oops! Lymetutu
I'm writing to tell you of a possible cure for chronic lyme. I've been sick for over 25 years. Nobody is more skeptical of people claiming to have a cure than me. You have nothing to lose by checking this out. Technically it is not a cure. It controls the symptoms.
Dr. David Moskowitz at Genomedics in St. Louis has the answers. I will let him speak for himself concerning theories, etc. But it has to do with immunity, receptors and inflammation. The drug is an ACE inhibitor. It is labelled for treating high blood pressure. It's inexpensive and safe.
I started taking cozaar about one month ago. At first I didn't think it was working, but after 2 weeks it was like a miracle. Now I'm pain free. Muscles relaxed. Skin conditions cleared up. My mouth had been unsymmetrical for 25 years - it is now symmetrical. The trigeminal neuralgia is gone. Fibromyalgia is gone. Fatigue is gone. I had ached for years. The aching is gone. I'm still having headaches, but they have improved. Many other symptoms have cleared up.
Please - write to Dr. Moskowitz. [email protected] or go to his website at www. genomedics.com
Give it a try. He will work with your local doctor. Don't quit for a month. I want to read about other patients results with cozaar.
Good luck,
A 25 year lyme patient
I hope you've had lengthy treatment with antibiotics also.
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oops!
Lymetutu
[This message has been edited by Lymetoo (edited 25 April 2004).]
quote:
Originally posted by Lymetoo:
Sounds interesting. I'm a skeptic until I check it out! Just wondering though, how much does this drug lower the BP?? Mine is already too low.I hope you've had lengthy treatment with antibiotics also.
Yes, I've had lengthy antibiotics. 13 months and just quit.
My blood pressure is on the low side. I don't get dizzy, but it does drop at times. It's a small price to pay. Take it at bedtime. Take smaller doses, etc.
quote:
Originally posted by Lymelighter:
What did "cozaar" cost you, or was it given as part of a clinical trial and thus gratis?
I had free samples for the first month. I just filled a Rx and it cost $59.39 (without insurance) for a 2 month supply.
The sarcoidosis patients there use mainly Benicar. They use it to relieve symptoms generally, but with a focus on preventing the misery of herx.
You started feeling better two weeks ago and subsequently quit antibiotics? If you were miserable three weeks ago from a Lyme infection, why would you quit antibiotics now? The ACE inhibitors don't kill bacteria.
I'm thinking about testing this approach to relieve symptoms, but I don't see how this would negate the need for antibiotics.
Your testimony is greatly appreciated. I was on the fence about trying ARBs, but now I think I will.
quote:
Originally posted by phage:
The use of ACE inhibitors for controlling inflammation is also described at length at www.sarcinfo.comThe sarcoidosis patients there use mainly Benicar. They use it to relieve symptoms generally, but with a focus on preventing the misery of herx.
You started feeling better two weeks ago and subsequently quit antibiotics? If you were miserable three weeks ago from a Lyme infection, why would you quit antibiotics now? The ACE inhibitors don't kill bacteria.
I'm thinking about testing this approach to relieve symptoms, but I don't see how this would negate the need for antibiotics.
Your testimony is greatly appreciated. I was on the fence about trying ARBs, but now I think I will.
I wanted Dr. Moskowitz to speak for himself about his theory, but I will say this:
He believes certain disease organisms make us sick, but don't cause the damage we see in West Nile and others (lyme?). These organisms cause over reaction of the immune system. Whereas, all the other doctors are trying to kill the organism he is trying to turn off the over reactive immune system.
I quit the antibiotics because they were not helping and it's not good to be on them forever. It was time to go another route. I do believe (but have no proof) that it is good to try to kill the spirochete first. But nobody knows if and when the antibiotics kill the very last trace of spirochetes in lyme patients. The debate will go on and on.
quote:
Originally posted by Lymelighter:
Perhaps this is a question for Dr. M: Cozaar and "Ace inhibitors" have been around for awhile. Does this company have a novel protocol with Cozaar for Lyme, or is it simply a new off-label use for an "old" drug?
Dr. M has a for profit research business. At this time he is not charging for the trials. He is testing cozaar on a wide variety of diseases. Lyme wasn't on the list, but I wrote to him and asked him to try it on me. He is very interested. He wants the patent for using cozaar to treat these diseases. But first he has to have the data to support his claim.
It is an off-label use of cozaar at this time. Cozaar has been around for a long time.
I'm not selling anything. Dr. M is not selling anything.
Dr. Moskowitz IS selling something. He hopes to eventually market the use of ACE inhibitors for a profit. Nothing inherently wrong with that, but I have a few concerns. His site says:
"GenoMed invites physicians to join its Clinical Outcomes Improvement NetworkTM in order to bring the latest in genomics-based medicine to your patients. Of the $800 annual subscription fee paid by your patient to belong to GenoMed's COIPTM, the physician is paid $200 in exchange for managing the patient and updating GenoMed on the patient's clinical course. Thus, a physician with 1,000 hypertensive or diabetic patients in his/her panel could earn an extra $200,000 annually while delivering superior outpatient preventive care."
Apparently, the "Clinical Outcomes Improvement Program" (a term that is actually trademarked) is not a formal clinical trial. Will the patients who purchase this membership first be informed that their own physicians are receiving a financial incentive for promoting the therapy? There is a conflict in such a patient/physician relationship that I doubt will be made transparent. Will the "clinical outcomes" be reported in an unbiased way?
Might he eventually promote this therapy for "post-lyme" symptoms to the exclusion of antibiotics? The last thing we need is a company with a financial interest in rejecting evidence of chronic lyme infection.
It turns out that ACE inhibitors and ARBs are separate classes of drugs that nonetheless achieve similar anti-inflammatory effects. I checked Dr. Moskowitz's patent applications and it appears that he claims a right to the use of ARBs only when combined with the ACE inhibitors. But the people at www.sarcinfo.com use the ARBs quite successfully without combining them with the ACE inhibitors. So why would anyone pay Dr. Moskowitz's licensees' for the privilege of using ACE or ACE+ARB when ARBs alone will work?
The mere discussion here of the possible use of ARBs for Lyme should constitute "public disclosure" and should therefore preclude any right to patent the use of ARBs for Lyme. I'm therefore uncomfortable with the prospect of a company with the incentive to marginalize the evidence that ARBs may be an effective surrogate for ACE inhibitors.
If you want info on this from people who in fact have no financial incentives, see www.sarcinfo.com They explain the rationale behind this approach in much greater depth than you will find at Dr. Moskowitz's web site.
quote:
Originally posted by phage:
I did some snooping.Dr. Moskowitz IS selling something. He hopes to eventually market the use of ACE inhibitors for a profit. Nothing inherently wrong with that, but I have a few concerns. His site says:
"GenoMed invites physicians to join its Clinical Outcomes Improvement NetworkTM in order to bring the latest in genomics-based medicine to your patients. Of the $800 annual subscription fee paid by your patient to belong to GenoMed's COIPTM, the physician is paid $200 in exchange for managing the patient and updating GenoMed on the patient's clinical course. Thus, a physician with 1,000 hypertensive or diabetic patients in his/her panel could earn an extra $200,000 annually while delivering superior outpatient preventive care."
Apparently, the "Clinical Outcomes Improvement Program" (a term that is actually trademarked) is not a formal clinical trial. Will the patients who purchase this membership first be informed that their own physicians are receiving a financial incentive for promoting the therapy? There is a conflict in such a patient/physician relationship that I doubt will be made transparent. Will the "clinical outcomes" be reported in an unbiased way?
Might he eventually promote this therapy for "post-lyme" symptoms to the exclusion of antibiotics? The last thing we need is a company with a financial interest in rejecting evidence of chronic lyme infection.
It turns out that ACE inhibitors and ARBs are separate classes of drugs that nonetheless achieve similar anti-inflammatory effects. I checked Dr. Moskowitz's patent applications and it appears that he claims a right to the use of ARBs only when combined with the ACE inhibitors. But the people at www.sarcinfo.com use the ARBs quite successfully without combining them with the ACE inhibitors. So why would anyone pay Dr. Moskowitz's licensees' for the privilege of using ACE or ACE+ARB when ARBs alone will work?
The mere discussion here of the possible use of ARBs for Lyme should constitute "public disclosure" and should therefore preclude any right to patent the use of ARBs for Lyme. I'm therefore uncomfortable with the prospect of a company with the incentive to marginalize the evidence that ARBs may be an effective surrogate for ACE inhibitors.
