 My theory on the development of FM and CFS  I have decided to share my theory about the development and etiology of FM and CFS. I developed this theory from all the information I have read on these conditions, from my personal experiences pertaining to people with CFIDS (including my sister), conversations with various researchers and medical professionals regarding CFIDS, and experience with several coworkers who experienced "symptoms", and from experience with some "symptoms" of my own. (What can I say I had a very stressful job!) At this time I am not aware of any specific research being done relating to all the details of my theory but there is research being done pertaining to parts of it.  What I am concluding is there are several factors which contribute to the development of CFIDS (chonic fatigue immune deficiency syndrome- FM & CFS). Some research has concluded that FM & CFS has a hereditary factor. It tends to run in families. In identical twins where one has it the percentage is high that the other twin has it (however it's not 100%) . I think that there is a genetic predisposition in that in order to get CFIDS you have to have it in your genes. If it's not there then you won't get it no matter what. Sort of like the cancer virus. Some smokers smoke heavily all their lives and never develop lung cancer. Some people get lung cancer who never smoke. Why? because you have to have the gene or predisposition to get it. I personally think there is a link between environmental pollutants, poor nutritional quality of our food today, lack of rest & high degree of stress compounded by genetic querks, injury and/or illness. Basically some of us have "abnormalities" that normally don't bother us such as alpha waves in our delta sleep or undiagnosed neurally mediated hypotension. However all the compounding negative environmental factors aggravate these abnormalities then a significant event happens (major injury, pregnancy, illness, etc.) which triggers the CFS &/or FM, much like extended periods of stress can trigger other autoimmune diseases such as Hashimoto's Thyroiditis. I'm a science writer for ... one of the 27 institutes and centers of the NIH. My main "beat" is diabetes, endocrinology, and metabolic diseases." There you have it, a professional's opinion. What triggers CFIDS? This is where research may go off in different directions. There are a number of events and illnesses which can trigger it. What's the common bond? I think it has to do with the hormonal levels triggered by stress (cortisol), hormonal changes caused by pregnancy or unusual imbalances in the body, attacks on the body by severe illnesses and major trauma to the body such as auto accidents and surgeries. These things causes changes in the chemistry of the body which can activate the CFIDS gene. I also think environmental factors (pollution, food perservatives, ozone layer changes, etc) do aggravate and add stress to the biological functioning of the body. These environmental factors may even stress the body's immune system, thus weakening it to be more prone to be adversely effected by severe emotional stress, illness or trauma. How does this cause symptoms of CFIDS? These changes first alter the nervous system which first produce an hyperactive fight or flight response. The nervous systom is on high alert and the person experiences symptoms such as nervousness, aggitation, sensation that electricity may be running through the nerves (not necessarily pain at this point but an underlying sensation that something is a little off with the CNS). Reflexes are probably hyperactive. (The patient may actually kick the doc who is checking the knee reflex.) The classic cognitive problems develop (concentration, memory, processing and retaining information, etc.) This may be to a significant degree that it actually may begin effecting job performance and daily life activities. This influences the moods and as a result depression and anxiety may develop. Then the other classic symptoms of CFIDS develop as a result of these changes over a period of time or to the severity of the changes. CFIDS can be a develop gradually or occur suddenly. Some people are able to work and carry on what appears to be a normal life while others are often bedridden or on disability. What causes the difference in degree of symptoms? Well, I believe stress and life events are a major factor. I have noticed people with CFIDS (at least all the ones I know & have met) tend to be very caring people. They take on people's worries and often strive to help people while prone to neglect their own needs. They tend to be emotionally aware and often sensitive to people's feelings. These characteristics tend to leave the person prone to worry and take on other people's problems. They are very friendly and open to people leaving room for emotional wounds by unthinking people. This tends to set the stage for increase stress hormones due to increase worry and wanting to please others who may or may not recipicate the same feelings. As a result they develop