Discussion in 'Fibromyalgia Main Forum' started by Nanie46, May 30, 2009.
Lyme does not cause CFS/FM but there are some overlapping symptoms. Saying Lyme is causing FM/CFS is very different than saying Lyme can be mistaken for something else. This is true for a lot of conditions.
You can also have CFS/FM plus Lyme.
If someone truely has Lyme and that is the reason for the symptoms, it means you have lyme and not CFS/FM.
This is an important distinction.
While I have heard the name Hortolf, I did not realize that he is into alternative approaches for treating patients.
He also does not believe in long term antibiotic therapy.
I disagree that that the lyme bacteria cannot cause a CFS or a FMS. They are both syndromes (sets of symptoms) with various causes, one of which can be the borrelia bacteria....just like it could be a virus or something else.
Let's say that EBV caused a CFS. A person still has the syndrome of symptoms but the cause is a virus.
A person can develop a fibromyalgia syndrome or a chronic fatigue syndrome from a bacterial infection also.......lyme is really a city in CT.
They still have a FMS or a CFS, just like they might still have migraines or tremors, but the cause is the bacteria.
My Dr agrees that borrelia burgdorferi causes fibromyalgia syndromes and chronic fatigue syndromes.
There are other infections that could cause those sets of symptoms also.
Do I have a fibromyalgia syndrome??? Yes, and the cause is the borrelia burgdorferi bacteria.
There were other infections mentioned on the site also.
Personally, I don't think the division between CFS and Lyme disease is all that clearcut. This division has resulted from votes by committees, but what's really going on it nature may be different. I offered the paper below at the Reno CFS conference. Since then I've heard from a few Lyme disease and CFS physicians, and this hypothesis seems to be holding up.
Is There a Link between Lyme Disease and Chronic Fatigue Syndrome?
Richard A. Van Konynenburg, Ph.D.
9th International IACFS/ME Conference
March 12-15, 2009
Introduction and Background
There are currently two prominent case definitions for chronic fatigue syndrome (CFS): the international research case definition of 1994, sponsored by the Centers for Disease Control and Prevention (CDC) , and the Canadian myalgic encephalomyelitis/chronic fatigue syndrome clinical working case definition of 2003 , which is intended to be used in clinical diagnosis.
The diagnosis of chronic fatigue syndrome is not always clear-cut when either of these definitions is used, because there is no accepted diagnostic test. Rather, the diagnosis is made on the basis of clinical judgment as to whether the specified symptom-based criteria are satisfied, after the exclusion of other known disorders that could account for the symptoms. Active Lyme disease is specified as one of the exclusionary disorders in both these case definitions for CFS. However, there is considerable overlap between the symptoms of CFS and those experienced by patients with Lyme disease. According to the guidelines of the International Lyme and Associated Diseases Society, “The clinical features of chronic Lyme disease can be indistinguishable from fibromyalgia and chronic fatigue syndrome .”
The diagnosis of Lyme disease is not always clear-cut, either, and the appropriate diagnostic criteria for it continue to be a subject of controversy. On the one hand, there are the criteria recommended by the Centers for Disease Control and Prevention (CDC) , which are in agreement with a set of guidelines established by the Infectious Disease Society of America (IDSA) , and on the other hand, there is the set of criteria recommended by the International Lyme and Associated Diseases Society (ILADS) . In some cases the onset of Lyme disease is accompanied by a characteristic rash (erythema migrans), and there is general agreement that when it is present, it establishes the diagnosis. History of having a tick bite is also an important factor in diagnosis. However, the rash does not occur in all the cases (The ILADS estimates less than 50%, while the IDSA offers a higher estimate), and many patients with Lyme disease do not recall having had a tick bite. When the rash and memory of a tick bite are not present and Lyme disease is suspected, serological testing is performed. Unfortunately, the available tests lack sensitivity, and there is also disagreement between these guidelines over which tests and which criteria for interpreting them should be used.
This difficulty in differential diagnosis has resulted in the situation that many patients who were initially diagnosed as having CFS have later (in many cases several years later) been found by serological testing to have Lyme disease. This is regrettable, because unrecognized and untreated Lyme disease can be progressive and can have very serious consequences.
