Fibromyalgia, a chronic pain condition commonly thought to originate in the brain, might actually be a disorder of the immune system, according to a new study.
Research published in the Journal of Clinical Investigation suggests that many symptoms of fibromyalgia are caused by antibodies that increase the activity of pain-sensing nerves throughout the body.1 According to the findings, these antibodies seem to cause the increased sensitivity to pain, pressure, and cold characteristic of fibromyalgia, along with the muscle weakness, reduced movement, and fatigue also seen with the disease.
The news could be a breakthrough for those who suffer from Fibromyalgia Syndrome (FMS), a condition whose causes are still being studied. About 2% of adults worldwide live with fibromyalgia (including some 4 million people in the U.S.4). The prevalence rises to 10-30% among people diagnosed with rheumatological conditions.2 About 80% of those with fibromyalgia are women.2
A research team from King’s College London, the University of Liverpool, and the Karolinska Institute injected mice with antibodies (immunoglobulin G) from people living with fibromyalgia and saw the mice develop symptoms of the disease. The mice became highly sensitive to pain and cold, their grip strength diminished, and their range of activity lessened as they became more lethargic, compared to mice injected with immunoglobulin G from people without fibromyalgia, or mice injected with serum from people with fibromyalgia with the antibodies removed.3
The findings suggest that therapies that reduce antibody levels in patients with fibromyalgia may be used to create effective treatments.
“The implications of this study are profound. 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,” said David Andersson, PhD, the study’s principal investigator. “Our work has uncovered a whole new area of therapeutic options and should give real hope to fibromyalgia patients.”1
However, some who study fibromyalgia are not as convinced.
“I am skeptical that this single study is showing that fibromyalgia is an autoimmune disorder, because it is at odds with decades of studies and clinical experience suggesting otherwise,” said rheumatologist and pain researcher Daniel Clauw, MD, director of the Chronic Pain and Fatigue Research Center at the University of Michigan.5
Regarding the antibodies highlighted in the study, “It’s hard to imagine how they could cause, for example, sensitivity to bright lights or to odors, because that is clearly a brain problem. Some of the classic, key features of fibromyalgia really can’t be triggered by the mechanism that was being studied in this particular animal study,” Clauw said.
“Many of us in the fibromyalgia field are skeptical about whether these results will be replicated. So this study should be viewed as it is – provocative but needing to be replicated before concluding that we have gotten things wrong about fibromyalgia and nociplastic pain. No question, there is a low-grade inflammatory response in fibromyalgia, but it seems quite different than the inflammation seen in autoimmune disorders.”
- Fibromyalgia likely the result of autoimmune problems — ScienceDaily
- JCI – Passive transfer of fibromyalgia symptoms from patients to mice
- Fibromyalgia could be an autoimmune disorder, new research suggests | MDLinx
- Fibromyalgia | Arthritis | CDC
- SAA’s Virtual Seminar – Fall 2021 – SAA (spondylitis.org)
Spondylitis Association of America