DAN!, glutathione, Sam-E

January 3, 2006

On Tuesday, January 3, 2006, at 01:58 PM, rvankonynen wrote:

> On the list, I have been suggesting to PWCs for

> the past two months that they consider using the DAN! treatments in

> CFS. Several have started this, and early results sound promising,

> but I think we have to wait for a while yet to be sure.

Rich, do you have one link to a place where this info is summarized? I

am kinda too tired to go read an entire list worth of stuff, but

wondering if I should be paying more attention. I never notice any

benefits to taking glutathione or g-producing stuff, although I am

taking NAC and selenium now because of reading Wheldon's work on MS

treatment.

My ears perked up when you mentioned Sam-E. I am wondering whether it

might help my son with his moods. But I just don't know enough about it

to take any action. We have Lyme, but what some people might call a

brain herx could possibly be periods of time when there is some

deficiency, I am guessing.

- Kate D.

January 5, 2006

Hi, Kate.

I think the best place to go is

http://www.danwebsite.com

This site has videos of the talks given at the two most recent DAN!

conferences, and it's free. You just have to register, and they

will email you a password right away. Note that this group deals

with autism, not CFS, but it is my current belief that most of what

they talk about in terms of pathogenesis and treatment is relevant

to chronic fatigue syndrome as well.

If you want a good discussion of the methylation cycle and the

research on that, I suggest that you watch the talk by Jill at

the Boston conference.

It takes a long time to watch all the talks, but at least you won't

have to read a lot.

I may have said this before, but let me grant that there clearly are

differences in the symptomatology of autism and CFS. It is my

opinion that these differences result from the different ages of

onset. In autism, the child becomes ill before his or her brain is

fully developed. The interruption in normal brain development as

well as oxidative stress is probably what gives rise to the

characteristic brain-related symptoms of autism. When the

methylation cycle is blocked, SAMe, cysteine, glutathione, taurine

and sulfate can all go down, and the important functions that they

normally serve in the body will also then suffer. SAMe is important

for methylation reactions that are involved in making myelin and

neurotransmitters as well as making DNA for new cells. I think the

lack of methylation is a big part of what happens to the brain in

autism.

As you know, one of the main features of CFS is fatigue in the

skeletal muscles. By contrast, kids on the autism spectrum can be

hyperactive. I'm less sure of this, but I suspect that this results

from the skeletal muscles in the autistic child not being fully

developed yet, either, in terms of forming the red, slow-twitch

skeletal muscle cells. These are the muscle cells that make use of

oxidative metabolism, rather than glycolysis alone, as the fast-

twitch muscle cells do. I think that the fatigue in CFS involves

the slow-twitch skeletal muscle cells (which have Krebs cycles and

respiratory chains). Since I think the autistic kids are at an age

where they don't have so many of these yet, the physical fatigue

does not manifest in them as it does in PWCs.

You mentioned that you have Lyme disease. As you know, the

symptomatology of Lyme disease is very similar to that of CFS, to

the point that it is very difficult to do the differential

diagnosis, since even the best Lyme tests have false negatives. It

was very interesting to me to read recently in a post from Sheila on

the Experimental list that Dr. Gow's gene expression work in

Scotland is showing that the gene expression in Lyme disease

is " identical " to that in CFS. I haven't seen the data to back this

up yet, but if it's true, that means that the pathophysiology in

Lyme disease (at least that involving the cells they studied, which

were lymphocytes and monocytes) is the same as in CFS. That would

certainly explain the similarity in symptoms. The question is, how

does the Borrellia trigger the same gene expression and

pathophysiology as found in CFS? If it's true that the

pathophysiology in CFS stems from the same basic pathogenesis

mechanism as does autism (namely, a blockage in the methylation

cycle), then maybe that's what Borrellia does, too! I realize that

my logic is cantilevered pretty far out there, but I do think this

gedanken experiment makes sense. Time will tell.

Rich

>

> > On the list, I have been suggesting to PWCs for

> > the past two months that they consider using the DAN! treatments

in

> > CFS. Several have started this, and early results sound

promising,

> > but I think we have to wait for a while yet to be sure.

>

> Rich, do you have one link to a place where this info is

summarized? I

> am kinda too tired to go read an entire list worth of stuff, but

> wondering if I should be paying more attention. I never notice any

> benefits to taking glutathione or g-producing stuff, although I am

> taking NAC and selenium now because of reading Wheldon's work on

MS

> treatment.

