7th Annual BMRP Investigator Meeting - Abstract

 

Laura Mackner^1,a, Kathleen Pajer¹, Wallace Crandall² and Ronald Glaser³

 

¹Center for Biobehavioral Health and ²Division of Gastroenterology, Nationwide Children's Hospital (Columbus, Ohio, U.S.A.); ³Institute for Behavioral Medicine Research and Ohio State University (Columbus, Ohio, U.S.A.)

 

Youth with inflammatory bowel disease (IBD) are at significant risk for depression, and aspects of the inflammatory disease process may predispose them to depression symptoms. Two mechanisms may contribute to the development of depression in IBD: proinflammatory cytokines and a hypoactive hypothalamic-pituitary-adrenal (HPA) axis. Proinflammatory cytokines mediate inflammation and induce illness behaviors that mimic symptoms of depression. Individuals with inflammatory diseases also have hyporeactive HPA axes that fail to appropriately rein in the inflammatory process via cortisol. The hyporeactive HPA axis cannot respond appropriately to immune challenges or psychosocial stress, which may lead to vulnerability to both disease flares and depression symptoms. We are following children longitudinally to examine relationships between disease activity, proinflammatory cytokines, HPA axis functioning (cortisol), and depressive symptoms. Preliminary data indicate that children with active IBD have significantly more depression symptoms that are likely to be cytokine-related. During remission, our preliminary results suggest that there may be a shift in the specific symptoms that are endorsed, so that fewer cytokine-related symptoms are endorsed, and more “psychological” symptoms (e.g., hopelessness) are reported.

 

^aPrincipal Investigator