5 million in the U.S. have fibromyalgia – Arthritis Foundation
10 million in the U.S. have fibromyalgia – National Fibromyalgia Association
75-90% of those with fibromyalgia are women.
Percent estimated to suffer with fibromyalgia worldwide: 3-6%
Percent of U.S. physicians who think fibromyalgia is ‘real’: approx. 25%
Fibromyalgia is a complex, multi-focal disease of unknown cause.
Natural NF-kB inhibitors may be effective in reducing the pain of fibromyalgia because inflammation plays a key role in every aspect of this disease.
Banjo provides fast, effective relief from pain and inflammation because it enables your body’s immune system to function properly. It works just like the fruits and vegetables you eat every day – by naturally inhibiting NF-kB, the inflammation Master Switch.
Banjo works better because it combines the most effective natural extracts and delivers them in a form that ensures maximum bio-availability. You get the full spectrum of phytonutrients your body needs to turn off excess inflammation.
Scroll past "Thoughts on Fibromyalgia" to see posts related to fibromyalgia.
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I don't want to read - I just want relief from fibromyalgia.
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Fibromyalgia is a complex, multi-focal disease that is difficult to treat and for which there is no known cause.
In the alternative, fibromyalgia might better be characterized as a syndrome – a collection of signs and symptoms that tend to occur together but that might not spring from a common cause. Fibromyalgia may ultimately prove to be several distinct disease entities. Fibromyalgia may ultimately prove to be more like a neuropathic pain condition than a rheumatic condition.
Fibromyalgia clearly involves distinct processes: inflammation, pain transmission, pain sensation, tissue abnormalities – all seem to make some contribution to what is called fibromyalgia.
But a clear pattern has yet to emerge. As a result, even the science is scattered. Those researching the disease have little idea where to begin or where to focus their efforts.
There is no compelling argument that a single disease process is at work. Fibromyalgia may involve inflammatory, metabolic, genetic, environmental and other processes. Even infectious agents may play a role.
With the exception of 18 identified “tender points” used as a diagnostic aid, fibromyalgia is likewise not associated with any specific location.
More accurately, it is associated with multiple locations. Specific abnormalities associated with fibromyalgia have been identified in the skin, brain, spinal column, muscles, joints, connective tissue and blood – pretty much scattered across the entire body.
We don’t know much about fibromyalgia as yet. But we do know one thing – that it is real.
Overwhelming scientific evidence – including specific, measurable differences in chemical, structural, neurological and hematological profiles between fibromyalgia and non-fibromyalgia patients – proves that whatever fibromyalgia is – it is ’something.’ To think otherwise is to compound scientific ignorance with ignorant belief.
According to the theory advanced on this site (in brief) every ‘disease of inflammation’:
The following – if true – would support (but not ‘prove’) the theory in regard to fibromyalgia:
Over time we’ll show additional associations between fibromyalgia and inflammation. An attempt will be made to connect each discrete finding of fibromyalgia abnormalities to inflammation. This may not be possible – but even if every such finding can be linked to inflammation, it will remain uncertain how significant that inflammation is in the overall picture.
In any case, even based on what has been demonstrated thus far, the assertion that fibromyalgia is associated with inflammation is supported.
There is no explanation for the cause and progression of fibromyalgia whatsoever – consistent or inconsistent with the theory.
There is relatively little support for the theory that fibromyalgia can be successfully treated with the use of natural NF-kB inhibitors.But there is some support – some evidence that the addition of natural NF-kB inhibitors, dietary or otherwise, may provide some degree of symptomatic relief.
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This may, at least in part, explain certain neurotransmitter imbalances and other central nervous system abnormalities associated with inflammatory conditions.
The publication:
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Med Sci Monit. 2007 Dec;13(12):RA214-21.
Das UN.
UND Life Sciences, Shaker Heights, OH 44120, USA.
Insulin resistance, obesity, type 2 diabetes, high blood pressure, hyperlipidemias, metabolic syndrome X, and Alzheimer’s disease are characterized by low-grade systemic inflammation.
