I am beginning to wonder if I had lyme or
if that test (Igenex) could have been a
false positive. Now that I went on all
the antibiotics, I didn't come out on top.

Do you have a specific autoimmune disorder in mind? What are your main symptoms?

I promise you, if you can find that person, you will know a lot more than you do now.

It is also called Autonomic Response Testing, and your Autnomic Nervous System will tell the truth and you will get a sense of direction as to what you need to address.

There is besides others in your area a nice clinic in Washington, D.C. with very capable people doing this kind of testing. They certainly will be able to shed some light on all.

That has been proven with Rheumatoid Arthritis, the fluid from swollen joints fails Koch's theory, but the DNA evidence proves that there was a pathogen there.

ALS cases have recovered their damaged nervous systems once the pathogen is removed. I have read of a 70+ year old ALS man who was totally bedridden with less than 24 hours to live. After IV antibiotics, he was walking again!

Very confusing issue. But we have an appointment with Dr.J in Dec, so I hope he can shed some light on this subject.

For example, my first LLMD said it was
very unusual to have more symptoms occur
while on antibiotics. I was finding that
I had more tingling, burning going on in
my limbs, gut, throat. Those symptoms have
basically stopped since the antibiotics were
stopped.

Now, it seems I am intolerant (not necessarily allergic) to any medication,
which goes beyond the normal spectrum of
antibiotics. Every time I take a drug,
except for my asthma and Klonopin, I get
a "burning headache." I have also become
intolerant/allergic to fruits since going
off antibiotics.

This seems different than lyme symptoms,
and I have been told this by current LLMD--
one of the best. To me, I keep wondering
if my immune system has been damaged by
a certain drug protocol.

Has it caused something called Multiple
Drug Allergy Syndrome? Is it really an
immune system gone wrong, ie in the arena
of Lupus, etal.

Since I had to go off antibiotics a year
ago, I have had dry mouth syndrome, indicative of Sjorgen's, but yet my most
recent ANA and other testing is normal, not
pointing to these illnesses.

It has also been pointed out to me that I
could have central nervous system damage.
Supposedly I am in remission for lyme, still
have Babesia, but I can't take drugs for the
burning occurs in my head.

I tried Dr. Shoemaker's protocol, but again
drugs are hurting my body. Is this neuro-
toxin, I am not sure? Part of me now
believes this is something else. I just
want to know what.

And so, I have been going to both mainstream
and alternative doctors, and no one has been
able to put a spin on this.

quote:

---

Originally posted by bd:
I believe the scientific evidence, mostly PCR DNA tests, has proven that there is no such thing as a truely "autoimmune" condition. You can have an allergic reaction to an infection, your immune system can mistake part of you for a pathogen, but in every case, remove the pathogen and the condition goes away.

That has been proven with Rheumatoid Arthritis, the fluid from swollen joints fails Koch's theory, but the DNA evidence proves that there was a pathogen there.

ALS cases have recovered their damaged nervous systems once the pathogen is removed. I have read of a 70+ year old ALS man who was totally bedridden with less than 24 hours to live. After IV antibiotics, he was walking again!

DO NOT buy into the hogwash coming out of the medical establishment. They want you to believe that you just have to suffer and take pain killers. They will perscribe all sorts of toxic drugs to treat the symptoms, but will do nothing to treat the cause.

---

On the contrary; it is the other way around, as so many have pointed out: you are far more likely to be a false negative than a false positive.

One so-called "autoimmune" disease, that has never truly been proven to be autoimmune at all, is multiple sclerosis. In many cases, Lyme disease is probably misdiagnosed (and mistreated) as MS.

But don't take my word on that. You can get a more detailed summary in an editorial from the December 26, 2001 edition of Journal of the American Medical Association that was written by Dr. Donald Gilden, M.D., a full joint professor of neurology and microbiology who has been chair of the department of neurology since 1985 at University of Colorado Medical School. Dr. Gilden's credentials can be found in the following 2 links:
http://www.uchsc.edu/sm/neuro/gilden_donald.htm (general profile)
http://www.uchsc.edu/sm/neuro/PDFs/gilden.don.pdf (curriculum vitae)

Dr. Gilden's editorial is very blunt and to the point on this issue: there has never been any proof of true autoimmunity in MS, no actual identification of immune markers on the surfaces of myelin, oligodendrocytes, etc.

It is interesting to note the chronological context of Dr. Gilden's comments: just a couple years before, preliminary results of "The Lesion Project" had revealed 4 different patterns of histology in MS patients, with much attention paid to oligodendrocyte (myelin-producing and regenerating cells) status in the vicinity of the lesions. Preliminary findings for the Lesion Project are summarized here:
http://www.neurologyreviews.com/aug02/nr_aug02_mslesion.html

and the abstract to the original article can be found here:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10581222&dopt=Abstract

Note the quoted pattern of unsubstantiated logic in the summary; note the "automatic presumption of autoimmune" in the summary and in the abstract:

"Patterns 1 and 2 suggest that myelin is the target, while patterns 3 and 4 suggest the oligodendrocyte may be the target." "She explained that patterns 1 and 2 resemble autoimmune models of multiple sclerosis, while patterns 3 and 4 resemble viral, toxic, ischemic, or metabolic models."

Given those quotes, consider in particular the following quote from Dr. Gilden, whose research group has painstakingly sought to identify the actual antigens involved in MS inflammatory damage, which came nearly two years after the Lesion Project summary information had been published in the December, 1999 edition of the medical journal Brain:

"For example, the target antigen(s) in MS is unknown, and it has never been shown that abundant brain white matter proteins, such as myelin basic protein or myelin oligodendrocyte protein, bind to or absorb out the OGBs in MS."

What I find even more amazing is that an MS patient can bring to his or her neurologist a Western blot assay with 4 highly intense bands, each of which is specific for Lyme, and the neurologist can dismiss this evidence as "negative for Lyme;" yet that same neurologist can prescribe potentially dangerous immunosuppressive drug therapies to his or her heart's content without, as Dr. Gilden points out, a single documented case of an antibody directed against myelin, oligodendrocytes, or other living tissues affected in MS.
__________________________________________________________
(Selected passages from Dr. Gilden's editorial)

"Although the cause of MS is unknown, 2 leading theories are that the disease is infectious, probably viral, or that it is produced by a host-immune response to an infectious agent or autoantigen.5"

"Although many investigators believe that MS is an autoimmune disorder, largely by analogy with the prototype immunopathology, experimental allergic encephalomyelitis (EAE), proof is lacking."

"For example, the target antigen(s) in MS is unknown, and it has never been shown that abundant brain white matter proteins, such as myelin basic protein or myelin oligodendrocyte protein, bind to or absorb out the OGBs in MS."

"Careful examination of MS plaques has not revealed any IgG binding to the surface of intact myelin sheets, even in the presence of IgG-positive plasma cells15; thus, if antimyelin antibody contributes to myelin breakdown in chronic MS lesions, the determinant does not appear to be an antigen on the surface of intact healthy myelin sheaths."

"...for the 2 instances in which the specificity of CSF OGBs was studied, they represented antibody directed against the agent that causes disease."

"For example, the OGBs in the CSF of patients with SSPE are antibody directed against measles virus.9 Similarly, the OGBs in cryptococcal meningitis were shown to be completely removed by absorption with cryptococcal antigen but not by absorption with Candida antigen, ruling out the possibility that cryptococci nonspecifically absorb the IgGs.10"

"Other examples of the specificity of OGBs in CNS infectious disorders include the fact that the oligoclonal IgG in human T-lymphotrophic virus 1 (HTLV-1) myelopathy is directed against HTLV-1 virus;11 that the oligoclonal IgG in the CSF of patients with mumps meningitis is directed against mumps virus;12 and that the oligoclonal IgG in the CSF of neurosyphilis patients is directed against Treponema pallidum, the cause of syphilis.13 In addition, progressive multifocal leukoencephalopathy is an exclusively human demyelinating disease that has been proven to be caused by a virus.14"

"Furthermore, there is no immune-mediated animal model of MS, and the collective abundant data gathered on immunogenetic background, macrophage function, specific T-cell subpopulations, and cytokine and chemokine responses in EAE and MS patients have failed to clarify the nature of disease production."

"Equally discouraging is that the multiple immunosuppressive and immunomodulating agents used to treat MS have not produced the gratifying response often seen in myasthenia gravis, a proven autoimmune disease. Moreover, although EAE can be induced in syngeneic recipients by adoptive transfer of lymphocytes from animals sensitized with whole brain white matter or myelin basic protein, there is only a single report of demyelination produced by passive transfer of antibody from MS patients.16"

"Although seemingly heretical, it was recently suggested that a moratorium be placed on the autoimmune hypothesis in MS to redirect funds for research on novel approaches to the problem.17"

______________________________________________________
(Full editorial)

Journal of the American Medical Association
Vol. 286 No. 24, December 26, 2001

Editorial

Viruses and Multiple Sclerosis

Donald H. Gilden, MD

Multiple sclerosis (MS) is the most common demyelinating disease of humans. In the United States alone, the prevalence is 250 000 to 350 000 cases.1 Based on data accumulated in 1994, the annual cost was estimated at more than $34,000 per person, translating into a conservative estimate of a national annual cost of $6.8 billion and a total lifetime cost per
case of $2.2 million.2 Most MS patients are young. Disease usually begins between ages 15 and 45 years and has a relapsing-remitting course, although a substantial proportion of patients develop chronic progressive disease.

