Re: Looking for THINKERS and I know you are here

[Guest guest]

Sorry link doesn't take you there. It does take you to the website,

then go to Medical Questions and the to " Mino & Doxy.... How do they

work? "

[Guest guest]

I would love it if you are up to the challenge to take a look at the discussion and offer what you can. We already know what the Lyme specialists say, so not really looking for that. This is one of those times when we need to think outside the box yet again. Thinking outside the box is what some of you do best here, so that is why I am here and asking.Here is a link to the discussion: http://flash.lymenet.org/ubb/ultimatebb.php?ubb=get_topic;f=1;t=044540.What I got out of it, is that I am now confused about Mino and IL-10. I don't understand whether IL-10 is good or bad and whether the fact that Mino increases it is good or bad. I can see how it might be bad.http://www.rheumatology.org/public/factsheets/minocycline.asp"Minocycline decreases the production of substances causing inflammation, such as prostaglandins and leukotrienes, while increasing production of interleukin-10, a substance in the blood that decreases inflammation."Buthttp://www.jem.org/cgi/content/full/194/10/f53"In part through inhibition of IL-12 production and of costimulatory molecule expression on antigen-presenting cells, IL-10 has an overall suppressive effect on the generation of Th1 responses. In addition, IL-10 profoundly affects the bactericidal activity of phagocytic cells, allowing intracellular survival of pathogens such as Mycobacterium tuberculosis (2) and Leishmania major (3). In addition to inhibit the intracellular bactericidal mechanisms, IL-10 was shown to prevent TNF-mediated apoptosis of M. tuberculosis infected macrophages thus possibly facilitating the maintenance of a chronic infection (4)."Maybe this would clear up my confusion, but I doubt I can plow through it!:1: Immunol Rev. 2004 Dec;202:223-36.     Interleukin-10 in viral diseases and cancer: exiting the labyrinth?    Vicari AP, Trinchieri G.    Schering-Plough Laboratory for Immunological Research, Dardilly, France. alain.vicari@...    Interleukin-10 (IL-10) is unique among cytokines, as it is considered both as a potent immunostimulatory and immunosuppressive factor. This complex biology has been particularly challenging when trying to define the useful or harmful role of IL-10 in chronic viral diseases and cancer. In the present review, we emphasize how these multiple roles define IL-10 as an adaptive molecule, constantly tuning the host response against dangerous and resourceful pathogens.    PMID: 15546396 [PubMed - indexed for MEDLINE]- Kate

[Guest guest]

The causes of death of bacteria facing abx in vitro are not terribly

clear. Well, lets stick to tetracyclines. They inhibit protein

synthesis. For at least several kinds of bacteria (100% of the cases

I know), temporary inhibition of protein synthesis does not kill the

cell, not even if total protein syntehsis shutdown is acheived.

Yet, there are concentrations of tetracyclines that will kill cells

in MBC assays. This is probably because they are not equipped to

adjust that rapidly to the inhibition of protein synthesis. It would

probably be physically possible a priori for a cell to adjust to this

and remain alive, but they arent equipped to do so, so they cant and

dont, and they die.

This depends on growth rate. At a slower growth rate they have more

time to adjust. This is probably why most abx are poorly lethal in

vitro at slow growth rates (for most bacteria in most systems I've

learned about, anyway). Also, adding the abx more gradually might

also decrease the lethality, I would imagine. I'm not aware of any

such experiments, but I suppose I could just do them myself, as

nothing could be simpler. In MBC assays I believe the cells (around

10^5) are added to the abx-containing broths. So they face the abx

immediately. But their growth rate would depend on whats going on in

the culture they were inoculated from. This is something I should

look into more.

Anyway, in vivo its a different story. Most intracellular bacteria

may need to synthesize certain proteins at a certain rate in order to

withstand hostile host molecules, and prevent autonomous or CTL-

assisted programmed cell death. If tetracycline inhibition of protein

synthesis impinges on this significantly, bacterial death may occur.

Now, heres the part youll be interested in most. The amount of

inhibition of protein synthesis by tetracyclines is not a linear

function of the concentration of the drug. In other words, doubling

the concentration of tetracycline does make a 2x change in the level

of protein synthesis inhibition. It can be less or more than 2. The

amount of inhibition of protein synthesis by tetracyclines can be

understood rather completely. It depends on

1. The concentration of the drug in the bacterial cell. Some think

that tetracyclines become concentrated in bacterial cells because

they are taken up actively. I dont know if this has ever been

resolved.

2. The concentration of tRNAs in the cell. Tetracycline competes with

tRNAs for a binding site on the ribosome. The concentration of tRNAs

may or may not be lower in slow-growing bacteria such as I theorize

to cause our conditions.

3. The concentration of active ribosomes in the bacterial cell. Also

probably lower in slow bacteria.

Thats it, throw in the inhibition constant (Ki) for tetracycline and

you can calculate the amount of inhibition youre getting.

Basically, bottom line, if youre looking at a 3 mg dose of mino vs a

200 mg dose, whether this makes a huge difference in the amount of

protein synthesis inhibition basically depends on whether the

resulting concentration in the target cell crosses the Ki when you go

from a 3 mg dose to a 200 mg dose. I would guess that it does. Maybe

I can work it out later... I dont mind as this is just the sort of

thing I am working on now. When the concentration is near the Ki,

thats where changes in concentration make a really big difference in

the effect you get.

If it does cross the Ki, I would basically conclude that its really

unlikely that 3 mg of mino can kill any bacteria.

> Hi, been awhile, but I have been thinking and I was finally able to

> form enough of a thought to pose a question. I have been diagnosed

> with Lyme and I already knew that I had Myco Fermentans. Was

> infected with the Lyme at least 38 years ago.

>

> I have always been curious as to why I have achieved such a high

> state of remission, yet I take nano doses of Minocycline, like 3

> mgs. every other day. The sole reason I take such small doses is I

> can't stand herxing, and so I take only what I need to, in order to

> bring on a tolerable herx. And I do herx herx at this low of a

dose,

> makes me real cranky.

>

> I have read that Mino some how prevents replication and I also read

> somewhere that it prevents Mycoplasma from re-entering new healthy

> cells once they have used another cell up. This leaves them exposed

> and without a cell wall. One of two things happens, they die of

> their own accord or they are now visible to our own immune system,

> both of which seem like real good things.

>

> I am not the only one that very low dose mino ellicits a response

> and others are making some serious headway. Thing is, this flies in

> the face of all we are being told which is, massive ABX are a must.

>

> So I posed a questioned on the Lyme board and some of you may have

> already seen it. I know that there are some REALLY smart people

that

> frequent this board and was hoping that some of you may be able to

> add to the discussion, which so far has no real explanation as to

> why this might work.

>

> I would love it if you are up to the challenge to take a look at

the

> discussion and offer what you can. We already know what the Lyme

> specialists say, so not really looking for that. This is one of

> those times when we need to think outside the box yet again.

> Thinking outside the box is what some of you do best here, so that

> is why I am here and asking.

>

> Here is a link to the discussion:

> http://flash.lymenet.org/ubb/ultimatebb.php?

> ubb=get_topic;f=1;t=044540

>

[Guest guest]

> What I got out of it, is that I am now confused about Mino and IL-

10.

> I don't understand whether IL-10 is good or bad and whether the fact

> that Mino increases it is good or bad. I can see how it might be bad.

Make sure your source is talking about a reasonable concentration of

mino. Norman posted a classic example last week at cpnhelp. There was

this experiment on mino inhibiting yada yada, but the concentration

where it did so effectively was like 50x higher than the serum

concentration you get from a therapeutic dose. People will cite this as

if it has some kind of relevance to medicine.

Theres a large lit on immunomod by abx. I have an entire book about it

from the library. I dont know if all or most of the lit suffers from

these kind of errors, or not... havent spent much time on this topic

yet.

[Guest guest]

Have these on file but havent really been thru em yet:

tetracyclines Ki:

http://www.pubmedcentral.gov/picrender.fcgi?artid=557307 & blobtype=pdf

uptake/concentration in bx:

http://www.pubmedcentral.gov/picrender.fcgi?artid=252046 & blobtype=pdf

[Guest guest]

Ok , these are my questions so far. Testing ABX in a test tube

would seem wholly different then what happens in our bodies. Toward

the end of that thread I comment on this. In one thing someone

offered a test that was done on sheep blood, using differing doses

of ABX. Higher doses seemed to be better. But in our bodies, is

something else occuring that just couldn't possibly happen in a test

tube, like antibody production?

From what I understand Mino doesn't behave at all like other ABX, it

doesn't kill the pathogens directly. Is that correct? The protien

synthisis inhibition, what does that mean for a cell wall deficient

organism? I am not clear on that. Does it leave them stranded, open

to an acitve immune system?

Wonder what would prevent this protien synthisis in some to a

greateregree then in others? Is it a matter of the ABX penetrating

the pathogen?

If 3 mgs. isn't killing anything, any ideas what bring on the herx

symptoms and then a long remission to follow?

ectionAndInflammation2 , " "

<usenethod@...> wrote:

>

> The causes of death of bacteria facing abx in vitro are not

terribly

> clear. Well, lets stick to tetracyclines. They inhibit protein

> synthesis. For at least several kinds of bacteria (100% of the

cases

> I know), temporary inhibition of protein synthesis does not kill

the

> cell, not even if total protein syntehsis shutdown is acheived.

