1. Introduction

Stress pervades the daily lives of Americans and is a major contributor to unfavorable pain experiences.1,2,22,50,55,63,66 Yet despite the prevalence of stress, not all people experience pain in response to stressful situations.11,37 One potential factor that may differentially contribute to future pain outcomes in relation to stress is stress reactivity—the extent to which one responds to a stressor physiologically, cognitively, behaviorally, and/or emotionally.3,21,26,56,57 Physiological measures of stress reactivity predict a range of negative health-related, and notably, pain experiences including recurrent abdominal pain, reduced condition pain modulation, and greater likelihood of musculoskeletal pain and pain severity.3,13,14,19,37,46,56,64 However, prior research used laboratory-based assessments measured in response to an applied controlled stressor, which is time consuming and unfeasible in a clinical setting. One potential time-efficient and cost-efficient clinical alternative measure of stress reactivity is self-perceived stress reactivity (SPSR)—the personal appraisal of how and to what extent one cognitively and emotionally responds and reacts to stressors—which is associated with poor health and pain outcomes such as pain intensity and frequency among people with fibromyalgia and recurrent abdominal pain among children.14,34,35,58,61,72,74 Importantly, SPSR correlates with physiological stress reactivity while also being distinguishable from the exposure to stressful experiences themselves.14,17,25,31,33,39,43,57

Furthermore, addressing patient stress reactivity through mindfulness-based and cognitive behavioral therapy is recognized as a beneficial target for those with chronic pain, leading to a range of improved pain experiences.6,10,12,23,51 However, the utility of SPSR as a predictive risk factor for chronic pain development has yet to be explored.

In this study, we conduct secondary analyses of the Midlife in the United States (MIDUS) national survey to test our hypothesis that greater SPSR would be associated with increased odds for the development of chronic pain.52,53

2. Methods 2.1. Participants

Data were taken from MIDUS waves 2 (2004–2005) and 3 (2013–2014) (chronic pain and SPSR questions were added at wave 2).52,53 The MIDUS is an ongoing longitudinal study assessing sociodemographic, behavioral, and health data gathered through telephone surveys using random digit dialing and mailed questionnaires. Wave 2 contained 4963 participants; we selected only those who reported not having chronic pain at wave 2 and had data for all variables of interest at both waves, resulting in n = 1512. Participants' ages at wave 2 ranged from 30 to 83 years (M = 54.80 ± 11.30). The MIDUS assessed sex, racialized identity, education, and marital status using forced multiple choice items (Table 1).53 This analysis of open-source data was determined exempt by Texas A&M University's Institutional Review Board.

Table 1 - Participant demographics cross sectionally within wave 2 of the Midlife in the United States national survey for those without chronic pain. Participant demographics N (%) Sex  Female 806 (53.3)  Male 706 (46.7) Racialized identity  White 1423 (94.1)  Black 48 (3.2)  Native American/Alaska Native 5 (0.3)  Asian or Pacific Islander 7 (0.5)  Multiracial 11 (0.7)  Other 18 (1.2) Educational attainment  Professional degree 90 (6.0)  Master's degree 198 (13.1)  Some graduate school 63 (4.2)  Bachelor's degree 371 (24.5)  2-y degree 105 (6.9)  3+ y of college (no degree) 52 (3.4)  1–2 y of college (no degree) 230 (15.2)  High school graduate 344 (22.8)  High school equivalency credential (GED) 12 (0.8)  Some high school (no degree) 36 (2.4)  Junior high school 7 (0.5)  Some grade school or no school 4 (0.3) Marital status  Married 1120 (74.1)  Divorced 164 (10.8)  Widowed 86 (5.7)  Never married 123 (8.1)  Separated 19 (1.3)
2.2. Measures 2.2.1. Chronic pain

Chronic pain was assessed using the question “Do you have chronic pain, that is do you have pain that persists beyond the time of normal healing and has lasted from anywhere from a few months to many years?” Values were recoded from the MIDUS data sets so that odds ratios of >1 would reflect increased odds of developing chronic pain (ie, “yes” = 2, and “no” = 1).

