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Hi guys, Welcome to another episode
of The Factor podcast. I'm your host,
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Jessica Riddle. Welcome and thanks for
listening. Today we unpack a new
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training with doctor Navaz Habib, a
Toronto based chiropractor, acupuncturist, and functional
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medicine practitioner that has dedicated his career
to the study of the vegus nerve.
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In part one of this two episode
series, we'll explore how the vegus nerves
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regulatory pathways impact inflammation, the role
of acetacholine in modulating immune responses, and
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how these mechanisms can be leveraged to
improve conditions such as autoimmune disorders, neurological
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diseases, and more. I know
you hear me say this a lot,
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but this episode is truly jam packed
with insides that can help you approach your
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patient care a little differently. Be
sure to hit that bookmark or download link
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so you can listen more than once. Let's dive in. Thank you so
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much, Jessica. I'm excited to
be here and excited to share some of
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the amazing research and findings that I've
had in incorporating vegas nerve stimulation into my
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practice. I am a chiropractor,
I'm based in Toronto, Canada. Graduated
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in twenty ten from Canadian Memorial Chiropractic
College. Was actually lucky enough to be
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the class valedictorian of my year and
that was wonderful. I have since and
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I'll just give you a brief breakdown. I have been an associate, I've
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owned a chiropractic practice, I've sold
a chiropractic practice, and have shifted into
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working with Page via telemedicine and working
more with consulting clients all around the world
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with regards to their vegus nerve and
optimizing their overall health. It's been an
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interesting shift and it's been a positive
one. And I'm excited to kind of
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tell you a little bit about the
Vegas nerve a little bit more because I
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think it's something that we tended to
scoot by in understanding in our school,
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and it's one of those things that
I think if we give it a little
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bit more attention, we'll realize just
how important it truly is to creating an
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optimal environment for help. So the
Vegas nerve, what happens in Vegas,
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not the city, obviously, is
we have communication by direction, communication between
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many different organs and the brain.
Eighty percent of the information on the vegas
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nerve is actually afferent, meaning coming
from all of the organs sharing status information
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from the organs back to the brain. That's a big component. We tend
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to think of parasympathetic as being much
more efferent in its pathway, being much
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more from the brain to the body, and only fifteen percent of the information
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on the vegas nerve is actually parasympathetic
efferient information. This is where we get
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this rest digest information from the brain
to the organs. An really important area
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here is the actual inflammatory control via
the cholinergic anti inflammatory pathway also known as
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the CIP. This is a really
important thing to understand because when it comes
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to chronic health conditions that a lot
of our patients are dealing with, whether
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they be autoimmune or inflammatory in nature, always have the lack of control of
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inflammation as the pathway to the disease
progression. So this is a really important
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area to fully understand, and the
control of inflammation is the primary job of
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the vegus nerve within the body.
This is where we have that specific effect
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of being able to limit the amount
of damage that inflammation can do. Inflammation
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is a necessary piece to the optimization
of our body puzzle. But the control
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of inflammation is what often needs to
be talked about, and that's what the
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job of the vegas nerve is.
For the math people out there, that's
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only ninety five percent of the role. So four percent of the information here
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is motor information and that's specifically going
to the and laryngeal muscles. Those are
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the muscles of the airway, throat
and vocal cords. So maintaining the openness
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and patentness of an airway is the
job of the motor component of the vegas
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nerve, and as well as having
a bit of a role to play in
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vocal pitch and tone. So being
able to go really really low or really
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really high with my voice is there
because I have motor control of the laryngeal
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muscles that tension and pull on the
vocal cords themselves to create tension allowing for
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pitch to change. The last area
here is one percent of the information is
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actually sensory information from the skin of
the ear and actually in a very particular
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area, and this is an area
that acupuncture has been utilizing for generations to
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help improve vegas nerve stimulation. Or
vegas nerve function. There's actually a few
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points in there, particularly vegas nerve
points, and another one with the name
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of shen Men which is right in
that center area, and that's an area
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that will play a really positive role
in improving vegas nerve function overall. Next,
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we want to get into the pathway
that I talked about, and that's
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the coal energic anti inflammatory pathway.
It's actually multiple directions and that's what's really
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exciting about it. So the vegas
nerve has inputs going in primarily to the
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nucleus tractus solitarius in the brain stem
and then coming from the dorsal motor nucleus
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in vegas in the brain stem and
coming out. Okay, so this is
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where the inputs and the outputs are
being relayed to within the brain stem nuclei.
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The vegus nerve courses down sends a
signal out to the lungs, has
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a direct branch that goes to this
celiac ganglion and the celiac superior mesenteric plexus
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ganglia just go to the celiac ganglion
to make it easy, and over here
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it releases a setyl coline. This
is the reason for the name coal ergic.
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In the coal energic ante inflammatory pathway, it uses a setyl coling.
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The vegus nerve only uses a setl
coline as it's neurotransmitter of choice. It
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also then has a direct branch to
the entirety of the gut, and this
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is very important. The gut brain
connection is physically made up by the vegus
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nerve, and we know that seventy
percent of our immune cells by volume are
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located in the gut and the gut
lining. So this is an important area
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for controlling signals to be sent via
setal coline, and so this is an
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important area to look at from a
physical standpoint. The fun relay here is
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as the vagus nerve sends acetyl coline, if we look back at the celiac
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ganglion, we then see that the
acetylcholine is released to attach to the splenic
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nerve. The splenic nerve is actually
a sympathetic nerve, not parasympathetic. It's
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a sympathetic nerve. And what's really
exciting here is when the acetyl coline is
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released into this area, it actually
hijacks that splenic nerve and turns it into
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a parasympathetic functional nerve, which is
really cool. The splenic nerve will then
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release neuropenephron at the spleen level,
activating a set of T cells called chat
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cells. Okay, and they have
a beta two andronergic receptor on them that
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the norropinephrine attaches to. Then these
T cells, these chat cells become hyperactivated
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and they become activated to release a
seal coline. You can see what those
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red dots coming down the pathway from
the T cells, and these acetyl coline
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will make its way too splenic and
other local tissue macrophagers. So any organs
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that don't have direct innervation from the
vegas nerve, we know a lot of
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the visceral organs do. Almost every
single one has a direct innervation, but
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the bone, the muscle directly to
areas within other organs and tissues that are
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not directly innovative innervated by the vegas
nerve, including the skin, will get
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the signal of acetyl coline through the
bloodstream via these chat cells being released in
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the spleen and then these local tissue
macrofages, all of them have this alpha
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seven nicotinic acetal coldine receptor. You
can see within that red box, each
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of these splinic and local tissue macrophagers
contains that particular receptor, and that receptor
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is the target of the acetal colding
that's being released both directly from the vegus
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nerve in particular organs, and then
without it being in the vegas nerve directly
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where it goes out through splenic amplification. The other tissues will receive this acetyl
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coline signal, and that acetyl coline
signal goes to those macrofagists to tell them
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we need to shut down or decrease
the amount of inflammation that's happening. And
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then, as you can see also
within that red box, we're able to
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decrease the release of TNF, alpha
ail one and aisle six. These are
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very very well known inflammatory side of
kinds. These are inflammatory signaling molecules that
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we don't want to have going off
and becoming rampant drivers of an inflammatory response.
