You already know what it’s like. You spent years being told it was anxiety. Or deconditioning. Or just something you’d grow out of. You might have fainted in a supermarket queue and been sent home with advice to drink more water. You might have left consultation after consultation with a printout about pacing and a referral to physiotherapy that had a six-month waiting list. And somewhere in the middle of all that, you started wondering whether the medical system actually had any idea what was wrong with you.
For those with POTS, EDS, and related conditions, that experience is pretty much universal. I’ve lost count of the number of clients who’ve told me their GP had never heard of POTS, or had heard of it vaguely but didn’t feel confident enough to actually diagnose it. Diagnostic delay of five years or more. Specialists who exist in theory but have waiting lists measured in years. It’s not a comfortable picture.
So when a group of eleven authors (cardiologists, neurologists, and autonomic specialists across Australia, Sweden, Canada, the United States, and the United Kingdom) put together a state of the art review of POTS published in February 2026, it was worth paying attention to. That’s exactly what this post is going to do.
We’re going to look at what’s actually in the Lau et al. 2026 review [1], what’s genuinely changed, what remains frustratingly unresolved, and what it means for those with hypermobility who are navigating this alongside everything else. We’ll also be honest about where the science is still catching up, and where the gap between what the guidelines say and what patients can actually access remains pretty wide.
A quick note before we go further: this post is educational. It’s not medical advice, it doesn’t replace a clinical assessment, and it shouldn’t be used to self-diagnose or change any treatment you’re currently receiving. If you’re concerned about POTS or dysautonomia, please work with a healthcare professional who knows your full picture.
So, if you’re ready to actually understand what 2026’s best thinking on POTS looks like, let’s go. And if you want a broader overview first, our POTS resource hub is a good starting point.
What Is the 2026 POTS State-of-the-Art Review?
Published in Heart, Lung and Circulation in February 2026, the paper by Lau et al. is what’s called a state-of-the-art review [1]. That means it’s not a clinical trial. It’s not a meta-analysis. It’s a synthesis of the current evidence base, written by a team of experienced clinicians, intended to bring together what we know about POTS diagnosis, mechanisms, and management into one coherent document.
The authorship team is significant, though. You’ve got Dennis Lau leading the team out of Australia, Artur Fedorowski from Sweden (one of the most prolific POTS researchers in the world), Satish Raj from Canada, Svetlana Blitshteyn from the US, Lesley Kavi from the UK, and Celine Gallagher as the senior author anchoring the work back in Australia, with several other clinicians across those same centres in between. This is not a fringe or single-centre paper. It draws on 119 references, making it one of the more comprehensive recent reviews of the condition. When researchers of this calibre sit down together to write a synthesis paper, the result tends to shape how clinicians think about a condition for years to come.
Why does it matter? Because this is the kind of paper that feeds into how clinicians think about POTS. It shapes training, it influences referral pathways, it’s the sort of document that a GP might eventually see cited in a continuing medical education module. It matters because, for a lot of people, getting a POTS diagnosis at all still depends on whether their doctor has seen recent literature.
And the diagnostic picture has, genuinely, shifted.
The Simplified Diagnostic Approach: GPs Can Now Diagnose POTS
One of the most practically important changes in the 2026 review is its endorsement of the active standing test as the primary diagnostic tool for POTS, not the tilt table test [1].
This might sound like a technicality. It isn’t. The tilt table test requires specialist equipment, a cardiology or autonomic unit, and often a referral that takes months or years to come through. The active standing test requires none of that. A patient lies down for five to ten minutes. Heart rate and blood pressure are measured. They stand up. Measurements are repeated at one, three, five, and ten minutes. That’s it.
Now, the diagnostic threshold remains the same: a heart rate increase of 30 beats per minute or more in adults, or 40 beats per minute or more in adolescents aged 12 to 19, within ten minutes of standing, without a sustained drop in blood pressure [1]. The duration criterion also remains: these symptoms need to be present for at least three months (some guidelines use three to six months) and not just an acute response to illness or dehydration.
I actually had one client bring the Lau paper into her GP appointment on her phone. The GP read the abstract, did the active standing test there and then, and she had her diagnosis within twenty minutes. That’s how it should work. The fact that the review endorses the active standing test as sufficient for diagnosis means, in theory, that a GP with a blood pressure monitor and a stopwatch can diagnose POTS in a consulting room. That’s a meaningful shift, for patients who’ve been sitting on a waiting list for a tilt table test, it changes what they can reasonably ask for.
