Re: CFS and DAN! treatments for autism

January 6, 2006

RIght on, I've been saying this lately too. I hae a couple of points

of refining:

1) In some ways the kids are worse off and in some ways better off.

Their brains are affected, but their immune systems are still

relatively resilient. For some midlife or older adults with decades of

CFS it may be much more difficult

2) I think lyme is involved in at least 50% of adult CFS situations

and lyme itself downregulates immunity, allowing other pathogens to

piggyback and skewing the immune system and once you have that, you

may end up getting some of the methylation defects merely from

overburdening of toxins. You can end up with a similar skewed pathway

but for different reasons and it may be that, at least if you have

lyme, if you could tolerate years of abx (which I can't) that alone

would slowly get you well. Some of the autistic kids DO have lyme and

this is still overlooked by DAN community

3) There will be other CFS situations where a toxic exposure

(pesticides, molds) will be the primary cause.

4) No matter what, restoring the methylation pathways restores

detoxification ability and that is important. Now in looking back I

realize I had lyme since age 21--then when I got re-bit with a much

more virulent tick with lyme and babesia later, is when I got really

ill. But now I look back and realize, a summer at Yale at 21, was when

my health really started going kaflooey (after that). And the amalgams

I had tolerated perfectly well as a teenager, became intolerable. I

couldn't detox the leaking mercury because I had biotoxins from

chronic lyme, and then couldn't fight of strep and fungus as well, and

had those biotoxins too.

So whatever the way you get there, you need to support detox.

I still think glutathione is only a piece of the puzzle, you need all

those pathways working, not just the endpoint, although glutathione is

useful. But for instance if I had to choose btw magnesium and

glutathione, I'd choose the former, in terms of effect on my health.

Luckily I don't have to choose.

It seems others are having this same insight on this and other lists,

and its a very useful one (autism/CFS). In fact, when I did my first

hyperbaric oxygen 5 years ago, the doctor, who specialized in treating

autistic kids, said exactly what you're saying now. He said, CFS is

autism but without all those vaccinations.

>

> Hi, all.

>

> I am posting the following message to several CFS internet lists,

> based on the experiences that many of you have shared with me.

> Thank you, and I hope this really flies:

>

> I have been researching chronic fatigue syndrome for over eight

> years. As regular readers may recall, I had developed a hypothesis

> for the pathogenesis of chronic fatigue syndrome that prominently

> featured the depletion of glutathione, and I presented a poster

> paper on it at the AACFS (now the IACFS) meeting in October, 2004,

> in Madison, Wisconsin. This paper can be found at

>

> http://www.cfsresearch.org/cfs/research/treatment/15.htm

>

> Anecdotal experience of people in the internet

> group and others who took my hypothesis seriously and acted upon it

> suggested that while some were able to raise their glutathione

> levels by various means and experienced benefit from doing so,

> others were not able to do so. At the time of writing my poster

> paper, I was aware of this, and I acknowledged in the conclusions of

> the paper that there appeared to be things that were blocking the

> raising of glutathione in CFS. At that time, I was not sure

> specifically what they were. I also knew that there was evidence

> for a genetic predisposition in CFS, but I did not know the details

> of the genetic variations involved.

>

> Since then, I became aware of the work of S. Jill et al. in

> autism (Am J Clin Nutr. 2004 Dec;80(6):1611-7). They found that

> glutathione was also depleted in autistic children, that this

> resulted from a partial block in the methylation (also called

> methionine) cycle, that this partial block resulted in part from

> genetic variations in the genes for certain enzymes and proteins

> associated with the sulfur metabolism (I don't think the genetic

> part is published yet), and that it interfered with the conversion

> of methionine to cysteine, which is the rate-limiting amino acid for

> the synthesis of glutathione. They found that by using certain

> supplements they could lift the block in the methylation cycle and

> restore the glutathione level.

>

> In response to learning of this work, I became very interested in

> possible parallels between chronic fatigue syndrome and autism. I

> went on to attend the conference of the Defeat Autism Now! project

> in Long Beach, California in October, 2005. As a result of this

> experience, I became convinced that the genetic predisposition found

> in autism must be the same or similar to that in a major subset of

> chronic fatigue syndrome, and that the resulting biochemical

> abnormalities were also the same or similar. As far as I know, the

> genetic variations in people with CFS have not yet been studied in

> detail or published, but I am optimistic that this will occur soon,

> because of the rapid advances in the technology for doing so, and

> the current active interest of at least three groups in the U.S. and

> the U.K. in genomic aspects of CFS.

>

> There are obviously also major differences between chronic fatigue

> syndrome and autism. I believe that these result primarily from the

> different ages of onset. Autistic children experience onset early

> in life, before their brains are fully developed. I believe that

> this gives rise to the very different brain-related symptoms seen in

> autistic children from those seen in adults with CFS. However,

> there are many similarities in the symptomatology and the

> biochemistry of these two disorders as well, including oxidative

> stress, buildup of toxins, immune response shift to Th2, and gut

> problems, for examples.

>

> The triggering factors for autism and chronic fatigue syndrome are

> also largely different. There appears to be substantial evidence

> now that vaccinations (containing either a mercury-based

> preservative or live viruses, many given at the same time) were

> responsible for triggering many of the cases of autism in

> genetically-susceptible children. In CFS, a variety of triggering

> factors (physical, chemical, biological, or psychological/emotional)

> have been shown to be involved in various cases. All of these

> factors have in common the tendency to deplete glutathione. It

> appears that once glutathione drops sufficiently in a genetically

> susceptible person, the methylation cycle goes down, and the result

> is a depletion of several important metabolites in the sulfur

> metabolism, including S-adenosylmethionine (SAMe), cysteine,

> glutathione, taurine and sulfate. The depletion in these

> metabolites causes an avalanche of pathogenesis, since they all have

> very important functions in the body, and I think that much of this

> pathogenesis is common between autism and CFS. In autism, I think

> the loss of methylation capacity because of the drop in SAMe is

> responsible for much of the interference with normal brain

> development.

>

> I think that the reason why the people who have developed CFS as

> adults did not develop autism as children (even though I suspect

> that they have the same or similar genetic predisposition) is that

> when they were children, not as many vaccinations were required.

> The schedule of vaccinations required for children in the U.S. has

> grown substantially in the past two or three decades, as has the

> incidence of autism. I think this is also true in the U.K.

>

> My main message is that a great deal has already been worked out in

> autism by the people in the Defeat Autism Now! project, and that I

> believe that the CFS community would benefit greatly by looking

> carefully at what they have already done. They have found

> supplements that will compensate for the genetic variations and

> correct these biochemical irregularities. They are also detoxing

> heavy metals. The results in many autistic children have been

> astounding.

>

> So I want to encourage everyone who has an interest in CFS to look

> at the results of the DAN! project in autism. You can view videos

> of the talks given at the latest two DAN! conferences on the

> internet at no cost (unless you are paying for the internet time!).

> Go to this site:

>

> http://www.danwebcast.com

>

> You can choose either the later Long Beach conference or the earlier

> Boston conference. They cover much of the same material, but both

> are worthwhile to watch. If you want to see a good explanation of

> the methylation cycle research, go to the Boston meeting first, so

> you will be able to view the talk by Jill , who did not attend

> the Long Beach meeting.

>

> After selecting one of the conferences, go to the lower left and

> register. This is free. They will email a password to you right

> away, and then you can choose a talk to watch.

>

> Beyond this, I also want to recommend a book. This is a new book

> (Sept. 2005). It is by Jon Pangborn, Ph.D. and Sydney Baker, M.D.,

> a biochemist and an autism clinician, respectively. It is available

> on Amazon for people within the U.S. For people outside the U.S.,

> it can be obtained from the following website by means of PayPal:

>

> http://www.autismresearchinstitute.com

>

> The cost for the book is $30 U.S.

