or not will depend on situational characteristics, but it appears a rather consistent finding that having an anger inhibition tendency is a vulnerability factor for daily pain.

In agreement with the state-by-trait matching hypothesis of anger expression (Engebretson et al., 1989, Burns et al., 2006), less everyday pain was observed in women who showed both a general tendency to express anger and actual expressed anger in everyday life. Yet this finding does not necessarily generalize to male patients with chronic pain. Anger expression may be more detrimental for men than for women (Burns et al., 1996, Burns et al., 1998). Moreover, the relationship between anger expression and health consequences is likely not linear; both ruminating on anger (Bushman et al., 2005) and the mere expression of anger without cognitive processing (Bushman, 2002) have been suggested to be maladaptive. That anger expression predicted less pain suggests potential beneficial effects of therapeutic emotional expression as observed before in a variety of populations, including fibromyalgia (Smyth et al., 1999, Pennebaker et al., 2001, Gillis et al., 2006). Expressing one’s anger may protect against rumination, solve an emotionally troublesome situation, and decrease anger intensity, which may all lead to less pain.

Our study also provided insight into pain fluctuations of female patients with fibromyalgia. The pain levels were highest on Fridays and lowest on Sundays, which might reflect a gradually increasing pain during the work week. However, patients who worked did not show a more pronounced week rhythm than unemployed patients (data not shown). Potentially, relaxing activities and quality time during the weekends of both working and non-working women may reduce the pain.

This study is the first to examine both the general tendency to regulate anger (trait anger regulation) and its actual regulation in anger-arousing situations (state anger regulation) in a single study. Although it was found that individuals with a higher trait tendency to inhibit or express anger showed corresponding behaviour in the majority of anger days (80% for anger inhibition and 63% for anger expression), in about one third of these anger days, both anger inhibitory and expressive strategies were used. This implies that anger inhibition and expression cannot be regarded as opposite extremes of one dimension.

Consistent with studies on trait and state coping (Stone et al., 1998), the modest association between trait and state anger regulation indicates a rather limited validity of trait measures of anger regulation in predicting state anger regulation in daily life. In particular, anger expression showed only a small correlation between trait and state measures. This may support the contention that the urge to express anger could be prevented by its potential negative social consequences (Brosschot and Thayer, 1998, Porter et al., 1999), whereas anger inhibition is socially desirable, especially in women (Burns et al., 1998).

Strengths of our study include the large, representative sample of women with fibromyalgia and the use of a daily diary approach, which has a high ecological validity, minimizes recall bias, and extends previous cross-sectional and experimental research findings. A drawback of having participants think about a single positive or negative emotional event is that we were unable to examine specific anger-provoking experiences that might be most relevant to anger management. Some patients may have had a bias to select only events that did not elicit anger. The two items that were selected to measure state anger regulation may not reflect the whole scope of anger inhibition or expression. The use of different items may give a somewhat different picture. Although prospective research provides more insight into temporal relationships than cross-sectional research, only experimental research permits causality to be determined. Our results may reflect, for instance, that higher pain levels impact the actual or recalled anger and anger regulation strategies. Due to our choice to include a large number of participants, it was not feasible to use ecological momentary assessment methodologies with palmtop computers to obtain tight control over daily compliance with the study regimen; however, paper-and-pencil diary studies have yielded equivalent findings to electronic studies, suggesting their validity (Green et al., 2006).

Future research could provide more insight into who is at risk for the potential pain-amplifying effects of anger and its inhibition. Expanding to other populations (e.g., males, other chronic diseases) will provide knowledge on the generalizability of findings and assessing the regulation of other emotions (e.g., sadness or fear) will provide information on the specificity of anger effects. Specific mechanisms underlying the anger–pain association could be examined in an experimental anger induction study that includes potential mediators such as sympathetic nervous system functioning or reactivity of neural areas that are involved in both anger and pain (Eisenberger and Lieberman, 2004, Geenen et al., 2009). By including trait and state anger regulation in such studies, the proposed idea that anger regulation may prevent or exacerbate the pain-enhancing effects of anger could be substantiated.

Knowledge of the present study could be used in clinical encounters with female patients with fibromyalgia. Anger and its suppression are prevalent in this patient group (Sayar et al., 2004, Van Middendorp et al., 2008), which makes their potential impact on functioning relevant. Psychological education and interventions that focus on changing thoughts and behaviour of patients with fibromyalgia vary greatly on outcomes, with potentially better outcomes in patients with high levels of psychological distress (Van Koulil et al., 2007). The present findings suggest a therapeutic focus on anger and its regulation in patients with fibromyalgia who tend to inhibit anger. Specifically, we suggest a twofold strategy. First, one could attempt to reduce the frequency of experiencing anger in easily-angered patients by altering relationships, cognitions, and unresolved emotional conflict that lead them to encounter, elicit, or interpret anger-inducing situations. Second, patients high on trait anger inhibition could be taught to respond to anger in adaptive ways with healthy expression, including appropriate assertion or sharing of feelings with appropriate targets.

To conclude, the present study showed that anger and a general tendency to inhibit anger predict heightened pain in daily life for a large portion of female patients with fibromyalgia. Furthermore, anger expression in combination with actual anger-expressive behaviour, may prevent or reduce this pain amplification. In addition to focusing on preventing or attenuating anger in easily-aroused patients, psychological education and therapy could focus on healthy anger expression to mitigate the symptoms of fibromyalgia.

Acknowledgements 

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This study was financially supported by the Dutch Arthritis Association. We thank the rheumatologists and Leslie Beks of the University Medical Center Utrecht, the rheumatologists and secretaries of the Diakonessenhuis Utrecht, and the rheumatologists of the Flevo Ziekenhuis Almere for their help in recruitment of patients, and Mariëlle de Bruijn, Rianne Burger, Juliette Libier, Eveline Rijken, and Bob Scheerder for their help in data collection and data entrance.

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a Department of Clinical and Health Psychology, Faculty of Social and Behavioral Sciences, Utrecht University, P.O. Box 80.140, 3508 TC Utrecht, The Netherlands

b Department of Psychology, Wayne State University, Detroit, USA

c Department of Methodology and Statistics, Utrecht University, The Netherlands

d Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, The Netherlands

Corresponding Author InformationCorresponding author. Tel.: +31 30 253 3027; fax: +31 30 253 4718.

PII: S1090-3801(09)00073-1

doi:10.1016/j.ejpain.2009.03.007


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