Welcome to From the Spectrum Podcast. This is a podcast about autism. It is my
goal to explain what is autism. I intend to use a mixture of scientific literature,
personal experience, and opinion. With opinion, I will explain why I feel the
way I do and 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 discuss biological aspects implicating the excitation
and inhibition balance. The EI balance is a worthy discussion with autism,
and a lengthy discussion. Today's episode will be part one of a two-part series covering the EI
balance. Notice not all of these topics of our biological mechanisms covered, or a cause
of all cases of autism. Autism is a genetic patchwork, not one gene, and not all gene
implications reach autistics in the same manner. The cause of all autistic phenotypes are unknown.
I want to warn you, you need to know some literature, and even some literature I have
shared on autism are attempts to create pharmacological help. This has concerns.
This has concerns because of our medical paradigm, which likes and maybe even prefers
prescriptions as the first line, as something that gets lots of financial backing.
And it isn't hard to know why. I want you to understand autism, and I want you to make informed
decisions. For the excitation and inhibition, we will discuss sensory, social, emotional,
emotional, mnemonics, and some specific cell types, glutamate and GABA. We will cover cortical
networks, memory, information processing, pattern learning, and plasticity. No, neuroplasticity,
which is how we are shaped, shaped in our ways, our preferences, habits, comfort, and more.
We will cover brain derived neutropic factor, or BDNF, and N-Methyldeaspartate, or NMDA,
and AMPA. Now feel free to look up the long form scientific nomenclature of AMPA. It is long,
and maybe not necessary for our discussion. However, those three receptors, or biological
components, are excitation. We will also discuss neuromodulators and melanin. And we will also
discuss certain brain regions, some of these we have mentioned before. With the EI balance,
or imbalance, too much excitation creates a noisy brain. Think unstable cortex, lots of energy
potential. Now imagine the EI balance. I will use balance, but it's basically an imbalance.
Think about a C-cell. Excitation on one side, inhibition on the other side.
Remember, excitation turns cells on, activates regions and systems. The cell is named glutamate.
Inhibition turns regions and systems off, inactivates, or quiets things. This cell is called GABA.
Glutamate is excitation, GABA is inhibition. This imbalance is either an increase in excitation,
or a reduction in inhibition. This implicates perception, memory, cognition, and motor control.
Think about stemming, think learning about a world around that seems chaotic and overwhelming,
and our future preferences of what we are and who we are. You will hear cortical and subcortical.
Cortical is the cortex. Think of what makes humans the superior species on earth. This is where our
higher order functions occur, things like decision making and functioning and language and so forth.
Subcortical is below the cortex, used for memory, emotion, pleasure, valence, or how we perceive
our feelings. Evolutionary, subcortical areas are much older. Think reflexes. Think people being
more impulsive or lacking emotional regulation. The cortical areas intends to quiet the emotions
and feelings of the subcortical area. Let's quiet things so we can properly evaluate things.
Remember, synaptic processes are where cells travel to connect and communicate. In the brain,
areas become preferred. The more synaptic thickness or morphology exist at those connections.
The brain and the nervous system passes things off to what is easiest for them.
We are who we are for that reason. EI imbalance implicates synaptic and myelination functions.
Remember myelin. Turns a gravel road into a paved road to improve the cells' travel.
Subcortical areas and cortical areas communicate back and forth to each other.
Ultimately, it wants to quiet the noise while considering survival functions.
Now you can see, people with and without autism can have trouble with this.
The EI imbalance is not just present in autism.
Cortical areas are hypersensitive to sensations. These perceptual areas that allow the person
to properly evaluate the sensations they are receiving from the outside world.
This is all sensations, or some with autism have trouble with certain sensations
and are better at others. GABA is crucial for sensory processing.
A lack of GABA implicates downstream processing and quieting cognitive behaviors.
GABA modulates the flow of information in the thalamus, a place that processes all sensations
and helps modulate our attention. Now, we are talking about autism, which means we are born
with it or it is developed early, likely on that critical period, that early stage of our
critical development. If sensations are overwhelming or perceived as difficult at this time of the
critical period, it implicates maturation of these processes, the process of developing.
When exposed to challenging exposure, this closes the window of the critical period
prematurely. In other words, our perception of the sensory going on implicates how long the
critical period lasts. Some things to know, the critical period is an accelerated time,
meaning lots of learning and understanding and development. GABA, which is inhibitory,
remember GABA is inhibitory, GABA in the critical period is excitatory.
