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.