In addition, in cases in which Lyme disease has been recognized and treated, some of the patients have continued to experience symptoms. There is a disagreement within the medical community as to whether these patients continue to be infected with Borrelia burgdorferi (Bb), the bacteria that causes Lyme disease, and/or with one or more of the tick-borne coinfections, and thus are suffering from “chronic Lyme disease ,” or whether the bacteria have been eradicated, and the patients are therefore suffering from “post-Lyme disease syndrome .”
Two years ago the present author proposed a hypothesis for the etiology and pathogenesis of CFS, called the Glutathione Depletion—Methylation Cycle Block (GD-MCB) hypothesis . This hypothesis has been found to be consistent with the results of a clinical study of a treatment based upon it . The GD-MCB hypothesis proposes that a variety of stressors that place demands on glutathione can bring about the onset of CFS in genomically predisposed individuals.
The present paper elaborates the GD-MCB hypothesis by describing a specific biochemical link between Lyme disease and CFS, such that patients who are genomically predisposed to developing CFS can and do progress into CFS when they have contracted Lyme disease. They thus suffer from Lyme disease and CFS simultaneously (in spite of the artificial exclusion of active Lyme disease in the case definitions for CFS). If they are successfully treated for Lyme disease, this hypothesis holds that a significant fraction of them can and do continue to suffer from CFS, which must also be specifically treated. Another paper at this conference describes a clinical study of a treatment for CFS that appears to be promising .
Summary of the CDC-sponsored international research case definition for chronic fatigue syndrome 
This definition excludes other known conditions that could account for the symptoms, and then defines a case of CFS as involving the presence of the following:
“1) clinically evaluated, unexplained, persistent or relapsing chronic fatigue that is of new or definite onset (has not been lifelong); is not the result of ongoing exertion, is not substantially alleviated by rest; and results in substantial reduction in previous levels of occupational, educational, social or personal activities; and 2) the concurrent occurrence of four or more of the following symptoms, all of which must have persisted or recurred during 6 or more consecutive months of illness and must not have predated the fatigue: self-reported impairment in short-term memory or concentration severe enough to cause substantial reduction in previous levels of occupational, educational, social or personal activities; sore throat; tender cervical or axillary lymph nodes; muscle pain; multijoint pain without joint swelling or redness; headaches of a new type, pattern or severity; unrefreshing sleep; and postexertional malaise lasting more than 24 hours.”
Having had Lyme disease that was “treated with definitive therapy before development of chronic symptomatic sequelae” does not exclude a patient from the diagnosis of CFS under this definition.
Summary of the Canadian ME/CFS clinical working case definition 
This definition specifies that a patient with ME/CFS will meet criteria for fatigue, post-exertional malaise and/or fatigue, sleep dysfunction, and pain; will have two or more neurological/cognitive manifestations and at least one symptom from two of the categories of autonomic, neuroendocrine and immune manifestations. In addition, the illness must have persisted for at least six months.
Symptoms in the various categories are delineated in detail in the definition. In this definition, active Lyme disease is listed among the infectious diseases to be excluded during diagnosis, but the definition also states, “If the potentially confounding medical condition is under control, then the diagnosis of ME/CFS can be entertained if the patient meets the criteria otherwise.”
Summary of the IDSA Guidelines for diagnosis of Lyme disease 
If erythema migrans rash is present, clinical diagnosis of Lyme disease can be made without laboratory confirmation. If not, evidence from laboratory testing is required.
These guidelines specify two-tier testing: First, a polyvalent enzyme-linked immunosorbent assay (ELISA) is to be performed. If the ELISA is positive or equivocal, it is to be followed with IgM and IgG western blots as specified by the CDC . These are considered positive if 5 out of 10 IgG bands or 2 out of 3 IgM bands are positive.
Summary of the IDSA proposed definition for “post-Lyme disease syndrome” 
According to the IDSA, in order for a case to be diagnosed as “post Lyme disease syndrome,” there must have been a documented episode of early or late Lyme disease, using the above criteria, and there must have been a generally accepted treatment regimen that resolved or stabilized the objective manifestations of Lyme disease. In addition, there must have been onset of any of the following symptoms within 6 months of the diagnosis of Lyme disease, and persistence of continuous or relapsing symptoms for at least a 6-month period after completion of antibiotic therapy:
Widespread musculoskeletal pain
Complaints of cognitive difficulties
These symptoms must be of such severity that, when present, they result in substantial reduction of occupational, educational, social or personal activities.
There are a number of exclusions in this proposed definition, among them being a diagnosis of fibromyalgia or chronic fatigue syndrome before the onset of Lyme disease.
