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This article is part of our comprehensive guide to hypermobility and Ehlers-Danlos syndrome.
Weight is one of the stranger things about hypermobile Ehlers Danlos syndrome. Some people lose weight they then can’t put back on, some people gain weight they can’t shift no matter what they do, and a fair few manage both over the space of a few years without changing much at all about how they live. What the evidence actually supports though, is not one clean line running from the connective tissue to the bathroom scales. It’s a pile of comorbidities that travel with hEDS, each one of which pushes weight one way or the other, and quite a lot of which turn up more often in those with hypermobility than in anyone else [1][2].
So, the short answer to whether Ehlers Danlos syndrome can cause weight gain or weight loss is yes, but nearly always through something else: the gut, what eating has quietly turned into, the medication list, the sleep, the fatigue, and how much you’re actually able to move. Which is better news than a single unfixable mechanism would be really, as most of the things doing the pushing can actually be got at.
hEDS also sits right across the weight range, and almost nobody mentions it. In one large group of people with hEDS, getting on for half were overweight or obese [3], while in a separate group of women with EDS the average body weight sat lower than in the comparison group [4]. Both of those are true at the same time, which is why “EDS doesn’t cause weight gain” and “everyone with EDS is underweight” manage to be wrong in exactly the same way.
Most of it starts in the gut
Gut symptoms are the best supported explanation for weight change in hEDS and hypermobility spectrum disorders, and they’re extremely common. Abdominal pain, feeling full after a few mouthfuls, nausea, reflux, constipation and diarrhoea all turn up more in hypermobile groups than in non hypermobile ones, and disorders of gut brain interaction are particularly common [5][6][7]. And that isn’t just a quirk of who ends up in a specialist clinic either, as early satiety and fullness after eating were already raised in university students who had no EDS diagnosis at the time they were assessed [8].
Now, none of that on its own changes anybody’s weight, what changes weight is what those symptoms do to eating over months and years, and that part has been measured. In a large group of people with hEDS, most had changed their diet in the previous year and most regularly skipped meals, and altered diet went along with reflux, functional dyspepsia, reported MCAS and features of avoidant restrictive food intake [9]. In a closely related group, chronic nausea and functional dyspepsia predicted the meal skipping, and close to a third of those who had changed their diet reported needing some form of nutrition support [10].
The two directions come out clearly enough once the actual dietary patterns get looked at, as a “low food intake” pattern carried the worst nutrient shortfalls and the most nutrition support use, while a “refined and highly processed” pattern carried the highest body weight [3][11]. Same condition, same symptom burden, two completely different places to end up. One person stops eating because eating hurts, while another ends up living on the four things that don’t, and those are almost always the soft, beige, calorie dense ones (toast, crisps, ice cream, the usual suspects), because that’s what a nauseous stomach will accept late at night.
In younger groups with hypermobility the picture is much the same, with constipation, difficulty swallowing and delayed stomach emptying all common enough that they shouldn’t be put down to fussiness [12].
Coeliac disease, bacterial overgrowth, and actual malabsorption
True malabsorption does happen, it’s just a much smaller part of this than the internet suggests. Current gastroenterology guidance for hEDS and HSD says coeliac testing can reasonably be considered earlier than usual where the gut symptoms are varied, while stopping short of supporting routine testing for disaccharidase deficiencies or other diet mediated mechanisms in everyone [1].
Coeliac disease does turn up alongside EDS more often than you’d expect by chance, both in large outpatient datasets and in hospital records [13][14]. Those are associations though, not proof that the connective tissue is causing malabsorption, and surveillance bias is a live concern in this particular literature, as people already under investigation for one thing get investigated for everything [13]. Where coeliac disease is present, weight loss and micronutrient deficiency follow in the general population, although being overweight at diagnosis is increasingly recognised too [15].
Small intestinal bacterial and fungal overgrowth is the other one people ask about, and in symptomatic adult EDS groups, positive testing has ranged from roughly a third to about half depending on whether it was breath testing or a duodenal sample, with methane predominant overgrowth going along with constipation [16][17].
What that means for weight specifically in hEDS is still an inference rather than a measurement though, as the link from overgrowth to bloating, altered motility, malabsorption and disturbed appetite signalling comes from general population work rather than from anyone with hEDS [18][19].
When eating itself becomes the problem
In women with EDS, gut symptoms and food allergies or intolerances went along with restricted eating and with body weight, and that group carried more eating disorder history and more current risk than the comparison group [4]. In women with self reported EDS, gut problems were linked specifically to painful eating, fearful eating, and turning up the volume on ordinary body sensations [20]. Which is to say the food avoidance looks like it’s driven by the symptoms rather than by anything to do with how somebody wants to look.
