by Leon Chaitow ND DO, Copyright 2008
The most frequent gastrointestinal problem for which specialist advice is sought is irritable bowel syndrome (IBS). The major symptoms include abdominal discomfort or pain, intermittent diarrhoea or constipation, bloating and distension.Sometimes an initial distinction can be made between IBS and organic bowel disease by virtue of the presence (in IBS) of the associated symptoms of urinary frequency, premature satiety ('feeling full'), backache and fatigue (Maxton et al 1991).
In fibromyalgia (FMS) and chronic fatigue syndrome (CFS), the patient with IBS is far more likely to be a young adult female, displaying no clear laboratory evidence for the problem, and with no obvious pathology (Yunus 1989).
There are various schools of thought as to the cause(s) of IBS:
Stress-related inﬂuences including anxiety/ hyperventilation (Schleifer 2002)
Allergy, sensitivity inﬂuences (particularly wheat, corn, dairy products, coffee, tea, citrus fruits) possibly effected by enzyme or HCl imbalances (Jones et al 1982)
Infection and possible overgrowth, by fungi and/or bacteria; or parasitic infection (particularly Giardia, threadworms, Ascaris and Amoeba). Yeast overgrowth in particular has been blamed for damaging gut mucosa and precipitating malabsorption, and consequent allergic responses, including IBS symptoms (Phaosawasdi 1986). British physicians Stephen Davies and Alan Stewart state: ‘Apart from the simple matter of overgrowth with candida, some people are hypersensitive to it. … the main places candida takes hold are the GI tract, the mouth and the vagina. It has been reported that some people with the symptoms of IBS are allergic to the yeast’ ( Davies & Stewart 1988)
Use of antibiotics (Henry 1995).
Antibiotics usage can trigger a sequence which results in yeast overgrowth followed by bowel irritability. Dr John Henry (1995), chief medical editor for the British Medical Association’s book A New Guide to Medicines and Drugs, who is not antagonistic to the use of antibiotics, says:
‘A risk of antibiotic treatment, especially if it is prolonged, is that the balance of micro-organisms normally inhabiting the body may be disturbed. In particular antibiotics may destroy bacteria that limit the growth of Candida, a yeast often present in the body in small amounts. This can lead to overgrowth of Candida in the mouth, vagina, or bowel.’
Dr Joseph Pizzorno, of Bastyr University, Seattle, indicates the implications of this as follows:
'In a study of 55 injured patients admitted to the trauma service of a hospital, all were given broad spectrum antibiotic therapy during some point of their stay. 67% developed elevated candida antigen levels in their blood during their hospital stay, indicating that candida were overgrowing in their intestines (and/or the vagina in women). The researchers also found that the white blood cells of patients with candida antigens were not able to inhibit candida albicans growth as effectively as white blood cells from patients who did not have candidal antigens in their blood. In other words, when patients receive antibiotics, the level of candida in their intestines increases so much, and the intestines become so damaged, that fragments of the candida leak into their bloodstream and inhibit the function of their immune system.' (Pizzorno 1996)
A meta-analysis, published in the British Medical Journal (D’Souza et al 2002), has shown a clear linkage between antibiotic use and the onset of acute diarrhoea (which as noted above is often a precursor of IBS), and importantly highlights the value of probiotics in prevention of this when antibiotics have to be used.
When local gut irritation (caused by hypersensitivity of gastrointestinal mechano- and chemoreceptors caused by initial trauma) prevails, it is thought that visceral hyperalgesia may occur leading to central sensitization (visceral afferents inﬂuence dorsal horn neurons which subsequently affect the hypothalamus) (Mayer 1993).
This (visceral hyperalgesia) model is what Goldstein (1996) calls a ‘bottom-up’ version of what he sees as a ‘top-down’ process in his neurosomatic model of FMS aetiology : ‘Thalamic and dorsal horn dysregulation in IBS would stem from prefrontal cortical dysfunction in this paradigm. There is no … reason to complicate matters by invoking some peripheral lesion, although some may occur, just as primary immune dysfunction may occasionally cause CFS, and post-traumatic myofascial pain syndrome may produce ﬁbromyalgia.’
