Re: ACE inhibitors vs ARBs in high-risk patients

[Guest guest]

That's a good article. I wonder what Dr,. Wonder would put his

patients on?B12 injections seem to be his CFS wonder drug, Oh and

the 2 or 3 antidepressants to protect the brain, the only problem

was he discovered the brain ain't being protected.

So at a glance what would your reserach recommend?

I don't mind doing the smart age related disease drugs..

tony

> This is a pretty recent review of the comparative cardio-

protective

> effects of ACE inhibitors and ARBs, finding superior protection

for

> the ACE inhibitors based on studies performed to date.

>

> Ann Pharmacother. 2005 Mar;39(3):470-80. Epub 2005 Feb 8.

>

> Angiotensin receptor blockers versus ACE inhibitors: prevention of

> death and myocardial infarction in high-risk populations.

>

> Epstein BJ, Gums JG.

>

> Department of Pharmacy Practice, College of Pharmacy, University

of

> Florida, 625 SW 4th Avenue, Gainesville, FL 32601-6430, USA.

> epstein@c...

>

> OBJECTIVE: To determine, through a review of the medical

literature,

> whether there is adequate evidence to support the use of

angiotensin

> receptor blockers (ARBs) in place of angiotensin-converting enzyme

> (ACE) inhibitors in high-risk populations, focusing on the

> prevention of death and myocardial infarction (MI).

>

> DATA SOURCES: Original investigations, reviews, and meta-analyses

> were identified from the biomedical literature via a MEDLINE

search

> (1966-August 2004). Published articles were also cross-referenced

> for pertinent citations, and recent meeting abstracts were

searched

> for relevant data.

>

> STUDY SELECTION AND DATA EXTRACTION: All articles identified

during

> the search were evaluated. Preference was given to prospective,

> randomized, controlled trials that evaluated major cardiovascular

> endpoints and compared ARBs with ACE inhibitors, active controls,

or

> placebo.

>

> DATA SYNTHESIS: The renin-angiotensin system plays a pivotal role

in

> the continuum of cardiovascular disease and represents a major

> therapeutic target in the treatment of patients at risk for

vascular

> events. While ACE inhibitors have been definitively shown to

prevent

> death and MI, studies with ARBs in similar populations have not

> reduced these endpoints. In clinical trials that enrolled patients

> with heart failure, post-MI, diabetes, and hypertension, ARBs did

> not prevent MI or prolong survival compared with ACE inhibitors,

> other antihypertensives, or placebo.

>

> CONCLUSIONS: ACE inhibitors and ARBs should not be considered

> interchangeable, even among patients with a documented history of

> ACE inhibitor intolerance. ARBs can be considered a second-line

> alternative in such patients with the realization that they have

not

> been shown to prevent MI or prolong survival.

>

> Publication Types:

> Review

> Review, Tutorial

>

> PMID: 15701766 [PubMed - indexed for MEDLINE

[Guest guest]

I'm not sure how this study is relevant to PWC in general?

Regarding the objective of the study: As far as I know, the makers

of ARBs have never promoted the drugs for high risk heart patients.

They're only supposed to be used to lower bp in people with

moderately high blood pressure. Not people with very high bp who are

considered at " high risk " for MI or death.

I'm also curious about the earlier statement that was made regarding

the risks of ARBs. Is there new information? I know a lot of claims

have been made without any scientific evidence to support those

claims. My own experience has been just the opposite of those

claims. i.e. My alderesterone, kidneys and liver all are fine

according to tests. My b vitamins are pretty much where they've

always been since I started testing. In fact, I'm depleted in fewer

of the Bs now, than I've been in the past. I've been on an ARB

(benicar), for over a year with no apparent side effects (except for

fatigue and dizziness during the first few weeks adjusting to the

high doses of the drug) and no lessening of symptom relief over a

year later. As a matter of fact, my kidneys and liver are looking

better than ever. Sure, it's 'possible' that there's some kind of

unseen damage being done, but that's purely speculation, since tests

do not bear this out.

I know that many of us have concerns about the person who introduced

the ARBS as a part of a certain controversial protocol, but for some

people the benefits of the ARB are quite extraordinary, and I'd hate

to see these drugs not given a fair and objective chance if they can

potentially help a lot of people, as they've helped me.

We take risks with lots of commonly prescribed drugs. Antibiotics,

anti-fungals, blood thinners, pain killers, anti-depressants, anti-

inflammatories, anti-seizure meds, migraine meds, anti-malarials,

anti-parsitics, among others. These drugs are known to have risks,

and yet we decide that the calculated risks are worth the results.

It makes sense to warn people of the known risks of a drug. For

instance, warnings about the tendon risk of chloroquinolone drugs,

like Cipro and Levaquin, is sensible, since this risk is proven.

Trying to objectively analyze a protocol, where it holds up and

where it doesn't makes sense. Speculation on potential risks makes

sense too, if there's some indication that the risk may be real. But

we need to be careful that we don't cause alarm by suggesting risk

that is based on nothing more than our own personal beliefs or bias.

Unfortunately, I do think this has happened to a certain degree with

ARBs and Benicar. It would be really terrible if some people's

personal distaste for a particular creator of a certain protocol

prevented further research into a potentially helpful drug.

penny

[Guest guest]

I have no bias. I wondered why my Doc put me on Zestril and has never mentioned Benicar. I just want to know why I am being put on medications. The wonder of the internet and this group is- if you don't understand something you can ask.

Mariepenny <pennyhoule@...> wrote:

I'm not sure how this study is relevant to PWC in general? Regarding the objective of the study: As far as I know, the makers of ARBs have never promoted the drugs for high risk heart patients. They're only supposed to be used to lower bp in people with moderately high blood pressure. Not people with very high bp who are considered at "high risk" for MI or death. I'm also curious about the earlier statement that was made regarding the risks of ARBs. Is there new information? I know a lot of claims have been made without any scientific evidence to support those claims. My own experience has been just the opposite of those claims. i.e. My alderesterone, kidneys and liver all are fine according to tests. My b vitamins are pretty much where they've always been since I started testing. In fact, I'm depleted in fewer of the Bs

now, than I've been in the past. I've been on an ARB (benicar), for over a year with no apparent side effects (except for fatigue and dizziness during the first few weeks adjusting to the high doses of the drug) and no lessening of symptom relief over a year later. As a matter of fact, my kidneys and liver are looking better than ever. Sure, it's 'possible' that there's some kind of unseen damage being done, but that's purely speculation, since tests do not bear this out. I know that many of us have concerns about the person who introduced the ARBS as a part of a certain controversial protocol, but for some people the benefits of the ARB are quite extraordinary, and I'd hate to see these drugs not given a fair and objective chance if they can potentially help a lot of people, as they've helped me.We take risks with lots of commonly prescribed drugs. Antibiotics, anti-fungals, blood thinners, pain killers,

anti-depressants, anti-inflammatories, anti-seizure meds, migraine meds, anti-malarials, anti-parsitics, among others. These drugs are known to have risks, and yet we decide that the calculated risks are worth the results.It makes sense to warn people of the known risks of a drug. For instance, warnings about the tendon risk of chloroquinolone drugs, like Cipro and Levaquin, is sensible, since this risk is proven. Trying to objectively analyze a protocol, where it holds up and where it doesn't makes sense. Speculation on potential risks makes sense too, if there's some indication that the risk may be real. But we need to be careful that we don't cause alarm by suggesting risk that is based on nothing more than our own personal beliefs or bias. Unfortunately, I do think this has happened to a certain degree with ARBs and Benicar. It would be really terrible if some people's personal distaste for a particular creator

of a certain protocol prevented further research into a potentially helpful drug.penny__________________________________________________

[Guest guest]

Marie, I didn't say or mean to imply that you have any kind of bias.

