Klimas said that she's identified different protocols for different types of CFS patients: Pre-menopausal women, post-menopausal women, men, and one more group.
The protocol you tried was for GWS, which her modeling suggest is very different that CFS. GWS has way too much molecular signaling, like signal overload. CFS has very little molecular signaling, everything quiet. So how you reset or restart the HPA axis may be different: shut it down for a while (GWS) vs jump start and shock it to turn it back on (CFS).
@raghav - I feel like I should know the answer to this, but I don't - was Nancy Klimas going to use the same protocol for GWS and ME/CFS patients? she has said they have a lot similarities but also huge differences too.
eta: it looks like @junkcrap50 just answered my question
I saw in a video presentation of Nancy Klimas(Not able to locate it), where she made a comparison of GWS and ME /CFS and said even though they are vastly different in the blood analyses, they will both respond to the same protocol. I will try to locate it. But searching through videos is a painful process.
I did see one of her videos (and I totally agree that searching through videos is a painful process! ) in which she talked about GWS and ME/CFS, their similarities and differences. But I don't remember her saying that they would respond to the same protocol. We could have watched different videos, or, perhaps even more likely, I just don't remember that part - my memory is atrocious.
So if you're correct, that is more discouraging. But kudos to you for giving it a try!
@Mary I saw in a video presentation of Nancy Klimas(Not able to locate it), where she made a comparison of GWS and ME /CFS and said even though they are vastly different in the blood analyses, they will both respond to the same protocol. I will try to locate it. But searching through videos is a painful process.
@raghav, It may have been that when Klimas said they might both respond to the same protocol that what she was actually thinking of is postmenopausal women with ME/CFS, because the upcoming clinical trial she's doing for postmenopausal ME/CFS women is apparently going to use the same sequential protocol of etanercept followed by mifepristone that's being used right now for the clinical trial for men with Gulf War Illness (GWI).
She (or her staff) has said at least a couple of times in different places that postmenopausal women, premenopausal women, and men with ME/CFS may all need a different therapy. For example, in the latest update from her group they say;
We have established 3 models that require different clinical approaches – post-menopausal women model differently than pre-menopausal women, and men model differently than women.
I think there's a decent chance that mifepristone might be used as part of the treatment regardless of subgroup, because that drug has the ability to correct abnormal cortisol/HPA axis states whether high, low, or inappropriately normal. For correction of the immune component, though, some groups may require something different than etanercept, or something in addition to etanercept, or perhaps a different treatment order (e.g., using the mifepristone first). Also, some patients may need to be modeled individually for individualized treatment.
Note also that the same computer modeling that determined that the sequential use of etanercept followed by mifepristone should cause remission in men with GWI (and which has already been shown to cause remission in the very good GWI mouse model) is also indicating that multiple cycles of that sequential treatment may be necessary to effect the remission. The model predicts one cycle to cause remission only 40% of the time. One additional cycle (i.e., course of treatment with etanercept then mifepristone) increases the probability of remission to 63%. Four cycles increase the chance of remission to over 80%. (Reference) And again, this is for GWI men (and perhaps by extension to postmenopausal ME/CFS women).
Perhaps @Belbyr might be able to find out some additional info from Dr Klimas on how the treatments might potentially be different for ME/CFS men and premenopausal women.(?)
@nandixon I too thought of the idea of multiple cycles to bring it under control. I think that is why the monitoring period of 4 months post protocol. But if getting funds for even one cycle is that difficult then I dont know what to say.
Or perhaps that is why it is so expensive, it is adding in the use of multiple cycles..?
I remember her saying in, was it 3 or 4 years? They went from a computer sim to a human trail in GWS. If there is any good news to come out of these small trials, I'm sure the flood gates will open up in terms of awareness and funds.
Is your free testosterone level also below normal as well?
As of 2014, for the HPA axis, the hypothalamic-pituitary-gonadal (HPG) axis and the immune system, respectively, Klimas had found :
Experimental data for endocrine-immune markers measured in male GWI subjects showed the greatest alignment with predictions of a naturally occurring alternate steady state presenting with hypercortisolism, low testosterone and a shift towards a Th1 immune response. In female CFS subjects, expression of these markers aligned with an alternate homeostatic state displaying hypocortisolism, high estradiol, and a shift towards an anti-inflammatory Th2 activation.
(I believe in the above instance that the female CFS patients may have been a mixture of pre- and postmenopausal women, since they're just described as having an average age of 50, but I'm not sure.)
I haven't been able to determine what Klimas has found the HPA, HPG and immune system profile to be for ME/CFS males, except that they appear to have at least some immune shift towards the proinflammatory TH1 state, but it is different than in GWI males.