There’s a catch, though, and it’s an honest one: having the diagnostic criteria available to a GP doesn’t automatically mean GPs will feel confident applying them. Training, awareness, and willingness to diagnose a condition that a lot of doctors still consider specialist territory are all separate problems from having a simple test. We’ll come back to that tension later. The shift in the guidelines is real, it matters for access.
The review also places greater emphasis on symptom burden, not just heart rate numbers [1]. This is part of a broader move toward recognising that the lived experience of POTS is not fully captured by one physiological threshold. A lot of patients have significant symptoms before they technically hit 30 beats per minute. Others hit 30 beats per minute without the same symptom burden. The 2026 paper acknowledges this, though as we’ll discuss, the move toward more patient-reported measures cuts both ways.
For those with hypermobility, this diagnostic update is particularly relevant. Awareness and willingness to use the test in primary care remain pretty uneven, though. Hypermobility-related diagnoses are already challenging to get, and the diagnostic tools used for hypermobility are imperfect in similar ways. Having a simpler POTS test that a GP can administer at least removes one layer of the barrier.
The Shift Toward Patient-Reported Symptoms: Good for Access, Tricky for Precision
The 2026 review places much more weight on the patient’s subjective experience of symptoms than older POTS criteria did [1]. That’s broadly a good thing. When it comes to conditions that cause brain fog, fatigue, palpitations, nausea, and coat hanger pain, relying purely on objective measurements in a controlled clinical environment has always been a bit inadequate.
Well, there’s a tension here that the review doesn’t fully resolve, and that’s worth being honest about.
When you broaden diagnostic criteria to include more subjective symptom burden, you make it easier for people to receive a diagnosis. That’s the access benefit. More patients get identified, more patients get treatment, fewer people spend a decade being dismissed. The review explicitly notes that awareness of POTS has grown significantly, in part because of long COVID, and that expanded diagnostic capacity is urgently needed [1].
The thing is, a broader, more symptom-led approach also risks grouping together people who have fundamentally different underlying problems. POTS is not one condition. The mechanisms driving it vary considerably between individuals. And if everyone with a racing heart upon standing gets the same label, treatment planning becomes murkier, it’s not that the symptoms aren’t real, it’s that the physiological drivers are different and respond to different interventions.
To be honest, this isn’t a new problem. Previous guidance from the Canadian Cardiovascular Society [3] and from the 2019 NIH Expert Consensus meeting [2] both grappled with the heterogeneous nature of POTS. The 2026 review hasn’t solved it. What it has done is acknowledge it more explicitly and push toward subtype-informed care, which is the right direction. Whether that nuance translates into clinical practice is a different question entirely.
POTS Is Not One Condition: Understanding the Three Subtypes
This is probably the section that will matter most if you’re trying to understand your own presentation (or that of someone you care for). The 2026 review reinforces what researchers have been working toward for some years: that POTS is best understood as a final common pathway for several distinct physiological problems [1][4]. It’s a bit like saying “headache” is a diagnosis. Technically true, practically not very useful on its own.
There are three main subtypes described. They overlap in a lot of people. And understanding which one (or which combination) is driving a person’s POTS is what makes a difference to treatment.
Hyperadrenergic POTS
In hyperadrenergic POTS, the sympathetic nervous system is pretty much in overdrive. Norepinephrine levels, the main stress-response neurotransmitter, are elevated when standing, often significantly so [1]. What this looks like in practice: a heart rate that climbs sharply and often stays high, blood pressure that can spike rather than drop, significant anxiety-like symptoms, palpitations that feel dramatic, and sometimes flushing or tremor.
This subtype is also the one most commonly associated with mast cell activation syndrome. The connection isn’t fully mapped but it’s clinically recognised: mast cells release vasoactive substances that can trigger or amplify sympathetic overactivation. One study of 69 POTS patients found that 42% showed markers consistent with mast cell activation disorder, though worth flagging that only the subgroup reporting additional symptoms like flushing, rashes or GI issues were actually tested, so this isn’t a clean prevalence figure for POTS across the board [10]. Even with that caveat, it’s not a small number. It’s also why the POTS-EDS-MCAS trifecta is such a clinically meaningful concept for a lot of people, and why treating just one piece of it so often falls short.
