The phenotype of recovery XII: A reinforcer pathology perspective on associations between delay discounting and pain catastrophizing in substance use disorder recovery.

Table 1 summarizes sample characteristics, including demographic data, delay discounting, all pain variables, and QOL, stratified by remission status. Overall, 50.6% of the sample was in remission (n=86). Further, the sample was, on average, 44.44 years old, 51.2% women, 86.5% white, and 94.7% not Hispanic or Latino. DSM-5 lifetime SUD and sustained remission prevalences are shown in Table 2 . Supplemental Table 1 displays associations between delay discounting and pain indices. Univariate logistic regressions examined the relationship between sustained remission status and delay discounting, all pain variables, pain catastrophizing, and demographic characteristics ( Table 3 ). Significant negative associations were found between sustained remission and delay discounting (OR=0.958, 95% CI [0.936, 0.980], p <.001) as well as pain catastrophizing (OR=0.989, 95% CI [0.982, 0.995], p =.001). Individuals who were older (OR=1.01, 95% CI [1.00, 1.04], p <.001), female (OR=1.18, 95% CI [1.02, 1.37], p =.032), or had higher income (OR=1.02, 95% CI [1.00, 1.04], p =.013) were more likely to be in sustained remission while being Black or African American (OR=0.739, 95% CI [0.562, 0.971], p =.032) was associated with less likelihood of being in remission. Univariate linear regressions examined the relationship between each QOL domain and delay discounting, the pain variables, as well as the demographic characteristics ( Table 4 ). For physical QOL, significant negative associations were found for pain status (i.e., having chronic pain; F(1,168)=17.59, p <.001), pain catastrophizing (F(1,168)=47.67, p <.001), pain interference (F(1,168)=50.11, p <.001), pain intensity (F(1,168)=28.48, p <.001), and delay discounting (F(1,168)=15.22, p< .001). Significant positive associations were found for age (F(1,168)=18.81, p< .001), income (F(1,168)=44.29, p< .001), years of education (F(1,168)=12.54, p< .001), and poly-SUD status (F(1,168)=7.84, p =.006). For psychological QOL, significant negative associations were found for pain catastrophizing (F(1,168)=54.17, p< .001), pain interference (F(1,168)=7.54, p =.007), and delay discounting (F(1,168)=18.74, p< .001). Significant positive associations were found for age (F(1,168)=32.81, p< .001), income (F(1,168)=15.92, p< .001), and years of education (F(1,168)=8.11, p =.005). For social QOL, a significant negative association was found for pain catastrophizing (F(1,168)=31.41, p< .001), pain interference (F(1,168)=4.46, p =.036), and delay discounting (F(1,168)=4.25, p= .041) while a significant positive association was found for age (F(1,168)=7.66, p =.006) and income (F(1,168)=12.30, p< .001). For environmental QOL, significant negative associations were found for pain interference (F(1,168)=12.97, p <.001), pain intensity (F(1,168)=6.44, p =.012), pain catastrophizing (F(1,168)=41.32, p< .001), and delay discounting (F(1,168)=38.40, p< .001). Significant positive associations were found between poly-SUD (F(1,168)=19.08, p <.001), being female (F(1,168)=48.49, p <.001), income (F(1,168)=38.32, p< .001), and years of education (F(1,168)=14.39, p< .001). Multivariate linear regression with model selection identified covariates of interest for the mediation analysis, using the variables from the model with the lowest BIC. For sustained remission status the model with the lowest BIC included age ( p =.002). For physical QOL the optimal model included pain status ( p =.004), pain interference ( p <.001), and income ( p <.001). For psychological QOL the optimal model included age ( p <.001). For social QOL the optimal model included income ( p <.001). Finally, for environmental QOL the optimal model included age ( p =.002). We examined the mediating effect of pain catastrophizing (M) on the relationship between delay discounting (X) and: sustained remission (Y1), physical QOL (Y2), psychological QOL (Y3), social QOL (Y4), and environmental QOL (Y5). After controlling for the relevant covariates, pain catastrophizing significantly mediated the relationship between delay discounting and physical QOL ( ꞵ =−0.051, 99% CI: −0.183, −0.018, p =.044), psychological QOL ( ꞵ =−0.082, 99% CI: −0.231, −0.043, p =.009), social ( ꞵ =−0.077, 99% CI: −0.121, −0.019, p =.018), and environmental QOL ( ꞵ =−0.062, 99% CI: −0.232, −0.040, p =.014). Pain catastrophizing did not mediate the relationship between delay discounting and sustained remission ( p >.05). The significant findings are displayed in Figure 1A – 1D .

