For today's episode, we will cover autism and Parkinson's.
A major region of interest for both autism and Parkinson's is the basal ganglia.
And sticking with this theme, we will cover some more basal ganglia, specifically the
substantia nigra. The substantia nigra is in the midbrain, sometimes called the mesencephalon,
sometimes called the tegmentum, and sometimes referred to as a region of the brainstem.
Essentially, the substantia nigra is towards the top of the brainstem.
The translation of substantia nigra is black substance or black matter.
This is because of the neuromellin. Remember neuromellin's roles, and it is black.
Because it is black, it receives all, all frequencies of light.
Other nature uses it, because it is black. It was selected for specific roles.
Before I say the roles, this is true with the locus serilius as well.
Same area and same black substance. Same cause for the black.
Neuro-mellin. Remember the locus serilius for epinephrine
and norepinephrine. You could call it brain adrenaline.
And that internal calculator we covered with the astrocytes, a type of glia cell.
This internal calculator that we covered was calculating effort versus outcome.
And if the outcome does not match, the glia shuts the locus serilius off.
So melanin. The synthesis of melanin comes from tyrosine,
an aromatic amino acid. Those GV light detectors 200 nanometer to
400 nanometer light. And tyrosine peaks at 280 nanometer.
The strongest wavelength that arrives on terrestrial land from the sun.
280 nanometer light starts the UVB range, which is 280 nanometer to 315.
Remember nanometer. There's 1000 nanometers in one micron.
And the sheet of paper is 80 to 90 microns. 80 to 90 millimeters.
These are very small and it fits the theme because of how small, how upstream we are
going into our biology. The reason I say that is, this is as upstream
as we can think about going, at least for humans and our ability to measure and see things.
This is quantum biology. Environmental signals.
How living organisms on earth are created. The sources of energy.
How cells receive energy. Which provides energy to the living organism.
At the atomic level. How the powerhouses of the cells.
Remember the mitochondria. How the powerhouses of the cells receive
the energy, the powers to power the powerhouses.
Cells respond to environmental signals. Remember the two episodes on mitochondria.
And remember the cause of autism episode. Water production is coming from cytochrome
c-oxidase. And a decrease of this water production from
the mitochondria equals less energy. This is huge for today's topic.
Autism is underdeveloped cells. Parkinson's is that process running in reverse.
Cells die because they lose energy. Melanin drives transduction.
A transfer of energy from the environment. Into and through our biology.
That's it. That's all you need to know about this.
That's all you need to know about autism. If you can't go here.
If you don't allow yourself to go here. And allow yourself to understand this.
You won't understand anything with our health and life.
You will not understand autism. You might think that the research in autism
is pretty lost. It seems like there's so much to cover.
It seems like we're not getting anywhere. And this is true.
Centralized autism research misses this in large part.
It misses there is no power to the so called powerhouse of the cell.
And if you think about an infective fix. The treatment for Parkinson's is deep brain stimulation.
An electrode placed in these areas to supplement the loss of energy.
Energy lost from our modern environments that neglect the environment we evolved under.
Humans do this and no other species will do this.
Okay the rows of neuro melanin this dark pigment.
It's an antioxidant properties. Neuro melanin is our greatest defense to environmental toxins.
It binds metals. This is a huge topic in current autism.
It's well established. It is well recognized and accepted.
That environmental toxins cause autism or increase the risk of autism.
But what's missing is what's changed. A top topic in autism research.
It binds to atom and ions. And it makes it less reactive.
Less toxic. Less harmful.
Other ways of describing this are binding or sequestering.
This allows detox of the cells. Thereby it's a neuro protection.
A common and a region of interest for health is ROS reactive oxygen species or redox.
Okay so a lot here and we cannot cover this. ROS is a very linksy discussion.
But ROS can be harmful to mitochondria and cells and proteins, lipids and DNA.
Next is free radicals. This is of interest. We've covered some free radicals when discussing
blue light, teculite and or isolated wavelengths of light.
The primary region of interest here. The primary region of interest for modern health.
Next for melanin is a neuronal regulation. Another easy connection especially with dopamine.
Also electrons, the energy source from earlier. What powers the powerhouses?
For cytochrome c-oxidase. Reverse engineer the ATP process to the electron transport
chain. To those cycles pumping out enzymes and ions and so forth.
All the way back to pyruvate and TCA cycle, nurek acid. Which is a very hot topic in Parkinson's.
Just reverse this final output of the mitochondria, the ATP, in this back track and you can find
implications here from the loss of environmental signals from the loss of transduction.
And remember chromophores. The red light chromophores on cytochrome c-oxidase and the vitamin D receptors.
More and more on this light topic. And humanity has seen rapid changes in light over the past
130 years. The question is, what do you think light is?
