Welcome to From the Spectrum Podcast.
This is a podcast about autism.
It is my goal to explain what is autism.
I plan to use a mixture of scientific literature, personal experience, and opinion.
With opinion, I will explain why, I will give examples.
I will provide links to various references for each episode.
For each episode, we will discuss various aspects of autism.
For today's episode, we will explore autism's development in the embryo.
We will cover common biology already discussed, such as cell proliferation, differentiation,
migration, neurogenesis, synapogenesis, and synaptic function, and the development of
neural networks.
Think cells migrating to common cells that create whole brain regions, or organs, or tissues.
The process of stem cell into a specialized cell, and how they migrate to each other to
form different aspects of the human body.
This episode will expand on the cause of autism episode to explain more detail.
This episode fills in what is happening simultaneously and slightly downstream.
The cause of autism episode explained how our living organism is created, at least an introduction
to it.
This episode picks up essentially the developed cell, and this is regardless of normal developed
or abnormal developed.
In addition, we will cover specific timelines of cell life and the embryo, and into about
three years old postnatal.
As to remember from cause of autism, let's call them ingredients, light, as the driving
force of living organisms.
Remember the energy source, the electromagnetic strip, the photoelectric effect, and water,
magnetism, and the elements from the periodic table.
Remember we use some of these elements, and then a subset of the ones that we do use, a
subset we use a lot of those.
But also remember melanin as the target for that light, and melanin being black, to absorb
all of the light's spectrum.
Don't think it's black for this.
Think.
Our body, our biology, our evolution, chose melanin to do this role.
Remember POMC, as the source for melanocyte stimulating hormones, alpha, beta, and gamma.
These are in cells, organs, and tissues, all through the body.
Later, I will show you how this is proven as an implication to autism, accidentally.
In a paper we will spend most of the episode reviewing.
The paper proves light and melanin is a cause without saying it is a cause.
Remember vitamin A and tryptophan, and their roles in eye development.
Eye development generates brain development.
Vitamin D and tryptophan, and the skin.
TPH1 for the skin and gut, which helps create our body.
And TPH2 for helping to develop the brain.
TPH is tryptophan hydroxylase.
And remember proteins are semiconductors.
And remember the amino acids.
We have 20 amino acids.
Tryptophan and methionine are codes for DNA and protein sequencing.
Tryptophan and methionine are special, whereby they have one codon.
And they sequence proteins and DNA.
Tyracine is the special start signal.
Tyrosine is huge too.
Remember the aromatic amino acids.
All of these so called ingredients use certain wavelength of light.
They require the certain wavelength of light to function.
We've covered, and I would even say we've established, common themes in the biological
development are implications to the cell and the synapses.
These are common themes with autism.
The cell meaning proliferation, differentiation, migration, development, and the synapses.
Development, growth, and the functions.
So let's explore something.
Autism spectrum disorder, living biology.
This is the paper I want to review from Transin neuroscience.
It is a paper from Cell Press.
Recently there's a conceptual and paradigm shifts towards a focus on the abnormal prenatal
processes underlying autism within each individual.
From specific abnormal development to early clinical stages.
Remember cells divide.
They increase in number.
So cell proliferation.
Increasing cells as a result of growth and division.
Proliferation is becoming mature.
Cells become specialized, unique, or distinct types.
These are stem cells can become nerve cells, which we mostly discuss in the podcast.
They can become immune cells, muscle cells, organ cells, blood cells, epithelial cells,
which is important in the light as a cause, hypothesis, and melanin is inside all of these
cells.
Migration, once mature and specialized.
Into one of those previous mentioned cell types, migration is like building blocks that
allow a formation to occur.
Such as creating the nervous system, or an organ, tissues, or muscles, and so on.
Let's review some timelines and the developmental milestones.
First trimester, starting at roughly four weeks.
Proliferation and neurogenesis occurs.
The beginning of neurons, or cells.
Lasting to around 26 weeks.
This is prenatal.
This is the embryo.
Cell migration begins at 10 weeks or so.
And this lasts until 32 weeks.
The second trimester, neuro-ight overgrowth at 14 weeks to roughly three years of age.
So roughly at the end of the critical period that we've discussed quite frequently.
And synaptogenesis and synapsis function begins at 20 weeks until around age three.
And the third trimester, neural networks, the formation and functioning.
Once specialized, they start to begin these networks that develops the nervous system and
so on.
