What is the science saying about fibromyalgia?
Fibromyalgia is diagnosed based on signs and symptoms rather than a test.
There is no test.
For some people this presents a challenge because of a need for ‘concrete’ proof.
There is a feeling that it has to be proved to others because there is nothing to see. You can’t see pain or tiredness or any other inner experiences.
Despite being invisible to the naked eye, they exist as you know.
The stress of trying to persuade people that they really do exist contributes to the suffering.
And then the fight for support in the different ways that are necessary: health, financial, social, occupational etc.
As such, fibromyalgia is an umbrella term and when you fit a certain criteria, this is the term used.
There is absolutely nothing wrong with that approach as long as you receive the support and guidance you then need to move forward.
In my experience of helping many people with fibromyalgia, the diagnosis or labelling can sometimes help and sometimes hinder until it is understood and the path ahead is illuminated.
Many people understandably turn to the internet. This is risky. It is easy to find stories that are unhelpful, and a range of dubious treatment offerings and promises.
None of those stories are you. You are unique on your own path with your own needs to be met.
If you have been reading Fibromyalgia 28 each day, you will have come across the Royal College of Physicians diagnosis and clinical guidelines on Day 2.
Science
I have structured this in bullet points to highlight some key areas rather than a large body of text.
I hope that works for you, so that it gets straight to the point.
There have been many studies looking at fibromyalgia in different ways: e.g./ basic science, treatments, drugs.
For today I am focusing on basic science.
In no particular order of importance. And this is not a comprehensive review. It is a selection.
Fibromyalgia: Genetics and epigenetics insights may provide the basis for the development of diagnostic biomarkers (2019)
- Genetic factors are possibly responsible for up to 50% of the disease susceptibility
- Gene-environmental interaction has been proposed to trigger epigenetic changes (genes are turned on and off by environmental factors, i.e. your lifestyle, situations)
- In particular, genes implicated in stress, DNA repair, and the autonomic system (flight-fright-freeze)
- Paper here
r.s.
In my experience, listening to people who I work with, stress is a major player in the evolving situation. Typically this is chronic stress that is gradually having an impact. There are many reasons and they are individual to the person. Looking at these and how you can create new habits and responses is an important part of creating the conditions to get better.
Adrenergic dysfunction in patients with myalgic encephalomyelitis/chronic fatigue syndrome and fibromyalgia: A systematic review and meta-analysis (2024)
- Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM) are co-morbid disorders with overlapping symptoms
- A meta-analysis of 37 studies, encompassing 543 ME/CFS patients and 651 FM patients, compared with 747 and 447 healthy controls, respectively
- Studies investigating peripheral biological markers of adrenergic function in patients with ME/CFS or FM compared to healthy controls at baseline were included
- Higher baseline adrenaline levels and atypical responses to exercise in ME/CFS indicate that sympathetic dysfunction, underscored by adrenergic abnormalities, is more involved in the pathophysiology of ME/CFS rather than FM
- FM patients showed no significant differences at baseline but exhibited a diminished adrenaline response to exercise
- This meta-analysis highlighted differences between ME/CFS and FM with regards to the sympathetic nervous system
- Paper here
Passive transfer of fibromyalgia symptoms from patients to mice (2021)
- Authors of this study identified antibodies from patients with FMS that produce FMS in mice
- IgG from FMS patients produced sensory hypersensitivity by sensitising nociceptive neurons in mice
- IgG purified from the serum of individual FMS patients and healthy control (HC) subjects was given to female mice by (intraperitoneal) injection for 4 consecutive days
- Because IgG antibodies taken from patients with FMS, but not controls, stimulated certain cells to become activated in a way known to mediate chronic pain, these findings reveal a role for IgG in the pathophysiology of FMS
- Paper here
Hyperexcitable C nociceptors in fibromyalgia (2014)
- To test the hypothesis that peripheral C nociceptor function may be abnormal in fibromyalgia and that C nociceptor dysfunction may contribute to the symptoms
- They recorded the activity of C nociceptors of 30 female patients meeting criteria for fibromyalgia and compared them with recordings from 17 female patients with small-fibre neuropathy and 9 female controls
- Findings: the majority of fibromyalgia patients have abnormal C nociceptors
- Authors conclusion: abnormal peripheral C nociceptor ongoing activity and increased mechanical sensitivity could contribute to the pain and tenderness suffered by people with fibromyalgia
- Paper here
r.s.
