A Molecular Revolution
We are in the midst of a molecular revolution. Instead of plucking out individual factors and studying them, researchers are ploughing through immense amounts of data to try and get at the molecular roots of illness. They’re using genetic, gene expression, metabolomic, proteomic or other data are trying to determine which genetic variations are present, which genes are being expressed abnormally, which metabolic products are being produced, which proteins are found in unusually high (or low) levels, etc.
Once that data is in pathway or other analyses are done to determine where the body is taking a hit. They often highlight specific genes, metabolites, or proteins which seem to play a particularly important role.
Over the last couple of years a Swedish research group has done a series of proteomic studies on women with chronic widespread pain/fibromyalgia. Theoretically, because proteins do the work in cells they should be very illuminating, but proteome analyses are complex, expensive and tricky and we don’t see too many of them.
The results have been illuminating.
Study #1 – Muscle Damage
The group’s exploration of the proteins in the trapezius muscle should put to rest any ideas that problems with muscle functioning are not present in FM. The six proteins that stood out suggested that an inflammatory process in the muscles in people with FM is putting them under stress, interfering with energy production and causing muscle damage. The fact that levels of those proteins were strongly associated with pain intensity indicated that they likely contributed to the muscle pain experienced in FM.
The muscle findings make sense given the voluminous list of studies finding issues with the muscles in FM including the muscle membranes (3 studies), a muscle reflex, increased lactate and glutamate levels, muscle activity, reduced ATP production, muscle oxygenation, muscle contractibility (2 studies), muscle strength, neuromuscular control, psychomotor retardation, etc. (That was just through 2010).
(Note that these findings suggest that the pain in FM is not simply the result of central sensitization; i.e. amped up pain-sensing processes in the brain and spinal cord; it is also being produced by the muscles.)
Freedom from Fibro Summit Encore Weekend – Watch Any Presentation
Watch any of the 40-plus presentations from Dr. Murphree’s Freedom from Fibro Summit for free this encore weekend. If exploring alternative health options is something for you – or if you just want to explore what’s out there – Dr. Murphree’s Summits provide a great overview of the possibilities this large field of medicine presents.
The Summit provides simple techniques to reduce pain and anxiety, provides updates on the latest research, diet options (one of which has helped me greatly), ways to boost energy, the latest on fibromyalgia research (my presentation), etc.
Click here to check out the encore weekend and here to see a prior blog on it.
Study #2 – Neuroinflammation
Just about every protein in the 2017 cerebrospinal fluid study pointed an arrow straight at neuroinflammation. The most important factor, insulin-like growth factor 2 (IGF2), is believed to trigger microglial cells – the key inflammation producers in the brain – to produce nerve pain.
Other proteins were associated with reduced anti-inflammatory activity, hypoxia (low oxygen levels), damaged glial cells, inflammatory brain disorders, neuronal damage in neurodegenerative disorders, reduced neuro-protection, etc. It was a witches’ brew of bad news for the brains of FM patients.
The study suggested that an inflamed, possibly hypoxic (low oxygen) brain was getting tweaked to produce pain and more pain; i.e. it agreed with a recent study which suggested that neuroinflammation is alive and well in FM.
The Plasma Study
A Swedish team has done three proteomic studies in three different compartments of FM – the muscles, the cerebral spinal fluid and the blood (plasma).
The muscle study suggested that an inflammatory process is creating problems with energy production and causing muscle damage. Other studies finding a multitude of problems in FM patients’ muscles back up the Swedish team’s findings.
The cerebral spinal fluid findings provided a witches’ brew of bad news. The signs of inflammation, low oxygen levels, damage glial cells and problems with neuronal protection all suggested neuroinflammation is alive and well in FM.
The plasma study findings mirrored those of the first two studies. Inflammation and problems with energy production were strongly indicated.
The three proteomic studies suggest that an inflammatory process affecting metabolic energy production may be widespread in fibromyalgia.
Similar findings occurring in chronic fatigue syndrome (ME/CFS) suggest ME/CFS and FM are, as suspected, closely related and that research efforts in one will likely benefit the other.
Pain and Rehabilitation Centre, Department of Medical and Health Sciences, Linköping University, Linköping, Sweden. Frontiers in Psychology: published: 29 November 2018 doi: 10.3389/fpsyg.2018.02400
The Swedish group’s most recent proteomic study – on the plasma – attempted to determine if proteins in the blood of people with CWP/FM were associated with the amount of pain they were in and whether they were experiencing anxiety, low mood, etc. (Being in chronic pain puts people at a much increased risk of having a mood disorder – go figure… Plasma is the fluid part of the blood which contains the white and red blood cells and platelets.)