2.2.2. Stress reactivity

Self-perceived stress reactivity was assessed using 3 items of its subscale of the Multidimensional Personality Questionnaire—Brief Form (MPQ-BF) included in the MIDUS.48 Items (eg, “I sometimes get myself into a state of tension and turmoil as I think of the day's events”) were scored on a scale of 1 (true of you) to 4 (false) but were reverse scored so that higher values represent greater endorsement of that domain (α = 0.722). Items were summed to create final SPSR scores.

2.2.3. Covariates

Self-rated physical health and mental health were separately reported (“In general, would you say your [physical health/mental or emotional health] is excellent, very good, good, fair, or poor?”) on a scale of 1 (excellent) to 5 (poor). Body mass index was calculated within the MIDUS by dividing the participants' self-reported weight (recorded in lbs., converted to kilograms) from their self-reported height (recorded in inches, converted to meters squared). Depression was assessed using the World Mental Health Organization's Composite International Diagnostic Interview Short Form (WHO CIDI-SF) and was calculated as the accumulated “yes” responses to 7 questions assessing both depressed affect (eg, “During 2 weeks in the past 12 months, when you felt sad, blue or depressed, did you lose interest in most things?”) and anhedonia (eg, “During 2 weeks in the past 12 months, when you lost interest in most things, did you have a lot more trouble concentrating than usual?”).32 Totals ranged from 0 to 7, with higher scores indicating greater depression. Anxiety was assessed using the WHO CIDI-SF, which measures the frequency of responses to 10 items (eg, “How often over the past 12 months you were restless because of your worry”) using a scale of 1 (most days) to 4 (never). Anxiety scores were calculated as the total number of “most days” responses.32Number of chronic conditions was operationalized as the number of chronic conditions (eg, asthma, stroke, ulcers) from a list of 30 that participants experienced in the past 12 months.

2.3. Analysis plan

A binary logistic regression was conducted to determine the predictive value of SPSR at wave 2 on the development of chronic pain at wave 3 using SPSS (version 25; IBM Corp, Armonk, NY). Demographics and covariates were included in the equation along with SPSR, modeled after prior research.7,15

3. Results

The absolute risk of participants developing chronic pain from wave 2 to wave 3 was 25.3%. Results of binary logistic analysis showed that higher SPSR at wave 2 was associated with increased odds of developing chronic pain at wave 3 controlling for all other variables, including anxiety and depression (odds ratio (OR) = 1.085, 95% confidence interval (CI) (1.021–1.153), P = 0.008; Table 2). The number of chronic conditions was the only other significant predictor (OR = 1.118, 95% CI (1.045–1.197; P = 0.001).

Table 2 - Binary logistic regression with self-perceived stress reactivity, demographics, and covariates predicting the odds for the development of chronic pain between waves 2 and 3 of the Midlife in the United States national survey. Odds ratios for the development of chronic pain Variables Mean (σ) Range OR 95% CI P BMI 27.232 (4.946) 15.60–48.84 0.999 0.974, 1.024 0.930 Depression 0.44 (1.484) 0–7 1.025 0.944, 1.114 0.555 Anxiety 0.07 (0.611) 0–8 0.896 0.732, 1.098 0.290 Physical health 2.11 (0.868) 1–5 1.123 0.947, 1.332 0.181 Mental health 1.97 (0.844) 1–5 1.025 0.858, 1.223 0.788 # Chronic conditions 1.73 (1.933) 0–30 1.118 1.045, 1.197 <0.001 Stress reactivity 5.2 (1.05) 3–12 1.085 1.021, 1.153 0.008

Includes participant variable descriptive statistics for participants who reported not having chronic pain at wave 2 and who also had complete data at wave 3.

95% CI, 95% confidence interval; BMI, body mass index; OR, odds ratio. Bold values indicate significant predictors of chronic pain.

