I'm Dr. Chris Masterjohn of
chrismasterjohnphd.com and this is
Episode 55 of Mastering Nutrition, Part 3
of our series Nutrition in Neuroscience.
This is Mastering Nutrition with Chris Masterjohn.
Take control of your health.
Master the science and apply it like a pro.
Are you ready?
Welcome to Part 3 of the Safari through the
leading textbook Neuroscience, where
I as your tour guide point out all of the
stuff relevant to nutrition.
In part one we talked about the basic
mechanisms of how neurons
communicate information from one place
to another, and the roles of
nutrition in that process.
In part 2, we talked about all the major
neurotransmitters, the roles of nutrition
in making them, metabolizing them,
clearing them, making them function properly.
In part 3 we are talking
about our five senses: touch, sight,
hearing, smell, and taste. The roles of
salt, potassium, magnesium, calcium, and
vitamin A in making those things happen.
How touch can go wrong in chronic pain.
Nutritional strategies to deal with
chronic pain both at the site of the
pain and in how your central nervous
system is interpreting it.
The role of vitamin A in preventing night blindness,
and it's very closely related role
in setting your circadian rhythm.
How vitamin K2, magnesium, and vitamin A
could perhaps play a role in preventing some
types of hearing loss. Capsaicin the
thing that makes hot peppers hot and how
it really is literally hot as far as
your nervous system is concerned.
The use of topical capsaicin to manage pain.
A speculation about why some anorexics may
crave spicy foods because they're missing
the literal heat from low body fat levels,
and low metabolic rates.
All this and much more in this episode.
Remember for this and all my other
content you can get early ad-free content
with transcripts, and other premium features
at chrismasterjohnphd.com/pro.
Using: MASTERINGNUTRITION
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Without further ado here's a word from my
sponsors and then we dig in to the five senses.
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All right, we have covered the
neurotransmitters. Now let's look at some
specific topics, some specific problems
to solve if you will.
And the first thing that we'll talk about is pain.
Now pain is closely related to your
sense of touch. You have a sense of touch
that we think of when something touches
the outside of your body and that's
technically tactile sensation, and we
could refer to that as exteroception,
meaning perceiving our environment.
Then there's the closely related
proprioception which is a sense of our
selves, and the space that we occupy, and
the relation of one body part to another
within the space inside of ourselves.
Proprioception and exteroception or
tactile sensation are both using very
similar systems, and these are mediated
by mechanoreceptors.
Mechanoreceptors are receptors where a membrane
stretching will open an ion channel
that allows positively charged ions to flow through.
So this is acting extremely
similarly to neurotransmitter receptors
it's just that the stimulus for opening
the ion channel is not a chemical, it is
a physical mechanical process of the
membrane that contains the receptor stretching.
Proprioception just has the same types
of mechanoreceptors, but instead of
being in the surface of our body they
are in our muscles to sense the length
of the muscle, in our tendons to sense
the tension that the muscle
is placing on the tendon, and they're
in our joints to sense our proximity to the
end of our range of motion.
If we compare tactile sensation in our skin
to pain reception in our skin,
we get a general model of the
difference between this normal touch
sensation and pain. So in the case of the
mechanoreceptors that mediate tactile
sensation on the surface of our body we
have specialized cells that have the
mechanoreceptors that have a milieu that
is designed to increase sensitivity and
to decrease the threshold required to
generate an action potential. By contrast
when we experience pain
we have nociceptors or pain receptors
that are on unspecialized low
sensitivity neurons where you need
a much stronger stimulus to generate an
action potential that will make its way
into the central nervous system. And that
kind of makes sense right if you, if you
just touch someone lightly on the hand
it's not going to hurt because, because of
those specialized nerves with
mechanoreceptors that are designed to be
super sensitive. But if you keep pushing
hard enough you will hurt that person
because now you start activating these
pain receptors or nociceptors on the
unspecialized low sensitivity neurons
that only get activated when you have
a great enough stimulus to overcome that
threshold. There's two different sets of
fibers. The first one generates first pain
which when it's weak
it causes tingling, and when it's strong
enough causes sharp pain. And then
there's another one, another set that is
responsible for so-called second pain or
or dull pain and this is a chronic
dull pain as opposed to an acute, short,
sharp pain. If you take that model you
can say that there is similar,
a similar comparison could be
made for how we feel pain deeper in our
muscles for example, or in our joints
and so on. So the first thing that I find
nutritionally interesting is this
textbooks discussion of capsaicin, the
thing that's responsible for the
sensation of hotness in a hot pepper.
