Hypermobility, EDS and Constipation: Why Your Gut Won’t Cooperate and What Actually Works

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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)

• 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
• Endometriosis, hypermobility and EDS: where the connective tissue link holds up, and where it doesn’t - 1 October 2026

Constipation is one of the most common gut problems in hypermobility and Ehlers-Danlos syndrome, and it’s also one of the worst handled, largely because nearly all of the advice on offer was built for a different problem entirely. In women with long standing constipation who also have hEDS or HSD, the thing that really stands out isn’t a slower gut and it isn’t a structural fault in the pelvis, it’s a rectum that under reports what’s sitting in it ^[1]. Whole gut transit wasn’t delayed any more often than in other constipated women, and the structural imaging wasn’t any worse either, yet reduced rectal sensation turned up in more than twice as many of them ^[1]. That difference matters a great deal, as fibre, water and a bit more walking do very little indeed for a signalling problem at the exit, and the exit is pretty much the one place most people get told not to look.

The current expert guidance for hypermobile EDS now says this out loud, as where somebody has lower gut symptoms, and particularly that feeling of never quite emptying, the recommended next step is testing the anorectum with manometry, a balloon expulsion test or defecography, because pelvic floor dysfunction and reduced rectal sensation are common in this group ^[2]. That’s a genuine shift in position, and in our experience it hasn’t really reached many appointments yet, which is why so many people are still on their fourth round of sachets with nobody having measured anything.

The evidence underneath all of this is uneven, and unevenly spread too. One mechanism has been measured directly in hypermobile groups ^[1], a couple of the others have only ever been reasoned about, and the pathophysiology of gut problems in hEDS and HSD is still described as poorly understood ^[2]. Meanwhile several of the treatments that get recommended the most confidently have either a pretty thin base underneath them or a result pointing the other way entirely, and one of the warnings that gets repeated absolutely everywhere turns out to be backwards.

How Common Constipation Actually Is in Hypermobility

The headline gap is 73% against 16%: roughly three quarters of those with HSD or hEDS report constipation, against about one in six of people without either ^[3]. Gaps that size don’t happen by accident, and constipation sits alongside abdominal pain, bloating and reflux as one of the gut complaints that keeps turning up right across the Ehlers Danlos syndromes, rather than being a quirk of one subtype ^[4].

Take the numbers themselves gently though, as most of what we have is questionnaires, and most of it comes from people who had already been referred somewhere, which is a very different population from everybody walking around with hypermobile joints and no diagnosis. The evidence base is still plainly described as limited and heterogeneous ^[3]. So the direction is solid, the precision really isn’t, and anybody quoting the 73% as though it were a population figure is overselling it.

There’s also a reporting problem underneath the numbers, and it runs in both directions. Plenty of people never mention constipation at an appointment, because it’s embarrassing, because it’s been going on for fifteen years and has quietly become normal, or because the appointment was booked for a shoulder that keeps coming out and there were only ten minutes. Others mention it and get handed a leaflet. Either way the symptom gets logged as minor when it very often isn’t, and people end up managing something quite serious on their own with whatever they read on the internet at two in the morning.

What that prevalence does earn is a change in how seriously the symptom gets taken. Constipation in this community is routinely treated as a lifestyle matter, something to be sorted out with more fruit and a bigger water bottle, and the frequency with which it turns up alongside everything else suggests it belongs with the rest of the multi system picture rather than in the diet advice pile.

Where the Problem Usually Sits

Now, there are four or five mechanisms proposed for gut problems in hEDS and HSD, and they are nowhere near equally well supported. One of them has been measured directly and stands out clearly, two of them are plausible and largely unproven, and one is an association nobody can explain yet. Sorting them out matters, as the mechanism decides the treatment, and getting that wrong is how somebody ends up three years into fibre supplements for a coordination problem.

Reduced Rectal Sensation

Rectal hyposensitivity is the term you’ll see on a report, and what it means is that the rectum needs more filling than it should before it tells the brain anything at all. The urge arrives late, faintly, or not at all. You don’t get the signal that says go now, so you don’t go, and the stool sits there getting drier and harder while the whole thing becomes self reinforcing.