If you want info on this from people who in fact have no financial incentives, see www.sarcinfo.com They explain the rationale behind this approach in much greater depth than you will find at Dr. Moskowitz's web site.
Being skeptical is one thing. But you are way beyond skeptical. I was very clear that Dr. M is in this for a profit. But that profit comes in the future. Someone will patent the protocol and someone will become wealthy. Sorry - capitalism thrives.
Every doctor in the world is trying to make a profit. You won't find the details at his website. He will be publishing results (not lyme) soon. The section you read about costs is not what I experienced. Those are for other trials.
I have paid nothing to Dr. M for this treatment. My local doctor has paid nothing to Dr. M. I have paid for a Rx at a local drug store. Which is a lot cheaper than antibiotics. I have been so sick for so many years I don't care who profits as long as they make me well.
All I tried to do was relate my experience to this group. I don't care if you believe my story. I'm sure there are some in this group who will try to verify my results. And I wish them success. I wish you the best of luck with the sarcinfo group.
I do believe your story, which is why I said I intend on trying the approach.
My post was not an attack on your character or motives. It questioned the ethics of this company if in fact it is paying kickbacks to physicians without the knowledge of patients. That's not capitalism, that's a breach of the patient/physician relationship. It's also indicative of what Lyme patients may expect in the future if they ever gain this company's attention in a big way. My concern about their financial incentives is a possible FUTURE incentive for downplaying the need to treat the infection with antibiotics.
I also wanted to make clear that there is a better source of info (not necessarily more valid, just much more in-depth) than Dr. Moskowitz's site. If people want to understand the rationale behind the approach they can learn much more about it at SarcInfo. I was also pointing out that should this company ever market ACE inhibitors to Lyme patients (in the future), ARBs may be a cheaper surrogate since it doesn't look like ARBs will be patented for this. It's just a heads-up.
I'm on your side.
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oops!
Lymetutu
I did go to sarcinfo and skimmed the article. Very promising and is the same idea.
I don't think we can stop the way medicine is chasing after protocol patents.
To read an interview with Dr. M go to http://www.immunesupport.com/library/showarticle.cfm/id/5007
There is also an article (will have to search for it) about how he quit the VA clinic because the feds were cutting off the ACE Rxs for his patients (kidney patients). They relapsed without the drug.
quote:
Originally posted by Lymetoo:
j123, if you've had Lyme for 25 yrs and you've only been on abx for 13 months, then you'd be VERY fortunate to be able to stop them now. If/when those symptoms return, be sure to get right back on the abx!
Maybe the goal isn't to kill the spirochete. Maybe the spirochete messed up our immune systems. Antibiotics never cured me. If my symptoms returned I don't think antibiotics would help me.
I got Lyme after that, and I've been taking abx for l4 months, so if Cozaar does what this doc projects it will do for Lyme, I can expect to be "cured".
I'm for it! I can say that Cozaar does keep blood pressure in range. Good drug.
I hope this doc is right.
lifeline
quote:So what would you do, then? Sorry, I don't mean to be the Devil's Advocate...just haven't heard of anyone being cured after 25 yrs of Lyme and 13 months of abx. Call me jealous! I hope you remain WELL!
Originally posted by J123:
If my symptoms returned I don't think antibiotics would help me.
------------------
oops!
Lymetutu
[This message has been edited by Lymetoo (edited 25 April 2004).]
I agree with you completely.
Dr. (PHD) Trevor Marshall (www.sarcinfo.com)
suffered with Sar for decades.
His abx protocol coupled with the ARB (Benicar) has helped many people who have Sarc. There has been a pathogen(s) discovered in people with Sarc (and some test
+ for Lyme). It works in conjunction with the abx (and reduces the pain -inflammation- from a herx).
Dr. Marshall has published his protocol, and sells ** no ** products. Sarcinfo is helping
people educate themselves, theirr Drs (who are willing to listen) and these people are improving.
As I have said many times before ad nauseum - the overlap of symptoms between Sarc and Lyme are quite amazing.
The information (about Benicar) is getting out there though - and I will not be surprised if eventually the LLMDs incorporate it in their therapy.
Barb
[This message has been edited by free2reckon (edited 13 May 2004).]
quote:So what would you do, then? Sorry, I don't mean to be the Devil's Advocate...just haven't heard of anyone being cured after 25 yrs of Lyme and 13 months of abx. Call me jealous! I hope you remain WELL!
Originally posted by Lymetoo:
[QUOTE]Originally posted by J123:
[b] If my symptoms returned I don't think antibiotics would help me.
[/B][/QUOTE]
Thank You. If the symptoms return I'll do what I've always done. Pray for a cure. 6 weeks ago I was so sick and so tired of hurting I was hoping to die. All the other medications in the past did little to help me.
We need a break through and this may be it.
It may well control the symptoms, but be aware of the "side effects".
Before you make a decision to try a drug be sure to understand the risks/complications that may be involved.
This is not unlike knowing if you chose to use abx, the importance of adding probiotics. Learn all you can before making a decision.
A brief search re: ACE inhibitors follows:
In addition, some ACE inhibitors are used to treat congestive heart failure or may be used for other conditions as determined by your doctor.
The exact way that these medicines work is not known. They block an enzyme in the body that is necessary to produce a substance that causes blood vessels to tighten.
Other medical problems-- The presence of other medical problems may affect the use of the ACE inhibitors. Make sure you tell your doctor if you have any other medical problems, especially:
Diabetes mellitus (sugar diabetes)--Increased risk of potassium levels in the body becoming too high, or increased effect of insulin on control of blood sugar
Heart or blood vessel disease or
Low sodium diet--Lowering blood pressure may make problems resulting from these conditions worse
Kidney disease or
Liver disease--ACE inhibitors' effects may be increased because of slower removal of medicine from the body
Kidney transplant--Increased risk of kidney disease caused by ACE inhibitors
Systemic lupus erythematosus (SLE)--Increased risk of blood problems caused by ACE inhibitors
Previous reaction to any ACE inhibitor or previous occurrence involving hoarseness; swelling of face, mouth, hands, or feet; or sudden trouble in breathing--Reaction is more likely to occur again
What are the side effects of ACE inhibitors?
ACE inhibitors are relatively well-tolerated by most individuals. Nevertheless, they are not free of side effects, and some patients should not use ACE inhibitors. ACE inhibitors usually are not prescribed for pregnant patients because they may cause birth defects.
Individuals with severe kidney problems and people who have had a severe reaction to ACE inhibitors probably should avoid them. The most common side effects are cough, elevated blood potassium levels, low blood pressure, dizziness, headache, drowsiness, weakness, abnormal taste (metallic or salty taste), and rash.
It may take up to a month for coughing to subside, and if one ACE inhibitor causes cough it is likely that the others will too. The most serious, but rare, side effects of ACE inhibitors are kidney failure, allergic reactions, a decrease in white blood cells, and swelling of tissues (angioedema).
With which drugs do ACE inhibitors interact?
ACE inhibitors have few interactions with other drugs. Since ACE inhibitors may increase blood levels of potassium, the use of potassium supplements, salt substitutes (which often contain potassium), or other drugs that increase the body's potassium may result in excessive blood potassium levels.
ACE inhibitors also may increase the blood concentration of lithium (Eskalith) and lead to an increase in side effects from lithium. There have been reports that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDS) such as ibuprofen, indomethacin, and naproxen may reduce the effects of ACE inhibitors; however, there is no conclusive evidence that this interaction, if it exists, is important."
Just a "heads up".
It may well control the symptoms, but be aware of the "side effects".
Before you make a decision to try a drug be sure to understand the risks/complications that may be involved.
You are right. Everyone should be aware of the dangers of every medication.
Many of the diseases in your list are the very diseases that ACE inhibitors help. Look at the research.
Once again, my symptoms were becoming intolerable and I'd rather reach for a cure even if there are risks involved. Some of you have not had chronic lyme for many years. For those of you who have not experienced enough lyme misery - you will as the years go by. Chronic lyme only gets worse.
This drug has been used on millions of patients with few serious problems. There are various ACE inhibitors. The new ones have fewer side effects.
I've been talking to Dr. Trevor Marshal this past week.
Folks, IMO, this is vital information and extremely important work.
I am extremely impress with Dr. Marshall and his sarcoidosis work.
To Scott and Barb,
Keep up the good work. Keep posting info on Dr. Marshall and sarcoidosis.
