Joint Hypermobility, hEDS, and Anxiety – The Brain-Body Connection

As time passes, we have found more and more support for the fact that the mind and body are connected. What affects us physically affects us mentally, and vice versa. When we consider the autonomic nervous system, we know that we have "fight or flight", aka the sympathetic mode, and "restoration/relaxation", aka the parasympathetic mode. That means that if our mind is relaxed, our body will also relax, we will breathe deeper and slower, our blood will flow throughout our entire body, we will digest food more easily, and more. If our mind races, our heart rate increases, we breathe faster and more shallow, and our fingers and toes get cold because our blood is rushing to the core parts of our body. This also works in reverse- if we are in pain, our body is naturally in fight or flight, and therefore our mind feels stressed. Whereas, if we focus on relaxing the body through slow breathing, releasing muscle tension, or something else, we will find that our mind slows down as well.

It is essential to take that a step further. People will often hear that their health issues are coming from anxiety, depression, or trauma. While this can be true, unfortunately, it is often overstated and used more as a dismissal rather than an accurate and helpful note for treatment purposes. In the last couple of decades, researchers have begun to show the link between health issues causing mental health concerns, which is not shocking to anyone who has ever experienced a chronic health issue. Understandably, having to deal with constant pain and illness can lead to anxiety and depression, just due to the nature of existing when you don't feel well all the time and the amount of time it takes to manage health issues and grieving changes in life.

But again, what if we take it one more step.... which is linking specific physical health issues to mental health issues due to differing brain structures, hormones, neurotransmitters, and more. Researchers have demonstrated links between certain physical health conditions and changes in the brain and, therefore, mental wellness. Still, in recent years, the relationship between joint hypermobility (including hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorder) and Attention Deficit/Hyperactivity Disorder (ADHD) and Anxiety has been explored.

Joint hypermobility (as seen in HSD or hEDS) frequently goes hand-in-hand with neurodevelopmental conditions. Recent studies show people with ADHD are several times more likely to be hypermobile (and vice versa), and many hypermobile teens (30–45%) have ADHD.

Anxiety disorders are also about four times more common in hypermobile individuals. So the question is- why?

This blog post is focused on the connection between anxiety and hEDS/HSD, but check out my other blog post for the connection between ADHD and hEDS/HSD.

hEDS and Anxiety

People with hypermobile joints don’t only face physical symptoms – they also have markedly higher rates of anxiety disorders. Estimates suggest individuals with joint hypermobility are up to 4 times more likely to experience anxiety or panic disorders than the average person​

Many hypermobile folks report chronic anxiety, and conversely, anxiety clinics often find an overrepresentation of people who turn out to be extraordinarily flexible. This link has prompted researchers to dig deeper: what is it about hypermobility that might feed into feelings of anxiety?

Understanding this overlap sets the stage for exploring why it exists. The answer, emerging from recent research, seems to lie in how our brains process emotions, sensations, and focus in the context of a bendy body.

Recent studies using brain imaging and other neurological tests have started to unravel how joint hypermobility might be linked to differences in brain structure and function. In other words, the connection between a flexible body and traits like anxiety or ADHD may be partly due to how the brain is wired and how it processes bodily information.

Hypermobility and Anxiety: Fear and Bodily Signals on Overdrive

If you have ever felt anxious because your heart was racing, you’ve experienced how closely physical sensations tie into anxiety. People with hypermobility (especially in hEDS) often deal with unique bodily feelings – frequent dizziness, heart palpitations, pain, or gastrointestinal issues – due to things like dysautonomia (imbalances in the autonomic nervous system). Researchers theorized that hypermobile individuals might have brains that react more strongly to such internal sensations and to potential threats, making them prone to anxiety. Functional MRI (fMRI) studies are now confirming this brain-body connection in anxiety:

Overactive “Fear Centers”: A 2025 study led by Dr. Jessica Eccles examined brain activity in hypermobile people with anxiety. When shown emotional stimuli (like expressive faces), those with joint hypermobility and generalized anxiety disorder (GAD) had higher activation in the left amygdala – the brain’s “fear center” that processes threats – compared to non-hypermobile people​.

Heightened Internal Awareness: The same study found that hypermobile individuals also showed extra activation in the insula, specifically the mid-insula and anterior insula.​ The insula is a region that acts as the brain’s internal sensor; it helps monitor bodily states (like heartbeat, gut feelings, pain signals) and contributes to how we feel emotions in the body. Increased insula activity suggests that hypermobile people’s brains may be hypersensitive to internal bodily signals, which can fuel anxiety. In fact, those with more extreme joint flexibility showed the most significant insula activation, hinting that the “bendier” the body, the more responsive the brain’s internal alarm system might be.

