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Childhood trauma and risk for chronic fatigue syndrome: Association with neuroendocrine dysfunction

Heim C, Nater UM, Maloney E, Boneva R, Jones JF, Reeves WC
Archives of General Psychiatry 2009; Vol. 66 (1): 72-80.

Summary

CFS affects up almost 3% of the US adult population. A quarter of those suffering the illness are unemployed or receiving disability and families in which a member has CFS loose about $20,000 annually in earnings and wages. The causes and mechanisms involved in the illness remain unknown and effective prevention/treatment is elusive. Identifying risk factors for CFS is critical to guide pathophysiological research and devise therapeutic targets. It is increasingly clear that persons with CFS have altered responses to physical, mental, and emotional stressors. Moreover, physical, infectious, and emotional stressors are risk or triggering factors of CFS. A large body of evidence shows that stress early in life (such as childhood abuse, neglect and loss), within a genetic window of vulnerability, permanently programs an individual’s responsiveness to subsequent stress throughout the lifespan. These long-term consequences of early life stress occur through direct effects on brain circuits involved in the mediation of cognitive-emotional regulation, vigilance, arousal, and the integration of endocrine, autonomic, and immune regulatory systems. Of note, similar changes in these circuits and regulatory outflow systems have been implicated in the pathophysiology of CFS. The current study confirms and extends results from early studies of CFS. We found that severe childhood trauma, in particular sexual abuse, emotional abuse, and emotional neglect were associated with a 6-fold increased risk for CFS and risk of CFS increased with increasing severity of the childhood abuse. In addition, neuroendocrine dysfunction, manifested by decreased salivary cortisol awakening response, was associated with childhood trauma in CFS, likely reflecting a biological correlate of vulnerability due to early developmental insults. The findings from this study are particularly important because we evaluated persons with CFS and well controls identified from the general Georgia population rather than clinical settings. Thus, the results can be generalized to the population of persons suffering from CFS. Our findings lend further support for the hypothesis that CFS represents a disorder of adaptation that is promoted by early environmental insults, leading to failure to compensate in response to challenge. The hypocortisolism likely reflects a marker for the risk of developing CFS rather than being a sign of the syndrome itself.

Abstract

Context: Childhood trauma appears to be a potent risk factor for chronic fatigue syndrome (CFS). Evidence from developmental neuroscience suggests that early experience programs the development of regulatory systems that are implicated in the pathophysiology of CFS, including the hypothalamic pituitary-adrenal axis. However, the contribution of childhood trauma to neuroendocrine dysfunction in CFS remains obscure.

Objective: To replicate findings on the relationship between childhood trauma and risk for CFS and to evaluate the association between childhood trauma and neuroendocrine dysfunction in CFS.

Design, Setting, and Participants: A case-control study of 113 persons with CFS and 124 well controls identified from a general population sample of 19,381 adult residents of Georgia.

Main Outcome Measures: Self-reported childhood trauma (sexual, physical, and emotional abuse; emotional and physical neglect), psychopathology (depression, anxiety, and posttraumatic stress disorder), and salivary cortisol response to awakening.

Results: CFS cases reported significantly higher levels of childhood trauma and psychopathology than controls. Exposure to childhood trauma was associated with 6-fold increased risk for CFS. Sexual abuse, emotional abuse and emotional neglect were most effective in discriminating CFS cases from controls. There was a graded relationship between exposure level and CFS risk. Risk for CFS conveyed by childhood trauma further increased with the presence of posttraumatic stress disorder symptoms. Only CFS cases with childhood trauma exposure, but not CFS cases without exposure, exhibited decreased salivary cortisol concentrations after awakening compared to controls.

Conclusion: Our results confirm childhood trauma as an important risk factor of CFS. In addition, neuroendocrine dysfunction, a hallmark feature of CFS, appears to be associated with childhood trauma, possibly reflecting a biological correlate of vulnerability due to early developmental insults. Our findings are critical to inform pathophysiological research and devise targets for the prevention of CFS.

Page last modified on January 5, 2009


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