a pattern of worry and taking on problems and worries which they really do not need to. The biological changes occure in the body over a period of years maybe setting up a certain personality type or traits. Some, as they begin to experience the negative consequences of stress (may be physical, emotional, or socially), will adjust and develop more effective coping and problem solving skills resulting in a lowerer level of stress and stress hormones. Some people tend to appear to create worse problems. Needless to say more stress causes more problems and moodiness. This worsens the symptoms. Stress reduction activities and effective coping and problem solving skills decrease stress which decreases the stress hormones which decrease the adverse effects. Lowly Cytokine May Play Role In Controlling Neurotransmitters "Researchers here in collaboration with a group in California have discovered that a protein normally thought only to be a component in the immune system actually plays a key role in regulating neurotransmission in the central nervous system -- the CNS -- as well. The protein, tumor necrosis factor alpha, or TNF-alpha, has long been known to be a key player in controlling cell death but this new finding offers new insights into how cells interact within the human nervous system. Understanding this new role of TNF-alpha may provide researchers with possible new approaches to treating illnesses such as dementia, Alzheimer's disease, stroke, epilepsy and spinal cord injury." This may account for the neurological effects of CFIDS, FM & Hashimoto's as well as other autoimmune diseases. What can the person with CFIDS do to decrease stress? Decrease stress in your life. Don't worry about things you have no control over. Resolve conflicts and problems you have control over. Learn the difference. Take advantage of your bad memory in forgiving and forgetting. Make the best out of bad situations. Learn from them. Don't blame others. Take responsibility for your own self and actions. Role with the pounches. Educate yourself on your condition. Be patient with the ignorant and patiently educate them. Take care of yourself. Get proper sleep and rest. Eat nutritious foods. Avoid problem foods. Cut back on activities when needed. Listen to your body's needs but sometimes you have to ignore it's whinning. Accept the fact medical science has not progressed to the point of "fixing" CFIDS or FM(and many other syndrome conditions) so you have to learn what works best with you. Is there anything that can be done about CFIDS & FM? As of today (3/30/02), I'm afraid the answer is no as far as finding a cure. Research is being done but no solid answers are found yet to be an effective treatment cure for CFIDS or FM. Some people find things that has helped them but there are many who tried the same treatment but found it didn't help them. I will include links to sites that may be of help to reduce severity of symptoms and promote overall health. A visitor to my site emailed me her thoughts about FM. I agree with her that food does effect our health and can irritate the GI system which effects nutritional absorption which over time effects the levels of electrolytes and other chemical and hormonal levels in the body leading to increase or development of new symptoms. In other words it can lead to worsening of FM symptoms or development of other conditions, such as anemia. There is a doctor who has put forth a theory about the origin of Fibromyalgia and chronic fatigue syndrome. He has been successfully treating himself, and many others, for these diseases for forty years. He has written a book that outlines his theory and very simple medication for REVERSING the disease. I know it really works! My daughters and I are feeling great because of it. The book is What Your Doctor May Not Tell You About Fibromyalgia by Dr. R. Paul St. Amand and Claudia Merek. Another book of useful information is The Inflamation Syndrome by Jack Challem – what you eat greatly affects how you feel. I mention these here because hypothyroidism seems to be an integral part of fibro/CFIDS. Many autoimmune diseases can be eased by watching what you eat. Hope this is helpful. Detection of Actin Fragments in Serum: A Rapid Screening Test to Aid in the Diagnosis of Chronic Fatigue Syndrome "Since the original identification of the abnormal low molecular weight (LMW) RNase L protein by researchers at Temple University in 1995(2), intense research has focused on defining the origins of this protein. Within the 12 months of 2000, researchers at Temple University, Montpellier University, and R.E.D. Laboratories independently determined that the appearance of the LMW RNase L protein was due to proteolysis of native RNase L. Further research performed at R.E.D. Laboratories has identified one of the proteases responsible as calpain (calcium-activated neutral proteinase)." This lead to the development of "The Fragmented Actin Serum Test (FASTest™) Actin fragments present in serum are measured by Western blot using an antibody specific for