>

> Yet, there are concentrations of tetracyclines that will kill

cells

> in MBC assays. This is probably because they are not equipped to

> adjust that rapidly to the inhibition of protein synthesis. It

would

> probably be physically possible a priori for a cell to adjust to

this

> and remain alive, but they arent equipped to do so, so they cant

and

> dont, and they die.

>

> This depends on growth rate. At a slower growth rate they have

more

> time to adjust. This is probably why most abx are poorly lethal in

> vitro at slow growth rates (for most bacteria in most systems I've

> learned about, anyway). Also, adding the abx more gradually might

> also decrease the lethality, I would imagine. I'm not aware of any

> such experiments, but I suppose I could just do them myself, as

> nothing could be simpler. In MBC assays I believe the cells

(around

> 10^5) are added to the abx-containing broths. So they face the abx

> immediately. But their growth rate would depend on whats going on

in

> the culture they were inoculated from. This is something I should

> look into more.

>

> Anyway, in vivo its a different story. Most intracellular bacteria

> may need to synthesize certain proteins at a certain rate in order

to

> withstand hostile host molecules, and prevent autonomous or CTL-

> assisted programmed cell death. If tetracycline inhibition of

protein

> synthesis impinges on this significantly, bacterial death may

occur.

>

> Now, heres the part youll be interested in most. The amount of

> inhibition of protein synthesis by tetracyclines is not a linear

> function of the concentration of the drug. In other words,

doubling

> the concentration of tetracycline does make a 2x change in the

level

> of protein synthesis inhibition. It can be less or more than 2.

The

> amount of inhibition of protein synthesis by tetracyclines can be

> understood rather completely. It depends on

>

> 1. The concentration of the drug in the bacterial cell. Some think

> that tetracyclines become concentrated in bacterial cells because

> they are taken up actively. I dont know if this has ever been

> resolved.

>

> 2. The concentration of tRNAs in the cell. Tetracycline competes

with

> tRNAs for a binding site on the ribosome. The concentration of

tRNAs

> may or may not be lower in slow-growing bacteria such as I

theorize

> to cause our conditions.

>

> 3. The concentration of active ribosomes in the bacterial cell.

Also

> probably lower in slow bacteria.

>

> Thats it, throw in the inhibition constant (Ki) for tetracycline

and

> you can calculate the amount of inhibition youre getting.

>

> Basically, bottom line, if youre looking at a 3 mg dose of mino vs

a

> 200 mg dose, whether this makes a huge difference in the amount of

> protein synthesis inhibition basically depends on whether the

> resulting concentration in the target cell crosses the Ki when you

go

> from a 3 mg dose to a 200 mg dose. I would guess that it does.

Maybe

> I can work it out later... I dont mind as this is just the sort of

> thing I am working on now. When the concentration is near the Ki,

> thats where changes in concentration make a really big difference

in

> the effect you get.

>

> If it does cross the Ki, I would basically conclude that its

really

> unlikely that 3 mg of mino can kill any bacteria.

>

>

>

>

> > Hi, been awhile, but I have been thinking and I was finally able

to

> > form enough of a thought to pose a question. I have been

diagnosed

> > with Lyme and I already knew that I had Myco Fermentans. Was

> > infected with the Lyme at least 38 years ago.

> >

> > I have always been curious as to why I have achieved such a high

> > state of remission, yet I take nano doses of Minocycline, like 3

> > mgs. every other day. The sole reason I take such small doses is

I

> > can't stand herxing, and so I take only what I need to, in order

to

> > bring on a tolerable herx. And I do herx herx at this low of a

> dose,

> > makes me real cranky.

> >

> > I have read that Mino some how prevents replication and I also

read

> > somewhere that it prevents Mycoplasma from re-entering new

healthy

> > cells once they have used another cell up. This leaves them

exposed

> > and without a cell wall. One of two things happens, they die of

> > their own accord or they are now visible to our own immune

system,

> > both of which seem like real good things.

> >

> > I am not the only one that very low dose mino ellicits a

response

> > and others are making some serious headway. Thing is, this flies

in

> > the face of all we are being told which is, massive ABX are a

must.

> >

> > So I posed a questioned on the Lyme board and some of you may

have

> > already seen it. I know that there are some REALLY smart people

> that

> > frequent this board and was hoping that some of you may be able

to

> > add to the discussion, which so far has no real explanation as

to

> > why this might work.

> >

> > I would love it if you are up to the challenge to take a look at

> the

> > discussion and offer what you can. We already know what the Lyme

> > specialists say, so not really looking for that. This is one of

> > those times when we need to think outside the box yet again.

> > Thinking outside the box is what some of you do best here, so

that

> > is why I am here and asking.

> >

> > Here is a link to the discussion:

> > http://flash.lymenet.org/ubb/ultimatebb.php?

> > ubb=get_topic;f=1;t=044540

> >

>

[Guest guest]

Kate, what I am seeing around is that possibly the lower doses of

Mino won't cause this immune suppression. Most of what we read is

about your typical doses, no one other then our kind of doctors ever

think of using micro doses, and then pulsed at that.

>

> >

> > I would love it if you are up to the challenge to take a look at

the

> > discussion and offer what you can. We already know what the Lyme

> > specialists say, so not really looking for that. This is one of

> > those times when we need to think outside the box yet again.

> > Thinking outside the box is what some of you do best here, so

that

> > is why I am here and asking.

> >

> > Here is a link to the discussion:

> > http://flash.lymenet.org/ubb/ultimatebb.php?

> > ubb=get_topic;f=1;t=044540

> >

> >

> > .

>

> What I got out of it, is that I am now confused about Mino and IL-

10.

> I don't understand whether IL-10 is good or bad and whether the

fact

> that Mino increases it is good or bad. I can see how it might be

bad.

>

> http://www.rheumatology.org/public/factsheets/minocycline.asp

> " Minocycline decreases the production of substances causing

> inflammation, such as prostaglandins and leukotrienes, while

> increasing production of interleukin-10, a substance in the blood

> that decreases inflammation. "

>

> But

> http://www.jem.org/cgi/content/full/194/10/f53

> " In part through inhibition of IL-12 production and of

costimulatory

> molecule expression on antigen-presenting cells, IL-10 has an

overall

> suppressive effect on the generation of Th1 responses. In

addition,

> IL-10 profoundly affects the bactericidal activity of phagocytic

> cells, allowing intracellular survival of pathogens such as

> Mycobacterium tuberculosis (2) and Leishmania major (3). In

addition

> to inhibit the intracellular bactericidal mechanisms, IL-10 was

shown

> to prevent TNF-mediated apoptosis of M. tuberculosis infected

> macrophages thus possibly facilitating the maintenance of a

chronic

> infection (4). "

>

> Maybe this would clear up my confusion, but I doubt I can plow

> through it!:

> 1: Immunol Rev. 2004 Dec;202:223-36.

> Interleukin-10 in viral diseases and cancer: exiting the

labyrinth?

> Vicari AP, Trinchieri G.

> Schering-Plough Laboratory for Immunological Research,

Dardilly,

> France. alain.vicari@...

>

> Interleukin-10 (IL-10) is unique among cytokines, as it is

> considered both as a potent immunostimulatory and

immunosuppressive

> factor. This complex biology has been particularly challenging

when

> trying to define the useful or harmful role of IL-10 in chronic

viral

> diseases and cancer. In the present review, we emphasize how

these

> multiple roles define IL-10 as an adaptive molecule, constantly

> tuning the host response against dangerous and resourceful

pathogens.

>

> PMID: 15546396 [PubMed - indexed for MEDLINE]

>

> - Kate

>

[Guest guest]

Have you been over to the Road Back forums (RA)? They've been discussing low dose mino forever it seems. http://www.roadback.org/index.cfm/fuseaction/home.main.html penny jellybelly92008 <herranenb@...> wrote: Kate, what I am seeing around is that possibly the lower doses of Mino won't cause this immune suppression. Most of what we read is about your typical doses, no one other then our

kind of doctors ever think of using micro doses, and then pulsed at that.>> >> > I would love it if you are up to the challenge to take a look at the> > discussion and offer what you can. We already know what the Lyme> > specialists say, so not really looking for that. This is one of> > those times when we need to think outside the box yet again.> > Thinking outside the box is what some of you do best here, so that> > is why I am here and asking.> >> > Here is a link to the discussion:> > http://flash.lymenet.org/ubb/ultimatebb.php?> > ubb=get_topic;f=1;t=044540> >> >>

> .> > What I got out of it, is that I am now confused about Mino and IL-10. > I don't understand whether IL-10 is good or bad and whether the fact > that Mino increases it is good or bad. I can see how it might be bad.> > http://www.rheumatology.org/public/factsheets/minocycline.asp> "Minocycline decreases the production of substances causing > inflammation, such as prostaglandins and leukotrienes, while > increasing production of interleukin-10, a substance in the blood > that decreases inflammation."> > But> http://www.jem.org/cgi/content/full/194/10/f53> "In part through inhibition of IL-12 production and of costimulatory > molecule expression on antigen-presenting

cells, IL-10 has an overall > suppressive effect on the generation of Th1 responses. In addition, > IL-10 profoundly affects the bactericidal activity of phagocytic > cells, allowing intracellular survival of pathogens such as > Mycobacterium tuberculosis (2) and Leishmania major (3). In addition > to inhibit the intracellular bactericidal mechanisms, IL-10 was shown > to prevent TNF-mediated apoptosis of M. tuberculosis infected > macrophages thus possibly facilitating the maintenance of a chronic > infection (4)."> > Maybe this would clear up my confusion, but I doubt I can plow > through it!:> 1: Immunol Rev. 2004 Dec;202:223-36.> Interleukin-10 in viral diseases and cancer: exiting the labyrinth?> Vicari AP, Trinchieri G.> Schering-Plough Laboratory for Immunological Research, Dardilly, > France.

alain.vicari@...> > Interleukin-10 (IL-10) is unique among cytokines, as it is > considered both as a potent immunostimulatory and immunosuppressive > factor. This complex biology has been particularly challenging when > trying to define the useful or harmful role of IL-10 in chronic viral > diseases and cancer. In the present review, we emphasize how these > multiple roles define IL-10 as an adaptive molecule, constantly > tuning the host response against dangerous and resourceful pathogens.> > PMID: 15546396 [PubMed - indexed for MEDLINE]> > - Kate>

[Guest guest]

I have Penny. In fact the RBF was my first stop after ending up in

the ER after having been given full dose Doxy. I was on low dose

Mino for Myco Fermentans, long before I found I have Lyme. Thing is

low dose Mino is NOT what the LLMDs recommend. Rather the majority

of them insist that the opposite, massive doses is essential. So I

am trying to fit together my experience with my Lyme diagnosis.

