If you want to look at stress or stressors then its best to avoid BPS entirely. A broken bone, a car accident, a stabbing, an ebola infection, a lightning strike, all fit in BPS. Its so broad its meaningless.
Second, that ebola infection ... thats multiple stressors right there. A stab wound ... more stressors. Ditto all other physical trauma. The stressor thing is also too broad. Now focusing on cortisol is fine as a theoretical approach ... but its been looked at for a very long time. Heck, it was the basis for many ideas on ME in the 70s, at least in the thoughts of doctors. Decades later and we have ... what? They stopped using cortisol to treat ME at around that time.
Now there is unpublished UK research that we have cortisol resistance due to elevated beta cortisol receptors. I want to see that published so we can look at the data. This however does not tell us if this is primary, or secondary, or even tertiary to the disease process.
A great many patients with ME and CFS have more or less normal cortisol as well. It takes a larger cohort to identify subtle deficits, including circadian deficits, and it looks secondary, at best, not primary. It probably contributes to symptoms.
Now there might be subgroups where cortisol issues are a big thing. This applies to many theories of ME and CFS, not just cortisol.
Please go back to the original post, above for the premise. It is that ‘Bio’ part: a child is abused. S/he grows up with major stress disorders as a result (some manifest overtly; others are deeply buried within). It first attacks the gut, then the hypothalamus, and then all sorts of immune hyper dysfunction follows. This is what the PTSD (BPS) model parallels, only accelerated. Not Wessely’s theories!
There are a number of studies related to these immune system dysfunctions, coming back around from losing speed in the early 90’s, not 70’s. (I was part of the more recent CFS outbreak from Incline Village in the mid 80’s, when the CDC was only then called into investigate, which we all now know they bumbled.)
IAE, here’s just one or two of a number of articles (abstract form) supporting the role of Stress in CFS, which we can further build upon:
Does hypothalamic–pituitary–adrenal axis hypofunction in chronic fatigue syndrome reflect a ‘crash’ in the stress system?
Boudewijn Van Houdenhove a,*, Filip Van Den Eede b, Patrick Luyten c
a Department of Liaison Psychiatry, University Hospitals K.U. Leuven, Herestraat 49, B-3000 Leuven, Belgium
b Collaborative Antwerp Psychiatric Research Institute, Department of Psychiatry, Antwerp University Hospital, Antwerp, Belgium c Department of Psychology, K.U. Leuven, Leuven, Belgium
article info
Article history:
Received 18 November 2008 Accepted 21 November 2008 Available online xxxx
summary
The etiopathogenesis of chronic fatigue syndrome (CFS) remains poorly understood. Although neuroen- docrine disturbances – and hypothalamic–pituitary–adrenal (HPA) axis hypofunction in particular – have been found in a large proportion of CFS patients, it is not clear whether these disturbances are cause or consequence of the illness. After a review of the available evidence we hypothesize that that HPA axis hypofunction in CFS, conceptualized within a system-biological perspective, primarily reflects a funda- mental and persistent dysregulation of the neurobiological stress system. As a result, a disturbed balance between glucocorticoid and inflammatory signaling pathways may give rise to a pathological cytokine- induced sickness response that may be the final common pathway underlying central CFS symptoms, i.e. effort/stress intolerance and pain hypersensitivity. This comprehensive hypothesis on HPA axis hypo- function in CFS may stimulate diagnostic refinement of the illness, inform treatment approaches and suggest directions for future research, particularly focusing on the neuroendocrine–immune interface and possible links between CFS, early and recent life stress, and depression.
And more familiar psychiatric reference results, paralleling the above hypothesis:
Childhood Trauma Raises CFS Risk
Researchers Also Say Stress Is a Factor in Chronic Fatigue Syndrome
By
Daniel J. DeNoon
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This article is from the WebMD News Archive
This content has not been reviewed within the past year and may not represent WebMD's most up-to-date information.
FROM THE WEBMD ARCHIVES
Nov. 6, 2006 -- Childhood trauma raises a person's risk of
chronic fatigue syndrome by three- to eightfold, CDC researchers find.
Another study, based on data from the Swedish twin registry, shows stress to be a triggering factor for chronic
fatigue syndrome (CFS). It also shows that emotional instability is a significant CFS risk factor, although genetic and family factors determine whether this personality trait leads to
fatigue.
"Our observations lend 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," conclude CDC researcher Christine Heim, PhD, and colleagues.
"Stress is a significant risk factor for
chronic fatigue-like illness, the effect of which may be buffered by genetic influences," conclude Karolinska Institute researcher Kenji Kato, PhD, and colleagues. "Emotional instability assessed 25 years earlier is associated with chronic fatigue through genetic mechanisms contributing to both personality style and expression of the disorder."
This also represents an assault on the immune system going unresolved. By inference, if you subscribe to mainstream CFS etiology you also buy into the possibility of the viability of BPS as a cause since it’s the other side of the viral/immune system etiology which all our wonderful clinicians treat but can’t cure. This is simply a call to look down this rabbit hole since we’re not finding any along the viral tracks!