Summary of the ILADS guidelines for diagnosis of Lyme disease 
The position of the ILADS on diagnosis of Lyme disease is different from that of the IDSA.
The ILADS maintains that Lyme disease is a clinical diagnosis, which includes a consideration of symptoms, and tests should be used to support rather than supersede the physician’s judgment. Burrascano, an ILADS board member, has presented a list of 60 symptoms found in Lyme disease .
Erythema migrans rash is diagnostic, but is absent in over 50% of cases.
Diagnosis of Lyme disease by the two-tier confirmation fails to detect up to 90% of cases.
Sensitivity and specificity for both the IgM and IgG western blots range from 92 to 96% when only two specific bands are positive.
Overlap in symptoms between Lyme disease (including “chronic Lyme disease” and “post-Lyme disease syndrome”) and CFS
A comparison of Burrascano’s symptoms list for Lyme disease  with the discussion of symptoms in the Canadian criteria for CFS  reveals that these two disorders have a large number of symptoms in common, and very few if any that are specific to one or the other of these disorders. Similarly, a comparison of the IDSA proposed definition for “post-Lyme disease syndrome”  and the Canadian criteria for CFS  shows that the symptoms specified in the former are also prominently found in the latter.
Etiology of Lyme disease
It is well-established that the Borrelia burgdorferi bacterium is responsible for causing Lyme disease , and that there are several other tick-borne diseases that can be present with Lyme disease as coinfections [5,8].
Etiology of CFS, and the Glutathione Depletion—Methylation Cycle Block (GD-MCB) hypothesis for CFS
The etiology of CFS is not agreed upon. As noted above, the present author has proposed a hypothesis for CFS called the Glutathione Depletion—Methylation Cycle Block hypothesis , which proposes that the etiology of CFS consists of genetic predisposition combined with the effects of some combination of a variety of stressors (physical, chemical, biological and/or psychological/emotional) that lead to the depletion of glutathione, which in turn causes a partial block in the methylation cycle. A updated review of the GD-MCB hypothesis follows:
• An individual inherits a genomic predisposition (polymorphisms in several of certain genes) toward developing CFS. (This genomic factor is more important for the sporadic cases than for the cluster cases of CFS.)
• The person then experiences some combination of a variety of possible stressors (physical, chemical, biological, and/or psychological/emotional) that place demands on glutathione. [As will be discussed later, this is the point at which Lyme disease can come into this pathogensis.]
• Glutathione levels drop, producing oxidative stress, removing protection from cobalamin (vitamin B12) and allowing toxins to accumulate.
• Toxins react with cobalamin, lowering the rate of formation of methylcobalamin.
• Lack of sufficient methylcobalamin inhibits the activity of methionine synthase, placing a partial block in the methylation and folate cycles.
• Sulfur metabolites drain excessively through the transsulfuration pathway to form cysteine.
• Much of the cysteine is oxidized to cystine because of the state of high oxidative stress, and is therefore not available for the synthesis of glutathione. An alternative pathway initiated by cystathionine gamma lyase diverts the cystine into formation of hydrogen sulfide and thiosulfate, and the latter is excreted in the urine.
• An interaction (vicious circle) is established between the partial block in the methylation cycle and the depletion of glutathione, and this is what causes the disorder to become chronic.
• A wide range of symptoms results from these chronic abnormalities in the basic biochemistry of the cells.
• The dysfunction of the detoxication system and the immune system that results from this vicious circle mechanism allows toxins and infections to accumulate over time, which increasingly produce effects of their own.
• Treatment should be directed primarily at increasing the activity of methionine synthase. The resulting normalization of the methylation cycle, the folate metabolism and glutathione levels will restore function to the immune system and the detoxication system as well as to a wide range of other parts of the overall biochemistry.
• It can be expected that die-off of pathogens and mobilization of stored toxins will initially produce some exacerbation of symptoms, but improvements will be experienced as the body burdens of toxins and active infections are decreased.
Included among the biological stressors that place demands on glutathione are infections, such as that produced by Borrelia burgdorferi. In other words, the possibility that Lyme disease could lead to CFS was part of the GD-MCB hypothesis as proposed. The biochemical mechanism of the proposed link between Lyme disease and CFS is elaborated in more detail below.