My comments were based on the post about the study comparing ACE

inhibitors and ARBs, as well as the fact that I've seen a lot of

bias against ARBs ever since a certain controversial protocol came

out which has an ARB central to it. There are quite a few sites

where that protocol is panned, and the ARB is panned by association,

when it may not be prudent to do so.

I was also questioning how a study, that compares ACE inhibitors to

ARBs for effectiveness in high risk heart patients, applies to PWC,

when most of us are not dx'd with any kind of high risk heart

disease.

Also, please remember that none of us can really answer why your

doctor prescribed meds for you, as none of us are doctors. We can

discuss theories and our own experiences, but we can never give

medical advice. I would be very interested to hear more about your

doctor's approach. He sounds very innovative.

penny

> I have no bias. I wondered why my Doc put me on Zestril and has

never mentioned Benicar. I just want to know why I am being put on

medications. The wonder of the internet and this group is- if you

don't understand something you can ask.

[Guest guest]

Penny,

I do believe your comments were addressed not to Marie, but to me.

You say you don't see how the study I posted is relevant to " PWC in

general. " I never claimed it was. That is not even a meaningful

category to me - nor do I know of one serious scholar of CFS who

believes it is a monolithic condition.

But if Cheney is right, there is a substantial subset of " CFS " that

is a variant form of heart failure. And that, by itself, seems

enough to me to make the study relevant. In fact, in crude terms

what Cheney is suggesting (as posts by Sue and others have

informed us) is that for a block of CFS patients fatigue and

enforced inactivity are the only thing preventing a potentially

fatal cardiomyopathy from ending their lives.

Marie posted about having been prescribed an ACE inhibitor. She

seemed curious to know more about it, and the study seemed a way of

adding a little light there and also referring back to the recent

discussions here and elsewhere about this cardio-centric model of

CFS.

Now, as to my comments about ARBs in the context of infection:

There's a large body of hopeful sounding research on ARBs as useful

treatment components in a number of conditions. Persistent,

debilitating, bacterial infection is not one of them.

My reservations about ARBs are specific to patients struggling to

clear chronic, debilitating, bacterial infections. I believe there

is enough evidence that ARBs suppress key components of the immune

system to give us pause. It has nothing to do with my feelings about

the founder of the MP and his foibles.

Here, for whatever degree of attention you may choose to give it, is

some of the data which lead me to these reservations. A lot of it is

complex, and when it seems appropriate I will summarize or comment

to clarify what I think I am seeing in this data. PubMed IDs and/or

links are given for every reference, and I welcome you or anyone

else to review them in full and offer your own interpetations.

PubMed ID 15250470, " Effect of angiotensin II and losartan on the

phagocytic activity of peritoneal macrophages from Balb/C mice. "

" Mice peritoneal macrophages were cultured for 48 h and the

influence of different concentrations of AII...and/or losartan...,

an AT1 angiotensin receptor antagonist, on phagocytic activity and

superoxide anion production was determined. "

" A stimulatory effect on phagocytic activity (P < 0.05) was observed

with AII concentrations. The addition of losartan to the cell

cultures blocked (P < 0.001) the phagocytosis indicating the

involvement of AT1 receptors. "

PubMed ID 151648, " Unexpected News In Renal Fibrosis. "

The " unexpected news " was the result of a study in which bone marrow

transfer made it possible to create mice whose macrophages HAD no

AII Type 1 receptors: a perfect " angiotensin blockade. " A group of

these mice, and a control group of mice with wild-type macrophages,

were both provoked with a 'unilateral ureteral obstruction' to

determine the inflammatory response.

Had the general assumptions are how kidney inflammation works been

valid, the blockade mice would have had less white cell infiltration

and less fibrosis.

They did indeed have fewer white cells infiltrating the inflamed

tissue. But they had more, not less, fibrosis.

" How could infiltrating macrophages have antifibrotic action? Given

the myriad actions described for these cells, the possibilities are

many, but it could simply be due to their ability to phagocytize

dead cells and cellular debris.Indeed, analysis of macrophage

function by Nishida et al. (11) revealed that macrophages lacking

Agtr1a have reduced migratory capacity and decreased phagocytic

activity, a characteristic that could also be elicited in wild-type

macrophages by the angio-tensin II receptor antagonist losartan. "

The above is from a commentary in the same issue of The Journal of

Clinical Investigation in which the study itself was published.

That study is available in its full text version at:

http://www.pubmedcentral.gov/articlerender.fcgi?artid=151648

PubMed ID is 151648, if you wish to view the abstract instead.

" Absence of angiotensin II type 1 receptor in bone marrow–derived

cells is detrimental in the evolution of renal fibrosis "

The authors describe how previous studies had found an association

between white cell infiltrates in the kidneys and fibrosis, but

lacked any method for distinguishing what the actual role of AII-

influenced macrophage activity was.

By using bone marrow transfer to create mice whose macrophages were

impervious to AII, this study was able to isolate that role.

" When the bone marrow was transplanted from Agtr1–/– into Agtr1+/+

wild-type mice, the accumulation of macrophages in the kidney

occurring in response to an obstructive insult was substantially

attenuated, whereas renal interstitial fibrosis and profibrotic

activity were enhanced. "

" This divergence between macrophage accumulation and fibrosis was

evident in late stages (day 14) but not in early stages (day 5) of

UUO. Since infiltrating macrophages are thought to be a critical

determinant of fibrogenesis, these data suggest that the Agtr1 on

bone marrow–derived macrophages promotes preservation of the renal

parenchyma during the evolution of renal fibrosis in obstructive

nephropathy. "

In other words, the macrophage activity spurred specifically by

angiotensin II was protective and anti-fibrotic.

" Further analyses revealed impaired phagocytic capability of Agtr1–/–

macrophages both in vitro and in vivo (Figure 8). We also found

that in vivo administration of losartan to Agtr1+/+ mice reduced

phagocytic capability of Agtr1+/+ macrophages to a level similar to

that of Agtr1–/– macrophages (Figure 8), suggesting that angiotensin

II acts on the Agtr1 on macrophages in vivo and stimulates

phagocytic capability. "

" Our finding that attenuated macrophage accumulation is associated

with accelerated renal fibrosis, therefore, provides a unique

insight into the function of macrophages. It is notable that a

salutary function of macrophages has been described in the process

of wound healing (12–15, 44). Thus, macrophages have been shown to

promote provisional ECM deposition in early stages of wound healing

(12, 13), whereas in later stages, macrophages are thought to play

an essential role through phagocytic clearance of ECM fragments and

apoptotic cells (13, 44). "

" Collectively, a possibility arises that diminution in the quantity

and/or quality of functioning macrophages, as seen in the present

study, leads to sustained profibrotic activity in the resident renal

cells. "

So: even in a clinical area where ARBs were widely assumed to be

benign, their suppressive effect on macrophage recruitment and

function turned out, at the longer 15-day interval, to produce a

more destructive outcome.

Now, when we turn to the challenge of clearing infection, we find

that these same functions are of critical importance.