Stronger Brain Connectivity for Self-Awareness: Beyond isolated brain regions, researchers noted differences in how brain areas communicate. Hypermobile participants showed stronger connections between the amygdala and the precuneus (a region involved in self-awareness and shifting attention)​. This could mean that bodily threat signals (amygdala) are more tightly linked to self-focused attention in hypermobile folks, potentially making it hard to ignore anxious feelings. Essentially, the brain’s threat radar and its self-monitoring systems may be unusually in sync in people with hypermobility, which might explain why anxiety comes so easily.

One thing that is interesting about this is that, like all emotions, anxiety has an important purpose. I always tell clients that it would actually be a bad thing if we said "Poof! You no longer have any anxiety!" We need anxiety, to a degree, to stay safe. With any chronic illness, you need to be in tune with your body to understand what causes your symptoms to flare and how to intervene early if your body feels "off". So the stronger connectivity between the amygdala and the precuneus, extra activation in the insula, and higher activation in the left amygdala may actually help people be more in tune with early detection of potential flares in symptoms and understanding of triggers. The problem is, the anxiety being heightened goes past the "sweet spot" of being helpful, and causes issues.

These neural findings map onto real-world symptoms: if your “fear center” fires up quickly and your body-sensing brain regions are ultra-attuned, you’re likely to feel anxious more often. Notably, this fMRI research helps explain why joint hypermobility has been linked to anxiety disorders (like panic disorder and GAD) so frequently – the brain circuits for fear and bodily sensation seem to be tuned a bit differently.

On a hopeful note, understanding this brain pattern suggests new treatment angles. For example, interventions like biofeedback or neurofeedback might be used to help hypermobile individuals calm their amygdala and insula activity, potentially reducing anxiety symptoms​. Simply recognizing that their anxiety has a physical, brain-based component can be empowering for patients – it’s not “all in your head” in the dismissive sense, but rather a genuine mind-body interaction.

Why Might Connective Tissue and Brain Traits Be Linked?

Interoception and Autonomic Factors: One research angle focuses on the feedback loop between body and brain. People with hypermobility often experience dysautonomia – their heart rate and blood pressure can fluctuate abnormally (as in POTS, postural orthostatic tachycardia syndrome), and they might have gastrointestinal or immune issues. These constant physical stressors bombard the brain with sensory information. Over time, the brain of a hypermobile person might become trained to be hyper-vigilant about bodily sensations. The heightened insula activity seen in the fMRI study​ supports this – hypermobile individuals may have a heightened sense of what’s happening inside their body (called interoception). While being in tune with your body can be good, like I stated above, in this case, it may overshoot, leading to anxiety (every flutter or pain is perceived as a threat). Essentially, the connective tissue disorder sets off a cascade of physical symptoms, and the brain responds in kind, affecting mood and attention.

When I have a client begin working with me who shows physical symptoms of anxiety in a pattern that is irregular and not easy to identify patterns or triggers, and also does not experience cognitive symptoms of anxiety, I have dysautonomia on my mind as a potential diagnosis to assess for. This particular pattern tends to raise a red flag for me to consider whether dysautonomia might be playing a role.

Collagen in the Nervous System: Connective tissue isn’t just in the joints – collagen is also present in our brains and nerves. One hypothesis is that the collagen abnormalities in hEDS (and related conditions) directly lead to subtle changes in the brain’s anatomy. For example, collagen is a component of the corpus callosum (the bridge between the brain’s hemispheres) and the supporting structure of white matter tracts. If collagen is weaker or disorganized, the brain’s wiring could be formed a bit differently. In hEDS, impaired collagen might alter how certain brain regions connect, or how robust those connections are.  This theory is consistent with the MRI findings of structural differences (in the amygdala, ACC, etc.) described above. In short, the same tissue quirk making one’s joints extra flexible might also be shaping the brain’s connective framework, leading to differences in function.

None of these theories alone can fully explain the connection, and likely it’s a mix of factors. The take-home message is that the overlap between hypermobility and anxiety is real and biologically based. The brain and body are in constant conversation, and differences in our connective tissue may alter that dialogue in ways that shape how we feel and behave.

What does this mean for clients, therapists, and other medical providers?