This is mediated by the vanilloid
receptor known also in the abbreviated
form as TRPV1. This mediates pain not
only in response to capsaicin, but in
response to hot temperatures that are
above 110 degrees Fahrenheit,
or 43 degrees Celsius.
What I find fantastically amazing about
this is that this is literally showing
you that peppers are literally hot.
So they're not literally hot in the sense
of physics, like the capsaicin is not
actually over the temperature of
110 Fahrenheit, but they are
literally hot in the sense of your
nervous system and perception because
the receptor that mediates pain in
response to intense heat is the receptor
that is activated by capsaicin. So --one
way-- another way to say that would be
to say that capsaicin is hijacking the
receptor that mediates pain and response
to intense heat. But it's still the same
sensation. Now if you eat a lot of hot
foods you will develop a tolerance for
the hot foods. It will take more of the
hotness to make it feel like a hot food.
That's because capsaicin down-regulates
the receptor. It's sort of like we talked
about before, organophosphates
cause paralysis by blasting your
muscles with so much acetylcholine that
they need to down--regulate their
acetylcholine receptors so that they
aren't as easily stimulated and they get
paralyzed. Similarly if you eat a lot of
hot foods your your hot pain receptors
go down in your mouth and you are less
sensitive to the capsaicin. Well this
logic has been used to use capsaicin topically
to relieve chronic pain. The logic here
is that something in chronic pain,
something's wrong with your pain receptors.
And so for some reason
whatever that pain stimulus is isn't
down-regulating the receptor, but
capsaicin will. And so you put the
capsaicin on, it hurts because that's
what capsaicin does, but the pain in
response to capsaicin for whatever reason
is more effective at mediating
the down-regulation of the receptor
than whatever it is that's causing the
chronic pain. You could think of this
kind of like hormesis.
Hormesis is the principle that's a little bit
of something that is bad for you
is good for you.
And the reason is that if you have
something that's bad for you your body
reacts to it by adjusting its defenses
against it. In some senses you could
think of exercise as hormesis because
you don't get strong from lifting
weights you get strong from going home
and resting after you lifted weights.
That's providing that stimulus that your
body then reacts to with increased
fitness. A better model of hormesis would
be the polyphenols found in fruits and
vegetables. Now we all think of these, not
all, most of us think of these as good
for you, but the way that they're good
for you is that they act as toxins, but
they're the toxins that our bodies
have been used to consuming, and being
exposed to in the environment for
you know, all of human existence.
As a result we are very well adapted to them
and when we consume them, even though
they have toxic effects like if you were
to dump a buttload of these polyphenols
onto a cell you might kill the cell,
only a little bit of these get into our
circulation and get into our tissues
and we react with greater
antioxidant defense, greater detoxification
capabilities, and so on and so forth.
And so cigarette smoke does not
appear to be hormetic because people
that smoke get cancer from it. And so
there is no known dose of cigarettes
that you can smoke that is good for you.
So you eat fruits and vegetables and
they're toxic, but they cause a greater
up-regulation of the defenses
than they do toxicity.
You smoke cigarettes and it causes
greater toxicity than up-regulation of
the defense's, so one is hormetic and one
is toxic at those doses. So capsaicin is
sort of like a reverse hormesis. What
it's doing is it is instead of causing
you to up-regulate defenses it's causing
you to down-regulate pain receptors, but
it's the same, it's almost the same
principle, it's just in the opposite
direction. Now there are several other
things that I find very interesting
about this hot receptor thing. And this
relates to a conversation that
I had with one of my friends and
colleagues that I'll get to in a moment
about cravings that anorexics can have
for hot foods.
Before I get to that I have to talk a
little bit about interoception.
so in addition to exteroception, the
sense of touch, tactile sensation, and
proprioception, the sense of self and the
space that we in our body parts
occupy and their relation to one another,
interoception is our sense of the
--physiological environment -- the
physiological state within the body.
