Cold showers come up in our inbox a lot. Cold plunges, ice baths, cryotherapy chambers, the seven minute Wim Hof breathing thing, the “11 minutes a week” claim that’s been doing the rounds on every wellness podcast for the last few years. Someone with fibromyalgia or hypermobility reads about it, sees a video of a man in shorts roaring in a barrel of ice, and asks the very fair question. Is this actually going to help my pain, or is it another wellness fad?
Short answer. The evidence is thinner than the marketing suggests, the popular claims often don’t survive a look at the primary papers, and the safety picture for people with hEDS, POTS, MCAS, or significant central sensitisation is genuinely more complicated than the wellness internet lets on. That doesn’t make cold exposure useless. It does mean the “everyone should be cold plunging” pitch isn’t honest.
This is a full rewrite of an older post we had on this site. We’ve gone back through the literature, pulled in the EDS angle that wasn’t in the original, and stripped out the bits that didn’t age well. What you’re reading now is what we’d tell a client in person, with the actual papers handed to you.
If you’ve got fibromyalgia, hypermobility, hEDS, POTS, MCAS, or some combination of those, read this all the way through before you turn the shower dial to cold. Some of what’s below will change the calculus. Some of it might make you reconsider what your local cryotherapy place is selling.
Why people with fibro and EDS keep asking about cold showers
When it comes to chronic pain, people will try almost anything that looks plausible and costs nothing. A cold shower is free. It feels like it’s doing something. The wellness internet has spent the last five years promoting it as a kind of shortcut for inflammation, mood, focus, immunity, and pain. So the question lands in our inbox on a weekly basis.
For fibromyalgia specifically, there’s an extra layer. Many of those with fibro have allodynia, the experience of normal touch becoming painful. We’ve covered allodynia in detail elsewhere. Cold is one of the modalities people try when their skin is hypersensitive to clothing, water, or temperature changes. Sometimes it helps a bit. Sometimes it makes everything worse. The reason for the inconsistency turns out to be relevant to the whole evidence base.
For those with hEDS or hypermobility spectrum disorder, the picture is different again. Cold intolerance is a recognised symptom in this population. Raynaud’s overlap is common. POTS overlap is common. MCAS overlap is common. The POTS, EDS and MCAS trifecta is something we’ve written about at length. Any conversation about cold exposure has to take all of that into account.
So the question isn’t “are cold showers good or bad”. The question is “what does cold actually do to a nervous system that’s already running with central sensitisation, autonomic dysregulation, and in many cases small fibre damage”. That’s the version we’re going to answer.
What the cold shower evidence actually shows (and who it’s been tested on)
Here’s the catch. The largest randomised controlled trial of cold showers ever conducted didn’t include a single person with fibromyalgia. Not one [2].
That trial is Buijze and colleagues, 2016, published in PLOS One. The Dutch team randomised 3,018 healthy adults aged 18 to 65 without severe comorbidity to a routine hot to cold shower (30, 60, or 90 seconds of cold at the end of a hot shower) or a control group, for 30 consecutive days, with optional continuation for 60 days afterwards. The primary outcome was illness days and sickness absence from work [2].
The result. A 29% reduction in sickness absence from work in the cold shower groups compared to control. That’s a real effect, and that’s the headline you’ll see quoted everywhere. What gets quoted less often. No difference in work productivity. No difference in self reported illness days. And again, healthy Dutch adults. Not a fibro population. Not an EDS population. Not anyone with chronic pain, dysautonomia, or mast cell issues.
This is the biggest, best designed cold shower trial that exists. And it doesn’t tell us much about whether cold showers help fibromyalgia. The honest answer to “what does the cold shower evidence show for fibro” is: there is no direct cold shower trial in fibromyalgia. Anyone who tells you otherwise is extrapolating from healthy populations, which is exactly the move that gets us into trouble in this space.
The closest we can get is the whole body cryotherapy literature, which has actually been studied in fibro. So let’s look at that.
