Living with Fibromyalgia: The Guide

What is fibromyalgia, in plain English?

Fibromyalgia is a long term condition in which the nervous system amplifies ordinary input from the body, so that pressure and movement hurt far more than they should, usually alongside heavy fatigue, sleep that leaves you no better off, and a head that won’t hold a thought.

There’s no blood test and no scan for it. Somebody makes the call by looking at how widespread the pain is, how heavy the fatigue, the sleep and the fog have been, and whether it’s run for at least three months. And if you were ever examined by somebody pressing a thumb into a list of spots, that’s gone. The current criteria don’t contain a tender point count at all [1].

Two things follow from how it’s classified now. It isn’t what’s left over once everything else has been crossed off, so the diagnosis still stands when you’ve got other conditions alongside it [1]. And the World Health Organization files it as a pain condition in its own right rather than as a symptom of something nobody has found yet [2]. That’s the difference between a condition and an unfinished search.

Is fibromyalgia a real condition?

Fibromyalgia is a real condition with measurable biology behind it, and it stopped being filed under medically unexplained a long time ago [3].

Press on somebody with fibromyalgia and it takes noticeably less pressure before it hurts, which was measured back in the early nineties and has held up ever since [4][5]. It isn’t only pressure either, and it isn’t confined to the tender spots the old diagnosis revolved around, because test it properly and heat and cold come out the same way, in more than one part of the body [6][7]. That last part is what rules out the muscles. A problem in the muscle doesn’t change how cold feels.

Put somebody in a scanner and hurt them, and the networks that handle it work harder, with less help from the circuits that normally settle things back down [8].

What none of that gives you is a test you can wave at anybody. It’s measured across groups rather than in one person, and some of it may belong to long term pain generally rather than to fibromyalgia in particular [9]. The gap between real and provable inside a ten minute appointment is where nearly all of the dismissal happens.

If my scans and bloods are normal, where is the pain coming from?

Your scans and bloods come back normal because they’re built to find damage and inflammation, and fibromyalgia is neither. They answered their question honestly enough. It just wasn’t the question you walked in with.

They’re still worth doing, because they catch the things that do show up, and inflammatory arthritis and thyroid disease are worth getting out of the way [10]. Nothing in a routine workup was ever designed to measure how a nervous system is handling what it’s being sent, though, and that’s where this one lives [8].

There is something physical underneath it that the standard tests go nowhere near. Around half of people with fibromyalgia turn out to have changes in the smallest nerve fibres in the skin and the eye, the ones that carry temperature and the first hint that something is wrong [11][12]. Before anybody gets excited, that figure swings enormously depending on which study you read, and the people who have those changes report much the same pain as the people who don’t [12][13][14]. So it’s a real finding, it isn’t a diagnosis, and nobody is going to offer you the biopsy.

Which brings up the blood test you may have seen advertised. It tells people with fibromyalgia apart from healthy people fairly well, then falls over against lupus and rheumatoid arthritis, which is the only comparison a clinic actually needs [15]. No blood marker anybody has looked at performs well enough to diagnose this [16].

What is central sensitisation, and does it mean it is in my head?

Central sensitisation is your nervous system turning its own volume up, and no, it doesn’t mean the pain is in your head. Central here means the spinal cord and the brain, which is where pain gets produced in everybody, including the pain from a broken leg.

Two things get measured. Repeated pressure stacks up into more pain than it should instead of settling down, and pain in one place does less to quieten pain somewhere else, which is the body’s own damping system failing to pull its weight. Both turn up in fibromyalgia, moderately rather than dramatically [17].

There are limits to the idea though, and they’re worth knowing before anyone sells it to you as an explanation for everything. Central sensitisation is a construct built out of several tests that mostly agree with one another rather than something anybody can point at on a scan, and plenty of people with fibromyalgia come out normal on the individual pieces of it [18][19].

None of which makes it psychological. A nervous system amplifying a real signal from real tissue is biology doing something, not biology making something up.

Is fibromyalgia an autoimmune or inflammatory disease?

Fibromyalgia isn’t an autoimmune or an inflammatory disease, and the largest piece of evidence anybody has argues against it fairly hard.

The genetics were read across 2.5 million people. If this were autoimmune, the inherited risk ought to sit in the immune system, and it doesn’t. Nothing turned up in the stretch of DNA where autoimmune conditions usually announce themselves, and nothing in the immune cells either. What came out instead was the brain and nothing but the brain [20]. The authors are careful with that and so should we be, because their sample was mostly of European ancestry, and another group using a looser definition of who counts as having fibromyalgia did find an immune signal [20].

Inflammation doesn’t rescue the idea either. A few inflammatory markers do run slightly higher on average, and the review that pooled them said plainly that not one of them is specific to fibromyalgia [16]. Nothing there you could diagnose anybody with.

Then there’s the mouse study, which is the one most likely to get reported at you badly. Antibodies taken from the blood of people with fibromyalgia were injected into mice, and the mice became sensitive to pressure and cold and lost grip strength. Take the same blood, strip the antibodies out of it, and nothing happens, which is what lifts it from interesting to causal [21].

Three things get left off when that study is quoted at you. It’s mice. The effect wore off within two to three weeks. And it didn’t work by inflaming anything, because not one of the inflammatory messengers measured in the blood moved and the spinal cord showed no reaction at all. The only thing that stirred was the support cells the antibodies had attached themselves to, right where they landed [21]. So even in the version of events where antibodies cause the pain, inflammation isn’t the route it takes.

In people, a subgroup does carry raised antibodies against the support cells that wrap the sensory nerves, and that subgroup reports worse symptoms. People waiting for a knee replacement, who are in plenty of genuine pain, show nothing of the sort, so it isn’t simply a marker of hurting [22]. A subgroup, though. Not a diagnosis, not a test, and not yet a treatment.

So if somebody tells you fibromyalgia is an autoimmune disease, they’re ahead of the evidence. If somebody tells you there’s nothing immune about it whatsoever, so are they.

Is fibromyalgia genetic?

Fibromyalgia runs in families, and there’s no single gene behind it and nothing you can go and be tested for.

Having a sibling with fibromyalgia puts your own risk at roughly 13 times everybody else’s [23]. Measure the common inherited variation directly though, and it accounts for only about a tenth of why one person develops it and another doesn’t [20]. Genes load the dice. They don’t deal the hand.

That same study turned up 26 separate places in the DNA that each nudge the risk along a little, and the genes involved were overwhelmingly ones that do their work in the brain and the nervous system rather than in muscle [20]. Which is a decent argument in itself about what sort of condition this is.

One last thing, if you’re a man with fibromyalgia, or simply tired of hearing it called a women’s condition. Genetically it came out indistinguishable between men and women, so the lopsidedness in the research is a shortage of men in the data rather than a different disease [20].

How is fibromyalgia diagnosed?

Fibromyalgia is diagnosed by scoring what you report against a checklist, and no blood test, scan or examination forms any part of it. Two numbers come out. One counts how many areas of your body hurt. The other scores how bad the fatigue, the unrefreshing sleep and the trouble thinking have been. Clear the thresholds on both, with everything sitting at a similar level for three months, and you meet the criteria [25].

Which is why two clinicians can see the same person and come to different answers. Three thousand adults in American primary care were scored against the criteria and then asked whether a doctor had ever told them they had fibromyalgia, and the two lists barely overlapped. Only a third of those carrying the diagnosis met the criteria, and only a third of those who met the criteria had ever been given it [26].

Why is there no blood test for fibromyalgia?

There’s no blood test for fibromyalgia, including the one you can buy. That test measures signalling chemicals released by immune cells, and against healthy people it performs well, picking out 93 in every 100 of those with fibromyalgia and correctly clearing 89 in every 100 of those without [15].

Healthy people aren’t the comparison that matters. Nobody arrives at a rheumatology clinic wondering whether they’re well. They arrive wondering whether this is lupus. Run the same test against people who actually have lupus or rheumatoid arthritis and it clears only 71 and 69 in every 100 of them [15]. Pool every other candidate marker anybody has measured in blood and the verdict is the same: plenty differ between groups on average, not one is specific to fibromyalgia [16].

What happened to the tender points?

The tender point examination was dropped from the criteria in 2010, and what it turned out to be measuring is the reason why. The old test was a thumb pressed at 4 kg into eighteen named spots, with pain required at eleven of them [27]. Across 177 adults at two general practices in north west England, the count climbed with depression, fatigue and poor sleep whether or not the person was in any pain, and 60 per cent of those who did have chronic widespread pain scored under eleven [28]. So it was missing a good share of the people it was built to find.

It leaned female too, because women are more sensitive to that kind of pressure. Under the tender point criteria fibromyalgia came out at 13.7 women to every man, under the 2010 version 4.8 to one, and under the 2011 self report version 2.3 to one [25]. A fair amount of this looking like a women’s condition was the examination.

Who diagnoses fibromyalgia in the UK, and how do I get referred?

In the UK your GP is the way in, and it’s usually somebody in a hospital clinic who ends up naming it. Of 85 people in Scotland with the diagnosis, 34 per cent had been given it in primary care and 54 per cent in secondary care, most of those by a rheumatologist [29].

The NHS tells you to start with your GP, says plainly that there’s no specific test, and describes an examination and blood tests to rule other things out [30]. NICE leaves how hard to look for another cause to a judgement taken with you rather than to a fixed list [31]. So referral is the usual route rather than the backstop, and asking which criteria you’re being assessed against is a perfectly fair question. Among 1,622 doctors across eight countries, 45 per cent had never heard of them [24].

What gets ruled out before fibromyalgia is given?

What gets ruled out are the conditions that cause the same widespread pain and do show up on a test. Polymyalgia rheumatica, inflammatory arthritis of the spine, coeliac disease, low vitamin D and a short list of neurological conditions are the usual ones [32]. Your medication gets checked too, and that’s the one people forget, because statins cause muscle pain in 2 to 10 per cent of those taking them [32]. What isn’t on the list is a Lyme test, unless you’ve actually had Lyme disease [32].

Then it stops, because fibromyalgia isn’t what’s left over once the list runs out. Finding something else doesn’t cancel it, and the NHS says so in as many words: if you’re found to have another condition, you could still have fibromyalgia as well [30].

Is a fibromyalgia diagnosis even worth having?

A fibromyalgia diagnosis is worth having for what it stops. The rolling investigation ends, and six symptoms stop being chased as six unrelated problems. What it doesn’t appear to come with is relief.

In Scotland, 85 people with the diagnosis were set against 110 who met the criteria and had never been given it. On symptom impact, quality of life and satisfaction with life the two groups came out the same, and the ones holding the diagnosis reported the worst experiences of care in the study [29].

Nor does the name arrive with any teaching attached. Of 1,626 people in Norway who already had it, one in three still didn’t understand why they were in pain, and more than half didn’t know what they could do to get better [33]. Which is more or less the gap this page exists to close.