Price et al (2006) have concluded that a combination of research studies of human IBS patients, as well as animal studies, strongly point to a mechanism wherein both primary visceral hyperalgesia, and secondary widespread cutaneous hyperalgesia, are dynamically maintained by tonic impulse input from the non-inflamed colon and/or rectum. They suggest that secondary hyperalgesia is likely to be at least partly related to sensitization of spinal cord dorsal horn neurons, and in this respect might be similar to other persistent pain conditions such as fibromyalgia.
Questions to ask in irritable bowel syndrome
In order to make sense of irritable bowel conditions the following differentiations need to be made by means of questioning, examination, testing and, if necessary, hospital investigation:
Is the problem related to gynaecological, urinary, liver or biliary, musculoskeletal or purely gastrointestinal factors?
Is it modiﬁed by menstruation, defecation, urination, certain foods (fatty, etc.), work, rest?
Do emotions relating to work, family, relationships, other factors inﬂuence the problem?
Is there evidence of infection (particularly bacterial or yeast overgrowth), inﬂammation, trauma, neoplasm, metabolic disturbance, degenerative disease?
Is there a link between IBS and use of steroid medication or antibiotics?
What is the status of the gut ﬂora and what can be done to enhance normal gut ecology?
Treatment should depend upon the answers to these questions.
How common is IBS in association with FMS?
Between 20 and 32% of patients with irritable bowel syndrome have been found to suffer from FM and 4.2–11% from CWP. (Lubrano et al 2001, Whitehead et al 2002)
Using Insurance data (US provider) a large cohort of 97,593 people with IBS, and a comparison cohort of 27,402 people receiving routine medical services, were evaluated for coexisting conditions. People in the IBS cohort had a 40% to 80% higher prevalence odds of migraine, fibromyalgia, and depression in comparison to people without IBS. (Cole et al 2006)
· Clauw (1995) found 60% of his surveyed FMS patients to have IBS symptoms
· The Forrest Hospital survey found over 50% with IBS (Fibromyalgia Network Newsletter 1999)
· Jessop observed that of her in excess of 1000 patients with CFS and FMS, fully 82% had yeast cultured, and 30% had parasites, in their purged stool samples (Fibromyalgia Network Newsletters 1990–94).
· Prior to the onset of their CFS/FMS, Jessop’s patients were recorded as having had a high proportion of IBS (89%) with 80% reporting a history of ‘constant gas’ or bloating, and 58% chronic constipation.
Comment: Sensitization mechanisms appear to offer an explanation between the known high incidence of IBS in individuals with a diagnosis of FMS.
Infection and FMS
Goldenberg (1994) describes two possible pathways via which infection could be associated with FMS:
1. An infectious agent directly invades tissues or activates immune mediators (cytokines) and produces the symptoms of pain and neural dysfunction.
2. An infection triggers an adaptive response which leads to the symptom picture. In this model infection is just one possible trigger resulting in avoidance (‘sickness’) behaviour involv-ing altered sleep patterns, emotional changes, increased muscle tension and reduced activity.
Goldenberg says that the ﬁrst model is unsupported by any evidence of the presence of infectious agents in either peripheral tissues of the nervous system. The provocation of cytokine production (such as interleukin-2) does, however, result in symptoms similar to FMS and CFS.
Both models are worthy of further research, although Goldenberg is clear that, ‘It is unlikely that a single infection is the cause of most cases of ﬁbromyalgia. Studies of the complicated integration of mind, body and patient’s psychological milieu are more likely to provide meaningful answers to all potential factors, including infections, that may be associated with ﬁbromyalgia.’
British physician Anne Macintyre (Macintyre 1993), herself afﬂicted with myalgic encephalomyelitis (aka CFS), writes:
'The incidence of new cases [of ME] peaks in late summer and autumn, coincident with the peak time of year for enteroviral infections. It is likely that enteroviral infection accounts for the majority of ME illness in this country [UK], even if other factors (stress, trauma) are present. There may also be a genetic predisposition, evidenced by the higher than expected number of parents with ME whose children also develop it some years after the parents.' (Dowsett 1990)
The evidence for a link between infection and FMS and CFS seems to be compelling in some individuals, however the issue is extremely controversial, and the evidence is coonflicting, as outlined below.
