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Welcome to From the Spectrum Podcast.

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This is a podcast about autism.

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It is my goal to explain what is autism.

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I plan to use a mixture of scientific literature, personal experience, and opinion.

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With opinion, I will explain why, I will give examples.

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I will provide links to various references for each episode.

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For each episode, we will discuss various aspects of autism.

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For today's episode, we will explore autism's development in the embryo.

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We will cover common biology already discussed, such as cell proliferation, differentiation,

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migration, neurogenesis, synapogenesis, and synaptic function, and the development of

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neural networks.

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Think cells migrating to common cells that create whole brain regions, or organs, or tissues.

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The process of stem cell into a specialized cell, and how they migrate to each other to

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form different aspects of the human body.

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This episode will expand on the cause of autism episode to explain more detail.

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This episode fills in what is happening simultaneously and slightly downstream.

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The cause of autism episode explained how our living organism is created, at least an introduction

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to it.

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This episode picks up essentially the developed cell, and this is regardless of normal developed

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or abnormal developed.

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In addition, we will cover specific timelines of cell life and the embryo, and into about

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three years old postnatal.

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As to remember from cause of autism, let's call them ingredients, light, as the driving

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force of living organisms.

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Remember the energy source, the electromagnetic strip, the photoelectric effect, and water,

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magnetism, and the elements from the periodic table.

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Remember we use some of these elements, and then a subset of the ones that we do use, a

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subset we use a lot of those.

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But also remember melanin as the target for that light, and melanin being black, to absorb

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all of the light's spectrum.

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Don't think it's black for this.

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Think.

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Our body, our biology, our evolution, chose melanin to do this role.

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Remember POMC, as the source for melanocyte stimulating hormones, alpha, beta, and gamma.

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These are in cells, organs, and tissues, all through the body.

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Later, I will show you how this is proven as an implication to autism, accidentally.

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In a paper we will spend most of the episode reviewing.

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The paper proves light and melanin is a cause without saying it is a cause.

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Remember vitamin A and tryptophan, and their roles in eye development.

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Eye development generates brain development.

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Vitamin D and tryptophan, and the skin.

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TPH1 for the skin and gut, which helps create our body.

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And TPH2 for helping to develop the brain.

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TPH is tryptophan hydroxylase.

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And remember proteins are semiconductors.

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And remember the amino acids.

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We have 20 amino acids.

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Tryptophan and methionine are codes for DNA and protein sequencing.

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Tryptophan and methionine are special, whereby they have one codon.

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And they sequence proteins and DNA.

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Tyracine is the special start signal.

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Tyrosine is huge too.

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Remember the aromatic amino acids.

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All of these so called ingredients use certain wavelength of light.

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They require the certain wavelength of light to function.

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We've covered, and I would even say we've established, common themes in the biological

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development are implications to the cell and the synapses.

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These are common themes with autism.

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The cell meaning proliferation, differentiation, migration, development, and the synapses.

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Development, growth, and the functions.

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So let's explore something.

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Autism spectrum disorder, living biology.

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This is the paper I want to review from Transin neuroscience.

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It is a paper from Cell Press.

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Recently there's a conceptual and paradigm shifts towards a focus on the abnormal prenatal

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processes underlying autism within each individual.

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From specific abnormal development to early clinical stages.

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Remember cells divide.

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They increase in number.

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So cell proliferation.

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Increasing cells as a result of growth and division.

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Proliferation is becoming mature.

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Cells become specialized, unique, or distinct types.

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These are stem cells can become nerve cells, which we mostly discuss in the podcast.

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They can become immune cells, muscle cells, organ cells, blood cells, epithelial cells,

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which is important in the light as a cause, hypothesis, and melanin is inside all of these

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cells.

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Migration, once mature and specialized.

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Into one of those previous mentioned cell types, migration is like building blocks that

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allow a formation to occur.

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Such as creating the nervous system, or an organ, tissues, or muscles, and so on.

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Let's review some timelines and the developmental milestones.

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First trimester, starting at roughly four weeks.

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Proliferation and neurogenesis occurs.

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The beginning of neurons, or cells.

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Lasting to around 26 weeks.

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This is prenatal.

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This is the embryo.

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Cell migration begins at 10 weeks or so.

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And this lasts until 32 weeks.

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The second trimester, neuro-ight overgrowth at 14 weeks to roughly three years of age.

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So roughly at the end of the critical period that we've discussed quite frequently.

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And synaptogenesis and synapsis function begins at 20 weeks until around age three.

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And the third trimester, neural networks, the formation and functioning.

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Once specialized, they start to begin these networks that develops the nervous system and

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so on.

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This starts at 32 weeks and essentially this is continuous through the lifespan.