Avoidant restrictive food intake disorder, ARFID, is the label for exactly that: restricting food because of fear, disgust or lack of appetite rather than because of how you want to look. About a third of a large hEDS and HSD group screened positive for it, and the single strongest predictor of ending up needing nutrition support was fear of eating [9]. Across the broader literature, ARFID can lead to weight loss, nutritional deficiency, reliance on supplements or tube feeding, and real social cost, though it’s a mixed bag and assessment of it still varies a lot between services [21]. In gut clinics specifically, the fear of aversive consequences pattern is the common one, and the people with both tend to sit at a lower body weight with poorer quality of life [22].
If you’ve ever been told you have an eating disorder when what you actually have is a stomach that punishes you for eating, then the difference matters, because the treatment for the two is not the same.
Elimination diets, histamine, and what MCAS can and can’t explain
Mast cell activation syndrome is where most of the confident internet claims about EDS and weight live, and it’s the weakest part of the evidence. The overlap between hEDS, HSD and MCAS gets discussed constantly, and the current guidance still describes the biological mechanisms behind it as limited and evolving [1][23]. When the link between mast cell disorders, hereditary alpha tryptasemia, POTS and EDS was looked for systematically, it came back unconfirmed [24].
Histamine intolerance sits in a similar place, as there’s no validated biomarker for it, so it’s diagnosed on clinical pattern and on response to a low histamine diet [25]. And the published low histamine diets are all over the place, with a good number of the excluded foods not actually being consistently high in histamine, which raises the fairly obvious possibility of people cutting out food for no gain [26]. Current guidance does say elimination diets can be considered for gut symptoms in hEDS and HSD with suspected MCAS, but it says it with a condition attached, which is that they’re delivered alongside nutritional counselling precisely so they don’t tip into restrictive eating [1]. That condition is the part that gets dropped.
The direct link between mast cells and metabolism is where there’s real biological plausibility, and almost none of it is in EDS. In animals, removing or stabilising mast cells reduced diet induced obesity and the inflammation that goes with it [27]. In human obesity, mast cells are more abundant in fat tissue and track with fibrosis and insulin resistance [28]. But in children, a whole body marker of mast cell burden didn’t rise across lean, overweight and obese groups at all [29], so the human picture isn’t one directional, and none of it was measured in anybody with hEDS.
Histamine does regulate appetite in the brain, mind you, and this is the one thread that connects to something you might be taking. Signalling at the H1 receptor damps food intake down, and reduced histamine tone or H1 blockade goes along with increased appetite and weight gain [30]. That work is animal and neurobiology work rather than anything measured in EDS, so treat it as a reason to suspect something rather than a reason to believe it, though it does lead somewhere practical.
The medicine cabinet does more of this than anyone tells you
Several drug classes used around hEDS comorbidities are associated with weight gain in the general population, and the same ones come up over and over [31]. None of this is a reason to stop taking them. The point is that when your weight moves and the medication changed three months earlier, you’ve got somewhere to look.
– Antihistamines: They block the H1 receptor, which is the same receptor that damps appetite down [30], and a lot of people with hEDS are taking them daily, often for years, for suspected MCAS [1].
– Antidepressants: These differ a great deal by drug rather than as a class, as across a very large group of adults starting them, some carried noticeably more weight gain over six months than others, with bupropion the outlier in the opposite direction [32]. The best predictor of which ones do it turns out to be how strongly the drug blocks H1, which is the same mechanism again [33].
– Gabapentin and pregabalin: Weight gain and fluid retention in the ankles are both common with these in chronic pain populations, and the gain looks dose related [34][35]. Which matters, as they’re prescribed so widely for hypermobility pain.
– Beta blockers: The effect here is real but modest, as averaged across trials running six months or more the excess came out at a bit over a kilo [36], which is enough to notice and not enough to panic over.
– Corticosteroids: These have the clearest metabolic signal of the lot. Excess glucocorticoid action is strongly linked to abdominal fat, insulin resistance and disordered blood lipids [37], and in a large general population cohort, starting them went along with greater long term weight gain and a bigger waist, most of all in women and in people already carrying weight [38].
All of that was measured in general populations rather than in hEDS specifically though, so treat the list as things to go and check rather than things proven to be doing it to you.
Sleep, fatigue, and the movement that quietly disappears
Sleep in EDS is bad, and bad in a way that matters metabolically. In one survey of people with EDS, most weren’t getting anything close to a full night, and the majority were lying awake for more than half an hour before they got off [39]. Pain tracks straight through it too, as in a large group of adults with self reported hEDS, the more frequent the pain the longer the wait to fall asleep [40].
Now, what short sleep does to appetite has been tested properly, just not in us. Restricting sleep in healthy adults makes them hungrier, pushes daily intake up by a couple of hundred calories, and drops insulin sensitivity [41], and shorter sleep goes along with higher ghrelin, which is the hormone that makes you want to eat [42]. That’s general population work, so the step across to hEDS is an inference, but it’s a reasonable one given how much worse the sleep is to start with.