So if you look at where these pain
receptors feed into the brain they have
they feed into the brain with
information from other TRPs, so this was
TRPV1, there are other similar receptors
with TRP you know denoted something else,
one that responds to noxious cold which
is below 17 Celsius or below freezing.
But then there are innocuous warm
receptors, and innocuous cool receptors.
So altogether we have noxious heat,
noxious cold, innocuous warm, innocuous cool.
Then we have puria receptors that sense itch,
which have some overlapping,
some of these receptors overlap
with the pain response. And then all
these different sensations
of warm, hot, cold, cool get integrated
along with along with information from
lactic acid that's released during
exercise and some of the other
metabolites that could be released
during tissue damage or intense exercise
into a part of the spinal cord known as
the anterolateral system. And the name
for the integration of all this information
is interoception, a sensation of the
physiological state of the body.
So I had a discussion with Briana Theroux,
who has been working for me for the last
year and a half and recently opened her
own business after completing her
Certificate in the Psychology of Eating.
She's now doing coaching with clients
especially with especially around the
the psychological aspects of managing
your diet. You can find her at
brianatheroux.com
I'll link to her site in the show notes.
But what she said to
me when we were talking about this was
she's worked with anorexics who really
crave spicy food could that be related?
And it seems to me to make a lot of
sense because if the anterolateral
system in the spinal cord is integrating
hot, cold, warm, and cool with information
about the body's temperature, and if your
metabolic rate is going to decrease the
generation of heat, and if your low body
fat levels are going to decrease your
insulation so that your body temperature
actually does drop, then wouldn't that
indicate cravings for the thing that
activates the warm and hot receptors?
And if capsaicin is activating the hot
receptors it seems like it could fit
into a calculation in your spinal cord
to sort of fool the sense of your body
temperature in a way,
by actually being calculated as literal heat
in that center. So if you're
anorexic and you have a low body fat,
and you have low heat generation, and you
have low heat retention, and your body is
cooler, you crave the heat provided by
that food because it literally is
incorporated as information about
temperature in your spinal cord.
Besides topical capsaicin what else
might we do for pain?
Well we have to think about how we get
overly sensitized to pain.
And there's two different things
going on one in the peripheral nervous
system meaning --outside this-- outside the
brain and spinal cord, and the other in
the central nervous system meaning the
brain and spinal cord. In the peripheral
nervous system the primary things that
are sensitizing your pain receptors are
things that are released from
inflammation and tissue damage. One of
those is hydrogen ions which is acidity.
Acidity will sensitize the pain
receptors. This might make a case
for pH balance. When I think about pH balance
I think about measuring your urine pH,
probably it's going to be below 6 in the
morning when you first see it up, but
most of the day especially after your
first meal it should be in the sixes
probably between 6.4 and 6.8. And if it's
not you could try bicarbonate on an
empty stomach, but when you do start with
a quarter teaspoon, measure your urine pH
continually every time you pee until
you get the dose and timing right. You
have to see not only where does that
amount of bicarbonate bring you, but also
how long does the effect last, and,
and that's one way to address urine pH.
I found that my urine pH ran acidic
until I corrected a zinc deficiency, so
that's another thing to think about. But
I don't know how important that would be
only because probably the major effect
of acidity is going to be very local to
the tissue damage. So while your systemic
pH might alter a tiny, tiny bit in
response to the bicarbonate,
it might not have a huge effect at the
local site of tissue damage. The second
thing that I would try is to manage your
anti, I shouldn't say anti, manage --your--
the fatty acids that help you resolve
inflammation. So I'm generally against
anti-inflammatory things and that's
because I believe that most chronic
inflammation is a result of not having
properly resolved the inflammation. A lot
of anti-inflammatory things like most of
the non-steroidal anti-inflammatory
drugs --will-- they will lower your peak
inflammation, but they will actually
promote long-term chronic low-level
inflammation, because they also prevent
you from resolving the inflammation.
Arachidonic acid from liver and egg
yolks is necessary for the initiation
and resolution of inflammation.