The pathologic hallmark of MS is the plaque, an area of white matter demyelination often accompanied by inflammation. The inflammatory infiltrates are composed of T lymphocytes, some B cells and plasma cells, and activated macrophages or microglial cells.3 Although it is generally believed that inflammation is an obligatory and possibly primary feature of
demyelination in MS, myelin destruction also may proceed despite a nearly complete lack of lymphocytic infiltration, suggesting a role for endogenous glia, such as microglia or astrocytes, as a source of injury mediators.3 Immunoglobulin G and complement are localized primarily at the periphery of plaques.4

Although the cause of MS is unknown, 2 leading theories are that the disease is infectious, probably viral, or that it is produced by a host-immune response to an infectious agent or autoantigen.5

Results from 3 different areas of investigation argue for a viral cause of MS. First, epidemiologic analysis of all cases of MS in the Faroe Islands in 1920-1977 indicated a point-source epidemic of MS, probably introduced by British groups or their baggage; thus, MS in the Faroes appeared to be a transmissible, most likely infectious disease.6 Second, studies of identical twins in which one has MS have shown that only 30% of the other twins develop disease, suggesting that more than a putative susceptible genotype determines disease.7 Third, although the protein of normal human cerebrospinal fluid (CSF) contains up to 13% IgG, the CSF of MS patients contains 15% to 30% IgG and sometimes more, as well as oligoclonal bands (OGBs).8 The latter are found almost exclusively in central nervous system (CNS) disorders of infectious origins, such as
neurosyphilis, tuberculous and fungal meningitis, some acute viral CNS infections, and subacute sclerosing panencephalitis (SSPE), a chronic encephalitis caused by measles virus.

Furthermore, for the 2 instances in which the specificity of CSF OGBs was studied, they represented antibody directed against the agent that causes disease. For example, the OGBs in the CSF of patients with SSPE are antibody directed against measles virus.9 Similarly, the OGBs in cryptococcal meningitis were shown to be completely removed by
absorption with cryptococcal antigen but not by absorption with Candida antigen, ruling out the possibility that cryptococci nonspecifically absorb the IgGs.10 Other examples of the specificity of OGBs in CNS infectious disorders include the fact that the oligoclonal IgG in human T-lymphotrophic virus 1 (HTLV-1) myelopathy is directed against HTLV-1 virus;11 that the oligoclonal IgG in the CSF of patients with mumps meningitis is directed against mumps virus;12 and that the oligoclonal IgG in the CSF of neurosyphilis patients is directed against Treponema pallidum, the cause of syphilis.13 In addition, progressive multifocal leukoencephalopathy is an exclusively human demyelinating disease that has been proven to be caused by a virus.14

Although many investigators believe that MS is an autoimmune disorder, largely by analogy with the prototype immunopathology, experimental allergic encephalomyelitis (EAE), proof is lacking. For example, the target antigen(s) in MS is unknown, and it has never been shown that abundant brain white matter proteins, such as myelin basic protein or myelin oligodendrocyte protein, bind to or absorb out the OGBs in MS. Careful
examination of MS plaques has not revealed any IgG binding to the surface of intact myelin sheets, even in the presence of IgG-positive plasma cells15; thus, if antimyelin antibody contributes to myelin breakdown in chronic MS lesions, the determinant does not appear to be an antigen on the surface of intact healthy myelin sheaths.

Furthermore, there is no immune-mediated animal model of MS, and the collective abundant data gathered on immunogenetic background, macrophage function, specific T-cell subpopulations, and cytokine and chemokine responses in EAE and MS patients have failed to clarify the nature of disease production. Equally discouraging is that the multiple immunosuppressive and immunomodulating agents used to treat MS have not produced the gratifying response often seen in myasthenia gravis, a proven autoimmune disease. Moreover, although EAE can be induced in syngeneic recipients by adoptive transfer of lymphocytes from animals sensitized with whole brain white matter or myelin basic protein, there is only a single report of demyelination produced by passive transfer of
antibody from MS patients.16

Although seemingly heretical, it was recently suggested that a moratorium be placed on the autoimmune hypothesis in MS to redirect funds for research on novel approaches to the problem.17

Various microorganisms have been associated with MS, but none has been tightly linked to disease. The most recent organism to be implicated is Chlamydia pneumoniae, a gram-negative bacterium. Since the original detection of C pneumoniae DNA and antibody in the CSF of some MS patients,18 various laboratories around the world have attempted to confirm this potentially important finding. However, multiple studies have indicated a lack of any significant association between C pneumoniae and MS.19 In the past decade, 2 human herpesviruses also have been associated with MS. One is human herpesvirus 6 (HHV-6), the cause of roseola, and the other is Epstein-Barr virus (EBV), the cause of infectious mononucleosis. The detection of fingerprints of these 2 ubiquitous viruses known to be latent in blood B-EBV or T-HHV-6 cells is intriguing, since the primary encounter with either virus usually occurs before or during puberty, the same time that
epidemiologic evidence indicates exposure to the disease-causing agent of MS. However, HHV-6 is found not only in the brain and CSF of MS patients, but also in neoplastic and normal brain,20 suggesting that the detection of virus reflects its reactivation from latency and blood T-cell trafficking through brain. Furthermore, no EBV-specific RNA was detected in 10 MS patients' brains by in situ hybridization.21

In this issue of THE JOURNAL, a prospective serologic study of 62 439 women by Ascherio et al22 found significant elevations in serum anti-EBV antibody titers before onset of MS, particularly antibody to the EBV nuclear antigen 2 (EBNA-2). While the findings would suggest a role of EBV in the etiology of MS, CSF data would be helpful, since the IgG in MS patients' brain tissue and CSF is synthesized intrathecally and may more accurately reflect the immune response at the site of disease. While the neurotropism of EBV and its ability to produce serious neurologic disease at all levels of the human neuraxis have been documented,23 if EBV or any other virus causes MS, it should be possible to demonstrate that MS OGBs contain antibody directed against the suspected agent.

Many viruses and pathogens have been associated with MS, although none has been tightly linked to disease.24 The potential to identify rare or low-abundance pathogens has improved, and the molecular virologic strategies and techniques available today allow studies of virus detection not possible 20 years ago. For example, the ability to prepare and characterize libraries of genes from human tissue based on a difference in their genes or gene products allowed the isolation of complementary DNA clones derived from hepatitis C virus (HCV).25 Those cDNA clones were obtained without prior knowledge of the virus, the viral genome, or presence of circulating viral antibodies. The abundance of HCV-specific RNA from infected animals was ultimately determined to be only approximately 0.00001% or 1:107. Combined cloning in expression vectors (even without subtraction hybridization) and immunologic screening led to the identification of an
HCV-specific clone in approximately 106 recombinant phage.

Some of these strategies already have been applied to MS. Cloning of IgG genes in brain tissue (and CSF) of MS patients has revealed the presence of overrepresented heavy-chain sequences expressed at multiple plaque sites. Alignment of the heavy-chain sequences to their closest germline counterparts revealed clonal amplification and extensive somatic mutation, features of an antigen-driven response.26 Comparison of the IgG heavy-chain sequences in MS and SSPE again revealed features of an antigen-driven response in both diseases. Since the antigen in SSPE is known to be measles virus, the parallel findings in MS suggest an antigen-driven immune response,27 rather than a nonconventional mechanism of B-cell activation. This concept warrants further analysis of the specificity of IgG in brain tissue and CSF in MS. Although the cause of MS is not likely to be found under the EBV lamppost, the search for a viral cause of MS must continue.

Author/Article Information

Author Affiliation: Departments of Neurology and Microbiology, University of Colorado Health Sciences Center, Denver.

Corresponding Author and Reprints: Donald H. Gilden, MD, Department of Neurology, University of Colorado Health Sciences Center, 4200 E Ninth Ave, MS B182, Denver, CO 80262 (e-mail: [email protected]).

Editorials represent the opinions of the authors and THE JOURNAL and not those of the American Medical Association.

Funding/Support: This editorial was supported in part by Public Health Service grant NS 32623 from the National Institutes of Health.

Acknowledgment: I thank Marina Hoffman for editorial review and Cathy Allen for preparing the manuscript.

REFERENCES

1.
Anderson DW, Ellenberg JH, Leventhal CM, Reingold SC, Rodriguez M, Silberberg DH.
Revised estimate of the prevalence of multiple sclerosis in the United States.
Ann Neurol.
1992;31:333-336.
MEDLINE

2.
Whetten-Goldstein K, Sloan FA, Goldstein LB, Kulas ED.
A comprehensive assessment of the cost of multiple sclerosis in the United States.
Mult Scler.
1998;4:419-425.
MEDLINE

3.
Lassmann H, Raine CS, Antel J, Prineas JW.
Immunopathology of multiple sclerosis: report on an international meeting held at the
Institute of Neurology of the University of Vienna.
J Neuroimmunol.
1998;86:213-217.
MEDLINE

4.
Lumsden CE.
The immunogenesis of the multiple sclerosis plaque.
Brain Res.
1971;28:365-390.
MEDLINE

5.
Gilden DH, Devlin ME, Burgoon MP, Owens GP.
The search for virus in multiple sclerosis brain.
Mult Scler.
1996;2:179-183.
MEDLINE

6.
Kurtzke JF, Hyllested K.
Multiple sclerosis in the Faroe Islands, I: clinical and epidemiological features.
Ann Neurol.
1979;5:6-21.
MEDLINE

7.
Spielman RS, Nathanson N.
The genetics of susceptibility to multiple sclerosis.
Epidemiol Rev.
1982;4:45-65.
MEDLINE

8.
The proteins of cerebrospinal fluid: findings in multiple sclerosis.
In: McAlpine D, Lumsden CE, Acheson ED, eds. Multiple Sclerosis: A Reappraisal. 2nd ed.
Edinburgh, Scotland: Churchill Livingstone; 1972:368-398.