Recent studies showed that the plasma and tissue activities of two enzymes, butyrylcholinesterase and acetylcholinesterase, are both elevated in patients with Alzheimer’s, diabetes, high blood pressure, insulin resistance, and hyperlipidemia. High levels of these two enzymes result in low plasma and tissue levels of acetylcholine (ACh).
The “cholinergic anti-inflammatory pathway” mediated by acetylcholine acts by inhibiting the production of pro-inflammatory mediators, probably by inhibiting NF-kB.
ACh is a neurotransmitter and regulates the levels and activities of serotonin, dopamine and other neuropeptides and thus, modulates both immune response and neurotransmission.
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The central nervous system (CNS = brain and spinal cord) can regulate peripheral inflammation, but the pathways and mechanisms by which it does so remain unclear.
The study summarized below investigates the possibility that the neurotransmitter acetylcholine (ACh) exerts an anti-inflammatory effect via binding to a specific receptor found primarily on the synovial lining of rheumatoid arthritis and osteoarthritis joints.
That possibility is confirmed by observations of reduced pro-inflammatory cytokine activity as a result of such binding.
While the authors suggest that the receptor identified in rheumatoid arthritis and osteoarthritis joints might be a potential target for drug development, I am curious if a similar mechanism might explain the connection between observed neurotransmitter abnormalities seen in fibromyalgia and the persistence of peripheral inflammation.
The publication:
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Arthritis Rheum. 2008 Nov;58(11):3439-49.
Waldburger JM, Boyle DL, Pavlov VA, Tracey KJ, Firestein GS.
University of California, San Diego, La Jolla, CA, USA.
OBJECTIVE: The central nervous system can regulate peripheral inflammation, but the neuronal routes from the central nervous system to the peripheral tissue, as well as the messengers, remain poorly defined. One candidate is the cholinergic pathway, which releases acetylcholine (ACh). This neurotransmitter can bind to the alpha7 cholinergic receptor (alpha7R) expressed by nonneuronal cells and reduce inflammation.
To test this possibility, we evaluated the expression of alpha7R and its potential role as a target in rheumatoid arthritis (RA).
RESULTS: Protein and mRNA for alpha7R were demonstrated in RA and osteoarthritis synovium, mainly in the intimal lining. ACh significantly reduced the production of pro-inflammatory mediators. The effect was blocked when the alpha7 receptor was blocked.
CONCLUSION: Alpha7R is a potential therapeutic target for inflammatory diseases.
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IL-10 is an important anti-inflammatory messenger in the body. It helps turn inflammation off.
In the study summarized below it was found in lower than normal levels in fibromyalgia patients.
The publication:
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Arthritis Rheum. 2006 Aug;54(8):2656-64.
Uçeyler N, Valenza R, Stock M, Schedel R, Sprotte G, Sommer C.
Julius-Maximilians Universität, Wurzburg, Germany.
The term chronic widespread pain refers to a group of painful diseases of poorly understood pathophysiology. One major subgroup is fibromyalgia.
Among other hypotheses, a potential pathophysiologic role of cytokines in chronic widespread pain has been proposed. This study was designed to investigate whether cytokine profiles differ in patients with chronic widespread pain by looking at levels of IL-2, IL-4, IL-8, IL-10, tumor necrosis factor alpha (TNF), and transforming growth factor beta1 (TGFbeta1.)
Significantly lower levels of IL-4 and IL-10 were found for those patients with chronic widespread pain.
CONCLUSION: Chronic widespread pain is associated with a lack of antiinflammatory and analgesic Th2 cytokine activity, which may contribute to its pathogenesis.
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This is an essential publication because it:
Under certain conditions, sugars can bind with proteins or fats to create an AGE. The reaction forming an AGE can happen in food before it is eaten, or it can happen inside the body after sugar is consumed.
Fructose is said to form AGEs 10x more easily than glucose. So consuming a lot of high fructose corn syrup (e.g. as in soda) might not be a good thing – because AGEs are bad for us.