Neuropathic POTS
Neuropathic POTS arises when there is partial sympathetic denervation in the lower limbs. In plain terms: the nerves that would normally cause blood vessels in the legs and abdomen to constrict when you stand up aren’t doing their job properly. Blood pools downward instead of being redirected, venous return to the heart drops, and heart rate climbs to compensate [1][11].
Interestingly, if you’ve ever wondered why your legs go mottled or your feet go an odd colour when you’ve been standing for a bit, this is part of the reason. The blood isn’t going where it should. It’s sitting in the lower limbs because the vascular tone isn’t doing the redirecting it’s supposed to.
Research using skin biopsies has shown structural and functional small fibre abnormalities in a significant proportion of people with this subtype [11]. The 2013 study by Gibbons et al. found distinct structural differences in the neuropathic POTS group compared to non-neuropathic POTS patients. More recent work by Qu and Hakonarson [14] notes that small fibre neuropathy and neuropathic POTS share common features with autoimmune processes, which is relevant given that neuropathic POTS is often seen post-infection, including post-COVID [7].
This is, incidentally, one of the clearest connections between POTS and the neurological symptoms a lot of people experience. Small fibre neuropathy affects unmyelinated C-fibres and thinly myelinated A-delta fibres, which carry pain, temperature, and autonomic signals. When those fibres aren’t working well, the effects ripple out in ways that are easy to misread as psychological or non-specific. That’s part of why these presentations get missed for so long.
Hypovolemic POTS
In hypovolemic POTS, the circulating blood volume is genuinely depleted, by around 13% on average compared to healthy controls, based on plasma volume studies [1]. The renin-aldosterone system, which normally acts to retain fluid and maintain blood pressure, appears to be under-responsive. The result is that when upright, there simply isn’t enough blood in circulation to maintain adequate pressure and perfusion, so heart rate increases to compensate.
This is the subtype most directly addressed by salt and fluid loading strategies. Increasing dietary sodium and fluid intake raises plasma volume, which can meaningfully reduce orthostatic tachycardia. The 2026 review supports this as an initial management strategy, alongside compression garments and physical manoeuvres [1]. Salt loading works for some people, for others it does almost nothing, and that difference largely comes down to which subtype is dominant.
Look, these subtypes are not mutually exclusive. A significant number of people have features of more than one. The 2026 paper acknowledges that the same person might have hypovolemia and neuropathic denervation and mast cell activity all contributing simultaneously. This is part of why POTS can be so difficult to treat: there is not one lever to pull. The problem with the problem is that it’s rarely just one problem.
The EDS and Hypermobility Connection
The 2026 review explicitly acknowledges connective tissue disorders (including Ehlers-Danlos syndrome and hypermobility spectrum disorders) as a recognised driver of POTS [1][5]. That’s not surprising to anyone who works in this space, but it’s worth noting that this is now clearly established in a major clinical review rather than being treated as an anecdotal association. We see this in the studios pretty regularly: someone comes in having been told to just exercise more, and they’re crashing after every session because nobody accounted for the orthostatic piece.
The connection makes physiological sense when you think about it. The blood vessels are partly made of connective tissue. In hypermobile Ehlers-Danlos syndrome and related conditions, that connective tissue is structurally different: more elastic, less rigid [5]. Veins in the lower limbs that would normally provide resistance to blood pooling become more compliant. Blood pools downward more easily. Venous return drops. The heart races to compensate. That’s POTS.
And it doesn’t stop there. When it comes to autonomic dysregulation in hypermobility, it goes beyond just blood vessel compliance. The heart rate variability patterns seen in hypermobility often reflect reduced parasympathetic tone and heightened sympathetic reactivity, a setup that makes the body less able to adapt smoothly to position changes. Add in the fact that mast cell density is higher in connective tissue, and the POTS-EDS-MCAS overlap becomes less of a coincidence and more of a predictable convergence of mechanisms.
The Grigoriou et al. 2015 paper, which is one of the references cited in the 2026 review, documented the clinical association between POTS and Ehlers Danlos syndrome from an orthopaedic perspective, highlighting the practical challenges that arise when both conditions coexist [5]. The broader clinical implication, which the 2026 review reinforces, is that POTS management in people with connective tissue disorders needs to account for the joint instability, pain, and postural challenges that are part of daily life for someone with hypermobile EDS. That’s a point that gets missed in generic POTS management. Often spectacularly missed.