>

> My ears perked up when you mentioned Sam-E. I am wondering whether

it

> might help my son with his moods. But I just don't know enough

about it

> to take any action. We have Lyme, but what some people might call

a

> brain herx could possibly be periods of time when there is some

> deficiency, I am guessing.

>

> - Kate D.

>

January 5, 2006

On Thursday, January 5, 2006, at 01:53 PM, rvankonynen wrote:

> As you know, one of the main features of CFS is fatigue in the

> skeletal muscles. By contrast, kids on the autism spectrum can be

> hyperactive. I'm less sure of this, but I suspect that this results

> from the skeletal muscles in the autistic child not being fully

> developed yet, either, in terms of forming the red, slow-twitch

> skeletal muscle cells. These are the muscle cells that make use of

> oxidative metabolism, rather than glycolysis alone, as the fast-

> twitch muscle cells do. I think that the fatigue in CFS involves

> the slow-twitch skeletal muscle cells (which have Krebs cycles and

> respiratory chains).

Well, if Lyme is doing a similar thing, it would explain why my son and

I don't have much stamina, yet I am relatively strong as far as a

short-term effort goes. Even as a teen, when I suspect I already had a

suppressed Lyme infection, I noticed that in Gymnastics I had to always

put my most difficult move early in a routine because I could barely

make it through the routine. Still, I had some pretty impressive

strength moves. It all makes sense now, if I am understanding that

fast-twitch muscles might be responsible for bursts of strength,

whereas endurance comes from slow-twitch muscles. This is a new concept

for me, so correct me if I am understanding that wrong.

Thanks for the link.

- Kate

January 5, 2006

Dear Rich

The essence of hyperactivity is not well established to my mind but I

believe it is more neurological than physical. Some of us are blessed (or

cursed) with remitting/relapsing CFS. In my periods of remission I am

classically hyperactive, in my relapses the hyperactivity is masked by lack

of energy and pain but the innate restlessness is evident ( at least to

me). In ADHD the tell-tales in adults are often fidgeting, finger tapping

and foot movements while sitting. I suspect that the overt symptoms of

hyperactivity may well reflect an inner mental state or lack of neurological

homeostasis ( the concept of failure of neurological inhibition) . This is

related to the concepts of sensory overload and salience problems . ADHD,

autism and CFS sufferers often have issues of photophobia, light

sensitivity (including Irlen Syndrome) auditory hypersensitivity

(hyperacusis and auditory processing problems) proprioceptive and tactile

issues. All these return to saliency problems and the inability to inhibit

response to stimuli. It has been hypothesised that the primary problem in

CFS is in fact, this mechanism where CFS sufferers are unable to

appropriately interpret normal neurological feedback from all organ

systems. There is probably a great deal of truth in this as many of us can

perform under testing, at a rate much higher than we believe possible,

especially muscle testing.

This explanation does nothing to provide an explanation for a mechanism for

CFS and is dismissive of the impact of the problem caused by the disease.

My own thoughts are that there is an underlying susceptibility to

disregulation , probably genetic, which in the face of insult, leads to

neurological sequelae including ADHD and other symptoms of disinhibition.

This fails to account for the immunological facets of these presentations.

There is no doubt in my mind that Iodine deficiency is linked to early

neurological development. What is less understood is the effect of estrogen

dominance on thyroid function during gestation. It appears to me that high

estrogen/low progesterone can explain many of the correlations seen with

autistic spectrum disorders as this situation inhibits thyroid function, Low

thyroid function during pregnancy inhibits neurological development of the

fetal brain.

Given the proliferation of xenoestrogens in the environment as well as other

hormone mimetics, a plausible explanation exists to explain the increase in

autistic spectrum disorders.

It has also been claimed that the performance in the USA scholastic aptitude

tests done by adolescents has declined steadily since the introduction of

DDT ( a known hormone mimetic) See http://www.ourstolenfuture.org/, also

print, Colborn , Myers and Dumanoski. See also " Hormonal Chaos " by Sheldon

Krimsky and other works by Sherril Selman etc.

Regards

Windsor

[infections] Re: DAN!, glutathione, Sam-E