Creatine for Hypermobility, Fibromyalgia and Chronic Pain: What the Research Actually Shows

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Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

Latest posts by Adam Foster (see all)

• Fibromyalgia and Central Sensitisation, What Is It in Plain English? - 8 October 2026
• Which supplements are worth taking when you’re hypermobile - 4 October 2026
• Hypermobile Wrists: Why They Hurt, Which Brace to Use, and How to Build Control - 4 October 2026

Creatine is the supplement we get asked about more than all of the others put together, and the asking has got considerably louder over the past couple of years, as creatine has gone from something sold in big tubs to men who deadlift, into something written up in the press for fatigue, brain fog and chronic illness. It comes up in the studios, it comes up in the workshop questions, and it turns up in our inbox most weeks of the year. So, the short answer first and then the long one, as the long one is where the useful bits actually live.

Creatine is about as safe as a supplement gets, at least in the groups where it has actually been looked at properly ^[1][2], and it does reliably put more fuel into muscle, and in fibromyalgia it did improve strength ^[3][4]. What it doesn’t do, on the evidence that exists, is reliably reduce pain ^[4][5]. And for hypermobility or Ehlers-Danlos syndrome specifically, the direct evidence is essentially absent, which is not a sentence you’ll find on very many supplement websites.

Nearly everything useful in this article comes from research in the conditions next door, so fibromyalgia, ME/CFS, post viral fatigue, arthritis, and healthy adults. Every time we’re borrowing from a neighbouring group we’ll say so out loud, rather than quietly letting it read as though somebody had studied you.

What follows is what creatine actually does inside a body, why the safety question is genuinely settled while the pain question genuinely isn’t, what the fibromyalgia and post viral fatigue research found, why the brain fog claims are real but rather oversold, and how to take it sensibly if you decide to. You’ll also come away with a fairly clear idea of where the data stops, which matters a great deal in a field where most of what gets written is wishful thinking wearing a lab coat.

What Creatine Actually Does In A Body

Your body already makes creatine. It’s put together mainly in the liver, the kidneys and the pancreas, and then carried into the cells that need it by a dedicated transporter, which is a detail worth holding onto, as it means getting creatine into a tissue is an active process rather than just a matter of having enough of it floating about ^[6].

Once it’s inside a cell, creatine kinase runs a reversible reaction between creatine and phosphocreatine, and that reaction is what lets a cell regenerate ATP very quickly when demand suddenly rises ^[6]. In plain terms, creatine isn’t a painkiller and it isn’t a fuel in the way that food is, it’s a buffer, a small local reservoir that smooths out the gap between how fast a tissue needs energy and how fast it can make it ^[6].

The vast majority of the body’s creatine, around 95 per cent of it, sits in skeletal muscle, with much smaller amounts in the brain and elsewhere ^[7]. The brain manages its own supply somewhat separately, which is why brain creatine gets measured with scanning rather than a blood test, and why it behaves rather differently from the creatine sitting in your quadriceps ^[8].

Supplementing raises muscle creatine and phosphocreatine pretty dependably ^[3]. Brain creatine appears to rise too, though usually by less and considerably less predictably, and that difference between the two tissues is doing a great deal of quiet work underneath the headlines about creatine and the brain ^[9].

What Happens When There Isn’t Any

Some of the more convincing mechanistic evidence comes from the other direction entirely, from what goes wrong when creatine is missing rather than what improves when it’s added. In animals bred without the ability to make creatine, energy metabolism in muscle goes badly wrong and a muscular dystrophy develops, and feeding creatine back reverses it ^[10]. Break the transporter instead, so creatine is made but can’t get into the cells that need it, and you get impaired motor function alongside disrupted muscle energy handling, again in animals ^[11].

That has been shown in animals though, and nobody has tested whether any of it holds in people, so it isn’t a fact about you and we’re not going to present it as one. What it does tell you is that the creatine system is load bearing, and when it’s genuinely broken the consequences turn up in muscle and in movement, which is at least a coherent reason to wonder whether topping it up matters in conditions where energy handling looks a bit off.