9.
Vandvik B, Norrby E, Nordal HJ, Derge M.
Oligoclonal measles virus-specific IgG antibodies isolated from cerebrospinal fluids, brain
extracts, and sera from patients with subacute sclerosing panencephalitis and multiple
sclerosis.
Scand J Immunol.
1976;5:979-992.
MEDLINE

10.
Porter KG, Sinnamon DG, Gillies RR.
Cryptococcus neoformans-specific oligoclonal immunoglobulins in cerebrospinal fluid in
cryptococcal meningitis.
Lancet.
1977;1:1262.
MEDLINE

11.
Grimaldi LM, Roos RP, Devare SG, et al.
HTLV-1-associated myelopathy: oligoclonal immunoglobulin G bands contain anti-HTLV-1
p24 antibody.
Ann Neurol.
1988;24:727-731.
MEDLINE

12.
Vandvik B, Norrby E, Steen-Johnsen J, Stensvold K.
Mumps meningitis: prolonged pleocytosis and occurrence of mumps virus-specific
oligoclonal IgG in the cerebrospinal fluid.
Eur Neurol.
1978;17:13-22.
MEDLINE

13.
Vartdal F, Vandvik B, Michaelson TE, Loe K, Norrby E.
Neurosyphilis: intrathecal synthesis of oligoclonal antibodies to Treponema pallidum.
Ann Neurol.
1982;11:35-40.
MEDLINE

14.
Padgett BL, Walker DL, ZuRhen GM, Eckroade RJ, Dessel BH.
Cultivation of papova-like virus from human brain with progressive multifocal
leukoencephalopathy.
Lancet.
1971;1:1257-1260.
MEDLINE

15.
Prineas JW, Kwon EE, Cho E-S, et al.
Immunopathology of secondary-progressive multiple sclerosis.
Ann Neurol.
2001;50:646-657.
MEDLINE

16.
Saeki Y, Mima T, Sakoda S, et al.
Transfer of multiple sclerosis into severe combined immunodeficiency mice by mononuclear
cells from cerebrospinal fluid of the patients.
Proc Natl Acad Sci U S A.
1992;89:6157-6161.
MEDLINE

17.
Steiner I, Wirguin I.
Multiple sclerosisin need of a critical reappraisal.
Med Hypotheses.
2000;54:99-106.
MEDLINE

18.
Sriram S, Stratton CW, Yao S, et al.
Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.
Ann Neurol.
1999;46:6-14.
MEDLINE

19.
Tsai JC, Gilden DH.
Chlamydia pneumoniae and multiple sclerosis: no significant association.
Trends Microbiol.
2001;9:152-154.
MEDLINE

20.
Cuomo L, Trivedi P, Cardillo MR, et al.
Human herpesvirus 6 infection in neoplastic and normal brain tissue.
J Med Virol.
2001;63:45-51.
MEDLINE

21.
Hilton DA, Love S, Fletcher A, Pringle JH.
Absence of Epstein-Barr virus in multiple sclerosis as assessed by in situ hybridisation.
J Neurol Neurosurg Psychiatry.
1994;57:975-976.
MEDLINE

22.
Ascherio A, Munger KL, Lennette ET, et al.
Epstein-Barr virus antibodies and risk of multiple sclerosis: a prospective study.
JAMA.
2001;286:3083-3088.
ABSTRACT | FULL TEXT | PDF | MEDLINE

23.
Majid A, Galetta SL, Sweeney CJ, et al.
Epstein-Barr virus myeloradiculitis and encephalomyeloradiculitis.
Brain.
2002;125:1-7.

24.
Johnson RT.
Viral Infectious of the Nervous System.
2nd ed. Philadelphia, Pa: Lippincott-Raven; 1998.

25.
Choo Q-L, Kuo G, Weiner A, Overby L, Bradley D, Houghton M.
Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome.
Science.
1989;244:359-362.
MEDLINE

26.
Owens GP, Kraus H, Burgoon MP, Smith-Jensen T, Devlin ME, Gilden DH.
Restricted use of VH4 germline segments in an acute multiple sclerosis brain.
Ann Neurol.
1998;43:236-243.
MEDLINE

27.
Smith-Jensen T, Burgoon MP, Anthony J, Kraus H, Gilden DH, Owens GP.
Comparison of IgG heavy chain sequences in MS and SSPE brains reveals an
antigen-driven response.
Neurology.
2000;54:1227-1232.
MEDLINE

On the contrary; it is the other way around, as so many have pointed out: you are far more likely to be a false negative than a false positive.

One so-called "autoimmune" disease, that has never truly been proven to be autoimmune at all, is multiple sclerosis. In many cases, Lyme disease is probably misdiagnosed (and mistreated) as MS.

But don't take my word on that. You can get a more detailed summary in an editorial from the December 26, 2001 edition of Journal of the American Medical Association that was written by Dr. Donald Gilden, M.D., a full joint professor of neurology and microbiology who has been chair of the department of neurology since 1985 at University of Colorado Medical School. Dr. Gilden's credentials can be found in the following 2 links:
http://www.uchsc.edu/sm/neuro/gilden_donald.htm (general profile)
http://www.uchsc.edu/sm/neuro/PDFs/gilden.don.pdf (curriculum vitae)

Dr. Gilden's editorial is very blunt and to the point on this issue: there has never been any proof of true autoimmunity in MS, no actual identification of immune markers on the surfaces of myelin, oligodendrocytes, etc.

It is interesting to note the chronological context of Dr. Gilden's comments: just a couple years before, preliminary results of "The Lesion Project" had revealed 4 different patterns of histology in MS patients, with much attention paid to oligodendrocyte (myelin-producing and regenerating cells) status in the vicinity of the lesions. Preliminary findings for the Lesion Project are summarized here:
http://www.neurologyreviews.com/aug02/nr_aug02_mslesion.html

and the abstract to the original article can be found here:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10581222&dopt=Abstract

Note the quoted pattern of unsubstantiated logic in the summary; note the "automatic presumption of autoimmune" in the summary and in the abstract:

"Patterns 1 and 2 suggest that myelin is the target, while patterns 3 and 4 suggest the oligodendrocyte may be the target." "She explained that patterns 1 and 2 resemble autoimmune models of multiple sclerosis, while patterns 3 and 4 resemble viral, toxic, ischemic, or metabolic models."

Given those quotes, consider in particular the following quote from Dr. Gilden, whose research group has painstakingly sought to identify the actual antigens involved in MS inflammatory damage, which came nearly two years after the Lesion Project summary information had been published in the December, 1999 edition of the medical journal Brain:

"For example, the target antigen(s) in MS is unknown, and it has never been shown that abundant brain white matter proteins, such as myelin basic protein or myelin oligodendrocyte protein, bind to or absorb out the OGBs in MS."

What I find even more amazing is that an MS patient can bring to his or her neurologist a Western blot assay with 4 highly intense bands, each of which is specific for Lyme, and the neurologist can dismiss this evidence as "negative for Lyme;" yet that same neurologist can prescribe potentially dangerous immunosuppressive drug therapies to his or her heart's content without, as Dr. Gilden points out, a single documented case of an antibody directed against myelin, oligodendrocytes, or other living tissues affected in MS.
__________________________________________________________
(Selected passages from Dr. Gilden's editorial)

"Although the cause of MS is unknown, 2 leading theories are that the disease is infectious, probably viral, or that it is produced by a host-immune response to an infectious agent or autoantigen.5"

"Although many investigators believe that MS is an autoimmune disorder, largely by analogy with the prototype immunopathology, experimental allergic encephalomyelitis (EAE), proof is lacking."

"For example, the target antigen(s) in MS is unknown, and it has never been shown that abundant brain white matter proteins, such as myelin basic protein or myelin oligodendrocyte protein, bind to or absorb out the OGBs in MS."

"Careful examination of MS plaques has not revealed any IgG binding to the surface of intact myelin sheets, even in the presence of IgG-positive plasma cells15; thus, if antimyelin antibody contributes to myelin breakdown in chronic MS lesions, the determinant does not appear to be an antigen on the surface of intact healthy myelin sheaths."

"...for the 2 instances in which the specificity of CSF OGBs was studied, they represented antibody directed against the agent that causes disease."

"For example, the OGBs in the CSF of patients with SSPE are antibody directed against measles virus.9 Similarly, the OGBs in cryptococcal meningitis were shown to be completely removed by absorption with cryptococcal antigen but not by absorption with Candida antigen, ruling out the possibility that cryptococci nonspecifically absorb the IgGs.10"

"Other examples of the specificity of OGBs in CNS infectious disorders include the fact that the oligoclonal IgG in human T-lymphotrophic virus 1 (HTLV-1) myelopathy is directed against HTLV-1 virus;11 that the oligoclonal IgG in the CSF of patients with mumps meningitis is directed against mumps virus;12 and that the oligoclonal IgG in the CSF of neurosyphilis patients is directed against Treponema pallidum, the cause of syphilis.13 In addition, progressive multifocal leukoencephalopathy is an exclusively human demyelinating disease that has been proven to be caused by a virus.14"

"Furthermore, there is no immune-mediated animal model of MS, and the collective abundant data gathered on immunogenetic background, macrophage function, specific T-cell subpopulations, and cytokine and chemokine responses in EAE and MS patients have failed to clarify the nature of disease production."

"Equally discouraging is that the multiple immunosuppressive and immunomodulating agents used to treat MS have not produced the gratifying response often seen in myasthenia gravis, a proven autoimmune disease. Moreover, although EAE can be induced in syngeneic recipients by adoptive transfer of lymphocytes from animals sensitized with whole brain white matter or myelin basic protein, there is only a single report of demyelination produced by passive transfer of antibody from MS patients.16"

"Although seemingly heretical, it was recently suggested that a moratorium be placed on the autoimmune hypothesis in MS to redirect funds for research on novel approaches to the problem.17"

______________________________________________________
(Full editorial)

Journal of the American Medical Association
Vol. 286 No. 24, December 26, 2001

Editorial

Viruses and Multiple Sclerosis

Donald H. Gilden, MD

Multiple sclerosis (MS) is the most common demyelinating disease of humans. In the United States alone, the prevalence is 250 000 to 350 000 cases.1 Based on data accumulated in 1994, the annual cost was estimated at more than $34,000 per person, translating into a conservative estimate of a national annual cost of $6.8 billion and a total lifetime cost per
case of $2.2 million.2 Most MS patients are young. Disease usually begins between ages 15 and 45 years and has a relapsing-remitting course, although a substantial proportion of patients develop chronic progressive disease.

