Pain Severity and Mental Health of Lifetime Trauma Exposed Young Adults: The Role of Emotion Dysregulation

Abstract

Traumatic events are clinically significant experiences for young adults, associated with an increased risk of adverse mental health outcomes and poorer well-being. Little work has explored the underlying relationships of mental health problems in the context of pain in this population. Therefore, the present study sought to examine the role of emotion dysregulation and its sub-facets in the relation between individual differences in the severity of pain experienced and traumatic stress and anxiety/depressive symptoms in a sample of trauma-exposed young adults (N = 566; 81.40% female, Mage = 21.37, SD = 2.84). Results revealed that individual differences in pain severity had a significant indirect effect on the indices of mental health of trauma-exposed young adults through emotion dysregulation. Findings are discussed in the context of developing specialized prevention and treatment programs targeting emotion regulation and its specific facets to improve the mental health of trauma-exposed young adults.

Keywords

trauma pain emotion dysregulation mental health young adults

Introduction

Traumatic events are clinically important experiences for young adults (Allen Mallett et al., 2019; Arnett, 2007; Breslau et al., 1991; Hawdon & Ryan, 2012). Severe weather events, sudden injury and life-threatening accidents, sudden loss, sexual assault, and natural disasters are common types of trauma experienced by young adults (Allen Mallett et al., 2019; Breslau et al., 1991; SAMHSA, 2023). Certain subpopulations may experience other specific types of trauma, including sexuality-based discrimination trauma and re-settlement trauma (Gušić et al., 2017; Huxley, 2013). The experience of trauma among young adults is clinically important because such trauma-exposed people are at an increased risk of personal, occupational, educational, and health-related problems (Ghafoori et al., 2014; Kim et al., 2019; Sienkiewicz et al., 2020). Additionally, among young adult matriculating college students, trauma experiences have been shown to confer worse substance use and mental health outcomes throughout college (Read et al., 2012), and the accumulation of such traumatic experiences has been shown to confer greater risk of PTSD into adulthood (Ogle et al., 2014). Therefore, understanding the mechanisms that may contribute to these greater risks of adverse mental health outcomes and PTSD among this population may provide researchers and clinicians with new avenues for clinical treatment.

Although research consistently links trauma to mental health concerns, some subpopulations may be at increased risk for adverse psychological experiences in the context of chronic pain (e.g., veterans and refugees; Baker et al., 2009; Siqveland et al., 2017). Trauma exposure and symptoms of PTSD have been identified as vulnerability factors for clinical pain problems (Siqveland et al., 2017). Theory-based models posit that PTSD symptoms and pain commonly co-occur and reinforce each other through a mutual maintenance model, such that PTSD symptoms increases the risk of more intense and disabling pain, and pain may also increase the risk of PTSD symptoms following trauma exposure (Liedl et al., 2010; Norman et al., 2008; Sharp & Harvey, 2001). More specifically, the mutual maintenance model claims that PTSD symptoms, such as re-experiencing and arousal, can contribute to the development and persistence of chronic pain, while chronic pain can, in turn, exacerbate PTSD symptoms through mechanisms such as attentional bias and heightened arousal (Sharp & Harvey, 2001). This mutual maintenance model has been demonstrated in young adult populations. For instance, the work by Clapp et al. (2008) demonstrated significant interactions between pain and PTSD symptom clusters, such as emotional numbing and hyperarousal, in young adults. Similarly, a study by Andreski et al. (1998) found strong associations between PTSD and medically unexplained pain in a young adult population. These studies highlight the importance of considering the bidirectional relationship between PTSD and chronic pain, especially in younger populations. Additionally, pain is one of the most reported health problems by patients experiencing PTSD (Asmundson & Katz, 2009; Gasperi et al., 2021; Moeller-Bertram et al., 2012), with the occurrence of pain being shown to increased traumatic symptom severity (Asmundson & Katz, 2009). Though the relationship between pain and PTSD symptoms is well documented and the occurrence of pain experienced by individuals with PTSD is commonly reported, there has been little exploration of mediators among trauma-exposed young adults in terms of pain experience and mental health problems (e.g., depression, anxious arousal, and PTSD symptom severity; Moeller-Bertram et al., 2012). This limitation is unfortunate, as mediators can help explicate the mechanisms within the population of trauma-exposed young adults with pain who may be at greater risk for more severe mental health symptoms and problems. While studies with adult chronic pain and PTSD populations have been explored (Powers et al., 2014), similar attention has not been seen for young adult populations.

