Cause/Trigger list
A. HYPOTHESES ("THEORIES") (pathogenesis; etiology)
A.1. CSS, central sensitization syndrome, central sensitivity syndrome (pain only)
The Science of Fibromyalgia (CSS)
Inflammation of the glia as cause or effect?
A.2. Autoimmune (e.g. - perhaps! - biomarkers cytokines (e.g. IL-6) / chemokines)
It’s completely open whether biomarkers such as these have to do with the causes or rather with effects / consequences…
Newest study: Goebel et al 2021: https://www.jci.org/articles/view/144201 FMS-IgG causes “sensitivity to pressure and cold” and reduces “movement grip strength” in mice, AI-treatment helped.
A.3. SFN = Small Fiber Neuropathy (pain)
2021 Advances in the Management of Small Fiber Neuropathy - PubMed
2020 Fibromyalgia syndrome-A laser-evoked potentials study unsupportive of small nerve fibre involvement - PubMed unsupportive
2019 Current Diagnosis and Treatment of Painful Small Fiber Neuropathy - PubMed
2018 Fibromyalgia and small fiber neuropathy: the plot thickens! - PubMed
2015 The Role and Importance of Small Fiber Neuropathy in Fibromyalgia Pain - PubMed
2014 Small nerve fiber involvement in patients referred for fibromyalgia - PubMed subset
A.4. AV-shunt-disorder
Biotech Research 2013/2016: Hand nerves increased in FM (was: New Research) - #35 by JayCS
A.5. Neuroendocrine
Psychological stress and fibromyalgia: a review of the evidence suggesting a neuroendocrine link
A.6. Mitochondria/ATP/Q10
Many studies about Q10 & FM mention this connection as a cause (or biomarker?).
View held by Bodo Kuklinski, Rostock.
A.7. Underlying issues like chronic pain, sleep disorder, low GABA, other diseases (e.g. SPD)
Due to @Sheila_W 's idea: Fibromyalgia References: Causes, symptoms, treatments (to be intertwined) - #21 by JayCS
When people occasionally seem to have been healed or find other underlying issues
Chronic pain idea: Cfs - #6 by SK1
GABA improves 10+ of my symptoms
Now I’ve got my pains down, it often feels like that a sleep disorder is the main part of my fibro.
Stiff Person’s Disorder (cf. @Freedom): Good news! I don’t have Stiff Person’s Syndrome
A.8. genetic predisposition: twins; translocator protein gene
Occurs more in some families, also in twins. 15% increased likelihood in twins https://www.painscale.com/article/7-possible-causes-triggering-fibromyalgia-pain
translocator protein gene, Kosek 2016: The translocator protein gene is associated with symptom severity and cerebral pain processing in fibromyalgia - PubMed
translocator protein gene Fanton 2021 (with Kosek) The translocator protein gene is associated with endogenous pain modulation and the balance between glutamate and GABA in fibromyalgia and healthy subjects: a multimodal neuroimaging study - PubMed TSPO is important for pain, so meds shd target that.
A.9. (Not accepted in any way: Extinction memory damage, EMD
New hypothesis on the origin of FMS and related diseases → The EMD hypothesis)
A.10. (Unclear idea: HPV vaccination syndrome)
HPV vaccination syndrome: A clinical mirage, or a new tragic fibromyalgia model - PubMed 2018.
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B. BIOMARKERS ('tests' for FMS, more validation needed)
B.1. Proinflammatory/neuroinflammatory cytokines (IL-6, IL-8) / chemokines / mast cells...
cf. EpicGenetics new blood test for Fibromyalgia - #18 by JayCS
Fibro doesn’t cause inflammation in the normal sense, but recent research has shown some neuroinflammatory markers (Des).
Neuroinflammation in Fibromyalgia
Study on Fibromyalgia and cytokines" 2014
Current evidence suggests that cytokines and especially chemokines may have a role in the pathogenesis of this syndrome. Cytokines are small soluble factors that work as immune system messengers. They can be classified as pro-inflammatory and anti-inflammatory cytokines. Chemokines are a special kind of pro-inflammatory cytokines that guide the movement of circulating mononuclear cells to the injured side. Some pro-inflammatory cytokine levels (i.e. IL-1RA, IL-6, and IL-8) and, recently, some chemokines’ levels have been found to be increased in patients with fibromyalgia. Thus, herein we review the current knowledge regarding the role of cytokines in fibromyalgia patients and their possible clinical relevance.
“Low-grade chronic inflammation mediated by mast cells in fibromyalgia: role of IL-37”: Mast cells are involved in FM by releasing proinflammatory cytokines, chemokines, chemical mediators, and PGD2. Ah, I’d heard of mast cells before.