The omega-3 fatty acids especially DHA from
fish or algal oil, to a lesser extent
from pastured egg yolks and maybe
pastured butter fat, but primarily from
from fish or algal oil is going to be
the thing that's missing for a lot of
people because a lot of people get
enough omega-6 arachidonic acid,
and they don't get enough of the omega-3.
So if you don't include omega-3 fatty acids in
your diet, including them may help.
There's a product from Metagenics
called Specialized Pro Resolving
Mediators or SPM. I haven't seen this
studied, but what it's doing is it's
providing the actual compounds that you
make from the fatty acids and that might
help jump-start the process of resolving
inflammation. If these things don't work
then I think another way to try to
jumpstart the resolution of inflammation
would be, and I advise more caution about
this and make sure you talk to your
doctor if there's, if there's any
possibility that you might have negative
reactions to aspirin, but in this
approach I would combine
asprin with fish oil and glycine along
with the pH protocol for the urine with
bicarbonate that I had just mentioned.
And here's the logic. Although most
non-steroidal anti-inflammatory drugs,
most over-the-counter anti-inflammatory
drugs, including acetaminophen, which is
not technically called an NSAID,
but has similar concerns,
most of them block the production of resolvins
that resolve inflammation. Aspirin on
the other hand actually promotes the
production of resolvins and the EPA
in the fish oil is only converted into
resolvins in the presence of aspirin.
Now this is something that is very
unique about aspirin which is
acetylsalicylic. The effect is from the
acetyl part of the aspirin not from the
salicylate. And so you cannot mimic this
with the natural salicylates that are
found in foods because foods do not
contain acetylsalicylic. Also one of the
things that worries me about aspirin is
that after the acetyl group acetylates
the Cox enzyme which causes it to
make the resolvins, it leaves behind
salicylate which actually can decrease
the amount of the Cox enzyme available.
And so while you're making the Cox
enzyme make resolvins you're also
decreasing its expression which seems
like, it seems like you're shooting yourself
in the foot with with that. So I think what
you really want to happen
with the aspirin is that you want to
acetylate the Cox enzyme, make the resolvins
from the omega-6, the omega-3
the EPA, the DHA with the fish oil, and
then you just want to get rid of the
salicylate altogether. How do you get rid
of salicylate? The most important thing
is your urine pH. By bringing the pH
of your urine from 6 to 7 you'll
increase the rate at which you get rid
of salicylate 17 fold. If you bring your
urine pH up to 8 you increase the
removal of salicylate through your urine
25-fold. And then the glycine is because glycine
will quickly metabolize the salicylate
into the glycinated form that is
detoxified more easily and is inactive.
I don't know how much to dose this because
there just isn't adequate data, but what
I would do is the aspirin I would start
with the lowest dose of baby aspirin,
and work your way up slowly. And the
fish oil I would dose at maybe one to three grams
of omega-3 fatty acids a day. And the
glycine I would say take probably shoot
for three grams with each time that you
take the aspirin. Now the downside, apart
from the potential to thin your blood of
course, is that a certain percentage of
people react to aspirin with asthma. And
in self-reported use only about one or
two percent of people make this
complaint, but when they give people
aspirin in a controlled setting and
measure asthmatic responses in a
laboratory it's actually like ten or
twenty percent of people that respond to
aspirin this way. And I think that's
because aspirin uses glycine in its
detoxification and depletes glycine, and
glycine is involved in the synthesis of
glutathione in the lung which is your
primary bronchodilator. So I think
including the glycine in this protocol
--will-- I suspect will prevent any risk of
developing asthma in response to the
aspirin. So --I don't-- I wouldn't jump to
this particular thing, but I think if
you're in a lot of pain and you're
looking for a fairly natural root cause
way to go about clearing it up
then I think after you try some of the
the more gentle measures like improving
your omega-3 fatty acid intake then this
aspirin, plus fish oil, plus glycine, plus
bicarbonate protocol might be worth trying.
That's for peripheral sensitization to pain.