Creatine also does rather more than shuttle energy about inside a single cell, as it turns out. It gets described these days as a systemic regulator sitting in the middle of a much wider metabolic network, rather than as a purely local buffer, and that reframing is a good part of why the research has spread out from sport into so many unrelated conditions ^[12]. All very interesting, and still a very long way from proof that it helps with any of them.

Now, that’s the whole mechanistic case. We know the tank fills, we’re much less sure what filling it does for symptoms, and that gap is now being pointed out fairly bluntly in the brain creatine work itself, where the enthusiasm has rather run ahead of the measurements ^[13].

Safety Is The Part That Is Actually Settled

The safety case for creatine is far stronger than the efficacy case for anything it’s currently being sold for, and it’s worth separating the two, because “it probably won’t hurt you” and “it will help you” are very different sentences.

Short and long term use has been judged safe and well tolerated in healthy people and in several groups with health conditions, including use at up to 30 grams a day for five years, which is a much larger dose over a much longer stretch than anyone reading this is ever likely to take ^[1]. When every controlled comparison anyone could find was pooled together, there was no increase in how commonly side effects were reported, or how often, compared with placebo ^[2][14].

There is one honest wrinkle in all of that, as gut complaints and muscle cramping did turn up slightly more often at the level of what got written down in reports, though the difference didn’t hold once people were counted rather than reports, and the gaps were small either way ^[2]. Dose and duration also don’t show any consistent pattern of more exposure producing more meaningful side effects ^[15].

Practically, that wrinkle is worth taking seriously even though it’s a small one, as gut trouble is already the norm rather than the exception with hypermobility, and a supplement that upsets an already unhappy stomach gets abandoned in week two regardless of what it might have done by week twelve.

None of this is new either, which is worth knowing when somebody tells you creatine hasn’t been around long enough to be sure about. The safety questions were being picked over pretty carefully well over a decade ago, and the answers haven’t moved a great deal since ^[16]. It has also been given across a fairly wide spread of health conditions, muscular, neurological and metabolic, which is a large part of why the tolerability data is so much richer than the data on whether it actually works for anything ^[17].

Kidneys, And The Blood Test That Looks Alarming

The kidney worry is the one that gets repeated most, usually by somebody who heard it from somebody else, and the controlled evidence doesn’t support it. Pooling everything available, there’s no sign that the doses and durations studied cause kidney damage ^{[18][19][20][21][22]}.

The myth has been gone over directly more than once and the pattern is always the same: the theoretical worry is understandable, the measured kidney outcomes don’t follow it, and the belief survives mostly because of the blood test artefact below ^[23].

What does happen is a lab artefact, and it catches people out constantly. Creatine converts to creatinine, creatinine is exactly what a routine kidney blood test measures, so taking creatine can push your serum creatinine up without anything at all having gone wrong with your kidneys ^[18][19]. If you’re hypermobile you probably get bloods done more often than most, so tell whoever is ordering them that you’re taking it, otherwise you risk a phone call about your kidney function that nobody needed to make (and that call never seems to land on a Monday morning).

The longer term picture points the same way, as no clinically meaningful kidney or liver abnormalities turned up in women footballers followed across a full season, in people with motor neurone disease taking 10 grams a day for the best part of a year, or in college footballers using between 5 and 20 grams a day for up to five and a half years ^[24][25][26].

Now, the caveat, and it’s a real one rather than a legal one. Almost all of that reassurance comes from healthy people, or from groups being medically supervised for something else, and established kidney disease is repeatedly flagged as the situation where the evidence thins out and caution is warranted ^[27][28]. So if you’ve got kidney disease, or you take medication that leans on your kidneys, that’s a conversation with a clinician who knows your bloods rather than a decision to make off the back of an article.

Pain, Which Is The Part Everybody Wants And The Evidence Doesn’t Give

In fibromyalgia, given over sixteen weeks and against a placebo, muscle phosphocreatine went up, leg press, chest press and isometric strength all improved, and pain did not change ^[4]. Not reduced a bit, not reduced in some subgroup worth getting excited about, no general change in pain at all, and no general improvement in thinking, sleep or quality of life either ^[4].