So, what does this mean practically? It means that for those with hypermobility, the route to better POTS management isn’t just about autonomic medicine. It’s about the whole system. Joint support. Load management. Understanding what drives flares and why cardiovascular symptoms often get worse when musculoskeletal symptoms are worse. These aren’t separate problems. They’re different expressions of the same underlying picture.
Exercise Therapy: What the 2026 Review Actually Says
Let’s be clear about what the 2026 review says about exercise, because there’s a version of this that gets oversimplified into “just exercise more” and that version causes harm.
The review supports individualised, graded exercise programmes as a key part of non-pharmacological POTS management [1]. The key words there are “individualised” and “graded.” Not generic. Not standard cardio. Not “go for a jog and you’ll feel better.” Structured, progressive, monitored exercise that starts where the patient actually is, which for a lot of people with POTS means starting supine or semi-recumbent.
The rationale is pretty straightforward when it comes to why exercise matters: POTS is associated with deconditioning in many cases, not because patients are lazy or haven’t tried to exercise, but because orthostatic intolerance makes upright activity feel genuinely terrible, so people naturally reduce it, which worsens the deconditioning, which worsens the POTS. Breaking that cycle requires an approach that starts well below the threshold of symptom provocation and builds incrementally [9].
The 2011 study by Fu et al. [9] is worth being precise about, because it often gets summarised as a head-to-head trial and it wasn’t. All 19 participants first went through a short drug phase (propranolol versus placebo in a crossover), then all 19 went on to complete a three-month exercise training programme. So the same people did both, one after the other. It’s a sequential within-subject comparison, not a parallel randomised exercise-versus-drug study. With that caveat firmly in place, the finding was still that the exercise phase produced greater improvements in symptoms and cardiac function than the medication phase did, and that finding has held up in the wider literature since. That said, the finding that exercise outperformed pharmacotherapy has held up. The 2026 review references feasibility data showing 76% completion in the original structured research-setting programme, which drops to 41% in community settings, a gap worth being honest about [1,15].
But this is critical: the review also emphasises that post-exertional malaise must be accounted for [1]. Pacing strategies are not optional extras. They’re central to whether an exercise programme is safe and sustainable for someone with POTS, particularly those who have overlap with ME/CFS features or who have long COVID-related POTS. Pushing through fatigue in this population doesn’t build resilience. It creates crashes. Full stop.
So, the structure the review supports looks like this: endurance-based activity three times a week, resistance training twice a week, starting at light to moderate intensity, using recumbent positions initially (rowing machines, recumbent bikes, swimming) and progressing gradually to more upright exercise as tolerance builds [1]. That’s a very different prescription from “walk more.”
For those with hypermobility, there’s an additional layer. Exercise has to account for the first step that often gets missed, which is understanding load tolerance before adding cardiac stress. Joint instability, proprioceptive deficits, and pain all affect how exercise is tolerated and how it should be modified. The generic POTS exercise protocols in the literature weren’t designed with hEDS in mind. Adapting them requires clinical judgement, not just a handout.
CO2, Breathing, and POTS: A Connection That Keeps Growing
Now, one of the areas where the 2026 review’s discussion connects with an emerging body of research (and with what we cover in depth elsewhere on this site) is the relationship between carbon dioxide regulation, breathing patterns, and POTS.
Orthostatic tachycardia is only part of the picture when it comes to what drives symptoms in POTS. A significant proportion of people with POTS hyperventilate when they stand up, not because they’re anxious, but because the autonomic and cardiovascular changes of standing trigger an increase in respiratory rate [12]. That hyperventilation lowers blood CO2 levels, a state called hypocapnia. And hypocapnia causes cerebral blood vessels to constrict, reducing blood flow to the brain even further than the positional changes already have. Brains, eh?
Research by Stewart and Pianosi [12] framed postural orthostatic tachycardia syndrome as potentially a respiratory disorder in significant part, arguing that the breathing dysregulation isn’t just a symptom but may actually be a driver of the tachycardia and cerebral hypoperfusion that define the condition. The 2024 work by Novak et al. [13] went further, showing that POTS and hypocapnic cerebral hypoperfusion without tachycardia may represent a spectrum of the same underlying disorder, with reduced orthostatic cerebral blood flow as the key unifying feature.