4. Discussion

Stress is a common experience for people living in the United States and is a major contributor to unfavorable pain outcomes.1,22,50,55,63,66 Stress reactivity—one component of the stress experience—has been shown to predict future health outcomes (including pain).46,56,64 Physiological reactivity in response to laboratory-controlled stress predicts the presence, frequency, and severity of various types of pain among both healthy and chronic pain populations; however, administering these laboratory tests in a clinical setting has limited viability.29,46,71 Here, we show that SPSR may be a clinically relevant tool for identifying who may be at risk for developing chronic pain.

There are several possible explanations for why higher SPSR might contribute to pain outcomes. Maintaining a prolonged cognitive and emotional focus on stressors may sustain underlying physiological responses that over time accumulate into allostatic load.16,20,45,68 In turn, allostatic load and dysregulated immune response predict unfavorable pain outcomes.8,9,59,60 High SPSR may also motivate coping behaviors such as smoking and alcohol consumption, which can impact health over time.42,47,65,73 Poststressor rumination also affects sleep quality, a known risk factor for pain.18,27,72

Separately, self-perceptions are frequently associated with a range of health outcomes, particularly among older adults; negative self-perceptions of one's health and aging predict future mortality, physical functioning, and disability independent of objective health markers, such as the number of other chronic conditions.4,5,31,41,44,54 Self-perceptions (eg, of self-worth and pain sensitivity) have also been shown to predict pain outcomes, including pain disability and intensity.24,36,40,67 It is possible that self-perceptions reflect an interoceptive awareness of how one's body and mind react to various situations, tracking negative health processes and highlighting targets for intervention.

A notable limitation to the generalizability of the present results is the lack of racialized diversity in this large national sample. Racialized stressors that are associated with pain disparities are therefore underrepresented in this data set and may differentially influence stress reactivity.15,28,30,38,69,70 In addition, recent or general experiences of stress were not assessed and controlled for; it is possible that those higher in SPSR encounter more stressors in their lives, influencing and overwhelming their vigilance for and response to stress. However, previous research demonstrates that perceptions of personal stress responses predict future health outcomes independently from the stressor itself, although outcomes are most likely among those who report both high levels of stress and SPSR.31 A person's self-awareness of their stress response, regardless of the source of stress, may therefore differentiate levels of relative risk for future pain outcomes. Self-perceived stress reactivity was also assessed in the MIDUS using select items of its scale; using the full stress reactivity subscale of the MPQ-BF or the Perceived Stress Reactivity Scale may more accurately tap SPSR.48,58 The type of chronic pain that participants developed was not measured, nor was the date of onset of that pain between waves; SPSR may differentially contribute to various pain conditions and do so over varying time frames, limiting the precision of the pain measurement used. Finally, this study relied upon subjective report; future work may include physiological measures in conjunction with SPSR to further assess discriminative and predictive validity in relation to pain outcomes.

Clinical approaches to chronic pain, such as cognitive behavioral therapy and mindfulness-based stress reactivity, have recognized the importance of reducing stress reactivity to relieve pain and promote mental health.6,10,12,23,51 The current findings suggest that SPSR may also help contribute to preemptive risk assessment for chronic pain development. With increased need and use of virtual assessment and care, SPSR may be a time and cost-efficient tool for predicting pain outcomes in research and clinical contexts.49,62

Disclosures

The authors have no conflict of interest to declare.

