I thought I had CFS (HHV-6, CMV, Myco, Candida) but recently had an equivocal Igenex IGM (the IGG had a few positive/equivocal bands). I have all the symptoms: arrythmmias, vertigo, fatigue, GI problems, twitching all over, sweats, panic attacks, etc ...

I am not sure when I got this but think it was quite a few years ago and have never been treated with abx, but a few short weeks with orals for other problems (myco pneumoniae last year).

Anyway, my d levels are very high (1,25 D 87!!!) and I am thinking about Marshall as it seems everyone here relapses and is constant abx combos anyway. Why aren't more patients trying Marshall??

I hate to avoid sunlight, but if I can cure this in a year I would do it.

My LLMD wants me to do IV but I already have gallbladder polyps and am thinking it might be better to try IM Bicillin first.

Right now I am doing IV C w/ Glutathione and alot of immune building supplements. My energy is better overall, but I am having some majpr neuro and fatigue issues this week that came out of nowhere. I have not worked in over a year.

My Dr. said I was not ready for abx when I came in and wanted to build me up first, but anymore delay might not be such a good thing. I don't think orals are such a good idea right now as my IGA for Candida was high.

Any thoughts for a newbie who has never done any long term abx????

I think I might also have babs or another form of myco because I have occasional night sweats, but my pcr was negative.

I live in Upstate NY and may have to go out of state to do a Bowen.

Am waiting on my CD57.

Thanks for any advice!

I am prepping to go on it myself...after some IV Claforan to knock my bacterial load down.

You may think of hitting the Babs for 2 or 3 months before doing the MP.

I just did....2 months Mepron/Zithro/Biaxin...

Just a thought from someone who was infected North East of Syracuse.

To my knowledge, there is no modified MP and the staff would be quick to say so. They encourage people to follow it to the letter. I have no problem modifying my lifestyle, heck, lyme has already done that . . . So I am willing to modify, so that I can heal.

Your lab results would indicate that you are a good candidate. Did you post your results on the MP site?

My only concern about the protocol is for people living alone as they adjust to the protocol. It might take some preparation of quick frozen meals etc for when you don't feel good. But people herxing would have to do the same.

I was for some months on the board staff at the marshall protocol site. Here are some things you may want to consider:

The Marshall Protocol was originally developed as a treatment for Sarcoidosis. Many people are under the impression that the MP is a proven cure for that disease, with lots and lots of Sarc patients in remission.

That is not, in fact, the case. It came to light recently that only about 50 of the 200 hundred Sarcoidosis patients who started the MP have been on it for the minimum 18 months needed to obtain symptomatic remission. There is anecdotal evidence that many are doing well, but no systematic review of their progress has yet been undertaken.

Nearly all of those 50 are still on antibiotics and Benicar, some after more than 2 years on the MP. We know virtually nothing about what will happen when the drugs are discontinued.

We know much, much less about how the MP will turn out to work as a treatment for Lyme disease.

We do not, in fact, even know when a systematic review of patient experiences on the Marshall Protocol will be undertaken.

When it was learned that even the Sarc outcomes were not really known, some site members recently offered to help with an informal survey, to help fill the information gap until funding for a formal study is available. That offer was rejected, forcefully, by Dr. Marshall, and discussion of the matter was closed.

Are there reasons to hope that the MP will help at least some Lyme patients? Sure there are. But you must go into this understanding that the MP is a very, very experimental treatment.

Should you decide to proceed, here are some things you may want to consider:

Some Lyme patients have experienced fairly severe problems adjusting to Benicar. The theory of the MP holds, in part, that Benicar will help bring your 1,25-D down rapidly and thus allow your immune system to more effectively kill borrelia.

Your 1,25-D level is quite high. You might want to implement the lifestyle changes first: eliminate vitamin D rich foods, avoid sun exposure and bright light in the eyes. The theory is that this allows you to bring your 1,25-D level down more gradually, so you don't get zapped by rapid adjustments in other hormones and a sudden surge of bug killing.

You might think about combining this pre-MP stage with antibiotics, in what ever form your Lyme doc thinks best, to bring down your bacterial load and further cushion yourself from abrupt changes on the Mino/Benicar combo.

There is a lot of anecdotal evidence that Lyme patients who don't avoid sun and vitamin D rich foods pay a very high price. You will be told again and again by staff: these are not optional items, combining Benicar and antibiotics without making the lifestyle changes will not only not work but may well make you utterly miserable.

What matters most of all, though, is having a competent LLMD who really understands both your illness and the MP.

To sum up: I would advise you not to consider the MP unless the following things are true:

1) You are prepared to practice strict sun avoidance, wear NOIR sunglasses indoors and out, and purge your diet of vitamin-D rich foods and supplements, and maintain that lifestyle for 18 months or longer.

2) You are ready to implement those steps first, before starting on the Benicar, to gradualize the lowering of your 1,25-D level

3) You have no qualms about committing to a treatment protocol that at this stage has to be considered wholly experimental

4) You have an LLMD who really 'gets' the MP and gives you a clear assessment of its strengths and weaknesses compared to other treatments.

I am not on the MP, and never have been. My perspective is based on studying the science, writing about it a bit, being invited to join the board staff, asking lots of questions there about what was and was not known, and reading a TON of patient progress reports.

By the time I was diagnosed with Lyme at the beginning of October, I had decided that the MP was too experimental, and I was too sick, to make it a treatment of choice. For that reason, among others, I resigned from the MP board.

I know there are Lymies here like Shelley, who are very enthusiastic about the MP. Nothing I've said is meant to suggest that they're wrong. At this point, we simply do not know.

I wish you all the best, whatever treatment you decide to pursue.

Personaly I am not on board but if you want be a guinee pig go for it its your life.

Its still abx's, his benicar he's saying takes away the pain its your choice but for me untill there is some clinical studies buy MD's LLMD's Iam not on board.Thats published

That being said heres something else that might be why it helps.
Another peculiar observation of these bacteria is seen inside the bacteria. When the genetic control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase Inhibitors (ciprofloxin) the bacteria start to produce bacterio-phage. A phage is a virus that specifically attacks bacteria. In this case there are two distinct forms. This means the Lyme bacteria at one time were attacked by viruses. It was able to suppress them, but the DNA to make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this phage could one day be beneficial to treating chronic Lyme patients? (JTBD 94)

What happens when the infection gets to the brain? In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite to the brain in just a few days. (41,60, abstract 644) While we know these bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect. When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood brain barrier. (E.g. Il-6, Tumor Necrosis Factor-alpha, Il-1, Transforming Growth Factor-beta etc.) In addition to affecting the blood brain barrier, these cytokines can make us feel ill, and give us fevers. (54,60,) (JID 1996:173, Jan)

Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can't enter either, making treatment of the brain especially hard. For the first ten days of a Lyme infection, the blood brain barrier is virtually nonexistent. This not only allows the Lyme bacteria to get in, but also immune cells that can cause inflammation of the brain. (41) *Note: The breakdown of Bb was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive Iodine. The CSF was tested, and then the animals were infected with Bb. Then the CSF was tested everyday for several weeks. The result: No cross over of Iodine in the control group, 100% crossover in the infected group for 10 days. The infection had the same result as injecting the radioactive iodine directly into the brain. (60)

When the human brain becomes inflamed, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson's Disease, MS, ALS, and is responsible for the dementia that occurs in AIDS patients. What quinolinic acid does is stimulate neurons to repeatedly depolarize. This eventually causes the neurons to demyelinate and die. People with elevated quinolinic acid have short-term memory problems. (27,29-37,40-42,74,75, 82-84,87-90)

This means: If we think of all of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can't learn anything. If all of the lines going out are busy, we can't recall any memories. Our thinking process becomes impaired.

A second impairment to clear thinking that Lymies experience is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computer Tomography scanner (SPECT scans), we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal "swiss-cheese" pattern of blood flow. The cortical, or thinking region of the brain, was being deprived of good circulation; the occipital (eyesight) regions had an increase flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes. (91)

Since benicar expands blood vessels this may help improve memory quickly also possiblely let certain abx's cross blood brain barrier.

But like I said need studies published.

I am in pretty much the same boat as you. I decided to go with MP. In my mind it is the first explanation of cause and effect for Lyme that makes detailed scientific sense. My stomach was shot from abx. I'd had no significant reaction to 5 months of heavy duty oral abx and my LLMD wanted me to start IV.

I did not want to go down the IV road. Avoiding Vit. D in foods is not a big deal. Avoiding light is more difficult but do-able, especially as winter approaches here in the northeast USA. I have not eaten any D in 2 months and have been wearing my glasses all the time for a month.

My new Dr. will I hope start me on MP drugs in a week. My LLMD was unwilling to educate herself and dismissed MP out of hand.

If you read the posts on the MP board you will learn that deviating from the MP can be dangerous, so don't look for shortcuts.

Your D 1,25 of 87 is huge. My reading of 52 was > 99% of the population. You must be > 99.9%.

There are some good points in the previous posts about unproven treatment, lack of data, etc. By all means feel free to wait the 5-10 years necessary to prove MP to the medical community if you wish. Personally I've been sick too long to wait that long.

I've read phases 1-3, got phaes 2-3 from someone else who is now on no. 2.

With no problems while taking meds, it's a 2.5 - 4 year commitment on MP. So it's a big time commitment.

Just depends on how you herx while going thru entire thing plus how long you have had lyme disease.

I lost what I typed earlier as I am copying/pasting something from my private emails about my meds, etc.

I'm not on MP, but I read their daily "digest" and contribute my progress in their OFF TOPIC area.

Here is what my LLMD put me on:

BIAXIN 500 mg/twice daily: take for 3 days and then 2 days off;

DOXYCYCLINE 100 mg/twice daily: take for 2 days and then 2 days off;

then I start the biaxin again, and follow by doxy -- it's called PULSING.