Think about it. Are we using the way we evolved? Or have we changed light as a convenience?
What do you think light is? And is it the same today versus evolution of life on earth?
This is so simple. If you understand Dr. Jack Kruse's orange tree example.
If you buck the sun from an orange tree, will it produce the same amount of fruit? And even
if the production of the fruit and also for the oranges coming in being bloomed, will those
be fully developed? Or maybe they're not fully developed?
I use an example of this in the episode with Dr. Richard Frye when we discussed understanding
the roles and sensitivity of mitochondrial functioning. And I use this example for describing
autism and Alzheimer's. And there's a short on YouTube that you can find if you're interested.
In this. With neuro melanin, with Parkinson's, hypoxia of these pigmented neurons break
down melanin. The source, the power and the electrons. This creates a loss of dopamine.
Now, it's common that people think Parkinson's is a loss of dopamine. And that's true. But
research often misses the neuro melanin aspect of this, this component of this biological
energy, these biological concepts. So let's go upstream in the biological path.
The eyes, hair and skin. This is the starting points, the starting lines. Think about this
in a linear path. If the first domino doesn't hit the next, what happens?
The eyes, we have melanin here. Of course we do. Lots of melanin. We have melanopsin.
And we have the retinal pigmental epithel, or RPE. With this linear path, the goal here
for this energy transduction is to remain efficient and powerful down the line, down
the path. To answer the question earlier, what is light? Melanin is chosen here because
it is a dark pigment and absorbs all frequency of light. In the summer, if you go outside
anywhere black versus white, there's going to be a big difference, a noticeable difference.
This is why the pupil is black. This is why Mother Nature chose neuro melanin for this
role. Melanin and the pupil are black to receive the full light frequencies. So light is electromagnetic
field containing a wave and a particle, a photon, a wave particle duality. Waves have
the information, photons carry the energy. In the linear example of the photon, or photons,
getting the first domino, the eye, skin or hair has to be, it must be, as much power
as possible, to power the downstream processes. Biologically, this is how we make the dopamine,
serotonin, proteins, whatever the example like these you want to use. Vitamin D is a
popular example. Most people understand sunlight and vitamin D. You can see the cause of autism
episode for more detail on this and also autism and gastrointestinal problems episode. There's
a lot of this transduction happening in the gut. Artificial light versus sunlight is the
cause. UV light wavelengths keep the melanin and dopamine optimized in the mid-bring. The
Substantia Nigra for this Parkinson's discussion. Tyrosine is an aromatic amino acid. Remember
those UV light wavelengths? Do you think artificial light is optimizing these biological processes?
Don't miss the wavelengths throughout the light spectrum. This is why I ask, what do you think
light is? This is also occurring on the skin with melanocytes. Something well known in autism
research is thyroid and the correlation with the risk. Thyroid is tyrosine and iodine. Iodine
is well established in autism as well. This is hitting us right in the face. Thyroid and
Parkinson's is similar. There are strong data here. People with hypothyroidism have an increased
risk of Parkinson's. Mothers with hypothyroidism, their offspring will have a higher risk of autism.
This is all right here in front of us. We have all of these siloed data and research studies,
but we cannot connect them because we don't go upstream. Because research has this centralized
framework and it's very confusing. Now in our modern world, the thyroid is a pretty frequent lab
test because the rates of thyroid are increasing. It's pretty common to find people, especially
adults, with hypothyroidism. We can think about the hypothalamus as the control center for the
body's hormones and then it communicates to the pituitary. Based off of these lab tests,
you're probably even familiar in your own medical history. You know about T3 and T4. The 3 and the
4 represents iodine. So the T3 is tyrosine, tyroxine, and iodine. If you look up autism research,
one of the ways to mitigate the risk of autism is to supplement iodine. Another way that we
mitigate risk factors for autism are supplementing with things like tyroxine, medication. This is
well established and it works. It mitigates the risk of autism when the mother is supplementing
with these medications. So the important part here is the rows of T3, the rows of the thyroid with
neuronal function and motor function. This is well established, but I don't think it's well
understood or appreciated. So the rows of T3 here for brain development, this is during the
fetal development. During fetal development and even in through early childhood, this T3 is critical
for brain growth. It has a big influence on cell differentiation and migration. Remember the episode
on autism and the embryo and the episode covering the placenta. This is a key region of interest
here. This is going to be when autism is developing in the living organism. So the T3 with
the differentiation and migration, autism research has well established data on these being a problem
in autism. In addition, T3's role with maturation of neurons, also another well established data
point in autism. Now the overarching goal here with this process, building the brain development
is for cognitive functions. We think about autism, it's underdeveloped, it's a neurodevelopmental
problem. T3 also helps with neuronal activity. So once the cell, the neuron is formed, T3 regulates
the gene expression in the neuron and this affects neurotransmitter synthesis and receptor
expression and synaptic plasticity. All of these things are well established in the autism data.