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Okay, so that's really important.
If we go back towards the brain
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here, you'll notice that at the
NTS we have the input coming in from
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the vagus nerve and then we have
a relay pathway with a green arrow that
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goes up to the hypothalamus. And
this is really really important because not only
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do we have an acetyl coline release
going down from the brain to the rest
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of the body, we actually have
a signal coming up to the brain as
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well. And if we remember the
name of these macrofages that are within the
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brain and the central nervous system are
the microglia, and acetyl colin is released
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from certain areas called particularly the nucleus
Bacillus of maynards within the brain. There's
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not going to be a test on
this later, don't worry, but that
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area is necessary for releasing acetyl colin
locally within the brain, within the central
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nervous system, and that acetyl coline
helps to manage the inflammation within the brain.
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This is huge because this is an
area that needs to be addressed in
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many many health conditions, whether they
be neurodegenerative in nature like Alzheimer's or Parkinson's,
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or dementia or TBI concussion, stroke, whiplash. Those types of injuries
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can also severely increase the inflammatory response
within the brain, and so the vegus
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nervous heavily heavily involved in the release
of that acetyl colin in the brain as
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well. We also get direct signals
up to the hypothalamus which actually activates corticotrope
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and releasing hormone CR, which then
sends a signal to the pituitary gland to
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release adrenal corticotropic hormone ACT, which
is the yellow dots and the green arrow
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that goes down to the adrenals,
and this actually activates glucocorticoid release to help
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to shut down that inflammatory response as
well. So the glucocorticoids help in a
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secondary manner in affecting those local tissue
macrofashes and helping to downregulate the inflammatory response.
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So this is a really, really
awesome picture of what the colonergic anti
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inflammatory pathway looks like. And it
can get deep. And I realize this
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is not an easy thing to fully
understand, but I'm going to do my
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best to help you see this.
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dot com today. Now back to
the show. The target of the coolinergic
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anti inflammatory system or the pathway is
the marvelous macrophage. The macrophage is the
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organ that is necessary to be controlled
in this pathway. It is the main
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cell of the innate immune system.
It is the main one that goes and
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identifies the sources of threat to our
bodies and when it senses threat, it
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is activated into a state called M
one. We'll talk about that in a
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moment. And what it does is
it signals of inflammatory cytokines out to bring
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other immune cells locally to the area, adaptive immune cells and other innate immune
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cells as well. This is the
target. When we can control this cell
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through vegas nerve activation, vegas nerve
stimulation and the release of acetyl cooldine,
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we can have a phenomenal response on
controlling the severity of inflammatory response that our
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body creates. There are tissue resident
macrofages everywhere. They all have very similar
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jobs in similar roles, but they're
called different things. In different tissue.
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In the skin, they're called dermal
macrophage or Lungerhund cells. In the lung
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they're alveolar, interstitial, and pulmonary
intravascular macrophages. In the liver their cupfour
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cells. In the heart, there
are multiple different types. In the brain
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they're microglia, and the kidney they're
kidney macrophages. In the muscle, there's
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three different types CD eleven C plus
CD eleven B plus F four to eighty.
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We've got in the bone stromo macrophages, and then one that's missing from
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this list is actually osteoclasts are macrofages
within the bone. Osteoclasts that we know
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are necessary to create osteoporosis or to
maintain the shape of bone by breaking it
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down slightly. In the lymph nodes, we've got subscapular macrofages. In the
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spleen, we've got the red pulp, the white pulp, and the marginal
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zone macrophages. In the intestine,
we've got lemon appropriate macropages and sub mucosal
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This is where seventy percent of our
immune cells by volume are located within the
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body, is in the intestinal walls
and then within the pancreas. There are
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pancreatic macrofages as well. These tissues
are everywhere. These cells are necessary as
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not only the detectors of threat,
but they really do help to focus on
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identifying and maintaining the function of the
organ that they're located in. And this
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is a necessary piece to understand because
this is the target of control from the
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vegus nerve. This is the names
of all of the target cells of the
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vagus nerve col energic anti inflammatory pathway. The directly innervated tissues are cns,
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the blood vessels, lungs, liver, gut, and then the spleen via
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the splinic ganglion are the directly innervated
but then via splinic amplification, we send
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signals out to the skin, the
sirosa, the muscle, atipose tissue,
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and bone. And this is important
to understand. So these are the target
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cells of that entire cool energic anti
inflammatory pathway. It can be dysfunctional in
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many different conditions, whether autoimmune in
ra sl ms, asthma, type one
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diabetes, vascular conditions like athrosclerosis,
digestive conditions very very important here, irritable
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bowel crones colitis, metabolic conditions,
obesity, type two diabetes, naffled Nash,
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neurological conditions, Alzheimer's autism, schizop
me a dimension, dementia at Parkinson's,
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and then even hormonal effects as well, indometriosis being an inflammatory condition as
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well. So these are all conditions
that may have some specific piece to the
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or dysfunction going on and a lack
of control of the inflammatory process locally within
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a particular organ or within a particular
area. Macrifages have different states that they
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will work on. So an M
zero macriphage, the blue guy that you
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see at the top of the screen
here, that one has not been differentiated
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yet into a state of being fight
or fix state. Okay, But there
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are certain signals that will drive an
M not or an M zero macrofage into
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a different statelypopolysach right LPs A,
IFN gamma, which take the M zero
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macrifage to the left side of the
screen here will turn on what's called M
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one state or M one macrofash state, and these are very high expression pro
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inflammatory cell functions. These guys are
meant to fight, They're meant to send
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a signal of us of inflammatory cytokines
out into the bloodstream into every area to
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have them bring in more inflammatory and
immune cells locally to the area where they've
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discovered said threat. The M two
macrofages we can shift to using IL four
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and ILE ten, which are which
we know are anti inflammatory cytokines, and
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these guys helped differentiate them or M
zero macrofashes into M two M two are
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known as the fix macrifages, not
the fight guys, are the fixed guys,
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and then these will further differentiate depending
on other signals that are there present
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locally. They can go into M
two A, M t B, M
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two C, and M two D
and a lot of these are regulatory or
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focused on debris removal. They use
the same tools as during inflammation, but
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they do it in a very controlled
manner and what their job is to help
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regulate and control and optimize the function
of particular organs. And so the regulatory
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effect of these will come from whichever
signals are being sent, whether ile thirteen,
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IO four, IRF four, TLR, golobulin complexes, group of cordocoids,
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Ile ten to TGF beta, or
A two A R as well.
