In one of your posts on this thread, you shared that you follow a very comprehensive program and that this(benecar, ect.) is the missing part.

Would you mind sharing what your program entails...its possible that what you are doing "combined" with Marshalls protocol is whats helping and not just Marshalls protocol....

Marnie, magnesium depletion does *not* cause all the symptoms of this chronic infection.

You asked how symptoms can come and go quickly and how this ties into pain from inflammation.

The magnitude of inflammation can change rapidly. And the severity has to build up to a certain threshold level before you have pain - and then it can subside somewhat, pain may subside - the inflammation may below the threshold for pain - but still there.

Think of the inflammation that causes hardening of the arteries - you don't feel that untill it's almost too late.

But inflame a nerve ending - and you know about that pain right away.

Barb

It may cause some initial dizziness but as you get well, that resolves and the hypoperfusion begins to improve.

My peripheral perfusion has dramatically improved in only 3 days.

Benicar can be used in cases of hypotension.

You are correct...we are going to have to educate our MDs so they know this is safe to do. They are ignorant about this.

Help them help us!

Scott

Scrambled said, Some of us have neurally mediated hypotension (NMH). This is very common in CFS, and is also seen in lyme, according to Dr. B's guidelines. We get light-headed after standing, tachacardia, increased thirst. Some of us drink salt water/electrolyte mixtures to keep our blood pressure up. I even infuse fluids IV.

Surely this drug would be contraindicated for those of us with this problem. In any case, I don't think my doctor would prescribe a drug to lower my blood pressure when it is already low, I am light headed, and asking for IV fluids.>

I refer you to my Lyme report posted in the files section of Eurolyme group:
http://health.groups.yahoo.com/group/EuroLyme/

I include some of my regimen in there...I need to update this info...it changes so quickly it's hard to keep up with.

Scott

quote:

---

Originally posted by Byron2:
Scott...

In one of your posts on this thread, you shared that you follow a very comprehensive program and that this(benecar, ect.) is the missing part.

Would you mind sharing what your program entails...its possible that what you are doing "combined" with Marshalls protocol is whats helping and not just Marshalls protocol....

Thanks,
Byron

---

Marshall's program advises to use just BENICAR without the added diuretic.

quote:

---

Originally posted by bpeck:
J123:

You asked how symptoms can come and go quickly and how this ties into pain from inflammation.

The magnitude of inflammation can change rapidly. And the severity has to build up to a certain threshold level before you have pain - and then it can subside somewhat, pain may subside - the inflammation may below the threshold for pain - but still there.

Think of the inflammation that causes hardening of the arteries - you don't feel that untill it's almost too late.

But inflame a nerve ending - and you know about that pain right away.

Barb

---

I still don't understand. What causes the inflammation to be reduced below the threshold? It seems once the cascade starts and the trigger remains in place that the cascade will continue or worsen, but in fact it improves. (Compare it to sarc.)
Does pain caused by hardening of the arteries improve without treatment? Why does a trigger mess up the cascade one day and not the next? Something is causing the cascade to be interrupted (I'm glad it is). It's been my belief that it may have to do with borrelia activity in our cells. Is it possible that the cascade only occurs when borrelia divide? Could that correlate to migrating symptoms - depending on which population is dividing (brain, joints, muscle,etc)?

1) When I first got lyme, I did a ton of research (I even tried hyperbaric within the first few weeks, and had meningeal/neck pain after a hyperbaric session that indicated to me that the antibiotics were not effectively penetrating my CNS and it had already disseminated within just 2 weeks). That first summer I had a ton of inflammatory symptoms particular muscle pain, fibro etc all over. I tried questran at one point but did not know about sugar-free compounded questran so all I had available to me was the questran that contains sugar. Within an hour of my first dose of questran my pain magically went away. Now remember, I wasin the acute stages of early infection. I tried to continue the questran but the sugar present in it exacerbated yeast problems making bladder pain and problems etc so I went off.

2) Rosanne, and James JOhnson, and others who got well on ICHT saw their symptoms miraculously resolve after a few weeks of treatment. What does this say? That the entire inflammatory cascade can be effectively reversed within weeks if the infection itself is eradicated.