So what’s the clinical relevance? Well, if part of what’s maintaining POTS symptoms is a habitual pattern of over-breathing that lowers CO2 and impairs cerebrovascular regulation, then addressing breathing mechanics is a legitimate therapeutic target. This is one of the threads we explore in detail in our piece on CO2 tolerance, breathlessness, and chronic pain. The overlap with POTS is not coincidental.
For those with hypermobility, breathing pattern disorders are also pretty common, related to rib hypermobility, thoracic instability, and the way the body uses accessory breathing muscles when primary mechanics are less efficient. This doesn’t mean breathing retraining fixes POTS. It means it may be one component of a more complete picture, especially for people whose symptoms are particularly driven by breathlessness, brain fog on standing, or significant fatigue.
Interestingly, the 2026 review doesn’t cover this territory in depth [1]. But the research base is moving in this direction, it’s a gap worth filling for patients who want to understand the full landscape of what’s happening in their nervous system.
Multidisciplinary Care: What It Means, and Why Most Patients Won’t Get It
The 2026 review calls for multidisciplinary care as the ideal model for POTS management [1]. In theory, that means a primary team of a GP working alongside a trained autonomic physician, supported by specialist nurses, allied health professionals, extended appointment times, and regular follow-up for monitoring and medication adjustment.
In practice, for most people reading this, that’s not what’s available.
The review itself acknowledges the “dearth of specialists in autonomic medicine” [1]. That’s not just a British understatement. It’s a genuine structural problem that no amount of guideline updating will solve without investment in training pathways, dedicated clinics, and the administrative infrastructure to support complex chronic illness care. The paper advocates for expanded services and notes the urgent need driven in part by the long COVID patient population, but advocacy and implementation are different things.
So, what this means for patients is that the guidelines represent an ideal that most healthcare systems aren’t currently equipped to deliver. That’s worth knowing. Not so that you give up, but so that you can be strategic about what you’re actually trying to access. Getting a GP confident enough to diagnose using the active standing test, and getting a referral to a physiotherapist experienced with dysautonomia, may be more achievable in the near term than finding an autonomic specialist with a reasonable waiting time. The guidelines move the goalposts, but the distance between the goalposts and where most patients actually start hasn’t disappeared.
Oh, and there is also an important point about the psychological and gastrointestinal dimensions of Postural Orthostatic Tachycardia Syndrome that the 2026 review addresses [1]. Both are frequently present. Gut motility is regulated by the autonomic nervous system, so it shouldn’t be surprising that a condition characterised by autonomic dysregulation causes nausea, bloating, early satiety, and bowel irregularity. Likewise, the review acknowledges the significant psychological burden of POTS: not as a cause, but as a consequence of living with a condition that is poorly understood, poorly managed, and often initially dismissed. The distinction matters. Anxiety and depression in POTS are largely secondary to the illness burden, not primary drivers of it [6].
For those with hypermobility, the overlap with sleep disturbance, blood pressure dysregulation, and the general systemic load of managing multiple interacting conditions makes the case for multidisciplinary care even stronger, and its absence even more consequential.
What About Long COVID, Paediatric POTS, and HPV-Related Cases?
The 2026 review dedicates specific attention to several special populations that have either grown in prominence or required adjusted diagnostic thresholds [1].
Long COVID: The paper draws on the work of Seeley et al. [7], first published online in 2023 and formally printed in the 2025 journal volume, which found a high incidence of autonomic dysfunction and POTS in patients presenting with post-COVID sequelae. This has been one of the pretty significant developments of the past few years: the number of people developing dysautonomia following COVID-19 infection is substantial enough to have changed how autonomic medicine is resourced in some centres. The 2026 review recommends that clinicians maintain a high index of suspicion for POTS in anyone presenting with prolonged post-COVID fatigue and orthostatic symptoms [1].
Paediatric POTS: In adolescents aged 12 to 19, the diagnostic threshold is higher, at 40 beats per minute rather than 30, to account for the higher resting heart rate variability typical in this age group [1]. The review notes that paediatric POTS requires particular sensitivity, both diagnostically and in terms of management, given the impact on school attendance, physical activity, and social development. These are kids who are being pulled out of their normal lives, the stakes are real.
HPV vaccine-associated cases: The review acknowledges POTS occurring in the context of HPV vaccination as a recognised phenomenon, citing Blitshteyn et al. [8]. This is an area where the evidence is complex: the absolute number of cases is small relative to the vaccination uptake, and a causal mechanism has not been definitively established, but clinicians are advised to take these presentations seriously and investigate appropriately.