In constipated women with hEDS or HSD, reduced rectal sensation turned up in 43.3% of them, against 20.1% of constipated women who weren’t hypermobile, and it held up again in a separate second group, which is what stops it being a fluke of one unit ^[1]. It was also the only thing that was strikingly over represented, as whole gut transit and the structural pictures were no worse than in anybody else with constipation ^[1]. So the honest phrasing is that reduced rectal sensation is over represented, rather than that it’s the master mechanism, as nobody has shown it explains the whole symptom picture.

Keep the scope in mind though. Those were women, already constipated, already through the door of a specialist gut unit, so it’s a finding about that group rather than a prevalence figure for everybody with hypermobility. What it does do is tell you where to look first, and it explains a symptom pattern that a lot of people recognise instantly: no urge for days, no obvious slowness on the days it works, and a persistent sense that nothing has finished.

It’s worth being clear about what the urge actually is, as it’s easy to assume it’s a simple stretch alarm. Stool arriving in the rectum stretches the wall, receptors report the stretch, and the brain builds that into the sensation that tells you to find a toilet in the next ten minutes. When the reporting side of that is dim, the stretch is still happening, and nothing is wrong with the stool, the volume or the timing, it’s the message about it that’s quiet. And because the message is quiet rather than absent, it tends to get drowned out by everything else competing for your attention, which in this community is usually pain, fatigue and a heart rate doing something unhelpful.

So, that’s also why so many people describe only going when it becomes unavoidable, as if the early, polite version of the urge never registers, the only signal you ever get is the late one, by which point the stool has been sitting there long enough to be genuinely hard work.

The practical consequence is blunt. Bulking agents add volume to a system that isn’t reporting volume properly, and stimulants push stool down to a rectum that doesn’t then ask you to do anything about it. Neither of them addresses the reason the message is faint, which is why the standard ladder can look like it’s failing for no reason at all.

The Pelvic Floor Working Against You

Dyssynergic defecation is the other half of the outlet story, and it’s mechanically the opposite of what you’d expect. Instead of the pelvic floor and anal sphincter relaxing as the abdomen presses down, they hold on, or they actively squeeze harder. You push, the exit tightens, nothing moves, so you push harder, which tightens it further. It’s a coordination fault rather than a weakness, which is why it responds to retraining rather than to more effort.

It’s common in chronic constipation generally, common enough that it’s one of the first things a gut physiology unit looks for ^[5]. And the part that matters most for anybody trying to work this out at home is that symptoms on their own cannot reliably separate it from a genuinely slow gut, which is exactly why it gets diagnosed on anorectal physiology and not on a description ^[5][6]. Straining for twenty minutes, needing to press on the perineum, the feeling of a blockage that isn’t a blockage, sitting there scrolling until your legs go numb, none of those are specific enough to settle it, however convinced you or your GP happen to be.

The word most people reach for here is weakness, and it’s the wrong one. A pelvic floor doing this, is usually working extremely hard, just at the wrong moment, which is why pelvic floor exercises aimed at strength can make the problem worse rather than better. The aim is the opposite skill, which is letting go on demand while the abdomen presses, and that’s a coordination job most of us have never had to think about consciously in our entire lives. It’s surprisingly hard to learn without feedback, as you can’t see it, and the internal sense of what your pelvic floor is up to is famously unreliable.

That’s also the reason the current hEDS guidance points at the tests rather than at a treatment ^[2]. Where reduced sensation and poor coordination are both common, and where neither can be identified from the outside, testing is the thing that changes what you do next. Everything else is a guess with sachets attached.

Connective Tissue in the Gut Wall

The gut is full of connective tissue, and the intuitive story more or less writes itself. Laxer tissue makes a floppier tube, a floppier tube propels less efficiently, and so the gut is slower and baggier in the same way the joints are looser. It’s a tidy story, and it’s the one most often given in appointments.