T3 also acts as a neuro protector, similar to the neuro melanin and T3 has roles with
reducing oxidative stress and aiding in repair processes after cell injury. T3 has roles with
metabolism and energy, which is well established. Delay public likely knows this. However, it's
the metabolic rate of the neurons influencing the energy availability for the neuronal firing
and maintaining of the neuronal health, cell health. These are all have big implications
with the synaptic transmission as well. And the gene expression. So if you're thinking
T3 and the pituitary and the hypothyroidism, that's all associated with hormones and that's
correct. T3 acts as a connector, like a node here that's connecting the hormones and all
of these growth factors and the neuronal activity. Now if you go downstream with these implications,
it's easier for the lay public and will just anybody to observe these, you might think of
them as such as cognitive impairments or mood swings, some neurological symptoms even. One
might go to the doctor and say, I just haven't been feeling well. My energy is low. I'm irritable.
And they will do lab work. And they well indeed, it'll show your TSH might be seven or eight
or nine or whatever it is. And then they'll put you on and you might be prescribed a couple
of micrograms, 7500 micrograms of this medication. Now you can also understand the relationship
here with the motor functioning. At the upstream level here, everything's related to cell health,
the development of cells. If we lack energy, the cell lacks energy. So it's always coming
back to the lack of or the loss of energy. For autism, this is happening in the womb
early in development on this linear timeline. And we can move this out, stretch the timeline
across these basal ganglia areas and understand the problems here with the efficiency of this
pathway. Something that's looking at us right in the face with this data are the environment
of the pregnant mother has changed drastically. The rates of autism matches the type of environment.
The mothers are in and it's not a direct shot at the mother. It's just the modern world,
the modern environment. We are losing energy to the environment. Now if you talk to a researcher
on mitochondria, they might think, yeah, it's a mitochondrial dysfunction, but they
might not know why. And that's not a shot against them either. It's just the centralized
framework that determines which lens are we looking through? What are we looking at? What
are we looking for? It's very siloed. It's very narrow. It almost lacks depth if I had
to sum it up. Now remember thyroid, row, and the biosynthesis of tyrosine here as well.
I cannot harp on this enough. Remember the biosynthesis of tyrosine making thyroxine
and making al-dopa, which is common with the Parkinson's theme and making dopamine and
epinephrine and melanin. Melanin is the missing row here. It's the underrated row. Remember
melanin's row with water. So the mitochondria is here once again. And the regions with this
most neuro melanin are centered in the midbrain areas that contains lots of other water in
the brain. The melanin and water interaction equals more electrons. Remember light changes
the physics of water. This is what it is all about. Electrons and the environmental signals.
And remember the water being produced out of mitochondria. As we age, roughly each decade
of life, we lose roughly 10% of the water being produced in mitochondria. And this occurs
across the lifespan. 10% roughly every 10 years. So we are losing energy naturally. This
is entropy. This is senescence. This is life, aging and life. Check this with hetero plasmy.
If you want a good marker, a good biological marker, look into hetero plasmy. Now with
disease and other insults and such, we can lose more frequency of water. This rate can
be increased. Now you can even begin to understand the other neurodegenerative problems and why
the rates of these are increasing. Okay, I said in a previous episode because we are
covering the basal ganglia quite extensively here. I would cover the direct pathway and
the indirect pathway in the basal ganglia. So I'll do that now. Quick recap on the basal
ganglia. There are five subcortical nuclei all working together to orchestrate movements.
The basal ganglia is our go, no go areas. And this is where motivation and movements converge.
But remember, the definition of motivation here is not defined by us and our ability
to think and create. With our human cortex, motivation here is defined by the specific
living organism. The nervous system just wants to respond. So that is the definition
that you need to consider for motivation. The nervous system is just going to respond
based off of what it knows. This is a very different definition of motivation. So remember
the five subcortical areas. There are inputs, so the cadet nucleus and the pudiment. And
then we have the globus pallidus internal and globus pallidus external. These form a
triangle, two separate nuclei forming a triangle. And we also have the subthalamic nucleus,
which is the personal assistant essentially to the thalamus. And of course the substantiate
nigra, the two nuclei here, the reticulata and the compacta. So these are all orchestrating
movements based off of the environmental signals and the perception of the living organism's
nervous system. We are orchestrating movements here. The direct pathway is trying to facilitate
movements by reducing inhibitory outputs from these basal ganglia nuclei into the thalamus.