Think about it. Perhaps the purpose is to not limit the processing of physical phenomena
of the outside world. GABA turns or is created excitatory to accelerate that development period.
Think about how easy it is for children to learn in this time, including multiple languages.
Also, brain-derived, new tropic factor is the primary signaling source in the critical period.
BDNF is powerful for the human brain. It's powerful because it regulates myelin.
In autistic brains, data show larger brains in childhood. They are larger, in large part,
because of myelination. BDNF also is a component of neuronal growth, neuroplasticity, learning and
memory, which is essentially neuroplasticity. BDNF helps regulate glucose. BDNF are similar
to insulin-like growth factors and act on survival genes. Therefore, BDNF are crucial
for cell survival. Remember last episode, remember the rapamycin, the mTOR, discussion and autophagy.
BDNF is critical for metabolism. Remember the discussions on brain energy, how the brain
changes blast-out energy. BDNF has a high affinity, meaning it loves the tyrosine-kines receptor.
Something highlighted in research about neurodevelopmental conditions is that tyrosine
receptor over expression of BDNF is shown in epilepsy. Remember they commentize with autism
in epilepsy. So earlier I just mentioned tyrosine. Tyrosine makes dopamine, epinephrine, and nor
epinephrine, which is essentially adrenaline, and it also makes melanin. Tyroxine, all more components
of functioning and functioning with energy. Melanin and dopamine does much more than what you know
in the human body. For melanin, you probably know about hair, eye, and skin color, which is mainly
alpha-melanocyte-stimulating hormones, or AMSH, which is cleaved from POMP-C in the hypothalamus.
I know, irrelevant information may be here for our discussion, but I am autistic and I love that
topic. We're going to talk about some dark and deep melanin though, much different than the skin,
hair, and eye color. We're going to talk about how melanin is used for energy and cells firing
and functioning. Melanin comes from tyrosine. Tyrosine, like tryptophan from our last episode,
is an aromatic amino acid, meaning it activates for UVB light, which is around 260 to 280 nanometer
light. Starting in the eye, a source for many complications for autism. Think eye contact
and looking inattentive and simply the eyes are a source of most of our sensations. We navigate the
world in large part through the eyes. And think about development. Let's think about how the eyes
help our downstream processes in development. Sunlight hits the eyes and regulates development.
Physiology, neurotransmitters, remember the tyrosine and the tryptophan. So here we're talking about
groups like monoamines and catecholamines, which are a group of neuromodulators lumped together
based off of different functions. Now, the human body has about 40 days worth of catecholamines.
These things are deletable and renewable. And without any chronic disease or lesion,
we can always make more of these. But we can see, such as during the winter time,
when the UV light is not as present, people's moods and the way we act and feel suffers.
And that's because these aromatic amino acids require the UVB light range for activation.
In addition, it helps development of the hormones and the energy, including metabolism. In contrast,
modern light implicates those above, especially at the wrong time of day.
Remember, autism was first observed in the late 1930s. So the 1930s is one to about one and a
half generations after electricity and the power grid, 1893. Know this. I have to play a brief game
of the tug of war with barbed wire here. As society is exposed to more artificial light,
especially blue light, and we are less exposed to sunlight, diagnoses of autism increase.
And this is a sharp increase. The light for the developing child is vast. Maybe everything.
Remember, the brain and skin come from the same place and are connected through neuroectoderm.
The skin is the largest endocrine organ in the entire body. It's a solar panel for the energy hog
that is our brain. Those aren't my words, but they are accurate words. Now back to melanin.
In the eye, melanin comes from the retinopigment epithelium, or RPE for short. It provides dark
pigments for the light receptors in the retina. Also, melanopsin, which regulates all
non-image forming processes with physiology and hormones and such, that is done by a
monosynaptic connection, which is bizarre in our biology. Monosynaptic means a direct connection,
and this spaces out from the back of the eye to the midbrain and the hypothalamus. It's a long
connection. In the hypothalamus, there's a nuclei called supracrasmatic nucleus, or SCN for short.
The hypothalamus is subcortical and a place where endocrine processes meet cellular processes,
so they can orchestrate together in perfect synchrony to carry out the biological processes
in perfect concert. The SCN controls this. The SCN is the master clock of our biology.