This starts at 32 weeks and essentially this is continuous through the lifespan.
The paper distinguishes epoch one as trimesters one, two, and three.
And epoch two, trimester three.
So trimester three is split between both epochs.
Epoch two is trimester three into early postnatal periods.
Let's call it that three years old.
Epoch two is more brain specific or if another type of health condition implications to these
areas occur.
Remember, autism just shows up.
It doesn't necessarily mean if you have a problem.
It doesn't necessarily mean that problem will cause autism.
It might cause something else, something similar.
And this is the case with most health conditions if we go that far upstream.
For our topic, autism is a brain development is a region of interest.
This is covered in previous episodes, episode three, four, and five and in autism and light,
the cause of autism episode.
Disruptions here include neuro-right overgrowth, synaptogenesis and wiring or connecting those
highways of communication.
Remember I said highway, but some connections could be more like a gravel road.
Remember myelin.
Remember these connections differ.
And this is how cells communicate.
At each synapses, a cell receives a brief summary about what must be occurring for this cell
to connect here.
With each connection, the summary adds and creates a story.
Another implication or expanding on the migration slash brain development because this is the
process these cells are migrating and creating the brain.
Brain development and dysfunction with how our regions or networks form.
Of course, that ought to make sense to us.
However, the crucial part is the timing of it.
Remember these episodes, autism and adaptive responses, autism and silence network.
Remember our discussion with Dr. Leanna Hernandez and the boy versus girl differences.
Back to the silence network, remember the UCLA paper came out in 2024.
The paper I am mostly referencing about being able to predict profound autism.
Remember the conversation with Dr. Catherine Lord and I mentioned this.
It has to do with the brain organoid.
The paper predicting profound autism and this paper from trends in neuroscience discussing
the embryo is from the same researcher.
This researcher does wonderful work from UC San Diego.
Okay, the trends in neuroscience paper.
This paper mentions risk genes, a common topic with autism research.
Specific risk genes are risk genes that we've covered on the atomic level and with general
descriptions in mostly episodes 3, 4 and 5.
These include phosphorus, phosphorylation and p10 and protein kinase B.
These involve cellular metabolism.
Previously I said autism and type 1 diabetes could be related upstream.
These are the regions of interest.
Diabetes will involve POMC too, a product cleaved from POMC for insulin.
That's my thought.
Remember implications upstream look differently downstream.
They have different so called clinical presentations or different health complications.
Now I didn't say autism and type 1 diabetes are the same or one increases the risk for
the other.
I'm saying upstream.
Many shared regions of interest are present.
Anyway, I won't mention the trends of these each over the past 50 years or even let's
say the past 20 years.
Again, at least not now.
Also MTOR is involved here in the paper.
I mentioned possible hope with MTOR when originally discussing p10, a paper from Cell Press.
This was in episode 3 at the beginning.
Lastly from the risk genes discussed is a pathway that play a critical role with embryonic
development.
Everything mentioned, I believe, are components of the cell development.
And this risk gene also contains mitogenic processes.
Mitogenic mitosis.
This requires UV light.
This is the spot to explore for autism.
The time is in the embryo.
We've connected early findings postnaturally at 6 weeks old.
Two studies.
We've discussed two studies here.
The Sanis Network from UCLA and the brain organoids mentioned earlier predicting profound
or more severe autism from UC San Diego.
I bring this up for two reasons.
One to expand and prove light as a large possibility as the cause of autism.
And two, funding and research must go here and stay here until proven otherwise.
This stuff on older children or adolescents, this research likely will not provide much
to the world.
At least not at this time.
Research ought to move to the pregnant woman because at this point every child seems to
be at risk for autism.
If we go by the 1 in 20 boys data and the possible misdiagnosed girls from the gendar
findings, it appears the assessment tools are boy biased because the diagnosis result
is boy biased.
But if girls or females have more social motivation that autistic boys are similar or more social
motivated based on brain imaging and connectivity, then non-autistic girls and non-autistic
boys that data could be misleading too.
Regardless, I don't want to discuss assessments now.
The timeline ought to go to the embryo and the cause is cell dysfunction in this development.
Okay, let's discuss some specifics of abnormal brain development in the prenatal.
These are postmortem, proliferation, these are averages.
Autistic children have 67% more prefrontal neurons than non-autistic.
This includes 79% more in the dorsolateral prefrontal cortex.