References [1]. Abdallah CG, Geha P. Chronic pain and chronic stress: two sides of the same coin? Chronic Stress 2017;1:247054701770476. [2]. American Psychological Association. Stress in America 2021: pandemic impedes basic decision-making ability, 2021. Available at: https://www.apa.org/news/press/releases/2021/10/stress-pandemic-decision-making. Accessed January 15, 2022. [3]. Aslaksen PM, Flaten MA. The roles of physiological and subjective stress in the effectiveness of a placebo on experimentally induced pain. Psychosomatic Med 2008;70:811–8. [4]. Benyamini Y, Burns E. Views on aging: older adults' self-perceptions of age and of health. Eur J Ageing 2020;17:477–87. [5]. Blazer DG. How do you feel about? Health outcomes in late life and self-perceptions of health and well-being. Gerontologist 2008;48:415–22. [6]. Bogart RK, McDaniel RJ, Dunn WJ, Hunter C, Peterson AL, Wright EF. Efficacy of group cognitive behavior therapy for the treatment of masticatory myofascial pain. Mil Med 2007;172:169–74. [7]. Boring BL, Maffly-Kipp J, Mathur VA, Hicks JA. Meaning in life and pain: the differential effects of coherence, purpose, and mattering on pain severity, frequency, and the development of chronic pain. J Pain Res 2022;15:299–314. [8]. Borsook D, Maleki N, Becerra L, McEwen B. Understanding migraine through the lens of maladaptive stress responses: a model disease of allostatic load. Neuron 2012;73:219–34. [9]. Borsook D, Youssef AM, Simons L, Elman I, Eccleston C. When pain gets stuck: the evolution of pain chronification and treatment resistance. PAIN 2018;159:2421–36. [10]. Crofford LJ. Psychological aspects of chronic musculoskeletal pain. Best Pract Res Clin Rheumatol 2015;29:147–155. [11]. Davis MC, Zautra AJ, Smith BW. Chronic pain, stress, and the dynamics of affective differentiation. J Pers 2004;72:1133–60. [12]. Davis MC, Zautra AJ, Wolf LD, Tennen H, Yeung EW. Mindfulness and cognitive-behavioral interventions for chronic pain: differential effects on daily pain reactivity and stress reactivity. J Consult Clin Psychol 2015;83:24–35. [13]. Dorn LD, Campo JC, Thato S, Dahl RE, Lewin D, Chandra R, Di Lorenzo C. Psychological comorbidity and stress reactivity in children and adolescents with recurrent abdominal pain and anxiety disorders. J Am Acad Child Adolesc Psychiatry 2003;42:66–75. [14]. Dufton LM, Dunn MJ, Slosky LS, Compas BE. Self-reported and laboratory-based responses to stress in children with recurrent pain and anxiety. J Pediatr Psychol 2010;36:95–105. [15]. Edwards RR. The association of perceived discrimination with low back pain. J Behav Med 2008;31:379–89. [16]. Epel ES, Crosswell AD, Mayer SE, Prather AA, Slavich GM, Puterman E, Mendes WB. More than a feeling: a unified view of stress measurement for population science. Front Neuroendocrinol 2018;49:146–69. [17]. Evans BE, Greaves-Lord K, Euser AS, Tulen JHM, Franken IHA, Huizink AC. Determinants of physiological and perceived physiological stress reactivity in children and adolescents. PLoS One 2013;8:e61724. [18]. Finan PH, Goodin BR, Smith MT. The association of sleep and pain: an update and a path forward. J Pain 2013;14:1539–52. [19]. Geva N, Defrin R. Opposite effects of stress on pain modulation depend on the magnitude of individual stress response. J Pain 2018;19:360–71. [20]. Gianferante D, Thoma MV, Hanlin L, Chen X, Breines JG, Zoccola PM, Rohleder N. Post-stress rumination predicts HPA axis responses to repeated acute stress. Psychoneuroendocrinology 2014;49:244–52. [21]. Goldfarb EV, Seo