The study recruited participants (N=283) from the International Quit and Recovery Registry (IQRR; https://www.quitandrecovery.org/ ) online community of more than 10,000 individuals who self-identify as being in recovery from SUD. The IQRR offers monthly assessments investigating recovery-related factors. Participants are awarded an online badge and 400–1000 points for each assessment completed, and points can be redeemed for monetary compensation (100 points = $1.00). For further details regarding the IQRR see (Athamneh et al., 2020; Craft et al., 2021 ; Dwyer et al., 2023 ). Inclusion criteria for the present study included being 18 years or older, having a lifetime history of at least one SUD (as defined by The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition [DSM-5]; American Psychiatric Association, 2013 ), and self-identifying as being in recovery from substance use. Initiating recovery was defined by a participant endorsing that they have taken steps toward actively changing substance use behaviors and making efforts to reduce or cease substance use. Individuals were excluded (n=50) if they reported that they had never experienced physical pain (other than everyday aches and pains such as minor headaches) at some point in their lives. The data analyzed in this study was collected between March and May of 2020. The Institutional Review Board at Virginia Tech approved this study. Participation was voluntary and consent was implied through the submission of the survey. Participants successively chose between an immediately available, but smaller hypothetical monetary reward ($500 initial), and a delayed, larger reward ($1000) across seven randomized delays (1 day, 1 week, 1 month, 3 months, 1 year, 5 years, and 25 years). Within each delay, the smaller reward was adjusted based on the response pattern across the six trials until reaching an indifference amount. The indifference amount reflects the point at which the immediate, smaller, and delayed, larger rewards are subjectively equal in value. Subsequently, the study used Mazur’s hyperbolic discounting function ( Mazur, 1987 ) S V = A 1 + k D to fit the discounting curve to the indifference point for each delay. S V reflects the immediate reward’s subjective value (i.e., indifference amount), A is the objective, full-magnitude value, D is the time delay to the reward receipt, and k is an index of the discounting function (higher k values represent higher delayed rewards discounting). The study natural log transformed (ln( k )) All k values to stabilize the variance and normalize the data. The BPI is a validated self-report questionnaire that assesses the presence and severity of pain. All participants were asked (yes/no) if they had “ever experienced pain (other than everyday aches and pains such as minor headaches) at some point in their lives”. Individuals who responded “no” were not eligible to participate (see inclusion criteria). Respondents are asked on an 11-point scale to rate their current and average pain as well as their past 24-hour worst and least pain. A pain intensity score is calculated as the average across these four responses ( Cleeland & Ryan, 1991 ). Respondents also report how much their pain interferes with their ability to function over the past 24 hours across seven areas (i.e., general activity, mood, walking ability, normal work, interpersonal relations, sleep, and enjoyment of life). Past-day pain interference is the average score across these seven areas. For both pain indices, the higher the scores, the greater the pain severity. Chronic pain status was defined based on the duration respondents experienced pain ( International Association for the Study of Pain Task Force on Taxonomy, 1994 ; Treede et al., 2015 ). To assess chronic pain status, individuals were asked “How long have you experienced this pain?” (less than 1 month ago; at least 1 month but less than 3 months; at least 3 months but less than 6 months; at least 6 months but less than 1 year; 1 year or more). Individuals who endorsed experiencing pain for at least three months were considered to have chronic pain ( Treede et al., 2015 ). All other individuals were considered to have non-chronic pain. The PCS is a validated 13-item self-report questionnaire that assesses pain-related catastrophic thinking. Respondents were asked to indicate on a 5-point Likert scale how often (0=”not at all”, 4=”all the time”) they have thoughts and feelings related to three domains (rumination, magnification, and helplessness) when they experience pain. Items related to rumination include statements such as, “I can’t stop thinking about how much it hurts”; magnification items include statements such as, “I become afraid that the pain will get worse”; and finally, helplessness-related items include