For central sensitization to pain part of the way
you become sensitized is in an LTP like
process. Remember long-term potentiation
or LTP increases the sensitivity of
a pathway and it's mediated by NMDA
receptors. And what happens,
what theoretically can happen is that if
you don't have enough magnesium
the magnesium is not blocking the NMDA
receptor, and so the NMDA receptor is
inappropriately activated and that gives
you a greater LTP like response to
reinforce the pain pathway than you
would otherwise have if you had adequate
magnesium. So addressing a magnesium
deficiency might help.
Additionally, inadequate inhibitory signaling from
glycine and GABA could be involved, and
glycine and GABA supplementation could
help, but remember if, if the case is loss
of the proper chloride distribution
glycine and GABA theoretically might not
help or maybe even might make it worse
in which case addressing electrolyte
imbalances and energy problems might
help restore the function of glycine and GABA.
The endocannabinoids have-have
anti-pain effects and so arachidonic
acid and DHA like I had talked about
before in that section might also help.
And of course if endocannabinoids help,
then cannabinoids from cannabis might also help,
and that might be a rationale for using CBD oil.
So that was a longer discussion of touch
and its relation to pain. Let's go
through some of the other senses to look
at how nutrition can be important in
basic perception of our other senses.
These sections will be shorter.
So in vision light is focused by many of the
parts of our eye on our retina.
The retina is the innermost, meaning the most
to the back layer of the eye, and the
retina is considered part of the central
nervous system because of how it arises
in embryonic development. Within the
retina there are photoreceptors known as
rods and cones as well as several other
cell types. Usually in a neuron the
default state is to have the membrane
polarized and in response to a receptor
activation if you meet a certain
threshold of depolarization you generate
an all-or-nothing action potential.
In the photoreceptors several of these
things are reversed. So first of all the
default state is to be depolarized,
and in darkness there is a constant
activation of neurotransmitter in
response to that darkness in the default state.
Light actually suppresses the
release of neurotransmitter, but it
doesn't do so in a threshold mediated
way. In other words it's not an
all-or-nothing deactivation of the
neuron. Rather there's a graded decrease
in transmitter release in response to
a graded increase in light within an
individual photoreceptor. In darkness we
have a constant production of cyclic GMP.
Cyclic GMP is a nucleotide like ATP.
ATP is adenosine triphosphate. ADP as
adenosine diphosphate. AMP is adenosine
monophosphate. GTP is guanosine
triphosphate. GDP is guanosine
diphosphate. GNP is guanosine
monophosphate. GMP can be processed to
form into a ring structure called cyclic GMP.
And this is an example of a second
messenger system. The cGMP activates
in a channel in the membrane that imports
sodium and calcium, because positive
charge is coming into the cell the
default state is depolarized. There's also a channel
that's independent of cGMP that lets
potassium go out, and that potassium
export just is not great enough to
overcome the depolarizing effect of the
sodium and calcium import. But it becomes
relevant when the cGMP signal is lost.
When light comes in to the photoreceptor
it strikes a photo pigment that contains
an opsin protein and retinal which is a
form of vitamin A. The role of the opsin
protein is to tune the retinal, the vitamin A
to react to a specific band of
light wavelength. When the retinal
absorbs a photon within that band of
wavelength it converts from 11-sis-retinal
to all- trans-retinal because one
of the double bonds within the molecule breaks.
That is a form of isomerization,
same molecule different conformation.
The isomerization of the retinal,
the vitamin A, activates a protein called transducin.
Transducin activates a phosphodiesterace
that hydrolyzes cGMP, breaks it apart
using water. Because the cGMP is lost and
the cGMP is normally what keeps the
calcium sodium importer open, to the
extent the cGMP has lost the calcium
sodium importer closes, that leads to
a loss of the depolarizing default state.
The potassium export channel stays open
leading to a hyperpolarizing of the cell.
The reason you have this cascade, the
reason that you have transducin, and
then the phosphodiesterase, and making it
complicated like this is because it
allows amplification. The isomerization
of one retinal molecule can activate as
many as 800 transducin molecules. Each
of which can hydrolyze 6 cGMPs, which
translates all together into a closure
of 200 ion channels or 2% of the ion
channels in the membrane and the
photoreceptor for each
time that a photon is absorbed by
retinal or vitamin A. That slows the
release of neurotransmitter which
translates into a signal that travels
down the optic nerve into the brain.