I will be totally honest about my cozaar results. Last night I had a muscle cramp in my leg. But I still feel good - no fatigue, no aching, etc. My symptoms always had a vague "cycle". It's almost like the symptoms try to break thru when I would be due for another bout, but for the most part don't. Maybe more needs to be learned about dose and timing...
I'm sure some are saying "I knew the symptoms would return". Remember, this is not a cure. Whatever causes the symptoms (spirochete, toxins, autoimmunity, etc) is still there. If I get 90% control of symptoms I'm thrilled...
[This message has been edited by free2reckon (edited 13 May 2004).]
(angiotensin-converting enzyme inhibitor , drug used to reduce elevated blood pressure (see hypertension ), to treat congestive heart failure , and to alleviate strain on hearts damaged as a result of a heart attack (see infarction ). ACE inhibitors block production of an enzyme that helps convert the protein angiotensin 1 into angiotensin 2, a protein that makes blood vessels constrict and promotes retention of fluid, raising blood pressure. Thus ACE inhibitors act to widen the blood vessels and make it easier for the heart to pump blood through the body. captopril (Capoten), ramipril (Altace), and enalapril (Vasotec) are commonly used ACE inhibitors. Angiotensin receptor blockers (ARBs), such as losartan (Cozaar) and valsartan (Diovan), reduce hypertension by displacing angiotensin 2 from receptors on the surface of cells. ARBs are used as alternatives to the less expensive ACE inhibitors because they have fewer side effects.
From:
Columbia Encyclopedia, Sixth Edition, Copyright (c) 2004.
I apologize - cozaar is an ARB.
background info on ACE inhibitors (and ARBs)
[This message has been edited by free2reckon (edited 13 May 2004).]
[This message has been edited by free2reckon (edited 13 May 2004).]
[This message has been edited by free2reckon (edited 13 May 2004).]
>As I have said many times before ad nauseum - the overlap of symptoms between Sarc and Lyme are quite amazing.
It's hard to believe it when you read it. Some of the posts at SarcInfo look like they've be cut from Lymenet and pasted into the sarcinfo forum, and vice versa.
Scott said:
>So, the puzzle is coming together and I'm am very excited for all of us.
In trying to uncover the source of my misery I spent some time reviewing the information at SarcInfo and was very excited because it explained so much. Still, there were pieces missing. I then got mired down in a CFS/FM forum before dontlikeliver finally went there and clued me in to Lyme. Together lymenet and sarcinfo gave me, I think, the whole picture.
J123,
If you look at the "Problems w/ Sunlight" thread you'll see that only 3 days ago Barb raised the issue of SarcInfo and I said I would like to know if Lymies would respond well to ARBs. Voila!--2 days later, here you were testifying to their effectiveness. I never doubted your story. It's unfortunate that antibiotics have failed you. If memory serves, Dr. Marshall has said that about 5% of sarcoiders are not helped by antibiotics until they have the ARB in place. This may or may not apply to you but it's worth investigating. In either case, suggesting that active Borrelia infection can be left unchecked by antibiotics is alarming. Perhaps Lymies can live a long, symptom-free life with only an ARB, but it sounds risky and many here may have unfairly dismissed your testimony as soon as they read the speculation that antibiotics may not be necessary. I believe that Lymies will be vastly more receptive to SarcInfo than to Genomedics because SarcInfo uses ARBs with antibiotics, not in lieu of them. Please keep us updated on your experience with ARBs.
>As I have said many times before ad nauseum - the overlap of symptoms between Sarc and Lyme are quite amazing.
I spent some time studying Dr. Marshall's paper "New Treatments Emerge as Sarcoidosis Yields Up its Secrets". It's an excellent paper.
First, even though lyme and sarc share many symptoms I believe they are different diseases. The SarcInfo FAQs states that once-a-day dosing of Benicar will make sarc symptoms worse. In my case I was using cozaar once per day and my symptoms improved dramatically. Thus I don't have sarc. I was also taking Zithromax and had no herx at that time.
Secondly, Dr. Marshall's Angiotensin Hypothesis is great work. Follow the pathway and you end up with a cascade of cytokines (which are known to cause inflammation). In the case of sarcoidosis the culprit seems to be Gamma Interferon. I'm speculating that lyme damage involves the same pathway, but another cytokine is involved. For ARBs to control symptoms in a wide variety of diseases (as is being reported) something in general is shared by all these diseases. The key could be A-II binding at receptors. Why are some diseases controlled with once-a-day dosing but others require 4 doses per day? Is Benicar that different from Cozaar? I don't think we are at the point of predicting which brand will work best, but I'll be the first to switch if Benicar is superior.
As to antibiotics. I was on IV rocephin for 10 weeks, followed by Doxy and Zithromax for an additional 12 months. If spirochetes are capable of forming alternate forms(as reported), we really don't know how to kill them. I never said I don't believe in antibiotics. I said they didn't cure me. Certainly I had enough antibiotics to have knocked the spirochetal population in body down and I should have felt much better until the population built back up. Since sarccoidosis is triggered or caused by different bacteria than lyme my statements do not apply to any disease other than lyme. There is so much variation in borrelia that my statements may only apply to my case. In the case of lyme I think a lot has to do with the timing. How long a person is infected prior to treatment is relevant. It may also have to do with genetics, both human and borrelia variation. Let's not forget the possibility of toxins. Maybe ARBs will control lyme without antibiotics. Time will tell.
I do have some relevant observations to relate concerning my experience on cozaar. I'll write later. It will deal with the 6-8 hour dosing issue.
For all of you who want to take antibiotics - do it. Everyone should make their own decisions. Please post the results. If you discover a cure and it's an antibiotic I'll take it and thank you from the bottom of my heart.
Go for it. Try an ARB.
quote:
Originally posted by lymerx:
This discussion is very interesting. I have been taking zestril (an ace inhibitor) for 10 years now for HBP. I have had lyme for 4 years. I have taken antibiotics the whole time (also herbs and rife for 3 months). I had some joint pain early on but it subsided and left me with neuro symptoms and sinus symptoms. I wonder if the fact that I have been taking low doses of the ace inhibitor drug for HBP all this time may have been a help, may have limited my inflammatory symptoms. Any ideas? lymerx
This is good information. Can you tell us the dose - timing, # per day? What are your specific symptoms?
[This message has been edited by J123 (edited 26 April 2004).]
In answer to your question, I take 12 mgs of zestoretic (zestril with a diuretic) once a day. That's a small dose. 4 years ago I got the bite and the bullseye rash and a diagnosis of lyme. At that time I had some toe pain, leg weakness, depression, panic attacks, hip pain, eye symptoms, and sinus symptoms. After 6 months the toe pain left, and the weakness, and the depression, but I was left with sinus and eye dryness, and some pain in my spine. This is passing now that I have been using rife and magnetic pulsing and samento along with bicillin and zithromax. I'm 90% better. And all through this I have done that little bit of zestril or zestoretic. I do wonder if that has kept my joint pain to a minimum. thanks for asking, lymerx
25 mg once per day
No change in symptoms the first 6 days
Day 7-10 - much better, slight fatigue, some aching, ear ringing (it's normal for me to be slightly better some days - so I didn't consider this a cozaar effect)
Day 11- worse; fibromyalgia spots, ache, bad ear ringing, neck pain with headache, fatigue; symptoms worse at certain times of day (for days 7-11); realized cozaar effects may last only about 8 hours - made a mental note to pay attention to time of symptoms
Day 12 - woke with no pain (very unusual); took cozaar 9 am; 11 hours later I started aching; how do I test this idea that it lasts only 8 hours? (talking to myself)Decided to take the dose at a different time of day to see if the symptoms were delayed by an equal amount of time. And the answer is yes.
Day 13 - extreme aching started in evening (about 12 hours after dose) couldn't sleep at all
Day 14- aching even after cozaar, but much worse after 10 hours. Ready to give up on cozaar!!
Day 15 - Much better; slight SOB, slight headache; 12 hours after cozaar upper back/chest muscles pulling
Day 16 - ear ringing; good day; 8 hours after cozaar muscles pulling; many muscles cramping; getting fibromyalgia like spot in left upper arm and shoulder blade.
Day 17 - woke with muscles hurting, etc bad headache after taking cozaar; ear ringing 10 hours after cozaar; In the past fibromyalgia spots would last 3+ days.