statements such as, “there is nothing I can do to reduce the intensity of my pain.” In addition to the three subscales, the measure yields a total score (range: 0–52). In the present study, the total score was used to represent overall pain catastrophizing. Participants were asked to report (yes/no) which substances (i.e., alcohol, cannabis, cocaine, dissociative anesthetics, hallucinogens, inhalants, nicotine, opioids and prescription pain relievers, stimulants, and/or tranquilizers) they had used problematically in their lifetime. For each substance the participants endorsed using problematically, they were asked about the 11 DSM-5 symptoms. Participants who endorsed at least 2 symptoms were considered to have a lifetime history of SUD for that substance. If an individual met criteria for 2 or more lifetime SUDs they were also coded as an individual with poly-SUD. Individuals were considered to be in remission if they endorsed no symptoms other than craving in the past 12 months (i.e., sustained remission) across all substances in which they met the lifetime SUD criteria. (WHOQOL-BREF; “Development of the World Health Organization WHOQOL-BREF Quality of Life Assessment. The WHOQOL Group,” 1998 ). The WHOQOL-BREF is a 26-item validated self-report scale that captures a respondent’s subjective QOL across four domains. The physical health domain includes questions related to activities of daily living, pain/discomfort, energy, fatigue, and mobility. The psychological domain contains questions about emotions, thinking, motivation, concentration, self-esteem, and spirituality. The social relationship domain includes questions about social support, personal relationships, and sexual activity. Finally, the environmental domain includes questions related to home environment, finances, access to health care, safety, and transportation. Higher scores on each domain reflect a higher subjective QOL. Each domain was considered independently, as recommended in the guidelines of the WHOQOL user manual ( Division of Mental Health and Prevention of Substance Abuse World Health Organization, 1998 ). Two data cleaning procedures were implemented for quality control. Individuals who did not provide complete data (n=4) and individuals who provided non-systematic discounting data (Johnson & Bickel, 2008; n=59) were excluded, leaving a final analytical sample of 170 participants. Sample demographics, as well as delay discounting, all pain indices (i.e., pain catastrophizing, chronic pain status, pain intensity, and pain interference), remission status, and QOL domains, are summarized using frequency and percentage or mean and standard deviation. The study conducted univariate logistic regressions with delay discounting, the pain indices, demographics, and polysubstance-SUD (poly-SUD) status as the explanatory measures and sustained remission status as the outcome measure. Univariate linear regressions were conducted with delay discounting, all pain indices, demographics, and poly-SUD status as the explanatory measures, and each QOL domain (i.e., physical, psychological, social, and environmental) as the outcome measures. Hayes’ method ( Hayes, 2017 ) examined whether pain catastrophizing (M) mediated the relationship between delay discounting (X) and 1) sustained remission (Y1), 2) physical QOL (Y2), 3) psychological QOL (Y3), 4) social QOL (Y4), and 5) environmental QOL (Y5). Indirect effects were evaluated using a bootstrapping approach, with 10,000 bootstrap random samples to determine 99% confidence intervals (given multiple comparisons). All results were reported as standardized estimates. For each dependent measure, we performed an exhaustive search of the model space using multivariable logistic (Y1) and linear (Y2 - Y5) regression with chronic pain status, pain intensity, pain interference, demographics, and poly-SUD status as independent variables. The variables included in the model with the lowest Bayesian Information Criterion (BIC) were included as covariates for each mediation model. The study conducted all data analyses using R version 4.2.1 ( R Core Team, 2022 ). Mediation analyses were performed using the lavaan package ( Rosseel, 2012 ).

This study found that among individuals in SUD recovery reporting pain, 1) pain catastrophizing mediated the relationship between delay discounting and QOL such that individuals with a greater immediacy bias reported higher pain catastrophizing and poorer QOL and 2) greater delay discounting and pain catastrophizing were associated with a decreased likelihood of sustained SUD remission. The findings suggest that interventions that target both delay discounting and maladaptive cognitive and emotional responses to pain may lessen the negative impact of pain on SUD recovery and improve several SUD recovery outcomes.

