No, it’s not in your head!
This post presents the popular science of my PhD thesis, aiming to shed light on fibromyalgia (FM) and challenge the outdated views associated with it.
Up until recently FM patients faced stigma by clinicians who would believe that the patients’ symptoms were merely psychological or all in their head. While it is true that pain is both a sensorial and emotional experience, recent studies have proven that the nervous system, which is responsible for sending bidirectional messages amongst the brain, spinal cord and peripheral organs, is altered in FM. Additionally, studies have found alterations in patients’ skin, muscle, and blood of FM patients. These findings shifted the focus of research towards understanding how these peripheral changes outside the brain could explain the pain in FM.
One of the main key findings of this thesis is that injecting antibodies (proteins that normally defend our body) from FM patients into mice can cause symptoms that mimic the ones experienced by FM patients, such as increased sensitivity to cold temperature and touch, reduced nerve fibers in the skin, and decreased overall activity. These antibodies lost their original function to help protect our body from pathogens and are instead detrimental for the body, interacting with satellite glial cells (SGCs), which support neurons in the dorsal root ganglia, which is a key area for pain transmission. This interaction correlates with disease severity in FM patients.
FM is an heterogenous disease, and beyond its cardinal symptoms, comorbidities can vary greatly from person to person. Therefore, patients need to be stratified and receive individualized treatment. Besides autoimmunity, this thesis also further explores changes in lipids (fatty substances responsible for a variety of functions in our body). In FM, changes in lysophosphatidylcholine, triglycerides, sphingomyelin, and lysophosphatidic acid can play a role in chronic pain in FM, by direct- or indirectly interacting with pain neurons.
Overall, this thesis has challenged the outdated view of FM and contributed to its understanding, opening new possibilities for developing treatments for this challenging disease. The thesis can be found here.
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