Been on this for 3 months now.

2 months ago put on benicar 20 mg/day .. half in am/pm. It does make me dizzy so I take it before going to bed & around 7 am going back to bed until 10-noon! Benicar helps me to get some good sleep minus all my pee calls 5-8/night!

I had the "western blot IGM & IGG" blood tests tested at IGENEX blood research lab in Palo Alto, Calif., www.igenex.com and a special request form needs to be printed plus prepayment unless on medicare.

or at MD Labs, New Jersey; www.mdl.com or net.

IGX does not take insurance but tests ALL 16 protein bands.

MDL does take most insurance companies & said it tests ALL 16 bands too.

I'm having quality days; I'm a statistic for those who really have this bad & bedridden for weeks, months, & years! I've just learned to live with this for so many years...34.

I'm on 2 antibiotics: biaxin & doxycycline plus benecar for my lyme plus 5 others.

I'm herxing/side effects but nothing intolerable except my entire right arm is 24/7 pain plus my back, neck, & groin area.

I was rereading my note below. Finally made a call yesterday about neuro psychiatric testing for lyme brain or early onset AD and checking out various psychologists.

End of month I'm having a sleep apnea study done too. Thought of doing this for years, but hadn't pushed it.

Talk about expensive $2400 1 night; $2100 for 2nd night if needed plus drs. fees!

I'm still fighting to get SS disability after 4 yrs., 3 months. Off work 6 yrs.

My Phoenix SSD lawyer quit me at the time of my lyme dx. So what a year!

Dx w/type 2 diabetes in Jan. 04; July w/lyme.

Iowa Sen. Tom Harkin's DM office, Rob, has been so helpful to me on my SSD case. I wrote head judge and sent him my lyme dx & all drs. reports my lawyer hadn't sent.

I asked judge if he they would reopen my
1st case, in Virginia's appeals council almost 2.5 yrs!

Some of you said abx had decimated your stomach, but failed to mention this is still abx + Benicar.

Shelley,

How long have you been on The MP? I don't understand when people say they are feeling better on it when everyone is supposed to be herxing "comfortably" all the time. You are not supposed to be feeling better from what I understand, and if you are then it's time to increase the dosage to herx level or move on to the next abx.

There is at this time NO KNOWN absolute treatment for Lyme.

None.

They are ALL argumentative...or, unproven.

None are definitive.

The ones that work...work for those that have been able to define which ones are built for them...

What kind of heart symptoms do you experience?

I am worried about the heart stuff because I used to get chest pain spasms (very cardiac feeling!) in the sun and also PSVT, PVC's, PAC's and short runs of A-FIB. For some reason this has cleared up lately, though it always comes back. Because of my high D-levels I am worried about the heart herx alot and don't want to die of a heart attack, failure etc...

I am in my thirties and not too worried after having a negative angiogram, but know I have inflammation.

I might try IM Bicillin or IV first as I never have done any abx treatment and maybe by some chance of luck I'll get it with that. I've talked to people who have gone into remission this way.

Any other way to get the D-Levels down?

Thanks!

Those things are a real pain in the butt for some people. I'm not one of them, cuz I'm housebound and horribly photosensitive anyhow. Miss eating eggs and fish, but life goes on.

I've chosen to stick to those elements of the MP for several reasons:

1) It's within my budget
2) It doesn't require a doctor's approval
3) It seems very unlikely to cause me any harm
4) There is some chance it will aid my immune system in mounting a more effective defense against the evil little buggers.

In other words, I'm pretty sure a lot of the science of the MP is solid, as far as it goes. Does that make me want to rely on it for treatment at this stage of my disease? No. Frankly the propsect strikes me as insane. But that's based on a very individual assessment of my own health, as much as (or more than) my assessment of the MP.

It is true that all Lyme treatments leave much to be desired. It is also true that the MP is more unproven than most.

Of course we lament high relapse rates. The fact is, though, that one can find thousands of case histories and medical abstracts where extreme Lyme manifestations like vision and hearing loss, parasthesia, neuropathy, loss of mobility and psychosis have been reversed by high dose oral or IV antibiotics. That doesn't make those treatments an adequate answer to Lyme disease, but it is a hell of a lot more than has so far been demonstrated for the MP. Patients and physicians need to keep that squarely in mind, when considering this protocol.

TXLymeMom's daughter is doing very well. Her progress reports are among the most hopeful I've seen for any MP patient, regardless of diagnosis. But for every one of her there are ten patients who aren't getting better in any discernible way at all, and her progress is frankly outpacing what the experience of even Sarcoidosis MP patients would lead one to expect. I tend to think her extensive prior abx treatment has a lot to do with that.

Full Disclosure:

The excerpts you post below are very interesting. Could you post the entire article, including footnotes?

I want to share it with my daughter, who is graduating from med school this spring & beginning a residency in psychiatry. She is writing a paper on psychiatry & lyme disease.

Thank you!!

Tempe

quote:

---

Originally posted by treepatrol:

Another peculiar observation of these bacteria is seen inside the bacteria. When the genetic control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase Inhibitors (ciprofloxin) the bacteria start to produce bacterio-phage. A phage is a virus that specifically attacks bacteria. In this case there are two distinct forms. This means the Lyme bacteria at one time were attacked by viruses. It was able to suppress them, but the DNA to make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this phage could one day be beneficial to treating chronic Lyme patients? (JTBD 94)

What happens when the infection gets to the brain? In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite to the brain in just a few days. (41,60, abstract 644) While we know these bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect. When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood brain barrier. (E.g. Il-6, Tumor Necrosis Factor-alpha, Il-1, Transforming Growth Factor-beta etc.) In addition to affecting the blood brain barrier, these cytokines can make us feel ill, and give us fevers. (54,60,) (JID 1996:173, Jan)

Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can't enter either, making treatment of the brain especially hard. For the first ten days of a Lyme infection, the blood brain barrier is virtually nonexistent. This not only allows the Lyme bacteria to get in, but also immune cells that can cause inflammation of the brain. (41) *Note: The breakdown of Bb was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive Iodine. The CSF was tested, and then the animals were infected with Bb. Then the CSF was tested everyday for several weeks. The result: No cross over of Iodine in the control group, 100% crossover in the infected group for 10 days. The infection had the same result as injecting the radioactive iodine directly into the brain. (60)

When the human brain becomes inflamed, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson's Disease, MS, ALS, and is responsible for the dementia that occurs in AIDS patients. What quinolinic acid does is stimulate neurons to repeatedly depolarize. This eventually causes the neurons to demyelinate and die. People with elevated quinolinic acid have short-term memory problems. (27,29-37,40-42,74,75, 82-84,87-90)

This means: If we think of all of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can't learn anything. If all of the lines going out are busy, we can't recall any memories. Our thinking process becomes impaired.

A second impairment to clear thinking that Lymies experience is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computer Tomography scanner (SPECT scans), we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal "swiss-cheese" pattern of blood flow. The cortical, or thinking region of the brain, was being deprived of good circulation; the occipital (eyesight) regions had an increase flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes. (91)

Since benicar expands blood vessels this may help improve memory quickly also possiblely let certain abx's cross blood brain barrier.

But like I said need studies published.

[This message has been edited by treepatrol (edited 18 November 2004).][/B]

---

Lyme disease is a multi-system disease which can seemingly affect virtually every tissue,
and every organ of the human body. It is a disease which can be mild to some, and
devastating to others. It can cripple and disable, or fog your mind. It can affect men,
woman, and children, and even your family dog and can be devastating to horses and
cattle. (1-5,7-19) You may test negative for the disease, and still have it, or test positive
and be symptom free. Some will get symptoms within days of a tick bite, while others
may have it for years before they are even diagnosed. Some Lyme patients are told they
have fibromyalgia, chronic fatigue syndrome, depression, MS, ALS or some other disease
of unknown origin. (See abstracts of the 1996 International Lyme Conference) There are
some studies which support the theory that the infection can be transmitted from mother
to the unborn fetus, and may even cause still birth and has been implicated in some
SIDs deaths. (MacDonald-20,52; 45,53)

Why is Lyme disease such a mystery? Why does it mimic so many other disease? Why
is it so difficult to detect? The reasons come from the microbiology of the bacteria that
causes Lyme Disease. This paper will look at the biology of this bacteria and the
consequences of the organism's unique microbiology on human victims.

Lyme disease is caused by a spiral shaped bacterium known as a spirochete. Diseases
that are caused by spirochetes are notorious for being relapsing in nature, difficult to detect,
and great imitators of other diseases. Syphilis, Tick-Borne Relapsing Fever, and Leptospirosis
are other examples of spirochetal diseases. Lyme disease is caused by a bacteria called
Borrelia burgdorferi, named after the man who isolated it from a Deer Tick in 1981, Dr. Willy
Burgdorfer. The following is a tutorial to help explain away the mysteries of this bacteria, and
the why it causes so much controversy between patients and the medical community. (1)

The Structure of the Lyme Bacteria

The structure of the Lyme spirochete, is unlike any other bacteria that has ever been studied
before. It is one of the largest of the spirochetes (0.25 microns x 50 microns) It is as long, as
a fine human hair is thick. Borrelia burgdorferi is a highly motile bacteria, it can swim extremely
efficiently through both blood and tissue because of internal propulsion. It is propelled by an
internal arrangement of flagella, bundled together, that runs the length of the bacteria from tip
to tip. Like other Borrelia bacteria Borrelia burgdorferi has a three layer cell wall which helps
determine the spiral shape of the bacteria. What makes this bacteria different from other
species, is that it also has a clear gel-like coat of glyco-proteins which surround the bacteria.
This extra layer is sometimes called the Slime Layer or S-layer.