Whole body cryotherapy in fibromyalgia: what’s actually been studied
Whole body cryotherapy (WBC) means standing in a chamber cooled to between minus 110 and minus 140 degrees Celsius for two to three minutes. It’s not the same as a cold shower. It’s not the same as a cold plunge. It’s a specific, expensive intervention done in clinics and a few sports facilities. But it’s the closest thing we have to a properly studied cold exposure for fibromyalgia, so it’s the right place to start.
The Rivera trial in 2018 is one of the better designs we’ve got. Open randomised crossover, 60 fibro clients, cryosauna cabin versus rest. The VAS pain score difference was 3.0 in the WBC group versus 0.3 in the rest group after the first sequence. FIQ scores improved. The investigators noted a residual effect of WBC, which meant they could only analyse the first sequence cleanly [18]. So a real signal, decent sample size, but a methodological wrinkle that limits the strength of the conclusion.
The Klemm trial in 2021 is the one that matters most for the long term question. 23 women with fibro and 30 healthy controls, six sessions over six weeks at minus 130 degrees Celsius. Primary outcome was pain on a 100mm VAS. Pain improved significantly after three and six sessions. FIQ improved. Cytokine profiles shifted. And then the follow up. Three months after WBC was stopped, the clinical benefits did not persist [10]. The pain came back. The cytokines settled. The intervention worked while it was being delivered, and then it stopped working when it stopped being delivered.
That’s a really important detail. A treatment that works for as long as you’re doing it isn’t the same as a treatment that produces lasting change. In a chronic condition, that distinction matters financially, practically, and in terms of how you think about what’s actually happening at the neural level.
Vitenet 2018 was a small short report RCT showing health related quality of life improvement after WBC in fibro [22]. Useful confirmatory signal. Bettoni 2013 reported pain and quality of life improvement in 100 fibromyalgic clients, half receiving cryotherapy, half not [23]. The Bettoni paper is often cited as evidence for WBC, but it wasn’t a randomised trial. Participants were “addressed to” cryotherapy rather than randomised, which means selection bias is on the table. Worth knowing if you’re reading the citation list on a cryotherapy centre’s website.
The most recent piece is Verme and colleagues, 2024. They followed up two groups of 23 people, one receiving WBC as part of a multidisciplinary programme, one receiving the rehab programme alone. WBC added benefits in pain, general wellbeing, and sleep quality that lasted three to four months after the sessions ended [21]. Better persistence than the Klemm follow up data, but still a finite benefit, and still in the context of a broader rehab programme rather than as a standalone treatment.
So, the honest summary. WBC in fibromyalgia has small to moderate short term effects on pain and quality of life. The effects don’t necessarily persist past a few months. It’s expensive, requires repeated sessions, and is delivered in specialised facilities. Compared to a free cold shower, it’s a completely different intervention. So when someone uses the WBC data to justify cold showers for fibro, they’re connecting two studies that were never connected in the first place.
Cain and colleagues published a 2025 systematic review and meta analysis of cold water immersion effects on health and wellbeing more broadly, drawing on the wider literature [1]. It’s a sober read. The effects on inflammation, immunity, and mood are not as straightforward as the popular narrative suggests, and the populations studied are mostly healthy adults rather than chronic pain groups. Worth flagging because that review is what people should read first before they start quoting individual studies out of context.
The bigger picture: aerobic exercise wins, every time
Before we go any further, a piece of context that often gets dropped in these conversations. The EULAR revised recommendations for the management of fibromyalgia were updated in 2017 by an 18 member panel from 12 European countries, led by Macfarlane. They reviewed the evidence across pharmacological and non pharmacological treatments. The only intervention that received a “strong for” recommendation was aerobic and strengthening exercise [12].
Not cryotherapy. Not cold showers. Not heat, hydrotherapy, biofeedback, hypnotherapy, balneotherapy. When it comes to what actually moves the needle in fibromyalgia, the strong recommendation was exercise.
