Hypermobility in Pole Dance

Updated: Aug 20, 2021

Today’s blog is undeniably a big one. It’s on a topic that’s quite important to myself and to numerous polers, patients and colleagues around me, so I hope you’re able to take time out of your day to join me on this journey and learn about the zebra in the room. If you’re a hypermobile aerialist out there, trust me when I say this is not a blog that you want to TL;DR. There’s a lot of new information in this blog so I just suggest taking it in bit by bit and stepping away and coming back later if you feel overwhelmed at all. A reminder that The Pole Physio is here to help if you have any concerns or if this blog triggers you in any way.

Alright zebras, let’s do this!

Hypermobility disorders are frustratingly hard to diagnose, let alone define. The lack of knowledge out there on these syndromes makes for a challenging time for patients and therapists alike. In fact, it usually takes on average 15-20 years for these disorders to be diagnosed from onset of symptoms, meaning most patients get diagnosed well into their 40s.

With the average age of a pole dancer/aerialist sitting in their late 20s, you can see why this can be a huge issue in our community. Most hypermobile aerialists are unaware they even have one of these disorders and really struggle through their artform due to their underlying problem until they are diagnosed much later on in life.

We are going to deep dive today and uncover what hypermobility really is, spanning from asymptomatic joint laxity to connective tissue disorders such as Ehlers-Danlos Syndrome (EDS).

Let’s start with a few definitions to get everyone up to speed…

Flexibility – Flexibility is one’s ability to change their joint’s position/range of motion into a pre-determined end range position, i.e. the ability to bend forward or reach overhead. The capacity of our body for flexibility comes from multiple structures including muscles, connective tissues, joints and nerves and is controlled almost entirely by the nervous system

. Joint Hypermobility (JH) – In the physio world joint hypermobility is defined as greater than average range of motion directly as a result of connective tissue laxity (i.e joint looseness). This is laxity of the ligaments and capsules that usually help to passively stabilise the joint and is NOT related to the flexibility of surrounding muscles.

For many pole dancers and contortionists, hypermobility can be beneficial. An example of this in pole dancing is our hip range far exceeding the range of the normal population to produce those gorgeous flexy splits.

Another great example of joint hypermobility outside the pole studio, is actually in baseball where a pitcher’s shoulder external rotation can increase to 135 degrees when the normal is only 90 degrees. Baseball pitchers have trained to increase their range of motion to improve their sport specific skill of throwing. Incredible!

But what’s important to know is that the terms flexibility and hypermobility are NOT interchangeable! If your body is hypermobile, you’re not automatically guaranteed to be flexible. Our nervous system will step in if it detects any sense of joint hypermobility via a process of neuro regulation.

If the brain senses any joint hypermobility and potential instability, the nervous system activates the surrounding muscles to act as a protective mechanism and will tighten up those muscles which leads to less flexibility. So, in certain cases of hypermobile shoulders, the body reduces the active range available to protect the shoulder from dislocation.

Fascinating right?! Now that we have that understanding, let’s focus more on hypermobility.

Hypermobility spectrum disorder

The focus of today’s blog is on Hypermobility Spectrum Disorders (HSD). Remember this abbreviation because I’ll use it a lot! HSD are in basic terms defined as conditions in people who present with joint hypermobility (greater than average range of motion) with additional symptoms/signs (we will discuss these shortly). In short HSD = JH +/- symptoms.

The challenging part of this spectrum of hypermobile disorders is that symptoms may not present in people until their 30s, even 40s, and not even pose an issue for them until well into the future. So why do we worry about something when symptoms may not be present? Well the more educated the pole community are about these conditions, the quicker polers will be to pick up on symptoms if they occur, access help and prevent the commonly described ‘hitting the wall’ that athletes with HSD experience when their bodies start to feel like they just break down. And the more knowledgeable instructors are, the better they will be at assisting their hypermobile students and understanding their learning and physical needs.

The Hypermobility Spectrum From March 2017, a new classification system for hypermobility disorders was determined, with benign joint hypermobility syndrome (general hypermobility) now falling under the umbrella of HSD.

To recognize the continuum of joint hypermobility, the hypermobility spectrum was created, ranging between, at one end, asymptomatic joint hypermobility —someone who has no symptoms apart from their joints’ capacity to move beyond normal limits—through to hypermobile Ehlers-Danlos Syndrome (EDS), at the other end (another abbreviation to remember!).