>

> This is an excellent book. It is a reference book, full of good

> information and good science, explained clearly. This book deals

> very practically with developing a treatment program for an

> individual child. I think that most of it will turn out to apply

> directly to adults with CFS as well.

>

> Although I have been suggesting consideration of the DAN! treatments

> to people with CFS for only about two months, and it is too soon to

> draw conclusions, early feedback is very encouraging. While I am

> going out on a limb in announcing this on Co-Cure now, I don't want

> to wait any longer, because I think this could help a lot of

> people. Of course, we should all keep in mind that with the current

> case definition of CFS we have a very heterogeneous population, and

> the DAN! treatments may not help all PWCs, but I am convinced that

> they will help a substantial subset. So I want to encourage you to

> look into this in the strongest way I can. It could be the answer

> for many of you.

>

> Rich Van Konynenburg, Ph.D.

>

January 6, 2006

Hi, Jill.

Thanks for the comments. I think you made some good points. I have

a lot to learn about autism, since I really haven't studied it much

until recently. I just think I've heard enough to know that there

are powerful parallels with CFS.

Yes, I'm not the first person to make a connection between autism

and CFS. It just took me a little longer to get there. But I would

say that most of the CFS research and clinical community isn't there

yet, and if things continue to look good with these treatments, I'm

planning to try to get the word to them.

Rich

> >

> > Hi, all.

> >

> > I am posting the following message to several CFS internet

lists,

> > based on the experiences that many of you have shared with me.

> > Thank you, and I hope this really flies:

> >

> > I have been researching chronic fatigue syndrome for over eight

> > years. As regular readers may recall, I had developed a

hypothesis

> > for the pathogenesis of chronic fatigue syndrome that

prominently

> > featured the depletion of glutathione, and I presented a poster

> > paper on it at the AACFS (now the IACFS) meeting in October,

2004,

> > in Madison, Wisconsin. This paper can be found at

> >

> > http://www.cfsresearch.org/cfs/research/treatment/15.htm

> >

> > Anecdotal experience of people in the internet

> > group and others who took my hypothesis seriously and acted upon

it

> > suggested that while some were able to raise their glutathione

> > levels by various means and experienced benefit from doing so,

> > others were not able to do so. At the time of writing my poster

> > paper, I was aware of this, and I acknowledged in the

conclusions of

> > the paper that there appeared to be things that were blocking

the

> > raising of glutathione in CFS. At that time, I was not sure

> > specifically what they were. I also knew that there was

evidence

> > for a genetic predisposition in CFS, but I did not know the

details

> > of the genetic variations involved.

> >

> > Since then, I became aware of the work of S. Jill et al.

in

> > autism (Am J Clin Nutr. 2004 Dec;80(6):1611-7). They found that

> > glutathione was also depleted in autistic children, that this

> > resulted from a partial block in the methylation (also called

> > methionine) cycle, that this partial block resulted in part from

> > genetic variations in the genes for certain enzymes and proteins

> > associated with the sulfur metabolism (I don't think the genetic

> > part is published yet), and that it interfered with the

conversion

> > of methionine to cysteine, which is the rate-limiting amino acid

for

> > the synthesis of glutathione. They found that by using certain

> > supplements they could lift the block in the methylation cycle

and

> > restore the glutathione level.

> >

> > In response to learning of this work, I became very interested

in

> > possible parallels between chronic fatigue syndrome and autism.

I

> > went on to attend the conference of the Defeat Autism Now!

project

> > in Long Beach, California in October, 2005. As a result of this

> > experience, I became convinced that the genetic predisposition

found

> > in autism must be the same or similar to that in a major subset

of

> > chronic fatigue syndrome, and that the resulting biochemical

> > abnormalities were also the same or similar. As far as I know,

the

> > genetic variations in people with CFS have not yet been studied

in

> > detail or published, but I am optimistic that this will occur

soon,

> > because of the rapid advances in the technology for doing so,

and

> > the current active interest of at least three groups in the U.S.

and

> > the U.K. in genomic aspects of CFS.

> >

> > There are obviously also major differences between chronic

fatigue

> > syndrome and autism. I believe that these result primarily from

the

> > different ages of onset. Autistic children experience onset

early

> > in life, before their brains are fully developed. I believe

that

> > this gives rise to the very different brain-related symptoms

seen in

> > autistic children from those seen in adults with CFS. However,

> > there are many similarities in the symptomatology and the

> > biochemistry of these two disorders as well, including oxidative

> > stress, buildup of toxins, immune response shift to Th2, and gut

> > problems, for examples.

> >

> > The triggering factors for autism and chronic fatigue syndrome

are

> > also largely different. There appears to be substantial

evidence

> > now that vaccinations (containing either a mercury-based

> > preservative or live viruses, many given at the same time) were

> > responsible for triggering many of the cases of autism in

> > genetically-susceptible children. In CFS, a variety of

triggering

> > factors (physical, chemical, biological, or

psychological/emotional)

> > have been shown to be involved in various cases. All of these

> > factors have in common the tendency to deplete glutathione. It

> > appears that once glutathione drops sufficiently in a

genetically

> > susceptible person, the methylation cycle goes down, and the

result

> > is a depletion of several important metabolites in the sulfur

> > metabolism, including S-adenosylmethionine (SAMe), cysteine,

> > glutathione, taurine and sulfate. The depletion in these

> > metabolites causes an avalanche of pathogenesis, since they all

have

> > very important functions in the body, and I think that much of

this

> > pathogenesis is common between autism and CFS. In autism, I

think

> > the loss of methylation capacity because of the drop in SAMe is

> > responsible for much of the interference with normal brain

> > development.

> >

> > I think that the reason why the people who have developed CFS as

> > adults did not develop autism as children (even though I suspect

> > that they have the same or similar genetic predisposition) is

that

> > when they were children, not as many vaccinations were

required.

> > The schedule of vaccinations required for children in the U.S.

has

> > grown substantially in the past two or three decades, as has the

> > incidence of autism. I think this is also true in the U.K.

> >

> > My main message is that a great deal has already been worked out

in

> > autism by the people in the Defeat Autism Now! project, and that

I

> > believe that the CFS community would benefit greatly by looking

> > carefully at what they have already done. They have found

> > supplements that will compensate for the genetic variations and

> > correct these biochemical irregularities. They are also

detoxing

> > heavy metals. The results in many autistic children have been

> > astounding.

> >

> > So I want to encourage everyone who has an interest in CFS to

look

> > at the results of the DAN! project in autism. You can view

videos

> > of the talks given at the latest two DAN! conferences on the

> > internet at no cost (unless you are paying for the internet

time!).

> > Go to this site:

> >

> > http://www.danwebcast.com

> >

> > You can choose either the later Long Beach conference or the

earlier

> > Boston conference. They cover much of the same material, but

both

> > are worthwhile to watch. If you want to see a good explanation

of

> > the methylation cycle research, go to the Boston meeting first,

so

> > you will be able to view the talk by Jill , who did not

attend

> > the Long Beach meeting.

> >

> > After selecting one of the conferences, go to the lower left and

> > register. This is free. They will email a password to you

right

> > away, and then you can choose a talk to watch.

> >

> > Beyond this, I also want to recommend a book. This is a new

book

> > (Sept. 2005). It is by Jon Pangborn, Ph.D. and Sydney Baker,

M.D.,

> > a biochemist and an autism clinician, respectively. It is

available

> > on Amazon for people within the U.S. For people outside the

U.S.,

> > it can be obtained from the following website by means of PayPal:

> >

> > http://www.autismresearchinstitute.com

> >

> > The cost for the book is $30 U.S.