It’s also mostly unproven. Laxer connective tissue is listed as one plausible contributor to gut symptoms in hEDS and HSD, and in the very same breath the pathophysiology is described as poorly understood and the evidence as limited ^[3][4][2]. Nobody has pinned the mechanism down, and the more detailed versions of the story, the ones about altered peristalsis or a specific change in how compliant the gut wall is, are extrapolations rather than measurements.

That distinction is worth holding onto, as the laxity story is the one that most often gets used to explain why nothing can be done. A structural explanation sounds permanent, a sensory or coordination problem sounds fixable, and the mechanism that has actually been measured in this population is the second kind, which in our opinion is a considerably better place to be looking.

The Autonomic Overlap With POTS

POTS travels with hypermobility often enough that most people reading this already know the pairing, usually from the inside. Gut symptoms are heavier in HSD and hEDS where POTS is also in the picture, and functional gut disorders turn up more in the hypermobility related conditions when POTS comes with them ^[7]. In one specialist hEDS group, having POTS independently predicted abnormal results on dysmotility testing, which is a step beyond the two simply appearing together ^[8].

The mechanism, though, is genuinely unsettled. The direct biological link between hypermobility, POTS and gut symptoms is described as uncertain and still evolving ^[2][7], and that group came through a tertiary referral centre, which is the sickest and most investigated end of the population rather than a typical one. So two things turn up together, reliably, and nobody has shown which one is driving the other, or whether something upstream is quietly driving both.

Now, there’s a practical knot in the middle of this that rarely gets named. Eating makes orthostatic symptoms worse for a lot of people, as blood heads to the gut and there’s less available for everything else, so meals get smaller and later and a great deal more erratic. Smaller, more erratic meals give the bowel less to work with and less of a routine to hang a habit on. Then the constipation gets treated as a diet problem, and more food is exactly the thing that feels impossible. It’s a loop, and in our opinion it’s one of the main reasons gut advice lands so badly in this group.

We’d treat the overlap as a reason to sort out the autonomic side properly, rather than as an explanation for the gut on its own. If standing up makes you feel terrible and eating makes you feel worse, those two facts are probably related, and treating only one of them tends to produce about half a result.

Visceral Hypersensitivity, and Why It’s Borrowed

Visceral hypersensitivity means the gut’s own sensory system reporting ordinary events as painful ones. Normal filling, normal gas, normal movement, all of it arriving as pain or as an urgent problem. Disorders of gut brain interaction, abdominal pain and sensitisation are all common in hEDS and HSD, and they get discussed at length ^[3][4].

What hasn’t been done is showing that visceral hypersensitivity is a dominant, measured driver of constipation in hypermobile groups specifically. The material available is drawn from IBS and from the wider gut brain literature, so this one is an extrapolation. It’s a reason to suspect it rather than a reason to believe it, and that distinction gets lost constantly in this space.

And yes, it sits a bit oddly next to reduced rectal sensation, since the same person can have a rectum that reports filling poorly and a gut that reports pain very readily indeed. Those are different sensory channels doing different jobs, so having both isn’t a contradiction, just deeply unfair. We’d treat them as two separate problems needing two separate approaches, though that’s our reading of it rather than something anybody has measured in this population.

Gastroparesis and the Upper Gut

Gastroparesis comes up constantly in hypermobility circles, and it’s worth being straight about what’s actually known. The overlap between the Ehlers-Danlos syndromes, POTS and upper gut symptoms including delayed gastric emptying is recognised and discussed as a real clinical problem rather than a fringe one ^[9]. Abnormal results on dysmotility testing are common in specialist hEDS groups, and POTS predicted them ^[8].

What none of that gives you is a prevalence figure for the hypermobile population, or a mechanism. The link is described as poorly understood, which is the same verdict the connective tissue story gets ^[9]. So the honest position is that upper gut dysmotility is clearly part of the picture for some people, and that we can’t tell you how many, or why.