This study investigated associations between delay discounting, pain catastrophizing, sustained SUD remission, and QOL among individuals in SUD recovery. Pain catastrophizing significantly mediated the relationship between delay discounting and physical QOL, psychological QOL, social, and environmental QOL, with significant indirect effects accounting for 30.5%, 31.2%, 77%, and 17.0% of the total effects, respectively. Further, while pain catastrophizing did not mediate the relationship between delay discounting and sustained remission, lower delay discounting and pain catastrophizing were significantly associated with an increased likelihood of sustained remission. To our knowledge, this is the first study to report significant associations between delay discounting, pain catastrophizing, and QOL among individuals in recovery from SUD. Our study aligns with previous research showing that delay discounting is associated with QOL ( Athamneh et al., 2022 ; Einarsson, 2018 ; Rubenis et al., 2018 ) and SUD remission and SUD symptom severity ( Athamneh et al., 2023 ; Athamneh et al., 2022 ; Craft et al., 2021 ; Dwyer et al., 2023 ; García-Pérez et al., 2020 ; Kräplin et al., 2020 ). Discounting rates identified in the present study among those in remission ( MD =−6.28, SD =2.42) and not in remission ( M =−4.57, SD =3.54) are similar to other investigations. For example, Dwyer et al., (2023) found that individuals in early remission and not in early remission had mean discounting rates of −6.52 and −4.16, respectively. These findings also align with a broader literature showing that individuals in remission have lower delay discounting rates compared to those not in remission from opioid use disorder ( Craft et al., 2022 ) and that ex-smokers exhibit lower discounting rates compared to current smokers ( Bickel et al., 1999 ). Taken together, the findings of this study support that delay discounting is a behavioral marker of addiction and recovery outcomes ( Athamneh et al., 2022 ; Bickel et al., 2014 ). Greater pain catastrophizing has been robustly shown to be related to poor QOL. Specifically, pain catastrophizing leads to pain hypervigilance which together negatively impacts physical and mental QOL ( Wong et al., 2014 ). Further, greater pain catastrophizing is associated with decreased QOL in chronic pain patients ( Lamé et al., 2005 ; Merlijn et al., 2006 ; Tran et al., 2015 ), medical conditions such as endometriosis ( McPeak et al., 2018 ), hip osteoarthritis ( Hayashi et al., 2019 ), chronic rhinosinusitis ( Kazi et al., 2021 ), fibromyalgia ( Galvez-Sánchez et al., 2020 ; Libby & Glenwick, 2010 ), and mental health disorders and symptomatology ( Chung et al., 2012 ; Slawek et al., 2021 ). For example, Slawek et al., (2021) conducted a latent class analysis of pain catastrophizing, anxiety, depression, posttraumatic stress disorder (PTSD), and attention-deficit/hyperactivity disorder (ADHD) on a sample of patients on opioid treatments for pain. The authors found that the group characterized by high pain catastrophizing/high mental health symptoms had the poorest QOL compared to groups lower in pain catastrophizing. Our findings extend this body of research, identifying pain catastrophizing as a barrier to SUD recovery. While research on the relationship between pain catastrophizing and delay discounting is relatively limited, a prior investigation comparing discounting of monetary gains and losses among adults with and without chronic pain noted that while differences in discounting among pain groups were not observed, pain catastrophizing exerted a moderating effect. Specifically, individuals with chronic pain and high pain catastrophizing discounted monetary losses at a greater rate relative to individuals without chronic pain and low pain catastrophizing ( Mistretta et al., 2022 ). Mistretta and colleagues’ findings suggest that pain status/pain intensity coupled with pain catastrophizing drive effects of reward processing and punishment, rather than pain status or intensity alone. Importantly, converging neural findings in both chronic pain as well as delay discounting highlight overlapping patterns of aberrant neural activation. As individuals transition from acute to chronic pain, neural activation shifts from primarily somatosensory regions to limbic areas ( Apkarian et al., 2013 ). Conversely, individuals who prefer smaller, immediate reward exhibit hyperactivation of limbic and paralimbic regions ( McClure et al., 2004 ), providing a neurobiological basis for the behavioral economic findings we reported. The present findings in context of the broader literature demonstrate the potential utility of applying a Reinforcer Pathology framework to understanding the cognitive-emotional experience