It should be noted that a proposed link between infection and FMS does not necessarily mean that the infection is the cause of FMS; it may simply reﬂect the presence of opportunistic organisms, taking advantage of lowered immune function, or of local environmental situations.
Clearly concurrent infections add to the burden of symptoms.
Eliminating chronic infections, whether viral, bacterial or fungal, requires possibly targeting the organism, but most certainly should involve enhancing the immune system’s ability to exercise control of the invading pathogen.
Gran (2003) has performed a useful epidemiological survey of fibromyalgia patients. He found that in infectious disorders, FMS has been detected in 5–16% of patients with hepatitis C (Goulding et al 2001), in 11–29% of individuals with HIV infection (Buskila et al 1990), in 19% of those acute viral infection (Rea et al 1999) and in 8% of cases of Lyme disease.(Dinerman & Steere 1992)
In their study Rae et al (1999) observed that while 19% of patients exhibited clinical evidence of FMS at presentation, at 2 and 6 months, only 3 and 1%, respectively, suffered from FMS.
Bennett et al (2007) report that 43% of survey responders noted that infections worsened their symptoms and 26.7% noted that 'acute illness (unspecified nature) was the perceived trigger for the onset of their FMS.
The Fibromyalgia Network survey (1999) contained the information that 43% of responders reported fever blisters prior to the onset of symptoms (suggesting viral infection). Additionally 20% reported a diagnosis of mononucleosis, 9% herpes, 7% hepatitis, 1% Lyme disease - prior to the onset of their FMS symptoms.
Bacterial infection (mycoplasma)
· Root-Bernstein (1993) explains some of the characteristics of these unusual bacteria: 'Mycoplasma is a genus name for [approximately] 50 different species of bacteria. Mycoplasmas differ from most other bacteria in being relatively small and lacking an outer cell wall. They are often among the most difﬁcult bacteria to isolate. They can cause a range of disease manifestations, including pneumonia, when present in the lungs, and proctitis, when they infect the rectum. Animals infected with Mycoplasmas often become immune suppressed.'
· Microplasmata are primitive bacteria that have the ability to incorporate into their own surface structures parts of host cell membranes that contain important host membrane antigens, creating the opportunity for autoimmune responses (Baseman & Tully 1997). These micro-organisms are now considered important pathogens involved in various chronic illnesses including (in many individuals) CFS and FMS by some researchers and clinicians (Nicolson et al 2000, 2002, 2003).
There is controversy over the claims by some (see notes on Nicolson’s work below) that mycoplasma infection is commonly systemic in people with CFS, FMS and Gulf War syndrome (GWS). The treatment protocol recommended for systemic mycoplasma infection involves up to a year of multiple antibiotic use.
There is also a contrary viewpoint which suggests that the testing methods used by proponents of the mycoplasma aetiology theory are ﬂawed, and that the antibiotic protocols recommended are dangerous to the individual, creating havoc with their internal ecology, and promoting even greater antibiotic resistance, something which is causing great concern as ever more ‘superbugs’ evolve (see notes on Urnovitz’s critique of the mycoplasma theory, and Lo’s research, below).
· Speciﬁcally in relation to CFS, Nicolson et al (2002) offer these observations about the mycoplasmata: 'In CFS patients we have found that chronic infections are a rather common feature of the illness. Previously we studied American and European CFS patients and found that most had Mycoplasmal infections. … When we examined the incidence of particular Mycoplasmal infections in CFS, we found that most patients had multiple infections (two or more species of Mycoplasma), which were for the most part combinations of M. fermentans and other Mycoplasma species. For example, in studying the prevalence of multiple Mycoplasmal co-infections we found that double or triple infections occurred only when one of the species was M. pneumoniae and/or M. fermentans. In a study on European CFS patients a slightly different picture was found. Examining 261 consecutive patients seen at a CFS clinic in Belgium 68.6% of patients were found to have one or more species of Mycoplasma in their blood. In contrast to North American patients, however, the most common species found was M. hominis. This could indicate differences in demography and exposures between North American and Belgian CFS patients. We also found that more than 50% of North American patients with rheumatoid arthritis had Mycoplasmal infections, and in the majority of these patients multiple infections with more than one species was found (18). Mycoplasmas are found commonly in the oral cavity, urogenital tract and as symbiotic gut ﬂora, but some species can cause acute and chronic illnesses when they penetrate into the blood vascular system and systemically colonize organs and tissues. For example, M. penetrans, M. fermentans, M. hominis and M. pirum can enter a variety of tissues and cells and cause systemic signs and symptoms. Mycoplasmas have also been shown to have a complex relationship with the immune system. They are very effective at evading host immune responses, and synergism with other infectious agents has been seen.'