NICE’s 2021 guideline on chronic primary pain (NG193) covers chronic pain without a clear identifiable cause, which includes fibromyalgia. The recommendations centre on supervised group exercise, acceptance and commitment therapy, cognitive behavioural therapy, and acupuncture. Cold therapy is not specifically discussed [14]. The 2017 international classification of the Ehlers-Danlos syndromes from the international EDS consortium doesn’t specifically address cold exposure as a management strategy either [13].
This matters because the framing of cold therapy in the wellness internet often positions it as a major lever for fibromyalgia. The guidelines don’t agree. They view it, where they view it at all, as one of many options without strong evidence, sitting well behind the exercise based interventions that actually have the strongest data.
None of which means cold is useless. It means that if you’re choosing where to spend your finite energy and money in managing fibromyalgia, the EULAR and NICE guidance is pointing you at progressive exercise first, not cold plunges. We’ve written a long piece on pacing for fibromyalgia and EDS, which covers the exercise side of things in depth.
The CPM problem: why cold doesn’t work the way it does in everyone else
This is the section that, for many readers, will change how you think about cold exposure. So bear with the technical language for a few paragraphs. It matters.
Conditioned pain modulation (CPM) is the nervous system’s built in pain dampening mechanism. The classic experiment goes like this. You experience a painful stimulus in one body part. Then a second painful stimulus, usually cold, is applied somewhere else. In healthy people, the second stimulus activates descending inhibitory pathways from the brain, and the first stimulus suddenly feels less painful. The cold is acting as a “counter irritant” that turns down the pain volume elsewhere. This is one of the proposed mechanisms by which cold exposure might help chronic pain.
In fibromyalgia, CPM is well documented to be impaired. Jarrahi and colleagues in 2018 used functional MRI to study what happens in the brain during a cold water pressor test in 8 people with fibromyalgia versus 11 healthy controls. The result. Healthy brains showed activation in the central executive network during cold exposure. Fibro brains didn’t. The descending inhibitory response that should turn down pain via CPM was absent or aberrant in the fibro group [8].
That’s a small study. But it lands on top of a much bigger pile of evidence that CPM is broken in fibromyalgia. The implication is awkward for the cold therapy narrative. If the mechanism by which cold “should” help pain (descending inhibition) is the very mechanism that’s disrupted in fibro, the rationale gets shaky. You’re applying a stimulus that depends on intact inhibitory pathways to a nervous system whose inhibitory pathways aren’t intact.
Now layer on small fibre damage. Galosi and colleagues published a 2022 systematic review and meta analysis of 20 studies including 903 fibromyalgia clients, looking at small fibre nerve impairment. The estimated prevalence of somatic small fibre impairment, assessed by skin biopsy, corneal confocal microscopy, and microneurography, was 49% (95% CI 39 to 60%). The estimated prevalence of autonomic small fibre impairment, assessed by HRV, sympathetic skin response, skin conductance, and tilt testing, was 45% (95% CI 25 to 65%) [6].
So roughly half of those with fibromyalgia have measurable small fibre impairment. Oaklander’s 2013 paper in Pain made this point earlier with skin biopsy data, arguing that some illnesses currently labelled as fibromyalgia are actually small fibre polyneuropathy [15]. The picture has only firmed up since.
What does this mean for cold exposure? Small fibres are the nerves that carry cold, warmth, and pain. If they’re damaged, the perception of cold isn’t normal. The thresholds shift. The signalling is altered. The “cold as a generic stress to which the nervous system adapts” framing doesn’t apply cleanly when the cold sensing infrastructure itself is partially compromised. We’ve written about the underlying chronic pain mechanisms in fibro and hypermobility separately, but the small fibre piece is one of the threads that runs through both conditions.
So when somebody with fibromyalgia steps under a cold shower, what they’re experiencing isn’t quite what the wellness influencer in the cold plunge video is experiencing. The substrate is different. The processing is different. The expected benefit is harder to assume.
