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ORIGINAL ARTICLES |
From the Departments of Psychiatry (M.B.M., K.C.L., J.M.F., S.S.G.), Psychology (M.B.M.), and Dentistry (W.M.), University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Address correspondence and reprint requests to Susan S. Girdler, PhD, University of North Carolina at Chapel Hill, CB #7175, Medical Research Building A, Chapel Hill, NC 27599-7175. E-mail: susan_girdler{at}med.unc.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONNOTESREFERENCES |
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Methods: Fifty-one African Americans (24 men, 27 women) and 55 people from other ethnic groups (primarily Caucasian; 26 men, 29 women) were tested twice for pain sensitivity to tourniquet ischemia, thermal heat, and cold pressor tests, once following mental stress and once following rest control. Resting and stress-induced blood pressure (BP), plasma norepinephrine (NE), and cortisol were assessed.
Results: In response to all three pain tests, African Americans had lower pain tolerance relative to Caucasian/Others after both rest and stress. Only the non–African American group showed the expected inverse relationship between BP and pain sensitivity. African Americans had lower cortisol concentrations at rest and stress and showed blunted NE and systolic BP responses to stress. Only in Caucasians/Others was the relationship seen between higher stress-induced BP, cortisol, and NE levels and greater pain tolerance.
Conclusions: The results suggest that there are alterations in endogenous pain regulatory mechanisms involving BP, cortisol, and NE in African Americans. Such dysregulation may contribute to the greater rate of clinical pain symptoms they experience. It is hypothesized that greater chronic stress in African Americans may be a contributing factor to the alterations in pain regulation.
Key Words: African Americans • pain sensitivity • blood pressure • norepinephrine • cortisol
Abbreviations: ANOVA = analysis of variance; BP = blood pressure; NE = norepinephrine; SBP = systolic blood pressure; SIA = stress-induced analgesia; TSST = Trier Social Stress Test; LC = locus coeruleus.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONNOTESREFERENCES |
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Only a small handful of studies have examined biological mechanisms that may contribute to these ethnic differences in pain sensitivity. There is a well-documented relationship between higher blood pressure (BP) levels and reduced pain sensitivity in both hypertensive (11–13), and normotensive individuals (14–16). However, this relationship has been documented only in primarily Caucasian samples. Only two studies of which we are aware have examined relationships between BP and pain sensitivity in biethnic samples. Although one found that lower pain intensity and unpleasantness ratings on an individualized scale correlated with higher ambulatory systolic blood pressure (SBP; 17) and the other (9) also found an inverse relationship between thermal heat pain-intensity ratings and resting SBP levels in the laboratory, neither of these studies examined the BP–pain sensitivity relationship as a function of ethnicity. This may be important because African Americans differ in BP regulatory mechanisms (18–20), which may play a role in their greater prevalence rates for hypertension (21). Thus, examination of BP–pain regulatory mechanisms separately in African Americans may have implications for ethnic differences in clinical and experimental pain.
Related to potential ethnic differences in BP–pain sensitivity relationships, another endogenous pain regulatory factor that may differ by ethnicity involves stress-induced analgesia (SIA). Although SIA has been well documented in animals (22), fewer studies have investigated SIA in humans, particularly in response to psychological stress (16,23,24). To our knowledge, there have been no studies to date that have investigated the role of SIA in modulating pain perception in African Americans. The pain modality itself may also moderate ethnic differences in pain sensitivity because different experimental pain tests have been shown to activate different endogenous pain mechanisms. For example, sensitivity to tourniquet-induced ischemic pain involves endogenous opioid mechanisms (25–27), whereas sensitivity to cold pressor pain may be mediated by systemic vascular resistance and noradrenergic mechanisms (23). The vast majority of laboratory-based studies on ethnic differences in pain perception have employed only a single pain test, such as thermal heat pain (7–9), pressure pain (10), cold pressor pain (28), or ischemic pain (1), limiting comparisons across studies.