D, Sinha R. Sex differences in neural stress responses and correlation with subjective stress and stress regulation. Neurobiol Stress 2019;11:100177. [22]. Greenwood-Van Meerveld B, Johnson AC. Mechanisms of stress-induced visceral pain. J Neurogastroenterol Motil 2018;24:7–18. [23]. Greeson J, Eisenlohr-Moul T. Mindfulness-based stress reduction for chronic pain. In: Baer RA, editor. Mindfulness-based treatment approaches: Clinician's Guide to Evidence Base and Applications. San Diego, CA: Elsevier Inc., 2014. p. 269–92. [24]. Guite JW, Logan DE, Sherry DD, Rose JB. Adolescent self-perception: associations with chronic musculoskeletal pain and functional disability. J Pain 2007;8:379–86. [25]. Hellhammer J, Schubert M. The physiological response to Trier Social Stress Test relates to subjective measures of stress during but not before or after the test. Psychoneuroendocrinology 2012;37:119–24. [26]. Henderson RK, Snyder HR, Gupta T, Banich MT. When does stress help or harm? The effects of stress controllability and subjective stress response on Stroop performance. Front Psychol 2012;3:1–15. [27]. Herrero Babiloni A, De Koninck BP, Beetz G, De Beaumont L, Martel MO, Lavigne GJ. Sleep and pain: recent insights, mechanisms, and future directions in the investigation of this relationship. J Neural Transm 2020;127:647–60. [28]. Himmelstein MS, Young DM, Sanchez DT, Jackson JS. Vigilance in the discrimination-stress model for Black Americans. Psychol Health 2015;30:253–67. [29]. Janssens KAM, Oldehinkel AJ, Verhulst FC, Hunfeld JAM, Ormel J, Rosmalen JGM. Symptom-specific associations between low cortisol responses and functional somatic symptoms: the TRAILS study. Psychoneuroendocrinology 2012;37:332–40. [30]. Jones SCT, Anderson RE, Gaskin-Wasson AL, Sawyer BA, Applewhite K, Metzger IW. From “crib to coffin”: navigating coping from racism-related stress throughout the lifespan of Black Americans. Am J Orthopsychiatry 2020;90:267–82. [31]. Keller A, Litzelman K, Wisk LE, Maddox T, Cheng ER, Creswell PD, Witt WP. Does the perception that stress affects health matter? The association with health and mortality. Health Psychol 2012;31:677–84. [32]. Kessler RC, Andrews G, Mroczek D, Ustun B, Wittchen H-U. The World health organization composite international diagnostic Interview short-form (CIDI-SF). Int J Methods Psychiatr Res 1998;7:171–85. [33]. Kühnel A, Kroemer NB, Elbau IG, Czisch M, Sämann PG, Walter M, Binder EB. Psychosocial stress reactivity habituates following acute physiological stress. Hum Brain Mapp 2020;41:4010–23. [34]. Lee YR. Fibromyalgia and childhood abuse: exploration of stress reactivity as a developmental mediator. Develop Rev 2010;30:294–307. [35]. Limm H, Angerer P, Heinmueller M, Marten-Mittag B, Nater UM, Guendel H. Self-perceived stress reactivity is an indicator of psychosocial impairment at the workplace. BMC Public Health 2010;10:14–8. [36]. Linton SJ, Shaw WS. Impact of psychological factors in the experience of pain. Phys Ther 2011;91:700–11. [37]. Martin JB, Pihl RO. Influence of alexithymic characteristics on physiological and subjective stress responses in normal individuals. Psychother Psychosom 1986;45:66–77. [38]. Mathur VA, Trost Z, Ezenwa MO, Sturgeon JA, Hood AM. Mechanisms of injustice: what we (do not) know about racialized disparities in pain. PAIN 2022;163:999–1005. [39]. McInnis PM, Braund TA, Chua ZK, Kozlowska K. Stress-system activation in children with chronic pain: a focus for clinical intervention. Clin Child Psychol Psychiatry 