(See diagram 1) (45,46,59) Flagella runs internal from tip to tip DNA containing BLEB, newly
formed - Shed BLEB - Glyco-Protein Slime Layer (exaggerated In the example for illustrative
purpose) - Receptors in tips -
This means: This extra layer of glyco-proteins (exaggerated in thickness here) may act like
a stealthy coat of armor, that protects and hides the bacteria from the immune system. The
human immune system uses proteins that are on the surface of the bacteria as markers,
and sends attacking antibodies and killer T-cells to those markers, called outer surface
protein antigens (OSP antigens). This nearly invisible layer is rarely seen in washed cultures,
but can be seen regularly in tissue biopsies.(46)

The Lyme bacteria is different from other bacteria in its arrangement of DNA. Most bacteria
have distinct chromosomes that are found floating around inside the cytoplasm. When the
bacteria starts to divide it forms a new cell wall in the middle and begins to split in two, the
chromosomes also divide, and the new copies of the chromosomes enter the new cell. The
arrangement of DNA within Borrelia burgdorferi however; is radically different from other
bacteria. It is arranged along the inside of the inner membrane of the cell. It looks something
like a net embedded just underneath the skin of the bacteria. (46)

This means: We really don't understand the mechanisms of how Bb regulates its genetic
material during its division.

The bacterial DNA is uniformly embedded inside the inner membrane of the Bb bacteria,
like nylon stocking.

Another unique feature to Borrelia burgdorferi are Blebs.

This bacteria replicates specific genes, and inserts them into its own cell wall, and then
pinches off that part of its cell membrane, and sends the Bleb into the host. Why it does
this we don't know? But we do know that these blebs can irritate our immune system.
Dr. Claude Garon of Rocky Mountain Laboratories has shown that there is a precise
mechanism that regulates the ratio of the different types of blebs that are shed. (46)
In other bacteria the appearance of blebs often means the bacteria can share genetic
information between themselves. We don't know if this is possible with Borrelia species.
There have been reports of a granular form of Borrelia, which can grow to full size, fully
autonomous spirochetes and can reproduce. These granules are so small that they can
be filtered and separated from live adult spirochetes by means of a micro-pore filter. The
granular/spore form of Borrelia burgdorferi is still being debated. (Stealth Pathogens Lida
Mattman Ph.D 66, Phillips/Mattman 98, Preac-Mursic)

The division time of Borrelia burgdorferi is very long. Most other pathogens such as
Streptococcus, or Staphylococcus, only take 20 minutes to double, the doubling time
of Borrelia burgdorferi is usually estimated to be 12-24 hours. Since most antibiotics
are cell wall agent inhibitors, they can only kill bacteria when the bacteria begins to
divide and form new cell wall.(35,59-62)

This means: Since most antibiotics can only kill bacteria when they are dividing, a slow
doubling time means less lethal exposure to antibiotics. Most bacteria are killed in
10-14 days of antibiotic. To get the same amount of lethal exposure during new cell
wall formation of a Lyme spirochete, the antibiotic would have to be present 24 hours
a day for 1 year and six months!

Staphylococcus Lyme spirochetes

* Note: Antibiotics kill bacteria by binding to RNA rich organelles inside the bacteria called
ribosomes*, and interupting the formation of cell wall proteins, or proteins involved in cell
metabolism. (See LD Survival Manual) Some newer antibiotics kill by disrupting DNA/RNA
synthesis. (Cipros and other quinilones interrupt DNA gyrase and enzyme that unwinds DNA
for replication)

If a bacteria is in a non-metabolic state (dormant) no antibiotic is effective. To be lethal the
antibiotic must be absorbed and processed through the bacteria's metabolic machinery
and cause a disruption of metabolism.

Unlike antiseptics, antibiotics don't kill on contact. If there are any dormant bacteria hidden
in sequestered sites, then regardless of the length of treatment, antibiotics can fail until the
bacteria become metabolically active. (The Forgotten Plague see reference to Tuberculosis)

A ribosome translates messenger RNA into proteins. In other words, cellular genes are
expressed as proteins that are created at the site of the ribosomes.

Ribosomes are protein creating factory assembly lines. Like other spirochetes, such as
those that cause Syphilis, the Lyme spirochete can remain in the human body for years
in a non-metabolic state. We know this because patients with ACA rash for years are often
culture positive when the skin is biopsied and cultured. Non metabolic bacteria is essentially
suspended animation. The bacteria does not metabolize in this state, antibiotics are not
absorbed or effective. When the conditions are right, those bacteria that survive, can seed
back into the blood stream and initiate a relapse. It is a beautiful and patient survival
mechanism. (59-62,70)

This means: Just because a person is symptom free for long lengths of time doesn't mean
they aren't infected. It may simply be a matter of time before the re-emergence of sequestered
non-metabolic bacteria. Whereas viral infections often impart a lifelong immunity, and may
suppress subsequent relapses or reinfections. Lyme like other bacterial infections, does not
impart an active immunity for long a period of time. People are often reinfected with Lyme.
A relapse of symptoms could actually be thought of as a reinfection or a reseeding of infection
from immune privileged sites.(96)

POLYMORPHISM: The ability of a bacteria to change its structural identity. During cell
division this bacteria has the ability to change its cell wall structure, and surface antigens
thus making it more difficult for the human immune system to recognize. Like its cousins,
the RELAPSING FEVER

SPIROCHETES , the Lyme spirochete has a sequence of surface antigens it can choose
to express or not express. There are more than two dozen species of Relapsing Fever
Borrelia bacteria which have been clearly identified. We are now beginning to see a similar
diversity within the Lyme spirochete family as well. Polymorphism makes recognition and
identification more difficult, it is like a criminal putting on a new disguise after every time he
has committed a new crime. While there are four generally accepted genospecies of Lyme
disease Borrelia burgdorferi, afzellii, garinii, and lonstarrii, there are hundreds of identified
strains of the first three species. Borrelia spirochetes are polymorphic because they have
built in genetic mechanisms to vary their antigens.

This Means: Just as the immune system recognizes the bacteria and tries to kill it.
The bacteria changes its clothes and fools the immune system and survives a little longer.
Soon the bacteria finds safer areas of the body to hide in and the immune system stops
looking for it. But another aspect of polymorphism is that once the cell changes it may
become even more lethal to some cells. For example when Borrelia burgdorferi was
introduced into the mouse via the blood stream, the bacteria traveled to the brain. But
the bacteria recovered from the brain was more adapted to the brain and could no longer
be killed from antibodies in the bloodstream. Polymorphism is a clever way to survive
and may offer reasons to multiple symptoms.

CELL WALL DEFICIENT SPIROCHETES:

The nice clearly definable spiral shape of the Lyme spirochete is formed by the presence
of the bacteria's cell wall. Without this cell wall to determine its shape, the bacteria only
has a thin pliable membrane to hold its structure together. When the bacteria turns off its
genes that govern cell wall synthesis, the bacteria can change from a spiral shape, to a
sphere. These spherical forms are known as L-forms or Cell Wall Deficient (CWD) forms.
They represent a new hazard in the diagnosis and treatment of common diseases.

Many doctors and microbiologists have a hard time understanding that spirochetes can
actually be fuzzy blobby looking spheres, but they are a reality. As a defense mechanism to
mammalian immune systems, the Lyme spirochete has learned to turn off its group of genes
that result in cell wall formation. This also eliminates all associated cell wall antigens.

How does a microbiologist recognize Borrelia burgdorferi once it is no longer a spirochete?
In order to prove that these spheres floating around in human blood are actually spirochetes
is difficult because they do not culture well. Instead a microbiologist will make a wet mount
of the infected blood on a slide, and then add acrodine orange stain to stain the nucleic acids.
Then a second stain that is specific for Borrelia burgdorferi is added. It is prepared by first
making a monoclonal antibody specific to a Borrelia membrane antigen. Then that monoclonal
antibody is tagged with a fluorescent dye. When this dye is added to the wet mount slide it
stains only the Borrelia species of bacteria. Suddenly what was once totally invisible in blood
by normal staining techniques, becomes visible. Spirochetes can in fact become cell wall
deficient spheres.

Another technique to identify spheroplasts as being Borrelia bacteria is to take antibodies
unique against Borrelia and tag them with inert gold spheres. Then culture the L-forms with
the antibody-tagged-gold . When these cultures are viewed under electron-microscopes, the
gold can clearly be seen attached to the membrane indicating that the antibody has attached
to a protein specific to Borrelia. Therefore the spheroplasts must have once been spirochetes.

The most compelling evidence of spirochetes reverting from its classical form to L-forms and
back to the classical form, is sometimes seen in live wet mounts. Occasionally L-forms can
be observed producing a classical form spirochete that is actually in the process of being
extruded from the membrane of the L-form. In other words the bacteria can revert back and
forth from L-forms to spirochetes by a method other than normal binary fission. It appears that
the membrane its self can yield an intact spirochete without creating the normally obligatory
process of binary fission. Binary fission starts with the host cell splitting itself in half with a
cell wall, and then creating an identical clone cell, but when L-forms reproduce they don't
always form identical clones. (Lida Mattman, Stealth Pathogens, Detroit 1997 lecture and
video, Mattman/Phillips 98)

This means: Cell wall inhibiting antibiotics such as Rocephin and amoxicillin, are ineffective
since they depend on inhibiting cell wall formation to induce cell lysis. This means most
antibiotics used in treatment of Lyme disease may have a built in deficiency when confronting
L-forms. Other antibiotics such as doxycycline and clarithromycin which are protein inhibitors,
may have to be used when cell wall agents fail. Diagram: The Cell Wall Deficient form of
Borrelia burgdorferi, or the L-form lacks its normal spiral architecture due to the lack of
structural rigidity that is maintained by the structural presence of a cell wall. The bacteria
reverts back to a simpler spherical form.

