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Food allergies affect up to 8% of children in the United States and may occasionally lead to severe life-threatening reactions. Because there is currently no cure for food allergies, strict avoidance of the allergen-containing foods is the only means of preventing an allergic reaction. Consumers rely on food manufacturers to reliably track and declare the presence of food allergens in products. Over the past 10 to 20 years, the food industry has increasingly adopted allergen control approaches in its processing facilities. However, the major industry costs related to food allergen management have not been fully described. The objective of this study was to characterize the factors that contribute to the economic impact of food allergen control practices on the food industry. A focus group (n = 100) was conducted with food industry professionals to identify key areas of cost for food allergen management. A survey based on the domains identified was then developed and disseminated to a convenience sample (n = 50) of quality control food industry specialists with knowledge of their company's food allergen management practices. Nearly all companies (92%) produced food products containing one or more of the top eight allergenic foods recognized by the U.S. Food and Drug Administration or sesame seeds. Cleaning procedures, employee training, and the potential for a recall due to allergen cross-contact were most frequently rated as the important factors in food allergen management. Recalls due to food allergen cross-contact, cleaning procedures, equipment and premises design, and employee training were ranked as the greatest allergen management expenses. Although 96% of companies had a food allergen control plan in place, nearly half (42%) had at least one food allergen-related recall within the past 5 years. The industry appears to endorse a willingness to unify precautionary allergen labeling to communicate a clear message more effectively to consumers.

Use of opioid analgesics for management of chronic nonmalignant pain has become common, yet there are presently no well-validated predictors of optimal opioid analgesic efficacy. We examined whether psychosocial factors (eg, depressive symptoms) predicted changes in spontaneous low back pain after administration of opioid analgesics, and whether endogenous opioid (EO) function mediated these relationships. Participants with chronic low back pain but who were not chronic opioid users (N = 89) underwent assessment of low back pain intensity pre- and post-drug in 3 (counterbalanced) conditions: (1) placebo, (2) intravenous naloxone, and (3) intravenous morphine. Comparison of placebo condition changes in back pain intensity to those under naloxone and morphine provided indexes of EO function and opioid analgesic responses, respectively. Results showed that (1) most psychosocial variables were related significantly and positively to morphine analgesic responses for low back pain, (2) depressive symptoms, trait anxiety, pain catastrophizing, and pain disability were related negatively to EO function, and (3) EO function was related negatively to morphine analgesic responses for low back pain. Bootstrapped mediation analyses showed that links between morphine analgesic responses and depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability were partially mediated by EO function. Results suggest that psychosocial factors predict elevated analgesic responses to opioid-based medications, and may serve as markers to identify individuals who benefit most from opioid therapy. Results also suggest that people with greater depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability may have deficits in EO function, which may predict enhanced response to opioid analgesics.

Poor sleep quality among people with chronic low back pain appears to be related to worse pain, affect, poor physical function, and pain catastrophizing. The causal direction between poor sleep and pain remains an open question, however, as does whether sleep quality exerts effects on low back pain differently across the course of the day. This daily diary study examined lagged temporal associations between prior night sleep quality and subsequent day pain, affect, physical function and pain catastrophizing, the reverse lagged temporal associations between prior day pain-related factors and subsequent night sleep quality, and whether the time of day during which an assessment was made moderated these temporal associations. Chronic low back pain patients (n = 105) completed structured electronic diary assessments five times per day for 14 days. Items included patient ratings of their pain, affect, physical function, and pain catastrophizing. Collapsed across all observations, poorer sleep quality was significantly related to higher pain ratings, higher negative affect, lower positive affect, poorer physical function, and higher pain catastrophizing. Lagged analyses averaged across the day revealed that poorer prior night sleep quality significantly predicted greater next day patient ratings of pain, and poorer physical function and higher pain catastrophizing. Prior poorer night sleep quality significantly predicted greater reports of pain, and poorer physical function, and higher pain catastrophizing, especially during the early part of the day. Sleep quality × time of day interactions showed that poor sleepers reported high pain, and negative mood and low function uniformly across the day, whereas good sleepers reported relatively good mornings, but showed pain, affect and function levels comparable to poor sleepers by the end of the day. Analyses of the reverse causal pathway were mostly nonsignificant. Sleep quality appears related not only to pain intensity but also to a wide range of patient mood and function factors. A good night’s sleep also appears to offer only temporary respite, suggesting that comprehensive interventions for chronic low back pain not only should include attention to sleep problems but also focus on problems with pain appraisals and coping.