native G-actin. Blood is drawn from the patient into a serum separator tube to allow the blood to clot and serum is collected by centrifugation. An aliquot of serum is then mixed with denaturing agents and allowed to migrate through a SDS polyacrylamide gel to separate actin proteins based on molecular weight. After electrophoresis, the proteins are transferred to a solid support which is then allowed to react with antibody and coloration agents. Molecular weight size markers and positive and negative controls are included with each assay. Preliminary data indicate the following: Negative: Ratio <0.1 - 1.9 Positive: Ratio = 2.0 or greater" http://molecular.biosciences.wsu.edu/Faculty/pall/pall_cfs.htm College of Science School of Molecular Biosciences, Washington State University, Pullman, WA 99164-4660 USA Novel chronic fatigue syndrome (CFS) theory finally produces detailed explanations for many CFS observations: ---------------------------------------------------------------------------------- A novel theory of the cause of CFS has been published which is supported by diverse biochemical and physiological observations of CFS, while providing explanations for five of most difficult puzzles about this medical condition. The theory has been published by Dr. Martin L. Pall (Professor of Biochemistry and Basic Medical Sciences, Washington State University) in several publications (1-4,9). The theory starts with the observation that infections that precede and may therefore induce CFS and related conditions act to induce excessive production of inflammatory cytokines that induce, in turn, the inducible nitric oxide synthase (iNOS). This enzyme, in turn, synthesizes excessive amounts of nitric oxide which reacts with another compound (superoxide) to produce the potent oxidant peroxynitrite (see Fig. 1). Peroxynitrite acts via six known biochemical mechanisms to increase the levels of both nitric oxide and superoxide which react to produce more peroxynitrite (Fig. 1 - [JvR: not reproducible] ). In this way, once peroxynitrite levels are elevated, they may act to continue the elevation, thus producing a self-sustaining vicious cycle (ref.1). It is this cycle, according to the theory, that maintains the chronic symptoms of CFS and it is this cycle, therefore, that must be interrupted to effectively treat this condition. Twelve different observations on chronic fatigue syndrome and its symptoms provide support for this theory: 1. The levels of neopterin, a marker for the induction of the inducible nitric oxide synthase are reported to be elevated in CFS (1). 2. Mitochondria are reported to be dysfunctional in CFS and mitochondria are known to be attacked by peroxynitrite and also by nitric oxide (1). 3. Both cis-aconitate and succinate levels are reported to be elevated in CFS and the enzymes that metabolize these two compounds are known to be inactivated by peroxynitrite (1). 4. The four inflammatory cytokines implicated have been reported to been reported to be elevated in 10 different studies of CFS (1,2). 5. These same inflammatory cytokines have been reported to induce fatigue when injected into humans (1). 6. An animal (mouse) model of CFS has "fatigue" induced by a bacterial extract that can induce both the inflammatory cytokines and also the inducible nitric oxide synthase. 7. Polyunsaturated fatty acid pools are reported to be depleted in CFS and such polyunsaturated fatty acids are known to be oxidized by oxidants such as peroxynitrite. 8. Anecdotal evidence has suggested that antioxidants such as coenzyme Q-10, flavonoids and glutathione precursors may be useful in CFS treatment, consistent with a role for an oxidant such as peroxynitrite. 9. Women are reported to produce more nitric oxide than men, possibly explaining the gender bias seen in CFS. A similar gender bias is seen in autoimmune diseases characterized by excessive peroxynitrite (i.e. lupus, rheumatoid arthritis). 10. Cases of CFS are associated with high levels of deleted mitochondria DNA, suggesting but not proving that mitochondrial dysfunction can produce the symptoms of CFS (1). 11. Biochemical similarities "depletion of lutamine and cystine pools" have been reported in CFS and several diseases characterized by elevated peroxynitrite levels, suggesting a similar biochemical basis for all of these conditions (1). 