The bacteria is held together by a much more fragile 3 layer membrane stains semipermeable
3-layer membrane. Just beneath this membrane with acrodine orange is the bacteria's genetic
material, from which new cell synthesis seems to originate from a simple amorphous
membrane, the bacteria can give rise to the classical cell wall spiral shaped bacteria.

A Classical form arising from an L-form: Membrane antigens used to create monoclonal
antibody stain.

Cell Walled Classical Form (Gold tagged antibody to Borrelia burgdorferi)

In what form does the bacteria exist in the human body? A pioneering study on L-forms
of spirochetes, was done on tissues from a tertiary syphilis patient. A syphilitic aorta from
the heart of a human patient was dissected and analyzed for the presence of L-forms. What
was seen was that within the lumen of the artery or within the bloodstream, the classical form
was predominant. As you traveled into the vessel through the endothelium and into the
basement membrane, you found a progression of morphogenic forms. The spirochete slowly
went through a transition from a spiral shaped bacteria to a small sphere.

This means: The preferred form of the bacteria may be dependent on its physical
surroundings. In some tissues it prefers the classical form, in other tissues it reverts
to a cell wall deficient form. While such a dimorphism has long been accepted for yeast
and fungal infections such as Candida infections. It is only just now being accepted as
occurring in Borrelia species. (A yeast can also have a separate rhyzome fungal form
and a fungus can revert to a spore forming form!) Motility: How does the Lyme bacteria
travel from the bloodstream to other tissues? While we have known for a long time that
the Lyme spirochete can show up in the; brain, eyes, joints, skin, spleen, liver, GI tract,
bladder, and other organs, we didn't understand the mechanism by which it could travel
through capillaries, and cell membranes. (Abstract 644) Then Dr. Mark Klempner presented
at the 1996 LDF International Lyme Conference an interesting paper that gave us part of the
answer.

Many researchers have observed that the Lyme spirochete attaches to the human cells
tip first. It then wiggles and squirms until it enters the cell. What Dr. Klempner showed
was that when the spirochete attached to the human host cell, it caused that cell to release
digestive enzymes that would dissolve the cell, and allow the spirochete to go where ever it
pleases. This is very economic to the bacteria to use our own cell's enzymes against us,
because it does not need to carry the genes and enzymes around when it travels. Dr.
Klempner also showed that the spirochete could enter cells such as the human fibroblast
cell (The skin cell that makes scar tissue.) and hide. Here the pathogen was protected from
the immune system, and could thrive without assault. More importantly when these
Bb-fibroblast cultures were incubated with Rocephin (ceftriaxone), two thirds of the
cultures still gave rise to live spirochetes after two weeks, and in later experiments
for more than 30 days.

If we can't kill it in a test tube at these high concentrations of Rocephin in four weeks,
how can we hope to kill it in the human body? (22,48,79,80,)

This means: The infection can enter the best tissue that is optimal for its survival. Once
it gains an intracellular position, it may evade the immune system, and antibiotics therapy,
by remaining sequestered away from these hostile environs.

Another interesting observation about this bacteria is how it interacts with our body's
immune system; Dr. David Dorward of Rocky Mountain Labs made a video tape of how
Borrelia burgdorferi acts when surrounded by B-cells. (The type of white blood cell that
makes antibody.) The spirochete attached tip first, entered the B lymphocyte, multiplied
and ruptured the cell. It repeated this process for three days until the B-cells were able to
come to an equilibrium. A matter of concern was that some of the spirochetes were able to
strip away part of the B-cell's membrane, and wear it like a cloak. (Dorward, Hulinska 1994
LDF Conference Vancouver BC)

This means: If this spirochete is evolved enough to attack our B-lymphocytes, then it
may also be evolved in other ways that we do not yet understand. It is for certain that
its ability to kill B-lymphocytes, evolved as part of a defense mechanism to evade its
own destruction. The observation that it can use the B-cell's own membrane as camouflage,
indicates that it may be able to go undetected by our immune system.

Receptors:
It now appears that there are specific receptors in the Lyme spirochete to attach to endothelial
cells, N-Acetyl-glucasamine, B-cells, glial cells, nerves, and neurons.

The way our immune system is supposed to work , is that it recognizes foreign invaders as
being different from self, and it attacks the infection. Unfortunately the immune system
sometime attacks our own cells. This called autoimmune disease. If a foreign invader
has a chemical structure similar to our own tissue antigens, our bodies sometimes make
antibodies against our own tissues. In people with Lyme disease scientists have discovered
auto-antibodies against our own tissues including: (23,28,38-40,43,45,56,57,60,88)

* Nerve Cells (Axons)
* Cardiolipid
* Myelin (also seen in MS)
* Myelin Basic Protein (also seen in MS)
*Neurons (brain cells)

When the immune system finds a foreign invader, it tags that invader in a number of ways.
A cell called the macrophage can engulf the bacteria, and then communicate to other
immune cells the exact description of the bacteria. Another cell might mark the cell with
antibody which attracts killer T-cells. Some types of T-cells communicate to other cells
what to attack, and regulates the immune assault. But sometimes the body can produce
a type of antibody that doesn't attack or help. A blocking antibody will attach and coat the
intruder, but it won't fix compliment, and it shields the bacteria from further immune
recognition. In Lyme we have seen quantities of IgG4 blocking antibody such as is
seen in some parasitic infections. (Tom Schwann RML 92 LDF Conference)

* Note: Compliment is a term used for a series of 18 + digestive proteins that are only
activated by signals from our immune system, such as compliment fixing antibodies
that attach to foreign antigens.

In order for the immune system to make an attacking antibody, the immune system
must first find an antigen which it can attack. Unfortunately as seen by freeze fracture
electron microscope, photographs of the Lyme bacteria, show that most of the antigens
are on the inside of the inner membrane, and not on the outside. (60) This makes the
bacteria less visible to the immune system and more difficult to attack. The most intriguing
fact about Borrelia spirochetes, is their well documented ability to change the shape of their
surface antigens when they are attacked by the human immune system. When this occurs
it takes several weeks for the immune system to produce new antibodies. During this time
the infection continues to divide, and hide. (1,47,63,66)

It appears that Borrelia are able to change their surface antigens many times, and can do
it quickly. In one study by Dr. Andrew Pachner MD, he infected mice with a single strain of
Borrelia burgdorferi. After several weeks he was able to isolate two slightly different forms
of the bacteria. The bacteria from the bloodstream was attacked and killed by the mouse's
immune sera, but the bacteria isolated from the mouse's brain was unaffected by the
immune sera. The bacteria isolated from the mouse's brain had a new set of surface
antigens. It appears that contact with the CNS caused the bacteria to change its appearance.
Since the brain is isolated from the immune system, and is an immune privileged site, the
bacteria became its own separate strain. (47,97) This means: Infections of the bloodstream
may be different from the infections that are sequestered in the brain. While we continue to
have active immunity in the bloodstream, the brain has no immune defenses except for
circulating antibodies. So if those circulating antibodies are ineffective to attack the bacteria
in the brain, then the brain is left without any defenses, and the infection goes unabated.

Another peculiar observation of this bacteria is seen inside the bacteria. When the genetic
control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase
Inhibitors (ciprofloxin) the bacteria start to produce bacterio-phage. A phage is a virus that
specifically attacks bacteria. In this case there are two distinct forms. This means the Lyme
bacteria at one time was attacked by viruses, it was able to suppress them, but the DNA to
make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this
phage could one day be beneficial to treating chronic Lyme patients? (JTBD 94)

What happens when the infection gets to the brain?

In the case of Lyme disease every animal model to date shows, that the Lyme spirochete
can go from the site of the bite, to the brain in just a few days. (41,60, abstract 644) While
we know this bacteria can breakdown individual cell membranes, and capillaries, its entrance
into the brain is too pronounced for such a localized effect. When the Lyme bacteria enters
the human body, we react by producing several immune regulatory substances known as
cytokines and lymphokines. Several of these act in concert to break down the blood brain
barrier. (eg. Il-6, Tumor Necrosis Factor-alpha, Il-1, Transforming Growth Factor-beta etc. )
In addition to affecting the blood brain barrier, these cytokines can make us feel ill, and give
us fevers. (54,60,) (JID 1996:173, Jan)

Since the brain has no immune system, it prevents infection by limiting what can enter
the brain. The capillary bed that surrounds the brain, is so tight that not even white blood
cells are allowed to enter. Many drugs can't enter either, making treatment of the brain
especially hard. For the first ten days of a Lyme infection, the blood brain barrier is virtually
non existent. This not only allows the Lyme bacteria to get in, but also immune cells that
can cause inflammation of the brain. (41, see LDSM 95 for diagram)

*Note: The breakdown of BBB was shown to occur by tagging WBCs, albumin, and other
substances known not to cross the BBB with radioactive Iodine. The CSF was tested, and
then the animals were infected with Bb. Then the CSF was tested everyday for several weeks.
The result: No cross over of Iodine in the control group, 100% crossover in the infected group
for 10 days. The infection had the same result on the BBB, as if you were injecting the
radioactive iodine directly into the brain. (60)

When the human brain becomes inflamed, cells called macrophages respond by releasing
a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson's Disease, MS,
ALS, and is responsible for the dementia that occurs in AIDS patients. What quinolinic acid
does, is to stimulate neurons to repeatedly depolarize. This eventually causes the neurons
to demyelinate and die. People with elevated quinolinic acid have short term memory
problems. (27,29-37,40-42,74,75, 82-84,87-90)