The hEDS angle: cold isn’t a neutral stimulus when your thresholds are already lowered
Now the hypermobility piece, which the original version of this post completely missed. The most relevant paper here is Di Stefano and colleagues, 2016, in the European Journal of Pain. They studied 27 adults with what was then called joint hypermobility syndrome or Ehlers-Danlos syndrome hypermobility type, now reclassified as hEDS or hypermobility spectrum disorder under the 2017 framework [13].
The participants underwent quantitative sensory testing including thermal pain thresholds, nerve conduction studies, and laser evoked potentials. The findings. Lowered cold pain thresholds. Lowered heat pain thresholds. An increased wind up ratio, which is a marker of temporal summation of pain, suggestive of central sensitisation. And critically, no evidence of somatic nerve damage on nerve conduction or laser evoked potentials. So the pain hypersensitivity in this group isn’t being driven by peripheral nerve injury. It’s being driven by central sensitisation in nervous systems with otherwise intact peripheral wiring [5].
What does “lowered cold pain threshold” mean in practice? It means the temperature at which cold starts to feel painful is lower (closer to room temperature) than in controls. The same cold stimulus that’s “bracing” to a healthy person is “painful” to someone with hEDS or HSD. That’s not a metaphor. That’s the QST data.
Now layer on small fibre neuropathy, which Cazzato and colleagues showed in 2016 is a common feature of Ehlers Danlos syndromes [3]. So in the hEDS population, you’ve got central sensitisation plus an elevated rate of small fibre impairment plus lowered cold pain thresholds. Apply cold to that nervous system, and the response isn’t the response you’d get from an athlete in a sports rehab context. It’s potentially an amplified, prolonged, less tolerable response.
This is the bit the cold therapy narrative usually skips. The studies that get cited for benefit are done on healthy young people. The biology of people with hEDS or fibro isn’t the same as the biology of healthy young people. The dose, the duration, and the response will all differ. Pretending otherwise isn’t evidence based, it’s wishful thinking.
POTS, dysautonomia, and the standing problem
If you’ve got POTS, standing under a cold shower is not a neutral act. Here’s why.
POTS, postural tachycardia syndrome, is defined by a heart rate increase of at least 30 beats per minute within 10 minutes of standing, in the absence of orthostatic hypotension, with chronic symptoms of orthostatic intolerance. The prevalence in hEDS is high. De Wandele and colleagues, 2014, documented dysautonomia and its underlying mechanisms in hEDS, and the picture of autonomic dysfunction in this population is well documented [4]. Hakim and colleagues in 2017 wrote the AJMG review on cardiovascular autonomic dysfunction in hEDS specifically, summarising the prevalence of postural tachycardia, orthostatic intolerance, and the associated symptoms [7]. We’ve covered the 2026 POTS guideline updates separately, but the autonomic baseline matters here.
The cold pressor response in humans causes peripheral vasoconstriction, a rise in blood pressure, and an increase in sympathetic nervous system activity. Šrámek and colleagues mapped human physiological responses to immersion in water of different temperatures back in 2000, and the noradrenaline and dopamine responses are well documented [20]. Cold drives the sympathetic system. That’s the whole biochemical mechanism that the wellness industry has built its narrative on.
Now think about that in POTS. The autonomic regulation is already dysregulated. The sympathetic response is often already exaggerated. The orthostatic response is already abnormal. You’re standing in a shower. You’re cold. Peripheral blood vessels constrict. Then the shower stops. You step out into a warm room. Peripheral vessels dilate. Blood pools in the lower limbs. In POTS, this is exactly the kind of cardiovascular challenge that triggers symptoms (presyncope, syncope, tachycardia, palpitations).
This isn’t a theoretical concern. It’s the well known mechanism for why people with POTS feel worse with rapid temperature changes, hot showers, hot baths, and yes, standing cold showers in many cases. Our post on POTS and exercise gets into the orthostatic stress angle in more detail.