Remember the subdivisions.
The dorsolateral prefrontal cortex is involved with things like working memory and task switching,
planning, inhibition, and interestingly, abstract thinking and a 29% increase in the medial
prefrontal cortex, that subdivision that we discussed in autism and adaptive responses.
Now you hear that there's an increase of neurons in these different subdivisions for
autistics.
But this does not mean that these areas are better.
They are, they function better.
Remember the poor connections out of these areas.
30% more overall in the cerebral and 57% more von economo neurons or cells.
These are spindle neurons.
Remember from Autism and Adaptive Responses episode.
There is an increase of these spindle neurons in the insula.
Remember the insula, that hotspot, that regional hub that receives bodily information, brain
information and integrates it with how the living organism is navigating society, navigating
the outside world.
And the ACC.
Remember in the adaptive responses episode.
When we make healthy and adaptive responses to the flexible rules that are going on in
socialness, going on in society, the outside world is very unpredictable.
When we make healthy choices, the medial prefrontal cortex and the ACC lead the way.
They lead those adaptive responses.
However, whenever we have trouble with responding to the environment or responding to our body,
the insula kind of overtakes the prefrontal cortex and that ACC.
And it kind of leads the way.
It allows the body to overtake the brain essentially.
And these are specialized cells that are only found in larger primates.
They're not across all species or even all mammals.
These are involved in social emotional processes.
So social emotional processes.
It sounds like an autistic phenotype description.
A highlight of these data are this occurs between 10 and 20 weeks in the embryo.
But postnatal.
Okay, now a common theme with autism is excitation.
The excitation inhibition balance or imbalance.
Cell proliferation regarding excitatory cells.
A recent study exploring 102 common risk genes linked to autism.
71 of those 102 are involved in excitatory cells in the cortex.
Add this to the data of inhibitory implications in the striatum.
And with two glia cells, oligo dendrocytes and astrocytes.
Remember the striatum.
A hot spot for motivation and movement.
Motor movement.
Also think the reward areas.
Remember the discussion of the nucleus accumbens.
And then those stimulus responses.
So here we just mentioned the ventral and the dorsal striatum.
They are reflexes and deliberate, go directed activities here.
These include socialness.
These also include what is salient to us.
And for autistics, what is salient is mostly staying within ourselves.
In one or few interest at a time.
Remember that biology that gives us autism allows us to be comfortable within ourselves.
That's preferred.
When I say motivation, it is not limited to deliberate wants or deliberate needs or likes.
I think what motivates the nervous system to return to comfort.
Those actions become the motivation.
I know some discussion on genes.
And I know it is a hot spot for research and funding.
I don't love it.
You heard Dr. Lord say, she is unsure if this is the way.
What it will even do.
My position is I would rather spend time and money understanding the cause.
Such as the artificial light over the genetic implications.
I understand the genetics are implicated.
The genes are implicated.
The cells are dysfunctioned in various ways.
But why?
I suspect this is because medical treatment can be designed, developed and sold.
Sold at large volumes.
Then profit.
Profit is our medical paradigm.
The most popular medications for autism.
Yes, that's interesting, right?
The most popular come from anti-psychotic classification.
These are anti-psychotics.
Given to autistic individuals, there are a couple of different things wrong here.
One, the family, the loved ones of the autistic children, they are vulnerable.
They want their child to have relief, to be able to fit in in society.
They want their pain and struggles to be reduced or eliminated.
And the medical profession with their training is designed to prescribe medications.
Try this.
Try an anti-psychotic or SSRI or antidepressant.
Because the child needs to interact more.
The child needs more friends to be able to be comfortable interacting.
The child needs more diverse interests.
They need more hobbies.
The child receives complications in social settings whenever there is over-stimulation.
So let's try medication to calm the child, to calm the individual so that they can fit
in better and easier to be around and be accepted in society.
I only bring this up because I have concerns.
I have disagreements with medication use for autism, especially medications that were developed
for other conditions.
We mostly just throw medications at everything.
Try it and if it doesn't work, we'll try something else.
And I'll tell you two reasons why it's concerning to me.
It's very suspicious.
One is rarely do you get any informed consent.
You just get the prescription and maybe the physician or the PA or the NP, etc.
will give you just a off the top contour, just a few side effects or a few implications
that that happen in a very questionable trial.
The second thing is the second concern and probably even more concerning than the informed
consent is the medical paradigm, the accreditation.
