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» LymeNet Flash » Questions and Discussion » Medical Questions » Stricker article confused even me!

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Author Topic: Stricker article confused even me!
Danser
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After reading the rebuttals to the Stricker article, I was sick to my stomach and my first reaction was anger . . . but then, a tiny niggling doubt . . . perhaps my husband doesn't have chronic lyme afterall.

Perhaps there is NO chronic lyme and we are chasing the wrong diagnosis.

Perhaps this is why after one year of antibiotic treatment, he has had NO improvement.

Part of me prefers the lyme dx because unlike CFS or FMS . . . we are told that there IS an end in sight.

I have been to lyme conferences and read here and truly I believe that chronic lyme exist and that my husband indeed is infected with Bb and other TBD's. I just wanted to let you know that even knowing all that, I found some of the replies compelling and momentarily it took my hope away.

[ 07. August 2006, 08:14 AM: Message edited by: Danser ]

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luvs2ride
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Danser,

Just as we need doctors to think outside the box, we too need to think outside the box. It is quite possible the lyme bacteria we were infected with opened the pathway to other pathogens. Perhaps the abx really did kill the lyme and what we are fighting now are side effects of the abx. Please listen.

10 years ago I came down ill with the typical lyme symptoms, flu like, chronic fatigue, joint pain. Even though the ELISA test was negative, that did not stop my doctor from treating me. In fact, he started the doxy the day he drew blood explaining to me the test are very inaccurate. It took 6 mths of oral abx to get me well.

Over the next 10 years I developed migraines, hearing loss, shortterm memory problems, stiff neck, hot flashes (in fact I described it as always hot with an occasional cold flash). 2 yrs ago, I developed mental confusion, another flu like virus (strep ruled out) and WHAM! Horrific migratory joint pain.

2 LLMDs diagnosed chronic lyme. Igenex said I've had lyme (CDC positive) but indecisive as to whether I have lyme now (CDC negative). Still, clinically I had all the signs. This go round I was treated strictly with alternative meds because they said abx were no good on chronic lyme.

Immediately all my symptoms disappeared except the joint pain which increased. Rheum. Arthritis was diagnosed. I began to research outside the lyme box and discovered a whole world of possible causes to my joint pain.

Testing has born out the following: 3 out of 5 root canals are infected (2 opinions obtained the same results) Leaky Gut Syndrome confirmed. Systemic Yeast confirmed. Heavy metal toxicity confirmed. Parasites found and cleaned out quickly. Systemic yeast and metals are going to be a long slow process.

I could write a book on all I have learned through this illness. Here is my conclusion, be it right or wrong.

I believe 10 yrs ago I had lyme. 6 mths of abx cured the lyme, but nothing was done to offset the abx damage to my gut. I had yeast problems prior to this and had them afterward. The standard 1 dose Diflucan was given. I no longer had vaginal yeast infections after this.

I believe the vaginal area was spared because the gut was leaking the yeast out into my bloodstream instead of remaining in the gut. Hence, the migraines, hearing loss, shortterm memory and stiff neck issues. Allergies flared and asthma was diagnosed. Eventually I suffered an HP Ulcer. Diflucan was administered (1 dose) for yeast.

I had always been a very good eater but now I was craving sweets and carbs constantly and weight gain occured. Fall of 04 Shingles hit. Aug 05, the chronic lyme diagnosis.

Yeast has the exact same symptoms as Lyme. Clincically, how can a doctor differentiate?

When I learned I had RA, I found a LGS connection. This doctor espoused a vegan diet. I tried it and within 2 weeks I had 75% improvement. That was Jan, 06. I found an integrative doctor who specializes in nutrition and systemic yeast. We have been working together since April and I am thriving. The arthritis is nearly gone and the little that remains is not stopping me from any of my activities. (I ride horses which is a very physically demanding sport).

I do seriously doubt that lyme is my problem. I believe most of us here at lymenet need to fix our guts, even if lyme is the problem. Fixing the gut will begin the road to recovery. For myself, it seems to be the recovery.

Look beyond Lyme.

--------------------
When the Power of Love overcomes the Love of Power, there will be Peace.

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Lymetoo
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I think I could have gotten off abx earlier if I had realized that yeast was a major factor in how I felt.

That is why I'm the "yeast queen" around here!! I try to get people to realize how serious it is and how seriously ill it can make you feel!!

I have also recently discovered that I have celiac disease. Had I known that earlier, much of my lingering muscle and joint pain would have phased itself out as well!

Gluten can even cause sensitive individuals to have BRAIN FOG. Sound familiar!?

Anyway, I do hope everyone will address all the things that are keeping them from getting well!!

--------------------
--Lymetutu--
Opinions, not medical advice!

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Blackstone
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Would one of you be so kind as to tell us about the tests for systemic yeasts, heavy metals, celiac and so forth?

Edit: Also, what kind of dentist diagnosed you with infected root canals? Dentist? Oral surgeon? Or one of those "biodentists" who use the cavitat?

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Lymetoo
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For yeast and celiac, you can do your own "test"...Go on the anti-yeast diet and see how you feel.

Go on the no gluten diet and see how you feel. YOu have to be SURE not to comsume even a crumb of wheat. I felt better in ONE week!

Go here for more info:
www.celiac.com or google it.
There are tests you can get thru www.enterolab.com

For the yeast, check this stuff out:

Candida diet and elimination:
http://flash.lymenet.org/ubb/Forum1/HTML/021412.html
http://www.wholeapproach.com/diet/
Lyme symptoms list compared with yeast symptoms
http://flash.lymenet.org/ubb/Forum1/HTML/021202.html

"Successful control and elminiation of a Candida Albicans overgrowth requires a multifaceted program as described below. Failure to follow ALL the steps simultaneously will result in slow progress and will lengthen healing time significantly. The program should be tailored to the individual and must balance the need to eliminate the Candida and deprive it of its food source while insuring proper nutrition for the individual."

Five Steps to Candida Elimination:

1. You must starve it into submission by eliminating its food source.

2. You must kill it with anti-fungal herbs and supplements. [e.g....garlic, onion, caprylic acid, Pau D'Arco capsules or tea, clove, grapefruit seed extract, olive leaf extract, oil of oregano, tea tree oil, Echinacea, Goldenseal, black walnut, MSM, barberry root, uva ursi, neem leaf, biotin]

3. You must reestablish the proper balance and quantity of probiotic bacteria in the digestive tract. [...multi-strain lactobacillus acidophilus and bifidus capsules with FOS should be taken between meals to maximize repopulation of the digestive tract by beneficial bacteria.]