How often do fibromyalgia and hypermobility turn up together?

Fibromyalgia and joint hypermobility overlap a lot, and how much depends almost entirely on who gets counted and where. Eleven studies have been pulled together on this, nine of them setting a fibromyalgia group against a group without it, and hypermobile joints turned up in anywhere from 8 to 64 of every 100 people with fibromyalgia depending on which one you read [34].

That spread is definition rather than disagreement. Every one of those studies used criteria written before the 2017 rewrite, and the threshold for counting as hypermobile got applied the same way to a twenty year old as to a sixty year old. The review’s own authors say figures taken with the current criteria could come out very different [34].

Going the other way round, in a specialist clinic that assessed people against the current hypermobility criteria and had a doctor confirm the fibromyalgia, 56 in every 100 had both and 24 had hypermobility on its own [35]. Across the wider literature on hypermobile adults, fibromyalgia shows up in anywhere from 5 to 41 of every 100 [36].

The catch sits under all of it. Those numbers come out of clinics, and people reach specialist clinics by being complicated. Nobody has taken a general adult population, examined everybody and reported how the two actually sit together. So the overlap is real, and nobody can tell you its true size.

Could my fibromyalgia actually be hypermobility?

Usually it’s both rather than one instead of the other, and finding hypermobility underneath a fibromyalgia diagnosis doesn’t cancel the diagnosis. The two labels answer different questions. Fibromyalgia is a judgement about how widespread the pain is and how heavy the fatigue, the sleep and the fog have been. Hypermobility is a statement about your connective tissue and how far your joints travel. You can meet both at once, and plenty of people do.

They aren’t one condition wearing two names though. Seventy two women with the hypermobile type of Ehlers-Danlos were set against sixty nine with fibromyalgia and sixty five with rheumatoid arthritis, and physical function came out much the same in the hypermobile and the fibromyalgia groups, while the fibromyalgia group reported more severe pain, more interference with daily life and more distress tied to it [37]. Both groups were struggling. They weren’t struggling in the same shape.

Hypermobility has been sitting on the published list of things worth considering in anybody with widespread pain for years, under its older names [32]. So the question worth taking into an appointment isn’t which of the two you’ve got. It’s whether anybody has checked the second one.

How would I know if I am hypermobile?

The usual first check is the Beighton score, a quick count of how far five joints travel, and there’s a version of it you can do yourself at the kitchen table. It scores nine things: each little finger bending back on itself, each thumb folding down towards the forearm, each elbow and each knee going past straight, and your palms flat on the floor with your knees locked [38].

Where the line falls depends on your age. The current criteria put it at six or more out of nine before puberty, five or more from puberty up to fifty, and four or more after that [39]. That sliding scale exists because the score drops steadily as you get older, and by seventy hardly anybody scores above two [40]. So being told you aren’t hypermobile at forty five says very little about what you were at fifteen, which is why there are also five questions about what you used to be able to do. Two yes answers out of those five picks up around 80 to 85 of every 100 hypermobile people on its own [39].

What the test leaves out matters more. It covers fingers, thumbs, elbows, knees and the spine, and that’s the whole list [38]. Shoulders, hips, jaw and ankles are nowhere in it, and the score doesn’t track how loose any of them are [40]. Two people with a genetically confirmed connective tissue condition scored three and four on it [40]. And the floor touch is the weakest item of the lot, because tight hamstrings stop most hypermobile people doing it at all [40].

A high score tells you something. A low one clears you of very little.

Does it change what helps, if I am both?

Being both changes the order of the work more than the work itself, and the trial that would settle it hasn’t been run. No fibromyalgia study has split people by whether they’re hypermobile and then checked whether the treatment landed any differently.

What has been looked at is whether hypermobile people do badly in ordinary pain rehabilitation, and the answer is more interesting than yes or no. In a Swedish registry, 406 people with Ehlers-Danlos or hypermobility spectrum disorder went through interdisciplinary pain rehabilitation alongside thousands with other chronic pain conditions, and everybody improved. On quality of life, mental health and vitality the hypermobile group did as well as anyone else, while on pain, on physical function and on how much the pain got in the way, the group with spinal pain improved more than they did [41]. Hold that loosely, because the groups started from different places, which the authors point out themselves, and only four in ten of the hypermobile group were still answering a year later [41]. Turning up was never the problem. Of 335 people in an American pain programme, 60 were hypermobile, and they enrolled, attended and graduated at rates no different from everybody else, though that one picked hypermobility out of diagnostic codes rather than by examining anyone [42].

The reason we change the order is the signal. Laxer tissue blurs the information coming out of a joint before it ever reaches the brain, so the brain is working from a worse picture of where that joint actually is, and a worse picture makes for a worse decision about what to do next. Load a system that isn’t sure where it is and you get exactly what walks into our studios: gripping, bracing, holding everything slightly too tight all day, and far more fatigue than the activity accounts for. So the sensory and control work goes in front of the loading rather than instead of it.

The evidence for that is thin and points the right way. Of the four hypermobility trials that measured how accurately people could sense where a joint was, three found it improved with training [43]. Pool all the controlled work on conservative treatment and you get eleven studies, three of which showed a real advantage over no treatment at all, on joint position sense, muscle endurance, pain, physical function and standing balance [44]. Every one of the eleven had exercise at its centre, most stopped measuring the day treatment finished, and the review calls the overall evidence weak [44].

On safety, which is the question we get asked most: across ten rehabilitation studies in Ehlers-Danlos covering 330 people, exactly one non-serious adverse event was put down to the treatment [43]. The reviewers won’t call that a safety finding and they’re right not to, because there are too few studies and they measure too many different things [43]. The best single trial on the pile ran sixteen weeks of heavy shoulder strengthening in a hundred people with hypermobile, painful shoulders, and there wasn’t one serious adverse event in either arm. More muscle soreness and more headaches in the heavier group, and two people who stopped because of them [45]. Closest to the actual question, a study of adolescents with fibromyalgia compared those with hypermobile joints against those without and still backed the same neuromuscular and exercise work for both, with the group too small to be certain about it [46].

So nothing here says be careful with you. It says start where the signal is, and expect sore rather than damaged.

Why does nobody check?

Nobody checks because examining your joints isn’t part of a fibromyalgia workup, and there’s nothing in the system to force the issue. There’s no blood test for hypermobile Ehlers-Danlos, no scan and no gene, so the whole thing rests on somebody deciding to look [39]. Inside a ten minute appointment about widespread pain, that decision doesn’t get made.

The gap has been measured, once, and in a small way. Sixty three people carrying a diagnosis of fibromyalgia, ME/CFS or both were examined properly. Fifty one met the older criteria for symptomatic hypermobility and eleven met the 2017 criteria for hypermobile Ehlers-Danlos, and of everybody who turned out to have symptomatic hypermobility, fewer than one in four had ever been told [47]. The authors are careful that this is a small study with a smaller control group, and their conclusion is that recognition has to improve rather than that a precise share is being missed [47].

What it costs is years. Among 505 adults who did eventually get a hypermobile Ehlers-Danlos diagnosis, the run to it averaged about ten years and roughly sixteen clinicians, and the number of clinicians halved the moment the diagnosis existed [48]. More than half were diagnosed by a geneticist in the end, and one in twenty by a GP [48]. That’s a survey of people who got there, so it describes the route rather than the odds.

The naming doesn’t help either. The criteria were rewritten in 2017, and the newer label for the commonest version of this, hypermobility spectrum disorder, has since been used more often as a loose description than as a formal diagnosis, with a standard tool for making it still outstanding [49]. The NHS page a GP is most likely to point you at still runs under the older name, joint hypermobility syndrome [50].

None of that is anybody being lazy. It’s a condition with no test, a name that moved, symptoms that arrive one specialty at a time, and an examination nobody has been prompted to do.

What do I do with this if I think it applies to me?

Score yourself first and take the number in with you, because a filled in answer is harder to wave away than a question. There’s a version of the Beighton score drawn as line pictures and built to be done at home, and put against a clinician who didn’t know the answers, in 50 adults, it caught 87 of every 100 the clinician scored as hypermobile and correctly cleared 99 of every 100 who weren’t [38]. Add the five questions about what you could do when you were younger, because what was true at fifteen still counts [39].

Then ask. The NHS says a GP will usually check your joints using the Beighton scoring system, may send you for a blood test or an X-ray to rule other things out, and can refer you on to physiotherapy, occupational therapy or podiatry [50]. That’s what the service says it does. Whether it happens inside your ten minutes is a different question, and walking in with a score already written down is the thing most likely to move it along.

Keep the expectations level about what the assessment actually gets you. There’s no medication for hypermobility, no test that confirms it, and nothing that arrives attached to the word. What it gets you is a reason for the pattern you’ve been living inside, and a better place to start from than being told to stretch.

What is the difference between fibromyalgia and ME/CFS?

Fibromyalgia and ME/CFS are separate diagnoses covering a great deal of the same ground, and which one gets written down often comes down to which symptom you led with. Fibromyalgia is scored on how widespread the pain is and how heavy the fatigue, the unrefreshing sleep and the fog have been [25]. ME/CFS turns on a different cluster, heavy fatigue, sleep that doesn’t restore you and difficulty recovering after exertion, and it’s that last one the criteria insist on [51]. So one of them requires that you hurt in a lot of places and the other requires that exertion sets you back. Somebody who does both can clear both, and plenty do.

There isn’t one set of ME/CFS criteria either, which is where a good deal of the confusion comes from rather than from the conditions themselves. Three sets are in common use, all three require that symptoms get worse after exertion, and how much the two diagnoses appear to overlap shifts depending on which set the clinic in front of you happens to be working from [51].

The symptom everybody reaches for as the dividing line is the crash after exertion, and it divides them less cleanly than you’d want. Pool the studies that put people with one or the other through a single bout of exercise and measured their pain afterwards, 15 studies covering 306 people against 292 healthy controls, and pain rose more in both groups than in the controls [52]. A crash after activity tells you something real is happening. It doesn’t tell you which of the two you’ve got, and there’s a section further down this page on fatigue, fog and the crash where that gets taken apart properly.

What turns on the answer is smaller than it looks. The two names route you to different clinics and different leaflets, and the work in front of you overlaps heavily either way. The one thing worth getting straight is whether exertion reliably sets you back a day or two later, because that changes how anything active has to be built, whichever word ends up on the letter.

Can you have fibromyalgia and an autoimmune condition at the same time?

You can have fibromyalgia and an autoimmune condition at the same time, and in rheumatology clinics a sizeable minority do. Whether fibromyalgia is itself autoimmune is settled further up this page, and the answer there was no. This is the other question, and this one has numbers.