> >

> > This is an excellent book. It is a reference book, full of good

> > information and good science, explained clearly. This book

deals

> > very practically with developing a treatment program for an

> > individual child. I think that most of it will turn out to

apply

> > directly to adults with CFS as well.

> >

> > Although I have been suggesting consideration of the DAN!

treatments

> > to people with CFS for only about two months, and it is too soon

to

> > draw conclusions, early feedback is very encouraging. While I

am

> > going out on a limb in announcing this on Co-Cure now, I don't

want

> > to wait any longer, because I think this could help a lot of

> > people. Of course, we should all keep in mind that with the

current

> > case definition of CFS we have a very heterogeneous population,

and

> > the DAN! treatments may not help all PWCs, but I am convinced

that

> > they will help a substantial subset. So I want to encourage you

to

> > look into this in the strongest way I can. It could be the

answer

> > for many of you.

> >

> > Rich Van Konynenburg, Ph.D.

> >

>

January 6, 2006

You're right, and I can think of somebody who could set up a

conference with lyme experts and DAN experts. Perhaps we should do

that, it could be exciting. I'll think about that.

> > >

> > > Hi, all.

> > >

> > > I am posting the following message to several CFS internet

> lists,

> > > based on the experiences that many of you have shared with me.

> > > Thank you, and I hope this really flies:

> > >

> > > I have been researching chronic fatigue syndrome for over eight

> > > years. As regular readers may recall, I had developed a

> hypothesis

> > > for the pathogenesis of chronic fatigue syndrome that

> prominently

> > > featured the depletion of glutathione, and I presented a poster

> > > paper on it at the AACFS (now the IACFS) meeting in October,

> 2004,

> > > in Madison, Wisconsin. This paper can be found at

> > >

> > > http://www.cfsresearch.org/cfs/research/treatment/15.htm

> > >

> > > Anecdotal experience of people in the internet

> > > group and others who took my hypothesis seriously and acted upon

> it

> > > suggested that while some were able to raise their glutathione

> > > levels by various means and experienced benefit from doing so,

> > > others were not able to do so. At the time of writing my poster

> > > paper, I was aware of this, and I acknowledged in the

> conclusions of

> > > the paper that there appeared to be things that were blocking

> the

> > > raising of glutathione in CFS. At that time, I was not sure

> > > specifically what they were. I also knew that there was

> evidence

> > > for a genetic predisposition in CFS, but I did not know the

> details

> > > of the genetic variations involved.

> > >

> > > Since then, I became aware of the work of S. Jill et al.

> in

> > > autism (Am J Clin Nutr. 2004 Dec;80(6):1611-7). They found that

> > > glutathione was also depleted in autistic children, that this

> > > resulted from a partial block in the methylation (also called

> > > methionine) cycle, that this partial block resulted in part from

> > > genetic variations in the genes for certain enzymes and proteins

> > > associated with the sulfur metabolism (I don't think the genetic

> > > part is published yet), and that it interfered with the

> conversion

> > > of methionine to cysteine, which is the rate-limiting amino acid

> for

> > > the synthesis of glutathione. They found that by using certain

> > > supplements they could lift the block in the methylation cycle

> and

> > > restore the glutathione level.

> > >

> > > In response to learning of this work, I became very interested

> in

> > > possible parallels between chronic fatigue syndrome and autism.

> I

> > > went on to attend the conference of the Defeat Autism Now!

> project

> > > in Long Beach, California in October, 2005. As a result of this

> > > experience, I became convinced that the genetic predisposition

> found

> > > in autism must be the same or similar to that in a major subset

> of

> > > chronic fatigue syndrome, and that the resulting biochemical

> > > abnormalities were also the same or similar. As far as I know,

> the

> > > genetic variations in people with CFS have not yet been studied

> in

> > > detail or published, but I am optimistic that this will occur

> soon,

> > > because of the rapid advances in the technology for doing so,

> and

> > > the current active interest of at least three groups in the U.S.

> and

> > > the U.K. in genomic aspects of CFS.

> > >

> > > There are obviously also major differences between chronic

> fatigue

> > > syndrome and autism. I believe that these result primarily from

> the

> > > different ages of onset. Autistic children experience onset

> early

> > > in life, before their brains are fully developed. I believe

> that

> > > this gives rise to the very different brain-related symptoms

> seen in

> > > autistic children from those seen in adults with CFS. However,

> > > there are many similarities in the symptomatology and the

> > > biochemistry of these two disorders as well, including oxidative

> > > stress, buildup of toxins, immune response shift to Th2, and gut

> > > problems, for examples.

> > >

> > > The triggering factors for autism and chronic fatigue syndrome

> are

> > > also largely different. There appears to be substantial

> evidence

> > > now that vaccinations (containing either a mercury-based

> > > preservative or live viruses, many given at the same time) were

> > > responsible for triggering many of the cases of autism in

> > > genetically-susceptible children. In CFS, a variety of

> triggering

> > > factors (physical, chemical, biological, or

> psychological/emotional)

> > > have been shown to be involved in various cases. All of these

> > > factors have in common the tendency to deplete glutathione. It

> > > appears that once glutathione drops sufficiently in a

> genetically

> > > susceptible person, the methylation cycle goes down, and the

> result

> > > is a depletion of several important metabolites in the sulfur

> > > metabolism, including S-adenosylmethionine (SAMe), cysteine,

> > > glutathione, taurine and sulfate. The depletion in these

> > > metabolites causes an avalanche of pathogenesis, since they all

> have

> > > very important functions in the body, and I think that much of

> this

> > > pathogenesis is common between autism and CFS. In autism, I

> think

> > > the loss of methylation capacity because of the drop in SAMe is

> > > responsible for much of the interference with normal brain

> > > development.

> > >

> > > I think that the reason why the people who have developed CFS as

> > > adults did not develop autism as children (even though I suspect

> > > that they have the same or similar genetic predisposition) is

> that

> > > when they were children, not as many vaccinations were

> required.

> > > The schedule of vaccinations required for children in the U.S.

> has

> > > grown substantially in the past two or three decades, as has the

> > > incidence of autism. I think this is also true in the U.K.

> > >

> > > My main message is that a great deal has already been worked out

> in

> > > autism by the people in the Defeat Autism Now! project, and that

> I

> > > believe that the CFS community would benefit greatly by looking

> > > carefully at what they have already done. They have found

> > > supplements that will compensate for the genetic variations and

> > > correct these biochemical irregularities. They are also

> detoxing

> > > heavy metals. The results in many autistic children have been

> > > astounding.

> > >

> > > So I want to encourage everyone who has an interest in CFS to

> look

> > > at the results of the DAN! project in autism. You can view

> videos

> > > of the talks given at the latest two DAN! conferences on the

> > > internet at no cost (unless you are paying for the internet

> time!).

> > > Go to this site:

> > >

> > > http://www.danwebcast.com

> > >

> > > You can choose either the later Long Beach conference or the

> earlier

> > > Boston conference. They cover much of the same material, but

> both

> > > are worthwhile to watch. If you want to see a good explanation

> of

> > > the methylation cycle research, go to the Boston meeting first,

> so

> > > you will be able to view the talk by Jill , who did not

> attend

> > > the Long Beach meeting.

> > >

> > > After selecting one of the conferences, go to the lower left and

> > > register. This is free. They will email a password to you

> right

> > > away, and then you can choose a talk to watch.

> > >

> > > Beyond this, I also want to recommend a book. This is a new

> book

> > > (Sept. 2005). It is by Jon Pangborn, Ph.D. and Sydney Baker,

> M.D.,

> > > a biochemist and an autism clinician, respectively. It is

> available

> > > on Amazon for people within the U.S. For people outside the

> U.S.,

> > > it can be obtained from the following website by means of PayPal:

> > >

> > > http://www.autismresearchinstitute.com

> > >

> > > The cost for the book is $30 U.S.

