Re: Immune modulators, once more on ARBs, tony on IS vs pathos

[Guest guest]

I agree strongly with Tony's " Our immune system isn't taking care of

the pathogens we are trying to remove with drugs, as you can observe

the biggest problem lies in the late delivery and too short a

duration of treatment. "

However, that actually says nothing about where the problem is at

the macro level. I think the argument is pretty strong, that our

immune systems aren't what they used to be, and that this relates to

a combination of toxic pollutants and maladaptive ways of living

that are themselves virus-like in the manner of their spread.

I love the sentence from Civilization and It's Discontents where

Freud worries outloud about collective neurosis and points out that

it would be impossible to diagnose, because no background of

normality would exist.

I think we're seeing that worry establish itself as a tangible fact.

I was uber-impressed with Cheney's discussions of cardiomyopathy in

CFS, and have great respect for Rich's work on glutathione,

precisely because stuff like this lets you look at disease from the

perspective of health in a way that's still possible, using specific

patient populations and well-matched controls, and plot a graded

curve that does justice to the range of severity and the

pervasiveness of lower-grade chronic fatigue, ADD, arthalgia, etc in

modern societies.

I also understand why some here get frustrated on other sites where

pathogens are not the focus of discussion, and wish we could clone

Tony and put one in every ID practice.

But there is no point, it is absolutely a sterile exercise, to ask

which matters more, the presence of pathogens or the absence of a

robust/adaptible enough immune system to fend them off. Kind of like

debating between the value of air and water.

I also don't think we can know, via some remote diagnostic genius,

which emphasis is appropriate for any given patient at any given

time, and should exercise restraint in doubting what others choose

to focus on.

What matters to me is whether there is some valid reason for

thinking something will be helpful. I do not see a valid reason to

believe that ARBs will ever help anyone clear any infection of any

kind whatsoever. Sorry, J, but I've read those damn JOIR papers

and their citations up down and sideways and there isn't any science

to pull apart.

The citations in the paper you mention, if you actually read them,

demonstrate:

1) That angiotensin II increases host resistance, and losartan

decreases it (that's the Belline reference, look it up if you don't

believe me);

2) Two species of mycoplasma neither of which has ever been accused

of making anyone ill bind Angiotensin II;

3) Applying ARBs has absolutely no effect on this AII-binding by

microbes.

Not only do the references not agree with the argument, but the

argument is badly at odds with itself.

He spends paragraphs establishing that mammalian and microbial AII

receptors have absolutely nothing in common, structurally or

genetically, which makes it really unsurprising that ARBs, which

target mammalian receptors, don't do diddly squat to what appear to

be RARE microbial AII binding sites.

The coy little reference to Benicar not being available when these

studies were done has no weight - the author himself has established

the reasoning that tells us it's likely to make you win the lottery

as stop those two non-pathogenic myco's from doin' their thing

4) At least one of the studies he cites looked at a bonafide

pathogenic myco, M. hominins, and guess what, it didn't bind AII at

all.

You can play with that paper and the others from now till hell

freezes over, but it won't add up to an argument for any

antibacterial property of ARBs, putative or otherwise.

ARBs do have documented effects on host resistance to infection, and

they're consistently negative.

ABSs do modulate the immune system, but not in a way that would shut

down cytokine cascades, which are mainly triggered by tlrs, not AII

type 1 receptors, which are primarily involved in getting

macrophages to infection sites and putting them to work cleaning up

the mess. There's some cytokine production that results from

macrophages ingesting bugs and toxins, but it's necessary - those no

other way we know of to get the crap out of your body, the abx

unfortunately don't neutralize the toxins or make the bug corpses

vanish.

I know some people feel better on them, and no, I don't know why, I

just know there's no documented immune modulating effect that

provides anything like a convincing explanation.

The strongest theoretical argument would be no migration and

phagocytosis = no gobbling up of bugs that end up colonizing

macrophages, but you'd want to be REAL damn sure that the only bugs

you had to worry about were white cell parasites, because your

ability to cope with motile spirochetes or methicillin resistant

staph or even, according to a study I haven't posted yet, YEAST,

goes kaput. and i think you would be wanting some real high dose abx

treatment as well, plus a whole lot of D to promote inflammatory

cell apoptosis, unless you're a hypercalcemic sarcie in which case

even I admit there could be situations where ARBs are the lesser of

the available evil, depending heavily on how you conceptualize that

disease, because the 'evidence' from sarcinfo reports is not real

compelling.

Also, if you look at the only attempt to test this outsie of sarc,

the MP.com site itself, I read every damn progress report for

several months there and the numbers expressing improvement and the

numbers expressing exacerbation within the same dx cancel each other

out, making for no correlation between ARBs and reduction in immune

mediated inflammation.

Add to this that there AII type 1 receptors here there and

everywhere whose function no one's real sure of and it would take a

far more rigorous, systematic analysis of 'responders' vs 'non-

responders' to get any clue what the difference is.

Based on reports of both much worse and much improved PMS, I

strongly suspect hormones are involved in some cases. It's also

likely that immune system energy demands go way down due to reduced

activity, which combined with hormonal shifts could easily cause

some people to feel a whole lot more energetic. Meanwhile, if

Nishida's study turns out to be predictive of humans, and most renal

therapies are developed from such studies, we can expect to see a

lot of uglies down the road. frankly, immune modulating with Pop

Tarts would make more sense to me.

But one ugly duckling of an immune mod does not discredit the whole

concept, and there's no question, no debate at all in microbiology,

that some bugs have evolved to trigger inflammation as a way of

diverting immune system resources. Lyme appears to be one of them,

but it does it via TLRs, as do just about every pathogenic beastie

known to man, so again, shutting down AII type 1 receptors on

macrophages does not cut the mustard as a strategy.

if we could nudge rather than shove the immune system when it gets

stuck responding to pathogen cues that would be groovy but not a lot

of great drugs for that, and no evidence I know of that ARBs have

that effect.

Barb Peck's done a masterful job of documenting the value of HCQ in

alkalizing the cell compartment to maximize both antibiotic and

antifungal drug action against bugs, but it also has an immune mod

effect which I don't entirely understand. i think it might be an

interesting one to look at.

Personally, I'm in the part of the spectrum where you really do have

to look at mitochondrial issues, the immune system doesn't run on

fumes and unfortunately neither does the brain or any other vital

organ I know of and the evidence - which we're just figuring out how

to gather - of mitochondrial dysfunction in the real bad cases is

strong enough that the taxonomy is now classifying these grizzly

things as mitochondrial disorders, so you might take all Tony's abx

and still not get better if you don't address that somehow (though

my guess is without the abx you're also what's for dinner).

Pardon my bluntness, but this kind of back and forth just needs to

get somewhere. If Pippet or Penny have an ARB's save the day study

with specific positive results for reducing pathogen loads hidden up

their sleeves now would be a good time, otherwise anything other

than 'i feel better' to cancel out a lot of studies that make ARbs

look like infection prolongation tablets, something of a peer

reviewed variety or we could conceivably focus more on something

less problmeatic not to mention speculative. and no, Pippet, I do

not agree that taking abx for culture or even serology confirmed

infections and taking ARBS are equally experimental.

vitamin D for infection is more speculative than abx but also quite

consistent with every review of its immunological properties I could

find, and i've got like a zillion of them on my PC and posted at

least a dozen goodies in the old site, available for foraging in the

archives.

i would soften my stand on arbs considerably if someone could

produce even a sniffly hamster who cleared its bugs faster on arbs,

instead of slower or not at all, which is what the animal studies

i've read consistently find, and what is suggested by the 54% drop

in CD36 macrophage scavenber receptors on hypertensive doses of

Losartan in humans.

i know scott's breezed through and said oh yes, having great luck

with arbs, we are, but he does that, all yoda-like, and i respect

him lots but i never know who 'we' are and there's never anything

like data. i think the fluc stuff he's focusing on may actually

produce some data to expand on Schardt's which would be lovely.

i also think scott and penny and paul j and pippet are all splendid,

i just don't agree with them at all about arbs - there is nothing

remotely personal about it.

apologies for sleep deprived typing and possible rhetorical excess,

i think i may have at least sub-clinical tonyitis, we're agreeing

too much, something sure must be wrong.

S.

> > ...The main

> > > theme of posts here are direct abx treatment , but it's clear

to

> > me that

> > > AB'x's will only ever be partially effective ..at some point

the

> > IS will

> > > need to kick in to finish the job ..Can the IS kick in or is

it

> too

> > > stressed? Is the anergy we display too profound ...I believe

> that

> > Immune

> > > modulators are an essential part of treatment ... any

> > comments ...