The Søberg 2021 winter swimming study often cited in this space (the source of the “11 minutes a week” claim) studied young, healthy, winter swimming men with no clinical comorbidities [19]. The participants in that study could tolerate a cold shock response without orthostatic instability because their autonomic regulation was intact. Extrapolating from those results to someone with hEDS plus POTS is not a small leap. It’s an enormous one.
MCAS, cold urticaria, and the mast cell problem
Cold urticaria is a recognised condition in which cold exposure triggers mast cell degranulation, producing hives, itch, swelling, and in some cases more systemic reactions including hypotension and anaphylaxis. It’s not rare. It’s not always benign. And it overlaps significantly with the wider mast cell activation syndrome (MCAS) picture that’s increasingly recognised in the hEDS population. We’ve explained MCAS at length in a separate post, and the mast cell connection with fibromyalgia is something we’ve also covered.
The thing is, MCAS doesn’t always present with the textbook anaphylaxis case. A lot of those with MCAS get flushing, palpitations, fatigue, brain fog, GI symptoms, or just feeling “off” after a trigger. Cold can be one of those triggers. And in the EDS-spectrum population, where the prevalence of MCAS is elevated, cold exposure isn’t a benign experiment.
So if you’re seriously considering cold showers and you’ve got any MCAS picture, the order of operations matters. Talk to your GP or specialist first. If you’re already on antihistamines for MCAS, you’ve already got a flag waving. Adding a known mast cell trigger to your day on purpose isn’t an obviously good idea.
Raynaud’s phenomenon, where small arteries in the fingers and toes spasm in response to cold or stress, is also more common in the EDS spectrum than in the general population. If you’ve got Raynaud’s, deliberately exposing your hands and feet to repeated cold isn’t going to do them any favours.
The wellness narrative versus the data: three claims that don’t hold up
Now, the bit that always annoys us. The cold therapy narrative on social media has accumulated a layer of pseudo physiology that doesn’t survive contact with the primary papers. Three claims in particular are worth pulling apart, because you’ll see them quoted everywhere.
Claim 1: “Cold plunging releases endorphins”
This is repeated so often it sounds like settled science. The actual data is messier. Reed and colleagues in 2023 published a study in the Journal of Thermal Biology that measured beta endorphin response to acute cold water immersion. The result. No change in beta endorphin at any timepoint measured. There was a single mood effect (reduced negative affect at 180 minutes post immersion) but no evidence of the endorphin mediated mechanism that gets talked about [16].
That’s one study, but it’s a clean prospective measurement of the exact claim, and it didn’t replicate the popular narrative. The wider literature on cold and beta endorphin in humans is thin and not as conclusive as you’d think from how often the claim gets made. Cold raises noradrenaline. That’s well documented. Whether it raises beta endorphin in any meaningful way after a typical home cold shower is genuinely uncertain.
Claim 2: “11 minutes of cold per week is the optimal dose”
This figure traces back to Søberg and colleagues, 2021. The actual paper is a study of brown adipose tissue thermoregulation in young, healthy, winter swimming men in Copenhagen [19]. The “11 minutes” number was an observation about the average cold exposure time of the winter swimmers in that specific study. It was not a prospective dose response trial. It was not derived from a chronic pain population. It was not even framed by the authors as a clinical recommendation.
What happened is that the number got picked up by podcasts, condensed into “Søberg’s protocol”, and turned into a clinical guideline. It isn’t one. It’s a descriptive observation from a brown fat study in young Danish men. If you’ve got fibromyalgia or hEDS, that data doesn’t apply to you in any meaningful way. The wellness internet’s habit of converting descriptive observations from healthy populations into prescriptive protocols for everyone else is one of the recurring problems in this space.
Claim 3: “Cold is anti-inflammatory”
Sometimes. Sometimes not. It’s dose dependent and context dependent. Klemm 2021 did show cytokine shifts after WBC in fibro, including changes in IL 6, IL 1, TNF alpha, and IL 10 [10]. But cold water immersion in healthy participants can also cause acute rises in inflammatory markers in the immediate window after exposure, before any longer term shifts occur. The 2025 Cain systematic review reads the broader literature carefully and the picture is mixed, not the clean “cold reduces inflammation” line that gets quoted [1].