Of 316 people with lupus scored against the fibromyalgia criteria at a clinic visit in one American centre, 17 in every 100 met them [53]. Across several Italian centres, 267 people with Sjögren’s disease were scored the same way and 30 in every 100 met them [54]. People reach specialist clinics by being complicated, so read those as what a rheumatologist sees rather than as your own odds.

What matters is what the second diagnosis does to the measurement of the first. Most disease activity scores mix two things together: what the inflammation is doing, and what you report feeling. Fibromyalgia pushes the reported half up and leaves the inflamed half exactly where it was. In that Sjögren’s group, the score built from the person’s own account of pain, dryness and fatigue came out higher when fibromyalgia was present, while the score the clinician builds from organ involvement sat at the same level in both groups [54]. Same measured disease activity, worse number. Steroid use was higher in the fibromyalgia group too, about three times the odds once age and disease duration were accounted for [54]. That’s an association rather than proof anybody was overtreated, and it’s the shape you’d expect if they were.

The second label also lands badly, which is worth saying out loud. Of 1,269 people with autoimmune rheumatic disease surveyed through patient organisations, a quarter had been given a fibromyalgia diagnosis as well, and more than half of those doubted it, with one in five believing something else explained their symptoms better [55]. That’s a self selected survey of people motivated enough to answer one, so it tells you how the diagnosis gets received rather than how often it’s wrong. The useful sentence in the appointment isn’t that your lupus is flaring. It’s that the half of the score you fill in has a second cause, and that treating the inflammation harder won’t reach it.

Is long COVID the same thing as fibromyalgia?

Long COVID and fibromyalgia aren’t the same thing, and on symptoms alone they’re genuinely hard to tell apart, which is a fact about the definitions rather than about you. Both capture fatigue, sleep that doesn’t refresh, trouble thinking and pain in several places at once. Apply the fibromyalgia criteria to people with long COVID and a fair number will meet them, because the criteria were built to be met by exactly that pattern.

That has been done. Of 198 adults in Israel who’d been in hospital with COVID and had no fibromyalgia diagnosis beforehand, phoned about five months after they went home, 15 in every 100 met the fibromyalgia criteria, and among the women it was 26 in every 100 [56]. Fatigue, unrefreshing sleep and cognitive trouble were all more common than the pain itself. There was no uninfected comparison group, so what that gives you is how many met the criteria afterwards, not how many met them because of the infection.

Nobody has run the study that would answer the causal question for fibromyalgia, and the review that went looking says the literature is too fragmented to pool, with screening questionnaires, widespread pain and the full criteria all treated as interchangeable when they aren’t [57]. The nearest controlled work measured ME/CFS instead, and it disagrees with itself in a way that’s worth understanding. One study followed 11,785 people from the point of infection against 1,439 who were never infected, and the infected group went on to develop ME/CFS at about three times the rate [58]. Another followed 4,738 people who’d all turned up acutely unwell, split only by whether their COVID test came back positive, and found no difference at all across twelve months [59]. The comparison group is the whole argument. Set a post infection group against well people and the infection looks like the cause. Set it against people who were ill with something else and the something else does just as much work.

So if your widespread pain started after an infection and has stayed for months, the fibromyalgia criteria will probably fit you, and meeting them describes where you are rather than explaining how you got there. The practical difference between the two labels is mostly which service you end up in.

Where do POTS and MCAS fit in?

POTS and MCAS sit alongside fibromyalgia rather than replacing it, and they’re also the two labels on this page most likely to have been handed out, or refused, on a basis nobody wrote down. They aren’t the same kind of problem, so take them separately.

POTS has a short, measurable definition. Lie down, stand up, and if your heart rate climbs by at least 30 beats a minute within ten minutes of standing, without your blood pressure dropping, and that’s been going on for at least three months, that’s POTS [60]. The same position statement advises against running a tilt table as routine, so standing is the test, and it costs a blood pressure cuff and ten minutes.

Nobody has stood up a group of people with fibromyalgia and counted. Going the other way round there are figures: pool 19 studies and 8,268 people with POTS and 22 in every 100 also carried a fibromyalgia diagnosis, with joint hypermobility at 31 in 100 in the same pooled group [61]. Almost all of that comes from specialist clinics and much of it is self reported, and the authors say plainly that the reliability of the whole pile is low [61]. So the overlap is real and the size of it isn’t established, which by now will sound familiar.

MCAS is the harder one, and the difficulty is in the criteria rather than in the people being assessed. Nobody has measured the chemicals mast cells release in a group of people with fibromyalgia, so there’s no figure to give you at all. What has been measured is how far the answer moves when you change the rule. In 100 young people with POTS, 2 met the strictest published criteria, 37 met a middle version and 87 met the loosest, clinical one [62]. Same hundred people, three answers, and not one of them produced the blood result the strictest criteria ask for [62]. Hold that study at arm’s length too, because its own authors flag that one of them helped write the criteria being tested [62].

So hold an MCAS label loosely in both directions. Being given one off a symptom list isn’t the same as it having been measured, and being refused one because a single blood test came back normal isn’t the same as not having it. POTS is the one worth actually chasing, because the test is cheap, the answer is a number, and what follows from it is different from anything on a fibromyalgia plan.

Why do so many of us turn out to be autistic or ADHD?

Autism and ADHD do turn up more often around chronic widespread pain than in the general population, and almost everything that’s actually been counted was counted in hypermobility rather than in fibromyalgia. That distinction matters here, because the section above is about how much hypermobility sits underneath a fibromyalgia diagnosis without anybody noticing.

The hypermobility figures are the sturdier ones. Of 201 children seen at a Swedish paediatric department for hypermobility, 16 in every 100 had a confirmed ADHD diagnosis against 5.8 in every 100 of all children in the same area, and autism ran at 7.2 against 2.6 [63]. Looked at from the other end in adults, 199 autistic people examined against 419 community controls came out with roughly three times the odds of hypermobile joints, and about five times once those joints were also causing symptoms [64].

In fibromyalgia itself the direct work is a good deal thinner. On ADHD there’s one clinic study worth having: 78 women with fibromyalgia in Turkey assessed by a psychiatrist alongside 54 healthy volunteers, ADHD at 29.5 per cent against 7.4 [65]. On autism there’s nothing of that kind, only questionnaires, and the best of them says so itself. 260 people with fibromyalgia scored higher than 139 controls on an autistic traits questionnaire, and the authors had no way of knowing which of them were actually autistic [66]. Nobody has counted.

Three explanations are on the table and they aren’t exclusive. Measurement is the first: trouble concentrating, poor sleep, sensory sensitivity and fatigue all score on both sides, so a fibromyalgia symptom set pushes an autism or ADHD screening score up without anything else being true. Shared ground is the second, and that’s where the hypermobility findings sit. The third has nothing to do with biology at all. Both diagnoses get missed in women for decades, and a woman who has already had to fight for one assessment knows how to ask for the next one. That last one is what we see rather than a published finding, and we’d rather label it than slip it past you.

What a diagnosis gets you here isn’t a different pain. It’s a different account of why the pacing advice keeps failing. A plan that assumes you’ll remember it, a programme built on a steady weekly rhythm, a gym with strip lighting and three conversations going on at once: all harder than they look if you’re autistic or you have ADHD, and none of it anywhere in the fibromyalgia literature. Worth pursuing if you want it. It won’t change the fibromyalgia.

Could this be perimenopause instead?

Perimenopause produces widespread aching, broken sleep, fatigue and trouble thinking, so it belongs on the list of things worth ruling in before fibromyalgia gets settled on, and for a lot of women in their forties both are happening at once. The pain isn’t a minor feature of it either. Pool 16 studies and 5,836 women going through the transition and 71 in every 100 reported musculoskeletal pain, with the odds of it running about 60 per cent higher than in women who hadn’t started [67].

What separates the two is what perimenopause brings that fibromyalgia doesn’t. A cycle that’s changed in length, timing or heaviness. Hot flushes and night sweats arriving on their own schedule rather than tracking what you did the day before. And an end, eventually, which fibromyalgia doesn’t have.

The part worth knowing before you go in is that there’s no blood test to ask for, and that’s deliberate rather than an oversight. NICE says to identify perimenopause without laboratory tests in otherwise healthy people aged 45 and over who have menopause associated symptoms, going on recently started hot flushes and night sweats plus any change in the cycle, and it names six tests not to use at all in that age group [68]. A hormone level is only suggested between 40 and 45, or under 40 [68]. So if you’re 47 and you’ve been told your bloods came back normal so it can’t be the menopause, that isn’t what the guideline says.

How often one of these gets mistaken for the other has never been measured, in either direction. Nobody has counted how many times pain, fatigue or fog got put down to the wrong one, which is a gap in the literature rather than a gap in your notes, and it means nobody can tell you the odds that yours was.

So the move isn’t to pick one. It’s to get the perimenopause question asked properly, because unlike most things on this page it has a clear answer and a short list of things that follow from it, and then to look at what’s left over. What to do about the hormonal side, and whether hormone treatment does anything for the pain, is a separate question with its own section further down.

Widespread pain, and why it moves

Nobody has shown that fibromyalgia pain migrates around the body within one person, which is quite something given how often you’ll hear it said. Hardly anybody has measured the same person’s pain map twice. Of 42 studies that collected more than one body drawing, 38 were snapshots and only two followed a single individual over time [69]. So the most repeated claim about this condition rests on what people report rather than on anything anybody has tracked.

What has been mapped is where it sits. In digital pain drawings the commonest places were the neck and upper back, at around three quarters of people, with the lower back just behind [70]. Neck, shoulders and back come up far more often than anywhere else, and the jaw, chest and abdomen sit well down the list.

And it’s genuinely spread out rather than merely scoring as spread out. Of 5,011 people meeting the 2011 criteria, almost every single one had pain in at least four of the five body regions [71].

The nearest thing to an answer on movement comes from a different condition entirely. Twelve weeks of repeated drawings in people with spinal referred pain showed the size of the painful area changing while the shape of it stayed much the same [72]. That isn’t fibromyalgia, and it’s as close as anybody has got.

Why does my skin hurt to be touched?

Skin that hurts to be touched is a real and measurable finding in fibromyalgia, and it turns up in a minority rather than in everybody. The word for pain from something that shouldn’t hurt, a shirt sleeve or a light stroke across the forearm, is allodynia.

When it gets tested with a brush rather than asked about, the numbers come out lower than you’d expect. Of 87 people put through a full sensory examination of the hand, about a third had either brush pain or an outsized response to a pinprick [73], and a second group of 76 landed in much the same place [74].

What’s close to universal is pressure. Press on people with fibromyalgia and they report pain at lower force than controls, at essentially every site tested rather than only the sore ones [5]. Reviewers counting up what actually gets measured found pressure in 84 studies and brush type testing in 10 [75], which is worth knowing on its own. The thing everybody talks about is the thing least often measured.

