Some people who were extraordinarily bendy as children are now adults with four diagnoses that each explain part of how they feel. The party trick and the exhaustion are frequently the same story — and almost nobody makes the connection.
You probably knew one at school. The child who could bend their thumb to their forearm, put their palms flat on the floor without effort, do the splits without warming up. It was a party trick. Nobody thought anything of it.
Some of those people are entirely fine and always will be. And some of them are now adults in their thirties or forties who have been round several specialists, been told their tests are normal, and collected three or four diagnoses that do not quite explain how they feel.
Connective tissue has an image problem. It sounds like packaging — the stuff between the interesting parts.
It is not. It is the scaffold everything else is built on and inside. It is in the walls of your blood vessels, the structure of your gut, the pelvic floor, the skin, the ligaments, the tissue surrounding every organ. Alfred Pischinger described the extracellular matrix as the neglected half of physiology, and he had a point — vast research effort goes into cells, and comparatively little into the environment those cells sit in.
Hypermobility is not a joint condition that occasionally causes other problems. It is a whole-body tissue difference where the joints are simply the most visible part.
Widespread pain, so: fibromyalgia.
Bloating, alternating bowel habit, reflux — the gut wall is connective tissue too — so: IBS.
Light-headedness on standing, palpitations, heat intolerance, exercise intolerance, so: anxiety.
Persistent exhaustion, so: chronic fatigue.
Each one describes a real experience and each treats it as a separate problem.
And the joint hypermobility usually is not mentioned at all, for a reason that is almost funny — the person does not think of it as a symptom. It is just how their body has always been. You do not report the thing that has been normal since childhood. So the one finding that might connect the other four never makes it into the conversation.
One point each side for: the little finger extending beyond ninety degrees; the thumb touching the forearm; the elbow hyperextending past ten degrees; the knee hyperextending past ten degrees. One final point for palms flat on the floor with knees straight.
Thresholds vary with age and sex — broadly five or more in adults, six before puberty, four after fifty.
Two limitations matter more than the score does.
It assesses nine joints. If your hypermobility sits mainly in your shoulders, hips, spine or jaw, you can score low and still be hypermobile.
And it measures current range. Someone who was extraordinarily bendy at fifteen and has stiffened with age, injury or years of guarding can score two and have a lifelong history that is entirely relevant.
So the historical questions matter as much as the examination. Were you double-jointed as a child? Could you do the splits, or contortionist tricks? Do joints slip out or feel like they might? Do you bruise easily? Do your scars heal wide or unusually?
And an important caveat: none of this is a diagnosis. Hypermobile Ehlers-Danlos syndrome has formal international criteria requiring proper assessment and, crucially, the exclusion of other heritable connective tissue disorders — some of which carry serious cardiovascular risk and need genetics and cardiology input. Recognising a pattern and diagnosing a condition are different jobs. I do the first and refer for the second.
Three things turn up together often enough that anyone working in this area notices: symptomatic hypermobility, dysautonomia, and mast cell activation.
Dysautonomia — most commonly discussed as POTS — is a sustained heart rate rise on standing without a corresponding blood pressure drop, with light-headedness, palpitations, exercise intolerance, brain fog and heat intolerance. Diagnosis is a medical assessment.
Mast cell activation presents as flushing, itching, unexplained abdominal pain, rhinitis, headache, and reactions to foods, smells, temperature change or exercise that do not follow a classical allergy pattern. Reactions that are variable rather than consistent to the same trigger are characteristic.
Contested
Now the honest part, because this is where a lot of writing on the topic overreaches. The co-occurrence is well described. The mechanism connecting them is not established, and several competing explanations exist. Anyone presenting a confident causal story linking all three is going beyond what is known.
Mast cell activation syndrome specifically is a contested diagnosis. Two sets of consensus criteria exist and they disagree substantially — the stricter version requires a documented tryptase rise during an episode plus objective response to treatment, while the looser symptom-based version, far more widely used in functional practice, is not accepted by many allergists and immunologists.
Hereditary alpha-tryptasemia is a real, established entity — extra copies of a particular gene producing a persistently raised baseline tryptase, present in a meaningful slice of the population, with overlapping symptoms. A baseline serum tryptase is a simple blood test available through a GP. In an area thick with unfalsifiable claims, that is a measurement worth having.
Lifelong hypermobility, present since childhood, points toward something congenital in how the collagen was built. Hypermobility that appears in adulthood is a different question — because tissue laxity emerging in someone’s thirties after an illness, an infection, or a particular medication is a different clinical situation from tissue laxity they have always had.
Where I would be careful is with the confident lists. You will find sources attributing acquired hypermobility to mould, Lyme, Bartonella, heavy metals and fluoroquinolone antibiotics. Of those, the fluoroquinolone connection has the most substance — that class carries recognised regulatory warnings about tendon rupture and connective tissue effects, and it is a real consideration in anyone whose symptoms began after a course. The rest are clinical assertion rather than established causation.
The useful version is narrower: note when it started, and what was happening at the time. That is information. Attributing it to a specific exposure usually is not.
This is where recognition earns its keep, because a lot of standard advice is actively wrong for this group.
The instinct with a stiff person is to stretch them. The instinct with a bendy person should be the opposite. Stretching a hypermobile joint into more range is not neutral — it is usually the wrong direction.
What is needed is stability, control and proprioception: strength through range rather than range itself. Closed-chain work before open. Ballistic end-range stretching avoided. Progress slowly, because connective tissue adaptation is slower here and flare-ups follow overload more readily.
Which is why yoga sometimes makes hypermobile people worse. Not always, and not everyone — but a practice built around achieving greater range, in someone whose problem is excess range without control, can be exactly wrong.
Nutrition needs realism. Collagen synthesis requires vitamin C, copper, glycine and manganese among others, and adequacy matters. But adequacy is not the same as therapy, and I want to be plain: you cannot supplement your way out of a heritable difference in how collagen is built. Anyone selling that is selling something. What is reasonable is ensuring the raw materials are not limiting — which is a modest claim and an honest one.
Absorption cannot be assumed. Gut symptoms are common in this group, which means nutrient markers need reading with that in mind, and a low result may be an absorption problem rather than an intake one.
And elimination diets deserve real caution. Where food reactions are prominent and variable rather than consistent, that pattern may reflect mast cell activity rather than true food sensitivity. Responding by cutting foods narrows the diet, worsens the gut, and does not address what is driving it. This is a situation where aggressive restriction can do genuine harm.
Pacing over pushing. Where fatigue and post-exertional worsening are present, the graded exercise caution that applies in ME/CFS applies here.
The RCCX gene cluster hypothesis — proposing a shared genetic basis for hypermobility, autoimmunity and psychiatric conditions — is an unvalidated research proposal, not an established finding. An interesting idea. Not a thing to build a protocol on, and presented as settled far more often than it should be.
And collagen protocols promising structural change. Reasonable nutritional adequacy, yes. Restructured connective tissue, no.
Nothing here is a diagnosis, and hypermobility is common — plenty of hypermobile people are entirely well and always will be. The pattern only matters when it comes with symptoms.
But if it does, the most useful thing you can do is get the whole picture assessed together rather than in four separate appointments. Mention the childhood flexibility, even though it does not feel like a symptom. Ask about a baseline tryptase if the reaction pattern fits. And ask your GP about proper assessment rather than accepting a fourth label.
Because the frustrating thing is not that this is untreatable. It is that it is frequently unrecognised — and being recognised changes the advice you are given quite substantially.
If you have collected several diagnoses that each explain part of how you feel, that is the useful question.
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