4. You must reestablish proper levels of all B vitamins (yeast free) and utilize other immune enhancing supplements to boost immune system function. [e.g ... B complex vitamins (yeast free), biotin, beta 1-3 glucan, colostrum, maitake mushroom, vitamins A, C, E, zinc and selenium]

5. You must cleanse and heal the digestive tract to promote proper elimination of toxins and Candida and assimilation of nutrients. [e.g...chlorophyll, MSM, omega 3 fatty acids found in flax seed and salmon oils, GLA found in borage, evening primrose and black currant oils. Pantothenic acid, digestive enzymes between meals]

There are tests for yeast, but I wouldn't rely on them. The best way is to follow the diet in my opinion.

Also, I've recently discovered Theralac....Awesome stuff!!

www.theralac.com

--------------------
--Lymetutu--
Opinions, not medical advice!

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Danser
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I don't know about the yeast connection. You'd think he'd have felt worse . . . or better and then worse for it to be yeast.

Before we went with the lyme dx, he was tested for celiac disease and the results were negative.

We haven't gone the route of metal toxicity yet. We really weren't sure if we'd done enough with lyme. Besides the fact that he was only treated for one week for babesia - with oral quinine and IV clindamycine.

I'm hoping his new LLMD will help us figure out all this mess. His appt. is tomorrow but he's still in the hospital from the pulmonary embolism. His coumadin levels aren't high enough for them to release him.

I'm tired, distresed, depressed and discouraged right now. Sometimes I wonder if I have lyme since I feel so exhausted lately. But in reality, I'll bet it's just having the entire weight of the family, home and my husband's care on my shoulders.

It'd be nice if I could find a doctor to help lead the way.

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Lymetoo
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quote:
Originally posted by Danser:
I don't know about the yeast connection. You'd think he'd have felt worse . . . or better and then worse for it to be yeast.


The only way to know is to follow the diet.

I'm sorry the weight of the world is on your shoulders. That's pretty darned stressful! [group hug]

--------------------
--Lymetutu--
Opinions, not medical advice!

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Blackstone
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Theoretically, shouldn't Diflucan taken daily for a period of time wipe out any systemic yeast problem there is?
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LYMESCIENCE
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quote:
Originally posted by Danser:
After reading the rebuttals to the Stricker article, I was sick to my stomach and my first reaction was anger . . . but then, a tiny niggling doubt . . . perhaps my husband doesn't have chronic lyme afterall.

Perhaps there is NO chronic lyme and we are chasing the wrong diagnosis.

Perhaps this is why after one year of antibiotic treatment, he has had NO improvement.

Part of me prefers the lyme dx because unlike CFS or FMS . . . we are told that there IS an end in sight.

I have been to lyme conferences and read here and truly I believe that chronic lyme exist and that my husband indeed is infected with Bb and other TBD's. I just wanted to let you know that even knowing all that, I found some of the replies compelling and momentarily it took my hope away.

I'm sorry you've been through such a ringer of an experience.

I've read the rebuttles and have not been the least impressed. In fact, it leaves me quite unimpressed with the rebuttal given.

Let me start with the president of the IDSA and the claims he made.


"The July 31 Other Opinion article by Dr. Raphael B. Stricker is filled with inaccuracies and misleading information that can only contribute to the public's misunderstanding and unfounded fears about Lyme disease.

For example, the "small group of scientists" whom Dr. Stricker states are impeding effective treatments for the disease is in fact the 8,000-member Infectious Diseases Society of America, the nation's largest professional association of infectious disease experts.

Ironically, it is Dr. Stricker who represents "a small group of scientists." The International Lyme and Associated Diseases Society, of which he is president, has approximately 200 members, many of whom have a vested interest in promulgating long-term treatment for Lyme disease because they make their living off such treatment. Here's what else Courant readers need to know:

The IDSA Clinical Practice Guidelines for Lyme disease, which Dr. Stricker dismisses, were developed by a panel of world-renowned experts in Lyme disease, doctors who are researchers and who regularly treat Lyme disease patients.

The guidelines were created based on stringent rules of evidence-based medicine, which includes a thorough and objective review of published scientific research. This comprehensive review also included research submitted by members of Dr. Sticker's organization. The guidelines undergo a rigorous peer review and must ultimately be approved by the IDSA board of directors, who are all infectious-disease specialists and leaders in the field.

Despite claims that many people suffer from "chronic Lyme disease," a thorough review of published research reveals no credible scientific evidence that the disease persists after appropriate antibiotic treatment indicated in the IDSA guidelines.

There is valid scientific evidence documenting that more than 50 percent of patients diagnosed with "chronic Lyme disease" never actually had any form of Lyme disease. In one published scientific study, the majority of such patients were found to have conditions that, because of the misdiagnosis of chronic Lyme disease, were not properly diagnosed or treated.

In fact, Lyme disease is a tick-borne bacterial infection. In the vast majority of cases (95 percent to 98 percent), the disease is successfully treated with a two-week course of oral antibiotics. A small number of patients may require longer treatment of up to one month. These facts are supported overwhelmingly by the most current published studies.

There are a very few patients treated for Lyme disease who continue to have symptoms after the recommended treatment. The long-term antibiotic therapy advocated by Dr. Stricker and his colleagues can endanger these individuals, cause needless suffering and may promote the development of drug-resistant "superbugs."

We encourage anyone who is diagnosed with so-called chronic Lyme disease to get a second opinion. We strongly advise that people with Lyme disease avoid long-term antibiotic treatment, which is ineffective, costly and potentially very dangerous.

IDSA members have been at the forefront of preventing and treating Lyme disease. Our singular mission is to find out what is best for patients. We believe that our guidelines represent the best that science has to offer.

For reliable, scientific-based information on Lyme disease, we would direct your readers to sources such as the websites of the American College of Physicians (www.acponline.org) and the U.S. Centers for Disease Control and Prevention (www.cdc.gov), as well as that of IDSA (www.idsociety.org).

Martin J. Blaser, M.D.
President
Infectious Diseases Society of America
Alexandria, Va."

Claim 1:
For example, the "small group of scientists" whom Dr. Stricker states are impeding effective treatments for the disease is in fact the 8,000-member Infectious Diseases Society of America, the nation's largest professional association of infectious disease experts.

