Fibromyalgia: Research Update
Chester J. Zelasko, Ph.D. | September 12, 2007

“Fibromyalgia: a disease of unknown etiology.” It seems amazing that the cause of a condition that affects 15-20 million people could be so difficult to discover. First recognized as a syndrome in 1987, the cause of fibromyalgia is yet unknown. This Newsletter will review some of the most-recent research on the possible causes of fibromyalgia.

The Possible Suspects
Several factors have been examined for their role in fibromyalgia; one of the most researched is sleep deprivation. We live in a society continuously on the go: work, children, spouse, church, volunteer activities, parents, hobbies, and on and on. Completing all the must do things generally means that something must suffer, and for many, it’s sleep. We just don’t get enough good-quality sleep.

The allergic response to environmental factors has also been implicated as a potential cause for fibromyalgia. The factors could be dietary or chemical in nature. The result is an increase in the release of inflammatory enzymes. In conjunction with the allergic response, fibromyalgia is also being examined as an autoimmune disorder. An autoimmune disorder means the body manufacturers antibodies that attack the body’s own tissues--in the case of fibromyalgia, the muscles and joints seem to be most at risk for attack.

There’s also a genetic component to fibromyalgia. Several genes have been implicated, especially genes related to the inflammatory process. Single nucleotide polymorphisms (SNPs) of inflammatory genes such as IL-6, IL-8 and IL-1R may be contributing factors to the development of fibromyalgia.

With the possible suspects in mind, let’s examine the most recent science to see the current direction of fibromyalgia research.

The Pain Hypotheses
In an interesting article published in Medical Hypotheses, Dr. Sota Omoigui suggests that all pain is the result of the inflammatory process (1). This theory of pain and inflammation applies to fibromyalgia as well as arthritis, interstitial cystitis, migraines, bursitis, and more. If this theory proves to be correct, the treatment plan becomes clear: control the inflammation, control the pain. What’s much less clear is how to control the inflammation in every case, because each gene mentioned above works differently. What works for one inflammatory gene may or may not work for others. Until specific interventions are developed for each type of inflammation, Dr. Omoigui proposed that all pain be controlled through medications or surgery.

Trace Minerals
Researchers in Sweden examined the quantities of nearly 30 trace minerals in the blood, urine, and drinking water of people with fibromyalgia (2). There were significantly higher concentrations of the minerals cadmium, cobalt, copper, iron, selenium, silicon, and zinc in the blood of those with fibromyalgia compared to controls. The urinary excretion of these trace minerals, in addition to silver, was slightly lower than that of control subjects; no differences in trace minerals were found in the water supply. Because all trace-mineral levels were within the national and international guidelines for safety, researchers concluded the hypothesis that trace mineral abnormalities contribute to the development of fibromyalgia could not be supported.

That conclusion might be premature. In a paper published in Best Practice & Research Clinical Rheumatology, Dr. D. Buskila proposed that environmental factors may trigger the development of pain syndromes, including fibromyalgia, in genetically predisposed individuals (3). The subtle differences in people’s ability to metabolize trace minerals may be a precipitating environmental factor for fibromyalgia with the right genetic SNPs. More research needs to be done to identify the proper genetic patterns, but for now no potential explanation that may affect inflammatory genes should be eliminated.

Sensory-Motor Conflict
In one of the more fascinating research protocols I’ve read, scientists examined differences in somaesthetic responses (in simplest terms, the mental image of the body created by the brain from sensory inputs) between subjects with fibromyalgia and normal volunteers. Subjects with fibromyalgia responded differently to sensory input to their muscular system when they performed opposite movements with their arms or legs while being allowed to view only one arm or one leg--the right arm didn’t know what the left arm was doing. (The subjects were at the end of a wall with their arms or legs on opposite sides and their head on one side so they could see only one arm or leg; that side of the wall was mirrored so they could see the arm or leg even better.) In people with fibromyalgia, when asked if there were any sensations that they felt in the arm or leg they couldn’t see, most rated the pain and discomfort level higher than in the arm or leg they could see.

What conclusions could be drawn from a study like this? Perhaps people with fibromyalgia may have a more sensitive nervous system. Because the nervous system controls the muscular system, changes in sensory perception could result in increased pain, which is one of the most severe symptoms associated with fibromyalgia.

Bottom Line
The research to find the cause of fibromyalgia is interesting and frustrating at the same time. It’s interesting in that so many potential causes are being examined; the difficult part is separating cause from effect. For example, is a specific genetic pattern a contributing factor to sleep deprivation, which then initiates the inflammatory process in response to the lack of sleep? Or is it the sleep deprivation that causes the inflammatory process in those with the right genetic pattern--but only after exposure to certain trace minerals? You can see how complicated this can be. The most encouraging note is that there’s hope for fibromyalgia sufferers because with new potential causes, there will be new treatment options. And the search for definitive answers continues.

References:
  1. Omoigui S. The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response. Part 2 of 3--Inflammatory profile of pain syndromes Med Hypotheses. 2007. [Epub Aug 27].

  2. Buskila D. Genetics of chronic pain states. Best Pract Res Clin Rheumatol. 2007;21(3):535-47.

  3. Rosborg, I et al. Trace element pattern in patients with fibromyalgia. Sci Total Environ. 2007. [Epub Aug 20].

  4. McCabe, CS, et al. Somaesthetic disturbances in fibromyalgia are exaggerated by sensory-motor conflict: implications for chronicity of the disease? Rheumatology. 2007. [Epub September 1].
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