The same people, over the same sixteen weeks, got measurably stronger and felt no better. So, whatever creatine is doing inside a fibromyalgia muscle, and it is doing something, as the phosphocreatine measurements moved, it isn’t reaching whatever generates the pain ^[4]. Which is genuinely useful negative information, as it rules out the simplest version of the story, the one where fibromyalgia pain is a muscle running out of fuel and creatine just fills the tank back up.

Earlier and friendlier looking fibromyalgia results, which get quoted a great deal, had improvements in pain, sleep, disability and quality of life over eight weeks. There was no comparison group though, and it was called preliminary at the time, as the group was small and people dropped out of it ^[29]. So it’s supportive, it’s weak, and where it disagrees with the placebo comparison, the placebo comparison wins.

Widening out beyond fibromyalgia doesn’t rescue it either. Across chronic musculoskeletal pain treated in rheumatology, which takes in fibromyalgia, osteoarthritis, rheumatoid arthritis and juvenile idiopathic arthritis, the pattern is strength gains with inconsistent effects on pain, and the evidence on pain and inflammation is limited and all over the place ^[5].

The anti inflammatory story, which is the usual explanation offered for why creatine ought to help pain, has much the same problem. Pooling the controlled work on inflammatory markers, there’s no meaningful ongoing effect on CRP or IL-6 ^[30]. That doesn’t prove creatine does nothing to inflammation in every possible circumstance, but it does mean the specific mechanism people reach for to explain a pain benefit hasn’t shown up in humans, which is a bit of a problem when the pain benefit hasn’t reliably shown up either.

Supplements in fibromyalgia as a whole sit in much the same place, as there’s no shortage of plausible candidates with a decent mechanism behind them, and very little that survives contact with a control group ^[31]. Which isn’t the same as saying nothing works, by the way, it’s saying the research is thin, small and scattered, and thin research always favours whoever is selling something.

So, the honest version of it. If your question is “will creatine reduce my pain”, the answer at the moment is not reliably, and anyone telling you otherwise is either quoting the uncontrolled work or quoting nothing at all.

Strength And Function, Where It Does Earn Its Keep

That isn’t the same as creatine being irrelevant to you, and the difference between the two is where most of the confusion about creatine lives.

In fibromyalgia, the same sixteen weeks that gave no pain benefit did give better muscle phosphocreatine and better strength, in the same people ^[4]. Pooling the broader work in people at risk of losing physical function, creatine comes out as helpful for physical function specifically ^[32]. So the thing it seems to move is capacity, what your muscles can do and for how long, rather than how much it hurts while they do it.

Pain and capacity are not the same variable and they don’t always travel together, which matters a great deal if you’re hypermobile. Plenty of the people we work with, aren’t primarily limited by how much something hurts on the day, they’re limited by how little they can do before everything gets worse, and by how long it takes to get back afterwards.

Now, in our opinion, that’s where creatine is most likely to be doing something for this population, as a small help with the training rather than a treatment for the symptom. But that is an inference and we’re marking it as one, as nobody has tested it. What has been shown is better strength in fibromyalgia and better physical function in groups losing it ^[4][32]. Whether that translates into getting more out of your rehab when you’re hypermobile is currently a reasonable guess and nothing sturdier than that.

There’s a very practical reason to get that distinction right, as if you start creatine expecting less pain, you’ll give it six weeks, notice your pain is much the same, and bin it, and you’ll have missed the only thing it was ever plausibly going to do for you. Whereas if what you’re tracking is how much you got through in a week, and how flattened you were two days later, you’re at least measuring in units the evidence has something to say about.

And a caution on that, in our experience rather than from any of the research. Feeling capable of more, while your tissue tolerance hasn’t actually changed, is the precise recipe for the boom and bust pattern most of those with hypermobility already know far too well, and it’s the most common way we see a decent week turn into a rotten fortnight. If creatine does buy you a little more capacity, our advice would be to spend it on doing your rehab more consistently, rather than on doing far more of it in one afternoon.

An energy buffer doesn’t give your brain a clearer signal from a joint and it doesn’t teach a better movement strategy, and those two things are still where the actual work is for hypermobility. Creatine isn’t a shortcut round any of that, and we’ve never met anyone whose problem was a phosphocreatine deficit in their hamstring!