This means: If we think of all of our brain cells like telephone lines, we can visualize
the problem. If all of the lines coming in are busy we can't learn anything. If all of the
lines going out are busy, we can't recall any memories. Our thinking process becomes
impaired. A second impairment to clear thinking that Lymies experience, is the restriction
of proper circulation within the blood vessels inside the brain. Using an instrument called
the Single Photon Emission Computer Tomography scanner ( SPECT scans), we are able
to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the
brains of chronic neurological Lyme patients was an abnormal ``Swiss-Cheese'' pattern of
blood flow. The cortical or thinking region of the brain was being deprived of good circulation,
the occipital (eyesight) regions had an increase flow. This could help explain why most Lyme
patients complain of poor concentration, and overly sensitive eyes. (91)

Lyme Tests

There's a Lyme test, so what's the problem? There are several Lyme tests, but most
of them are dependent on the body's ability to make antibody against this bacteria. As
we have seen this may be a problem. There is the S-layer protecting the bacteria, the
surface antigens are not readily exposed, there may be a blocking antibody, the bacteria
might be inside a human cell, the bacteria might be down regulating the immune system
through cytokines, the bacteria might have altered its antigenic appearance to fool the
immune system, the bacteria might be cloaked in B-cell membrane, the bacteria might
be hiding in joints, tendons, white blood cells, skin cells, and the brain, and finally the
bacteria may have shed its cell wall making rendering it in effect invisible. Remember
if even just one spirochete survives, it could cause a relapse. Then there is another
problem, the tests that detect antibody can only detect free uncomplexed antibody.
(23,25,55,70)

When an antibody is formed it is meant to latch on to something and never let go until
it is destroyed. Like a lock and key, antibodies fit their associated antigens. Once the
antibody attaches to the antigen it is no longer a detectable antibody, because it has
now become an antibody-antigen complex. This complex is not measurable using today's
commercially available tests. Also as the amount of antigen increases, the amount of
antibody can decrease because the antigen will trap out the available antibody and
sequester it. So a person who has a bad infection, but is making a limited amount
of antibody, can be overwhelmed by antigen thus making antibody detectable only
if you can detect the complex.

Ab + Ag = Ab/Ag-complex
Antibody + Antigen = Antibody/Antigen---complex--
(free) (free) (complexed)

Free antibodies are detectable with the current Lyme tests, but antigen/antibody
complexes are undetectable using either the ELISA or Western Blot tests.

This means: People who have the worst infections may have the lowest antibody
titers, and test negative because the bacteria ``load'' overwhelms the antibodies present.

* Note: It takes four weeks from the day of the tick bite to test positive.

There are two main categories of Lyme tests, the most common and least specific
is the Enzyme Linked Immune Sera Assay or ELISA, the other is an Immuno Blot
or Western Blot. The Western Blot essentially makes a map of the different antibodies
we make to the bacteria. The map separates the antibodies by size and weight and is
reported in units called kilo daltons or kDa. For example a Western Blot may report bands
at 22, 25, 31, 34, 39, and 41 kDa. Each of these bands represents an antibody response
to a specific protein found on the spirochete. The 41 band indicates an antibody to the
flagella protein, and is non specific. The 31 kDa band represents the OSP-A protein
and is specific for Borrelia, as is the 34 band OSP-B, and 25 kDa OSP-C.

In 1994 the NIH decided that there should be consistency between labs reporting
Lyme Disease Western Blots, and that a specific reporting criteria should be established.
This sounds good, but one could argue they made a bad situation worse. The consensus
of the Dearborn MI. committee decided to set the standards for a positive test based on
the number of specific bands that appear, and where as every lab prior to this hearing had
accepted bands 25, 31, and 34 as specific and significant. The NIH without any clear
reasoning disqualified those bands as even being reportable. The result was, what had
been a fair-good test had now become poor or even useless. Many labs stopped reporting
the actual bands and simply reported the test as positive or negative, thus preventing
any further interpretations. (90)

(Diagram of Western Blot)Band 41 kDa Flagellin
OSP-B Antigen 34 OSP-A Antigen 31 kDa
OSP -C Antigen 23

How badly did the NIH boot strap this test? The following is an analysis of the new
guidelines presented as an abstract and lecture at the 1995 Rheumatology
Conference in Texas. 1995 Rheumatology Symposia Abstract # 1254
Dr. Paul Fawcett et al.

This was a study designed to test the recently proposed changes to Western Blot
Interpretation. The Second National Conference on Serological Testing for Lyme Disease,
sponsored by the NIH. The committee proposed limiting the bands that could be reported
in a Western Blot for diagnosis of Lyme Disease. A IgG Western Blot must have five or
more of these bands: 18, 23,28, 30, 39, 41, 45, 58, 66, and 93 kda. An IgM Western Blot,
must have two or more of the following three bands: 23, 39, 41.

Conspicuously absent are the most important bands 22, 25, 31, and 34 which include OSP-A,
OSP-B and OSP-C group antigens. The three most widely accepted and recognized antigens.
These antigens are so immuno reactive that they were the antigens chosen for human vaccine
trials. Yet they are not considered important enough to include in the diagnostic criteria?
Why?

This abstract showed that under the old criteria, all of 66 pediatric patients with a history
of a tick bite and, Bull's Eye rash who were symptomatic, were accepted as positive
under the old Western Blot interpretation. Under the newly proposed criteria only 20
were now considered positive. That means 46 children who were all symptomatic,
would probably be denied treatment! That's a success rate of only 31 %.

66 Children with Bull's Eye rash Old W. Blot Criteria 100 % positive
New NIH Criteria 31% positive
The number of false positives under both criteria was ZERO %

* Note: A misconception about Western Blots is that they have as many false
positives as false negatives. This is not true. False positives are rare.

The conclusion of the researchers was: ``the proposed Western Blot Reporting
Criteria are grossly inadequate, because it excluded 69% of the infected children.
'' The Accuracy of Laboratories Using the ELISA/EIA Lyme Tests

We are told by manufactures, health departments, and clinics that the Lyme
ELISA tests are good, and that they are useful, but in two blinded studies that
tested laboratories accuracy, they failed miserably. In two studies by Lorie
Bakken MS/MPH she showed that there was not only inaccuracy and inconsistency
between competing laboratories, but also between triple identical samples sent to the
same lab. In other words identical samples often resulted in different results! In the
latest study by the College of American Pathologists, 516 labs were tested. The
overall result was terrible, there were almost equal numbers of false positives as
false negatives. Overall the labs were 55 % inaccurate! You are actually better
off to flip a coin!

(98, 99) 98- Bakken LL, Callister SM, Wand PJ, Schell RF. Interlaboratory
Comparison of Test Results for the Detection of Lyme Disease by 516 Participants
in the Wisconsin State Lab of Hygiene/College of American Pathologists Proficiency
Testing Progrm. J Clin Microbiol 1997; Vol 35, No 3:537-543

Repeatedly there have been patients who are seronegative for antibodies, yet culture
positive. Despite this our medical community is dependent on these tests and rely
upon them as though they were 100 % accurate. No matter how bad the tests are,
as long as we have them doctors will use them. This is why doctor Samual Donta MD
asked for a complete ban of the Lyme ELISA test at the 1996 LDF Lyme Conference,
at least until the tests could be standardized and made reliably accurate. He found that
in his long term treatment study, that some ELISA tests were more than 70 % inaccurate.
Yet many doctors continue to rely upon these tests as though they were the last word in
diagnosis, and all too often it is.

The worst problem for chronic Lyme patients is that after they are treated with antibiotics,
they are told they are cured, even if they have a recurrence of symptoms. There is a persistent
dogma in medicine that 28 days of IV antibiotics cures all Lyme Disease. In fact the on going
six year old Nantucket Island Lyme Treatment Study, showed IV antibiotics to have the highest
relapse rate in late Lyme disease! This was because doctors put too much faith in IV antibiotics,
as being so powerful, that they did not follow up IVs with oral antibiotics. The key to treating late
Lyme appears to be the length of antibiotic treatment, not the method. If IVs are followed up by
six months or more of oral antibiotics, the relapse rate dropped to 13%. (Dr. Leslie Fein MD,
MPH, Magnarelli MD, MPH 96 LDF Conference)

I have included in the references, several published studies, case histories and abstracts,
that deal with culture positive patients who had been previously treated aggressively with
antibiotics, often including Intravenous antibiotics. Most of these cases are patients who
are seronegative for any Lyme antibodies, yet are culture positive. If we are repeatedly
culturing this bacteria out of patients who have been treated, and who are negative by
all other tests, we need to re-think our understanding of this disease! We need to treat
symptoms not tests, we need to recognize that while Lyme is a treatable disease, it
in some cases appears to be incurable. I would not like to be the doctor who under
treats this disease, now knowing that relapses are potentially more dangerous than
treating until the symptoms are gone. (4,6,42,49,67,68,70-96) Too often I have seen
the word cured used in Lyme Disease Studies, only to find that the researchers have
redefined the word cure to mean seronegative. Seronegativity is not synonymous with
cure. The numerous culture positive cases in recent years should have negated that
kind of logic years ago, and yet in 1997 researchers are still publishing studies that
use antibodies, and PCR as the end point for cure. Its time to ask the patients one
simple question: How are you feeling?

So lets say hypothetically you are bit by an infected tick, you get a rash, you get sick,
and you have a positive test. So you get 2-4 weeks of antibiotics, and you get better,
but then you get sick again. No problem you go back to your doctor and he says ``Well,
we better give you another Lyme test'' and its negative? Why? Even though you have
an active infection, the antibiotics cleared that infection from your blood stream. That
is where your immune system is. The rest of the pathogens are hiding from the immune
system inside your joints, your tendons, and your brain. Only now you don't have
antibiotics to fight the infection, or any antibodies!