Ironically, it is Dr. Stricker who represents "a small group of scientists." The International Lyme and Associated Diseases Society, of which he is president, has approximately 200 members, many of whom have a vested interest in promulgating long-term treatment for Lyme disease because they make their living off such treatment."

Rebuttal: This only implies Dr. Stricker was correct regarding those who have become medical revisionists. Only a group with significant power such as one who represents the nations largest infectious disease society would be capable of weilding such power with such little science.

A further example of the polical as opposed to scientific clout of this organization lies in the position of the writer as head of the NYU school of medicine.

Furthermore, his 200 vs 8000 idea is misleading at best, and false advertising at worst. The IDSA does have 8000 members, but the readers are left with the idea that all these members study and activily involve themselves with the Science of tick-bourne infectious diseases.

Unfortunatly, readers would have then been mislead. The large group of IDSA physicans do not in fact treat large groups of Lyme disease patients, nor are many of them involved in research dedicated to this particular disease.

In contrast to misleading claims, the ILADS is not a comprable organization of ID physicans interested in the totality of infectious diseases. They focus on one disease, namley Lyme and its associated diseases. They include multidisciplinairy specialities not limited to the thinking imposed by a single group of physicans.

Science has proven many times over that divergent opinions covering divergent topics of a diverse subject yeilds data much closer to objective truth.

The IDSA has failed at providing such opinions. In fact, the IDSA came upon its Lyme Disease guildlines not per the 8000 member discussion that these claims imply, but rather the inclusion of those listed below directly from the guildlines they promote.

GUIDELINES FROM THE INFECTIOUS DISEASES SOCIETY OF AMERICA
Practice Guidelines for the Treatment of Lyme Disease
Gary P. Wormser,1 Robert B. Nadelman,1
Raymond J. Dattwyler,2 David T. Dennis,6
Eugene D. Shapiro,7 Allen C. Steere,9
Thomas J. Rush,5 Daniel W. Rahn,10
Patricia K. Coyle,3 David H. Persing,11
Durland Fish,8 and Benjamin J. Luft4
1Division of Infectious Diseases, Department of Medicine, New York
Medical College, Valhalla, 2Division of Allergy, Immunology
and Lyme Disease, Department of Medicine, 3Department
of Neurology, and 4Department of Medicine, Health Sciences Center,
State University of New York at Stony Brook, and 5private practice,
Briarcliff Manor, New York; 6Division of Vector-Borne Infectious
Diseases, National Center for Infectious Diseases, Centers for Disease
Control and Prevention, Fort Collins, Colorado; Departments
of 7Pediatrics and 8Epidemiology and Public Health, Yale University
School of Medicine, New Haven, Connecticut; 9Tufts University
School of Medicine, New England Medical Center, Boston,
Massachusetts; 10Office of Medical Management, Medical College
of Georgia, Augusta; and 11Diagnostics Development, Corixa
Corporation, and Infectious Disease Research Institute,
Seattle Life Sciences Center, Seattle, Washington


Perhaps my math is incorrect, but my count is 12, which falls very short of 8000.

Conversly, every member of the 200 member ILADS focus directly on Lyme Disease, and are involved with a very high number of clinical cases.

Also, it seems like a conflict of interest for the Head of the Lyme Disease program for the IDSA also happens to work at the same college as the president of the IDSA. Certainly, the proximity of these individuals geographically would imply that Wormser has the undevoted attention of the Martin J. Blaser, M.D. as they work at the same institution.

If Wormser is critasized, then the university is critisized. As Martin J. Blaser, M.D. has the need to protect both his society and the grants his unversity recieves (not to mention the protection of his job if such critasicms infuriate the board of directors at the NY college of medicine) then his opinion on this subject is far from unbiased.

Claim 2:
The guidelines were created based on stringent rules of evidence-based medicine, which includes a thorough and objective review of published scientific research. This comprehensive review also included research submitted by members of Dr. Sticker's organization. The guidelines undergo a rigorous peer review and must ultimately be approved by the IDSA board of directors, who are all infectious-disease specialists and leaders in the field.

Despite claims that many people suffer from "chronic Lyme disease," a thorough review of published research reveals no credible scientific evidence that the disease persists after appropriate antibiotic treatment indicated in the IDSA guidelines"

So, that begs the question, what citations are present in this well developed peer review.

It is suprising that so many citations provided are of the same pannel who wrote the guildlines. Apparently, they can be trusted to meet the standards of rigourous science.