Self-report measures of emotional expression are common, but their validity to predict objective emotional expression, particularly of anger, is unclear. We tested the validity of the Anger Expression Inventory (AEI; Spielberger et al., 1985)), Emotional Approach Coping Scale (EAC; Stanton, Kirk, Cameron & Danoff-Burg, 2000), and Toronto Alexithymia Scale-20 (TAS-20; Bagby, Taylor, & Parker, 1994) to predict objective anger expression in 95 adults with chronic back pain. Participants attempted to solve a difficult computer maze by following the directions of a confederate who treated them rudely and unjustly. Participants then expressed their feelings for 4 minutes. Blinded raters coded the videos for anger expression, and a software program analyzed expression transcripts for anger-related words. Analyses related each questionnaire to anger expression. The AEI anger-out scale predicted greater anger expression, as expected, but AEI anger-in did not. The EAC emotional processing scale predicted less anger expression, but the EAC emotional expression scale was unrelated to anger expression. Finally, the TAS-20 predicted greater anger expression. Findings support the validity of the AEI anger-out scale but raise questions about the other measures. The assessment of emotional expression by self-report is complex and perhaps confounded by general emotional experience, the specificity or generality of the emotion(s) assessed, and self-awareness limitations. Performance-based or clinician-rated measures of emotion expression are needed.

The development of an injectable biomaterial that supports cell survival and maintains or promotes nucleus pulposus (NP) phenotype could aid delivery of cells to degenerated NPs causing low back pain. Mesenchymal cells were loaded and grown in a synthetic peptide gel, PuraMatrix ® . Cells were observed within the gels over 0–28 days, and accumulation of glycosaminoglycans were detected by histological staining. The mechanical properties of the cell-loaded constructs, and the change of the mechanical properties were studied using stress relaxation of the gels under compression and confinement. The PuraMatrix ® gel was shown to relax fast on compression indicating that the fluid could easily flow out of the gel, and thus indicating the presence of large pores/voids. The presence of these pores/voids was further supported by high mobility of dextran molecules, determined using fluorescence recovery after photo bleaching. The stress required to deform the cell-loaded constructs to a specific strain increases at day 21, at which point the presence of glycosaminoglycans within the cell-loaded constructs was also observed. The results provide evidence of changes in mechanical properties of the PuraMatrix ® matrix upon excretion of the extracellular matrix by the cells.

Recent studies suggest that participant expectations influence pain ratings during conditioned pain modulation testing. The present study extends this work by examining expectancy effects among individuals with and without chronic back pain after administration of placebo, naloxone, or morphine. This study aims to identify the influence of individual differences in expectancy on changes in heat pain ratings obtained before, during, and after a forearm ischemic pain stimulus. Participants with chronic low back pain (n = 88) and healthy controls (n = 100) rated heat pain experience (i.e., “test stimulus”) before, during, and after exposure to ischemic pain (i.e., “conditioning stimulus”). Prior to testing, participants indicated whether they anticipated that their heat pain would increase, decrease, or remain unchanged during ischemic pain. Analysis of the effects of expectancy (pain increase, decrease, or no change), drug (placebo, naloxone, or morphine), and group (back pain, healthy) on changes in heat pain revealed a significant main effect of expectancy (p = 0.001), but no other significant main effects or interactions. Follow-up analyses revealed that individuals who expected lower pain during ischemia reported significantly larger decreases in heat pain as compared with those who expected either no change (p = 0.004) or increased pain (p = 0.001). The present findings confirm that expectancy is an important contributor to conditioned pain modulation effects, and therefore significant caution is needed when interpreting findings that do not account for this individual difference. Opioid mechanisms do not appear to be involved in these expectancy effects.