2020;25:78–97. [40]. Meiselles D, Aviram J, Suzan E, Pud D, Eisenberg E. Does self-perception of sensitivity to pain correlate with actual sensitivity to experimental pain? J Pain Res 2017;10:2657–63. [41]. Menec VH, Chipperfield JG, Perry RP. Self-perceptions of health: a prospective analysis of mortality, control, and health. J Gerontol B Psychol Sci Soc Sci 1999;54B:85–93. [42]. Mezuk B, Abdou CM, Hudson D, Kershaw KN, Rafferty JA, Jackson JS, Lee H. “White Box” epidemiology and the social neuroscience of health behaviors: the environmental affordances model. Soc Ment Health 2013;3:79–95. [43]. Morgan ES, Umberson K, Hertzog C. Construct validation of self-reported stress scales. Psychol Assess 2014;26:90–9. [44]. Moser C, Spagnoli J, Santos-Eggimann B. Self-perception of aging and vulnerability to adverse outcomes at the age of 65-70 years. J Gerontol B Psychol Sci Soc Sci 2011;66B:675–80. [45]. Ottaviani C, Thayer JF, Verkuil B, Lonigro A, Medea B, Couyoumdjian A, Brosschot JF. Physiological concomitants of perseverative cognition: a systematic review and meta-analysis. Psychol Bull 2016;142:231–59. [46]. Paananen M, O'Sullivan P, Straker L, Beales D, Coenen P, Karppinen J, Pennell C, Smith A. A low cortisol response to stress is associated with musculoskeletal pain combined with increased pain sensitivity in young adults: a longitudinal cohort study. Arthritis Res Ther 2015;17:355–11. [47]. Parkerson HA, Zvolensky MJ, Asmundson GJG. Understanding the relationship between smoking and pain. Expert Rev Neurotherapeutics 2013;13:1407–14. [48]. Patrick CJ, Curtin JJ, Tellegen A. Development and validation of a brief form of the multidimensional personality questionnaire. Psychol Assess 2002;14:150–63. [49]. Perez J, Niburski K, Stoopler M, Ingelmo P. Telehealth and chronic pain management from rapid adaptation to long-term implementation in pain medicine: a narrative review. Pain Rep 2021;6:e912–9. [50]. Puschmann AK, Drießlein D, Beck H, Arampatzis A, Catalá MM, Schiltenwolf M, Mayer F, Wippert PM. Stress and self-efficacy as long-term predictors for chronic low back pain: a prospective longitudinal study. J Pain Res 2020;13:613–21. [51]. Rosenzweig S, Greeson JM, Reibel DK, Green JS, Jasser SA, Beasley D. Mindfulness-based stress reduction for chronic pain conditions: variation in treatment outcomes and role of home meditation practice. J Psychosomatic Res 2010;68:29–36. [52]. Ryff C, Almeida D, Ayanian J, Binkley N, Carr DS, Coe C, Davidson R, Grzywacz J, Karlamangla A, Krueger R, Lachman M, Love G, Mailick M, Mroczek D, Radler B, Seeman T, Sloan R, Thomas D, Weinstein M, Williams D. Midlife in the United States (MIDUS 3), 2013-2014. Ann Arbor, MI: Inter-University Consortium for Political and Social Research, 2017. [53]. Ryff C, Almeida DM, Ayanian J, Carr DS, Cleary PD, Coe C, Davidson R, Krueger RF, Lachman ME, Marks NF, Mroczek DK, Seeman T, Seltzer MM, Singer BH, Sloan RP, Tun PA, Weinstein M, Williams D. Midlife in the United States (MIDUS 2), 2004-2006. Ann Arbor, MI: Inter-University Consortium for Political and Social Research, 2017. [54]. Sargent-Cox KA, Anstey KJ, Luszcz MA. The relationship between change in self-perceptions of aging and physical functioning in older adults. Psychol Aging 2012;27:750–60. [55]. Sawicki CM, Humeidan ML, Sheridan JF. Neuroimmune interactions in pain and stress: an interdisciplinary approach. Neuroscientist 2021;27:113–28. [56]. Schlotz W. Stress reactivity. In: Gellman MD, Turner JR, editors. Encyclopedia of behavioral medicine. New York, NY: Springer, 2013. p. 1891–4. [57]. Schlotz W, Hammerfald K, Ehlert U, Gaab J. Individual differences in the cortisol response to stress in young healthy men: testing the roles of perceived stress reactivity and threat appraisal using multiphase latent growth curve modeling. Biol Psychol 2011;87:257–64. [58]. Schlotz W, Yim IS, Zoccola PM, Jansen L, Schulz P. The Perceived Stress Reactivity Scale: measurement invariance, stability, and validity in three countries. Psychol Assess 2011;23:80–94. [59]. Sibille KT, McBeth J, Smith D, Wilkie R. Allostatic load and pain severity in older adults: results from the English Longitudinal Study of Ageing. Exp Gerontol 2017;88:51–8. [60]. Slade GD, Sanders AE, By K. Role of allostatic load in sociodemographic patterns of pain prevalence in the U.S. population. J Pain 2012;13:666–75. [61]. Suarez K, Mayer C, Ehlert U, Nater UM. Psychological stress and self-reported functional gastrointestinal disorders. J Nervous Ment Dis 2010;198:226–9. [62]. Tauben DJ, Langford DJ, Sturgeon JA, Rundell SD, Towle C, Bockman C, Nicholas M. Optimizing telehealth pain care after COVID-19. PAIN 2020;161:2437–45. [63]. Timmers I, Quaedflieg CWEM, Hsu C, Heathcote LC, Rovnaghi CR, Simons LE. The interaction between stress and chronic pain through the lens of threat learning. Neurosci Biobehav Rev 2019;107:641–55. [64]. Turner AI, Smyth N, Hall SJ, Torres SJ, Hussein M, Jayasinghe SU, Ball K, Clow AJ. Psychological stress reactivity and future health and disease outcomes: a systematic review of prospective evidence. Psychoneuroendocrinology 2020;114:104599. [65]. Umberson D, Liu H, Reczek C. Stress and health behaviour over the life course. Adv Life Course Res 2008;13:19–44. [66]. Vachon-Presseau E. Effects of stress on the corticolimbic system: implications for chronic pain. Prog Neuropsychopharmacol Biol Psychiatry 2018;87:216–23. [67]. Valeberg BT, Høvik LH, Gjeilo KH. Relationship between self-reported pain sensitivity and pain after total knee arthroplasty: a prospective study of 71 patients 8 weeks after a standardized fast-track program. J Pain Res 2016;9:625–9. [68]. Verkuil B, Brosschot JF, de Beurs DP, Thayer JF. Effects of explicit and implicit perseverative cognition on cardiac recovery after cognitive stress. Int J Psychophysiol 2009;74:220–8. [69]. Walsh KT, Boring BL, Nanavaty N, Guzman H, Mathur VA. Sociocultural context and pre-clinical pain facilitation: multiple dimensions of racialized discrimination experienced by Latinx Americans are associated with enhanced temporal summation of pain. J Pain 2022;23:1885–93. [70]. Ward C, Szabó Á, Schwartz SJ, Meca A. Acculturative stress and cultural identity styles as predictors of psychosocial functioning in Hispanic Americans. Int J Intercult Relat 2021;80:274–84. [71]. Wingenfeld K, Heim C, Schmidt I, Wagner D, Meinlschmidt G, Hellhammer DH. HPA axis reactivity and lymphocyte glucocorticoid sensitivity in fibromyalgia syndrome and chronic pelvic pain. Psychosomatic Med 2008;70:65–72. [72]. Zachariae R, Zachariae H, Blomqvist K, Davidsson S, Molin L, Mørk C, Sigurgeirsson B. Self-reported stress reactivity and psoriasis-related stress of Nordic psoriasis sufferers. J Eur Acad Dermatol Venereol 2004;18:27–36. [73]. Zale EL, Maisto SA, Ditre JW. Interrelations between pain and alcohol: an integrative review. Clin Psychol Rev 2015;37:57–71. [74]. Zautra AJ, Hamilton NA, Burke HM. Comparison of stress responses in women with two types of chronic pain: fibromyalgia and osteoarthritis. Cogn Ther Res 1999;23:209–30.