12. Because peroxynitrite is a potent oxidant, this theory predicts that oxidative stress will be elevated in CFS. There was no direct evidence for this when the theory was published but three subsequent papers have reported substantial evidence for such oxidative stress in CFS (5-7A). These results, may therefore, be considered to confirm important predictions of the theory, although the authors were unaware of this theory when they initiated these studies. CFS puzzles explained by the elevated nitric oxide/peroxynitrite theory: There are five different puzzles of CFS that are explained by this theory. The first of these, the chronic nature of CFS, is explained by the self-sustaining vicious cycle that is central to this theory. The second is how infection and other stress which often precede CFS may produce CFS. This theory predicts that each of these can lead into this mechanism by inducing excessive nitric oxide. Infection is not the only stress that may be involved in this way: both physical trauma and severe psychological trauma can produce excessive nitric oxide synthesis (2). In addition, tissue hypoxia may induce this cycle by increasing levels of superoxide (the other precursor of peroxynitrite) (2). A third puzzle about CFS is how it leads to the many biochemical/physiological correlates reported to occur in CFS. This is discussed with the list of 12 such correlates described above. A fourth puzzle about CFS is how the diverse symptoms of this condition may be generated. It turns out that a variety of factors, including nitric oxide, superoxide, oxidative stress and mitochondrial/energy metabolism dysfunction may have important roles (2). For example, nitric oxide is known to stimulate the nociceptors that initiate the perception of pain, and therefore excessive nitric oxide may cause the multi-organ pain associated with CFS (2). Nitric oxide has a central role in learning and memory and so its elevation may also provide a partial explanation for the cognitive dysfunction characteristic of CFS (2). Other symptoms explained by this theory include orthostatic intolerance, immune dysfunction, fatigue and post-exertional malaise (2). The immune dysfunction reported in CFS, may allow for opportunistic infections to develop, such as mycoplasma or HHV6 infections, which may exacerbate the basic CFS mechanism by increasing inflammatory cytokine synthesis. What about multiple chemical sensitivity, posttraumatic stress disorder and fibromylagia? A fifth puzzle regarding CFS is its variable symptoms and, most importantly, its association with three other conditions of equally puzzling etiology, multiple chemical sensitivity (MCS), posttraumatic stress disorder (PTSD) and fibromylagia (FM). The theory explains the variable symptoms, from one case to another, in part, by a somewhat variable tissue distribution of the elevated nitric oxide/peroxynitrite. A common etiology (cause) for CFS with MCS, PTSD and FM has been suggested by others (discussed in refs 4,9). A common causal mechanism for these four conditions is suggested not only by the association among these different conditions (many people are afflicted by more than one) but also by the overlapping symptoms typically found in these four conditions (see refs. 4 and 9 for discussion). These overlaps raise the question about whether MCS, FM and PTSD may be caused by excessive nitric oxide and peroxynitrite. Each of these four conditions is reported to be often preceded by and possibly induced by exposure to a relatively short-term stress that can induce excessive nitric oxide synthesis. Pall and Satterlee (4) present a substantial case for an excessive nitric oxide/peroxynitrite cause for multiple chemical sensitivity (MCS), including the following: * Organic solvents and pesticides whose exposure is reported to precede and presumably induce multiple chemical sensitivity, are also reported to induce excessive nitric oxide synthesis. Such chemicals are also reported to induce increased synthesis of inflammatory cytokines which induce, in turn, the inducible nitric oxide synthase (leading to increased synthesis of nitric oxide). * Neopterin, a marker of induction of the inducible nitric oxide synthase, is reported to be elevated in MCS. * Markers of oxidative stress are reported to be elevated in MCS, as predicted if excessive peroxynitrite is involved. * In animal models of MCS, there is convincing evidence for an essential role for both excessive NMDA activity (where such activity is known to induce excessive nitric oxide) and for excessive nitric oxide synthesis itself. If one blocks the excessive nitric oxide synthesis in these animal models, the characteristic biological response is also blocked. This and other evidence shows the nitric oxide has an essential role (4). Somewhat similar evidence is available suggesting an elevated nitric oxide/peroxynitrite mechanism for both PTSD and FM (9). PTSD is thought to be induced by excessive NMDA stimulation, which, as discussed above, is known to produce excessive nitric oxide and peroxynitrite (9). Two inflammatory cytokines known to induce increased synthesis of nitric oxide have been reported to be elevated in PTSD. PTSD animal model studies have reported an essential role for both excessive NMDA stimulation and nitric oxide synthesis in producing the characteristic biological response. Interestingly, a recent study of FM implicates elevated nitric oxide and also elevated NMDA stimulation (8), and such NMDA stimulation is known to increase nitric oxide synthesis. As in the other conditions discussed here, there is a pattern of evidence from studies of FM patients, consistent with the proposed nitric oxide/peroxynitrite mechanism (9). The theory that elevated nitric oxide/peroxynitrite