The Communal Coping Model characterizes pain catastrophizing as a coping tactic whereby pain expression elicits assistance and empathic responses from others. Married couples (N = 105 couples; 1 spouse with chronic low back pain) completed electronic daily diary assessments 5 times/day for 14 days. In these diaries, patients reported pain catastrophizing, pain, and function, and perceived spouse support, perceived criticism, and perceived hostility. Non-patient spouses reported on their support, criticism, and hostility directed toward patients, as well as their observations of patient pain and pain behaviors. Hierarchical linear modeling tested concurrent and lagged (3 hours later) relationships. Principal findings included the following: a) within-person increases in pain catastrophizing were positively associated with spouse reports of patient pain behavior in concurrent and lagged analyses; b) within-person increases in pain catastrophizing were positively associated with patient perceptions of spouse support, criticism, and hostility in concurrent analyses; c) within-person increases in pain catastrophizing were negatively associated with spouse reports of criticism and hostility in lagged analyses. Spouses reported patient behaviors that were tied to elevated pain catastrophizing, and spouses changed their behavior during and after elevated pain catastrophizing episodes. Pain catastrophizing may affect the interpersonal environment of patients and spouses in ways consistent with the Communal Coping Model. Perspective Pain catastrophizing may represent a coping response by which individuals’ pain expression leads to assistance or empathic responses from others. Results of the present study support this Communal Coping Model, which emphasizes interpersonal processes by which pain catastrophizing, pain, pain behavior, and responses of significant others are intertwined.