In a study by Dr. Musher MD, he looked at incompletely treated Tertiary Syphilis patients,
and compared them to those Tertiary Syphilis patients that never got antibiotics. He found
that the incompletely treated group went into dementia faster. Why? Because they had no
natural immunity left. Their ability to make sufficient antibody was diminished, because the
antibiotics eliminated the stimulus from the blood stream, but the infection was still hidden
in the brain!

(35,61,62,65,74,83)
Conclusion: Lyme is an extremely complex disease that can cause long term chronic
infections. Patients can be seronegative yet culture positive (even after aggressive antibiotic
therapy). The infection enters the brain early in the infection (within days). The sequestered
bacteria within the CNS can be so different from the initial infection that serum antibodies
are ineffective. Incomplete antibiotic treatment of Lyme Encephalitis can harm the patient.

For a historical account of where the medical community got off on the wrong foot with
the truth about Lyme disease, and why they continue to support the fallacies, read the
history of Lyme Disease in the Lyme Disease Survival Manual, by Tom Grier

Tom Grier
Duluth, MN,
USA

quote:

---

Originally posted by shelley:
Tree,
I just read your post. How do you know Benicar expands blood vessels?

That is interesting.

---

What is olmesartan?
* Olmesartan is in a class of drugs called angiotensin II receptor antagonists. Olmesartan prevents the constriction (narrowing) of blood vessels (veins and arteries). http://benicar.drugs.com/

;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;;; http://www.frx.com/products/benicar.html
BENICAR and BENICAR HCT are indicated for the treatment of hypertension. BENICAR lowers blood pressure by blocking the angiotensin II receptor. (((It also interrupts the release of the hormone which causes salt retention and increased blood volume.))) BENICAR HCT combines BENICAR with the diuretic (water pill) hydrochlorothiazide for additional blood pressure lowering.

- The CWD forms of the bacteria have actually been photographed living inside immune system cells, never mind all the places Tom's article mentions.

A minority of people are doing pretty well or very well on the protocol. Most of these people have made progress on other therapies, but may have relapsed or reached a plateau.

The majority of people posting results have either dropped out or are struggling or seeing little change.

What does this mean?
There SHOULD be many failures...why? MANY people will run to try it..and a LOT of them...shouldn't be doing it...for a number of reasons.

For example;

1-They don't meet the minimum criteria...but insist on doing it anyway....they fail.

2-Once they begin...they don't follow the protocol as it is laid out...they fail.

3-They claim to do the protocol...and are actually 'winging' it....and fail.

4-They have such a positive response in the beginning that they don't finish the protocol...and fail.

I have seen this time and time again.

i am personally guilty of it...I went for Rife...bought a Plasma Rife...was doing FANTASTIC on it...followed the directions of the manufacturer...and then listened to two outside opinions that told me to either slow down..or actually stop. well...I did both...slowed down..and stopped occassionally....and, I failed.

This was my fault...and as soon as I get my Rife back from a tune up...I'm going back at it.

Trout

Was looking at the Marshall protocol and was interested in it... but I cannot stop the antibiotics, need them. I will die if I stop the Doxy, so can one do the MP with the minocycline alone?

I read that mino is better then Doxy...

any thoughts?

thanks,

Benicar and total D avoidance are the backbones of the Marshall Protocol, so the answer is no to doing it with Minocin alone.

While I say that, I will say also that a number of RA (Rheumatoid Arthritis) patients have had success using low dosed pulsed Minocin alone. http://www.rheumatic.org/ http://www.roadback.org/

Trevor Marshall, the man behind the Marshall Protocol discovered a link between dysregulated D-metabolism that drives runaway inflammation in patients with infections due to CWD (cell wall divergent) bacteria.

I wish you GREAT LUCK on the MP.

!

Life can be a living hell on these antibiotics sometimes, and hope that the MP
works for you.

There is also Rifing if the MP does not work. I am thinking myself about the MP, but am not sure I can stop the antibiotics at this time. Rifing is on my list as well.

Good luck, and hope things go well for you.

Chronic severe pain from herxing has really taken its toll on my mind.

all the best,

quote:

---

Originally posted by Health:
Hello,

Was looking at the Marshall protocol and was interested in it... but I cannot stop the antibiotics, need them. I will die if I stop the Doxy, so can one do the MP with the minocycline alone?

I read that mino is better then Doxy...

any thoughts?

thanks,

Trish

---

Trish,
Here's what I would try to do if I were you. I'd try to switch from doxycycline to minocycline as a first step. Remember, though, that minocycline has twice the tissue penetration and several times the killing effect of doxy, so the dosage will be lower.

Something else you can do is start by cutting out dietary sources of Vit D and all vitamin & mineral supplements with vit D added. You can buy Kroger brand of organic whole milk withOUT vit D added at most Kroger stores. The FDA requires that Vit D be added to all other milk which has had its fat content altered, so that's why you have to look for whole organic milk in order to find Vit-D FREE milk.

Learn to observe the effects of sun exposures. Usually this is a delayed effect, so it's very easy to overlook this and to fail to make the connection. In fact, a good way to prove this effect to yourself is a challenge -- which is easier to do during the summer. Our daughter deliberately exposed herself to sunbathing during our family's July 4th outing in order to see how much it bothered her because she knew she was going to be starting the MP a few weeks later and it was her last chance to so this.

Prior to starting Benicar, the effects of the sun are less apparent and more subtle. They are usually delayed by at least a day, or even longer. I could try to explain why it's delayed, but I'm tired tonight and don't want to overtax my weary brain cells, so I'll wimp out this time by simply saying that you should expect the reaction to be delayed and don't worry too much about why this is.

By switching to minocycline from doxy, then the next step is easier. You'll need to stop all antibiotics for a one week wash-out period, prior to starting Benicar. Usually, most folks need only one week on Benicar alone before they can add back in the minocycline -- except that the Benicar plus minocyclien is such a potent combination that a mere 25 mg dose of minocycline every other day will knock you on your caboose.

If you live alone, the first few weeks can be very difficult. You may be too dizzy to drive to do your own grocery shopping. You might need a friend to check in on you daily to be sure that you have essential food items and to run errands for you, maybe even to bring you a prepared meal. Not everyone has such a difficult adjustment at first, but you need to be aware that some people do have this much trouble, so you need to figure out how you are going to manage to cope successfully if your first week or two is as rough as this.

Maybe later, I'll try to compose more about how to know whether you are a good candidate for the MP, but in brief summary, I'd say that one of the first criteria to ask yourself is, "Is this a good time in my life for me to succeed with this right now?" You need to be free to really hit the couch and give into it for as long as it takes to get through the initial adjustment period -- which can be anywhere form 1-2 weeks up to 1-2 months.

After that, the benefits are so rewarding that you have no more doubts about it. You start to feel better than you can remember feeling and you want to keep moving forward.

Avoiding sun and bright lights and wearing NoIR sunglasses is a key essential element. In fact, one MP-friendly doc will no longer even write an Rx for Benicar unless the patient brings in a pair of NoIR sunglasses during an office visit to prove that s/he is really serious about doing it right.

Another thing if you are planning to start, be sure that you have printed out and read all of the essential materials first, ahead of time, because after you start, you won't feel like spending very much time in front of the computer looking for answers to questions which you forgot to study in advance. Keep a printed copy available which you can read over and over and over again. You'll need the Phase I Guidelines and the FAQ and probably quite a few other goodies which are now posted at the MP website.

thanks so much for that post. Really really
helpful for me.

I am having a tough time even getting the Doxy I am on now, so will wait to get the lyme test done first, then ask the LLMD to treat me with mino. I dont know if he will, as he thinks I dont have lyme... but I have to get someone to treat me, so will have to find a way.

That is a good idea to switch to the mino first, then the benicar. I thought that one had to be on the benicar for 3 months, then start the mino. I did not know it was only one week. I must have read it wrong, will go and read it when I am more able to retain info.

I get sick within 10 mins of lying in the sun. I was sick today just lying inside by the window in the sun.... I had the sun all over my body, and when I went to my room had to ly down, then 2 hours later my mind was so foggy and drug like.
So, my reaction to the sun is not delayed, it is immediate, and this makes me wonder if it is not a herx?

I will study the marshall protocol more.

I was also thinking, about the dry eyes, the severe sjgrodens syndrome i had in the summer, and sometimes have now....
it is maybe? the inflammation that is plugging up the tear ducts or saliva ducts, so then the tears dont flow, and the saliva does not, the lungs dry up.. By killing the infection, or with the use of the benicar, the inflammation goes down, and the tears start.

thanks ever so much, really wonderful for you to write that for me.

quote:

---

Originally posted by Health:
That is a good idea to switch to the mino first, then the benicar. I thought that one had to be on the benicar for 3 months, then start the mino. I did not know it was only one week. I must have read it wrong, will go and read it when I am more able to retain info.

I get sick within 10 mins of lying in the sun. I was sick today just lying inside by the window in the sun.... I had the sun all over my body, and when I went to my room had to ly down, then 2 hours later my mind was so foggy and drug like.
So, my reaction to the sun is not delayed, it is immediate, and this makes me wonder if it is not a herx?
Trish

---

Trish,
Some of the Sarc patients who weren't able to persuade their docs to prescribe Benicar at first, especially a couple of years ago when it was still such a new drug on the market, started out with minocycline first in order to lower their bacterial load in hopes it would make their adjustment to Benicar later a little easier. That approach seems to have worked quite well for them.

Anything one does prior to starting Benicar is called Pre-Phase I of the MP. Even something as simple as avoiding all sources of vit D, both dietary and exposures to sun and bright lights, counts as being on Pre-Phase I of the program.

