Dr. Joseph W. Ditre is an Assistant Professor of Psychology at Syracuse University. His research cuts across basic and applied work in the areas of health psychology and behavioral medicine, with an emphasis on the intersection of addictive behaviors and comorbid medical disorders. He has established a programmatic line of research that applies a multi-method approach to the study of complex and potentially bi-directional relations between the experience of acute/chronic pain and the use/misuse of addictive substances (e.g., nicotine/tobacco, alcohol, cannabis, prescription opioid medications), with the ultimate goal of translating these findings to inform the development of novel treatments for individuals with co-occurring pain and substance use disorders.
Joseph W. Ditre, Emily L. Zale, Jesse D. Kosiba, Martin J. De Vita, & Lisa R. LaRowe
To develop a human laboratory model of pain and smoking, and conduct the first assessment of experimental pain reactivity following a nicotine deprivation manipulation.
To test the hypothesis that current daily tobacco smokers who are randomized to overnight smoking abstinence (vs. continued ad lib smoking) would evince greater capsaicin-induced sensitivity to pain, neurogenic inflammation, and secondary hyperalgesia.
A recently proposed reciprocal model suggests that pain and smoking behavior interact in the manner of a positive feedback loop, resulting in greater pain and the maintenance of tobacco dependence. There is also reason to believe that abstaining from smoking may increase pain, which in turn may precipitate relapse. Increased pain as a function of smoking abstinence would likely undermine the goals of both pain and tobacco cessation interventions.
Results and Significance
Daily tobacco smokers (N = 165; 43% female; M CPD = 22) were randomized to either nicotine deprivation (12-24 hours smoking abstinence), minimal deprivation (2 hours smoking abstinence), or continued smoking conditions prior to undergoing pain induction using a capsaicin model that approximates key features of clinical pain. Results indicated that nicotine deprivation (relative to continued smoking) increased spontaneous pain intensity and unpleasantness ratings, neurogenic inflammation (area of visible flare), and secondary hyperalgesia (area of sensitivity to mechanical stimulation), thus implicating both central and peripheral mechanisms of action (ps < .05). The effects of nicotine deprivation on pain intensity/unpleasantness ratings were further shown to be mediated by severity of nicotine withdrawal (ps < .05). These findings suggest that smokers with co-occurring pain may experience a variety of negative pain-related sequelae during the early stages of a quit attempt. Smokers in pain may benefit from tailored cessation and relapse-prevention interventions that account for the antithetical influence of smoking abstinence-induced amplification of pain.