This is clarified, for example, in PubMed ID PMID: 15100000:

" Macrophages play a critical role in protection against MRSA

[methicillin resistant Staphylococcus aureus] administered directly

into the jejunum. LTA recognition sites (probably type A scavenger

receptors) on macrophages are required for binding and phagocytosing

MRSA. "

In PubMed ID: 16061696, published just this month:

" Response to Staphylococcus aureus requires CD36-mediated

phagocytosis triggered by the COOH-terminal cytoplasmic domain. "

" In transfection assays, the mammalian Croquemort paralogue CD36

confers binding and internalization of Gram-positive and, to a

lesser extent, Gram-negative bacteria. By mutational analysis, we

show that internalization of S. aureus and its component

lipoteichoic acid requires the COOH-terminal cytoplasmic portion of

CD36, specifically Y463 and C464, which activates Toll-like receptor

(TLR) 2/6 signaling. Macrophages lacking CD36 demonstrate reduced

internalization of S. aureus and its component lipoteichoic acid,

accompanied by a marked defect in tumor necrosis factor-alpha and IL-

12 production. As a result, Cd36(-/-) mice fail to efficiently clear

S. aureus in vivo resulting in profound bacteraemia. "

CD36, it turns out, is specifically inhibited by ARBs. See PubMed

ID: 10873620

" Losartan inhibits cellular uptake of oxidized LDL by monocyte-

macrophages from hypercholesterolemic patients "

" " CD36 (an Ox-LDL receptor) mRNA expression in human monocyte-

derived macrophages [HMDM] obtained after losartan treatment was

decreased by 54% compared to HMDM obtained before treatment. "

This is a perfect example of how a medical journal article can wax

enthusiastic about ARBs, and in its own context be perfectly

correct, while at the same time providing us with information that

should make anyone whose primary health issue is INFECTION think

twice.

S.

> > I have no bias. I wondered why my Doc put me on Zestril and has

> never mentioned Benicar. I just want to know why I am being put on

> medications. The wonder of the internet and this group is- if you

> don't understand something you can ask.

[Guest guest]

Hi Penny,

I hope you didn't think I was taking offense. I wasn't.

Sorry also if it sounded like I was asking for medical advice. I know better than that. Most all of what I know about BP medications has come from reading on this site and the not to be mentioned site so it came as a surprise when the Dr. ordered a BP med that had not been mentioned here. He must be getting his information from somewhere and I wondered if anyone knew anything about why he might choose Zestril. I did not post the information on his handout to get a vote on whether I should take the medication. I thought some people on the post might be interested in the approach this Dr. is taking.

Yes, I feel very fortunate to have found this Dr. It was quite serendipitous as I went looking for a rhuematologist who could help me with my knee pain.. I do have some osteo damage to my knees but the pain was primarily due to inflammation and swelling and I realize now it was due to infection. Since taking antibiotics almost all the time for a year I can walk. The pain is reduced to only pain upon touching. A year ago before I found this Dr. I was getting more and more crippled from the pain and was having a lot of difficulty getting around.

I had felt fortunate before because I had found a Dr. who treated CFS. He was a good Dr. but reluctant to put me on long term antibiotics ( I had asked for them). The new Dr. is willing and is constantly researching and adding things to the protocol. .

Didn't mean to ramble. I DO feel fortunate to have found this Dr. However as all of you know we must continue to do our own research. My education is not in bio or medical sciences so I appreciate feed back from this group. Thanx so much for the reponse. .

Marie

Marie, I didn't say or mean to imply that you have any kind of bias. My comments were based on the post about the study comparing ACE inhibitors and ARBs, as well as the fact that I've seen a lot of bias against ARBs ever since a certain controversial protocol came out which has an ARB central to it. There are quite a few sites where that protocol is panned, and the ARB is panned by association, when it may not be prudent to do so. I was also questioning how a study, that compares ACE inhibitors to ARBs for effectiveness in high risk heart patients, applies to PWC, when most of us are not dx'd with any kind of high risk heart disease. Also, please remember that none of us can really answer why your doctor prescribed meds for you, as none of us are doctors. We can discuss theories and our own experiences, but we can never give medical advice. I would be very interested to hear more about your doctor's

approach. He sounds very innovative.penny> I have no bias. I wondered why my Doc put me on Zestril and has never mentioned Benicar. I just want to know why I am being put on medications. The wonder of the internet and this group is- if you don't understand something you can ask.__________________________________________________

[Guest guest]

Penny I sort of read into the post that the arb doesn't make a huge

difference to overall herat deaths. This is like saying it's not

doing anything bad- but doesn't lower 'this death rate'.I found it

interesting because all my realtives that have had arb's swear by

how good they have been.But if it truly doesn't cut the deaths which

is a little strange -WHY!!! would be a good place to start asking

the tough questions.

I suppose it may boil down to when the heart is diagnosed as very

ill, it doesn't fare well- up to this point it may have been awesome.

just thinking out loud.

> I'm not sure how this study is relevant to PWC in general?

>

> Regarding the objective of the study: As far as I know, the makers

> of ARBs have never promoted the drugs for high risk heart

patients.

> They're only supposed to be used to lower bp in people with

> moderately high blood pressure. Not people with very high bp who

are

> considered at " high risk " for MI or death.

>

> I'm also curious about the earlier statement that was made

regarding

> the risks of ARBs. Is there new information? I know a lot of

claims

> have been made without any scientific evidence to support those

> claims. My own experience has been just the opposite of those

> claims. i.e. My alderesterone, kidneys and liver all are fine

> according to tests. My b vitamins are pretty much where they've

> always been since I started testing. In fact, I'm depleted in

fewer

> of the Bs now, than I've been in the past. I've been on an ARB

> (benicar), for over a year with no apparent side effects (except

for

> fatigue and dizziness during the first few weeks adjusting to the

> high doses of the drug) and no lessening of symptom relief over a

> year later. As a matter of fact, my kidneys and liver are looking

> better than ever. Sure, it's 'possible' that there's some kind of

> unseen damage being done, but that's purely speculation, since

tests

> do not bear this out.

>

> I know that many of us have concerns about the person who

introduced

> the ARBS as a part of a certain controversial protocol, but for

some

> people the benefits of the ARB are quite extraordinary, and I'd

hate

> to see these drugs not given a fair and objective chance if they

can

> potentially help a lot of people, as they've helped me.

>

> We take risks with lots of commonly prescribed drugs. Antibiotics,

> anti-fungals, blood thinners, pain killers, anti-depressants, anti-

> inflammatories, anti-seizure meds, migraine meds, anti-malarials,

> anti-parsitics, among others. These drugs are known to have risks,

> and yet we decide that the calculated risks are worth the results.

>

> It makes sense to warn people of the known risks of a drug. For

> instance, warnings about the tendon risk of chloroquinolone drugs,

> like Cipro and Levaquin, is sensible, since this risk is proven.

>

> Trying to objectively analyze a protocol, where it holds up and

> where it doesn't makes sense. Speculation on potential risks makes

> sense too, if there's some indication that the risk may be real.

But

> we need to be careful that we don't cause alarm by suggesting risk

> that is based on nothing more than our own personal beliefs or

bias.

>

> Unfortunately, I do think this has happened to a certain degree

with

> ARBs and Benicar. It would be really terrible if some people's

> personal distaste for a particular creator of a certain protocol

> prevented further research into a potentially helpful drug.