They cannot prescribe prescriptions fast enough.
So over time, they developed these nursing roles that are the role is to prescribe medications.
They are trained and their role is to prescribe medication, medication management.
Look at the health trends.
Look at around that society to observe each other.
Let's go back to 1960 and then 1980 and near 2000 and 2022.
And let's break down age from birth to nine years old to 10 to 19 years old to 20 to 29
years old.
So on until we get to 90 years old.
Let's look at the number of prescriptions given in each decade of lifespan from the
60s, the 80s, the 2000s, 2020s.
That increase is going to be wild and nothing's changed.
Nobody's healthier.
Just today, neuroscience news released a, they highlighted an article.
This is cancer drug as a possible autism treatment.
Okay.
One, how is this even discovered and what is going to be the purpose here?
But two, more discerning is clicking on that link.
It's not even autism.
The cancer drug would help Rett's syndrome, which has been kind of compared to autism.
And it's a separate thing.
It's a syndrome.
Syndrome's mean not a lot is known about it or what you do about it.
This came from UC San Diego as well.
This was very disappointing in my opinion.
However, remember, autism just shows up in human biology and human evolution.
Everything in the normal biological processes changed.
That change appears to be light and all of the new health trends supports both.
Both meaning the change and the profit.
This specific paper from trends in neuroscience highlights autism as a multi-organ disorder.
Of course, the primary one is the brain, meaning the biggest complication in autism is the brain.
But this is huge.
It is huge because of the light story and melanin and POMC.
The paper highlights all of these separate organs implicated in the autistic phenotype
and the autistic individual.
And there's a large list.
Now it doesn't mean that every one of these are implicated or abnormal, but there are
a lot of shared implications throughout the body, which we've discussed.
We've discussed in this episode even.
The what is going on upstream, those implications will show up differently and sometimes in multiple
ways.
You've heard of sequela or you've heard of a health condition causing other health
conditions.
All of these areas are dependent of melanin and the light to drive nonlinear optics.
Amazingly, this is amazing to me.
I was reviewing melanin and leukocytes.
Just chuck it up to one of those B3 fixated interest.
I'm just looking at melanin and where it is throughout the whole body.
And I just happened to stumble upon this this week.
Melanin and leukocytes from the 1960s.
This has already been known since the 1960s.
How many people know about melanin being in white blood cells?
And for those listening, leukocytes are white blood cells.
How many researchers and scientists on autism know about melanin being in white blood cells?
They know autism is linked to immune and inflammation.
This is huge.
These are huge findings.
This proves.
This suggests these immune problems and the inflammation problems.
And we've discussed the mitochondria problems and all of these cell implications and subnaptal
genesis and subnaptic connections.
All of these are kind of dysfunctioned.
But now they're linking other bodily processes, other organs and tissues that are seemingly
unrelated.
This supports the light theory.
Light is the only thing at this current moment that is making sense.
The past three episodes we've outlined some critical things here about the causes, about
what's implicated in these causes, and understanding even the rates of diagnosis, and how much
light has changed during this timeline since the 1930s.
Not only has the light changed, but the amount of time and how humans have shifted behaviors
more indoors under artificial light and surrounded by technology light and less time outside.
And this is showing up now in the lineage.
Remember those timelines discussed previously?
Remember that blue light chromophore, melanopsin?
Remember it wasn't discovered until 1998 and then fully understood the sequencing until
years after that, a couple of years after 1998 in the early 2000s.
But now it's known to be across various aspects of the brain, deep inside the brain in roughly
30 regions of the brain.
It's in tissues and organs, epithelial cells.
And remember it's a chromophore, so it activates based off of specific light wavelengths.
And the melanopsin is around 480, it peaks at 480 nanometer, which is blue light.
Modern light is blue light.
It's in the shorter wavelengths.
And our shifts to this type of lighting runs parallel with the rates of autism.
The timelines fit.
Lastly, this blue light wavelength light shuts down.
It implicates palm C. The pro-opioid melanochortin subdivision of the hypothalamus that cleaves
many crucial parts of our biology, including the melanocyte-stimulating hormones.
This is underrated in the research of autism.
This ought to have attention, but it has no attention.
And that is a concern to me.
So I hope to help bring attention of autism and light, but not only just autism.
The health implications, because of how the human body uses light.
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Thank you for listening to From the Spectrum Podcast.