Re: Chronic Lyme disease and the Yasko treatment program

[Guest guest]

Rich,

What dose of selenium would you suggest trying? I don't recall if

the Autism book discusses selenium and dosages, but I will check.

Thanks!

>

> Hi, all.

>

> I've been doing some more study of chronic Lyme disease and have

> been thinking about why the Yasko treatment program might be

helpful

> to someone with this disorder.

>

> As we know, Sue T. has been reporting considerable improvement on

> the Yasko treatment program, and as we also know, she has tested

> positively for Lyme disease in the past and has been ill for a long

> time. So what's going on here?

>

> As some of you may recall, I posted some information about Lyme

> disease and glutathione depletion back in January. I've pasted it

at

> the end of this message for those who would like to review it.

>

> In that earlier post, I reviewed published literature showing that

> Borrelia burgdorferi (the bacteria responsible for Lyme disease)

> depletes glutathione in the host, and it appears to suppress the

> activity of glutathione peroxidase over the longer term, even after

> antibiotic treatment.

>

> With glutathione peroxidase suppressed, we can expect that the

> levels of hydrogen peroxide would be higher in the host, because

the

> job of glutathione peroxidase is to eliminate hydrogen peroxide.

>

> O.K., here's something I just found out: Borrelia burgdorferi is

> encouraged to assume its cystic form when hydrogen peroxide is

> elevated, and when the cystic forms are placed back in a medium

with

> low hydrogen peroxide, they revert back to the spirochete form. (R.

> Murgia and M. Cinco, 2004, PMID: 14961976).

>

> Now, I think this is really interesting. I think it suggests that

> the reason Borrelia burgdorferi is able to hang on in a person's

> body and produce chronic Lyme disease is that it suppresses the

> activity of glutathione peroxidase, which allows hydrogen peroxide

> to build up, and then the hydrogen peroxide signals the bacteria to

> assume the cystic form. This protects them from the immune system

> and, to a large extent, from antibiotics as well, and that's why

> chronic Lyme is such a difficult disease to knock out.

>

> As I said in my earlier post (below), I don't know how Bb

suppresses

> glutathione peroxidase, but I suspect that it might do it by

> hoarding selenium, as Prof. Harry has theorized as the

> pathogenesis mechanism for some viruses, including HIV. Of course,

> as we know, the buildup of mercury, as occurs when glutathione is

> depleted and a person is exposed to mercury from amalgams, fish, or

> other sources, will tie up selenium as well. This may be part of

> the synergism that Dr. Yasko has found between pathogens and heavy

> metals.

>

> In any case, it seems to me that the key to knocking out chronic

> Lyme disease might be to lower the levels of hydrogen peroxide, so

> that Bb will revert to the spirochete form and can be attacked by

> the immune system and by antibiotics. To do this, both the

activity

> of glutathione peroxidase and the level of glutathione must be

> brought up to normal. How do we do this?

>

> I think supplementation with selenium would be a good thing to try

> for restoring the activity of glutathione peroxidase.

>

> What about glutathione? Well, in the case of many of the people

> with chronic Lyme disease, I suspect that we are dealing with a set

> of polymorphisms in the enzymes impacting the methylation cycle

that

> enable the development of a vicious circle mechanism when the

> glutathione level drops low enough, i.e. the same mechanism that

> occurs in many cases of autism and chronic fatigue syndrome. (This

> certainly seems to have been true in the case of Sue T.) If this

is

> true, then it will be necessary to deal directly to bypass these

> polymorphisms, such as is done in the Yasko treatment program.

>

> What I'm suggesting then, is that the people with chronic Lyme

> disease might also be brought under the " Yasko tent. " This might

be

> the key to making the Borrelia more vulnerable to the immune system

> and to the antibiotics, so that this disease can be knocked out

more

> effectively.

>

> I would appreciate comments on this hypothesis.

>

> Rich

>

>

> Here is my earlier post from last January:

>

> 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, 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

> cysteine 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

> principal 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

> nicotinamide adenine dinucleotide), 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 disease, such as antibiotic therapy, detoxing

of

> neurotoxins, or other approaches to deal with the bacteria

> themselves or to 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

>

[Guest guest]

A good hypothesis, Rich, except that chronic lyme disease is usually

not just borrelia burgdorferi. I've concluded that from six years of

my own history and listening to many many other histories very

closely. Just one strain of lyme, even given our polymorphisms, almost

never throws us into this kind of global disability. Burgdorfer found

six bugs in the tickgut in the 1980's. Google Eva Sapi, she's at Univ

of Connecticut and associated with Yale, or I'll email you her URL

privately. YOu might want to talk with her, I intend to at some point

as she's finally doing the work that should have been done twenty

years ago. She's trying to isolate the other organisms. Some are

commonly talked about and its my personal opinion that babesia is

extremely bad and synergistic with lyme. It releases some kind of bad

toxin from its plastid, and its very oxidizing to red blood cells and

damages their glutathione which they are then not very well able to

recycle. If you can do some pubmed research on babesia in any form,

and/or I'll email you some stuff. Please work this into your

hypothesis. If you don't find enuf info on babesia it's possible to

study malaria although one recognizes that drawing parallels is a

little bit dicey. In addition, there's something about the mycotoxins

involved with borrelia, and anergy to fungus. I posted some stuff

Kathleen (very brilliantly) wrote about this.

So there is a whole picture that is complex that has to do with

borrelia, babesia, and downstream issues with fungi that are directly

related to the infection, not just indirectly as opportunistic stuff.

In addition, lymies seem to get strep problems, from what I've seen,

not always, but mysteriously frequently, AND shingles, especially in

the kids. Dr. the lyme pediatrician long ago commented on the

strange connection btw varicella ie shingles, and his kids--way too

many had shingles. And adult lymies get it mysteriously often.

THere may be some completely unidentified virus in the ticks too.

So you've got vulnerable polymorphisms, maybe already metal issues,

and then you get a particular SOUP of bugs either from repeated

tickbites or ticks with multiple bugs (it is increasingly likely to

get several bugs in a mere single tickbite these days).

So to understand this is more complex than just borrelia.

It would be GREAT if you would help on that. If I can send along any

info I have I will look for it.

Okay, back to sleep.

>

> Hi, all.

>

> I've been doing some more study of chronic Lyme disease and have

> been thinking about why the Yasko treatment program might be helpful

> to someone with this disorder.

>

> As we know, Sue T. has been reporting considerable improvement on

> the Yasko treatment program, and as we also know, she has tested

> positively for Lyme disease in the past and has been ill for a long

> time. So what's going on here?

>

> As some of you may recall, I posted some information about Lyme

> disease and glutathione depletion back in January. I've pasted it at

> the end of this message for those who would like to review it.

>

> In that earlier post, I reviewed published literature showing that

> Borrelia burgdorferi (the bacteria responsible for Lyme disease)

> depletes glutathione in the host, and it appears to suppress the

> activity of glutathione peroxidase over the longer term, even after

> antibiotic treatment.

>

> With glutathione peroxidase suppressed, we can expect that the

> levels of hydrogen peroxide would be higher in the host, because the

> job of glutathione peroxidase is to eliminate hydrogen peroxide.

>

> O.K., here's something I just found out: Borrelia burgdorferi is

> encouraged to assume its cystic form when hydrogen peroxide is

> elevated, and when the cystic forms are placed back in a medium with

> low hydrogen peroxide, they revert back to the spirochete form. (R.

> Murgia and M. Cinco, 2004, PMID: 14961976).

>

> Now, I think this is really interesting. I think it suggests that

> the reason Borrelia burgdorferi is able to hang on in a person's

> body and produce chronic Lyme disease is that it suppresses the

> activity of glutathione peroxidase, which allows hydrogen peroxide

> to build up, and then the hydrogen peroxide signals the bacteria to

> assume the cystic form. This protects them from the immune system

> and, to a large extent, from antibiotics as well, and that's why

> chronic Lyme is such a difficult disease to knock out.

>

> As I said in my earlier post (below), I don't know how Bb suppresses

> glutathione peroxidase, but I suspect that it might do it by

> hoarding selenium, as Prof. Harry has theorized as the

> pathogenesis mechanism for some viruses, including HIV. Of course,

> as we know, the buildup of mercury, as occurs when glutathione is

> depleted and a person is exposed to mercury from amalgams, fish, or

> other sources, will tie up selenium as well. This may be part of

> the synergism that Dr. Yasko has found between pathogens and heavy

> metals.

>

> In any case, it seems to me that the key to knocking out chronic

> Lyme disease might be to lower the levels of hydrogen peroxide, so

> that Bb will revert to the spirochete form and can be attacked by

> the immune system and by antibiotics. To do this, both the activity

> of glutathione peroxidase and the level of glutathione must be

> brought up to normal. How do we do this?

>

> I think supplementation with selenium would be a good thing to try

> for restoring the activity of glutathione peroxidase.

>

> What about glutathione? Well, in the case of many of the people

> with chronic Lyme disease, I suspect that we are dealing with a set

> of polymorphisms in the enzymes impacting the methylation cycle that

> enable the development of a vicious circle mechanism when the

> glutathione level drops low enough, i.e. the same mechanism that

> occurs in many cases of autism and chronic fatigue syndrome. (This

> certainly seems to have been true in the case of Sue T.) If this is

> true, then it will be necessary to deal directly to bypass these

> polymorphisms, such as is done in the Yasko treatment program.

>

> What I'm suggesting then, is that the people with chronic Lyme

> disease might also be brought under the " Yasko tent. " This might be

> the key to making the Borrelia more vulnerable to the immune system

> and to the antibiotics, so that this disease can be knocked out more

> effectively.

