The new issue of *Archives of General Psychiatry* (vol. 66, #1) includes
an article: “Childhood Trauma and Risk for Chronic Fatigue Syndrome:
Association With Neuroendocrine Dysfunction.”

The authors are Christine Heim; Urs M. Nater; Elizabeth Maloney;
Roumiana Boneva; James F. Jones; & William C. Reeves.

Here’s the abstract:


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.


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 control
subjects 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


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.


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.