Could low dose Mino work for other Lymies too?

> >

> > >

> > > I would love it if you are up to the challenge to take a look

at

> the

> > > discussion and offer what you can. We already know what the

Lyme

> > > specialists say, so not really looking for that. This is one of

> > > those times when we need to think outside the box yet again.

> > > Thinking outside the box is what some of you do best here, so

> that

> > > is why I am here and asking.

> > >

> > > Here is a link to the discussion:

> > > http://flash.lymenet.org/ubb/ultimatebb.php?

> > > ubb=get_topic;f=1;t=044540

> > >

> > >

> > > .

> >

> > What I got out of it, is that I am now confused about Mino and

IL-

> 10.

> > I don't understand whether IL-10 is good or bad and whether the

> fact

> > that Mino increases it is good or bad. I can see how it might be

> bad.

> >

> > http://www.rheumatology.org/public/factsheets/minocycline.asp

> > " Minocycline decreases the production of substances causing

> > inflammation, such as prostaglandins and leukotrienes, while

> > increasing production of interleukin-10, a substance in the

blood

> > that decreases inflammation. "

> >

> > But

> > http://www.jem.org/cgi/content/full/194/10/f53

> > " In part through inhibition of IL-12 production and of

> costimulatory

> > molecule expression on antigen-presenting cells, IL-10 has an

> overall

> > suppressive effect on the generation of Th1 responses. In

> addition,

> > IL-10 profoundly affects the bactericidal activity of phagocytic

> > cells, allowing intracellular survival of pathogens such as

> > Mycobacterium tuberculosis (2) and Leishmania major (3). In

> addition

> > to inhibit the intracellular bactericidal mechanisms, IL-10 was

> shown

> > to prevent TNF-mediated apoptosis of M. tuberculosis infected

> > macrophages thus possibly facilitating the maintenance of a

> chronic

> > infection (4). "

> >

> > Maybe this would clear up my confusion, but I doubt I can plow

> > through it!:

> > 1: Immunol Rev. 2004 Dec;202:223-36.

> > Interleukin-10 in viral diseases and cancer: exiting the

> labyrinth?

> > Vicari AP, Trinchieri G.

> > Schering-Plough Laboratory for Immunological Research,

> Dardilly,

> > France. alain.vicari@

> >

> > Interleukin-10 (IL-10) is unique among cytokines, as it is

> > considered both as a potent immunostimulatory and

> immunosuppressive

> > factor. This complex biology has been particularly challenging

> when

> > trying to define the useful or harmful role of IL-10 in chronic

> viral

> > diseases and cancer. In the present review, we emphasize how

> these

> > multiple roles define IL-10 as an adaptive molecule, constantly

> > tuning the host response against dangerous and resourceful

> pathogens.

> >

> > PMID: 15546396 [PubMed - indexed for MEDLINE]

> >

> > - Kate

> >

>

[Guest guest]

Well, that is certainly the marshall protocol's theory, that low dose mino works for everything. My experience does not bear that out, but I react badly to mino (at any dosage), whereas others react well. It's a strange drug, I know that and an I.D. doc I know will tell you the same. It can cause temporary lupus and create pseudotumor cerebri which can actually kill you, while it clears up your acne. I personally hate minocycline because it makes me so sick. I'm interested in it but I hate it. My daugher did well on it. Of course, most docs say it clears acne and relieves RA pain due to it's anti-inflammatory effects. I find that really hard to believe. penny p.s. I don't know about minocycline, but a substance identified as being the same as tetracycline was discovered in 10,000 year old bones, which means somehow a form occurred

naturally and also that it was capable of penetrating bone (which is big) and that it didn't go away even after 10,000 years. Anyone have the paper on that? Makes you wonder what minocycline can do. jellybelly92008 <herranenb@...> wrote: I have Penny. In fact the RBF was my first stop after ending up in the ER after having been given full dose Doxy. I was on low dose Mino for Myco Fermentans, long before I found I have Lyme. Thing is low dose Mino is NOT what the LLMDs recommend. Rather the majority

of them insist that the opposite, massive doses is essential. So I am trying to fit together my experience with my Lyme diagnosis. Could low dose Mino work for other Lymies too?> >> > >> > > I would love it if you are up to the challenge to take a look at > the> > > discussion and offer what you can. We already know what the Lyme> > > specialists say, so not really looking for that. This is one of> > > those times when we need to think outside the box yet again.> > > Thinking outside the box is what some of you do best here, so > that> > > is why I am here and asking.> > >> > > Here is a link to the discussion:> > > http://flash.lymenet.org/ubb/ultimatebb.php?> > > ubb=get_topic;f=1;t=044540> > >> > >> > > .> > > > What I got out of it, is that I am now confused about Mino and IL-> 10. > > I don't understand whether IL-10 is good or bad and whether the > fact > > that Mino increases it is good or bad. I can see how it might be > bad.> > > > http://www.rheumatology.org/public/factsheets/minocycline.asp> > "Minocycline decreases the production of substances causing > > inflammation, such as prostaglandins and leukotrienes, while > > increasing production of interleukin-10, a substance in the blood > > that decreases

inflammation."> > > > But> > http://www.jem.org/cgi/content/full/194/10/f53> > "In part through inhibition of IL-12 production and of > costimulatory > > molecule expression on antigen-presenting cells, IL-10 has an > overall > > suppressive effect on the generation of Th1 responses. In > addition, > > IL-10 profoundly affects the bactericidal activity of phagocytic > > cells, allowing intracellular survival of pathogens such as > > Mycobacterium tuberculosis (2) and Leishmania major (3). In > addition > > to inhibit the intracellular bactericidal mechanisms, IL-10 was > shown > > to prevent TNF-mediated apoptosis of M. tuberculosis infected > > macrophages thus possibly facilitating the maintenance of a > chronic > >

infection (4)."> > > > Maybe this would clear up my confusion, but I doubt I can plow > > through it!:> > 1: Immunol Rev. 2004 Dec;202:223-36.> > Interleukin-10 in viral diseases and cancer: exiting the > labyrinth?> > Vicari AP, Trinchieri G.> > Schering-Plough Laboratory for Immunological Research, > Dardilly, > > France. alain.vicari@> > > > Interleukin-10 (IL-10) is unique among cytokines, as it is > > considered both as a potent immunostimulatory and > immunosuppressive > > factor. This complex biology has been particularly challenging > when > > trying to define the useful or harmful role of IL-10 in chronic > viral > > diseases and cancer. In the present review, we emphasize how > these > > multiple roles define IL-10 as an adaptive molecule, constantly >

> tuning the host response against dangerous and resourceful > pathogens.> > > > PMID: 15546396 [PubMed - indexed for MEDLINE]> > > > - Kate> >>

[Guest guest]

Can I ask what you mean when you say you react badly? Cuz I react

really bad to it too. So bad that I am still only up to 10 mgs. on

Mon. Wed. Fri.

As far as it preventing inflammation. One of the few times I ever

have experienced actual inflammation is when on Mino. It starts in

the joints of my toes and then into my ankles. Interstingly enough

that is where my pain started when I first started showing symptoms

over 25 years ago. Last time I took the mino, about 6 weeks ago, I

got the inflammation in my wrists and one wrist developed a ganglion

cyst, hot hot and painful. Went away in about 4 weeks after stopping

the mino. Also ended up with a very uncomfortable case of

Costochondroitis which I have never experienced before while on the

Mino.

Is this possibly an allergic reation, I really don't think so. I

react to Doxy and Diflucan in EXACTLY the same way. Identical

herxing it looks like.

I know this is what Marshall believes, but trust me I am not a

supporter of his protocol at this time if you remember. It still

amazes me to this day, that I never got banned, because I was

definely a thorn in his and Meg's side. My questions were really

sincere though.

This low dose Mino thing has been my experience quite some time

before I ever heard of Trevor Marshall. Thing is, what he says in

this particular instance makes sense in my case. Even his graphs of

Mino declining and killing mor on day 2....that's me for sure. It

also builds up the longer I take it, just like he says. What can I

say???

> > >

> > > >

> > > > I would love it if you are up to the challenge to take a

look

> at

> > the

> > > > discussion and offer what you can. We already know what the

> Lyme

> > > > specialists say, so not really looking for that. This is one

of

> > > > those times when we need to think outside the box yet again.

> > > > Thinking outside the box is what some of you do best here,

so

> > that

> > > > is why I am here and asking.