>

> penny

[Guest guest]

Remember that this was only dealing with high risk patients. ARB's

are supposed to be for light or moderate hypertension. They have

little or no effect on kinins which rise in many heart problems and

with increased endotoxins. The ACE inhibitors significantly reduce

kinins. It makes sense that ACE inhibitors would offer more

protection for high risk cases, and that a Dr. would prescribe them

for a patient with a high level of toxins.

For lower risk, moderate hypertension, the ARB's would still offer

the benefits of lowered blood pressure.

> > I'm not sure how this study is relevant to PWC in general?

> >

> > Regarding the objective of the study: As far as I know, the

makers

> > of ARBs have never promoted the drugs for high risk heart

> patients.

> > They're only supposed to be used to lower bp in people with

> > moderately high blood pressure. Not people with very high bp who

> are

> > considered at " high risk " for MI or death.

> >

> > I'm also curious about the earlier statement that was made

> regarding

> > the risks of ARBs. Is there new information? I know a lot of

> claims

> > have been made without any scientific evidence to support those

> > claims. My own experience has been just the opposite of those

> > claims. i.e. My alderesterone, kidneys and liver all are fine

> > according to tests. My b vitamins are pretty much where they've

> > always been since I started testing. In fact, I'm depleted in

> fewer

> > of the Bs now, than I've been in the past. I've been on an ARB

> > (benicar), for over a year with no apparent side effects (except

> for

> > fatigue and dizziness during the first few weeks adjusting to

the

> > high doses of the drug) and no lessening of symptom relief over

a

> > year later. As a matter of fact, my kidneys and liver are

looking

> > better than ever. Sure, it's 'possible' that there's some kind

of

> > unseen damage being done, but that's purely speculation, since

> tests

> > do not bear this out.

> >

> > I know that many of us have concerns about the person who

> introduced

> > the ARBS as a part of a certain controversial protocol, but for

> some

> > people the benefits of the ARB are quite extraordinary, and I'd

> hate

> > to see these drugs not given a fair and objective chance if they

> can

> > potentially help a lot of people, as they've helped me.

> >

> > We take risks with lots of commonly prescribed drugs.

Antibiotics,

> > anti-fungals, blood thinners, pain killers, anti-depressants,

anti-

> > inflammatories, anti-seizure meds, migraine meds, anti-

malarials,

> > anti-parsitics, among others. These drugs are known to have

risks,

> > and yet we decide that the calculated risks are worth the

results.

> >

> > It makes sense to warn people of the known risks of a drug. For

> > instance, warnings about the tendon risk of chloroquinolone

drugs,

> > like Cipro and Levaquin, is sensible, since this risk is proven.

> >

> > Trying to objectively analyze a protocol, where it holds up and

> > where it doesn't makes sense. Speculation on potential risks

makes

> > sense too, if there's some indication that the risk may be real.

> But

> > we need to be careful that we don't cause alarm by suggesting

risk

> > that is based on nothing more than our own personal beliefs or

> bias.

> >

> > Unfortunately, I do think this has happened to a certain degree

> with

> > ARBs and Benicar. It would be really terrible if some people's

> > personal distaste for a particular creator of a certain protocol

> > prevented further research into a potentially helpful drug.

> >

> > penny

[Guest guest]

So . Are you basically saying that unchecked inflammation is

fine, and all the evidence pointing to inflammation being a major

cause of heart disease (and other illnesses) is inaccurate or

irrelevant?

Do any of the studies you posted claim that the ARBs have the

ability to block ALL angiotensin II entirely? It seems to me these

mice were genetically manipulated to produce zero angiotensin. ARBs

block the receptors of angiotensin. I don't think angiotensin itself

is being eliminated entirely with ARBs, is it?

If we are producing too much of some substance which is causing

numerous inflammatory symptoms, pain, and even death by heart

attack, doesn't it make sense to decrease that substance a bit?

Besides, the ARBs must not be decreasing AII entirely (or more

accurately, blocking the AII receptors), as that first study on high

risk heart patients seems to suggest.

Lastly, how do you explain my improvement? I have a diagnosed long

term, entrenched infection, and despite using an ARB for over a year

now (which you are suggesting is bad for long term infections), my

infection is definitely decreasing, as is my inflammation (I'm

reducing the ARB dosage) while my energy and cognitive levels are up

and appear to be increasing. I'm even tolerating a little exercise.

I definitely feel that I'm steadily improving and on the best road

to health I've taken yet.

I agree that we need to investigate all aspects of any drug, pro and

con, especially a new experiemental one. But I'd feel a lot better

if you were showing studies on both sides of the issue, rather than

only pointing to ones that support your theory that ARBS are harmful.

penny

p.s. Serious scholars of CFS (all 2 or 3 of them) do recognize the

fact that we share many of the same symptoms (this is how we get the

dx plus the fact that our tests usually show negative for most known

illness markers). Despite the similarity in symptoms we do not

respond the same way to most treatments. So far, serious scholars of

CFS haven't found any cure, --they're still looking for a definite

cause or causes, so in general, any pronouncements they make

generally fall into the wait-and-see category.

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

> I do believe your comments were addressed not to Marie, but to me.

>

> You say you don't see how the study I posted is relevant to " PWC

in

> general. " I never claimed it was. That is not even a meaningful

> category to me - nor do I know of one serious scholar of CFS who

> believes it is a monolithic condition.

>

[Guest guest]

I agree. This is a great question. Why do ARBs make people feel

better? To be honest, they're only mildly effective as blood

pressure reducers, and are only used on people with mildly elevated

bp. Something is definitely going on, and the lowered bp may just be

a minor side effect. There's been some speculation that ARBs are

actually affecting the brain's receptors in some way. The

interesting thing to me is that after a year, I'm getting the same

benefit as when I started (on half the amount of the drug). The only

other drugs that don't lose their effectiveness over time are

hormones. Everything else I've taken has eventually been

circumvented by my illness and become useless against my symptoms.

penny

" dumbaussie2000 " <dumbaussie2000@y...> wrote:

> Penny I sort of read into the post that the arb doesn't make a

huge difference to overall herat deaths. This is like saying it's

not doing anything bad- but doesn't lower 'this death rate'.I found

it interesting because all my realtives that have had arb's swear

by how good they have been.But if it truly doesn't cut the deaths

which is a little strange -WHY!!! would be a good place to start

asking the tough questions.

[Guest guest]

This is interesting. I have just stopped taking eprosartan as I felt I was losing ground on it. Two weeks down the track I am now convinced this is the case. There are gains to be had perhaps but disproportionate to the cost. I welcome the next breakthrough. Eprosartan was a part answer but it was also the prompt to ask further questions.

Regards

Windsor

[infections] Re: ACE inhibitors vs ARBs in high-risk patients

I agree. This is a great question. Why do ARBs make people feel better? To be honest, they're only mildly effective as blood pressure reducers, and are only used on people with mildly elevated bp. Something is definitely going on, and the lowered bp may just be a minor side effect. There's been some speculation that ARBs are actually affecting the brain's receptors in some way. The interesting thing to me is that after a year, I'm getting the same benefit as when I started (on half the amount of the drug). The only other drugs that don't lose their effectiveness over time are hormones. Everything else I've taken has eventually been circumvented by my illness and become useless against my symptoms.penny

[Guest guest]

It sounds like some build resistance to the therapy? I was sure that

when I first took benicar it did a wonderfull job on inflammation

clamping, down the road though this was lost, so I stopped. feeling

it wasn't going to bare fruit.