Hypothesis for a link between Lyme disease and CFS
The present author proposes that Lyme disease can lead to CFS in individuals who are genomically predisposed to developing glutathione depletion and a partial block in the methylation cycle under the influence of stressors. This occurs because the Borrelia burgdorferi bacterium depletes glutathione in its hosts. In such cases, Lyme disease and CFS exist together as comorbid conditions, so that CFS is a component of what has been called “chronic Lyme disease.” If the Lyme disease is successfully treated, the CFS continues to be present chronically unless specifically and effectively treated, because of the ongoing vicious circle interaction between glutathione depletion and the partial methylation cycle block. The resulting condition then constitutes what has been called “post-Lyme disease syndrome,” which falls into the category of the post-infective fatigue syndromes.
Evidence in support of this hypothesis
Sambri and Cevenini  found in culture experiments that Borrelia burgdorferi (Bb) requires that cysteine be supplied exogenously, and is not able to make use of either methionine or cystine as a cysteine source. They also found that cysteine diffuses passively into Bb, i.e. there is no active transporter protein. This requirement of Bb for exogenous cysteine is important, because it means that Bb must take cysteine from its host. Cysteine is the rate-limiting amino acid for the synthesis of glutathione in human cells, and if it becomes depleted, this synthesis will be inhibited .
It has been found that Bb uses cysteine in the synthesis of several of its essential proteins: outer surface protein A (OspA), outer surface protein B (OspB), coenzyme A, a hemolysin and others [10,12]. Bb does not use glutathione for its control of its redox potential, as do human cells. Instead, it uses reduced coenzyme A (CoASH) .
Pancewicz et al. have found that Bb does in fact lower the cysteine and glutathione levels in its human host, and also inhibits the activity of glutathione peroxidase . Because glutathione peroxidase, with the help of glutathione, normally converts hydrogen peroxide to water, thus eliminating its contribution to oxidative stress, low glutathione and low activity of glutathione peroxidase will allow a rise in hydrogen peroxide concentration and a rise in oxidative stress .
Although Bb appears to be more resistant than other bacterial pathogens to reactive oxygen species, it does incorporate unsaturated fatty acids in its membranes, and these are vulnerable to oxidative attack . It has been observed that elevation of hydrogen peroxide causes Bb to assume its cyst form , in which it is less vulnerable to environmental threats , including antibiotics . Perhaps this self-actuated mechanism serves to promote the survival of Bb in its host.
It is known that the immune system is dysfunctional in CFS, and the GD-MCB hypothesis  suggests that this results from glutathione depletion and disruption of the folate metabolism. Glutathione is particularly important for the function of the T lymphocytes , and folate is needed in the synthesis of DNA and RNA, necessary for the proliferation of T cells . Thus, the biochemical mechanism suggested in the GD-MCB hypothesis can be expected to have a deleterious effect on the cell-mediated (Th1) immune response, which is needed to counter intracellular pathogens. Bb has been found to be able to reside intracellularly , and it has been shown that Th1 types of responses are required for optimum eradication of Bb . Therefore, this immune dysfunction may help Bb to continue to survive in the body of the host, which is relevant to chronic Lyme disease.
The major overlap in symptoms between CFS on the one hand, and both chronic Lyme disease and post-Lyme disease syndrome on the other, as described earlier, is also evidence that supports this hypothesis.
In this regard, a study was performed by Gaudino et al.  that compared a group of patients judged to have post-Lyme disease syndrome (though the authors acknowledged that the possibility of ongoing infections could not be ruled out) with a group who met the research case definition for CFS  but did not have histories suggestive of Lyme disease. The authors found that both groups experienced severe fatigue, myalgia, headaches, and perceived cognitive problems. Eighty-four percent of the post-Lyme patients also met the research case definition for CFS. They did not find significant differences between the two groups in terms of psychiatric illness.
Despite the overlap in symptoms, they did find that some symptoms distinguished the two groups. Fever, sore throat, tender lymph nodes and unrefreshing sleep were found to be significantly more common among the patients with CFS. They also found that post-Lyme patients showed more global cognitive impairment.