is responsible for the etiology of CFS, MCS, PTSD and FM appears to be the only mechanism to be proposed that explains the multiple overlaps among these four conditions. While the pattern of evidence supporting it cannot be considered definitive, the many types of evidence providing support for this view must be considered highly suggestive. What does this proposed mechanism suggest about CFS treatment? As discussed in ref 1, there are a number of agents that may be useful in the treatment of CFS, based primarily on anecdotal evidence, that are expected to lower the consequences of the proposed nitric oxide/peroxynitrite mechanism. Possibly the most intriguing such mechanism relates to the widespread use of vitamin B12 injections in treatment of CFS (3). Two forms of vitamin B12 are being used here, hydroxocobalamin, which is a nitric oxide scavenger and cyanocobalamin, which is converted to hydroxocobalamin by Pall human cells (3). These observations suggest that the nitric oxide/peroxynitrite proposed mechanism for CFS makes useful predictions for effective treatment. It is hoped that this proposed mechanism may allow us to optimize the use of these and other agents for treatment of CFS and related conditions. References: 1. Pall ML. Elevated, sustained peroxynitrite levels as the cause of chronic fatigue syndrome. Medical Hypotheses 2000;54:115-125. http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=10790736&form=6&db=m&Dopt=b 2. Pall ML. Elevated peroxynitrite as the cause of chronic fatigue syndrome: Other inducers and mechanisms of symptom generation. Journal of Chronic Fatigue Syndrome, 2000;7:45-58. http://listserv.nodak.edu/scripts/wa.exe?A2=ind0103C&L=co-cure&P=R1753 3. Pall ML. Cobalamin used in chronic fatigue syndrome therapy is a nitric oxide scavenger. Journal of Chronic Fatigue Syndrome, 2001;8:39-44. 4. Pall ML, Satterlee JD. Elevated nitric oxide/peroxynitrite mechanism for the common etiology of multiple chemical sensitivity, chronic fatigue syndrome and posttraumatic stress disorder. Annals of the New York Academy of Science, 2001;933:323-329. http://listserv.nodak.edu/scripts/wa.exe?A2=ind0205B&L=co-cure&P=R2378 5. Richards RS, Roberts TK, Mathers MB, Dunstan RH, McGregor NR, Butt HL. Investigation of erythrocyte oxidative damage in rheumatoid arthritis and chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome 2000;6:37-46. 6. Richards RS, Roberts TK, McGregor NR, Dunstan RH, Butt HL. Blood parameters indicative of oxidative stress are associated with symptom expression in chronic fatigue syndrome. Redox Rep 2000;5:35-41. http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=10905542&form=6&db=m&Dopt=b 7. Fulle S, Mecocci P, Fano G, Vecchiet I, Vecchini A, Racciotti D, Cherubini A, Pizzigallo E, Vecchiet L, Senin U, Beal MF. Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome. Free Radicals in Biology and Medicine 2000;15:1252-1259. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11118815&dopt=Abstract 7A. Keenoy BM, Moorkens G, Vertommen J, DeLeeuw I. Antioxidant strotus and lipoprotein oxidation in chronic fatigue syndrom. Life Sciences 2001;68:2037-2049. 8. Larson AA, Giovengo SL, Russell IJ, Michalek JE. Changes in the concentrations of amino acids in the cerebrospinal fluid that correlate with pain in patients with fibromyalgia: implications for nitric oxide pathways. Pain 2000;87:201-211. http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=10924813&form=6&db=m&Dopt=b 9. Pall ML. Common etiology of posttraumatic stress disorder, fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity via elevated nitric oxide/peroxynitrite, Medical Hypotheses, 2001;57:139-145. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11461161&dopt=Abstract --------------------------------------------- Co-Cure Web Site Exercise Prescription for Fibromyalgia: A Plan for Patients From Beginner to Advanced by Colleen Black-Brown "Editor's Note: The following information has been prepared by the author for health care professionals as a guide to developing exercise programs for their fibromyalgia patients. We recommend that you discuss exercise with your health care professional before beginning a program. The cause of FM has not been pinpointed but what has been found to be true is that the fitness or aerobic capacity of fibros is ½ to that of normal individuals. Also, strength levels are significantly less in fibros (fibromyalgia patients) compared to age and sex matched 'normal' individuals. Mannerkorpi reported that FM patients demonstrate 30-50% reduction in aerobic capacity, reduced range of motion (ROM), and some reduction in muscle strength and endurance. Since these people in general are less fit they may not all be able to tolerate normal progressions in a one-size-fits-all exercise prescription. Because each fibro is unique and has varying degrees of pain and fatigue and what seems an unlimited number of symptoms, I have designed four different phases of FM. From this model we will be able to prescribe an exercise program more effectively