Posttraumatic Oxytocin Dysregulation: Is It a Link Among Posttraumatic Self Disorders, Posttraumatic Stress Disorder, and Pelvic Visceral Dysregulation Conditions in Women?

Abstract

This article explicates a theory that oxytocin, a sexually dimorphic neurotransmitter and paracrine hormone, is a plausible mechanism linking early relational trauma with posttraumatic self disorders (e.g., dissociation, somatization, and interpersonal sensitivity), posttraumatic stress disorder, and pelvic visceral dysregulation disorders (e.g., irritable bowel syndrome, chronic pelvic pain, interstitial cystitis, and hyperemesis gravidarum). This posttraumatic oxytocin dysregulation disorders theory is consistent with the historical and contemporary literature. It integrates attention to psychological and physical comorbidities and could account for the increased incidence of these disorders among females. Specific propositions are explored in data from studies of traumatic stress and women's health.

Keywords:

• affect regulation
• attachment theory
• chronic pelvic pain
• dissociation
• hyperemesis gravidarum
• interstitial cystitis
• irritable bowel syndrome
• oxytocin
• posttraumatic stress
• women's health

Grant support for the empirical data included in this article comes from the following sources: National Institutes of Health Grant M01-RR00042 to the University of Michigan General Clinical Research Center, National Institutes of Health Grant U013786 to the University of Michigan Office of the Vice President for Research, National Institute of Nursing Research's MESA Center for Health Disparities Grant 1P20 NR008367, and National Institute of Nursing Research Grant R01 NR008767. This work used the Chemistry Core of the Michigan Diabetes Research and Training Center funded by Grant DK020572 from the National Institute of Diabetes and Digestive and Kidney Diseases. The content is solely the responsibility of the author and does not necessarily represent the official views of the National Institutes of Health. Michigan Medicaid data were made available by Health Management Associates, Inc., Lansing, Michigan, with the expert support of Dennis Roberts, PhD. Some of the analyses were supported by a dissertation grant from the Blue Cross and Blue Shield of Michigan Foundation, and others were completed while Dr. Julia Seng was a Pfizer Postdoctoral Fellow. The author would especially like to thank Janis Miller, Mickey Sperlich, Rachel Jeltema, and C. Sue Carter.