Fatigue Is The More Interesting Story

Fatigue is where this gets properly interesting, and it’s also where you need to keep the hedges firmly in place.

The rationale is decent, as conditions like ME/CFS, post viral fatigue and fibromyalgia have all been argued to involve some sort of bioenergetic disturbance, altered phosphocreatine handling, or regional differences in brain creatine, and if any of that is right then an energy buffer is at least aiming at the correct target ^[3][17][33].

Notice that fibromyalgia sits in that list too, which means the same bioenergetic argument is being made for a pain condition and for the fatigue conditions at once ^[3][17]. The results have gone rather differently in the two, and that split is informative all by itself, as a mechanism that’s meant to explain both should probably have delivered in both.

What’s been done in people is early, small, and pointing in a consistent direction, which is about the most you can say for it.

In ME/CFS, 16 grams a day for six weeks raised creatine in two frontal brain regions, reduced fatigue, improved hand grip strength and improved some reaction time measures ^[34]. There was no comparison group though, and the need for one was stated outright at the time, so treat it as a hint rather than a finding ^[34].

In post COVID fatigue, 4 grams a day over six months, this time with a placebo comparison, raised creatine in thigh muscle and in selected brain white matter, reduced general fatigue by three months, and improved several symptoms including body aches, headache and difficulty concentrating by six months ^[35]. The group was tiny though, so it’s an encouraging signal rather than something to build a plan on.

In long COVID over four weeks, 6 grams a day was associated with lower fatigue scores and higher handgrip strength, while a much larger daily dose wasn’t clearly better, and the side effects that turned up were minor and passed ^[36]. That’s one of the very few hints anywhere in this literature that more is not automatically better.

The tissue measurements did move, as creatine went up in muscle and in brain regions, and those are scans rather than questionnaires ^[34][35]. The fatigue improvements are questionnaires, which honestly isn’t a criticism, as fatigue is a subjective experience and there’s no blood test for it, though it does mean the softer outcome is the one carrying the claim. Where both moved together, as they did in post COVID fatigue, that’s a slightly stronger position than either on its own ^[35].

What would shift our view is fairly specific and fairly obvious: the same sort of doses, given to a decent sized group, with a placebo comparison, in a fatigue condition, measuring the tissue and the symptom at once. That’s an entirely doable piece of work and somebody will get round to it eventually.

Put it together and you’ve got three early looks, in three different fatigue conditions, all pointing the same way, none of them big, and not one of them in hypermobility. Consistent direction across small studies is worth something, it’s just not worth anything like what the internet currently charges for it.

Brain Fog, Real But Oversold

The cognitive claims are where creatine marketing has got completely out of hand (it is now being sold for more or less everything above the neck), and the underlying evidence is a good deal more interesting and much more modest than the headlines.

Pooling the controlled work in adults, there were genuine effects on memory, on attention time and on processing speed time, and no meaningful improvement in overall cognition or in executive function, with the confidence in those results sitting at moderate for memory and low for everything else ^[37]. Another pooling landed in a similar place, short term memory and reasoning may improve while other domains stay conflicting or unchanged, particularly in young healthy people who presumably didn’t have a great deal of room to improve ^[38].

Then it gets properly contested, as looking specifically at healthy people, the cognitive evidence has been judged equivocal overall, with the better case sitting in stressed states, sleep deprivation, low oxygen, mental fatigue, rather than in ordinary everyday thinking ^[39]. The claim has also been formally assessed in Europe and judged not established, meaning a cause and effect relationship between creatine and improved cognitive function isn’t considered to have been shown, which is why you won’t see it on a label there ^[40].

Where the stressed state case does hold up, it holds up reasonably well. During sleep deprivation, a single large dose of 0.35 grams per kilogram of bodyweight improved processing speed and cognitive performance, and altered measures of high energy phosphates in the brain at the same time ^[41]. Benefits under low oxygen, under sleep deprivation and during long mentally demanding tasks get summarised repeatedly ^[42][43]. Nobody has settled on how you’d actually dose creatine to raise brain creatine in the first place though, which is a slightly awkward thing not to know about an intervention people are already selling for the brain ^[9][13].