AGEs link with other AGEs, so when they are present in sufficient concentration in a tissue they can all link together – resulting in a ’stiffer’ and less functional tissue.
AGEs are also bad because they cause inflammation – by binding to a specific receptor on the cell surface.
A large body of evidence suggests that AGEs are an important cause of almost all diabetes complications. Diabetics have much higher levels of AGEs because excess blood sugar results in an excess of AGEs. That is one reason why it is important for diabetics to keep their blood sugar under control.
When the AGE binds to RAGE it results in activation of NF-kB.
Activation of NF-kB results in inflammation.
Activation of NF-kB also results in the production of more receptors – more RAGE.
So a self-perpetuating, vicious cycle can emerge. AGE binds to RAGE which results in more inflammation AND more RAGE – the additional RAGE then binds to more AGE leading to more NF-kB activation, more inflammation and more RAGE…
This is very bad.
Besides diabetes, other chronic, inflammatory conditions that have been linked to RAGE include atherosclerosis, congestive heart failure and Alzheimer’s disease.
RAGE is not generally thought to be significant in fibromyalgia, but the study summarized below suggests that it might be of importance.
In studying the muscle tissue of fibromyalgia patients it was found that the level of AGEs were increased, and that this increase was associated with collagen changes (AGE modified collagen,) NF-kB activation and, perhaps most significantly, with the presence of RAGE.
As noted above, by activating NF-kB, RAGE can initiate a vicious cycle of localized inflammation.
The authors suggest that AGEs found in excess in the muscle of fibromyalgia patients may impact the disease:
Inhibition of NF-kB might therefore be of substantial benefit in relieving the pain and inflammation of fibromyalgia.
The Publication:
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Scand J Rheumatol. 2005 Nov-Dec;34(6):460-3.
Rüster M, Franke S, Späth M, Pongratz DE, Stein G, Hein GE.
Department of Internal Medicine III, Friedrich-Schiller-University of Jena, Germany.
OBJECTIVES: To compare levels of CML, an AGE (advanced glycation end product) present in the muscle tissue and in the serum of patients with fibromyalgia (FM) vs. healthy controls.
METHODS: The serum levels of CML were measured in 41 patients with FM and 81 healthy controls. The presence of CML, nuclear factor kappa B (NF-kB), the AGE receptor (RAGE), collagen types I, II, VI, and CD68-positive monocytes/macrophages in muscle tissue of 14 patients with FM was investigated.
RESULTS: Patients with FM showed significantly increased serum levels of CML and more CML, activated NF-kB and CD68-positive monocytes/macrophages in the muscle. The collagens and CML were found together, suggesting that the AGE modifications were related to collagen. RAGE was absent in controls but a faint and patchy staining was seen in FM.
CONCLUSIONS: In the connective tissue of fibromyalgic muscles there was more activated NF-kB and more of the CML AGE. Higher CML levels were found in fibromyalgia patients. RAGE was only found in the muscle of fibromyalgia patients – it was not found in those who did not have fibromyalgia.
AGE modification of proteins causes reduced solubility and high resistance to proteolytic digestion of the altered proteins (e.g. AGE-modified collagens).
AGEs can stimulate different types of cells by activation of the transcription factor NF-kB, mediated by specific receptors of AGEs (e.g. RAGE) on the cell surface.
Both mechanisms may contribute to the development, perpetuation, and spreading of pain characteristic in FM patients.
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This is an essential publication because it supports the benefits of diet in providing symptom relief in fibromyalgia and rheumatoid arthritis.
In a nutshell 
those suffering with fibromyalgia or rheumatoid arthritis experienced a substantial improvement in their conditions when they switched to a raw, vegan diet. Specifically, they experienced a decrease in pain and stiffness and self-perception of their health was improved.
The problem, of course, is that this diet represents a substantial and some would say extreme departure from our ‘normal’ diet. A vegan diet includes no animal products whatsoever – no milk, eggs, butter. The “living food” diet studied here included only raw foods – no cooking whatsoever.