Meanwhile there's an immediate effect to
shut down that transduction pathway as
soon as communication from one photon
makes its way up the optic nerve.
What happens is on the one hand there's an
enzyme that phosphorylates the opsin
protein preventing it from activating
transducin anymore, and the all-trans-retinal
transfers back to a patch of
cells known as the pigmented epithelium
where inside these cells they'll convert
the all-trans-retinal back to the 11-sis-retinal
and then shuttle it back to
the photoreceptor with a binding protein.
All of this is best studied in rods
which are responsible for the perception
of basic outlines of shape in dim light.
And in here we see the opsin protein
called rhodopsin, but in cones which are
responsible for color vision we have red
opsins, green opsins, and blue opsins that
mediate RGB color vision. On top of all
of this we have the least studied one
which is in specific cells called
intrinsically photosensitive retinal
ganglion cells or ipRGCs. We have an
opsin known as melanopsin.
And melanopsin acts in just the
same way, but instead of
translating light into vision, it translates
the effective blue light into
a signal that tells our brain that it's
daytime out, and this is responsible for
our circadian rhythm, our body knowing
when it's daytime and when it's nighttime.
No one really knows how
melanopsin is prioritized in this scheme,
but one thing is very clear that the
cones get priority over vitamin A during
vitamin A deficiency. And the reason is
that it's utterly devastating to lose
the ability to see during bright daylight in
full vision, but it's not that bad to lose
your night vision. And if you think about
this outside the context of artificial
lighting this should be super obvious.
Before artificial lighting when did you
do all your survival critical tasks?
During the day. Even now it's devastating
to lose daytime vision. You are legally
blind if you have something that
compromises your daytime vision. If you
have night blindness you just need to
turn your high beams on at night, or you
know, I mean it's a problem, but it's
nowhere near as devastating as losing
your daytime vision. And the logic here
is that with a limited vitamin A supply
if you have to lose part of your vision
you're going to lose your ability to see in
dim light when it's less survival critical,
and you're going to preserve your
ability to see in the daytime. If you
have night blindness there's probably a 95% chance
that you need more vitamin A
in your diet, sometimes it's zinc, but
night blindness is a huge giveaway of a
potential vitamin A deficiency. Vitamin A
does other things that maintain the eye
like it prevents dryness in the eye.
It promotes the immune defense in the eye.
And there are much worse things that can
happen to your eye if you're severely
vitamin A deficient, but if you're just
a little bit deficient night blindness is
often the first thing to happen. Now the
question becomes what is more survival
critical? Having a well working circadian
rhythm or being able to see in dim light?
Is it possible that the first thing to
go is actually your circadian rhythm?
I don't know the answer to that, but if you
have problems in training your circadian
rhythm with standard approaches, like put
blue blockers on at night and get
morning sunlight, --if these -- and do these
at a very consistent time of a day.
If these things don't help you get on
a rhythm where you're getting tired and
falling asleep at the same time every
day and you're waking up at the same
time every day then something's missing
in how the light is communicating to
your brain and vitamin A could be
the problem.
So that's how we see. What about how we hear?
Well inside our ears
we have hair cells that have tiny cilia
like hairs that protrude into a chamber
that is very sodium poor and potassium rich.
The hairs are graded in height so
that you have one hair that's short, then
you have one that's a little bit higher,
one that's a little bit higher, one that's
a little bit higher, and then in the back
you have the highest hair in each
cluster. And that's so that they can
detect movement in a directional manner.
They can detect movement that goes
towards the tallest hair or away from
the tallest hair. When the movement goes
towards the tallest hair it opens a
potassium channel and when the movement
comes away from the tallest here it
closes the potassium channel. The cell
body of the hair cell is exposed on the
other side to a second chamber that is
very rich in sodium and poor in
potassium like most other extracellular
fluids. When potassium enters the hair
cell that depolarizes the membrane.
The depolarization of the membrane opens a
voltage-gated calcium channel that
causes calcium to come in to the cell
body and that triggers neurotransmitter release.