It helps to separate the two ends of the gut in your own head as well, as they get merged constantly. Delayed gastric emptying and a rectum that doesn’t report filling are different problems, in different organs, needing different treatment, and it’s entirely possible to have one, both or neither. Somebody who feels full after four mouthfuls and somebody who hasn’t had an urge in four days, are describing completely different things, even when the letter at the end of it says dysmotility for both.

We’d push back on the speed at which the label gets applied though. Nausea, early fullness and bloating are miserable and they’re also extremely non specific, and working out whether the stomach is genuinely emptying slowly is a testing question rather than a symptom question. That’s the same trap as at the other end of the gut, where the description feels diagnostic and isn’t. In our opinion gastroparesis is the most over assumed diagnosis in this whole area, which is not at all the same as saying it’s rare.

Why the Standard Ladder Keeps Failing

The usual sequence goes fibre, then water, then a stool softener, then a stimulant, then a shrug. Every step on that ladder is aimed at the same assumption, which is that the stool is too hard or the gut is too slow, and neither of those is the thing that’s over represented in constipated hypermobile women, as transit wasn’t slower and the structural pictures weren’t worse ^[1].

So, somebody with a faint urge and a pelvic floor that won’t let go can climb the entire ladder, do everything correctly, and get precisely nowhere, because every rung was built for a different problem. Worse, the failure gets read as a personal one. You get told you can’t be taking it properly, or that you need to be more consistent, or that it’s stress, and after a few rounds of that most people stop raising it at all.

The second thing the ladder does is hide the diagnosis. A stimulant laxative will eventually produce a bowel movement in somebody with dyssynergia, which looks like the treatment working and means only that enough pressure got applied to overcome a tight exit. The coordination problem is still there, it’s still making every attempt exhausting, and nothing about the sachet has changed it. Symptoms don’t separate these mechanisms from each other ^[5][6], and a partial response to an empirical treatment doesn’t either.

And it runs on for years. The pattern we see most often is somebody who has been through four or five products, escalating in strength, with the gaps between them getting shorter, who has never had a single measurement taken of what their rectum senses or what their pelvic floor does when they push. None of that is a failure of effort on anybody’s part, it’s a ladder with no diagnostic step in it.

The Testing, and What Each One Tells You

Three tests carry most of the weight, and the current expert guidance for hEDS names them directly for anybody with lower gut symptoms such as incomplete emptying, precisely because pelvic floor dysfunction and reduced rectal sensation are prevalent here ^[2]. Knowing what they are makes it considerably easier to ask for them without being fobbed off.

– Anorectal manometry: a thin catheter measures pressures in the rectum and anal canal, at rest and while you bear down. It’s the test that shows whether the pelvic floor and sphincter are letting go or holding on, so it’s how dyssynergia is identified. It’s also where sensation gets measured, by inflating a small balloon until you can feel it, which is what produces a hyposensitivity result.

– Balloon expulsion: a small filled balloon in the rectum, and a clock. It’s crude, it’s quick, and it’s genuinely useful, as it answers the plainest possible version of the question, which is whether you can get something out at all.

– Defecography: imaging while you actually empty. It’s the one that finds structural problems, prolapse and the rest. Worth knowing that in constipated hypermobile women the structural findings weren’t more common than in other constipated women ^[1], so a tidy defecography result isn’t the end of the search, it just moves the search back to sensation and coordination.

The reason to want these rather than another empirical trial of something is that symptoms cannot separate the mechanisms ^[5][6]. Slow transit, poor coordination and reduced sensation all produce a person who doesn’t go often enough and feels awful, and they respond to completely different treatments. Guessing does have a hit rate, it just isn’t a very good one.

On the day itself, none of the three is anywhere near as bad as it sounds, which is worth saying because the names are alarming and the descriptions online are worse. Manometry is a thin flexible catheter rather than a scope, and it takes about twenty minutes of being asked to squeeze, relax and bear down while a machine records what actually happens. Balloon expulsion is over in a couple of minutes. Defecography is the undignified one, and it’s also the one you’ll be given clear instructions for in advance. Nobody enjoys any of it, and most people who’ve had it done say the worst part was the waiting list.

