Re: CFS 2005 - The Year in Review/Cort&All

[Guest guest]

Hi, Cort & all.

Great to see the excellent choice for " Paper of the Year " from the Phoenix

Rising CFS Newsletter. These Baraniuk et al findings of PWCs having cerebral

spinal fluid evidence of amyloid or misfolded protein build-up, known to savage

brain cells and function, is in sync with the glutathione depletion-methylation

block hypothesis for CFS, conjoining the views of Rich and Dr Amy Yasko as the

upstream explanation for why heat shock proteins, which manage proper folding of

cellular proteins, fail in CFS.

It would be interesting to know if kids with Autism show evidence of amyloid

build-up, which I think if they did, this would greatly cinch the CFS as well as

Alzheimer's connection despite the disparate ages of overt symptom onset among

these three disorders. I just read that Alzheimer's researchers have been

making a paradigm shift in their views and have now zeroed in on heat shock

proteins in this disorder by specifically identifying heat shock factor 1(HSF-1)

as key to breaking-up amyloids once they have formed.

They've learned this becomes low in Alzheimer's and that HSF-1 depends on

phosphorylation of the genes for it for it be produced. However, I don't see

them making the further upstream connection to, in my reading as a layman, the

issue of ATP production for this all important phosphorylation to occur.

http://en.wikipedia.org/wiki/Phosphorylation

http://en.wikipedia.org/wiki/Heat_shock_proteins

Are glutathione status and methylation critical to the level of phosphorylation

needed to make heat shock proteins? Anyway, here is the article regarding the

HSF-1 finding in Alzheimer's:

http://www.msnbc.msn.com/id/14290153/

[Guest guest]

, that's very interesting. Rich, can we add such a question to

your questions for Amy Yasko? I also have some questions for you to

add for her whenever you ask our questions:

Deth was talking about phosphorylation and the d4 receptor at one point.

>

> Hi, Cort & all.

>

>

>

> Great to see the excellent choice for " Paper of the Year " from the

Phoenix Rising CFS Newsletter. These Baraniuk et al findings of PWCs

having cerebral spinal fluid evidence of amyloid or misfolded protein

build-up, known to savage brain cells and function, is in sync with

the glutathione depletion-methylation block hypothesis for CFS,

conjoining the views of Rich and Dr Amy Yasko as the upstream

explanation for why heat shock proteins, which manage proper folding

of cellular proteins, fail in CFS.

>

>

>

> It would be interesting to know if kids with Autism show evidence of

amyloid build-up, which I think if they did, this would greatly cinch

the CFS as well as Alzheimer's connection despite the disparate ages

of overt symptom onset among these three disorders. I just read that

Alzheimer's researchers have been making a paradigm shift in their

views and have now zeroed in on heat shock proteins in this disorder

by specifically identifying heat shock factor 1(HSF-1) as key to

breaking-up amyloids once they have formed.

>

>

>

> They've learned this becomes low in Alzheimer's and that HSF-1

depends on phosphorylation of the genes for it for it be produced.

However, I don't see them making the further upstream connection to,

in my reading as a layman, the issue of ATP production for this all

important phosphorylation to occur.

>

>

>

> http://en.wikipedia.org/wiki/Phosphorylation

> http://en.wikipedia.org/wiki/Heat_shock_proteins

>

>

>

> Are glutathione status and methylation critical to the level of

phosphorylation needed to make heat shock proteins? Anyway, here is

the article regarding the HSF-1 finding in Alzheimer's:

>

>

>

> http://www.msnbc.msn.com/id/14290153/

>

>

>

>

>

[Guest guest]

Hi, Jill and .

O.K., I'll add it to the list.

Rich

> >

> > Hi, Cort & all.

> >

> >

> >

> > Great to see the excellent choice for " Paper of the Year " from

the

> Phoenix Rising CFS Newsletter. These Baraniuk et al findings of

PWCs

> having cerebral spinal fluid evidence of amyloid or misfolded

protein

> build-up, known to savage brain cells and function, is in sync with

> the glutathione depletion-methylation block hypothesis for CFS,

> conjoining the views of Rich and Dr Amy Yasko as the upstream

> explanation for why heat shock proteins, which manage proper

folding

> of cellular proteins, fail in CFS.

> >

> >

> >

> > It would be interesting to know if kids with Autism show

evidence of

> amyloid build-up, which I think if they did, this would greatly

cinch

> the CFS as well as Alzheimer's connection despite the disparate

ages

> of overt symptom onset among these three disorders. I just read

that

> Alzheimer's researchers have been making a paradigm shift in their

> views and have now zeroed in on heat shock proteins in this

disorder

> by specifically identifying heat shock factor 1(HSF-1) as key to

> breaking-up amyloids once they have formed.

> >

> >

> >

> > They've learned this becomes low in Alzheimer's and that HSF-1

> depends on phosphorylation of the genes for it for it be produced.

> However, I don't see them making the further upstream connection

to,

> in my reading as a layman, the issue of ATP production for this all

> important phosphorylation to occur.

> >

> >

> >

> > http://en.wikipedia.org/wiki/Phosphorylation

> > http://en.wikipedia.org/wiki/Heat_shock_proteins

> >

> >

> >

> > Are glutathione status and methylation critical to the level of

> phosphorylation needed to make heat shock proteins? Anyway, here

is

> the article regarding the HSF-1 finding in Alzheimer's:

> >

> >

> >

> > http://www.msnbc.msn.com/id/14290153/

> >

> >

> >

> >

> >

>

[Guest guest]

johnson <cortttt@...> wrote:

I dont know how or if glutathione depletion contributes to a possible

amyloidosis in CFS but I am most intrigued by the evidence of low blood flows

and circulatory problems in CFS since normal blood flows are needed to wash

these protein aggregations of the blood vessel.

***I'm intrigued about this too. And right now on this list I appear to be the

poster child for the point that repleting glutathione will raise blood volume

and long established low blood pressure to normal levels, so there is one

possible way low glutathione could contribute to insufficient blood flows not

clearing out this gunk in the CFS brain.

***Also interesting to this point is the fact that cortisol, known to be low

later on in the pathophysiology of CFS, helps reduce inflammation and limit cell

adhesion(clumping), and there is evidence that low glutathione reduces HPA axis

hormone production by way of allowing increased oxidative stress that does the

damage reducing function.

HPA hormones AVH as well as MSH along with cortisol among others are commonly

reported low in test results for PWCs.

***I won't get into how mercury build-up can add to the gunk and inflammation,

but it certainly is looking like those almost two decades of brain scan studies

showing hypoperfused areas and spots in PWC brains are hints of islands of

concentrated blockages needing to be cleared out for

healthy-free-flowing-function.

***Establish healthy glutathione status with corresponding healthy blood

volume/blood pressure-cardiac function and clear out this brain clog by whatever

other methods(ie, chelation and/or deeper nutrigenomic compensation) that work,

and I think you're no longer a PWC. You're out of the CFS hole!

davidhall2020@...wrote>>

These Baraniuk et al findings of

> PWCs

> > having cerebral spinal fluid evidence of amyloid or misfolded

> protein

> > build-up, known to savage brain cells and function, is in sync with

> > the glutathione depletion-methylation block hypothesis for CFS,

> > conjoining the views of Rich and Dr Amy Yasko as the upstream

> > explanation for why heat shock proteins, which manage proper

> folding

> > of cellular proteins, fail in CFS....