In addition to examining the mutual maintenance of pain and PTSD symptoms, it is crucial to consider the long-term effects of chronic pain and traumatic stress on young adults. Chronic pain and PTSD can significantly impact the developmental trajectory of young adults, leading to long-term psychological, social, and functional impairments. Chronic pain and stress during formative years can disrupt crucial developmental milestones, leading to persistent mental health issues such as anxiety and depression. This disruption underscores the need for early, developmentally appropriate interventions to mitigate these long-term impacts (McEwen, 1998). The Generated Stress Model (Conway et al., 2012) suggests that individuals may perpetuate their symptoms by engaging in stressful or stress-inducing situations, thereby maintaining a cycle of chronic stress and symptom exacerbation. This model is particularly relevant for young adults, who are in a critical developmental stage and may be more vulnerable to the effects of chronic pain and PTSD. The generated stress model highlights the role of self-perpetuated stress in the ongoing experience of mental health issues. Individuals with a history of depression may be more likely to generate stress in their lives, contributing to the persistence of their depressive symptoms (Hammen, 1991). By incorporating a developmental perspective, our study highlights the importance of early intervention strategies aimed at breaking this cycle. Addressing the interplay between chronic pain and PTSD in young adults not only aids in symptom management but also supports healthier developmental outcomes, thereby reducing the long-term burden of these conditions.

One promising construct for better explicating the pain-mental health relationship is emotion dysregulation, defined as difficulties in employing a set of abilities wherein one experiences, monitors, evaluates, and modifies emotions to accomplish goals (Gratz & Roemer, 2004). According to one empirically supported model, emotion dysregulation involves dysfunction in the domains of emotional awareness and acceptance, access to a variety of effective strategies to regulate emotions, the ability to control impulsive behaviors, and behave in accordance with one’s desired goals, despite experiencing adverse emotions (Atherton et al., 2015; Gratz & Roemer, 2004). The model suggests that deficits in any or all the domains previously mentioned would indicate the existence of emotion dysregulation, which could then lead to worse mental health outcomes and exacerbate symptoms already present within individuals (Gratz & Roemer, 2004). Chronic pain has been demonstrated to alter the levels of serotonin and norepinephrine in the brain, contributing to the development of depression and anxiety, which are closely linked to emotion dysregulation (Delgado, 2000). Additionally, chronic pain can lead to structural and functional changes in the brain, particularly in areas involved in emotion regulation, such as the prefrontal cortex and hippocampus (Apkarian et al., 2011). Greater emotion dysregulation has demonstrated a consistent and moderate association with mental health problems, including PTSD symptoms (Tripp et al., 2015), anxiety/depression (Hofmann et al., 2012; Mennin et al., 2005), and poorer quality of life across clinical and non-clinical samples (Fox et al., 2007; Powers et al., 2015; Trent et al., 2019). Emotion dysregulation is also associated with pain-related complaints across numerous domains (e.g., pain intensity, pain catastrophizing, and pain disability) in clinical and non-clinical pain samples, including trauma-exposed samples (Powers et al., 2014; Zaorska et al., 2020). Further, pain could serve as a stressor, depleting emotion regulation capacities (Johns et al., 2008; Narita et al., 2015; Riquino et al., 2018).

Despite this knowledge, no work has examined emotion dysregulation as a mechanistic factor involved in the pathway from the experience of pain to poorer mental health among trauma-exposed young adults. Theoretically, emotion dysregulation may be one explanatory factor involved in the experience of pain concerning PTSD symptoms, anxiety, and depressive symptoms among trauma-exposed young adults. Specifically, the cumulative stress associated with severe pain among trauma-exposed young adults may reduce regulatory capacities and cause an increase in emotion dysregulation (Latini & Costigan, 2022). Such process, in turn, could lead to emotional vulnerability and a surge in PTSD and anxiety/depressive symptoms (Cisler & Olatunji, 2012; Elwood et al., 2009). To demonstrate, a trauma-exposed young adult with higher levels of experienced pain is apt to respond to such somatic stress with an overall reduced capacity to regulate their emotions in the face of such stress (i.e., cumulative stress effects; Abravanel & Sinha, 2015; Tran et al., 2020). Such a decreased capacity to regulate emotions, in turn, could be associated with experiencing more severe negative PTSD symptoms in the context of trauma. Further, given the transdiagnostic nature of the emotion regulation construct, this individual could experience exacerbation in commonly co-occurring symptoms of anxiety and depression. According to this viewpoint, emotion dysregulation may explain, in part, the pathway from the experience of more severe pain to the indices of mental health in trauma-exposed young adults.