The spectrum of joint hypermobility disorders now includes:

Asymptomatic joint hypermobility

  • Asymptomatic localised joint hypermobility (1 joint)

  • Asymptomatic peripheral joint hypermobility (hands and feet)

  • Asymptomatic generalised joint hypermobility (5 or more joints)

Symptomatic hypermobility spectrum disorder

  • Historical hypermobility spectrum disorder (H-HSD)

  • Localised hypermobility spectrum disorder (L-HSD) (1 joint)

  • Peripheral hypermobility spectrum disorder (P-HSD) (hands and feet)

  • Generalised hypermobility spectrum disorder (G-HSD) (5 or more joints)

It’s really important to note that this spectrum does not infer any greater severity at one end of the spectrum compared to the other. A person with HSD can have severe problems whilst a person with EDS can have minor problems. It simply is a spectrum of similar but distinguishable disorders based on diagnoseable traits.

And now this is where things can get a tad confusing…

You don’t actually need to be hypermobile to have a HSD.

As mentioned earlier, range of motion of a joint may be limited secondary to lack of flexibility of the soft tissues around a joint. Perhaps you had surgery at a young age and lost that joint’s mobility. Or you have shortened muscles of the biceps as your body’s protective response to keep you from dislocating your shoulders. So just because you’re not flexible, don’t automatically rule out HSD or EDS if other symptoms are present.

Understanding Asymptomatic vs Symptomatic Hypermobility

A great number of pole dancers, aerialists or contortionists have some level of hypermobility. In fact, some would say hypermobile people are drawn to this artform because of the way their body moves. But hypermobility is still very poorly understood in this world. When hypermobility is discussed with patients, common responses I receive are:

“I’m hypermobile – I always twinge my ankles”

“I’m double jointed”

“Isn’t that a good thing for pole. I wish I was hypermobile”

For those who experience symptomatic hypermobility, these types of reactions can be quite frustrating, particularly as hypermobility can cause quite debilitating acute and chronic style pain. Just remember hypermobility is a spectrum with mild to extreme hypermobility and asymptomatic to severely symptomatic hypermobility. So, comparing your mobility levels with the next person doesn’t tell you whether you’ve got a HSD.

How does hypermobility/HSD occur? Joint hypermobility can occur via joint trauma such as injury, or from repetitive joint stress/load from training which leads to increased mobility. However, HSDs are secondary to autosomal dominant hereditary connective tissue disorders that affect the connective tissue of a joint, specifically the collagen.

Understanding connective tissue, muscle and collagen Connective tissue is a type of tissue in the body that connects, separates and supports the joints. Examples of connective tissue are tendons, fascia, joint capsule and ligaments. Skeletal muscle is another type of tissue of the body that performs voluntary contractile actions under control of the somatic nervous system to move the body through space. Both connective tissue and skeletal muscle are built via the foundation blocks of collagen.

Collagen is the most represented protein in the human body (30% of the protein concentration). It is an incredibly important component of the extracellular matrix of our skeletal muscle and connective tissue and is mainly responsible for their functionality in terms of force transmission, flexibility, stiffness and adaptation.

Our skeletal system is actively and passively supported by our connective tissue so we can function day to day. In connective tissue disorders, there is an issue with the connective tissue (usually a lack of collagen), which then leads to laxity/hypermobility of that joint’s surrounding passive (and sometimes active) structures. Without our passive support system in place, joints become incredibly mobile and are able to access greater than usual range of motion, aka joint hypermobility – which is why HSD/EDS patients need to rely heavily on their active support system, aka the skeletal muscles, to stabilise their joints.

Asymptomatic HSD So you don’t have any symptoms other than hypermobility of a few joints? Then you will likely be classified under asymptomatic HSD. Why is hypermobility a disorder? Well if managed correctly, it’s not an issue! But it’s the genetic collagen deficiency which leads to the secondary hypermobility that’s the issue and why it’s classified as a disorder.

In fact, asymptomatic HSD is thought to occur in 4 to 13% of the population (Simpson, 2006), with a higher prevalence in women from an Asian, African and/or Middle Eastern background. Diagnosis of asymptomatic joint hypermobility is made via a process of exclusion and requires a battery of medical tests and physical exams.