The other half of it is what happens to movement. Fatigue in EDS has a long list of contributors, including sleep disorders, pain, deconditioning, autonomic dysfunction, bowel dysfunction and nutritional deficiency [43], and orthostatic intolerance, pain and reduced activity between them account for a substantial chunk of how severe that fatigue gets [44]. Adolescents with HSD or hEDS spend more time sedentary and less time in anything vigorous than their peers [45], and adults with the hypermobility type were found to do less habitual physical activity as well [46]. Less movement, worse sleep, more pain, less movement, and the useful thing about a loop is that you can get at it in more than one place.
Feeding tubes and TPN, and why the order matters
Feeding tubes are not a standard feature of EDS, and anybody presenting them as one is wrong. What’s true is that some people with hEDS or HSD develop symptoms, dysmotility or restrictive eating severe enough that nutrition support becomes the sensible option [47], and in a large hEDS group, around a quarter had used artificial nutrition at some point and a smaller number were on it at the time [48].
The reasons for starting it aren’t what people assume. Low body weight was the most commonly reported reason, but significant weight loss was another, and so was symptom burden with no weight loss at all, and some people were overweight when support began [48]. Tube feeding in hEDS is about not being able to sustain intake, hydration or stable nutrition, which is a much wider thing than being too thin.
The order goes mouth, then gut, then vein. Feeding into a working gut is preferred because it uses a functional digestive system and is safer and simpler than feeding into a vein [49], and the European position on it is blunt: long term parenteral nutrition shouldn’t be used where oral or enteral feeding is still possible [50][51]. And it does work, as in gastroparesis managed in a stepwise way, weight gain happened across all the treated groups, including the people who ended up with a tube, even where the nausea and pain improved a good deal less than the weight did [52].
The other side of it is the treatment burden, which is real. Most enteral tube users in that hEDS group reported tube related complications, and around half of those with a line did too [48]. Jejunal tubes in particular are maintenance heavy, with dislodgement, clogging and leakage the common problems [53].
Which is why the current argument is that escalation happens too early in some cases, and that coordinated gut, nutrition and psychological assessment belongs before non oral nutrition support rather than after it [47]. More specifically, the advice is now to screen for ARFID and for shape and weight driven eating disorders before anybody goes near long term parenteral support [50]. And there’s at least one paediatric hEDS account of oral intake being restored with physiotherapy, feeding therapy, psychology and motility directed medication instead of a surgical tube [54]. None of that is an argument against tubes for the people who need them, as most of those using artificial nutrition in that hEDS group reported tolerating it well and felt it improved their quality of life [48], it’s an argument for doing it in the right order.
What actually helps
– Stop making the number on the scales the target: The thing that’s actually moving is your intake and your symptoms, and weight is the readout rather than the problem. Chasing the readout while the reflux, the nausea and the fear of eating carry on unchanged is how people end up more restricted and no lighter.
– Get the gut symptoms properly named: Reflux, functional dyspepsia, constipation, delayed emptying and swallowing difficulty are all specific things with specific management, and current guidance sets out what’s worth assessing in hEDS and what isn’t [1]. “IBS, try peppermint” is not an assessment.
– Go through the medicine cabinet with whoever prescribes it: Not to stop anything unilaterally, as that’s a bad idea with several of these, but to find out whether a weight change lines up with a start date or a dose change [31].
– Treat fear of eating as its own problem: If eating has become frightening rather than just uncomfortable, that’s ARFID shaped, it’s common in this population, and it’s the strongest single predictor of needing nutrition support [9]. It also responds to the right help, which is not a weight management referral [50].
– Be careful with elimination diets, and don’t run one on your own: Low histamine diets in particular are inconsistent about what they exclude [26], and guidance only supports them alongside nutritional counselling [1]. A dietitian who knows hypermobility is worth a great deal more here than a list off a forum.
– Protect the sleep before you touch the diet: Short sleep pushes appetite up and insulin sensitivity down in healthy people [41], and pain is already stretching out how long it takes you to get off [40]. Sorting the sleep doesn’t fix this on its own, but everything else is harder on five hours a night.
– Move in a way you can repeat: Activity is lower in hypermobile groups and it’s part of what drives the fatigue [44][45]. In our opinion the useful target isn’t intensity, it’s repeatability, so something you can do again in two days rather than something that costs you the rest of the week.
Weight in hEDS has this many inputs, and the ones doing the work in your case are probably not the ones doing the work in somebody else’s. If your weight has moved and nobody has explained why, the list above is where to start looking, and the answer is usually two or three of them at once rather than one.
The Fibro Guy
References
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