of pain in SUD recovery. Specifically, individuals in SUD recovery who have an immediacy bias (i.e., greater delay discounting) may render short-term events (e.g., pain) more salient. As such, individuals with higher delay discounting may be more vulnerable to over-attending to their immediate environment and resultantly, experiencing pain with a greater emotional valence. The present findings highlight the potential therapeutic utility of intervening on both delay discounting and pain catastrophizing in SUD recovery. Our findings underscore the potential value of interventions targeting both delay discounting and pain catastrophizing in individuals with lifetime SUDs and pain. Several studies have demonstrated reductions in delay discounting and substance use following SUD treatment, including contingency management ( García-Pérez et al., 2020 ) and episodic future thinking (EFT; Athamneh et al., 2022 ; Ruhi-Williams et al., 2022 ; Snider et al., 2016 , 2021 ; Stein et al., 2018 ). EFT involves mentally projecting oneself into the future and vividly imagining positive and meaningful experiences ( Patel & Amlung, 2020 ; Peters & Büchel, 2010 ; Ruhi-Williams et al., 2022 ), thereby shifting attention towards distal, prosocial outcomes and making longer-term benefits of recovery more salient and rewarding. Notably, one study investigated EFT as a treatment for pain and found that EFT not only reduced pain severity in a rate-dependent manner (i.e., individuals reporting the worst pain experienced the greatest reductions in pain posttreatment), reductions in delay discounting mediated reductions in pain severity ( Craft et al., 2020 ). In this, investigations of whether EFT can ameliorate pain catastrophizing is a promising avenue for future research. Moreover, we identified that individuals who are younger, male, and lower income reported reduced rates of remission. Thus, these demographic groups who are also experiencing pain in SUD recovery may particularly benefit from treatments targeting delay discounting and pain catastrophizing to improve remission rates. Overall, this field is still nascent and would benefit from further investigation on the interaction between delay discounting and pain catastrophizing, with a particular emphasis on understanding potential moderating effects of chronic pain etiology and substance use type (e.g., opioid vs cannabis). Several limitations of the study should be noted. First, our results were based on a cross-sectional assessment and did not establish causality. Future longitudinal investigations are necessary to determine the validity of our mediation model. Such research would contribute to a better understanding of the complex dynamics between pain, psychological factors, and QOL as well as hold direct clinical importance for developing effective interventions. Second, while this study assessed the mediating role of overall pain catastrophizing, we did not investigate potential effects of pain catastrophizing subscales (i.e., rumination, magnification, and helplessness). Future investigation of these components will help further refine understanding of catastrophizing in the context of recovery. Third, our mediation models accounted for a relatively low amount of the indirect effect; thus, a significant portion of the variance is unexplained. Fourth, most participants in our sample were self-selected, middle-aged, and white; therefore, the generalizability of the findings may be limited. Fifth, ~20% (n=59) of individuals were excluded from our analysis because they provided non-systematic delay discounting data. However, previous investigations have found that excluding similar proportions of data due to non-systematic delay discounting results in improved data quality ( Craft, Tegge, Freitas-Lemos, et al., 2022 ; Yeh et al., 2022 ). Further understanding other factors associated with non-systematic discounting and the extent to which random responding on discounting tasks correlates with responding on other measures is important. Sixth, our group has published extensive research on delay discounting using the IQRR as a crowdsourcing platform. Therefore, some overlap in our samples may exist and findings regarding associations between delay discounting and SUD remission as well as quality of life could potentially be confirmatory. However, this is a larger issue for online research - for example, while Amazon Mechanical Turk has advertised a participant pool of ~500,000 participants, researchers have reported that the pool available at any time is closer to ~7,000 (Stewart et al. 2012). Lastly, this study was conducted during the early part of the COVID-19 pandemic and we did not account for potential impact of COVID-19 on substance use and quality of life outcomes.