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49. Massarotti EM, Luger SW, Rahn DW, et al. Treatment of early Lyme disease.
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50. Nadelman RB, Luger SW, Frank E, et al. Comparison of cefuroxime axetil
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51. Luger SW, Paparone P, Wormser GP, et al. Comparison of cefuroxime axetil
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52. Luft BJ, Dattwyler RJ, Johnson RC, et al. Azithromycin compared with
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53. Dattwyler RJ, Luft BJ, Kunkel M, et al. Ceftriaxone compared with doxycycline
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54. Centers for Disease Control and Prevention. Prevalence and impact of chronic
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55. Buchwald D, Umali P, Umali J, Kith P, Pearlman T, Komaroff AL. Chronic
fatigue and the chronic fatigue syndrome: prevalence in a Pacific Northwest
Health Care System. Ann Intern Med 1995; 123:81-8.
56. Wang TJ, Sangha O, Phillips CB, et al. Outcomes of children treated for
Lyme disease. J Rheumatol 1998;25:2249-53.
57. Wolfe F, Cathey MA. Prevalence of primary and secondary fibrositis. J
Rheum 1983; 10:965-8.
58. Reidenberg MM, Lowenthal DT. Adverse nondrug reactions. N Engl J Med
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59. Verbrugge LM, Ascione FJ. Exploring the iceberg. Common symptoms and
how people care for them. Med Care 1987; 25:539-69.
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61. Steere AC, Malawista SE, Newman JH, Spieler PN, Bartenhagen NH. Antibiotic
therapy in Lyme disease. Ann Intern Med 1980; 93:1-8.
62. Nowakowski J, McKenna D, Nadelman RB, et al. Two weeks' therapy with
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63. Nowakowski J, Nadelman RB, Forseter G, McKenna D,Wormser GP. Doxycycline
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65. Dever LL, Jorgensen JH, Barbour AG. Comparative in vitro activities of
clarithromycin, azithromycin, and erythromycin against Borrelia burgdorferi.
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66. Hansen K, Hovmark A, Lebech A-M, et al. Roxithromycin in Lyme borreliosis:
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study and a clinical trial in patients with erythema migrans. Acta Derm
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67. Wormser GP. Lyme disease: insights into the use of antimicrobials for prevention
and treatment in the context of experience with other spirochetal
infections. Mt Sinai J Med 1995; 62:188-95.
68. Dattwyler RJ, Grunwaldt E, Luft BJ. Clarithromycin in treatment of early
Lyme disease: a pilot study. Antimicrob Agents Chemother 1996; 40:468-9.
69. Nowakowski J, McKenna D, Nadelman RB, Cooper D, Bittker S, Holmgren
D, Pavia C, Johnson RC, Wormser GP. Failure of treatment with cephalexin
for Lyme disease. Arch Fam Med 2000; 9:563-7.
70. Agger WA, Callister SM, Jobe DA. In vitro susceptibilities of Borrelia burgdorferi
to 5 oral cephalosporins and ceftriaxone. Antimicrob Agents
Chemother 1992;36:1788-90.
71. Steere AC, Pachner AR, Malawista SE. Neurologic abnormalities of Lyme
disease: successful treatment with high-dose intravenous penicillin. Ann
Intern Med 1983; 99:767-72.
72. Wormser GP. Treatment and prevention of Lyme disease, with emphasis on
antimicrobial therapy for neuroborreliosis and vaccination. Semin Neurol
1997; 17:45-52.
73. Pfister HW, PreacMursic V,Wilske B, Einhaupl KM. Cefotaxime vs penicillin
G for acute neurologic manifestations in Lyme borreliosis: a prospective
randomized study. Arch Neurol 1989; 46:1190-4.
74. Mullegger RR, Millner MM, Stanek G, Spork KD. Penicillin G sodium and
ceftriaxone in the treatment of neuroborreliosis in children: a prospective
study. Infection 1991; 19:279-83.
75. Pfister H-W, Preac-Mursic V, Wilske B, Schielke E, Sorgel F, Einhaupl KM.
Randomized comparison of ceftriaxone and cefotaxime in Lyme neuroborreliosis.
J Infect Dis 1991; 163:311-8.
76. Dotevall L, Alestig K, Hanner P, Norkrans G, Hagberg L. The use of doxycycline
in nervous system Borrelia burgdorferi infection. Scand J Infect
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77. Dotevall L, Hagberg L. Successful oral doxycycline treatment of Lyme disease-
associated facial palsy and meningitis. Clin Infect Dis 1999; 28:
569-74.
78. Karlsson M, Hammers-Berggren S, Lindquist L, Stiernstedt G, Svenungsson
B. Comparison of intravenous penicillin G and oral doxycycline for treatment
of Lyme neuroborreliosis. Neurology 1994; 44:1203-7.
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randomized comparison of doxycycline and penicillin G. J Neurol 1989;
236:464-9.
80. Clark JR, Carlson RD, Sasaki CT, Pachies AR, Steere AC. Facial paralysis
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81. Steere AC, Batsford WP, Weinberg M, et al. Lyme carditis: cardiac abnormalities
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tection of Borrelia burgdorferi by polymerase chain reaction in synovial
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LYMESCIENCE
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Claim 3:There is valid scientific evidence documenting that more than 50 percent of patients diagnosed with "chronic Lyme disease" never actually had any form of Lyme disease. In one published scientific study, the majority of such patients were found to have conditions that, because of the misdiagnosis of chronic Lyme disease, were not properly diagnosed or treated.

Rebuttal: So, where does this evidence come from. That's right, only one study.
http://tinyurl.com/prqb4

BTW, this study has serious flaws and has not been reproduced. To my knowledge 1993 is not what many would consider the most current scientific knowledge.

LYMENET RESPONSE TO
'THE OVERDIAGOSIS OF
LYME DISEASE'

Carl Brenner
Marc C. Gabriel
John S. O'Donnell
Editors, The LymeNet Newsletter

May, 1993


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Abstracts:


Although Lyme disease has been recognized as a distinct clinical entity for nearly 20 years (1), there are still gaping holes in our knowledge about the most fundamental questions of incidence, diagnosis and treatment. This is due primarily to the many difficulties posed by the nature of the illness (non-specific symptoms, protean manifestations, long latency period and/or apparent asymptomatic infection in some individuals, etc.) and our limited arsenal in the areas of both testing and treatment. The resulting knowledge gap leaves room for reasonable people to disagree on almost every facet of Lyme disease research.

A recent study by Steere et al. (2) published in the April 14, 1993 issue of the Journal of the American Medical Association (JAMA) suggests that Lyme disease is widely overdiagnosed. Because the study's conclusions are so striking and its primary author is considered one of the world's leading experts in Lyme disease research, the publication of this article has generated considerable medical and media attention and will likely have significant impact on how Lyme disease is perceived in both the medical and lay communities.

We believe that the study contains multiple serious flaws which leave its conclusions unsupported. We are concerned that this paper's publication may lead to ill-advised complacency about Lyme disease in this country, may compromise patients' access to treatment at all stages of the disease -- thus exposing more of them to the risk of potentially devastating long term sequelae -- and may even influence the amount and direction of future allocations of funds for Lyme disease research. We thus feel it imperative to address the methodological and philosophical flaws in this work.

Our specific concerns about the Steere et al. paper are as follows:

Serology:

The authors report that 98% of the patients (176 out of 180) found to have active Lyme disease, but none of the patients (0 out of 452) who had never had Lyme disease but who were evaluated for suspected Lyme at their clinic, were seropositive by enzyme-linked immunosorbent assay (ELISA) and/or Western Blot. If this is correct, it means the authors have developed an extremely sensitive and specific group of tests that vastly outperform any of the existing antibody tests or testing protocols that have been reviewed in the Lyme literature. Indeed, the authors state that of the 452 patients in the study who were determined to have never had Lyme disease, 203 (45%) had obtained "false" positive results from another laboratory.