> > >

[Guest guest]

I found what you had to say a bit warped. How can you give credit to

anyone in any line of business that doesn't take the time to work

out what's the next cab of the rank thing to be done when presented

with a problem.I mean just about every cfs patient on most forums

got ill and never got over it, none of there doctors did any viral

swabs or bacterial swabs to determine firstly what struck, and

secondly how to get rid of it.The blood tests ordered don't give you

information- there a good baseline on life and death but not

designed to work out what your cause is.How many people walk in and

get blood cultures.NONE as far as what I observed.I mean carry the

flag for an excuse to keep us ill- please.I walk into a doctors

office and observe a person looking for a chance to make a couple of

pathology kick back dollars, someone also expected to tow the party

line, spread the patient around so everyone can get there pound of

flesh. I don't see a doctor do a viral swab and say you have

enterovirus 19 blah blah blah that normally lasts a couple of weeks

and goes away and you get on with your life.It's funny but the

powers that be don't see the healthy dollar in getting a patient

a 'diagnosis' or 'well quick'.You can stick up for them all you like

but when you have the power of observing the behind the scenes stuff-

like myself- you just want to spit on all of them.There's a

bacteria called strep throat that is fine when your healthy but

alway's sets up shop when your immune system is down. The problem

with this bacteria is it weakens you slowly over time and you pay

for it, so it's basically killing you slowly, not causing massive

discomfort all the time..Aboriginal children in australia have a

high incidence of strep throat due to bad hygeine practises and they

also have kidney disease, diabetes, and heart disease at a very

early age, they also have an early death rate. Then someone will

come out and tell us we live too clean and aren't exposed to many

bacteria.This person that does this science doesn't carry a culture

swab, they come to all these hypothesis.

Cheney and lapp the cfs men don't ever give antibiotics or

antivirals.What do the patients look like when first presenting,

obstructed airways, sinus, sore red throat,strong irregular

pulse,low blood pressure, inflammation everywhere- what do they want

to call that 'klonopin disease'.This is a baseline of somethings not

right..please let's get it right, we just don't look 'THAT ILL'.but

we do need to make the point that buddy your not doing your job in

your line of work- if I was this incompetent I wouldn't get paid at

the end of the week, wheras you make more.

> > > ...The main

> > > > theme of posts here are direct abx treatment , but it's

clear

> to

> > > me that

> > > > AB'x's will only ever be partially effective ..at some point

> the

> > > IS will

> > > > need to kick in to finish the job ..Can the IS kick in or is

> it

> > too

> > > > stressed? Is the anergy we display too profound ...I believe

> > that

> > > Immune

> > > > modulators are an essential part of treatment ... any

> > > comments ...

> > > >

[Guest guest]

, I've never claimed that ARBs are reducing my pathogen load.

Why do you keep attributing opinions to me that I don't have? (It's

frustrating, to say the least.) As a matter of fact, I've said just

the opposite. In my own experience, the ARBs seem to have nothing to

do with my pathogen load. ABX is the important player when it comes

to my pathogens. I've said this countless times. I've ONLY shared

that ARBS are apparently impacting an excessive inflammatory

condition (a natural immune system response) that's actually been

giving me the most nasty symptoms and doing the most quantifiable

damage.

Inflammation can be a killer too. You know this. Inflammation around

the brain, the heart, etc. kills. That's why Moscowitz is encouraged

by ARB's effectiveness against illnesses like SARS and West Nile

Virus. Focusing on a few people's unsubstantiated belief that ARBs

are killing bugs is really beside the point. It's fine to argue with

those who claim such a thing, but that's not what most ARB

researchers are claiming or interested in. They're looking at

inflammation. Anti-aging, etc. " How is it working? " " What does it do

and why? " Not, " why doesn't it kill bacteria. " In my case, it does

almost everything I need except relieve fatigue. That takes abx. The

right abx for me, not the right abx for someone else. In addition,

I'm becoming convinced that the residual stamina issues I have are

related to my heart, and some kind of additional help is needed

there.

You can't seriously evaluate the effectiveness of an ARB based on

reports of people who are using it only in combination with certain

other drugs, as is the case on the site and " research " you refer to.

People could be completely misunderstanding which drug they're

reacting to, or which combination of drugs. Those people are heavily

influenced by what other people are telling them to think about the

experiences they're having. As far as I'm concerned, none of the

reports on that site can be considered as hard evidence of anything.

All we can do is try to glean some information from people's

experiences and keep an open mind.

I also disagree that we should only be concerned with the immune

system (which is the current trend by far). It IS important for

people to look at both the immune system AND the pathogens. So far,

very few people in these communities are paying any attention

whatsoever to the pathogens. That's like plotting warfare against an

unknown enemy.

You " believe " that our immune systems are weaker than they used to

be, but do you have any proof? It's a BELIEF. It seems to me that

history has shown our immune systems typically get stronger after

exposure to MOST pathogens. A first round of something might wipe

out a population, but the next generation often adapts to deal with

it. I agree, we've probably created conditions giving these bugs

more access, and we've undoubtedly created stronger bugs with all

kinds of misguided practices, but we have to recognize the fact that

these ARE strong bugs, no matter how strong our immune systems are.

Some bugs are stronger. Some bacteria have adapted to withstand

incredibly high temperatures, or ice. You name it, they adapt. Our

bodies aren't nearly THAT adaptable. That's why bacteria will be

around long after the human species is extinct, IMO. We have to know

enough about our enemy to fight effectively.

Otherwise, I agree with most of what you're saying.

penny

P.S. , From a certain eastern thought perspective, you recieve

the same level of benefit when you rejoice in someone else's success

or happiness as that person themselves received. I'm always happy

when someone feels better, for whatever reason, whether it works for

me or not. I try to focus my time on how to make that happen for

more people, not on knocking down the few successes people do have

if they don't work or make sense to me. Minocyline practically

killed me, but it turned my daughter's life around. I'm not going to

tell people they shouldn't do Minocycline, only that results may

vary. People SHOULD be aware of that.

" Schaafsma " <compucruz@y...> wrote:

> I agree strongly with Tony's " Our immune system isn't taking care

of the pathogens we are trying to remove with drugs, as you can

observe the biggest problem lies in the late delivery and too short

a duration of treatment. "

>

> However, that actually says nothing about where the problem is at

> the macro level. I think the argument is pretty strong, that our

> immune systems aren't what they used to be, and that this relates

to a combination of toxic pollutants and maladaptive ways of living

> that are themselves virus-like in the manner of their spread.

>

>> I also understand why some here get frustrated on other sites

where pathogens are not the focus of discussion, But there is no

point, it is absolutely a sterile exercise, to ask

> which matters more, the presence of pathogens or the absence of a

> robust/adaptible enough immune system to fend them off. Kind of

like debating between the value of air and water.

>

I do not see a valid reason to believe that ARBs will ever help

anyone clear any infection of any kind whatsoever.

[Guest guest]

--- In infections , " penny " <pennyhoule@y...>

wrote:

>I've ONLY shared

> that ARBS are apparently impacting an excessive inflammatory

> condition (a natural immune system response) that's actually been

> giving me the most nasty symptoms and doing the most quantifiable

> damage.

Penny:

Just to understand, didn't you recently post that your CRP, homocysteine and

some

other measure of inflammation were actually quite elevated? Did your SED rate

go

down or some other measure of inflammation with this ARB thing relative to

before

treatment? How are you measuring inflammation? And how do you make the

attribution that it is ARB versus any other therapy you are using concurrently?

These

data would be very helpful in understanding this.

Thanks,

DM.

[Guest guest]

Hello , What a war & peace post, very impressive , hands up on the ARB’s & bacteria . at the end of the day the question is.. do the bloody things work [ARB’s]…the answer is yes they bloody do, big time If they don’t work for you find out why.

Lets just remind ourselves that we are in the midst of a medical denial that puts the Helicobactor debacle the cause of ulcers in the very deep shade….Yeast is endemic ..Doctors have acknowledged this fact privately to me they didn’t need to ,it’s common knowledge , our political representatives are under siege from affected people wanting more action .. Is it a coincidence that the incidence of Lyme, Autism , or any other so called auto-immune condition is skyrocketing ..of course not …you will not find any pubmed extract on endemic yeast ..so frankly bollocks to the docs [or most of em],they have their heads three feet down in the sand …It’s all been said before ,but I say look to your gut dysbiosis treat that BEFORE you embark on any other course of action …

And yes I found myself agreeing with Tony’s last few posts they seemed sensible ..Wonder why ..You don’t think he’s sickening for something do you?..