Just incredable how some, possably the man himself, could still feel

the clamping. Oh! I also felt the detrimental effects of having a

80/50 blood pressure reading meant I wasn't supplying blood to

places that it was much needed.

> This is interesting. I have just stopped taking eprosartan as I

felt I was losing ground on it. Two weeks down the track I am now

convinced this is the case. There are gains to be had perhaps but

disproportionate to the cost. I welcome the next breakthrough.

Eprosartan was a part answer but it was also the prompt to ask

further questions.

> Regards

> Windsor

> [infections] Re: ACE inhibitors vs ARBs

in high-risk patients

>

>

> I agree. This is a great question. Why do ARBs make people feel

> better? To be honest, they're only mildly effective as blood

> pressure reducers, and are only used on people with mildly

elevated

> bp. Something is definitely going on, and the lowered bp may

just be

> a minor side effect. There's been some speculation that ARBs are

> actually affecting the brain's receptors in some way. The

> interesting thing to me is that after a year, I'm getting the

same

> benefit as when I started (on half the amount of the drug). The

only

> other drugs that don't lose their effectiveness over time are

> hormones. Everything else I've taken has eventually been

> circumvented by my illness and become useless against my

symptoms.

>

> penny

[Guest guest]

> I agree. This is a great question. Why do ARBs make people feel

> better? To be honest, they're only mildly effective as blood

> pressure reducers, and are only used on people with mildly

elevated

> bp. Something is definitely going on, and the lowered bp may just

be

> a minor side effect. There's been some speculation that ARBs are

> actually affecting the brain's receptors in some way.

Penny, part of the answer may be matrix metalloproteinases (MMPs).

These can affect signalling pathways and open the blood brain

barrier. They can also cause problems in other organs. They increase

in the presence of macrophage produced TNF-alpha, and can be reduced

with the use of ARBs. ACE inhibitors seem to have no effect. There

seems to be a lot of research interest in them in the last few years.

There has also been a recent discovery of a AT4 receptor in the

brain. " There is support for an inhibitory influence by AngII

activation of the AT1 subtype, and a facilitory role by AngIV

activation of the AT4 subtype, on neuronal firing rate, long-term

potentiation, associative and spatial learning. " (The brain

angiotensin system and extracellular matrix molecules in neural

plasticity, learning, and memory. - PMID: 15142685). It appears that

inhibitting AT1 receptors may improve brain function.

[Guest guest]

Hi Penny,

You don't appear to have understood my post. It was long, technical,

and perhaps the key points were not made clear enough, so I will try

again, while at the same time answering your questions as best I can.

Penny said:

> So . Are you basically saying that unchecked inflammation is

> fine, and all the evidence pointing to inflammation being a major

> cause of heart disease (and other illnesses) is inaccurate or

> irrelevant?

replies:

Did I say that? No, I didn't.

What I did say was that when inflammation is the result of

infection, and resolving inflammation requires clearing infection,

there is evidence that ARBs may be counterproductive.

Penny said:

> It seems to me these mice were genetically manipulated to produce

zero angiotensin.

replies:

They did nothing to change the amount of angiotensin II the mice

produced. They replaced their macrophages, by bone marrow transfer,

with macrophages that have no angiotensin II RECEPTORS.

It was the only way to be certain which macrophage activities were a

result of having those macrophage AII receptors stimulated, and what

the effect would be of having them blocked.

The effect was: a reduction of macrophage numbers in the inflamed

area, AND a significant increase in fibrosis, a kind of scarring

that results when inflammation is not resolved properly, in a manner

that preserves the architecture of the inflamed tissue or organ.

Penny wrote:

Do any of the studies you posted claim that the ARBs have the

ability to block ALL angiotensin II entirely?

replies:

What the study found was that the identical result occurred when

control mice, whose macrophages had AII receptors, were treated with

losartan. So as far as macrophage function is concerned, and the

corresponding ability to resolve inflammation sucessfully, yes, the

effect of the ARB was equivalent to a total blockade.

It is a very striking finding, which probably explains why the

journal publishing the study devoted an editorial to the results. I

included their comments in my post, because they describe the real

importance of this finding in clear terms:

" How could infiltrating macrophages have antifibrotic action? Given

the myriad actions described for these cells, the possibilities are

many, but it could simply be due to their ability to phagocytize

dead cells and cellular debris.Indeed, analysis of macrophage

function by Nishida et al. (11) revealed that macrophages lacking

Agtr1a {that's the macrophage AII receptor, Penny} have reduced

migratory capacity and decreased phagocytic activity, a

characteristic that could also be elicited in wild-type

macrophages by the angio-tensin II receptor antagonist losartan. "

In response to my last two citations, Penny wrote nothing at all,

probably because I did such a poor job explaining the Nishida

finding that she never got past it. I believe, however, that these

additional citations lend more weight and urgency to my concerns:

PubMed ID: 16061696, published just this month:

" Response to Staphylococcus aureus requires CD36-mediated

phagocytosis triggered by the COOH-terminal cytoplasmic domain. "

" Macrophages lacking CD36 demonstrate reduced internalization of S.

aureus and its component lipoteichoic acid, accompanied by a marked

defect in tumor necrosis factor-alpha and IL-12 production. As a

result, Cd36(-/-) mice fail to efficiently clear S. aureus in vivo

resulting in profound bacteraemia. "

PubMed ID: 10873620

" CD36 (an Ox-LDL receptor) mRNA expression in human monocyte-

derived macrophages [HMDM] obtained after losartan treatment was

decreased by 54% compared to HMDM obtained before treatment. "

Penny wrote:

> If we are producing too much of some substance which is causing

> numerous inflammatory symptoms, pain, and even death by heart

> attack, doesn't it make sense to decrease that substance a bit?

replies:

I don't quite understand your point here. If you want to decrease

Angiotensin II levels, the logical drug of choice would not be an

ARB, which only achieves that effect over a very long period

(initially, blocking receptors causes AII plasma levels to spike),

but an ACE inhibitor, which begins reducing the level of circulating

Angiotensin II immediately, by inhibiting the enzyme needed to

produce it.

Penny wrote:

> Lastly, how do you explain my improvement?

replies:

Respectfully, Penny, you are not the only patient with evidence of

infection who attempted high-dose ARB therapy. Your response is not

unique, but of the cases I've reviewed it is also far from typical.

Many patients, including some members of this list, not only saw

symptoms multiply and increase in severity but months after ceasing

ARB treatment had not gotten back to baseline.

I don't know anything about the measurement of your bacterial load,

but if you want to provide some lab data that you think shows

increased clearance of bacterial during your year on Benicar, and a

breakdown of how your antibiotic treatment has changed during the

same interval, I'd be willing to look at that.

I am very glad you are feeling better, but as I say, many with

strong evidence of pathogenic bacterial infection tried the same

high-dose ARB therapy and felt substantially worse.

> I agree that we need to investigate all aspects of any drug, pro

and con, especially a new experiemental one. But I'd feel a lot

better if you were showing studies on both sides of the issue,

rather than only pointing to ones that support your theory that ARBS

are harmful.

>

replies:

Penny, the question I undertook to address was not whether ARBs are,

in every possible clinical situation for which they might be

prescribed, helpful or harmful.