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So these will differentiate the function of
these to do very specific tasks using the
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same tools that any macrofage would.
Okay, so we often think of the
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macrifages as being these magical engulfers of
threats to us. But that's only one
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job. The regulatory job. The
fixed job is the one that we've often
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overlooked, and it's the role of
acetyl colding to help to actually shift from
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M one state macrofages, which are
the pro inflammatories, into the M two
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state macrophages. You'll see that with
the green line going across vegas nerve stimulation
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is one of the best ways to
do this. This has been proven.
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I've got a great research study below
that I'm going to share. This is
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a really amazing tool. And then
when we have the presence of lots of
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M two macrophage, is that it's
actually inhibitory to the production of M one
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high inflammatory macrophages as well, and
that's indicated by the red line below there.
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Okay, so these are important pieces
to understand, and it's the job
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of the vegas nerve when working to
help to shift these cells from M one
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state to M two state and from
fight to fix the cellular effects. This
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is how it actually works. Remember
we mentioned that alpha seven nicotinic acetyl coline
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receptor on the pathway. What it's
doing. When acetyl coline hits that particular
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receptor, it has two very particular
things that it can change. Number One,
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it can go down the camp C
FOSS pathway, which is the first
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pathway on the left. Here you'll
see that it activates CAMP which goes into
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the nucleus and activates sea fire CFOs, and that will lead to a decrease
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in the transcription of a factor known
as Nfkapa B. NF kapa b,
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when activated, sends out the cytokinds
that are inflammatory the ile one IILE six
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or excuse me, il yeah,
io one, io six okay, and
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TGF or tnf alpha as well.
The second pathway is a cetylcholine will hit
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that same receptor and activate the JACK
two STAT three pathway, and that will
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actually result in the decreased gene transcription
of inflammatory side of kinds as well,
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So we're actually regulating and decreasing the
amount of inflammatory side of kinds that will
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be released. There is one more
scenario, and this is an interesting one
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that most people don't understand as yet, but that alpha seven nicotinic acetylcholine receptor
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is also present not only on the
cell surface, but it's also present on
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the surface of mitochondria. How many
of us have heard about mitochondrial health and
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the importance of maintaining good mitochondrial health
for longevity, for energy, for overall
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optimal function, and metabolic ideals.
Well, when there's a lot of ATP
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that's present around the cell surface,
ATP will activate a channel here that allows
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acetylcholine to enter the cell directly and
that will activate the alpha seven nicotinic acetylcholine
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receptor on the mitochondria. When that
receptor is activated, it actually decreases and
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shuts down the release of mitochondrial DNA. This is a very common pathway by
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which we trigger an inflammosome or trigger
this NFAPA B gene transcription occurrence that takes
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place. If mitochondrial DNA is released, it will lead to the inflammosome and
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the release of inflammatory cytokines into surrounding
areas. But when we activate the acetolcholine
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receptor on the mitochondria, that shuts
down the mitochondria DNA release. That allows
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for the to remain within the mitochondria
that allows for optimal function to be restored,
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and we don't trigger an inflammasome.
We actually don't allow this pathway to
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begin. And one of the best
ways that I've found to help do this
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is through cervical transcutaneous vegus nerve stimulation. Okay, so the vagus nerve is
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sending these acetylcholine signals out to all
of these tissues, particularly those macrifages,
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to help with the regulation and control
of inflammation. When we don't have an
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optimally working vegus nerve, the control
of inflammation is going to be reduced.
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Use of electrical currents to help to
stimulate nerves is something that we've all seen
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00:22:42.680 --> 00:22:48.079
many times. How many practices use
a tends unit or interferential current or other
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electrical stimulation tools like a pointer plus
on acupuncture or something along those lines.
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This is a tool that directly targets
the vagus nerve. So it's electrical stimulation
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of vagel fibers. The aentiilateral circle
spine to find where your vegas nerve is
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literally find your pulse and it's right
beside there. I'm going to show you
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a really cool image so this is
a great area to access the vegas nerve.
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And what you'll find is about ninety
to ninety five percent of the fibers
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on vegas nerve are found within the
neck and not anywhere else. It's easily
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accessible within the crotted sheet. You'll
see on the next slide that we've got
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the crowded artery, the jugular vein, and the vegas nerve that are nice
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00:23:30.720 --> 00:23:37.039
and wound type. Together, we're
going to be able to activate both afferent
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and epherentt exonal fibers. Interestingly,
there are only one hundred thousand fibers on
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00:23:41.519 --> 00:23:45.680
the left side vegas nerve and two
hundred thousand on the right side vegas nerve.
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Two hundred thousand plus. They're realizing
there's more on the right. For
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whatever reason, I wasn't there for
the design process and it's something that we're
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still trying to figure out why.
So where is the vegas nerve I just
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00:23:56.400 --> 00:24:00.400
mentioned this. It's within the carotid
sheet, just behind our certoclidomastoid muscle,
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00:24:00.440 --> 00:24:06.279
the SCM muscle. If you ever
push against your head, you can push
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your head against your hand, excuse
me, you'll notice that your SCM muscle
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00:24:08.599 --> 00:24:12.440
pops up. If you just pop
in front of that SCM muscle, you'll
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be able to find your pulse.
Your pulse, your feeling is the common
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00:24:17.480 --> 00:24:22.200
carotid artery, the CCA that's present
on this ultrasound image. You'll see the
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IGV there as well. That's the
internal jugular vein, and then right behind
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00:24:26.200 --> 00:24:30.440
it, that thick tissue that's outlined
in yellow, that is the vegas nerve.
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00:24:30.480 --> 00:24:34.440
So if you feel your pulse,
you're very very close to your vegus
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nerve as well. The thing that
really introduced me to the importance of the
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vegas nerve was that it was the
only nerve coursing down through the neck present
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00:24:44.480 --> 00:24:48.079
within this carotid sheet. It's the
only tissue there. We know how important
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00:24:48.079 --> 00:24:52.400
the common CA and internal jugular vein
are, but how many of us have
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00:24:52.480 --> 00:24:56.119
forgotten that the vegus nerve is part
of that sheet and so so important to
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00:24:56.160 --> 00:25:00.680
our overall health and survival. So
just great to see there. It's literally
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00:25:00.759 --> 00:25:04.279
right behind the anterior fibers of the
stern cloudomastoid, and so if you just
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00:25:04.359 --> 00:25:07.599
kind of give it a little push
out of the way, you'll be able
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00:25:07.640 --> 00:25:11.440
to find the pulse and you're right
there on your vegas nerve. How does
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00:25:11.799 --> 00:25:15.640
non invasive vegus nerve stimulation work?