>

> I would appreciate comments on this hypothesis.

>

> Rich

>

>

> Here is my earlier post from last January:

>

> 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, 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

> cysteine 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

> principal 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

> nicotinamide adenine dinucleotide), 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 disease, such as antibiotic therapy, detoxing of

> neurotoxins, or other approaches to deal with the bacteria

> themselves or to 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

>

[Guest guest]

Hi, Rich.

Okay. So here is my response for you regarding this Lyme-Yasko treatment

scenario, with some info about my case you may or may not have forgotten.

Of course I've long been diagnosed with CFS. I also was diagnosed with lyme by

one LLMD, by one non-LLMD as well as had lyme ruled-out for me by another LLMD

and a CFS specialist who happened to be Dr Cheney.

Aside my many other tests and history indicating CFS as my primary diagnosis, I

had three western blots from three seperate testing labs show positivity for

lyme in me while tests for lyme co-infections showed negative. Long story

short, I did lots of many several antibiotics intended to treat chronic lyme to

no avail, except one, a sulfa antibiotic(the name illudes me at the moment).

And the outstanding benefit from this one abx lasted just one day on the fifth

day of use after an oral surgery when I also happen to be on my sixth month of

ampligen and had completed my 26th of 40 dives of hyperbaric oxygen

therapy(HBOT). As I had not noticed any benefit like this one day from

ampligen, a previous oral surgery(same kind) and HBOT up to this point, it seem

as if they didn't directly cause the herx that I experienced for ten minutes on

this fifth day of the sulfa abx use resulting in a complete release of my key

right side brain pain and fatigue, which allowed for one very good refreshing

night of sleep and an excellent following day(I literally felt like I popped

completely out of the CFS hole, albeit short lived).

I think connected to this moment is the fact that I do now know I have a CYP2C9

SNP which makes several drugs, including specifically sulfa abxs, more potent

and potentially more toxic at normal recommended doses. This makes me think,

given the back drop of your glutathione depletion-methylation block hypothesis

for CFS and the current symptom benefit RenewPro provides me now similar to what

Ampligen provided then, that the sulfur based sulfa abx at souped-up levels in

my body may have indeed caught an infection of some sort, perhaps lyme, off

guard.

As I do now as I was then, I was taking a daily multi with selenium in it and I

can conceive of how glutathione peroxidase might have come up a bit and hydrogen

peroxide brought down a bit in this overall scenario temporarily, causing lyme

to go to spriochette form just long enough for

my immune system with the sulfa abx to do some killing of it. I can also

conceive that my glutathione status overall must still have been low at that

time, despite Ampligen's downstream benefit to my RnaseL enzyme system and the

sulfur provided by this one sulfa abx, and this combined with now suspected

heavy metal toxin

build-up might be why this amazing pop out the CFS hole could not hold despite

continuing on with these efforts.

As far as the HBOT, I think I've read since doing it that it can potentially

increase oxidation which seems to rule it out as a good help for CFS, but

perhaps there is another take on it that I'm not aware? Whatever the case, as

you can see I like many PWCs haven't been afraid of throwing everything,

including the kitchen sink, the bathtub and The House(a good down payment for

one at least!), at CFS inorder to get well, but more importantly, do my

connections jibe with what you're thinking may be possible with Yasko treatments

for lyme?

I've never felt confident that lyme must be THE infection in me connected to my

symptoms, but I see a potential for it given this new information about higher

hydrogen peroxide levels encouraging its stealthy cystic form.

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

>

> Hi, all.

>

> I've been doing some more study of chronic Lyme disease and have

> been thinking about why the Yasko treatment program might be helpful

> to someone with this disorder.

>

> As we know, Sue T. has been reporting considerable improvement on

> the Yasko treatment program, and as we also know, she has tested

> positively for Lyme disease in the past and has been ill for a long

> time. So what's going on here?

>

> As some of you may recall, I posted some information about Lyme

> disease and glutathione depletion back in January. I've pasted it at

> the end of this message for those who would like to review it.

>

> In that earlier post, I reviewed published literature showing that

> Borrelia burgdorferi (the bacteria responsible for Lyme disease)

> depletes glutathione in the host, and it appears to suppress the

> activity of glutathione peroxidase over the longer term, even after

> antibiotic treatment.

>

> With glutathione peroxidase suppressed, we can expect that the

> levels of hydrogen peroxide would be higher in the host, because the

> job of glutathione peroxidase is to eliminate hydrogen peroxide.

>

> O.K., here's something I just found out: Borrelia burgdorferi is

> encouraged to assume its cystic form when hydrogen peroxide is

> elevated, and when the cystic forms are placed back in a medium with

> low hydrogen peroxide, they revert back to the spirochete form. (R.

> Murgia and M. Cinco, 2004, PMID: 14961976).

>

> Now, I think this is really interesting. I think it suggests that

> the reason Borrelia burgdorferi is able to hang on in a person's

> body and produce chronic Lyme disease is that it suppresses the

> activity of glutathione peroxidase, which allows hydrogen peroxide

> to build up, and then the hydrogen peroxide signals the bacteria to

> assume the cystic form. This protects them from the immune system

> and, to a large extent, from antibiotics as well, and that's why

> chronic Lyme is such a difficult disease to knock out.

>

> As I said in my earlier post (below), I don't know how Bb suppresses

> glutathione peroxidase, but I suspect that it might do it by

> hoarding selenium, as Prof. Harry has theorized as the

> pathogenesis mechanism for some viruses, including HIV. Of course,

> as we know, the buildup of mercury, as occurs when glutathione is

> depleted and a person is exposed to mercury from amalgams, fish, or

> other sources, will tie up selenium as well. This may be part of

> the synergism that Dr. Yasko has found between pathogens and heavy

> metals.

>

> In any case, it seems to me that the key to knocking out chronic

> Lyme disease might be to lower the levels of hydrogen peroxide, so

> that Bb will revert to the spirochete form and can be attacked by

> the immune system and by antibiotics. To do this, both the activity

> of glutathione peroxidase and the level of glutathione must be

> brought up to normal. How do we do this?

>

> I think supplementation with selenium would be a good thing to try

> for restoring the activity of glutathione peroxidase.

>

> What about glutathione? Well, in the case of many of the people

> with chronic Lyme disease, I suspect that we are dealing with a set

> of polymorphisms in the enzymes impacting the methylation cycle that

> enable the development of a vicious circle mechanism when the

> glutathione level drops low enough, i.e. the same mechanism that

> occurs in many cases of autism and chronic fatigue syndrome. (This

> certainly seems to have been true in the case of Sue T.) If this is

> true, then it will be necessary to deal directly to bypass these

> polymorphisms, such as is done in the Yasko treatment program.

>

> What I'm suggesting then, is that the people with chronic Lyme

> disease might also be brought under the " Yasko tent. " This might be

> the key to making the Borrelia more vulnerable to the immune system

> and to the antibiotics, so that this disease can be knocked out more

> effectively.

>

> I would appreciate comments on this hypothesis.

>

> Rich

[Guest guest]

Hi Rich,

I do have a concern about this hypothesis. Here is what I wrote earlier

from Jill April talk:

" I just wanted to comment on something I learned from watching the

presentations from the April DAN! Conference. In Jill second

presentation, she suggested that the methylation cycle is not

malfunctioning in girls b/c of the effects of estrogen in upregulating

the enzymes. She said she doesn't know yet what the cause is in girls.

This is consistent with my normal creatinine. A friend who is very sick

just found out her creatinine is normal, after 6+ years of CFS "

Has Sue T had her glutathione measured to see if it has come up ?

[Guest guest]

>In any case, it seems to me that the key to knocking out chronic Lyme

>disease might be to lower the levels of hydrogen peroxide, so that Bb

>will revert to the spirochete form and can be attacked by the immune

>system and by antibiotics. To do this, both the activity of

>glutathione peroxidase and the level of glutathione must be brought up

>to normal. How do we do this?

Rich,

The production of hydrogen peroxide by neutrophils is inhibited by the

imidazole class of abx (and by some other abx like minocycline-see many studies

on acne). I guess this observation is the basis for the old refrain from

non-LLMDs: " it's the anti-inflamatory effects of the abx that is suppressing

your symptoms although all the bugs are gone and you're just producing

inflammation in the absence of bacteria "

Quote from the acne study below:

" Metronidazole, which is effective in the treatment of acne, markedly

inhibited ROS generated by neutrophils. The drug is known to have no significant

effect on the growth of Propionibacterium acnes. "

Many chronic Lyme patients and treating physicians have, in recent years,

found the imidazoles to be a valuable addition to the abx regimens for their

cyst busting properties (as per Brorsons) but the suppression of the production

of hydrogen peroxide by PMN might indeed be part of the reason for the good

results seen with the imidazoles.

I personally notice a very rapid improvement in my most obvious

inflammatory symptoms after starting an imidazole (within hours) FWIW

Rich, do you have specific refs to the relationship btwn Bb and selenium

depletion?

Nelly

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search & DB=PubMed

Report

Increased hydrogen peroxide generation by neutrophils from patients with

acne inflammation

Hirohiko Akamatsu, MD, PhD, Takeshi Horio, MD, PhD, and Kazuhiro Hattori,

MD, PhD

Abstract

BackgroundReactive oxygen species generated by neutrophils are closely

correlated with the pathogenesis of a variety of inflammatory skin diseases. The

aim of this study was to investigate the possible role of reactive oxygen

species generated by neutrophils in the mediation of acne inflammation.

