Re: RichV: Pragmatic question on DNA/RNA testing...

[Guest guest]

Hi, Ken.

***I certainly share your desire to prevent PWCs from being ripped

off by something that would not clearly lead to a choice of

treatment that has a good chance of being effective for them.

***I think there are some distinctions that need to be made

concerning the issues you raised. See comments at asterisks below.

>

> Rich,

> I have several questions about DNA/RNA testing -- I know that

it's

> a new " dot-com " for biotech firms, hence a lot of hard sell is

being

> done by some of them.

***Yes, I think you're right. It's a very " hot " field right now.

I have read many NewScientist articles that

> time and again has found DNA and RNA modification in response to

> environmental influences and even **disease**.

***It's true that DNA molecules can be altered by environmental

influences, including viruses, chemicals and ionizing radiation.

This is more frequent in somatic cells than in germ cells, and it is

the basis for producing cancers, for example.

I recall a few years

> back one of the variation found for CFIDS caused me to do some

> digging and the variation was also found in many natives in

Bolivia.

> The variation appear to be one that allows the body to handle low

> oxygen levels -- hence the hypoxia (low tissue oxygen levels) of

> CFIDS was causing intragenerational mutations/evolution to occur

in

> some CFIDSers.

***I think several things are mixed together here. First, genetic

variations are changes that have occurred in the past in the germ

cells of one's ancestors and have survived to produce offspring.

Those are rare events, and not the same as the mutations in somatic

cells in an individual during their life that we just talked about,

such as the ones that lead to cancer. I'm not familiar with the

particular variation you are referring to here, but the explanation

could be that those who inherited that particular variation from

their ancestors were more predisposed to developing CFS than other

people who didn't inherit that one, for some reason. I don't think

this should be interpreted as suggesting that the genome (i.e. the

set of genes in all their somatic and germ cells) in particular PWCs

changed during their lifetimes in response to having CFS. That

doesn't happen. That was the error made by Lysenko in the old

Soviet Union, whose influence set back Soviet genetics for decades.

>

> The OLD premise of DNA/RNA testing was that this was static or

very

> slowly changing...

***That old premise is still true.

more and more papers are appearing that indicate

> significant DNA/RNA mutations can occur within a few years -- and

far

> more importantly, that the mutations are not RANDOM, but very much

in

> response to the environment, almost, cough cough " intelligent

design " .

***Again, I think there are two things mixed together here. On the

one hand there are mutations that occur in the DNA of somatic cells

of living individuals, that are caused by environmental influences,

but these are not changes in the germline. On the other hand, if

you are talking about a life form that goes through many generations

rapidly, and you are looking at changes over many generations when

this lifeform is in an environment that has been changed from what

it was in the past, then yes, there will be natural selection of

random mutations, and the mutations that help the lifeform to

survive and reproduce under the new environmental conditions will

become part of the genome of the surviving population. But if

you're talking about humans, the generation time is too long to see

most such effects. I think that Berg used to make the

argument, though, that the reason for so many people having

hypercoagulation mutations was that the people who had them survived

the bloody battles in Europe many years back. But again, that would

have been a selection from a population that had random mutations,

not the environment causing the changes in DNA.

>

> My conclusion was that DNA/RNA testing in CFIDS must be carefully

> intrepretted to not be viewed as a pre-existing DNA condition, but

a

> post-condition DNA condition unless pre-existing DNA is available

and

> also tested.

***Again, in view of what I've tried to explain above, I think the

DNA is constant in an individual, except for a low rate of random

mutations in somatic cells. When a blood sample is taken, there are

a large number of white blood cells in it, and when the DNA is

amplified, even though it's conceivable that an occasional mutation

might have occurred in one of these cells at the exact location of

the SNP you are looking for, there are enough other cells present to

overwhelm it, and the result is going to be that you will get a

result that is characteristic of the genome that the person

inherited. Any somatic mutations will be down in the noise.

Yes, there are some genetic states (for example the

> Prothrombin 20210 coagulation effect) that occurs in some CFIDSer -

> and those are *likely* pre-existing DNA.

***I think I've covered this above.

>

> So my question to you is simple:

>

> 1) What are the treatment plan that REQUIRES DNA/RNA testing

before

> starting? Ampligen and RNASE-L would be one such case. Are there

> other demonstrated plans?

***Dr. Amy Yasko recommends getting DNA testing done before starting

her treatment program. There are actually aspects that can be

started before one has the results, but before starting some of the

treatments, for example those that are directed at supporting the

methylation cycle, it is important to know if you have an

upregulating genetic variation in the enzyme cystathionine beta

synthase, for example. Several people on this list have turned out

to have such a SNP. It is possible to attempt the treatments

without getting the DNA testing first, but it is more hit-or-miss

that way.

>

> My general feeling is that PAYING for testing is a waste of money

IF

> it does not IMMEDIATELY results in a demonstrated treatment plan

that

> is effective.

***Of course, you are certainly entitled to hold that view, and I

encourage everyone to think it over for themselves.

***So far we have only one case that has proceeded through the

treatment far enough to find out how well it has worked. She has

reported that she believes very strongly that it has been worth the

money. She reported that last Saturday night she was able to

go " fast dancing " for four hours, and still felt fine on Sunday.

This week she has been camping. Before this, she wrote that she had

been riding horses. This is a person who was house-bound before.

***I think it will take some time to see whether others have similar

experiences, but I am hopeful. There is quite a bit of experience

from autism to draw upon, however, and I think the genetic test

results so far are showing that the same SNPs are present in CFS as

in autism. And the test results do tell you immediately which path

to follow for treatment. The treatment itself, though, takes some

time to shift the metabolism back in the correct direction. I think

there is quite a bit of momentum in the abberent gene expression,

and this has to be nudged back, rather than being changed overnight.

Doing testing if it is part of a research study and

> FREE -- would be recommended.

***That would certainly be wonderful, but I don't know who would

fund it.

>

> To me, the literature cause me to view this DNA/RNA with a lot of

> caution...

***I agree that we need to be cautious, but I think the literature

requires careful interpretation, and it's important to decipher what

it is actually saying. I do appreciate your concern about this,

Ken, and I have thought long and hard about it, too, but so far it's

looking good to me.

>

> Comments?

>

***Rich

[Guest guest]

Rich or anyone- for those of us who aren't familiar w/ Amy or this

thread, could someone give a rough description of the

treatment protocol? What I mean is, are we talking herbs, minerals,

anti-virals, antibiotics, etc. or some combination of the above or

something completely different.

The reason I ask is that I know some on this list are dead set

against any prescription drugs. Personally, valgancyclovir sounds

a little scary to me although it sounds like I am in the CFS subset

that might benefit from it. Thanks,

Mike C. (A link to the treatment protocol would also be great)

In , " rvankonynen " <richvank@...>

wrote:

> > So my question to you is simple:

> >

> > 1) What are the treatment plan that REQUIRES DNA/RNA testing

> before

> > starting? Ampligen and RNASE-L would be one such case. Are

there

> > other demonstrated plans?

>

> ***Dr. Amy Yasko recommends getting DNA testing done before

starting

> her treatment program. There are actually aspects that can be

> started before one has the results, but before starting some of

the

> treatments, for example those that are directed at supporting the

> methylation cycle, it is important to know if you have an

> upregulating genetic variation in the enzyme cystathionine beta

> synthase, for example. Several people on this list have turned

out

> to have such a SNP. It is possible to attempt the treatments

> without getting the DNA testing first, but it is more hit-or-miss

> that way.

> >

> > My general feeling is that PAYING for testing is a waste of

money

> IF

> > it does not IMMEDIATELY results in a demonstrated treatment plan

> that

> > is effective.

[Guest guest]

Nice dialogue, to which I wish to add a few thoughts.

1) We are in the beginning of understanding connections between adult

chronic illnesses like lyme/cfids, and the autism model. Doctors and

researchers I have spoken with, and only a few thus far, readily admit

that although COMT and MTHFR mutations are the most important ones

they have found thus far, there will be more revealed over time. We

have much to discover. In fact, this biomedical approach is only

recently being integrated by researchers

2) In this biomedical approach to autism, many would agree with what

is implicit in Ken's post, or in one of Kurt's a while ago. Many of

the kids, for instance, improve markedly on gluten and casein free

diets, and then the now typical interventions like folinic acid or

methylB12. I spoke with someone yesterday whose son responded very

well to methyl b12, and natural antimicrobials. I spoke also with a

doc who is passionate about treating the kids, very knowledgeable and

credentialed, but farms out the more complex cases when necessary.