It is difficult to accept uncritically the authors' claim that their antibody testing protocols are superior to others currently in use. Independent reviews of a wide variety of today's antibody detection tests -- immunofluorescent assays, enzyme-linked immunosorbent assays and assorted immunoblots -- have indicated generally dismal performance, marked by significant interlaboratory and intralaboratory variability (3-5). The authors offer no independent evaluations or persuasive arguments to distinguish their tests from others in current use. Instead, it appears that Steere and his co-authors are relying inappropriately on imperfect testing techniques -- from a single laboratory -- to make the diagnosis of Lyme disease. The presumption seems to be that their tests are better than others because the correlation between seropositivity and actual Lyme disease is highest; on the other hand, the definition of "actual Lyme disease" in the study is derived almost exclusively from their test results. The reasoning is entirely circular.

Moreover, the nearly exclusive reliance on serologies for diagnosis leads to the systematic underestimation of the prevalence of seronegative Lyme disease. This point cannot be overemphasized. Although false negative serologies are widely recognized as common in early Lyme disease, it is often claimed that they are extremely rare phenomena later in the course of the illness (6-8). The many cases of seronegative, culture-positive "late" Lyme disease that have been identified and reported (9-12), however, make this claim even more untenable than it is unverifiable. In one study on transplacental transmission of Borrelia burgdorferi (10), over half of the mothers who had adverse pregnancy outcomes and whose fetuses or neonates demonstrated the presence of B. burgdorferi were themselves seronegative. Thus, when the study population is determined by factors other than serology -- when the inevitable bias toward seropositivity is removed -- the true incidence of seronegative Lyme disease emerges.

One example from this study merits special attention:

"A 24-year old white woman was admitted in February 1985 in labor at term of her pregnancy. Ultrasound examination showed that the fetus was dead when she arrived at the hospital. Following the delivery of her stillborn infant and completion of the fetal autopsy, a retrospective interview established that she had acquired Lyme borreliosis in the first trimester of her pregnancy outside of Salt Lake City, Utah. Postpartum serological studies yielded conflicting results because the Centers for Disease Control found strongly reactive results by IFA and ELISA, as did the New York State Department of Health; however, the Yale University laboratory of Dr. Allen Steere could detect no evidence of specific antibodies for B. burgdorferi. Fetal viscera showed B. burgdorferi in the liver, adrenal, brain, heart and placenta. . . "

The implications of this finding for the patients studied in "The Overdiagnosis of Lyme Disease" are obvious and profound, given that over a quarter of the study population was determined by the authors to have received "false positive" test results from other laboratories. False negatives in Dr. Steere's laboratory may very well account for a significant portion of the discrepancy among results.

Steere et al. further compromise their estimates of the numbers of patients with Lyme disease by creating inappropriate conditions for diagnosis which in some cases are impossible to meet. The authors state that "a history of exposure in an area where B. burgdorferi has been recovered from ticks" was required for a diagnosis of Lyme disease in their study. This approach systematically excludes all patients from areas that have not been investigated for B. burgdorferi infestation. In light of the fact that thousands of clear-cut cases of Lyme disease, complete with physician-verified erythema migrans, and/or clinical findings and positive serologies, have been reported from "non-endemic" and unstudied areas, such a restriction is inappropriate. The patient in the study quoted above apparently contracted Lyme disease in Utah and was also seronegative on Dr. Steere's ELISA. Either of these two factors alone would have been sufficient in Steere et al.'s JAMA study to exclude the diagnosis of Lyme disease, though of course the patient clearly did suffer from B.burgdorferi infection.

It is remarkable that the authors made no attempt to use any direct testing methods, such as culture, histological tissue examination, or antigen or nucleic acid detection systems, to verify the accuracy of their diagnoses. Although the latter techniques are relatively new, several tests of considerable utility have been reported (13-15). If one is carrying out a study that purports to be the final word on the correct diagnosis of a disease, every effort should be made to use the latest and most accurate diagnostic techniques before publishing the study. The diagnostic criteria and methods used by Steere et al. are both outdated and marred by an unacceptable level of subjectivity on the part of the researchers.

Response to Treatment:

Steere et al. divide their patient population into three categories: patients with active Lyme disease, patients with a history of Lyme disease and another current illness, and patients with another illness. Interestingly, of the patients thought to have active Lyme disease, at least 52 had already been antibiotically treated before evaluation by the authors. Thus, Steere et al. implicitly acknowledge that treatment failures are a common phenomenon in Lyme disease.

Yet under the study protocols, lack of responsiveness to antibiotic therapy is a primary criterion for the determination that active Lyme disease is not present: "We did not find age, sex, or duration of symptoms to be of help in diagnosing fibromyalgia, but the presence of tender points upon examination and lack of response to antibiotic therapy were important clues in diagnosing fibromyalgia." These criteria are clearly not consistent with the authors' own findings regarding the prevalence of treatment failures among patients whom they determined to harbor active disease; further, it is well known that every one of the primary symptoms associated with fibromyalgia or chronic fatigue syndrome (persistent headache, fatigue, myalgias, arthralgias, sleep disturbance, etc.) are common in active Lyme disease and cannot be used for differential diagnosis. Finally, in cases where the patient did improve with antibiotic therapy but relapsed afterwards, the authors conclude anecdotally that the positive response was probably due to the placebo effect.

We strongly take issue with the fact that the alternate interpretation for these treatment responses -- that borrelial infection persisted after antibiotic treatment -- is completely ignored. There are now culture-confirmed treatment failures in the medical literature for all stages of Lyme disease [9,12,16-19], sometimes even after long term, high-dosage antibiotic therapy [17-19]. Other studies employing the polymerase chain reaction have indicated the persistence of B.burgdorferi-specific DNA in the cerebrospinal fluid of many patients who remain symptomatic after antibiotic therapy [15]. In light of these findings, the authors' exclusive interpretation that treatment failure was due to misdiagnosis seems rather reckless. Although persistent symptoms after treatment by no means implies the continued presence of B. burgdorferi, unresponsiveness to short term antibiotic therapy cannot be interpreted to exclude it.