Mycoplasmata and FMS
· According to Nicolson et al (1998), mycoplasmal infection has been observed in approximately 70% of FMS, 60% of CFS, and 50% of Gulf War Syndrome (GWS) and rheumatoid arthritis patients. Many of these patients were found to have principally one infectious species of mycoplasma, M. fermentans. (See also the notes on thyroid dysfunction linking mycoplasmal infection with hypo-thyroidism (Sack et al 1989).
· According to Nicolson & Nicolson (1995), the majority of patients with conﬁrmed pathogenic mycoplasmal infections eventually recover 50–100% of their premorbid health on therapies that are directed speciﬁcally against their chronic infections, rather than against possible psychological problems. The recommended treatment (Nicolson & Nicolson 1995) for conﬁrmed mycoplasmal blood infections is long-term antibiotic therapy, usually involving multiple 6-week cycles of doxycycline (200–300mg/day) together with a number of other antibiotics. They justify this protocol as follows: 'Multiple [antibiotic] cycles are required, because few patients recover after only a few cycles, possibly because of the intracellular locations of the infections, the slow-growing nature of these microorganisms and their inherent insensitivity to antibiotics. We now recommend that patients who have been diagnosed with blood infections receive continuous oral antibiotics for at least 6 months before using the 6-week cycles of treatment. … Although patients starting such therapy usually have Herxheimer [die-off] reactions and feel initially worse due to die-off or release of toxic materials from damaged microorganisms, they eventually stabilize within days to a few weeks and then slowly begin to recover. Unfortunately, the treatment requires long-term therapy, and recovery is usually very slow. Patients that have been sick for many years are unlikely to recover within a year of therapy.'
Note: Doxycycline is one of the tetracyclines, with untoward reactions generally typical of that class of antibiotics, with an increasing degree of resistance being manifested by organisms sensitive to it (O’Grady et al 1997).
· In addition to the antibiotic attack, Nicolson et al (1998) also recommend nutritional support for the immune system when treating mycoplasma infection: 'In addition to antibiotics, patients with CFS, FMS or GWI have nutritional and vitamin deﬁciencies that must be corrected. For example, these patients are often depleted in vitamins B, C and E and certain minerals. Unfortunately, patients with these chronic illnesses often have poor absorption. Therefore, high doses of some vitamins must be used, and others, such as vitamin B complex, cannot be easily absorbed by the gut, so sublingual natural B-complex vitamins in small capsules or liquids should be used instead of oral capsules that are swallowed. General vitamins plus extra C, E, CoQ-10, beta carotene, folic acid, bioﬂavoids and biotin are best. L-cysteine, L-tyrosine, L-carnitine and malic acid such as zinc, magnesium, chromium and selenium. Some recommend doses as high as 300mg/day sodium selenite for a few days, followed by lower maintenance doses. Antibiotic use that depletes normal gut bacteria can result in over-growth of less desirable bacteria. To supplement bacteria in the gastrointestinal system yogurt and especially Lactobacillus acidophilus, tablets are recommended. One product is a mixture of Lactobacillus acidophillus, Lactobacillus biﬁdus and FOS (fructoologosaccharides) to promote growth of these ‘friendly’ bacteria in the gut. In addition, a number of natural remedies that boost the immune system, such as ginseng root, herbal teas, whole lemon/olive extract drink or an extract of olive leaves with antioxidants are available and are potentially useful, especially during or after antibiotic therapy has been completed. Although these products appear to help some patients, their clinical effectiveness in GWI/CFS/FMS patients has not been evaluated. They appear to be useful during therapy to boost the immune system, or after antibiotic therapy in a maintenance program to prevent relapse of illness.'