One thing to keep in mind though. If you have a habit of bracing or holding your breath under stress, which a lot of those with hypermobility do, that habit will turn up on the test, and it should. The point of measuring is to catch what your body does when it’s asked to empty, including the bits you’d rather it didn’t do.

In our experience the obstacle is access rather than argument. Anorectal physiology sits in a small number of specialist gut units, the waits are long, and a GP may never have referred anyone for it in their career. It helps enormously to ask for the specific test by name, to say which symptom pattern you have, and to mention that testing is what the current hEDS guidance recommends for lower gut symptoms ^[2]. That last part is the bit that actually moves things, as it turns a request into a guideline question.

Fibre, Done Honestly

Fibre works for chronic constipation, on average, and that result has been replicated rather than resting on one hopeful finding ^[10][11]. Supplementing it improves the overall response rate, how often people go, and stool consistency, with the best supported version being psyllium at more than 10 g a day for at least four weeks ^[10]. It also increases flatulence, consistently, which is not a small consideration if bloating is already one of your main complaints ^[10]. In the general guidance for chronic constipation, fibre sits in the first line, and soluble fibre is the type with the strongest support behind it ^[12][13].

The benefit isn’t even across fibre types or across symptoms. Soluble and viscous fibres have the best evidence for stool frequency, consistency and straining, while insoluble fibre is either conflicting or lower certainty depending on which comparison you look at ^[14][15]. Practically, that means bran is not interchangeable with psyllium, and the advice to eat more fibre without naming a type is close to useless.

Fibre is also better matched to some versions of constipation than others, as it suits the pattern dominated by infrequent, hard stools and straining, and it suits the pattern dominated by incomplete emptying and bloating considerably less well ^[10]. And the second pattern, unfortunately, is the one that’s over represented in hypermobility.

Where fibre clearly doesn’t help is the coordination problem. When dyssynergia itself was corrected in people who had it, their symptoms improved, and adding fibre supplements didn’t produce the same effect ^[16]. Scope on that one, as it was done in people who had functional dyspepsia alongside their constipation and dyssynergia, and the symptom that shifted was the fullness ^[16]. But the direction is clear enough, and it’s mechanistically fairly obvious once you’ve accepted that a tight exit doesn’t care how bulky the stool is.

Tolerability is a great deal more formulation dependent than fibre’s reputation suggests. Some mixes and some doses improved bloating rather than worsening it, so the gas problem isn’t a fixed property of all fibre at all doses ^[17][18]. If psyllium wrecked you at a heaped spoonful, that’s information about that dose of that fibre, and not a verdict on the entire category.

So, the accurate version is narrower than the one usually given in either direction. Fibre remains evidence based for chronic constipation overall, and in hypermobility with prominent incomplete emptying, a poor or absent urge, or suspected dyssynergia, fibre on its own can miss the main mechanism and make the bloating worse ^[10][12]. There is no hypermobility specific evidence comparing a fibre first approach against a mechanism first one, so a blanket rule in either direction goes well beyond what’s actually been shown ^[12][15]. Try it, choose soluble, build the dose slowly, give it four weeks, and don’t let it be the only thing anybody ever suggests.

If you’re going to give fibre a proper go, the details matter more than the decision does. Psyllium above 10 g a day for at least four weeks is the version with the evidence, and both halves of that are usually the bit people skip ^[10]. Two weeks at a heaped teaspoon isn’t a trial of psyllium, it’s a trial of your own tolerance for a new texture. Build the dose up over a fortnight rather than starting at the target, take it with considerably more water than feels necessary, and expect the gas to be worse in the first week or two before it settles ^[10]. If it hasn’t done anything after a month at a proper dose, that’s a real answer and you can stop.

Water, Footstools and the Rest of the Standard Advice

Water first, as it’s the advice everybody has already had. Hydration is sensible and genuine dehydration is worth fixing, and that’s about as far as the evidence goes, because the stronger evidence base sits with laxatives and with treatment aimed at the mechanism rather than with drinking more ^[12][19]. Extra water above your usual intake isn’t a treatment. It’s also cheap and harmless, so nobody’s telling you to stop, but it shouldn’t be occupying a year of your life while nothing at all gets tested.