This will send a signal up to the cortex for responses deemed necessary or efficient or
practical, useful for the living organism. The start is neurons from the cortex. Of
various areas of the cortex and some from the thalamus and some from the substantiate
nigra providing dopamine. These inputs are not exhaustive, but just kind of to explain
the pathway. The direct pathway acts as more of the goal signal. So we are receiving excitatory
dopamine from the substantiate nigra. This is D1 like dopamine, excitatory. The dorsal
striatum then will communicate with the globus pallidus internal and the substantiate nigra
reticulata. It communicates to these two subdivisions by inhibiting them. It puts a break on them.
Because the roles of the globus pallidus internal and the substantiate nigra reticulata is normally
to interact with the thalamus. So the dorsal striatum will shut these two nuclei off and
that frees up the thalamus. And the thalamus being less inhibited can then communicate
back to the cortex, exciting the cortex and promoting movements. This pathway removes
the break, removes the no-go side. The indirect pathway is a little bit more communication.
It inhibits or kind of slows down movements, acting as a break. So one is a go side and
one is a no-go side. Similar to the direct pathway, signals come in to the input area,
the cadet and the containment, from the cortex and the thalamus and the midbrain. The dorsal
striatum will then speak to the globus pallidus external and it will inhibit the external area.
By inhibiting the globus pallidus external, it will free up the subthalamic nucleus. It
allows this area to be more active. The subthalamic nucleus will then speak to the globus pallidus
internal and the substantia nigra reticulata, essentially giving them free will, giving
them a go ahead signal to activate. Remember the direct pathway inhibited these. So here
we are exciting these two areas. The globus pallidus internal and the substantia nigra
reticulata then speaks to the thalamus, the main goal. And these two nuclei to the thalamus
says stop. This is a no-go. And because the thalamus is inhibited or stopped, it can suppress
or even slow down movements. It controls the movements. The indirect pathway is the no-go.
And it uses the D2 like dopamine, the inhibitory dopamine. What the basal ganglia is trying
to accomplish here is fine tuning of motor control. Remember the goal of the central
nervous system is designed to move the living organism. What these two pathways are doing
is fine tuning of that motor control, this action selection. And remember the dorsal
striatum is an area where go directed movements and behaviors are located and also habit formation.
More habits reside here. There's a lot of communication from sensory motor regions and
the dorsal lateral side of the striatum, the DLS. Whereas the go directed resides more
in the dorsal medial striatum, which is more cadet. So cadet is more go direction and the
putamen is more habit formation. It's where habits live. And that's the goal of the central
nervous system though. We want to build learning and then send those down into habits. And
these areas of the basal ganglia and this direct pathway and indirect pathway, this is
how we can grasp our motor signals being processed and leading to how we coordinate downstream
behaviors downstream movements. Now Parkinson's here is a loss of timing and loss of energy.
Now with everything with the substantia nigra compacta and reticulata, you can start to
understand why the substantia nigra here losing energy, losing its ability, its efficiency.
It cannot conduct this pathway correctly. It loses its ability to coordinate these two
direct pathway and indirect pathway. And if you think about it with all the, with the
motor movements associated with Parkinson's and autism, this is pretty common and easy
to understand here. The substantia nigra is lacking here and all of these downstream processes
are off. So with autism, we get these stereotyped motor movements and stimming and repetitive
restricted behaviors and so forth. In both Parkinson's and autism, it's easy to see.
We love it when we can see things and observe and evaluate things. It's easy to see the
motor movements here, the abnormal motor movements. In autism, it's well established that there's
an increase of this D2 like dopamine facilitated through the dorsal striata and is implicated
in the indirect pathway. We cannot inhibit motor movements. And over time, remember the
discussions on neuroplasticity. These motor movements can actually become calming. We
learn how to do these for calming and they also remember the habit formation. We do these
out of habit now. The more we do things, the easier it is to form the habit, which is the
goal of the central nervous system because it doesn't want to work. It just wants to
respond. And considering that the substantia nigra is not optimized, the transduction is
not capable. It's loss of energy is very implicated here. This is what it's all about. If you
look at go versus no go and put them on a seesaw, the fulcrum there, the thing that
is balancing on is the substantia nigra and the dopamine coming out of the substantia nigra
and into these other nuclei facilitating these movements. If you are listening to the episode
or listening to the podcast, please feel free to leave a review or rating. In podcasting,
reviews, ratings and downloads are huge. And I very much appreciate your feedback. You
can contact me on X at RPS 47586 and we can discuss anything about autism. I very much
appreciate your comments and interaction. You can check out the hop link so you can have
links to all of the shows across various podcasts. You can contact me on YouTube. Check out the
YouTube channel and tick tock. I guess I'll try out tick tock. I'll see how that goes.
I don't love it. But anyways, thank you for listening to From the Spectrum podcast.