Additional support for the mycoplasma hypothesis include:
A further study by Nicolson et al (2003) reported a 52% prevalence of mycoplasmal infection among 200 patients with CFS; simultaneously 7.5% of the same patients were found to show evidence of infection with Chlamydia pneumoniae and 30.5% infection with Human Herpes Virus-6 (HHV-6). Prevalence of infection among 100 control patients in this study was low: 6% were infected with Mycoplasma, 1% with Chlamydia and 9% were infected with HHV. The study reports that patients with co-infections tended to suffer from more severe signs and symptoms.
In a review Endresen (2003) pointed out that the incidence of Mycoplasma infection among patients with CFS was around 50%, and was much higher than the rate in healthy controls which was around 10%. Many of the patients with CFS appeared to improve after antibiotic treatment aimed against Mycoplasma.
Noting that Nicolson reported chronic active infection by plausible organisms, (mycoplasmids and others) in approximately half of the thousands of GWS patients he has surveyed, Garrison and Breeding (2004) state:. 'Because of reliance on DNA probes, and other hyper-specific technologies, his methodology eliminates the false positives of other methods, but will underestimate the true numbers of patients with chronic infection.' (Italics added).
The contrary view on mycoplasmata
In contrast to the view promoted by Nicolson (with some support from others).
· Urnovitz (2002) who has conducted his own research into GWS and myscoplasma (Urnovitz et al 1999), is scathing about the idea that systemic mycolpasmal infection is widespread: 'My position on the role of mycoplasma in CFS and GWS was stated under oath to the US Congress in January 2002: ‘… The mycoplasma causal theory for GWS was based on poorly conducted research and the claims had never been validated. Finally, an excellent controlled scientiﬁc experiment has put this matter to rest’ (Lo et al 2000). In other words, I believe the controlled study, using conventional clinical laboratory methods, has done an excellent job in suggesting that mycoplasma plays little or no role in GWS. So, why does one study using a well-established clinical laboratory method claim no role for this organism, while another research team claims GWS and CFS patients have ‘systemic infections’?'
· Urnovitz’s main criticism of papers which support the mycoplasma aetiology for FMS, etc., relates to the evidence apparently gained from polymerase chain reaction (PCR) tests: 'So what is the problem with the mycoplasma papers? The abstracts of these studies seem to always claim that the patients are suffering from ‘systemic infections.’ If there were a truly systemic infection, where are the data showing the results of mycoplasma cultures? Correlating PCR tests with microbial culture data is standard clinical laboratory practice……….The authors correctly used the PCR technique as a pre-screen for culture. (Waring et al 2001). All that is published in the mycoplasma PCR papers [that promote the mycoplasma aetiology theory] are tables and charts claiming to show what percentage of patients is ‘positive,’ but never any correlative culture data. We cannot ﬁnd any proper validation study comparing PCR and mycoplasma culture data for any of the mycoplasma species that some researchers claim are causing systemic infections in CFS and GWS patients. The only proper conclusion that can be drawn from these GWS/CFS studies is: a large percentage (not even close to 100%) of CFS and GWS patients have genetically reactive samples, i.e., inconclusive laboratory results.' (Urnovitz 2002)
· Urnovitz (2002) is also concerned at the damage which could be caused by the treatment protocol advised for attacking mycoplasma infection. He expresses the problem cogently: 'The argument is that, since the antibiotics can kill bugs like mycoplasma, it must be the fact that mycoplasma is being killed by the antibiotics that’s making the patients feel better. Not only is this a circular argument, we’re learning that the conventional wisdom that antibiotics work solely on microbes is inaccurate. The reasoning behind requiring manufacturers to describe an antibiotic’s adverse side effects in package inserts is that these chemotherapeutic agents work on human genetic and protein material as well as microbial material. The number and severity of these adverse side effects is why regulatory agencies demand rigorous clinical trials on chemotherapeutic agents before they are allowed on the market. One cannot conclude that patients feel better on an antibiotic because it is killing mycoplasma without a shred of clinical microbiological evidence. Our concern is that this unethical, off-label prescribing of antibiotic combinations will have signiﬁcant adverse side effects on the patients taking them, as we have seen in the failure of anti-retrovirals prescribed to ‘treat’ HIV.'