In addition, the use of psychiatric symptoms to exclude the diagnosis of Lyme disease (". . . psychiatric disorders such as anxiety, depression or somatization clearly played a role in the illness of some of these patients . . . ") is entirely inappropriate. Controlled studies have indicated that a high percentage (66%) of seropositive Lyme disease patients report an episode of major depression during the course of their illness, most (90%) for the first time [20]. A wide variety of minor and major psychiatric disorders have been reported in Lyme disease [21-23], similar to the findings in neurosyphilis [24]. The authors may be unaware of these findings or may be ignoring them; in either case, the study's patient evaluation techniques are compromised. Also disturbing is the authors' classification of the neurological sequelae that developed in 15 of the 156 patients who were determined to have previous Lyme disease and another current illness. Although discussion of these patients' symptoms was vague, the syndromes listed in the accompanying table -- vertigo, peripheral neuropathies, radiculopathy and seizure disorder -- have all been described in patients with active Lyme disease [7,8,25]. Steere and his colleagues ruled out active disease in these patients because "neurological test results for Lyme disease were negative." Such a conclusion is insupportable, as there are many reports of culture-positive and PCR-positive patients with active disease and normal neurological findings [15,26,27]. Further, many clinical findings in Lyme disease, such as Bell palsy or Lyme meningitis, often resolve even without treatment [8], but this certainly cannot be equated with microbiological "cure." The presence of subjective symptoms in combination with the absence of clinical findings after treatment is frustrating for both physician and patient, but it is clearly inappropriate to simply declare the patient borrelia-free in these circumstances. Finally, even if the authors are correct and active disease was not present in any of these 15 patients, the incidence of serious neurological sequelae in the "post-Lyme" patient population implies that the "post-Lyme syndrome" can be quite severe. The shunting of these patients into the "non-Lyme" category gives the impression that Lyme disease could not have been responsible for any of their symptoms, an extremely questionable conclusion that suggests that Lyme disease and its sequelae are more benign than they really are. On a broader level, the authors are asking us to believe that one-fifth of the entire study population had a history of Lyme disease, were all cured, and then went on to develop a variety of other illnesses, virtually all of which have identical symptoms to active Lyme disease. This strains credulity.

Implications and Conclusions:

The methodology used by Steere et al. for categorizing diagnoses with adverse antibiotic treatment outcomes can thus be summarized as follows:
Treatment failures occurred in other physicians' treatment of Lyme disease.
However, treatment failures apparently never occurred when the authors treated Lyme disease.
In cases where Lyme disease was diagnosed in a patient who did not improve permanently with short term antibiotic therapy, the determination was made retrospectively that Lyme disease was not present.

Rather than engaging in a serious attempt to explore the rate of treatment failure in their study by utilizing direct detection methods, the authors chose to rely entirely on anecdotal observations and then reported these as objective fact: These patients do not have Lyme disease. This retrospective determination was made despite ongoing unchanged symptomatology, despite extensive literature documenting culture-confirmed persistent infection following antibiotic treatment, and without investigation via direct methods for the presence of B. burgdorferi. That this is offered as "science" in a leading medical journal is appalling.

Interestingly, the authors never followed up on the patients who were determined to have active Lyme disease and who were therefore treated with "appropriate" antibiotic regimens. Did all of these patients recover completely? If so, it would imply that Lyme disease is always easily cured, an assumption that is belied by both the medical literature and the authors' own willingness to re-treat. If there were later relapses, then the authors' contention that treatment failures are due primarily to misdiagnosis is obviously false, unless they had been mistaken in their diagnosis of Lyme disease in these patients, in which case the diagnostic conclusions of the study are rendered useless. No matter how these questions are answered, the internal contradictions of the study are exposed.

It is no longer acceptable to continue to deny that treatment failures often occur in Lyme disease. The literature now provides substantial documentation on this point, and is beginning to elucidate the mechanisms responsible. Early dissemination of B. burgdorferi to the central nervous system [27,28] and intracellular localization and persistence [29,30] have been identified as contributors to treatment failure in Lyme disease. Instead of anecdotal and subjective "studies" like "The Overdiagnosis of Lyme Disease," we urgently need to know the true incidence of Lyme disease, the percentage of patients in whom the Lyme spirochete survives after therapy, and the efficacy of further antibiotic treatment in these patients. Some authors are already attempting to come to terms with these issues [31,32]. Unfortunately, Steere et al. clearly are not. Instead, the authors have employed a flawed methodology that "defines away" Lyme disease and does a disservice both to patients and to unwary physicians who as a result of this article may adopt an inappropriately skeptical approach to the diagnosis [33].


--------------------------------------------------------------------------------


REFERENCES

1. Steere AC, Malawista SE, Snydman DR, et al. Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthritis Rheum 1977;20:7-17.

2. Steere AC, Taylor E, McHugh GL, et al. The overdiagnosis of Lyme disease. JAMA 1993;269:1812-6.

3. Hedberg CW, Osterheim MT, MacDonald KL, et al. An interlaboratory study of antibody to Borrelia burgdorferi. J Infect Dis 1987;155:1325-7.

4. Proceedings of the First National Conference on Lyme Disease Testing.. CDC/ASTPHLD, November, 1990.

5. Bakken LL, Case KL, Callister SM, et al. Performance of 45 laboratories participating in a proficiency testing program for Lyme disease serology. JAMA 1992;268:891-5.

6. Dattwyler RJ, Volkman DJ, Luft BJ et al. Seronegative Lyme disease: dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi. N Engl J Med 1988;319:1441-6.

7. Steere AC. Lyme disease. N Eng J Med 1989;321:586-96.

8. Rahn DW, Malawista SE. Lyme disease: recommendations for diagnosis and treatment. Ann Intern Med 1991;114:472-81.

9. Preac-Mursic V, Weber K, Pfister HW, et al. Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme borreliosis. Infection 1989;17:355-9.

10. MacDonald AB. Gestational Lyme borreliosis: implications for the fetus. Rheumatic Disease Clinics of North America 1989;15:657-77.

11. Lavoie PE, et al. Culture positive seronegative transplacental Lyme borreliosis infant mortality. Arthritis Rheum 1987; 3(Suppl):S50.

12. Hupl Th, Krause A, Rittig M, et al. Persistence of Borrelia burgdorferi in chronic Lyme disease: altered immune regulation or evasion into immunologically privileged sites? (Abstr. 149, Fifth Int'l Conf. on Lyme Borreliosis, Arlington VA 1992.)

13. Dorward DW, Schwan TG, Garon CF. Immune capture and detection of Borrelia burgdorferi antigens in urine, blood or tissues from infected ticks, mice, dogs and humans. J Clin Microbiol 1991;29:1162-70.

14. Rosa PA, Schwann TG. A specific and sensitive assay for the Lyme disease spirochete Borrelia burgdorferi using the polymerase chain reaction. J Infect Dis 1989;160:1018-29.