Words such as ‘abnormal’ concern me (philosophically and practically) because people can take this as ‘I am abnormal’. Instead, it maybe more useful to think of these as possible changes in the way human biology works as a means to survive and protect. Nociceptors are there as part of a threat detection system, not in isolation to other systems. It is useful for this change because it creates awareness that you need to do something, that you have need to be met. One of the main issues for people is the challenge of understanding what these needs are and how to meet them. This is what we do in part and in detail and specifically with Pain Coaching. This exemplifies why understanding your pain and symptoms is a key start point.
Small fibre pathology in patients with fibromyalgia syndrome (2013)
- A case-control study investigating the function and morphology of small nerve fibres in 25 people with fibromyalgia
- The results were compared with data from 10 patients with depression without pain and with healthy control subjects matched for age and gender
- People with fibromyalgia syndrome had increased neuropathic pain questionnaire scores compared with people with depression and with control subjects
- A reduction in dermal unmyelinated nerve fibre bundles was found in skin samples of people with fibromyalgia syndrome
- Impaired small fibre function in patients with fibromyalgia syndrome, pointing towards neuropathic type pain in fibromyalgia
- Compared with control subjects, people with fibromyalgia but not those with depression had impaired small fibre function, with increased cold and warm detection thresholds in quantitative sensory testing
- Paper here
The Influence of Pro-inflammatory Cytokines and Genetic Variants in the Development of Fibromyalgia: A Traditional Review (2020)
- The objective of this review article is to provide a brief overview of the pro-inflammatory cytokines commonly associated with fibromyalgia, as well as to look into the genes that have shown some level of involvement in the development of fibromyalgia and its symptomatology
- Pro-inflammatory cytokines could be essential in the pathophysiology of fibromyalgia
- It is not unusual to see autoimmune co-morbidities in people diagnosed with fibromyalgia
- Some studies have shown a positive association between serum and cerebrospinal fluid levels of cytokines and pain severity, while others have shown little to no evidence in the correlation between them
- Due to the strong association of genetic variants with chronic pain disorders, pain-related gene polymorphisms are now considered to be key in the mechanism behind the pathogenesis of fibromyalgia
- It has been well documented in multiple studies that inheritance of pain-related genes contributes up to 50% in the development of chronic pain
- The aetiology of fibromyalgia is most likely the outcome of multiple interactions between psychological, neurobiological, environmental triggers and genetic susceptibility, the latter in particular due to the observed, high familial predisposition in fibromyalgia
- Paper here
r.s.
Humans are complex. There are always a range of factors and variables. Chronic pain and conditions that feature chronic pain are complex. There is no absolute separation of these factors, and certainly trying to separate body and mind takes you down the wrong path. In fact, I would go so far to say that there is no mind-body connection either. Just one experience of what it is like to be you, in the world you experience in that moment. This is key because in terms of helping you move forward, to ease your pain and symptoms, you focus on your aspirations and goals and the steps to take in that direction, beginning with this one now. You feel pain and other symptoms, not your body parts or your mind, and neither is it in your mind as imagined. Together we look at the specific ways you can transform your experiences for the better.
And just because you may have the genes, or there is a family history of chronic pain, it does not mean you have to follow that route. Your route is different to your ancestors and the way you live. You can choose to live the best way you can in terms of what you do and how you do it. This is under your control.
I hope this information is helpful.
The depth into which people like to go to understand the science varies. You don’t need to get a science degree!
However, knowing that many body systems work together to generate your experiences in a complex and dynamic way, is a good start. It is a good foundation to understand the many different ways you can ease your pain and symptoms and improve your life.
Thank you very much.
r.s.
If you have just joined, we started on Day 1 here.
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🎥 Pain in the Person ~ two short films: https://youtu.be/zidJbZHEGzM
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