The footstool is the interesting one, as it’s sold as the highest yield thing you can possibly do and the evidence for that is mixed. Defecation posture has been linked with functional constipation, in children ^[20]. When a footstool was actually tested in adults who were constipated, it changed the posture without improving how long a balloon took to expel or how easy emptying felt ^[21]. So it’s low cost, low risk, possibly helpful for you personally, and not the lever the internet says it is.

Now, sitting time deserves a mention too. Where the urge signal is faint, a lot of people compensate by sitting and waiting, sometimes for half an hour, which produces sore legs and a worse habit rather than a result. We’d rather see a short, unhurried attempt at a consistent time of day than a long session built on hope, though that’s a practical preference rather than something with a trial behind it.

And exercise, which gets recommended universally and is worth doing for about nine other reasons. Where fatigue and orthostatic symptoms are already limiting, telling somebody to walk more as a constipation treatment is asking for a cost they may not be able to pay, for a benefit nobody has demonstrated in this population.

What the Evidence Supports Trying

Roughly in order of how well supported each one is, rather than in the order they usually get suggested.

Magnesium Oxide

Magnesium oxide has the cleanest result of anything on this list. Magnesium oxide and senna both clearly beat a placebo, with about 68% to 69% of people improving overall on either against 11.7% on the placebo ^[22]. That’s a large difference, in a fair comparison, for a cheap and widely available thing.

Now, the form matters a good deal more than most people realise, as that was magnesium oxide specifically. The supplement aisle is full of citrate, glycinate, malate, taurate and threonate (and there will be another one along by the time you read this), all of which have been marketed at this community at some point, and none of which were the thing being compared. Glycinate in particular gets recommended for sleep and for cramp, and then quietly expected to do a job it was never tested for. If the aim is the bowel, the oxide is the one with the evidence.

Senna came out about the same ^[22], which is worth saying plainly given how much fear there is around stimulant laxatives in this community. The idea that they’ll wreck your gut for good, is much stronger than the evidence behind it, and for a lot of people occasional use is a reasonable part of a plan rather than a failure.

On the practical side, magnesium oxide is cheap, it’s available without a prescription, and the dose that works varies enormously between people, so it’s worth starting low and adjusting. Loose stool is the signal you’ve gone past your dose rather than a sign it isn’t working. And if you have kidney problems, magnesium is one to check with a pharmacist first rather than to work out yourself, as it’s cleared by the kidneys.

Osmotic Laxatives

Polyethylene glycol, PEG, sold as macrogol on a UK prescription and under a handful of brand names over the counter, has strong evidence behind it and a strong recommendation in the current guidance for chronic idiopathic constipation ^[23][24]. The evidence base for laxatives generally is a good deal better than the evidence base for the lifestyle advice that usually precedes them ^[12], which is close to the reverse of the order they get offered in.

It’s also boring, and boring is probably why it gets skipped in favour of something with a nicer label and a mushroom on the packaging! Worth knowing that it works on stool consistency, so it addresses the hard and infrequent version of the problem much better than it addresses the outlet version. If your stool is already soft and you still can’t get it out, more PEG isn’t the answer to that, and taking more of it is how people end up with soft stool they still have to strain for.

Pelvic Floor Biofeedback and Sensory Retraining

For dyssynergia, biofeedback outperforms PEG and laxatives ^[5]. It’s the strongest treatment result in this entire area and also the hardest one to actually get hold of, which is a fairly grim combination. It involves a small number of sessions with a specialist, learning to relax the pelvic floor and coordinate it with abdominal pressure, usually with visual feedback so you can see what your body is genuinely doing rather than what you think it’s doing.

