By Katie Hardy and Henry Pollard
The stress response is a natural reaction by the body, against potentially harmful stimuli to enhance the chance for survival. Persistent activation of the stress response can cause changes to homeostatic mechanisms. The study of stress neurophysiology, in the evaluation of the manifestation of disease in the body, suggests that these chronic changes have detrimental effects on sub cortical structures. Furthermore, there is much scientific support for the notion that chronic activation of supraspinal systems will lead to maladaptation of homeostatic mechanisms, causing the impairment of processes within the body, and ultimately leading to visceral disorders. The chiropractic profession for many years has alluded to chronic change of neurophysiological pathways as a potential explanation of visceral disorders, but the profession has typically described these in terms of somatovisceral or viscerosomatic reflex activity. Change in supraspinal neurophysiological efferent activity is increasingly being used to explain "stress" related disease. The chiropractic profession should consider investigating such stress responses by conducting spinal manipulative therapy trials that evaluate supraspinal effects of manipulation. Such research may help elucidate key mechanisms associated with the change of visceral disorders noted by some chiropractors following manipulative therapy.
Read more...
Be the first to rate this post
- Currently 0/5 Stars.
- 1
- 2
- 3
- 4
- 5
|
Exposure to stressful events during development has consistently been shown to produce long-lasting alterations in the hypothalamic-pituitary-adrenal (HPA) axis, which may increase vulnerability to disease, including posttraumatic stress disorder and other mood and anxiety disorders. Recently reported genetic association studies indicate that these effects may be mediated, in part, by gene×environment interactions involving polymorphisms within two key genes, CRHR1 and FKBP5. Data suggest that these genes regulate HPA axis function in conjunction with exposure to child maltreatment or abuse. In addition, a large and growing body of preclinical research suggests that increased activity of the amygdala-HPA axis induced by experimental manipulation of the amygdala mimics several of the physiological and behavioral symptoms of stress-related psychiatric illness in humans. Notably, interactions between the developing amygdala and HPA axis underlie critical periods for emotional learning, which are modulated by developmental support and maternal care. These translational findings lead to an integrated hypothesis: high levels of early life trauma lead to disease through the developmental interaction of genetic variants with neural circuits that regulate emotion, together mediating risk and resilience in adults. Depression and Anxiety Depression and Anxiety 26:984-992, 2009. Published 2009 Wiley-Liss, Inc.
| Charles F. Gillespie, M.D. Ph.D. 1, Justine Phifer, B.A. 1, Bekh Bradley, Ph.D. 1 2, Kerry J. Ressler, M.D. Ph.D. 1 3 4 * |
1Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia
2Atlanta Veterans Affairs Hospital, Atlanta, Georgia
3Yerkes National Primate Research Center, Emory University, Atlanta, Georgia
4Howard Hughes Medical Institute, Chevy Chase, Maryland
|
http://www3.interscience.wiley.com/journal/122596389/abstract?CRETRY=1&SRETRY=0
|
Be the first to rate this post
- Currently 0/5 Stars.
- 1
- 2
- 3
- 4
- 5