Depression, anxiety, and somatoform disorders are among the most prevalent psychiatric disorders; they have overlapping symptoms, and they frequently co-occur. In many respects, however, somatoform disorders, such as somatization disorder, have received the least attention from researchers. First, relatively few randomized controlled trials have been undertaken on these disorders, although some presumably related conditions, such as fibromyalgia, now have Food and Drug Administration approved drug treatments. Second, there are comparatively few studies of the neurobiology of these conditions, although there have been significant advances in the clinical neuroscience of pain. Third, there are few animal models of somatoform disorders, although, again, there have been important advances in the basic neuroscience of pain. Alvarez et al. (1) potentially provide new insights into this field by using a rodent model of early-life stress, restriction of nesting material (2,3). Maternal separation is a well-known model of early adversity, but the neonatal limited bedding (NLB) paradigm seems especially useful insofar as it results in erratic maternal care (rather than no care) and like other validated early-life stress models is accompanied by alterations in behavior and cognition, as well as in regulation of the hypothalamic-pituitary-adrenal axis (2,3). Furthermore, while maternal separation leads to inconsistent changes in pain thresholds, earlier work from the authors’ laboratory indicated that animals subjected to NLB demonstrate clear hyperalgesia and nociceptor sensitization later in life (4). Importantly, the NLB model is consistent with human studies demonstrating associations between early-life adversity and subsequent pain symptoms. And in the current publication, Alvarez et al. (1) contribute to understanding the underlying mechanisms that govern the association between early-life stress and subsequent hyperalgesia. In particular, they elegantly demonstrate roles for interleukin-6 and for the adrenal catecholamine system. These findings are broadly consistent with a growing animal and human literature demonstrating links between early exposure to environments characterized by adversity and subsequent disruptions in the endocrine, immune, and monoamine systems (5,6). More work will be needed to understand the precise genetic contributors and gene-environment interactions that lead to somatic symptoms. Indeed, the work of Alvarez et al. (1) would seem to provide a useful base for helping to build a translational neuroscience approach to DSM-IV somatization disorder or pain disorder. This would be consistent with a growing vision of psychosomatic medicine resting on a foundation of fundamental neuroscience (7). Such a vision nevertheless faces a number of challenges.