MethodsBacterial phagocytotic stimuli, mediated by opsonin activity, were

applied to whole blood, and neutrophil hydrogen peroxide production was

measured.

ResultsPatients with acne inflammation showed a significantly increased

level of hydrogen peroxide produced by neutrophils compared to patients with

acne comedones and healthy controls. There were no marked differences in the

level of hydrogen peroxide produced by neutrophils between patients with acne

comedones and healthy controls. In addition, patients with acne inflammation

treated by oral administration of minocycline hydrochloride, a drug that

inhibits hydrogen peroxide generation by neutrophils, showed a significant

decrease in the ability of neutrophils to produce hydrogen peroxide in

accordance with a decrease in the inflammatory activity of acne lesions.

ConclusionsThe present study seems to suggest that acne inflammation is

mediated in part by hydrogen peroxide generation by neutrophils.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search & DB=pubmed

The Possible Role of Reactive Oxygen Species Generated by

Neutrophils in Mediating Acne Inflammation

H. Akamatsu, T. Horio

Department of Dermatology, Kansai Medical University, Osaka, Japan

Dermatology 1998;196:82-85 (DOI: 10.1159/000017876)

Abstract

The purpose of this study was to investigate the possible role of

reactive oxygen species (ROS) generated by neutrophils in mediating acne

inflammation. Antibiotics used for the treatment of acne significantly inhibited

ROS generated by neutrophils, when compared to other antibiotics. Metronidazole,

which is effective in the treatment of acne, markedly inhibited ROS generated by

neutrophils. The drug is known to have no significant effect on the growth of

Propionibacterium acnes. The proportion of linoleic acid is markedly decreased

in acne comedones. Linoleic acid significantly suppressed ROS generated by

neutrophils. The ability of neutrophils to produce ROS was significantly

increased in patients with acne inflammation. These results seem to reveal the

involvement of ROS generated by neutrophils in the disruption of the integrity

of the follicular epithelium, which is responsible for inflammatory processes of

acne.

Author Contacts

Hirohiko Akamatsu, MD

Department of Dermatology, Kansai Medical University

10-15, Fumizono-cho

Moriguchi 570 (Japan)

Tel. 6 992 1001, Fax 6 992 5965

[Guest guest]

Hi Rich,

Thanks for your hypothesis which is probably one of the clues of the Lyme

problem. As Jill

wrote, unfortunately, the sickest chronic Lymies are those who catch a soup of

different micro-organisms. In my case, after I had tried the anti-malaria

treatments, it

became evident that the BIG devil inside my body is babesiosis. Maybe there is

also a

mechanism which allows babesiosis to raise levels of H2O2 or something else that

put the

two of them bugs out of reach of antimicrobials.

Worse: I assume antibiotics contribute to impair enzymes (in quantity or in

quality, I don't

know) and help raise H2O2 levels in the body. From my personal experience, I

didn't have

burning in the legs (free-radicals) before I used abx against Lyme disease. Nor

did I feel

pinpoints all over my skin when ozone was in the atmosphere at an unusual level

(I am

presently a walking ozonometer...) As I wrote before, my burning sensations due

to H2O2

free-radicals have improved using MSM, much more than with other antioxidants

like GSH,

SOD or ginkgo. But I am unable to reach a conclusion there. I have bought my

Lyme brain

a biochemistry book about enzymes, now it has to read it...

Sylvie

[Guest guest]

Hi Sylvie,

I've been completely flumuxed by the burning in my palms and soles of my feet

since treating lyme with antibiotics. I NEVER had this symptom before in the

past few decades of this illness. Your post is a revelation for me. Do you

really think it's the babesia critter that can cause all this even if one has

been infected with it for so many years? And why after antibiotics? Did the

lyme control it somehow or did the antibiotics change the terrain? I also get a

strong prickling sensation in my; hands when I take a deep breath. Does this

happen to you? This symptom has got me guessing for too long. I was tested for

the babesia and my LLMD said it was cleared.

Edy

Sylvie <funnyb1331@...> wrote:

Hi Rich,

Thanks for your hypothesis which is probably one of the clues of the Lyme

problem. As Jill

wrote, unfortunately, the sickest chronic Lymies are those who catch a soup of

different micro-organisms. In my case, after I had tried the anti-malaria

treatments, it

became evident that the BIG devil inside my body is babesiosis. Maybe there is

also a

mechanism which allows babesiosis to raise levels of H2O2 or something else that

put the

two of them bugs out of reach of antimicrobials.

Worse: I assume antibiotics contribute to impair enzymes (in quantity or in

quality, I don't

know) and help raise H2O2 levels in the body. From my personal experience, I

didn't have

burning in the legs (free-radicals) before I used abx against Lyme disease. Nor

did I feel

pinpoints all over my skin when ozone was in the atmosphere at an unusual level

(I am

presently a walking ozonometer...) As I wrote before, my burning sensations due

to H2O2

free-radicals have improved using MSM, much more than with other antioxidants

like GSH,

SOD or ginkgo. But I am unable to reach a conclusion there. I have bought my

Lyme brain

a biochemistry book about enzymes, now it has to read it...

Sylvie

[Guest guest]

Can one's H2O2 levels be tested for?

davidhall2020 <davidhall@...> wrote: Hi, Rich.

Okay. So here is my response for you regarding this Lyme-Yasko treatment

scenario, with some info about my case you may or may not have forgotten.

Of course I've long been diagnosed with CFS. I also was diagnosed with lyme by

one LLMD, by one non-LLMD as well as had lyme ruled-out for me by another LLMD

and a CFS specialist who happened to be Dr Cheney.

Aside my many other tests and history indicating CFS as my primary diagnosis, I

had three western blots from three seperate testing labs show positivity for

lyme in me while tests for lyme co-infections showed negative. Long story short,

I did lots of many several antibiotics intended to treat chronic lyme to no

avail, except one, a sulfa antibiotic(the name illudes me at the moment).

And the outstanding benefit from this one abx lasted just one day on the fifth

day of use after an oral surgery when I also happen to be on my sixth month of

ampligen and had completed my 26th of 40 dives of hyperbaric oxygen

therapy(HBOT). As I had not noticed any benefit like this one day from ampligen,

a previous oral surgery(same kind) and HBOT up to this point, it seem as if they

didn't directly cause the herx that I experienced for ten minutes on this fifth

day of the sulfa abx use resulting in a complete release of my key right side

brain pain and fatigue, which allowed for one very good refreshing night of

sleep and an excellent following day(I literally felt like I popped completely

out of the CFS hole, albeit short lived).

I think connected to this moment is the fact that I do now know I have a CYP2C9

SNP which makes several drugs, including specifically sulfa abxs, more potent

and potentially more toxic at normal recommended doses. This makes me think,

given the back drop of your glutathione depletion-methylation block hypothesis

for CFS and the current symptom benefit RenewPro provides me now similar to what

Ampligen provided then, that the sulfur based sulfa abx at souped-up levels in

my body may have indeed caught an infection of some sort, perhaps lyme, off

guard.

As I do now as I was then, I was taking a daily multi with selenium in it and I

can conceive of how glutathione peroxidase might have come up a bit and hydrogen

peroxide brought down a bit in this overall scenario temporarily, causing lyme

to go to spriochette form just long enough for

my immune system with the sulfa abx to do some killing of it. I can also

conceive that my glutathione status overall must still have been low at that

time, despite Ampligen's downstream benefit to my RnaseL enzyme system and the

sulfur provided by this one sulfa abx, and this combined with now suspected

heavy metal toxin

build-up might be why this amazing pop out the CFS hole could not hold despite

continuing on with these efforts.

As far as the HBOT, I think I've read since doing it that it can potentially

increase oxidation which seems to rule it out as a good help for CFS, but

perhaps there is another take on it that I'm not aware? Whatever the case, as

you can see I like many PWCs haven't been afraid of throwing everything,

including the kitchen sink, the bathtub and The House(a good down payment for

one at least!), at CFS inorder to get well, but more importantly, do my

connections jibe with what you're thinking may be possible with Yasko treatments

for lyme?

I've never felt confident that lyme must be THE infection in me connected to my

symptoms, but I see a potential for it given this new information about higher

hydrogen peroxide levels encouraging its stealthy cystic form.

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

>

> Hi, all.

>

> I've been doing some more study of chronic Lyme disease and have

> been thinking about why the Yasko treatment program might be helpful

> to someone with this disorder.

>

> As we know, Sue T. has been reporting considerable improvement on

> the Yasko treatment program, and as we also know, she has tested

> positively for Lyme disease in the past and has been ill for a long

> time. So what's going on here?

>

> As some of you may recall, I posted some information about Lyme

> disease and glutathione depletion back in January. I've pasted it at

> the end of this message for those who would like to review it.

>

> In that earlier post, I reviewed published literature showing that

> Borrelia burgdorferi (the bacteria responsible for Lyme disease)

> depletes glutathione in the host, and it appears to suppress the

> activity of glutathione peroxidase over the longer term, even after

> antibiotic treatment.

>

> With glutathione peroxidase suppressed, we can expect that the

> levels of hydrogen peroxide would be higher in the host, because the

> job of glutathione peroxidase is to eliminate hydrogen peroxide.

>

> O.K., here's something I just found out: Borrelia burgdorferi is

> encouraged to assume its cystic form when hydrogen peroxide is

> elevated, and when the cystic forms are placed back in a medium with

> low hydrogen peroxide, they revert back to the spirochete form. (R.