One finding does come with a comparison group. After a brushstroke, three quarters of people with fibromyalgia still felt something afterwards, against a quarter of controls [76]. The sensation outlasts the touch. Why that happens is a mechanism question, and it gets taken apart further down this page.

Headaches and migraine

Migraine turns up alongside fibromyalgia far more often than chance allows, and the cleanest evidence for it is that each one raises the odds of later getting the other. Across two population cohorts, people with fibromyalgia went on to develop migraine at about 1.9 times the rate of people without it, and people with migraine went on to develop fibromyalgia at about 1.5 times the rate [77]. Those are the two numbers worth having, because both carry a comparison group and neither depends on who happens to turn up at a headache clinic.

Which kind of headache matters more than the label does. Across a Chinese multicentre headache cohort, fibromyalgia was around two and a half times as common in chronic migraine as in episodic migraine, with the same pattern in tension type headache [78]. It tracks with how often you get the headache.

One catch is worth saying out loud. The criteria used to diagnose fibromyalgia count headaches as one of the scoring symptoms, so a study that recruits people using those criteria is always going to find a lot of headaches [79].

Painkillers are the other half of it. In a tertiary headache clinic in Egypt, 43 in every 100 people whose headaches were being driven by their own medication had musculoskeletal pain or fibromyalgia, against about one in five of those whose weren’t [80]. One clinic, one study, and the direction is exactly what you’d expect of a group taking a lot of analgesia.

Back pain

Back pain is so close to universal in fibromyalgia that the more useful question runs the other way, which is how often an unrecognised fibromyalgia is sitting inside a back pain clinic. In one chronic low back pain population, roughly fifteen in every hundred screened positive for fibromyalgia while the clinic’s own records had it written down for three [81]. Same people, two numbers, and the gap is everybody nobody asked.

The part that changes a decision is what happens after spinal surgery. Around one in five people going in for spinal surgery meet the fibromyalgia criteria, and across orthopaedic surgery generally the ones who do come out with less satisfaction, more pain, worse function, more opioid prescribing and more complications than the ones who don’t [82]. A group scored before their operation makes the point harder still: those meeting the criteria beforehand had no improvement in symptom severity afterwards at all [83].

Injections aren’t the alternative either, and not because of the fibromyalgia. Pooled across the trials, epidurals, nerve blocks and radiofrequency procedures for ongoing spine pain mostly fail to beat a dummy procedure in anybody [84].

None of that says don’t have the operation. It says the fibromyalgia question is worth asking before it rather than after.

Chest and rib pain

Chest and rib pain is part of fibromyalgia for a lot of people, and nobody has counted it properly. No study in this evidence set measured how common chest wall pain is in fibromyalgia against any comparison group, so there’s no figure to give you. The diagnostic criteria do treat the chest as somewhere you can hurt while deliberately leaving it out of the regional count, which exists partly so a chest wall problem doesn’t get quietly absorbed into a fibromyalgia score [79].

The safety half is thinner still. Nobody has measured whether a fibromyalgia label delays cardiac investigation. Nobody has measured how many people with fibromyalgia arriving with chest pain turn out to have a cardiac cause. And no feature has been shown to separate chest wall pain from heart pain in this group. That’s an absence of evidence rather than a reassurance, and we aren’t going to dress it up as one.

So the rule is the ordinary one. The NHS says to call 999 for sudden chest pain or discomfort that doesn’t go away, for pain spreading to an arm, the neck, jaw, stomach or back, and for chest pain with sweating, nausea, light headedness or breathlessness [85]. Having fibromyalgia changes none of that, and years of being told everything is the fibro is exactly what makes people sit on it.

Heart risk is a separate question and it should stay separate. The only pooled work here looked at death rates rather than heart attacks, and the studies disagreed with each other too much to conclude anything [86].

Sciatica type pain down the leg

Pain running down the leg is common in fibromyalgia, and how often it’s genuinely coming from a trapped nerve root rather than being referred from somewhere else has never been measured. No study here put a number on it. Nor has anybody tested whether having fibromyalgia changes what a straight leg raise or a nerve conduction study shows, which is the obvious thing to check given how often both get done in this group.

What has been described is how fibromyalgia differs from small fibre neuropathy, the other condition that produces burning legs. Fibromyalgia tends to arrive with pain in a lot of places plus bowel and sleep trouble. Small fibre neuropathy tends to arrive with numbness and pins and needles plus something measurably wrong on testing [87].

Restless legs is the one everybody asks about, and this evidence set came back with no usable figure against a comparison group, so we aren’t going to print one.

The thing not to sit on is weakness. The NHS says to go to A and E or call 999 for sciatica on both sides, for weakness or numbness in both legs that’s severe or getting worse, for numbness around the genitals or the back passage, and for new trouble starting to pee or controlling your bladder or bowels [88]. None of that is fibromyalgia, whatever else is.

Eye pain and visual symptoms

Eye symptoms in fibromyalgia are common, mostly surface discomfort and light sensitivity, and one finding in this literature is serious enough to be worth knowing about. Light sensitivity has the clearest comparison of the lot: in a blinded neurological examination, seven in ten people with fibromyalgia reported it against six in every hundred pain free controls [89].

Dry, gritty, sore eyes come next. Against controls, people with fibromyalgia score worse on the standard dry eye questionnaire, their tear film breaks up faster, and the density of the small nerves in the cornea is lower [90]. That last part is the same small nerve story running through the rest of this page.

Eye pain itself has barely been studied against anybody, and focusing problems haven’t been measured in fibromyalgia at all. Both are gaps rather than negatives.

The finding that changes something is optic neuritis, which is inflammation of the nerve at the back of the eye. In a nationwide South Korean cohort it ran at about twice the rate seen in people with other chronic pain, which is the comparison that counts rather than a comparison with healthy people [91]. It’s still uncommon. It just isn’t nothing.

So the line is this. The NHS says 999 or A and E for eye symptoms that start suddenly or for any loss of vision, and urgent same day advice for severe eye pain, new light sensitivity, a very red eye or changes to your vision including how you see colour [92]. None of that gets filed under fibromyalgia.

Itching

Itching with nothing to see on the skin is a recognised part of fibromyalgia, and it’s one of the few symptoms on this page with a proper case control study behind it. In a dermatology comparison, around seven in ten people with fibromyalgia reported itch, well above the controls, along with burning, sweating and numbness [93]. Set against that, a review of hospital notes found unexplained itch written down for about three in every hundred [94]. Those two numbers don’t contradict each other. One study asked and the other read the file, and the gap between them is how often nobody thinks to ask.

What causes it hasn’t been worked out, and three explanations are on the table. Skin in fibromyalgia has been reported to carry more mast cells, which are the cells that release histamine. Around half of people with fibromyalgia have measurable changes to the small nerve fibres in the skin, which is the same finding sitting behind the burning and the pins and needles [11]. And the third is the medication, because gabapentin, pregabalin, opioids and antidepressants are all common in this group and every one of them can cause itch.

Nobody has separated those three. The only detailed case on record is one person with widespread itch, no rash, normal routine bloods and clearly reduced nerve fibre density on a skin biopsy, whose itch started before the opioid and carried on while it was stopped, and who got no relief from antihistamines, steroids, gabapentin or pregabalin [95]. That’s one person. It tells you the nerve version is possible and absolutely nothing about how often.

The practical bit is that itch with no rash is worth mentioning to somebody rather than absorbing into the diagnosis. It has its own list of causes, and already having fibromyalgia rules out exactly none of them.

Numbness, tingling and the zaps

Numbness and pins and needles are among the commonest symptoms in fibromyalgia and among the hardest to interpret, because they’re also one of the things the diagnosis gets scored on. In a blinded neurological examination, just over half the people with fibromyalgia reported tingling in the arms or legs against four in every hundred pain free controls [89]. That gap is real. The 2010 and 2016 criteria count numbness and tingling among the symptoms that earn you the diagnosis though, so any study recruiting that way is partly selecting for it [79].

Standard nerve tests usually come back normal. Of 33 people with fibromyalgia and pins and needles, the tests showed no widespread nerve damage, though carpal tunnel syndrome turned up in about one in seven and a nerve trapped somewhere in about one in four [96]. A second small series found every test normal despite three quarters of the group describing pins and needles and burning [97].

The smallest nerve fibres are a different matter, and they don’t show up on those tests at all. On skin biopsy, 41 in every 100 people meeting the fibromyalgia criteria had damage to those fibres against 3 in every 100 controls [98], and pooled across studies it comes out at around half [11].

How many of those turn out to have a separate and treatable cause behind them hasn’t been measured in fibromyalgia. That’s the number that would actually be worth having, and nobody has it.

The symptoms nobody warns you about

The symptoms nobody mentions when fibromyalgia gets written on the letter are mostly the ones below the waist and above the neck, and four of them have real comparison group evidence behind them.

Jaw pain is the first. Of 71 people with fibromyalgia against 151 without, pain in the jaw joint, jaw locking and grinding the teeth both asleep and awake were all more common [99].

Bladder is second and it carries the sharpest number on this page. Among women arriving at a clinic with urinary symptoms, overactive bladder was found in about six in ten of those with fibromyalgia against under three in ten of the controls, who’d come in with similar complaints [100]. A comparison group with the same symptom is a much harder thing to argue with than a comparison against well people.

Irritable bowel is third, at 43.7 in every 100 against 1.9 in a group with small fibre neuropathy [87]. That comparator is another nerve condition rather than the general population, so read it as something that separates the two diagnoses rather than as your own odds.

Pelvic floor trouble is fourth. Women with fibromyalgia report more leaking, more prolapse and more pain with sex than controls [101], and a separate controlled study put urinary incontinence at 60 in every 100 against 25 [102].

Then a middle tier. Dizziness and unsteadiness: people with fibromyalgia score worse than controls on a balance questionnaire [103], and that blinded examination found poor balance in nearly two thirds of them against four in every hundred controls [89]. Tinnitus: 31.1 in every 100 against 3.5, although that was children and teenagers in a single clinic [104].

Below that it thins out fast, and we’d rather say so than pad the list. Swallowing trouble gets reported by about half of people in surveys, with no control group anywhere in it [105]. Easy bruising, dry mouth and voice changes came back with nothing usable at all. They may well be real. Nobody has counted them.

Why do my scans come back normal?

Scans come back normal in fibromyalgia because they photograph tissue, and the change that produces the pain is in how the nervous system handles what the tissue sends. An MRI of your knee shows you the knee. It can’t show you the junction in the spinal cord where the signal from that knee gets amplified on its way up.

That amplification has been measured in ways that don’t rely on anybody taking your word for it. The reflex that whips your leg away from something sharp is wired through the spinal cord, it fires before you’ve had a thought about it, and its threshold can be measured in units. In fibromyalgia that threshold is lower [106]. A reflex has no opinion about your diagnosis.