There was one heartwrenching story she mentioned which I will not

investigate further, but this boy has such serious gut damage, most

likely from the vaccines/his genetics, that he has chronic

esophagitus. For four years it was so painful he could not sleep well.

On a casein and gluten free diet he improved, and it was discovered

that instead of being retarded he has an IQ of 150 (genius) but the

area where he lives is so prejudiced against the whole idea of no milk

no wheat it is apparently nigh impossible for the mom to keep him on

the diet. He is in such pain from esophagitus he sometimes tries to

sleep standing up with his head on his dresser.

I mention this because for the kids, as for us, there will be a

bellcurve of response. This is to be expected. Some of us will be

harder cases than others. Some of us will have issues that have not

been figured out yet, or mutations that haven't been focussed on. This

is true with all treatment approaches.

After watching the Yasko DVDs I could not make a case, in my case, for

not getting genetic testing. I don't expect it to be the ansewr to

everything, but to give me insights I wouldn't have had before and

make my journey a little more directed.

It is also nice for me, anyway, to know why I have intuitively avoided

and then gravitated to certain things. Why have I avoided maltodextrin

(turns out to be an excitotoxin), to the point where I get the

sleeping pill from a specific pharmacy that gets it from Mylar, a

generic drug maker that fills with lactose, not maltodextrin...why do

I drink strong (two teabags steeped for five minutes) decaffeinated

green tea every morning (theanine...Yasko talks about). Why, when I

finally decided to try ARG's niacin, did i feel my mood improve (the

body needs b3 and will break down trytophan to make it, then you will

have less serotonin)...But these are things I tripped across. You

don't 'trip' across methyl b12...

> >

> > Rich,

> > I have several questions about DNA/RNA testing -- I know that

> it's

> > a new " dot-com " for biotech firms, hence a lot of hard sell is

> being

> > done by some of them.

>

> ***Yes, I think you're right. It's a very " hot " field right now.

>

> I have read many NewScientist articles that

> > time and again has found DNA and RNA modification in response to

> > environmental influences and even **disease**.

>

> ***It's true that DNA molecules can be altered by environmental

> influences, including viruses, chemicals and ionizing radiation.

> This is more frequent in somatic cells than in germ cells, and it is

> the basis for producing cancers, for example.

>

> I recall a few years

> > back one of the variation found for CFIDS caused me to do some

> > digging and the variation was also found in many natives in

> Bolivia.

> > The variation appear to be one that allows the body to handle low

> > oxygen levels -- hence the hypoxia (low tissue oxygen levels) of

> > CFIDS was causing intragenerational mutations/evolution to occur

> in

> > some CFIDSers.

>

> ***I think several things are mixed together here. First, genetic

> variations are changes that have occurred in the past in the germ

> cells of one's ancestors and have survived to produce offspring.

> Those are rare events, and not the same as the mutations in somatic

> cells in an individual during their life that we just talked about,

> such as the ones that lead to cancer. I'm not familiar with the

> particular variation you are referring to here, but the explanation

> could be that those who inherited that particular variation from

> their ancestors were more predisposed to developing CFS than other

> people who didn't inherit that one, for some reason. I don't think

> this should be interpreted as suggesting that the genome (i.e. the

> set of genes in all their somatic and germ cells) in particular PWCs

> changed during their lifetimes in response to having CFS. That

> doesn't happen. That was the error made by Lysenko in the old

> Soviet Union, whose influence set back Soviet genetics for decades.

> >

> > The OLD premise of DNA/RNA testing was that this was static or

> very

> > slowly changing...

>

> ***That old premise is still true.

>

> more and more papers are appearing that indicate

> > significant DNA/RNA mutations can occur within a few years -- and

> far

> > more importantly, that the mutations are not RANDOM, but very much

> in

> > response to the environment, almost, cough cough " intelligent

> design " .

>

> ***Again, I think there are two things mixed together here. On the

> one hand there are mutations that occur in the DNA of somatic cells

> of living individuals, that are caused by environmental influences,

> but these are not changes in the germline. On the other hand, if

> you are talking about a life form that goes through many generations

> rapidly, and you are looking at changes over many generations when

> this lifeform is in an environment that has been changed from what

> it was in the past, then yes, there will be natural selection of

> random mutations, and the mutations that help the lifeform to

> survive and reproduce under the new environmental conditions will

> become part of the genome of the surviving population. But if

> you're talking about humans, the generation time is too long to see

> most such effects. I think that Berg used to make the

> argument, though, that the reason for so many people having

> hypercoagulation mutations was that the people who had them survived

> the bloody battles in Europe many years back. But again, that would

> have been a selection from a population that had random mutations,

> not the environment causing the changes in DNA.

> >

> > My conclusion was that DNA/RNA testing in CFIDS must be carefully

> > intrepretted to not be viewed as a pre-existing DNA condition, but

> a

> > post-condition DNA condition unless pre-existing DNA is available

> and

> > also tested.

>

> ***Again, in view of what I've tried to explain above, I think the

> DNA is constant in an individual, except for a low rate of random

> mutations in somatic cells. When a blood sample is taken, there are

> a large number of white blood cells in it, and when the DNA is

> amplified, even though it's conceivable that an occasional mutation

> might have occurred in one of these cells at the exact location of

> the SNP you are looking for, there are enough other cells present to

> overwhelm it, and the result is going to be that you will get a

> result that is characteristic of the genome that the person

> inherited. Any somatic mutations will be down in the noise.

>

> Yes, there are some genetic states (for example the

> > Prothrombin 20210 coagulation effect) that occurs in some CFIDSer -

>

> > and those are *likely* pre-existing DNA.

>

> ***I think I've covered this above.

> >

> > So my question to you is simple:

> >

> > 1) What are the treatment plan that REQUIRES DNA/RNA testing

> before

> > starting? Ampligen and RNASE-L would be one such case. Are there

> > other demonstrated plans?

>

> ***Dr. Amy Yasko recommends getting DNA testing done before starting

> her treatment program. There are actually aspects that can be

> started before one has the results, but before starting some of the

> treatments, for example those that are directed at supporting the

> methylation cycle, it is important to know if you have an

> upregulating genetic variation in the enzyme cystathionine beta

> synthase, for example. Several people on this list have turned out

> to have such a SNP. It is possible to attempt the treatments

> without getting the DNA testing first, but it is more hit-or-miss

> that way.

> >

> > My general feeling is that PAYING for testing is a waste of money

> IF

> > it does not IMMEDIATELY results in a demonstrated treatment plan

> that

> > is effective.

>

> ***Of course, you are certainly entitled to hold that view, and I

> encourage everyone to think it over for themselves.

>

> ***So far we have only one case that has proceeded through the

> treatment far enough to find out how well it has worked. She has

> reported that she believes very strongly that it has been worth the

> money. She reported that last Saturday night she was able to

> go " fast dancing " for four hours, and still felt fine on Sunday.

> This week she has been camping. Before this, she wrote that she had

> been riding horses. This is a person who was house-bound before.

>

> ***I think it will take some time to see whether others have similar

> experiences, but I am hopeful. There is quite a bit of experience

> from autism to draw upon, however, and I think the genetic test

> results so far are showing that the same SNPs are present in CFS as

> in autism. And the test results do tell you immediately which path

> to follow for treatment. The treatment itself, though, takes some

> time to shift the metabolism back in the correct direction. I think

> there is quite a bit of momentum in the abberent gene expression,

> and this has to be nudged back, rather than being changed overnight.

>

> Doing testing if it is part of a research study and

> > FREE -- would be recommended.

>

> ***That would certainly be wonderful, but I don't know who would

> fund it.

> >

> > To me, the literature cause me to view this DNA/RNA with a lot of

> > caution...