> Murgia and M. Cinco, 2004, PMID: 14961976).

>

> Now, I think this is really interesting. I think it suggests that

> the reason Borrelia burgdorferi is able to hang on in a person's

> body and produce chronic Lyme disease is that it suppresses the

> activity of glutathione peroxidase, which allows hydrogen peroxide

> to build up, and then the hydrogen peroxide signals the bacteria to

> assume the cystic form. This protects them from the immune system

> and, to a large extent, from antibiotics as well, and that's why

> chronic Lyme is such a difficult disease to knock out.

>

> As I said in my earlier post (below), I don't know how Bb suppresses

> glutathione peroxidase, but I suspect that it might do it by

> hoarding selenium, as Prof. Harry has theorized as the

> pathogenesis mechanism for some viruses, including HIV. Of course,

> as we know, the buildup of mercury, as occurs when glutathione is

> depleted and a person is exposed to mercury from amalgams, fish, or

> other sources, will tie up selenium as well. This may be part of

> the synergism that Dr. Yasko has found between pathogens and heavy

> metals.

>

> In any case, it seems to me that the key to knocking out chronic

> Lyme disease might be to lower the levels of hydrogen peroxide, so

> that Bb will revert to the spirochete form and can be attacked by

> the immune system and by antibiotics. To do this, both the activity

> of glutathione peroxidase and the level of glutathione must be

> brought up to normal. How do we do this?

>

> I think supplementation with selenium would be a good thing to try

> for restoring the activity of glutathione peroxidase.

>

> What about glutathione? Well, in the case of many of the people

> with chronic Lyme disease, I suspect that we are dealing with a set

> of polymorphisms in the enzymes impacting the methylation cycle that

> enable the development of a vicious circle mechanism when the

> glutathione level drops low enough, i.e. the same mechanism that

> occurs in many cases of autism and chronic fatigue syndrome. (This

> certainly seems to have been true in the case of Sue T.) If this is

> true, then it will be necessary to deal directly to bypass these

> polymorphisms, such as is done in the Yasko treatment program.

>

> What I'm suggesting then, is that the people with chronic Lyme

> disease might also be brought under the " Yasko tent. " This might be

> the key to making the Borrelia more vulnerable to the immune system

> and to the antibiotics, so that this disease can be knocked out more

> effectively.

>

> I would appreciate comments on this hypothesis.

>

> Rich

[Guest guest]

Hi, Edy.

Probably the best indicator would be a test for malondialdehyde. This

is a lipid peroxide. When hydrogen peroxide is elevated, it tends to

react with lipids, and that should raise this parameter. It can be

measured in the urine.

Rich

>

> Can one's H2O2 levels be tested for?

[Guest guest]

Hi Edy,

I have met many other babesiosied Lymies who had the burning feet syndrome. It

gets

better with anti-malaria treatments like Mepron or quinine or artemether. I

usually have

burning soles too, my palms are so and so. Till I was treated for Lyme disease,

I was in a

state of equilibrium, having a suffering but still normal life. I was diagnosed

for borreliosis

only, and treated for it. Then my body's equilibrium broke, I developped FM,

CFS, full

blown babesiosis, and the Lyme was not even eradicated. As you write, I think

abx modify

the terrain. I think they are weapons studied on people previously in good

health, not on

chronic depleted unbalanced cases like us. I have almost been killed by the

Bactrim-Rulid

protocole and I still don't know why (nobody knows). When it happened, I thought

of

enzyme poisoning (my own enzymes), I even discussed it with my university

biochemistry

teacher, but he couldn't say if I was right or wrong.

I don't have your hand prickling sensation, but I have a weird itching of a very

precise

place in the right palm (on the heart line between the two last fingers).

Sometimes it can

be so unbearable I scratch till the skin peels off... The point is an

acupuncture one, located

on the lung meridian. I don't know what it means and why it itches, except that

it could be

related to breathing.

How could you doc say that your babesiosis has cleared?

Sylvie

>

> Hi Sylvie,

>

> I've been completely flumuxed by the burning in my palms and soles of my

feet since

treating lyme with antibiotics. I NEVER had this symptom before in the past few

decades

of this illness. Your post is a revelation for me. Do you really think it's

the babesia critter

that can cause all this even if one has been infected with it for so many years?

And why

after antibiotics? Did the lyme control it somehow or did the antibiotics

change the

terrain? I also get a strong prickling sensation in my; hands when I take a

deep breath.

Does this happen to you? This symptom has got me guessing for too long. I was

tested

for the babesia and my LLMD said it was cleared.

>

> Edy

[Guest guest]

Right: I'm almost 100% convinced that anybody with chronic " lyme " also

has babesia. This is why I think a responds to zithromax but can't

get off it--it suppresses enough borrelia and babesia but does not

kill them.

Vulnerable genetics also plays a definite role--my friend works out

with a 70 year old guy who has had lyme six or seven times and babesia

once and got over them all....

Nonetheless, babesia is a much overlooked foe in this 'tickborne'

syndrome. And its a known oxidizer of glutathione in the red blood cell.

>

> Hi Rich,

>

> Thanks for your hypothesis which is probably one of the clues of the

Lyme problem. As Jill

> wrote, unfortunately, the sickest chronic Lymies are those who catch

a soup of

> different micro-organisms. In my case, after I had tried the

anti-malaria treatments, it

> became evident that the BIG devil inside my body is babesiosis.

Maybe there is also a

> mechanism which allows babesiosis to raise levels of H2O2 or

something else that put the

> two of them bugs out of reach of antimicrobials.

>

> Worse: I assume antibiotics contribute to impair enzymes (in

quantity or in quality, I don't

> know) and help raise H2O2 levels in the body. From my personal

experience, I didn't have

> burning in the legs (free-radicals) before I used abx against Lyme

disease. Nor did I feel

> pinpoints all over my skin when ozone was in the atmosphere at an

unusual level (I am

> presently a walking ozonometer...) As I wrote before, my burning

sensations due to H2O2

> free-radicals have improved using MSM, much more than with other

antioxidants like GSH,

> SOD or ginkgo. But I am unable to reach a conclusion there. I have

bought my Lyme brain

> a biochemistry book about enzymes, now it has to read it...

>

> Sylvie

>

[Guest guest]

Hi Sylvie,

I took mepron for about 3 or 4 months and then was retested through Igenex.

Still had the BB big time, but the babesia was gone, or so my doc thought so the

plan was to then totally focus on the Lyme. Unfortunetly my body had had enough

of the ABX and I simply cannot tolerate them anymore. We've tried many

different ones and the result is always the same. I now have an epi pen by the

bed as I have now become so sensitized to so many things I simply cannot believe

it. The most recent being the nightshade family of food! If it weren't so

uncomfortable I'd make a joke about it.

So now I'm only doing Hyperbaric and some cats claw. One thing I've gotten

from this list is some undecidedness. I know I have lots of pathagens and

through testing lots of methylation issues and genes missing or working badly.

The Yasko protocol has my attention, but I just don't know what to address

first. I can't seem to find a guide and my brain can't show me the way to go,

so.........I read and read and read.

Edy

Sylvie <funnyb1331@...> wrote:

Hi Edy,

I have met many other babesiosied Lymies who had the burning feet syndrome. It

gets

better with anti-malaria treatments like Mepron or quinine or artemether. I

usually have

burning soles too, my palms are so and so. Till I was treated for Lyme disease,

I was in a

state of equilibrium, having a suffering but still normal life. I was diagnosed

for borreliosis

only, and treated for it. Then my body's equilibrium broke, I developped FM,

CFS, full

blown babesiosis, and the Lyme was not even eradicated. As you write, I think

abx modify

the terrain. I think they are weapons studied on people previously in good

health, not on

chronic depleted unbalanced cases like us. I have almost been killed by the

Bactrim-Rulid

protocole and I still don't know why (nobody knows). When it happened, I thought

of

enzyme poisoning (my own enzymes), I even discussed it with my university

biochemistry

teacher, but he couldn't say if I was right or wrong.

I don't have your hand prickling sensation, but I have a weird itching of a very

precise

place in the right palm (on the heart line between the two last fingers).

Sometimes it can

be so unbearable I scratch till the skin peels off... The point is an

acupuncture one, located

on the lung meridian. I don't know what it means and why it itches, except that

it could be

related to breathing.

How could you doc say that your babesiosis has cleared?

Sylvie

>

> Hi Sylvie,

>

> I've been completely flumuxed by the burning in my palms and soles of my feet

since

treating lyme with antibiotics. I NEVER had this symptom before in the past few

decades

of this illness. Your post is a revelation for me. Do you really think it's the

babesia critter

that can cause all this even if one has been infected with it for so many years?

And why

after antibiotics? Did the lyme control it somehow or did the antibiotics change

the

terrain? I also get a strong prickling sensation in my; hands when I take a deep

breath.

Does this happen to you? This symptom has got me guessing for too long. I was

tested

for the babesia and my LLMD said it was cleared.

>

> Edy

[Guest guest]

>In any case, it seems to me that the key to knocking out chronic Lyme >disease might be to lower the levels of hydrogen peroxide, so that Bb >will revert to the spirochete form and can be attacked by the immune >system and by antibiotics. To do this, both the activity of >glutathione peroxidase and the level of glutathione must be brought up >to normal. How do we do this?