The pathologic hallmark of MS is the plaque, an area of white matter demyelination often accompanied by inflammation. The inflammatory infiltrates are composed of T lymphocytes, some B cells and plasma cells, and activated macrophages or microglial cells.3 Although it is generally believed that inflammation is an obligatory and possibly primary feature of
demyelination in MS, myelin destruction also may proceed despite a nearly complete lack of lymphocytic infiltration, suggesting a role for endogenous glia, such as microglia or astrocytes, as a source of injury mediators.3 Immunoglobulin G and complement are localized primarily at the periphery of plaques.4

Although the cause of MS is unknown, 2 leading theories are that the disease is infectious, probably viral, or that it is produced by a host-immune response to an infectious agent or autoantigen.5

Results from 3 different areas of investigation argue for a viral cause of MS. First, epidemiologic analysis of all cases of MS in the Faroe Islands in 1920-1977 indicated a point-source epidemic of MS, probably introduced by British groups or their baggage; thus, MS in the Faroes appeared to be a transmissible, most likely infectious disease.6 Second, studies of identical twins in which one has MS have shown that only 30% of the other twins develop disease, suggesting that more than a putative susceptible genotype determines disease.7 Third, although the protein of normal human cerebrospinal fluid (CSF) contains up to 13% IgG, the CSF of MS patients contains 15% to 30% IgG and sometimes more, as well as oligoclonal bands (OGBs).8 The latter are found almost exclusively in central nervous system (CNS) disorders of infectious origins, such as
neurosyphilis, tuberculous and fungal meningitis, some acute viral CNS infections, and subacute sclerosing panencephalitis (SSPE), a chronic encephalitis caused by measles virus.

Furthermore, for the 2 instances in which the specificity of CSF OGBs was studied, they represented antibody directed against the agent that causes disease. For example, the OGBs in the CSF of patients with SSPE are antibody directed against measles virus.9 Similarly, the OGBs in cryptococcal meningitis were shown to be completely removed by
absorption with cryptococcal antigen but not by absorption with Candida antigen, ruling out the possibility that cryptococci nonspecifically absorb the IgGs.10 Other examples of the specificity of OGBs in CNS infectious disorders include the fact that the oligoclonal IgG in human T-lymphotrophic virus 1 (HTLV-1) myelopathy is directed against HTLV-1 virus;11 that the oligoclonal IgG in the CSF of patients with mumps meningitis is directed against mumps virus;12 and that the oligoclonal IgG in the CSF of neurosyphilis patients is directed against Treponema pallidum, the cause of syphilis.13 In addition, progressive multifocal leukoencephalopathy is an exclusively human demyelinating disease that has been proven to be caused by a virus.14

Although many investigators believe that MS is an autoimmune disorder, largely by analogy with the prototype immunopathology, experimental allergic encephalomyelitis (EAE), proof is lacking. For example, the target antigen(s) in MS is unknown, and it has never been shown that abundant brain white matter proteins, such as myelin basic protein or myelin oligodendrocyte protein, bind to or absorb out the OGBs in MS. Careful
examination of MS plaques has not revealed any IgG binding to the surface of intact myelin sheets, even in the presence of IgG-positive plasma cells15; thus, if antimyelin antibody contributes to myelin breakdown in chronic MS lesions, the determinant does not appear to be an antigen on the surface of intact healthy myelin sheaths.

Furthermore, there is no immune-mediated animal model of MS, and the collective abundant data gathered on immunogenetic background, macrophage function, specific T-cell subpopulations, and cytokine and chemokine responses in EAE and MS patients have failed to clarify the nature of disease production. Equally discouraging is that the multiple immunosuppressive and immunomodulating agents used to treat MS have not produced the gratifying response often seen in myasthenia gravis, a proven autoimmune disease. Moreover, although EAE can be induced in syngeneic recipients by adoptive transfer of lymphocytes from animals sensitized with whole brain white matter or myelin basic protein, there is only a single report of demyelination produced by passive transfer of
antibody from MS patients.16

Although seemingly heretical, it was recently suggested that a moratorium be placed on the autoimmune hypothesis in MS to redirect funds for research on novel approaches to the problem.17

Various microorganisms have been associated with MS, but none has been tightly linked to disease. The most recent organism to be implicated is Chlamydia pneumoniae, a gram-negative bacterium. Since the original detection of C pneumoniae DNA and antibody in the CSF of some MS patients,18 various laboratories around the world have attempted to confirm this potentially important finding. However, multiple studies have indicated a lack of any significant association between C pneumoniae and MS.19 In the past decade, 2 human herpesviruses also have been associated with MS. One is human herpesvirus 6 (HHV-6), the cause of roseola, and the other is Epstein-Barr virus (EBV), the cause of infectious mononucleosis. The detection of fingerprints of these 2 ubiquitous viruses known to be latent in blood B-EBV or T-HHV-6 cells is intriguing, since the primary encounter with either virus usually occurs before or during puberty, the same time that
epidemiologic evidence indicates exposure to the disease-causing agent of MS. However, HHV-6 is found not only in the brain and CSF of MS patients, but also in neoplastic and normal brain,20 suggesting that the detection of virus reflects its reactivation from latency and blood T-cell trafficking through brain. Furthermore, no EBV-specific RNA was detected in 10 MS patients' brains by in situ hybridization.21

In this issue of THE JOURNAL, a prospective serologic study of 62 439 women by Ascherio et al22 found significant elevations in serum anti-EBV antibody titers before onset of MS, particularly antibody to the EBV nuclear antigen 2 (EBNA-2). While the findings would suggest a role of EBV in the etiology of MS, CSF data would be helpful, since the IgG in MS patients' brain tissue and CSF is synthesized intrathecally and may more accurately reflect the immune response at the site of disease. While the neurotropism of EBV and its ability to produce serious neurologic disease at all levels of the human neuraxis have been documented,23 if EBV or any other virus causes MS, it should be possible to demonstrate that MS OGBs contain antibody directed against the suspected agent.

Many viruses and pathogens have been associated with MS, although none has been tightly linked to disease.24 The potential to identify rare or low-abundance pathogens has improved, and the molecular virologic strategies and techniques available today allow studies of virus detection not possible 20 years ago. For example, the ability to prepare and characterize libraries of genes from human tissue based on a difference in their genes or gene products allowed the isolation of complementary DNA clones derived from hepatitis C virus (HCV).25 Those cDNA clones were obtained without prior knowledge of the virus, the viral genome, or presence of circulating viral antibodies. The abundance of HCV-specific RNA from infected animals was ultimately determined to be only approximately 0.00001% or 1:107. Combined cloning in expression vectors (even without subtraction hybridization) and immunologic screening led to the identification of an
HCV-specific clone in approximately 106 recombinant phage.

Some of these strategies already have been applied to MS. Cloning of IgG genes in brain tissue (and CSF) of MS patients has revealed the presence of overrepresented heavy-chain sequences expressed at multiple plaque sites. Alignment of the heavy-chain sequences to their closest germline counterparts revealed clonal amplification and extensive somatic mutation, features of an antigen-driven response.26 Comparison of the IgG heavy-chain sequences in MS and SSPE again revealed features of an antigen-driven response in both diseases. Since the antigen in SSPE is known to be measles virus, the parallel findings in MS suggest an antigen-driven immune response,27 rather than a nonconventional mechanism of B-cell activation. This concept warrants further analysis of the specificity of IgG in brain tissue and CSF in MS. Although the cause of MS is not likely to be found under the EBV lamppost, the search for a viral cause of MS must continue.

Author/Article Information

Author Affiliation: Departments of Neurology and Microbiology, University of Colorado Health Sciences Center, Denver.

Corresponding Author and Reprints: Donald H. Gilden, MD, Department of Neurology, University of Colorado Health Sciences Center, 4200 E Ninth Ave, MS B182, Denver, CO 80262 (e-mail: [email protected]).

Editorials represent the opinions of the authors and THE JOURNAL and not those of the American Medical Association.

Funding/Support: This editorial was supported in part by Public Health Service grant NS 32623 from the National Institutes of Health.

Acknowledgment: I thank Marina Hoffman for editorial review and Cathy Allen for preparing the manuscript.

REFERENCES

1.
Anderson DW, Ellenberg JH, Leventhal CM, Reingold SC, Rodriguez M, Silberberg DH.
Revised estimate of the prevalence of multiple sclerosis in the United States.
Ann Neurol.
1992;31:333-336.
MEDLINE

2.
Whetten-Goldstein K, Sloan FA, Goldstein LB, Kulas ED.
A comprehensive assessment of the cost of multiple sclerosis in the United States.
Mult Scler.
1998;4:419-425.
MEDLINE

3.
Lassmann H, Raine CS, Antel J, Prineas JW.
Immunopathology of multiple sclerosis: report on an international meeting held at the
Institute of Neurology of the University of Vienna.
J Neuroimmunol.
1998;86:213-217.
MEDLINE

4.
Lumsden CE.
The immunogenesis of the multiple sclerosis plaque.
Brain Res.
1971;28:365-390.
MEDLINE

5.
Gilden DH, Devlin ME, Burgoon MP, Owens GP.
The search for virus in multiple sclerosis brain.
Mult Scler.
1996;2:179-183.
MEDLINE

6.
Kurtzke JF, Hyllested K.
Multiple sclerosis in the Faroe Islands, I: clinical and epidemiological features.
Ann Neurol.
1979;5:6-21.
MEDLINE

7.
Spielman RS, Nathanson N.
The genetics of susceptibility to multiple sclerosis.
Epidemiol Rev.
1982;4:45-65.
MEDLINE

8.
The proteins of cerebrospinal fluid: findings in multiple sclerosis.
In: McAlpine D, Lumsden CE, Acheson ED, eds. Multiple Sclerosis: A Reappraisal. 2nd ed.
Edinburgh, Scotland: Churchill Livingstone; 1972:368-398.