Depolarization also opens
voltage-gated potassium channels in the
cell body and calcium opens calcium
regulated potassium channels in the cell
body, and those together allow potassium
to leave the cell into the potassium
poor chamber leading to repolarization.
So to visualize this think of this
stack of hairs of graded height. On the
top you have potassium rich fluid and on
the bottom you have potassium poor fluid.
The potassium first flows in to
depolarize and then it continues down
into the bottom chamber
repolarize, and that's how you get
movement coming in to move the hairs
that leads to neurotransmitter release,
and as soon as that movement stops the
repolarization resets everything.
So notably you need enough calcium and
potassium for your hearing to work.
And although I don't know any evidence that
not getting enough potassium in your
diet compromises your hearing, maybe it
does, and there is some evidence that
certain subsets of the genetic defects
that cause hearing loss do so by
compromising the transport of potassium
between cells. There are many causes of
hearing loss, but among them
there is atherosclerotic damage to
the micro vasculature, the small blood
vessels that nourish the ears, and there
is ossification of the inner ear bones,
meaning they get they get jammed up with
too much calcium. That could indicate
a role for vitamin K2, magnesium, and maybe
vitamin A, since these nutrients are
known to prevent calcium from getting
into the wrong places. On the topic of
vitamin K2, this is something that's
found in animal fats and fermented foods,
and I have a very in-depth analysis of
vitamin k2 called:
The Ultimate Vitamin K2 Resource
at chrismasterjohphd.com/K2
I'll link to that as well as resources on
magnesium and vitamin A, calcium and potassium,
all important to hearing, in the show notes.
Moving on to smell. There are 950 odorant
receptor genes in humans. About 40% of
them are expressed, the others are
pseudogenes meaning genes, but they don't
actually express a protein. So we have
altogether about 400 different odorant
receptors. And these are expressed in
a way that each neuron in the olfactory
system expresses only one specific receptor.
Some of those receptors are
highly specific to one chemical. Some of
them are rather broad in their specificity.
But this allows us to have relatively
specific senses of smell for thousands
of different things.
The olfaction mechanism, the mechanism
of our sense of smell, is very similar
to how light affects the photoreceptors
in the eyes. But instead of, but instead of a photon
in general turning down transmission,
a highly specific odorant molecule binds
to a receptor to turn up transmission.
So it's sort of the reverse
of what happens in the eye.
An odorant binds to a receptor which activates a
protein called G ulf.
Some jokester named this so it spelled Gulf.
Anyway it activates adenylate cyclase
and that causes you to take AMP and
make cyclic AMP that activates a channel
that brings sodium and calcium into the cell.
The calcium activitates a chloride channel
that in this case lets chloride out of the cell
rather than in.
All of this which depolarizes the
membrane and that leads to action
potentials that reach the brain and
release glutamate there.
And then there's taste.
We have taste buds on our tongue,
on our palate, on our epiglottis, and on our
esophagus, and these taste buds have
taste cells. These taste cells have micro
villi which are very small finger-like
projections that have taste receptors.
Unlike the 400 odorant receptors that we
have, we have just five classes of taste receptors.
Tastes for: salty, sour, sweet, bitter, and umami.
In the case of salty and sour we have salt
or the hydrogen ions from the acidity of the sourness
that travel right through the ion channels.
So instead of something
activating an ion channel to open, the
ion channels are just open
and the ions directly flow through them
and that's what transmits the taste of
those signals. In the case of sweet,
bitter, and umami we have them binding to
receptors that generate some kind of
intracellular process to allow an influx
of calcium to act as a second messenger.
In both cases depolarization of the
membrane lets calcium in to release
neurotransmitters and the
neurotransmitters are not exactly worked
out for all of them, but GABA, ATP, and
serotonin are all thought to play
important roles in taste perception.
This episode is brought to you by
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Heart is uniquely rich in coenzyme Co Q10 which
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For example natives of the Arctic had very
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Vitamin C is important to far more parts
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In his epic work Nutrition and Physical Degeneration,
Weston Price recorded a story of natives
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What they did was they went
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But even the birds took what they
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Price reported that once the zookeeper started
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The problem I often encounter though is that many
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Let's face it if you weren't raised on them
it can be very hard to acquire a taste for them.
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