Additional studies that fail to support the mycoplasma hypothesis include:
Vernon et a (2003) found no evidence of infection with Mycoplasma species among 34 patients with CFS
A rigorous, placebo-controlled double-blind study focused on 491 patients with detectible blood Mycoplasma DNA, suffering from Gulf War syndrome, a condition with many characteristics of FMS and CFS, including pain ( Donta et al 2004). These patients received doxycycline, 200 mg per day or placebo for 12 months. No statistically significant difference was found between doxycycline and placebo groups, while side effects such as nausea and photosensitivity were more common among patients receiving doxycycline.
These negative results obtained by Donta et al contrast with the positive results reported by Nicolson (1998) where antibiotic use was far more extensive and prolonged, supported by a comprehensive nutritional support protocol (see above)
Comment: The analogy of ﬂies swarming round a pile of garbage comes to mind when considering that unhealthy, possibly toxic, and/or nutritionally deﬁcient, immune compromised tissues might provide a ﬁne environment for opportunistic organisms (viruses, fungi, mycoplasmata, etc.). Can infectious agents cause conditions such as FMS? Or is it not more likely that the situation which allows the active presence of these organisms is associated with many of the underlying aetiological features of conditions such as FMS and CFS, and that the organisms, while certainly adding to the adaptive burden, may not, in themselves, be causal?
Even Nicolson & Nicolson (1995), who enthusiastically recommend antibiotic therapy in treating mycoplasmal infections, acknowledge that these organisms are unlikely, in themselves, to offer an explanation for FMS:
'Do chronic infections explain illnesses like FMS? It is unlikely that there is only one, or even a few explanations for complex chronic illnesses like FMS or CFS. Rather, these illnesses are probably due to a combination of multiple toxic exposures, chemical and biological, in combination with genetic susceptibility (immune systems and/or detoxiﬁcation systems, cellular metabolism) that determines whether a person becomes chronically ill. These considerations probably also play an important role in determining who will recover to various extents on different types of therapy.'
The possibility of viral infection being associated with the onset of FMS has been discussed as a trigger impacting someone genetically predisposed to FMS, as a factor in promoting neurohumoral dysfunction, as a feature creating excessive immune response demands, as a precursor to widespread allergy and central neurological dysfunction, etc.
In a preliminary study Tennant & Herman (2004) noted that 7 patients with FMS, who had experienced numerous symptomatic treatments and were maintained with opioids at 400 - 1000mg/dl of morphine equivalence were studied. They report that : 'Pain control was judged to be poor to fair. Subjects demonstrated positive serum titers at least two times normal to two or more of the following viral agents: (1) cytomegalus; (2) rubella; (3) varicella; (4) herpes simplex; (5) Ebstein Barr. Titers indicated either previous or possibly current infection. Patients were treated with either acyclovir, 400 to 1000mg/d, or valacyclovir, 500 to 1000mg/d. After one month patients were evaluated for pain reduction, endurance, well-being, and side-effects. If improved pain control was reported, viral suppression was indefinitely continued. All patients reported improvement in pain control, endurance, energy, and well-being. Two patients reported decrease in cervical lymph node size. Discontinuation of viral suppression for one week, in three patients, resulted in a resurgence of pain and other symptoms. This preliminary study suggests that fibromyalgia patients with severe persistent pain and positive viral titers may experience enhanced pain control with viral suppression therapy. It also suggests that there is some unclear neuro-mechanism by which a previous or current viral infection may produce pain.'
Some of the major inﬂuences of viral infection suggested by various researchers to be linked to CFS/FMS are summarized below:
HHV6, a lymphotrophic herpes virus, has been found to be more prevalent in FMS/CFS patients than in controls, with elevated antibody titers being observed (Buchwald et al 1992).