Interesting to me cos of my whole-body cryotherapy is this one: Serial whole-body cryotherapy in fibromyalgia is effective and alters cytokine profiles" - very new: Adv Rheumatol. 2021 Jan 13;61(1):3.
Plasma Cytokine Levels in Fibromyalgia and Their Response to 15 Weeks of Progressive Resistance Exercise or Relaxation Therapy - PubMed 2018, done 2010, exercise made no difference.
Comparison of the Levels of Pro-Inflammatory Cytokines Released in the Vastus Lateralis Muscle of Patients with Fibromyalgia and Healthy Controls during Contractions of the Quadriceps Muscle--A Microdialysis Study - PubMed Christidis 2015 no correlation with muscle pain.
Also wondering if GABA and its derivatives are related to this, cf. the updated GABA-thread GABA & derivatives, gabapentin (Neurontin), pregabalin (Lyrica), phenibut, baclofen, picamilon
B.2. Salivary Biomarkers
Application of Salivary Biomarkers in the Diagnosis of Fibromyalgia - PubMed
B.3. Muscle pressure
Evidence that Muscle Pressure is Almost Three Times Higher than Expected in the Trapezius Muscle Opens a Pathway to Identify Fibromyalgia Pain with a Definitive Test
https://www.jrheum.org/content/jrheum/early/2020/12/10/jrheum.191068.full.pdf
https://doi.org/10.3899/jrheum.191068
https://frankleavitt.weebly.com
Painfully High Muscle Pressures in Fibromyalgia Put Old Paradigm to the Test - Health Rising Criticism that the biomarker doesn’t explain much and treatments such as Mg and HBOT (oxygen) to improve consequent muscle oxygen is not mentioned in the study.
(My answer here: Pardon Our Interruption)
B.4. Less gut bacteria & serum: molecular biomarkers and altered glutamate metabolism
Gut microbiome and serum metabolome analyses identify molecular biomarkers and altered glutamate metabolism in fibromyalgia - PubMed 2019:
We found that the diversity of bacteria is reduced in fibromyalgia patients. The abundance of the Bifidobacterium and Eubacterium genera (bacteria participating in the metabolism of neurotransmitters in the host) in these patients was significantly reduced. The serum metabolome analysis revealed altered levels of glutamate and serine, suggesting changes in neurotransmitter metabolism. The combined serum metabolomics and gut microbiome datasets showed a certain degree of correlation, reflecting the effect of the microbiome on metabolic activity. We also examined the microbiome and serum metabolites, cytokines and miRNAs as potential sources of molecular biomarkers of fibromyalgia.
Conclusions: Our results show that the microbiome analysis provides more significant biomarkers than the other techniques employed in the work. Gut microbiome analysis combined with serum metabolomics can shed new light onto the pathogenesis of fibromyalgia. We provide a list of bacteria whose abundance changes in this disease and propose several molecules as potential biomarkers that can be used to evaluate the current diagnostic criteria.
B.5 Hormones: serotonin, noradrenaline, dopamine, cortisol...
Hormones “Research has found people with fibromyalgia have abnormally low levels of the hormones serotonin, noradrenaline and dopamine in their brains.”
“Some researchers have also suggested that changes in the levels of some other hormones, such as cortisol, which is released when the body is under stress, may contribute to fibromyalgia.” (Des)
B.6 protein backbones and pyridine-carboxylic acids using vibrational spectroscopy
Hackshaw 2019 et al. Metabolic fingerprinting for diagnosis of fibromyalgia and other rheumatologic disorders - PubMed
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C. Possible general STARTING POINTS
C.1. Virus Infections:
such as flu, swine flu, Epstein-Barr-Virus (EBV).
But the connection is only slight:
Real studies are >30 years old and don’t really see much of a connection
1987: The "chronic, active Epstein-Barr virus infection" syndrome and primary fibromyalgia - PubMed
1989: The chronic fatigue syndrome: definition, current studies and lessons for fibromyalgia research - PubMed
These are the newest connections made:
EBV Is The Possible Cause Of Fibromyalgia, Research - Fibromyalgia Resources
Epstein Barr Virus and Fibromyalgia Connected - Wellness Resources
(interesting to me, as I’m using glutamate and serotonin increasing amino acids like GABA, whilst catecholamines are also something Trudy Scott recommends amino acids for.)