-----Original Message-----From: infections [mailto:infections ]On Behalf Of SchaafsmaSent: 20 August 2005 17:43infections Subject: [infections] Re: Immune modulators, once more on ARBs, tony on IS vs pathosI agree strongly with Tony's "Our immune system isn't taking care of the pathogens we are trying to remove with drugs, as you can observe the biggest problem lies in the late delivery and too short a duration of treatment."However, that actually says nothing about where the problem is at the macro level. I think the argument is pretty strong, that our immune systems aren't what they used to be, and that this relates to a combination of toxic pollutants and maladaptive ways of living that are themselves virus-like in the manner of their spread.I love the sentence from Civilization and It's Discontents where Freud worries outloud about collective neurosis and points out that it would be impossible to diagnose, because no background of normality would exist.I think we're seeing that worry establish itself as a tangible fact.I was uber-impressed with Cheney's discussions of cardiomyopathy in CFS, and have great respect for Rich's work on glutathione, precisely because stuff like this lets you look at disease from the perspective of health in a way that's still possible, using specific patient populations and well-matched controls, and plot a graded curve that does justice to the range of severity and the pervasiveness of lower-grade chronic fatigue, ADD, arthalgia, etc in modern societies. I also understand why some here get frustrated on other sites where pathogens are not the focus of discussion, and wish we could clone Tony and put one in every ID practice.But there is no point, it is absolutely a sterile exercise, to ask which matters more, the presence of pathogens or the absence of a robust/adaptible enough immune system to fend them off. Kind of like debating between the value of air and water.I also don't think we can know, via some remote diagnostic genius, which emphasis is appropriate for any given patient at any given time, and should exercise restraint in doubting what others choose to focus on.What matters to me is whether there is some valid reason for thinking something will be helpful. I do not see a valid reason to believe that ARBs will ever help anyone clear any infection of any kind whatsoever. Sorry, J, but I've read those damn JOIR papers and their citations up down and sideways and there isn't any science to pull apart.The citations in the paper you mention, if you actually read them, demonstrate:1) That angiotensin II increases host resistance, and losartan decreases it (that's the Belline reference, look it up if you don't believe me);2) Two species of mycoplasma neither of which has ever been accused of making anyone ill bind Angiotensin II;3) Applying ARBs has absolutely no effect on this AII-binding by microbes.Not only do the references not agree with the argument, but the argument is badly at odds with itself.He spends paragraphs establishing that mammalian and microbial AII receptors have absolutely nothing in common, structurally or genetically, which makes it really unsurprising that ARBs, which target mammalian receptors, don't do diddly squat to what appear to be RARE microbial AII binding sites.The coy little reference to Benicar not being available when these studies were done has no weight - the author himself has established the reasoning that tells us it's likely to make you win the lottery as stop those two non-pathogenic myco's from doin' their thing4) At least one of the studies he cites looked at a bonafide pathogenic myco, M. hominins, and guess what, it didn't bind AII at all.You can play with that paper and the others from now till hell freezes over, but it won't add up to an argument for any antibacterial property of ARBs, putative or otherwise.ARBs do have documented effects on host resistance to infection, and they're consistently negative.ABSs do modulate the immune system, but not in a way that would shut down cytokine cascades, which are mainly triggered by tlrs, not AII type 1 receptors, which are primarily involved in getting macrophages to infection sites and putting them to work cleaning up the mess. There's some cytokine production that results from macrophages ingesting bugs and toxins, but it's necessary - those no other way we know of to get the crap out of your body, the abx unfortunately don't neutralize the toxins or make the bug corpses vanish.I know some people feel better on them, and no, I don't know why, I just know there's no documented immune modulating effect that provides anything like a convincing explanation.The strongest theoretical argument would be no migration and phagocytosis = no gobbling up of bugs that end up colonizing macrophages, but you'd want to be REAL damn sure that the only bugs you had to worry about were white cell parasites, because your ability to cope with motile spirochetes or methicillin resistant staph or even, according to a study I haven't posted yet, YEAST, goes kaput. and i think you would be wanting some real high dose abx treatment as well, plus a whole lot of D to promote inflammatory cell apoptosis, unless you're a hypercalcemic sarcie in which case even I admit there could be situations where ARBs are the lesser of the available evil, depending heavily on how you conceptualize that disease, because the 'evidence' from sarcinfo reports is not real compelling.Also, if you look at the only attempt to test this outsie of sarc, the MP.com site itself, I read every damn progress report for several months there and the numbers expressing improvement and the numbers expressing exacerbation within the same dx cancel each other out, making for no correlation between ARBs and reduction in immune mediated inflammation.Add to this that there AII type 1 receptors here there and everywhere whose function no one's real sure of and it would take a far more rigorous, systematic analysis of 'responders' vs 'non-responders' to get any clue what the difference is. Based on reports of both much worse and much improved PMS, I strongly suspect hormones are involved in some cases. It's also likely that immune system energy demands go way down due to reduced activity, which combined with hormonal shifts could easily cause some people to feel a whole lot more energetic. Meanwhile, if Nishida's study turns out to be predictive of humans, and most renal therapies are developed from such studies, we can expect to see a lot of uglies down the road. frankly, immune modulating with Pop Tarts would make more sense to me.But one ugly duckling of an immune mod does not discredit the whole concept, and there's no question, no debate at all in microbiology, that some bugs have evolved to trigger inflammation as a way of diverting immune system resources. Lyme appears to be one of them, but it does it via TLRs, as do just about every pathogenic beastie known to man, so again, shutting down AII type 1 receptors on macrophages does not cut the mustard as a strategy.if we could nudge rather than shove the immune system when it gets stuck responding to pathogen cues that would be groovy but not a lot of great drugs for that, and no evidence I know of that ARBs have that effect.Barb Peck's done a masterful job of documenting the value of HCQ in alkalizing the cell compartment to maximize both antibiotic and antifungal drug action against bugs, but it also has an immune mod effect which I don't entirely understand. i think it might be an interesting one to look at.Personally, I'm in the part of the spectrum where you really do have to look at mitochondrial issues, the immune system doesn't run on fumes and unfortunately neither does the brain or any other vital organ I know of and the evidence - which we're just figuring out how to gather - of mitochondrial dysfunction in the real bad cases is strong enough that the taxonomy is now classifying these grizzly things as mitochondrial disorders, so you might take all Tony's abx and still not get better if you don't address that somehow (though my guess is without the abx you're also what's for dinner).Pardon my bluntness, but this kind of back and forth just needs to get somewhere. If Pippet or Penny have an ARB's save the day study with specific positive results for reducing pathogen loads hidden up their sleeves now would be a good time, otherwise anything other than 'i feel better' to cancel out a lot of studies that make ARbs look like infection prolongation tablets, something of a peer reviewed variety or we could conceivably focus more on something less problmeatic not to mention speculative. and no, Pippet, I do not agree that taking abx for culture or even serology confirmed infections and taking ARBS are equally experimental.vitamin D for infection is more speculative than abx but also quite consistent with every review of its immunological properties I could find, and i've got like a zillion of them on my PC and posted at least a dozen goodies in the old site, available for foraging in the archives.i would soften my stand on arbs considerably if someone could produce even a sniffly hamster who cleared its bugs faster on arbs, instead of slower or not at all, which is what the animal studies i've read consistently find, and what is suggested by the 54% drop in CD36 macrophage scavenber receptors on hypertensive doses of Losartan in humans.i know scott's breezed through and said oh yes, having great luck with arbs, we are, but he does that, all yoda-like, and i respect him lots but i never know who 'we' are and there's never anything like data. i think the fluc stuff he's focusing on may actually produce some data to expand on Schardt's which would be lovely.i also think scott and penny and paul j and pippet are all splendid, i just don't agree with them at all about arbs - there is nothing remotely personal about it.apologies for sleep deprived typing and possible rhetorical excess, i think i may have at least sub-clinical tonyitis, we're agreeing too much, something sure must be wrong. S.> > ...The main> > > theme of posts here are direct abx treatment , but it's clear to > > me that> > > AB'x's will only ever be partially effective ..at some point the > > IS will> > > need to kick in to finish the job ..Can the IS kick in or is it > too> > > stressed? Is the anergy we display too profound ...I believe > that > > Immune> > > modulators are an essential part of treatment ... any > > comments ...> > >

[Guest guest]

Penny, we must be at peace. If you have a stack of grievances with

me, write to me about them privately and I pledge, I will work right

throught them with you. I feel the need to say publically that I

have no ill will toward you at all, and no desire to cast doubt on

the assessment you make of your own health and response to

medications.

I do not really understand the personal dimension of this. As a Lyme

patient and friend to many Lyme patients, nothing is more common

than diverse, even opposite responses to a drug. This is true even

when the drug is an antibiotic! How much more room is there for

variability when it is a non-discriminating blocker of a type of

receptor found all over the human body?

We could not talk at all, us Lyme patients, if we did not take as a

given that what is efficacious in one patient may well not be in

another.

So it is, how to say, unexepected, a sort of continuing cognitive

dissonance, this sense I have from you and from J. that your

self-assessed positive response to this drug somehow establishes a

logical expectation that others will respond the same way. That is

to me just sort of unresolvably odd.

Now I don't know about J., but I am pretty sure that you must

have read at some point the progress reports on mp.com, perhaps not

with the compulsiveness I did (I am compulsive, it is not a virtue,

but a habit).

And it is pretty clear in some of those cases, because of the

sequence in which the protocol was begun, that Benicar, not anything

else, made some of these people feel like total hell. And I know

some of them. Well enough to trust their assessments, which I would

do anyway, because patients I think owe that to each other, but in

some cases I really do feel I know them well enough to get in their

skins as to how they registered and interpreted their response.

And it was horrid. And you do not seem to live in the world that I

do, where this in fact occurred, and was by all appearances at least

as common as the positive response that you had.

For me, in your shoes, this would not I think present a problem.

What the hell do I care, with symptoms like these, if what helps me

makes someone else feel like hell? After all, I am not pushing it on

them, I am just gratefully using it myself.

There is some other territory you get to, and J. gets to, some

set of assumptions which after all the posts we've had on this I am

no closer to understanding than before.