> > > >

> > > > Here is a link to the discussion:

> > > > http://flash.lymenet.org/ubb/ultimatebb.php?

> > > > ubb=get_topic;f=1;t=044540

> > > >

> > > >

> > > > .

> > >

> > > What I got out of it, is that I am now confused about Mino and

> IL-

> > 10.

> > > I don't understand whether IL-10 is good or bad and whether

the

> > fact

> > > that Mino increases it is good or bad. I can see how it might

be

> > bad.

> > >

> > > http://www.rheumatology.org/public/factsheets/minocycline.asp

> > > " Minocycline decreases the production of substances causing

> > > inflammation, such as prostaglandins and leukotrienes, while

> > > increasing production of interleukin-10, a substance in the

> blood

> > > that decreases inflammation. "

> > >

> > > But

> > > http://www.jem.org/cgi/content/full/194/10/f53

> > > " In part through inhibition of IL-12 production and of

> > costimulatory

> > > molecule expression on antigen-presenting cells, IL-10 has an

> > overall

> > > suppressive effect on the generation of Th1 responses. In

> > addition,

> > > IL-10 profoundly affects the bactericidal activity of

phagocytic

> > > cells, allowing intracellular survival of pathogens such as

> > > Mycobacterium tuberculosis (2) and Leishmania major (3). In

> > addition

> > > to inhibit the intracellular bactericidal mechanisms, IL-10

was

> > shown

> > > to prevent TNF-mediated apoptosis of M. tuberculosis infected

> > > macrophages thus possibly facilitating the maintenance of a

> > chronic

> > > infection (4). "

> > >

> > > Maybe this would clear up my confusion, but I doubt I can plow

> > > through it!:

> > > 1: Immunol Rev. 2004 Dec;202:223-36.

> > > Interleukin-10 in viral diseases and cancer: exiting the

> > labyrinth?

> > > Vicari AP, Trinchieri G.

> > > Schering-Plough Laboratory for Immunological Research,

> > Dardilly,

> > > France. alain.vicari@

> > >

> > > Interleukin-10 (IL-10) is unique among cytokines, as it is

> > > considered both as a potent immunostimulatory and

> > immunosuppressive

> > > factor. This complex biology has been particularly challenging

> > when

> > > trying to define the useful or harmful role of IL-10 in

chronic

> > viral

> > > diseases and cancer. In the present review, we emphasize how

> > these

> > > multiple roles define IL-10 as an adaptive molecule,

constantly

> > > tuning the host response against dangerous and resourceful

> > pathogens.

> > >

> > > PMID: 15546396 [PubMed - indexed for MEDLINE]

> > >

> > > - Kate

> > >

> >

>

[Guest guest]

If you look up studies on the side effects of minocyline, pseudotumor cerebri is cited, which is another name for intracranial pressure or hypertension. Those are the symptoms I have. Severe headache, nausea, light sensitivity, dizziness, malaise, etc. It's actually a very dangerous reaction which can cause permanent blindness or death. Minocycline can also mess with your thryoid. I had a thyroid storm while on minocycline, which is another symptom that can kill you. You can see why I don't much care for minocycline. penny jellybelly92008 <herranenb@...> wrote: Can I ask what you mean when you say you react badly? Cuz I react really bad to it too. So bad that I am still only up to 10 mgs. on Mon. Wed. Fri. As far as it preventing inflammation. One of the few times I ever have experienced actual inflammation is when on Mino. It starts in the joints of my toes and then into my ankles. Interstingly enough that is where my pain started when I first started showing symptoms over 25 years ago. Last time I took the mino, about 6 weeks ago, I got the inflammation in my wrists and one wrist developed a ganglion cyst, hot hot and painful. Went away in about 4 weeks after stopping the mino. Also ended up with a very uncomfortable case of Costochondroitis which I have never experienced before while on the Mino.Is this possibly an allergic reation, I really don't think so.

I react to Doxy and Diflucan in EXACTLY the same way. Identical herxing it looks like.I know this is what Marshall believes, but trust me I am not a supporter of his protocol at this time if you remember. It still amazes me to this day, that I never got banned, because I was definely a thorn in his and Meg's side. My questions were really sincere though.This low dose Mino thing has been my experience quite some time before I ever heard of Trevor Marshall. Thing is, what he says in this particular instance makes sense in my case. Even his graphs of Mino declining and killing mor on day 2....that's me for sure. It also builds up the longer I take it, just like he says. What can I say??? > > >> > > >> > > > I would love it if you

are up to the challenge to take a look > at > > the> > > > discussion and offer what you can. We already know what the > Lyme> > > > specialists say, so not really looking for that. This is one of> > > > those times when we need to think outside the box yet again.> > > > Thinking outside the box is what some of you do best here, so > > that> > > > is why I am here and asking.> > > >> > > > Here is a link to the discussion:> > > > http://flash.lymenet.org/ubb/ultimatebb.php?> > > > ubb=get_topic;f=1;t=044540> > > >> > > >> > > > .> > > > > > What I got out of it, is that I am now confused about Mino and > IL-> > 10.

> > > I don't understand whether IL-10 is good or bad and whether the > > fact > > > that Mino increases it is good or bad. I can see how it might be > > bad.> > > > > > http://www.rheumatology.org/public/factsheets/minocycline.asp> > > "Minocycline decreases the production of substances causing > > > inflammation, such as prostaglandins and leukotrienes, while > > > increasing production of interleukin-10, a substance in the > blood > > > that decreases inflammation."> > > > > > But> > > http://www.jem.org/cgi/content/full/194/10/f53> > > "In part through inhibition of IL-12 production and of > >

costimulatory > > > molecule expression on antigen-presenting cells, IL-10 has an > > overall > > > suppressive effect on the generation of Th1 responses. In > > addition, > > > IL-10 profoundly affects the bactericidal activity of phagocytic > > > cells, allowing intracellular survival of pathogens such as > > > Mycobacterium tuberculosis (2) and Leishmania major (3). In > > addition > > > to inhibit the intracellular bactericidal mechanisms, IL-10 was > > shown > > > to prevent TNF-mediated apoptosis of M. tuberculosis infected > > > macrophages thus possibly facilitating the maintenance of a > > chronic > > > infection (4)."> > > > > > Maybe this would clear up my confusion, but I doubt I can plow > > > through it!:> > > 1: Immunol Rev. 2004

Dec;202:223-36.> > > Interleukin-10 in viral diseases and cancer: exiting the > > labyrinth?> > > Vicari AP, Trinchieri G.> > > Schering-Plough Laboratory for Immunological Research, > > Dardilly, > > > France. alain.vicari@> > > > > > Interleukin-10 (IL-10) is unique among cytokines, as it is > > > considered both as a potent immunostimulatory and > > immunosuppressive > > > factor. This complex biology has been particularly challenging > > when > > > trying to define the useful or harmful role of IL-10 in chronic > > viral > > > diseases and cancer. In the present review, we emphasize how > > these > > > multiple roles define IL-10 as an adaptive molecule, constantly > > > tuning the host response against dangerous and resourceful

> > pathogens.> > > > > > PMID: 15546396 [PubMed - indexed for MEDLINE]> > > > > > - Kate> > >> >>

[Guest guest]

> But in our bodies, is

> something else occuring that just couldn't possibly happen in a

test

> tube, like antibody production?

Yes, the cells are under stress from all kinds of nasty molecules and

other threats. They have to keep up with all that.

> From what I understand Mino doesn't behave at all like other ABX,

it

> doesn't kill the pathogens directly. Is that correct?

High concentrations will kill. Indirect and direct are both

conceivable, I think. I'd have to check the numbers. Indirect is

probably more important (a guess). However, mino/tetracyclines are

not unique in this regard; several other drugs can be the same way.

> The protien

> synthisis inhibition, what does that mean for a cell wall deficient

> organism? I am not clear on that. Does it leave them stranded, open

> to an acitve immune system?

Pretty much the same as for a cell-wall-normal organism. Yes, it

should make it harder for them to deal with the threats posed by

immunity.

> Wonder what would prevent this protien synthisis in some to a

> greateregree then in others? Is it a matter of the ABX penetrating

> the pathogen?

There are basically 4 considerations that bear on the effect on

protein synthesis. First the molecule has to get into the space where

the bacterium is (probably in a host cell). Most abx do that pretty

well.

Then it has to get into the bacterial cell. This is potentially a

problem. But some drugs, possibly including tetracyclines, actually

get superconcentrated in the bacterial cell.

Then it has to bind to the ribosome. This depends on the ribosomes

shape. All bacterial ribosomes are similar, but they have small

differences that can affect how tightly a tetracycline molecule

binds. The binding is not permanent. The tetracycline molecule will

bind on and then come off many times. While it is on the ribosome

cant work.

Finally, if the bug has genetic resistance, none of this will work.

The resistance can work in numerous ways. The bug might lack the

protein that takes up the drug. Or it might have another one that

spews it out. Or it might break down the drug, or it might have a

small change in the target shape so that the drug cant bind there.

> If 3 mgs. isn't killing anything, any ideas what bring on the herx

> symptoms and then a long remission to follow?

What exactly do you take (how often and for how long), and what do

you experience when? Do you do 3 mg daily? How long do you herx and

when do you start feeling better? Does the herx stop if you stop the

drug? Does the herx fade out eventually if you *dont* stop the drug?

[Guest guest]

Marshall's graphs of drug concentration are fair enough, but they don't

explain why a lower dose would be more potent than a higher one. And

there's an alternative explanation which seems more direct: the

Herxheimer reaction is on the second day because it takes that long for

the bacteria to die.