>

> ***I agree that we need to be cautious, but I think the literature

> requires careful interpretation, and it's important to decipher what

> it is actually saying. I do appreciate your concern about this,

> Ken, and I have thought long and hard about it, too, but so far it's

> looking good to me.

> >

> > Comments?

> >

> ***Rich

>

[Guest guest]

She has a PhD and an ND (naturopathic) and although she obviously

likes amoxicillin for strep, she tends to naturopathic interventions.

She does seem to like low dose EDTA but I think Garry Gordon makes a

bath product called Beyond Clean that has EDTA In it...she mentioned

one kid who, when his mom ran out of that, regressed...she's not heavy

into drugs, which is great fo rme in any case.

> > > So my question to you is simple:

> > >

> > > 1) What are the treatment plan that REQUIRES DNA/RNA testing

> > before

> > > starting? Ampligen and RNASE-L would be one such case. Are

> there

> > > other demonstrated plans?

> >

> > ***Dr. Amy Yasko recommends getting DNA testing done before

> starting

> > her treatment program. There are actually aspects that can be

> > started before one has the results, but before starting some of

> the

> > treatments, for example those that are directed at supporting the

> > methylation cycle, it is important to know if you have an

> > upregulating genetic variation in the enzyme cystathionine beta

> > synthase, for example. Several people on this list have turned

> out

> > to have such a SNP. It is possible to attempt the treatments

> > without getting the DNA testing first, but it is more hit-or-miss

> > that way.

> > >

> > > My general feeling is that PAYING for testing is a waste of

> money

> > IF

> > > it does not IMMEDIATELY results in a demonstrated treatment plan

> > that

> > > is effective.

>

[Guest guest]

Jill and all-I agree, this is a great discussion. I do have one

question that I would like to get a response from Rich on or anyone

else who cares to chime in.

Within the last month or so Rich wrote, and I paraphrase, " recently,

I have come to believe that CFS and autism are the same thing. The

difference being the age of onset " .

Surely, IMO, what Rich means is that CFS and autism are the same thing

for a *subset* of CFS patients. I can't see the correlation between

the autism symptoms and most symptoms that are reported w/ CFS.

Just to take one, for example, do autistic folks have post exertional

fatigue? They do have gut problems, but not all CFS patients have

this symptom.

Am I off base? Anyone?

Mike C

>

> Nice dialogue, to which I wish to add a few thoughts.

>

> 1) We are in the beginning of understanding connections between adult

> chronic illnesses like lyme/cfids, and the autism model. Doctors and

> researchers I have spoken with, and only a few thus far, readily

admit

**disease**.

> >snip<<<

[Guest guest]

The idea is that a similar constellation of mutations in the

methylation cycle can lead to autism or chronic fatigue or chronic

lyme etc, under circumstances where the right environmental insults

are present. The autism is a result of damage to the developing brain.

> >

> > Nice dialogue, to which I wish to add a few thoughts.

> >

> > 1) We are in the beginning of understanding connections between adult

> > chronic illnesses like lyme/cfids, and the autism model. Doctors and

> > researchers I have spoken with, and only a few thus far, readily

> admit

> **disease**.

> > >snip<<<

>

[Guest guest]

Yes, I think I have said that a bunch of times repeatedly, that we are

just beginning.

The methylation defects are definitely not sufficient. You have to

have some kind of load on the system that crashes it, such as mercury

poisoning, or perhaps too many biotoxins from bad infections. Once you

get past a certain point, problems that were chronic become global.

In fact, in some instances it could have been highly adaptive. I don't

want to go into that right now but there are some cool ideas out there.

> > >

> > > Nice dialogue, to which I wish to add a few thoughts.

> > >

> > > 1) We are in the beginning of understanding connections between

> adult

> > > chronic illnesses like lyme/cfids, and the autism model. Doctors and

> > > researchers I have spoken with, and only a few thus far, readily

> > admit

> > **disease**.

> > > >snip<<<

> >

>

>

>

>

[Guest guest]

Kurt-I am glad you posted this. I am always concerned that members

just joining this list will read recent posts and think that

whatever the current thread is, like mold, EMFs, Lyme, etc. is all

the list is about without taking the

time to look at old posts. Then they may start treatments based

on whatever is being talked about currently. Ciguatera comes to

mind as something that was discussed but didn't pan out.

Mike C.

In , " Kurt R " <kurt@...> wrote:

>

> Mike, Jill,

>

> I think we need to be careful in this discussion because nothing is

> 'proven' here yet regarding autism and CFS. Certainly the

similarities

> are striking, but so are the differences. We are just speculating.

>

> My own speculation is that in the end the methylation issue will

turn

> out to be a necessary but not sufficient condition for CFS. In

other

> words, you can not get CFS unless you have methylation defects.

> However, not everyone with methylation defects will get CFS. Until

> people with other diseases are genetically profiled, we should not

> presume that this is 'the' original cause. For instance, there

could be

> quite a few toxin-related diseases that share methylation defects

with

> autistic children. The development of CFS may require MUCH more

than

> just methylation defects. And you can not just call any other

> conditions 'triggers' because some of them may ALSO be necessary

for

> CFS. In other words, I could say that the cause of a car accident

is

> riding in a car. After all, that is a necessary condition. And I

could

> say that failing to observe the traffic laws leading to accident

was

> just the trigger. See my point? We do not yet know enough about

this

> to be assuming that these methylation mutations lead to or cause

CFS.

> Adults with CFS have a heaping load more pathological exposures

than

> autistic children.

>

> Personally, I believe we will also eventually learn of other

necessary

> genetic problems for CFS. The opera is not over yet, far from it.

>

> --Kurt

[Guest guest]

> I can't see the correlation between

> the autism symptoms and most symptoms that are reported w/ CFS.

> Just to take one, for example, do autistic folks have post exertional

> fatigue?

Hi Mike C,

I've wondered the same thing.

Sue ,

Upstate New York

[Guest guest]

" Kurt R " < wrote:

> Mike, Jill,

> I think we need to be careful in this discussion because nothing is

> 'proven' here yet regarding autism and CFS. Certainly the

similarities are striking, but so are the differences. We are just

speculating.

> My own speculation is that in the end the methylation issue will

turn out to be a necessary but not sufficient condition for CFS. In

other words, you can not get CFS unless you have methylation defects.

However, not everyone with methylation defects will get CFS. Until

people with other diseases are genetically profiled, we should not

presume that this is 'the' original cause. For instance, there

could be quite a few toxin-related diseases that share methylation

defects with autistic children. The development of CFS may require

MUCH more than just methylation defects. And you can not just call

any other conditions 'triggers' because some of them may ALSO be

necessary for CFS.

In other words, I could say that the cause of a car accident is

riding in a car. After all, that is a necessary condition. And I

could say that failing to observe the traffic laws leading to

accident was just the trigger. See my point? We do not yet know

enough about this to be assuming that these methylation mutations

lead to or cause CFS.

Adults with CFS have a heaping load more pathological exposures than

autistic children. Personally, I believe we will also eventually

learn of other necessary genetic problems for CFS. The opera is not

over yet, far from it.

--Kurt

VERY well put!

I can't even conceive how someone who has seen CFS in it's original

form could even bring to mind such a comparison or make such a

statement.

Imagine an autistic child throwing a tantrum.

That would lay a CFSer out for a month or more, if it were even

possible to expend energy in this fashion.

One might say that CFS and autism have certain immunological

similarities, or that the basis shares common methylation

dysregulation, but the idea of even uttering the concept that they

are the same condition is compelling evidence that the illness that

is being conceptualized is absolutely nothing like CFS.

At least, it has no similarities at all to the illness of the

people who first received the term " CFS " .

One who has seen CFS simply wouldn't put it this way unless the

illness WAS the same.

" The fat lady ain't singing yet! "

-

[Guest guest]

Hi, Mike.

Yes, what I mean to say is that the genetic predisposition and much

of the biochemistry are the same in a major subset of autism and a

major subset of CFS. The symptoms and signs differ because of the

difference in age at onset. If onset occurs early in life, before

the brain is fully developed, then there will be additional symptoms

and signs that result from the interruption in brain development.