It should be noted that the CFS research case definition  described earlier, which was used for patient selection in this study, specifically lists sore throat, tender lymph nodes and unrefreshing sleep among eight symptoms, four of which must be present to diagnose CFS. The more recent Canadian diagnostic case definition for ME/CFS  specifies a broader definition for sleep dysfunction and combines sore throat and tender lymph nodes together under “immune manifestations.” The immune manifestations are then grouped together with two other categories of symptoms, and the definition requires only that at least one symptom from two of these three categories must be present. Since there are 21 symptoms listed in these three categories, it is likely that patients in a group selected using the Canadian criteria for CFS would be less likely to exhibit sore throat, tender lymph nodes and unrefreshing sleep than a group selected using the CFS research case definition. In view of this, the differences found in this study between these symptoms in post-Lyme disease syndrome and CFS do not appear to be very robust. In addition, while this study found little cognitive deficit in the CFS patients, an earlier study in CFS reported poor performance on reaction time and attention , in disagreement with this study. It therefore appears that CFS and post-Lyme disease syndrome are essentially indistinguishable on the basis of comparison of symptoms.
Implications for the debate concerning “chronic Lyme disease” vs. “post-Lyme disease syndrome”
In view of the hypothesized link between Lyme disease and CFS, it seems possible that either chronic Lyme disease or post-Lyme syndrome could be present in a given case that began with Lyme disease and progressed into CFS, depending on whether or not Borrelia burgdorferi had subsequently been eradicated. If Bb were still present, the condition would properly be called chronic Lyme disease. If Bb had been eradicated, the patient would still have CFS, which would persist because of the vicious circle mechanism described in the GD-MCB hypothesis. Therefore, the patient would have post-Lyme disease syndrome, which is a post-infective fatigue syndrome, a recognized category within CFS .
Testing this hypothesis
This hypothesis can readily be tested by means of the commercially available methylation pathways panel , which is increasingly being used in CFS and autism. This panel measures metabolites in the methylation cycle and the folate metabolism, as well as the reduced and oxidized forms of glutathione, and will reveal whether glutathione depletion and/or a partial block in the methylation cycle are present. This panel could be used on patients believed to have either chronic Lyme disease or post-Lyme disease syndrome, to find out whether this hypothesis is valid for these patients.
Implications for treatment
If this hypothesis is valid, it suggests that treatment of “chronic Lyme disease” or “post-Lyme disease syndrome” should include treatment to lift the partial methylation cycle block. Such treatment of patients with combined diagnoses of chronic fatigue syndrome and fibromyalgia has been subjected to a clinical research study, and the results are reported in another paper at this Conference .
A link has been hypothesized between Lyme disease and chronic fatigue syndrome (CFS). This link is based on the Glutathione Depletion—Methylation Cycle Block (GD-MCB) hypothesis for CFS . The GD-MCB hypothesis proposes that in a person who is genomically predisposed, stressors that place demands on glutathione can cause it to become depleted, and can lead to a partial block in the methylation cycle. The resulting vicious circle interaction maintains CFS as a chronic condition. The present paper suggests that Lyme disease is one of the stressors that can produce this vicious circle interaction in the body of a person who is genomically predisposed. It is suggested that this leads to chronic Lyme disease. If the Borrelia bacteria are subsequently eliminated by treatment, the patient then has post-Lyme disease syndrome. Post-Lyme disease syndrome is one of the post-infective fatigue syndromes, a category of disorders within chronic fatigue syndrome . A commercial test panel is available to test this hypothesis , and treatment to lift the methylation cycle block and to restore glutathione is available  if these are found to be present.
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[This Message was Edited on 05/31/2009]
Thanks for your reply and posting your paper Rich.
I still disagree, and so does my Dr. He says it is a matter of semantics and that is why many people go undiagnosed as far as the cause of their illness.
FMS and CFS officially have no known cause which means Dr's just haven't figured it out.
Those syndromes most certainly have a cause.
I assure you that I do have a FMS and it was caused by a bacterial illness. When the infection is properly treated the FMS can resolve.
Unfortunately, most people with FMS or CFS never find the cause of their symptoms and therefore never recover.
My office visits are coded as FMS, CFS and Lyme.
In reality, no one knows the exact cause of either CFIDS/ME nor FMS. They often go hand in hand with other conditions, like MS, Lupus, Lyme, etc. As stated, some docs and researchers have set out parameters for describing, and diagnosing, these illnesses. This is often done for practical reasons, expecially after other similar conditions have been eliminated.
There are still docs out there who swear they "know" what causes our illnesses. I take them with a grain of salt. We do know that some treatments address the symptoms of our illnesses but that no one treatment seems to work for everyone all the time. To date, no one has a sure cure although, one of these treatments may eventually prove to be a cure or, at least, drive the symptoms into remission.
