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Latest News

The latest news on fibromyalgia syndrome and chronic fatigue syndrome is posted below in support of Fibromyalgia Network's mission to educate patients and the media with ad-free reporting.

Contact: Kristin Thorson, Editor • Phone: (800) 853-2929
E-mail: editor@fmnetnews.com • Website: www.fmnetnews.com

» News Archives

A Little Omega-3 Could Reduce Your Pain and Fatigue

Posted: January 29, 2010

Omega-3 fatty acid (FA) supplements can benefit your joints and cardiovascular system, but what about the pain of fibromyalgia? A small, one-month study involving 12 fibromyalgia patients showed improvements in tender point pain counts, chest expansion (e.g., less muscle tightness), and perceived fatigue levels.1 Even total cholesterol dropped with the supplementation of 1,500 mg per day of the combined two key omega-3 FAs: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Vegetable oils are not a source of EPA or DHA. Fish oils that have been processed and encapsulated increase the concentration of these two essential omega-3 FAs. The manner in which omega-3 FAs work to relieve fibromyalgia or neuropathic-type pain is not clear. However, a recent case series report on the use of omega-3 FAs to substantially reduce the neuropathic pain and restore function in five patients (one with fibromyalgia), is quite impressive.2

While omega-3 FAs are known to exert anti-inflammatory effects, which can then lead to pain relief, inflammation is not generally present in patients with neuropathic or fibromyalgia pain. The Canadian research team that published the case series suggests that EPA and DHA could possibly work by reducing the release of pain-promoting cytokine substance from the white blood cells. These cytokines are suspected to play a major role in the production of neuropathic and fibromyalgia pain.

Two of the patients in the case series had cervical neck pain due to injuries sustained from a motor vehicle accident (a common occurrence in fibro). A third patient was an auto mechanic with carpal tunnel syndrome due to repetitive strain of his job, another was a nurse with an arm injury from lifting patients that developed into fibromyalgia, and the fifth subject was a burn patient. All five patients had tried lots of therapies before being placed on EPA/DHA in amounts from 2,400 mg to 7,200 mg per day.

Prior to supplementing with the omega-3 FA, the fibromyalgia patient could barely do household chores, such as vacuuming the carpet, and her pain was 8 on a scale of 0 to 10 (where 0 is no pain and 10 is worst possible pain). After taking the EPA/DHA for seven months, her function and grip strength were much improved and she rated her pain 3 on the scale.

Both cervical neck pain patients took 4,800 mg per day of EPA/DHA, and after eight months muscle strength, grip strength, and function were restored. One returned to ice hockey and the other resumed actively working out in the gym. In fact, the latter patient boosted his daily dose to 7,200 mg and noticed "sharper brain function and feeling clear-headed." The mechanic took 3,000 mg of EPA/DHA per day and after eight months was back to full-time work. The burn patient initially took 2,400 mg of EPA/DHA and slowly increased to high-dose omega-3 FAs. After several months his pain was reduced in half.

All of these patients had serious pain, but after many months of omega-3 FA therapy, their pain levels slowly came down and their function returned. This is only a small sampling of patients, and the study lacks a control group for comparison so the results are strongly biased in favor of the patient feeling better. However, some of the parameters for patient improvement represented objective measures, and the increased physical functioning of these patients after many months of omega-3 FA supplementation was quite dramatic.

"It is important to recommend a high-quality brand of omega-3," writes the authors. "A product with a higher concentration of EPA/DHA per serving is advisable over a similar product with a lower concentration," they add, because fish oils may contain heavy metal impurities(such a mercury) and it is best to limit the number of capsules needed per day. With regards to purity, the authors recommend the website www.ifosprogram.com, which lists omega-3 products that have been independently tested for contaminants. Click on the Consumer Report tab for free information. If you are diabetic or trying to loose weight, beware that each capsule will likely contain about 10 calories.

Other recommendations provided by the research team to help ensure greater success with treating your pain:

  1. Ozgocmen S, et al. Int J Clin Pharmacol Ther 38:362-3, 2000.
  2. Ko GD, et al. Clin J Pain 26:168-72, 2010.

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Could Fibro Make Arthritis Worse?