When it comes to chronic pain populations, the assumption that “anti inflammatory equals less pain” is itself questionable. Fibromyalgia pain isn’t primarily inflammatory in the classical sense. The central sensitisation model doesn’t reduce to inflammation. So even if cold does shift some cytokines, the link from that to reduced fibro pain is not the direct line the marketing implies.
What cold actually does to the nervous system (the part that’s genuinely interesting)
None of the above means cold is doing nothing. It’s doing a lot. Some of it is potentially useful. Some of it is potentially harmful in our population. Knowing which is which is the bit that matters.
Cold immersion triggers the cold shock response below roughly 15 degrees Celsius. The first 30 seconds in cold water cause an involuntary gasp, hyperventilation, a sharp rise in heart rate, and a spike in noradrenaline. Šrámek 2000 mapped this across different water temperatures [20]. That stress response is what underlies most of the “cold is good for you” claims. The argument is that controlled, brief exposure to that stress builds resilience by training the nervous system to recalibrate faster.
There’s something to this. In healthy populations. The question is whether the same hormetic principle applies when the nervous system you’re stressing is already running with autonomic dysregulation, central sensitisation, or both. The honest answer is we don’t know, because nobody’s run the trials. The default assumption from the wellness internet is “yes, of course”. The default assumption from where we sit, looking at the safety data, is “be very careful, because the stress you’re applying could push an already dysregulated system further off track”.
What’s much more interesting, and much less talked about, is the face and neck cooling pathway. This is a completely different mechanism from whole body cold immersion. Apply cold specifically to the face (cheeks, forehead, around the eyes), particularly with breath hold, and you trigger the mammalian dive reflex. The vagus nerve, which is the main parasympathetic nerve in the body, gets activated. Heart rate slows. Blood pressure can transiently rise. Sympathetic tone drops.
Jungmann and colleagues showed in a 2018 randomised trial that cold stimulation increased cardiac vagal activation in healthy participants [9]. Richer and colleagues in 2022 published a randomised study of 28 healthy participants showing that the cold face test reduced acute psychosocial stress responses, with significant reductions in cortisol and improvements in heart rate variability [17]. We’ve written about HRV and fibromyalgia separately, but the autonomic angle is the part of cold exposure where there’s actually plausible mechanistic benefit.
The face cold approach is, in our view, the more sensible starting point for anyone in our audience who wants to experiment. It’s localised. It doesn’t trigger the whole body cold shock response. It doesn’t require standing in a cold environment for extended periods, which sidesteps the POTS issue. And the existing evidence (in healthy people, granted) is that it can produce real autonomic shifts without the same level of cardiovascular risk.
Splash cold water on your face. Hold a cold pack on your cheeks and forehead for 30 seconds. If you want to be fancy, fill a sink with cold water and dunk your face for 10 to 15 seconds, eyes open or closed. This is the bit of the cold therapy world that has the most defensible mechanistic basis and the lowest safety footprint for our population. It’s also the bit that the cold plunge industry doesn’t talk about much, because it doesn’t sell barrels.
WBC safety: what’s actually been reported
If you’re considering paying for whole body cryotherapy at a local centre, you should know what the safety literature says. Legrand and colleagues, 2023, published a scoping review of WBC safety risks from an international consortium of researchers. Going through 5 case reports and 2 RCTs, they documented 16 total adverse events from true WBC exposure [11]. Most were mild (cold induced headache, dizziness, long lasting shivering, reactive hypertension). A small number were serious. One case of transient global amnesia in a 63 year old man (full resolution within 24 hours). One intracerebral haemorrhage in a 61 year old woman with prior ocular migraine history. One moyamoya angiopathy event in a 32 year old woman during a 4 minute session. One abdominal aortic dissection in a 56 year old man with a hypertension history. The authors’ overall conclusion was that risks are within acceptable limits when contraindications are screened, but the serious events tell you that screening matters. WBC isn’t risk free, and the people most at risk are often the people not being screened properly.