Well, this was a sham study that
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00:25:15.799 --> 00:25:22.079
was done where they actually stimulated over
the sterno clidum mastoid versus over the carotid
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00:25:22.240 --> 00:25:26.880
artery area where they found the pulse. And what was found was when not
295
00:25:27.039 --> 00:25:32.119
obviously not within the sham activation,
but within the actual activation of the nerve
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00:25:32.839 --> 00:25:37.880
when they stimulated using the electrical device
to handheld electrical device, they had an
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00:25:37.920 --> 00:25:41.839
activation of particular brainstem nuclei. This
will go back to which ones we saw.
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00:25:42.240 --> 00:25:47.640
This is the nucleus of the solitary
tract the NTS nucleus tractus solitarius,
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00:25:48.680 --> 00:25:52.559
and we had activation of the dorsal
motor nucleus of vegas. This is cool
300
00:25:52.599 --> 00:25:56.519
because we know that we're getting activation
of the two nuclei, the primary tow
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00:25:56.680 --> 00:26:02.240
nuclei by which vegas nerve connects.
Okay, so this is really important.
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00:26:02.240 --> 00:26:06.759
We also got a little bit of
activation in vestibular nuclei and the medial longitudinal
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00:26:06.799 --> 00:26:10.400
fasciculus as well, and as well
a little bit in the spinal trigeminal which
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00:26:10.440 --> 00:26:15.559
is linked as well, and that's
actually the spinal trigeminal was not activation,
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00:26:15.599 --> 00:26:18.720
excuse me an inhibition that occurred in
the spinal trigeminal nerve. This is great
306
00:26:18.880 --> 00:26:25.000
for things like boos palsy or great
for kind of the trigeminal headaches that can
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00:26:25.039 --> 00:26:27.839
occur as well, and this is
a reason for why this particular tool is
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00:26:29.000 --> 00:26:33.160
used heavily in headache cases, migraine
in particular. So this was a great
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00:26:33.440 --> 00:26:37.119
study and it continued on to show
that not only is the effect local within
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the brain stem, but it actually
creates a biphasic response above in different areas
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00:26:44.039 --> 00:26:48.319
of the brain. So this was
a three phase response. They did fMRIs
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00:26:48.440 --> 00:26:52.359
between three and five minutes, seven
to nine minutes, and thirteen to fifteen
313
00:26:52.400 --> 00:26:57.240
minutes later, and what they found
was activation of the Rapie nuclei and substantion
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00:26:57.279 --> 00:27:03.200
niagra and the brain stem the early
phase, as well as the medial frontal
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00:27:03.240 --> 00:27:11.039
cortex and parasingulate cortex early phase.
Then we had inhibition initially and then activation
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00:27:11.160 --> 00:27:15.079
in the amid post VNS phase,
which is a seven to nine minute phase,
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00:27:15.119 --> 00:27:19.119
and we got activation of the ray
Fie nuclei, the VTA mental tech
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00:27:19.200 --> 00:27:23.119
megntal area, and then we had
it in the hypothalamus and the acc as
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00:27:23.200 --> 00:27:27.200
well. Above this was an activation
that occurred, and then we had a
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00:27:27.200 --> 00:27:33.680
calming effect almost throughout the entire cortex, particularly the precuneus and parasingulate cortex had
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00:27:33.680 --> 00:27:38.599
an inhibitory response, and then we
had activation in the brain stem at the
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00:27:38.720 --> 00:27:44.480
VTA, the pag, the substantia
niagra, and the Rayphi nuclei. This
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00:27:44.799 --> 00:27:48.799
helps to tell us exactly how this
system works. This is a neuromodulatory activation
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00:27:49.319 --> 00:27:55.759
that's occurring. We're getting activation of
dopamine response, of nouerpenephrine response, and
325
00:27:55.839 --> 00:28:00.200
of serotonin response within the brain.
And once we go and see as well,
326
00:28:00.519 --> 00:28:06.599
you'll notice that the nucleus bacillis of
mainards becomes activated in particular, and
327
00:28:06.640 --> 00:28:11.240
that's where we get the acetal colon
release within the CNS. When we do
328
00:28:11.279 --> 00:28:15.839
this, what we're essentially getting is
an activation of acetyl colonorropin effrin and serotonin
329
00:28:15.880 --> 00:28:19.680
within the brain and they're going to
have effects on the cortex, the singulate
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00:28:21.000 --> 00:28:26.519
gyrus, the amygdala, and the
hippocampus. The hippocampus being heavily involved in
331
00:28:26.640 --> 00:28:33.720
that pituitary response and in the production
of memory as well. The cortices are
332
00:28:33.720 --> 00:28:40.880
going to be affected with positive income
from nouropin, ephrin and five HT serotonin.
333
00:28:40.960 --> 00:28:44.440
So we're going to become activated because
of the nourop and ephron and mood
334
00:28:44.480 --> 00:28:48.880
and affect would generally be improved with
the introduction of the five HT which is
335
00:28:49.000 --> 00:28:53.880
the precursor to serotonin. And then
it also will go and affect the thalamus,
336
00:28:53.960 --> 00:28:57.599
which is going to allow for improvements
in sleep, a motion, arousal,
337
00:28:57.640 --> 00:29:00.519
plasticity, and memory. So this
is a great area to kind of
338
00:29:00.519 --> 00:29:06.720
look at. The brainstem is where
the effect primarily will occur, and you'll
339
00:29:06.720 --> 00:29:11.240
notice that transputaneous vagus nerve stem will
have this particular effect both afferently and have
340
00:29:11.359 --> 00:29:26.839
effects peripherally through the effherent pathway that's
getting signaled as well. That's it for
341
00:29:26.920 --> 00:29:30.759
today's episode. Be sure to tune
in for part two, where doctor Habib
342
00:29:30.799 --> 00:29:37.400
will share compelling case studies and practical
tips, including therapies like diaphragmatic breathing,
343
00:29:37.799 --> 00:29:42.759
dietary changes and vague nerve exercises.
Plus we'll discuss the promising effects of music
344
00:29:42.880 --> 00:29:52.400
on vagus nerve activation and dive into
detailed mechanisms involving microphasescholinergic pathways, and neurotransmitters.
345
00:29:52.759 --> 00:29:56.279
You won't want to miss it.
Episode eighty four launches in two weeks.
346
00:29:56.839 --> 00:29:59.880
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so be sure to check those out.