It's true in both CFS and autism that symptoms can vary somewhat

from one person to another. But the underlying genetic variations

and much of the biochemistry appear to be the same.

On the question of autism and fatigue, either in general or post-

exertional, that's a difficult question to answer, because babies

can't tell you they are fatigued, and because the ways in which they

manifest fatigue are different from the ways adults do. Some autism

mothers say that their kids really are fatigued, but it is masked by

the fact that the more fatigued they become, the more it is

manifested in hyperactivity. But they know from experience that

when they see this behavior, it means that their child is tired,

i.e. fatigued.

On the gut problems, it's true that not all PWCs have gut problems,

and not all autistic kids do, either. I'm beginning to suspect that

this depends on the serotonin situation, and that in turn will

depend on what set of genetic variations the person has. There are

quite a few different combinations of genetic variations that can

predispose a person to developing autism or CFS. There are subsets

in both.

Rich

>

> Jill and all-I agree, this is a great discussion. I do have one

> question that I would like to get a response from Rich on or anyone

> else who cares to chime in.

>

> Within the last month or so Rich wrote, and I

paraphrase, " recently,

> I have come to believe that CFS and autism are the same thing. The

> difference being the age of onset " .

>

> Surely, IMO, what Rich means is that CFS and autism are the same

thing

> for a *subset* of CFS patients. I can't see the correlation

between

> the autism symptoms and most symptoms that are reported w/ CFS.

> Just to take one, for example, do autistic folks have post

exertional

> fatigue? They do have gut problems, but not all CFS patients have

> this symptom.

>

> Am I off base? Anyone?

>

> Mike C

>

[Guest guest]

and Kurt,

This brings to mind another question as well. How can we compare DNA

in autistic children to the CFIDS population when we don't even know

what the heck the CFIDS population is? I mean we have been griping

about this for years. Who are we? Is fibro part of us? Is Lyme or

mycoplasma part of us? How about those viruses or ciguatera? Do we

all have the same DNA going on?

a

>

> " Kurt R " < wrote:

> > Mike, Jill,

> > I think we need to be careful in this discussion because nothing

is

> > 'proven' here yet regarding autism and CFS. Certainly the

> similarities are striking, but so are the differences. We are just

> speculating.

> > My own speculation is that in the end the methylation issue will

> turn out to be a necessary but not sufficient condition for CFS.

In

> other words, you can not get CFS unless you have methylation

defects.

> However, not everyone with methylation defects will get CFS.

Until

> people with other diseases are genetically profiled, we should not

> presume that this is 'the' original cause. For instance, there

> could be quite a few toxin-related diseases that share methylation

> defects with autistic children. The development of CFS may require

> MUCH more than just methylation defects. And you can not just call

> any other conditions 'triggers' because some of them may ALSO be

> necessary for CFS.

> In other words, I could say that the cause of a car accident is

> riding in a car. After all, that is a necessary condition. And I

> could say that failing to observe the traffic laws leading to

> accident was just the trigger. See my point? We do not yet know

> enough about this to be assuming that these methylation mutations

> lead to or cause CFS.

> Adults with CFS have a heaping load more pathological exposures

than

> autistic children. Personally, I believe we will also eventually

> learn of other necessary genetic problems for CFS. The opera is

not

> over yet, far from it.

> --Kurt

>

> VERY well put!

> I can't even conceive how someone who has seen CFS in it's

original

> form could even bring to mind such a comparison or make such a

> statement.

> Imagine an autistic child throwing a tantrum.

> That would lay a CFSer out for a month or more, if it were even

> possible to expend energy in this fashion.

> One might say that CFS and autism have certain immunological

> similarities, or that the basis shares common methylation

> dysregulation, but the idea of even uttering the concept that they

> are the same condition is compelling evidence that the illness that

> is being conceptualized is absolutely nothing like CFS.

> At least, it has no similarities at all to the illness of the

> people who first received the term " CFS " .

>

> One who has seen CFS simply wouldn't put it this way unless the

> illness WAS the same.

>

> " The fat lady ain't singing yet! "

> -

>

[Guest guest]

" pjeanneus " wrote:

>

> and Kurt,

> This brings to mind another question as well. How can we compare

DNA in autistic children to the CFIDS population when we don't even

know what the heck the CFIDS population is? > a

>

Well, a, Take a look at this interesting statement:

" Some autism mothers say that their kids really are fatigued, but it

is masked by the fact that the more fatigued they become, the more

it is manifested in hyperactivity. But they know from experience that

when they see this behavior, it means that their child is tired,

i.e. fatigued. "

" HYPERACTIVITY " ???

And this is an indication of " fatigue " ??

Now I hate to complain, but this indicates in no uncertain terms

that the writer is thinking of an illness that is ABSOLUTELY NOTHING

like CFS.

Let me repeat that:

ABSOLUTELY NOTHING LIKE CFS!!!

First of all, CFS means not being able to predict when you can

stand up, move, or sometimes even feed yourself.

And the sensation that prevents function is NOTHING like fatigue.

It is a neurological paralysis that take intense mental

concentration to overcome.

" Tired " has absolutely nothing to do with the central sensations

that are of critical importance to CFS.

These kinds of statements do not refer to any subset of CFS.

This only applies to " idiopathic fatigue " ,.

The mere attempt to describe CFS in terms of fatigue or " tired "

without making any effort to explain the devastating neurological

paralysis is a sure sign that the person has no conceptual model for

CFS, no matter how much they think they do.

-

[Guest guest]

Hi, .

Before you get too exercised over this (pun intended!) let me note

that early results of running the ATP Profile test on an autistic

child suggest that their mitochondria might be in much different

condition than those in adults with CFS, perhaps because they are so

young and have not yet suffered as much oxidative damage. But it's

a little early to reach conclusions on this. Comparing very young

children to adults introduces a lot of complicating factors.

Rich

> >

> > and Kurt,

> > This brings to mind another question as well. How can we compare

> DNA in autistic children to the CFIDS population when we don't

even

> know what the heck the CFIDS population is? > a

> >

>

> Well, a, Take a look at this interesting statement:

>

> " Some autism mothers say that their kids really are fatigued, but

it

> is masked by the fact that the more fatigued they become, the more

> it is manifested in hyperactivity. But they know from experience

that

> when they see this behavior, it means that their child is tired,

> i.e. fatigued. "

>

> " HYPERACTIVITY " ???

> And this is an indication of " fatigue " ??

> Now I hate to complain, but this indicates in no uncertain terms

> that the writer is thinking of an illness that is ABSOLUTELY

NOTHING

> like CFS.

> Let me repeat that:

> ABSOLUTELY NOTHING LIKE CFS!!!

> First of all, CFS means not being able to predict when you can

> stand up, move, or sometimes even feed yourself.

> And the sensation that prevents function is NOTHING like fatigue.

> It is a neurological paralysis that take intense mental

> concentration to overcome.

> " Tired " has absolutely nothing to do with the central sensations

> that are of critical importance to CFS.

>

> These kinds of statements do not refer to any subset of CFS.

> This only applies to " idiopathic fatigue " ,.

> The mere attempt to describe CFS in terms of fatigue or " tired "

> without making any effort to explain the devastating neurological

> paralysis is a sure sign that the person has no conceptual model

for

> CFS, no matter how much they think they do.

> -

>

[Guest guest]

" rvankonynen " wrote:

>

> Hi, .

Before you get too exercised over this (pun intended!) let me note

that early results of running the ATP Profile test on an autistic

child suggest that their mitochondria might be in much different

condition than those in adults with CFS, perhaps because they are so

young and have not yet suffered as much oxidative damage. But it's

a little early to reach conclusions on this. Comparing very young

children to adults introduces a lot of complicating factors.

> Rich

Rich,

It's very telling to see that MCSers are forced to say " Chemical

Injury " because the hidden insult in MCS is that the problem is put

upon your individual sensitivity rather than allowing for the

possibility that you were just a normal person struck down by an

overwhelming exposure.

If you recall the history of CFS, even though it struck athletes,

people blamed it on deconditioning and weakness.

Even though it struck people who were health conscious, they blamed

it on bad diet and drugs.

Even though it hit children, they blamed it on a lifetime of self

abuse.

Even though it happened overnight, they blamed it on deconditioning.