For people with chronic pain, anger-related factors are significantly associated with pain intensity, mood and physical function such that greater anger is related to poorer adjustment (Janssen, Spinhoven, & Brosschot, 2001; Kerns, Rosenberg, & Jacob, 1994; Nicholson, Gramling, Ong, & Buenevar, 2003; Wade, Price, Hamer, Schwartz & Hart, 1990). Evidence suggests that how anger is regulated – expression, inhibition – may have greater consequences for chronic pain patients’ pain and function than their level of state anger (Bruehl, Chung, & Burns, 2006; Bruehl, Burns, Chung, Ward, & Johnson, 2002; Burns et al., 2008). Anger expression may be related to pain and function along at least two pathways. First, it has been proposed that people who tend to verbally or physically express anger and who exhibit high pain sensitivity may be characterized by deficits in endogenous inhibitory mechanisms (Bruehl et al., 2002). Findings support this model and indicate that chronic pain patients and healthy people alike who are high in trait anger-expressiveness show evidence of deficient endogenous opioid function, thus leaving them with elevated pain sensitivity (Bruehl et al., 2002). Second, a symptom-specific reactivity model (Flor, Turk & Birbaumer, 1985) has been adapted for anger and chronic pain, and holds that anger arousal may lead to increases in muscle tension near the site of injury, and thereby increase pain (Burns, Bruehl, & Quartana, 2006). In the case of chronic low back pain (CLBP) patients, the relevant muscles would be in the low back (e.g., lower paraspinal [LP] muscles). Results support this model, and indicate that anger arousal among CLBP patients produces greater increases in LP muscle tension than sadness (Burns, 2006), and that CLBP patients with elevated trait anger-expressiveness showed greater increases in LP muscle tension during anger arousal than those low in trait anger-expressiveness (Burns et al., 2006). Anger inhibition may be related to pain and function also along at least two pathways. First, a thought suppression model (Wegner, 1994) was adapted for anger inhibition and pain, and holds that inhibiting anger has the ironic consequence of amplifying and maintaining anger which in turn exerts delayed negative effects on responses to later events (Burns, Quartana, & Bruehl, 2008). Thus, inhibiting anger can worsen later pain perception as ironically sustained thoughts of anger contaminate the experience of pain. Results support this model in that chronic pain patients and healthy people who inhibited anger during anger arousal showed greater increases in anger during anger-induction and reported greater anger and pain intensity during subsequent acute pain-induction than those who did not inhibit anger during anger arousal (Burns, 2008; Quartana & Burns 2007). Second, the symptom-specific reactivity model may also apply to anger inhibition. Findings showed that CLBP patients evinced greater increases in LP muscle tension while inhibiting anger during anger arousal than those not inhibiting, and these increases were shown to predict the frequency of observable pain behaviors during subsequent pain induction (Burns, Quartana, Gilliam, Matsuura, Nappi, & Wolfe, 2012). These conceptual models support hypotheses that both anger expression and inhibition can lead to increased pain sensitivity and intensity, and may do so via distinct pathways. Findings from numerous cross-sectional questionnaire and lab-based studies support these contentions (Bruehl et al., 2006; Burns et al., 2008). However, the questionnaire studies based on traits tell us little about the effects of actual anger regulation behaviors on pain and functioning, and although some lab-based studies did manipulate anger arousal, anger regulation behavior and pain in controlled conditions, ecological validity is limited by the artificial nature of the procedures. Thus, we know little about relationships between what people actually do in everyday life to regulate anger and their pain and function. Results of two recent daily diary studies help address this shortcoming. In the first study (van Middendorp, Lumley, Moerbeek, Jacobs, Bijlsma, & Geenen, 2010), results suggested that behavioral anger expression during an anger-provoking event during the day was related to elevated end-of-day pain. They also reported that state anger was related to higher end-of-day pain. This design did not include true lagged analyses, so it is not clear whether anger predicted pain or vice versa. In the second study (Bruehl, Liu, Burns, Chont, & Jamison, 2012), results of lagged analyses suggested that behavioral anger expression during one period was related to elevated pain in the subsequent period, providing the first evidence of a longitudinal effect. Their assessment was limited, however, only to anger expression and patient rated pain intensity, and, moreover, did not include state anger. In the present study, we used electronic diary methods to replicate and extend prior work, and evaluate the degree to which patient feelings of anger and behavioral anger regulation – both expression and inhibition – occurring in the course of daily life was related to both patient pain and function as rated by patients. In addition, these data were collected as part of a larger study that also included spouse ratings of patient pain and function (Burns et al., in press). Specifically, patients with chronic low back pain (CLBP) and their spouses completed electronic diary entries 5 times/day for 14 days using Personal Data Assistants (PDAs). On one level, if anger arousal and/or behavioral anger regulation, as it occurs in everyday life, are related to pain and function, then concurrent analyses would show relationships between increases in state anger, anger expression and/or inhibition and fluctuations in pain and function. Further, if anger arousal and/or behavioral anger regulation actually influence pain and function, then lagged analyses would show that initial increases in state anger, anger expression and/or inhibition predict later fluctuations in pain and function, particularly in the case of anger inhibition given prior evidence of delayed effects on pain (Burns et al. 2008) (i.e., anger → pain). Alternatively, it may be the case, as suggested by results of Feldman, Downey and Schiffer-Neitz (1999), that initial pain intensity could predispose someone to experience later anger and the need to regulate it, and thus initial increases in pain would predict later fluctuations in anger arousal, anger expression and/or inhibition (i.e., pain → anger). On another level, if increases in anger arousal, anger expression and/or inhibition are indeed related to changes in patient pain and function, these increases should be related to demonstrable pain and function changes that can be observed by reporters other than the patient. We hypothesized that patient-reported increases in their anger arousal, behavioral anger expression and/or inhibition would be related to spouse ratings of observable patient behavior. Finally, the need to regulate anger presupposes the presence of anger arousal. If patient behavioral anger regulation per se is a key phenomenon related to current and later pain and function, then anger regulation factors should exert unique effects beyond those attributable to anger arousal alone. To address this issue, we controlled for either concurrent state anger or lagged state anger where relevant. Note that because anger arousal is a core and necessary constituent of the phenomenon “anger regulation,” statistically controlling for state anger represents a conservative and stringent approach.