9.
Vandvik B, Norrby E, Nordal HJ, Derge M.
Oligoclonal measles virus-specific IgG antibodies isolated from cerebrospinal fluids, brain
extracts, and sera from patients with subacute sclerosing panencephalitis and multiple
sclerosis.
Scand J Immunol.
1976;5:979-992.
MEDLINE

10.
Porter KG, Sinnamon DG, Gillies RR.
Cryptococcus neoformans-specific oligoclonal immunoglobulins in cerebrospinal fluid in
cryptococcal meningitis.
Lancet.
1977;1:1262.
MEDLINE

11.
Grimaldi LM, Roos RP, Devare SG, et al.
HTLV-1-associated myelopathy: oligoclonal immunoglobulin G bands contain anti-HTLV-1
p24 antibody.
Ann Neurol.
1988;24:727-731.
MEDLINE

12.
Vandvik B, Norrby E, Steen-Johnsen J, Stensvold K.
Mumps meningitis: prolonged pleocytosis and occurrence of mumps virus-specific
oligoclonal IgG in the cerebrospinal fluid.
Eur Neurol.
1978;17:13-22.
MEDLINE

13.
Vartdal F, Vandvik B, Michaelson TE, Loe K, Norrby E.
Neurosyphilis: intrathecal synthesis of oligoclonal antibodies to Treponema pallidum.
Ann Neurol.
1982;11:35-40.
MEDLINE

14.
Padgett BL, Walker DL, ZuRhen GM, Eckroade RJ, Dessel BH.
Cultivation of papova-like virus from human brain with progressive multifocal
leukoencephalopathy.
Lancet.
1971;1:1257-1260.
MEDLINE

15.
Prineas JW, Kwon EE, Cho E-S, et al.
Immunopathology of secondary-progressive multiple sclerosis.
Ann Neurol.
2001;50:646-657.
MEDLINE

16.
Saeki Y, Mima T, Sakoda S, et al.
Transfer of multiple sclerosis into severe combined immunodeficiency mice by mononuclear
cells from cerebrospinal fluid of the patients.
Proc Natl Acad Sci U S A.
1992;89:6157-6161.
MEDLINE

17.
Steiner I, Wirguin I.
Multiple sclerosisin need of a critical reappraisal.
Med Hypotheses.
2000;54:99-106.
MEDLINE

18.
Sriram S, Stratton CW, Yao S, et al.
Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.
Ann Neurol.
1999;46:6-14.
MEDLINE

19.
Tsai JC, Gilden DH.
Chlamydia pneumoniae and multiple sclerosis: no significant association.
Trends Microbiol.
2001;9:152-154.
MEDLINE

20.
Cuomo L, Trivedi P, Cardillo MR, et al.
Human herpesvirus 6 infection in neoplastic and normal brain tissue.
J Med Virol.
2001;63:45-51.
MEDLINE

21.
Hilton DA, Love S, Fletcher A, Pringle JH.
Absence of Epstein-Barr virus in multiple sclerosis as assessed by in situ hybridisation.
J Neurol Neurosurg Psychiatry.
1994;57:975-976.
MEDLINE

22.
Ascherio A, Munger KL, Lennette ET, et al.
Epstein-Barr virus antibodies and risk of multiple sclerosis: a prospective study.
JAMA.
2001;286:3083-3088.
ABSTRACT | FULL TEXT | PDF | MEDLINE

23.
Majid A, Galetta SL, Sweeney CJ, et al.
Epstein-Barr virus myeloradiculitis and encephalomyeloradiculitis.
Brain.
2002;125:1-7.

24.
Johnson RT.
Viral Infectious of the Nervous System.
2nd ed. Philadelphia, Pa: Lippincott-Raven; 1998.

25.
Choo Q-L, Kuo G, Weiner A, Overby L, Bradley D, Houghton M.
Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome.
Science.
1989;244:359-362.
MEDLINE

26.
Owens GP, Kraus H, Burgoon MP, Smith-Jensen T, Devlin ME, Gilden DH.
Restricted use of VH4 germline segments in an acute multiple sclerosis brain.
Ann Neurol.
1998;43:236-243.
MEDLINE

27.
Smith-Jensen T, Burgoon MP, Anthony J, Kraus H, Gilden DH, Owens GP.
Comparison of IgG heavy chain sequences in MS and SSPE brains reveals an
antigen-driven response.
Neurology.
2000;54:1227-1232.
MEDLINE

Lyme and immune:

"The levels of antibodies (immunoglobulins) decrease in experimental animals (mice, rats and hamster) by up to 60% when the supply of magnesium is significant reduced.
There is a direct correlation between magnesium deficiencies in rats and reduced immune defense against allergic reactions and cancers, in particular leukaemia and lymphomas." http://www.1stvitality.co.uk/az/magnesium/

Our own antibodies are not "perfect" fighters against Bb, why?

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

In Lyme there are fewer antibodies to fight off Bb AND those that are made, are defective due to, it appears from the above medical abstract, a Ca and Mg deficiency!

With fewer highly targeted healthy antibodies, I believe the body sends out an overabundance of inflammatory cytokines (acids, neg. charges) to try to compensate.

My sister, a lyme pt. has now been "diagnosed" as having AIDS...autoimmune disease. She is now receiving Humira (shots) to block ONE inflammatory cytokine - TNF alpha.

This makes me very "nervous" since it is this cytokine that appears to be of greatest help in fighting Bb in studies with mice.

Down-regulation of mammalian cytokine production has been demonstrated during tick feeding. To examine the hypothesis that reconstitution of cytokines during tick feeding could facilitate immune containment of Borrelia burgdorferi, the following experiments were done.

C3H/HeJ mice were given cytokines for 10 days after Ixodes scapularis attachment. At day 21, ear biopsies were analyzed for B. burgdorferi.

***Polymerase chain reaction analysis indicated a PROTECTION RATE of 95% in mice receiving tumor necrosis factor (TNF)-alpha.***

Mice that received interleukin (IL)-2 or interferon (IFN)-gamma had infection rates of 30%-45% compared with 83% for untreated controls.

PMID: 8537658

The OVERABUNDANCE of TNF alpha can damage the optic nerve and cause joint damage. So this is a fine line. We need some TNF alpha, for sure, but need it to be regulated...and guess what does that...

RESTORE OUR OWN NUMBERS AND HEALTH OF OUR OWN ANTIBODIES TO FIGHT OFF THIS INFECTION.

Mice that received interleukin (IL)-2 or interferon (IFN)-gamma had infection rates of 30%-45% compared with 83% for untreated controls.

PMID: 8537658

The OVERABUNDANCE of TNF alpha can damage the optic nerve and cause joint damage. So this is a fine line. We need some TNF alpha, for sure, but need it to be regulated...and guess what does that...

RESTORE OUR OWN NUMBERS AND HEALTH OF OUR OWN ANTIBODIES TO FIGHT OFF THIS INFECTION >>

There is an interesting description of oligodendrocytes, the specialized cells that produce and replace myelin in the central nervous system, as they pertain to the pathology of MS, that mentions the postulated interplay of TNF in promoting apoptosis of the oligodendrocytes:

(taken from: http://webmail.optonline.net/en/mail.html?sid=nWiiTQRwpcg&lang=en&cert=false )

"What accounts for the destruction of oligodendrocytes in MS is not clear, though it would appear from recent work that oligodendrocytes are not immunologically inert and that, apoptosis - "programmed cell death" - is at least partially responsible."

"Apoptosis is a process whereby cells "commit suicide" in response to receiving signalling molecules, called cytokines, from other cells. The cytokines Tumour Necrosis Factor-alpha (TNF-alpha), LymphoToxin-alpha and -beta (LT-a and LT-b) and interferon-gamma (INF-g) all appear to be involved in the apoptosis of oligodendrocytes in multiple sclerosis."

There is also the potentially intended beneficial role of apoptosis, to clear the body of cells that have had foreign DNA (from opportunistic stealth pathogens like mycoplasmas) inserted into them, thus contaminating the cells and causing them to set off an immune response.

Get rid of the chronic infection(s) first, and then hope the body has enough of the requisite machinery left behind to clean up the debris and get the factory running again.

quote:

---

(wrong website link posted previously...)

There is an interesting description of oligodendrocytes, the specialized cells that produce and replace myelin in the central nervous system, as they pertain to the pathology of MS, that mentions the postulated interplay of TNF in promoting apoptosis of the oligodendrocytes:

(taken from: http://www.mult-sclerosis.org/oligodendrocyte.html )

"What accounts for the destruction of oligodendrocytes in MS is not clear, though it would appear from recent work that oligodendrocytes are not immunologically inert and that, apoptosis - "programmed cell death" - is at least partially responsible."

"Apoptosis is a process whereby cells "commit suicide" in response to receiving signalling molecules, called cytokines, from other cells. The cytokines Tumour Necrosis Factor-alpha (TNF-alpha), LymphoToxin-alpha and -beta (LT-a and LT-b) and interferon-gamma (INF-g) all appear to be involved in the apoptosis of oligodendrocytes in multiple sclerosis."

There is also the potentially intended beneficial role of apoptosis, to clear the body of cells that have had foreign DNA (from opportunistic stealth pathogens like mycoplasmas) inserted into them, thus contaminating the cells and causing them to set off an immune response.

Get rid of the chronic infection(s) first, and then hope the body has enough of the requisite machinery left behind to clean up the debris and get the factory running again.

[/B]

---

Targeted modulation of neuronal apoptosis in neurodegenerative disease:

That's a lot of information to absorb. One or two people said it here, and I agree, that you are much more likely to get a false negative than a false positive.

When did you get your Igenex test/results?
Which tests?
What bands showed up?
What was the intensity of the bands?

quote:

---

Originally posted by ArtistDi:

For example, my first LLMD said it was
very unusual to have more symptoms occur
while on antibiotics. I was finding that
I had more tingling, burning going on in
my limbs, gut, throat. Those symptoms have
basically stopped since the antibiotics were
stopped.
.