1
00:00:15.240 --> 00:00:19.480
Hi guys, Welcome to another episode
of The Factor podcast. I'm your host,
2
00:00:19.679 --> 00:00:24.559
Jessica Riddle. Welcome and thanks for
listening. Today we unpack a new
3
00:00:24.600 --> 00:00:30.280
training with doctor Navaz Habib, a
Toronto based chiropractor, acupuncturist, and functional
4
00:00:30.320 --> 00:00:35.119
medicine practitioner that has dedicated his career
to the study of the vegus nerve.
5
00:00:35.920 --> 00:00:40.240
In part one of this two episode
series, we'll explore how the vegus nerves
6
00:00:40.280 --> 00:00:47.679
regulatory pathways impact inflammation, the role
of acetacholine in modulating immune responses, and
7
00:00:47.799 --> 00:00:53.560
how these mechanisms can be leveraged to
improve conditions such as autoimmune disorders, neurological
8
00:00:53.600 --> 00:00:57.079
diseases, and more. I know
you hear me say this a lot,
9
00:00:57.280 --> 00:01:02.039
but this episode is truly jam packed
with insides that can help you approach your
10
00:01:02.079 --> 00:01:06.959
patient care a little differently. Be
sure to hit that bookmark or download link
11
00:01:07.159 --> 00:01:19.760
so you can listen more than once. Let's dive in. Thank you so
12
00:01:19.840 --> 00:01:23.239
much, Jessica. I'm excited to
be here and excited to share some of
13
00:01:23.280 --> 00:01:32.359
the amazing research and findings that I've
had in incorporating vegas nerve stimulation into my
14
00:01:32.599 --> 00:01:38.400
practice. I am a chiropractor,
I'm based in Toronto, Canada. Graduated
15
00:01:38.879 --> 00:01:44.280
in twenty ten from Canadian Memorial Chiropractic
College. Was actually lucky enough to be
16
00:01:44.599 --> 00:01:49.719
the class valedictorian of my year and
that was wonderful. I have since and
17
00:01:49.760 --> 00:01:53.680
I'll just give you a brief breakdown. I have been an associate, I've
18
00:01:53.680 --> 00:01:59.200
owned a chiropractic practice, I've sold
a chiropractic practice, and have shifted into
19
00:01:59.319 --> 00:02:07.120
working with Page via telemedicine and working
more with consulting clients all around the world
20
00:02:07.560 --> 00:02:12.240
with regards to their vegus nerve and
optimizing their overall health. It's been an
21
00:02:12.240 --> 00:02:15.319
interesting shift and it's been a positive
one. And I'm excited to kind of
22
00:02:15.360 --> 00:02:19.840
tell you a little bit about the
Vegas nerve a little bit more because I
23
00:02:19.840 --> 00:02:25.159
think it's something that we tended to
scoot by in understanding in our school,
24
00:02:25.719 --> 00:02:29.800
and it's one of those things that
I think if we give it a little
25
00:02:29.800 --> 00:02:32.759
bit more attention, we'll realize just
how important it truly is to creating an
26
00:02:32.800 --> 00:02:38.719
optimal environment for help. So the
Vegas nerve, what happens in Vegas,
27
00:02:39.080 --> 00:02:45.280
not the city, obviously, is
we have communication by direction, communication between
28
00:02:45.719 --> 00:02:51.759
many different organs and the brain.
Eighty percent of the information on the vegas
29
00:02:51.759 --> 00:02:57.039
nerve is actually afferent, meaning coming
from all of the organs sharing status information
30
00:02:57.199 --> 00:03:00.840
from the organs back to the brain. That's a big component. We tend
31
00:03:00.840 --> 00:03:07.159
to think of parasympathetic as being much
more efferent in its pathway, being much
32
00:03:07.199 --> 00:03:10.599
more from the brain to the body, and only fifteen percent of the information
33
00:03:10.759 --> 00:03:17.719
on the vegas nerve is actually parasympathetic
efferient information. This is where we get
34
00:03:17.719 --> 00:03:23.960
this rest digest information from the brain
to the organs. An really important area
35
00:03:24.000 --> 00:03:30.560
here is the actual inflammatory control via
the cholinergic anti inflammatory pathway also known as
36
00:03:30.560 --> 00:03:38.240
the CIP. This is a really
important thing to understand because when it comes
37
00:03:38.280 --> 00:03:42.840
to chronic health conditions that a lot
of our patients are dealing with, whether
38
00:03:42.840 --> 00:03:49.360
they be autoimmune or inflammatory in nature, always have the lack of control of
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00:03:49.400 --> 00:03:53.680
inflammation as the pathway to the disease
progression. So this is a really important
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area to fully understand, and the
control of inflammation is the primary job of
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the vegus nerve within the body.
This is where we have that specific effect
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of being able to limit the amount
of damage that inflammation can do. Inflammation
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is a necessary piece to the optimization
of our body puzzle. But the control
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of inflammation is what often needs to
be talked about, and that's what the
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job of the vegas nerve is.
For the math people out there, that's
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only ninety five percent of the role. So four percent of the information here
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is motor information and that's specifically going
to the and laryngeal muscles. Those are
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the muscles of the airway, throat
and vocal cords. So maintaining the openness
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and patentness of an airway is the
job of the motor component of the vegas
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nerve, and as well as having
a bit of a role to play in
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vocal pitch and tone. So being
able to go really really low or really
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really high with my voice is there
because I have motor control of the laryngeal
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muscles that tension and pull on the
vocal cords themselves to create tension allowing for
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pitch to change. The last area
here is one percent of the information is
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actually sensory information from the skin of
the ear and actually in a very particular
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area, and this is an area
that acupuncture has been utilizing for generations to
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help improve vegas nerve stimulation. Or
vegas nerve function. There's actually a few
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points in there, particularly vegas nerve
points, and another one with the name
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of shen Men which is right in
that center area, and that's an area
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that will play a really positive role
in improving vegas nerve function overall. Next,
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we want to get into the pathway
that I talked about, and that's
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the coal energic anti inflammatory pathway.
It's actually multiple directions and that's what's really
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exciting about it. So the vegas
nerve has inputs going in primarily to the
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nucleus tractus solitarius in the brain stem
and then coming from the dorsal motor nucleus
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in vegas in the brain stem and
coming out. Okay, so this is
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where the inputs and the outputs are
being relayed to within the brain stem nuclei.
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The vegus nerve courses down sends a
signal out to the lungs, has
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a direct branch that goes to this
celiac ganglion and the celiac superior mesenteric plexus
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ganglia just go to the celiac ganglion
to make it easy, and over here
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it releases a setyl coline. This
is the reason for the name coal ergic.