Therefore, though I am interested in symptomatic treatments, I am of two minds about the idea that the immune system has gone kaflooey and needs to be reigned in. Maybei t really does and this is an effective approach--there are many roads to Rome.

This is body chemistry. Everything is always in flux (the state of change within certain parameters).

Without a (bio) Chemistry background, I know it's going to be hard to understand some of this stuff.
Inflammation comes in many flavors.

What we are talking about here is chronic inflammation and the chemicals ( damaging oxygen free radicals, and other damaging chemicals) produced once it gets started.

Once these chemicals reach certain threholds- pain is usually produced ( and tissue damage can occur without the pain).

You ask " What causes an increase or decrease of inflammation"

That can be MANY things - every thing we put into our bodys affects the body. That's why there are so many ALT.MED remedies that DO work - they modulate chronic inflammation -
certain events/foods drugs exacerbate inflammation or dampen it depending on what's going on at the cellular level....
tissue type and individual immune system function also play a role in how these drug work.

Barb

Barb

I think you're very right to stress this, infectious and inflammatory processes are very complex, so many factors interacting! That's why I tend to be a bit cautious when people claim that "this is the answer and it is SIMPLE".

I know this is not going to help much, I truly hope this Benicar stuff is part of the answer for some of us at least.

And I hope it IS a free lunch!!

Once you get the epiphany of Dr. Marshall's discovery, it makes the complex problem much more simple to understand.

Actually, Benicar is a relatively simple way of stopping this problem.

It simply blocks angiotensin II type I receptors. This blockade stops the self-propelled inflammatory cascade from continuing.

I don't know what's so difficult to understand about that...aren't I being clear?

Don't make this harder than it really is.

The reason things appear complex is because folks don't have a good understanding of them.

When you really understand it well, you can simplify it.

This will help all of us...not just some!

We've been burned so many times with false hope.

Please comfort your skepticism and allow yourself to have some hope, at least one more time...because I'm confident that this is not a false hope.

I have a strong background in medicine, immunology and other sciences. I've studied this well and have a strong knowledge of this disease.

I'm sharing my investigations with LLMDs and helping them learn more.

I don't post messages on this site that I don't have good understanding about.

What's my incentive to give false hope...I won't do that to the people suffering with this disease!

I have never boasted on this site about any therapy as the potential cure...until now!

I'm delighted to be able to say, with confidence, that this protocol is the cure we've been looking for.

We all have a bright future again...

Thank God!

I haven't seen you talk about the dosing schedule he uses for abx, and whether it makes sense for Lyme.

I understand that the Benicar, by reducing inflammation, is supposed to make the abx more effective. I see that Marshall believes his entire protocol, exactly as it is, will be effective for Lyme. What do you think?

Barb, I've seen parts of your protocol, and I know you did nort follow Marshall's to the letter. What are the reasons you deviated, once you understood what he was doing?

Do you believe his protocol would be effective, or have thoughts on how it needs to be different for Lyme?

I've given my LLMD a copy of Marshall's articles, so hope to hear something of what he thinks, as well. I'll share that when I hear from him.

The effect of angiotensin II on platelet intracellular free magnesium and calcium ionic concentrations in essential hypertension.

Touyz RM, Schiffrin EL.

Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada.

OBJECTIVE: To assess the effects of angiotensin II on intracellular free Mg2+ and Ca2+ concentrations in platelets from normotensive and hypertensive subjects.

DESIGN AND METHODS: Seventeen normotensive, 25 untreated hypertensive and 18 treated hypertensive patients were studied. Intracellular Mg2+ concentrations were measured with the fluorescent dye mag-fura-2-acetyoxymethylester (AM) and intracellular Ca2+ concentrations with the fluorescent dye fura-2AM under basal conditions and after stimulation by angiotensin II, saralasin (angiotensin II antagonist), arginine vasopressin and endothelin-1.

The effects of increased extracellular Mg2+ concentrations on intracellular Mg2+ and Ca2+ concentrations were also determined.

RESULTS: The intracellular basal Ca2+ concentration was significantly higher in the untreated hypertensives compared with the normotensives and treated hypertensive subjects (150 +/- 14 nmol/l versus 120 +/- 17 nmol/l for normotensives and 124 +/- 8 nmol/l for treated hypertensives).