---

I dont know if this will help or not, but my LLMD doc at the time (back in 1990, when i was on IV Rocephin 2x daily) said that it was NORMAL to feel the symptoms get worse, as the disease was trying to fight against the antibiotics. I've found, even now, that when i go on oral courses to try to treat the still symptomatic problems i have, that the same reaction still occurs. That is until recently. Since I am kind of on the subject, has anyone had a problem with their bodies completely starting to react allergically to all antibiotics? I've always been allergic to Penicillan, however, I was put on biaxin for bronchitis, and had a sever allergic reaction to that, then i was put on anohter cephelosporin , and had a reaction to THAT. although not as sever as to the Biaxin. Could it be that since i have been on and off these types of drugs for so long, my body is finally saying " ENOUGH"??.. Ugh.. Thanks for if nothing else, letting me vent

I believe there is really no way to quickly resolve your questions or confusion. We continue to try to treat all possibilities w/out harming any of them either. So, no steroids for lupus becasue it's bad for Lyme. But Plaquenil is good for both and so are abx (some rheumatologists treat autoimmune stuff w/abx too). After 3 years of this, my vote is for Lyme, but we're still not doing that well either.

Taking abx is like Pandora's box. They uleash a lot of reaction from the bugs. I think that a worsening of symptoms actually may prove you have Lyme.

I had lyme testing done back in May 2002
and again in Feb. 2003. Back in May I was
positive, but will have to look up the bands
again. After 10 mos of antibiotics, the
lyme is now negative.

Something else happened to me, and I don't
know if the Mepron/Biaxin/Plaquenil combo
put my body on overload or what. After
that, I started having severe burning
headaches,and then seizue activity. My
present LLMD doesn't know what is making
my head do this, and he is one of the best,
so now I feel I don't know how to proceed.

To me, it seems like my immune system was
agitated and now has become hypersensitive
to drugs, even outside the class of antibiotics as well as fruits, which I was
never allergic to. It is so odd, because
even a very kind rheumatologist (who knew
about lyme) said that the elevated pancreas
levels, mouth dryness, etc. seemed like
lupus, but said the ANA tests were very
accurate. I don't come up positive.

So the question is: What in God's name
has happened to me? I didn't have any
headaches pre-treatment or seizures. I can't
take medicines any more and it is difficult
to chose foods that won't cause a reation.

It is important to understand the immune response/dysfunction to Lyme disease. It helps us understand treatment, prognosis, and symptoms.

Lyme disease triggers immune responses/inflammation/dysfunctions that can appear to be autoimmune-like but are not purely autoimmune. That is to say that the immune system is not attacking self without an extraneous stimulus or trigger. Rather, the damage comes from the immune system being coaxed by borrelia, more specifically a toxin or several toxins produced by borrelia.

Whether this inflammation/immune dysfunction can lead to an actual immune disease over time is debatable.

I favor persistent LD being the problem, not an actual autoimmune disease.

Treatment for autoimmune disease would be strongly contraindicated for chronic LD...such as corticosteroid therapy.

The inflammation/dysfunctioning immune response needs to be addresses with therapy, but the correct immune therapy, not an immuno-suppressing one that is used for autoimmune diseases.

Scott

Why not go see Dr. Cowden? I know you were thinking about it before.

Strong statement, but it can be corroborated by statements made by Sarah Navina, MD, Ming Yin, MD, PhD, and A. William Pasculle. ScD in their diagnosis of a case of babesiosis at the University of Pittsburgh Medical Center (UPMC rated #15 on the recent US News and World Report list of the "best of the best" hospitals in the nation; this is a world-class mainstream hospital whose presence on that list probably has little to do with "past reputation:" http://www.usnews.com/usnews/nycu/health/hosptl/honorroll.htm )

Pertinent passages from their babesiosis diagnosis, which can be found here (along with an informative diagram of the initiation and progression of the infection:
http://path.upmc.edu/cases/case332/dx.html

and
http://path.upmc.edu/cases/case332.html )

include the following statements:

"The clinical manifestations of babesiosis range from subclinical illness to a fatal fulminating disease [1] "

(note: fulminating = erupting suddenly and progressing very rapidly)

"Babesial infections are often not apparent [2]."

"THOSE AT GREATEST RISK OF FATAL DISEASE include individuals older than age 50 years; asplenic individuals; and
IMMUNOCOMPROMISED INDIVIDUALS AS A RESULT OF IMMUNOSUPPRESSIVE DRUGS, malignancy, or HIV infection. These patients may have serious illness, characterized by high fever and severe hemolytic anemia, that results in death or a prolonged convalescence. The case fatality rate for human babesiosis approaches 5% [1]."

"Approximately 20% of the cases of babesiosis have clinical and serologic evidence of concurrent Lyme
disease."

"Identification of the parasites in thin blood films requires a reasonable level of parasitemia, otherwise the parasites might be missed."

"The parasite represents a threat to the safety of the blood supply in that blood from asymptomatic humans can transmit Babesia to blood recipients. Such transmissions have occurred."

"Identification of human infection with Babesia spp. will probably increase as physicians and the public become more aware of the disease..." (that one should be all-capped)...

REFERENCES:

1.Meldrum, SC, Birkhead GS, White DJ, et al. Human babesiosis in New York state: an epidemiologic description of 136 cases. Clin Infect Dis 1992; 15:1019 23.

2.Krause PJ, Telford SR, Pollack RJ, et al. Babesiosis: an underdiagnosed disease of children. Pediatrics 1992; 89:1045 8.

To summarize; it is not trivial matter for a physician to misdiagnose and treat a chronic infection as an autoimmune disorder.

I've personally seen a MS patient with an unheeded positive Western blot assay. with medium to high intensity bands including high intensity 31 kDa IgG, go downhill extremely rapidly during a course of methotrexate therapy from a neurologist, who is among the many who dismiss this patient's Western blot results.

Other diagnoses of potential interest from UPMC physicians that concern diagnostic differentiation of MS, Lyme disease-neuroborreliosis, and babesia. All of the photos are interactive; click on them to enlarge. Note in particular the expanded views of the CSF assays in case 59, the case ultimately diagnosed as Lyme disease-neuroborreliosis, which can be found at the following 2 links:

"Multiple sclerosis-pattern:" http://path.upmc.edu/cases/case59/images/micro1.jpg

"Neuroborreliosis pattern:" http://path.upmc.edu/cases/case59/images/micro2.jpg

http://path.upmc.edu/cases/case336.html
(acute demyelinating disease (2003); established by histology)
http://path.upmc.edu/cases/case332.html
(babesiosis (2002); established by parasite assay of blood)
http://path.upmc.edu/cases/case79.html
(multiple sclerosis (1996); established by histology)
http://path.upmc.edu/cases/case59.html
(Lyme disease - neuroborreliosis (1996); established by diffuse CSF oligoclonal band pattern

Many abx. deplete the vits. and minerals too!!!

Restore the level and your symptoms will vanish.

It will take about 6 months. Best to take small doses more often (several times a day)with a very, very small amt. of B6 to carry it into the cells (may skip B6 if eating something that has B6 in it at that time).

Allergies, headaches, seizures are all CAUSED by a Mg deficiency. You do NOT have an autoimmune disease, you have a Mg deficiency.

Every single one has prescribed Plaquenil. Plaquenil is the first line choice of treatment for lupus, RA. etc.As we all know, Plaquenil is also used in Lyme treatment (helping drugs go into cells by altering Ph) and is also an anti-malarial that may help w/Babesia. It has anti-inflammatory properties and is a mild immuno-suppressant.

I think that Lyme triggers auto-immune activity is some of us (w/genetic markers) and that the auto-immune activity is very real and must be treated along w/the Lyme, until sufficient headway is made w/Lyme t eatment to try to see if the auto-immune problems are improved. (Labs can help w/theis assessment)

If you don't treat the autoimmune stuff going on, you may end up w/permanent damage from it, regardless of the outcome w/the Lyme.

One of my doctors has suggested vasculitis.
Now the point is that drugs probably caused
this vasuculitis, and at any rate, I can't
take small amounts of drugs (antibiotics
and anti-reflux) and at one point even
supplements when I first had this horrible
head burning.

Every LLMD has said this heading burning is
not lyme. Three LLMDS have said no lyme
now. The burning is constant, unlike lyme
symptoms that seem more transient.

I have started to seize again. This was
after 4 days of Prevacid, Carafate and what
preceded the seizure was head burning after
ingesting the drugs.

Something is SO wrong. This is not just
a neurotoxin thing.

I take IM shot of Magnesium and several of
B12. This seems to happen because the
drugs seem to injure something in my brain that is already impaired.

I will just be beside myself if I have
permanent central nervous system damage as
suggested by a highly regarded LLMD. Other
ideas have been that I developed Multiple
Drug Allergy Syndrome, but my former allergist said he is not sure about that because it seems more complex and multi-organ.

It is difficult to remain strong day in and
out without really knowing the underlying
cause. It is now a year that I have been
like this. All I know is that when I was
put on Mepron, Biaxin and Plaquenil, something was happening in my head. I could
feel that something was going deeper into
my brain and suddenly the head burning began
and has never quite ended.

I have started to seize again. This was
after 4 days of Prevacid, Carafate and what
preceded the seizure was head burning after
ingesting the drugs.

Something is SO wrong. This is not just
a neurotoxin thing.

I will just be beside myself if I have
permanent central nervous system damage as
suggested by a highly regarded LLMD.

Other
ideas have been that I developed Multiple
Drug Allergy Syndrome, but my former allergist said he is not sure about that because it seems more complex and multi-organ. >>

If what you have is an allergy or intolerance to a certain type of drug, maybe the Nambudripad Allergy Elimination Technique (NAET) could help you, but you are even less likely to get a physician to endorse or recommend NAET since it is completely alternative therapy.

I've been treated successfully by this method, and in extreme cases patients have even been desensitized to chemotherapy and radiation therapy drugs by appropriately-designed NAET protocols.