The brain shows it too, though only while something is actually being done to you. Give people with fibromyalgia the same pressure as anybody else, or less, and the regions that handle pain respond more, which is one of the more consistent findings in the imaging work, while scans taken with people lying quietly at rest disagree with each other far more [8]. So a clear MRI isn’t evidence against you. It’s the right answer to a question about tissue, and fibromyalgia isn’t a tissue problem in the way a torn tendon is.

Why does the pain move around?

Fibromyalgia pain seems to move around because the threshold for hurting has dropped right across the body, so it takes far less than usual for any one area to cross it, and which area does on a given day depends on what that area has been through. As the symptom map above says, nobody has actually tracked that movement inside one person [69], so take what follows as the mechanism behind what people describe rather than a measured map of it.

Start at the spinal junction again. As the receiving nerve cell there becomes more excitable, the patch of body it answers for gets bigger [107]. A cell that used to cover an area the size of a coin ends up covering one the size of your palm, and it fires more easily than it did. Repeat that at enough junctions and the map of where you hurt grows without anything new going wrong in any of those places.

Repeated input stacks up as well. Give anybody a steady run of short heat pulses and the pain climbs with each one even though the heat doesn’t change. Twenty six people with fibromyalgia reached that wound up state at lower intensities than 23 people without it, held it there longer, and their hands and feet behaved much the same as each other [108]. Sensitivity to pressure and temperature turns up well outside the sore areas too [109]. That’s a setting on the whole system rather than a fault in one shoulder.

Then there’s what feeds it. Sleep is one of the bigger ones, because poor sleep weakens the brakes the brain puts on incoming input, and deliberately depriving people of sleep can bring on fibromyalgia like pain and tenderness [110]. Input from the body keeps it going too, since numbing a painful muscle with local anaesthetic has reduced sensitivity at sites well away from the injection [111]. A long drive, a bad night and a cold week each land somewhere different. On a system set this high, any one of them is enough.

Why does being touched hurt?

Ordinary touch hurts in fibromyalgia because touch, which was never meant to produce pain, gets pulled into the machinery that does. Touch travels on its own nerve fibres, separate from the nociceptors, and once the junctions in the spinal cord are wound up, what arrives on those fibres can get handled as though it were a threat [106]. The word for pain from something that shouldn’t hurt at all is allodynia.

The symptom map left one thing hanging, which is why the feeling outlasts the touch. Wound up junctions don’t only respond more, they keep responding after the input has stopped, and those aftersensations run larger and longer in fibromyalgia than in people without it [108]. The brakes are part of it as well, because the system that ought to quieten one sensation while something else is going on works less well here, by a moderate amount rather than a huge one, and it varies a great deal from one person to the next [17][19].

None of which makes your partner’s hand a threat. It means the system handling it has been set to over report, and a setting is something that can change, which matters for the last question on this list.

Does it mean damage is being done?

Fibromyalgia doesn’t wear your joints, muscles or anything else away, and pain that gets worse isn’t a sign that it has started to. It’s understood as pain that’s been amplified, rather than pain being driven by damage or inflammation in the tissue [3].

The one physical finding with real support behind it is the change in the smallest nerve fibres in the skin, which turns up in around half of people [11][12] and is covered in the first section of this guide. It’s a fair question whether that’s damage that keeps going. The best answer so far comes from one group followed for 18 months, whose nerve fibre counts didn’t fall over that time while their pain, their nerve type symptoms and their fatigue improved [112]. One study is one study, and it still points away from a slowly advancing nerve disease. Fibromyalgia and small fibre neuropathy overlap without being the same condition, which is worth knowing if anybody treats a biopsy result as the whole diagnosis [87].

So hurting when you move isn’t the same as harming when you move. In a sensitised system those two have come apart, and the volume of the pain is telling you about the setting rather than about the state of the tissue. That isn’t a licence to push through a flare, and this bit is our clinical experience rather than a trial: a wound up system can usually be wound up further, and the next couple of days tend to pay for it. What you can put down is the fear that every bad day is leaving a permanent mark.

What has childhood got to do with it?

Hard things in childhood raise the odds of developing fibromyalgia as an adult, and that’s a statement about a nervous system that was loaded early rather than about pain that’s been imagined.

Pool the studies comparing adults with fibromyalgia against people without it, look only at what happened in childhood, and the odds of having been physically abused come out about three times higher, with emotional abuse close to twice [113]. Those studies relied on people remembering though, and the pooled figures weren’t adjusted for anything else that might explain them, which is exactly where the objection about memory bites. The better answer to it comes from UK GP records, where maltreatment had been written into the notes before anybody had fibromyalgia, and those adults went on to be diagnosed with it at about twice the rate of matched adults with no such record [114]. A Finnish population study found the same direction across six different kinds of childhood difficulty [115]. Written down at the time, by somebody who had no idea what would happen next, is a much harder thing to explain away.

What happens in between is a good deal less settled. The usual explanation is that the systems handling threat, meaning the stress hormones, the autonomic nervous system and the brain’s own brakes on pain, get calibrated early and carry that setting forward [116][117]. One comparison of people with and without fibromyalgia found the link ran through how stressed people felt, with no sign that it ran through cortisol [118]. That’s a single study, so hold it loosely.

Raised odds across a group tell you nothing about any one person’s history, in either direction. And none of this makes it psychological. A stress system that was set high in childhood is biology, it’s measured in the body, and the pain it helps produce is real pain.

Is any of this reversible?

The amplification behind fibromyalgia can shift, because it’s the nervous system adapting rather than tissue breaking, though fibromyalgia rarely simply switches off, and the lab measures of that amplification don’t always move when people feel better.

Over 10 to 12 years in a Swedish group of women, 16 in every 100 saw their pain at least halve, and lower stress levels were what predicted it [119]. Over shorter stretches people tend to settle into a pattern and stay there. In one analysis of trial participants roughly a third were on a path of some improvement and two thirds on one of none [120], and in a large cohort most people stayed in the same severity group from one six month check to the next [121]. That’s slower and rarer than anybody would like. It’s also not the steady decline people get warned about.

The lab measures are messier still. Pooling nine trials, treatment didn’t shift the measures of wind up or of the brain’s own brakes overall, though the treatment arms that did improve them by at least a tenth were more likely to produce a meaningful drop in pain, which the authors frame as possible rather than established [122]. In a trial of 116 people with fibromyalgia everybody exercised, and all four groups improved in pain, fatigue and quality of life by much the same amount, while brain stimulation improved the brakes on top and added nothing at all to how people actually felt [123]. Pressure thresholds are the ones that move most readily, and exercise combined with psychological treatment raised them in people with long term musculoskeletal pain without shifting the other two [124].

So you don’t need a lab to declare your nervous system fixed before you’re allowed to feel better, and people do get better without it. What tends to move things is the unglamorous work in the rest of this guide: sleep, a graded way back into movement, and the load sitting around you, worked on together rather than one at a time.

What is a fibromyalgia flare?

A flare is a period when your symptoms are clearly worse than your usual, and that’s as precise as the research gets. There’s no agreed number of points on any scale that marks one, and no consensus definition from the groups who set outcome standards for fibromyalgia trials. The questionnaire used most in those trials couldn’t establish a threshold for meaningful change even while it was being validated [126].

So studies pick their own. The one prospective diary cohort counted any obvious worsening of usual symptoms and ignored anything lasting under a day [125], which means two studies reporting flare rates aren’t necessarily counting the same event. Worth holding on to the next time somebody quotes you a flare statistic.

How long does a flare last?

One cohort has measured it prospectively, and it came out at a mean of 11 weeks, from 92 people in Madrid keeping diaries for six months. About three quarters had at least one flare, averaging two each across those six months, and a quarter had only small fluctuations [125].

Handle the 11 weeks carefully though. The spread around it was 13 weeks, flares still running when the diaries stopped were left out altogether, and several of the paper’s own figures don’t reconcile. No second cohort has measured duration, so there’s nothing to check it against.

What sets a flare off?

Stress, overdoing it and bad sleep are what people report, and reporting isn’t the same as measuring. In the diary cohort the commonest reported triggers were sustained stress lasting over a month, sudden intense stress, physical overexertion and a change in the weather, each named by roughly a third to a half of people [125]. Those are perceptions collected afterwards, which is a polite way of saying they’re what people reckon.

Measured work does exist, and it tracks next day symptoms rather than flares, so none of it tells you what starts one. Weather is the one worth naming, because it gets asked about constantly. A study matching daily reports against meteorological records found pain did rise as barometric pressure fell, by an amount so small it’s hard to feel, and a minority of people moved the other way entirely [127].

Should I exercise during a flare?

Nobody has tested it. No study has taken people with fibromyalgia in a flare and compared carrying on, cutting back and stopping against how long the flare then ran.

What’s known is more general. Across the aerobic exercise trials people leave at much the same rate as controls, 20 in every 100 against 17 [128]. And a single low intensity bout of resistance work in one arm left pain and fatigue in that arm raised across the next three days in people with fibromyalgia, where controls were back to normal the following day [129]. That’s the mechanism behind exercise made it worse, and it isn’t the same finding as exercise being a bad idea.

What actually helps once you are in one?

Nothing has been tested against how long a flare lasts. Not a written flare plan, not heat, not rest against modified activity, not taking something as needed. Anti inflammatories have no trustworthy evidence of benefit for fibromyalgia pain at any point, and paracetamol on its own doesn’t even appear in the Cochrane overview of fibromyalgia drug trials [130].

In the diary cohort most people rested and most took a painkiller, and nobody recorded whether either of those helped [125]. So anything you read about managing a flare is reasoning from mechanism rather than a trial result, and we’ll keep saying so.

How do I tell a flare from things getting permanently worse?

Mostly by how long it runs, because nobody has published anything better. With no agreed definition there’s no test and no cutoff, so duration is what’s left. A bad few weeks that comes back towards your usual is a flare. A worse baseline that holds for months is something else, and worth taking to somebody.

The second half of this matters more. New symptoms outside your usual pattern deserve a fresh look rather than being filed under flare, because a fibromyalgia label doesn’t stop anything else happening, and nobody has measured what gets missed once it’s sitting on your notes.

Why am I this tired when I have not done anything?

The fatigue in fibromyalgia stays heavy even when the pain is quiet, which is the part that makes it look like it came from nowhere. Among 266 people in Beijing whose fibromyalgia was in remission or mild, fatigue scores still ran well above those of people whose rheumatoid arthritis was in remission, and close to twice those of healthy controls [131]. In a survey of 105 people in Northern Ireland, fatigue averaged 8.5 out of 10 [132].

It moves about as well. In 256 people rating themselves daily for up to three months, roughly a quarter to a third of the variation in symptoms happened within the same person from one day to the next [133]. So an average is a poor description of any particular day here, and a plan built on one will keep missing.