If the bacteria are dying on the second day, then the Herxheimer reaction

is arriving after most of the minocycline has left, which probably means

that you're getting less of whatever anti-inflammatory effects the

minocycline may have, to mitigate the herx.

If you care to test this, you can try cutting that 10mg dose in quarters

(use a razor blade if you have to), and taking 2.5 mg twice daily. If

it's correct, you'll get less herx.

But you might also get less progress. One reason that taking the

antibiotic every other day may help is that if one keeps up a constant

level of the antibiotic, the bacteria may go into a dormant state, in

which they sit there not doing much but not dying, either. (This has

been pretty well demonstrated in the case of Chlamydia pneumoniae, which

you probably have some of, because most people do, although that doesn't

mean it's your main problem.) With pulsing, on the other hand, the

bacteria may wake up as the pulse fades away, then get hammered again by

the next pulse -- with, each time, a certain proportion of them dying

rather than shutting down cleanly.

If this is the case, you'll get a lot less herx from taking minocycline

twice daily, not just a little less herx. You might even find that you

can build up to the usual doses.

On Fri, Jun 09, 2006 at 01:31:25AM -0000, jellybelly92008 wrote:

>Can I ask what you mean when you say you react badly? Cuz I react

>really bad to it too. So bad that I am still only up to 10 mgs. on

>Mon. Wed. Fri.

>

>As far as it preventing inflammation. One of the few times I ever

>have experienced actual inflammation is when on Mino. It starts in

>the joints of my toes and then into my ankles. Interstingly enough

>that is where my pain started when I first started showing symptoms

>over 25 years ago. Last time I took the mino, about 6 weeks ago, I

>got the inflammation in my wrists and one wrist developed a ganglion

>cyst, hot hot and painful. Went away in about 4 weeks after stopping

>the mino. Also ended up with a very uncomfortable case of

>Costochondroitis which I have never experienced before while on the

>Mino.

>

>Is this possibly an allergic reation, I really don't think so. I

>react to Doxy and Diflucan in EXACTLY the same way. Identical

>herxing it looks like.

>

>I know this is what Marshall believes, but trust me I am not a

>supporter of his protocol at this time if you remember. It still

>amazes me to this day, that I never got banned, because I was

>definely a thorn in his and Meg's side. My questions were really

>sincere though.

>

>This low dose Mino thing has been my experience quite some time

>before I ever heard of Trevor Marshall. Thing is, what he says in

>this particular instance makes sense in my case. Even his graphs of

>Mino declining and killing mor on day 2....that's me for sure. It

>also builds up the longer I take it, just like he says. What can I

>say???

>

>

>> > >

>> > > >

>> > > > I would love it if you are up to the challenge to take a

>look

>> at

>> > the

>> > > > discussion and offer what you can. We already know what the

>> Lyme

>> > > > specialists say, so not really looking for that. This is one

>of

>> > > > those times when we need to think outside the box yet again.

>> > > > Thinking outside the box is what some of you do best here,

>so

>> > that

>> > > > is why I am here and asking.

>> > > >

>> > > > Here is a link to the discussion:

>> > > > http://flash.lymenet.org/ubb/ultimatebb.php?

>> > > > ubb=get_topic;f=1;t=044540

>> > > >

>> > > >

>> > > > .

>> > >

>> > > What I got out of it, is that I am now confused about Mino and

>> IL-

>> > 10.

>> > > I don't understand whether IL-10 is good or bad and whether

>the

>> > fact

>> > > that Mino increases it is good or bad. I can see how it might

>be

>> > bad.

>> > >

>> > > http://www.rheumatology.org/public/factsheets/minocycline.asp

>> > > " Minocycline decreases the production of substances causing

>> > > inflammation, such as prostaglandins and leukotrienes, while

>> > > increasing production of interleukin-10, a substance in the

>> blood

>> > > that decreases inflammation. "

>> > >

>> > > But

>> > > http://www.jem.org/cgi/content/full/194/10/f53

>> > > " In part through inhibition of IL-12 production and of

>> > costimulatory

>> > > molecule expression on antigen-presenting cells, IL-10 has an

>> > overall

>> > > suppressive effect on the generation of Th1 responses. In

>> > addition,

>> > > IL-10 profoundly affects the bactericidal activity of

>phagocytic

>> > > cells, allowing intracellular survival of pathogens such as

>> > > Mycobacterium tuberculosis (2) and Leishmania major (3). In

>> > addition

>> > > to inhibit the intracellular bactericidal mechanisms, IL-10

>was

>> > shown

>> > > to prevent TNF-mediated apoptosis of M. tuberculosis infected

>> > > macrophages thus possibly facilitating the maintenance of a

>> > chronic

>> > > infection (4). "

>> > >

>> > > Maybe this would clear up my confusion, but I doubt I can plow

>> > > through it!:

>> > > 1: Immunol Rev. 2004 Dec;202:223-36.

>> > > Interleukin-10 in viral diseases and cancer: exiting the

>> > labyrinth?

>> > > Vicari AP, Trinchieri G.

>> > > Schering-Plough Laboratory for Immunological Research,

>> > Dardilly,

>> > > France. alain.vicari@

>> > >

>> > > Interleukin-10 (IL-10) is unique among cytokines, as it is

>> > > considered both as a potent immunostimulatory and

>> > immunosuppressive

>> > > factor. This complex biology has been particularly challenging

>> > when

>> > > trying to define the useful or harmful role of IL-10 in

>chronic

>> > viral

>> > > diseases and cancer. In the present review, we emphasize how

>> > these

>> > > multiple roles define IL-10 as an adaptive molecule,

>constantly

>> > > tuning the host response against dangerous and resourceful

>> > pathogens.

>> > >

>> > > PMID: 15546396 [PubMed - indexed for MEDLINE]

>> > >

>> > > - Kate

>> > >

[Guest guest]

Jelly:

I do not think you are herxing from the tiny dose of Mino you are

taking weekly. That dose of Mino is not high enough to kill a large

number of organisms, and have their die-off elicit an immune response

(which is the definition of herx). Take note of Mino's therapeutic

level in the quote below.

See Reference 1:

QUOTE:

Following a single dose of two 100 mg minocycline HCL capsules

administered to ten normal adult volunteers, serum levels ranged from

0.74 to 4.45 mg/mL in one hour and attained peak levels between 2 and

3 hours; after 12 hours, they ranged from 0.34 to 2.36 mg/mL.

Therapeutic levels are 1-2 mg/mL. The serum half life following a 200

mg dose in 12 normal volunteers ranged from 11 to 17 hours, in 7

patients with hepatic dysfunction ranged from 11 to 16 hours and in 5

patients with renal dysfunction ranged from 18 to 69 hours. Between

55% and 76% of an administered dose is bound by serum proteins.

END QUOTE

REFERENCE 1:

http://www.medsafe.govt.nz/Profs/Datasheet/m/Minotabtab.htm

In the early days, before the birth of the MP, I supplied Marshall

with alot of the full peer-reviewed papers (Antimicrobial

Chemotherapy Journals) he uses to support his use of small doses of

some antibiotics.

There are alot of peer reviewed papers on the use of low dose Zith to

keep the offending pathogen in cystic fibrosis in colony form

(meaning the dose is just high enough so the bug doesn't replicate).

Bactrim is used a the low control dose to keep AIDS patients free

from sysptoms of pathogenic invaders, and Mino has been used for

years and years at 20 to 50 mg per day to keep acne at bay.

There is a ton of medical literature out there on Minocycline.

There are also many articles which show that quote small doses of

SOME antibiotics do kill the VARIANT of some organisms... but Lyme

organism is not one of the organisms small doses of any antibiotic

can kill.

Minocycline is an immune modulator as well as an antimicrobial.

Minocycline also has several immunosuppressive qualities, not all of

which are understood. It is much more likely in my opinion, that it

is one of the immunosuppressive mechanisms- possibly still unknown -

that mino expresses that may be the reason people are feeling better

on these tiny doses. Minocycline is an immune modulator as well as

an antimicrobial.

I don't even know how you can cut a capsule of mino down to 3

milligrams.. that assuming that each grain in the capsule (or tablet)

is perfectly uniform.

I have asked time and time again for some one to show me proof from a

manufacturer than you can even cut a tablet sucessfully down to be

able to measure it by the milligram.

So, in summary Jelly, I am not disputing that you feel better on your

current regime, part of which may be taking a tiny portion of any

medication. But I just can not make the assumptions for results you

are making based soley on observation and subjective reports

regarding these tiny antibiotic amounts.

I think before I could go into arguing my case against the

antimicrobial efficacy of a 3 milligram dose of Mino- I'd first have

to have someone show me there is such a thing as a true 3 milligram

oral dose.

I'd love to see a lab analyse a 3 milligram dose of Mino cut down

from a 100mg pill or capsule to see what's REALLY in that small

sample.

Sorry,

Barb

>

> Hi, been awhile, but I have been thinking and I was finally able to

> form enough of a thought to pose a question. I have been diagnosed

> with Lyme and I already knew that I had Myco Fermentans. Was

> infected with the Lyme at least 38 years ago.

>

> I have always been curious as to why I have achieved such a high

> state of remission, yet I take nano doses of Minocycline, like 3

> mgs. every other day. The sole reason I take such small doses is I

> can't stand herxing, and so I take only what I need to, in order to

> bring on a tolerable herx. And I do herx herx at this low of a

dose,

> makes me real cranky.