The Pain Proteins
First they compared the proteins found in plasma from people with CWP/fibromyalgia and healthy controls. Then they determined whether the abnormally expressed (either high or low) proteins in the CWP/FM patients were associated with either increased pain intensity or mood issues. If the same protein had lower levels in people with less pain and higher levels in people with more pain, the protein was assumed to be associated with pain.
The results were intriguing, given previous studies suggesting that coagulation issues could impact ME/CFS/FM. Fibrinogen – a part of the blood coagulation cascade – was elevated. So was a substance, kinnenogen-1, which triggers the release of bradykinin – an inflammatory agent which does many things, including cause pain, and is involved in mast cell degranulation.
Lower levels of a broad-based anti-inflammatory, alpha-1-antitrypsin, that has been associated with fibromyalgia before suggested that the CWP/FM patients were failing to keep inflammation in check. The authors believed these three factors signaled an increase in inflammation.
Ceruloplasmin was the big surprise. A copper transporter, it’s never been associated with increased pain intensity but has been found to be elevated in FM. One of the group’s past studies found that several forms of it were associated with widespread pain.
The really exciting outcome, though, was the finding that most proteins associated with increased pain were involved in metabolism; i.e. energy production. Proteins involved in energy metabolism have showed up in two trapezius muscle studies, and this plasma study – suggesting that in the pain of fibromyalgia, energy production problems play a key role.
The Distress Proteins
Two tests of psychological distress indicated, as expected, that psychological distress (anxiety and depression) were elevated in the CWP/FM patients. We think of psychological states as being manifestations of mood, but they have a physiological overlay; i.e. changes in our physiology can contribute to mood changes and vice versa.
The study found that proteins involved in inflammation (complement) and iron metabolism were associated with increased levels of psychological distress.
Proteomic analyses are rare which makes it all the more encouraging that this Swedish team’s findings are broadly consistent with other kinds of analyses. A similar picture showing up in the muscles, brain and plasma of CWP/FM patients suggests that FM is probably a systemic inflammatory and metabolic disease. Inflammation was the high note – it was found in all three compartments of the body – while problems with energy metabolism were found in two of them, as well in the two muscle studies.
These studies suggest that at its molecular roots, fibromyalgia – a pain and fatigue-producing disorder which includes sleep, cognitive, gut and stimuli problems – looks quite a bit like chronic fatigue syndrome (ME/CFS) – a fatiguing and pain-producing disorder which also produces sleep, cognitive, gut and stimuli problems.
Neuroinflammation, energy production, small fiber neuropathy, central sensitization and micro-circulation problems appear to be present in both. Both diseases appear to feature failures in the anti-oxidant and anti-inflammatory systems. My guess is that orthostatic intolerance will at some point be confirmed in FM.
Jarred Younger has suggested that the difference may come down to the microglia being tweaked one way in FM and in a slightly different way in ME/CFS. However it turns out, at the molecular level, at least, a similar pattern is showing up in these two diseases and that’s good news for both of these severely underfunded diseases.
That suggests it’s a good idea to keep up with the research on both diseases, and that breakthroughs in one disease may benefit the other. Ron Tompkins’s deep exploration of the muscles in ME/CFS at the Open Medicine Foundation-funded ME/CFS Collaborative Research Center at Harvard, could, for instance, provide key insights that apply to both diseases. Similarly, the cascade of new pain drugs the NIH’s Heal Initiative will hopefully produce may be helpful in ME/CFS as well.
- Next up – Fibromyalgia – a mitochondrial disorder?
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Cort, do we have any idea how many people have both FM and CFS, or just one or the other?
I remember decades ago a dr I was seeing first told me I had FM years after I got CFS. At the time, I was so sick with CFS, FM didn’t matter to me at all.
Good question. The numbers on both vary – ME/CFS – from just under a million to 2.5 million and FM – 3 1/2 million to ten million.
I don’t know what percentages of each disease are co-morbid with each other though.