on an individual basis." Fibromyalgia: Colleen' s Story Site by the arthur of the site above. "Colleen is a specialist in the causes and treatment of fibromyalgia. Since 1997, she has been designing and conducting research and intervention programs for fibromyalgia clients using the F.L.I.P. approach (Fibromyalgia Lifestyle Intervention Program). Her initial interest in fibromyalgia was sparked when she experienced a major flare–up of this debilitating condition in 1995. She and her husband, Dr. Barry Brown, are widely renowned for their efforts to increase public understanding of the positive impact that sound exercise can have on reducing the symptoms of fibromyalgia." Additional Information & Research Sites on FM & CFIDS Toxic Chemicals Seen Contributing To Increased Childhood Illness Artical describing how chemicals are adversely effecting children's health. "In addition to cancer-causing substances, Landrigan warned of "endocrine disrupting" chemicals, which he said may be linked to premature puberty in girls, growing numbers of testicular cancer in boys and penis malformation in a condition known as hypospadia. The last condition has doubled, from approximately 40 incidents per 10,000 live boy births to around 80 incidents per 10,000 births in Atlanta between 1968 and 1983, according to a study by the Centers for Disease Control and Prevention." This is an interesting tid bit of information I got from a Co-Cure newsletter which contained a segment on Dr. Kenny De Meirleir. "Dr. De Meirleir says that CFS is no longer a diagnosis by exclusion due to the 8 makers for the disease. One marker which he talks of repeatedly, is the well- known 37 kDa RNAse. This half-broken down RNAse is diagnosed in 88% of CFS patients." (note the artical above on RNase.) "Only on specific request does he disclose the other markers, and then more vaguely he mentions "disturbances in the anti-viral pathway", "fragments of nucleotides floating in the serum", "disturbances in the proteinKinase pathway", "depletion of natural killer (NK) cells, or the opposite, too many NK cells", "disturbance of the ratio of CD4/CD8 cells, the ratio can go either way". What I think he says, is that this is not as straight forward as the 37kDa marker, but in his hands a diagnosis of CFS _can_ be made biochemically." (During a twin study 4/98 my CD4/CD8 ratio just happened to be 3.12 normal range= 1-2 Is this a response to getting over a cold, a common change in Hashimoto's or hypothyroidism or a change that is occuring in everyone due to environmental factors? It's an interesting finding. When asked about Ampligen he emphasizes that it is the immune modulating effect of the drug, rather that the anti-viral effect, that is responsible for the sometimes miraculous effect on CFS symptoms (cognitive symptoms in particular). The Ampligen trial that we are all waiting for (the US based, double-blind placebo controlled, phase III trial), will be finished and the results known by late 2002/early 2003." Nightingale Research Foundation Dedicated to the study and treatment of M.E. / CFS (also known as Myalgic Encephalomyelitis, Chronic Fatigue Syndrome, CFIDS, Fibromyalgia, and Post-Viral, Post-Toxic, Post-Immunization, Post-Traumatic Brain Syndromes)"M.E./CFS is an acquired brain dysfunction and results in a rapid and persistent exhaustion of both physical and cognitive abilities, an autonomic disregulation and a reduction of more than 50% of the individual's previous ability to carry out work, school or social activities. This Central Nervous System dysfunction can be exacerbated by levels of physical, sensory, cognitive, or emotional stress that would have been of no consequence in the same patient prior to the infectious or traumatic injury." The National CFIDS Foundation Good information under "online library" & "misc information" includes research on CFIDS. CFS Association of Minnesota Site provides information & Links. "What are the main symptoms of CFS? Persons with CFS often function at much lower levels of activity than they were capable of before becoming ill. Patients often report various nonspecific symptoms, including weakness, muscle pain, impaired memory or mental concentration, insomnia, and post-exertional fatigue lasting more than 24 hours. In some cases, CFS can persist for years. Some people with CFS have symptoms that are always present but vary in intensity. Others alternate between episodes of illness and well-being, and recurrences may be either at random or in cycles. Symptoms generally worsen after minimal activity or exercise. The degree of disability varies widely. Some patients continue to function at home and at work, although at a reduced level of activity. Others are severely disabled and cannot perform many routine activities of daily living." Fibromyalgia Network Site includes research, advocacy, support, & medical information on FM & CFIDS as well as quarterly newsletter. CFS study They are looking at aspects of memory in CFS/ME. "We not only need those who have CFS/ME, but people who do not have