> > >

> > > This is an excellent book. It is a reference book, full of good

> > > information and good science, explained clearly. This book

> deals

> > > very practically with developing a treatment program for an

> > > individual child. I think that most of it will turn out to

> apply

> > > directly to adults with CFS as well.

> > >

> > > Although I have been suggesting consideration of the DAN!

> treatments

> > > to people with CFS for only about two months, and it is too soon

> to

> > > draw conclusions, early feedback is very encouraging. While I

> am

> > > going out on a limb in announcing this on Co-Cure now, I don't

> want

> > > to wait any longer, because I think this could help a lot of

> > > people. Of course, we should all keep in mind that with the

> current

> > > case definition of CFS we have a very heterogeneous population,

> and

> > > the DAN! treatments may not help all PWCs, but I am convinced

> that

> > > they will help a substantial subset. So I want to encourage you

> to

> > > look into this in the strongest way I can. It could be the

> answer

> > > for many of you.

> > >

> > > Rich Van Konynenburg, Ph.D.

> > >

> >

>

January 7, 2006

Hi, Rich.

" rvankonynen " <richvank@a...> wrote:

> I think that the reason why the people who have developed CFS as

> adults did not develop autism as children (even though I suspect

> that they have the same or similar genetic predisposition) is that

> when they were children, not as many vaccinations were required.

> The schedule of vaccinations required for children in the U.S. has

> grown substantially in the past two or three decades, as has the

> incidence of autism. I think this is also true in the U.K.

***I saw a local(Silicon Valley-California) TV news documentary about six years

ago which focused on the growing epidemic of autism occurring in children in the

U.S.. This documentary featured a young successful high-income couple, both

engineers, who had three of their four kids come down with autism here in the

valley.

***In the process of telling and interviewing this couple about their great

struggle with their entrenched family health crisis, this piece underscored the

fact that engineers and those in similar technical fields had a higher rate of

autism occurring in their kids than the general population. They also drew

attention to the fact that Silicon Valley seemed to have four times the rate of

autism cases occurring compared to the national average, itself showing stunning

increases.

***At any rate, when I was talking with Dr Cheney in 2002 about his suspicions

about mercury and vaccines connection to autism(and mercury's link to CFS), I

recalled having seen this documentary. I then spontaneously stated to him that

the upswing in affluence in my area over the last 20 years, due to the

tremendous upswing in world-wide demand for computers(ie, the PC and IT

revolutions), has probably created this increase in autism by allowing new

families benefitting greatly financially from this to go for all the gold

standard and cutting edge vaccinations unlike any other group.

***At alarming rates, natural attraction to technology and having the means to

turn every modern stone available to give every chance for good health in their

kids backfired!

Dr Cheney seemed to concur that my observation was quite plausable and it now

seems to fit in with what you suspect is the case.

***Interesting to note. The thrust of that documentary at that time, in terms

of a suspected etiology for autism, was leaning towards attributing genetic

brain traits in engineer types as being more vulnerable to mutations

predisposing autism, nothing related to vaccinations and engineer types capacity

or inclination to get ALL the ones available for their kids.

January 7, 2006

, both can be true.

As noted at conferences, DAN and Yasko's, the parents will usually

have issues. After all, they're carrying the genes their kids

inherited. And it is true that high functioning asperger's types,

" techy nerds " , are drawn to those professions and do very well in

them. At the same time, they might've just had techy nerd kids, not

autistic kids, if not for toxins, vaccinations, live viruses and

mercury in the vaccinations, infections like lyme and strep getting

more widespread and antibiotic resistant etc.

You find almost no autism in the Amish and they don't vaccinate their

kids and there will be some decent studies underway soon (the research

into the Amish has been fairly loose/sloppy so far).

> > I think that the reason why the people who have developed CFS as

> > adults did not develop autism as children (even though I suspect

> > that they have the same or similar genetic predisposition) is that

> > when they were children, not as many vaccinations were required.

> > The schedule of vaccinations required for children in the U.S. has

> > grown substantially in the past two or three decades, as has the

> > incidence of autism. I think this is also true in the U.K.

>

> ***I saw a local(Silicon Valley-California) TV news documentary

about six years ago which focused on the growing epidemic of autism

occurring in children in the U.S.. This documentary featured a young

successful high-income couple, both engineers, who had three of their

four kids come down with autism here in the valley.

>

> ***In the process of telling and interviewing this couple about

their great struggle with their entrenched family health crisis, this

piece underscored the fact that engineers and those in similar

technical fields had a higher rate of autism occurring in their kids

than the general population. They also drew attention to the fact that

Silicon Valley seemed to have four times the rate of autism cases

occurring compared to the national average, itself showing stunning

increases.

>

> ***At any rate, when I was talking with Dr Cheney in 2002 about his

suspicions about mercury and vaccines connection to autism(and

mercury's link to CFS), I recalled having seen this documentary. I

then spontaneously stated to him that the upswing in affluence in my

area over the last 20 years, due to the tremendous upswing in

world-wide demand for computers(ie, the PC and IT revolutions), has

probably created this increase in autism by allowing new families

benefitting greatly financially from this to go for all the gold

standard and cutting edge vaccinations unlike any other group.

>

> ***At alarming rates, natural attraction to technology and having

the means to turn every modern stone available to give every chance

for good health in their kids backfired!

> Dr Cheney seemed to concur that my observation was quite plausable

and it now seems to fit in with what you suspect is the case.

>

> ***Interesting to note. The thrust of that documentary at that

time, in terms of a suspected etiology for autism, was leaning towards

attributing genetic brain traits in engineer types as being more

vulnerable to mutations predisposing autism, nothing related to

vaccinations and engineer types capacity or inclination to get ALL the

ones available for their kids.

>

January 12, 2006

Hi Rich,

> Yes, I'm not the first person to make a connection between autism

> and CFS...But I would say that most of the CFS research and clinical

> community isn't there

> yet, and if things continue to look good with these treatments, I'm

> planning to try to get the word to them.

I hope you can include the chronic Lyme research and clinical community!

Sue ,

Upstate New York

January 13, 2006

Hi, Sue.

I don't know yet how applicable the DAN! autism treatments will be

in Lyme disease. Maybe they will turn out to be helpful there,

too. If so, I certainly would plan to spread the word.

Rich

>

> Hi Rich,

>

> > Yes, I'm not the first person to make a connection between autism

> > and CFS...But I would say that most of the CFS research and

clinical

> > community isn't there

> > yet, and if things continue to look good with these treatments,

I'm

> > planning to try to get the word to them.

>

> I hope you can include the chronic Lyme research and clinical

community!

>

> Sue ,

> Upstate New York

>

January 13, 2006

Rich, Sue,

What are your thoughts on the article below re cysteine triggering hemolysis

in-vitro of blood infected with Borrelia burgdorferi?

Nelly

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=1639493 & query_hl=1 & itool=pubmed_docsum

See full text article at:

http://www.pubmedcentral.gov/picrender.fcgi?artid=257305 & blobtype=pdf

Hemolytic activity of Borrelia burgdorferi.

LR, Austin FE.

Department of Microbiology and Immunology, School of Medicine, University of

Louisville, Kentucky 40292.