What is fibro fog, and is it damage?

Fibro fog is a real and measurable drop in cognitive performance, and nothing so far suggests it’s damage. Pool 37 case control studies, 964 people with fibromyalgia against 1,025 age matched controls, and performance came out worse in every domain tested, with the widest gap in holding back an automatic response and the narrowest in switching between tasks [134]. A 2025 pooling of 26 studies found verbal working memory clearly impaired while visual working memory came out no different from controls [135].

On the damage question, 18,898 UK Biobank adults were followed for a median of about two and a half years, and once everything else was accounted for, a higher fibromyalgia index score didn’t predict any further decline in executive function [136]. So it’s a real deficit, and it doesn’t appear to be heading anywhere worse.

What is post exertional malaise, and do I have it?

Post exertional malaise is a delayed and outsized worsening of symptoms after exertion, and in fibromyalgia it’s barely been measured as a syndrome in its own right. What has been measured is what a single bout of exercise does.

Pool 15 case control studies of people with fibromyalgia or ME/CFS and pain rose more after exercise than it did in controls, with a far bigger gap between 8 and 72 hours afterwards than in the first two hours [52]. The delay is the whole character of the thing. In fibromyalgia alone, one light set of resistance work in a single arm left pain and fatigue in that arm raised at day one and again at day three, where matched controls had already settled [129].

How do I tell post exertional malaise from deconditioning?

You can’t reliably tell them apart yet, and anybody offering you a clean test is ahead of the evidence. The test usually named is two day cardiopulmonary exercise testing, and in fibromyalgia it exists only in two conference abstracts, which can’t carry a result. In ME/CFS it’s contested: 55 matched pairs showed peak oxygen uptake falling 6 per cent on day two with no change in controls [137], while a replication in 58 people found no change in either group [138].

Fitness does come out lower in fibromyalgia than in controls, across a review of 79 studies [139], and the arrow runs both ways. Widespread pain predicts later inactivity [140], and among 75,485 Norwegian women the very lowest activity levels went with about a third higher chance of reporting fibromyalgia later [141]. So being less fit is part of the picture, it isn’t the explanation on its own, and it isn’t a diagnosis anybody should be handing you.

Does that mean I have ME/CFS rather than fibromyalgia?

Meeting one set of criteria doesn’t rule out the other, and how far the two overlap depends almost entirely on which criteria get used. Of 60 people diagnosed with fibromyalgia at a Turkish hospital clinic, 8 also met the Fukuda criteria for chronic fatigue syndrome [142]. Among 595 people with ME/CFS across seven American specialist clinics, 45 per cent also had fibromyalgia [143].

And in a Norwegian pain clinic, of 33 people with chronic widespread pain, 82 per cent met the 2016 fibromyalgia criteria while 30 per cent met the Canadian criteria for chronic fatigue syndrome [144]. Which label you end up with turns partly on which questionnaire you happened to be handed.

What helps the fog?

Two things have improved measured cognitive performance in a randomised trial, and neither is large or replicated. Four weeks of daily home based transcranial direct current stimulation, a weak electrical current run across the scalp, beat a sham version in 36 women on the trial’s main cognitive outcome [145]. Repetitive transcranial magnetic stimulation in 40 people beat sham on word list recall at one month and again at three [146].

Against that, cognitive behavioural therapy aimed at the pain improved attention no more in 69 women than a fibromyalgia education class did [147]. And most fibromyalgia trials of sleep treatment, medication and exercise never measure cognition at all, which is the bigger problem of the two. Nobody finds an effect on something they aren’t looking at.

Why is my sleep never refreshing?

Because the problem is continuity rather than quantity. Pool 19 polysomnography studies against healthy controls and people with fibromyalgia spent longer awake after first dropping off, slept less in total, had lower sleep efficiency, more light stage 1 sleep and less slow wave sleep [148].

Fragmentation is the part that shows up most reliably. In one case control study awakenings, arousals and the arousal index were all higher, and the difference held even after everybody with sleep apnoea had been excluded [149]. Set against ordinary insomnia, fibromyalgia was marked less by total time awake than by frequent short bouts of waking [150], and a large study recording sleep at home rather than in a lab found the same pattern once age, weight and antidepressant use were accounted for [151].

So it isn’t the length of the night. It’s that the night keeps getting interrupted, and the deep stage that does most of the restoring is the one that loses out. What people report is still usually worse than what the machines pick up [148], which means a sleep study reading near normal doesn’t settle the question either.

What is actually happening to sleep in fibromyalgia?

There’s no single fibromyalgia sleep signature, and the one you’ll have read about is a good deal weaker than its reputation. Alpha wave intrusion into deep sleep, usually called alpha delta sleep, was described early and in striking numbers, with phasic alpha in half of one fibromyalgia sample and tonic alpha in a fifth [152], and it’s been repeated ever since as though it were diagnostic.

It isn’t. Against osteoarthritis with disturbed sleep, alpha delta levels came out statistically similar [153]. Against generalised musculoskeletal pain there was no significant difference at all [154]. Only 36 per cent of people in one treatment trial had it to begin with, and it tracked neither severity nor response [155]. And you can produce it in healthy volunteers simply by disrupting their deep sleep [156]. It’s a marker of broken sleep rather than a marker of fibromyalgia.

Does poor sleep cause the pain, or the other way round?

Both, and on average the arrow running from sleep to pain is the stronger of the two. Pool 16 longitudinal cohorts and 116,746 people and sleep problems at the start predicted chronic musculoskeletal pain later, more strongly over the shorter term than over the longer [157]. Among 14,172 Norwegian women followed for 11 years, one insomnia symptom went with a 39 per cent higher rate of later reporting fibromyalgia and two or more with 86 per cent, though the diagnosis there was self reported [158].

Day to day it reads the same way. Across 11 diary studies, nine found last night’s sleep predicted today’s pain more reliably than today’s pain predicted tonight’s sleep [159]. And deprive healthy volunteers of sleep and their pain thresholds drop while their own pain inhibition weakens [160][161].

Studies pointing the other way do exist [162], and none of this makes fibromyalgia a sleep problem with pain attached. What it does mean is that sleep is worth working on in its own right, rather than parked until the pain settles.

Is napping making it worse?

Nobody has tested that in fibromyalgia, so anybody telling you to stop is extrapolating. Cutting daytime sleep is a standard component of cognitive behavioural therapy for insomnia, bundled in with sleep restriction and stimulus control, and those packages do improve sleep in fibromyalgia [163][164]. No trial in this evidence set has pulled the napping component out and tested it on its own.

That leaves a practical rule rather than a finding. If you nap long and late and then lie awake at two in the morning, it’s worth a fortnight without to find out. If you nap because you’re wrecked and it buys you the rest of the afternoon, a leaflet isn’t a reason to stop.

What actually helps?

Get screened before you get treated, because a real share of this is a separate and treatable sleep disorder. Obstructive sleep apnoea turns up in 45 to 66 per cent of fibromyalgia clinic samples that actually tested for it [165][166], and restless legs in about a third, against 3 per cent of controls [167]. Those are referred samples rather than population rates, so read them as a reason to ask rather than as your own odds.

After that, cognitive behavioural therapy for insomnia has the most consistent non drug sleep benefit [163], although in 113 adults with both it improved sleep without beating the comparison arm on pain [164]. Exercise helps sleep a little, varies by type, and fades once you stop [168][169].

Of the drugs, pregabalin has the clearest sleep evidence, at roughly 19 fewer minutes awake on polysomnography [170], which is a real effect and not a big one. Duloxetine doesn’t reliably improve sleep at all [163][171]. So the order worth following is apnoea and restless legs first, then the behavioural work, then a conversation about a tablet, rather than the other way round.

Why does heat wipe me out?

Heat intolerance in fibromyalgia is partly a thermoregulation problem and partly a pain processing one, and the two turn up together. Autonomic symptom questionnaires in fibromyalgia cohorts come back with orthostatic intolerance, sweating problems and poor heat tolerance well above what you’d expect [176][177]. Measured directly, the sympathetic control of sweating looks blunted: lower resting skin conductance, weaker reactivity, and the usual relationship between sweating, arousal and body temperature missing altogether [178].

Underneath that sit the small nerve fibres. Pooled biopsy studies put small fibre impairment at roughly half of fibromyalgia cohorts, and impairment of the autonomic ones at about 45 per cent [179][180], and those are precisely the fibres running your sweating and the width of your blood vessels. Add heat hyperalgesia on top [181] and the heat is both harder to shed and more painful while you’re shedding it. Which is the whole explanation for having to go and sit down.

Why am I cold all the time?

Cold intolerance has firmer experimental backing than almost any other sensory complaint in fibromyalgia. A systematic review found reduced cold pain thresholds in 14 of the 17 studies that measured them [181]. In the lab, people with fibromyalgia tolerate cold for less time, rate it as more unpleasant, and show an exaggerated response to the thermal grill illusion, where warm and cold bars interleaved get read as pain [182][183]. Cold is also one of the most commonly named symptom triggers, with warmth named as the relief [184][185].

A subgroup may be genuinely vascular, since a 1991 study found 41 per cent had an abnormal Nielsen test [186], though that’s one old study and nobody has replicated it. And cold hands and feet aren’t specific to fibromyalgia anyway. Raynaud’s, thyroid disease and anaemia all produce them [187][188], and all three are worth excluding before you settle on this as the answer.

Are cold showers or ice baths worth it?

Nobody has tested a cold shower or an ice bath in fibromyalgia, so anybody selling you one is extrapolating. What has been tested is whole body cryotherapy, which isn’t the same thing at all: a few supervised minutes in a chamber, at a temperature no bath reaches. A randomised crossover trial in a cryosauna improved pain and Fibromyalgia Impact Questionnaire scores over the first treatment period [189], a second study reported the same for pain and mobility but exists only as a conference abstract [190], and the reviews call it promising and thin in the same breath [191][192].

The cold water immersion literature is mostly healthy adults, and mostly about wellbeing rather than pain [193]. It isn’t harmless either. Immersion sets off a cold shock response with hyperventilation and autonomic stress [194][195], and cold is contraindicated outright in Raynaud’s, cold urticaria and cryoglobulinaemia [191].

Warm water has the better fibromyalgia evidence [196][197], which is a duller recommendation and a considerably easier one to keep up in February.

Why do noise and light hurt now?

Sound and light sensitivity in fibromyalgia are measurable rather than merely reported. In quantitative sensory testing, people with fibromyalgia needed noticeably lower sound pressures than controls before calling a noise mild, moderate or intense [198]. For light, discomfort arrived at substantially lower intensities, at levels most people would call an ordinarily lit room [199].