Thank you Cort and Happy Holidays as you folk say?. I will print this article out for my doc hope he is receptive, he believes in ME/CFS enough to put me on LDN 4 mg ( doesn’t help with pain but helps stress and emotional resilience for me) but not fibro. I just did a little cobweb sweeping for Christmas. Bad idea but my poor husband has driven 2 hours for food supplies, as well as making me a new bathroom so I don’t have to walk downstairs at night and also does a full time job working on computer from home he’s a champion. Now I’m in severe pain, can’t stay upright and muscles weak and shaking. I have terrible trouble with trapezius but worse with pyriformis and gluteus muscles. Thank you again, good luck with your fund raising I will contribute again next year.
Thanks Peach! I have high hopes that the Heal Initiative will bring good news in the form of more effective pain reducing drugs with fewer side effects over the next couple of years.
Hang in there!
I strongly believe they are two different conditions, and it is not possible to distinguish who has “both” until it is understood exactly what each of the two conditions is.
I believe FM is a dysfunction in muscle fascia and interstitial fluids, that people have a genetic vulnerability to. If you don’t have the genetic vulnerability, you won’t get FM. CFS is straight-out energy metabolism dysfunction, but one consequence of this dysfunction is elevated levels of many of the same toxins that accumulate in FM. The energy metabolism dysfunction in CFS probably has a genetic vulnerability component too.
Some very unlucky people could have both dysfunctions. But many people whose dysfunction is purely FM, not CFS, are misdiagnosed as having CFS as well, because the fascia adhesiveness greatly increases the effort required for movement, leading to genuine premature exhaustion. Chronic pain itself is exhausting, as is chronic inappropriate (involuntary) muscle tension.
Some people with CFS may be misdiagnosed as having FM as well, simply because the toxin elevation ends up causing symptoms like FM. But real FM involves the toxins causing lumps of adhered muscle tissue at vulnerable locations (the famous “tender points”). You might be in muscle pain from the toxins, but if you don’t have these palpable lumps of adhered muscle tissue, you don’t have FM.
Then again, even the label “FM” might officially mean something else, and we need a different label for the condition involving the adhered muscle tissue vulnerability. If, for example, FM actually means “heightened CNS”, which is what it has been taken to mean by many researchers, then it is about as useful as a “disease” label, as “headache” is. If you have a “headache”, you want to know what is causing it. If you have “FM” and this means “heightened CNS”, then again, the cause of it could be a number of different things. But one of the most likely causes is chronic REAL pain; failure to recognise this is gross dereliction by experts and researchers.
In most people with “FM”, the chronic real pain is from toxicity, adhered muscle tissue sticking and pinching, and lumps of adhered muscle tissue extremely sensitive (like a raw wound) to the pressures and tensions of attempted movement.
In people vulnerable to ME I strongly believe high levels of oxidative stress to be very bad for starting and maintaining the disease. Once ME starts I believe it generates copious amounts of oxidative stress, strongly helping to maintain the disease.
In people vulnerable to FM I also suspect it to be at least important too.
If so, people with either a big/major vulnerability to either ME or FM and at least a minor vulnerability to the other disease could have one disease trigger the other.
How do you feel about the importance of oxidative stress for increasing risk for FM in people vulnerable to it? And how do you feel about this mode of one disease triggering the other in those vulnerable?
It’s going to be interesting. Symptomatically I certainly fit the muscle sticking and pinching set. Then there are all the other symptoms – the orthostatic intolerance, sympathetic nervous system overdrive, cognitive issues that I wonder if are common to all forms of the diseases (or not??)
Thanks, Cort – you certainly “get it” when you refer to muscles “sticking and pinching”. I’d say you have FM, whether you have CFS as well, or not.
Dejurgen; yes I certainly believe that chronic stress is one of the triggers for FM. I understand CFS less, but it is probably a factor there too. How I think it constributes to the onset of FM, is simply that the stress results in inappropriate muscle tension, and the fascia with its proneness to “sticking”, does indeed get stuck, in the “muscle tense” position. The reason I still believe that a genetic vulnerability is a precondition, is that I know people who are basket-cases of chronic stress for years, who do not get FM. You can visibly see their tensed muscles, and they do experience pain from the constant tension, but they still have good limb range of mobility, no lumps of permanently adhered muscle tissue, and they respond to massage therapy. People with FM do not respond; the lumps and bands and so on refuse to resolve regardless of the skill of the therapist.
So I think that someone with CFS and the toxicity that accompanies it, will only get FM as well if they have the genetic vulnerability.
There may be coincident factors required in any case; in my own case and many others in these discussions, the FM started after an operation, an accident, an infection, or combinations of these things at the same time as chronic stress.