You can find out more here:
http://www.naet.com

There is also a book, "Say Goodbye to Illness" by Dr. Devi Nambudripad, D.C., Ph.D.

The success you can achieve with NAET is definitely practitioner-dependent; there are some who are extremely good and some who seem to be practically reading off their course notes as they do the procedure.

What would happen if you pursued this would be to first screen with muscle-resistance testing (MRT) what you allergic or intolerant to. Then the things you are allergic or intolerant to are "cleared" by an acupressure (some use acupuncture) technique that is completely painless, non-invasive and drug-free (I've never had the acupuncture configuration).

Apparently it goes something like this. If you hold in your hand a closed glass vial that contains something you are not allergic to or intolerant of, and hold out your opposite arm, your arm will be "strong" and resist the downward pressure the practitioner exerts in screening for allergy or intolerance.

If, however, you are allergic or intolerant to the substance in the vial, the magnetic field of that substance, which penetrates the glass, your skin and perturbs the electrochemical currents in your nervous system, sends a signal to your brain. The brain immediately "closes" all of the acupressure "points" in your body. If the substance was introduced inside your body, all of the above would happen, and you would actually manifest symptoms of an allergic attack or intolerance. With the substance isolated in a glass vial, however, you can safely screen for the "brain signalling" without placing yourself at risk of undergoing an allergic attack or an episode of intolerance.

To treat the allergy or intolerance, once they have been identified, the practitioner has you hold the vial containing the substance in one hand while manually "opening" all of your acupressure points. The brain apparently "stores" this phenomenon in "memory" so that the next time you encounter the substance, your body will not launch an allergic attack or manifest intolerance.

It sounds far-fetched, but when done appropriately it works, plain and simple.

If one truly had an autoimmune reaction against myelin or another body tissue, for that matter, the NAET procedure, in theory, could be utilized with samples of those tissues to "reprogram" the body, safely and without potentially dangerous drugs with unpredictable side effects, to no longer attack the tissue.

The discoverers of NAET did a controlled clinical trial in collaboration with the American Medical Association in late 1999 to test the use of NAET + chemotherapy and radiation therapy for cancer vs. chemotherapy and radiation therapies alone. A number of patients with a number of different types of cancers were given one of the following: 1) conventional therapy alone, 2) conventional therapy + NAET, 3) conventional therapy + sham procedure resembling NAET, or 4) NAET alone.

The initial controlled trials were conducted at University of California-Berkely and University of Pennsylvania Hospitals. The results of the preliminary trials were: patient groups with conventional therapy alone maximum less than 50% in remission; patients with conventional therapy + NAET minimum 89% in remission, and the results of the 3rd and 4th groups were not released. Further trials were planned at Johns-Hopkins, and Mayo Clinic and Cleveland Clinic were "watching closely, but not getting involved just yet."

But then, mysteriously, all information concerning this phenomenon simply vanished, and nothing more was said or done.

NAET practitioners such as the one who treated me could no longer get access to information on what was going on, but my NAET practitioner continued using NAET on her own to treat cancer patients. One man, in particular, was "full of cancer" and was brought into remission, with nothing but the NAET procedure, before he even had a chance to report for conventional therapy.

So the technique has tremendous potential, and I've seen it work on myself. For instance, I used to get an oozing red rash on my forearms, even when I wore shirtsleeves, if I pushed a lawnmower under evergreen trees. After being treated by NAET, I was able to deliberately rub evergreen needles and branches on my arms without getting a rash.

There is a "relative" of NAET, called Jaffe-Mellor Technique (JMT), http://www.jmt-jafmeltechnique.com/
in which a NAET-like protocol is used to treat patients against stealth pathogens believed to be responsible for various chronic diseases, including autoimmune disorders. This is also a practitioner dependent procedure. I know of a JMT practitioner in Utah who claims she can produce near-miraculous results in more than 90% of the lupus patients she treats, no matter how long they've had the disease and no matter how advanced or serious the disease progression is.

The results she gets with rheumatoid arthritis, osteoarthritis, multiple sclerosis, etc. are not as overwhelming as what she claims to get for lupus. But the originators of JMT are very adamant that the term "autoimmune" is a misnomer.

Perhaps JMT is a technique that could desensitize the body to foreign DNA, entrapped pathogens, or the like in healthy cells, which may be the true origin of what may be incorrectl referred to as "autoimmune." But the offending pathogen(s) must first be identified correctly. In like fashion, successful deployment of NAET requires successful identification of the offending toxin or allergen, with attention paid to the possibility of interplay of metabolic byproducts (i.e., you may not be allergic to milk itself, but if you drink a large quantity after your stomach has "shut down" for the evening after 7 PM or so, or if you have a large bowl of late-night ice cream, you may react with intolerance to what the milk or cream transforms into over time).

Here's the documentation:

"New hypothesis: Adrenal insufficiency caused chronic fatigue
When hypomagnesia is present, or/and the ratio magnesium/calcium is low (lots of calcium, relatively low magnesium levels), the excess calcium levels will cause excess calcium influx into all living cells. This is because magnesium, can only act as a calcium-channel blocker if it is in the right balance with calcium. The calcium influx will cause nitric oxide (NO) synthesis inside the cells. The NO suppresses the adrenals, causing adrenal sufficiency. The low cortisol levels will further increase NO synthesis. This is because the low cortisol levels are making the immune system hyper. This means upregulated nitric oxide and other cytokines. The increased nitric oxide levels will further depress the adrenals. Vicious Cycle." http://www.newtreatments.
org/cfs

This therapy uses this knowledge (positive and negative charges - the acid/base balance) to heal...via COMBINED routes...INCLUDING NUTRITION.

I know who your LLMD is...and that said; how frustrating have HIM not know what this is!!!

In my opinion he is either #1 or #2 in the Lyme world.

Now.....you and I have gotten to know each otherr very well thru this...you showed me what my TRUE dx was...

YOU SAVED MY LIFE>>>>

I am improving...slowly, yet I am so very humbled by your fight with this illness.

I say to you now....this is from the bottom of my heart and soul....

My symptoms increase when on abx, also.....

YOU HAVE LYME>>>>>>>>>> I think it is just in some morphed form right now.....could also be BARTENELLA!!!!!!

Gotta Go,

I love you Sis',

Kent

You can find out more in the JMT practitioner testimonies, toward the end, here:
http://www.jmt-jafmeltechnique.com/index_files/index_practitioner_area.html

My NAET practitioner has, since 1999-2000, practiced an "advanced" form of NAET that does not require the use of vials, and more importantly does not require each allergen / antigen to be treated separately, with a "25 hour clearance" interval for the body to remove all immune complexes involving the antigen (so, for instance, if you had a single treatment for milk, you would have to avoid all physical contact with milk or anything containing milk or dairy for 25 hours after the treatment).

My NAET practitioner informed Jaffe-Mellor of this technique, which she in turn learned from a chiropractor in California named John Lubecki, when she "exchanged notes with them" somewhere around that time, but I don't know for sure what the "advanced" JMT technique is or how it is accomplished, but JMT practitioners sound excited about it.

The advanced NAET technique involves a white "box" that is about the size of a typical car alarm actuator that you may have on your keychain. Inside this white "box" are electromagnetic "imprints" of 4,000 different antigens. The practitioner, using a special device with flashing red lights (that looks like a prop from the 1966-67 "Batman" TV show), is able to program the white box "to you," and in a single NAET treatment desensitize you to everything imprinted in that white box.

In followup treatments, if necessary, the practitioner can imprint other items that you may react to that may not have been present initially. You keep the white box with you, and do a "supporting" treatment (15 seconds or less) to yourself with it everyday to ensure that your treatment stays active. The patient is also provided with a "black box." An illustration of how the black box, which is always carried on one's person (or in a handbag, etc.) works is as follows: suppose one is eating mints and suddenly has an acute, severe attack of heartburn. Simply place a mint on top of the black box for about 15-30 seconds, and then ingest the mint. The heartburn will stop, immediately.

I had the advanced NAET procedure technique after about 55 single NAET treatments. I spent more than $2,000 on the single treatments, but only about $250 on the one-shot treatment. I've used the black box to arrest asthma attacks by rubbing the black box over my chest while an asthma attack is setting in; the asthma was reversed, and the phlegm loosened and was eliminated, within 15 minutes. I still keep an inhaler handy just in case, but have never had to use one since I've had the black box. As for followup white box treatments: when I first moved to a desert climate and had an adverse reaction to the local pollens. I swabbed some of the pollen off my car into a vial and took it to my practitioner the next time I was in the area and she imprinted it into my "white box." I had no further adverse reactions to the desert pollen after that.

If interested, you can find out more about advanced, "vial-free" NAET therapy, or perhaps receive a referral to a NAET practitioner near you, try the following email address:

That's an interesting phenomenon. I agree that unhealthy cells have to be "ID'd and removed," but so often it seems that apoptosis (programmed cell death) is being cited as a "primary destroyer," just as what is initially a perfectly normal immune response to pathogen(s) is being cited as an "out of control, autoimmune response."

There is an informative link to an actual diagnosis of a babesiosis case at the University of Pittsburgh Medical Center. It includes initial patient symptoms and provides the final diagnosis, including a relatively rigorous description of the disease and the various symptoms that can be presented. It can be found here:
http://path.upmc.edu/cases/case332.html
(babesiosis (2002); established by parasite assay of blood)

I haven't had the time to read through all of the posts on this thread so if I repeat what somebody else said, I apologize.

I saw a well-known and well respected immunologist about the time I got diagnosed with Lyme. He explained that it was a little known fact that there can be an autoimmune component to Lyme Disease. I read the same information in a book called The Road to Immunity written by one of the Bock brothers. So it isn't always an either/or situation. You can have Lyme AND an autoimmune disorder.

This is true in my case -- I have an autoimmune disorder called antiphospholipid antibody syndrome so I have to be careful about up-regulating my immune system with certain herbs such as echinacea.