Only one study of which we are aware has examined ethnic differences in response to multiple pain modalities. Campbell et al. (6) found that, in response to heat, cold, and ischemic pain, African American men and women had similar thresholds to Caucasian men and women but significantly lower pain tolerance to all tests. Thus, the study by Campbell et al. (6) confirms the robustness of the earlier work documenting reduced pain tolerance but not pain threshold in African Americans. Consequently, the purpose of this study was to extend the work of Campbell et al. (6) by examining ethnic differences in endogenous pain regulatory mechanisms, including BP-related hypoalgesia and SIA, during heat pain, cold pain, and ischemic pain. Additionally, because increased concentrations of catecholamines, as well as cortisol, are associated with reduced pain sensitivity in both animals and humans (23,29,30), we examined the relationship of resting and stress-induced plasma norepinephrine (NE) and cortisol to pain tolerance separately in African Americans versus non–African Americans.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONNOTESREFERENCES |
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All subjects were medically healthy, with no more than mildly elevated BP (<160/90 mm Hg) as determined during an initial screening session. Only four subjects (two Caucasian/Others and two African Americans) had elevated BP, defined as SBP >135 mm Hg and/or DBP >85 mm Hg. Additionally, subjects were not taking any prescription medication, including oral contraceptives, and not taking any over-the-counter medication on a regular basis (e.g., nonsteroidal anti-inflammatory agents, antihistamines). All women reported regular menstrual cycles. Excluded from participating were subjects with chronic pain conditions (e.g., temporomandibular joint disorder, fibromyalgia, arthritis) and those exhibiting signs of depression or anxiety. Individuals with Hamilton scale (31) depression ratings greater than seven (indicating mild depression) or anxiety ratings greater than nine (indicating symptoms of anxiety) were excluded.
The protocol was approved by the institution’s institutional review board, and all subjects provided informed, written consent before participating. Subjects received $500 compensation.
Procedures
In order to minimize any influence that novelty of exposure to the laboratory and pain testing apparatuses would have on pain perception, during an initial screening session subjects were shown the laboratory and the pain-testing equipment, subjects had the procedures described to them, and then underwent a preliminary thermal pain threshold assessment. Women were tested at 1 of 3 points in their menstrual cycle (early follicular, n = 20; late follicular, n = 20; luteal n = 16) in randomized order, with phase of cycle subsequently confirmed using serum estradiol and progesterone concentrations.
To examine decreases in pain sensitivity following mental stress compared with pain testing following rest (i.e., SIA), pain testing occurred twice, once following a modified Trier Social Stress Test (TSST) and once following a time equivalent Rest Control Period. The order of Stress versus Rest was fully counterbalanced within gender and ethnic groups.
For all subjects, laboratory testing began between 12 PM and 2 PM. Immediately on arrival, all subjects were instrumented for cardiovascular monitoring. An intravenous line (IV) was then established in an arm vein, and once in place, a curtain was drawn to hide the IV and arm and to minimize awareness of blood sampling.
The sequence of laboratory events was as follows: (1) instrumentation for BP and other monitoring; (2) IV setup and recovery from venipuncture (10 minutes); (3) baseline (10 minutes quiet rest); (4) modified TSST (20 minutes); (5) recovery (10 minutes); (6) pain testing; (7) stress testing if event #4 was rest control or rest control if event #4 was stress testing (20 minutes); (8) recovery (10 minutes); and (9) pain testing. These events are described fully below.
Baseline
Immediately following the IV setup, 20 minutes of quiet rest followed. The first 10 minutes served as recovery from venipuncture, whereas the last 10 minutes constituted baseline. BPs were taken at minutes 1, 3, 5, 7, and 10 and averaged to yield mean baseline rest values. Blood was sampled at minute 10 for baseline NE and cortisol.
The TSST
A modified version of the TSST was employed (to include serial addition as opposed to serial subtraction). The TSST is a stress test that reliably induces large and consistent hypothalamic-pituitary-adrenocortical and cardiovascular responses (32–34). The TSST involved the following components: (1) pretask instructions (5 minutes), during which time subjects are introduced to the "selection committee" who would listen to their job talk. Subjects were also given the instructions for the mental arithmetic task; (2) speech preparation period (5 minutes), during which time subjects were left alone to prepare their talk; (3) job speech (5 minutes): immediately following the preparation period, the selection committee returned to the testing room and asked the subject to deliver his/her talk describing to the committee why he or she would be the perfect applicant for the position. If the subject finished before 5 minutes, the committee responded in a standardized way, with prepared questions to ensure that the subject spoke for the entire period. Talks were tape recorded, and subjects had the opportunity to earn up to $10 based on the committee’s ratings of their speech. BPs were taken at minutes 1, 3, and 5 of speech, and blood was sampled for plasma NE at the end of minute 2; and (4) paced auditory serial-addition task (PASAT; 35) (8.5 minutes): involves the tape-recorded presentation of numbers from 1 to 9. Subjects add each number presented on the tape to the immediately preceding number and to state the answer aloud. There are four series of numbers, with progressively shorter interdigit intervals. The experimenter remained in the room to monitor performance. Subjects had the opportunity to earn up to $10 based on total number of correct additions. BP was taken once each series, and blood was sampled for plasma NE at the end of minute two.