Nearly all previous work on emotion dysregulation and pain has focused on the higher-order emotion dysregulation construct. However, in the context of differential roles of different aspects of emotion dysregulation in contributing to various aspects of the mental health of trauma-exposed individuals, there is a clear need for research to better understand emotion dysregulation facets and their potential unique roles in explaining the pain-mental health relationship among trauma-exposed young adults (Carter et al., 2020; Deckert et al., 2020; Kerig et al., 2009; Khakpoor et al., 2019; Palus et al., 2012).This approach allows for a fine-grained examination of how different facets of emotion dysregulation in the context of pain contribute to various aspects of the mental health of trauma-exposed young adults in one overarching model.

Therefore, the current study sought to examine the explanatory role of emotion dysregulation and its facets (in one overarching model) in the relationship between pain severity and traumatic stress, as well as anxiety/depressive symptoms (as the most common comorbidities of PTSD symptoms; Cisler & Olatunji, 2012; Elwood et al., 2009) among trauma-exposed young adults. We focused on pain severity as the most clinically relevant index of pain among young adults (Graham & Streitel, 2010) and aim to fill in gaps in literature through 2 avenues: (1) exploring potential underlying mechanisms (emotion dysregulation) between the relationship of pain and traumatic symptom severity, anxiety, and depressive symptoms and (2) illuminating potential pathways for clinicians and researchers to better identify and treat trauma exposed young adults. Additionally, models of moderated mediation were conducted in an exploratory fashion examining the potential moderators of gender, trauma severity (only for depression and anxiety models), and trauma type (interpersonal vs. not) in the relationship between pain severity. These models were exploratory in nature given the dearth of preexisting work on this subject, however we chose these potential moderators based on prior literature demonstrating their relevant associations with the outcomes of interest (Asghari et al., 2013; Girgus & Yang, 2015; Haldane & Nickerson, 2016). We hypothesized that greater pain levels would be indirectly associated with greater traumatic stress and anxiety/depressive symptoms via emotion dysregulation. Our additional focus on these mental health symptoms are due to them being reported as the most common symptoms experienced among trauma-exposed individuals, including young adults (Breslau et al., 1991; Foa et al., 1997; Vrana & Lauterbach, 1994; Whetten et al., 2008). While no formal hypothesis was presented for the exploratory models of moderated mediation regarding gender and trauma type, it was considered that specific group differences may contribute to unique outcomes of depression, anxiety, and trauma severity. For trauma severity as a potential moderator (only being utilized in models where depression and anxiety were outcome variables), it was hypothesized that an increase in trauma severity and emotion dysregulation could have compounding effects in model pathways that may be greater than singular effects.

Methods

Participants

The present sample is a subset of participants from a larger study (n = 1138) of mental health among students at a large, southwestern university. Participants were 568 undergraduate college students (81.3% female, Mage = 21.15, SD = 2.38; Range = 18–29) who reported at least one lifetime traumatic event as determined by the Posttraumatic Diagnostic Scale (Foa et al., 1997). As part of the larger study, participants received extra credit toward their psychology course as compensation and were recruited via flyers and postings on the extra credit website. Exclusion criteria for the larger study included being younger than age 18 years and non-proficiency in English (to ensure comprehension of study questions). The current study consisted of an ethno-racially diverse sample: 38.7% Hispanic (n = 220), 25.90% Asian/Pacific Islander (n = 147), 20.80% non-Hispanic White (non-Hispanic; n = 118), 10.60% Black (non-Hispanic; n = 60), 3.2% other (n = 18), and 0.90% (n = 5) American Indian/Alaskan Native. Among the participants, 16.1% reported experiencing moderate to severe pain on average in the last 3 months. A total of 24.5% of the sample presented scores above the clinical cut-off score of 27 on the measure of PTSD (see below). 64.6% (n = 367) of the sample reported experiencing 1 traumatic event in their lifetime, 20.6% (n = 117) reported experiencing 2 traumatic events in their lifetime, 7.6% (n = 43) reported experiencing 3 traumatic events in their lifetime, and 7.2% (n = 41) reported experiencing 4 or more traumatic events in their lifetime. Of the traumatic events reported, 13.6% (n = 77) reported experiencing a serious life threatening illness, 10.6% (n = 60) reported experiencing physical assault, 16.7% (n = 95) reported experiencing sexual assault, .5% (n = 3) reported experiencing military combat or lived in a war zone, 10.6% (n = 60) reported experiencing child abuse, 22.5% (n = 128) reported experiencing a serious accident (serious injury or death), 45.4% (n = 258) reported experiencing a natural disaster, and 7.6% (n = 43) reported experiencing other traumatic events (home invasion, multiple surgeries, etc.).