In each of these special populations, the core message is the same: don’t wait for a textbook presentation before investigating. The range of POTS presentations is wider than a lot of clinicians expect, and the cost of missing it, in terms of years lost to misdiagnosis, is high.
The Honest Gap: What the 2026 Review Doesn’t Fully Solve
Credit where it’s due: the Lau et al. 2026 review is a genuinely useful document. It pulls together a complex field with clarity, it acknowledges heterogeneity, it endorses more accessible diagnostics, and it’s honest about the resource gap between what patients need and what services can currently provide [1].
But there are gaps, and it’s worth naming them.
The diagnostic precision problem: Broadening access to POTS diagnosis through simpler, more subjective criteria is a trade-off. It helps more people get identified, but it also risks creating a large, heterogeneous population under the same label who may not all benefit from the same management approach. Fedorowski [4] and Olshansky et al. [6] have both written about the risk of oversimplifying POTS as a single entity when the underlying mechanisms are diverse. The 2026 review is aware of this, it doesn’t fully resolve the tension between widening the diagnostic net and maintaining mechanistic precision, though.
The implementation gap: Guidelines describe ideal care. They don’t create the capacity to deliver it. Recommending multidisciplinary teams and regular follow-up is only meaningful if those teams exist and can be accessed. For most patients, particularly outside major urban centres, they can’t.
The hypermobility-specific gap: The review acknowledges connective tissue disorders as a driver of POTS [1][5], but it doesn’t provide specific guidance on how to modify exercise programmes, diagnostic approaches, or management priorities for people who have POTS alongside hypermobile EDS or HSD. That’s a meaningful omission for a population that represents a substantial proportion of POTS patients, particularly women in their 20s and 30s.
The MCAS evidence gap: The review acknowledges MCAS as a co-occurring condition with POTS, particularly in the hyperadrenergic subtype [1]. The evidence base for MCAS in POTS remains a bit uneven, though. The Kohno et al. 2021 data [10] is significant, but as more recent systematic work has noted, studies in this area use varying diagnostic criteria, making it difficult to draw firm conclusions about prevalence and mechanism. What is clear is that clinicians should ask about MCAS symptoms in POTS patients, particularly those with the hyperadrenergic presentation. What remains less clear is exactly how to diagnose and treat it consistently.
And these aren’t criticisms of the authors. They’re reflections of where the science genuinely is. A 2026 state-of-the-art review can only synthesise what’s been studied, and some of the most clinically relevant questions haven’t yet been answered at the level of evidence that would allow firm recommendations.
What This Means for You, Practically Speaking
If you’re someone with POTS (or you suspect you might have it), here are the practical takeaways from the 2026 review that are worth knowing.
So, first things first. You don’t need a tilt table test to be diagnosed. The active standing test is now the endorsed primary diagnostic tool. If your GP is willing and has a blood pressure cuff and a stopwatch, they have what they need. You can point them to the Lau et al. 2026 paper if that’s helpful.
And your symptom experience matters, not just your heart rate numbers. The shift toward recognising symptom burden as central to POTS means that a clinician who dismisses your experience because “your heart rate only went up 28 beats per minute” is working from outdated thinking. Symptoms matter.
Now, there are likely multiple things going on, not just one. If you have hypermobility and POTS, you may also have features of MCAS, small fibre neuropathy, and breathing pattern dysregulation all interacting. Understanding the picture is more useful than chasing a single diagnosis or single intervention.
But exercise can help, and it has to be the right kind. Graded, recumbent-start, paced exercise is very different from generic exercise advice. When it comes to exercise in POTS, if you’ve been told to “just exercise more” and it’s made you worse, that’s not evidence that exercise doesn’t work, it’s evidence that the exercise approach was wrong. The first step in POTS and exercise is often the most important one to get right.
Salt and fluid management has a role, but it’s subtype-dependent. For those with hypovolemic features, salt loading strategies can make a meaningful difference. For those with predominantly hyperadrenergic POTS, the picture is more complicated and the same approach may not be as effective.
And finally: if you’re also navigating menopause or perimenopause alongside hypermobility and POTS, the hormonal dimension is real and often underappreciated. Oestrogen has pretty significant effects on vascular tone, autonomic regulation, and mast cell activity. The intersection of menopause, hypermobility, and dysautonomia is an area where clinical guidance is still catching up to patient experience.