Protein is a serious major issue in Ehlers Danlos Syndrome in fact some researchers believe something is wrong with the Protein signaling…Fibro is another name Label for EDS there is no difference they are the same illness.They also believe this to be the cause mixed signaling
I mentioned some time back to Jarrod about EDS his response was he would look at Proteins so he knows proteins are involved in EDS I even said these were all the same illness from ME/CFS Fibro EDS just different name labels…He likely new Protein is tied to inflammation they go hand in hand
We could really use more proteomic studies. They are apparently the hardest and most expensive studies to do but if they’re done right they seem to present the clearest clues. Instead of scads of genes you get a few proteins – which do, after all, the work of the cells.
As I suspected, ceruloplasmin has a relation to oxidative stress. But rather then contributing to it, it seems to fight it. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3593134/
“In conclusion, our findings suggest that CP was an antioxidative biomarker which controls oxidative stress, whereas ferritin was a marker which may participate in the generation of oxidative stress.”
With CP equal to ceruloplasmin
“Non-ceruloplasmin copper, the free form, is a potent pro-oxidant than the protein bound copper.”
it seems that increased levels of ceruloplasmin bind and protect against the strong oxidative effect of free copper.
And thanks for reporting on “The fact that levels of those proteins were strongly associated with pain intensity indicated that they likely contributed to the muscle pain experienced in FM.” Let’s hope it start to finally get to doctors worldwide at more then a snails pace.
You made my day Cort ;-).
Ha, ceruloplasmin is elevated perhaps in an attempt to fight off oxidative stress and/or bind with copper.
Check this out from an endometriosis study
AIM: To compare patients with advanced stage endometriosis with control patients without endometriosis with respect to serum Copper (Cu) and Ceruloplasmin (Cp) levels and oxidative stress markers in order to evaluate the importance of these parameters in the pathogenesis of endometriosis.
RESULTS: Serum TOS, OSI, Cu, Cp, TG, TC, LDL were significantly higher, whereas TAS, PON-1 activity and HDL were significantly lower, in women with advanced-stage endometriosis than in control groups.
CONCLUSIONS: Cu and Cp appear to be associated with the etiopathogenesis of and oxidative stress in endometriosis.
It also plays an important role in removing excess iron deposits. Such deposits can be caused by neutralizing damaged heme (due to ROS) or due to damaged RBC (due to ROS) falling apart and releasing there heme.
“When ceruloplasmin is unavailable, transport of iron out of the body’s tissues is impaired. The resulting iron accumulation damages cells in those tissues, leading to neurological dysfunction, and the other health problems seen in aceruloplasminemia.”
“may experience involuntary muscle contractions (dystonia) of the head and neck, resulting in repetitive movements and contortions. Other involuntary movements may also occur, such as rhythmic shaking (tremors), jerking movements (chorea), eyelid twitching (blepharospasm), and grimacing. Affected individuals may also have difficulty with coordination (ataxia). Some develop psychiatric problems and a decline of intellectual function (dementia)”
“Affected individuals also have changes in the light-sensitive tissue at the back of the eye (retina) caused by excess iron.”
-> someone asked a related question on this in another recent blog, don’t remind which one.
Cort, with reference to these new findings, I thought you would be interested in reading this section of a book which has some relevance. Scroll down to the section on Neurophysiological aspects of muscle/TrPs. Also further down under Muscle pain.
This has been a channel of research for years, routinely belittled by the know-it-all “CNS primary cause” charlatans who dominate the institutions. But it is the RIGHT channel of research!
In my own case, I have proven that these toxic adhesions in the muscle fascia are resolvable by de-toxing, diet, the right kind of hands-on therapies, intelligent supplementation (guided by HTMA), hydration, the right kind of movement therapies, and the right kind of exercise (lots, at low intensity). Everything is explainable by the very simple hypothesis of “toxic overload”, adhesiveness, and “flushing it out” if you can. The toxic overload is everywhere, but the interstitial spaces and the muscle fascia are the unique, probably genetically-originated problem in people with FM. The great majority of people are lucky enough to not have this vulnerability, hence the skepticism about toxins, stress, etc (because “thousands of people live this way and it doesn’t do US any harm” therefore it’s all in YOUR “head”)
“…Note that these findings suggest that the pain in FM is not simply the result of central sensitization; i.e. amped up pain-sensing processes in the brain and spinal cord; it is also being produced by the muscles…”
Prime importance! I have been suggesting for a long time that the CNS being sensitized is an EFFECT of the real, chronic pain in muscle tissue, NOT “the cause”. CNS’s can get sensitized in prisoners of totalitarian regimes being subjected to regular torture, too. Why is this so hard for the mainstream medical research profession to grasp?