Zones of beta-hemolysis occurred around colonies of Borrelia burgdorferi grown

on Barbour-Stoenner- medium containing agarose and horse blood. Blood

plates were inoculated with either the infective strain Sh-2-82 or noninfective

strain B-31 in an overlay and incubated in a candle jar. Both strains of B.

burgdorferi displayed beta-hemolysis after 1 to 2 weeks of incubation. The

hemolytic activity diffused out from the borrelial colonies, eventually

resulting in lysis of the entire blood plate. Hemolysis was most pronounced with

horse blood and was less intense with bovine, sheep, and rabbit blood. Hemolysis

was enhanced by hot-cold incubation, which is typical of phospholipase-like

activities in other bacteria. Further characterization of the borrelial

hemolysin by using a spectrophotometric assay revealed its presence in the

supernatant fluids of stationary-phase cultures. *****Detection of the borrelial

hemolytic activity was dependent on activation of the hemolysin by the reducing

agent cysteine.***** This study provides the first evidence of hemolytic

activity associated with B. burgdorferi.

PMID: 1639493 [PubMed - indexed for MEDLINE]

Re: CFS and DAN! treatments for autism

Hi, Sue.

I don't know yet how applicable the DAN! autism treatments will be

in Lyme disease. Maybe they will turn out to be helpful there,

too. If so, I certainly would plan to spread the word.

Rich

>

> Hi Rich,

>

> > Yes, I'm not the first person to make a connection between autism

> > and CFS...But I would say that most of the CFS research and

clinical

> > community isn't there

> > yet, and if things continue to look good with these treatments,

I'm

> > planning to try to get the word to them.

>

> I hope you can include the chronic Lyme research and clinical

community!

>

> Sue ,

> Upstate New York

>

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.

January 13, 2006

They will be applicable and I " ll tell you why:

1) Most lymies have heavy metal issues, like the autistic kids. It's

either a prior existing problem that was silent, and/or, something

about lyme and biotoxins so downregulates the system that it begins to

collect metals because its so pressured

2) Many lymies probably have methylation issues. I found it

fascinating that both mercury and strep inhibit the same enzyme--I

forget the initials, you may remember, RIch, dpp4-----whatever it is.

A crucial enzyme in methylation/immunity. Probably lyme does too,

then, why not? I'll bet there is a profound link there

3) Having a good methylation cycle can only help. What is CFS anyway?

CHronic infection. What is lyme? Chronic infection. They overlap,

often are the same, otherwise, they're just different bugs. The

autistic kids have chronic infection too. Their guts are a mess. They

often have strep, fungi etc. Some have lyme.

4) Some of the therapies they're using, targetted to immunity, like

oralgam are interesting.

I see nobody responded back about that bovine serum product--I'm

wondering.

Rich could you do me a favor I don't have the time. Can you contact

Boyd Haley and interview him and post it back to us here? I want to

know as much as possible about that chelator and his hopes for it. I

know he can't reveal what it is. If we could get a safe strong

chelator that would be great.

> >

> > Hi Rich,

> >

> > > Yes, I'm not the first person to make a connection between autism

> > > and CFS...But I would say that most of the CFS research and

> clinical

> > > community isn't there

> > > yet, and if things continue to look good with these treatments,

> I'm

> > > planning to try to get the word to them.

> >

> > I hope you can include the chronic Lyme research and clinical

> community!

> >

> > Sue ,

> > Upstate New York

> >

>

January 13, 2006

Thats very upsetting. Its bad enough babesia ruins the red blood

cells. Once again, a reason hyperbaric is so helpful.

> >

> > Hi Rich,

> >

> > > Yes, I'm not the first person to make a connection between autism

> > > and CFS...But I would say that most of the CFS research and

> clinical

> > > community isn't there

> > > yet, and if things continue to look good with these treatments,

> I'm

> > > planning to try to get the word to them.

> >

> > I hope you can include the chronic Lyme research and clinical

> community!

> >

> > Sue ,

> > Upstate New York

> >

>

> 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.

>

January 13, 2006

Rich

A+++

If you were closer, I'd plant one on your forehead.

mjh

" The Basil Book "

http://foxhillfarm.us/FireBasil/

January 13, 2006

Hi, Nelly, Sue, Sheila and the group.

Thanks very much for posting this. It has really stimulated my

thinking about why Lyme disease is symptomatologically so similar to

CFS.

First, some review. As we all know, it has been terribly difficult

to do the differential diagnosis between Lyme disease and CFS. The

symptoms overlap considerably and even the best of the lab tests do

not have the sensitivity and selectivity we would all like to see.

Symptoms are manifestations of the pathophysiology of a disease,

i.e. how the functioning of the body of the sick person is abnormal

as a result of the disease. Therefore, if we see that the symptoms

of two diseases are very similar, we should suspect that they must

have some aspects of pathophysiology in common.

Pathophysiology is intimately involved with abnnormal gene

expression in the cells of the sick person, because gene expression

is a reflection of how the cell is conducting its business, and the

misconduct of the business of the cell is pathophysiology.

Because of this, I was quite struck some time ago when Sheila

reported that Dr. Gow said in a recent talk that he had found that

the gene expression pattern in peripheral blood mononuclear cells

(monocytes and lymphocytes) is " identical " in CFS and Lyme disease.

This implies that the pathophysiology of these two disorders in

these cell types is the same. (Note that we can't say anything

about what's going on in other cell types in the body in these two

disorders from this work. There are no doubt different things that

happen in other cell types between Lyme and CFS, and so this is not

saying that the two are identical in every way. But in these

mononuclear cells, this is saying that the pathophysiology of the

two is the same.)

As you know, I am of the firm view that in at least a large subset

of CFS there is glutathione depletion. In another subset, it looks

as though there are genetic variations in the enzymes that make use

of glutathione (glutathione transferases and glutathione

peroxidases), and the results in terms of pathophysiology are much

the same, even though the first group has low glutathione, and the

second group may have elevated glutathione. In either subset, the

people do not have normal glutathione function.

As you also know, based on the work by the DAN! project in autism, I

now believe that the basic abnormalities in the biochemistry in

autism and CFS are the same or similar. The glutathione depletion

brings down the methylation cycle, and a vicious circle develops

that produces a host of problems because of the depletion of SAMe

(the main methylator in the body), cysteine, glutathione, taurine

and sulfate.

So, if the pathophysiology of CFS involves the inability to use

glutathione effectively, whether because glutathione itself is

depleted or because the enzymes that use it have below-normal

activity, and if the pathophysiology of CFS and Lyme are indeed

identical, then it follows that there must be a problem with the

glutathione system in Lyme disease as well.

With that introduction, let me now review some things I found in the

literature, including the paper to which you (Nelly) drew my

attention. I will give the PubMed ID numbers for the references

that support these statements.

(PMID 1477785) First, in in vitro experiments it has been found

that the growth of Borrelia burgdorferi (Bb), the bacterium that

causes Lyme disease, in the culture medium is decreased by 80% if

cysteine is not present in the culture medium.

(PMID 147785) It has been found that cysteine diffuses passively

into Bb, i.e. there is no active transporter protein that pumps it

into the bacterium.

(PMID 1477785) It has been found that Bb incorporates cysteine in

three of its proteins. One has a mass of 22 kilodaltons. The

others have been identified as outer surface protein A (Osp A), with

a mass of 30 kilodaltons, and outer surface protein B (Osp , with

a mass of 34 kilodaltons.

(PMID 1639493) Bb produces a water-soluble hemolysin. This is a

substance that is able to break down red blood cells and release

their hemoglobin. It is likely that this substance incorporates a

cyteine residue, and this cysteine must be in its reduced state in

order for the hemolysin to break down red blood cells.

(PMID 16390443) Bb does not produce glutathione, which is the

principle non-protein thiol (substance containing an S-H or

sulfhydryl group) in human cells. Instead, Bb cells have a high

concentration (about 1 millimolar) of reduced coenzyme A (CoASH).

Bb also produces a CoA disulfide reductase enzyme that has the

responsibility to keep CoASH in its chemically reduced form, so it

can function. This enzyme is in turn reduced by NADH (reduced

nicotinic acid diethylamide), which is reduced by metabolism of Bb's

fuel. (This is analogous to glutathione reductase in human cells,

which requires NADPH, which in turn is reduced by the pentose

phosphate shunt on glycolysis, which metabolizes glucose as fuel.)