Stress Recovery (10 Minutes)
Subjects rested quietly alone. Blood was sampled at the end of this period in order to capture the delayed plasma cortisol response to the TSST (33,34).
Pain-Testing Procedures
Immediately after the recovery periods that followed both the TSST and the rest control period, subjects were exposed to the three different pain tests. One of three task orders (i.e., 1, tourniquet, thermal, cold; 2, thermal, cold, tourniquet; or 3, cold, tourniquet, thermal) was randomly assigned to each subject, ensuring that equal numbers of men and women and African Americans and Caucasian/Others received each of the three orders.
The Submaximal Effort Tourniquet Procedure
In this procedure, as described previously (36), a tourniquet cuff was positioned on the subject’s arm and the arm placed to the side. Before inflating the tourniquet cuff to 200 mm Hg (Hokanson E20 Rapid Cuff Inflator), the subject’s arm was raised for 30 seconds to promote venous drainage, and then the cuff was inflated, the experimenter’s stopwatch started, and the arm returned to the side. To promote forearm ischemia, subjects engaged in 20 handgrip exercises at 30% of their maximum force with an intersqueeze interval of 2 seconds. Subjects were instructed to indicate when the sensations in their arm first became painful (pain threshold) and when they were no longer willing or able to tolerate the pain (pain tolerance). A maximum time limit of 20 minutes was enforced, though subjects were not informed of this limit.
Hand Cold Pressor
The apparatus for the cold pressor consisted of a container filled with ice and water that was maintained at 4°C as recorded immediately before initiating the test. The use of a water circulator prevented the water from warming near the subject’s hand. At the onset of the test, subjects were instructed to submerge their hand to the marked line on their wrist and to remain still. Subjects were instructed to indicate to the experimenter when the sensations in their hand first became painful (pain threshold) and to also indicate when they were no longer willing or able to tolerate the pain by saying "stop" (pain tolerance). A maximum time limit of 5 minutes was imposed, though subjects were not informed of this limit.
Thermal Heat Pain Testing
Thermal heat pain threshold and tolerance were determined by an ascending method of limits using a 1-cm-diameter contact thermode with the capability for a rise time of 10°C/second. The thermode was controlled by a personal computer, and thermal probe applied to the left volar forearm. During the pain testing, an adapting temperature of 38°C was maintained for 10 seconds. Then, the temperature increased directly to 41.5°C and from that point on increased 0.5°C every 5 seconds until it reached 53°C or until the subject reached his/her tolerance. To determine thermal pain onset (threshold), subjects were instructed to press a mouse button (which terminated the stimulus) when the thermal percept first became painful. This was repeated three times and averaged to calculate thermal pain thresholds. Then, three series to determine average thermal pain tolerance were conducted by instructing the subject to press a mouse button when they were no long able to tolerate the pain.
Physiological Recording Procedures
The SunTech Exercise blood pressure monitor, Model 4240 (SunTech Medical Instruments, Inc., Raleigh, NC) provided the automated measurements of BP during baseline and stress testing. Before initiating the baseline period, five standard stethoscopic BPs were taken simultaneously with the automated pressures to ensure correct microphone placement and cuff position.
Hormone and Neuroendocrine Assays
Plasma cortisol was determined using radioimmunoassay (RIA) techniques (ICN Biomedical, Inc.). The sensitivity of the assay is 0.07 µg/dl and the specificity high, showing 0.05% to 2.2% cross-reactivity with most similar compounds. Plasma NE concentrations were determined using the high performance liquid chromatography (HPLC) technique. The lower limit of quantification with this system is 25 pg/ml, and the intra- and interday coefficients of variation are less than 10%.