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The paper distinguishes epoch one as trimesters one, two, and three.

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And epoch two, trimester three.

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So trimester three is split between both epochs.

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Epoch two is trimester three into early postnatal periods.

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Let's call it that three years old.

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Epoch two is more brain specific or if another type of health condition implications to these

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areas occur.

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Remember, autism just shows up.

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It doesn't necessarily mean if you have a problem.

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It doesn't necessarily mean that problem will cause autism.

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It might cause something else, something similar.

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And this is the case with most health conditions if we go that far upstream.

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For our topic, autism is a brain development is a region of interest.

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This is covered in previous episodes, episode three, four, and five and in autism and light,

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the cause of autism episode.

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Disruptions here include neuro-right overgrowth, synaptogenesis and wiring or connecting those

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highways of communication.

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Remember I said highway, but some connections could be more like a gravel road.

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Remember myelin.

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Remember these connections differ.

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And this is how cells communicate.

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At each synapses, a cell receives a brief summary about what must be occurring for this cell

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to connect here.

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With each connection, the summary adds and creates a story.

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Another implication or expanding on the migration slash brain development because this is the

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process these cells are migrating and creating the brain.

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Brain development and dysfunction with how our regions or networks form.

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Of course, that ought to make sense to us.

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However, the crucial part is the timing of it.

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Remember these episodes, autism and adaptive responses, autism and silence network.

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Remember our discussion with Dr. Leanna Hernandez and the boy versus girl differences.

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Back to the silence network, remember the UCLA paper came out in 2024.

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The paper I am mostly referencing about being able to predict profound autism.

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Remember the conversation with Dr. Catherine Lord and I mentioned this.

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It has to do with the brain organoid.

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The paper predicting profound autism and this paper from trends in neuroscience discussing

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the embryo is from the same researcher.

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This researcher does wonderful work from UC San Diego.

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Okay, the trends in neuroscience paper.

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This paper mentions risk genes, a common topic with autism research.

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Specific risk genes are risk genes that we've covered on the atomic level and with general

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descriptions in mostly episodes 3, 4 and 5.

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These include phosphorus, phosphorylation and p10 and protein kinase B.

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These involve cellular metabolism.

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Previously I said autism and type 1 diabetes could be related upstream.

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These are the regions of interest.

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Diabetes will involve POMC too, a product cleaved from POMC for insulin.

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That's my thought.

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Remember implications upstream look differently downstream.

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They have different so called clinical presentations or different health complications.

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Now I didn't say autism and type 1 diabetes are the same or one increases the risk for

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the other.

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I'm saying upstream.

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Many shared regions of interest are present.

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Anyway, I won't mention the trends of these each over the past 50 years or even let's

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say the past 20 years.

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Again, at least not now.

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Also MTOR is involved here in the paper.

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I mentioned possible hope with MTOR when originally discussing p10, a paper from Cell Press.

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This was in episode 3 at the beginning.

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Lastly from the risk genes discussed is a pathway that play a critical role with embryonic

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development.

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Everything mentioned, I believe, are components of the cell development.

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And this risk gene also contains mitogenic processes.

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Mitogenic mitosis.

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This requires UV light.

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This is the spot to explore for autism.

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The time is in the embryo.

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We've connected early findings postnaturally at 6 weeks old.

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Two studies.

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We've discussed two studies here.

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The Sanis Network from UCLA and the brain organoids mentioned earlier predicting profound

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or more severe autism from UC San Diego.

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I bring this up for two reasons.

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One to expand and prove light as a large possibility as the cause of autism.

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And two, funding and research must go here and stay here until proven otherwise.

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This stuff on older children or adolescents, this research likely will not provide much

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to the world.

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At least not at this time.

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Research ought to move to the pregnant woman because at this point every child seems to

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be at risk for autism.

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If we go by the 1 in 20 boys data and the possible misdiagnosed girls from the gendar

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findings, it appears the assessment tools are boy biased because the diagnosis result

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is boy biased.

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But if girls or females have more social motivation that autistic boys are similar or more social

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motivated based on brain imaging and connectivity, then non-autistic girls and non-autistic

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boys that data could be misleading too.

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Regardless, I don't want to discuss assessments now.

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The timeline ought to go to the embryo and the cause is cell dysfunction in this development.

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Okay, let's discuss some specifics of abnormal brain development in the prenatal.

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These are postmortem, proliferation, these are averages.

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Autistic children have 67% more prefrontal neurons than non-autistic.

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This includes 79% more in the dorsolateral prefrontal cortex.

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Remember the subdivisions.