The best way to take minocycline for this purpose is to take 100 mg every other day (qod), which is called "pulsing" it -- because it actually increases the killing effect to do it this way, and you actually Herx more if you pulse it that if you take it daily. Taking minocycline daily fosters its anti-inflamatory DMARD effect instead of enhancing its bacteriostatic effect. (DMARD = disease modifying anti-rheumatic drug; ie, an "anti-inflamatory" drug)

Belinda at SarcInfo was one of the very earliest patients to do this. She's a fellow Texan and I'm had the privilege and pleasure of meeting her. She looks and feels great now, although she is still continuing on the MP/Benicar program. Here pulmonary sarc diagnosis was life-threatening at the time that she started the MP program. One would never be able to tell that now, though, just two years later.

She did 4 months of pulsed minocycline at 100 mg qod, before stopping the minocycline for a one week wash-out period, prior to starting Benicar.

You will definitely want to start with taking Benicar q6h (every six hours) instead of q8h (every 8 hours) due to the severity of your symptoms. Keep that in mind when you approach your doc. Benicar is much harder for Canadians to obtain because they have to import it from Germany since it's not in the Canadian formulary.

Regarding your immediate reaction to the sun, let me explain it this way. Folks who are really, really, really sick tend to have more immediate reactions to the sun. Most folks are only really, really sice, so their sun reactions are delayed instead of immediate. That's an overly simplistic explanation, but it will have to do.

Since your eyes bother you so much, be sure to start first of all with purchasing at least a couple of pairs of NoIR sunglasses. You need different shades for different purposes. If you can afford to do so, get all three shades -- 2%, 10% and 40%. They will all come in handy. It depends on your lifestyle as to which one's you'll need the most. If you hardly ever leave the house at all, then you might not need the darkest 2% shade and could get by for very brief periods outside with just the 10% shades instead. A lot of folks save their errands until nighttime because driving around in a car exposes you to a lot of light.

It can be hard driving a car in heavy traffic with the really dark 2% shade so you might want to find a friend to chauffeur you if you have to drive any long distance so that you can wear the darkest 2% shade while riding as a passenger in the car. Even when driving at night with on-coming headlights, you'll probably need either the 10% or the 40% shades on. Again, having a chauffer helps because then you can wear the darker shades and not worry about knocking down a pedestrian because you glasses are too dark to use safely when driving a car.

You'll find the link to info on NoIR sunglasses at both websites:
www.sarcinfo.com
www.marshallprotocol.com

The number one main reason why people fail therapy on the MP is that they don't "get it" when it comes to strict avoidance of sun and bright lights. Some folks think they are being strict enough when they really aren't. After you finally begin to experience the benefits of the program, then you no longer resent the inconvenience of the lifestyle changes or even question its necessity because by then you are seeking ways to improve your compliance by learning how to do it more carefully -- including knit-picky little details like driving gloves and neck scarves and sun hats with a dark brim to avoid reflected sunlight from striking your face. You turn into a fanatical cave-dwelling vampire because you feel so much better when you do.

At first, while your high 1,25-D level is dropping, you might feel worse at first, because a falling 1,25-D level allows the body's immune system to kick in and start killing CWD critters, so you can Herx just from nothing but sun-avoidance measures alone, even without the minocycline or the Benicar.

Can yo tell me more about that, if you don't mind!!!!!!!!! I'd like to have one done, especially now that I've been on abx since late August.

I have thrush and major stomache problems and I think it's all from Candida!!!!

Thank you soooooooo much,,,,Jamoie

Sure happy too .. another person from my area is on MP and got her phase 2 instuctions. She emailed it to us locals on her email support group list. Some folks were having serious problems, and she wanted us to be ware of things..... I believe I deleted that message; so that info is in my brain fog only...ok.

I believe it was at the bottom where it stated what periods of time were possibly involved for phases 2 and 3 plus adding in phase 1.

Phase 2 is not posted on MP; moderators send it privately to those who have reached this step.

I feel the longer someone has had chronic lyme, the longer it will be for them to get thru the MP completely.

If you've been bitten early, your chances are better at curing it. Betty G., Iowa

Many times I don't go back to a post I've replied too, so if I do not respond, please send me a private email ok.

I don't understand. I hear from people on the Marshall Protocol who said "they feel great". I thought everyone were supposed to raise the abx to a comfortable level of herxing all the time. Trevor has even said this, "make sure you are comfortably herxing with the abx".

How can you feel great at any stage, since you should be herxing comfortably all the time??

Also, how did you survive without leaving the house during the day????

I don't know how I would function without a walk or a breath of fresh air.

This seems to go against alot of my beliefs for getting well, but I know there is truth to it.

I just don't know how people can psycholgically handle living in a cave all the time. I am worried about my mental health with this.

Thanks for any feedback!

Inflammation is a nec. part of the healing process. It is, and always has been, a necessary step.

But too much inflammation = big OUCH.

Soooooo, okay reduce it. But don't block it entirely.

Humira and Remicade block TNF alpha. You FEEL really good when taking them. The side effects are TB and cancer. This is KNOWN.

Benicar blocks angiotensin.

The question is: why are these (angiotensin and TNF alpha) elevated in the first place?

What is the ROOT of the problem?

From my Updated nutshell post:

1. "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."
PMID: 8390527

It appears:
(1)Mg ++ charge levels low -> increase in Ca ++ charge (not good) -> stimulates angiotensin II (a protein, -- charge)-> TNF Alpha (a pro inflammatory cytokine, ++ charge)

Get your Mg level back up. That is the ROOT of the problem. How?...that becomes the problem!!! Impossible to do orally.

Please read my Updated Nutshell post and pay close attention to the BENEFITS of TNF alpha. It's not all bad.

The body is chosing ways to save/protect us.

A LOT of ACIDS react with the minerals/positive charge (glycogen is pos. charge also) to make hydrogen. CoQ10 carries hydrogen into the cells to react with free oxygen radicals to make H2O2. H2O2 is capable of knocking out most bacteria, viruses and even some spores.

But the cells can't stay acidic or they will die. (H2O2 is acidic.) So in steps catalase, an ENZYME (and you know what controls the enzymes) to break it down from H2O2 to H2O and O. Soooo for every 2 hydrogens we get into the cells, we get rid of ONE free radical (most are oxygen) and these damage the cells. Obviously we are normally making a LOT of hydrogen every second. Free radicals are very elevated in lyme.

In order to make CoQ10 (when we exercise) we need B6, which in turn needs Mg.

This bug picked THE most critical mineral to deplete for us.

The second worse mineral to deplete would be calcium since it takes Mg and Ca to make HEALTHY ANTIBODIES.

Do you see WHY the macrophages produced the acid? To react with stored minerals to make hydrogen...to combine with oxygen...as an attempt to knock off the pathogen.

The body is searching for alternative paths since with Mg low...few healthy antibodies can be made. And they are HIGHLY TARGETED.

P.S. Cancer doctors in Romania CURED 2 lyme patients, albeit only 2 and at early stage (rash), in 3 weeks by combining very large Mg doses and abx. These patients tested positive at the beginning and negative at the end. Furthermore, there is a U.S. Patent, titled: Magnesium for AUTOIMMUNE by Dr. Valletta. He CURED RA, ulcerative colitis and invasive cancer in 6 months time using (IV doses at first) Mg pyrophosphate and sublingual B6.

These are very very important documents. Who will listen and follow up? A relatively cheap cure for more than one disease seems to already exist.

I hope someone at Johns Hopkins is reading this board. This seems to be (to me at least) the only research facility that is dedicated to finding nutritional healing routes.

see article below
http://www.journal-inflammation.com/content/1/1/3

Cancer, inflammation and the AT1 and AT2 receptors

Abstract

The critical role of inappropriate inflammation is becoming accepted
in many diseases that affect man, including cardiovascular diseases,
inflammatory and autoimmune disorders, neurodegenerative conditions,
infection and cancer.

This review proposes that cancer up-regulates the angiotensin II
type 1 (AT1) receptor through systemic oxidative stress and hypoxia
mechanisms, thereby triggering chronic inflammatory processes to
remodel surrounding tissue and subdue the immune system. Based on
current literature and clinical studies on angiotensin receptor
inhibitors, the paper concludes that blockade of the AT1 receptor in
synergy with cancer vaccines and anti-inflammatory agents should
offer a therapy to regress most, if not all, solid tumours.

With regard to cancer being a systemic disease, an examination of
supporting evidence for a systemic role of AT1 in relationship to
inflammation in disease and injury is presented as a logical
progression. The evidence suggests that regulation of the mutually
antagonistic angiotensin II receptors (AT1 and AT2) is an essential
process in the management of inflammation and wound recovery, and
that it is an imbalance in the expression of these receptors that
leads to disease.

In consideration of cancer induced immune suppression, it is further
postulated that the inflammation associated with bacterial and viral
infections, is also an evolved means of immune suppression by these
pathogens and that the damage caused, although incidental, leads to
the symptoms of disease and, in some cases, death.

Mg testing is notoriously INACCURATE. It is an intracellular mineral.

This is far far greater than can be supplemented orally or even IM for that matter.

And...the level must be maintained until the infection has cleared.

These IV doses and monitoring would require hospitalization.

Valletta, U.S. patent - Mg for autoimmune - used IV DOSES of Mg pyrophosphate and sublingual B6 for the first 3 months. He cured RA, ulcerative colitis and INVASIVE bowel cancer.

And...you went to Italy. Speeding up glycolysis uses Mg. This further depleted your stored levels.

Having Mg given by NB (Tammi)prior to ICHT not only PROTECTED her, but helped this therapy work better. Very, very risky. DNP is in a category with cyanide. TOO ACIDIC. TOXIC.