The obvious reality is that very few people will ever attempt such an extreme dietary modification, and fewer still will adhere to it. Nonetheless, it is one option, and might result in general improvement in conditions related to inflammation other than those specifically studied.
As an alternative, one might want to add more fruits and vegetables to the diet, especially fresh, raw fruits and vegetables. Supplements might be considered as well.
The publication:
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Toxicology. 2000 Nov 30;155(1-3):45-53.
Hänninen, Kaartinen K, Rauma AL, Nenonen M, Törrönen R, Häkkinen AS, Adlercreutz H, Laakso J.
Department of Physiology, University of Kuopio, Finland.
Plants are rich natural sources of antioxidants in addition to other nutrients. Interventions and cross sectional studies on subjects consuming uncooked vegan diet called living food (LF) have been carried out. LF is an uncooked vegan diet and consists of berries, fruits, vegetables and roots, nuts, germinated seeds and sprouts, i.e. rich sources of carotenoids, vitamins C and E.
The efficacy of LF in rheumatoid diseases was studied as an example of a health problem where inflammation is one of the main concerns.
The subjects eating LF showed highly increased levels of beta and alfa carotenes, lycopen and lutein in their sera. As the berry intake was 3-fold compared to controls the intake of polyphenolic compounds like quercetin, myricetin and kaempherol was much higher than in the omnivorous controls.
Those with fibromyalgia who changed to the LF diet experienced a decrease of their joint stiffness and pain as well as an improvement in perceived health and quality of life.
Rheumatoid arthritis patients eating the LF diet also reported similar positive responses and the objective measures supported this finding. The improvement of rheumatoid arthritis was significantly correlated with the day-to-day fluctuation of subjective symptoms.
In conclusion the rheumatoid patients subjectively benefited from the vegan diet. The improvements were consistent with objective measures.
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Fibromyalgia is associated with increased levels of corticotropin-releasing hormone – corticotropin-releasing hormone has been shown to activate NF-kB.
Fibromyalgia is associated with increased levels of substance P, which is also known to activate NF-kB.
Fibromyalgia is associated with inflammation, as evidenced both by the frequent occurrence of other inflammatory conditions in those with fibromyalgia, and by the observation that pro-inflammatory cytokines are found at higher levels in the blood and cerebro-spinal fluid (CSF) of fibromyalgia patients.
The author of the study briefly summarized below suggests the use of anti-inflammatory supplements in the treatment of fibromyalgia and notes that these may be safely combined with other treatments.
The publication:
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Int J Immunopathol Pharmacol. 2006 Jan-Mar;19(1):5-10.
Lucas HJ, Brauch CM, Settas L, Theoharides TC.
Special Clinic for FMS and CFS, Trier, Germany.
Fibromyalgia (FMS) is a debilitating disorder characterized by chronic diffuse muscle pain, fatigue, sleep disturbance, depression and skin sensitivity.
Patients with fibromyalgia often have other conditions as well, especially migraines, interstitial cystitis and irritable bowel syndrome.
The cause of fibromyalgia is still unknown, but there is evidence of increased corticotropin-releasing hormone (CRH) and substance P (SP) in the CSF of FMS patients, as well as increased SP, IL-6 and IL-8 in their serum.
Increased numbers of activated mast cells were also noted in skin biopsies. The hypothesis is put forward that FMS is a neuro-immunoendocrine disorder where increased release of CRH and SP from neurons in specific muscle sites triggers local mast cells to release proinflammatory and neurosensitizing molecules.
Recent nutraceutical formulations containing the natural anti-inflammatory and mast cell inhibitory flavonoid quercetin hold promise since they can be used together with other treatment modalities.
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Fibromyalgia is associated with increased levels of “substance P” – a neurotransmitter and neuromodulator that is found in the brain and spinal cord and that is associated with inflammatory processes and especially pain processes.
Pregabalin is used in the treatment of seizure, neuropathic pain and fibromyalgia. It is thought to act by binding to a specific receptor on nerve cells and reducing or slowing nerve transmissions in the central nervous system.