They couldn't make up their mind if it was from being lazy, or from

being burned out - so they blamed both simultaneously - while

ignoring our past history of activity.

The list of " misunderstandings " goes on.

No matter how much you describe it as being unlike any sort of

fatigue you have ever felt in your life, not even quantitatively

different, it was QUALITATIVELY and COMPLETELY different as an

undescribable and unknown sensation for which we have no words -

because we never felt anything like this before.

So one has to bear in mind that when someone makes a comparison

between autism and CFS, it's important to remember that this strikes

in a manner that is nothing like autism, and leaves sufferers

complaining of sensations that are also nothing like autism.

You may recall that " CFS " got going when Dr noted that

clusters of illness were occurring among closeknit groups:

The girls basketball team and the Truckee teachers.

The very fact that the illness could do this is an indication that

it has much less respect for individual tolerances and variations

that people who hope it's a rare genetic illness would hope for.

The illness just plain raced through groups in a manner unlike

anything an individual problem could ever do.

Isn't that amazing?

That's the very fluke that brought Polly Murrays attention to Lyme.

She could see that no matter what the symptoms were, the illness

wasn't spreading in a way that a genetic " JRA " illness could.

This whole Autism/CFS line of reasoning is very interesting, but

the " thrust " of the logic involved and the way it is expressed

brings up the very reason that MCSers want the world to understand

that their illness is " Chemical INJURY " :

The illness isn't spreading nearly like an individual susceptibility

as much as it appears to be something that can overwhelm just about

anybody at any time without much warning.

-

[Guest guest]

> >

> > Jill and all-I agree, this is a great discussion. I do have one

> > question that I would like to get a response from Rich on or

anyone

> > else who cares to chime in.

> >

> > Within the last month or so Rich wrote, and I

> paraphrase, " recently,

> > I have come to believe that CFS and autism are the same thing.

The

> > difference being the age of onset " .

> >

> > Surely, IMO, what Rich means is that CFS and autism are the same

> thing

> > for a *subset* of CFS patients. I can't see the correlation

> between

> > the autism symptoms and most symptoms that are reported w/ CFS.

> > Just to take one, for example, do autistic folks have post

> exertional

> > fatigue? They do have gut problems, but not all CFS patients have

> > this symptom.

> >

> > Am I off base? Anyone?

> >

> > Mike C

> >

>

[Guest guest]

Interesting little anecdote I just heard...the Mom of an autistic

child just got a tickbite and came down with horrific lyme which has

already gone to her heart.

IE we may indeed discover similar mutations as Rich is suspecting.

> > > Mike, Jill,

> > > I think we need to be careful in this discussion because nothing

> is

> > > 'proven' here yet regarding autism and CFS. Certainly the

> > similarities are striking, but so are the differences. We are just

> > speculating.

> > > My own speculation is that in the end the methylation issue will

> > turn out to be a necessary but not sufficient condition for CFS.

> In

> > other words, you can not get CFS unless you have methylation

> defects.

> > However, not everyone with methylation defects will get CFS.

> Until

> > people with other diseases are genetically profiled, we should not

> > presume that this is 'the' original cause. For instance, there

> > could be quite a few toxin-related diseases that share methylation

> > defects with autistic children. The development of CFS may require

> > MUCH more than just methylation defects. And you can not just call

> > any other conditions 'triggers' because some of them may ALSO be

> > necessary for CFS.

> > In other words, I could say that the cause of a car accident is

> > riding in a car. After all, that is a necessary condition. And I

> > could say that failing to observe the traffic laws leading to

> > accident was just the trigger. See my point? We do not yet know

> > enough about this to be assuming that these methylation mutations

> > lead to or cause CFS.

> > Adults with CFS have a heaping load more pathological exposures

> than

> > autistic children. Personally, I believe we will also eventually

> > learn of other necessary genetic problems for CFS. The opera is

> not

> > over yet, far from it.

> > --Kurt

> >

> > VERY well put!

> > I can't even conceive how someone who has seen CFS in it's

> original

> > form could even bring to mind such a comparison or make such a

> > statement.

> > Imagine an autistic child throwing a tantrum.

> > That would lay a CFSer out for a month or more, if it were even

> > possible to expend energy in this fashion.

> > One might say that CFS and autism have certain immunological

> > similarities, or that the basis shares common methylation

> > dysregulation, but the idea of even uttering the concept that they

> > are the same condition is compelling evidence that the illness that

> > is being conceptualized is absolutely nothing like CFS.

> > At least, it has no similarities at all to the illness of the

> > people who first received the term " CFS " .

> >

> > One who has seen CFS simply wouldn't put it this way unless the

> > illness WAS the same.

> >

> > " The fat lady ain't singing yet! "

> > -

> >

>

[Guest guest]

And in adults. This is exactly what happened to me last night,

actually. Unaware that I was approaching the point of collapse until I

actually did collapse, in fact, as I approached that point, I got so

overstimulated and over-reactive that I got into an argument and

probably looked like the picture of energy. A few minutes later I

realized I had been approaching this point all weekend, that my

muscles were weak, that my whole body was buzzing, and that I had that

familiar feeling that comes sometimes on too little sleep and too much

activity, since getting lyme, where if I don't rest with NO

STIMULATION or NOISE of any kind, I feel like I will collapse.

> >>

> >> and Kurt,

> >> This brings to mind another question as well. How can we compare

> > DNA in autistic children to the CFIDS population when we don't even

> > know what the heck the CFIDS population is? > a

> >>

> >

> > Well, a, Take a look at this interesting statement:

> >

> > " Some autism mothers say that their kids really are fatigued, but it

> > is masked by the fact that the more fatigued they become, the more

> > it is manifested in hyperactivity. But they know from experience that

> > when they see this behavior, it means that their child is tired,

> > i.e. fatigued. "

> >

> > " HYPERACTIVITY " ???

> > And this is an indication of " fatigue " ??

> > Now I hate to complain, but this indicates in no uncertain terms

> > that the writer is thinking of an illness that is ABSOLUTELY NOTHING

> > like CFS.

> > Let me repeat that:

> > ABSOLUTELY NOTHING LIKE CFS!!!

> > First of all, CFS means not being able to predict when you can

> > stand up, move, or sometimes even feed yourself.

> > And the sensation that prevents function is NOTHING like fatigue.

> > It is a neurological paralysis that take intense mental

> > concentration to overcome.

> > " Tired " has absolutely nothing to do with the central sensations

> > that are of critical importance to CFS.

> >

> > These kinds of statements do not refer to any subset of CFS.

> > This only applies to " idiopathic fatigue " ,.

> > The mere attempt to describe CFS in terms of fatigue or " tired "

> > without making any effort to explain the devastating neurological

> > paralysis is a sure sign that the person has no conceptual model for

> > CFS, no matter how much they think they do.

> > -

> >

> >

> >

> >

> >

> >

> > This list is intended for patients to share personal experiences

> > with each other, not to give medical advice. If you are interested

> > in any treatment discussed here, please consult your doctor.

> >

[Guest guest]

I would say the fatigue (and probably the endocrine and neurological

symptoms) are closer to the kind of problems people have when they are

deprived of sleep for days on end. Rats who are not allowed to sleep

will get all kinds of immune system problems and strange behaviors and

eventually their systems break down and they die. Soldiers can be

severely sleep deprived. I'm not talking about a couple hours short,

or a bad night or two. I suppose a normal person could simulate CFIDS

type fatigue if they wree deprived of sleep for 3-4 days.

>

> This is one of my big fears. If I get overtired I crash so badly I

can barely move. My face buzzes, my eyes won't stay closed and I feel

like I want to yawn, but can't. It's an awful feeling and all I can

do is lie down and wait for it to pass. I have a personality in me

that is like a security guard and will rarely let me get to that

point. I also agree completely with . Fatigue doesn't even get

close to describing the exhaustion.

>

[Guest guest]

What's even more alarming than the hideous way in which you were

treated, Edy, is that this was the treatment for a bona fide " nutcase. "

Normal everyday garden-variety average people have the most

incredible, and incredibly damaging, responses to things they don't

understand.