I think people feel more secure when someone tells them, he or she absolutely knows something about our illnesses. Part of dealing with out illnesses is getting to the point where we can admit that no one knows for sure what causes them and no one has a cure. That is not to say we should ever stop researching and trying treatment options. I continue to heal but it has taken a very comprehensive approach, using a lot of different treatment protocols, including the methylation treatment. Perhaps, had I started with the methylation treatment protocol, the other treatments may have been unnecessary. I will never know for sure. I only learned of the methylation protocol since you have been here. It may prove to be a cure in the long run.
I think we could argue til the cows come home here about who knows what, but I don't think it is helpful. Your info is always helpful and appreciated. Thanks for posting.
all of the lengthy post information here; I'm too unwell today. I just want to add my two cents about Holtorf's hormone and longevity center:
I spent upwards of $10,000 last year at the Holtorf Medical Center in Torrance. It's extremely expensive; they sell supplements at twice the price Prohealth does, for example.
I had a lot of hope that the treatment would work--anti-virals followed by anti-biotics; bio identical hormone replacement, etc. All the literature on the website and in the office seems to support a thorough, organized treatment approach.
When I didn't respond to the treatment protocol, they basically threw up their hands and said, "well what do you want to do??" I'm not the doctor . . . I was really disappointed, and I have no idea where to go now for help
You said in the thread above:
"While I have heard the name Hortolf, I did not realize that he is into alternative approaches for treating patients.
He also does not believe in long term antibiotic therapy."
If you've heard of the name Holtorf but didn't know he's into alternative approaches then how do you know he does not believe in long term antibiotic therapy? That seems to be a strange statement to make when Dr Holtorf posted the following on his website:
"Lyme Disease Often Missed as a Cause of Chronic Fatigue Syndrome.
Lyme disease is caused by a spiral shaped bacteria (spirochete) called Borrelia burgdorferi. They can be transmitted by tics, but also by mosquitoes. The spirochets have been called “the great imitators” because they can mimic virtually any disease, which is why they are often misdiagnosed. Anyone with chronic illness and especially those with chronic fatigue syndrome and fibromyalgia need to consider Lyme disease as the cause.
Patients with chronic Lyme disease most commonly have fatigue, joint and muscle pain, sleep disorders and cognitive problems (brain fog). In addition, infection with Borrelia often results in a low grade encephalopathy (infection of the brain) that can result in depression, bipolar disorder, panic attacks, numbness, tingling, burning, weakness, twitching and is associated with neurological disorders such as multiple sclerosis, dementia such as Alzheimer’s disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease). In addition, this infection often results in hormonal deficiencies, abnormal activation of coagulation and immune dysfunction, which potentiate the symptoms. Patients with chronic Lyme disease often complain of “strange” or “weird” symptoms that that cannot be explained even after going to numerous doctors and often results in the patient being told that it must be psychological. Patients are often told that they are hypochondriacs and are referred to psychiatrists and counselors.
Because the symptoms are so variable, patients are usually not even considered for testing or treatment. Even if testing is done, however, standard testing will miss over 90% of cases of chronic Lyme disease. The standard testing is an immunoassay test of IgG and IgM antibodies and then a Western blot for confirmation. The problem is that these tests were designed to detect acute Lyme disease and are very poor at detecting chronic Lyme disease. In addition, doctors (infectious disease, internists, family practice, etc) most often use the Center for Disease Control (CDC) criteria to define a positive test. This criteria was never meant to be used for diagnosis, but rather for epidemiological surveillance (tracking data). If one uses an expanded Western blot with revised requirement criteria for diagnosis, studies have demonstrated an improved sensitivity of detection and a low false-positive rate.
There are also a number of coinfections that are commonly transmitted along with the Lyme bacterium, including Bartonella, Babesia, Ehrlichia and others. There are also different species in different parts of the country, making testing difficult and insensitive. As with Borrelia, the coinfections have a very high percentage of false-negative results (test negative despite infection being present).