Frequently Asked Questions
Yes. The 2026 Lau et al. state-of-the-art review endorses the active standing test as the primary diagnostic tool for POTS. A patient lies down for five to ten minutes, then stands, and heart rate and blood pressure are measured at intervals up to ten minutes. A heart rate increase of 30 beats per minute or more in adults (40 or more in adolescents) without orthostatic hypotension, persisting for at least three months, meets the diagnostic criteria. No specialist equipment is required. Your GP can administer this test in a standard consultation room.
Yes, it matters considerably. Hyperadrenergic POTS is driven by sympathetic overactivation with elevated norepinephrine and is often associated with mast cell activity. Neuropathic POTS involves partial sympathetic denervation in the lower limbs causing blood pooling. Hypovolemic POTS involves genuinely reduced blood volume and responds well to salt and fluid strategies. Many people have features of more than one subtype. Identifying the dominant mechanism helps direct treatment. Salt loading that helps hypovolemic POTS may not be as useful in hyperadrenergic presentations, for example. A clinician experienced in autonomic medicine can help identify your subtype.
Yes. There is a well-established association between hypermobile EDS, hypermobility spectrum disorders, and POTS, acknowledged in the 2026 review and supported by earlier research. The mechanisms include increased vascular compliance due to connective tissue laxity, autonomic dysregulation, and the co-occurrence of mast cell activation syndrome. People with hypermobility presenting with orthostatic symptoms should be assessed for POTS as part of their clinical picture, and POTS management should account for the musculoskeletal and connective tissue context.
Because the type and intensity of exercise matters enormously. Generic exercise advice (walking, gym classes, upright cardio) can worsen POTS symptoms because it doesn’t account for orthostatic intolerance or the risk of post-exertional malaise. The evidence-based approach starts with recumbent or semi-recumbent exercise (rowing machine, recumbent bike, swimming), uses a graded progressive structure, includes pacing strategies, and is individualised to the person’s current tolerance. Starting too hard too fast is not a modified protocol: it’s the wrong protocol entirely.
A significant proportion of people with POTS hyperventilate on standing, which lowers CO2 levels in the blood (hypocapnia). Hypocapnia causes cerebral blood vessels to constrict, worsening brain perfusion on top of the already-reduced blood flow from the positional change. Research suggests this breathing dysregulation may be both a symptom and a driver of the tachycardia and cognitive symptoms in POTS. Breathing retraining to restore CO2 tolerance may be a useful component of management for some individuals, particularly those with prominent breathlessness, brain fog on standing, or fatigue.
Post-COVID POTS is a recognised clinical entity. Research shows a high incidence of autonomic dysfunction, including POTS, in people with post-acute sequelae of COVID-19. The mechanisms are thought to include post-viral autonomic neuropathy, immune dysregulation, and possibly mast cell activation. The 2026 Lau et al. review recommends that clinicians maintain a high index of suspicion for POTS in anyone with prolonged post-COVID symptoms involving fatigue, brain fog, and orthostatic intolerance.
Closing Thoughts
The 2026 Lau et al. review represents a meaningful step forward in how POTS is understood and how it should be managed [1]. The endorsement of simpler diagnostics, the acknowledgement of heterogeneity and subtypes, the emphasis on individualised exercise programming, and the recognition of connective tissue disorders as a driver are all important moves in the right direction.
But it also reflects the honest state of a field that is still catching up to the complexity of what patients actually experience. The gap between what guidelines recommend and what healthcare systems can deliver is real. The diagnostic precision questions haven’t been fully resolved. And the specific needs of people with hypermobility navigating POTS alongside Ehlers-Danlos and MCAS aren’t yet fully addressed in the mainstream literature.
What we can do (and what this site tries to do) is give you the most accurate, current picture of where the science stands. Not to replace clinical care, but to help you walk into consultations better informed, ask better questions, and understand what’s actually being proposed and why. Because when it comes to conditions this complex, understanding is itself a form of support.
The POTS-EDS-MCAS trifecta is a real clinical entity. The research is starting to reflect that more fully. And for those with hypermobility who have spent years being told these things are unrelated, or unlikely, or exaggerated: 2026 looks like the science is, slowly but surely, catching up.
— The Fibro Guy Team —