Symptomatic HSD What’s more is that collagen and connective tissue is found all throughout the body (in the digestive tract, skin, heart and even eyes), so HSD does not just affect the joints, it can also affect skin elasticity, digestion, eye function and even heart function. And this is how a range of symptoms arise. So dependent on which protein is affected by the disorder, a person can experience a range of symptoms.

It’s important to distinguish asymptomatic hypermobility syndromes from other disorders out there such as symptomatic HSD, Ehlers-Danlos Syndrome (EDS), osteogenesis imperfecta, Rheumatoid Arthritis, Lupus Erythematosus and Marfan Syndrome as these syndromes do share similar features. These other conditions can be ruled out along with infection, inflammatory and autoimmune based disorders via blood tests, molecular/genetic tests and review by a specialist (usually a geneticist/rheumatologist).

Ehlers-Danlos Syndrome

Well done for getting this far – it’s a lot of information to take in. But I’m sure you’ll agree it’s all very important and relevant for all aerialists out there. We’re now moving on to discussing one of the most common hypermobility syndromes: Ehlers-Danlos Syndrome (EDS). EDS are a group of inherited connective tissue disorders that are varied in how they affect the body and in their genetic causes. They are characterized by:

  1. Joint hypermobility

  2. Skin hyperextensibility (skin that can be stretched further than normal)

  3. Tissue fragility (ease of bruising)

The incidence of EDS, including all subtypes in the general population, is best estimated to be between 1 in 2500 and 1 in 5000 in the general population, and I imagine this number is closer to 1 in 250-500 in the pole and aerial community (no research to confirm).

Per the 2017 consensus, there are 13 different subtypes of EDS. Each EDS subtype has a set of clinical criteria that help guide diagnosis. A patient’s physical signs and symptoms will be matched up to the major and minor criteria to identify the subtype that is the most complete fit.

There is substantial symptom overlap between the EDS subtypes and the other connective tissue disorders including hypermobility spectrum disorders, as well as a lot of variability, so a definitive diagnosis for all the EDS subtypes (except for hypermobile EDS) requires genetic and molecular testing.

Types of EDS include:

  • Classical EDS (cEDS)

  • Classical-like EDS (clEDS)

  • Cardiac-valvular EDS (cvEDS)

  • Vascular EDS (vEDS)

  • Hypermobile EDS

  • Arthrochalasia EDS (aEDS)

  • Dermatosparaxis EDS (dEDS)

  • Kyphoscoliotic EDS (kEDS)

  • Brittle Cornea Syndrome (BCS)

  • Spondylodysplastic EDS (spEDS)

  • Musculocontractural EDS (mcEDS)

  • Myopathic EDS (mEDS)

  • Periodontal EDS (pEDS)

The most concerning of these diagnoses is the vascular EDS, which significantly reduces the last span of a person to an average of 48 years secondary to increased elasticity of the vascular structures which makes for an ineffective pumping system of blood vessels. This is why all hypermobile patients should be further assessed by their GP for cardiovascular issues, including assessment with an ECG and echocardiogram.

Hypermobile EDS Hypermobile EDS (hEDS) remains the only EDS without a confirmed cause/molecular marker. This means that this is the only form of EDS that currently cannot be diagnosed via testing, i.e there is currently no protein or molecular marker in the system to test for, so hEDS is a diagnosis made by ruling out all other possible diagnosis and ruling in certain hEDS criteria. And the essential difference between the diagnosis of HSD and symptomatic hEDS lies in the stricter criteria for hEDS, i.e if all possible disorders are ruled out for the patient and they don’t tick all the boxes for hEDS but exhibit clear cut symptoms of hypermobility disorders then they are diagnosed with HSD.

Diagnosing EDS/HSD

To confirm a diagnosis of EDS, specialist physicians will conduct a physical examination, and possibly skin biopsies, blood and urine tests, imaging tests, and genetic testing. Features clinicians will look for include:

  • Generalised joint hypermobility (diagnosed via Beighton’s or five-point questionnaire)

  • Unusually soft or velvety skin

  • Mild skin hyperextensibility (stretchiness)

  • Unexplained stretch marks without a history of significant gain or loss of body fat or weight

  • Spots on the heel (Bilateral piezogenic papules)

  • Recurrent or multiple abdominal hernia(s)

  • Poor wound healing/scarring

  • Pelvic floor, rectal, and/or uterine prolapse

  • Dental crowding and high or narrow palate

  • Long fingers

  • Arm span-to-height ≥1.05

  • Cardiovascular concern (via ECG/Echo)

  • Positive family history, with one or more first degree relatives independently meeting the current diagnostic criteria for EDS

  • Musculoskeletal pain in two or more limbs, recurring daily for at least 3 months

  • Chronic, widespread pain for ≥3 months

  • Recurrent joint dislocations or frank joint instability, in the absence of trauma

If you think you exhibit any of these symptoms, it’s important you don’t try to diagnose yourself, but instead seek assistance from a healthcare professional that can assist. This may be a GP who has a specialist interest in hypermobility disorders, but usually is from a specialist such as a geneticist, rheumatologist, immunologist, sports physician or musculoskeletal physician.