Treatment of chronic Lyme disease can also be very problematic as the Borrelia bacteria can transform from the standard cell wall form to a non-cell wall form (l-form) and also into a treatment resistant cyst. Standard antibiotic treatments are only effective against the cell wall form and are ineffective against the L-forms and cystic forms that are usually present in chronic Lyme disease. Consequently, the usual 2-4 weeks of intravenous or oral antibiotics can be of little benefit. Even the use of longer courses of oral or intravenous antibiotics for months or years can be ineffective as well if used a the sole major therapy. A multi-system integrative approach can, however, dramatically increase the likelihood of successful treatment. This includes using a combination of synergistic antibiotics that are effective against the l-forms and cystic forms, immune modulators, directed anti-Lyme nutriceuticals, anticoagulants, hormonal therapies and prescription lysosomotropics (medications that increase the effectiveness and penetration of antibiotics into the various forms of the Borrelia spirochete). To adequately detect and treat chronic Lyme disease, physicians must understand that standard testing will miss the majority of these patients and standard treatment will fail the majority of time. One must undergo more specialized testing and treatment to achieve success in the majority of these patients. "
Thanks much for posting this website link. I didn't read some of the replies here in depth, but I would just mention briefly a couple of my own thoughts.
CFIDS/ME and/or FM seems to usually be initiated by some kind of shock to the system. I think of this shock as the catalyst that sends a long row of dominos toppling, with the dominos being our bodies various systems, e.g., immune, digestive, hormonal, neurological communication, detoxification, etc.
Depending on individual resilience, these toppled dominos will take us into varying degrees of CFIDS / FM. In the end, I don't think it matters all that much what the initial shock was, (whether viral, bacterial, emotional, physical injury, etc.) the downward spiral was begun and then continues indefinitely, usualy long after the initial shock.
Regarding Lyme & CFIDS. I have been diagnosed with Lyme, but I think the initial shock that started my CFIDS was a head injury and whiplash as a teenager. So I believe I have Lyme and CFIDS. I suspect that if I am successful at eliminating the Lyme bacteria from my body, some of my problematic symptoms will improve. But unless I'm able to reverse decades of major system dysfunction, I'll likely continue to deal with CFIDS.
As far as Lyme initiating CFIDS. The evidence appears to be pretty overwhelming that this is often the case. In my case, I believe CFIDS, with the associated immune dysfunction, made me vulnerable to Lyme. I also believe that any number of other viruses or bacteria can initiate CFIDS. Just my own personal views, nothing else.
Thanks Rich, Munch and Mikie for your replies. Always appreciate your insights.
Regards, Wayne[This Message was Edited on 06/01/2009]
A lot of god information here. Rich I am impressed by all the work you've done.
Nanie this was a great link. I had a feeling several months ago when I read one of your posts on Lyme, that you were correct about not just treating the symptoms of FM but the causes, whatever those might be.
As I was reading the site by Dr Holtorf I came across the name of the infection I had been diagnosed with: Mycoplasma Fermenans (incognitus strain). I got this dx about 13 years ago, when I first had FM symptoms. I was treated with 12 months of Doxycycline.
It didn't help. My doctor had said the test had showed the antibodies for resisting this infection and he concluded that it had come and gone. Sorta like a post-lyme situation maybe?
I was tested for Lyme and it was negative, but the lab work wasn't sent to the correct facility.
Debilyn I was sorry to read about you disappointing experience at that center. The results on the website were phenomenal .Sometimes, unfortunately, that is the case. Maybe some others here, more knowledgeable than I, can point you in another direction.
I don't want to throw the baby out with the bathwater though and so am going to use some of the information contained in the studies. I will talk to my doc about implementing a multifaceted approach, not just to treat the symptoms as he has already done, but to treat the underlying causes.
I want to explore the bio identical hormones, further thyroid testing and possibly treatment, cortisol, and Xyrem. Maybe not all at the same time, I will have to see.
Wayne what does your treatment regimen consist of?
thanks again for all the info Nanie
Hi Vivian, Hi All,
Regarding my treatment regimen -- Hard to know what to say. Part of me has settled into a bit of a resignation in the past few months. The main reason being is that I feel I've lost more ground with my cognitive function. I just can't do the type of research I could sometimes do in the past, try to look at information from various angles, and then come up with some kind of game plan. I just don't have the resiliency to do that these days.
My main objectives recently are to just make it through my days somewhat intact. Not always an easy task. I've cut down on my supplements because of expense and energy. I'm now only taking digestive enzymes and some green tablets. I suspect dropping some of my supplements has led to some of my decline, although I went through some pretty stressful months recently.