British research implicates enteroviruses which have been found to be more prevalent in stools as well as muscle biopsies, with blood antigens also higher (Behan 1993)
An association has been recognized between hepatitis C infection (particularly in women) and fibromyalgia. (Buskila et al 1997)
A study conducted in Spain however found no increase in the prevalence of hepatitis C among patients diagnosed with fibromyalgia as compared with healthy controls. (Narvaez et al 2005)
Fibromyalgia symptoms have also been increasingly described in patients with hepatitis B infection. (Adak et al 2005)
Buskila et al (1990) and Simms et al (1992) have both reported on the presence of FMS symptoms in patients infected by HIV.
Chronic coxsackie B virus infection has been shown to mimic FMS symptoms (Nash 1989). See also the notes on post polio syndrome, below.
Parvovirus has likewise been associated with FMS (Leventhal 1991).
‘Post polio syndrome’
Another infectious hypothesis exists, involving what has been called ‘post polio syndrome’ (PPS). Bruno (2001) asserts that something ‘unexpected, frightening and totally unrecognized happened after the polio vaccine was distributed: the number of cases of CFS/ME went through the roof.’
Bruno reports that British infectious disease specialist Elizabeth Dowsett plotted the cases of CFS/ME she and CFS/ME pioneer Melvin Ramsay had seen in their practice since 1919 against reported cases of polio in England. When the Salk and then Sabin vaccines virtually eliminated British polio cases in the early 1960s, the number of CFS/ME patients increased dramatically. Throughout the world 32 CFS/ME outbreaks were recorded after the polio vaccine was distributed. So something other than the poliovirus was causing CFS/ME.
The suggestion is that the vaccine that eliminated polio had an unintended consequence. The elimination of the poliovirus left a vacuum that was ﬁlled by enteroviruses that inhabited the gut and were able to multiply, spill into the bloodstream and enter the spinal cord and brain.
In 1990 Dr Dowsett looked for antibodies to non-polio enterovirus in her CFS/ME patients. Fifty percent had antibodies to the ﬁrst non-polio enterovirus ever discovered – the coxsackie B virus. Apparently neuron damage, weakness, paralysis and symptoms of brain fatigue caused by non-polio enteroviruses can be so similar as to be indistinguishable from the actions of polioviruses. One coxsackie virus, named A7, produces paralytic symptoms so similar to polio that it has been named poliovirus type IV (see Nash’s (1989) linking of this virus with FMS, cited above).
The hypothesis is that the ‘disguised form’ that polio may now be taking is not a disguise at all, but replacement by another enterovirus. This suggests that the oral polio vaccine is ‘causing’ chronic fatigue syndrome by making way for other enteroviruses to grow in the intestines and be able to do damage such as that caused by the poliovirus, except that with CFS/ME the damage is most frequently found in brain-activating system neurons, leading to fatigue, not in the spinal cord causing paralysis.
A review in 2006 by Ablin et al that has evaluated an infectious etiology for FMS concluded that [an infectious] causation remains tentative and that evidence of the utility of antibiotic or anti-viral treatment in fibromyalgia or CFS is lacking - as a result of contradictory research studies.
Comment: Anecdotal connections between infection and FMS are common. Studies are cointradictory. Antiviral and antibiotic medication alone do not seem to offer predictable benefits. There is more to learn about the possibile etiological role of infectious agents in the evolution of FMS and CFS.
© Leon Chaitow 2008
About the Author:
Leon Chaitow ND DO is a respected osteopathic and naturopathic practitioner and teacher. He is author of over 60 books, including Fibromyalgia Syndrome: A Practitioners Guide to Treatment (for Elsevier), and also Fibromyalgia & Muscle Pain, a self-treatment guide (for Thorsons/HarperCollins).
He is editor of the peer reviewed Journal of Bodywork & Movement Therapies (Elsevier) and was for many years senior lecturer, on the Therapeutic Bodywork degree courses, which he helped to design, at the School of Integrated Health, University of Westminster London, where is now a Honorary Fellow. He continues to teach and to practice part time in London, when not in Corfu, Greece where he focuses on his writing.
His website is available at www.leonchaitow.com - which contains book details, as well as direct links to Amazon pages for purchase of these.
His blog is available via google at :http://chaitowschat-leon.blogspot.com/