Re: Infections/NCF?/madijen

[Guest guest]

Hi, Madijen.

" madijen " <madijen@...> wrote:

>

> I don't usually post here but have been reading all the infection

> posts. I have had CFIDS for 19 years or more and was diagnosed at the

> Cheney Clinic by Dr. Lapp. Over 30years ago I started with FM.

> 18months ago I was diagnosed with Mycobacterium Avium Complex (MAC)

> and also another mycobacterium called Mycobacterium Fortuitum. I have

> been on multiple antibiotics for over a year. I have experienced no

> change in my CFIDS/FM symptoms.

***I was diagnosed in similar fashion with a mycobateria also at one point.

I took multiple antibiotics for it as well for supposed chronic lyme infestation

and NADA. No one bit of improvement.

***I later re-tested fro the mycobacteria infection and it was apparent the

antibiotic therapy had completely wiped it flat line. It was not the cause of

my CFS as been speculated.

***BTW, nondenatured whey will do the same thing as the antibiotics do with

mycobacteria. It will flat line them.

> Why is it that there has been very little discussion about the

> announcement coming out of NCF?

***It's not standing out as a strong hypothesis, as presented by they're

announcement, that the virus they're noticing PWCs have been exposed to is the

cause of CFS. There have been various viruses that have been proven that we've

been exposed to, but none ever seem to end up being shown as causal, so how is

this one really any different I guess is the question that is giving people

pause.

Postive and even negative views should

be out there on these boards online and it has been strangely quiet. Is everyone

doubting that this announcement will hold up like so many

> disappointments in the past?

***I don't have a reason to doubt they're finding of exposure. However, I don't

see the announcement outlining a hypothesis of chronic pathology that follows

from exposure to this virus, but more making an assertion that there is possibly

one.

***Also and maybe what I'm getting at is it would be helpful to us for the NCF

to explain the mechanism of STAT-1 in more detail, particularly how it gets

produced in the cell and the mechanism of its depletion. The nature of their

suggested causal hypothesis regarding this virus in CFS essentially relies on

what is going on with STAT-1 in us.

***At first blush by my layman's reading of STAT-1 is it seems this protein

depends a lot on ATP to get made. If this is right, this potentially creates a

problem with NCF's hypothesis because it's becoming fairly evident that PWCs are

ATP production challenged to start, given the glutathione status and methylation

issues tying back to genetics.

***STAT-1 depletion then seems to be more of a downstream terrain issue and this

virus of note possibly just adding insult to injury by creating further

depletion, but not properly characterized as THE cause of it in PWCs. I'd like

to here the NCF say more about they're finding and aswage this concern that the

gene variant/metabolic predispostions may be the more relevant issue when it

comes to STAT-1 status.

I just find it very strange that the

> cfids community is so quiet about this announcement.

***

[Guest guest]

The basis of the NCF speculation is DeMeirleir's work on RNaseL and

stat 1. Cort has written an outstanding summary of

DeMeirleir's book. You can find the section relating to the question

of stat 1 degradation and whether it is viral or bacterial at this

link:

http://www.phoenix-cfs.org/The%20SITE/CFSABAVII.htm

FACTORS INFLUENCING CYTOKINE PRODUCTION

Viruses

Viral reactivation is an important factor for most CFS patients.

That CFS patients evidence increased rates of viral reactivation yet

do not display an increased prevalence of specific viruses, suggests,

however, that viral reactivation is not causative in CFS. Instead

viral reactivation is a co-morbid feature of the disease; that is,

the underlying disease process in CFS contributes to the increased

incidence of viral reactivations found in CFS. (Interestingly enough)

different viruses trigger different parts on the interferon/2-

5OAS/RNaseL enzyme system. The potential therefore exists for each

to alter that system, and therefore the body chemistry of the CFS

patient, and thus the symptoms the CFS patient experiences in

distinct ways.

Viral reactivation or infection in CFS is, therefore, likely not only

to cause different symptoms in CFS patients, but also variations in

lymphocyte activity and probably cytokine production and

biochemistry. The variable results seen in many CFS studies may be

the result of a heterogeneous co-morbid disease process that has yet

to be accounted for.