Data Reduction and Analyses
Our first analytical strategy involved comparing groups for differences that existed in demographic and baseline measures. For each dependent measure, a 2 (Gender) x 2 (Ethnicity) analysis of variance (ANOVA) was employed. Next, we examined differences in pain sensitivity. Initial analyses confirmed expected gender differences in all three pain tests, with men having higher pain thresholds (F(1,101) = 9.12 to 12.61, p < .01) and pain tolerance (F(1,101) = 9.37 to 24.63, p < .01). Additionally, as expected, women had lower baseline and stress BP, NE, and cortisol concentrations than men (F(1,87) = 4.48 to 51.83, p < .05). There were no Gender x Ethnicity interactions for any dependent variable. Therefore, for analytical simplicity, gender was not considered further in the model as an independent variable. Thus, we examined differences in pain threshold and tolerance separately for each pain test, using a 2 (Ethnicity) x 2 (Time Point: Threshold/Tolerance) x 2 (Stress/Rest) repeated-measures ANOVA, with Threshold/Tolerance and Stress/Rest as repeated factors. Where significant interactions emerged, subsequent simple effects analyses were conducted in order to explore those effects.
We then examined ethnic differences and stress effects for neuroendocrine variables. A 2 (Ethnicity) x 2 or 3 (Condition: Baseline, Stress; 3 time points for BP and NE, 2 time points for cortisol) ANOVA was used. As before, subsequent simple effects analyses were employed to examine significant interactions.
In order to investigate relationships between physiological measures and pain sensitivity, a series of Pearson product moment correlational analyses were employed. To reduce type I error rates, we focused exclusively on differences between African Americans and Caucasian/Others, collapsing across gender, and focused exclusively on baseline and the speech stressor.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONNOTESREFERENCES |
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There were ethnic differences in education because African Americans were more likely than Caucasians/Others to have attended some college but not receive a degree (18/51 versus 10/55; 
2 (1) = 3.97, p < .05), and they were also less likely than Caucasians/Others to have done postgraduate work at a university (10/51 versus 22/55; 2 (1) = 5.22, p < .05). There were no ethnic differences between African Americans and Caucasians/Others in the proportion who did not complete high school (0/51 versus 1/55), or whose highest level of education was a high school degree (3/51 versus 1/55), trade school or business college (2/51 versus 0/55), or a 4-year college degree (18/51 versus 21/55).
Effects of Ethnicity on Pain Sensitivity
Ischemic Pain
Threshold and Tolerance
Ischemic pain threshold and tolerance values following the rest control period (top panel) and following mental stress (bottom panel) are depicted in Figure 1. Analyses revealed a significant Time Point x Ethnic interaction (F(1,99) = 13.23, p < .001). In order to explore this interaction, simple effects analyses were conducted separately for pain threshold and tolerance. These analyses revealed that following both stress and rest African Americans had lower pain tolerance than Caucasian/Others (F(1,102) = 2.62, p = .10), while no ethnic differences existed at threshold. There was no evidence for SIA during ischemic pain testing in either ethnic group.
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Cold Pain
Threshold and Tolerance
Similar to the ischemic pain task, a Time Point x Ethnic interaction also emerged (F(1,102) = 7.48, p < .01). African Americans were more sensitive to cold pain at tolerance (F(1,103) = 7.92, p < .01) but not at threshold (see Figure 2), and this was evident after both stress and rest. For neither ethnic group was there evidence of SIA during cold pain testing.
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Thermal Heat Pain
Threshold and Tolerance
Similar to the ischemic and cold pain tests, there was a trend for a Time Point x Ethnic interaction (F(1,102) = 3.44, p < .07). African Americans had lower heat pain tolerance (F(1,102) = 5.00, p < .05) but not threshold (see Figure 3). Again, stress versus rest did not influence these results. For neither ethnic group was there any evidence for SIA during thermal heat pain testing.