The basal intracellular Mg2+ concentration was significantly lower in the untreated hypertensive compared to the normotensive and treated hypertensive groups (0.37 +/- 0.08 mumol/l versus 0.58 +/- 0.09 mumol/l for normotensives and 0.52 +/- 0.11 mumol/l for treated hypertensives). In the hypertensive groups, inverse correlations were found between intracellular Ca2+ and intracellular Mg2+ concentrations (r = -0.44, P < 0.05) and between intracellular Mg2+ and diastolic blood pressure (r = -0.35, P < 0.05), while a positive correlation was found between intracellular Ca2+ and systolic blood pressure (r = 0.41, P < 0.05).

Exposure of the platelets to 1 nmol/l angiotensin II significantly increased intracellular Ca2+ and significantly decreased intracellular Mg2+ concentrations in all three groups. The angiotensin II-evoked effect on intracellular Ca2+ was exaggerated in the untreated hypertensives and blunted in the treated patients (basal versus stimulated: 150 +/- 14 versus 217 +/- 20 nmol/l in untreated hypertensives; 124 +/- 8 versus 140 +/- 10 nmol/l in treated hypertensives).

Saralasin (0.1 mumol/l) abolished the effects of angiotensin. Arginine vasopressin (1 mumol/l) increased the intracellular Ca2+ concentration, whereas endothelin-1 (1 nmol/l) had no significant effect on either intracellular Ca2+ or intracellular Mg2+.

Increasing extracellular Mg2+ concentrations led to significant reductions in intracellular Ca2+ concentrations in all groups and a significant elevation of the intracellular Mg2+ concentration in the untreated hypertensive patients only.

CONCLUSIONS: These data demonstrate a relationship between angiotensin II and intracellular magnesium and calcium. In hypertension, angiotensin II-stimulated calcium responses may be related to simultaneously decreased intracellular magnesium concentrations.

Q: I haven't seen you talk about the dosing schedule he uses for abx, and whether it makes sense for Lyme.

A: I am taking low-dose mino with the Benicar. I'll add azithromycin later and then maybe cotrimoxazole at some point...I don't know for sure yet.

Marshall's abx protocol makes perfect sense when you understand the pathogenesis of this disease.

Remember the BLPs (bacterial lipoproteins)in my study on pathogenesis....they trigger this whole disease...I had already figured out that the best abx protocol for us was low-doses of bacterial protein synthesis inhibitors...ie, tetracyclines, macrolides, co-trimoxazoles.

These all inhibit the pathogens ability to make BLPs...which trigger the inflammation and disease. So, I agree with Marshall use of low-dose bacteriostatic abx.

Q: I understand that the Benicar, by reducing inflammation, is supposed to make the abx more effective. I see that Marshall believes his entire protocol, exactly as it is, will be effective for Lyme. What do you think?

A: Yes, it should be very effective for chronic borreliosis...I also use a lot of alternative and supportive therapy, but this is a major part of what I believe is the best conventional therapy.

I appreciate your trust...

I read the sarcinfo website and everything Dr Trevor Marshall a few months ago and I think I understand what he and you are saying.
It is just that you make certain leaps of faith that I am not prepared to make like being sure that there is no brain infection in Lyme (only BLPs and toxins that give us our brain symptoms), and I would like to be surer of this before I embark on taking a sartan-type drug to block inflammation

you write:

>It simply blocks angiotensin II type I >receptors. This blockade stops the self->propelled inflammatory cascade from >continuing.

>I don't know what's so difficult to >understand about that...aren't I being >clear?
Nothing hard to understand there, that is simple, I got that much from Dr Trevor Marshall ages ago,and you are prbbly quite right that such inflam cascades are taking place in PWLyme and causing symptoms.

My questions are:
What proof do you have that it is the main or even only process that is at play in the pathogenesis of our illness?
Do you have proof that these inflammatory cascades (triggered by BLPs) are JUST having deleterious effects (eg could we imagine that the cascade of cytokine is in fact play a part in keeping bugs in check, and that we might fare badly in the medium term without these cascades?