the condition, and who are currently healthy. The project is based at the University of Northumbria, Newcastle Upon Tyne. We are hoping to make this the largest study of it's kind, but for that, we really do need your help." Tip of the Day for May 09, 2003 According to the renowned CFS & FM physician Charles Lapp, M.D., "I can never emphasize enough that taking periodic rest breaks, limiting activities, and maintaining low level aerobic activities is the very most important treatment for both CFS and FM. Unfortunately, many sufferers are unwilling to accept these drastic lifestyle changes. There is no drug, no potion, no supplement, herb or diet that even competes with lifestyle change for the treatment of CFS or FM. The next most important step is to minimize stress, optimize your support systems, and to maintain a positive attitude despite adversity. I have never seen a study that proves these points, but I can assure you from experience that pushing and crashing, denial, depression, and a negative attitude are all formulas for disaster, and I have never seen a patient who practiced them and yet recovered. Drugs, supplements, and alternative therapies are only supportive and symptomatic treatments that make the path toward recovery more bearable. But they do make it more bearable for most." Endometriosis Linked to Autoimmune and Other Chronic Diseases Including Chronic Fatigue Syndrome & Fibromyalgia "Women with endometriosis frequently suffer from autoimmune inflammatory diseases, hypothyroidism, fibromyalgia, Chronic Fatigue Syndrome, allergies and asthma," according to Ninet Sinaii, from the National Institute of Child Health and Human Development in Bethesda, Maryland, based on the results of a 2002 survey. "These findings also suggest a strong association between endometriosis and autoimmune disorders and indicate the need to consider the co-existence of other conditions in women with endometriosis." Fibromyalgia and Sleep Deprivation: Fatigue Can Be Dangerous About 90 percent of people with fibromyalgia syndrome suffer from consistent sleep deprivation, according to the Fibromyalgia Network, a nonprofit organization headquartered in Tucson, Arizona. Lack of sleep exacerbates the fatigue, stiff joints and depression common with fibromyalgia (FM), a disease that affects 3.7 million people. What many people with FM might not know is that when fatigue compromises your cognitive functioning, it can be dangerous. "DANGERS OF FATIGUE Fatigue isn’t just a matter of being sleepy. Fatigue can be dangerous as well. "People with FMS should be cautious about making long road trips, as well as operating heavy or dangerous equipment," said Winkler. The four signs of fatigue include: 1. Lack of attention 2. Memory loss 3. Frustration with coworkers or friends 4. Poor concentration In many cases, a person with fibromyalgia suffers from sleep disorders beyond insomnia. Adults with fibromyalgia may suffer from a lack of deep sleep as well as from constant waking throughout the night. Deep, restorative sleep, also known as delta sleep, is the most crucial stage of sleep. It is during this stage that the body recovers energy and repairs muscle tissue. Without delta sleep, a person with fibromyalgia might sleep eight hours yet wake feeling unrefreshed. This sleep problem can be difficult to detect - let alone treat. In addition, a person with FMS may have traditional sleep disorders, as well such as apnea, or obstructed breathing, and periodic limb movement [including Restless Legs Syndrome]." New Theory Links Neurotoxins with Chronic Fatigue Syndrome, Lyme, MCS and Other Mystery Illnesses "Two doctors believe they've discovered a new brand of illness and a new way for pathogens to make people sick. They also have an FDA-approved treatment that was effective in a small, preliminary clinical trial. neurotoxic /nõr'ò tok'sik/, anything having a poisonous effect on nerves and nerve cells, such as the effect of lead on the brain and nerves. -The Mosby Medical Encyclopedia" Disability Info Free Medicines.org Men With Fibro Teens with CFS/FMS Made for teens, by a teen. Chemical Sensitivities The pain is real, but is fibromyalgia a condition? Depends who you ask "The research findings are beginning to change a few minds, said Laurence Bradley, a psychologist and professor of medicine at the University of Alabama's medical school in Birmingham. He also does research into fibromyalgia. "I think there is much more acceptance of this now than there was 10 years ago when I first got involved in the research," he said. Some of the most recent evidence comes from an experiment in which Clauw and a colleague, Richard Gracely, used a device to apply pressure to the thumbnails of a group of subjects, half of them with a fibromyalgia diagnosis, half without. The researchers watched the activity in the subjects' brains with a magnetic resonance imaging machine. The differences were impressive, according to Clauw. The fibromyalgia patients were quicker to report pain. More significantly, the brain scans bore out