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Cardiovascular and Neuroendocrine Reactivity to Stress
BP
Both stressors significantly increased SBP (F(2,206) = 567.26, p < .0001) and DBP (F(2,206) = 590.17, p < .0001) in both ethnic groups relative to baseline levels. A significant Condition x Ethnic interaction was observed for SBP (F(2,206) = 4.56, p < .05). Although no significant differences existed between African Americans and Caucasians/Others in absolute levels of SBP at baseline (115 versus 113 mm Hg, respectively), speech stress (139 versus 142 mm Hg), or math stress (131 versus 134 mm Hg), subsequent ANOVAS comparing groups for reactivity (stress-baseline) revealed that this interaction resulted from African Americans having blunted SBP reactivity to the speech stressor (mean change = +24 mm Hg versus +28 mm Hg) relative to Caucasians/Others (F(1,105) = 5.54, p < .05). There were no significant ethnic differences involving DBP.
NE
Both stressors significantly increased plasma NE in both ethnic groups relative to baseline levels (F(2,178) = 56.77, p < .0001). A significant Condition x Ethnic interaction was also observed for NE (F(2,178) = 4.62, p < .05). Although no significant differences existed between African Americans and Caucasians/Others in absolute levels of NE at baseline (182 versus 175 pg/ml, respectively), speech stress (219 versus 243 pg/ml), or math stress (213 versus 220 pg/ml), subsequent ANOVAS comparing groups for reactivity (stress-baseline) revealed that this interaction reflected blunted responses to speech (mean change = +37 pg/ml versus +68 pg/ml) and math (mean change = +31 pg/ml versus +45 pg/ml; F(1,89) = 5.38, p < .05) in African Americans relative to Caucasians/Others.
Cortisol
Cortisol significantly increased in response to the stressors in both ethnic groups relative to baseline (F(1,102) = 13.75, p < .001). However, African Americans exhibited lower cortisol concentrations at both baseline (7.28 versus 9.44 pg/ml) and stress (8.43 versus 11.01pg/ml) relative to Caucasian/Others (F(1,102) = 10.07, p < .01), though there were no ethnic differences in cortisol reactivity (stress-baseline).
Relationship of Physiological Variables to Pain Sensitivity
BP
As summarized in Table 2, only Caucasian/Others showed the expected positive correlations between baseline SBP and pain tolerance (r = +0.30 to +0.50, p < 0.05) and stress SBP and pain tolerance (r = +0.32 to +0.49, p < 0.05), regardless of whether testing followed stress or rest. For African Americans, there was no evidence that baseline or stress SBP related to pain sensitivity (r = –0.14 to +0.11). Correlations relating SBP reactivity (speech stress-baseline) and pain tolerance values were also conducted post hoc. SBP reactivity was significantly correlated with pain tolerance in the thermal task only in the Caucasian/Others sample (r = +0.38, p < .01), but not in the African Americans (r = –0.14 and –0.23). For neither group were any robust relationships observed involving DBP levels or reactivity and pain sensitivity.
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For the significant correlations involving SBP and pain sensitivity (Table 2), group differences in the magnitude of correlation coefficients were examined using Fisher’s r to z transformation. These analyses revealed that the correlation coefficients relating baseline SBP to pain tolerance were significantly greater in Caucasians/Others than African Americans for both the tourniquet and cold pressor tasks following rest and stress (z = –3.4 to –1.8, p < 0.05) and tended to be higher for the thermal task following rest (z = –1.3, p < .10). The correlation coefficients relating speech stress SBP and pain tolerance were significantly greater in Caucasians/Others than African Americans for the tourniquet and thermal tasks following both rest and stress (z = –3.3 to –2.5, p < 0.01) and tended to be higher for the cold pressor following both rest and stress (z = –1.4 and –1.3, p < 0.10).
NE
There was little evidence that baseline NE correlated with pain sensitivity in either group, though African Americans showed unexpected negative and potentially spurious correlations involving baseline NE. Greater stress NE concentrations were related to higher pain tolerance to all three tests, but only in Caucasian/Others (r = +0.28 to +0.35, p < 0.05), whereas this relationship was absent in African Americans (r = –0.22 to –0.11). Additionally, NE reactivity to speech stress was positively correlated with pain tolerance to the cold pressor task following both rest and stress (r = +0.34 and +0.38, p < 0.05), as well as thermal heat pain tolerance following rest (r = +0.32, p < .05) in Caucasian/Others, but not in African Americans (r = –0.19 to +0.27).