Posted: December 31, 2009

Most people assume that as they age, the wear and tear on their joints will eventually lead to osteoarthritis (OA). Indeed, OA is the leading cause of pain and disability around the world, but have you ever considered if having fibromyalgia puts you at greater risk of developing OA? Or, could your fibro make your OA more painful and disabling? And even if the radiographic images of your painful knees or hips don't reveal the true severity of how much aggravation these joints cause, scientists believe that there is another factor that you and your doctor have overlooked.

Initially, research on OA focused solely on the joints involved. When X-rays and tests did not correlate with the patient's pain severity and disability, the focus shifted to evaluating psychological factors. Depression and anxiety do make the pain of OA worse, just as these two symptoms might cause a slight increase in the pain of fibro. However, looking at the psyche or joint does not present the full picture of what is going on in people with OA, according to a published editorial by Daniel J. Clauw, M.D., "Pain and Rheumatology: Thinking Outside the Joint."1 With close to 20 years of experience in fibromyalgia research, Clauw, of the University of Michigan, understands that issues pertaining to chronic pain involve the central nervous system and are influenced by a person's genetics.

Commenting on the radiographic evidence that joint damage in OA does not usually match the patient's report of pain, Clauw states:

"Population-based studies suggest that there is a significant disparity between the degree of peripheral damage noted on radiographs and the pain and functional limitations that patients with this condition experience. The most dramatic evidence of this is that 30-60% of individuals with moderate to severe radiographic changes of OA are completely asymptomatic, and approximately 10% of individuals with moderate to severe knee pain have normal radiographs."

Clauw points out that one regulatory system working in the spinal cord to filter out pain does not function properly in fibromyalgia and OA patients. This means that the noxious signals generated by minor joint deterioration will be perceived by the brain as painful. However, for the person with a normal functioning pain inhibitory system, these noxious signals would be filtered out and the person would not feel any discomfort in the joint. Given that this part of the pain inhibitory system isn't working in people with fibromyalgia, it would mean that even OA could produce much more pain than what the doctor might predict from your X-rays.

Problems within the pain control system may help explain why your OA is particularly painful, but what about the prevalence? Does having fibromyalgia place you at greater risk for developing OA? Perhaps. Based on a report by Michael T. Smith, Ph.D., of Johns Hopkins Medical Center, the common denominator that may contribute to OA pain and disease severity is disrupted sleep.2

In 2007, Smith showed that disruption of sleep in healthy people could cripple their pain inhibitory system and cause them to develop achy muscles.3 Smith adds: "All of the studies describing sleep disturbance in individuals with knee OA report a robust relationship between pain severity and sleep disturbance." He goes on to say that sleep studies in OA (which are very scarce) show that patients have trouble staying asleep throughout the night and that the findings are comparable to people with fibromyalgia.

So sleep impairments, or all the tossing and turning at night, interfere with your pain inhibitory system and this leads to more painful OA. The disruption of sleep has also been shown to produce and release into the bloodstream more inflammatory substances, in particular interleukin-6 (IL-6). Smith points to a recent study that followed middle-aged women for 15 years to see if any blood markers could predict the development of knee OA.4 The authors found that increasing levels of IL-6 in the blood corresponded to increasing radiographic evidence of knee OA. Unfortunately, sleep quality or pain levels were not assessed, but Smith connects the dots in his report.

When sleep disruption and chronic pain persist, they set up a vicious cycle that leads to more pain, more inflammation, and less physical activity. After all, joint pain and sleep loss will both interfere with a person's ability to function. As a result, the patient may start to gain weight. The issue is not really the weight gain, but rather, the sleep disorder that is at the root of the problem. Levels of IL-6, the inflammatory substance found to correspond with the development of OA, were also shown to be elevated in people with fibromyalgia and could place you at higher risk of developing OA.

"Aggressive management of sleep disorders should be a critical component of the comprehensive treatment of rheumatologic patients and older adults," writes Smith. If you are experiencing joint pain in addition to the muscle aches of fibromyalgia, don't just talk to your doctor about pain-relieving treatments. Make sure that everything is being done to ensure that you have the best quality sleep possible. A good night sleep seems to be key to relieving OA and fibromyalgia pain.