15. Keller TL, Halperin JJ, Whitman M. PCR detection of Borrelia burgdorferi DNA in cerebrospinal fluid of Lyme neuroborreliosis patients. Neurology 1992;42:32-42.

16. Schmidli J, Hunzicker T, Moesli P, et al. Cultivation of Borrelia burgdorferi from joint fluid three months after treatment of facial palsy due to Lyme borreliosis. J Infect Dis 1988;158:905-6.

17. Hassler D, Riedel K, Zorn J, et al. Pulsed high-dose cefotaxime therapy in refractory Lyme borreliosis (letter). Lancet 1991;338:193.

18. Liegner KB, Rosenkilde CE, Campbell GL, et al. Culture-confirmed treatment failure of cefotaxime and minocycline in a case of Lyme
meningoencephalomyelitis in the United States. (Abstr. 63, Fifth Int'l Conf. on Lyme Borreliosis, Arlington VA 1992.)

19. Masters E, Lynxwiler P, Rawlings J. Spirochetemia two weeks post cessation of six months of continuous p.o. amoxicillin therapy. (Abstr.
65, Fifth Int'l Conf. on Lyme Borreliosis, Arlington VA 1992.)

20. Fallon BA, Nields JA. Psychiatric manifestations of Lyme borreliosis:Part I, A controlled study of major depression. (Abstr. 47, Fifth Int'l Conf. on Lyme Borreliosis, Arlington VA 1992.)

21. Barnett W, Sigmund D, Roelke U, et al. Endogenous paranoid-hallucinatory syndrome caused by Borrelia encephalomyelitis. Nervenarzt 1991;62:445-7.

22. Roelcke U, Barnett W, Wilder-Smith E, et al. Untreated neuroborreliosis: Bannwarth's syndrome evolving into acute schizophrenia-like psychosis. J Neurol 1992;239:129-31.

23. Fallon BA, Nields JA, Burrascano JJ, et al. The neuropsychiatric manifestations of Lyme borreliosis. Psychiatric Quarterly 1992;63:95-117.

24. Rundell JR, Wise MG. Neurosyphilis: a psychiatric perspective. Psychosomatics 1985;26:287-95.

25. Reik L, Smith L, Khan A, et al. Demyelinating encephalopathy in Lyme disease. Neurology 1985;35:267-9.

26. Pfister H-W, Preac-Mursic V, Wilske B, et al. Latent Lyme neuroborreliosis: presence of Borrelia burgdorferi in the cerebrospinal fluid without concurrent inflammatory signs. Neurology 1989;39:1118-20.

27. Luft BJ, Steinman CR, Neimark HC, et al. Invasion of the central nervous system by Borrelia burgdorferi in acute disseminated infection. JAMA 1992;267:1364-7.

28. Garcia-Monco JC, Villar BF, Alen JC, et al. Borrelia burgdorferi in the central nervous system: experimental and clinical evidence for early invasion. J Infect Dis 1990;161:1187-93.

29. Ma Y, Sturrock A, Weis JJ. Intracellular localization of Borrelia burgdorferi within human endothelial cells. Infect Immun 1991;59:671-8.

30. Georgilis K, Peacocke M, Klempner MS. Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. J Infect Dis 1992;166:440-4.

31] Brenner C. Lyme disease: asking the right questions. Science 1992;257:1845-7.

32. Liegner KB. Lyme disease: the sensible pursuit of answers. J Clin Microbiol, in press.

33] Tuohy L. Victim of Lyme disease settles malpractice suit. Hartford Courant. May 18. 1993, p. C8.

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quote:
Originally posted by LYMESCIENCE:
Claim 3:There is valid scientific evidence documenting that more than 50 percent of patients diagnosed with "chronic Lyme disease" never actually had any form of Lyme disease. In one published scientific study, the majority of such patients were found to have conditions that, because of the misdiagnosis of chronic Lyme disease, were not properly diagnosed or treated.

The reality is that there is no definite method that can distinct with certainty between active Bb, inactive Bb and absence of Bb. So it can't be determined with certainty that one doesn't have Lyme disease.

It is likely that false diagnoses of Lyme happen, but the opposite happens too. That's what you get with a disease so hard to diagnose and treat as Lyme.

It is the art of medicine to find the most likely diagnosis, while physicians should always be prepared to change it when appropriate. A diagnosis is not per se definite.

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minimonkey
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Thanks, Lymescience!!!!!!!!!

It is very much a "caveat emptor" situation when reading scientific literature --- so very much of it is horribly biased and has conflicts of interest that stretch far and wide. The body of literature surrounding Lyme is the epitome of this.

Interestingly, the literature coming out of countries other than the US in the last 10 years or so is overwhelmingly pointing to chronic lyme as being a very real condition, with active, ongoing spirchetal infection. I notice that the Steere camp doesn't include any of those studies in their peer reviewed body of literature..... they really are perverting "science" about as much as it can be perverted, IMO.

All that said, I too would be wondering what was going on if I had been treated for a year with no improvement whatsoever....

There are so many co-infections and hormonal disturbances and other things that can accompany chronic lyme -- I do believe it is necessary to address the whole picture.

Yes, a run with daily diflucan will go a long way to clearing up systemic yeast, assuming it is a strain of yeast that is not resistant to diflucan. Sometimes it is necessary to use other antifungal agents in addition to diflucan -- and dietary changes, probiotics, etc are imperative to a successful yeast treatment, too.

My personal opinion is that after a year of treatment with no results, I'd be searching for other possible problems and solutions as well as wanting to try a different treatment approach to the lyme, as well.... just my 2 cents.

--------------------
"Looks like freedom but it feels like death..
It's something in between, I guess"

Leonard Cohen, from the song "Closing Time"

Posts: 822 | From California | Registered: Jan 2006  |  IP: Logged | Report this post to a Moderator
luvs2ride
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Blackstone,

My doctor used a bloodtest called High Resolution Blood Morphology. They prick your finger and study the blood under a special microscope. My doctor did it on a television screen so I could see what he sees. It was very interesting even though nothing about my blood was good.

Both white and black yeast were present. Black yeast is extremely rare and can produce instant death if it gets to the brain. Parasites and bacteria were in my bloodstream as well. My red blood cells were both clumping and linking which are bad. My White Blood Cells were nearly comatose. Just barely moving. Spiderweb looking lines indicated my liver was stressed. The technician running the test was very good at showing and explaining it all to me. The doctor came in, looked it over, turned to me and said "You are very sick.". Yep, I didn't need a bloodtest to know that one.