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In the coal energic ante inflammatory pathway, it uses a setyl coling.
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The vegus nerve only uses a setl
coline as it's neurotransmitter of choice. It
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also then has a direct branch to
the entirety of the gut, and this
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is very important. The gut brain
connection is physically made up by the vegus
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nerve, and we know that seventy
percent of our immune cells by volume are
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located in the gut and the gut
lining. So this is an important area
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for controlling signals to be sent via
setal coline, and so this is an
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important area to look at from a
physical standpoint. The fun relay here is
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as the vagus nerve sends acetyl coline, if we look back at the celiac
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ganglion, we then see that the
acetylcholine is released to attach to the splenic
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nerve. The splenic nerve is actually
a sympathetic nerve, not parasympathetic. It's
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a sympathetic nerve. And what's really
exciting here is when the acetyl coline is
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released into this area, it actually
hijacks that splenic nerve and turns it into
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a parasympathetic functional nerve, which is
really cool. The splenic nerve will then
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release neuropenephron at the spleen level,
activating a set of T cells called chat
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cells. Okay, and they have
a beta two andronergic receptor on them that
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the norropinephrine attaches to. Then these
T cells, these chat cells become hyperactivated
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and they become activated to release a
seal coline. You can see what those
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red dots coming down the pathway from
the T cells, and these acetyl coline
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will make its way too splenic and
other local tissue macrophagers. So any organs
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that don't have direct innervation from the
vegas nerve, we know a lot of
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the visceral organs do. Almost every
single one has a direct innervation, but
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the bone, the muscle directly to
areas within other organs and tissues that are
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not directly innovative innervated by the vegas
nerve, including the skin, will get
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the signal of acetyl coline through the
bloodstream via these chat cells being released in
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the spleen and then these local tissue
macrofages, all of them have this alpha
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seven nicotinic acetal coldine receptor. You
can see within that red box, each
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of these splinic and local tissue macrophagers
contains that particular receptor, and that receptor
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is the target of the acetal colding
that's being released both directly from the vegus
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nerve in particular organs, and then
without it being in the vegas nerve directly
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where it goes out through splenic amplification. The other tissues will receive this acetyl
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coline signal, and that acetyl coline
signal goes to those macrofagists to tell them
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we need to shut down or decrease
the amount of inflammation that's happening. And
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then, as you can see also
within that red box, we're able to
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decrease the release of TNF, alpha
ail one and aisle six. These are
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very very well known inflammatory side of
kinds. These are inflammatory signaling molecules that
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we don't want to have going off
and becoming rampant drivers of an inflammatory response.
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Okay, so that's really important.
If we go back towards the brain
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here, you'll notice that at the
NTS we have the input coming in from
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the vagus nerve and then we have
a relay pathway with a green arrow that
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goes up to the hypothalamus. And
this is really really important because not only
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do we have an acetyl coline release
going down from the brain to the rest
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of the body, we actually have
a signal coming up to the brain as
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well. And if we remember the
name of these macrofages that are within the
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brain and the central nervous system are
the microglia, and acetyl colin is released
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from certain areas called particularly the nucleus
Bacillus of maynards within the brain. There's
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not going to be a test on
this later, don't worry, but that
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area is necessary for releasing acetyl colin
locally within the brain, within the central
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nervous system, and that acetyl coline
helps to manage the inflammation within the brain.
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This is huge because this is an
area that needs to be addressed in
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many many health conditions, whether they
be neurodegenerative in nature like Alzheimer's or Parkinson's,
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or dementia or TBI concussion, stroke, whiplash. Those types of injuries
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can also severely increase the inflammatory response
within the brain, and so the vegus
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nervous heavily heavily involved in the release
of that acetyl colin in the brain as
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well. We also get direct signals
up to the hypothalamus which actually activates corticotrope
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and releasing hormone CR, which then
sends a signal to the pituitary gland to
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release adrenal corticotropic hormone ACT, which
is the yellow dots and the green arrow
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that goes down to the adrenals,
and this actually activates glucocorticoid release to help
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to shut down that inflammatory response as
well. So the glucocorticoids help in a
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secondary manner in affecting those local tissue
macrofashes and helping to downregulate the inflammatory response.
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So this is a really, really
awesome picture of what the colonergic anti
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inflammatory pathway looks like. And it
can get deep. And I realize this
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is not an easy thing to fully
understand, but I'm going to do my
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best to help you see this.
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00:11:52.480 --> 00:11:56.200
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click the new certifications link in our
show notes or visit online dot Sports Hyphenseminars
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00:12:18.480 --> 00:12:28.840
dot com today. Now back to
the show. The target of the coolinergic
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anti inflammatory system or the pathway is
the marvelous macrophage. The macrophage is the
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organ that is necessary to be controlled
in this pathway. It is the main
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cell of the innate immune system.
It is the main one that goes and
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identifies the sources of threat to our
bodies and when it senses threat, it
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is activated into a state called M
one. We'll talk about that in a
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moment. And what it does is
it signals of inflammatory cytokines out to bring
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other immune cells locally to the area, adaptive immune cells and other innate immune
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cells as well. This is the
target. When we can control this cell
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through vegas nerve activation, vegas nerve
stimulation and the release of acetyl cooldine,
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we can have a phenomenal response on
controlling the severity of inflammatory response that our
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body creates. There are tissue resident
macrofages everywhere. They all have very similar
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jobs in similar roles, but they're
called different things. In different tissue.
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In the skin, they're called dermal
macrophage or Lungerhund cells. In the lung
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they're alveolar, interstitial, and pulmonary
intravascular macrophages. In the liver their cupfour
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cells. In the heart, there
are multiple different types. In the brain
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they're microglia, and the kidney they're
kidney macrophages. In the muscle, there's
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three different types CD eleven C plus
CD eleven B plus F four to eighty.