The contraindication lists that have been developed for WBC by international consensus include uncontrolled hypertension, recent cardiac events, Raynaud’s, cold urticaria, severe peripheral artery disease, cryoglobulinaemia, and others. A lot of those contraindications apply to the EDS and POTS population at higher rates than to the general population. If you’re considering WBC, the centre offering it should be screening for these. Most do. Some, frankly, don’t.
This isn’t a “scary stories” section. Most WBC sessions are uneventful. The issue is that “most” isn’t “all”, and the rate of serious events isn’t zero. When the expected benefit is modest and short lived, the risk benefit calculation is more delicate than the marketing makes out.
So, should you try cold showers if you’ve got fibro or EDS?
The honest answer, which is the only kind we do. When it comes to cold therapy in this population, it depends. Mostly, on what else is going on.
If you have fibromyalgia alone, no POTS, no MCAS, no Raynaud’s, no cardiac history, and you’re curious, you can try a short cold rinse at the end of a normal shower and see what happens. Start with 10 seconds. Pay attention to how you feel during, immediately after, and over the next few hours. Some people in this group will get a temporary mood lift, alertness, or sense of “feeling more themselves”. Some will feel worse. Both are valid data points. There’s no moral imperative to push through if it doesn’t work for you.
If you have hEDS with POTS, the calculation changes. Standing cold exposure carries real orthostatic risk. If you want to try cold, do it seated. Sit on a stool in the shower, run the water cold over your legs first, build up over several sessions, never go from cold to hot rapidly in standing. Better still, start with face cold (the vagal route), not whole body. The face approach gets you most of the plausible benefit with much less of the cardiovascular load.
If you have MCAS or cold urticaria, the honest answer is don’t. Or if you really want to test, do it in clinical supervision with antihistamine cover, knowing the mechanism you’re triggering on purpose. This isn’t gatekeeping. It’s basic safety logic.
If you have Raynaud’s, avoid hand and foot cold specifically. If you want to experiment with cold for autonomic or mood effects, keep your hands and feet warm and use face cooling instead.
For anyone in this audience, what we’d say. Cold isn’t a primary treatment. It isn’t the lever that’s going to change your fibromyalgia or your hEDS in any sustained way. The data doesn’t support that framing. What it can be, in some people, is a small additional tool, used carefully, with awareness of your specific physiology. It’s an experiment, not a protocol.
What actually changes the pain (the unglamorous bit)
Here’s the thing. The work that actually moves the needle on fibromyalgia and hEDS pain isn’t sexy. It’s progressive aerobic exercise, built up slowly, in the right dose, with proper pacing. It’s improving sleep. It’s addressing the autonomic dysfunction that drives so much of the symptom load in the hypermobility population. It’s rebuilding strength around the joints that have been deconditioned for years. It’s working on the central sensitisation directly, through graded exposure, motor learning, and the slow rewiring of how the nervous system processes input.
That’s the EULAR strong recommendation. That’s the NICE guidance. That’s what we do in the studios. It’s also what the cold plunge content on social media tends to obscure, because progressive exercise doesn’t lend itself to dramatic 60 second videos. Cold plunging does. So one gets the airtime, the other gets the boring evidence base.
If you’ve got fibromyalgia or hEDS and you’re choosing where to put your energy, put it into the exercise side first. Cold is at best a small adjunct, and at worst, in the wrong subpopulation, a way to make yourself feel substantially worse for the sake of a wellness narrative that wasn’t built for your physiology.
Our pacing guide covers the exercise build up in detail. The cold intolerance post and heat intolerance post address the wider thermoregulation picture in fibromyalgia. The brain fog post covers the cognitive side. All of them sit upstream of the cold question in terms of where to spend your effort.
Frequently Asked Questions
Are cold showers safe if I have POTS?