Day 18-20 - Same, but less intense symptoms
Day 21 - Very Good day; little pain; no SOB; slight headache in evening
Day 22 - Great day
Day 23 - Great day
Day 24 - noticed skin conditions are clearing up; patches of pimple like bumps are going away after years; my red, ugly, dirty elbows are even a little better (I've spent hours scrubbing them in the past); red tough patches on my ankles are normal looking again; leathery skin over areas of muscle loss are softer;
woke a little achy; Good day until 11 hours after cozaar- upper back pulling a little.
Day 25 - woke pain free; headache after cozaar; otherwise good
Day 26 - woke slightly cramped; felt good rest of day - have energy (very unusual), thinking better, no SOB, no fatigue, no pain; Was good in evening also
Day 27 - Fair day - some slight problems. Worked outside in hot sun (the sunny SE) and wasn't worn out. (That has never happened). Now I'm thinking maybe 2 doses per day would be better. I asked for medical advice and was told that there may not be a dose effect. I decided to try anyway and started with 25 mg morning and about 12 mg 12 hours later. Wanted to make sure it didn't drop my bp too much.
Day 28 - woke pain free (normally after working outside I'd hurt for days). Neck muscles tight, legs slight ache, but fair day
Day 29 - no pain; didn't take evening cozaar
Day 30 - L ear ringing; Great day - I mopped, vacuumed, cooked with no pain, no fatigue, no ache. Amazing - I haven't been able to be this active in years.
Day 31 - fibromyalgia trying to develop but never did. Good day
Day 32 - lower leg cramp, but only one. In the past I'd have cramp after cramp. Good day - no pain, no SOB or fatigue, have energy
Day 33 - another leg cramp; It's like the symptoms are trying to break thru but they aren't able to. Good day; lots of energy; no fatigue; no ache
Day 34 - good day; still going strong after working a 5 hour shift, working around house and being up 14 hours. (Ok - so I sat at the computer for 3 hours).
______
What have I learned?
1) It took a long time for it to kick in. You may have better results with ARBs if you follow Dr. Marshall's 3-4 doses per day protocol.
2) I don't think it lasts over 8-12 hours in the beginning at least. I have a lot to learn about dose.
3) It has not affected my headaches. Maybe they are less intense and maybe with more time they will clear up. I should mention that I have MS-like lesions in my brain.
4) Whatever you do - follow your doctor's advice
5) I hope some of you will work out the dose and timing issue. I had no one as a role model. The more who try ARBs and post results the more reliable the info becomes. We need others...
>In answer to your question, I take 12 mgs of zestoretic (zestril with a diuretic) once a day.
Maybe you should ask your doctor if you could take a larger dose, or two divided doses. Or maybe try the newer ARBs - but if the ACE works why change a good thing...what you are doing is working for you! I think the ACE inhibitor may have played a role.
The Sarclist posted the molecular diagrams a while back.
If the molecule is different, then it will probably latch on to receptors differently
than others. So while these are all ARBS they all aren't created equal.
Benicar is also taken slightly differently when used in conjunction with abx (as compared to being taken just for BP).
If any one on a BP med is thinking of switching to Benicar as a trial (to see if it alleviates lyme symptom inflammation )- please contact Trevor Marshsll first, and have him consult with your Doc. as dosage and timing of dose is important.
Barb
I even did 4.5 months of IV Rocephin 2gms daily and about 6 months of Flagyl included in the many abx I have tried.
The is a very interesting subject and we all need to familarize ourselves with this information.
I will be studying up on this and see if it is something that might be good for me. Especially, if this is something without narcotics, and it is, that will work for my severe and chronic pain.
Again, Thanks and I look forward to reading more about this...to google I go.
Rosemary
Benicar has a mechanism by which inflammation is reduced, thereby allowing the immune system (and abx) to be more effective on the bugs, and the mucoid (or non mucoid) films they create around themselves.
The other BIG misunderstanding, is how the hormone 1,25-D (the component of the Vit D metabolism) works in the the body.
In the inflammation pathway of chronic disease, this hormone (1,25-D) is thought to be manufactured (nor only by UV exposure) but also by inflammation itself in certain cells and organs (like the kidney).
Take a look at the site listed below... it may read over your heads, but it's worth a read anyway.
This is a complicated subject, and alot of Drs. don't understand it - so don't feel bad if it's confusing.
Basically - Trevor Marshall is saying - reduce the inflammation the correct way (by limiting the over production of certain inflammatory hormones) and the abx will be able to work better to kill the pathjogen, and so will your immune system.
http://www.joimr.org/phorum/read.php?f=2&i=38&t=38
Http:// www.chestjournal.org/cgi/eletters/123/1/18
http://
clinmed.netprints.org/cgi/content/full/2003010001
http://
biochemistry.ucr.edu/faculty/norman.html
Barb
[This message has been edited by bpeck (edited 27 April 2004).]
http://flash.lymenet.org/ubb/Forum1/HTML/024816.html
I have a few questions, as I have started reading over the site and do not fully understand all the connections yet, but they are as follows:
1) A friend's son developed sarcoidosis some years ago, they spent summers on shelter island and even tho they religiously did tick checks i now wonder if he had a manifestation of lyme or rickettsia. Anyway, he took Hoxsey's formula and got well and has been well ever since. I want to go look at Hoxsey's formula agian, it's usually used for cancer, but it has powerful detox mechanisms. I'd like for us all to try and figure out why different methods of detox are working and what they might share in common. That would include herbs as in Hoxseys' formula. My reasoning is even though apparently you can take these arbs with low blood pressure, some people with lyme apparently have really bad neurally mediated hypotension...we don't know how this would affect them. Though there is overlap in the 2 diseases...they are not the same in most cases
2) WHy would Patricia Kane's therapy be working well in some cases--how does THAT therapy get rid of BLP's, as it apparently must be doing, and if Scott is talking to these doctors, does he mind asking them about that? Can we figure out how different approaches are affecting the same pathway? Is there any way to replicate Kane's therapy orally (seems not).
3) Why would a low-carbohydrate diet be so important? It seems to me it's not just because glucose feeds all kinds of bugs. There seems to be a more direct correlation. Can we speculate on that? How could insulin be tied in to this inflammatory pathway?
4) WHy did questran work in some? Did it just bind the BLP's? If so why didn't it work in all? Why did some get worse on questran?
5) WHy does bee venom work for some? And samento? Are either of these affecting this inflammatory pathway?
6) The sunlight problem--most lymies don't have it--so I assume that active form of Vitamin D is not involved for us.
I probably shoudl've waited to post until I'd read further and understand better.
Also, I'm going to link this thread to Byron's naturalhealthcare thread, I'd like to see what he thinks.
This is good work.
quote:
Originally posted by treepatrol:
CWD forms its all LYME or cousins of it.
How do you know that?
"People who take so-called ACE-inhibitors for the treatment of high blood pressure should not take magnesium supplements. ACE-inhibitor medications tend to
***concentrate magnesium in the body***
and by taking additional magnesium you could develop problems."
www.health24.co.za/
dietnfood/What_is
_in_food/ 15-1167
-1172,13249.asp
Am J Hypertens. 1997 Feb;10(2):145-51. Related Articles, Links
The alterations in insulin sensitivity during angiotensin converting enzyme inhibitor treatment are related to changes in the calcium/magnesium balance.
Haenni A, Berglund L, Reneland R, Anderssson PE, Lind L, Lithell H.
Department of Geriatrics, Uppsala University, Sweden.
The present analysis was undertaken to investigate the relations between alterations in mineral factors, especially the balance between serum calcium and magnesium concentrations (S-Ca and S-Mg, respectively), and variables reflecting glucose and lipid metabolism during angiotensin converting enzyme (ACE) inhibitor treatment.
A total of 96 patients with essential hypertension, participating in four double-blind studies with four different ACE inhibitors and similar protocols, were included.
At the end of the initial placebo period and at the end of the period of active drug treatment, a hyperinsulinemic euglycemic clamp test was carried out, lipoprotein status was assessed, and the concentrations of serum electrolytes were measured.
The serum ACE activity was determined in the group treated with fosinopril. Changes in insulin sensitivity index (M/I) were directly correlated to alterations in S-Mg (r = 0.24, P < .02), and inversely correlated to changes in S-Ca (r = -0.19, P = .07) and the ratio between serum calcium and magnesium concentrations (Ca/Mg) (r = -0.27, P < .008). The change in total serum triglycerides (S-Tg) was inversely correlated to the change in S-Mg (r = -0.35, P < .0005), and directly correlated to the change in Ca/Mg ratio (r = 0.36, P < .0004). The reduction in serum ACE activity correlated to a more pronounced increase in S-Mg r = -0.62, P < .002), and decrease in the Ca/Mg ratio (r = 0.73, P = .0002).