>

> You know what I mean. I ended up in the phyche ward at the hospital

for 5 days once because I hadn't slept for 3 nights. I thought I

would die. The hospital thought I was depressed and wouldn't let me

stay in bed during the day and I had to lie on a cold, hard floor from

8 in the morning til 10 at night in the " community " room. They

thought I was out of my mind when I said I had CFS. Treated me like a

nutcase. Which at that point I was. All I wanted was to be drugged

into a 3 day sleep.

>

[Guest guest]

" jill1313 " <jenbooks13@...> wrote:

>

> I would say the fatigue (and probably the endocrine and neurological

> symptoms) are closer to the kind of problems people have when they are

> deprived of sleep for days on end. Rats who are not allowed to sleep

> will get all kinds of immune system problems and strange behaviors and

> eventually their systems break down and they die. Soldiers can be

> severely sleep deprived. I'm not talking about a couple hours short,

> or a bad night or two. I suppose a normal person could simulate CFIDS

> type fatigue if they wree deprived of sleep for 3-4 days.

>

>

Funny you should mention that.

I went through many sleep deprivation exercises in the Army.

One lasted for five days before I hit my limit during Operation

Reforger (REturn of FORces to GERmany) in '75. An exercise that

simulated a NATO invasion of Europe in response to a soviet incursion.

I would often refer to that exercise and say " I've been set on fire,

had broken bones, Hangovers from drinking Ouzo all night in Crete, and

been kept awake for five days on military missions, and if you put them

all together, it still wouldn't feel as bad as CFS " .

The military often pushed people to the limit, just to weed out the

ones who broke down first. I got to see what happened, and it was

absolutely nothing like CFS.

Although to someone who doesn't believe a thing you say, that is the

mental image they would call to mind even if you tell them that

you've " been there and done it " and " that ain't it " .

It is infuriating that you can explain the neuro-paralytic dysfunction

in very clear terms, and yet people will STILL say " So you mean, VERY,

VERY tired " .

NO. Nothing like tired. Nothing like anything I ever felt.

Looks more to me like a stroke victim who struggles, but cannot find

the words to speak, and cannot move.

-

[Guest guest]

You really don't have to wait. There are several books on the subject.

Methylation is not a new thing. I got a book on it in 1999. ALso check

homocysteine, a closely related topic.

mjh

" The Basil Book "

_http://foxhillfarm.us/FireBasil/_ (http://foxhillfarm.us/FireBasil/)

I dont know alot about methylation - I'm waiting for Rich to write a paper

on it - but I would not go so far to say that every CFS patient has problems

with methylation. I would suggest that some do and treatments based on those

problems will be helpful in that case.

[Guest guest]

Hi, Cort.

>

> I just think it takes a huge leap of faith to believe that autism -

one of the most profoundly disturbing brain diseases - and CFS are

similar in pathology.

***If by " pathology " here you are referring to the popular meaning

of pathology that refers to how the tissues look structurally,

especially the brain tissue, then I would not suggest that these two

disorders show the same pathology. If, however, you mean

pathogenesis, then I think there is evidence for a great deal of

similarity between a major subset of autism and a major subset of

CFS. If you want to know what that evidence is, I suggest that you

listen to the interview that Laurette Janak and I did with Teri

Small in early June. You can hear it by going to the archives at

http://www.autismone.org/radio, clicking on the left arrow to get to

the June calendar, and then clicking on the bold times of day for

the interview with our names on it. Then click on the upper Play

arrow, and you can listen to it. It's three hours long, and we

reviewed lots of evidence.

Rich got interested in autism by learning that glutathione can be

helpful in autism. But does this mean the two have similar causes?

***That fact by itself doesn't, no.

That GSH is depleted in both?

***The work of S. Jill et al., published near the end of 2004,

showed that glutathione is depleted in autism. I realize that you

don't agree that the literature shows that glutathione is depleted

in a major subset of CFS, but we've been over that several times in

the past. I think it is also relevant that several people on this

list, including yourself, as I understand it, have tested low for

glutathione.

Or is it more likely at this point thiat they share another

common factor such as increased oxidative stress?

***They do in fact both share oxidative stress, and in many cases

that is intimately tied up with glutathione depletion, since

glutathione is the basis for the antioxidant enzyme system.

>

> We know that glutathione is very helpful in some CFS patients,

moderately helpful in others and not helpful in others.

***The work of Amy Yasko has shown why some people do not do well

with supplementation of glutathione. They have a SNP that causes

upregulation of the enzyme cystathionine beta synthase. This causes

an overload of the sulfite oxidase enzyme and leads to rises in

sulfites and hydrogen sulfide, which produce symptoms.

The research evidence for low glutathione levels in CFS is very

mixed with most studies showing normal glutathione levels.

***A great deal of the body of research in CFS on a whole range of

topics is mixed. As I've argued in the past, this is a result of

the broad research case definition for CFS, which results in a very

heterogeneous population for study. When studies are done with

relatively low budgets and are thus forced to limit the number of

patients in the group studied, the result of these two factors is

that there is too much scatter in the data and the averages of

different studies will not agree. This is a well-understood problem

in scientific research. You must have a tight definition if you want

to get crisp and definitive results. Unfortunately this is not

currently the case in CFS, and as a result we have a large body of

research that is not only worthless, but unfortunately worse than

worthless, because it is very difficult to test a hypothesis against

research that argues in both directions. This is the tragedy of CFS

research. The CDC does not want to change the definition, according

to Leonard , because it would render all previous research

useless. What they don't want to face is that that is already true.

This is not to say GSH cannot be very helpful in CFS; CFS has

consistently been shown to be a disease of high oxidative stress and

GSH is the main detoxifier in the body - it stands to reason that it

would be helpful. I wouldn't be surprised if GSH supplementation

helps to some degree in many chronic diseases. Whether or not it is

central in CFS is an entirely different proposal.

***What we are working on now is not supplementing glutathione, but

going after the root causes of the vicious circle that keeps

glutathione from rising naturally to a normal level.

>

> To be blunt about it a good number of studies have looked at

antioxidants levels (GSH included) and there doesn't seem to be a

rush in the research community to study it. - we are the ones that

are most interested in it. Even Dr. Cheney - who brought whey

protein to the fore in CFS - did not list it among his top 4

treatments. I know there are people who have gotten a great deal of

help from glutathione - I dont want to dissuade anybody from trying

this excellent compound - but I dont see the evidence that indicates

it is central to CFS.

***In many scientific fields it is the case that important things go

unrecognized for a long time. Then, one day, someone figures it

out, and that starts a scientific revolution. The fact that this

has gone unrecognized does not provide evidence that it is invalid.

In fact, in the presence of the lack of progress in CFS for many

years, one should expect that whatever is important has gone

unrecognized. Again, we have moved beyond trying to build

glutathione by supplementing it, to dealing with the genetically-

based vicious circle that holds it down.

>

> While it is true that autistic people share some symptoms with

CFS patients so do fibromyalgia syndrome patients, irritable bowel

syndrome patients, myofascial pain syndrome and people with

overtraining syndorme. The symptomatic overlap between overlap

between orthostatic intolerance and CFS is simply amazing. Besides

their movement difficulties MS patients can experience overwhelming

fatigue. CFS patients also share numerous symptoms with what is

called 'sickness behavior' - which refers to the acute stages of

infection we are all familiar with. Most of the symptoms in CFS are

fairly and a fair number of diseases have many of them. It would be

interesting to see in post exertional fatigue is present in autism -

it appears to be in FMS.

***Some recent posts on the lists have been discussing fatigue in

autism. There does seem to be some evidence for it.

>

> I dont know alot about methylation - I'm waiting for Rich to

write a paper on it - but I would not go so far to say that every

CFS patient has problems with methylation. I would suggest that some

do and treatments based on those problems will be helpful in that

case.

***I think it is going to be a while before I will be able to do

that Cort! I have too many other commitments right now. But you

can get some good, easy-to-follow explanations of it if you watch

the free videos of talks given by Jill and by Deth at

the recent DAN! conferences (http://www.danwebcast.com). I don't

think that all the PWCs who meet the Fukuda et al. criteria have

methylation cycle blocks, either, but a large proportion appear to.

