The first time is stumbled upon the connection between the vagus nerve and hyper-mobility was during a webinar. The guest speaker mentioned that cervical compression was one of the most common causes of vagus nerve compression and therefore dysfunction. They mentioned that is was the likely link between Ehlers-Danlos syndrome (a condition characterised by extreme hyper-mobility of the tissue) and the extremely low cardiac vitality and chronic fatigue experienced by these patients. They often experience shallow breathing, a very slow heart rate, slow gastric motility etc.
I was already beginning to come to the realisation that tissue in one part of the body was likely to do the exact same thing in another part of the body. A prime example of this is the connection between leaky gut and a leaky blood brain barrier.
On a very simplified level, your body has a number of wide spread endocrine (or hormonal) signals. Your body also has a finite amount of tissue types (not every part of your body uses a unique tissue type). So, when endocrine signals are wide spread across similar tissue types in various different locations, you are going to get a very similar response at a tissue level, regardless of where that tissue is located. Structural similarities exist between the intestinal and blood brain barriers (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4604320/). Hence we see similar reactions to both of these barriers under the influence of things such as stress (i.e. cortisol), Inflammation (from various inflammatory mediators such as IL6) or toxicity (such as from alcohol.)
Now that you understand that, lets move back over to the relationship between the vagus nerve and fascia.
Your vagus nerve and fascia are both PREDOMINANTLY sensory organs. This means that their largest job is feeding information back to a control centre.
Firstly, fascia is EVERYWHERE. It innovates every part of your body, providing a visco-elastic framework for mechanotransduction. This allows your body to translate movement into hormonal and chemical signalling to the brain. You stand on your leg, fascia is jolted. This jolt is translated to chemical signals and the body knows that it is time for the next step... in you stepping.
Secondly, your vagus nerve is also EVERYWHERE. The vagus nerve helps to communicate changes in the fascia to your brain. So, once you take that step, the vagus nerve assists in the communication process.
If you were to get hit in your kidney, your fascia would sense that, then your vagus nerve would sense the fascia and then stimulate the appropriate branch of the nervous system. Some may fight, some may take flight, and others may shut down completely. This reaction is dependent on a number of things leading up to the injury.
So, where does hyper-mobility come into play?
Consider a patient with a compressed vagus nerve. Now, the electrical impulses are not making it around the body properly.
Your fascia is a sensory organ, its job is to tell you when you have extended your elbow to its appropriate range of motion. Or, when your knee has reached the appropriate range of motion during walking.
You vagus nerve is responsible for carrying those signals.
If your vagus nerve is compressed, your ability to sense your body in space (proprioception) is wildly diminished.
Now consider also the relationship between the vagus nerve and hyper-permeable tissue such as the gut and brain. Is it possible that a dysfunctional vagus nerve could contribute to the flaccidity of other tissues such as fascia?
In my practice, I notice that women become more hyper-mobile in the period of time leading up to their cycles. This shows an anecdotal example of widespread endocrine signals having a widespread effect on certain tissue types.
Babies can indeed be born with vagus nerve and fascial dysfunction. Is it possible that when in utero, if a foetus develops under conditions with elevated stress and toxins, alongside a predisposed genetic pattern, that the foetus could develop a dysfunctional vagus nerve system, and therefore dysfunctional fascia/hyper-mobility?
These are just hypothesis at this point.
But, it is important to begin unravelling why so many more children are being born with hyper-mobility in todays society. It is also important to note that many adults continue to get increasingly mobile, even though that should not be the case.
The kinesthetics quotient and overall physical connectivity of humans today is far from where it used to be.
Perhaps taking a more fascial/biomechanics approach and supporting the vagus nerve is a major missing piece in the puzzle of solving tissue dysfunctions such as hyper-mobility.
Hope this was interesting! Reach out if you have any thoughts.
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