Measures

Graded Chronic Pain Scale (GCPS)

(Von Korff et al., 1992) The graded chronic pain scale is an eight-item self-reported measure (e.g., “How would you rate your pain RIGHT NOW?”, “In the last 3 months, how would you rate your WORST pain?”, “in the last 3 months, ON AVERAGE, how would you rate your pain?”, etc.) assessing the impact of chronic pain on daily life. The original version of the measure was incorporated, where participants are asked to rate the number of days over the last 180 days they have experienced pain, as well as the intensity of their pain and the disability due to pain over the last 3 months using a 0 (No pain) to 10 (Pain as bad as it can be) scale. Four items are used to assess current pain severity and another four items are used to assess current pain disability. The scale yields two subscales, pain disability and pain severity, which are computed by summing their respective 4 items, where higher scores indicate more severe pain and pain disability. The pain severity subscale was used in the current study (α = .88).

Difficulty in Emotional Regulation Scale (DERS)

Gratz & Roemer (2004); Victor & Klonsky (2016). The DERS-18 is an 18-item self-reported measure that asks respondents to indicate how often they experience each of the items (e.g., “I am clear about my feelings”, “When I’m upset, I feel out of control”, “When I’m upset, I feel ashamed with myself for feeling that way”, etc.) on a 5-point Likert scale of 1 (almost never) to 5 (almost always). The DERS-18 measures 5 factors of emotion dysregulation including non-acceptance of emotional responses, difficulties engaging in goal directed behavior, impulse control difficulties, limited access to emotion regulation strategies, and lack of emotional clarity. The DERS-18 total score (mean = 34.08, SD = 14.15) was used in the current study as an index of emotion dysregulation and all of its subscales were used for exploratory mediation analysis. As in past work among trauma exposed samples, the DERS-18 total score and its subscales demonstrated excellent internal consistency (α′s range .90–.95; Tull et al., 2007).

Posttraumatic Diagnostic Scale (PDS)

Foa et al. (1997). The PDS is a 49-item self-reported measure designed to assess the current severity of PTSD symptoms in participants. The scale is comprised of 4 sections: (1) a checklist of traumatic events the individual has experienced (i.e., “Have you ever experienced, witnessed, or been repeatedly confronted with any of the following, check all that apply:”) (2) identification of the most distressing traumatic event, (3) an assessment of PTSD symptoms (e.g., “How often have you experienced unwanted upsetting memories about the trauma in the last month?”), and (4) an assessment of the interference of symptoms (e.g., “How much have these difficulties been interfering with your everyday life, for example relationships, work, or other important activities?”). The assessment of PTSD symptoms yields a total score (the sum of all items assessing trauma severity) and three subscales: re-experiencing (e.g., “Bad dreams or nightmares related to the trauma”), avoidance (e.g., “Trying to avoid activities, situations, or places that remind you of the trauma or that feel more dangerous since the trauma”), and arousal (e.g., “Having intense negative feelings like fear, horror, anger, guilt or shame”), all of which can be computed from selective items from the assessment of PTSD symptoms. The number of traumatic events was computed from this measure. The most commonly reported symptom was “feeling very emotional upset when reminded of the trauma” and the average severity score was 17.13. The total score of trauma severity showed excellent internal consistency (α = 0.95) and was used in the current study.

Inventory of Depression and Anxiety Symptoms (IDAS)

Watson et al. (2007). The IDAS is a 64-item self- reported measure used to assess anxiety and depressive symptoms, rated on a 5-point Likert scale from 1 (Not at all) to 5 (Extremely). The scale yields 10 specific symptom scales: Suicidality, Lassitude, Insomnia, Appetite Loss, Appetite Gain, Ill Temper, Well-Being, Panic (anxious arousal; Stasik-O’Brien et al., 2019), Social Anxiety, and Traumatic Intrusions. Additionally, the IDAS has 2 global factors of General Depression and Dysphoria. For the current study, the General Depression (Cronbach’s α = 0.93), and Panic (Anxious Arousal; Cronbach’s α = 0.92) specific symptom scales were used.

Procedures

This study was approved by the institutional review board (IRB) at the university in which the study was conducted, and all study procedures complied with the IRB-approved protocol. After a complete discussion of the study objectives and procedures with potential participants, written informed consent was obtained. Specifically, each participant provided online informed consent before proceeding to an Internet-based self-report survey. All study measures were completed online. No identifying information was collected linking participants to survey responses. Validity questions (e.g., “For this question, please select answer choice 4”) were used to detect poor-quality responses. Additionally, we incorporated two recommended methods to check for careless responding: time to completion (i.e., extremely short responding time indicating careless or inattentive responding) and Mahalanobis distance, assessing the distance of a respondent’s data points from the mean of all respondents (multivariate outlier index; Goldammer et al., 2020). After incorporating such methods, no participant met criteria for careless responding, therefore no data was discarded.

