The well-accepted biopsychosocial model proposes that the experience of pain and responses to it result from a complex interaction of biological, psychological, and social factors. However, the separation of these constructs is substantially artificial, and we presume that psychological processes have biological effects, that biological processes affect an individual's psychosocial environment, and so on. Considerable research has demonstrated that pain-coping strategies influence perceived pain intensity and physical functioning, and individual differences in styles of pain coping even shape the persistence of long-term pain complaints in some populations. A good deal of this coping research has focused on catastrophizing, which is a generally maladaptive cognitive and emotional mental set that involves feelings of helplessness when in pain, rumination about pain symptoms, and magnification of pain-related complaints. Collectively, catastrophizing has been consistently associated with heightened experiences of pain across a variety of samples. Although catastrophic thinking regarding pain-related symptoms is often classified under the "psychologic" category within the broader biopsychosocial model, we propose that catastrophizing exerts biologic effects that may account for some of its negative consequences. In general, the cognitive and affective processes captured within the construct of catastrophizing may exert effects on the neuromuscular, cardiovascular, immune, and neuroendocrine systems, and on the activity in the pain neuromatrix within the brain. The interface between pain-related neurobiology and processes such as pain-related catastrophizing represents an important avenue for future pain research.