I know you seem very sure of yourself, but I, in the past heard exact same discourses re cortisone tx. I was mad not to take it, it was going to stop all my symptoms.

My other question is; HOW CAN YOU BE SURE THAT SOME OF US DO NOT ACTUALLY HAVE INFECTION IN THE BRAIN THAT WOULD NOT GET BETTER ON 25 mg OF MINOCYCLINE EVERY SECOND DAY! even with Benicar.

I have asked you this question several times but got no answer

Can you tell me this because I am very sick and I can fool around with new fads?

What you are writing might be enough for some people but I want more specific reasoning and data that clearly says: your symptoms that quack like brain infection are not really brain infection symptoms!

I will then gladly drop my highish dose abx and hit the Benicar and be happy ever after.

Nelly

PS does it work for other bugs? Have you looked into the pathogenesis of other TBDs?

I so appreciate your sharing this encouraging protocol. I'm going to talk to my doctor about it next week.

Do you think it will be a problem that I'm already on the low dose minocin? Will I have to stop, or can I just add the Benicar?

I'd also be interested in hearing your complete protocol.

I'm overly tired at the moment and having difficulty organizing the info, especially in a way that would make most sense to my doctor. What would you recommend would be the best information to take him, so that he can easily and quickly understand the protocol and the rationale behind it?

thanks,

Have you talked to Dr. C about any of this? Do you plan to?

You have done so much for the Lyme Community and Dr. C is one of the best LLMD's around - so I'm hoping you'll share this with him.

1) All drugs have side effects. No drug is simply benign. There will be a bellcurve here and some people will not tolerate the drug well at all, others will do fine with it. We need to know who those subsets of people are before we start assuming it's just fine to add this in to the protocol

2) Inflammation as you point out is a two edged sword. Our body definitely uses it to wall off bugs and keep them from spreading, as well as for lots of other reasons (inflammation attracts some of the cells that then kill the bugs). OTOH, it is true that chronic inflammation is deleterious and also quite possible that certain bugs might adapt and use the inflammation to sequester themselves from appropriate abx and other anti pathogenic meds

3) Another good point--for an infection disseminated throughout the CNS, what does low dose or pulsed abx do longterm?

4) Another very good question--how does benicar work in rickettsia, babesia, bartonella, etc. Do they all produce BLP's and/or the inflammatory cascade in us is so similar in each of those chronic infections that benicar is the choice?

I am not intending to do anything more than ask questions, as I usually do. I guess I will try to find some answers. It looks like this might be a very useful drug to add into the armementarium, like others; some find heparin helps, others find plaquenil helps, etc etc.

Perhaps it's even useful to help someone through a particular bad herx rather than being used daily longterm.

I discovered Trevor's Sarcinfo board
when I was about half way through my 1.5 years off and on abx for Lyme.

My Doc & I had already designed my protocol
(for Lyme) starting with *lower* doses of abx and pulsing them, then ramping them up to theraputic doses based on my body weight because my herxes were so bad ( and I had a ton of neuro symptoms).
My Abx were chosen by their tissue penetrating ability - working up to the drugs that penetrated better because we belived my Lyme bacterial load was SO high I couldn't withstand the better penetrating drugs to start with.

I started with DOxy and worked **up** to Mino. The additional drugs I used (Bactrim and Zith) to pulse in combo with Mino were the ones the MP recommended - But I had already researched them, and everything I seemed to be doing just FIT with what the Sarc people were doing (albiet not exactly).

I didn't need any convincing that inflammation played a big part in my on- going symptoms, and for years used ALT.MED and other therapies to try and dampen inflammation.

I was also already on very high doses ibuprofen as an anti-inflammatory because I already knew I was loaded with inflammation
with high COX2 production.
(I have pathology reports on tissues taken from my 3 major surgeries over a 20 year period).

After participating in the Sarclist - and realizing how much overlap of symptoms there was between Lupus, Sarc and Lyme - I starting thinking the MP protocol could work for Lymies for whom symptoms persisted after
long-term abx, and that inflammation control was the key. On several occassions I refered Lymenet to the Sarinfo list.