Philip, I agree with a lot of what you say except that there is a difference between chronic myofascial pain and chronic myofascial pain wth FM. FM perpetuates CMP whereas CMP alone can be treated with the therapies you mentioned. I believe in my case the FM started early in life and a chronic sustained fight and flight response results in chronically contractured muscles. I was able to exercise until not long after puberty when the hormones went awry. After that impossible. The works by Devin Starlanyl are worth looking at.
Thanks for the link Tricia. I, like Phil, do not understand why the myofascial findings are not followed up more. I think part of it is just very limited research funding which leaves lots of key areas unexplored.
I searched for NIH funded fibromyalgia studies – of the twelve I found six focused on behavioral aspects of FM. (:()
Thanks, Tricia. Yes, I agree. CMP exists in its own right. CMP and FM are not “interchangeable”, but FM involves CMP of the worst kind, which does not resolve with hands-on therapies.
CMP without FM, will resolve quickly. In my case, I only started to improve after 20 years of fruitless experimenting with self-helps and therapies, only getting worse. I believe I improved about 20% in the first year, and 20% in each year thereafter, “diminishing” not “straight-line” improvement (that is, five years later, I am still not 100% better). I believe what I had is full-blown FM, which I have discovered how to resolve very slowly with a lot of time and expense.
Absolutely, chronic stress with inappropriate muscle tension is involved in getting full-blown FM. I know others who have chronic stress and muscle tension, and they certainly get myofascial pain but it resolves with massage, and they do not get adhesions resulting in limited limb range of movement. So I am sure there are other factors, probably genetic vulnerability.
I found Starlanyl’s book on Trigger Point therapy and FM and MPS, very helpful, but I think it could be confusing to less knowledgeable people, and not helpful to those with full FM who will NOT respond to trigger point therapy, it will just be a whole lot of pain for no gain. Here is my review of the book, on Amazon:
The one thing I have changed my mind about since that review, is that it might be possible to have MPS but not be vulnerable to full-blown, intractable FM.
Very hard to believe that the periphery is not quite involved….
I’m just seeing this thread, so I wonder if you will see my question… do you mind sharing more specifically what has been working for you in terms of detoxing? When you say “the right kind of….” what do you mean? Many thanks, Jane
Interesting. I am meeting with a Thrombosis specialist to find out why I suddenly got a blood clot. They have no idea why this occurred given I have no family history. Wondering if my FM could be causing it.
Interesting; me too. Unexplained DVT’s. But in my case I started getting them after I’d improved considerably from my FM. It could be unrelated; a lot of people get unexplained DVT’s. I am resigned to being on anti-coagulant medication for life. Hoping for the best.
Have you thought of changing your gut bacteria makeup…this might be the game changer. I made my own FMT (fecal transplant) capsules and have recovered from ME/CFS for 8 months so far. Skype me at username KnowApr if you would like to know what I did. I share my story online, but Healthrising doesn’t allow links.
“Have you thought of changing your gut bacteria makeup…this might be the game changer. I made my own FMT (fecal transplant) capsules and have recovered from ME/CFS for 8 months so far. Skype me at username KnowApr if you would like to know what I did. I share my story online, but Healthrising doesn’t allow links.”
Yes I tried. What were your symptoms and were they triggered or made worse by sugars and starches in your diet? I would be curious of your approach?
I have discovered via both Ubiome testing ( and Excel download) that I have a large amount of Klebsiella Pn which I confirmed with the GI-Map test which roughly agreed. As it has increased ( being antibiotic resistant), my symptoms have dramatically worsened. I have done 3 FMTs via enema which did dramatically alter my ubiota ( as seen in Ubiome report and in Excel) but did nothing for the Klebsiella which I suspect may be in my small intestines as an overgrowth as Klebsiella SIBO. Klebsiella is notoriously a near superbug with Resistance to many antibiotics and evolves quickly via plasmid exchange.
I’ve also seen some other less than friendly bacteria that seem suspicious including in much lower quantities, C-Diff, Citrobactor freundii, and P. mirabilis. All these have the potential to trigger via molecular mimicry, a autoimmune like reaction.