Standing cold exposure is risky in POTS. The cold pressor response causes peripheral vasoconstriction, which then reverses when you step out into a warm room. Blood pools in the lower limbs, and people with POTS can get presyncope, syncope, or significant tachycardia on standing. If you want to try cold exposure with POTS, do it seated. Keep it short. Have someone nearby. Face only cold (splashing cold water on your face, holding a cold cloth on your forehead) is the lower risk option and may give you the autonomic benefits without the cardiovascular load.
Will cold showers reduce fibromyalgia pain long term?
The evidence doesn’t support that. There are no randomised controlled trials of cold showers specifically in fibromyalgia. The closest data is from whole body cryotherapy, where short term pain reductions are real but do not persist three months after the sessions stop [10]. The strongest evidence in fibromyalgia is for aerobic exercise, both in the EULAR 2017 recommendations and the NICE 2021 guideline on chronic primary pain [12, 14].
I have cold urticaria. Should I avoid cold exposure entirely?
Yes. Cold urticaria means your mast cells degranulate on cold exposure, releasing histamine and other mediators. Repeated or significant cold exposure can produce systemic reactions, and in some cases anaphylaxis. This is not a “push through it” scenario. If you’ve also got a broader MCAS picture, the same logic applies. Don’t deliberately trigger your mast cells in pursuit of a wellness goal.
Is whole body cryotherapy worth paying for if I have fibromyalgia?
The RCT data shows real short term pain and quality of life improvements after WBC in fibromyalgia [10, 18, 22]. The Verme 2024 follow up suggests benefits can last three to four months when WBC is added to a multidisciplinary rehab programme [21]. So if your local centre offers it as part of a broader programme and you can afford it, the evidence is reasonable. As a standalone treatment promised to “fix” fibromyalgia, the evidence isn’t there. And the safety contraindications (Raynaud’s, cold urticaria, recent cardiac events, uncontrolled hypertension) should be checked before signing up [11].
What about face cold or the diving reflex approach?
This is the option with the cleanest mechanistic story for our audience. Cold applied to the face (cheeks, forehead, around the eyes), particularly with breath hold, activates the vagus nerve via the mammalian dive reflex. Heart rate slows. Parasympathetic tone increases. Two small RCTs in healthy participants have shown changes in cardiac vagal activation and reductions in cortisol responses to stress with cold face exposure [9, 17]. We don’t have specific fibro or EDS data on this, but the safety profile is much better than whole body cold immersion for the POTS and MCAS subgroups. Splashing cold water on your face for 15 to 30 seconds is a reasonable, low risk way to experiment.
Does the “11 minutes of cold per week” rule apply to me?
Probably not. That figure comes from Søberg and colleagues, 2021, a study of brown adipose tissue in young, healthy, winter swimming men in Copenhagen [19]. It was a descriptive observation about how much cold those particular participants happened to be doing, not a prospective dose response trial, and not a clinical recommendation for chronic pain populations. The wellness internet turned it into a protocol. The paper didn’t. If you’ve got fibromyalgia or hEDS, treat the “11 minutes” figure as a marketing artefact rather than a clinical guideline.
The bottom line
Cold isn’t a miracle. It isn’t the lever. It isn’t the missing piece. When it comes to fibromyalgia and EDS, it can be a small adjunct for some people in our population, used carefully, with awareness of POTS, MCAS, Raynaud’s, cardiac history, and the broader autonomic picture. The biggest gains in fibromyalgia and hEDS still come from progressive exercise, sleep, pacing, and the slow rebuild of a nervous system that’s been dysregulated for years.
If you’re considering cold therapy, start with face cold rather than whole body. Sit, don’t stand. Keep it short. Stop if your body tells you to. And don’t expect it to do the heavy lifting that progressive exercise is actually built to do.
If you’ve got hEDS, hypermobility, fibromyalgia, POTS, or any combination of these and you want help rebuilding without the wellness internet’s bad advice, that’s what we’re here for. Take a look around the site, or get in touch through our studios if you’re ready to start.
— The Fibro Guy Team —