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We've got in the bone stromo macrophages, and then one that's missing from
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this list is actually osteoclasts are macrofages
within the bone. Osteoclasts that we know
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are necessary to create osteoporosis or to
maintain the shape of bone by breaking it
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down slightly. In the lymph nodes, we've got subscapular macrofages. In the
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spleen, we've got the red pulp, the white pulp, and the marginal
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zone macrophages. In the intestine,
we've got lemon appropriate macropages and sub mucosal
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This is where seventy percent of our
immune cells by volume are located within the
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body, is in the intestinal walls
and then within the pancreas. There are
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pancreatic macrofages as well. These tissues
are everywhere. These cells are necessary as
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not only the detectors of threat,
but they really do help to focus on
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identifying and maintaining the function of the
organ that they're located in. And this
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is a necessary piece to understand because
this is the target of control from the
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vegus nerve. This is the names
of all of the target cells of the
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vagus nerve col energic anti inflammatory pathway. The directly innervated tissues are cns,
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the blood vessels, lungs, liver, gut, and then the spleen via
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the splinic ganglion are the directly innervated
but then via splinic amplification, we send
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signals out to the skin, the
sirosa, the muscle, atipose tissue,
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and bone. And this is important
to understand. So these are the target
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cells of that entire cool energic anti
inflammatory pathway. It can be dysfunctional in
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many different conditions, whether autoimmune in
ra sl ms, asthma, type one
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diabetes, vascular conditions like athrosclerosis,
digestive conditions very very important here, irritable
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bowel crones colitis, metabolic conditions,
obesity, type two diabetes, naffled Nash,
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neurological conditions, Alzheimer's autism, schizop
me a dimension, dementia at Parkinson's,
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and then even hormonal effects as well, indometriosis being an inflammatory condition as
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well. So these are all conditions
that may have some specific piece to the
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or dysfunction going on and a lack
of control of the inflammatory process locally within
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a particular organ or within a particular
area. Macrifages have different states that they
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will work on. So an M
zero macriphage, the blue guy that you
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see at the top of the screen
here, that one has not been differentiated
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yet into a state of being fight
or fix state. Okay, But there
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are certain signals that will drive an
M not or an M zero macrofage into
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a different statelypopolysach right LPs A,
IFN gamma, which take the M zero
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macrifage to the left side of the
screen here will turn on what's called M
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one state or M one macrofash state, and these are very high expression pro
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inflammatory cell functions. These guys are
meant to fight, They're meant to send
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a signal of us of inflammatory cytokines
out into the bloodstream into every area to
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have them bring in more inflammatory and
immune cells locally to the area where they've
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discovered said threat. The M two
macrofages we can shift to using IL four
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and ILE ten, which are which
we know are anti inflammatory cytokines, and
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these guys helped differentiate them or M
zero macrofashes into M two M two are
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known as the fix macrifages, not
the fight guys, are the fixed guys,
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and then these will further differentiate depending
on other signals that are there present
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locally. They can go into M
two A, M t B, M
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two C, and M two D
and a lot of these are regulatory or
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focused on debris removal. They use
the same tools as during inflammation, but
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they do it in a very controlled
manner and what their job is to help
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regulate and control and optimize the function
of particular organs. And so the regulatory
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effect of these will come from whichever
signals are being sent, whether ile thirteen,
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IO four, IRF four, TLR, golobulin complexes, group of cordocoids,
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Ile ten to TGF beta, or
A two A R as well.
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So these will differentiate the function of
these to do very specific tasks using the
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same tools that any macrofage would.
Okay, so we often think of the
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macrifages as being these magical engulfers of
threats to us. But that's only one
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job. The regulatory job. The
fixed job is the one that we've often
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overlooked, and it's the role of
acetyl colding to help to actually shift from
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M one state macrofages, which are
the pro inflammatories, into the M two
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state macrophages. You'll see that with
the green line going across vegas nerve stimulation
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is one of the best ways to
do this. This has been proven.
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I've got a great research study below
that I'm going to share. This is
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a really amazing tool. And then
when we have the presence of lots of
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M two macrophage, is that it's
actually inhibitory to the production of M one
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high inflammatory macrophages as well, and
that's indicated by the red line below there.
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Okay, so these are important pieces
to understand, and it's the job
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of the vegas nerve when working to
help to shift these cells from M one
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state to M two state and from
fight to fix the cellular effects. This
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is how it actually works. Remember
we mentioned that alpha seven nicotinic acetyl coline
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receptor on the pathway. What it's
doing. When acetyl coline hits that particular
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receptor, it has two very particular
things that it can change. Number One,
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it can go down the camp C
FOSS pathway, which is the first
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pathway on the left. Here you'll
see that it activates CAMP which goes into
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the nucleus and activates sea fire CFOs, and that will lead to a decrease
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in the transcription of a factor known
as Nfkapa B. NF kapa b,
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when activated, sends out the cytokinds
that are inflammatory the ile one IILE six
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or excuse me, il yeah,
io one, io six okay, and
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TGF or tnf alpha as well.
The second pathway is a cetylcholine will hit
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that same receptor and activate the JACK
two STAT three pathway, and that will
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actually result in the decreased gene transcription
of inflammatory side of kinds as well,
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So we're actually regulating and decreasing the
amount of inflammatory side of kinds that will
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be released. There is one more
scenario, and this is an interesting one
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that most people don't understand as yet, but that alpha seven nicotinic acetylcholine receptor
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is also present not only on the
cell surface, but it's also present on
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the surface of mitochondria. How many
of us have heard about mitochondrial health and
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the importance of maintaining good mitochondrial health
for longevity, for energy, for overall
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optimal function, and metabolic ideals.
Well, when there's a lot of ATP
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that's present around the cell surface,
ATP will activate a channel here that allows
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acetylcholine to enter the cell directly and
that will activate the alpha seven nicotinic acetylcholine
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receptor on the mitochondria. When that
receptor is activated, it actually decreases and
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shuts down the release of mitochondrial DNA. This is a very common pathway by
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which we trigger an inflammosome or trigger
this NFAPA B gene transcription occurrence that takes
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place. If mitochondrial DNA is released, it will lead to the inflammosome and
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the release of inflammatory cytokines into surrounding
areas. But when we activate the acetolcholine
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receptor on the mitochondria, that shuts
down the mitochondria DNA release. That allows
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for the to remain within the mitochondria
that allows for optimal function to be restored,
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and we don't trigger an inflammasome.
We actually don't allow this pathway to
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begin. And one of the best
ways that I've found to help do this
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is through cervical transcutaneous vegus nerve stimulation. Okay, so the vagus nerve is
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sending these acetylcholine signals out to all
of these tissues, particularly those macrifages,
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to help with the regulation and control
of inflammation. When we don't have an
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optimally working vegus nerve, the control
of inflammation is going to be reduced.
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Use of electrical currents to help to
stimulate nerves is something that we've all seen
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many times. How many practices use
a tends unit or interferential current or other
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electrical stimulation tools like a pointer plus
on acupuncture or something along those lines.
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This is a tool that directly targets
the vagus nerve. So it's electrical stimulation
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of vagel fibers. The aentiilateral circle
spine to find where your vegas nerve is
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literally find your pulse and it's right
beside there. I'm going to show you
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a really cool image so this is
a great area to access the vegas nerve.