Data Analytic Plan

Analyses were conducted using SPSS version 24. First, a series of mediation analyses were conducted using the PROCESS macro, with pain severity as the predictor, emotion dysregulation as mediator, and PTSD, depressive, and anxious arousal symptoms as the dependent variables (see Figure 1; Hayes & Rockwood, 2017)¹. Next, to detect the unique explanatory role of each emotion dysregulation facet in the above relationships, another set of mediation analysis was conducted with a similar set of predictor and dependent variables, and all facets of emotion dysregulation as mediators in one overarching model (i.e. multiple mediation; see Figure 2). All mediation models were adjusted for the number of traumatic event exposures, age, and gender. Both direct and total effects for each model were reported. A pairwise deletion method of missing data was used for the study, where participants with complete data from variables of interest for specific analysis were included, while missing data from specific variables of analysis excluded them from that specific analysis. To detect the significance of the indirect effects in each model set, bootstrapping with 10,000 bootstrap re-samplings was conducted. Bootstrapping estimates the sampling distribution of an estimator based on re-sampling with replacement from the data set, which creates an empirically generated sampling distribution (Mooney et al., 1993). A bootstrapped confidence interval that does not include zero indicates a statistically significant indirect effect (Ditlevsen et al., 2005; Preacher & Kelley, 2011). To determine the magnitude of the effect present in the mediation models, completely standardized point estimates represented as the indirect effect of a one-unit change in the standardized predictor (1 unit = 1 standard deviation) on the standardized outcome were utilized. Scores were interpreted as small (0.01), medium (0.09) and large (0.25; Ditlevsen et al., 2005; Preacher & Kelley, 2011).

Results

Bivariate Correlations

Pain severity was statistically significantly positively correlated with emotion dysregulation (r = 0.19), anxious arousal (r = 0.24), general depression (r = 0.29), and PTSD symptoms (r = 0.22). Emotion dysregulation was statistically significantly positively correlated with anxious arousal (r = 0.41), general depression (r = 0.61), and PTSD symptoms (r = 0.43). All emotion dysregulation sub-facets were also statistically significantly positively correlated with pain severity (r’s range = .13–.19), anxious arousal (r’s range = .30–.40), general depression (r’s range = .50–.61), and PTSD symptoms (r’s range = .33–.46). See Table 1 for descriptive data and bi-variate relations.

Table 1.

Descriptive Statistics and Bivariate Correlations Between Study Variables.

Variables	1	2	3	4	5	6	7	8	9	10	11	12	13
1. Age	1	.003	.090*	.04	−.08	−.15**	−.06	−.03	−.09*	−.08*	.002	−.03	−.03
2. Gender		1	.02	.15**	.13**	.06	.14**	.13**	.15**	.10*	.19**	.14**	.08
3. N Traumas			1	.18**	.18**	.15**	.13**	.17**	.18**	.19**	.39**	.21**	.18**
4. Pain severity				1	.19**	.13**	.15**	.17**	.19**	.18**	.22**	.29**	.24**
5. DERS total					1	.74**	.87**	.92**	.95**	.88**	.43**	.61**	.41**
6. DERS clarity						1	.56**	.61**	.64**	.62**	.33**	.50**	.30**
7. DERS goal							1	.74**	.81**	.69**	.33**	.51**	.31**
8. DERS impulse								1	.88**	.79**	.39**	.54**	.40**
9. DERS strategies									1	.79**	.46**	.61**	.39**
10. DERS non-acceptance										1	.37**	.53**	.37**
11. PDS total score											1	.51**	.44**
12. IDAS general depression												1	.69**
13. IDAS anxious arousal													1
Mean (N)	21.15	462	1.61	24.49	34.08	4.25	7.22	5.85	10.78	6.52	17.13	46.33	13.02
SD (%)	2.38	81.3%	1.03	21.11	14.15	2.02	3.18	2.79	5.14	3.12	18.50	15.34	6.45

Note. gender (coded as Female = 1); N Traumas = number of traumatic events endorsed; DERS = Difficulties in Emotion Regulation Scale; PDS = Posttraumatic Diagnostic Scale; IDAS General Depression & IDAS Anxious Arousal = Inventory of Depression and Anxiety Scale. *p < .05; **p < .01.

Mediation Models

PTSD Symptoms

Regarding PTSD symptoms, there was a statistically significant total effect on pain severity (See Table 2; b = .12, SE = .03, p = <.001, 95% CI [.05, .19]). There was a statistically significant indirect effect of pain severity via emotion dysregulation for PTSD symptoms (b = .04, SE = .01, 95% CI [.01 .08]), completely standardized point estimate (β = .05). After accounting for the indirect effects of the mediator, the direct effect of pain severity on PTSD symptoms was statistically significant (b = .08, SE = .03, p = .02, 95% CI [0.01, .14]).