We conclude that the changes in the studied metabolic variables and serum ACE activity during ACE inhibitor treatment are related to alterations in mineral status and the balance between calcium and magnesium concentrations in serum.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 9037321
www.healthy.net/scr/column.asp?ColumnId=10&ID=97
Generally speaking, the rule of thumb is: if you have high BP, you need more Mg than Ca; if you have low BP, you need more Ca than Mg. We need both.
Bb SIGNIFICANTLY lowers our Mg levels as evidenced by the recent abstract from Romania and as stated by microbiologist, Dr. Gary Kaiser.
When Mg levels are low, calcium and potassium will rise at first, but eventually these will be deficient also. You cannot hold onto Ca or K without enough Mg.
"The spectrum of magnesium activities is impressive, indeed. For instance, magnesium inhibits platelet aggregation (quite like aspirin); thins the blood (as does Coumadin); blocks calcium uptake (such as Procardia); and relaxes blood vessels (as do ACE inhibitors). Of note, magnesium increases oxygenation in the heart muscle by improving cardiac contractability. It is for this reason that it is used frequently in emergency rooms to manage atrial defibrillation."
http://www.vitaminretailer.
com/SIE/articles/
HeartHealth.htm
[This message has been edited by free2reckon (edited 13 May 2004).]
quote:http://www.joimr.org/phorum/read.php?f=2&i=38&t=38
Originally posted by J123:
How do you know that?
This is the same lady who can take blood from you and in three days tell you if you have lyme by raising spirochetes from your blood which had none in it ie (blebs,Lforms) are there they revert back to spirochetes at least thats what I make out of it. http://www.fourwinds10.com/news/06-health/B-disease/2003/06B-02-01-03-microbiologist-Mattman-closing-lab.html
SarcInfo.com - How a Pathologist can see Bacteria causing Sarcoidosis
I just spent a fascinating afternoon with Dr Alan Cantwell, one of the first to report that a special type of bacteria had been found in the tissue of sarcoidosis patients. His first paper reporting these special pleomorphic bacteria was published in 1981, and a second paper in 1982. His discovery was ignored by Pulmonologists, although a number of other physicians have continued this work, with a detailed study of 20 patients and 20 controls in 1996, which clearly implicated bacteria as a likely cause of sarcoidosis. It was a bacteria similar to Mycobacterium Tuberculosis, but with an evolutionary adaptation that allows it to live without having a cell wall.
These special bugs are called "Cell Wall Deficient Bacteria" (CWD), and they have been found not only in Sarcoidosis, but also a number of other diseases, including Crohn's disease. There is a well written description of these bacteria at 'The Lyme Alliance'.
<--- A clump of tiny, round, 'coccoid forms', resembling minute granules, is at the far left of this image of a sweat gland from the skin of a lung sarc patient.
Here are the 'rod' bacteria more commonly seen by a pathologist --->
Dr Cantwell came under intense criticism when he reported that he could also find these bacteria in cancer patients, and from that time onwards he was ostracized by many in the medical profession. Dr Lida Mattman has managed to plot a course through the medical politics, and she is still working and researching today. Dr Phyllis E Pease has also continued to publish. Dr EA Moscovic has also published about CWD in Sarcoidois.
These CWD bacteria grow very slowly. Sometimes it can take months to culture them in a lab. That is one of the reasons that the labs don't find them during their standard tests for fungi and bacteria. These CWD have also been referred to as mycoplasma, L-forms, mollicutes,and nanobacteria. Milton Wainright referred to them as 'pleomorphic' in his recent article.
Alan gave us the benefit of his decades of research on cell wall deficient bacteria, explaining how any pathologist could see them under a microscope, and which stains should be used to make the bacteria show up amongst the tissue. If you look at the two images above, on the left you have a microscope photo, at 1000 times magnification, of the tissue surrounding the sweat gland from the skin of a lung sarcoidosis patient. The orifice for the sweat gland is the large open space at the lower right, the clump of tiny bacteria (called a coccoid form) is at the middle left. Click the image for an enlarged view. It is not easy to see these bacteria, but a good pathologist should be capable of doing it.
Normally the stain would show up the bacteria as red, (like the 'bacterial rods' on the right from the University of Wisconsin). But they show up as light pink, or, as in this slide, a purplish violet (a mixture of pink and blue).
Your pathologist might even be able to find these bacteria in old biopsy slides (some hospitals keep these for years). Here is some info that will help him find these tiny bugs (include this with Doc's pathology request)
The stains that are most useful to view the bacteria are:
1. Intensified Kinyoun
2. Giemsa
3. Fite-Faraco (often used with Leprosy biopsies)
They must be viewed under oil using an "oil immersion lens" at a magnification of 1000.
There are several books that will help a pathologist recognise the cell wall deficient bacteria:
1. Mattman LH: Cell Wall Deficient Forms. ISBN 0-8493-4405-0 (info from B&N.com)
2. Domingue G: Cell Wall Deficient Bacteria. (info from Amazon)
3. Xalabarder C: Publicaciones del Instituto Antituberculoso Francisco Moragas, Caja de Pensiones Para La Vejezy de Ahorros, Paseo de San Juan, 20, Barcelona-10: "L-Forms of Mycobacteria and Chronic Nephritis". 1970
Dr Alan Cantwell's book is interesting reading, and extremely provocative. It has photographs of the sarcoidosis microbes in it.
Now of course this topic is a little more complex than I have made it sound. The University of Wisconsin has an excellent description of the importance of the cell wall to a microbe, and why certain antibiotics, such as the penicillins, attack the microbe's cell wall. Microbes that have evolved to live without a wall are immune to attack by the penicillins (but apparently not immune to Minocycline). In fact the existence of your CWD mutations may be due to the use of the Penicillins on microbes for which the Tetracyclines should have been chosen in the first place.
Additionally, species of the E-coli Bacterium, as well as the Strep bacterium, have been found in a cell-wall deficient form, not just the Mycobacteria.
Hopefully this tutorial will give you and your pathologist the information needed to verify that these microbes were in fact in YOUR biopsy tissue, and that therefore Doc had better darn well think about trying some antibiotics to get rid of them...
Click on the images to get enlarged versions.
CWD Bacteria in the connective tissue of the skin biopsy sample taken from a skin sarcoidosis patient
Culture of CWD staph bacteria from this patient (cultures of these CWD bacteria typically take months to grow)
Bacteria in the lung tissue of a patient with systemic sarcoidosis
Bacteria in a sweat gland of the skin of the same (lung sarc) patient
Culture from the second patient
The Mattman Study
Jo Anne Whitaker, M.D.,' Eleanor G. Fort, B.G., M.T.' Minter H. Dopson,'' Lida H. Mattman, Ph.D.,``Sally M. Marlowe,N.P."
'Bowen Research and Training, Tarpon Springs, FL, USA, '' Chisolm Biological Laboratory,
Aiken, SC, USA `` Nelson Medical Research, Warren, MI, USA (4) Arthritis Pain Treatment Center, Clearwater, FL, USA
INTRODUCTION
Health is a state of balance. Because humans and microbes are often competitors, interactive co-evolution has resulted in multiple and varied defense mechanisms on the part of both. The body must juggle and perform delicate balancing acts to maintain adaptive successes in spite of constantly changing life situations.
Lyme Disease (LD), Fibromyalgia (FMS), Chronic Fatigue Syndrome (CFS), Gulf War Syndrome (CWS), and many similar chronic conditions affect multiple body systems often accompanied by extreme morbidity. Laboratory diagnostic methods presently in use are often undependable. We believe The Gold Standard Culture method developed by Lida Mattman, Ph.D. is the only consistently dependable procedure for the demonstration of the spirochete, Borrelia burgdorferi (Bb), the causative agent of LD. It is becoming increasingly obvious that the plethora of multiple clinical signs and symptoms associated with LD are also common to patients with FMS, CFS, GWS, and other commonly referred to as immune diseases. Most physicians do not consider LD to be a cause of these syndromes, thus, allowing untold numbers of direly ill patients to suffer without the antibiotic treatments which will improve their clinical situation, and, in some cases, cure their disease (acute LD).