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The dorsolateral prefrontal cortex is involved with things like working memory and task switching,

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planning, inhibition, and interestingly, abstract thinking and a 29% increase in the medial

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prefrontal cortex, that subdivision that we discussed in autism and adaptive responses.

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Now you hear that there's an increase of neurons in these different subdivisions for

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autistics.

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But this does not mean that these areas are better.

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They are, they function better.

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Remember the poor connections out of these areas.

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30% more overall in the cerebral and 57% more von economo neurons or cells.

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These are spindle neurons.

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Remember from Autism and Adaptive Responses episode.

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There is an increase of these spindle neurons in the insula.

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Remember the insula, that hotspot, that regional hub that receives bodily information, brain

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information and integrates it with how the living organism is navigating society, navigating

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the outside world.

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And the ACC.

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Remember in the adaptive responses episode.

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When we make healthy and adaptive responses to the flexible rules that are going on in

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socialness, going on in society, the outside world is very unpredictable.

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When we make healthy choices, the medial prefrontal cortex and the ACC lead the way.

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They lead those adaptive responses.

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However, whenever we have trouble with responding to the environment or responding to our body,

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the insula kind of overtakes the prefrontal cortex and that ACC.

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And it kind of leads the way.

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It allows the body to overtake the brain essentially.

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And these are specialized cells that are only found in larger primates.

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They're not across all species or even all mammals.

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These are involved in social emotional processes.

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So social emotional processes.

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It sounds like an autistic phenotype description.

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A highlight of these data are this occurs between 10 and 20 weeks in the embryo.

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But postnatal.

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Okay, now a common theme with autism is excitation.

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The excitation inhibition balance or imbalance.

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Cell proliferation regarding excitatory cells.

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A recent study exploring 102 common risk genes linked to autism.

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71 of those 102 are involved in excitatory cells in the cortex.

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Add this to the data of inhibitory implications in the striatum.

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And with two glia cells, oligo dendrocytes and astrocytes.

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Remember the striatum.

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A hot spot for motivation and movement.

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Motor movement.

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Also think the reward areas.

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Remember the discussion of the nucleus accumbens.

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And then those stimulus responses.

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So here we just mentioned the ventral and the dorsal striatum.

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They are reflexes and deliberate, go directed activities here.

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These include socialness.

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These also include what is salient to us.

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And for autistics, what is salient is mostly staying within ourselves.

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In one or few interest at a time.

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Remember that biology that gives us autism allows us to be comfortable within ourselves.

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That's preferred.

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When I say motivation, it is not limited to deliberate wants or deliberate needs or likes.

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I think what motivates the nervous system to return to comfort.

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Those actions become the motivation.

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I know some discussion on genes.

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And I know it is a hot spot for research and funding.

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I don't love it.

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You heard Dr. Lord say, she is unsure if this is the way.

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What it will even do.

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My position is I would rather spend time and money understanding the cause.

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Such as the artificial light over the genetic implications.

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I understand the genetics are implicated.

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The genes are implicated.

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The cells are dysfunctioned in various ways.

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But why?

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I suspect this is because medical treatment can be designed, developed and sold.

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Sold at large volumes.

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Then profit.

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Profit is our medical paradigm.

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The most popular medications for autism.

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Yes, that's interesting, right?

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The most popular come from anti-psychotic classification.

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These are anti-psychotics.

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Given to autistic individuals, there are a couple of different things wrong here.

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One, the family, the loved ones of the autistic children, they are vulnerable.

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They want their child to have relief, to be able to fit in in society.

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They want their pain and struggles to be reduced or eliminated.

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And the medical profession with their training is designed to prescribe medications.

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Try this.

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Try an anti-psychotic or SSRI or antidepressant.

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Because the child needs to interact more.

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The child needs more friends to be able to be comfortable interacting.

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The child needs more diverse interests.

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They need more hobbies.

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The child receives complications in social settings whenever there is over-stimulation.

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So let's try medication to calm the child, to calm the individual so that they can fit

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in better and easier to be around and be accepted in society.

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I only bring this up because I have concerns.

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I have disagreements with medication use for autism, especially medications that were developed

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for other conditions.

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We mostly just throw medications at everything.

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Try it and if it doesn't work, we'll try something else.

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And I'll tell you two reasons why it's concerning to me.

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It's very suspicious.

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One is rarely do you get any informed consent.

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You just get the prescription and maybe the physician or the PA or the NP, etc.

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will give you just a off the top contour, just a few side effects or a few implications

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that that happen in a very questionable trial.

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The second thing is the second concern and probably even more concerning than the informed

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consent is the medical paradigm, the accreditation.

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They cannot prescribe prescriptions fast enough.

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So over time, they developed these nursing roles that are the role is to prescribe medications.

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They are trained and their role is to prescribe medication, medication management.