Table 2.

Total, Direct, and Indirect Effects of Pain Severity on PTSD Symptom Severity, General Depression, and Anxious Arousal via Emotion Dysregulation.

Y	Model	b	SE	t	p	LLCI	ULCI
1. PTSD symptoms	PAIN → DERS-18 (a)	.09	.03	3.27	.001	.04	.15
	DERS-18 → PDS (b)	.43	.05	8.60	<.001	.33	.52
	Pain → PDS (c)	.12	.03	3.40	<.001	.05	.19
	Pain → PDS (c’)	.08	.03	2.39	.02	.01	.14
	Pain → PDS (ab)	.04	.01			.01	.08
2.General depression	DERS-18→ IDAS-GD (b)	.61	.04	16.24	<0.001	.54	.69
	Pain → IDAS-GD (c)	.18	.03	5.94	<.001	.12	.24
	Pain → IDAS-GD (c’)	.12	.02	4.85	<.001	.07	.17
	Pain → IDAS-GD (ab)	.06	.02			.02	.10
3. Anxious arousal	DERS-18→ IDAS-AA (b)	.17	.02	8.95	<.001	.13	.20
	Pain → IDAS-AA (c)	.06	.01	4.84	<.001	.04	.09
	Pain → IDAS-AA (c’)	.05	.01	3.85	<.001	.02	.07
	Pain → IDAS-AA (ab)	.02	.01			.01	.03

Note. a = Association of X with M; b = association of M with Y; c = Total association of X with Y; c’ = Direct association of X with Y controlling for M; ab = indirect effects of X on Y; Path a is equal in all models; therefore, it presented only in model 1. The standard error and 95% CI for ab are obtained by bootstrapping with 10,000 re-samples. DERS-18 = Difficulties in Emotion Regulation Scale; IDAS-AA = Inventory of Depression and Anxiety-Anxious Arousal Subscale; IDAS-GD = Inventory of Depression and Anxiety-General Depression Subscale; PDS = Post-Traumatic Diagnostic Scale; LLCI = lower bound of a 95% confidence interval; ULCI = upper bound;→ = association.

General Depression

For general depression, there was a statistically significant total effect on pain severity (See Table 2; b = .18, SE = .03, p = <.001, 95% CI [.12, .24]). There was also a significant indirect effect of pain severity, through emotion dysregulation, on general depression (b = .06, SE = .02, 95% CI [.02, .10]), completely standardized point estimate (β = .08). After accounting for indirect effects of the mediator, the direct effect of pain severity on general depression was statistically significant (b = .12, SE = .02, p = <.001, 95% CI [.07, .17]).

Anxious Arousal

Concerning anxious arousal, there was a statistically significant total effect on pain severity (See Table 2; b = .06, SE = .01, p = <.001, 95% CI [.04, .09]). In addition, there was a statistically significant indirect effect of pain severity, through emotion dysregulation, for anxious arousal (b = .02, SE = .01, 95% CI [.01, .03]), completely standardized point estimate (β = .05). After accounting for the indirect effects of the mediator, the direct effect of pain severity on anxious arousal was statistically significant (b = .05, SE = .01, p = <.001, 95% CI [0.02, .07]).

Multiple Mediation Models

PTSD Symptoms: Running the multiple mediation model for PTSD symptoms, limited access to emotion regulation strategies was the only statistically significant mediator in the model consisting of other subscales of emotion dysregulation (b = .06, SE = .02, 95% CI [.02, .11]). General Depression: Running the multiple mediation models for general depression saw two subscales emerge significant. Limited access to emotion regulation strategies was demonstrated to be a statistically significant mediator in the model (b = .04, SE = .02, 95% CI [.02, .08]) and lack of emotional clarity as well (b = .01, SE = .01, 95% CI [.002, .03]). For Anxious Arousal: The inability to control impulsive behaviors was the only statistically significant mediator (b = .01, SE = .005, 95% CI [.0001, .02]).