I am doing some low-dose MMS (3 drops/day) and am feeling it is keeping my Lyme somewhat in check until I can come up with some kind of comprehensive game plan for that. I really don't feel my body could handle the kinds of assaults antibiotics could have on my very fragile system, at least at this time. I'm also doing the methylation cycle supplements.
I've also been seeing a couple of different health care practitioners; one does interesting gentle touch chiropractic; the other is a Neurolink practitioner. Both are to some degree or another, working on some of the bioelectric components that I feel are a big issue for me.
I have two acquaintances who both believed the had developed CFS. One was a friend who began dating a woman with CFS, and feels he contracted it from her. He struggled for months trying to get well. He finally went to see a Korean acupuncturist who he said stuck about a hundred needles in his hands. He said he knew immediately that this therapy was going to work. He only need about 2-3 sessions, and all his symptoms went away. He remains healthy to this day.
Another man, an osteopath who does cranial/sacral work, said he too had become very sick for several weeks. He had all kinds of tests done to no avail. He could see all the symptoms were heading him toward a CFS diagnosis. He finally went to a homeopath who gave him a remedy which completely cleared up his symptoms in about 3 days.
The reason I'm sharing these stories is because I think it fits into the perspective of some kind of shock usually initiating CFS. I think when this shock occurs, it not only affects us physically, but also affects our bioelectrical systems, which most medical disciplines don't even take into consideration. But when two modalities such as acupuncture and homeopathy can affect seeming cures, it would seem that addressing bioelectric dysfunction may be a value.
I've tried so many different things, and have gotten to the point where I will likely put more focus on the bioelectrical components. If I can get some of my major systems up and running again, by whatever means, I think it will be important to be prepared to assist my body with some major detoxification. Which is why obtaining a far infrared (FIR) sauna has now become a priority for me.
I sometimes feel I'm languishing, but after reading what I've just written, it does appear I am moving forward after all, albeit somewhat haltingly at times. Like you, I feel I want to revisit some of my thyroid issues as well, but I'll just have to get to it when I can. Almost forgot, I am doing low-dose hydrocortisone (Cortef), and have done so for over ten years now. It's been a godsend for me.
Best, Wayne[This Message was Edited on 06/01/2009]
'Treatment of chronic Lyme disease can also be very problematic as the Borrelia bacteria can transform from the standard cell wall form to a non-cell wall form (l-form) and also into a treatment resistant cyst. Standard antibiotic treatments are only effective against the cell wall form and are ineffective against the L-forms and cystic forms that are usually present in chronic Lyme disease. Consequently, the usual 2-4 weeks of intravenous or oral antibiotics can be of little benefit. Even the use of longer courses of oral or intravenous antibiotics for months or years can be ineffective as well if used a the sole major therapy.'
So it looks like he is talking about using antibiotics as the only therapy and other therapies, which can be anything from bioidentical hormones, supplements, muscle testing, Armour thyroid. etc. are not scientifically proven to be effective.
This does indeed make me think he is not a credible doctor by my standards. I know other's may have different standards.
I have researched on the subject of diagnosis of lyme as well as the other theories that go with it. I still go by the IDSA.
I will not reply as it only bumps this post up nor read it again as it has taken too much space on this board and my time. At this point looks like this post should be heading for the Lyme board.
Thanks for your post. I understand that sliding down and don't quite know why feeling. I also have it at times. Some people might call it a flare but I don't think that quite describes it well enough for me.
Sometimes just making it through the day has to be good enough. I am constantly having to take measure of my pain and energy levels so I can adjust my schedule accordingly.
I have been under stress lately too. I seem to be ok during the crisis but have to take to my bed afterward.
I haven't tried different things like many here have. Most of them I am not familiar with and like you I don't believe I am able to think clearly enough to evaluate them adequately at this time. It's too bad really because, as you pointed out, we never know what just might work.
I don't know anything about bioelectric systems in our bodies. I have never heard of far infared sauna either. What do you hope this will do for you?
I don't know you and so am unable to comment on your previous cognitive functioning but from what I have seen on the boards for the last 6 months or so, you seem like a very intelligent person.
I know that it is hard for us to objectively evaluate how much mental capacity we have or have lost. I wonder what standard IQ tests would reveal. Most of us had them in school and know our approximate IQ.
I have a friend that administers IQ tests at her job, I could ask her to test me again, but I don't think I really want to know.
Best to you Wayne and all
love and hugs to all
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