Is there are cure for HSD/EDS? Unfortunately, no there is no silver bullet cure or drug for these disorders. However, holistic intervention from a symptomatic point of view can significantly improve a patient’s quality of life so they can continue doing everything they want to and need to do. More on this later.

Do we need a formal EDS diagnosis? A lot of patients with EDS have been given a primary diagnosis and have not undertaken formal testing with a geneticist. This may be due to a variety of reasons including the lack of access to clinicians that understand HSD/EDS conditions. And for many patients, they don’t feel they require a formal diagnosis as there is no medication to provide a simple cure for this disorder.

At the end of the day, regardless of the formal diagnosis, the focus remains on management of the condition.

Associated EDS conditions There is a range of conditions which can accompany EDS. While they’re associated with EDS, they’re not proven to be the result of EDS and they’re not specific enough to be criteria for diagnosis. These conditions may be even more debilitating than joint symptoms; they often impair daily life, and they should be considered and treated appropriately. Associated conditions include (but not limited to):

  • Anxiety

  • Cardiovascular problems – tachycardia, aortic root dilation and mitral valve prolapse

  • Cervico-cranial instability

  • Chiari malformation

  • Chronic degenerative joint disease

  • Chronic fatigue

  • Chronic pain syndrome

  • Depression

  • Dysautonomia

  • Functional gastrointestinal disorders – acid reflux and irritable bowel syndrome

  • Headaches

  • Hernias

  • Insomnia

  • Mast cell activation syndrome

  • Migraines

  • Neurodiversity – ADHD, Autism

  • Organ rupture

  • Orthodontia issues – crowding and high palate

  • Osteoporosis

  • Postural orthostatic tachycardia (POTS)

  • Pregnancy complications/Pre-term labour

  • Raynaud’s

  • Rectal or uterine prolapse/incontinence

  • Recurrent dislocations/subluxations

  • Respiratory and swallowing difficulties

  • Scoliosis

  • Skin scarring, stretching and slow wound healing

  • Small fibre neuropathy

The conditions listed in bold have been shown to have a very close link to EDS.

Did you know? A 2012 brain imaging study conducted by Dr Eccles and her colleagues found that individuals with joint hypermobility had a bigger amygdala? This is a part of the brain that is essential to processing emotion, especially fear. This is why hypermobility is highly linked to anxiety and depression.

In fact, research by Dr Eccles revealed that people with EDS are seven times more likely to be autistic, and six times more likely to have ADHD compared to the general population. There appears to be an incredibly important link between hypermobility and neurodivergence.

HSD/EDS and hormones The sex hormones, are divided into three types;

  • Androgens (mainly in males)

  • Oestrogens (mainly in females) and

  • Progestogens (also mainly in females)

The balance and change in levels of oestrogens and progestogens control the 28-day menstrual cycle in the female.

In hypermobile males the predominant androgen hormones have very little negative effect on collagen, with these hormones likely contributing to muscle bulking around the joints instead which is an ideal response.

In females though, it is quite a different story.

Whilst oestrogen tends to stabilise collagen levels, progestogens appear to destabilise or loosen them. Many hypermobile people, though not all, notice a worsening in symptoms including increased joint pain, clumsiness or a greater tendency to dislocate in the five days leading up to menstruation and in the few days after menstruation.

This is exactly the time when the progesterone compounds far exceed the stabilising oestrogen compounds and is particularly prevalent in collagen-based HSD/EDS.

Those females whose joints become worse at the time of menstruation often note that if their periods become irregular, for whatever reason, their joint symptoms not only become worse but, are worse for longer. This may be because in these people progesterone is present in high concentrations at times when it would not normally be present. Recurring irregularity of a period (<21 days and >35 days) requires assessment by a GP or gynaecologist.