Bisman Zebras- Hypermobility & EDS Support

03/03/2026

We have our monthly meet-up this coming Sunday, March 8th at Cappuccino on Collins in Mandan at 1pm. Everyone is welcome!

03/03/2026

Save the date for Wednesday, June 10th, 2026 for our second-annual awareness event. More details to come!

02/28/2026

Scientists found a biological "off-switch" for pain.

And it is significantly more active in males than females.

A groundbreaking study from Michigan State University reveals that pain recovery is not a passive process, but an active immune response driven by specific cells called monocytes. These cells produce interleukin-10 (IL-10), a signaling molecule that instructs pain-sensing neurons to quiet down after an injury. Researchers discovered that males possess significantly more active IL-10-producing monocytes than females, a difference directly linked to s*x hormones like testosterone. When these hormones were blocked in animal models, the male advantage in pain resolution disappeared, highlighting a biological mechanism rather than just a difference in perception or reporting.

The findings, confirmed in both mice and human patients, offer a long-sought explanation for why chronic pain disproportionately affects women. Because pain resolution depends on this active immune signaling, weaker IL-10 activity can cause discomfort to persist far longer than necessary. This discovery shifts the medical focus from merely blocking pain sensations to understanding why the biological "off-switch" fails to engage. By targeting this specific pathway, researchers hope to develop new non-opioid therapies that boost the body's natural ability to shut down pain before it becomes a chronic condition.

source: Michigan State University. (2026). Monocyte-derived IL-10 drives s*x differences in pain duration. Science Immunology.

02/24/2026

Do you get frustrated when pain is so hard to resolve? There are many areas of your brain involved in the processing of pain, and therefore, in the treatment of pain.

How pain signals travel in the body and brain

When something hurts, pain signals start in your nerves and travel to your spinal cord (or brainstem for the face). From there, the signal gets passed up to different parts of the brain.

Those brain areas:

Help you feel the pain

Attach emotion to it (like fear or distress)

Influence your thoughts about it

Affect motivation, stress response, and even reward systems

In other words, pain isn’t just a simple signal — it travels through a network of brain regions that shape how intense it feels and how upsetting it is. This is where psychology can come into play, by helping to change those signals.

Image from :
Sci Transl Med. Author manuscript; available in PMC: 2021 Dec 16.ublished in final edited form as: Sci Transl Med. 2021 Nov 10;13(619):eabj7360. doi: 10.1126/scitranslmed.abj7360

Fig. 3. Pain emotional and cognitive networks and treatments that can ameliorate chronic pain affect.

(A) Primary afferent neurons synapse onto second-order neurons in the spinal dorsal horn (DH) or the trigeminal nucleus caudalis (SpVC). These neurons, in turn, project to the lateral parabrachial nucleus (lPB) and the periaqueductal gray (PAG), which then connect with the anterior cingulate, insular, and prefrontal cortices, medial thalamus, amygdala, nucleus accumbens, and hypothalamus to generate and modulate pain experience. Note, mixed arrows indicate glutamatergic and GABAergic pathways. (B) Prevalent treatments for pain commonly use opioid receptor signaling to induce a prominent action on pain affect circuits. Investigative treatments include motor cortex stimulation (MC stim), dlPFC stimulation (dlPFC stim), neurofeedback, and cognitive behavior therapy (CBT) that act on frontal cortex circuits to modulate pain. In severe cases of intractable pain, cingulotomy reduces chronic pain. Frontal cortex modulation is hypothesized to relieve pain through descending pain control in the PAG, but notable connections to the medial and intralaminar thalamus (MT) and to the parabrachial nucleus could also play a role. ACC, anterior cingulate cortex; BLA, basolateral amygdala; CeA, central amygdala; IC, insular cortex; mPFC, medial prefrontal cortex; NAc, nucleus accumbens; Orb, orbitofrontal cortex; RVM, rostromedial ventral medulla; VTA, ventral tegmental area.

https://pmc.ncbi.nlm.nih.gov/articles/PMC8675872/figure/F3/

02/20/2026

Anyone see this? Short and sweet story but cool they realized what was happening!

Doctors saved a 29-year-old Bismarck man in the nick of time when they discovered a hidden, life-threatening condition. MORE: https://www.kfyrtv.com/2026/02/19/battling-through-marfan-syndrome/

02/19/2026

So many are sick right now. If you are, be gentle with yourself.

02/11/2026

01/23/2026

12/27/2025

“It’s just HSD.” — Please stop saying that. 🛑

There’s a widespread myth that Hypermobility Spectrum Disorder (HSD) is the “mild” version of hypermobile EDS (hEDS).
That is not what the science says.

Clinical reality:
Under the 2017 EDS Classification, the separation between hEDS and HSD was created mainly for research and genetic clarity, not to rank severity or suffering.

What research shows:
People with HSD experience:
• Comparable chronic pain levels
• Similar rates of joint instability and dislocations
• The same common comorbidities (POTS, MCAS, GI issues, fatigue)
• Similar impacts on daily function and quality of life

So what’s the difference?
Often it comes down to missing a few diagnostic checkboxes (like specific skin features or arm span ratios) — not symptoms, pain, or disability.

HSD is not a “lesser” condition.
It is not benign.
And it does not mean your pain is mild or imaginary.

Your symptoms are real.
Your diagnosis is valid.
You deserve proper care — regardless of the label.

👇 hEDS, HSD, or still stuck in diagnostic limbo?

12/05/2025