My question was:

For patients whose inflammation is due to infection, whose recovery

depends on clearing that infection, are the affects of ARBs on the

immune system more likely to be helpful or harmful?

I logged quite a few hours doing the research, and presented it

honestly. If you think I missed something important, post it. If you

think I misread the data I presented, provide you own reading of

that data.

Thanks much,

> penny

>

> p.s. Serious scholars of CFS (all 2 or 3 of them) do recognize the

> fact that we share many of the same symptoms (this is how we get

the

> dx plus the fact that our tests usually show negative for most

known

> illness markers). Despite the similarity in symptoms we do not

> respond the same way to most treatments. So far, serious scholars

of

> CFS haven't found any cure, --they're still looking for a definite

> cause or causes, so in general, any pronouncements they make

> generally fall into the wait-and-see category.

>

>

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

>

> > I do believe your comments were addressed not to Marie, but to

me.

> >

> > You say you don't see how the study I posted is relevant to " PWC

> in

> > general. " I never claimed it was. That is not even a meaningful

> > category to me - nor do I know of one serious scholar of CFS who

> > believes it is a monolithic condition.

> >

[Guest guest]

That was so long-'my goodness'.. Just curious as to the macrophages

clearing staph areus infections. I did notice while on arb's my

staph bacterial load was very evident, before this therpay I

struggled to grow anything. It seems the arb's gave the infection an

upper hand- even though suppressing the inflammation to a degree.

What's your take on this obvious change in my bacterial load.

> >

> > > I do believe your comments were addressed not to Marie, but to

> me.

> > >

> > > You say you don't see how the study I posted is relevant

to " PWC

> > in

> > > general. " I never claimed it was. That is not even a

meaningful

> > > category to me - nor do I know of one serious scholar of CFS

who

> > > believes it is a monolithic condition.

> > >

[Guest guest]

I'd say the guys who did the August 05 staph study nailed it: when

that macrophage scavenger receptor [CD36] doesn't work, staph

becomes a lot harder to clear.

Losartan reduces expression of CD36 on human macrophages by 54% at

the standard hypertensive dose. Don't know what dose you were

taking, but unless it was tiny based on this data I'd say you cut

your clearance rate, and it showed up in your cultures.

Think you're phrasing really gets it right: " the arb's gave the

infection an upper hand- even though suppressing the inflammation. "

As the Aug 05 study says, when the macrophages are blocked from

gobbling up the baddies, they don't generate the TNF-alpha and IL-12

that they would have, if they'd been functioning properly.

The thing is, in that case those inflammatory cytokines were needed,

to get the bugs and their toxins gone. Because the source of the

inflammation was infection, what we want is not to suppress that

inflammation but to RESOLVE it, by clearing the source.

> > >

> > > > I do believe your comments were addressed not to Marie, but

to

> > me.

> > > >

> > > > You say you don't see how the study I posted is relevant

> to " PWC

> > > in

> > > > general. " I never claimed it was. That is not even a

> meaningful

> > > > category to me - nor do I know of one serious scholar of CFS

> who

> > > > believes it is a monolithic condition.

> > > >

[Guest guest]

Thanks PAul

That really made it clear, my next challenge is going after

understanding steroids.I basically know how easy it is to stop

infections pumping there toxins and hence making you feel good.I

really think the steroids also work on this angle with bacteria, as

opposed to doing something to the immune system.

I would find them pretty useless in advanced disease but they seem

to have the ability to get people up and running for 10 years at

times.Actually had this dude with ankylosing spondylitis tell me how

he got an injection into the eyeball to fix his uveitis.His uveitis

hasn't bothered him for some time.

Anyway there's no harm done if we get a grip on the actual mechanism

of action as opposed to recommending or doing this therapy.

> > > >

> > > > > I do believe your comments were addressed not to Marie,

but

> to

> > > me.

> > > > >

> > > > > You say you don't see how the study I posted is relevant

> > to " PWC

> > > > in

> > > > > general. " I never claimed it was. That is not even a

> > meaningful

> > > > > category to me - nor do I know of one serious scholar of

CFS

> > who

> > > > > believes it is a monolithic condition.

> > > > >

[Guest guest]

Tony:

Hah!.. Here's what my Vet says about steroids:

" You can walk an animal into the autopsy room on them " .

No one really knows how they work completely.

And I refused that 5 inch long needle/steroid injection into the back

of the eyeball for posterior Uveitis.

Barb

Tony wrote:

my next challenge is going after

understanding steroids.I basically know how easy it is to stop

infections pumping there toxins and hence making you feel good.I

really think the steroids also work on this angle with bacteria, as

opposed to doing something to the immune system.

I would find them pretty useless in advanced disease but they seem

to have the ability to get people up and running for 10 years at

times.Actually had this dude with ankylosing spondylitis tell me how

he got an injection into the eyeball to fix his uveitis.His uveitis

hasn't bothered him for some time.

Anyway there's no harm done if we get a grip on the actual mechanism

of action as opposed to recommending or doing this therapy.

> > > > >

> > > > > > I do believe your comments were addressed not to Marie,

> but

> > to

> > > > me.

> > > > > >

> > > > > > You say you don't see how the study I posted is relevant

> > > to " PWC

> > > > > in

> > > > > > general. " I never claimed it was. That is not even a

> > > meaningful

> > > > > > category to me - nor do I know of one serious scholar of

> CFS

> > > who

> > > > > > believes it is a monolithic condition.

> > > > > >

[Guest guest]

Barb

'Why did it fix this guys uveitis. I'm not big on taking them I just

want to get a true feel for what there all about.This guy hasn't had

the condition come back and he was told he was going to go blind.

> > > > > >

> > > > > > > I do believe your comments were addressed not to

Marie,

> > but

> > > to

> > > > > me.

> > > > > > >

> > > > > > > You say you don't see how the study I posted is

relevant

> > > > to " PWC

> > > > > > in

> > > > > > > general. " I never claimed it was. That is not even a

> > > > meaningful

> > > > > > > category to me - nor do I know of one serious scholar

of

> > CFS

> > > > who

> > > > > > > believes it is a monolithic condition.

> > > > > > >

[Guest guest]

, I have very obvious indicators when my infection has the upper

hand. Bad fatigue, severe cognition problems, and a salty taste in

my mouth are a few.

Long before I took Benicar, but was on cipro (first time my symptoms

improved), then high dose i.v. abx, I could easily tell when my

bacterial load was being reduced. Better energy, better cognition,

fewer other symptoms like the salty taste, IBS, etc. This is why all

the supplements pretty much went out the window at that point. Huge

difference when I introduced abx. That's also why I knew I had an

infection before I had any tests to prove it, I knew it, based on my

postive reaction to abx.

So now, I'm on zithromax, diflucan and penicillin AND and benicar,

an ARB, and my energy has increased substantially, my cognition is

better, less mental fatigue, I'm even doing mild exercise (hiking)

and liking it for the first time in years. I KNOW when my infection

is decreasing from many years' experience of dealing and treating

it. You can talk to family and friends and ask them if I'm doing

better or not. Ask them if they think I should stop the antibiotics

or whether they're not doing me any good. Maybe I should just read

more books and studies, and not take any action, at least while my

cognitive abilities hold, which believe me, won't be for long if I

stop the abx now (I've already tried that too).