All cells, all tissues, and organs start with the master clock before those things take flight
and work, become active. There's a clock at the beginning of the process. That has to be
in sync. That needs to be in sync. Melanin and melanopsin are all over the brain.
It's important. Melanopsin was first discovered in the human eye in the retina in 1998 by Iggy
Provincio, and then critical discoveries in retinal ganglion cells during the next six, seven,
eight years or so. Melanopsin is still being discovered across the human body, including
in the brain, no fewer than about 30 regions in the brain in 2017 and 2018 or so, so not long ago.
This presents lots of curiosity and concern. The biggest concern is most, indeed most,
of artificial light is blue light. I'm talking about LED, tech screens, TV, that's blue light.
Light, like incandescent, is mostly red. Candles and fireplaces are mostly red and infrared.
In short, those longer wavelengths, red and infrared, they have less harm to the human
biology. There's less photonic energy. Furthermore, why modern light is so critical to melanopsin,
melanopsin activates for 480, about 460 to 480 nanometer light. That's blue light. So anytime
you have blue light exposed to the human body, it's implicating melanopsin somehow.
Evolutionary, we want that blue light because when we're outside, most of the light we see,
most of the color we see, is blue. Okay, why is this a topic? It is most certainly a topic
because of the implication to brain development at all stages of human life, from embryo to the
other end in older adults. And this covers from autism to neurocognitive or degenerative diseases,
like Alzheimer's and the dementias and so forth. All of these conditions are new in the medical
world. Melanin and melanopsin implicates all the things we covered with the synaptic development,
migration, cellular health, and so forth, including the neuroplasticity. Remember, becoming what we are
and continuously becoming what we are through changing from habits and learning. This is a
continuous process. Neuroplasticity doesn't stop. Implications in melanin and pom-C possibly
allows sensory cells to shift based on how it is perceiving the outside world, the outside
environment. Melanin dysfunction can also implicate cortical communication and connection.
Kids in developmental stages have broken processes in their skin, their eyes, and circulatory system,
which features the heart, blood vessels, and blood, making indifference to the outside sensations
and complications. Now we covered in criteria B some of these symptoms. Additionally, our modern light
implicates this melanopsin protein and downstream distal connections because all opsin have a weak
covalent bond to vitamin A or 11 cis retinal and blue light wavelength breaks this bond. It destroys
the blood vessels and this regulates plasticity and connections, including, certainly, including
complicating excitatory and inhibitory processes. Melanin is the screen. Sunlight is the light
beam and the sun is the projector and every piece of that three-step process must function properly
to organize our biology properly. Anything broken or time delayed presents chaos and just like that,
just like the warning earlier, the broken processes upstream can manifest differently downstream,
meaning there are many genetic implications to autism, but those same genetic implications
are also seen in other disorders and conditions like OCD, TICS, Tourette's, schizophrenia,
focal epilepsy, Vret syndrome, fragile X syndrome, and so forth. In other words, as we have problems
upstream in our biological processes, by the time we get downstream, they present differently. It
manifests differently. It can look different as the process unfolds. This explains the spectrum.
This explains why there are many inconsistencies with autism and a lot of unknown factors.
I know we covered a lot of biology here, a lot of areas, but understand humans evolved under the sun
and the sun was the primary light source. Today we have many light sources. We also have photo
receptors all over our body and the photo receptors in our biology that we have evolved
to become are implicated today. Recently things have changed. Our world and our environments
have changed. We cannot understand autism unless we understand these areas and the purpose of these
areas. And I'm talking about our biology. Despite melanopsin being discovered in 1998,
it predates humans. In other words, it is a crucial part of many species biology and development.
Before humans evolved on earth, other species, and that's not limited to just mammals,
have had melanopsin. Lastly, think about all of our new modern diseases such as autism,
diabetes, both type 1 and 2, obesity, all the recent new cancers and the rates of cancer,
and all of these new neurodegenerative conditions, all of these aging diseases that are just increasing
too quickly. Everything I just named are increasing much too quickly. I don't understand why we don't
look someplace else. Think about all the cardiovascular diseases. Melanopsin is in tissues. Our environment
is changing and so is our biology. If you would like to contact me, you can reach me by email
at info.fromthespectrumatgmail.com. And thank you for listening to part one of a two-part series
covering the excitation and inhibition. And most importantly, thank you for listening to From the
Spectrum podcast.