Childhood trauma and risk for chronic fatigue syndrome: association with neuroendocrine dysfunction.
BACKGROUND
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.


METHODS
A case-control study of 113 persons with CFS and 124 well control subjects identified from a general population sample of 19 381 adult residents of Georgia.


METHODS
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
Individuals with CFS reported significantly higher levels of childhood trauma and psychopathological symptoms than control subjects. Exposure to childhood trauma was associated with a 6-fold increased risk of 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. The risk of CFS conveyed by childhood trauma further increased with the presence of posttraumatic stress disorder symptoms. Only individuals with CFS and with childhood trauma exposure, but not individuals with CFS without exposure, exhibited decreased salivary cortisol concentrations after awakening compared with control subjects.


CONCLUSIONS
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. This possibly reflects a biological correlate of vulnerability due to early developmental insults. Our findings are critical to inform pathophysiological research and to devise targets for the prevention of CFS.
Heim
Christine
C
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Woodruff Memorial Research Bldg, Ste 4311, Atlanta, GA 30322, USA. cmheim@emory.edu
Nater
Urs M
UM
Maloney
Elizabeth
E
Boneva
Roumiana
R
Jones
James F
JF
Reeves
William C
WC
D000328:Adult; D001143:Arousal / Q000502:physiology; D016022:Case-Control Studies; D002648:Child; D002940:Circadian Rhythm / Q000502:physiology; D015673:Fatigue Syndrome, Chronic / Q000175:diagnosis / Q000503:physiopathology* / Q000523:psychology; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008016:Life Change Events; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D012307:Risk Factors; D012463:Saliva / Q000737:chemistry; D013313:Stress Disorders, Post-Traumatic / Q000175:diagnosis / Q000503:physiopathology* / Q000523:psychology
D006854:Hydrocortisone