The information Trevor had on excess Vit D production in the body exacerbating and perpetuating inflammation made sense to me because I *had* UV sensitivities in the past.

I did not use Benicar, but had I found Sarc info earlier, I would have used it...
and in the future - if I have symptoms return I will use it. (I'm still feeling great - no symptoms)

IMO, A Late stage Lymie's protocol based on Trevor's protocol may have to be tweaked - because by the time most long term Lymies find the Marshall protocol, their GI tracts are messed up from high dose long term abx...

So I dearly wanted a LLMD to talk to Trevor. I STILL want a reputable LLMD to talk to Trevor.

I know you guys know how MUCH I stressed
controlling the herx in Lyme (and NOT toughing through it).
This is one area where the Marshall protocol is so different than a Lyme protocol:
The Marshall protocol, puts a inflammatory blockage in place before abx, controls the HERX which controlls additional inflammation, which allows the body and the abx to be more efficient.

Control of inflammation is paramount.

Barb

I just touched a little on this Sat at our meeting...that was when you left to get your wife.

Yes, this will help the myriad of symptoms we deal with...and likely MCS too.

I agree with you that ALL lyme is NeuroLyme
and at least for the untreated - bacteria is **IN** the brain.

Symptoms are not just from inflammation - but more inflammation just makes everything worse... then you get sertain cells perpetuating more inflammation and it can be never ending for some people.

I know in my case I could not have tolerated Mino right out of the chute.
And I've told Trevor that.

I've already told ya'll I have a Lyme friend that had seizures from too fast a Lyme kill in the brain...

Thanks for the replies. I especially appreciate Barb's willingness to go into some of the details.

As they say, the devil is in the details.

I wonder how it could be worked if someone is already doing well on high dose abx. Would just adding in Benicar cause more intense herxing, because the abx would be more effective? Or would it simply keep the inflammation levels lowered?

I'm also interested in how this works in the CNS. And what about if someone is responding to a cephlasporin? Would that work with Benicar?

I know T. Marshall is very adament that ONLY his protocol works for everybody. Maybe he's right, but the truth is, nobody knows yet.

As I said, I've already given some of the sarcinfo to my LLMD. Unfortunately, he's not one of the biggies, so he may not have much influence. On the other hand, he is very open to new information, and is likely to give it a trial if he feels it is valid.

Q: My questions are:
What proof do you have that it is the main or even only process that is at play in the pathogenesis of our illness?

A: It's not the only process that is causing pathology, but it appears to be the only part that is self-perpetuating.

Q: My other question is; HOW CAN YOU BE SURE THAT SOME OF US DO NOT ACTUALLY HAVE INFECTION IN THE BRAIN THAT WOULD NOT GET BETTER ON 25 mg OF MINOCYCLINE EVERY SECOND DAY! even with Benicar.

A: I'm not sure... I'm not taking 25 mg ever other day...I'm taking 100 mg of mino every day. Benicar has the ability to modulate the immune system so it is able kill the infection much better and it also improves the ability of abx to kill pathogens...according to Dr. Marshall.

Q: Can you tell me this because I am very sick and I can fool around with new fads?

A: I'm asking you to trust me...this is no fad! I know many that read this information are very ill and suffer greatly. I have no incentive to give any of them false hope...why would I do such a cruel thing?

Q: does it work for other bugs? Have you looked into the pathogenesis of other TBDs?

A: it works well for all CWD pathogens, and likely many more. It's ideal for the chronic bacterial infections like borreliosis.

Q: Do you think it will be a problem that I'm already on the low dose minocin? Will I have to stop, or can I just add the Benicar?

A: Just add the Benicar along with the mino.

Q: I'd also be interested in hearing your complete protocol.

A: See my report on Eurolyme

Q: What would you recommend would be the best information to take him, so that he can easily and quickly understand the protocol and the rationale behind it?

A: This will be the toughest part for most of us. We'll need to give our LLMDs some information. Take Dr. Marshall's protocols with you. You can also have them contact him or me.

Q: Have you talked to Dr. C about any of this? Do you plan to?

A: I called him today...he's very excited about this new development. I've forwarded Dr. Marshall's protocol to him...please encourage him to investigate this with me more...we need all the help we can get.