Chronic pain is associated with elevated negative emotions, and resources needed to adaptively regulate these emotions can be depleted during prolonged pain. Studies of links between pain, function, and negative emotions in people with chronic pain, however, have focused almost exclusively on relationships among mean levels of these factors. Indexes that may reflect aspects of emotion regulation have typically not been analyzed. We propose that 1 index of emotion regulation is variability in emotion over time as opposed to average emotion over time. The sample was 105 people with chronic low back pain and 105 of their pain-free spouses. They completed electronic diary measures 5x/d for 14 consecutive days, producing 70 observations per person from which we derived estimates of within-subject variance in negative emotions. Location-scale models were used to simultaneously model predictors of both mean level and variance in patient negative emotions over time. Patients reported significantly more variability in negative emotions compared to their spouses. Patients who reported higher average levels of pain, pain interference, and downtime reported significantly higher levels of variability in negative emotions. Spouse-observed pain and pain behaviors were also associated with greater variability in patients' negative emotions. Test of the inverse associations between negative emotion level and variability in pain and function were significant but weaker in magnitude. These findings support the notion that chronic pain may erode negative emotion regulation resources, to the potential detriment of intra- and inter-personal function.

Long-term use of opioid analgesics may be ineffective or associated with significant negative side effects for some people. At present, there is no sound method of identifying optimal opioid candidates. Individuals with chronic low back pain (n = 89) and healthy control individuals (n = 102) underwent ischemic pain induction with placebo, opioid blockade (naloxone), and morphine in counterbalanced order. They completed the Spielberger Anger-Out subscale. Endogenous opioid function × Anger-out × Pain status (chronic pain, healthy control) interactions were tested for morphine responses to ischemic threshold, tolerance, and pain intensity (McGill Sensory and Affective subscales) and side effects. For individuals with chronic pain and healthy control participants, those with low endogenous opioid function and low anger-out scores exhibited the largest morphine analgesic responses, whereas those with high anger-out and low endogenous opioid function showed relatively weaker morphine analgesic responses. Further, individuals with chronic pain with low endogenous opioid function and low anger-out scores also reported the fewest negative effects to morphine, whereas those with low endogenous opioid function and high anger-out reported the most. Findings point toward individuals with chronic pain who may strike a favorable balance of good analgesia with few side effects, as well as those who have an unfavorable balance of poor analgesia and many side effects. Perspective We sought to identify optimal candidates for opioid pain management. Low back pain patients who express anger and also have deficient endogenous opioid function may be poor candidates for opioid therapy. In contrast, low back patients who tend not to express anger and who also have deficient endogenous opioid function may make optimal candidates for opioid therapy.

Factors underlying differential responsiveness to opioid analgesic medications used in chronic pain management are poorly understood. We tested whether individual differences in endogenous opioid inhibition of chronic low-back pain were associated with the magnitude of acute reductions in back pain ratings after morphine administration.In randomized counterbalanced order over three sessions, 50 chronic low-back pain patients received intravenous naloxone (8 mg), morphine (0.08 mg/kg), or placebo. Back pain intensity was rated predrug and again after peak drug activity was achieved using the McGill Pain Questionnaire-Short Form (Sensory and Affective subscales, VAS Intensity measure). Opioid blockade effect measures to index degree of endogenous opioid inhibition of back pain intensity were derived as the difference between predrug to postdrug changes in pain intensity across placebo and naloxone conditions, with similar morphine responsiveness measures derived across placebo and morphine conditions.Morphine significantly reduced back pain compared with placebo (McGill Pain Questionnaire-Short Form Sensory, VAS; P0.01). There were no overall effects of opioid blockade on back pain intensity. However, individual differences in opioid blockade effects were significantly associated with the degree of acute morphine-related reductions in back pain on all measures, even after controlling for effects of age, sex, and chronic pain duration (P0.03). Individuals exhibiting greater endogenous opioid inhibition of chronic back pain intensity reported less acute relief of back pain with morphine.Morphine appears to provide better acute relief of chronic back pain in individuals with lower natural opioidergic inhibition of chronic pain intensity. Possible implications for personalized medicine are discussed.