C.2. Psychological:
Trauma, stress, panic disorder,
bipolar disorder (The Co-Morbidity between Bipolar and Panic Disorder in Fibromyalgia Syndrome - PubMed)
C.3. Functional - intolerances, deficiencies:
10 causes: 1) gluten, 2) candida, 3) thyroid, 4) mg/D3/B12, 5) SIBO/leaky gut, 6) mycotoxins, 7) mercury fillings, (8) adrenal fatigue as result, 9) MTHFR mutations (B6, B12, folinic acid nec.)), 10) glutathione deficiency
10 Causes of Fibromyalgia Your Doctor May Not Know About = https://www.prohealth.com/library/10-causes-of-fibromyalgia-your-doctor-doesnt-know-about-32779
Mercury: Can mercury in amalgam fillings cause fibromyalgia? (from Plasmaboy)
SIBO
https://bodyecology.com/articles/the-hidden-cause-of-fibromyalgia-a-natural-treatment-for-pain/
Fructose (& fructans) decreasing serotonin
Fibromyalgia Syndrome: A Metabolic Approach Grounded in Biochemistry for the Remission of Symptoms = Fibromyalgia Syndrome: A Metabolic Approach Grounded in Biochemistry for the Remission of Symptoms - PubMed (2017): Improving the low serotonin=5-HT levels in FMS by reducing fructose (= some carbs) and increasing trytophan in food intake, instead of taking (L-)tryptophan(=Trp), might alleviate and also be better for the microbiota, interrupting a vicious circle.
“The core of the hypothesis is that a gastrointestinal malabsorption has a central role as a primarily cause of FMS and that it is mainly due to fructose. This way, the core of the treatment is the contrast of Trp malabsorption, favoring its normal absorption.”
“the hypothesis springs from the observation of marked worsening of pain and stiffness in a FMS patient after a breakfast of fruit, marmalade, and rye bread…”
" Although fructose malabsorption plays a primarily role, it appears reasonable that it is not the sole cause of FMS, mostly because the incidence of fructose malabsorption (28) is well greater than the FMS ones (4). Maybe, it can just be considered the main risk factor for FMS."
“Theoretically, the most efficacious management would be a fructose free, fructan restricted, lactose free, sorbitol free, aspartame free, low sucrose diet, together with proper Trp intake.”
" Excessive amount of fructose is very easy to be reached, as modern Western diets are rich in fructose due to industrial food containing high fructose corn syrup (HFCS), fresh fruit that naturally contains fructose, honey, soft drink, and beverages containing HFCS and saccharose (27, 28, 34, 47). In addition, wheat and the most of cereals, the most of legumes and many vegetables contain fructans (28), contributing to increase the total amount of ingested fructose.
Lactose might have the same consequences of fructose in the gut, especially if the enzyme lactase is deficient."
" Trp supplements (like Trp tablets) are not suggested in any way, as their intake has potential for important side effects by themselves or due to the interaction with serotonergic drugs, up to life-threatening effects related to serotonin syndrome (48).
Suggested food containing Trp are: meat, eggs, fish, rice, potatoes, dark chocolate, and walnuts."
"A further note concerns monosodium glutamate (MSG) and aspartame: their withdrawal from the diet is suggested too.
“the mean rate of 5-HT synthesis is significantly lower in women.”
“The association between decreased serum Trp concentrations and sugar (fructose and lactose) malabsorption was observed in experimental studies significant only in women.”
“Trp can only be transported across the blood–brain barrier in its free form by the competitive and non-specific l-type amino acid transporter” (16). “Trp reaches the brain when ingested food is rich in this amino acid and not excessively rich in other large neutral amino acid (LNAAs), that could compete with it” (15).
D. Causing LONG-TERM FLARES (weeks or months)
http://www.healthcentral.com/chronic-pain/c/5949/151398/fibromyalgia/
found by @Sheila_W here 10 Causes of Fibro Flares
Flares/flare-ups can take hours, days, months or years, can start 48h later than the trigger.
Journals, keeping a log, diary, blog can help identify triggers/causes.
- D.1. Illness, common cold…
- D.2. injury,
- D.3. long-term stress (often hard to identify)
- D.4. allergies, incl. seasonal,
- D.5. sleep problems
- D.6. vicious circles of sleep, stomach/gut problems, etc.
- D.7. hormonal changes (menstrual cycles, menopause, etc.)
- D.8. treatment changes
- D.9. meds/supps/herbs, even without changing them.
e.g. Statins may be a nocebo! https://jamanetwork.com/journals/jama/fullarticle/2779202 - D.10. traveling:
Travel often disrupts lifestyle factors like sleep, nutrition, environmental conditions and activity levels, which can bring on a flare-up. NAD+ for Fibromyalgia - NAD Amino Acid Fights Chronic Fatigue
E. Causing SHORT-TERM FLARES (hours or days)
E.1. Physicallly overdoing it/overexertion:
carrying on physical activities altho we are over our limits/capacities
E.2. Mental Stress
social: socializing/peopling
E.3. Weather, esp. temperature, esp. changes
Cold, hot, sunny, extremes, changes, wind, humidity, seasonal allergies, rainy
E.4. sensitivies: light, noise, smells
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E.5. changes in sleep routine
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Version 2021-08-11 = August 11th