Hypermobility and Anxiety: Why Some Bodies Feel Everything More Deeply

Joint hypermobility—often seen in Ehlers-Danlos Syndrome (EDS) or Hypermobility Spectrum Disorder (HSD)—is frequently misunderstood as just extra flexibility. In reality, it reflects broader connective tissue differences that can affect every system in the body: joints, gut, immune response, and even the brain. And one of the most consistent, yet least explained, symptoms is anxiety.

A newly published neuroimaging study in The British Journal of Psychiatry (Kamboureli et al., 2025) just gave us one of the most compelling brain-based explanations to date. The researchers looked at people with and without hypermobility, some with generalized anxiety disorder (GAD) and some without. When exposed to emotional facial expressions, people with both GAD and hypermobility had significantly increased activation in their amygdala (the brain’s threat detector) and insula (which tracks internal bodily states like heartbeat, pain, gut feelings, etc.). The more hypermobile someone was, the more reactive their insula—but only if they were also anxious.

This offers a biological explanation for something I hear patients describe all the time:

• “I feel everything too much.”

• “My body constantly feels like it’s under threat.”

• “I have panic symptoms but I’m not actually anxious.”

• “No one believes me.”

It’s not just “anxiety.” It’s the body and brain trying to make sense of overwhelming interoceptive input—and for those of us in psychiatry, this should fundamentally change how we approach these cases.

This aligns with emerging perspectives from the 2024 Mast Cell Masterminds conference that I have been watching the recordings of. Many of the speakers emphasized the role and overlap of mast cell activation syndrome (MCAS) in individuals with hypermobility and sensory sensitivity.

MCAS is a condition where mast cells—the immune cells that help detect threats and initiate inflammation—become overly reactive. Mast cells don’t just release histamine in your sinuses—they’re deeply integrated into the nervous system. They can release serotonin, histamine, prostaglandins, and more directly onto nerve endings, which contributes to a wide range of symptoms that are often misdiagnosed as “psychiatric” in origin:

• Sudden panic attacks or mood swings

• Migratory pain that doesn't follow a clear injury pattern

• Sensory overload (light, sound, smell, touch, EMFs)

• Cognitive dysfunction ("brain fog")

• Reactions to food or meds that vary day-to-day

• Insomnia, fatigue, or just… system overwhelm

So what does this mean for us as mental health providers? First, we have to stop framing complex bodily symptoms as just somatization or health anxiety. We need to expand our differential to include dysautonomia, MCAS, and connective tissue disorders—especially when the psychiatric treatments aren’t working or are making people feel worse. Second, we need to be open to the idea that mental health symptoms can emerge from immune dysregulation and interoceptive chaos.

Anxiety isn’t always “psychological.” It can be the brain responding to signals of inflammation, pain, and autonomic instability. And if we only treat the brain, we’re missing half the story.

If you’re a psychiatrist reading this:

• Start asking about joint hypermobility (can you touch your thumb to your wrist? Dislocations? Family history of Ehlers Danlos Syndrome or hypermobility?)

• Ask about flushing or itching, food sensitivities, allergic-like reactions that don’t test positive Watch for sensitivities to meds, especially SSRIs, which can sometimes worsen activation in MCAS

• Consider whether “resistance” might actually be physiological overwhelm

And if you’re someone living in one of these bodies—please know your experiences are real. You’re not broken or “too sensitive.” Your nervous system and immune system are trying to keep you safe in a world that hasn’t caught up to your biology yet.

Psychiatry and mental health care have a crucial role here—not only in helping regulate the nervous system through therapies like somatic work, IFS, or neuroplasticity training, but also in holding space for complexity without defaulting to psychological explanations for physiological symptoms.

Approaches that may support healing include:

• Low-histamine or low-salicylate trial diets

• Mast cell stabilizers (quercetin, cromolyn, ketotifen)

• Thoughtful pacing around root causes like mold, infections, or trauma

• Nervous system regulation tools

• Collaborative care with providers across disciplines

• Validating the whole picture, not just diagnosing pieces

The growing intersection of psychiatry, immunology, and connective tissue biology invites a new kind of mental health care—one that listens more closely to the body, makes space for uncertainty, and honors the lived experience of those whose systems feel everything a little more deeply. Beyond siloed care.

A kind reminder: This blog post is designed as a general guide. This is not a substitute for personalized medical advice, nor is a patient-physician relationship established in this blog post.

References:

Kamboureli, Christina Niki; Rae, Charlotte; Gould Van Praag, Cassandra; Harrison, Neil A; Garfinkel, Sarah N; Critchley, Hugo; et al. (2025). Neural processes linking joint hypermobility and anxiety: key roles for the amygdala and insular cortex. University of Sussex. Journal contribution. https://hdl.handle.net/10779/uos.28350236.v1