Chronic musculoskeletal pain can strain marriages, perhaps even to the point of engendering spouse criticism and hostility directed toward patients. Such negative spouse responses may have detrimental effects on patient well-being. While results of cross-sectional studies support this notion, we extended these efforts by introducing expressed emotion (EE) and interpersonal theoretical perspectives, and by using electronic diary methods to capture both patient and spouse reports in a prospective design. Chronic low back pain (CLBP) patients and their spouses (N = 105 couples) reported on perceived spouse behavior and patient pain 5 times/day for 14 days using Personal Data Assistants (PDAs). Concurrent and lagged within-couple associations between patient's perceptions of spouse criticism/hostility and patient self-reported pain and spouses’ observations of patient pain behaviors revealed that 1) patient perceived spouse criticism and hostility were correlated significantly with pain intensity, and spouse observed patient pain behavior was related significantly with patient perceived hostility at the same time point; 2) patient perceived spouse hostility significantly predicted patient pain intensity three hours later, and spouse observed pain behaviors significantly predicted patient perceived spouse hostility three hours later. Results support both EE and interpersonal models, and imply that a comprehensive model would combine these conceptualizations to fully illustrate how spouse criticism/hostility and patient pain interact to produce a negative spiral. Given that marital interactions are amenable to clinical intervention, improved insight into how spouse behavior and patient pain are tightly linked will encourage productive translational efforts to target this neglected area.

Predictors of responsiveness to opioid analgesic medications are not well understood. This study tested whether individual differences in endogenous opioid (EO) function are associated with analgesic responsiveness to morphine. In randomized, counterbalanced order over 3 sessions, 45 chronic low back pain participants and 31 healthy controls received an opioid antagonist (8 mg naloxone), morphine (0.08 mg/kg), or placebo. Participants then engaged in 2 laboratory-evoked pain tasks (ischemic and thermal). Outcomes included pain threshold, pain tolerance, and pain ratings. Indexes of EO function and morphine analgesic responsiveness were derived for each measure as the difference in pain responses between the placebo condition and naloxone or morphine condition, respectively. For all 7 pain measures across the 2 laboratory pain tasks, greater EO function was associated with significantly lower morphine analgesic responsiveness (P

OBJECTIVES Clinically feasible predictors of opioid analgesic responses for use in precision pain medicine protocols are needed. This study evaluated whether resting plasma β-endorphin (BE) levels predicted responses to an opioid analgesic, and whether chronic pain status or sex moderated these effects. METHODS Participants included 73 individuals with chronic low back pain (CLBP) and 88 pain-free controls, all using no daily opioid analgesics. Participants attended 2 identical laboratory sessions during which they received either intravenous morphine (0.08 mg/kg) or saline placebo, with blood samples obtained before drug administration to assay resting plasma BE levels. Once peak drug activity was achieved in each session, participants engaged in an ischemic forearm pain task (ISC) and a heat pain task. Morphine analgesic effects were derived reflecting the difference in pain outcomes between placebo and morphine conditions. RESULTS In hierarchical regressions, significant Type (CLBP vs. control)×BE interactions (Ps