Thank you Julie...I appreciate your encouragement.

Barb>

Exactly! Barb...

And without angiotensin II receptor blockade...there is no relief from this perpetual inflammatory cascade.

We have to stop pouring gas on the fire before we can put it out.

Scott

[This message has been edited by bpeck (edited 29 April 2004).][/B][/QUOTE]

Q: I wonder how it could be worked if someone is already doing well on high dose abx. Would just adding in Benicar cause more intense herxing, because the abx would be more effective? Or would it simply keep the inflammation levels lowered?

A: If you can already tolerate high doses of abx, you'll likely tolerate high doses of Benicar well and you'll likely have great results with it.

Q: I'm also interested in how this works in the CNS.

A: Benicar is great for symptoms of neuroborreliosis.

Q: And what about if someone is responding to a cephlasporin? Would that work with Benicar?

A: It's important to use bacteriostatic abx such as the tetracyclines, macrolides and cotrimoxazoles.

How would you know that?

And: If you can already tolerate high doses of abx, you'll likely tolerate high doses of Benicar well

How would you know that and what possible connection could there be between tolerating a drug that lowers blood pressure, and tolerating antibiotics?

Also the: I am asking you to trust me...

These are people on the internet whom you don't know personally and you are not a physician. Thank goodness you are adding in to your posts that they should bring Marhsall's material to their LLMD's. Let experienced doctors decide how and when and on whom to experiment with this protocol.

I have some time myself so I will put these questions to Marshall myself. I don't believe he could/would say the things being said on this thread, since he has little experience with lyme and limited if successful experience in sarcoidosis.

Try to temper your enthusiasm with a bit of caution, please. As Lisa who is a nurse pointed out on the other thread, she has seen benicar's side effects and would not give it to her children (advocating this drug for children before even seeing how it fares in adult lyme patients seems somewhat reckless to me.)

I stand firmly by my statements!

Q: IE this appears to be the only part of the inflammatory process that is self-perpetuating...

How would you know that?

A: Dr. Marshall's work clearly indicates this.

Q: And: If you can already tolerate high doses of abx, you'll likely tolerate high doses of Benicar well

How would you know that and what possible connection could there be between tolerating a drug that lowers blood pressure, and tolerating antibiotics?

A: It has to do with bacterial load and the body's tolerance to the BLPs being released. If you can already tolerate high doses of abx, you will be able to handle Benicar very well...and like me, will probably notice benefits with the first dose.

Q: Also the: I am asking you to trust me...

These are people on the internet whom you don't know personally and you are not a physician. Thank goodness you are adding in to your posts that they should bring Marhsall's material to their LLMD's. Let experienced doctors decide how and when and on whom to experiment with this protocol.

A: This group knows my work...they understand that I have an extremely strong medical background and that I have spent an enormous amount of time investigating the pathogenesis of this disease. I correspond with many of them via email.

I am teaching the LLMDs about my work by sharing this info with them.

Q: I have some time myself so I will put these questions to Marshall myself. I don't believe he could/would say the things being said on this thread, since he has little experience with lyme and limited if successful experience in sarcoidosis.

A: Good, for I know he'll echo my statements.

Q: Try to temper your enthusiasm with a bit of caution, please.

A: When in my opinion, the cure for our disease has been discovered, why are asking me to temper my enthusiasm?

Q: As Lisa who is a nurse pointed out on the other thread, she has seen benicar's side effects and would not give it to her children (advocating this drug for children before even seeing how it fares in adult lyme patients seems somewhat reckless to me.)

A: I disagree with Lisa and I'm not reckless...I'm knowledgable and confident!

Scott

Just a little history about Sarcoidosis
and the abx/Benicar therapy some are using.
I think there's about 100 people doing the "field trial" of abx, or abx and Benicar.
And a Very very large percent of those people
are ALOT better (go read the posts on Sarc info).

And these aren't just internet stories:
Their disease improvement can be documented with lung Xrays, and lung function.

Their blood is documented periodically as most of them (during flares) are lymphopenic (as I was) indicating supression of that class of cells.

AND, almost all have have documentation of the ratio between Vit D, and 1,25D dropping as their symptoms subside.