Have you checked your ubiota using Ubiome or the GI-Map test? Before and after?
looking at wikipedia I see this Klebsiella has a lot of potential to form biofilms. Biofilms appear much harder to remove from the body by both antibiotics and other means to get them out such as competition from other species.
I haven’t tried it yet, but Issie has written on ways to better target those biofilms. She claims it helps her but it’s no easy process. Googling Issie and biofilm and healthrising should get you there.
Ugh, I had a post all written up, and then hit the wrong button. Let’s see if I can get that thought back. I’m a 53 year old female, with fibro and moderate ME. Lately I have been having severe memory lapses, and I’ve even found myself getting lost in town, places I’ve been before are completely unfamiliar, even after someone tells me that I was just there last week (like a Dr. appointment.)
My spelling and grammar are getting worse, and I’m having more trouble finding words. My hands shake badly, making typing difficult.
I have not had a PET scan done yet, but my neurologist is leaning towards Early Onset Alzheimer’s. Have you seen any other cases that correlate the two, or am I just “lucky”?
I can live with pain, I can live with exhaustion, I can even live with basic brain fog. I cannot live with forgetting my entire life, standing on a street corner and crying.
Is there any kind of treatment or therapy that would help? If things get too bad, I have a bottle of sleeping pills on standby, just in case.
I would get a comprehensive neuropsychological assessment from an experienced neuropsychologist, probably at a university center, before I hit those sleeping pills (have some here myself LOL, chronic pain’s a bitch). At best, it might specify diagnosis, functional deficits, and possible brain areas that are affected, at worst, it could provide a baseline of cognitive functioning that you could use to monitor your condition/progress. Good luck.
Thanks for the input.
I would be very wary about an early onset Alzheimer’s diagnosis. The cognitive issues you’re relaying are very common in FM and ME/CFS. Getting lost is town – not remembering where your home is – I’ve heard that related MANY times in these diseases. The chance that your neurologist has any conception of what’s happening in ME/CFS is very, very low…
I wouldn’t put too much stock in that diagnosis – far more likely you’re suffering from significant brain fog.
Yep, at times I could not remember my own name if people asked. Even when trying for 5 minutes, I failed. Scaling back on working did wonders for that. That is one symptom gone.
Hello Yocheved, The other replies to your post ring true for me too. Yes, it is scary to have memory issues, and scary for a neurologist to suggest that diagnosis. There are studies that show that the memory issues of ME/CFS/Fibro are not the same as Alzheimer’s, and your issues sound like ME/Fibro — but I’m not a doctor. Please (A) go to a different specialist such as a neuropsychologist, (or neuropsychiatrist) for a neuropsychological assessment, as the retired psychologist above advised. Also please (B) look up the medicines you’ve been taking to find it any of them can compromise your memory or mental functioning. I was taking at least 2, 3, maybe 4 medicines that were linked to memory and impaired mental functioning (as well as increased risk of Alzheimer’s). I still have fibro fog and fatigue-triggered fog, but it is now way better than when I was taking diphenhydramine and amytriptylene. A big study by Dr. Shelly Gray, Univ. of Wash. linked a lot of popular — legal(!) — drugs with increased risk of Alzheimer’s, and it’s gotten people talking, and finding good substitutes that don’t fry our brains so much! There’s also a lot of anecdotal reporting about people being foggier on days when they take their decongestant, for instance. Unfortunately, it sounds like you got a scary diagnosis from somebody who is not well versed in ME/Fibro issues. Please keep going til you find someone who knows better. It’s worth it.
Happy to hear your fundraising is going well. I was able to contribute this year with gratitude.
Just a question on pain medication & FM. What to try & what seems to work?
Really, if the big three (Lyrica, Cymbalta, Milnacipran) aren’t working or even if they are – definitely try low dose naltrexone – https://www.healthrising.org/treating-chronic-fatigue-syndrome/drugs/low-dose-naltrexone-ldn-fibromyalgia-chronic-fatigue-syndrom/ and if you can get it, cannabis and CBD oil. We have blogs on both CBD oil and cannabis coming up.
Opioids are often not helpful if used continuously but can be a huge help for flares…
Also meditation and calming exercises – can certainly be helpful. If you can afford massage – that can relieve muscle pain.
Sleep hygiene is important.
Keep in mind the HEAL NIH campaign should come up with a number of new, better, pain killers over the next couple of years.