>

> I have read that Mino some how prevents replication and I also read

> somewhere that it prevents Mycoplasma from re-entering new healthy

> cells once they have used another cell up. This leaves them exposed

> and without a cell wall. One of two things happens, they die of

> their own accord or they are now visible to our own immune system,

> both of which seem like real good things.

>

> I am not the only one that very low dose mino ellicits a response

> and others are making some serious headway. Thing is, this flies in

> the face of all we are being told which is, massive ABX are a must.

>

> So I posed a questioned on the Lyme board and some of you may have

> already seen it. I know that there are some REALLY smart people

that

> frequent this board and was hoping that some of you may be able to

> add to the discussion, which so far has no real explanation as to

> why this might work.

>

> I would love it if you are up to the challenge to take a look at

the

> discussion and offer what you can. We already know what the Lyme

> specialists say, so not really looking for that. This is one of

> those times when we need to think outside the box yet again.

> Thinking outside the box is what some of you do best here, so that

> is why I am here and asking.

>

> Here is a link to the discussion:

> http://flash.lymenet.org/ubb/ultimatebb.php?

> ubb=get_topic;f=1;t=044540

>

[Guest guest]

On Fri, Jun 09, 2006 at 02:03:43PM -0000, Barb Peck wrote:

>Jelly:

>

> I do not think you are herxing from the tiny dose of Mino you are

>taking weekly. That dose of Mino is not high enough to kill a large

>number of organisms, and have their die-off elicit an immune response

>(which is the definition of herx). Take note of Mino's therapeutic

>level in the quote below.

That the therapeutic level is such-and-such doesn't mean that the drug

has no effect below that level. In any real-world bacterial population,

you'll have some bacteria which are just barely managing to exist, and

which thus don't take much to push over the edge. (You'll also have some

which just happen to be more sensitive to the antibiotic. Killing them,

and them only, breeds antibiotic resistance, which is a reason to avoid

low doses.) In someone who has a high bacterial load, even killing a

small proportion of the bacteria can be quite noticeable.

>I don't even know how you can cut a capsule of mino down to 3

>milligrams.. that assuming that each grain in the capsule (or tablet)

>is perfectly uniform.

>

>I have asked time and time again for some one to show me proof from a

>manufacturer than you can even cut a tablet sucessfully down to be

>able to measure it by the milligram.

Manufacturers aren't the only ones who can prove things. Besides,

manufacturers are scared to death of being sued, so are most unlikely to

tell you to do anything except take the pills exactly as the FDA has

approved them.

I opened up a 100mg minocycline capsule, to see just how hard this might

be. This is a generic, made by Danbury. The capsule opened after a bit

of pulling; it wasn't sealed. The contents are a fine powder, of uniform

color and consistency. It didn't come out too easily, but with a bit of

tapping I got almost all of it out. I first tried scraping up the pile

into a symmetrical shape, that I could cut in half by eye, using a razor

blade. It worked okay, except that some of it stuck to the razor blade.

So I tried again, using the edge of a piece of paper. Here's the result:

http://yarchive.net/photos/mino_cutting.jpg

As indicated, by successively bisecting, I got down to about 0.3 mg

before the exercise started to get silly. I was doing this entirely by

eye, so the last two piles, labeled " 0.3 mg " , might be anywhere from

about 0.2 mg to about 0.5 mg. To really check, I'd need a

laboratory-quality scale. The scale I have is only good enough to weigh

the whole pile: it weighed about 300 mg, so about a third of it is active

ingredient.

The only other thing that would need to be proven is that the powder is

all the same; but it'd be really weird if they put two different kinds of

powders, both the same color and consistency, into one capsule.

--

Norman Yarvin http://yarchive.net

[Guest guest]

Norman:

I agree with you regarding low dose and resistance formation.

And I have already stated that under certain circumstances low dose

can kill the variants of some organisms.

And we already know that RA patients take Mino (at doses of 100 to

200mg) for several years untill they cease to " feel better " . These

people (or their Drs) are weighing the risks (i.e. feeling better V

the chance of acquiring a super strain of some other unknown

organism).

While you may have been able to sucessfully divide the contents in a

mino capsule, and accurately weigh the final cut, it's the assumption

of active ingredients, meaured down to the milligram in that final

cut I question. Making the assumption that the active ingredients

are uniformly distributed throughout each grain is a leap of

(manufacturing) faith I'm not willing to take.

When there are a variety of unknowns, and a multitude of variables,

then statements regarding some final result cannot be

pronounced as fact.

I have long held the opinion, as still do, that the pronouncement

of " I'm herxing " has been the single most thing to cloud what's

really going on. It keeps the subject from being investigated

further.

I am perfectly willing to change my mind on any of my opinions if

someone gives me *some* data to go on.

Barb

> >Jelly:

> >

> > I do not think you are herxing from the tiny dose of Mino you

are

> >taking weekly. That dose of Mino is not high enough to kill a

large

> >number of organisms, and have their die-off elicit an immune

response

> >(which is the definition of herx). Take note of Mino's therapeutic

> >level in the quote below.

>

> That the therapeutic level is such-and-such doesn't mean that the

drug

> has no effect below that level. In any real-world bacterial

population,

> you'll have some bacteria which are just barely managing to exist,

and

> which thus don't take much to push over the edge. (You'll also

have some

> which just happen to be more sensitive to the antibiotic. Killing

them,

> and them only, breeds antibiotic resistance, which is a reason to

avoid

> low doses.) In someone who has a high bacterial load, even killing

a

> small proportion of the bacteria can be quite noticeable.

>

> >I don't even know how you can cut a capsule of mino down to 3

> >milligrams.. that assuming that each grain in the capsule (or

tablet)

> >is perfectly uniform.

> >

> >I have asked time and time again for some one to show me proof

from a

> >manufacturer than you can even cut a tablet sucessfully down to be

> >able to measure it by the milligram.

>

> Manufacturers aren't the only ones who can prove things. Besides,

> manufacturers are scared to death of being sued, so are most

unlikely to

> tell you to do anything except take the pills exactly as the FDA has

> approved them.

>

> I opened up a 100mg minocycline capsule, to see just how hard this

might

> be. This is a generic, made by Danbury. The capsule opened after

a bit

> of pulling; it wasn't sealed. The contents are a fine powder, of

uniform

> color and consistency. It didn't come out too easily, but with a

bit of

> tapping I got almost all of it out. I first tried scraping up the

pile

> into a symmetrical shape, that I could cut in half by eye, using a

razor

> blade. It worked okay, except that some of it stuck to the razor

blade.

> So I tried again, using the edge of a piece of paper. Here's the

result:

>

> http://yarchive.net/photos/mino_cutting.jpg

>

> As indicated, by successively bisecting, I got down to about 0.3 mg

> before the exercise started to get silly. I was doing this

entirely by

> eye, so the last two piles, labeled " 0.3 mg " , might be anywhere from

> about 0.2 mg to about 0.5 mg. To really check, I'd need a

> laboratory-quality scale. The scale I have is only good enough to

weigh

> the whole pile: it weighed about 300 mg, so about a third of it is

active

> ingredient.

>

> The only other thing that would need to be proven is that the

powder is

> all the same; but it'd be really weird if they put two different

kinds of

> powders, both the same color and consistency, into one capsule.

>

>

> --

> Norman Yarvin

http://yarchive.net

>

[Guest guest]

No need to feel sorry Barb, gives me stuff to think about. Whether

or not this is a herx....how would you explain?

Let me give somme back ground and I'll do it in a nut shell if I

can. I could write a book. Please read it, so you will know why I

really wonder what I did that has worked for me.

I've been infected with Lyme since I was about twelve. I could see

that it may have happened earlier as I lived at the base of the

angeles forest and used to ride my horse into heavy brush, build

forts in the bushes, etc. I have always been a sleeper. When we are

sure I was bitten, I had 15-20 ticks in my hair.

When I started having children is when I really started showing

signs of being sick. There was the usual stuff, flu like symptoms,

but then there was other stuff too that eventually came along. Never

ran fevers, never sweat, never got sick, anorexic thin, pale in

color with gray and blue undertones, hair falling out, ice cold

hands and feet, feet often turning black. Never bruised. I felt

absolutely toxic. Couldn't eat, couldn't digest fod. Migraines

nearly 24/7. Interstycial cystitis. Lips peeled all the time,

fingers puckery like I was always in water, etc, etc, etc. That was

all at my sickest which was about 12 years ago, and I had no answers.

Had started reading about Fibro and began to pursue that. I'm going

to list what I have done since then. First I was started on Elavil,

and it turned my life around. somehow it bought me time, because I

was knocking on deaths door now that I look back. I was still

declining slowly though. Heart rate was way up at a steady 120, and

Raynaud's was worsening. Found a great doctor who started looking

into a bunch of stuff.

First thing was hypercoagulation, I had it bad. Treat with heparin,

big change in phsycial appearance. Skin became alive and turned

normal in color. I was on that for about 10 months, then stopped,

hypercoagulation came right back. So it was assumed I had aquired

hypercoagulation from infection.

Next I was tested for Mycolasma and was positive for Fermentans and

Pnuemonia. We started treatment with full dose Doxy and that is when

I end up in the ER, with HR at 145 and BP plumitting. Could hardly

stand up. Nuerally mediated hypotension all over the place.