In this study it was shown to reduce the ability of substance P to activate NF-kB in cancer cells. it is reasonable to suspect that it would do the same in other, non-cancerous cells, and perhaps in all cells.
Given that pregabalin’s (Lyrica’s) mechanism of action is unknown, it may be that it exerts at some portion of its beneficial effect in fibromyalgia via inhibition of NF-kB.
The publication:
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J Cell Biochem. 2008 Oct 1;105(2):414-23.
Park S, Ahn ES, Han DW, Lee JH, Min KT, Kim H, Hong YW.
Dongduk Women’s University, Department of Applied Chemistry, Seoul, Korea.
Pregabalin and gabapentin are lipophilic amino acid derivatives of gamma-amino butyric acid that show anticonvulsant and analgesic activity against neuropathic pain.
In this study, their actions on substance P-induced NF-kB activation were investigated in human neuroblastoma and rat glioma cells and in both cases they were found to inhibit NF-kB activation.
These drugs also inhibited NF-kB activation in rat spinal dorsal root ganglia cells pre-treated in vitro with substance P. These results suggest a previously undefined role of pregabalin and gabapentin.
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Some fibromyalgia patients seem to respond relatively well to non-steroidal anti-inflammatory drugs (NSAIDs.)
Some fibromyalgia patients (about 30% in the study below) have evidence of neurogenic inflammation on skin biopsy. This might explain, at least in part, why some patients respond better than others to NSAIDs.
The role of inflammation in fibromyalgia remains unclear, but inflammation clearly plays some role, and may play a significant role, at least for a percentage of fibromyalgia patients.
The publication:
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J Rheumatol. 2003 Jan;30(1):146-50.
Salemi S, Rethage J, Wollina U, Michel BA, Gay RE, Gay S, Sprott H.
OBJECTIVE: To determine if abnormal collagen metabolism is correlated with neurogenic inflammation, a potential activator of collagen metabolism, in patients with fibromyalgia (FM).
RESULTS: Positive results were detected in skin tissues of FM patients for IL-1, IL-6, and TNF. None of the cytokines could be detected in healthy control skin.
CONCLUSION: The detection of cytokines in FM skin indicates the presence of inflammatory foci (neurogenic inflammation) in the skin of certain patients (about 30% of FM patients), suggesting an inflammatory component in the induction of pain. This may explain the response to nonsteroidal antiinflammatory therapy in a subset of FM patients.
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This is an essential publication because it clearly demonstrates that fibromyalgia is a disease of inflammation and that symptomatic relief can be achieved through the reduction of inflammation.
Higher than normal levels of pro-inflammatory cytokines in the blood indicate ongoing inflammation. When inflammation is relieved, as demonstrated by a reduction in those pro-inflammatory cytokines, symptoms improve – pain decreases.
IL-8 levels are high
TNF levels are high
IL-6 levels are normal
IL-4 levels are normal
IL-10 levels are normal (IL-10 is an anti-inflammatory cytokine)
TNF levels drop quickly, by 10 days, and remain low through 6 months after treatment.
IL-8 is substantially decreased by six months.
Pain reduction does not correlate with TNF levels.
Pain reduction does correlate with IL-8 levels.
The authors conclude that pro-inflammatory cytokines TNF and IL-8 are involved in FM, but that they most likely do not directly cause the pain of fibromyalgia.
Nonetheless, IL-8 may be very closely associated with pain, because the pain decreases when levels of IL-8 decrease.
IL-8 is frequently associated with inflammation. An excess of IL-8 has been demonstrated in certain cancers, inflammatory bowel disease, psoriasis and other ailments. Its excess clearly demonstrates an ongoing inflammatory condition.
The publication:
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J Rheumatol. 2008 Jul;35(7):1366-70. Epub 2008 Jun 1.
Wang H, Moser M, Schiltenwolf M, Buchner M.