Rich,

The production of hydrogen peroxide by neutrophils is inhibited by the imidazole class of abx (and by some other abx like minocycline-see many studies on acne). I guess this observation is the basis for the old refrain from non-LLMDs: "it's the anti-inflamatory effects of the abx that is suppressing your symptoms although all the bugs are gone and you're just producing inflammation in the absence of bacteria"

Quote from the acne study below:

"Metronidazole, which is effective in the treatment of acne, markedly inhibited ROS generated by neutrophils. The drug is known to have no significant effect on the growth of Propionibacterium acnes."

Many chronic Lyme patients and treating physicians have, in recent years, found the imidazoles to be a valuable addition to the abx regimens for their cyst busting properties (as per Brorsons) but the suppression of the production of hydrogen peroxide by PMN might indeed be part of the reason for the good results seen with the imidazoles.

I personally notice a very rapid improvement in my most obvious inflammatory symptoms after starting an imidazole (within hours) FWIW

Rich, do you have specific refs to the relationship btwn Bb and selenium depletion?

Nelly

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search & DB=PubMed

Report

Increased hydrogen peroxide generation by neutrophils from patients with acne inflammation

Hirohiko Akamatsu, MD, PhD, Takeshi Horio, MD, PhD, and Kazuhiro Hattori, MD, PhD

Abstract

BackgroundReactive oxygen species generated by neutrophils are closely correlated with the pathogenesis of a variety of inflammatory skin diseases. The aim of this study was to investigate the possible role of reactive oxygen species generated by neutrophils in the mediation of acne inflammation.

MethodsBacterial phagocytotic stimuli, mediated by opsonin activity, were applied to whole blood, and neutrophil hydrogen peroxide production was measured.

ResultsPatients with acne inflammation showed a significantly increased level of hydrogen peroxide produced by neutrophils compared to patients with acne comedones and healthy controls. There were no marked differences in the level of hydrogen peroxide produced by neutrophils between patients with acne comedones and healthy controls. In addition, patients with acne inflammation treated by oral administration of minocycline hydrochloride, a drug that inhibits hydrogen peroxide generation by neutrophils, showed a significant decrease in the ability of neutrophils to produce hydrogen peroxide in accordance with a decrease in the inflammatory activity of acne lesions.

ConclusionsThe present study seems to suggest that acne inflammation is mediated in part by hydrogen peroxide generation by neutrophils.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search & DB=pubmed

The Possible Role of Reactive Oxygen Species Generated by Neutrophils in Mediating Acne InflammationH. Akamatsu, T. HorioDepartment of Dermatology, Kansai Medical University, Osaka, Japan

Dermatology 1998;196:82-85 (DOI: 10.1159/000017876)

Abstract

The purpose of this study was to investigate the possible role of reactive oxygen species (ROS) generated by neutrophils in mediating acne inflammation. Antibiotics used for the treatment of acne significantly inhibited ROS generated by neutrophils, when compared to other antibiotics. Metronidazole, which is effective in the treatment of acne, markedly inhibited ROS generated by neutrophils. The drug is known to have no significant effect on the growth of Propionibacterium acnes. The proportion of linoleic acid is markedly decreased in acne comedones. Linoleic acid significantly suppressed ROS generated by neutrophils. The ability of neutrophils to produce ROS was significantly increased in patients with acne inflammation. These results seem to reveal the involvement of ROS generated by neutrophils in the disruption of the integrity of the follicular epithelium, which is responsible for inflammatory processes of acne.

Author Contacts

Hirohiko Akamatsu, MDDepartment of Dermatology, Kansai Medical University10-15, Fumizono-choMoriguchi 570 (Japan)Tel. 6 992 1001, Fax 6 992 5965

Free Abstract Article (Fulltext) Article (PDF 69 KB)

[infections] Chronic Lyme disease and the Yasko treatment program

Hi, all.Here's a repost from the Experimental list. Maybe it will be of interest to some people here:I've been doing some more study of chronic Lyme disease and have been thinking about why the Yasko treatment program might be helpful to someone with this disorder.As we know, Sue T. has been reporting considerable improvement on the Yasko treatment program, and as we also know, she has tested positively for Lyme disease in the past and has been ill for a long time. So what's going on here?As some of you may recall, I posted some information about Lyme disease and glutathione depletion back in January. I've pasted it at the end of this message for those who would like to review it. In that earlier post, I reviewed published literature showing that Borrelia burgdorferi (the bacteria responsible for Lyme disease) depletes glutathione in the host, and it appears to suppress the activity of glutathione peroxidase over the longer term, even after antibiotic treatment.With glutathione peroxidase suppressed, we can expect that the levels of hydrogen peroxide would be higher in the host, because the job of glutathione peroxidase is to eliminate hydrogen peroxide.O.K., here's something I just found out: Borrelia burgdorferi is encouraged to assume its cystic form when hydrogen peroxide is elevated, and when the cystic forms are placed back in a medium with low hydrogen peroxide, they revert back to the spirochete form. (R. Murgia and M. Cinco, 2004, PMID: 14961976).Now, I think this is really interesting. I think it suggests that the reason Borrelia burgdorferi is able to hang on in a person's body and produce chronic Lyme disease is that it suppresses the activity of glutathione peroxidase, which allows hydrogen peroxide to build up, and then the hydrogen peroxide signals the bacteria to assume the cystic form. This protects it from the immune system and, to a large extent, from antibiotics as well, and that's why chronic Lyme is such a difficult disease to knock out.As I said in my earlier post (below), I don't know how Bb suppresses glutathione peroxidase, but I suspect that it might do it by hoarding selenium, as Prof. Harry has theorized as the pathogenesis mechanism for some viruses, including HIV. Of course, as we know, the buildup of mercury, as occurs when glutathione is depleted and a person is exposed to mercury from amalgams, fish, or other sources, will tie up selenium as well. This may be part of the synergism that Dr. Yasko has found between pathogens and heavy metals.In any case, it seems to me that the key to knocking out chronic Lyme disease might be to lower the levels of hydrogen peroxide, so that Bb will revert to the spirochete form and can be attacked by the immune system and by antibiotics. To do this, both the activity of glutathione peroxidase and the level of glutathione must be brought up to normal. How do we do this?I think supplementation with selenium would be a good thing to try for restoring the activity of glutathione peroxidase.What about glutathione? Well, in the case of many of the people with chronic Lyme disease, I suspect that we are dealing with a set of polymorphisms in the enzymes impacting the methylation cycle that enable the development of a vicious circle mechanism when the glutathione level drops low enough, i.e. the same mechanism that occurs in many cases of autism and chronic fatigue syndrome. (This certainly seems to have been true in the case of Sue T.) If this is true, then it will be necessary to deal directly to bypass these polymorphisms, such as is done in the Yasko treatment program.What I'm suggesting then, is that the people with chronic Lyme disease might also be brought under the "Yasko tent." This might be the key to making the Borrelia more vulnerable to the immune system and to the antibiotics, so that this disease can be knocked out more effectively.I would appreciate comments on this hypothesis.RichHere is my earlier post from last January: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, 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 cysteine 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 principal 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 nicotinamide adenine dinucleotide), 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 disease, such as antibiotic therapy, detoxing of neurotoxins, or other approaches to deal with the bacteria themselves or to 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

[Guest guest]

Hi, Nelly.

Thank you very much for this information. This action of thess

specific antimicrobials may indeed be giving a clue that there is

something to this idea.

No, I don't have any references about selenium and Bb. I sure wish

I did. I'm only inferring that Bb manipulates selenium in order to

suppress glutathione peroxidase, because that is one way it could do

it.

Have you (or other Lymies you know of) tried supplementing selenium

in significant dosages, such as up to 600 micrograms per day?

Rich

>

> >In any case, it seems to me that the key to knocking out

chronic Lyme

> >disease might be to lower the levels of hydrogen peroxide,

so that Bb

> >will revert to the spirochete form and can be attacked by

the immune

> >system and by antibiotics. To do this, both the activity

of

> >glutathione peroxidase and the level of glutathione must be

brought up

> >to normal. How do we do this?

>

> Rich,

>

> The production of hydrogen peroxide by neutrophils is

inhibited by the imidazole class of abx (and by some other abx like

minocycline-see many studies on acne). I guess this observation is

the basis for the old refrain from non-LLMDs: " it's the anti-

inflamatory effects of the abx that is suppressing your symptoms

although all the bugs are gone and you're just producing

inflammation in the absence of bacteria "

>

> Quote from the acne study below:

> " Metronidazole, which is effective in the treatment of acne,

markedly inhibited ROS generated by neutrophils. The drug is known

to have no significant effect on the growth of Propionibacterium

acnes. "

>

> Many chronic Lyme patients and treating physicians have, in

recent years, found the imidazoles to be a valuable addition to the

abx regimens for their cyst busting properties (as per Brorsons) but

the suppression of the production of hydrogen peroxide by PMN might

indeed be part of the reason for the good results seen with the

imidazoles.

>

> I personally notice a very rapid improvement in my most

obvious inflammatory symptoms after starting an imidazole (within

hours) FWIW

>

> Rich, do you have specific refs to the relationship btwn Bb

and selenium depletion?

>

> Nelly

>

>

> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

CMD=search & DB=PubMed

>

> Report

> Increased hydrogen peroxide generation by neutrophils from

patients with acne inflammation

> Hirohiko Akamatsu, MD, PhD, Takeshi Horio, MD, PhD, and

Kazuhiro Hattori, MD, PhD

>

> Abstract

> BackgroundReactive oxygen species generated by neutrophils

are closely correlated with the pathogenesis of a variety of

inflammatory skin diseases. The aim of this study was to investigate

the possible role of reactive oxygen species generated by

neutrophils in the mediation of acne inflammation.