Shortly there after I had a sleep study, found I only slept stage 1

and a little 2, no dreaming, I already know that. BUT they also

found I was having ventricular tacycardia, also know as a malignant

arrythmia, deadly, sudden death stuff. Was sent to cardio who found

things looked normal so it I was told heart is irritable, but don't

know why. Likely nuero/electrical. Aslo had MVP.

So, what to do now. Kind afraid of ABX because reaction to Doxy was

so severe, possibly septic shock. I found RBF where I learned about

low dose Mino and have been doing that every since.

About 1 year ago I was diagnosed with Lyme, my daughter who would

have gotten lyme from me in utero is CDC positive. My mom who was

bitten in the same place as me, is also now CDC positive after

having a diagnosis of MS. LLMD, has been adjusting my hormones, put

me on Lopressor to reduce my heart rate a bit more, I had gotten it

down to 90.

That is ALL that I have done. Where am I health wise now in 3 years

of on and off ABX . No pain, that doesn't respond to a couple of

Advil, no headaches, I sweat like normal people, my hair has grown

back, I sleep all night without help, no elavil, hypercoagulation is

gone, no heparin, I am a normal weight, I have great energy, hike at

high alltidues, I have an appetiete, no nausea, color is good. I get

sick now on occasion, and I run low grade fevers, whccih tells me my

immune system in doing something. And very recently, my chiro and I

discovered when I asked for new exrays that my 37 degree scoliosis

has gone nearly straight???? When and why would that happen? could

it be the relaxing of my muscles? He has no idea, because scoliosis

is degenertive, supposedly.

When I take ABX, I get that familiar fluish achey feeling. I get

swelling in my larger joints. I get mild depression, and very

recently for the first time in my life, my glands are actually

swelling and getting sore. None of this stuff worked before. If I am

not herxing and getting well because of low dose mino, what could

the explanation to my good health be....relatively speaking.

I don't feel good on Mino, I feel awful, it is later that I feel

good after I stop and I can go months and months without relapse,

even under very stressful situations. The only reason, I go on ABX

is because of my heart rate, which I believe to be a good indicator

that there is still infection to some degree. Rapid heart rate is a

sign of infection.

You tell me, because I can think of no other explanation. It is also

believed that I am dealing with Babesia which may have been wiped

out by the heparin, and the more coinfections one has the sicker

they are expected to be. Well I am one of a handful that actually

looked like a toxic waste dump.

In regards to getting 3 mgs. I use capsules, with powder, actually

Minocycline not time released, and I talked with a pharmissist about

doing this. The powder is mixed in huge vats, not one capsule at a

time, so I don't worry about what is in each split dose anymore then

I worry about what is in a single capsule which has been split off

from a huge vat. I got 50 mg capsules and simply eyeballed dumping

them into 12-13 new gel caps. so like Norman, it may have been 2.5

in one and 3.2 in another, but close enough. I wasn't looking for

anything precise, just a lessening of the herx.

> >

> > Hi, been awhile, but I have been thinking and I was finally able

to

> > form enough of a thought to pose a question. I have been

diagnosed

> > with Lyme and I already knew that I had Myco Fermentans. Was

> > infected with the Lyme at least 38 years ago.

> >

> > I have always been curious as to why I have achieved such a high

> > state of remission, yet I take nano doses of Minocycline, like 3

> > mgs. every other day. The sole reason I take such small doses is

I

> > can't stand herxing, and so I take only what I need to, in order

to

> > bring on a tolerable herx. And I do herx herx at this low of a

> dose,

> > makes me real cranky.

> >

> > I have read that Mino some how prevents replication and I also

read

> > somewhere that it prevents Mycoplasma from re-entering new

healthy

> > cells once they have used another cell up. This leaves them

exposed

> > and without a cell wall. One of two things happens, they die of

> > their own accord or they are now visible to our own immune

system,

> > both of which seem like real good things.

> >

> > I am not the only one that very low dose mino ellicits a

response

> > and others are making some serious headway. Thing is, this flies

in

> > the face of all we are being told which is, massive ABX are a

must.

> >

> > So I posed a questioned on the Lyme board and some of you may

have

> > already seen it. I know that there are some REALLY smart people

> that

> > frequent this board and was hoping that some of you may be able

to

> > add to the discussion, which so far has no real explanation as

to

> > why this might work.

> >

> > I would love it if you are up to the challenge to take a look at

> the

> > discussion and offer what you can. We already know what the Lyme

> > specialists say, so not really looking for that. This is one of

> > those times when we need to think outside the box yet again.

> > Thinking outside the box is what some of you do best here, so

that

> > is why I am here and asking.

> >

> > Here is a link to the discussion:

> > http://flash.lymenet.org/ubb/ultimatebb.php?

> > ubb=get_topic;f=1;t=044540

> >

>

[Guest guest]

Wow Norman, I can't believe you went to all that trouble, but you

have proved that splitting can be done. Your way is far more precise

then mine, which just means eyeballing while dumping it into new

capsules. Thanks for sharing those pictures, awesome!

> >Jelly:

> >

> > I do not think you are herxing from the tiny dose of Mino you

are

> >taking weekly. That dose of Mino is not high enough to kill a

large

> >number of organisms, and have their die-off elicit an immune

response

> >(which is the definition of herx). Take note of Mino's

therapeutic

> >level in the quote below.

>

> That the therapeutic level is such-and-such doesn't mean that the

drug

> has no effect below that level. In any real-world bacterial

population,

> you'll have some bacteria which are just barely managing to exist,

and

> which thus don't take much to push over the edge. (You'll also

have some

> which just happen to be more sensitive to the antibiotic. Killing

them,

> and them only, breeds antibiotic resistance, which is a reason to

avoid

> low doses.) In someone who has a high bacterial load, even

killing a

> small proportion of the bacteria can be quite noticeable.

>

> >I don't even know how you can cut a capsule of mino down to 3

> >milligrams.. that assuming that each grain in the capsule (or

tablet)

> >is perfectly uniform.

> >

> >I have asked time and time again for some one to show me proof

from a

> >manufacturer than you can even cut a tablet sucessfully down to

be

> >able to measure it by the milligram.

>

> Manufacturers aren't the only ones who can prove things. Besides,

> manufacturers are scared to death of being sued, so are most

unlikely to

> tell you to do anything except take the pills exactly as the FDA

has

> approved them.

>

> I opened up a 100mg minocycline capsule, to see just how hard this

might

> be. This is a generic, made by Danbury. The capsule opened after

a bit

> of pulling; it wasn't sealed. The contents are a fine powder, of

uniform

> color and consistency. It didn't come out too easily, but with a

bit of

> tapping I got almost all of it out. I first tried scraping up the

pile

> into a symmetrical shape, that I could cut in half by eye, using a

razor

> blade. It worked okay, except that some of it stuck to the razor

blade.

> So I tried again, using the edge of a piece of paper. Here's the

result:

>

> http://yarchive.net/photos/mino_cutting.jpg

>

> As indicated, by successively bisecting, I got down to about 0.3 mg

> before the exercise started to get silly. I was doing this

entirely by

> eye, so the last two piles, labeled " 0.3 mg " , might be anywhere

from

> about 0.2 mg to about 0.5 mg. To really check, I'd need a

> laboratory-quality scale. The scale I have is only good enough to

weigh

> the whole pile: it weighed about 300 mg, so about a third of it is

active

> ingredient.

>

> The only other thing that would need to be proven is that the

powder is

> all the same; but it'd be really weird if they put two different

kinds of

> powders, both the same color and consistency, into one capsule.

>

>

> --

> Norman Yarvin

http://yarchive.net

>

[Guest guest]

Oh, one other thing Barb. What if mino doesn't kill the bacteria or

whatever. Problem with survial of the fitist wouldn't be a problem

if it was now the immune system that was actually killing. What if

it causes another reaction that leaves them more vulnearble?

Am I the only one who read the stuff about Mino locking out

Mycoplasma so that they are exposed to the immmune system? I could

just kick myself for not putting that where I could find it. I know

that I didn't get that from Marshall. I remember talking about it

way back on Immune Support.

> >

> > Hi, been awhile, but I have been thinking and I was finally able

to

> > form enough of a thought to pose a question. I have been

diagnosed

> > with Lyme and I already knew that I had Myco Fermentans. Was

> > infected with the Lyme at least 38 years ago.

> >

> > I have always been curious as to why I have achieved such a high

> > state of remission, yet I take nano doses of Minocycline, like 3

> > mgs. every other day. The sole reason I take such small doses is

I

> > can't stand herxing, and so I take only what I need to, in order

to

> > bring on a tolerable herx. And I do herx herx at this low of a

> dose,

> > makes me real cranky.

> >

> > I have read that Mino some how prevents replication and I also

read

> > somewhere that it prevents Mycoplasma from re-entering new

healthy

> > cells once they have used another cell up. This leaves them

exposed

> > and without a cell wall. One of two things happens, they die of

> > their own accord or they are now visible to our own immune

system,

> > both of which seem like real good things.

> >

> > I am not the only one that very low dose mino ellicits a

response

> > and others are making some serious headway. Thing is, this flies

in

> > the face of all we are being told which is, massive ABX are a

must.

> >

> > So I posed a questioned on the Lyme board and some of you may

have

> > already seen it. I know that there are some REALLY smart people

> that

> > frequent this board and was hoping that some of you may be able

to

> > add to the discussion, which so far has no real explanation as

to

> > why this might work.

> >

> > I would love it if you are up to the challenge to take a look at

> the

> > discussion and offer what you can. We already know what the Lyme

> > specialists say, so not really looking for that. This is one of

> > those times when we need to think outside the box yet again.