Whether the bugs infecting them are also some of the (co)infections infecting a Lymie, remains to be proven - but it's plausible that there the same (meaning CWD
variants of some species).

Secondly, the Sarc people have it pretty bad, as all the Sarc Docs in the US think it's autoimmune, and thats THAT. If any DOcs read the resarch and
admit there's been a CWD bacteria found in any biopsies - then it's handled like "post Lyme Syndrome".. the immune system gone awry.
They are conventional Docs afterall, and constrained by their training and their job description for the public.

Plus most people with Sarc have to wean off predisone, which isn't an easy task.

In my opinion, from what I've seen of the Lyme community and how the disease is treated - the inflammation part of the picture is not addressed, or given the significance it should be.. especially when it's even more elevated while herxing.

Also in my opinion, no ones really looking for the reason why a certain percentage of Lymies just don't respond to abx or can't get off them. I think this might be because the abx can't work because the inflammation is so high in these people... this is the connection I see

So- rather than argue about this - I'd like to see some of the LLMDs really take a look at what's working for these Sarc people.

In the mean time - as always- we all have to decide what we'll take or not take depending on the risks as we see them.

Barb

riversinger,

I don't think that's an accurate characterization of Dr. Marshall's position. He claims that his protocol is optimal for sarcoidosis. That's not saying much. The standard of care for sarcoidosis is prednisone. This drug has serious side effects and suppresses the immune system in a global sort of way. If the antigen that incites granuloma formation in sarcoidosis is, in fact, a microbe, then it is wreckless to give the microbe free reign through the use of prednisone. Merely telling sarcoid patients to get off prednisone would be enought to make Dr. Marshall's protocol superior to the standard of care.

This business about vitamin D dysregulation needs to be put in perspective. Originally, Dr. Marshall had nothing to do with showing this effect in sarcoidosis. There is complete consensus about the vitamin D dysregulation in sarcoidosis. Dr. Marshall's observation (concerning vitamin D) was more modest than that. He reasoned that, given the unregulated conversion of 25(D) to 1,25(D) in sarcoidosis, the best laboratory marker of the disease might be the ratio of 25(D) to 1,25(D). His work at SarcInfo bears this out. Dr. Marshall is a very sharp guy, but the D-ratio business is not the evidence of that. His D-ratio merely shows that he can do arithmetic, while his colleagues are sleepwalking.

What one wants to do then is individual, I think. What percentage of sarc individuals Marshall is treating are doing mino alone, and what percentage have added in benicar? Maybe that's on his website..I only recall that 50 had been treated (not 100)...and a reference to a pubmed abstract on mino that showed it helped at least some cases, although not all...it was a small study.

Walt Tarello, an italian DVM, has done some really good research into the infectious nature of CFS.

And it's animals that are often used for research. I don't think DVM's should be underestimated at all. Hey they were treating ulcers in pigs far before humans had the same treatment opportunities.

I'm very grateful to Scott, a DVM and medical researcher, for sharing his impressions and enthusiasm here with us about this protocol. And it's so encouraging that he's seeing such immediate effects, and understands the mechanisms behind it.

This week is the first week I've felt truly optimistic in a while. And that's because this is making sense, in my own realm of experience.

Thank you for those kind words of support, sometimes I wonder if I'm posting to the right group...I appreciate the support.

I'd really rather be golfing or fishing instead of doing this work...but I am compelled to help others.

After suffering with this disease, it was a clear calling to me that I am in need to help those suffering with this illness.

So, I try to help,

quote:

---

Originally posted by phage:
>I know T. Marshall is very adament that ONLY his protocol works for everybody. Maybe he's right, but the truth is, nobody knows yet.

riversinger,

I don't think that's an accurate characterization of Dr. Marshall's position. He claims that his protocol is optimal for sarcoidosis.

---

Phage,

I've been reading the sarcinfo site, and Trevor Marshall states very clearly in numerous places that his protocol is correct for Lyme as well as sarcoidosis. I actually searched for any reference to Lyme in particular.

He is in fact quite sharp in correcting people. I can understand, he has worked hard to establish this, and is concerned about what will happen if people try all kinds of variations.

