by Anushri Bhattacharya
The disease associated with abnormal processing of pain perception in humans, also known as Fibromyalgia is not such a rare disease after all, as it affects around 2%-8% of the general population (or 1 in 40 people) . Around 2% of the adult population in the US which is roughly around 4 million adults in the US fall victim to Fibromyalgia. Although the exact cause of fibromyalgia is not known, until now doctors and researchers have believed that this disease is due to a neurological disorder wherein the patient’s brain or spinal cord processes pain in an abnormal manner, which is why patients with fibromyalgia suffer from chronic widespread pain even during the absence of any physical injury (internal or external). However, last year (August 2021) a research study conducted by researchers at the King’s College London, showed that fibromyalgia may be a result of autoimmune problems rather than the currently held view, that it is caused in the brain.
If a person suffers from Fibromyalgia , then they experience chronic musculoskeletal pain and tenderness all over their body even when they are not sick or injured ; hence these patients are more sensitive to pain compared to others. Besides chronic pain, some common symptoms that accompany fibromyalgia are constant fatigue, sleep disorders, persistent headaches, body stiffness, tingling sensation/numbness. Sometimes, patients with fibromyalgia also face problems with concentration and memory, and may also have anxiety or depression. As mentioned previously, the exact cause is still unknown but some risk-factors related to fibromyalgia include age (usually affects middle-aged people 25-55 years old) , sex (more prevalent in women by 80%), and pre-existing conditions (like Lupus which is an autoimmune disease where one’s body attacks itself; or Rheumatoid arthritis increases an individual’s chance of developing fibromyalgia).
As we all know, the immune system is our body’s own ‘defence system’ against pathogens or foreign organisms that may invade our body and cause diseases. Previously done studies have shown that there is a correlation between patients with fibromyalgia and the immune system, more specifically these studies have shown that developing fibromyalgia may weaken our body’s immune system. Firstly, in various studies and experiments it has been observed that patients with fibromyalgia show an increased WBC (leukocyte) count along with cytokines which are chemical proteins secreted by helper T-cells (lymphocytic leukocytes), and these cytokines help regulate the immune system’s response to an infection or inflammation. This observation suggests that there is a correlation between developing fibromyalgia and the immune system response. Secondly, further studies have also shown that this condition restricts blood flow to the brain’s pain centre or ‘pain matrix’ (comprising of the anterior cingulate cortex, thalamus and insula) of the brain that consistently responds to painful stimuli. This in turn affects the neuron receptors and eventually leads to increased pain and stress levels which in turn weakens the brain’s immune system.
Moreover, fibromyalgia also results in an imbalance of hormones in the patient’s body, for instance, this condition causes a steep decline in cortisol (stress hormone) levels in the body, which in turn results in the increase in oestrogen levels and consequently, progestin (artificial progesterone in females) level decreases. This kind of fluctuation in hormone levels weakens the immune system as well, as the B-lymphocytes of the immune system are regulated by hormones like oestrogen and testosterone. Both specific and non-specific immune systems are influenced by hormones. Thus, dysregulation of hormone levels may lead to immune-mediated diseases including autoimmune diseases. Autoimmune disease is when the body’s immune system ‘malfunctions’, and attacks its own body instead of protecting it and this includes healthy cells and tissues of the body being destroyed/killed by the immune system.
The previously found correlation between fibromyalgia and the immune system led a research team of scientists from the University College London in collaboration with the University of Liverpool to conduct an experiment , and they now suggest that symptoms of fibromyalgia may occur when an individual’s antibodies increase the activity of pain-sensing neurons . In the experiment , the researchers chose the independent variable as the presence of antibodies from patients with fibromyalgia syndrome (FMS) or healthy patients; and the dependent variable was the change in level of sensitivity to unpleasant stimuli / pain. This study had 3 groups - first, a group of mice who were injected with fibromyalgia antibodies, this was the treatment group. Secondly, the control group comprised of mice who were injected with antibodies from healthy people who didn't have fibromyalgia; and the 3rd group comprised of mice who were injected with a serum from FMS patients but with their antibodies removed (sham group). It was observed that, in the treatment group, the mice with fibromyalgia antibodies rapidly developed an increased-sensitivity to cold and pressure (which demonstrate pain/ unpleasant stimuli here), and also displayed reduced movement, and grip strength ; thus became weaker. In contrast, the control group and sham group (with serum) mice remained unaffected. A second observation was also made; the treatment group mice with antibodies from an FMS patient , recovered right after the antibodies in the mice’s body died (as antibodies have a short lifespan of 2-3 weeks in this case , and die at the end of immune response in patients body) .
These observations thus led to the result that antibodies from a patient suffering from fibromyalgia syndrome are a major contributor to this disease fibromyalgia. This finding also suggests that therapies in which a patient’s antibody levels in the bloodstream are reduced , may prove to be an effective treatment for FMS. The results concluded that antibodies from FMS patients appear to sensitize nociceptors, which are nerves in the derma that send pain signals to the brain when they detect extremes of temperature and pressure or noxious chemicals. Moreover, adding to the reliability of the study, the people with fibromyalgia from whom the antibodies were taken were from the UK and Sweden, and patients from both these countries showed similar results.
In conclusion, with this experiment the team scientists and researchers now plan on further investigating factors that affect the antibodies of an FMS patient that induces fibromyalgia symptoms in the mice; and then perhaps conduct this experiment on humans to test the efficiency. Although these experiments were done in mice, they show some significant correlation of fibromyalgia which may result from immune system disorders or autoimmune disease. This may in turn help in improving therapeutic methods for treating fibromyalgia and probably even improved blood-testing methods of diagnosing this condition in the future.
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