My understanding of Lyme testing is that other things such as antinuclear antibodies can cause a falsely positive Elisa test -- that's why they run a Western Blot and also test us for things such as ANA, etc. -- to eliminate that false positive before making a diagnosis.

It's also my understanding that you are unlikely to get false positives on the key Lyme bands. This is just my recollection of what I've read on various sites, including Igenex, about western blot testing so you might want to check that out.

Please know that even when I don't email you regularly, I'm still sending you healing thoughts and wishes.

I can't just take things without knowing
why my head has been burning for a year. My
LLMD has tried the neurotoxin theory and
hormonal, but neither has really helped
without harming my body.

Something is awry besides any Babesia, etc.
I know my body and I know what a herx was,
and this is no herx. This headache is
perpetual, can cause vision to blur and everything is on my left side--the eye,
the numbness in my hand and my headache.

I will have to explore through different
physicians, and I feel compelled to do so
as I have two children that I am fighting
to be around for.

It is so hard some days to get through them,
and I still push myself to exercise when
I can, I teach from my studio and try to
do to cooking and homework with my kids. My
will has always been strong--right now--
stronger than my body. My head feels like
it will explode.

I wasn't trying to discourage you from exploring other things or encouraging you to take meds like abx which don't help. Really I'm not. I'm not one of the folks who think everybody has Lyme or that Lyme is the explanation for every illness out there.

You should listen to your own body and your intuition as they are some of the best guides you have.

I am just so tired of having to go on like
this without knowing what it is that I am
facing. When one of the best LLMDS out there
is stumped, I find that I must seek answers.

Once again-I maybe jumping in too late on this thread

Katydid-I totally agree with your post, and raise ya five!!

I had an immunilogist At U Of Michigan tell me to watch out for all those markers also-eps. if the lyme became *long standing* (didn't use the word chronic)

Also to keep an eye on my immune functions-because lyme can and will cause grave problems to the immune system

But everything was fine on that particular visit

3yrs later, and everything is *not so normal anymore*

IgG,IgM,IgA all low

Plus I also now test + for lupus, and have the MRI of a MS patient

5yrs of CDC lyme positives for bloodwork

LYME is definitely a muti-system infection, as I also have a spect scan that suggests vascular disease of the brain, and doppler studies to show occlussive disease in the legs

The immune system can be *misguided* in this disease, it can be hyperactive, or in my case, underactive

The vascular disease is due to the chronic inflammatory cascade

MRI-due to keetes crossing the blood-brain barrier

And the Lupus Testing-that one has us stumpped-other than multi-system damage due to the keetes

AS I stated earlier, all this same testing was normal back in 2001

What a difference 2yrs can make

With a paper *trail* like mine, we are becoming *The missing Link*

I am really beginning to believe B.B and other stealth pathogens do trigger the auto-immune process, it is the fault of the medical community-when it failed to follow up on promising studies, as far back as the 1940'slinking auto-immune diseases to keetes,ect

And for going exactly in the opposite direction, and down-regulating the immune system-instead of following up on a infectious process

It's not auto-immune in the true sense of the word-when there is a pathogen causing the body to attack organs and tissues-the immune system is trying to get at the foriegn envaders-but said immune system may become dysfunctional and remain hyperactive-and keep on "attacking" even once the pathogen has ceased to exsist in the body

The big Question in B.B, how do you really know when it is active infection, or immune dysfunction?

And there is the fact of chronic infection

This is the big issue pitting the medical establishment-many doctors do believe in chronic infection ,look to syphllis as a chronic keete model

but there are studies that suggest molucular mimicry-a type of auto-immune response

You overdid it with the drugs. Your body is sensitive and those drugs are tough and it was too much. I think some of your responses were also probably fungal but who knows.

Remember, the valium helped. Klonipin I think it was. Try that again.

You might look into Patricia Kane's work on lipid therapy. It seems to be a way to restabilize the cell membrane and help flush out neurotoxins, without relying too heavily on questran which many can't tolerate and which makes some worse.

You might also start doing some cleansing, with colonics, liver flushes, etc. I think Clarice posted about that.

Exercise increases the amt. of COQ10 which is a carrier of electromagnetic charges across the cell membrane. This helps to heal the cells.

One sided symptoms are most definitely an indication of an electrolyte imbalance.

Mg is needed for the formation of the myelin sheath.

The BBB is broken down early in this disease.

There is a tremendous increase in TNF alpha...one of the inflammatory cytokines with this disease. This is a "general attack". TNF alpha is a "helper".

This is probably due in part to the decrease in the numbers and "health" of our own HIGHLY TARGETED antibodies. This is due to a Mg deficiency...and is DOCUMENTED.

Marines (our own antibodies) are wounded and their numbers decreased due to a Ca and Mg deficiency, so the body sends in the Army (TNF alpha). (But the Marines do the best job.)

Early on the mitochondria (powerhouses) of the cells are damaged and later their numbers are reduced.

Early on the thymus gland shrinks due to a Mg deficiency. The body "knows" there is a major infection to fight and goes into a "protection" mode. Iron is also stored because most bacteria need it to replicate (not Bb). With the thymus involution (shrinking) = zinc implications.

Much Zinc is bound in neutophils (the most numerous of our WBCs) in order to prevent it from being used by the bug to replicate. Yes, we are zinc deficient because most is bound up. We NEED zinc, but so does the bug, so this becomes a problem.

It takes a LONG time (months) to restore the levels (storage) of Mg. So...does the body think the infection is still there (due to the Mg deficiency status) and keeps producing more and more TNF alpha? Or IS the infection still there?

Mg, B6 and COQ10 issue (not enough) - possibility.

More commonly known/felt as Chinese restaurant syndrome.

An unknown percentage of the population may react to MSG and develop MSG symptom complex, a condition characterized by one or more of the following symptoms:

burning sensation in the back of the neck, forearms, and chest
numbness in the back of the neck, radiating to the arms and back
tingling, warmth, and weakness in the face, temples, upper back, neck, and arms
facial pressure or tightness
chest pain
headache
nausea
rapid heartbeat
bronchospasm in MSG-intolerant people with asthma
drowsiness
weakness
http://www.fda.gov/
medbull/january96/msg.html

Or:

Cluster Headaches Intense and severe one-sided burning pain with sudden onset and fairly brief duration typify the pain of a cluster headache.

The above is a form of a migraine. Migraines are definitely Mg/B6 related.

Rx. for seizures is IV Mg sulfate.

You have wonderful responses & everyone of them are lightyears ahead of my knowledge about this.

I know you probably don't want to hear about another stupid product to take, but this one is a little different.

I've even thought of going to work at a Health Food Store where as an employee I could get these things for 50% off. These products would probably enable me to work because I'm unable to work now.

Here goes:
This is about the man who invented the flak-jacket during the Vietnam war. I think it was in the l990s he saw that children treated with chemotherapy were alive, but left with damaged immune systems.

He bought the pharmaceutical rights to refine a product called Beta Glucans. He wanted cancer patients to have something to build themselves up with, but they had to improve the product so children could tolerate it.

I believe it consist of only the cell wall of yeast. It does not add to yeast problems-----that's all been removed & was part of the refining process, I believe.

It's ridiculously expensive, but it does help-------if you're trying to strengthen the immune system. (It's not for dampening down the immune system).

It's called Beta Glucan Immunition (10 mg.)
NSC-100 Extra 30 count is $48.97, on sale.

If you go to their website they should have much more information. They are the scientists, not me.

Frank Jordan authored a book about these beta glucans which is probably available on the website. I've tried other brands, but they're not as potent.

Hearing everyone's stories makes me think I should try to find the money to purchase the Beta Glucans-----because I know they work. It's not an overnight cure-all, but in time your immunity will improve. It's a behind the scenes kind of thing. It does not work directly on infections, but on your immune system.

One of my many, former physicians had recovered from lymphoma & he used the Beta Glucans.

That website was: www.nsc24.com
if you want to research the product.

The only other thing I found to also help my immune system was MGN-3 capsules by Lane Labs.

You can order from Doctor's Trust Vitamins for $39.99 on sale; 50 caps at 250 mg. Their web is www.doctortrust.com

I'm sure you could pull up Lane Labs website & find more helpful information about the MGN-3 & exactly how it works.

It's just that they're so blasted expensive and our entire family of 3 has Lyme.

Just a thought for you; can't stand to hear someone suffering so. There's got to be answers out there. Keep looking.

Good luck,
Jan

quote:

---

Originally posted by ArtistDi:
My
will has always been strong--right now--
stronger than my body. My head feels like
it will explode.

The only time I get some relief is with
exercise, so I know something in my head
needs oxygen.

---

I had a headache for allmost two months when I came off abx's called llmd and got a appt I thoght my head was going to explode it hurt so bad even when I blinked lots of really bad pressure. I took motrin up to 1600mg a day it hurt bad. When I got to my llmd he said I had lyme induced encephilitis swelling it took dynabac another month too get it under control after that it slowly subsided but I kept on taking abx's and motrin and vicodine. I feel so sorry for you.

That worked for about 1 week, and then I crashed. 6 more weeks of IV helped me recover from that.

My new LLMD found an undetected mycoplasma infection in my brain and CNS which seems to explain my autoimmune symptoms.

that if anyone thinks they are going into
an autoimmune state... and they have been on antibiotics for quite some time....

dont forget about CANDIDA.

This can cause an autoimmune like condition.
It can get so out of control it can be unbearable. It is the toxins that make one just sick. I know for me, it made me just about crazy in the mind. The herxing has been unbearable again on the nystain, but it is getting better each day.

If one is reacting to all antibiotics after they have been on antibiotics a long time, consider a thourough candida program...
nystatin is excellent for me, and then there is the Diflucan and possible herbs from a ND.

I have experienced terrible candida while on antibiotics, and my diet has been very good, treating with the nystatin has really helped me.

I tend to agree with bd

Candida is an infection, and can cause problems as well, especially when one has been on long termm antibiotics...
candida will suppress the immune system which will then make it impossible to eliminate all of the lyme or other coinfections.