MATERIALS AND METHODS
(1) The Mattman Blood Culture Technique for identification of BB was used. Her success in producing positive cultures involved initiating growth in cell-wall deficient forms of the spirochete.
(2) LUAT (Lyme Urine Antigen Test) performed at Igenex.
(3) Peripheral Blood Smears with Giemsa Stain (4) Live cell analysis.
Results
103 subjects exhibiting clinical evidence of multiple body system involvement were studied. The Mattman Blood Culture was positive for Bb in 94 subjects. 37 subjects were tested by LUAT for Bb antigen and 19 of the 37 tested positive. Smears were done on blood taken from the subjects. There was evidence of bone marrow stimulation characterized by hypochromia, red blood cells (RBCs) inclusions (stippling or parasites) and large polychromatic RBCs Platelets and white blood cells appeared normal. Extreme fragility of RBCs was detected in many (nonspherocytic). Live Cell Analysis was also performed on the blood of the subjects and followed over 4 days ( same preparation). Upon standing, most striking was parasitization of RBCs by ring forms, and in many cases spirochetes emerging from RBCs. There existed extreme degradation of red blood cell membranes. Cystic and large L-Body forms were frequent.
Breakdown of diagnosis and the number of subjects:
Fibromyalgia - 30
Osteoarthritis - 1
Mixed Connective Tissue Disease - 3
Polymyalgia Rheumatica - 1
Ankylosing Spondylitis - 1
Lupus Erythematosus - 1
Palindromic Rheumatism - 1
Chronic Fatigue Syndrome - 8
Multiple Sclerosis - 40
Amyotrophic lateral Sclerosis - 17
DISCUSSION
When Fleming discovered the miracle drug, penicillin by mistake, he observed that it worked by altering the cell wall, thus, preventing replication. The Mattman Culture Method induces positive growth by supporting the cell-wall deficient forms. These forms are extremely stealthy in their proclivity for pleomorphism, suggesting other genera. The ambiance of their surrounding medium is probably responsible for these changes and migration to all part of the body in the interest of self-preservation. Without intact cell walls their receptors are disadvantaged.
It is essential that the "medical world" question the validity of present laboratory methods in detecting Bb and recognizes that Lyme disease, sometimes a killer but almost always a disabler, is a disease just as fearsome as "The Great Imitator", syphilis, and about to become just as widespread. Success in treating LD can best be achieved with early clinical diagnosis and the initiation of proper long-term antibiotic and antigen-specific Transfer Factor therapies. Until this is achieved, there will continue to be great cost not only to patients progressing to chronic neuroborreliosis, but also to the public health community. One of the most crucial diagnostic tools, the initiation of a trial antibiotic regimen and antigen-specific Transfer Factor therapies, and the resulting Herxheimer reaction (belived by may "Lyme Savvy" practitioners to be the best indicator of LD response) must be embraced and practiced. It is paramount to accept the fact that Lyme disease is the most common and rampant vector- borne infectious disease in the US.
Its not a far leap to think that lyme or one of it buddies is the cause of all this suffering.TBD
Heres some more. http://www.mercola.com/2001/jul/25/lyme_disease.htm
http://www.lymenet.de/mattms.htm
Update on Research Activities
Bowen Research and Training Institute, Inc. is a research facility in Palm Harbor , Florida . After finding that there were few accurate tests for Borrelia burgdorferi (Bb), researchers at Bowen Research and Training developed a new direct immunofluorescent test that identifies the Borrelia burgdorferi (Bb) antigen.
This research project has found the Bb antigen in whole blood, breast milk, amniotic fluid, placental tissue, semen, eye fluid, tooth, foot nodule, shoulder fluid, spinal fluid, finger joint fluid and African dust. This test, called the Rapid Identification of Borrelia burgdorferi (RIBb) test, looks for an antigen of the Bb spirochete. Findings are documented with digital photography.
This method of testing is of particular importance for Bb because current serology tests measure only antibody response beginning three to four (3-4) weeks following onset of active Lyme disease, whereas the antigen of Bb is present within twenty-four (24) hours of contracting the disease. In addition to the RIBb test, a buffy coat blood smear stained with Wright Giemsa is examined to identify other tick borne bacterial infections such as Human Granulocytic Ehrlichia (HGE), and Human Monocytic Ehrlichia (HME), which are seen in the white blood cells (WBC). The parasite Babesia is often seen intracellularly in the red blood cell (RBC). All three infections can be identified in the same individual.
We have now tested over 2900 specimens including over 700 very sick children from all geographic areas and, as previously described, all are positive for the Bb antigen. The RIBb test has been validated by Mattman's culture method, yielding the same results on over three hundred (300) same draw blood specimens. An independent laboratory using thirty (30) same draw blood specimens has also confirmed the RIBb test. Appropriate, specific and non-specific positive and negative controls are performed on each specimen.
We have recently developed a titration serial dilution method for quantitating the amount of Bb antigen in the blood. This may help to differentiate the carrier state from the patients with serious disease by comparing persistence of fluorescing structures. This method will also help us to determine the efficacy of antibiotic and other treatment therapies. We strongly recommend that physicians order the serial dilution RIBb test pre and post antibiotic therapy to determine the efficacy of treatment.
In 1998 Dr. Lida Mattman cultured Borrelia burgdorferi by supporting the growth of cell wall deficient organisms in 43 out of 47 blood samples from patients with the signs and symptoms of chronic Lyme disease. In that study there were 23 out of 23 negative controls in patients without signs and symptoms of Lyme disease. For the last four years Dr. Mattman has not had a negative culture for Borrelia burgdorferi. All specimens have cultured out cell wall deficient Borrelia burgdorferi organisms.
A large epidemiological study needs to be done with a sensitive specific test for Borrelia burgdorferi to help understand its many complexities.
This study should alert us that Lyme disease is a very serious problem, quite possibly the fastest growing epidemic in the world, and one that is very difficult to diagnose and treat. The RIBb test as well as the identification of the presence of other tick borne infections is vitally important so that the disease can be diagnosed early in order for treatment to be started immediately to prevent the morbidity of chronic Lyme disease and other tick borne diseases.
Jo Anne Whitaker, M.D.
That should keep ya busy 
TNF alpha is not all "bad":
Thus, one mechanism of action of TNF-alpha, SMase, and ceramide on thyroid FRTL-5 cells is to INHIBIT CALCIUM ENTRY.
PMID: 10092616
"We wanted to know if TNF-alpha was regulating the number of receptors on the cell surface," Bresnahan explained. "If the number of receptors increased, and if there was glutamate nearby to bind to them, that would allow more calcium into the cells, killing them."
Experiments at the Stanford lab were able to show that controlling the presence or activity of TNF-alpha had a direct relationship to the numbers of glutamate receptors on the cell surface and therefore on the amount of synaptic transmission.
"This showed that TNF-alpha, this cytokine that is supposed to come from the immune system and not have a role in transmitting information,
is actually a potent modulator of neurotransmitter interaction,"
Beattie said.
hdlighthouse.org/see/immune/tnf.htm
Through their ability to induce TNF production by macrophages, spirochete lipoproteins may play important roles in the development of the local inflammatory changes and the systemic manifestations that characterize syphilis and Lyme disease.
PMID: 1890308
Naturally...if Mg is "unavailable" the first thing to happen is Ca will try to go into the cells. The body tries to stop this. Ca levels rise, histamine kicks in, etc.
Need to get to the ROOT of the problem. Bb depletes a LOT of Mg. Restore the balance and maintain it so own healthy antibodies can do the job.
There is risk of cyst formation when Bb is in a nutrient deficient environment:
Cystic forms of Borrelia burgdorferi sensu lato: induction, development, and the role of RpoS.
Murgia R, Piazzetta C, Cinco M.
Dipartimento di Scienze Biomediche, sez. Microbiologia, Universita degli Studi di Trieste, Trieste, Italy. [email protected]
It has been demonstrated recently that cells of Borrelia burgdorferi sensu lato, the etiological agent of Lyme disease, transform from mobile spirochetes into nonmotile cystic forms in the presence of certain unfavourable conditions, and that cystic forms are able to reconvert to vegetative spirochetes in vitro and in vivo.
The purpose of this study was to investigate the kinetics of conversion of borreliae to cysts in different stress conditions such as starvation media or the presence of different antibiotics.
Using the same experimental conditions we also investigated the possible role in cyst formation of RpoS, an alternative sigma factor that controls a regulon in response to starvation and transition to stationary phase.