Again, it's the problem with the broad case definition.

>

> I think the methylation treatments will be like many treatment

protocols; each one helps some people in a moderate degree, a few

people will luck out and get really well and some wont get much of

a response to it at all.

***We will have to wait to see about this. I'm optimistic that

quite a few will be helped.

Why do I think t hat? Because there is little evidence as yet that

CFS is truly a hereditary disorder - the twin studies certainly dont

show that. Does this mean heredity doesnt play a role? No,

hereditary does play some role and it will good to know what role it

plays but it is not determinative. Just on personal level - my twin

brother does not have CFS. Somewhere along the line I bumped into

something really bad and he didnt - that I think is the difference

between us two.

***I think there is good evidence that both a genetic predisposition

and circumstances in the person's life are important in producing

onset of CFS. Again, bear in mind that the quality of the research

data base in CFS is poor, because of the broad case definition. I

think it is very possible that with two people having the same

genes, one could have onset and the other not, though both are

vulnerable from the standpoint of genetic predisposition. I think

this also offers hope to the one who had the onset, that once the

vicious circle is broken, his metabolic processes can be returned to

normal, so that he will enjoy the same state of health as the one

who never suffered onset (yet!).

>

> I think theres a long long way to go on our journey to

understand CFS. I dont think its going to be this easy. I do think

that detoxification is very important, however, and if methylation

fits into this detoxification scenario, then treatments addressing

it, along with GSH, will be another valuable addition to the CFS

treatment regime.

***I agree that detox is important. For many PWCs, it appears that

toxins played a major role in bringing down their glutathione,

setting off the vicious circle involving the methylation cycle, and

producing the onset and the chronicity of this disorder.

***Rich

>

[Guest guest]

Rich,

Thank you very much for clarifying that you are addressing a SUBSET of CFS. And

about the massive confusion in doing and intrepreting Research data due to the

Heterogeneous population under the CDC's changing and current CFS definition!!

I really hope that everyone takes note of your comments.

Thank you,

Katrina

P.S. I don't agree that CFS Researchers are not getting anywhere. ALot of work

is being done that we do not see, or is stalled for financial reasons only.

> >

> > I just think it takes a huge leap of faith to believe that autism -

> one of the most profoundly disturbing brain diseases - and CFS are

> similar in pathology.

>

> ***If by " pathology " here you are referring to the popular meaning

> of pathology that refers to how the tissues look structurally,

> especially the brain tissue, then I would not suggest that these two

> disorders show the same pathology. If, however, you mean

> pathogenesis, then I think there is evidence for a great deal of

> similarity between a major subset of autism and a major subset of

> CFS. If you want to know what that evidence is, I suggest that you

> listen to the interview that Laurette Janak and I did with Teri

> Small in early June. You can hear it by going to the archives at

> http://www.autismone.org/radio, clicking on the left arrow to get to

> the June calendar, and then clicking on the bold times of day for

> the interview with our names on it. Then click on the upper Play

> arrow, and you can listen to it. It's three hours long, and we

> reviewed lots of evidence.

>

> Rich got interested in autism by learning that glutathione can be

> helpful in autism. But does this mean the two have similar causes?

>

> ***That fact by itself doesn't, no.

>

> That GSH is depleted in both?

>

> ***The work of S. Jill et al., published near the end of 2004,

> showed that glutathione is depleted in autism. I realize that you

> don't agree that the literature shows that glutathione is depleted

> in a major subset of CFS, but we've been over that several times in

> the past. I think it is also relevant that several people on this

> list, including yourself, as I understand it, have tested low for

> glutathione.

>

> Or is it more likely at this point thiat they share another

> common factor such as increased oxidative stress?

>

> ***They do in fact both share oxidative stress, and in many cases

> that is intimately tied up with glutathione depletion, since

> glutathione is the basis for the antioxidant enzyme system.

> >

> > We know that glutathione is very helpful in some CFS patients,

> moderately helpful in others and not helpful in others.

>

> ***The work of Amy Yasko has shown why some people do not do well

> with supplementation of glutathione. They have a SNP that causes

> upregulation of the enzyme cystathionine beta synthase. This causes

> an overload of the sulfite oxidase enzyme and leads to rises in

> sulfites and hydrogen sulfide, which produce symptoms.

>

> The research evidence for low glutathione levels in CFS is very

> mixed with most studies showing normal glutathione levels.

>

> ***A great deal of the body of research in CFS on a whole range of

> topics is mixed. As I've argued in the past, this is a result of

> the broad research case definition for CFS, which results in a very

> heterogeneous population for study. When studies are done with

> relatively low budgets and are thus forced to limit the number of

> patients in the group studied, the result of these two factors is

> that there is too much scatter in the data and the averages of

> different studies will not agree. This is a well-understood problem

> in scientific research. You must have a tight definition if you want

> to get crisp and definitive results. Unfortunately this is not

> currently the case in CFS, and as a result we have a large body of

> research that is not only worthless, but unfortunately worse than

> worthless, because it is very difficult to test a hypothesis against

> research that argues in both directions. This is the tragedy of CFS

> research. The CDC does not want to change the definition, according

> to Leonard , because it would render all previous research

> useless. What they don't want to face is that that is already true.

>

> This is not to say GSH cannot be very helpful in CFS; CFS has

> consistently been shown to be a disease of high oxidative stress and

> GSH is the main detoxifier in the body - it stands to reason that it

> would be helpful. I wouldn't be surprised if GSH supplementation

> helps to some degree in many chronic diseases. Whether or not it is

> central in CFS is an entirely different proposal.

>

> ***What we are working on now is not supplementing glutathione, but

> going after the root causes of the vicious circle that keeps

> glutathione from rising naturally to a normal level.

> >

> > To be blunt about it a good number of studies have looked at

> antioxidants levels (GSH included) and there doesn't seem to be a

> rush in the research community to study it. - we are the ones that

> are most interested in it. Even Dr. Cheney - who brought whey

> protein to the fore in CFS - did not list it among his top 4

> treatments. I know there are people who have gotten a great deal of

> help from glutathione - I dont want to dissuade anybody from trying

> this excellent compound - but I dont see the evidence that indicates

> it is central to CFS.

>

> ***In many scientific fields it is the case that important things go

> unrecognized for a long time. Then, one day, someone figures it

> out, and that starts a scientific revolution. The fact that this

> has gone unrecognized does not provide evidence that it is invalid.

> In fact, in the presence of the lack of progress in CFS for many

> years, one should expect that whatever is important has gone

> unrecognized. Again, we have moved beyond trying to build

> glutathione by supplementing it, to dealing with the genetically-

> based vicious circle that holds it down.

> >

> > While it is true that autistic people share some symptoms with

> CFS patients so do fibromyalgia syndrome patients, irritable bowel

> syndrome patients, myofascial pain syndrome and people with

> overtraining syndorme. The symptomatic overlap between overlap

> between orthostatic intolerance and CFS is simply amazing. Besides

> their movement difficulties MS patients can experience overwhelming

> fatigue. CFS patients also share numerous symptoms with what is

> called 'sickness behavior' - which refers to the acute stages of

> infection we are all familiar with. Most of the symptoms in CFS are

> fairly and a fair number of diseases have many of them. It would be

> interesting to see in post exertional fatigue is present in autism -

> it appears to be in FMS.

>

> ***Some recent posts on the lists have been discussing fatigue in

> autism. There does seem to be some evidence for it.

> >

> > I dont know alot about methylation - I'm waiting for Rich to

> write a paper on it - but I would not go so far to say that every

> CFS patient has problems with methylation. I would suggest that some

> do and treatments based on those problems will be helpful in that

> case.

>

> ***I think it is going to be a while before I will be able to do

> that Cort! I have too many other commitments right now. But you

> can get some good, easy-to-follow explanations of it if you watch

> the free videos of talks given by Jill and by Deth at

> the recent DAN! conferences (http://www.danwebcast.com). I don't

> think that all the PWCs who meet the Fukuda et al. criteria have

> methylation cycle blocks, either, but a large proportion appear to.

> Again, it's the problem with the broad case definition.