> > Thinking outside the box is what some of you do best here, so

that

> > is why I am here and asking.

> >

> > Here is a link to the discussion:

> > http://flash.lymenet.org/ubb/ultimatebb.php?

> > ubb=get_topic;f=1;t=044540

> >

>

[Guest guest]

Fascinating stuff. How's your weight at the moment? I think the less

fat cells you have to harbour the toxins the better you respond.

Also if you keep the blood right long enough it goes on to repair

the body.The low dose mino is a very poor therapy choice that

doesn't have too many people swinging from the rafters in too many

forums IMO.I suppose a good environment and a bit of cardiovascular

exercise and eating don't do any harm either.

> > >

> > > Hi, been awhile, but I have been thinking and I was finally

able

> to

> > > form enough of a thought to pose a question. I have been

> diagnosed

> > > with Lyme and I already knew that I had Myco Fermentans. Was

> > > infected with the Lyme at least 38 years ago.

> > >

> > > I have always been curious as to why I have achieved such a

high

> > > state of remission, yet I take nano doses of Minocycline, like

3

> > > mgs. every other day. The sole reason I take such small doses

is

> I

> > > can't stand herxing, and so I take only what I need to, in

order

> to

> > > bring on a tolerable herx. And I do herx herx at this low of a

> > dose,

> > > makes me real cranky.

> > >

> > > I have read that Mino some how prevents replication and I also

> read

> > > somewhere that it prevents Mycoplasma from re-entering new

> healthy

> > > cells once they have used another cell up. This leaves them

> exposed

> > > and without a cell wall. One of two things happens, they die

of

> > > their own accord or they are now visible to our own immune

> system,

> > > both of which seem like real good things.

> > >

> > > I am not the only one that very low dose mino ellicits a

> response

> > > and others are making some serious headway. Thing is, this

flies

> in

> > > the face of all we are being told which is, massive ABX are a

> must.

> > >

> > > So I posed a questioned on the Lyme board and some of you may

> have

> > > already seen it. I know that there are some REALLY smart

people

> > that

> > > frequent this board and was hoping that some of you may be

able

> to

> > > add to the discussion, which so far has no real explanation as

> to

> > > why this might work.

> > >

> > > I would love it if you are up to the challenge to take a look

at

> > the

> > > discussion and offer what you can. We already know what the

Lyme

> > > specialists say, so not really looking for that. This is one

of

> > > those times when we need to think outside the box yet again.

> > > Thinking outside the box is what some of you do best here, so

> that

> > > is why I am here and asking.

> > >

> > > Here is a link to the discussion:

> > > http://flash.lymenet.org/ubb/ultimatebb.php?

> > > ubb=get_topic;f=1;t=044540

> > >

> >

>

[Guest guest]

jelly

You've got major heart issues going on and good medical book that

lists stuff on heart infections will clearly state- using

bacteriastatic antibiotics is not wise in heart infections-

bacteriacidal drugs are the only choice for heart infections.So

having a major reaction from minor dose gives an indication of

waking the vegetations on your mitral valve to give you all those

flutters.

Again your so lucky you have minimul fat cells which make your

condition pretty responsive.

> > >

> > > Hi, been awhile, but I have been thinking and I was finally

able

> to

> > > form enough of a thought to pose a question. I have been

> diagnosed

> > > with Lyme and I already knew that I had Myco Fermentans. Was

> > > infected with the Lyme at least 38 years ago.

> > >

> > > I have always been curious as to why I have achieved such a

high

> > > state of remission, yet I take nano doses of Minocycline, like

3

> > > mgs. every other day. The sole reason I take such small doses

is

> I

> > > can't stand herxing, and so I take only what I need to, in

order

> to

> > > bring on a tolerable herx. And I do herx herx at this low of a

> > dose,

> > > makes me real cranky.

> > >

> > > I have read that Mino some how prevents replication and I also

> read

> > > somewhere that it prevents Mycoplasma from re-entering new

> healthy

> > > cells once they have used another cell up. This leaves them

> exposed

> > > and without a cell wall. One of two things happens, they die

of

> > > their own accord or they are now visible to our own immune

> system,

> > > both of which seem like real good things.

> > >

> > > I am not the only one that very low dose mino ellicits a

> response

> > > and others are making some serious headway. Thing is, this

flies

> in

> > > the face of all we are being told which is, massive ABX are a

> must.

> > >

> > > So I posed a questioned on the Lyme board and some of you may

> have

> > > already seen it. I know that there are some REALLY smart

people

> > that

> > > frequent this board and was hoping that some of you may be

able

> to

> > > add to the discussion, which so far has no real explanation as

> to

> > > why this might work.

> > >

> > > I would love it if you are up to the challenge to take a look

at

> > the

> > > discussion and offer what you can. We already know what the

Lyme

> > > specialists say, so not really looking for that. This is one

of

> > > those times when we need to think outside the box yet again.

> > > Thinking outside the box is what some of you do best here, so

> that

> > > is why I am here and asking.

> > >

> > > Here is a link to the discussion:

> > > http://flash.lymenet.org/ubb/ultimatebb.php?

> > > ubb=get_topic;f=1;t=044540

> > >

> >

>

[Guest guest]

Years ago, I saw an orthopedist during an episode of back spasms so severe and painful that I couldn't stand or walk straight. He incorrectly told me that I had extreme scoliosis and my inability to stand straight couldn't possibly be caused by muscle spasms and that I'd just have to live with "scoliosis" for the rest of my life. Apparently he disregarded by assertions that I had periods of being able to walk normally. Just one more idiot to cross off my list (along with 2 other orthopedists who recommended surgery and 3 chiropractors who probably did more damage than good). After I recovered from what was actually a herniated disc with traction therapy, dxd by a sports medicine doc, my "scoliosis" disappeared and I've never walked crooked or needed adjustments again. penny

[Guest guest]

Real minocycline is actually made of tiny balls. I've heard people say that they actually count these tiny balls under a magnifying glass to split the doses, and I've also heard others say that there can be accuracy problems even with this method. I think Barb has a valid point. Especially if you truly believe 3 mgs has some kind of effect, then 4 mgs is a substantially larger dose. Maybe the tiny dose is enough to stir up your organisms' defenses causing an immune system activation? I don't see how 3 mgs can possibly be doing much on its own. Not against the resistant levels of the bacteria we're dealing with. I doubt if you're experiencing a "herx" in its true definition, which would mean causing enough of an organism die-off to cause a reaction to the toxins being released to make you feel sick. The misuse of this word, I think, to include any crummy

feelings, is causing all kinds of problems for people with infections. penny

[Guest guest]

Tony, I still do not see how you can support this view about fat cells. There's so much research to show that fat and cholesterol (which are usually linked) are both there to protect your body from toxin exposure. Elevated cholesterol is almost always linked to underactive thyroids, and is also believed by many to be some kind of protective mechanism. My doc says that if your thyroid output goes up, your cholesterol goes down automatically. Often the same with weight. I've been very thin and it didn't prevent me from getting sick. In fact I think it may have contributed to me getting sicker. I gain weight extremely easily, which is crazy considering the low caloric intake I have.. I believe it has something to do with my body's defenses. It could be some kind of self preservation mechanism, turning food into fat stores, rather than energy, since low energy also seems to be a defense mechanism. penny dumbaussie2000 <dumbaussie2000@...> wrote: Fascinating stuff. How's your weight at the moment? I think the less fat cells you have to harbour the toxins the better you respond. Also if you keep the blood right long enough it goes on to repair the body.The low dose mino is a very poor therapy choice that doesn't have too many people swinging from the rafters in too many forums IMO.I suppose a good environment and a bit of cardiovascular exercise and eating don't do any harm

either.> > >> > > Hi, been awhile, but I have been thinking and I was finally able > to > > > form enough of a thought to pose a question. I have been > diagnosed > > > with Lyme and I already knew that I had Myco Fermentans. Was > > > infected with the Lyme at least 38 years ago.> > > > > > I have always been curious as to why I have achieved such a high > > > state of remission, yet I take nano doses of Minocycline, like 3 > > > mgs. every other day. The sole reason I take such small doses is > I > > > can't stand herxing, and so I take only what I need to, in order > to > > > bring

on a tolerable herx. And I do herx herx at this low of a > > dose, > > > makes me real cranky.> > > > > > I have read that Mino some how prevents replication and I also > read > > > somewhere that it prevents Mycoplasma from re-entering new > healthy > > > cells once they have used another cell up. This leaves them > exposed > > > and without a cell wall. One of two things happens, they die of > > > their own accord or they are now visible to our own immune > system, > > > both of which seem like real good things.> > > > > > I am not the only one that very low dose mino ellicits a > response > > > and others are making some serious headway. Thing is, this flies > in > > > the face of all we are being told which is, massive ABX are a > must.> >

> > > > So I posed a questioned on the Lyme board and some of you may > have > > > already seen it. I know that there are some REALLY smart people > > that > > > frequent this board and was hoping that some of you may be able > to > > > add to the discussion, which so far has no real explanation as > to > > > why this might work.> > > > > > I would love it if you are up to the challenge to take a look at > > the > > > discussion and offer what you can. We already know what the Lyme > > > specialists say, so not really looking for that. This is one of > > > those times when we need to think outside the box yet again. > > > Thinking outside the box is what some of you do best here, so > that > > > is why I am here and asking.> > > >

> > Here is a link to the discussion: > > > http://flash.lymenet.org/ubb/ultimatebb.php?> > > ubb=get_topic;f=1;t=044540> > >> >>