Bacterial Toxins.

Bacterial toxins can induce cytokine activity. Skin coagulase-

negative staphylococci (CoNS) produces a membrane damaging toxin

that, the authors have found, is implicated in myofascial pain

syndrome (MFPS), a commonly occurring syndrome characterized by

muscle tenderness. That CFS patients with more toxin producing

strains of CoNS were found to have more severe core CFS symptoms,

and that toxin levels were associated with increased RNase L

activity, suggested that bacterial toxins are another co-morbid

condition that exacerbates CFS symptoms.

Another study indicated that CFS patients exhibit significant

disruptions of bowel microflora relative to controls.

Gastrointestinal upset was predominantly associated with general CFS

symptoms. CFS patients were significantly more likely than controls

to harbor Enterococcus and Staphylococcus spp. (the `bad' bacteria),

and significantly less likely to have Bifidobacterium or

Lactobaccillus spp. in their bowels.

>

> Hi, Madijen.

>

>

>

> " madijen " <madijen@> wrote:

> >

> > I don't usually post here but have been reading all the infection

> > posts. I have had CFIDS for 19 years or more and was diagnosed at

the

> > Cheney Clinic by Dr. Lapp. Over 30years ago I started with FM.

> > 18months ago I was diagnosed with Mycobacterium Avium Complex

(MAC)

> > and also another mycobacterium called Mycobacterium Fortuitum. I

have

> > been on multiple antibiotics for over a year. I have experienced

no

> > change in my CFIDS/FM symptoms.

>

>

>

> ***I was diagnosed in similar fashion with a mycobateria also at

one point.

> I took multiple antibiotics for it as well for supposed chronic

lyme infestation and NADA. No one bit of improvement.

>

>

>

> ***I later re-tested fro the mycobacteria infection and it was

apparent the antibiotic therapy had completely wiped it flat line.

It was not the cause of my CFS as been speculated.

>

>

>

> ***BTW, nondenatured whey will do the same thing as the antibiotics

do with mycobacteria. It will flat line them.

>

>

>

> > Why is it that there has been very little discussion about the

> > announcement coming out of NCF?

>

>

>

> ***It's not standing out as a strong hypothesis, as presented by

they're announcement, that the virus they're noticing PWCs have been

exposed to is the cause of CFS. There have been various viruses that

have been proven that we've been exposed to, but none ever seem to

end up being shown as causal, so how is this one really any different

I guess is the question that is giving people pause.

>

>

>

> Postive and even negative views should

> be out there on these boards online and it has been strangely

quiet. Is everyone doubting that this announcement will hold up like

so many

> > disappointments in the past?

>

>

>

> ***I don't have a reason to doubt they're finding of exposure.

However, I don't see the announcement outlining a hypothesis of

chronic pathology that follows from exposure to this virus, but more

making an assertion that there is possibly one.

>

>

>

> ***Also and maybe what I'm getting at is it would be helpful to us

for the NCF to explain the mechanism of STAT-1 in more detail,

particularly how it gets produced in the cell and the mechanism of

its depletion. The nature of their suggested causal hypothesis

regarding this virus in CFS essentially relies on what is going on

with STAT-1 in us.

>

>

>

> ***At first blush by my layman's reading of STAT-1 is it seems this

protein depends a lot on ATP to get made. If this is right, this

potentially creates a problem with NCF's hypothesis because it's

becoming fairly evident that PWCs are ATP production challenged to

start, given the glutathione status and methylation issues tying back

to genetics.

>

>

>

> ***STAT-1 depletion then seems to be more of a downstream terrain

issue and this virus of note possibly just adding insult to injury by

creating further depletion, but not properly characterized as THE

cause of it in PWCs. I'd like to here the NCF say more about they're

finding and aswage this concern that the gene variant/metabolic

predispostions may be the more relevant issue when it comes to STAT-1

status.

>

>

>

> I just find it very strange that the

> > cfids community is so quiet about this announcement.

>

>

>

> ***

>