Objective To determine the degree to which anger arousal and anger regulation (expression, inhibition) in the daily lives of people with chronic pain were related to spouse support, criticism, and hostility as perceived by patients and as reported by spouses. Method Married couples (N = 105, 1 spouse with chronic low back pain) completed electronic daily diaries, with assessments 5 times/day for 14 days. On these diaries, patients completed items on their own anger arousal, anger expression, and inhibition, and on perceived spouse support, criticism, and hostility. Spouses reported on their responses toward patients and their negative affect. Hierarchical linear modeling tested concurrent and lagged relationships. Results Patient-reported increases in anger arousal and anger expression were predominantly related to concurrent decreases in patient-perceived and spouse-reported spouse support, concurrent increases in patient-perceived and spouse-reported spouse criticism and hostility, and increases in spouse-reported negative affect. Relationships for anger expression remained significant with anger arousal controlled. These effects were especially strong for male patients. Spouses reported greater negative affect when patients were present than when they were not. Conclusions Social support may facilitate adjustment to chronic pain, with declining support and overt criticism and hostility possibly adversely impacting pain and function. Results suggest that patient anger arousal and expression may be related to a negative interpersonal environment for married couples coping with chronic low back pain.

The Screener and Opioid Assessment for Patients with Pain–Revised (SOAPP-R) predicts increased risk of opioid misuse in chronic pain patients. We evaluated whether higher SOAPP-R scores are associated with greater opioid reinforcing properties, potentially contributing to their predictive utility. Across 2 counterbalanced laboratory sessions, 55 chronic low back pain sufferers completed the SOAPP-R at baseline and measures of back pain intensity, evoked pain responsiveness (thermal, ischemic), and subjective opioid effects after receiving intravenous morphine (.08 mg/kg) or saline placebo. Morphine effect measures were derived for all outcomes, reflecting the difference between morphine and placebo condition values. Higher SOAPP-R scores were significantly associated with greater desire to take morphine again, less feeling down and feeling bad, and greater reductions in sensory low back pain intensity following morphine administration. This latter effect was due primarily to SOAPP-R content assessing medication-specific attitudes and behavior. Individuals exceeding the clinical cutoff (18 or higher) on the SOAPP-R exhibited significantly greater morphine liking, desire to take morphine again, and feeling sedated; less feeling bad; and greater reductions in sensory low back pain following morphine. The SOAPP-R may predict elevated opioid risk in part by tapping into individual differences in opioid reinforcing effects. Perspective Based on placebo-controlled morphine responses, associations were observed between higher scores on a common opioid risk screener (SOAPP-R) and greater desire to take morphine again, fewer negative subjective morphine effects, and greater analgesia. Opioids may provide the best analgesia in those patients at greatest risk of opioid misuse.

Our recent work indicates that endogenous opioid activity influences analgesic responses to opioid medications. This secondary analysis evaluated whether endogenous opioid activity is associated with degree of opioid analgesic adverse effects, and whether chronic pain status and sex affect these adverse effects.Using a double-blind, randomized, placebo-controlled, crossover design, 51 subjects with chronic low back pain and 38 healthy controls participated in 3 separate sessions, undergoing 2 laboratory-evoked pain tasks (ischemic and thermal) after receiving placebo, naloxone, or morphine. Endogenous opioid system function was indexed by the difference in pain responses between the placebo and naloxone conditions. These measures were examined for associations with morphine-related adverse effects.Chronic pain subjects reported significantly greater itching and unpleasant bodily sensations with morphine than controls (P0.05). Across groups, only 6 of 112 possible associations between adverse effects and blockade effects were significant. For the ischemic task, higher endogenous opioid function was associated with greater itching (visual analog scale [VAS]; P0.05), numbness (tolerance; P0.001), dry mouth (tolerance; P0.05), and unpleasant bodily sensations (VAS; P0.05). For the thermal task, higher endogenous opioid function was associated with greater numbness (VAS; P0.05) and feeling carefree (VAS; P0.05). There were no significant main or interaction effects of chronic pain status or sex on these findings.No consistent relationships were observed between endogenous opioid function and morphine-related adverse effects. This is in stark contrast to our previous observation of strong relationships between elevated endogenous opioid function and smaller morphine analgesic effects.