Maybe when you've personally been on a good antimicrobial for a

while, and know with certianty that you're feeling better due to a

reduction in your bacterial load, you'll understand where I'm coming

from. I don't need any tests to tell me if I'm feeling better or

killing bugs. I especially don't need to prove it to anyone else.

Remember, CFS is the illness that never tests positive for any known

disease, and yet we know we're slowly dying. Oh, right, it's all in

our heads. I keep forgetting. :-) I suppose my improvement is all in

my head too.

penny

> I'd say the guys who did the August 05 staph study nailed it: when

> that macrophage scavenger receptor [CD36] doesn't work, staph

> becomes a lot harder to clear.

>

[Guest guest]

Or maybe we need to do both. Reduce the inflammation and coagulation

just sufficiently to allow our IS to remain efficient whilst at the

same time using antimicrobial agents.

Since increasing my vit D and increasing my intake of nattokinase

which acts as a mild ACE inhibitor many of the problems associated

with these have improved. Even whilst having some iffy days my levels

of functioning are higher than the best days I had prior to looking

into a safer way to achieve this. My cervical spine is so bad the I

know from the consequences of that alone how high my genereal

inflammation levels are. What I am experiencing now is the lowest

they have been for very many years.

Cheers, Tansy

> > > >

> > > > > I do believe your comments were addressed not to Marie, but

> to

> > > me.

> > > > >

> > > > > You say you don't see how the study I posted is relevant

> > to " PWC

> > > > in

> > > > > general. " I never claimed it was. That is not even a

> > meaningful

> > > > > category to me - nor do I know of one serious scholar of

CFS

> > who

> > > > > believes it is a monolithic condition.

> > > > >

[Guest guest]

Hi Penny,

I've been offline for about a week focusing on building my business,

and on my education, but wanted to get back to you to thank you for

your ongoing information regarding Actomycosis testing, look forward

to hearing more of these details, and also thank you for this message

you posted below.

As another patient who does well on Benicar I feel the same way;

I would hate to see people not give it a chance because of their

personal feelings towards the protocol's originator.

ARBs, particularly Benicar, show alot of promise for the treatment of

Th1 diseases, and in fact, I have always thought, maybe more so than

for blood pressure-reduction (as they usually are second-line drugs

for hypertension rather than first-line).

I also agree with you that most of the claims regarding adverse

effects of Benicar, upon further investigation, really lacked

substance. I've always looked at every angle to be absolutely sure of

what the truth is about various theories and in fact have taken some

heat for being too impartial, but my (quietly) searching all sides of

an issue has actually strengthened my sureness that the science the

protocol is based on is dead on. My pouring through pieces of the

biochemistry in recent months helped me to understand on increasingly

deeper levels why it works. The bacteria are not only utilizing but

manufacturing more of our naturally occuring nutrients and hormones

for their own survival, and Benicar works by blocking the AT II Type

1 receptor, thus denying them one primary pathway through wich they

continue to fuel this process via our cytokines.

I did alot of reading the past few months on how different types of

bacteria operate, especially when they adapt to living inside

macrophages, and what I discovered is that although there is a

paucity of direct prior references to how Benicar works against

bacteria, there is quite alot of information about how bacteria

sustain themselves inside the body, adapt and use cell surface

proteins and various substrates to their advantage. One can then

infer certain core principles from this literature about Benicar's

ability to inhibit protein transcription. This is what has to be done

with a discovery so new. You won't find a big smoking gun; any one

study which says " Aha! Here is my proof! " but instead small parts of

supporting material contained in many studies.

Where things went wrong in people's understanding of Benicar was

mostly in the lack of precendent data (pre-MP). Lack of earlier data

got translated into an assumption of dangerousness, when in fact the

literature couldn't confirm or deny any such thing. The drug was too

new to have any information one way or another on long-term effects.

Although the Japanese study Ken cited stated Benicar reduced

Aldosterone levels at one year, some patients just ran with that and

failed to take note that the authors didn't ever say they felt it

lowered levels too much to be safe. What they heard instead was alarm

bells going off and at that point considered this

information " evidence " that the drug was dangerous to PWCs. Then

there was the skewed poll being circulated which listed the MP as

last in effectiveness playing on people's fears subliminally. (Of

course those who had positive experiences were not wanted as

participants, and votes were removed). These kinds of maneuvors stand

in the way of objective and fair evaluation by patients and in my

opinion should be strongly discouraged.

As a result there was a panic created which spread and was

catastrophized based purely on a kind of free-flowing mistrust, and

people got their belief (or lack thereof) in the man confused with

their belief in the science. I realize it takes an incredible amount

of inner strength and resources for most people to keep those two

issues seperate because patients often can't help but act on their

emotions, even if subconsciously. Intrinsically we want and expect

the messenger of some groundbreaking medical discovery to be

selfless, benevolent, kind, and one who cares about us as people, to

know that we are not just a number or a disposable " subject " to him.

That is deeply imbedded in our culture. We have grown up with images

of doctors and scientists as these almost God-like philanthropists

whose sole purpose in life is to help us, and it is disappointing to

find that these people don't always fit that stereotype.

I have felt the pull myself at times to reject the whole package

because of hurt feelings or my inability to live with the dichotomy

that is inherent in this treatment choice. Sometimes it is quite a

bitter pill to swallow because of such a strong association, but I

remind myself every day of where I was before I decided to do this,

how much my health has improved, and how much better I'm functioning.

No matter how deeply my feelings have been hurt (yes, me too), I

refuse to let that hurt dictate my healthcare decisions because to do

so would be self-destructive.

I have come to the conclusion that there are some scientists and

doctors who are just not capable of sustaining human connection and

empathy and they can only do one thing.

Hopefully that those patients who feel slighted can hang onto the

science as that one thing that they benefitted from if nothing else,

however dry, impersonal, or unemotional it might seem. We may not get

to choose who discovers what will make us better, but we can choose

to do whatever it takes to get well.

You make a very good point that people here subject themselves to all

kinds of possible risks with numerous other treatments, yet we don't

hear those treatments being so cynically scrutinized. I don't see

near as much energy being expended in disproving those treatments as

focused on the MP meds and lifestyle changes. There is definitely a

double-standard being applied and I thank you for having the

integrity as site administrator to point that out.

Sincerely,

Pippit

> I'm not sure how this study is relevant to PWC in general?

>

> Regarding the objective of the study: As far as I know, the makers

> of ARBs have never promoted the drugs for high risk heart patients.

> They're only supposed to be used to lower bp in people with

> moderately high blood pressure. Not people with very high bp who

are

> considered at " high risk " for MI or death.

>

> I'm also curious about the earlier statement that was made

regarding

> the risks of ARBs. Is there new information? I know a lot of claims

> have been made without any scientific evidence to support those

> claims. My own experience has been just the opposite of those

> claims. i.e. My alderesterone, kidneys and liver all are fine

> according to tests. My b vitamins are pretty much where they've

> always been since I started testing. In fact, I'm depleted in fewer

> of the Bs now, than I've been in the past. I've been on an ARB

> (benicar), for over a year with no apparent side effects (except

for

> fatigue and dizziness during the first few weeks adjusting to the

> high doses of the drug) and no lessening of symptom relief over a

> year later. As a matter of fact, my kidneys and liver are looking

> better than ever. Sure, it's 'possible' that there's some kind of

> unseen damage being done, but that's purely speculation, since

tests

> do not bear this out.