their claims. Activity in the pain-processing region of the brain was much greater in the fibromyalgia patients. The bottom line: The fibromyalgia patients' claims of greater pain were proven true by the MRI pictures. "The majority of the scientific community that studies pain didn't find this to be a revelation," he said. "This was an incremental step that corroborated a lot of things that had previously indicated abnormalities in people with fibromyalgia." There's more evidence that something's amok in the pain systems of people with fibromyalgia. Several studies have found they have two or three times the normal amount of Substance P, a compound involved in sending pain messages in the body. Researchers also have found that people with fibromyalgia have relatively low levels of several compounds that diminish pain sensation. One of them is the hormone cortisol, an anti-inflammatory compound that the body produces particularly when under stress. Another is the brain chemical serotonin. People with fibromyalgia also seem to have lower levels of endorphins, a family of compounds that elevate mood and dampen feelings of pain. Thomas Fasy is an associate professor of pathology at the Mount Sinai Medical School in New York City. He's been studying the apparent endorphin-deficiency in people with fibromyalgia. Given the high incidence of autoimmune conditions such as lupus and rheumatoid arthritis among people with fibromyalgia, Fasy wondered whether fibromyalgia might be another autoimmune condition. He's been studying samples of blood serum, looking for autoantibodies, chemical agents that might attack and destroy endorphin-type compounds, resulting in higher levels of pain. Fasy said the results of his study "are encouraging but not yet definitive." Wolfe, the skeptic, accepts that individual biochemistry varies. However, he said, the context and meaning of those numbers is clear as mud. "It doesn't tell us what came first, the chicken or the egg," he said. Studies so far suggest there's no single abnormality that causes all fibromyalgia, said Clauw, from the University of Michigan. Several mechanisms are involved in producing and transmitting pain signals. Any one of those, he said, could result in "the volume control turned up too loud" in a person's pain messaging system. It's estimated that fibromyalgia afflicts at least 2 percent of Americans, the vast majority of them women. One of them is Phyllis Woolard, of Kansas City, Kan. She says she feels largely recovered from her fibromyalgia, which for several years caused her intense pain that flared up with the slightest provocation. "I'd go to the doctor and he'd say, `Where does it hurt?' and I'd say, `All over. Just touch my flesh anywhere.' " Woolard's doctor called her condition fibromyalgia, but he didn't know what to do about it. He prescribed medications. She concocted mixtures of arthritis medicine and pain formulas and headache pills and muscle relaxants. "It's a little scary, looking back on it," she said. Baffled, the doctor suggested she search the Internet for help. About three years ago she found a fibromyalgia support group. She began drinking more water and taking vitamin- and mineral-laden nutritional supplements. Two years ago she met a chiropractor who advised her to avoid caffeine and heavily processed foods and certain chemicals to which, he claimed, she was allergic. Woolard underwent some treatments, including oral chelation and network spinal analysis, that are widely scorned in the medical establishment. Eventually Woolard felt good enough to stop wearing the face mask she'd used to protect herself from troublesome fumes and compounds. She resumed working. She now considers herself to be "80 percent recovered." The treatment of fibromyalgia, like nearly every aspect of this confounding condition, is at an embryonic stage. Certain anti-depressants, because they increase the amount of serotonin, are sometimes prescribed. Neurontin, a drug usually given to epileptics, also can relieve pain in some cases. Two of the most widely embraced treatment strategies are exercise and what Bradley calls "coping skills training." Exercise is recommended because a weak body is more prone to pain, he said. Activity also can be therapeutic because it naturally hikes endorphin levels. Teaching people to cope with their pain is a strategy used for other conditions, such as cancer, Bradley said. How people feel and think about their pain makes a difference. "People who believe they can manage their pain do manage their pain better," he said. Relaxation techniques and helping people focus on something other than their discomfort "helps people change their beliefs about their ability to manage their pain." In one respect Bradley agrees with the skeptics: There is a psychological component to fibromyalgia -- as there is to cancer or any number of other illnesses. But he and others would argue, that doesn't mean it's all in people's heads." Charlotte Area CFIDS/FMS Support Group 
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