Discussion

Consistent with the hypotheses, emotion dysregulation statistically significantly explained the relationship between pain severity and PTSD symptoms, anxiety, and depression among trauma-exposed young adults. These observed effects were evident above and beyond the variance accounted for by the number of lifetime trauma events, age, and gender. These results align with the view that emotion dysregulation may serve as a transdiagnostic mechanism underlying the pathway from pain severity to mental health among trauma-exposed young adults (Aaron et al., 2020; Riquino et al., 2018). Theoretically, it is possible that cumulative stress associated with the experiences of pain-related states may reduce the trauma-exposed young adults’ capacity to regulate their emotional responses in the face of negative emotional experiences (Abravanel & Sinha, 2015; Johns et al., 2008), hindering their ability for cognitive processing of the traumatic experiences and conferring risk for more severe PTSD symptoms and other related mental health-related outcomes (Carter et al., 2020). Accordingly, future work could usefully replicate and extend these findings using prospective and laboratory-based research designs to determine the causal pathways related to the observed associations. Caution should be taken when interpreting the results of the study when considering the cross-sectional nature and the potential for emotion regulation to be a collider with pain severity and trauma symptoms in the models (MacKinnon & Lamp, 2021). Additionally, trauma exposure could potentially be an unmeasured confounder, violating mediation assumptions which can impact the study’s findings. Future research looking to replicate results would benefit from collecting more comprehensive data on potential confounding variables, in order to better control for them. Additionally, future studies may elect to incorporate more rigorous data collection protocols (e.g., structured interview based) and advanced statistical techniques to help identify and mitigate the potential of confounding and colliding effects of pain severity and emotion regulation.

Examination of facets of emotion dysregulation demonstrated the unique explanatory role of limited access to emotion regulation strategies for the relationship between pain severity and PTSD and depressive symptoms of trauma-exposed young adults. Additionally, lack of emotional clarity also emerged significant for depressive systems of trauma exposed young adults. Yet, the association between pain severity and anxiety symptoms was explained by the facet of lack of impulse control. These observations generally align with past work that found that PTSD symptoms and depressive symptoms are mainly impacted by an individual’s inability to develop adaptive strategies to modulate the duration and/or intensity of these aversive emotional experiences (Carter et al., 2020; Fiedler et al., 2018; Kerig et al., 2009; Palus et al., 2012). In the absence of adaptive processing of information related to the experience of trauma, driven by the depletion of overall adaptive regulatory capacities due to pain, the individual would feel stuck in his negative cognitions related to the symptoms of PTSD and depression. Moreover, anxious arousal symptoms, as a rather somatic (vs. cognitive) aspect of anxiety symptoms, have been shown to be influenced by the trait-like inability to inhibit impulses in reaction to somatic symptom presentations (Dasch et al., 2008; Khakpoor et al., 2019; Palus et al., 2012). Impulsivity-driven depletion of resources due to pain could be a mechanistic factor in the development and maintenance of anxiety in trauma-exposed young adults. Future work could usefully examine the indirect pathways from the negative emotional experiences related to pain for each of these disorder-specific emotion dysregulation facets using a prospective design.

In regard to the exploratory models of moderated mediation, no models emerged statistically significant. There are multiple potential reasons for this observation. First, the entire sample was, by design, trauma exposed thereby potentially limiting variability in trauma severity and influencing interaction model results. Additionally, differences in interpersonal trauma endorsement versus non-interpersonal trauma or differences in gender may not be as relevant to the associated relationship between emotion dysregulation and outcomes of interest, especially given that emotion dysregulation is a common underlying transdiagnostic factor across trauma types. It is also possible that the interaction effect size was too small to be detected in the current study despite the large sample size. Researchers may want to take into account these considerations when interpreting study results.

Although not the study’s primary aim, some additional findings are worth consideration. First, 13.6% of the sample reported clinically relevant pain (Von Korff et al., 1992). This finding is in line with past work regarding the clinical significance of pain among trauma-exposed young adults (Gómez-Pérez & López-Martínez, 2013). Thus, the current study adds to the literature, highlighting the importance of investigations regarding the epidemiology and clinical implications of pain among trauma-exposed young adults. Second, pain severity and emotion dysregulation shared only 3.6% of the variance with each other. Thus, making these constructs are empirically distinct. Such data is consistent with the literature regarding the distinctive clinical relevance of these two constructs to different indices of mental health (Deckert et al., 2020).

The current study findings have some clinical implications for developing specialized treatments to address the mental health needs of trauma-exposed young adults. Specifically, identifying and targeting emotion dysregulation problems to increase trauma-exposed young adults’ capacity to respond to pain-related stress flexibly could have mental health benefits (Gómez-Pérez & López-Martínez, 2013; Reed et al., 2021; Tidmarsh et al., 2022). Psychological interventions such as cognitive-behavioral and dialectical behavioral therapies may be promising tactics for improving emotion dysregulation in the context of pain experience among trauma-exposed young adults (Breslau et al., 1991; Lindsey et al., 2007; Nelson et al., 2021; Tran et al., 2020). Furthermore, to provide more specificity to target emotion dysregulation processes implicated in pain-related mental health outcomes, preventive interventions could be honed to target the most relevant facets of the construct that underlies the relationship between pain and specific mental health-related outcomes. For example, limited access to emotion regulation strategies could be targeted in preventive treatments for PTSD symptoms, depression among trauma-exposed young adults how experience pain.