Fisher’s r to z transformation analyses confirmed that for all three pain tasks, following rest and stress, Caucasians/Others had significantly greater correlation coefficients relating stress NE to pain tolerance (z = –2.3 to –1.8, p < 0.05). Correlation coefficients relating NE reactivity to pain tolerance to the cold pressor task and thermal task were significantly larger for Caucasians/Others than African Americans (z = –2.3 to –1.9, p < 0.05) following both rest and stress.
Cortisol
Similar to effects seen for NE, baseline cortisol was not correlated with any pain tolerance measure for either group (see Table 2). However, greater stress cortisol levels were positively correlated with greater pain tolerance to the cold and thermal pain tests, but again this relationship was seen only in Caucasian/Others (r = +0.30 to +0.38, p < 0.05). No relationship between stress cortisol and pain tolerance was observed in African Americans (r = –0.07 to +0.15). In Caucasians/Others there was a significant positive correlation between cortisol reactivity to stress and pain tolerance but only during thermal heat pain following rest and stress (r = +0.28 to +0.29, p < 0.05). For the African American group, there were no significant correlations between cortisol reactivity and pain tolerance (r = –0.04 to +0.10).
Although the correlations were significant in Caucasians/Others but not in African Americans, Fisher’s r to z transformations failed to reveal any significant differences between Caucasians/Others and African Americans in the magnitude of the correlation coefficients relating cortisol to pain tolerance.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONNOTESREFERENCES |
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For example, although numerous studies have reported an inverse relationship between SBP levels and pain sensitivity (11–16), this relationship was observed in the present study for the primarily Caucasian group only but not African Americans. To our knowledge, there are no studies to date that have examined the relationship between BP and pain sensitivity separately in African Americans. The relationship between increased BP and reduced pain sensitivity is thought to be mediated by BP-induced stimulation of mechanoreceptive afferents (i.e., baroreceptors) because stimulation of these visceral afferents in animal models has been shown to diminish somatomotor reflexes indicative of analgesic-like effects (11,37). It has been shown that African Americans have decreased baroresponses to transient BP elevation relative to Caucasians during sleep (38) and that they show abnormal BP responses to postural changes, indicative of alterations in baroreceptor function (39). Thus, diminished baroreceptor function in African Americans may contribute to the absence of a relationship between BP and pain sensitivity. As has been postulated for the absence of BP–pain sensitivity relationships in chronic smokers, which may come about via frequent BP surges associated with chronic smoking (23), we speculate that larger stress-induced BP responses to real-life stress in African Americans, especially if occurring in the context of frequent stress exposure resulting from racism, poverty, crime, and/or lower SES (40), may repeatedly activate baroreceptor mechanisms and, over the long term, contribute to a desensitization of the baroreceptor reflex pathway and an uncoupling of BP-baroreceptor mechanisms. Consequently, this might explain the apparent paradox that African Americans have a higher prevalence of hypertension (21) but at the same time they show increased sensitivity to experimental pain and more clinical pain.
An alternative, though not mutually exclusive, explanation for the absence of any BP-related hypoalgesia in African Americans stems from our previous research documenting that plasma NE concentrations mediate the relationship between SBP and ischemic, as well as cold, pain tolerance in a primarily Caucasian sample of men and women (23). Thus, the blunted NE stress response that we observed in the African Americans may be a contributing factor to the absence of any BP–pain sensitivity relationship in that group.
There was also a striking absence of expected relationships involving plasma NE and cortisol concentrations and pain sensitivity in the African Americans that was observed in the primarily Caucasian group and which has also been documented in other primarily Caucasian samples (23,30). Although the absence of these relationships remains unexplained at present, the blunted NE response to stress and lower cortisol concentrations at both rest and stress in the African American group may play a role. Diminished NE responses in African Americans may reflect decreased activation of locus coeruleus (LC) neurons in brain, the major site of CNS adrenergic neurons. The LC receives projections from visceral baroreceptor afferents via the nucleus of the solitary tract and is among several regions sending neuronal projections to spinal cord (41). Thus, the LC plays an important role in modulating sensory input. Consequently, in addition to any direct role that desensitization in baroreceptor function in African Americans may have in their hyperalgesia (38,39), diminished stimulation of LC neurons and diminished activation of noradrenergic inhibitory pathways may also act to increase pain sensitivity in African Americans. This combination could account for both increased pain sensitivity and the absence of BP–pain sensitivity relationships in the African Americans.
