In an upcoming episode as part of a series covering autism in the Basil Ganglia, there
is an autism in Parkinson's episode.
For now, just think of the Basil Ganglia as our go no go area.
We'll cover that more in detail during these episodes.
Sometimes I feel like this data that we're parsing out here are looking at us right in
the face and we do nothing.
We miss it so badly.
It is so much that I envision a lost party shooting up flares or writing SOS or help
even on the beach and we don't have eyes on it.
There is a pressing issue in the future of autism in Parkinson's regarding how vulnerable
autistics are for various dementias.
While covering autism in Parkinson's, I can't help but mention something that is so simple.
But for whatever reason, it's neglected or ignorance, I'm not sure, but it prevents
any valuable connections.
In autism, we are already on a path of Parkinson's.
It's essentially a precursor to Parkinson's.
We have problems in the so-called indirect pathway of the Basil Ganglia.
In the episode of autism in Parkinson's, we'll parse out the direct pathway, our go area,
and the indirect pathway, our no go area in more detail.
But for today, there is a concern outside of that.
And that is thyroid.
Several things here are undisputed with autism, undisputed with Parkinson's, and undisputed
in both the autism in Parkinson's research, such as that indirect pathway.
Now, if you follow the long, and this is no shot against them, several guests have come
on and mentioned how hypothyroid is a biomarker and a risk for autism.
Risk the offspring.
Okay.
So data are impressive on this.
Those guests were not wrong.
And in Parkinson's, thyroid is a biomarker of Parkinson's, undisputed.
This is well researched.
If we parse out thyroid being synthesized from tyrosine and talk about the hypothalamus,
the body's control center of hormones, the sort signal for the hormones, essentially.
It's a hormone controller.
It signals to the pituitary for thyroid functioning.
And then we can talk about T3 and T4.
The iodine are involved here for the three and the four.
If you look at supplementing iodine during pregnancy, it's also used to mitigate the
risk of autism.
This stuff is pretty basic.
If we begin to travel into our biology and parse out the synthesis of tyrosines, involvement
in both dopamine, which is well researched, this molecule is well researched in Parkinson's.
It's probably the front runner.
Entirely involvement in melanin.
Okay.
Recently, recently there's been more involvement with neuro melanin in Parkinson's.
And this is the right track.
The reason why the substantia nigra and the basal ganglia, the reason why this is
black is because of the neuro melanin.
It's not really disputed either.
This is all accepted in the research.
I question the knowledge of melanin within autism research.
So the first question I want to ask is, what do you think neuro melanin is?
It's involvement in autism in Parkinson's is the flare being shot up right in the face
of this.
If you say Parkinson's is a disruption of dopamine in the substantia nigra and not
having an ability to orchestrate these different go, no go areas with D1 dopamine or D2 dopamine
excitation inhibition.
This partially in line with what we're talking about.
This is well accepted.
What is missing though is the true synthesis of these molecules and the environmental signals
that are required.
This is where we lose track.
This is where people get confused.
But it's not that complicated.
Two different things here, two different things that explains these problems, both autism
and Parkinson's is a loss of or a lack of energy from the environment.
Now we have to understand tyrosine, the aromatic amino acid, being a UV light detector, absorption
and emission of 200 nanometer to 400 nanometer light.
That's UV.
UV ranges.
That's not complicated.
If we talk about the synthesis of tyrosine into thyroxine and the relationship of the
iodine for T3 and T4, it is somewhat understood and accepted.
We can parse out T3 in this rose.
Here I'm going to read some notes from the episode on autism and Parkinson's.
For T3, brain development.
So during fetal development and early childhood, T3's role here is huge in cell differentiation
and migration.
Two very well understood and accepted facts about autism, well researched items.
Another thing is maturation of neurons.
Autism at its core is a collection of underdeveloped cells.
Neuronal activity.
T3 regulates gene expression in neurons.
And this affects neurotransmitter synthesis, receptor expression and synaptic plasticity.
All well understood and autism research.
Neuro protection effect.
Okay.
Neuromellin in here is huge with the neuro protection as well.
But this has roles with reducing oxidative stress.
So here we're probably talking a lot of mitochondria, which we'll talk about a lot in the episode.
And the metabolic rate of neurons and influencing energy availability.
So this has implications in neuronal firing and maintaining neuronal health.
In the episode, we'll talk about the clock timing, which is one of the factors.
The other factor is the energy.
So two different things here, the timing and the energy.
This is what we need to really parse out.
So what regulates these?
It's not complicated.
It's really not that complicated.
Synaptic transmission is huge with the gene expression.
So T3 can alter the efficiency of the synaptic transmission.
And here we're talking about, especially with the roles of the basal ganglia with learning
and memory.
This is huge for learning and memory.
But this is also huge.
Because T3 helps regulate this, helps conduct this.
Now what is missing in all of this that is so simple is a signal from the environment.
And that is light.
The second question I want to ask you, and I will leave it at that, is, what do you think
light is?