I understand " I took this drug, I felt better, I am glad about

that. " I do not understand " this drug kicks ass against

inflammation " when there are lots of people with obvious,

uncontestable inflammation and they take the drug and they are

worse.

I know patients who were so sold, and again Penny don't get

confused, I'm not saying YOU are like this, but I know patients who

were so effectively hooked by mp.com that they took the drug, felt

like hell, took the drug, felt like hell, for months. And now

say, 'that is the craziest, dumbest damn thing I have ever done.'

Now I think about you and the Minocycline. You took it, you felt

like hell. For how long I don't know, but I know that you stopped.

You stopped even though Barb Peck did well with Mino, and many

others. You stopped because it was clearly a mistake in your case.

And that is an antibiotic, for heaven's sake! That is something we

understand not anything like perfectly but far, far better than we

understand ARBs.

So within the intimate perimeter of your own experience there is

nothing I do not understand, no part of 'relief is good' that I do

not get, but how you get past that perimeter to any sort of broad

endorsement of the drug I simply do not comprehend.

I think Bleu just did a pretty good job of reminding us all what a

shrewd, tenacious agent of his own recovery he has been. He is one

who did not do well on Benicar. What happens to your respsect for

him, when you say there are no serious reports of adverse effects? I

do not follow, cannot track where your mind is going.

J. says, " Does it work. It sure does. If it doesn't work for

YOU, find out why. " Now you cannot be asked to answer for J, I

mention it only because I greet it with the same fundamental

bafflement. How did the burden fall on everyone who does not respond

as J. did, to figure out what's wrong with them? How did an

idiosyncratic response, which to date we cannot provide any

coherent, consistent explanation for, which not only diverges from

but inverts the response of many others, become normative?

I do not follow. I don't mean in the follow the leader sense, I

mean, I cannot see the path the mind is going on, when in the case

of a drug like Benicar it leaves the perimeter of individual

experience and says 'oh yes, this is the ticket for inflammation!'

or 'oh yes, this is a breakthrough for people with OUR illnesses!'

To me, it is like someone walking on wet sand, I can't follow where

they went because the ground is so subjective, so disconnected from

any objective reality, the footprints disappear after each step.

Now if you are coming to clarity about a subjective impression,

there is no reason I should be able to follow your footprints. And

we all have to do this. I have to do it in ways that my life may

very well depend on, I have to assess, is it right for me to say of

myself, this drug averts crisis in me more than it causes it? No

need for anyone to follow. Even my doctors have learned not to

question, if I say 'nope, that's a bad one' or 'yep, that one helps'

we just go with that.

But good lord, I would never hazard a guess what effect these things

would have in other people. I might go so far as to tell someone

with nearly identical sounding and extremely punishing

symptoms, 'look, this seems to help me, but i know for a fact it has

given other people some serious grief, but you might want to read up

on it or ask your doctor or whatever, and proceed cautiously, if

nothing else presents itself.'

I now know several patients, have communicated with them, who have

largely recovered from Lyme and attribute this primarily to

ceftriaxone, and it does not even occur to me to doubt it.

I know several patients, have communicated with them, who are

deteriorating, who say to me 'I think it all went to hell on

ceftriaxone,' and it does not even occur to me to doubt it.

And these are antibiotics, for heaven's sake, not exotic drugs that

go blocking willly-nilly receptors here there and everywhere about

which medical science has barely any clue, or none at all, what is

this for, why is this receptor here.

To sum up, there is a big difference between lacking respect for a

person (I do NOT lack respect for you, far from it) and being

incapable, flat incapable, of comprehending their thought process on

a particular question. When it comes to ARBs, we have a gap that is

a gap of understanding, and it is not for lack of effort on my part,

or your part, but in the end we simply do not understand each other.

And it isn't just you. I do not understand J. I do not

understand at all how either of you take one confident step outside

the perimeter of your immediate, subjective experience, and get

to " ARBs work, " whatever that even means, which I supsect if I spent

enough time interviewing each of you, would not be the same from one

to the other.

Now I also do not understand Marshall, the whole MP cult, but that

does not mean that I think you are like Marshall, or a cult member.

There is just a list of things that make no sense to me, and your

way of talking about ARBs is on that list. It doesn't prevent me

from distinguishing what you are saying from what the cultists are

doing, it doesn't cause me to look badly on you, it just causes you

to disappear, at a certain juncture, from my field of vision. I

don't know where you went. I don't know how you got from here to

there.

When I present the science, the studies I have been able to locate

that specify immune modulating effects of angiotensin II receptors,

and it is perfectly clear to me from those studies that if one were

to conclude anything, one would have to conclude they are designed

in such a way as to adversely effect the clearance of infection,

when I present that evidence that I have found, it is almost a

secondary gesture.

I mean, even without having done the research, and seen what it

says, the discrepancy in responses was already enough for me to

say " well hell, this obviously does NOT 'work' in the broad sense

people talk about at all, there is clearly NOT a mechanism which

insures that sufferers of inflammation experience less of it, rather

than more, when they take high doses of an angiotensin II blocker. "

The science helps me to understand the adverse response. It does not

help me, perhaps, quite as much as in some posts it seems to help

Ken, in understanding the positive response. I am referring to posts

where he suggested, and it's not unreasonable, that

immunosuppression is what is causing people to feel better. But that

assumes a certain level of infection, and that the infection will

exact a certain toll if the immune system is not impaired by ARBs,

and those are not assumptions I am comfortable making about the

people who have responded positively.

I could not swear that Lonestartick had a single spirochete left in

her body. I don't think she could, either. I sure as hell don't know

what you do and don't have in the way of pathogens in your body. You

might know. If you say you know, I won't dispute it. I might remind

you of saying, 'if you want to know, Tony has some good advice,'

because that is an objective procedure, not a subjective self-

assessment. But I do NOT, this is really crucial, I do not challenge

your authority within the perimeter of your intimate experience.

It's the steps beyond that, that leave me utterly bewildered, as

bewildered now as I was the first time this came up between us.

I may have been unfair to you. I may have lumped you together

unfairly with other people who I observe stating with great

confidence 'such and such is broadly true' on no apparent basis

other than 'such and such' appeared true to them in their own

experience.

There is really quite a lot of that in these discussions among the

ill. It drives me batty. What are these people smoking? Has

being 'outside the box', failing to fit the standard, preformed

diagnostic labels that most clinicians rely on, taught them nothing

about what DIFFERENCE means? I can have fits over it. I can have

fits, and do have fits, when it seems to me that some essential

lesson has been thrust in a person's face and yet they are in no

danger, apparently, of learning it.

I will say that if I have done that, if I have lumped you together

in a sloppy, thoughtless way with others who seem to extrapolate

from their own experience unhesitatingly, as if nothing else

existed, I am sorry, because you have shown more sense than that,

and perhaps on this question of ARBs you show more sense than that,

it is just very hard for me to see what kind of sense, exactly, it

is.

So I will just continue to encourage you, anytime you see a way to

show me how you get beyond the perimeter, and can make the broad

statement that this is a potent tool for people with 'our

illnesses', rather than a potent tool for you, to go ahead and show

me.

If I am blind, make me see.

I could well be! I am the man who tries to turn off his electric

toothbrush by squeezing the bathroom faucet handles tight! This

brain has glitches! Sometimes ALL this brain has is glitches!

But sometimes this brain can think pretty well, and I am not ready

just yet to give up using it in this forum, so unless it is

unacceptable to you I will just keep trying to say what I do and do

not understand about this ARB business, and how you speak about it,

and why.

I hope this is all ok, and not a reason for either of us to feel

threatened or insecure.

S.

Benicar is a different situation. It has no obvious value in the

treatment of infection OR inflammation. We have some people who've

had positive experiences. Some of them, and I am not putting you in

this category, have become evangelists for the drug. It will save

you from inflammation, they say.

This extrapolation from personal experience is alien to my way of

thinking. I do not understand it.

> > I agree strongly with Tony's " Our immune system isn't taking

care

> of the pathogens we are trying to remove with drugs, as you can

> observe the biggest problem lies in the late delivery and too

short

> a duration of treatment. "

> >

> > However, that actually says nothing about where the problem is

at

> > the macro level. I think the argument is pretty strong, that our

> > immune systems aren't what they used to be, and that this

relates

> to a combination of toxic pollutants and maladaptive ways of

living

> > that are themselves virus-like in the manner of their spread.

> >

> >> I also understand why some here get frustrated on other sites

> where pathogens are not the focus of discussion, But there is no

> point, it is absolutely a sterile exercise, to ask

> > which matters more, the presence of pathogens or the absence of

a

> > robust/adaptible enough immune system to fend them off. Kind of

> like debating between the value of air and water.

> >

> I do not see a valid reason to believe that ARBs will ever help

> anyone clear any infection of any kind whatsoever.