Although we observed that greater pain sensitivity in African Americans was true only for pain tolerance and not threshold, and this is consistent with other reports (6,8), the reasons for this finding are currently unknown. It has been suggested that differences in tolerance reflect the affective-motivational dimensions of pain (3,6,8,9,42), whereas differences in threshold reflect sensory-discriminative aspects (42). Thus, in addition to alterations in biological pain regulatory mechanisms, there may be ethnic differences in psychosocial factors that influence the affective motivational dimensions of the pain experience. It is well established that African Americans experience more psychosocial stress than Caucasians, including racism and bigotry (40), and experience more chronic stress, such as unemployment, poverty, lower social status, and substandard housing (40,43). Thus, we hypothesize that greater chronic stress in African Americans may differentially influence affective/motivational factors that impact the experience of pain. This supposition is supported by animal models showing that chronic stress produces long-term increases in pain sensitivity to noxious stimuli (44).
Although blunted SBP and NE reactivity to stress and lower cortisol levels seen in the African Americans in the present study may at first seem paradoxic because it has been shown that African Americans exhibit increased cardiovascular reactivity to laboratory stress (e.g., 40), other studies have found that greater cardiovascular and NE reactivity to stressors in African Americans may reside exclusively in African American men (20,45). Thus, the absence of greater stress reactivity in the present sample of African Americans may reflect our decision to combine the responses of men and women within ethnic groups. An alternative explanation stems from other studies documenting that individuals with higher levels of chronic stress exhibit lower levels of NE in response to acute stress (46), suggesting that chronic stress may diminish the ability of the individual to respond to new challenges (47). Therefore, the blunted SBP and NE reactivity to stress that we observed in the African Americans may be related to their higher prevalence of chronic stress, though this is a hypothesis that remains to be tested.
It is of interest that we found no evidence for SIA in any group. This cannot be explained by failure of the protocol to elicit a stress response because all subjects showed significant increases in BP, NE, and cortisol in response to the stressors. The failure to observe SIA in African Americans may be related to their blunted BP and NE stress response. However, it was surprising that we did not observe SIA in the Caucasian/Other sample, especially since they showed positive correlations between stress-induced SBP, NE, and cortisol and pain tolerance following stress. One possibility for our inability to detect any evidence for SIA may be related to the time course of events. Because pain testing occurred 10 minutes after the cessation of stressors, the possibility exists that recovery of cardiovascular and neuroendocrine levels prevented us from detecting SIA. Another potential explanation is that SIA may not be a particularly robust phenomenon in humans, at least under laboratory conditions. Indeed, whereas some laboratory studies in humans have documented SIA (16,24), others have found it in only subgroups of individuals (23), and at least 1 study found that participants were more sensitive to pain following stress testing (48). Thus, future parametric research on laboratory-induced SIA in humans is indicated.
In conclusion, the results of our study suggest that decreased tolerance to experimental pain in African Americans is due, in part, to alterations in endogenous pain-regulatory mechanisms. As such, our results may have implications for biological mechanisms contributing to the greater rates of clinical pain in African Americans. We must acknowledge certain limitations to our study, however. The generalizability of the results may be limited by the stringent exclusionary criteria and resulting homogeneity of the study sample. This is especially true regarding the exclusion of individuals with hypertension because hypertension rates are greater in African Americans (21). Thus, our findings for altered pain-regulatory mechanisms in African Americans may not generalize to a substantial subset of African Americans with hypertension. Our findings may also not generalize to African Americans with mood disturbance or chronic pain disorders, conditions for which alterations in pain sensitivity and endogenous pain-regulatory mechanisms have been documented in primarily Caucasian samples (49,50). Future studies designed to investigate ethnic differences in psychosocial factors and pain perception and whether alterations in biological pain regulatory mechanisms mediate the link between greater life stress and greater pain sensitivity in African Americans are needed to further our understanding of ethnic differences in the experience of pain.
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NOTES |
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This study was supported by NIH grants NIDA R01 DA13705 and GCRC RR00046. The authors are grateful to Dot Faulkner for her assistance with manuscript preparation.
DOI:10.1097/01.psy.0000188466.14546.68
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- and ß-adrenergic receptor agonists: effects of race in borderline hypertensive compared to normotensive men. Am J Hypertens 1993;6:630–5.[Medline]
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