>

> MethodsBacterial phagocytotic stimuli, mediated by opsonin

activity, were applied to whole blood, and neutrophil hydrogen

peroxide production was measured.

>

> ResultsPatients with acne inflammation showed a

significantly increased level of hydrogen peroxide produced by

neutrophils compared to patients with acne comedones and healthy

controls. There were no marked differences in the level of hydrogen

peroxide produced by neutrophils between patients with acne

comedones and healthy controls. In addition, patients with acne

inflammation treated by oral administration of minocycline

hydrochloride, a drug that inhibits hydrogen peroxide generation by

neutrophils, showed a significant decrease in the ability of

neutrophils to produce hydrogen peroxide in accordance with a

decrease in the inflammatory activity of acne lesions.

>

> ConclusionsThe present study seems to suggest that acne

inflammation is mediated in part by hydrogen peroxide generation by

neutrophils.

>

>

>

> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

CMD=search & DB=pubmed

>

> The Possible Role of Reactive Oxygen Species Generated

by Neutrophils in Mediating Acne Inflammation

> H. Akamatsu, T. Horio

>

> Department of Dermatology, Kansai Medical University,

Osaka, Japan

>

>

> Dermatology 1998;196:82-85 (DOI: 10.1159/000017876)

>

> Abstract

>

> The purpose of this study was to investigate the

possible role of reactive oxygen species (ROS) generated by

neutrophils in mediating acne inflammation. Antibiotics used for the

treatment of acne significantly inhibited ROS generated by

neutrophils, when compared to other antibiotics. Metronidazole,

which is effective in the treatment of acne, markedly inhibited ROS

generated by neutrophils. The drug is known to have no significant

effect on the growth of Propionibacterium acnes. The proportion of

linoleic acid is markedly decreased in acne comedones. Linoleic acid

significantly suppressed ROS generated by neutrophils. The ability

of neutrophils to produce ROS was significantly increased in

patients with acne inflammation. These results seem to reveal the

involvement of ROS generated by neutrophils in the disruption of the

integrity of the follicular epithelium, which is responsible for

inflammatory processes of acne.

>

> Author Contacts

>

> Hirohiko Akamatsu, MD

> Department of Dermatology, Kansai Medical University

> 10-15, Fumizono-cho

> Moriguchi 570 (Japan)

> Tel. 6 992 1001, Fax 6 992 5965

>

>

> Free Abstract Article (Fulltext) Article (PDF

69 KB)

>

>

>

>

>

>

> [infections] Chronic Lyme disease and

the Yasko treatment program

>

>

> Hi, all.

>

> Here's a repost from the Experimental list. Maybe it will be of

> interest to some people here:

>

> I've been doing some more study of chronic Lyme disease and have

> been thinking about why the Yasko treatment program might be

helpful

> to someone with this disorder.

>

> As we know, Sue T. has been reporting considerable improvement

on

> the Yasko treatment program, and as we also know, she has tested

> positively for Lyme disease in the past and has been ill for a

long

> time. So what's going on here?

>

> As some of you may recall, I posted some information about Lyme

> disease and glutathione depletion back in January. I've pasted

it at

> the end of this message for those who would like to review it.

>

> In that earlier post, I reviewed published literature showing

that

> Borrelia burgdorferi (the bacteria responsible for Lyme disease)

> depletes glutathione in the host, and it appears to suppress the

> activity of glutathione peroxidase over the longer term, even

after

> antibiotic treatment.

>

> With glutathione peroxidase suppressed, we can expect that the

> levels of hydrogen peroxide would be higher in the host, because

the

> job of glutathione peroxidase is to eliminate hydrogen peroxide.

>

> O.K., here's something I just found out: Borrelia burgdorferi is

> encouraged to assume its cystic form when hydrogen peroxide is

> elevated, and when the cystic forms are placed back in a medium

with

> low hydrogen peroxide, they revert back to the spirochete form.

(R.

> Murgia and M. Cinco, 2004, PMID: 14961976).

>

> Now, I think this is really interesting. I think it suggests

that

> the reason Borrelia burgdorferi is able to hang on in a person's

> body and produce chronic Lyme disease is that it suppresses the

> activity of glutathione peroxidase, which allows hydrogen

peroxide

> to build up, and then the hydrogen peroxide signals the bacteria

to

> assume the cystic form. This protects it from the immune system

> and, to a large extent, from antibiotics as well, and that's why

> chronic Lyme is such a difficult disease to knock out.

>

> As I said in my earlier post (below), I don't know how Bb

suppresses

> glutathione peroxidase, but I suspect that it might do it by

> hoarding selenium, as Prof. Harry has theorized as the

> pathogenesis mechanism for some viruses, including HIV. Of

course,

> as we know, the buildup of mercury, as occurs when glutathione

is

> depleted and a person is exposed to mercury from amalgams, fish,

or

> other sources, will tie up selenium as well. This may be part of

> the synergism that Dr. Yasko has found between pathogens and

heavy

> metals.

>

> In any case, it seems to me that the key to knocking out chronic

> Lyme disease might be to lower the levels of hydrogen peroxide,

so

> that Bb will revert to the spirochete form and can be attacked

by

> the immune system and by antibiotics. To do this, both the

activity

> of glutathione peroxidase and the level of glutathione must be

> brought up to normal. How do we do this?

>

> I think supplementation with selenium would be a good thing to

try

> for restoring the activity of glutathione peroxidase.

>

> What about glutathione? Well, in the case of many of the people

> with chronic Lyme disease, I suspect that we are dealing with a

set

> of polymorphisms in the enzymes impacting the methylation cycle

that

> enable the development of a vicious circle mechanism when the

> glutathione level drops low enough, i.e. the same mechanism that

> occurs in many cases of autism and chronic fatigue syndrome.

(This

> certainly seems to have been true in the case of Sue T.) If this

is

> true, then it will be necessary to deal directly to bypass these

> polymorphisms, such as is done in the Yasko treatment program.

>

> What I'm suggesting then, is that the people with chronic Lyme

> disease might also be brought under the " Yasko tent. " This might

be

> the key to making the Borrelia more vulnerable to the immune

system

> and to the antibiotics, so that this disease can be knocked out

more

> effectively.

>

> I would appreciate comments on this hypothesis.

>

> Rich

>

> Here is my earlier post from last January:

>

> 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, 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

> cysteine 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

> principal 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

> nicotinamide adenine dinucleotide), 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 disease, such as antibiotic therapy,

detoxing of

> neurotoxins, or other approaches to deal with the bacteria

> themselves or to 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

>

[Guest guest]

Rich,

I am supplementing selenium but "only" 100 or 200 mcg/day as well as often eating high selenium foods (garlic for eg). Can't tell if it's having any effect.

In fact the ONLY thing that has had a striking effect in my case is imidazoles, I have been trying to understand why for ever. Other meds or supps or any other interventions like massages help some but not in the same league. Problem is after a few days the toxic shock hits and the headaches I get are out of this world! If I manage to stay on for a few weeks (sometimes I can) then I feel toxic all over, yet I also feel it is getting to the core of my problem.

Worried about liver toxicity issues when on tinidazole for any length of time, so I really want to know what it is doing exactly, if it is doing smthng directly antimicrobial or if it is doing smthng indirectly like suppressing some inflam process for eg which I could achieve differently

Nelly

[infections] Chronic Lyme disease and the Yasko treatment program> > > Hi, all.> > Here's a repost from the Experimental list. Maybe it will be of > interest to some people here:> > I've been doing some more study of chronic Lyme disease and have > been thinking about why the Yasko treatment program might be helpful > to someone with this disorder.> > As we know, Sue T. has been reporting considerable improvement on > the Yasko treatment program, and as we also know, she has tested > positively for Lyme disease in the past and has been ill for a long > time. So what's going on here?> > As some of you may recall, I posted some information about Lyme > disease and glutathione depletion back in January. I've pasted it at > the end of this message for those who would like to review it. > > In that earlier post, I reviewed published literature showing that > Borrelia burgdorferi (the bacteria responsible for Lyme disease) > depletes glutathione in the host, and it appears to suppress the > activity of glutathione peroxidase over the longer term, even after > antibiotic treatment.> > With glutathione peroxidase suppressed, we can expect that the > levels of hydrogen peroxide would be higher in the host, because the > job of glutathione peroxidase is to eliminate hydrogen peroxide.> > O.K., here's something I just found out: Borrelia burgdorferi is > encouraged to assume its cystic form when hydrogen peroxide is > elevated, and when the cystic forms are placed back in a medium with > low hydrogen peroxide, they revert back to the spirochete form. (R. > Murgia and M. Cinco, 2004, PMID: 14961976).> > Now, I think this is really interesting. I think it suggests that > the reason Borrelia burgdorferi is able to hang on in a person's > body and produce chronic Lyme disease is that it suppresses the > activity of glutathione peroxidase, which allows hydrogen peroxide > to build up, and then the hydrogen peroxide signals the bacteria to > assume the cystic form. This protects it from the immune system > and, to a large extent, from antibiotics as well, and that's why > chronic Lyme is such a difficult disease to knock out.> > As I said in my earlier post (below), I don't know how Bb suppresses > glutathione peroxidase, but I suspect that it might do it by > hoarding selenium, as Prof. Harry has theorized as the > pathogenesis mechanism for some viruses, including HIV. Of course, > as we know, the buildup of mercury, as occurs when glutathione is > depleted and a person is exposed to mercury from amalgams, fish, or > other sources, will tie up selenium as well. This may be part of > the synergism that Dr. Yasko has found between pathogens and heavy > metals.> > In any case, it seems to me that the key to knocking out chronic > Lyme disease might be to lower the levels of hydrogen peroxide, so > that Bb will revert to the spirochete form and can be attacked by > the immune system and by antibiotics. To do this, both the activity > of glutathione peroxidase and the level of glutathione must be > brought up to normal. How do we do this?> > I think supplementation with selenium would be a good thing to try > for restoring the activity of glutathione peroxidase.> > What about glutathione? Well, in the case of many of the people > with chronic Lyme disease, I suspect that we are dealing with a set > of polymorphisms in the enzymes impacting the methylation cycle that > enable the development of a vicious circle mechanism when the > glutathione level drops low enough, i.e. the same mechanism that > occurs in many cases of autism and chronic fatigue syndrome. (This > certainly seems to have been true in the case of Sue T.) If this is > true, then it will be necessary to deal directly to bypass these > polymorphisms, such as is done in the Yasko treatment program.> > What I'm suggesting then, is that the people with chronic Lyme > disease might also be brought under the "Yasko tent." This might be > the key to making the Borrelia more vulnerable to the immune system > and to the antibiotics, so that this disease can be knocked out more > effectively.> > I would appreciate comments on this hypothesis.> > Rich> > Here is my earlier post from last January:> > 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, 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 > cysteine 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 > principal 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 > nicotinamide adenine dinucleotide), 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 disease, such as antibiotic therapy, detoxing of > neurotoxins, or other approaches to deal with the bacteria > themselves or to 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>