Several study limitations warrant consideration. First, due to the study’s cross-sectional design, the temporal sequencing of the involved variables, particularly the exact order of the hypothesized predictor and mediator, could not be determined. Future longitudinal design studies (e.g., lagged designs) are needed to elucidate the causal pathways among variables. Second, self-reported assessment methods increase concerns regarding the shared method variance bias. Future research could examine the above relationships using multi-assessment methods to minimize such bias. Third, the unbalanced gender distribution of the current study could limit the generalizability of the results. Future work should seek to replicate and extend the existing models to a more gender-balanced sample of trauma-exposed young adults. Fourth, we did not have data on the nature (i.e., acute vs. chronic) and location of pain experienced. Future work should document this information, which could help to understand better the nuances concerning the role of pain in trauma-related mental health outcomes. Fifth, the non-clinical nature of the sample prevents us from generalizing the findings to clinical populations. Future work should replicate these findings in trauma-exposed young adults with clinical levels of pain. Sixth, data was not available for the recency of the traumatic events experienced by participants and therefore could not be controlled for. Additional work would benefit from including this variable in models to better assess the robustness of study results.

Together, the present study offers novel empirical support for the explanatory role of emotion dysregulation in the path from pain severity to a wide range of mental health symptoms among trauma-exposed young adults. Further, specific facets of emotion dysregulation seem to play unique roles in these relationships. Future replications using prospective designs are needed to explicate the temporal ordering of the observed associations.

Supplemental Material

Supplemental Material - Pain Severity and Mental Health of Lifetime Trauma Exposed Young Adults: The Role of Emotion Dysregulation

Supplemental Material for Pain Severity and Mental Health of Lifetime Trauma Exposed Young Adults: The Role of Emotion Dysregulation by Jafar Bakhshaie, Eric A. Storch, Bryce K. Clasuen and Michael J. Zvolensky in Emerging Adulthood

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Transparency and Openness Statement

The raw data contained in this manuscript are not openly available due to privacy restrictions set forth by the institutional ethics board, but can be obtained upon reasonable request from the corresponding author following the completion of a privacy and fair use agreement. The analysis code/syntax used for the analyses are not openly available for download, but can also be obtained from the corresponding author upon reasonable request by the journal. All the materials used in this study, including study measures, may be openly available for download, however restrictions may be imposed by the governing institutions and authors that own such measures. The study did not include a pre-registration plan for data collection or analysis.

ORCID iD

Jafar Bakhshaie

Supplemental Material

Supplemental material for this article is available online.

Note

Author Biographies

Dr. Bakhshaie is an Assistant Professor for the Center for Health Outcomes and Interdisciplinary Research lab at Massachusetts General Hospital where he primarily focuses on disparities in medical and mental health comorbidity, pain and substance/opioid use, and transdiagnostic mechanisms of change in underserved medical populations. Dr. Bakhshaie’s current work focuses on the development and testing of scalable technology-enhanced cost-effective, mind-body interventions that target both the physical and psychological aspects of chronic and acute medical conditions.

Dr. Storch is a Professor and Vice Chair of psychiatry and behavioral sciences at Baylor College of Medicine and is an experienced Clinical Psychologist with expertise in the assessment and treatment of obsessive-compulsive and related disorders and anxiety disorders in children, adolescents, and adults. Dr. Storch is trained in cognitive behavior therapy and habit reversal training and has clinical interests spanning a broad range of foci, including exposure and response prevention therapy, CBT, and anxiety related therapies.

Mr. Clausen is a clinical research at the Research on Emotions Substance Treatment Outcomes and Racial Equity lab (RESTORE) at the University of Houston located in the department of psychology. Mr. Clausen’s research focuses health vulnerable populations and high-risk behaviors, looking at transdiagnostic mechanisms such as anxiety sensitivity, emotional regulation, and social determinants of health and how they confer risk to behaviors such as substance use, anxiety, and suicidality.

Dr. Zvolensky is a Distinguished Professor in the Department of Psychology at University of Houston and Director of the RESTORE Laboratory: Research on Emotion, Substance Treatment Outcomes, and Racial Equity. Dr. Zvolensky’s research focuses on anxiety and stress related psychopathology with substance use disorders and has a global aim of eliminating inequalities that exist in addictive behaviors and psychopathology across all populations.

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