Where the problem is reduced sensation rather than coordination, sensory retraining is the matching treatment, and sensory biofeedback does improve rectal hyposensitivity, whether it’s delivered with a barostat or with a simpler syringe method ^[25]. Take the usual scope with it though, as that was done in constipation with rectal hyposensitivity generally and not in hypermobility specifically ^[25]. Given that reduced sensation is the mechanism most clearly over represented here ^[1], the absence of a hypermobility specific test of the treatment that targets it is genuinely maddening.

Slow Breathing

Slow, deep breathing improved symptoms, bowel movements, rectal sensation thresholds and vagal activity in constipation predominant IBS ^[26]. That’s an interesting result, and it points at something real about the autonomic side of this.

It’s been looked at properly once, in a small group, in a related condition rather than in hypermobility, so treat it as a hint rather than a finding ^[26]. It costs nothing, it carries no risk, and it’s plausible given how much the autonomic picture overlaps here, which is about as strongly as we’re willing to put it.

Sacral Neuromodulation

Last on the list, and last for a reason. Long term outcomes for chronic refractory constipation are poor, with benefit sustained in only a minority and a heavy burden of adverse events and dropouts ^[27][12]. It’s a genuine last resort rather than an option being unfairly withheld from you, and anybody presenting it as a fix is well ahead of the evidence.

Medications That Make It Worse, and One That Probably Doesn’t

Medication load is one of the proposed reasons constipation is so common in this population, and it’s the one you have the most immediate control over, so it’s worth going through properly.

– GLP-1 agonists: semaglutide, liraglutide, tirzepatide and the rest. These clearly raise the risk of constipation against a placebo, and semaglutide carries one of the highest constipation signals in the group ^[28][29]. That isn’t a reason to refuse a drug you need, it’s a reason to have a constipation plan in place before you start rather than three miserable months in.

– First generation antihistamines: the sedating ones, and the ones a lot of people with suspected mast cell issues end up taking daily. Anticholinergic and histamine receptor effects can impair gut motility, so the concern is credible, though the evidence for it is indirect and comes from the constipation that accompanies antipsychotics rather than from anything done in hypermobility ^[30]. Credible and unproven, in other words, which is a fair reason to consider a less sedating option and not a reason to stop anything abruptly.

– Beta blockers: the warning you’ll see repeated everywhere, that beta blockade slows the gut and makes constipation worse, isn’t supported. In Parkinson’s disease, taking a beta blocker was associated with less constipation rather than more ^[31]. So the effect of beta blockade on the bowel is drug and population specific, and there’s no general warning to hand out. If you’re on propranolol for POTS and your bowels are awful, that’s worth investigating on its own terms rather than blaming the propranolol by default.

So, the wider point is that the medication picture in this community is usually a list of six to ten things, several of which were started years ago for a reason nobody has revisited since. A proper review of the list, with somebody who knows what they’re looking at, is one of the cheapest interventions available and one of the least often done.

Where to Start, and What to Ask For

– Work out which pattern fits you: the first is infrequent, hard stool with a lot of straining and a gut that feels slow. The second is a poor or absent urge, a persistent sense of not having finished, and needing to strain even when the stool is soft. The second pattern is the one that points at the outlet, and it’s the one where the generic advice has the least to offer. Symptoms won’t settle it on their own, which is the whole reason for testing ^[5][6].

– Ask for anorectal physiology by name if the second pattern fits: manometry, balloon expulsion, or defecography, and say that current hEDS guidance recommends them for lower gut symptoms including incomplete emptying ^[2]. A named test is much harder to wave away than a general complaint.

– Get something working in the meantime: magnesium oxide has the cleanest result ^[22], and PEG has the strongest guideline backing ^[23][24]. Neither of those needs to wait for a referral, and neither of them precludes the testing.

– Give fibre a fair go if the first pattern fits: soluble rather than insoluble, psyllium above 10 g a day, four weeks minimum, dose built slowly ^[10]. Expect more gas early on ^[10], and stop expecting it to fix a coordination problem it can’t reach ^[16].

– Chase the biofeedback if testing shows dyssynergia: it’s the treatment with the best result behind it for that mechanism ^[5], and sensory retraining is the equivalent where the finding is reduced sensation ^[25].