[Guest guest]

Yes, that's correct, those 2 inflammatory markers were elevated

(SED/ESR not tested), but the inflammatory symptoms themselves are

gone. So can't say exactly what's going on, but I do know when I

clearly DID have all these symptoms, my blood tests always showed

normal, so how reflective are they to begin with? I took Benicar for

several months with no other drugs at all so all the symptom relief

was definitely due to the ARB. Fatigue relief I get from

antibiotics. Benicar has relieved all kinds of ailments, far better

than any NSAIDs I've done. I'm able to sleep soundly again, the

joint and tendon are pain gone, life long neck pain gone, migraines

down to 1 per month (previously 5-7), no more teeth

grinding/chattering. Anxiety levels reduced. No more getting up in

the night to go to the bathroom. Reduced my thyroid meds. It's

remarkable how many of my symptoms were eliminated and remain gone

after 14 months on the drug with no weird side effects like the ones

that come with heavy duty pain or anxiety drugs. And better yet,

I've been able to reduce the Benicar by half over that time. Am

hoping to get it down to even less. What's weird, is when I started

the Benicar, I would have " spells " sometimes for several days where

some particular pain would increase dramatically. I could barely

walk on one foot for a few days, then it cleared up. Then it was my

thighs. Then it moved somewhere else. Eventually, every problem area

just kind of cleared. I don't know the mechanism exactly, but I'm

very grateful for the relief. It's improved my quality of life

tremendously. I'm not stressed, and depressed and distraught over

this illness like I've been. And now that I have some energy too, I

feel really hopeful.

penny

" duramater27 " <spam-barb@c...> wrote:

>> Penny:

>

> Just to understand, didn't you recently post that your CRP,

homocysteine and some other measure of inflammation were actually

quite elevated? Did your SED rate go down or some other measure of

inflammation with this ARB thing relative to before treatment? How

are you measuring inflammation? And how do you make the attribution

that it is ARB versus any other therapy you are using concurrently?

These data would be very helpful in understanding this.

[Guest guest]

, I really don't think you're reading my posts at all. Here's a

perfect example:

You wrote:

" ...this sense I have from you and from J. that your

self-assessed positive response to this drug somehow establishes a

logical expectation that others will respond the same way. That is

to me just sort of unresolvably odd. "

I have screamed from the tree tops that I make NO assumption

whatsoever that this will work for others. My daughter stoped the

drug after experiencing head pressure. My friend stopped after

experiencing nothing. I've only been saying that it works remarkably

well for me, and also for some others I know (most of whom are

afraid to speak up in the recent climate of anti-ARB tongue lashing

if they bring it up.) I think it will benefit us all to research

what's going on with this drug and WHY it works for some of us. Why

does think that it may be able to prevent cancer? He also

wrote, on the old forum, that he felt it could help with chronic

infections (from an inflammatory position). This guy did excellent

research. Let's encourage that, find out more. It seems possible

that Benicar (and other ARBS) have some kind of remarkable potential

at least for some people, but a lot more research needs to be done.

And objective discussion needs to be cultivated out here in forum

land, and that's not happening at all.

I no longer read the reports at mp.com. They were horrifying and

since I'm banned from that site and can't post my concerns, I don't

like reading them. But I also realize that those people are posting

about a combination of drugs, not one particular drug independently,

so they can't be seen as proof for or against any one drug.

penny

> > > I agree strongly with Tony's " Our immune system isn't taking

> care

> > of the pathogens we are trying to remove with drugs, as you can

> > observe the biggest problem lies in the late delivery and too

> short

> > a duration of treatment. "

> > >

> > > However, that actually says nothing about where the problem is

> at

> > > the macro level. I think the argument is pretty strong, that

our

> > > immune systems aren't what they used to be, and that this

> relates

> > to a combination of toxic pollutants and maladaptive ways of

> living

> > > that are themselves virus-like in the manner of their spread.

> > >

> > >> I also understand why some here get frustrated on other sites

> > where pathogens are not the focus of discussion, But there is no

> > point, it is absolutely a sterile exercise, to ask

> > > which matters more, the presence of pathogens or the absence

of

> a

> > > robust/adaptible enough immune system to fend them off. Kind

of

> > like debating between the value of air and water.

> > >

> > I do not see a valid reason to believe that ARBs will ever help

> > anyone clear any infection of any kind whatsoever.

[Guest guest]

Yu don't expect people to read all that do you. YOU WROTE A BOOK.

tony

> > > I agree strongly with Tony's " Our immune system isn't taking

> care

> > of the pathogens we are trying to remove with drugs, as you can

> > observe the biggest problem lies in the late delivery and too

> short

> > a duration of treatment. "

> > >

> > > However, that actually says nothing about where the problem is

> at

> > > the macro level. I think the argument is pretty strong, that

our

> > > immune systems aren't what they used to be, and that this

> relates

> > to a combination of toxic pollutants and maladaptive ways of

> living

> > > that are themselves virus-like in the manner of their spread.

> > >

> > >> I also understand why some here get frustrated on other sites

> > where pathogens are not the focus of discussion, But there is no

> > point, it is absolutely a sterile exercise, to ask

> > > which matters more, the presence of pathogens or the absence

of

> a

> > > robust/adaptible enough immune system to fend them off. Kind

of

> > like debating between the value of air and water.

> > >

> > I do not see a valid reason to believe that ARBs will ever help

> > anyone clear any infection of any kind whatsoever.

[Guest guest]

S. said:

" ABSs do modulate the immune system, but not in a way that would shut

down cytokine cascades, which are mainly triggered by tlrs, not AII

type 1 receptors, which are primarily involved in getting

macrophages to infection sites and putting them to work cleaning up

the mess. "

AT1 receptors not involved in inflammation? Sorry , not buying

that one. Check s paper and references, the science is

against you on this one.

TLRs can also lead to inflammation, but this is because they get

triggered by bacterial LPS, i.e: a direct response to bacteria.

The overall result is that if you block the macrophage AT1

receptors, you reduce the inflammation while still allowing an IS

response to bacterial presence through the TLR. Yes, you reduce the

IS ability to respond through the AT1 pathway, but that has not been

shown to be a major response pathway to either bacteriological or

viral infection.

If your reading of these studies is correct, then I would expect a

large percentage of the hundreds of people on high doses of Benicar

to be dropping due to out of control staph (and other) infections.

Yet this has not been the case.

Ken

[Guest guest]

S. said

" I now know several patients, have communicated with them, who have

largely recovered from Lyme and attribute this primarily to

ceftriaxone, and it does not even occur to me to doubt it.

I know several patients, have communicated with them, who are

deteriorating, who say to me 'I think it all went to hell on

ceftriaxone,' and it does not even occur to me to doubt it. "

Perhaps it should occur to you to doubt it. The site

http://www.niaid.nih.gov/research/lyme.htm discusses the 2000

ceftriaxone/doxy study which was stopped early due to lack of

effectiveness.

" After its review, the DSMB unanimously recommended that NIAID

terminate the treatment component of these studies. Their

preliminary analysis showed that after 90 days of continuous

antibiotic therapy there were no significant differences in the

percentage of patients who felt that their symptoms had improved,

gotten worse, or stayed the same between the antibiotic treatment

and placebo groups in either trial. "

" It is noteworthy that in both the NEMC and SUNY clinical trials

cited above, 40 percent of patients given placebo alone reported

improvement in their symptoms (placebo effect). "

This shows quite clearly the need for placebo controlled trials on

any of these treatments, whether ceftriaxone, fluconazole, MP or any

other. The need is even greater with CFS where the placebo effect

could be in excess of 60%. Patient reports of how they feel can not

be relied on.

Ken

[Guest guest]

Re the Klempner ceftriaxone/doxy study - there is a detailed demur

from ILADS which was posted on eurolyme about 10 days ago. I

didnt read it, nor have I read the Klempner studies. When I took in

the inadequate microbiological scholarship of Steeres editorials on

chronic lyme treatment, I felt I'd spent enough time on that crowd for

a while.

Its not like I think the studies are total fabrication. Its just that

to say I take them with a grain of salt is a gigantic understatement.

> " It is noteworthy that in both the NEMC and SUNY clinical trials

> cited above, 40 percent of patients given placebo alone reported

> improvement in their symptoms (placebo effect). "

This is no inordinate rate of placebo effect. Isnt it usually around

33% for most any treatment of anything?

> This shows quite clearly the need for placebo controlled trials on

> any of these treatments, whether ceftriaxone, fluconazole, MP or any

> other. The need is even greater with CFS where the placebo effect

> could be in excess of 60%. Patient reports of how they feel can not

> be relied on.

Where is 60% coming from?

To me, what cant be relied on is reports (including my own, I notice!)

of oncoming/building effects, where hope and random oscillation of

ones condition is a factor.

Hope operates differently in a disease which generates such extreme

desperation, which in turn tempts one to deceive oneself. This could

cause a high disposition to placebo effects in CFS, at least in the

short term. In the short run, I see people including myself nurture

treatment " responses " like wan flames.

I also dont doubt that solid, 100% real responses can later evaporate -

whether it happens by reproliferation of tx-resistant microbes, re-

regulation of neurotransmission that had been boosted by

antidepressants, or reduction of microbe populations causing un-

desensitization towards immunoactivating ligands like LPS, causing the

former level of inflammation to be restored despite the fewer bugs.