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Look at the health trends.

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Look at around that society to observe each other.

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Let's go back to 1960 and then 1980 and near 2000 and 2022.

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And let's break down age from birth to nine years old to 10 to 19 years old to 20 to 29

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years old.

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So on until we get to 90 years old.

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Let's look at the number of prescriptions given in each decade of lifespan from the

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60s, the 80s, the 2000s, 2020s.

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That increase is going to be wild and nothing's changed.

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Nobody's healthier.

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Just today, neuroscience news released a, they highlighted an article.

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This is cancer drug as a possible autism treatment.

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Okay.

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One, how is this even discovered and what is going to be the purpose here?

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But two, more discerning is clicking on that link.

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It's not even autism.

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The cancer drug would help Rett's syndrome, which has been kind of compared to autism.

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And it's a separate thing.

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It's a syndrome.

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Syndrome's mean not a lot is known about it or what you do about it.

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This came from UC San Diego as well.

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This was very disappointing in my opinion.

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However, remember, autism just shows up in human biology and human evolution.

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Everything in the normal biological processes changed.

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That change appears to be light and all of the new health trends supports both.

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Both meaning the change and the profit.

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This specific paper from trends in neuroscience highlights autism as a multi-organ disorder.

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Of course, the primary one is the brain, meaning the biggest complication in autism is the brain.

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But this is huge.

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It is huge because of the light story and melanin and POMC.

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The paper highlights all of these separate organs implicated in the autistic phenotype

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and the autistic individual.

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And there's a large list.

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Now it doesn't mean that every one of these are implicated or abnormal, but there are

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a lot of shared implications throughout the body, which we've discussed.

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We've discussed in this episode even.

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The what is going on upstream, those implications will show up differently and sometimes in multiple

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ways.

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You've heard of sequela or you've heard of a health condition causing other health

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conditions.

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All of these areas are dependent of melanin and the light to drive nonlinear optics.

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Amazingly, this is amazing to me.

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I was reviewing melanin and leukocytes.

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Just chuck it up to one of those B3 fixated interest.

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I'm just looking at melanin and where it is throughout the whole body.

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And I just happened to stumble upon this this week.

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Melanin and leukocytes from the 1960s.

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This has already been known since the 1960s.

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How many people know about melanin being in white blood cells?

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And for those listening, leukocytes are white blood cells.

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How many researchers and scientists on autism know about melanin being in white blood cells?

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They know autism is linked to immune and inflammation.

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This is huge.

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These are huge findings.

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This proves.

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This suggests these immune problems and the inflammation problems.

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And we've discussed the mitochondria problems and all of these cell implications and subnaptal

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genesis and subnaptic connections.

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All of these are kind of dysfunctioned.

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But now they're linking other bodily processes, other organs and tissues that are seemingly

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unrelated.

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This supports the light theory.

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Light is the only thing at this current moment that is making sense.

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The past three episodes we've outlined some critical things here about the causes, about

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what's implicated in these causes, and understanding even the rates of diagnosis, and how much

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light has changed during this timeline since the 1930s.

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Not only has the light changed, but the amount of time and how humans have shifted behaviors

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more indoors under artificial light and surrounded by technology light and less time outside.

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And this is showing up now in the lineage.

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Remember those timelines discussed previously?

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Remember that blue light chromophore, melanopsin?

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Remember it wasn't discovered until 1998 and then fully understood the sequencing until

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years after that, a couple of years after 1998 in the early 2000s.

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But now it's known to be across various aspects of the brain, deep inside the brain in roughly

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30 regions of the brain.

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It's in tissues and organs, epithelial cells.

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And remember it's a chromophore, so it activates based off of specific light wavelengths.

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And the melanopsin is around 480, it peaks at 480 nanometer, which is blue light.

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Modern light is blue light.

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It's in the shorter wavelengths.

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And our shifts to this type of lighting runs parallel with the rates of autism.

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The timelines fit.

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Lastly, this blue light wavelength light shuts down.

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It implicates palm C. The pro-opioid melanochortin subdivision of the hypothalamus that cleaves

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many crucial parts of our biology, including the melanocyte-stimulating hormones.

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This is underrated in the research of autism.

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This ought to have attention, but it has no attention.

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And that is a concern to me.

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So I hope to help bring attention of autism and light, but not only just autism.

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The health implications, because of how the human body uses light.

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If you are listening to the podcast or listening to the episode, please feel free to leave

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a review or rating.

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And podcasting reviews, ratings, and downloads are huge.

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And I very much appreciate your feedback.

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You can contact me on X or Facebook or email info.fromthespectrumatgmail.com.

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Thank you for listening to From the Spectrum Podcast.