Understanding this joint-brain connection has practical implications for both clinicians and individuals dealing with these overlapping conditions:

For one, it encourages a more holistic approach to treatment. A therapist seeing a patient with anxiety might consider asking about physical symptoms like joint pain or dizziness. Conversely, a doctor treating a teenager with hEDS for chronic pain might screen for ADHD or anxiety, rather than assuming the emotional symptoms are “just because of the pain.” This integrated perspective can prevent missed diagnoses and ensure better management. For example, if a hypermobile client’s panic attacks are partly driven by a highly reactive autonomic system, interventions could include not just therapy and medication, but also techniques to manage dizziness or heart rate changes (like gradual physical conditioning or beta-blockers).

Anxiety in hypermobile individuals might improve with interventions that also target their physical well-being (for instance, gentle exercise to stabilize joints and improve autonomic function can reduce overall anxiety levels). The key is recognizing the person as a whole: brain and connective tissue, mental health and physical health, rather than siloing these issues.

For people with hEDS, simply knowing that their mix of symptoms has a name and a reason can be validating. Many people with EDS or hypermobility have long struggled with being told their symptoms are “in their head.” The new research flips that script: yes, the brain is involved, but in an integrated way with the body – and importantly, these findings legitimize their experiences.

A client with hEDS who reads about the amygdala-insula study might realize, “My anxiety makes sense biologically, I’m not just overreacting.” This understanding can reduce self-blame and encourage individuals to seek comprehensive care.

The growing recognition of the hypermobility-neurodivergence connection is leading to more personalized interventions. Researchers are exploring treatments like biofeedback targeting specific brain networks (amygdala-insula) to reduce anxiety in hypermobile patients​

For now, the best approach is one that acknowledges both the mind and the body. As science continues to unravel this brain-body puzzle, individuals with joint hypermobility and co-occurring mental health conditions can feel validated that science is on their side, and clinicians can refine therapies to improve quality of life.

If you’re living with Ehlers-Danlos Syndrome, hypermobility, or anxiety—and you’re starting to notice how deeply your mind and body affect each other—you don’t have to navigate it alone. Therapy can help you make sense of your experience, manage the overwhelm, and build strategies that support both your physical and emotional well-being.

I offer specialized therapy for individuals managing the impacts of chronic conditions like EDS and dysautonomia. If you're ready to feel more grounded and understood, reach out for a free 15-minute consultation. Let’s work together to support your wellbeing.

Stay tuned for my next blog: Joint Hypermobility, hEDS, and ADHD.

References

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Bulbena-Cabré, A., & Bulbena, A. (2018). Anxiety and joint hypermobility: An unexpected association. Current Psychiatry Reports, 20(7), 55. https://doi.org/10.1007/s11920-018-0917-9

Csecs, J. L. L., Iodice, V., Rae, C. L., Brooke, A., Simmons, R., Quadt, L., & Eccles, J. A. (2021). Joint hypermobility links neurodivergence to dysautonomia and pain. Frontiers in Psychiatry, 12, 786916. https://doi.org/10.3389/fpsyt.2021.786916

Eccles, J. A., Owens, A. P., Mathias, C. J., Umeda, S., & Critchley, H. D. (2023). Joint hypermobility and anxiety disorders: A novel neuroconnective phenotype? Journal of Neurology, Neurosurgery & Psychiatry, 94(8), 617–626. https://doi.org/10.1136/jnnp-2022-329711

Farmer, A. D., Aziz, Q., & Grahame, R. (2020). Neurovisceral phenotypes in the expression of functional gastrointestinal disorders associated with joint hypermobility. Autonomic Neuroscience, 224, 102631. https://doi.org/10.1016/j.autneu.2020.102631

Glans, M. R., Bejerot, S., & Humble, M. B. (2018). Generalised joint hypermobility and neurodevelopmental traits in a non-clinical adult population. BMJ Open, 8(10), e023465. https://doi.org/10.1136/bmjopen-2018-023465

Kindgren, E., Pérez-Vigil, A., & Larsson, H. (2021). Comorbidity of Ehlers-Danlos syndrome and hypermobility spectrum disorders with neurodevelopmental disorders: A population-based cohort study. Frontiers in Psychiatry, 12, 803213. https://doi.org/10.3389/fpsyt.2021.803213

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Seneviratne, S. L., Maitland, A., & Afrin, L. (2021). Mast cell disorders in Ehlers-Danlos syndrome. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 187(4), 519–529. https://doi.org/10.1002/ajmg.c.31952