In Bb, CoASH is able to reduce hydrogen peroxide, as glutathione

peroxidase, together with glutathione, do in human cells.

(PMID 11687735) It has been found that when people were infected

with Bb and had the characteristic erythema migrans (bulls-eye

rash), the total thiol and glutathione in blood analysis were found

to be significantly decreased. The activity of glutathione

peroxidase was also significantly decreased. Malondialdehyde, a

marker for lipid peroxidation, was significantly elevated. After

antibiotic treatment with amoxycillin, which eliminated the acute

symptoms of Lyme disease, both the total thiol and the glutathione

levels recovered to normal. However, the glutathione peroxidase

activity was still significantly below normal, and the

malondialdehyde remained significantly elevated. This suggested

that Bb lowers the thiol and glutathione levels in its host, and

inhibits the activity of glutathione peroxidase.

I think this also suggests that while antibiotic therapy eliminates

acute Lyme symptoms and brings recovery of glutathione levels, the

Bb infection may still be suppressing the activity of glutathione

peroxidase, and this may be a mechanism involved in long-term (or

chronic or post-) Lyme disease.

One way in which a pathogen can inhibit its host's glutathione

peroxidase activity is to hoard selenium, because this is a cofactor

for that enzyme. You may recall that that is the mechanism that

Prof. Harry has hypothesized for HIV and AIDS

(http://www.hdfoster.com). I could not find any reference in the

literature connecting Bb and selenium, and I don't know whether

anyone has looked at that. Have any of you who are positive for

Lyme had your selenium level measured?

It seems pretty clear that Bb uses cysteine and that it depletes

glutathione and total thiol (which includes cysteine and protein

thiols as well as glutathione) in its host, at least in the acute

phase. It also suppresses the activity of glutathione peroxidase,

but I'm not sure whether it does it by lowering the host's selenium

level, or by some other means. This suppression appears as though

it could be chronic. I think there is a good chance that this

lowering of glutathione and/or suppressing of the activity of

glutathione peroxidase could very well be the explanation for the

similarities in symptomatology and the " identical " gene expression

in the peripheral blood mononuclear cells in CFS and Lyme disease.

It may also be that a host whose glutathione has been depleted by

other factors may be more vulnerable to developing Lyme disease,

once inoculated with Bb. I am speculating a little here, but this

is exciting!

If this is true, what are the consequences for treatment of long-

term Lyme disease, the subject that Sue raised? I think this

remains to be seen, but it does suggest that the DAN! autism

treatments may have a contribution to make in the treatment of long-

term Lyme disease as I've suggested that they also do in the

treatment of CFS. Before we can reach such a conclusion, though, I

think it behooves us to get more data on glutathione levels,

selenium levels, and glutathione peroxidase activity in people with

positive tests for long-term Lyme disease, as well as some

experience trying these treatments as part of the treatment of long-

term Lyme disease. I'm not suggesting that they would replace other

treatments for Lyme disase, such as antibiotic therapy, detoxing of

neurotoxins, or other approaches to deal with the bacteria

themselves or do deal with particular characteristics of Lyme

disease that are not found in autism or CFS. Nevertheless, these

treatments might make a significant impact. Time will tell. Thanks

for rattling my cage about this, Sheila, Sue and Nelly.

Rich

>

> Rich, Sue,

>

> What are your thoughts on the article below re cysteine triggering

hemolysis in-vitro of blood infected with Borrelia burgdorferi?

>

> Nelly

January 13, 2006

Hi, here's a correction. NADH is actually nicotinamide adenine

dinucleotide, not what I said it was. The brain is getting fried.

Sorry about that.

Rich

> >

> > Rich, Sue,

> >

> > What are your thoughts on the article below re cysteine

triggering

> hemolysis in-vitro of blood infected with Borrelia burgdorferi?

> >

> > Nelly

>

January 14, 2006

Hi, mjh.

Wow! This is getting mushy! Too bad we're two time zones apart!

Wait till my wife hears about this! Just kidding. Thank you!

Rich

>

> Rich

>

> A+++

>

> If you were closer, I'd plant one on your forehead.

>

> mjh

> " The Basil Book "

> http://foxhillfarm.us/FireBasil/

>

January 14, 2006

Hi, Jill.

I think your intuition about this is good. See my other postm

written a little while ago.

In regard to contacting Prof. Haley about how he's doing on new

methods of detoxing heavy metals, I realize that you are anxious to

know as much about that as possible and as soon as possible, and I

understand that. However, sorry, I don't think I will contact him.

Here's why: I was an experimental researcher for forty years

myself. It's a tough game, with a lot of hurdles, and a lot of

uncertainty about whether one has done everything correctly. One of

the things I hated most was when poeple kept bugging me about what

results I had. Then there are the political aspects, especially

when you are at a university. The institution puts things on you

like " publish or perish, " and patent issues. They don't want you to

tell people about your results until all the bases are covered.

I think that we can rest assured that Prof. Haley is highly

motivated to improve the situation on heavy metal detoxing and is

working on figuring it out and getting the word out about it at the

speediest rate he is able to.

I did send him several papers in support of my suggestion to look

into high-dose methyl B12 to remove inorganic mercury from the brain

several weeks back, because I thought that might help him, and I

haven't heard back from him yet on that, so I think he's probably

busy trying to figure it all out, and I don't think I'll bother him

again for a while. It's kind of like not messing with the goose

that laid the golden eggs. Do you know that story?

Rich

>

> They will be applicable and I " ll tell you why:

>

> 1) Most lymies have heavy metal issues, like the autistic kids.

It's

> either a prior existing problem that was silent, and/or, something

> about lyme and biotoxins so downregulates the system that it

begins to

> collect metals because its so pressured

>

> 2) Many lymies probably have methylation issues. I found it

> fascinating that both mercury and strep inhibit the same enzyme--I

> forget the initials, you may remember, RIch, dpp4-----whatever it

is.

> A crucial enzyme in methylation/immunity. Probably lyme does too,

> then, why not? I'll bet there is a profound link there

>

> 3) Having a good methylation cycle can only help. What is CFS

anyway?

> CHronic infection. What is lyme? Chronic infection. They overlap,

> often are the same, otherwise, they're just different bugs. The

> autistic kids have chronic infection too. Their guts are a mess.

They

> often have strep, fungi etc. Some have lyme.

>

> 4) Some of the therapies they're using, targetted to immunity, like

> oralgam are interesting.

>

> I see nobody responded back about that bovine serum product--I'm

> wondering.

>

> Rich could you do me a favor I don't have the time. Can you contact

> Boyd Haley and interview him and post it back to us here? I want to

> know as much as possible about that chelator and his hopes for it.

I

> know he can't reveal what it is. If we could get a safe strong

> chelator that would be great.

>

January 14, 2006

Before we can reach such a conclusion, though,

I

> think it behooves us to get more data on glutathione levels,

> selenium levels, and glutathione peroxidase activity in people

with

> positive tests for long-term Lyme disease, as well as some

> experience trying these treatments as part of the treatment of

long-

> term Lyme disease.

***I certainly think GSH is a valuable treatment for some CFS patients and I

dont want to be represented as someone being 'anti-GSH'. My concern is

theoretical and as such it is relatively minor in the scheme of things.