[Guest guest]

 Rich, What dose of Selenium do you

recommend per day?  What about NAC?   Patrice

From: infections [mailto:infections ] On Behalf Of rvankonynen

Sent: Sunday, September 03, 2006

9:59 PM

infections

Subject: [infections]

Chronic Lyme disease and the Yasko treatment program

Hi, all.

Here's a repost from the Experimental list. Maybe it will be of

interest to some people here:

I've been doing some more study of chronic Lyme disease and have

been thinking about why the Yasko treatment program might be helpful

to someone with this disorder.

As we know, Sue T. has been reporting considerable improvement on

the Yasko treatment program, and as we also know, she has tested

positively for Lyme disease in the past and has been ill for a long

time. So what's going on here?

As some of you may recall, I posted some information about Lyme

disease and glutathione depletion back in January. I've pasted it at

the end of this message for those who would like to review it.

In that earlier post, I reviewed published literature showing that

Borrelia burgdorferi (the bacteria responsible for Lyme disease)

depletes glutathione in the host, and it appears to suppress the

activity of glutathione peroxidase over the longer term, even after

antibiotic treatment.

With glutathione peroxidase suppressed, we can expect that the

levels of hydrogen peroxide would be higher in the host, because the

job of glutathione peroxidase is to eliminate hydrogen peroxide.

O.K., here's something I just found out: Borrelia burgdorferi is

encouraged to assume its cystic form when hydrogen peroxide is

elevated, and when the cystic forms are placed back in a medium with

low hydrogen peroxide, they revert back to the spirochete form. (R.

Murgia and M. Cinco, 2004, PMID: 14961976).

Now, I think this is really interesting. I think it suggests that

the reason Borrelia burgdorferi is able to hang on in a person's

body and produce chronic Lyme disease is that it suppresses the

activity of glutathione peroxidase, which allows hydrogen peroxide

to build up, and then the hydrogen peroxide signals the bacteria to

assume the cystic form. This protects it from the immune system

and, to a large extent, from antibiotics as well, and that's why

chronic Lyme is such a difficult disease to knock out.

As I said in my earlier post (below), I don't know how Bb suppresses

glutathione peroxidase, but I suspect that it might do it by

hoarding selenium, as Prof. Harry has theorized as the

pathogenesis mechanism for some viruses, including HIV. Of course,

as we know, the buildup of mercury, as occurs when glutathione is

depleted and a person is exposed to mercury from amalgams, fish, or

other sources, will tie up selenium as well. This may be part of

the synergism that Dr. Yasko has found between pathogens and heavy

metals.

In any case, it seems to me that the key to knocking out chronic

Lyme disease might be to lower the levels of hydrogen peroxide, so

that Bb will revert to the spirochete form and can be attacked by

the immune system and by antibiotics. To do this, both the activity

of glutathione peroxidase and the level of glutathione must be

brought up to normal. How do we do this?

I think supplementation with selenium would be a good thing to try

for restoring the activity of glutathione peroxidase.

What about glutathione? Well, in the case of many of the people

with chronic Lyme disease, I suspect that we are dealing with a set

of polymorphisms in the enzymes impacting the methylation cycle that

enable the development of a vicious circle mechanism when the

glutathione level drops low enough, i.e. the same mechanism that

occurs in many cases of autism and chronic fatigue syndrome. (This

certainly seems to have been true in the case of Sue T.) If this is

true, then it will be necessary to deal directly to bypass these

polymorphisms, such as is done in the Yasko treatment program.

What I'm suggesting then, is that the people with chronic Lyme

disease might also be brought under the " Yasko tent. " This might be

the key to making the Borrelia more vulnerable to the immune system

and to the antibiotics, so that this disease can be knocked out more

effectively.

I would appreciate comments on this hypothesis.

Rich

Here is my earlier post from last January:

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, 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

cysteine 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

principal 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

nicotinamide adenine dinucleotide), 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 disease, such as antibiotic therapy, detoxing of

neurotoxins, or other approaches to deal with the bacteria

themselves or to 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

[Guest guest]

Rich, I had my minerals, including selenium tested. All came back

normal. I don't know if the tests were accurate though. For magnesium

at least, it was the red-blood-cell level that was measured. I have

had a positive Lyme western blot IgM and have been ill for ten years.

- Kate D

On Sep 3, 2006, at 11:58 PM, rvankonynen wrote:

> Have any of you who are positive for

> Lyme had your selenium level measured?

[Guest guest]

Hi, Kate.

Thanks for the information. Do you know whether you have Babesia as

well?

Rich

> > Have any of you who are positive for

> > Lyme had your selenium level measured?

>

[Guest guest]

My selenium tested a little low, but no surprise. Everyone who's hypothyroid supposedly tests low. Supplementing with selenium can be tricky if you take too much. Kate <KateDunlay@...> wrote: Rich, I had my minerals, including selenium tested. All came back normal. I don't know if the tests were accurate though. For magnesium at least, it was the red-blood-cell level that was measured. I have had a positive Lyme western blot IgM and have been ill for ten

years.- Kate DOn Sep 3, 2006, at 11:58 PM, rvankonynen wrote:> Have any of you who are positive for> Lyme had your selenium level measured?

[Guest guest]

forgot to mention, since the question was relating selenium to lyme disease, that I have not been d'xd with lyme, tests were negative with two possible equivocal bands. But selenium supplementation has long been touted as an aid for hypothyroid people who seem to also be suffering from cfs. Kate <KateDunlay@...> wrote: Rich, I had my minerals, including selenium tested. All came back normal. I don't know if the tests were accurate though. For magnesium at least,

it was the red-blood-cell level that was measured. I have had a positive Lyme western blot IgM and have been ill for ten years.- Kate DOn Sep 3, 2006, at 11:58 PM, rvankonynen wrote:> Have any of you who are positive for> Lyme had your selenium level measured?

[Guest guest]

Hi, Patrice.

The Institute of Medicine recommends an upper limit for adults of

400 micrograms per day of selenium. I would go with that.

On NAC, it depends. If a person has a high body burden of mercury,

I wouldn't recommend taking NAC, because published work has shown

that it can move mercury into the brains of rats. If a person has

an upregulation polymorphism in their cystathionine beta synthase

(CBS) enzyme (which nine out of the eleven PWCs for whom I currently

have Yasko panel data do), then I wouldn't recommend NAC for that

person, either, because it is likely to raise their sulfite level

and give them headaches. This may not leave very many, but for the

rest, I would say about 1 gram per day of NAC.

Rich

>

> Rich, What dose of Selenium do you recommend per day? What about

NAC?

> Patrice

>

>

>

> _____

>

> From: infections

> [mailto:infections ] On Behalf Of

rvankonynen

> Sent: Sunday, September 03, 2006 9:59 PM

> infections

> Subject: [infections] Chronic Lyme disease and the

Yasko

> treatment program

>

>

>

> Hi, all.

>

> Here's a repost from the Experimental list. Maybe it will be of

> interest to some people here:

>

> I've been doing some more study of chronic Lyme disease and have

> been thinking about why the Yasko treatment program might be

helpful

> to someone with this disorder.

>

> As we know, Sue T. has been reporting considerable improvement on

> the Yasko treatment program, and as we also know, she has tested

> positively for Lyme disease in the past and has been ill for a

long

> time. So what's going on here?

>

> As some of you may recall, I posted some information about Lyme

> disease and glutathione depletion back in January. I've pasted it

at

> the end of this message for those who would like to review it.

>

> In that earlier post, I reviewed published literature showing that

> Borrelia burgdorferi (the bacteria responsible for Lyme disease)

> depletes glutathione in the host, and it appears to suppress the

> activity of glutathione peroxidase over the longer term, even

after

> antibiotic treatment.

>

> With glutathione peroxidase suppressed, we can expect that the

> levels of hydrogen peroxide would be higher in the host, because

the

> job of glutathione peroxidase is to eliminate hydrogen peroxide.

>

> O.K., here's something I just found out: Borrelia burgdorferi is

> encouraged to assume its cystic form when hydrogen peroxide is

> elevated, and when the cystic forms are placed back in a medium

with

> low hydrogen peroxide, they revert back to the spirochete form.