The useful part of that light study is what it ruled out. It found no sign of amplified processing in the visual system itself, and argued instead that light was abnormally engaging the brain’s pain modulating circuitry [199]. Smell makes the same point by failing the simple version: people report a heightened sense of smell, and objective testing finds identification scores that are if anything worse [200][201][202].

The senses haven’t got sharper. What the system does with the input afterwards has changed, which is the same sentence as the rest of this page.

Why does my skin itch with no rash?

Itch without a rash is a genuine fibromyalgia symptom in a minority, and the figure is smaller than the internet suggests. In a review of 845 confirmed fibromyalgia records, unexplained itch appeared in 3.3 per cent, burning skin or mucosal sensation in 3.4 per cent, and other unusual skin sensations in 1.7 per cent [203].

The likeliest mechanism is neuropathic, in the subgroup with small fibre pathology, since those fibres carry itch as well as pain and produce burning and odd sensations when they’re sensitised [180][204]. Plausible rather than demonstrated, because nobody has studied itch mechanisms in fibromyalgia directly [205][206].

Which is the argument for bloods first. Chronic itch with no rash warrants a full blood count, renal, liver, thyroid, glucose and iron studies, because thyroid disease, iron deficiency and liver or kidney problems all cause it [188][204]. None of those gets found by assuming it’s the fibro.

What does pacing actually mean?

Pacing is distributing activity against a limit you set in advance, rather than against how you happen to feel that morning. A concept analysis found the word being used for two quite different things, which is most of why the advice you get sounds contradictory: pacing as conserving a fixed supply, and pacing as a graded route to doing more [207].

The researchers who work on it have spent a decade arguing that it isn’t simply taking breaks and slowing down [211], and the frameworks that have actually been tested treat it as several behaviours running at once. Planning. Breaking tasks up. Adjusting goals. Accepting where the limit currently sits [212][213].

How do I find my baseline?

Your baseline is what you can do on a bad day without paying for it afterwards, which is a smaller number than anybody wants it to be. The method is to record what you actually do and what it costs for a week or two before changing a single thing, then set the limit at what the worst day could have absorbed rather than at the average [212][214].

It also isn’t one number. Physical, cognitive and sensory tasks have separate ceilings and separate recovery times, and a day spent entirely at a desk can cost as much as a day on your feet [210][215]. If your own judgement is the part you trust least, heart rate gives you something external to argue with [216][217].

Why do I crash two days later?

The delay is the defining feature of post exertional malaise, and it’s what separates it from ordinary tiredness. Symptoms worsen after exertion that used to be manageable, usually peaking somewhere between twelve and seventy two hours afterwards and lasting days rather than hours [209][218].

Two day cardiopulmonary exercise testing is where the clearest objective signal has come from, with second day performance in ME and CFS cohorts dropping in a way healthy controls don’t show [137][219][220]. Don’t lean on that too hard though, because a 2026 study running the same protocol found no difference between the two days [138]. The delay itself isn’t in question. The test meant to capture it is.

Does pacing mean giving up?

Pacing isn’t an agreement to do less forever, and the people who research it are the ones most irritated by that version of it. Every framework that has been tested contains progression: the limit is a starting line you build from once it holds steady, rather than a ceiling you sign for [211][212][213].

What changes is the shape. Instead of the overactivity that reliably comes before a crash [208][221], you get a flatter, duller, more repeatable output, which is the only state in which adding exercise is worth attempting at all [128][222]. The caveat worth having is that the trial evidence for pacing on its own is thin and the studies are small [223].

Why does pacing stop working when my physical pacing is fine?

Physical activity is one of several things drawing on the same supply, and it’s the only one most pacing advice tells you to track. Cognitive load is measurable in its own right here. In fibromyalgia, cognitive performance is poorer, and the deficit tracks with how the system responds to pressure rather than sitting off to one side of it [224][225].

Sensory load counts too, which is why an afternoon in a loud cafe isn’t a rest. In hypermobility, fatigue is both common and poorly explained by how much somebody has actually done [226][227].

And guilt isn’t a soft extra bolted on at the end. Self compassion is one of the few psychological variables in chronic illness with a decent effect behind it [228][229], which is a dry way of saying that spending the afternoon furious with yourself costs you something too.

What actually works for fibromyalgia pain?

Duloxetine, milnacipran and pregabalin are the only drugs with moderate to good evidence of substantial pain relief, and it arrives in about one adult in ten [130]. Substantial means your pain halving. The number of people you’d have to treat to get one of them there runs from about 7 to 14, the trials lasted four to twelve weeks, and nothing shows anything past six months. Serious adverse events were no commoner than on a dummy tablet.

Nothing trustworthy came out for amitriptyline, SSRIs, cannabinoids, gabapentin or anti inflammatories, and there’s no evidence at all about who benefits. Milnacipran has no UK licence either, so in practice that list of three is a list of two.

Amitriptyline

Amitriptyline produces the best looking numbers in fibromyalgia and the least trustworthy ones, which is awkward, because it’s the drug a UK GP is likeliest to start you on. The Cochrane overview gives it a number needed to treat of 4.1, better than anything else on the list, and then flags that same review as one of only two susceptible to publication bias [130].

A network comparison of 36 trials and 11,930 people found it beat everything else for sleep, fatigue and quality of life, while duloxetine won on the pain itself [230]. It’s prescribed off label, well below the doses depression needs, and the sleep effect is probably doing most of the work. Worth knowing when you’re judging whether it’s doing anything for you.

Duloxetine

Duloxetine’s own trial data holds the most honest finding in the fibromyalgia literature, and it’s sitting in a secondary outcome table. Across eighteen trials and 7,903 people, duloxetine and milnacipran got 31 per cent of participants to a halving of their pain against 21 per cent on placebo, which the reviewers judged not clinically relevant [171].

On exactly the same data, 52 per cent called themselves much or very much improved, against 29 per cent. That gap, between a pain score that barely moves and a person who says they feel better, is worth knowing exists, because it’s the gap you’re actually deciding about. Nineteen per cent stopped because of side effects, against 10 per cent on placebo.

Pregabalin and gabapentin

Pregabalin and gabapentin get named in the same breath and they aren’t the same proposition at all, because one has eight trials behind it and the other has one. On 450 mg of pregabalin, 24 per cent reached a halving of their pain against 14 per cent on placebo, while 150 mg beat placebo on nothing whatsoever [231]. Dizziness carries a number needed to harm of 3.7, so for roughly every four people treated, one extra gets it.

Gabapentin’s entire fibromyalgia evidence base is one trial of 150 people, rated very low quality [232]. A records study of 105,602 US patients found raised five year rates of pulmonary embolism on both, which is a cohort rather than a trial, and worth raising with somebody rather than panicking about [233].

Low dose naltrexone

Low dose naltrexone has two properly controlled trials behind it in fibromyalgia, and it lost to placebo in both. A Danish crossover trial of 58 people found no difference on its primary outcome [234]. A twelve month Spanish trial in 98 women, the longest run yet, found pain fell 0.33 points on naltrexone and 0.64 on placebo, with the adjusted difference favouring placebo, and nothing appearing at six or twelve months either [235].

Side effects were mild and no commoner than on placebo, which is the genuinely good thing about it. Cheap, well tolerated and not shown to work is an unsatisfying verdict, and it’s the one the evidence supports.

What about TONMYA, and can I get it in the UK?

TONMYA is bedtime sublingual cyclobenzaprine, licensed in the United States on 15 August 2025 and the first fibromyalgia drug approved there in over fifteen years [236]. You can’t get it here. Cyclobenzaprine holds no UK marketing authorisation in any form, and appears nowhere in the compendium of licensed UK medicines [237].

The trial it was licensed on randomised 457 people, and 22.5 per cent reached a halving of their pain against 13.3 per cent on placebo [238]. That’s pregabalin territory rather than a breakthrough. Nearly a quarter had their mouth go numb, and to the authors’ credit they went and checked whether that had unblinded people. The effect held.

Why do NSAIDs and opioids not work?

Anti inflammatories, the NSAIDs, and opioids fail here for two completely different reasons, and the opioid reason is that nobody has run the study. The anti inflammatories showed no benefit over placebo at either a 30 or a 50 per cent pain reduction [130]. EULAR found no systematic reviews at all for strong opioids [239], and the Cochrane review of oxycodone in fibromyalgia is one of the seven that turned up not a single eligible trial [130].

So the line isn’t that opioids have been shown not to work. It’s that prescribing into that gap, for a condition you’ll have for decades, is a very different sort of decision from prescribing into an evidence base.

Why do the side effects hit so hard?

Side effect burden in fibromyalgia has barely been studied directly, and the most revealing number available comes from a placebo group. In the pregabalin trials, 78 per cent of people on the drug reported at least one adverse event, and so did 77 per cent of the people on a dummy tablet [231]. Whatever that is, it isn’t pharmacology.

The real drug effects then stack on top: a number needed to harm of 3.7 for dizziness, and 19 per cent stopping duloxetine or milnacipran because of side effects against 10 per cent on placebo [171]. The overview is blunt that there’s no evidence on who’s going to get them [130], which means the only way to find out is still you, a start date and a fortnight.

Why do my symptoms get worse around my period?

Symptoms getting worse around a period is a real pattern for a lot of women with fibromyalgia, though not for all of them, and the studies that tracked it as it happened are small. In a one cycle diary study of 40 women, pain and fatigue ran highest in the menstrual and luteal phases [240]. The best measured study of the lot took blood every day for 25 days in just eight women: pain peaked during the period, was lowest in the middle of the luteal phase, and tracked progesterone and testosterone rather than oestrogen [241].

The other half of the literature disagrees. A study of 57 women found pain didn’t vary across the cycle at all [242], and when ovulation was confirmed and pain thresholds were tested in a lab, 74 women with fibromyalgia came out more sensitive than 74 controls all month, with no shift between phases [243].

So the pattern is real for some people and it isn’t universal, and nobody can tell you in advance which you are. Three months of tracking your own symptoms against your own cycle will answer it faster than the literature will.

Does fibromyalgia get worse in perimenopause and menopause?

Fibromyalgia does seem to get worse around menopause for some women, and no study has yet separated menopause from simply getting older, which is the part that matters. In 152 women with fibromyalgia, those past menopause reported more pain, roughly a quarter put the start of their symptoms at menopause, and a similar share said it worsened afterwards [240]. That’s memory, and it compares two groups rather than following anybody through.

Early menopause was recorded in 38.3 per cent of women with fibromyalgia against 13.4 per cent with rheumatoid arthritis, and hysterectomy in 16.5 against 6.0 per cent [244], which may say as much about gynaecological history as about hormones. Joint and muscle pain is commoner across the transition in women generally [67].

We found no study that followed women with fibromyalgia through the menopause and accounted for age. That’s the study that would settle it, and it hasn’t been done.

Does HRT help fibromyalgia?