We observed that beta-lactams penicillin G and ceftriaxone, the antibiotics of choice in Lyme borreliosis treatment, favoured the production of cysts
when used with serum-depleted BSK medium.
In contrast, we observed a low level of cyst formation in the presence of macrolides and tetracyclines. In order to elucidate the role of the rpoS gene in cyst formation we analyzed the reaction of the rpoS mutant strain in comparison with its wild-type in different conditions.
Under the same stimuli, both the wild-type borrelia and the rpoS knock-out isogenic strain produced cystic forms with similar kinetics, thus excluding the participation of the gene in this phenomenon.
Our findings suggest that cyst formation is mainly due to a physical-chemical rearrangement of the outer membrane of Borrelia burgdorferi sensu lato leading to membrane fusion and controlled by different regulation mechanisms."
This may be why the Romanian's treatment plan worked. They gave abx. ALONG WITH restoring the very deficient level of Mg.
[This message has been edited by Marnie (edited 27 April 2004).]
Is this BLP, TNF, pathway, cytokines, ARB all summed up somewhere in a book or something?
Im sure there are A LOT of people this would help, but PLEASE break it down!
I think I do understand about BLP, etc. If you want to get the word out, that is more than fascinating
but laymens terms might help for some people. I *can* research it to figure it all out. Some other people may be too sick to do that.. and some
people like me might try REALLY hard to understand only to go WHAT???
Mind the small people, will ya?
My ultimate question is where are we interrupting the inflammatory cascade--in all these different approaches--and what is the healthiest approach to do so? I personally am leery of taking benicar, or a drug, however I need to read more and understand a lot more before I conclude that. I still think the best idea is to eradicate the bug--if it can be done. OTOH, if the inflammatory cascade gets ahead of itself and perpetuates symptoms, that's no good. But are we sure that cascade is suppressing immunity? Anyway I have so many questions and not a lot of time to investigate right now but it is a very cool avenue of exploration.
[This message has been edited by free2reckon (edited 13 May 2004).]
No one book that I know of just lots of reading of different Drs observances.
[This message has been edited by treepatrol (edited 27 April 2004).]
[This message has been edited by free2reckon (edited 13 May 2004).]
I'll ans. Your questions as they relate to me, and/or my best understanding of what I know of the autoimmune disorders:
1) In Sarc the BP can also be very low. Benicar is still used, and BP is moniotored. In most
Of the traked cases it's normalized at some number. There were a fw people who experienced dizziness. Low Bp is not a show stopper.
2) In My opinion, Kanes therapy is a detox - getting rid of the residual crap the inflammatory process creates - so you feeling OK becuase you're staying even with the board. I don't think the Kane therapy affactes the Th1 inflammatory pathway. - or if it does - I've never seen it explained.
3) I'm not overweight - but I tried the low to no carb diet in the 80's. It didn't make a difference for me. Fasting did though. I used to think I was just allergic to all foods.
4) Can't answer this one - never took it or researched it.
5) It's been proven that Mellitin (a component of honey Bee Venom) will kill Babesia and Lyne in the blood concentration is high enough. Plus after a sting, the immune system is kicked into high gear - This is an Alt therapy that worked for me in the past - . I beleive to lower the burden.
I don't have an experience with Samento - other than a months trial (it did nothing for me)
But on Eurolyme, there has been alot of favorable discussion.
6) Personally - I had sunlight sensitivites big-time...Bad enough at time to make me really nauseous and vomiting. I also had swollen lacramil glands - these were the reason's they suspected Sarc - but I'd already had the Lupus diag... So they left it at that. This seemed to fluctuate over time.
Barb
not wanting to offend
I'm all for symptomatic treatment if it helps quality of life...anyway, I'll probably do a little research later this week or next week. I'm a "less is more" person (sort of like you)...right now hyperbaric is still holding me above water and I plan to add ozone back in. Not exactly looking forward to the latter as its such a powerful modality, but longterm, I believe it has the potential to get rid of so many varieties of bugs--and if we don't have the antigen, then we won't have the kaflooey response, as the sarc. articles point out. I found with only a few days of ozone, candida symptoms were ameloriated...but the die-off systematically warn't no fun...
Never had sunlight problems myself. Always feel better in the sun.
I'm glad Scott is feeling better on Day One. Anything that can improve a lymie is a good thing.
I'm not writing off Kane's protocol - I said I just never saw it explained as modulating the TH1 inflammatory pathway.
Treepatrol:
The theory is that if the inflammation is reduced, then your own immune system will be more robust. An immune system which is working well will work in conjunction with the antibiotics to kill the pathogen(s).
Barb
Tree doesnt. LOL I have no one to pick on today Tree
quote:
Originally posted by TheCrimeOfLyme:
I got it wahoo, I finally understand.Tree doesnt. LOL I have no one to pick on today Tree
NOW YA DID IT so your nose got sore and you decided to pick on me hahahaha 
[This message has been edited by treepatrol (edited 27 April 2004).]
Jen13,
SarcInfo didn't give me all the answers, just most of them. However, you guys gave me the critical missing pieces. Borrelia grows better at 34C than at 37C (ie, 98.6F). It also prefers less oxygen. I have seasonal and climactic variations in my symptoms. By the end of summer I feel pretty good. By winter I'm miserable again. I also feel much worse during cloudy/dark weather (loosely correlated with a drop in barometric pressure). I tried bright light "therapy" for Seasonal Affective Disorder for around six years and it didn't work. In fact, it made me worse. Here's what I believe happens to me:
Like many of you my body temperature is below normal. I think borrelia thrives in us for that reason. I think the reason I go into remission during summer is because of the heat, not having anything to do with light-mediated entrainment of circadian rhythm, as the SAD theory goes (which, by the way, I now believe is a pretty SAD theory).
Likewise, I feel better when the barometric pressure is high (loosely correlated with sunny weather). Again, this effect is not mediated by the presence/absence of entraining bright light. It's the dissolved oxygen that I think is at play.
You can imagine my frustration then at learning how the Sarc folks feel worse during sunny weather (this was before I knew about lyme) because that didn't seem to apply to me. Alas, there ARE sarc folks who feel worse during rainy weather. I found two posts about this--not many, but they were sarcoiders, nonetheless. One of the posts was on the SarcInfo site, and the moderators there discounted this patient's testimony. I emailed Dr. Marshall that I thought he was over-looking something. He replied, but is a very busy guy and didn't give much thought to the issue.
Several years ago, before I knew about SarcInfo and Lymenet, I tried one last desperate attempt to make the bright lights work. It was during winter when I was crashing. I worked my way up to 3 bright light boxes (22,500 lux in all) for over one hour a day. It was devasting. For the first time I became frankly disabled. My memory was so bad that I couldn't remember the first part of my sentence in order to relate it to the second part. I'm mean I couldn't communicate clearly to people. There were times I nearly passed out. The fatigue, nightsweats, etc. were brutalizing. It took months to regain my baseline misery. Obviously, I gave up on bright lights, but it would take me another year and half to realize what had happened.
During the beginning of last summer I started to mow the lawn (I avoid bright sunshine generally, because of mild photophobia) and became intensely thirsty for about two weeks. Importantly, I also had a strange metallic taste in my mouth. I went to the doc who tested me for diabetes which was negative (I was actually disappointed because I was willing to have diabetes if it at least explained my problems). The doc did, however, mention that a year and half earlier (during that horrible episode) I had high levels of phosphate and calcium. The doc was clueless, but it was critical. The hypervitaminos D that can occur during elevated inflammation (as with sarcoidosis) can result in elevated calcium and phosphorus. The World Sarcoidosis Society actually emphasizes how Sarcoidosis can mimick diabetes (which is what I went into the clinic to be checked for!). It can also cause a metallic taste.
I believe now that at the beginning of summer, when I wasn't yet in remission, the extra vitamin D precursor that resulted from sun exposure became rapidly converted to the active form (in an unregulated manner). I felt the effects, but after another month or so of summer heat the bacteria had taken up a defensive posture (cysts, L forms, whatever). But during the winter, when the infection was very active, I blasted myself with bright lights and the resulting D precursor was rapidly converted to the active 1,25(D) form.
I'm committed to Okam's razor (which says that the simplest explanation is usually correct). In this case, however, I believe that no less than three variables in the weather affect me. Temperature gives me a seasonal variation; superimposed on that is the more rapidly fluctuating barometer; and sunlight loads me up on vitamin D.