OTOH when somethings been working for someone consistently for many

months, thats pretty reliable to me. When this holds up during times

of strain, or seasons of discontent, that means even more. Considering

my immense weather response, we wont see until another Virginia

December what good my antimicrobial treatment has really done. I

expect to get sicker than I am now, but I truly doubt I'll be in the

same ballpark as last winter. If you are going to consider whether CFS

may have a tremendous placebo effect propensity, it seems important

not to be atemporal in this inquiry but to instead consider whether

those placebo effects would/do hold up over many months, which many

improvement reports do.

[Guest guest]

Interesting, I read all the posts on all the forums on people and

that drug and it doesn't win any votes I'm afraid. It's a good con

job drug, it gives you a few good days and hospitals love

adminstering it because the patient normally doesn't get noticed on

this therapy as it doesn't continue for long.There's a small

percentage of people possably not carrying pseudonomads that can

keep this drug working long term, if there are bacteria present that

can swap genetic info the drug can become useless quick.We have had

many friends lyme positive and negative that just don't get

anywhere. Also bone doctors know this drug doesn't fix anything and

don't touch it and generally laugh at it as being useless.I feel it

may have a role in a multi faceted drug attack.

tony

> S. said

> " I now know several patients, have communicated with them, who have

> largely recovered from Lyme and attribute this primarily to

> ceftriaxone, and it does not even occur to me to doubt it.

>

> I know several patients, have communicated with them, who are

> deteriorating, who say to me 'I think it all went to hell on

> ceftriaxone,' and it does not even occur to me to doubt it. "

>

> Perhaps it should occur to you to doubt it. The site

> http://www.niaid.nih.gov/research/lyme.htm discusses the 2000

> ceftriaxone/doxy study which was stopped early due to lack of

> effectiveness.

>

> " After its review, the DSMB unanimously recommended that NIAID

> terminate the treatment component of these studies. Their

> preliminary analysis showed that after 90 days of continuous

> antibiotic therapy there were no significant differences in the

> percentage of patients who felt that their symptoms had improved,

> gotten worse, or stayed the same between the antibiotic treatment

> and placebo groups in either trial. "

>

> " It is noteworthy that in both the NEMC and SUNY clinical trials

> cited above, 40 percent of patients given placebo alone reported

> improvement in their symptoms (placebo effect). "

>

> This shows quite clearly the need for placebo controlled trials on

> any of these treatments, whether ceftriaxone, fluconazole, MP or

any

> other. The need is even greater with CFS where the placebo effect

> could be in excess of 60%. Patient reports of how they feel can

not

> be relied on.

>

> Ken

[Guest guest]

There's a little tit bit missing, anyone that did saline IV's with

no drug should benefit, so the placebo group can make an honest I

feel better claim.

> Re the Klempner ceftriaxone/doxy study - there is a detailed demur

> from ILADS which was posted on eurolyme about 10 days ago. I

> didnt read it, nor have I read the Klempner studies. When I took

in

> the inadequate microbiological scholarship of Steeres editorials

on

> chronic lyme treatment, I felt I'd spent enough time on that crowd

for

> a while.

>

> Its not like I think the studies are total fabrication. Its just

that

> to say I take them with a grain of salt is a gigantic

understatement.

>

> > " It is noteworthy that in both the NEMC and SUNY clinical trials

> > cited above, 40 percent of patients given placebo alone reported

> > improvement in their symptoms (placebo effect). "

>

> This is no inordinate rate of placebo effect. Isnt it usually

around

> 33% for most any treatment of anything?

>

> > This shows quite clearly the need for placebo controlled trials

on

> > any of these treatments, whether ceftriaxone, fluconazole, MP or

any

> > other. The need is even greater with CFS where the placebo

effect

> > could be in excess of 60%. Patient reports of how they feel can

not

> > be relied on.

>

> Where is 60% coming from?

>

> To me, what cant be relied on is reports (including my own, I

notice!)

> of oncoming/building effects, where hope and random oscillation of

> ones condition is a factor.

>

> Hope operates differently in a disease which generates such

extreme

> desperation, which in turn tempts one to deceive oneself. This

could

> cause a high disposition to placebo effects in CFS, at least in

the

> short term. In the short run, I see people including myself

nurture

> treatment " responses " like wan flames.

>

> I also dont doubt that solid, 100% real responses can later

evaporate -

> whether it happens by reproliferation of tx-resistant microbes,

re-

> regulation of neurotransmission that had been boosted by

> antidepressants, or reduction of microbe populations causing un-

> desensitization towards immunoactivating ligands like LPS, causing

the

> former level of inflammation to be restored despite the fewer bugs.

>

> OTOH when somethings been working for someone consistently for

many

> months, thats pretty reliable to me. When this holds up during

times

> of strain, or seasons of discontent, that means even more.

Considering

> my immense weather response, we wont see until another Virginia

> December what good my antimicrobial treatment has really done. I

> expect to get sicker than I am now, but I truly doubt I'll be in

the

> same ballpark as last winter. If you are going to consider whether

CFS

> may have a tremendous placebo effect propensity, it seems

important

> not to be atemporal in this inquiry but to instead consider

whether

> those placebo effects would/do hold up over many months, which

many

> improvement reports do.

[Guest guest]

The saline point is a good one Tony. But it's the tip of the iceberg

where the flaws of this study are concerned.

Ken doesn't bother to mention that this was a study of patients who

had previously had short-term treatment and failed to sustain

recovery - the group least likely to respond to another round of

short-term treatment.

Nor does he mention that the main instrument used to compare the

treatment and placebo groups was a subjective self-assessment -

SF16 - exactly the kind of thing of 'how do you feel' thing he just

finished telling us is meaningless.

The authors were questioned about that by Bransfield, one of the

leading researchers on neurospychiatric manifestations of Lyme, and

responded that they had in fact performed a battery of other, more

objective cognitive performance tests - but chose not to publish

that data in their relentlessly hyped NEJM report. They also

apparently collected data on things like MMP levels, lord only knows

if we'll ever see it.

I don't believe Ken's a Lyme patient, so no reason to fault him for

knowing precious little about Lyme studies.

But what fascinates me is Ken's punchline:

" Patient reports of how they feel can not be relied on. "

I can't wait to hear what reliable criteria Ken thinks will

demonstrate the efficacy of the MP.

Cheers,

S.

> > Re the Klempner ceftriaxone/doxy study - there is a detailed

demur

> > from ILADS which was posted on eurolyme about 10 days ago.

I

> > didnt read it, nor have I read the Klempner studies. When I took

> in

> > the inadequate microbiological scholarship of Steeres editorials

> on

> > chronic lyme treatment, I felt I'd spent enough time on that

crowd

> for

> > a while.

> >

> > Its not like I think the studies are total fabrication. Its just

> that

> > to say I take them with a grain of salt is a gigantic

> understatement.

> >

> > > " It is noteworthy that in both the NEMC and SUNY clinical

trials

> > > cited above, 40 percent of patients given placebo alone

reported

> > > improvement in their symptoms (placebo effect). "

> >

> > This is no inordinate rate of placebo effect. Isnt it usually

> around

> > 33% for most any treatment of anything?

> >

> > > This shows quite clearly the need for placebo controlled

trials

> on

> > > any of these treatments, whether ceftriaxone, fluconazole, MP

or

> any

> > > other. The need is even greater with CFS where the placebo

> effect

> > > could be in excess of 60%. Patient reports of how they feel

can

> not

> > > be relied on.

> >

> > Where is 60% coming from?

> >

> > To me, what cant be relied on is reports (including my own, I

> notice!)

> > of oncoming/building effects, where hope and random oscillation

of

> > ones condition is a factor.

> >

> > Hope operates differently in a disease which generates such

> extreme

> > desperation, which in turn tempts one to deceive oneself. This

> could

> > cause a high disposition to placebo effects in CFS, at least in

> the

> > short term. In the short run, I see people including myself

> nurture

> > treatment " responses " like wan flames.

> >

> > I also dont doubt that solid, 100% real responses can later

> evaporate -

> > whether it happens by reproliferation of tx-resistant microbes,

> re-

> > regulation of neurotransmission that had been boosted by

> > antidepressants, or reduction of microbe populations causing un-

> > desensitization towards immunoactivating ligands like LPS,

causing

> the

> > former level of inflammation to be restored despite the fewer

bugs.

> >

> > OTOH when somethings been working for someone consistently for

> many

> > months, thats pretty reliable to me. When this holds up during

> times

> > of strain, or seasons of discontent, that means even more.

> Considering

> > my immense weather response, we wont see until another Virginia

> > December what good my antimicrobial treatment has really done. I

> > expect to get sicker than I am now, but I truly doubt I'll be in

> the

> > same ballpark as last winter. If you are going to consider

whether

> CFS

> > may have a tremendous placebo effect propensity, it seems

> important

> > not to be atemporal in this inquiry but to instead consider

> whether

> > those placebo effects would/do hold up over many months, which

> many

> > improvement reports do.

[Guest guest]

Tony - I thought of that too. Was wondering if anyone else would

notice.