  1. Clauw DJ, Witter J. Arthritis Rheum 60:321-24, 2009.
  2. Smith MT, et al. Curr Pain Headache Rep 13:447-54, 2009.
  3. Smith MT, et al. SLEEP 30:494-505, 2007.
  4. Livshits G, et al. Arthritis Rheum 60:2037-45, 2009.

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Effective Treatment Leads to Better Brain Function

Posted: November 20, 2009

The hippocampus in the center of your brain plays a vital role in memory and learning, reducing pain, and controlling (often dampening) your body's response to stress. Given that fibromyalgia patients have cognitive difficulties, severe pain, and a hyperactive stress response, clinician and researcher Patrick Wood, M.D., hypothesized in 2003 that this brain area would show chemical and structural abnormalities that corresponded to the symptoms. Funded by the American Fibromyalgia Syndrome Association (AFSA), Wood's project has led to the publication of three exceptional reports that illuminate what is happening in the brains of people with fibro.

Initially, Wood demonstrated that an important metabolite (NAA/Cr) was abnormally low in the hippocampus and was related to the severity of the fibromyalgia patients' symptoms.1 N-acetylasparate (NAA) represents how effectively your neurons are functioning and creatine (Cr) represents the amount of energy consumed. Computing the ratio of NAA to Cr is thought to help standardize individual results for more accurate comparisons. See the September 30, 2008 posting in our Latest News section for additional study info and what the results might mean for you.

Next, Wood showed that fibromyalgia patients had reduced gray matter in the hippocampus and it appears to be related to a loss of dopamine activity in this region.2 Hippocampal dopamine plays a strong role in the pain inhibitory system, so a drop in activity could help explain why fibromyalgia patients have pain all over.

Although loss of gray matter can sound scarey, it appears to be reversible. Wood’s most recent article offers proof that the brain imaging findings in the hippocampus are directly tied to the symptoms of fibromyalgia (at least in some people) and can be reversed with the proper therapy.3 According to a patient case report, a 47-year-old woman who exhibited an abnormally low NAA/Cr ratio was successfully treated by Wood. A follow-up image taken of her brain scan showed that the NAA/Cr value increased to normal.

Wood offers a detailed picture of a woman who was diagnosed by two different rheumatologists as having fibromyalgia before entering his study. After an automobile whiplash accident she reported symptoms of widespread pain, diffuse tenderness, disturbed sleep, severe fatigue, numbness and tingling sensations, frequent headaches, constipation-related irritable bowel syndrome, cold-sensitive extremities, and difficulty with concentration and short-term memory. No doubt these latter symptoms of fibro fog were very distressing given that she was employed as psychotherapist with a Ph.D. She also reported being premenopausal with irregular menstrual cycles, heavy bleeding, cramps, and premenstrual irritability.

On the first visit, her Fibromyalgia Impact Questionnaire (FIQ) score was 52 on a scale from 0 to 80, where 80 is the worst possible score. In addition, she had the following symptom scores on a scale from 0 to 10 (10 being the worst possible):

pain = 5.5
fatigue = 10
symptoms at rest = 10
stiffness = 8.5

The above scores all indicate a patient who is very significantly impacted by her fibromyalgia symptoms, but she was not depressed. Due to her menstrual symptoms, Wood tested her hormone levels and found that her estradiol (e.g., estrogen) was extremely elevated. Otherwise, her blood work was normal.

After agreeing to participate in the brain imaging study, her hippocampal NAA/Cr ratio was found to be very low at 1.07 (normal is around 1.34). Wood repeated the scan and the results were the same. Oddly, her Cr level was slightly elevated, which may have been a contributing factor to her low NAA/Cr ratio.

Soon after completing the study, she sought Wood's help in treating her fibromyalgia. Her pre-study symptom scores can be used as a baseline or basis for comparison.