He also may very well be right. We just don't have the documentation yet on the results in Lyme, so I am trying to understand the rationale that makes it a reasonable assumption.

I'm reading Marshall's papers, but they are technical, and it takes time for me to understand them.

I personally think it would make sense to do his entire protocol, which includes measuring the markers he uses to show inflammation, and then response to medication.

That is part of how we would know if it is applicable to Lyme.

But I am also trying to understand things like when and why it makes sense to take lower doses of abx. I know that he says it is to keep the herx, and thereby the inflammation down.

But if someone is already doing well on high dose abx, does that mean the conditions don't apply? That they have inflammation going on that is not noticed? That there is a different kind of infection being treated?

You ARE posting to the right place.

Please keep doing so.

I don't post on my experience with Rife very often since it doesn't involve jugs full of ABX and often turns into a bash-a-thon.

However, it has helped us immensely, and my wife has not required ABX for a year and remains remarkably symptom-free.

Please be assured that many are following this Benicar thread with great interest.

Let's keep spreading and sharing the information and let the results do the talking.

Dave

You got 90+ posts on just this one thread. Most are queries into this protocol. Looks like a number of us will be testing for D1,25. I hope people report their results. Sounds like you are on the right forum to me

I know you from this and other forums, and I believe you when you say you are on a mission to help people.

That's hard to say if the zestril has helped relieve your inflammation of the joints or not...it sure can't hurt.

Yes, Benicar helps me significantly with my neuro symptoms...yes, inflammation is causing these too.

Also, I have had my D tested:
D, 1,25 Dihydroxy 39.7 pg/ml (8-52)
D, 5 Hydroxy 26.5 ng/ml ( 8.9-46.7)

These were both within normal as was my D ratio (1.5)

So I don't know what to make of this. I did have a granuloma, I definately have numbness, tingling, neuropathy, jerks and twitches, arthralgias......and the list goes on. So given all this do you think Lyme or Sarcoidosis? Do I stay on DOxy which seems to be helping or switch to the Marshall protocol? Hard decision.

But I did see enough to feel compelled to just say thank you for sharing this, Scott..

and thank you to all who are contributing objectively to this discussion.

Alot of value here..

If your D test results are accurate, and
If you have only been symptomatic since the fall of 2003 - it is quite possible that you do not fall in the category of "chronically inflammed".

This doesn't mean that you won't have symptoms from an infection with Lyme (or something else)

Since you do not have a diganosis yet,
It's important to stay focussed on the good results your having with Doxy..
If you're seeing results, stay on the Doxy, and discuss all this info at your next appt. with your Dr.

You are the first person I know of to report D1,25 test results on Lymenet since this Marshall protocol was suggested (maybe I missed other posts). It is interesting that you were normal, when it sounds like you would have been a good candidate for abnormal values.

If you already have all these symptoms and the symptoms were caused by the inflammatory cascade, I don't understand why it matters 'how long' you have had it. Maybe Barb will explain more.

I have had my ACE vaues taken in the past -
(but I'd have to look them up to see what they were) . But ACE is not the same as the
D value measurement (and subsequent ratio).

And as a matter of interest, I came within a hare's breath of being diagnosed with Sarc, as I had the symptoms, high ANA, Sed rate, Uveitis...and sun sensitivity.

I haven't seen any data on the D ratio from Lyme patients - anywhere - even in the literature. That data from Lymies would be interesting.

Barb

It only makes sense to me that if people with lyme disease want to try the protocol that it would be best to follow the protocol that he put together, starting with the testing...

The testing would be revealing, especially if it coincided with marshall's results and if it didn't that would also give pause and give valuable information as well...perhaps data that Marshall would find useful in his research with lyme.

By posting the results it would help get a clearer picture of what is going on...

By the way, insurance probably won't cover the tests unless you have osteo problems or bp problems...the tests run about 180-250 dollars.

Byron

Any Dr. should know that if the D ratio is whacked - then osteopenia (OR worse osteoporosis) is the result because calcium is not utilized properly.

If that's suspected, then insurance should cover it, if that's why the test is ordered.

And that shouldnt make any diference as far as gender goes.