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And what you'll find is about ninety
to ninety five percent of the fibers
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on vegas nerve are found within the
neck and not anywhere else. It's easily
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accessible within the crotted sheet. You'll
see on the next slide that we've got
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the crowded artery, the jugular vein, and the vegas nerve that are nice
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and wound type. Together, we're
going to be able to activate both afferent
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and epherentt exonal fibers. Interestingly,
there are only one hundred thousand fibers on
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the left side vegas nerve and two
hundred thousand on the right side vegas nerve.
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Two hundred thousand plus. They're realizing
there's more on the right. For
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whatever reason, I wasn't there for
the design process and it's something that we're
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still trying to figure out why.
So where is the vegas nerve I just
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mentioned this. It's within the carotid
sheet, just behind our certoclidomastoid muscle,
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the SCM muscle. If you ever
push against your head, you can push
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your head against your hand, excuse
me, you'll notice that your SCM muscle
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pops up. If you just pop
in front of that SCM muscle, you'll
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be able to find your pulse.
Your pulse, your feeling is the common
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carotid artery, the CCA that's present
on this ultrasound image. You'll see the
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IGV there as well. That's the
internal jugular vein, and then right behind
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it, that thick tissue that's outlined
in yellow, that is the vegas nerve.
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So if you feel your pulse,
you're very very close to your vegus
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nerve as well. The thing that
really introduced me to the importance of the
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vegas nerve was that it was the
only nerve coursing down through the neck present
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within this carotid sheet. It's the
only tissue there. We know how important
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the common CA and internal jugular vein
are, but how many of us have
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forgotten that the vegus nerve is part
of that sheet and so so important to
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our overall health and survival. So
just great to see there. It's literally
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right behind the anterior fibers of the
stern cloudomastoid, and so if you just
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kind of give it a little push
out of the way, you'll be able
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to find the pulse and you're right
there on your vegas nerve. How does
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non invasive vegus nerve stimulation work?
Well, this was a sham study that
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was done where they actually stimulated over
the sterno clidum mastoid versus over the carotid
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artery area where they found the pulse. And what was found was when not
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obviously not within the sham activation,
but within the actual activation of the nerve
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when they stimulated using the electrical device
to handheld electrical device, they had an
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activation of particular brainstem nuclei. This
will go back to which ones we saw.
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This is the nucleus of the solitary
tract the NTS nucleus tractus solitarius,
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and we had activation of the dorsal
motor nucleus of vegas. This is cool
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because we know that we're getting activation
of the two nuclei, the primary tow
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nuclei by which vegas nerve connects.
Okay, so this is really important.
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We also got a little bit of
activation in vestibular nuclei and the medial longitudinal
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fasciculus as well, and as well
a little bit in the spinal trigeminal which
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is linked as well, and that's
actually the spinal trigeminal was not activation,
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excuse me an inhibition that occurred in
the spinal trigeminal nerve. This is great
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for things like boos palsy or great
for kind of the trigeminal headaches that can
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occur as well, and this is
a reason for why this particular tool is
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used heavily in headache cases, migraine
in particular. So this was a great
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study and it continued on to show
that not only is the effect local within
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the brain stem, but it actually
creates a biphasic response above in different areas
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of the brain. So this was
a three phase response. They did fMRIs
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between three and five minutes, seven
to nine minutes, and thirteen to fifteen
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minutes later, and what they found
was activation of the Rapie nuclei and substantion
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00:26:57.279 --> 00:27:03.200
niagra and the brain stem the early
phase, as well as the medial frontal
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00:27:03.240 --> 00:27:11.039
cortex and parasingulate cortex early phase.
Then we had inhibition initially and then activation
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00:27:11.160 --> 00:27:15.079
in the amid post VNS phase,
which is a seven to nine minute phase,
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00:27:15.119 --> 00:27:19.119
and we got activation of the ray
Fie nuclei, the VTA mental tech
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megntal area, and then we had
it in the hypothalamus and the acc as
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00:27:23.200 --> 00:27:27.200
well. Above this was an activation
that occurred, and then we had a
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calming effect almost throughout the entire cortex, particularly the precuneus and parasingulate cortex had
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an inhibitory response, and then we
had activation in the brain stem at the
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VTA, the pag, the substantia
niagra, and the Rayphi nuclei. This
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00:27:44.799 --> 00:27:48.799
helps to tell us exactly how this
system works. This is a neuromodulatory activation
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that's occurring. We're getting activation of
dopamine response, of nouerpenephrine response, and
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00:27:55.839 --> 00:28:00.200
of serotonin response within the brain.
And once we go and see as well,
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00:28:00.519 --> 00:28:06.599
you'll notice that the nucleus bacillis of
mainards becomes activated in particular, and
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00:28:06.640 --> 00:28:11.240
that's where we get the acetal colon
release within the CNS. When we do
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00:28:11.279 --> 00:28:15.839
this, what we're essentially getting is
an activation of acetyl colonorropin effrin and serotonin
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within the brain and they're going to
have effects on the cortex, the singulate
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00:28:21.000 --> 00:28:26.519
gyrus, the amygdala, and the
hippocampus. The hippocampus being heavily involved in
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00:28:26.640 --> 00:28:33.720
that pituitary response and in the production
of memory as well. The cortices are
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00:28:33.720 --> 00:28:40.880
going to be affected with positive income
from nouropin, ephrin and five HT serotonin.
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00:28:40.960 --> 00:28:44.440
So we're going to become activated because
of the nourop and ephron and mood
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00:28:44.480 --> 00:28:48.880
and affect would generally be improved with
the introduction of the five HT which is
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the precursor to serotonin. And then
it also will go and affect the thalamus,
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00:28:53.960 --> 00:28:57.599
which is going to allow for improvements
in sleep, a motion, arousal,
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00:28:57.640 --> 00:29:00.519
plasticity, and memory. So this
is a great area to kind of
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00:29:00.519 --> 00:29:06.720
look at. The brainstem is where
the effect primarily will occur, and you'll
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00:29:06.720 --> 00:29:11.240
notice that transputaneous vagus nerve stem will
have this particular effect both afferently and have
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00:29:11.359 --> 00:29:26.839
effects peripherally through the effherent pathway that's
getting signaled as well. That's it for
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00:29:26.920 --> 00:29:30.759
today's episode. Be sure to tune
in for part two, where doctor Habib
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00:29:30.799 --> 00:29:37.400
will share compelling case studies and practical
tips, including therapies like diaphragmatic breathing,
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00:29:37.799 --> 00:29:42.759
dietary changes and vague nerve exercises.
Plus we'll discuss the promising effects of music
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on vagus nerve activation and dive into
detailed mechanisms involving microphasescholinergic pathways, and neurotransmitters.
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00:29:52.759 --> 00:29:56.279
You won't want to miss it.
Episode eighty four launches in two weeks.
346
00:29:56.839 --> 00:29:59.880
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We'll see you next time. Hey
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