The words themselves are doing a lot of quiet work here. Attention time and processing speed time are measures of how fast a task gets finished, and they aren’t the same thing as the fog you get on a bad day, where the problem is usually holding onto a thread, finding a word, or remembering what on earth you walked into the kitchen for. The domain that comes closest to any of that is memory, which is also the only one where the confidence in the result rises above low ^[37].

The fair summary, then, is that creatine appears to do something small and real to a couple of fairly narrow cognitive measures in adults, and there’s no good reason yet to believe that translates into your brain working better on a flare.

So, for the fog that comes with fibromyalgia, hypermobility or long COVID: the stressed state finding is not the same thing as your fog, an acute sleep deprivation result in healthy adults tells you very little about a chronic problem in an unwell nervous system, and nobody has tested creatine on your version of it. The fatigue work above is a better reason for cautious interest than the cognition work is.

Hypermobility And EDS, Where The Evidence Simply Isn’t

The Ehlers-Danlos syndromes are a group of heritable connective tissue disorders, characterised by joint hypermobility, tissue fragility and symptoms that turn up across multiple systems rather than staying politely in the joints ^[44][45]. There is no specific medical therapy established for EDS itself, and that’s the context every single supplement conversation in hypermobility happens inside ^[44][46].

Which explains a fair bit about why supplements loom so large in this community. Where there’s a licensed treatment that works, people argue about the treatment. Where there isn’t one, the space fills up with whatever is cheap, available without a prescription and easy to try, and it gets filled fastest by whoever is most confident rather than by whoever is most careful. The published guidance for EDS is largely about managing consequences, so the pain, the injuries, the systems that misbehave, rather than about treating the tissue itself ^[46][44]. Creatine walks into that vacuum with a good safety record and a nice sounding mechanism, which is precisely the combination that gets oversold.

Chronic pain and fatigue are both common in hypermobile EDS ^[47]. Hypermobility itself also spans a range of traits, disorders and syndromes rather than being one clean category, which is part of why research in this space is so difficult to interpret and why studies that look similar often aren’t ^[48].

And the direct creatine evidence here isn’t thin, or mixed, or promising, it’s essentially absent.

Part of that problem sits upstream of creatine entirely. Hypermobility research has spent years wrestling with the fact that those with hypermobility aren’t one group, and that the labels keep moving, so two pieces of work that look like they studied the same thing often didn’t ^[48][45]. Even if somebody ran a creatine study in hypermobility tomorrow, the first argument about it would be over who was in it.

Pain and fatigue also arrive alongside gut problems, dysautonomia, poor sleep and a long list of other things in hypermobile EDS, and any one of those can generate fatigue on its own ^[47]. A supplement aimed at cellular energy is aimed at one possible contributor among many, which is worth keeping in mind before it quietly becomes the thing you’re relying on.

There are two lines of thinking that make creatine biologically interesting in hypermobile EDS specifically. Mitochondrial dysfunction has been mapped as a possible contributor, bridging cellular energetics and the genetic pathways involved ^[33], and fascial abnormalities have been proposed as another ^[49]. Both are explicitly hypothesis generating, both are labelled that way in the work itself, and neither is evidence that creatine helps anyone with hEDS, because that would require giving creatine to people with hEDS and seeing what happened, which has not been done.

A tidy mechanism is about the easiest thing in the world to sell, and it’s nowhere near the most reliable thing to buy, and this community has been sold a fair few of them over the years.

If You Decide To Try It

None of the above is us telling you not to take creatine. It’s cheap, the safety data is genuinely good in the groups studied, and if you want to try it on the strength of the fatigue and strength findings, that’s a defensible decision made with your eyes open. So, these are the forms and the doses the research actually used.

– The form: Creatine monohydrate, essentially throughout. It’s the form in nearly all the work above, it’s the cheapest, and the fancier versions on the shelf (and there are a lot of them now) are not what any of this evidence is based on ^[2][50].