> >

> > I think the methylation treatments will be like many treatment

> protocols; each one helps some people in a moderate degree, a few

> people will luck out and get really well and some wont get much of

> a response to it at all.

>

> ***We will have to wait to see about this. I'm optimistic that

> quite a few will be helped.

>

> Why do I think t hat? Because there is little evidence as yet that

> CFS is truly a hereditary disorder - the twin studies certainly dont

> show that. Does this mean heredity doesnt play a role? No,

> hereditary does play some role and it will good to know what role it

> plays but it is not determinative. Just on personal level - my twin

> brother does not have CFS. Somewhere along the line I bumped into

> something really bad and he didnt - that I think is the difference

> between us two.

>

> ***I think there is good evidence that both a genetic predisposition

> and circumstances in the person's life are important in producing

> onset of CFS. Again, bear in mind that the quality of the research

> data base in CFS is poor, because of the broad case definition. I

> think it is very possible that with two people having the same

> genes, one could have onset and the other not, though both are

> vulnerable from the standpoint of genetic predisposition. I think

> this also offers hope to the one who had the onset, that once the

> vicious circle is broken, his metabolic processes can be returned to

> normal, so that he will enjoy the same state of health as the one

> who never suffered onset (yet!).

> >

> > I think theres a long long way to go on our journey to

> understand CFS. I dont think its going to be this easy. I do think

> that detoxification is very important, however, and if methylation

> fits into this detoxification scenario, then treatments addressing

> it, along with GSH, will be another valuable addition to the CFS

> treatment regime.

>

> ***I agree that detox is important. For many PWCs, it appears that

> toxins played a major role in bringing down their glutathione,

> setting off the vicious circle involving the methylation cycle, and

> producing the onset and the chronicity of this disorder.

>

> ***Rich

> >

>

[Guest guest]

Hi, Cort.

***As usual, I appreciate your incisive comments.

>

> I have never had my GSH directly tested. I have indicators that a)

my GSH levels could be low and that my GSH

detoxification 'pathway?' is working fine - so I'm in the middle.

***Hmmm. I think it would be interesting to see the results of a

direct measurement. Your situation is sort of like a microcosm of a

lot of the CFS research. One paper says one thing, and another says

the opposite. The nice thing about studying an individual case,

though, is that you can nail down the facts for that person, since

you aren't averaging over a heterogeneous group.

>

> Thanks for the URL on the interview I missed it earlier.

***You're welcome. I can't brag about my public speaking

performance there, but I think the material we discussed is good

stuff.

>

> THeres a big difference between saying that depleted GSH is the

cause or a cause of CFS and saying that you have low GSH levels

because of increased oxidative stress. In the first the answer is

to fix the GSH problem, in the second you take care of the cause of

oxidative stress (as well as take GSH) - those are two very

different scenario's.

***This is kind of like the yin and the yang. I think that

oxidative stress and glutathione depletion are inseparable. I do

get your point, though. If you really do have a very strong

generator of oxidative stress, it will be difficult to beat it using

only attempts to build glutathione. Toxins are such a possibility.

I do think that they need to be attended to as well, particularly in

someone who has been ill for a long time and has therefore

accumulated a lot of toxins.

>

> The fact is that even with the poor definition and the poor

sample sets researchers have been able to find a number of

consistent abnormalities - Rnase L, NK cell dysfunction, cortisol to

some degree, impaired blood flows, choline spikes in the brain, -

GSH depletion is not one of them. This in itself implies it is not

central to CFS.

***I guess I would say that all of the things you mentioned have

been found in some PWCs, but not in all, including glutathione

depletion. What's more, I think the glutathione depletion--

methylation cycle block hypothesis can account for all of them and

tie them all together into a coherent cause and effect tree. If you

want me to go into detail on that, I can do so.

>

> I keep hearing that there is both a genetic component and an

environmental to CFS. I dont know what makes this noteworthy - that

is true for every disease that is not purely one or the other - and

that includes almost the diseases. Of course theres going to be some

connection. The question is how strong is the genetic component.? I

dont think we know that yet.

***I agree. I don't think it is particularly noteworthy that both

are involved. I think I have stated that both components are found

in most disease states, because they all involve the response of the

organism, and that is to some degree based on genetics, and most

also involve some environmental factor, such as a pathogen, a toxin,

a dietary deficiency, a trauma, etc. Believe it or not, I also

agree that we haven't yet seen the degree to which genetic

polymorphisms are involved in the various subsets of CFS. They

appear to be quite significant in the subset with low glutathione,

however.

>

> Maybe I'm nitpicking but how can you say with confidence that

if for MANY PWC's it appears that toxins brought down their GSH

levels and then set off their methylation problems, etc. when we a)

dont have any tests on toxin levels that I am aware of in CFS and

the evidence for GSH depletion is so poor and c) that there the

methylation stuff is simply theory right now. Its a nice theory -

its got a nice sweept to it but ou need alot to go right for that

theory to hold.

***I think the key words here are " it appears. " When I use those

words, I am not saying that this is proven. I'm saying that that's

how it appears to me at the present time. I am involved in

hypothesis-driven research, something that I think has been sorely

lacking in a lot of the biomedical fields in the past, but which has

been found to be very powerful in the physical sciences. By

developing hypotheses, we can project the science ahead much faster

than if we are afraid to suggest anything we can't yet prove. And

obviously the rest of the scientific method has to be used as well,

i.e. the comparison of hypothesis to observation and experiment.

But without a hypothesis, we don't know what observations to make.

It's a bit like the difference between the static trench warfare of

WW I and the action of Patton's Third Army in WW II. If you want

to know why it appears to me that toxins played an important role in

many cases, I can get into that. I think I have presented my

reasoning at every step of the way, for those who have been

following my posts, but I can repeat it if that would be helpful.

***Briefly, we do have chelator-provoked urine collection tests and

now the newer urinary porphryin tests that give good indications of

heavy metal body burdens, which appear to be some of the most

important in the pathogenesis and pathophysiology of CFS. There are

also tests for many other toxins, such as are offered by

http://www.nmslab.com in Pennsylvania or by http://www.biolab.co.uk

in London. Some PWCs have used these tests, and I have received

reports from them. So good toxicology testing is available.

***The evidence for glutathione depletion is no poorer, in my

opinion, than the evidence for many other aspects of CFS, and as I

have said, I believe that this results primarily from the broadness

of the current case definition. I find it most productive to look

at individual cases, where averaging does not occur, and you can get

a direct measurement of the glutathione level for that individual,

at a fairly reasonable cost.

***The " methylation stuff " is not simply theory. It has been borne

out in literally thousands of autistic patients so far, and the

combinations of SNPs found in the seventeen PWCs whose test results

I have seen up to now are the same ones that have been found in the

autistic patients.

>

> My stool test for heavy metals showed normal amounts of all of

them by the way and I have horrible chemical sensitivities. I dont

think the problem with MCS is detox - I think detox can help

obviously but I dont know that high levels of toxins are the cause

of MCS.

***It is well known among clinicians experienced in heavy metal

toxicology that the stool test does not reflect body burdens of

heavy metals. The best tests for that are the chelator-provoked

urine collection and the newer urinary porphryin test.

***I'm sorry that you suffer from MCS. As you may know, I attended

the workshop on developing a case definition for it about a week and

a half ago. I hope to finish the next installment of my report on

that meeting and post it here soon. It's beginning to look as

though there are at least two subsets within MCS. Some of the

people with MCS can trace their onset to a major acute exposure of a

particular chemical (my wife is in this subset, because of a big

ammonia exposure at work), after which they have been sensitive to

many different chemicals.

***Others report that there was no major acute exposure, but that

over time they gradually developed sensitivity to many chemicals.

***I suspect that the first group sustained an injury to a

protective membrane in their nasal passages, and this has enabled

inhaled chemicals since then to travel up the olfactory nerve

directly into the brain. This appears to be a very rapid process.

***I suspect that the second group has genetic polymorphisms in some

of their detox enzymes, and that this has allowed the buildup of

toxins in their bodies. I think this second subset does suffer from

toxin buildup. There are two studies so far that support this

proposition, one by Haley et al in Gulf War Illnesses, and

the other by Gail McKeown-Eyssen et al. in MCS.

***Rich