I dont know why, Rich, you are interested in testing GSH in Lyme patients. The

evidence of GSH depletion in CFS is meager and getting more meager all the time;

the recent McGregor paper reviewed in the second issue of the Phoenix Rising

newsletter found normal or increased GSH levels in the erythrocytes of CFS

patients. This duplicated the findings of an earlier study. Because your theory

does not seem to primarily based on evidence from studies on CFS patients I dont

see why GSH studies on Lyme disease patients would hold any sway. Maybe this is

a moot question anyway. The better question might be does GSH supplementation

work? and if so why it does it do so in the face of apparently normal GSH

levels? Basically I think you should throw out the low GSH depletion aspect and

concentrate that question.

I think a better case for GSH in CFS, given the most contrary findings thus

far and the mostly positive results from its use, would involve greatly

increased oxidative stress (?) that requires supplementation even if GSH levels

are normal (?) or your intriguing idea that CFS patients are unable to utilize

GSH efficiently. Perhaps methylation will fit in there somewhere - I havent

been able to keep up the methylation ideas.

Yours truly,

Cort

>

---------------------------------

Photos

Got holiday prints? See all the ways to get quality prints in your hands ASAP.

January 14, 2006

I agree Cort and I also don't see the point of separating lyme and CFS.

CFS is a description of symptoms. Lyme almost always results in CFS.

Lyme is the name of a town and the name given to a bacterial infection

" rediscovered " in Lyme, Connecticut. Lyme is not a description of

symptoms.

There is huge overlap btw lyme and CFS because almost all CFS involves

chronic infection and a lot of CFSer's main problem is tickborne

illness they just don't know it. Many were active hikers and

campers...in the woods...

>

> Before we can reach such a conclusion, though,

> I

> > think it behooves us to get more data on glutathione levels,

> > selenium levels, and glutathione peroxidase activity in people

> with

> > positive tests for long-term Lyme disease, as well as some

> > experience trying these treatments as part of the treatment of

> long-

> > term Lyme disease.

>

> ***I certainly think GSH is a valuable treatment for some CFS

patients and I dont want to be represented as someone being

'anti-GSH'. My concern is theoretical and as such it is relatively

minor in the scheme of things.

>

> I dont know why, Rich, you are interested in testing GSH in Lyme

patients. The evidence of GSH depletion in CFS is meager and getting

more meager all the time; the recent McGregor paper reviewed in the

second issue of the Phoenix Rising newsletter found normal or

increased GSH levels in the erythrocytes of CFS patients. This

duplicated the findings of an earlier study. Because your theory does

not seem to primarily based on evidence from studies on CFS patients I

dont see why GSH studies on Lyme disease patients would hold any sway.

Maybe this is a moot question anyway. The better question might be

does GSH supplementation work? and if so why it does it do so in the

face of apparently normal GSH levels? Basically I think you should

throw out the low GSH depletion aspect and concentrate that question.

>

> I think a better case for GSH in CFS, given the most contrary

findings thus far and the mostly positive results from its use, would

involve greatly increased oxidative stress (?) that requires

supplementation even if GSH levels are normal (?) or your intriguing

idea that CFS patients are unable to utilize GSH efficiently. Perhaps

methylation will fit in there somewhere - I havent been able to keep

up the methylation ideas.

> Yours truly,

> Cort

>

> >

>

> ---------------------------------

>

> ---------------------------------

> Photos

> Got holiday prints? See all the ways to get quality prints in your

hands ASAP.

>

January 15, 2006

Hi

Raising my Glutathione level has been FUNDAMENTAL in my recovery although i

also had to include a few other things to reverse the damage caused over

many years.

my regime:

1) Whey protein Isolate

2) lactoferrin

3) Coconut oil & lauricidin

4)Probiotics

5)Protein enzymes

6) Sea Salt or Recup

7) Calcium

8) CoQ10

9) Vit B complex & Vit C

10) Licorice

Regards

CS

January 15, 2006

Hi, Cort.

Thanks for your comments. I realize that we have differing views

about how the published glutathione data should be interpreted.

The best response I can give is to reiterate that one of the most

difficult problems in making use of nearly all the clinical data

published in CFS is that the current research case definition

produces a very heterogeneous population for study. As a result, it

is very difficult to obtain definitive clinical results, and any

interpretation of those that have been published must be done with a

great deal of judgment.

I might add that I have communicated in person and by email with

quite a few clinical researchers, and this is a problem I hear from

them quite often. One of the extreme cases is McCully. He

repeated the same type of clinical study, using the same criteria

for CFS patients, and got opposite results. To his credit, he had

the guts to publish both, but where does that leave us in trying to

reach a conclusion about his type of study in CFS?

The glutathione work isn't so different from this. As you may know,

one of the Australian papers reported that there was actually a

bimodal distribution. One subset was higher than normal, and the

other was lower than normal. Had they averaged them together, as is

done in a lot of CFS work, especially since there usually aren't a

very large number of subjects, they would have gotten insignificant

results. As it is, they caused me to wonder how there could be

these two groups.

As I started to get some gene polymorphism results for the

glutathione transferase enzymes in PWCs, it hit me! That's where

the hypothesis came from that you find " intriguing. " My point is

that it is not just an idea out of the blue. It's based on data,

and it also conforms to the science of the glutathone system, as we

understand it. It's what one would expect if these polymorphisms

occurred. What I'm using here is a systems approach and " gedanken "

or thought experiments. These are techniques that have been very

commonly used in physics for many years, but haven't been so useful

in the biomedical field until recent years, because there wasn't a

well enough developed body of theory to enable someone to use these

approaches. But now there is, and one can.

I don't know if you saw the latest issue of the newletter put out by

the Wisconsin CFS Support Group. They reviewed a very candid talk

that was given by Lenny there, and one of the things he said

was that he had tried to get the research case definition tightened

up, but the objection was that if that were done, the research

performed after that could not be compared with all the research

that had gone before! We are stuck with a research definition that

prevents definitive work from being done, in the interest of

preserving the " value " of work done with a definition that prevents

definitive work from being done. Does that make sense to you? I

think it's tragic.

In the face of this, I have taken the position that we need to put

together some comprehensive hypotheses that can be used to guide the

clinical research, as a way to ferret out the various subsets in the

defined population, and that's what I've been trying to do. You may

think that this is purely a " blue sky " activity, without relevance

to the real world. However, I don't see it that way. Any

comprehensive hypothesis must be self-consistent, and it must also

be in accordance with accepted science. Furthermore, there must be

at least a subset of the CFS population whose characteristics

conform to it, wherever " peg points " exist. One can't expect one

hypothesis to fit all PWCs, because not all are the same. Does

anyone on this list still doubt that, after so many here have shared

their experiences? One size definitely does not fit all in CFS.

There's another very good test of comprehensive CFS hypotheses. Do

they lead to anyone being helped? We have heard from quite a few on

this list who have been helped by raising there glutathione. I'm

very optimistic that incorporating the DAN! autism treatments will

help many more, and if this turns out to be true, no comprehensive

hypothesis would have a better confirmation than that.

I have no problem with anyone coming up with an alternate

comprehensive hypothesis for CFS, in fact I encouraged the people at

the last AACFS (now IACFS) conference to do just that. Maybe they

can fit another subset from the ones I've been trying to fit. If

so, more power to them. But they must satisfy the rigorous criteria

that I outlined above: self-consistency, conformance to known

science, and agreement with data from at least a subset of PWCs.

Rich

>

> Before we can reach such a conclusion, though,

> I

> > think it behooves us to get more data on glutathione levels,

> > selenium levels, and glutathione peroxidase activity in people

> with

> > positive tests for long-term Lyme disease, as well as some

> > experience trying these treatments as part of the treatment of

> long-

> > term Lyme disease.

>

> ***I certainly think GSH is a valuable treatment for some CFS

patients and I dont want to be represented as someone being 'anti-

GSH'. My concern is theoretical and as such it is relatively minor

in the scheme of things.