– Loading or not: The common approaches are either around 20 grams a day for 5 to 7 days followed by 3 to 5 grams a day, or simply 3 to 6 grams a day from the start with no loading phase at all ^[3]. Loading fills the muscle faster and it’s also where the gut complaints cluster, so if your digestion is already temperamental, which it is for a lot of those with hypermobility, skipping the loading phase costs you very little.

– The doses used in the conditions nearest to yours: 4 grams a day over six months in post COVID fatigue, 6 grams a day over four weeks in long COVID, 16 grams a day over six weeks in ME/CFS, and 10 grams a day for the best part of a year in motor neurone disease ^{[35][36][34][25]}. There’s no agreed dose for fatigue, and the higher doses are not obviously better ^[36].

– Brain dosing is an open question: If your interest is cognitive, be aware that how much creatine it takes to meaningfully raise brain creatine, and for how long, has not been established ^[9][39][43].

– Blood tests: Tell whoever orders your bloods. Creatine raises serum creatinine directly, which can look like a kidney problem and isn’t one ^[19].

– Kidney disease: If you’ve got established kidney disease, or medication that’s hard on your kidneys, this is a clinician’s call rather than yours or ours, as that’s precisely the group where the reassuring evidence runs out ^[27][28].

– What it costs: Plain monohydrate powder is one of the cheapest things on the supplement shelf, and it is the form nearly all of the research above used ^[2][50]. If you’re being charged a premium for a capsule, a blend, or a cleverly named variant with a longer word on the tub, you’re paying for marketing rather than for evidence, and the gap between the price of the plain tub and the price of the clever one is not a gap you are getting anything at all for.

– How long to give it: The fatigue work ran from four weeks out to six months, and the fibromyalgia strength changes came over sixteen weeks ^[36][35][4]. So a fortnight is not a trial of anything, and in our opinion anything much under a couple of months isn’t either.

– What to judge it on: In our opinion, judge it on what you can do rather than on how much you hurt, as strength and function are where the evidence actually sits, and pain is where it doesn’t ^[4][32].

– What it isn’t: It isn’t a treatment for hypermobility, it isn’t a substitute for the rehab, and there’s nothing here suggesting it does anything at all to connective tissue. It’s a possible small help with strength, and possibly with fatigue, and that’s the whole of the offer.

What Nobody Knows Yet

The genuinely useful shift over the past few years is that creatine has stopped being purely a sports supplement and started being taken seriously as a possible bioenergetic add on in chronic, fatigue linked conditions. That’s a real change, and it’s a good part of why so much has appeared in the press about it lately.

The open question is whether any of that translates into reliable symptom benefit in hypermobility and chronic pain, and right now it doesn’t translate, as nobody has run the study. What’s missing is creatine given to those with hypermobility, with a placebo comparison, measuring fatigue and function rather than only pain, and run for long enough to matter.

Another pooling of the work that already exists won’t answer it, and neither will a mechanism paper, however elegant it is, as a plausible pathway in a hypermobile cell is not the same thing as a person feeling better ^[33][49]. The gap is a clinical one and the only thing that closes it is somebody doing the clinical work, which is unglamorous, slow and expensive, and is why it keeps not happening.

Until somebody does that, everything anyone tells you about creatine and hypermobility is borrowed from a neighbouring condition, and it’s worth knowing which one you’re being handed.

The Fibro Guy

References

[1] Kreider, R.B., Kalman, D.S., Antonio, J., Ziegenfuss, T.N., Wildman, R., Collins, R. et al. (2017) ‘International Society of Sports Nutrition position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine’, Journal of the International Society of Sports Nutrition. https://doi.org/10.1186/s12970-017-0173-z

[2] Kreider, R.B., Gonzalez, D.E., Hines, K., Gil, A. and Bonilla, D.A. (2025) ‘Safety of creatine supplementation: analysis of the prevalence of reported side effects in clinical trials and adverse event reports’, Journal of the International Society of Sports Nutrition. https://doi.org/10.1080/15502783.2025.2488937

[3] Marshall, R.P., Droste, J.N., Giessing, J. and Kreider, R.B. (2022) ‘Role of Creatine Supplementation in Conditions Involving Mitochondrial Dysfunction: A Narrative Review’, Nutrients. https://doi.org/10.3390/nu14030529