>

> I know that many of us have concerns about the person who

introduced

> the ARBS as a part of a certain controversial protocol, but for

some

> people the benefits of the ARB are quite extraordinary, and I'd

hate

> to see these drugs not given a fair and objective chance if they

can

> potentially help a lot of people, as they've helped me.

>

> We take risks with lots of commonly prescribed drugs. Antibiotics,

> anti-fungals, blood thinners, pain killers, anti-depressants, anti-

> inflammatories, anti-seizure meds, migraine meds, anti-malarials,

> anti-parsitics, among others. These drugs are known to have risks,

> and yet we decide that the calculated risks are worth the results.

>

> It makes sense to warn people of the known risks of a drug. For

> instance, warnings about the tendon risk of chloroquinolone drugs,

> like Cipro and Levaquin, is sensible, since this risk is proven.

>

> Trying to objectively analyze a protocol, where it holds up and

> where it doesn't makes sense. Speculation on potential risks makes

> sense too, if there's some indication that the risk may be real.

But

> we need to be careful that we don't cause alarm by suggesting risk

> that is based on nothing more than our own personal beliefs or

bias.

>

> Unfortunately, I do think this has happened to a certain degree

with

> ARBs and Benicar. It would be really terrible if some people's

> personal distaste for a particular creator of a certain protocol

> prevented further research into a potentially helpful drug.

>

> penny

[Guest guest]

Hi Pippit,

I think you make some good points.

But it also needs to be recognized that the credibility problem

started with the originator of the protocol, because discussion was

constantly being censored, and negative reports were continuously

deleted or derided.

In my own case, an unsuccessful attempt to sue me was made over

postings made by various individuals on a public discussion forum,

as well as private email concerns I had written to another moderator

which were shared with the plaintiff. The suit was dismissed, but

the person behind the protocol still managed to manipulate the

system to get the discussion group shut down.

This kind of overreaction is unheard of in the scientific or medical

world. How many times do you hear of doctors suing patients? Let

alone chiming into public discussions to defend their positions, no

matter how annoying those patients or forum participants may be? How

many scientists do you know of who try to control every bit of

information around their research once it's been made public?

The problem we have here is that it's now very difficult to

objectively evaluate the integrity of a protocol when there's a

strong public perception that doubts the integrity of the originator.

As a result, we are distracted from our purpose by discussions that

easily deteriorate into emotional brawls based on personal

grievances or biases.

I'd very much like to be able to objectively discuss these drugs,

but due to the problem outlined above, discussion HAS to be

independent of the particular protocol in question. Other protocols

are fine to discuss, because trained scientists in the field don't

overreact to discussion.

It's pretty sad, because these tactics of squashing discussion and

criticism may have won a battle for the originator, --basically no

one discusses the protocol openly anymore, but in the long term, the

credibility of the protocol was seriously damaged due to a huge

backlash against those very tactics.

In the meantime, I think it would be great if you would post any

studies (that are peer reviewed in major medical journals) or other

information you've found that on these drugs or combinations of

drugs. This is the kind of objective stuff we need to be looking at.

Not self published or self referenced material.

penny

" granulomabuster " <pippit@b...> wrote:

> Hi Penny,

> As another patient who does well on Benicar I feel the same way;

> I would hate to see people not give it a chance because of their

> personal feelings towards the protocol's originator....

> ...As a result there was a panic created which spread and was

> catastrophized based purely on a kind of free-flowing mistrust,

and people got their belief (or lack thereof) in the man confused

with their belief in the science....

.... Intrinsically we want and expect the messenger of some

groundbreaking medical discovery to be selfless, benevolent, kind,

and one who cares about us as people, to know that we are not just a

number or a disposable " subject " to him....

....and it is disappointing to find that these people don't always

fit that stereotype.

>

> I have felt the pull myself at times to reject the whole package

> because of hurt feelings or my inability to live with the

dichotomy that is inherent in this treatment choice. Sometimes it

is quite a bitter pill to swallow because of such a strong

association, but I remind myself every day of where I was before I

decided to do this, how much my health has improved, and how much

better I'm functioning.

No matter how deeply my feelings have been hurt (yes, me too), I

> refuse to let that hurt dictate my healthcare decisions because to

do so would be self-destructive.

>

> I have come to the conclusion that there are some scientists and

> doctors who are just not capable of sustaining human connection

and empathy and they can only do one thing.

>

> Hopefully that those patients who feel slighted can hang onto the

> science as that one thing that they benefitted from if nothing

else, however dry, impersonal, or unemotional it might seem. We may

not get to choose who discovers what will make us better, but we can

choose to do whatever it takes to get well.

>

>

> Pippit

[Guest guest]

Pippet,

This post and your next one are

two of the best I have ever seen.

Thank you.

Roy

> > I'm not sure how this study is relevant to PWC in general?

> >

> > Regarding the objective of the study: As far as I know, the

makers

> > of ARBs have never promoted the drugs for high risk heart

patients.

> > They're only supposed to be used to lower bp in people with

> > moderately high blood pressure. Not people with very high bp who

> are

> > considered at " high risk " for MI or death.

> >

> > I'm also curious about the earlier statement that was made

> regarding

> > the risks of ARBs. Is there new information? I know a lot of

claims

> > have been made without any scientific evidence to support those

> > claims. My own experience has been just the opposite of those

> > claims. i.e. My alderesterone, kidneys and liver all are fine

> > according to tests. My b vitamins are pretty much where they've

> > always been since I started testing. In fact, I'm depleted in

fewer

> > of the Bs now, than I've been in the past. I've been on an ARB

> > (benicar), for over a year with no apparent side effects (except

> for

> > fatigue and dizziness during the first few weeks adjusting to the

> > high doses of the drug) and no lessening of symptom relief over a

> > year later. As a matter of fact, my kidneys and liver are looking

> > better than ever. Sure, it's 'possible' that there's some kind of

> > unseen damage being done, but that's purely speculation, since

> tests

> > do not bear this out.

> >

> > I know that many of us have concerns about the person who

> introduced

> > the ARBS as a part of a certain controversial protocol, but for

> some

> > people the benefits of the ARB are quite extraordinary, and I'd

> hate

> > to see these drugs not given a fair and objective chance if they

> can

> > potentially help a lot of people, as they've helped me.

> >

> > We take risks with lots of commonly prescribed drugs.

Antibiotics,

> > anti-fungals, blood thinners, pain killers, anti-depressants,

anti-

> > inflammatories, anti-seizure meds, migraine meds, anti-malarials,

> > anti-parsitics, among others. These drugs are known to have

risks,

> > and yet we decide that the calculated risks are worth the results.

> >

> > It makes sense to warn people of the known risks of a drug. For

> > instance, warnings about the tendon risk of chloroquinolone

drugs,

> > like Cipro and Levaquin, is sensible, since this risk is proven.

> >

> > Trying to objectively analyze a protocol, where it holds up and

> > where it doesn't makes sense. Speculation on potential risks

makes

> > sense too, if there's some indication that the risk may be real.

> But

> > we need to be careful that we don't cause alarm by suggesting

risk

> > that is based on nothing more than our own personal beliefs or

> bias.

> >

> > Unfortunately, I do think this has happened to a certain degree

> with

> > ARBs and Benicar. It would be really terrible if some people's

> > personal distaste for a particular creator of a certain protocol

> > prevented further research into a potentially helpful drug.

> >

> > penny