He explained yeast can only get into your bloodstream through the damaged gut wall, hence clear case of leaky gut.

Yes, Diflucan is an effective yeast killer and more is needed than the old standard 1 pill dose I had always been given.

One of the LLMD's prior to this doctor prescribed a 10 day dose of Diflucan at 100mg to follow a 3 week dose of Ketek. When I took the Diflucan, by day 3, the pain in my joints drove me to the floor. It felt like you had put electrodes in each of my finger joints and turned on the juice. This was what first made me believe yeast might be my problem.

The heavy metals were determined by a urine challenge test. The infected root canal teeth were tested by two separate biological dentist. One used ART testing and one sent me to an ElectroDermal Screener who uses EAV. No Cavitat.

The day I took the EAV test, I was feeling very good. When she finished that test (1 hr) I couldn't think or walk well at all. I was trying to give them my phone number and I gave 3 wrong numbers before I could give the correct one. I left their parking lot to go to my next appt and I had to call the doctor I was going to see and they literally had to direct me turn by turn as I drove to their office. I couldn't believe how badly I had been affected by this test. It really confirmed things for me.

My current doctor first tried to attack the yeast by using IV dioxychlor. Just 2 cc's put me into a lot of pain. He backed off and began supporting my liver and kidneys instead with IV lipostabil and glutathione. He said we have to get my elimination systems working full speed before we can kill anything because I wasn't expelling the die-off. He has been doing this now for 3 mths and I am so much better already. I believe my system is expelling some of the metals and toxins already. He begins real chelation next month. I have had my 3 remaining amalgams removed. Dr does not want me to pull my teeth yet as he thinks it will be too much for me to handle. I'm kind of chicken about it myself.

The parasites are the only thing he has killed so far. He did it early on with an herbal combination. At first I was having heavy feeling and discomfort in my colon. I got 5 colonics and had complete relief. For many weeks afterward, each time I would get the IV glutathione, I would have a heavy load of sesame seed looking things in my poop for a couple of days which I have read are the dead parasites. This no longer happens.

Two weeks ago I received the results of my food allergy bloodtest. I only have a mild reaction to gluten so was advised by the lab to eat it sparingly. However, I was highly reactive to some things I had been eating daily. Blueberries, Strawberries, chicken, lemon and lettuce. Also egg whites which are in just about everything. I told the doctor when I eliminate these, I will probably never have to see him again.

I'm avoiding these now and practicing a rotation diet. On the good side, I was able to add back some foods like dairy and beef. Yea!

Hope I answered everything. Like Lymetoo, I am feeling so much better these days. Almost normal. Almost.

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When the Power of Love overcomes the Love of Power, there will be Peace.

Posts: 3038 | From america | Registered: Oct 2005  |  IP: Logged | Report this post to a Moderator
Lymetoo
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quote:
Originally posted by Blackstone:
Theoretically, shouldn't Diflucan taken daily for a period of time wipe out any systemic yeast problem there is?

I agree! I still take it!

--------------------
--Lymetutu--
Opinions, not medical advice!

Posts: 94468 | From Texas | Registered: Feb 2001  |  IP: Logged | Report this post to a Moderator
Al
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When I was very young I was diagnosed with bleeding ulcers; First it was caused by milk, then it was caused by stress. Then then they cut out half of my stomach to reduce acid. My symptoms continued.
Guess what ! out of the entire medical field 2 doctors discovered that almost all ulcers are caused by a bactreium ( H.Pylori )and a few weeks of Abx. would cure them. These 2 doctors had to fight for years to have there discovery accepted by the medical know it alls. In fact one of these drs. gave himself an ulcer with this bacteria and then cured himself with Abx. to prove his findings
Today it is the accepted treatment.

I think lyme falls into this category.
Autopsys of people with lyme disease (who diden't have lyme) found Borelia in their orgens
and brains.

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klutzo
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Like many dx'd with FMS too, besides Lyme, I have vulvar vestibulitis. When deep tissue scraping showed the cause to be mutated yeasts, down deep in my tissues, I was put on Diflucan.

After only 24 hrs. on it, years of pain had cleared up and I thought I had finally found help, and might even get my sex life back. But by the time another 24 hrs. had passed, the pain was right back to baseline, and I was crushed.

My GYN then told me that 30% of people are resistant to Diflucan. So, it may not work for one out of 3 of us. For others, it can be a miracle, but make sure to get your liver checked while on it.

Danser, I was the opposite in attitude. I badly wanted to believe I only had FMS, not Lyme. I would rather have something I had been told would never kill me, than to think I had something progressive, that can cause MS, ALS, AZD, and so on, esp. since I am allergic to the ABX, and must depend only upon herbs.

However, just when I almost had myself convinced that the whole chronic Lyme thing was overplayed and did not apply to me, I developed an EM rash on my thigh.

My duck PCP said it was a granuloma annulare, BUT because it had doubled in size in only a couple of days, she said it could be a tick bite. It started as a raised red area, then opened out into a red, raised, bumpy ring, with a clear center, except for a tiny red spot. My understanding is that if the ring enlarges, that is always Lyme. It never got any larger than 2 inches in diameter though, and I thought Lyme EM's were always large.

During my herbal tx, this ring has come back a couple of times, always in the same place, and each time it is smaller and lasts a shorter amt. of time than the time before. I was told this could happen during herbal tx as the bacteria are forced out.

I live in a state where many docs claim that there is no Lyme. The point is when you have a migrating, raised, red ring like that, it becomes impossible to deny Lyme any longer, unless what I've been told is wrong.

I am still wishing I could deny it, so I understand the feeling you had after reading those letters. It is just too hard to have a disease where you are not only very sick, but punished for being so, instead of being supported.

Klutzo

Posts: 1267 | From Clearwater, Florida, USA | Registered: May 2004  |  IP: Logged | Report this post to a Moderator
TheCrimeOfLyme
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If ur husband was only treated for one week for babesia ( which does nothing) and he has made no improvement,

I would suggest he may still babesia. Im no doctor, but it sounds likely considering he is going no where in treatment.

Lyme attaches to babesia, can't get rid of one , have to get rid of both.

--------------------
You want your life back? Take it.

Posts: 3169 | From Greensburg, Pennsylvania | Registered: Jun 2003  |  IP: Logged | Report this post to a Moderator
   

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