Treatment Visit #1: Nighttime sympathetic nervous system hyperactivity may have interfered with her ability to sleep and the concept that beta-adrenergic receptors in the hippocampus could be bombarded with signals from the sympathetic system. So a beta-adrenergic receptor blocker was prescribed at bedtime (60 mg of long-acting propranolol or Inderal-LA). Wood speculated that her high estradiol level was causing central nervous system hyperactivity, which contributed to her menstrual symptoms and disrupted sleep (including next-day fatigue). He recommended that she take the over-the-counter supplement, indole-3-carbinol, to increase the speed at which the liver breaks down estrogen for excretion in the urine. In addition, he balanced the remaining estrogen with a prescription for natural progesterone at bedtime on days 12 through 26 of her cycle (formulated in slow-release 200 mg capsules at a compounding pharmacy).

Treatment Visit #2: After 10 weeks, she returned with a much improved FIQ score of 30 (it was 52 at the beginning). She reported less pain at rest, improved sleep, and much more energy. However, she still had residual menstrual cycle symptoms and trouble sleeping. Wood increased her nighttime progesterone to 300 mg for the second half of her cycle and placed her on a small nightly dose of Ambien (zolpidem 5 mg) to help her sleep.

Treatment Visit #3: At her 16-week follow-up, her FIQ was down to 19. She reported continued improvement in all symptom areas, so the decision was made to stick with the same therapies.

Treatment Visit #4: At her 28-week follow-up with Wood, her FIQ score was down to 8 and she reported being "essentially pain free." Her primary concern was constipation, dry mouth, and fatigue following exertion. He prescribed pyridostigmine, which works to increase the activity of acetylcholine, the main communication transmitter used by the parasympathetic nervous system (the one that helps with "rest and digest"). The drug's side effects of increased GI motility and saliva/tear production were thought to relieve her remaining symptoms. Indeed, the patient described this last addition to her therapy as the "crowning touch" in her complex, symptom-based regimen.

Treatment Visit #5: A few weeks after the fourth visit, Wood conducted a telephone follow-up consultation with the patient. She was virtually symptom free while remaining on the prescribed therapies. In addition to her full-time job, she had enrolled in a rigorous postgraduate certification program in her field. Wood asked to take another brain scan to look for evidence of change. Her NAA/Cr ratio increased to 1.34 (it had been 1.07) and the average for the healthy control group was also 1.34. During this follow-up brain scan the value of Cr dropped. This appears to be why the NAA/Cr increased to normal (at least in this particular patient).

"It is tempting to speculate that the clinical improvements experienced by this patient might be related to decreased hippocampal energy metabolism," writes Wood. In other words, by applying therapies that reduce the excitability or amount of activity in the hippocampus, the result should be a decrease in energy use (e.g., lower Cr values). This should also enable the hippocampus to recover from being overworked and to begin focusing on vital functions such as memory/concentration, pain control, and regulating the stress response system. With these processes operating optimally, the symptoms of fibromyalgia should improve.

While the regimen prescribed for this 47-year-old fibromyalgia patient successfully eliminated her specific symptoms and reversed her NAA/Cr hippocampal metabolite abnormality, keep in mind that each person with this condition is different. The key for treating physicians is to use strategies aimed at correcting the physiologic abnormalities associated with the disorder. In this particular case, the patient had hormonal imbalances associated with her menstrual cycle, symptoms suggesting a hyperactive sympathetic and underactive parasympathetic nervous system, and disrupted hippocampal functioning. All of these factors likely contributed to her pain, brain fog, sleep disorder, daytime exhaustion, and GI symptoms to varying degrees.

"Given the multiple interventions detailed herein," writes Wood, "it is admittedly difficult to parse out which specific agent may have contributed the greatest impact on the combined improvements. However, on the basis of this experience, therapeutic strategies aimed at demonstrable lesions associated with this unusual disorder seem to represent rational targets for pharmacologic interventions that warrant further investigation." In other words, more research on the hippocampus in fibromyalgia could lead to better treatments.

Other therapies that Wood often recommends to help restore the "health" of the hippocampus include omega-3 fish oils (especially EPA and DHA), acetyl-l-carnitine, and dopamine-like drugs (agonists such as Mirapex or Requip). The research for these three related reports was conducted while Wood was at Louisiana State University in Shreveport. He is now in private practice near Seattle, WA, with Andrew J. Holman, M.D. Wood's clinic is devoted entirely to the care of patients with fibromyalgia, and this case report emphasizes that patients with more forward-thinking doctors may have milder symptoms. In other words, the medications are important, but the skill with which your doctor uses them is equally important.