– Spend your cheap options on the cheap things: slow breathing costs nothing and might help ^[26], a footstool costs a fiver and the evidence is mixed ^[21], and neither is worth building a year around.

– Review the medication list: the GLP-1 and anticholinergic effects are real and worth planning for ^[28][29][30], and the beta blocker warning isn’t ^[31].

How to Describe It So You Get Taken Seriously

Given that the mechanisms can’t be told apart by symptoms ^[5][6], the job in an appointment isn’t to arrive with a diagnosis, it’s to describe the pattern precisely enough that somebody can see why testing is the sensible next step. Vague descriptions get vague answers, and constipation is a subject where most people have only ever had vague words for it.

– Say whether you get an urge at all: this is the single most useful thing you can report, and almost nobody is ever asked about it. No urge for days, a faint urge you can easily ignore, or a normal urge that you can’t act on are three different situations. The first two point at the sensory side.

– Describe the stool separately from the difficulty: soft stool that you still have to strain for, is a completely different finding from hard stool that comes out once it arrives. People routinely say constipated for both, and the two point in opposite directions.

– Say what you do to get it out: pressing on the perineum, changing position, using a finger, straining for twenty minutes, or needing to go back three times in a morning. Those are all recognised things and they all say outlet rather than transit. They’re also the details people leave out because they’re embarrassing, and they’re the ones most likely to get you tested.

– Give a rough timescale and what you’ve already tried properly: four weeks of psyllium at a real dose and a month of macrogol is a useful history. A vague year of trying things isn’t.

– Mention the rest of the picture: the hypermobility diagnosis, POTS if you have it, and the full medication list. Gut symptoms and autonomic symptoms travel together here ^[7], and the medication list is the fastest fixable part of the whole thing.

– Ask for the test by name: anorectal manometry, balloon expulsion, or defecography, and say the current hEDS guidance recommends them for lower gut symptoms including incomplete emptying ^[2].

None of that is about performing credibility, which is a grim thing to have to do and most of this community has had plenty of practice at it already. It’s that the specific words happen to map onto specific mechanisms, so a precise description does genuine diagnostic work in a way that a general one simply can’t.

What Nobody Knows Yet

The pathophysiology of gut problems in hEDS and HSD remains poorly understood, and that gets said directly rather than buried in a limitations paragraph ^[3][2][9]. That’s genuinely the state of the field at the moment.

The specific open question is which of the proposed hypermobility specific mechanisms beyond reduced rectal sensation, so the connective tissue changes, the autonomic dysfunction, the visceral hypersensitivity and the medication load, actually drive symptoms enough to change which treatment you’d pick ^[3][2]. Until somebody answers that, treatment selection in this population rests on one clearly measured finding and a lot of reasonable inference.

And the gap that irritates us most: sensory retraining is the treatment that directly targets the one mechanism clearly over represented in hypermobile constipation, and it has never been tested in hypermobility specifically ^[25].

The Fibro Guy

References

[1] Choudhary, A., Vollebregt, P.F., Aziz, Q., Scott, S.M. and Fikree, A. (2022) ‘Rectal hyposensitivity: a common pathophysiological finding in patients with constipation and associated hypermobile Ehlers–Danlos syndrome’, Alimentary Pharmacology & Therapeutics. https://doi.org/10.1111/apt.17104

[2] Aziz, Q., Harris, L.A., Goodman, B.P., Simrén, M. and Shin, A. (2025) ‘AGA Clinical Practice Update on GI Manifestations and Autonomic or Immune Dysfunction in Hypermobile Ehlers-Danlos Syndrome: Expert Review’, Clinical Gastroenterology and Hepatology. https://doi.org/10.1016/j.cgh.2025.02.015

[3] Thwaites, P.A., Gibson, P.R. and Burgell, R.E. (2022) ‘Hypermobile Ehlers–Danlos syndrome and disorders of the gastrointestinal tract: What the gastroenterologist needs to know’, Journal of Gastroenterology and Hepatology. https://doi.org/10.1111/jgh.15927