(R.

> Murgia and M. Cinco, 2004, PMID: 14961976).

>

> Now, I think this is really interesting. I think it suggests that

> the reason Borrelia burgdorferi is able to hang on in a person's

> body and produce chronic Lyme disease is that it suppresses the

> activity of glutathione peroxidase, which allows hydrogen peroxide

> to build up, and then the hydrogen peroxide signals the bacteria

to

> assume the cystic form. This protects it from the immune system

> and, to a large extent, from antibiotics as well, and that's why

> chronic Lyme is such a difficult disease to knock out.

>

> As I said in my earlier post (below), I don't know how Bb

suppresses

> glutathione peroxidase, but I suspect that it might do it by

> hoarding selenium, as Prof. Harry has theorized as the

> pathogenesis mechanism for some viruses, including HIV. Of course,

> as we know, the buildup of mercury, as occurs when glutathione is

> depleted and a person is exposed to mercury from amalgams, fish,

or

> other sources, will tie up selenium as well. This may be part of

> the synergism that Dr. Yasko has found between pathogens and heavy

> metals.

>

> In any case, it seems to me that the key to knocking out chronic

> Lyme disease might be to lower the levels of hydrogen peroxide, so

> that Bb will revert to the spirochete form and can be attacked by

> the immune system and by antibiotics. To do this, both the

activity

> of glutathione peroxidase and the level of glutathione must be

> brought up to normal. How do we do this?

>

> I think supplementation with selenium would be a good thing to try

> for restoring the activity of glutathione peroxidase.

>

> What about glutathione? Well, in the case of many of the people

> with chronic Lyme disease, I suspect that we are dealing with a

set

> of polymorphisms in the enzymes impacting the methylation cycle

that

> enable the development of a vicious circle mechanism when the

> glutathione level drops low enough, i.e. the same mechanism that

> occurs in many cases of autism and chronic fatigue syndrome. (This

> certainly seems to have been true in the case of Sue T.) If this

is

> true, then it will be necessary to deal directly to bypass these

> polymorphisms, such as is done in the Yasko treatment program.

>

> What I'm suggesting then, is that the people with chronic Lyme

> disease might also be brought under the " Yasko tent. " This might

be

> the key to making the Borrelia more vulnerable to the immune

system

> and to the antibiotics, so that this disease can be knocked out

more

> effectively.

>

> I would appreciate comments on this hypothesis.

>

> Rich

>

> Here is my earlier post from last January:

>

> 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, 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

> cysteine 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

> principal 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

> nicotinamide adenine dinucleotide), 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 <http://www.hdfoster.com> .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 disease, such as antibiotic therapy, detoxing

of

> neurotoxins, or other approaches to deal with the bacteria

> themselves or to 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

>

[Guest guest]

Hi Rich,

What's the GSH peroxidase all about, as opposed to catalse-

peroxidase? I asked my lecturer about this yesterday and he said the

GSH peroxidase and vit C peroxidase have their significance at lower

[H2O2], whereas catalse-peroxidase is more important at high [H2O2].

I'm not sure why this would be, since catalse-peroxidase is itself

so powerful an enzyme, but it might be of some use to think about.

Presumably one takes it from Pall and (separately) Spence that there

is oxidative stress in CFS, tho I haven't read those myself (by the

way, have you ever found a disconfirming followup of that work? I

haven't).

I guess one possibility might be that the host might inhibit it's

own GSH peroxidase in the course of an inflammatory response, in

order to increase the delivery of reactive intermediates to

microbes. If so, then the prediction would be that the diminution of

GSH peroxidase activity would also be found in other infections.

I am not too clear yet on reactive intermediates. Here's what I've

learned:

1. The hydroxyl radical probably doesn't diffuse too well because it

is so reactive.

2. Myeloperoxidase is considered by some to convert other reactive

intermediates to hypohalites, which are more stable and are

considered highly toxic (perhaps because they have time to diffuse

into a bacterial cell?). The oddity is that a lesioned

myeloperoxidase doesn't seem to cause any phenotype, whereas a

lesion in NADPH oxidase yields chronic granulomatous disease, ie

recurrant infections with fungi, etc.

I'm not sure exactly where iNOS and NADPH oxidase are located and

which reactive intermediates can cross membranes. Temporal matters

are also something to wonder about; presumably the long-term

production of reactive intermediates is different from what's seen

during the " oxidative burst " (alas, there's not so much

investigation into *chronic* intracellular bx, except Mtb).

The thing about the ultrastructure of chronic Bb infection is,

there's only one paper to my knowledge, and that's Nanagara. As I

recall, she tagged both apparantly cytosolic and apparantly

endosomic antigens.

>

> Hi, all.

>

> Here's a repost from the Experimental list. Maybe it will be of

> interest to some people here:

>

>

>

> I've been doing some more study of chronic Lyme disease and have

> been thinking about why the Yasko treatment program might be

helpful

> to someone with this disorder.

>

> As we know, Sue T. has been reporting considerable improvement on

> the Yasko treatment program, and as we also know, she has tested

> positively for Lyme disease in the past and has been ill for a

long

> time. So what's going on here?

>

> As some of you may recall, I posted some information about Lyme

> disease and glutathione depletion back in January. I've pasted it

at

> the end of this message for those who would like to review it.

>

> In that earlier post, I reviewed published literature showing that

> Borrelia burgdorferi (the bacteria responsible for Lyme disease)

> depletes glutathione in the host, and it appears to suppress the

> activity of glutathione peroxidase over the longer term, even

after

> antibiotic treatment.

>

> With glutathione peroxidase suppressed, we can expect that the

> levels of hydrogen peroxide would be higher in the host, because

the

> job of glutathione peroxidase is to eliminate hydrogen peroxide.

>

> O.K., here's something I just found out: Borrelia burgdorferi is

> encouraged to assume its cystic form when hydrogen peroxide is

> elevated, and when the cystic forms are placed back in a medium

with

> low hydrogen peroxide, they revert back to the spirochete form.

(R.

> Murgia and M. Cinco, 2004, PMID: 14961976).

>

> Now, I think this is really interesting. I think it suggests that

> the reason Borrelia burgdorferi is able to hang on in a person's

> body and produce chronic Lyme disease is that it suppresses the

> activity of glutathione peroxidase, which allows hydrogen peroxide

> to build up, and then the hydrogen peroxide signals the bacteria

to

> assume the cystic form. This protects it from the immune system

> and, to a large extent, from antibiotics as well, and that's why

> chronic Lyme is such a difficult disease to knock out.

>

> As I said in my earlier post (below), I don't know how Bb

suppresses

> glutathione peroxidase, but I suspect that it might do it by

> hoarding selenium, as Prof. Harry has theorized as the

> pathogenesis mechanism for some viruses, including HIV. Of

course,

> as we know, the buildup of mercury, as occurs when glutathione is

> depleted and a person is exposed to mercury from amalgams, fish,

or

> other sources, will tie up selenium as well. This may be part of

> the synergism that Dr. Yasko has found between pathogens and heavy

> metals.

>

> In any case, it seems to me that the key to knocking out chronic

> Lyme disease might be to lower the levels of hydrogen peroxide, so

> that Bb will revert to the spirochete form and can be attacked by

> the immune system and by antibiotics. To do this, both the

activity

> of glutathione peroxidase and the level of glutathione must be

> brought up to normal. How do we do this?

>

> I think supplementation with selenium would be a good thing to try

> for restoring the activity of glutathione peroxidase.

>

> What about glutathione? Well, in the case of many of the people

> with chronic Lyme disease, I suspect that we are dealing with a

set

> of polymorphisms in the enzymes impacting the methylation cycle

that

> enable the development of a vicious circle mechanism when the

> glutathione level drops low enough, i.e. the same mechanism that

> occurs in many cases of autism and chronic fatigue syndrome.

(This

> certainly seems to have been true in the case of Sue T.) If this

is

> true, then it will be necessary to deal directly to bypass these

> polymorphisms, such as is done in the Yasko treatment program.

>

> What I'm suggesting then, is that the people with chronic Lyme

> disease might also be brought under the " Yasko tent. " This might

be

> the key to making the Borrelia more vulnerable to the immune

system

> and to the antibiotics, so that this disease can be knocked out

more

> effectively.

>

> I would appreciate comments on this hypothesis.

>

> Rich

>

>

> Here is my earlier post from last January:

>

> 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, 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

> cysteine 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

> principal 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

> nicotinamide adenine dinucleotide), 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 disease, such as antibiotic therapy, detoxing

of

> neurotoxins, or other approaches to deal with the bacteria

> themselves or to 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

>

[Guest guest]

I have no idea what my selenium levels are.

What I do know is that whenever I feel an outbreak of Herpes Simplex I

coming on, I blast it with selenium, 3-400 mcgs BID-TID. Usually, I can

notice a difference in the sensitive area within 3 hours. Halts the

outbreak in it's tracks.

My husband has a history also and has been prescribed acyclovir which

didn't work but selenium does. Neither of us has had a full-blown cold-

sore since we started using selenium.

Robyn

[Guest guest]

Oh, they speculated that alot of the downregulations they noted might

well have to do with slowed metabolism. I guess slowed metabolism

would reduce the amount of oxidatives that the worm produces by its

own respiration... thus, the downreg of GSH function (if GST downreg

indeed results in that) might *not* imply that the worm is attempting

to increase the concentration of oxidative intermediates in order to

hit the bugs.