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A new study in The Journal of Clinical Investigation provides compelling evidence that fibromyalgia arises when the body’s own antibodies interact with pain-sensing neurons, increasing their sensitivity. This finding suggests that reducing antibody levels could help to treat the condition, bringing hope to large numbers of people around the world who have struggled to respond to existing therapies.
Fibromyalgia is a poorly understood condition that is characterized by heightened pain sensitivity, fatigue, muscle weakness, and emotional distress. A loss of nerve fibers in the skin has also been associated with more severe symptomology, although the cause of this pathology has until now eluded scientists.
To test the theory that the illness may be underpinned by autoimmune processes, the study authors injected mice with immunoglobulin antibodies collected from the blood plasma of fibromyalgia patients in the UK and Sweden. Within a short time, the rodents began to display signs of the condition, including increased sensitivity to pressure and cold, reduced movement and grip strength, and a loss of nerve fibers in the skin.
The researchers then repeated the experiment using antibodies from people that did not suffer from the condition, and again using plasma from fibromyalgia patients that had been cleared of immunoglobulin, and found that the mice did not develop any symptoms in either case. Furthermore, mice that had been injected with antibodies from fibromyalgia sufferers typically overcame their symptoms after two to three weeks, which is roughly how long it takes for immunoglobulin levels to drop.
Taken together, these findings indicate that immunoglobulin antibodies are the main driver of the illness, thereby confirming the autoimmune mechanism behind fibromyalgia.
In a statement, study author Dr. David Andersson explained that “previous exploration of therapies has been hampered by our limited understanding of the illness. This should now change.” “
Treatment for [fibromyalgia] is focussed on gentle aerobic exercises, as well as drug and psychological therapies designed to manage pain, although these have proven ineffective in most patients and have left behind an enormous unmet clinical need."
“Establishing that fibromyalgia is an autoimmune disorder will transform how we view the condition and should pave the way for more effective treatments for the millions of people affected.”
While more research is needed in order to determine exactly how immunoglobulin increases pain sensitivity, the study authors found that these antibodies bind to clusters of neurons in the spinal cord called dorsal root ganglions, sparking a cascade of interactions that may result in the hypersensitization of certain nerve fibers.
Fortunately, techniques to reduce antibody levels are already in existence and are regularly used to treat other autoimmune diseases. The study authors, therefore, speculate that applying such therapies to fibromyalgia could result in the development of an effective treatment for this debilitating condition.
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