OBJECTIVE: This prospective study examined circulating cytokines in patients with fibromyalgia (FM) over 6 months rather than at only one timepoint, and investigated correlations between serum cytokine concentrations and pain intensity in FM patients receiving multidisciplinary pain therapy.
RESULTS: On admission, serum levels of IL-8 and TNF-alpha, but not IL-6, were elevated in patients with FM.
No significant difference in IL-4 and IL-10 was found between FM patients and controls. High IL-8 levels remained consistent during the followup, but TNF-alpha was already reduced after 10 days and until 6 months after therapy.
After 6 months’ treatment with multidisciplinary pain therapy, IL-8 and TNF-alpha levels were significantly lower than at the beginning.
IL-8 but not TNF-alpha serum levels were correlated with pain intensity in FM patients after 6 months’ multidisciplinary pain therapy.
CONCLUSION: Our results suggest that proinflammatory cytokines TNF-alpha and IL-8 are involved in FM, but they do not apparently provoke the pain of FM directly. Multidisciplinary pain therapy modified the cytokine profile in patients with FM during the observation period.
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The publication:
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Cochrane Database Syst Rev. 2009 Oct 7;(4):CD007115.
Lunn MP, Hughes RA, Wiffen PJ.
BACKGROUND: Duloxetine is a balanced serotonin and noradrenaline reuptake inhibitor licensed for the treatment of major depressive disorders, urinary stress incontinence and the management of neuropathic pain associated with diabetic peripheral neuropathy. A number of trials have been conducted to investigate the use of duloxetine in neuropathic and nociceptive painful conditions.
OBJECTIVES: To assess the benefits and harms of duloxetine for treating painful neuropathy and different types of chronic pain.
MAIN RESULTS: Six trials were identified including 2220 participants. Three studies included participants with painful diabetic neuropathy and three treated participants with fibromyalgia.
Duloxetine at 60 mg daily is effective in treating painful diabetic peripheral neuropathy in the short-term to 12 weeks.
Duloxetine at 60 mg daily is also effective in fibromyalgia over 12 weeks and at 28 weeks.
Adverse events were common in both treatment and placebo arms but more common in the treatment arm with a dose dependent effect. Most side effects were minor, but 16% of participants stopped the drug due to side effects. Serious adverse events were rare.
AUTHORS’ CONCLUSIONS: There is moderately strong evidence that duloxetine 60 mg and 120 mg daily are efficacious for treating pain in diabetic peripheral neuropathy and fibromyalgia but 20 mg daily is not. Minor side effects are common at therapeutic doses but serious side effects are rare.
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Elevated cytokine levels were observed in fibromyalgia patients. The extent to which these were elevated was found to correlate with symptom severity.
These findings suggest that fibromyalgia is related to an inflammatory process, and that effective reduction in inflammation might be of value in relieving symptoms.
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The publication:
Clin Exp Rheumatol. 2007 Mar-Apr;25(2):225-30.
Bazzichi L, Rossi A, Massimetti G, Giannaccini G, Giuliano T, De Feo F, Ciapparelli A, Dell’Osso L, Bombardieri S.
OBJECTIVE: To examine the possible role of the soluble factor (mediators of inflammation in the bloodstream) in fibromyalgia (FM) by studying the correlation of cytokine levels with the patients’ clinical and psychiatric profile.
RESULTS: Higher levels of IL-10, IL-8 and TNF-alpha were found in FM patients than in controls. Significant correlations between the biochemical parameters and clinical data were found.
CONCLUSION: The higher levels of cytokines found in FM patients suggest the presence of an inflammatory response system. They support the hypothesis that cytokines may play a role in the clinical features of fibromyalgia.
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Inflammation initiated by nerve endings (neurogenic inflammation) can be observed on skin biopsy of those with fibromyalgia.
“It is now apparent that the role of peripheral nerve endings in fibromyalgia is much greater than previously thought.”
The publication:
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Med Hypotheses. 2007;69(1):141-4. Epub 2007 Jan 9.
Kim SH.
The mechanisms responsible for symptom expression in fibromyalgia (FM) are complex.