HRT has one placebo controlled trial in fibromyalgia, and it didn’t help the pain. Twenty nine postmenopausal women used oestrogen patches or placebo for eight weeks, and neither their own pain ratings nor the lab pain testing differed [245].

The positive results all come from weaker designs or from different drugs. An open study of oestrogen with micronised progesterone reported better impact scores and sleep after 12 weeks, with no placebo group to compare against [246]. A placebo controlled trial in 100 women was positive, but for raloxifene, an osteoporosis drug that isn’t HRT [247]. Testosterone has one uncontrolled 28 day study in 12 women [248].

We found no report of fibromyalgia getting worse after starting HRT, which is an absence of evidence rather than proof it never happens. So if HRT makes sense for your menopause symptoms, decide on that basis and treat anything it does for the pain as a bonus rather than the reason.

What happens in pregnancy and after birth?

Fibromyalgia usually gets harder through pregnancy rather than easier, and the months after the birth are often worse again, though most of that comes from one small study of women looking back. In interviews covering 40 pregnancies, nearly all reported worsening, the third trimester was the worst of it, and 33 were followed by worse symptoms within six months of the birth [249]. In 360 women assessed in the third trimester, those with fibromyalgia had more pain, disability, anxiety and depression than those without [250].

Across 12.6 million US births, fibromyalgia came with modestly higher odds of prematurity, an odds ratio of 1.35, and of restricted growth in the womb, 1.48 [251]. That’s an association from hospital records rather than a cause, and the size of it is modest. Breastfeeding lasted just as long in the one study that compared it [252].

Pelvic pain, painful periods and painful sex

Painful periods, bladder pain and painful sex are all commoner alongside fibromyalgia, and the overlap runs both ways, which is a reason to examine the pelvis properly rather than a reason to stop looking. In 98 women with fibromyalgia, 41 per cent had painful periods against 28 per cent of controls [253]. Fibromyalgia was reported by 17.7 per cent of women with bladder pain syndrome against 2.6 per cent of controls [254], and diagnosed in 7 per cent of an endometriosis cohort [255]. Women with fibromyalgia report more pain during sex [256].

It matters before surgery too. In women having a hysterectomy for chronic pelvic pain, each extra point on a widespread pain score raised the adjusted odds of still being in pain six months later by 27 per cent [257].

Endometriosis is still endometriosis, and it still needs finding. A fibromyalgia diagnosis explains a great many things, and it doesn’t explain a pelvis nobody has examined.

Does fibromyalgia get worse with age?

Not as a rule, though nobody has yet separated fibromyalgia from ageing itself. The largest follow up tracked 1,555 people for up to 11 years, and about a quarter had at least moderate improvement in pain while severity worsened for around a third [258]. Movement both ways around a flat average. A six centre study found pain, fatigue, sleep and mood essentially unchanged over seven years [271], though a UK hospital cohort is grimmer, with 60 per cent feeling worse at four years [272].

Compare age groups and older people report slightly less rather than more. The lowest burden fell between 60 and 70 in an Italian registry of 2,889 [273], a US clinic found younger people worse off [274], and pain, mood and sleep were all lower with age once other conditions were accounted for [275]. Those are snapshots though, not people followed as they aged, so read them as what an older group looks like rather than as what’s coming for you.

Can fibromyalgia go away?

It can, and the word the research uses is remission rather than cure. In that 11 year cohort, 44 per cent stopped meeting the criteria at least once, and most didn’t stay there [258]. A two year US study found 26.3 per cent no longer met the definition at follow up, while ten people crossed the other way and acquired it [276]. In UK chronic widespread pain rather than diagnosed fibromyalgia, 44 per cent no longer met the criteria 15 months on [259].

Over 10 to 12 years, 16 per cent of Swedish women got at least a halving of their pain [119]. And the most useful long number is Finnish: after 26 years, 11 per cent considered themselves healed, and 23 per cent had had at least one symptom free stretch lasting a year or more [277]. That’s the going away and coming back the forums describe and the clinic letters never mention.

Is there a cure, and what about the people who say they cured it?

No treatment has been shown to cure fibromyalgia, and the cleanest test of that is a withdrawal trial. People doing well on long term milnacipran lost their response once they were switched to placebo, and the authors concluded that even successful treatment hadn’t cured anything [260].

None of which makes the recovery stories lies. Some people do improve enormously: a group pain neuroscience education course in Spanish primary care got 39.7 per cent of people to a 50 per cent improvement in fibromyalgia impact, against 4.5 per cent on usual care [261]. Some had something else all along, and in UK general practice only 38.5 per cent of those carrying a fibromyalgia diagnosis met the criteria on reassessment [262].

And some bought a programme nobody has tested here. Pain reprocessing therapy, which sits behind a lot of the cure content online, has one single arm pilot of 35 adults and no randomised trial in fibromyalgia at all [263]. Worth knowing before you pay for one.

Can fibromyalgia shorten your life?

Fibromyalgia isn’t a fatal condition, and the mortality research is broadly reassuring with one exception. Following 8,186 patients for 35 years found deaths running slightly below the expected rate [264]. A study of 35,248 people found a small rise that mostly vanished once other conditions and physical function were accounted for [265]. Two pooled analyses disagree with each other, one finding a modest increase and the other finding nothing clear [86][266]. Cancer deaths aren’t raised and may be lower [265].

The exception is suicide, at around three times higher across the cohorts [86][264][265], and higher still among Danish women [267]. That’s a verdict on how people with this get treated rather than on the illness itself. If you’re anywhere near that, the Samaritans are on 116 123.

What makes it more likely to get better?

Sleep keeps reappearing. In the UK chronic widespread pain study, people reporting restorative sleep were twice as likely to stop meeting the criteria 15 months on [259]. A Canadian follow up over a mean of 40 months found younger age and less disturbed sleep predicted a better outcome [268], and in a Norwegian population study insomnia predicted developing fibromyalgia in the first place [278]. Lower stress at the outset predicted substantial pain improvement in Swedish women followed for 10 to 12 years [119], while depression at baseline predicts a worse result across the rehabilitation studies [269].

These are prospective associations rather than instructions, so don’t read them as a list of personal failings to correct. Where sleep is being wrecked by something treatable though, treat it: people with sleep apnoea who also met the fibromyalgia criteria and stuck with CPAP and exercise for three months improved on pain, fatigue, mood and pain threshold [270].

Does fibromyalgia go away with weight loss?

No study reports anybody losing weight and ceasing to have fibromyalgia, and symptoms do shift. About 36 per cent of people with fibromyalgia are obese, and a higher body mass index tracks weakly with worse symptoms [279]. The one randomised trial put 83 obese patients through six months of dietary weight reduction and found better fibromyalgia impact scores, fewer tender points and better sleep and mood than no weight loss [280].

A calorie restriction study found the biggest gains in those who lost at least a tenth of their body weight [281], and a very low energy diet improved symptoms inside three weeks, before much weight had actually gone, which suggests the weight itself may not be the active ingredient [282].

Bariatric surgery has one small retrospective series reporting less pain and tenderness [283], and in the wider surgical literature pain improves for a year or two and then partly comes back [284][285]. So it’s worth doing if it’s worth doing for its own reasons. It isn’t a cure.

Is fibromyalgia a disability in the UK?

Fibromyalgia can be a disability in law, and the Equality Act 2010 doesn’t work from diagnoses. Its test is an impairment with a substantial and long term adverse effect on your ability to carry out normal day to day activities [286], where long term means it has lasted, or is likely to last, twelve months [287].

Two clauses matter more than the label does. If the effect stops but is likely to recur, the Act treats it as continuing, which is written for exactly the conditions that come and go. And where medication is masking the effect, you’re judged on what would happen without it [287]. So no letter makes you disabled, and no clear blood test stops you being it.

Can I claim PIP with fibromyalgia?

Yes, because PIP isn’t awarded for conditions. You need to be 16 or over, under State Pension age, and to expect the difficulties to last at least 12 months, and in Scotland you claim Adult Disability Payment instead [288][301]. Points are scored across twelve activities, eight for the standard rate and twelve for the enhanced [289].

The clause that decides most fibromyalgia claims is reliability. A task counts only if you can do it safely, to an acceptable standard, repeatedly, and in under twice the time a non disabled person takes, on more than half the days in a year [290]. Managing it once on a good day isn’t managing it, and that’s the sentence worth having in your head while you fill the form in.

Of new claims cleared to July 2026, 34 per cent were awarded, down from 41 the year before [292]. Of PIP appeals heard between April and June 2026, 67 per cent went the claimant’s way [293].

What about Universal Credit and the work capability assessment?

It’s a separate claim with a separate question: not what daily life costs you, but whether you can work or prepare for work [296]. The extra health amount split in two on 6 April 2026. Report a condition before that date, or be assessed as severe and lifelong, or be nearing the end of life, and it’s £429.80 a month. Declare from that date without one of those and it’s £217.26 [295][296].

The severe lifelong test needs a condition that stops you working, lasts your whole life, won’t get better, and is formally diagnosed [296]. Fibromyalgia fluctuates and can improve, so it won’t usually meet it.

What adjustments can I ask for at work?

Anything that removes the disadvantage and is practical, affordable and safe. Employers have to make reasonable adjustments by law, and the duty covers employees, workers, contractors, the self employed and job applicants [297]. It bites once the employer knows, or could reasonably be expected to know [297].

Start with hours, a later start, hybrid or home working, a seat, and control over lighting and noise [297]. After seven days off you need a fit note, which can say you may be fit for work with changes, and if those changes can’t be agreed you’re treated as not fit for work [299]. Access to Work grants cover equipment, support workers and travel, and explicitly not reasonable adjustments, which your employer pays for [298].

Can I get a blue badge?

Not on the diagnosis, and there are two routes, of which most people only ever hear about one. In England you qualify automatically with eight points or more on the PIP moving around activity, or ten points under descriptor E of planning and following journeys [300].

Otherwise your council assesses you, and the criterion that fits is finding walking very difficult because of pain, breathlessness or the time it takes [300]. That route explicitly covers non visible conditions, and councils ask for your medication, your treatments and the professionals involved [300]. Scotland, Wales and Northern Ireland run their own schemes [300].

What do I do when the GP says there is nothing more they can offer?

Take it as a statement about the local service rather than about the evidence. NICE classes fibromyalgia as chronic primary pain and says to offer a supervised group exercise programme, and to consider acceptance and commitment therapy or CBT for pain, a short capped course of acupuncture, and an antidepressant such as amitriptyline or duloxetine after a proper discussion of the harms [31]. The same guideline tells prescribers not to start paracetamol, anti inflammatories, opioids, benzodiazepines or gabapentinoids for it [31].

So nothing more usually means nothing more they’re allowed to prescribe, which is a different sentence altogether. Ask for the named thing instead: a referral to a pain management programme [31].