Please take the time to investigate what SarcInfo says about vitamin D. In short, we have a reservoir of vitamin D precursor that the kidneys convert, in a regulated way, to the active form. During inflammation, the immune cells convert so much of the precursor to the active form that the kidneys lose control.
Also keep in mind that if you are already consuming lots of vitamin D that this may make the effects of sunlight less salient to you. For years I consumed mass quantities of eggs and fortified milk so I don't think that the vitamin D that sunshine added to my system was as noticeable as it would've been otherwise.
I had the seasonal problems also. But I had Lyme long enough to be able to see 24hr, weekly, yearly and every 4 to 5 year cycles of symptoms - varying from the slight to the very debilitating.
I knew the sunligh exacerbated some symptoms sometimes - but not always. I probably felt better FASTING because I wasn't ingesting any extra vit D.
Barometric swings (whichis really atmospheric pressure) will always affect fluids - and this will be felt in people who have slight eodema (swelling) from inflammation.
I imagine alot of things will fall into place when people really understand this.
Barb
You have my attention. I go through the same exact thing that you do. In fact, I had just started abx last April when weather was turning nice up here in PA and I felt GOOD up until November when it got really cold. All of Nov, Dec, Jan, Feb, I felt like complete crap.
Now that its breaking again, I feel "cured" and or in Remission.
So do I need in the winter months to take phosphorus and calcium to do something with the stored Vitamin D?
Im confused. Is there a safe way to counter the winter blues/intense lyme symptoms?
Thanks
quote:http://www.joimr.org/phorum/read.php?f=2&i=38&t=38
Originally posted by treepatrol:
[QUOTE]Originally posted by J123:
[b] How do you know that?
Thank You. That's exactly the type of info we need to see posted. I had read some of those reports. It will take me weeks or months to digest.
Are you saying all CWD are Borrelia sp.? Or are other bacteria capable of forming CWD forms? Just spirochetes?
[This message has been edited by free2reckon (edited 13 May 2004).]
Learning is always open minded or at least keep looking.
Or the the way the bible puts it.
Study to show thyself approved unto God, a workman that needeth not to be ashamed, rightly dividing the word of truth.
[This message has been edited by free2reckon (edited 13 May 2004).]
>Im confused. Is there a safe way to counter the winter blues/intense lyme symptoms?
I have a bachelor's degree in psychology and another one with a double major in chemistry and biology. I know what qualifies as science and what doesnt rise above the level of philosophy. Psychology is a load of crap. At the beginning of this nightmare I got snared by the psychiatrists and even got my degree in psychology to find out what's behind "major depression." Smoke and mirrors.
I eventually got bogged down in the CFS/FM forum for awhile, before finding out about Lyme. The CFS/FM folks tolerate a lot of psychobabble. I was thrilled to read all the responses to Dougie's "WOW- I didn't have Lyme after all" post. You guys really have backbone.
The short of it is, don't justify the term "winter blues." We're not "hibernating" as the SAD theorists like to say. What we experience is far worse than that. As long as they can minimize the severity of what we feel, by invoking terms like "blue" and "hibernating", then they will get away with this BS. I suspect that there may be a sea of Lymies who are trapped in the SAD paradigm because they don't know about Lyme.
I have yet to study the nuts and bolts of the angiotensin/Th1 issue but so far I have every reason to believe that Benicar + antibiotics is the way to go.
>So do I need in the winter months to take phosphorus and calcium to do something with the stored Vitamin D?
Vitamin D is a steroid that has both hormonal and autocrine/paracrine functions. One of the hormonal functions (of the active form) is to regulate the expression of proteins in the GI epithelia that control the transport of calcium and phosphate from food into the bloodstream. Hypervitaminosis D leads to the over-expression of these transporter proteins with a concommitent over-uptake of calcium and phosphate. The excess calcium can cause some of the hypervitaminosis D symptoms (which is only a subset of all my symptoms), but to the extent that I understand this issue, most of these particular symptoms are caused by the vitamin D directly. You'd want to verify this, though.
>I go through the same exact thing that you do.
I can't tell you how thrilled I am to finally meet up with people who know what I'm going through.
ARTHRITIS - Vitamin D - In a mouse model of arthritis in which animals were infected with Borrelia burgdorferi, arthritis was prevented by treatment with 1,25-(OH)2D3 beginning 14 days post- immunization and continuing for the duration of the experiment.
Mice with established collagen-induced arthritis were treated with 1,25(OH)2D3 or mock-treated. The 1,25(OH)2D3 treatment significantly decreased arthritis severity. The authors conclude that vitamin D or its analogs may have benefit in the treatment of arthritis.
"1,25-Dihydroxyvitamin D3 Prevents and Ameliorates Symptoms in Two Experimental Models of Human Arthritis," Cantorna, M. T., et al, Journal of Allergy and Clinical Immunology, January, 1997;S186/Abstract 750. (Address: M. T. Cantorna, Department of Biochemistry, University of Wisconsin, 1300 University Avenue, Madison, WI 53706 U.S.A.) 26690 [rhe]
The minerals calcium and magnesium are so essential to bodily function that whole books could be dedicated to their functional importance to anti-aging and the body's minute by minute requirements. In order for calcium to be absorbed, the body must have sufficient magnesium and Vitamin D.
http://www.hmscrown.
com/Cal_Mag.html
We are not talking about creating a deficiency of vit D in the body.
As long as there is chronic inflammation in the body, the bone turn over rate will be dysfunctional, regardless of the mineral status. That's why in young people (20's and 30s) who have endured long term chronic inflammation, so many have osteopenia.
I'm not sure if it's necessary for all the readers on the board to understand the role of ARBs and inflammation - but the Doctors should have the opportunity to read the protocol.
Barb
1,25-Dihydroxycholecalciferol prevents and ameliorates symptoms of experimental murine inflammatory bowel disease.
J Nutr. 2000 Nov;130(11):2648-52.
I think this may be the one you're thinking of:
J Nutr. 1998 Jan;128(1):68-72.
1,25-Dihydroxycholecalciferol inhibits the progression of arthritis in murine models of human arthritis.
Cantorna MT, Hayes CE, DeLuca HF.
They show that supplementation with 1,25-(OH)2D3 reduces borrelia-induced arthritis. It would've be nice if they would have actually measured the influence of borreliosis on vitamin D levels. That is, I'd like to know what the levels of 25(D) and 1,25(D) were independent of the supplementation.
Has anyone here with borrelia-induced arthritis tried supplementing with vitamin D? Should be easy to test.
Thanks for your reply. What I meant by "Blues" though however, has nothing to do with psychological problem, what I did mean however, was that I get symptoms in the winter, not of psychiatric nature.. neurological.
I was one of them with the backbone, trust me.
quote:
Originally posted by Marnie:
Re: vitamin D:ARTHRITIS - Vitamin D - The minerals calcium and magnesium are so essential to bodily function that whole books could be dedicated to their functional importance to anti-aging and the body's minute by minute requirements. In order for calcium to be absorbed, the body must have sufficient magnesium and Vitamin D.
http://www.hmscrown.
com/Cal_Mag.html
Well,
I guess that does it! I'm moving my computer desk outside! 
quote:
Originally posted by free2reckon:
Tree,This is how borrelia is causing the disease.
What you are not getting is that borrelia get's this inflammatory disease rolling out of control and it then becomes self propelled... a life unto it's own...on top of the borreliosis.
If we don't address this vital part of the disease, we will not be as successful as we should.
...and the Truth shall set you free, Amen!
Scott
I get it once the inflamation starts its a end to itself by adding this drug your calling (Benicar) blocks the angiotensin receptors BUT in some cases say you havent had any pain in the joints or anywhere else then it starts again say 8 months later Is it actually LYME or a reoccurrance of this ((self perpetuating Th1 inflammatory cascade ))??????????????????
[This message has been edited by free2reckon (edited 13 May 2004).]
quote:
Originally posted by free2reckon: If after that period of remission, symptoms reappear, that is likely an indication that the pathogen is again triggering the inflammatory cascade and disease.This is why we still need to continue the appropriate abx therapy, even while we are asymptomatic.
Scott[/B]
Iam not sure what if this reoccurence is caused by some other thing created by the first cascade effect?
Iam tired of science being so slow to figure these things out because the researchers may not have a epiphany on how to use science in its correct mode or imagination.
The act or power of forming a mental image of something not present to the senses or never before wholly perceived in reality that they working in.