>

> I dont know why, Rich, you are interested in testing GSH in Lyme

patients. The evidence of GSH depletion in CFS is meager and getting

more meager all the time; the recent McGregor paper reviewed in the

second issue of the Phoenix Rising newsletter found normal or

increased GSH levels in the erythrocytes of CFS patients. This

duplicated the findings of an earlier study. Because your theory

does not seem to primarily based on evidence from studies on CFS

patients I dont see why GSH studies on Lyme disease patients would

hold any sway. Maybe this is a moot question anyway. The better

question might be does GSH supplementation work? and if so why it

does it do so in the face of apparently normal GSH levels? Basically

I think you should throw out the low GSH depletion aspect and

concentrate that question.

>

> I think a better case for GSH in CFS, given the most contrary

findings thus far and the mostly positive results from its use,

would involve greatly increased oxidative stress (?) that requires

supplementation even if GSH levels are normal (?) or your intriguing

idea that CFS patients are unable to utilize GSH efficiently.

Perhaps methylation will fit in there somewhere - I havent been able

to keep up the methylation ideas.

> Yours truly,

> Cort

>

> >

>

> ---------------------------------

>

> ---------------------------------

> Photos

> Got holiday prints? See all the ways to get quality prints in

your hands ASAP.

>

January 15, 2006

my glutathione tested very low, there isn't much question my health has little

chance of returning (and not getting worse) without restoring it. Its crucial

for me as well, and all the methylation probs Rich talks about fit the picture

for me based on my organic acids and fatty acids and amino acids, vite and mins

testing... so I can back up everything Rich is saying with my lab results. So

dont' discount that folks.

Marcia

Re: Re: CFS and DAN! treatments for autism

Hi

Raising my Glutathione level has been FUNDAMENTAL in my recovery although i

also had to include a few other things to reverse the damage caused over

many years.

my regime:

1) Whey protein Isolate

2) lactoferrin

3) Coconut oil & lauricidin

4)Probiotics

5)Protein enzymes

6) Sea Salt or Recup

7) Calcium

8) CoQ10

9) Vit B complex & Vit C

10) Licorice

Regards

CS

January 19, 2006

rvankonynen <richvank@...> wrote: Hi, Cort.

Thanks for your comments. I realize that we have differing views

about how the published glutathione data should be interpreted.

***It's difficult to understand how to interpret it other than how I have.

The results are just not very convincing; of seven studies, one did find reduced

GSH overall - but there was no control group, two found reduced GSH in subsets

of CFS patient, one of which they believed was due to obesity and increased

oxidative stress. Two have found increased GSH, not in a subset but in all CFS

patients and one found a tendency towards increased GSH. In order to make a case

for GSH depletion you have to start getting creative.

It very well could be and I expect there are subsets of people with GSH

depletion - something must explain the positive results from using GSH - but

overall, at least based on the published results its pretty to marshall a

scenario of either widespread or substantial GSH depletion in a significant

number of CFS patients.

I agree we do have a big problem with heterogeneity in CFS. Reeves recently

came out with a study, using the CDC definition, that found no orthostatic

intolerance in CFS. Thats kind of mind boggling. We've had so many false leads

in CFS that are thought to be due to referral bias; people with certain kinds of

CFS gathering around specific researchers. Perhaps we'll come to the conclusion

that what we thought was referral bias was instead different subsets of CFS

patients with different triggers.

Then again you can't throw out the baby with bathwater. The definition wasnt

arrived at out of the blue. While there has been a great variability in some

test results there have been some fairly consistent findings; reduced NK cell

cytotoxicity, problems with serotonin, increased RNase L fragmentation,

increased choline levels in the basal ganglia, increased levels of TGF-beta and,

of course, increased oxidative stress in the muscles and the blood. This is one

thing that weakens the GSH depletion theory; given the consistently increased

oxidative stress one would think that GSH might be depleted simply due to the

stress that system is under. Anyway while the definition is certainly not

satisfactory it has been good enough right now to give us some consistent

results.

But the definition is a big problem that has to be fixed. It think they'll

probably wait until they have really good evidence that they have a really good

definition. Its really difficult to start over; the CDC is investing millions of

dollars in huge studies incorporating genomic proteomics and other data all

based on that definition. I wonder what 's new definition is? I'd love to

see it. He's certainly doing excellant work in that area. Spence recently

talked about heterogeneity problem in his Making the Breakthrough talk.

I really wanted to get that newsletter but I couldn't find it.

In the face of this, I have taken the position that we need to put

together some comprehensive hypotheses that can be used to guide the

clinical research, as a way to ferret out the various subsets in the

defined population, and that's what I've been trying to do. You may think that

this is purely a " blue sky " activity, without relevance

to the real world.

***Why would I do that? In order for your theory to be viable, however, it now

has to involve subsets doesnt it?

However, I don't see it that way. Any

comprehensive hypothesis must be self-consistent, and it must also

be in accordance with accepted science. Furthermore, there must be

at least a subset of the CFS population whose characteristics

conform to it, wherever " peg points " exist. One can't expect one

hypothesis to fit all PWCs, because not all are the same. Does

anyone on this list still doubt that, after so many here have shared

their experiences? One size definitely does not fit all in CFS.

****Of course not. My objection has been that you've ignored the negative

evidence for your theory about GSH while accentuating the positive. A reading of

your theory would suggest to someone uninformed about the issue that glutathione

depletion is normal in CFS - that is what I thought until I looked at the

studies.

There's another very good test of comprehensive CFS hypotheses. Do

they lead to anyone being helped? We have heard from quite a few on

this list who have been helped by raising there glutathione. I'm

very optimistic that incorporating the DAN! autism treatments will

help many more, and if this turns out to be true, no comprehensive

hypothesis would have a better confirmation than that.

***I agree with that. That is in fact the strongest evidence that glutathione

in one way or another plays a role in CFS and this is the reason I hope you

proceed with this and continue educating CFS patients about it. GSH

supplementation has helped some CFS patients alot; others a bit, some it has

even hurt a bit and others have had no response. What a mixed bag we are!

I have no problem with anyone coming up with an alternate

comprehensive hypothesis for CFS, in fact I encouraged the people at

the last AACFS (now IACFS) conference to do just that. Maybe they

can fit another subset from the ones I've been trying to fit.

***I'm surprised your suggesting that MAYBE they can (?) come up with other

subsets or hypotheses? Of course they can and have; there is RNase L, PKR,

theres alot of brain stuff going on, Ablashi has suggested subsets of CFS

patients have HHV-6, Chia -enterovirus, Kerr - parvovirus. The fact that

longitudinal studies have revealed that several pathogens (EBV, Ross River)

cause CFS in a subset of people with come down with them suggest there are

different viral triggers. There is evidence of toxin induced CFS as well.

Lange/Natelson have found a subset of CFS patients demonstrate encephalopathy.

Pall believes CFS is due to increased NO/ONOO. There are lots of potential

subsets and a good number of hypotheses.

If

so, more power to them. But they must satisfy the rigorous criteria

that I outlined above: self-consistency, conformance to known

science, and agreement with data from at least a subset of PWCs.

*** My problem has been YOUR lack of rigor in addressing evidence that is

contrary to your theory. If you're looking for agreement with the data emerging

now you have to more and more start to cherry-pick to find GSH depleted CFS

patients. This is why I think you have to find a way to make GSH work without

being depleted. I just went over the recent Jammes study; GSH was found to be

normal in CFS patients during exercise - in fact at the end of the paper the

authors stated there was a 'tendency' for GSH to be increased in CFS patients;

that was a large sample size - almost 50 CFS patients as I remember. Yet GSH

works for some patients and works well. I think your theory would be more viable

and valuable if you can find a way to explain this conundrum and I hope you will

continue to look at ways that could explain that.

Yours truly,

Cort.