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In an upcoming episode as part of a series covering autism in the Basil Ganglia, there

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is an autism in Parkinson's episode.

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For now, just think of the Basil Ganglia as our go no go area.

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We'll cover that more in detail during these episodes.

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Sometimes I feel like this data that we're parsing out here are looking at us right in

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the face and we do nothing.

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We miss it so badly.

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It is so much that I envision a lost party shooting up flares or writing SOS or help

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even on the beach and we don't have eyes on it.

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There is a pressing issue in the future of autism in Parkinson's regarding how vulnerable

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autistics are for various dementias.

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While covering autism in Parkinson's, I can't help but mention something that is so simple.

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But for whatever reason, it's neglected or ignorance, I'm not sure, but it prevents

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any valuable connections.

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In autism, we are already on a path of Parkinson's.

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It's essentially a precursor to Parkinson's.

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We have problems in the so-called indirect pathway of the Basil Ganglia.

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In the episode of autism in Parkinson's, we'll parse out the direct pathway, our go area,

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and the indirect pathway, our no go area in more detail.

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But for today, there is a concern outside of that.

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And that is thyroid.

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Several things here are undisputed with autism, undisputed with Parkinson's, and undisputed

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in both the autism in Parkinson's research, such as that indirect pathway.

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Now, if you follow the long, and this is no shot against them, several guests have come

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on and mentioned how hypothyroid is a biomarker and a risk for autism.

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Risk the offspring.

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Okay.

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So data are impressive on this.

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Those guests were not wrong.

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And in Parkinson's, thyroid is a biomarker of Parkinson's, undisputed.

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This is well researched.

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If we parse out thyroid being synthesized from tyrosine and talk about the hypothalamus,

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the body's control center of hormones, the sort signal for the hormones, essentially.

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It's a hormone controller.

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It signals to the pituitary for thyroid functioning.

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And then we can talk about T3 and T4.

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The iodine are involved here for the three and the four.

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If you look at supplementing iodine during pregnancy, it's also used to mitigate the

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risk of autism.

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This stuff is pretty basic.

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If we begin to travel into our biology and parse out the synthesis of tyrosines, involvement

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in both dopamine, which is well researched, this molecule is well researched in Parkinson's.

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It's probably the front runner.

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Entirely involvement in melanin.

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Okay.

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Recently, recently there's been more involvement with neuro melanin in Parkinson's.

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And this is the right track.

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The reason why the substantia nigra and the basal ganglia, the reason why this is

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black is because of the neuro melanin.

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It's not really disputed either.

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This is all accepted in the research.

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I question the knowledge of melanin within autism research.

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So the first question I want to ask is, what do you think neuro melanin is?

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It's involvement in autism in Parkinson's is the flare being shot up right in the face

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of this.

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If you say Parkinson's is a disruption of dopamine in the substantia nigra and not

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having an ability to orchestrate these different go, no go areas with D1 dopamine or D2 dopamine

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excitation inhibition.

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This partially in line with what we're talking about.

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This is well accepted.

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What is missing though is the true synthesis of these molecules and the environmental signals

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that are required.

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This is where we lose track.

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This is where people get confused.

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But it's not that complicated.

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Two different things here, two different things that explains these problems, both autism

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and Parkinson's is a loss of or a lack of energy from the environment.

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Now we have to understand tyrosine, the aromatic amino acid, being a UV light detector, absorption

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and emission of 200 nanometer to 400 nanometer light.

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That's UV.

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UV ranges.

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That's not complicated.

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If we talk about the synthesis of tyrosine into thyroxine and the relationship of the

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iodine for T3 and T4, it is somewhat understood and accepted.

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We can parse out T3 in this rose.

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Here I'm going to read some notes from the episode on autism and Parkinson's.

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For T3, brain development.

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So during fetal development and early childhood, T3's role here is huge in cell differentiation

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and migration.

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Two very well understood and accepted facts about autism, well researched items.

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Another thing is maturation of neurons.

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Autism at its core is a collection of underdeveloped cells.

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Neuronal activity.

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T3 regulates gene expression in neurons.

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And this affects neurotransmitter synthesis, receptor expression and synaptic plasticity.

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All well understood and autism research.

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Neuro protection effect.

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Okay.

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Neuromellin in here is huge with the neuro protection as well.

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But this has roles with reducing oxidative stress.

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So here we're probably talking a lot of mitochondria, which we'll talk about a lot in the episode.

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And the metabolic rate of neurons and influencing energy availability.

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So this has implications in neuronal firing and maintaining neuronal health.

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In the episode, we'll talk about the clock timing, which is one of the factors.

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The other factor is the energy.

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So two different things here, the timing and the energy.

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This is what we need to really parse out.

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So what regulates these?

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It's not complicated.

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It's really not that complicated.

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Synaptic transmission is huge with the gene expression.

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So T3 can alter the efficiency of the synaptic transmission.

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And here we're talking about, especially with the roles of the basal ganglia with learning

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and memory.

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This is huge for learning and memory.

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But this is also huge.

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Because T3 helps regulate this, helps conduct this.

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Now what is missing in all of this that is so simple is a signal from the environment.

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And that is light.

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The second question I want to ask you, and I will leave it at that, is, what do you think

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light is?