- The 60% is something that stuck with me from years ago, the

study was trying to show that it was all in our minds. I did not

agree with their conclusion, but it is something I keep in mind when

looking at all the supplements, treatments and protocols. I try to

separate my own changes into those that I feel certain are due to

treatment, and those that I hope are. I figure that I will be able

to clarify some of the hope issues by next spring.

> > Re the Klempner ceftriaxone/doxy study - there is a detailed

demur

> > from ILADS which was posted on eurolyme about 10 days ago.

I

> > didnt read it, nor have I read the Klempner studies. When I took

> in

> > the inadequate microbiological scholarship of Steeres editorials

> on

> > chronic lyme treatment, I felt I'd spent enough time on that

crowd

> for

> > a while.

> >

> > Its not like I think the studies are total fabrication. Its just

> that

> > to say I take them with a grain of salt is a gigantic

> understatement.

> >

> > > " It is noteworthy that in both the NEMC and SUNY clinical

trials

> > > cited above, 40 percent of patients given placebo alone

reported

> > > improvement in their symptoms (placebo effect). "

> >

> > This is no inordinate rate of placebo effect. Isnt it usually

> around

> > 33% for most any treatment of anything?

> >

> > > This shows quite clearly the need for placebo controlled

trials

> on

> > > any of these treatments, whether ceftriaxone, fluconazole, MP

or

> any

> > > other. The need is even greater with CFS where the placebo

> effect

> > > could be in excess of 60%. Patient reports of how they feel

can

> not

> > > be relied on.

> >

> > Where is 60% coming from?

> >

> > To me, what cant be relied on is reports (including my own, I

> notice!)

> > of oncoming/building effects, where hope and random oscillation

of

> > ones condition is a factor.

> >

> > Hope operates differently in a disease which generates such

> extreme

> > desperation, which in turn tempts one to deceive oneself. This

> could

> > cause a high disposition to placebo effects in CFS, at least in

> the

> > short term. In the short run, I see people including myself

> nurture

> > treatment " responses " like wan flames.

> >

> > I also dont doubt that solid, 100% real responses can later

> evaporate -

> > whether it happens by reproliferation of tx-resistant microbes,

> re-

> > regulation of neurotransmission that had been boosted by

> > antidepressants, or reduction of microbe populations causing un-

> > desensitization towards immunoactivating ligands like LPS,

causing

> the

> > former level of inflammation to be restored despite the fewer

bugs.

> >

> > OTOH when somethings been working for someone consistently for

> many

> > months, thats pretty reliable to me. When this holds up during

> times

> > of strain, or seasons of discontent, that means even more.

> Considering

> > my immense weather response, we wont see until another Virginia

> > December what good my antimicrobial treatment has really done. I

> > expect to get sicker than I am now, but I truly doubt I'll be in

> the

> > same ballpark as last winter. If you are going to consider

whether

> CFS

> > may have a tremendous placebo effect propensity, it seems

> important

> > not to be atemporal in this inquiry but to instead consider

> whether

> > those placebo effects would/do hold up over many months, which

> many

> > improvement reports do.

[Guest guest]

The double blind studies and just medical procedures in general are

an absolute wank.If you notice they keep doing double blind studies

until they get a certain amount of positive to introduce a drug into

the market.It often takes 20 double blind studies ignoring the 19

and showing the positive 20th as a reason to introduce a drug.

There's so much of medicine that's ugly and as we ourselves are

debating right now this double blind thing sucks.

I would concentrate on the eralier work of medicine which took a

pathogen reproduced the ilness in the animal model recovered the

organisms reproduced the ilness again and then I would have

treatment and something to overcome-NO PATHOGEN RECOVERABLE.Before

you bit my head off, this is done in tuberculosis.

> > > Re the Klempner ceftriaxone/doxy study - there is a detailed

> demur

> > > from ILADS which was posted on eurolyme about 10 days

ago.

> I

> > > didnt read it, nor have I read the Klempner studies. When I

took

> > in

> > > the inadequate microbiological scholarship of Steeres

editorials

> > on

> > > chronic lyme treatment, I felt I'd spent enough time on that

> crowd

> > for

> > > a while.

> > >

> > > Its not like I think the studies are total fabrication. Its

just

> > that

> > > to say I take them with a grain of salt is a gigantic

> > understatement.

> > >

> > > > " It is noteworthy that in both the NEMC and SUNY clinical

> trials

> > > > cited above, 40 percent of patients given placebo alone

> reported

> > > > improvement in their symptoms (placebo effect). "

> > >

> > > This is no inordinate rate of placebo effect. Isnt it usually

> > around

> > > 33% for most any treatment of anything?

> > >

> > > > This shows quite clearly the need for placebo controlled

> trials

> > on

> > > > any of these treatments, whether ceftriaxone, fluconazole,

MP

> or

> > any

> > > > other. The need is even greater with CFS where the placebo

> > effect

> > > > could be in excess of 60%. Patient reports of how they feel

> can

> > not

> > > > be relied on.

> > >

> > > Where is 60% coming from?

> > >

> > > To me, what cant be relied on is reports (including my own, I

> > notice!)

> > > of oncoming/building effects, where hope and random

oscillation

> of

> > > ones condition is a factor.

> > >

> > > Hope operates differently in a disease which generates such

> > extreme

> > > desperation, which in turn tempts one to deceive oneself. This

> > could

> > > cause a high disposition to placebo effects in CFS, at least

in

> > the

> > > short term. In the short run, I see people including myself

> > nurture

> > > treatment " responses " like wan flames.

> > >

> > > I also dont doubt that solid, 100% real responses can later

> > evaporate -

> > > whether it happens by reproliferation of tx-resistant

microbes,

> > re-

> > > regulation of neurotransmission that had been boosted by

> > > antidepressants, or reduction of microbe populations causing

un-

> > > desensitization towards immunoactivating ligands like LPS,

> causing

> > the

> > > former level of inflammation to be restored despite the fewer

> bugs.

> > >

> > > OTOH when somethings been working for someone consistently for

> > many

> > > months, thats pretty reliable to me. When this holds up during

> > times

> > > of strain, or seasons of discontent, that means even more.

> > Considering

> > > my immense weather response, we wont see until another

Virginia

> > > December what good my antimicrobial treatment has really done.

I

> > > expect to get sicker than I am now, but I truly doubt I'll be

in

> > the

> > > same ballpark as last winter. If you are going to consider

> whether

> > CFS

> > > may have a tremendous placebo effect propensity, it seems

> > important

> > > not to be atemporal in this inquiry but to instead consider

> > whether

> > > those placebo effects would/do hold up over many months, which

> > many

> > > improvement reports do.

[Guest guest]

Why would I bite your head off? What you say here makes sense. If I

were more energetic, I could talk to you a little about where the

animal studies have seemed to run into limitations, but nothing you

say here runs against the grain for me.

> > > > Re the Klempner ceftriaxone/doxy study - there is a detailed

> > demur

> > > > from ILADS which was posted on eurolyme about 10 days

> ago.

> > I

> > > > didnt read it, nor have I read the Klempner studies. When I

> took

> > > in

> > > > the inadequate microbiological scholarship of Steeres

> editorials

> > > on

> > > > chronic lyme treatment, I felt I'd spent enough time on that

> > crowd

> > > for

> > > > a while.

> > > >

> > > > Its not like I think the studies are total fabrication. Its

> just

> > > that

> > > > to say I take them with a grain of salt is a gigantic

> > > understatement.

> > > >

> > > > > " It is noteworthy that in both the NEMC and SUNY clinical

> > trials

> > > > > cited above, 40 percent of patients given placebo alone

> > reported

> > > > > improvement in their symptoms (placebo effect). "

> > > >

> > > > This is no inordinate rate of placebo effect. Isnt it

usually

> > > around

> > > > 33% for most any treatment of anything?

> > > >

> > > > > This shows quite clearly the need for placebo controlled

> > trials

> > > on

> > > > > any of these treatments, whether ceftriaxone, fluconazole,

> MP

> > or

> > > any

> > > > > other. The need is even greater with CFS where the placebo

> > > effect

> > > > > could be in excess of 60%. Patient reports of how they

feel

> > can

> > > not

> > > > > be relied on.

> > > >

> > > > Where is 60% coming from?

> > > >

> > > > To me, what cant be relied on is reports (including my own,

I

> > > notice!)

> > > > of oncoming/building effects, where hope and random

> oscillation

> > of

> > > > ones condition is a factor.

> > > >

> > > > Hope operates differently in a disease which generates such

> > > extreme

> > > > desperation, which in turn tempts one to deceive oneself.

This

> > > could

> > > > cause a high disposition to placebo effects in CFS, at least

> in

> > > the

> > > > short term. In the short run, I see people including myself

> > > nurture

> > > > treatment " responses " like wan flames.

> > > >

> > > > I also dont doubt that solid, 100% real responses can later

> > > evaporate -

> > > > whether it happens by reproliferation of tx-resistant

> microbes,

> > > re-

> > > > regulation of neurotransmission that had been boosted by

> > > > antidepressants, or reduction of microbe populations causing

> un-

> > > > desensitization towards immunoactivating ligands like LPS,

> > causing

> > > the

> > > > former level of inflammation to be restored despite the

fewer

> > bugs.