Substance use disorders (SUD) and physical pain are highly comorbid conditions, with over 70% of individuals with SUD also experiencing pain that interferes with functioning ( Jennings et al., 2022 ; Rosenblum et al., 2003 ; Witkiewitz & Vowles, 2018 ; Zale et al., 2015 ). Research on physical dimensions of pain show that pain severity and pain interference are associated with SUD relapse ( Griffin et al., 2016 ; Jakubczyk et al., 2016 ; Potter et al., 2015 ; Witkiewitz et al., 2015 ), while findings on the association between chronic pain and relapse are more mixed (Dhingra et al. 2015; Fox et al. 2012; Potter et al. 2015 ). One understudied pain index among individuals in SUD recovery is the cognitive/emotional experience of pain. Pain catastrophizing, the propensity to magnify the threat value of pain or the inability to inhibit thoughts regarding pain, and feelings of helplessness about pain ( Quartana et al., 2009 ), is related to poor health outcomes ( Slawek et al., 2021 ; Tran et al., 2015 ; Wong et al., 2014 ). Recovery from SUD is a multidimensional process involving not only reductions in substance use but also improvements in psychosocial functioning, including quality of life (QOL; National Institute on Drug Abuse, 2017 ; NIAAA Recovery Research Definitions, n.d. ; Witkiewitz et al., 2020 ). A more nuanced understanding of how pain catastrophizing impacts multidimensional aspects of SUD recovery may help improve SUD prognoses. Broadly, pain catastrophizing is related to reduced pain-treatment response including lower response to analgesics ( Mankovsky et al., 2012 ), worse pain severity ( Craner et al., 2016 ; Feinstein et al., 2017 ; Wertli et al., 2014 ), pain interference ( Craner et al., 2016 ), mental health symptomatology, particularly depression and suicidality ( Craner et al., 2016 ; Noyman-Veksler et al., 2017 ; Richardson et al., 2009 ), and poorer QOL ( Chung et al., 2012 ; Hayashi et al., 2019 ; Wong et al., 2014 ). Pain-related anxiety, a feature of pain catastrophizing, is also associated with opioid misuse ( Martel et al., 2013 ) and cigarette smoking relapse ( LaRowe et al., 2017 ). Moreover, one investigation of patients with chronic pain undergoing SUD treatment found that pain catastrophizing was related to greater pain interference, substance craving, as well as worse anxiety and mood symptoms ( Kneeland et al., 2019 ). Mechanistically, pain catastrophizing is associated with over-attending to affective and sensory pain stimuli, an attention bias that hinders the ability to inhibit pain-related thoughts ( Quartana et al., 2009 ; Van Damme et al., 2002 , 2004 ). Importantly, pain-associated negative emotions may exert stronger cognitive effects than pain itself, with a series of studies providing evidence that pain-related fear was more disabling than pain duration, pain intensity, or negative affect ( Crombez et al., 1999 ). One SUD framework that may inform our understanding of pain catastrophizing in SUD is the Reinforcer Pathology theory. Reinforcer Pathology is a behavioral economics-guided theory of decision-making that delineates how individuals place subjective value on the future to guide behavior ( Bickel et al., 2017 , 2019 , 2020 ; Bickel & Athamneh, 2020 ). Specifically, the temporal distance individuals’ factor into their decision-making (i.e., the temporal window) determines the subjective value of a reinforcer ( Bickel & Athamneh, 2020 ). The temporal window is indexed by delay discounting - a preference for smaller, immediate rewards over larger, delayed rewards - also referred to as an immediacy bias. In this, individuals with an immediacy bias confer greater value on unhealthy immediate, intense, and reliable reinforcers (e.g., substances) while undervaluing temporally extended prosocial reinforcers (e.g., improved health in SUD recovery). Greater delay discounting is a proposed biomarker of addiction ( Bickel et al., 2014 ) that is robustly associated with SUD, including substance use initiation ( Audrain-McGovern et al., 2009 ) and worse SUD severity and worse treatment outcomes ( Albein-Urios et al., 2012 ; Exum et al., 2023 ; Johnson et al., 2007 ). Conversely, lower DD is associated with an increased probability of SUD remission ( Athamneh et al., 2023 ; Athamneh et al., 2022 ; Craft et al., 2022 ; Dwyer et al., 2023 ), more time in recovery ( Craft et al., 2021 ), and better QOL ( Athamneh et al., 2022 ; Rubenis et al., 2018 ). Relationships between delay discounting and pain have also been characterized, with higher discounting rates associated with higher pain severity ( Craft et al., 2021 ; Tompkins et al., 2016 ; Wakaizumi et al., 2019 ), and recently, pain-related anxiety ( Białaszek et al., 2023 ) and pain catastrophizing ( Mistretta et al., 2022 ). The purpose of this study was to understand if the Reinforcer Pathology framework can be useful in understanding how the cognitive-emotional experience of pain affects recovery outcomes. Specifically, we examined the relationship between delay discounting, pain catastrophizing, and multidimensional SUD recovery outcomes including remission and QOL. In the context of pain, individuals with an immediacy bias may attend to their physical pain more and with a higher emotional valence (i.e., ruminating, magnifying, and feeling helpless) engendering a negative state that is related to poorer recovery outcomes such as reduced QOL and likelihood of remission. Thus, we hypothesized that greater discounting would be associated with greater pain catastrophizing as well as a reduced likelihood of remission and poorer QOL among individuals in SUD recovery.