  1. Wood PB, et al. J Pain 10(1):47-52, 2009.
  2. Wood PB, et al. J Pain 10(6):609-18, 2009.
  3. Wood PB, et al. Clin J Pain 25(9):810-4, 2009.

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Virus Linked to CFS

but is history repeating itself?

Posted: October 29, 2009

Earlier this month, a relatively new retrovirus called XMRV was reported to be found in 68 percent of 101 chronic fatigue syndrome (CFS) blood samples, while the viral infection was detected in only 3.7 percent of 218 healthy controls. Scientists at the Whittemore Peterson Institute in Reno, NV, whose medical director is Daniel Peterson, M.D., worked in collaboration with the Cleveland Clinic and the National Cancer Institute to generate this discovery published in the journal Science.1 Following the study, a press release from the Whittemore Peterson Institute stated the tests for XMRV were refined and now up to 95 percent of the CFS samples have evidence of the virus.

XMRV was originally discovered by researchers at the Cleveland Clinic in 2006 from prostate cancer tissue of men who had a specific genetic defect in their antiviral enzyme RNASE L.2 This enzyme destroys viruses by degrading RNA, their genetic machinery. A similar defect associated with a portion of CFS patients prompted researchers to suspect that XMRV might be linked to this illness, which then led to the report in Science. The relationship between prostate cancer and the virus is unknown, and it turns out that the RNASE L enzyme defect did not correlate with the presence of XMRV in the CFS patients studied.

Aside from XMRV, there are two other known retroviruses, HIV which causes AIDS and HTLV which causes leukemia. This family of viruses operate by inserting their genetic RNA material into their hosts' genetic DNA, causing permanent changes in the way the hosts' cells operate. Retroviral infections are serious business that cause lifelong diseases affecting the immune and neurological systems, unlike the common flu bug that usually only makes you ill for a few days. While the prospect of a viral cause may validate the symptoms of CFS and possibly fibromyalgia (a small sample of patients have tested positive), the study findings need to be confirmed and many more questions need to be answered.

Keep in mind that close to 4 percent of the healthy subjects turned up positive for XMRV. Does this mean that the virus is benign or will these subjects start to develop symptoms of CFS after some unknown environmental trigger? The role this virus might be playing in CFS is completely unknown. Is this some sort of "passenger" virus that happens to infect people with a dysfunctional immune system? Whether XMRV is involved in the generation of CFS symptoms remains unclear, but researchers appear confident that the virus is not airborne.

Depending upon your perspective, the report of a retroviral link to CFS can be exciting or alarming news. However, the history of CFS is paved with a number of viral claims by well-intended scientists that later turned out not to be the cause of this condition.

After the first outbreak of fatiguing illnesses occurred in Incline Village, NV, where Dr. Peterson was practicing in 1984, there were others that occurred elsewhere in the United States. The initial name was post-viral fatigue syndrome because the symptoms seemed like they were caused by a virus, but no specific agent could be identified. Then researchers claimed the illness was caused by the Epstein-Barr virus (EBV), the bug that causes mono, because almost every patient had antibodies to EBV. As it turned out, so did everyone else in the general population over the age of 6. Then came human herpes virus 6 (HHV-6), followed by HHV-7, an enterovirus that infected the muscles, cytomegalovirus (CMV), and others that were later found not to be the cause of CFS.

While the patients for the current study all met the CFS diagnostic criteria, the authors state, "Samples were selected from several regions of the United States where outbreaks of CFS had been documented." They go on to say that these are severely disabled patients with multiple immunological abnormalities and extremely low exercise capacities. It remains unknown how these CFS patients from the mid-1980s outbreaks compare to today's population of CFS patients or those with fibromyalgia.

Given the number of viral reports that have been associated with CFS, it would be prudent to wait for an independent laboratory to confirm the initial study that appeared this month in Science. This does not in any way diminish the potential significance of the research findings by the Whittemore Peterson Institute, but until more information is known, there is really nothing else we can do but wait.

  1. Lombardi VC, et al. Science 326:585-89, 2009.
  2. Urisman A, et al. PloS Pathogens 2:211-25, 2006.

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