> > > >

> > > > OTOH when somethings been working for someone consistently

for

> > > many

> > > > months, thats pretty reliable to me. When this holds up

during

> > > times

> > > > of strain, or seasons of discontent, that means even more.

> > > Considering

> > > > my immense weather response, we wont see until another

> Virginia

> > > > December what good my antimicrobial treatment has really

done.

> I

> > > > expect to get sicker than I am now, but I truly doubt I'll

be

> in

> > > the

> > > > same ballpark as last winter. If you are going to consider

> > whether

> > > CFS

> > > > may have a tremendous placebo effect propensity, it seems

> > > important

> > > > not to be atemporal in this inquiry but to instead consider

> > > whether

> > > > those placebo effects would/do hold up over many months,

which

> > > many

> > > > improvement reports do.

[Guest guest]

Unfortunaely we are the animals in our disease and looking for toxic

pathogens and there recovery is all I can vouch for in this

discussion.

Remember most here feel they have invisable battles- that they can

only swing and hit or swing and miss with therapies.So basically I'm

no good to anyone in the overall scheme of things.

You won't even share the therapy you opted for penicillin or

rocephin?

> > > > > Re the Klempner ceftriaxone/doxy study - there is a

detailed

> > > demur

> > > > > from ILADS which was posted on eurolyme about 10

days

> > ago.

> > > I

> > > > > didnt read it, nor have I read the Klempner studies. When

I

> > took

> > > > in

> > > > > the inadequate microbiological scholarship of Steeres

> > editorials

> > > > on

> > > > > chronic lyme treatment, I felt I'd spent enough time on

that

> > > crowd

> > > > for

> > > > > a while.

> > > > >

> > > > > Its not like I think the studies are total fabrication.

Its

> > just

> > > > that

> > > > > to say I take them with a grain of salt is a gigantic

> > > > understatement.

> > > > >

> > > > > > " It is noteworthy that in both the NEMC and SUNY

clinical

> > > trials

> > > > > > cited above, 40 percent of patients given placebo alone

> > > reported

> > > > > > improvement in their symptoms (placebo effect). "

> > > > >

> > > > > This is no inordinate rate of placebo effect. Isnt it

> usually

> > > > around

> > > > > 33% for most any treatment of anything?

> > > > >

> > > > > > This shows quite clearly the need for placebo controlled

> > > trials

> > > > on

> > > > > > any of these treatments, whether ceftriaxone,

fluconazole,

> > MP

> > > or

> > > > any

> > > > > > other. The need is even greater with CFS where the

placebo

> > > > effect

> > > > > > could be in excess of 60%. Patient reports of how they

> feel

> > > can

> > > > not

> > > > > > be relied on.

> > > > >

> > > > > Where is 60% coming from?

> > > > >

> > > > > To me, what cant be relied on is reports (including my

own,

> I

> > > > notice!)

> > > > > of oncoming/building effects, where hope and random

> > oscillation

> > > of

> > > > > ones condition is a factor.

> > > > >

> > > > > Hope operates differently in a disease which generates

such

> > > > extreme

> > > > > desperation, which in turn tempts one to deceive oneself.

> This

> > > > could

> > > > > cause a high disposition to placebo effects in CFS, at

least

> > in

> > > > the

> > > > > short term. In the short run, I see people including

myself

> > > > nurture

> > > > > treatment " responses " like wan flames.

> > > > >

> > > > > I also dont doubt that solid, 100% real responses can

later

> > > > evaporate -

> > > > > whether it happens by reproliferation of tx-resistant

> > microbes,

> > > > re-

> > > > > regulation of neurotransmission that had been boosted by

> > > > > antidepressants, or reduction of microbe populations

causing

> > un-

> > > > > desensitization towards immunoactivating ligands like LPS,

> > > causing

> > > > the

> > > > > former level of inflammation to be restored despite the

> fewer

> > > bugs.

> > > > >

> > > > > OTOH when somethings been working for someone consistently

> for

> > > > many

> > > > > months, thats pretty reliable to me. When this holds up

> during

> > > > times

> > > > > of strain, or seasons of discontent, that means even more.

> > > > Considering

> > > > > my immense weather response, we wont see until another

> > Virginia

> > > > > December what good my antimicrobial treatment has really

> done.

> > I

> > > > > expect to get sicker than I am now, but I truly doubt I'll

> be

> > in

> > > > the

> > > > > same ballpark as last winter. If you are going to consider

> > > whether

> > > > CFS

> > > > > may have a tremendous placebo effect propensity, it seems

> > > > important

> > > > > not to be atemporal in this inquiry but to instead

consider

> > > > whether

> > > > > those placebo effects would/do hold up over many months,

> which

> > > > many

> > > > > improvement reports do.

[Guest guest]

Just another tid bit, we are a strange lot and generally try and get

the patrients benefitting from any of these approaches on the phone.

generally we find they don't exist all these studies and double

blind placebo's are just hashed up junk. Basically there's no-one in

real world land benefitting from any of this otherwise we'd have

them on the phone, even visit them in there office in another state.

> > > > > Re the Klempner ceftriaxone/doxy study - there is a

detailed

> > > demur

> > > > > from ILADS which was posted on eurolyme about 10

days

> > ago.

> > > I

> > > > > didnt read it, nor have I read the Klempner studies. When

I

> > took

> > > > in

> > > > > the inadequate microbiological scholarship of Steeres

> > editorials

> > > > on

> > > > > chronic lyme treatment, I felt I'd spent enough time on

that

> > > crowd

> > > > for

> > > > > a while.

> > > > >

> > > > > Its not like I think the studies are total fabrication.

Its

> > just

> > > > that

> > > > > to say I take them with a grain of salt is a gigantic

> > > > understatement.

> > > > >

> > > > > > " It is noteworthy that in both the NEMC and SUNY

clinical

> > > trials

> > > > > > cited above, 40 percent of patients given placebo alone

> > > reported

> > > > > > improvement in their symptoms (placebo effect). "

> > > > >

> > > > > This is no inordinate rate of placebo effect. Isnt it

> usually

> > > > around

> > > > > 33% for most any treatment of anything?

> > > > >

> > > > > > This shows quite clearly the need for placebo controlled

> > > trials

> > > > on

> > > > > > any of these treatments, whether ceftriaxone,

fluconazole,

> > MP

> > > or

> > > > any

> > > > > > other. The need is even greater with CFS where the

placebo

> > > > effect

> > > > > > could be in excess of 60%. Patient reports of how they

> feel

> > > can

> > > > not

> > > > > > be relied on.

> > > > >

> > > > > Where is 60% coming from?

> > > > >

> > > > > To me, what cant be relied on is reports (including my

own,

> I

> > > > notice!)

> > > > > of oncoming/building effects, where hope and random

> > oscillation

> > > of

> > > > > ones condition is a factor.

> > > > >

> > > > > Hope operates differently in a disease which generates

such

> > > > extreme

> > > > > desperation, which in turn tempts one to deceive oneself.

> This

> > > > could

> > > > > cause a high disposition to placebo effects in CFS, at

least

> > in

> > > > the

> > > > > short term. In the short run, I see people including

myself

> > > > nurture

> > > > > treatment " responses " like wan flames.

> > > > >

> > > > > I also dont doubt that solid, 100% real responses can

later

> > > > evaporate -

> > > > > whether it happens by reproliferation of tx-resistant

> > microbes,

> > > > re-

> > > > > regulation of neurotransmission that had been boosted by

> > > > > antidepressants, or reduction of microbe populations

causing

> > un-

> > > > > desensitization towards immunoactivating ligands like LPS,

> > > causing

> > > > the

> > > > > former level of inflammation to be restored despite the

> fewer

> > > bugs.

> > > > >

> > > > > OTOH when somethings been working for someone consistently

> for

> > > > many

> > > > > months, thats pretty reliable to me. When this holds up

> during

> > > > times

> > > > > of strain, or seasons of discontent, that means even more.

> > > > Considering

> > > > > my immense weather response, we wont see until another

> > Virginia

> > > > > December what good my antimicrobial treatment has really

> done.

> > I

> > > > > expect to get sicker than I am now, but I truly doubt I'll

> be

> > in

> > > > the

> > > > > same ballpark as last winter. If you are going to consider

> > > whether

> > > > CFS

> > > > > may have a tremendous placebo effect propensity, it seems

> > > > important

> > > > > not to be atemporal in this inquiry but to instead

consider

> > > > whether

> > > > > those placebo effects would/do hold up over many months,

> which

> > > > many

> > > > > improvement reports do.

[Guest guest]

I thought the law was changed (or is being changed) that researchers

can no longer exclude previous work that does not support the findings

they present as proof of their claims. If this hasn't happened it

should.

penny

" dumbaussie2000 " <dumbaussie2000@y...> wrote:

>

If you notice they keep doing double blind studies

> until they get a certain amount of positive to introduce a drug into

> the market.It often takes 20 double blind studies ignoring the 19

> and showing the positive 20th as a reason to introduce a drug.