HAVE to make a LOT of hydrogen and have to get it INTO the cells to heal.But the cells can't remain acidic. Need Catalase to break down the H2O2 into H2O and O. Mg controls catalase and over 350 other enzymes.

To make hydrogen takes both...positive charges and a lot of negative ones. Then CoQ10 to carry the hydrogen INTO the cells. CoQ10 needs enough B6, which in turn needs additional Mg.

The "Universal Remedy" of old was:

Magnesium oxide, tannic acid and activated charcoal.

Mg + acids -> hydrogen (IF carried into the cells, INactivates PFK - Bb dependent on it). Then once destroyed (cell walls) -> toxic (outer cell walls, neg. charge - proteins). Activated charcoal to "mop up" the toxins (or possibly additional pos. charges).

Suki, my sister is blocking TNF alpha via Humira. She continues have problems...both knees replaced (doctor said worse knees he had ever seen - disintegrated).She continues to have edema (hyponatremia).

A low salt diet is Mg sparing. It may be the body dumps Na to conserve as much Mg as possible.

Get to the ROOT of the problem. These drugs...calcium channel blockers, angiotensin blockers, TNF alpha blockers...treat the symptoms, not the disease. They may help to "conserve" Mg temporarily, but the side effects concern me.

A long time ago, I took the 40+ lyme symptoms and linked them to Mg deficiency symptoms.

Even WHEN the infection is gone, the symptoms will remain UNTIL the very deficient Mg levels are restored. Inflammation will continue to happen. The body perceives it as still under attack.

Thanks for that post! All those complaints about Benicar have made me think twice!

I already have kidney problems according to my Dr. of Chinese Medicine and this info scares me.

I my need to go with IM Bicillin or an oral abx combo as I have Chronic Lyme and have never been treated.

I am seeing Dr. Dhonden (Tibetan herbalist) in NY this week and he should be able to give me an idea what to do.

On the Yahoo list infectionandinflamation ( I & I ) there been alot of discussion on this in the last few days.

This type of action bothers me, in the sense that it indirectly stifles what's said
about the many protocols that we all have knowledge of for fighting out respective diseases.

Even though libel or other civil actions are probably extremely hard to prove about stuff written on the internet, especially about something in the public domain, this type of action results in hardships - financial and emotional.

The Court's website was posted on the I & I list. The plaintiff (Trevor) lost at the hearing in favor of the defendant (Penny)(Penny was represented by a lawyer), and Trevor filed a motion to dismiss without prejudice right after that, and it was granted.

I just don't know what to think anymore.

One caution on confusing the MP with potential ARB therapies for cancer. In addition to emplyoying an ARB, Benicar, the MP strives to reduce the active hormone of vitamin D, 1,25-D, to an absolute minimum.

Whether this is helpful for Lyme patients is at this point unknown. For cancer patients, however, it is NOT recommended. 1,25-D plays a constructive role in the body's defense against cancer. Dr. Marshall acknowledges this. In breast cancer, for example, there is a strong correlation between declining 1,25-D and mortality.

Marshall claims that in patients with what he calls Th1 disease, Benicar helps reduce 1,25-D. It is important to understand, though, that no direct relationship has been demonstrated. Rather, a very specific disease process is described by Marshall, in which pockets of bacterial inflammation synthesize 1,25-D as part of an inflammatory cascade. By blocking the cascade, Benicar indirectly reduces the level of 1,25-D in the body.

So it is possible that in patients who don't have 'Th1 disease', ARBs won't have any effect on 1,25-D at all.

These are complicated distinctions, I realize, but they are also potentially quite important.

Marnie, thanks for that link to the Benicar complaints. It should be noted that those individuals are taking the standard FDA approved doses of 20 or 40mg. Dosing on the MP is much higher. The minimum Benicar dosing for the first 18 months is 120mg. Patients are encouraged to increase this to an 'optimal' dose of 160mg. Should they experience 'intolerable herxing', patients are further encouraged to take 40mg every 4 hours, or 240mg a day!

I have read the FDA safety review of Benicar and I am far from convinced that these MP doses are safe. The human trials of Benicar focused on doses of 40mg or less. There were some studies of 80mg, and even one of 160mg, but these were fairly short term - they can't tell us what to expect when a dose of 160mg is sustained for a year and a half, or longer.

In drug safety trials, animal studies are used to test dosages which for ethical reasons cannot be tested on humans. The FDA review of Benicar safety makes frequent mention of a 2 year study on rats. I haven't been able to identify the doses of Benicar they were given, but there were adverse effects, concentrated in the kidneys, like renal tumors and tubular cell hyperplasia.

The FDA took these outcomes seriously enough to request additional information and vote formally that the adverse impacts in the rat study were both real and relevant to man.

It is probably also worth noting that 1st of 2 reviews of medical data by the FDA, in which the animal studies are mentioned frequently, the "Summary and Recommendations" advise a lower starting dose than 20mg, and that "all patients be started on the lower dose."

In short, I can't see any way to read that FDA data that certifies the safety of the doses Marshall's protocol requires.

Paul

My doctor is willing to do and is doing the Marshall protocol, but not as long as the people have dental infections, cavitations, and show heavy metal and chemical toxicity.

As long as these are still in the body, as they are with almost everybody that is chronically ill, the body is doing battle and most of all, the minerals are out of sync and have to be brought back before successful detoxing can take place. That usually is impossible as long as the toxic dental conditions exist.

The mineral base, lack of some and too much of others, and allergies toward some, is underlying the bacterial infection. I do not believe that the lack of magnesium did only start with Lyme exposure.

We know that people with chronic exposure to mercury have low sodium and low calcium levels. Blood tests are no indication because the body will pull some of the minerals out of wherever it can find it - out of the bones, and a blood test is not really a true indication of the actual level and availability in all body parts. We know that calcium and mag work in tandem.

I truly wish the Rumanians had found the solution. Mag plays a role, but there is a whole lot more to it -- from my experience and what I hear from my doctor.

Take care.

How much IV mag do you think that it takes to bring levels back up

What about just doing an Iv push 3 x a week with mag/cal/b6/glute/vit C?

***Borrelia bergdorferi is a bacterium that doesn't even use iron as a cofactor for enzyme reactions. It instead uses magnesium.''

Doc Kaiser's Microbiology Home Page
Copyright � Gary E. Kaiser
All Rights Reserved
Updated: Jan. 21, 2002
http://www.cat.cc.md.us/courses/bio141/lecguide/unit2/innate/nutimm.html

If the above link does not work, type in the *** sentence to get to Dr. Kaiser's website. Yes, he misspelled bergdorferi.

Bb uses our supply of Mg. In addition, we need it to make ATP, activate enzymes, and most importantly...make HEALTHY antibodies.

Without enough Mg...the fab portion of the antibodies specifically made by us to destroy Bb is damaged. Up goes TNF alpha (one of it's jobs is to rid damaged antibodies).

PROOF:

Characterization of the physiological requirements for the bactericidal effects of a monoclonal antibody to OspB of Borrelia burgdorferi by confocal microscopy.

The bactericidal effect of Fab-CB2 is not dependent on the induction of spirochetal proteases but is dependent on the presence of Ca2+ and Mg2+.

Supplementation of Ca2(+)- and Mg2(+)-free medium with these cations ***restored the bactericidal effects of Fab-CB2.

The mechanism by which a Fab fragment of an antibody destroys a bacterium directly may represent a novel form of antibody-organism interaction.

PMID: 9125579

1. We have a microbiologist who comes out and clearly states Bb uses Mg for its enzyme reactions.

2. We have cancer doctors in Romania who restored very, very low Mg levels and cured lyme.

3. We have an Italian doctor who used Mg pyrophosphate and sub. B6 in large doses - maintained, IV at first- and he cured RA, ulcerative colitis and invasive bowel cancer in 6 months.

4. We have history...Mg chloride was used many years ago (Delbet et al)to cure many diseases...but vaccines were being developed...

The tide is turning slowly...

12/15/04...WebMD "Peanut Butter Packs a Healthy Punch"

Good nutrition and exercise to stay healthy and nutritional supplements (IV) to get healthy if we encounter very toxic pathogens. Safer, IMHO.

Restore the balance.

Look very closely at the % Mg serum drop that the Romanians discovered. If the normal male has 15 GRAMS of Mg stored in the body (less than 1% is in the serum)...how much has been pulled out of storage (liver likely)? How much and which Mg did they use? How often? I wish I knew.

Find Valletta's U.S. patent. Look at the doses and TIMING of the IV Mg.

The kidneys maintain the pH balance. They will dump excess Mg in a 2 hour time frame.

It APPEARS maintaining a slightly, I repeat, slightly, higher level of Mg/B6 in the blood stream for as many hours a day as possible is critical to healing.

In my updated nutshell post, find the mdschoice website to learn about the functions of Mg. Pay close attention to what it says about immunoglobulins (antibodies), proteins, enzymes, ATP, etc...amazing. Highlight the words you understand...skim the rest. Eventually this will all fall in place.

I'm gonna drill it into you until it does

;-D

Marnie-
Dr M only advocates the use of Benicar. Humira has different actions.

It is my understanding that the D levels are responsible for the loss of magnesium and calcium increase and when they are regulated then blood levels are normalised.

Sarcies can be at risk of kidney failure from high calcium levels and one of my friends says already the MP has helped this.

I am on the MP myself and though I do think I am improving on it so far (about 3 months in) I do have reservations about longterm safety and for that reason I only take the minimum dose - 40mgs X 3 a day.

Paulscha - Thanks for the info, I will look back on the I & I board. For me it is a matter of weighing up the risks of long term abx (Flagyl for instance has been linked to cancer and the high relapse rate of Lymies on penicilin) and the possible dangers of the MP!