The most consistently detected objective abnormalities in FM involve pain-processing systems. Up to recently, central nervous system was a primary focus of investigations in FM.
Although it is unlikely that FM occurs because of primary disorders of the peripheral tissues, there are still data to suggest that some abnormalities can be detected in the periphery. It is now apparent that the role of peripheral nerve endings in FM is much greater than previously thought.
This paper suggests that patients with FM represent a state of the dysfunction of descending, antinociceptive (anti-pain) pathways and low hypothalamic-pituitary-adrenal function. This state is further proposed to result in many skin biopsy findings associated with the disorder, including neurogenic inflammation.
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1. 25% of those with inflammatory bowel disease (IBD) develop symptoms or disease that does not directly affect the intestinal tract. This is a very high percentage.
2. These symptoms can occur before or at the same times as the IBD – not just after it. This suggests that whatever is causing the IBD is also causing the other symptoms or disease – not simply that IBD causes the other manifestations.
3. The severity of IBD and the other manifestations seem to move in parallel.
A fourth observation – that controlling the IBD controls the related symptoms/disease could be taken to mean either that the IBD causes the other symptoms/disease, so controlling IBD controls the other symptoms/disease, or that in treating IBD we are simultaneously treating the other conditions.
According to one theory, most of these inflammation-related disease conditions spring from a common underlying dysfunction of the immune system – primarily its inability to turn off. Since treatment for IBD is primarily directed against inflammation, the findings observed in this publication are consistent with that theory.
Of particular interest is that fibromyalgia is one condition that manifests as a result of, or with, IBD. There is some debate over whether fibromyalgia is related to inflammation and, if so, to what extent.
The publication:
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nflamm Bowel Dis. 2009 Apr 30;15(12):1915-1924. [Epub ahead of print]
Bourikas LA, Papadakis KA.
Extraintestinal manifestations develop in approximately 25% of patients with inflammatory bowel disease (IBD).
Musculoskeletal symptoms are the most common extraintestinal manifestations of IBD, often associated with colonic involvement, and present as either arthritis or fibromyalgia.
Musculoskeletal manifestations can precede or be synchronous with the development of bowel disease or develop following the diagnosis of IBD. Their clinical course often correlates with IBD activity but it can also be independent of the activity of bowel disease.
Controlling intestinal inflammation remains the cornerstone therapeutic approach for the musculoskeletal manifestations of IBD.
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Mugwort is an inhibitor of NF-kB, which accounts for its frequent historic use in herbal medicine in many countries.
In a process known as “moxibustion,” mugwort is burned – generally in a rolled up shape resembling a cigar. This burning ‘mugwort cigar’ is held near the patient’s skin at acupuncture points until it either warms or sometimes burns the skin.
It may be that the patient benefits from the inhalation of mugwort fumes/smoke or that in the warming process, when the mugwort is in direct contact with the skin, that some absorption of herbal actives takes place.
There is no good explanation of why this might work, and scant evidence – save the publication referenced below – that it does work.
Nonetheless, it is reported that 93% of fibromyalgia patients improved when moxibustion was combined with standard therapy, whereas only 57% improved with standard therapy alone.
The publication:
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Zhongguo Zhen Jiu. 2009 Mar;29(3):200-2.
Zhao RH, Zhu YB.
Department of Acupuncture, Workers Hospital of Jihua 3502 Occupational Apparel Ltd, Shijiazhuang, Hebei 050000, China
OBJECTIVE: To observe the clinical therapeutic effect of herb-partitioned moxibustion combined with medication on fibromyalgia syndrome.
METHODS: Sixty cases were randomly divided into a treatment group and an observation group, 30 cases in each group. The observation group was treated with oral administration of amitriptyline, and the treatment group with oral administration of amitriptyline and herb-partitioned moxibustion.
RESULTS: The total effective rate was 93.3% in the treatment group and 56.7% in the observation group.
CONCLUSION: The herb-partitioned moxibustion combined with medication is an effective therapy for fibromyalgia syndrome.
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