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

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With opinion, I will explain why I feel the way I do and 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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The From the Spectrum Podcast will mostly avoid causes of autism.

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And I will try avoiding the increase of diagnoses of late.

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This is like playing tug of war with barbed wire and I don't think I want to travel down

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that path.

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For today's episode, we will spend time preparing for a future episode on the balance, or imbalance,

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of excitation and inhibition.

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Inhibition is activating, turning cells on, and this can be locally, within a specific

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region of the brain, or brain areas, or this can be distal, or activating whole systems,

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regions, or critical parts of the nervous system.

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That is excitation.

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Inhibition is the complete opposite, inhibition turns cells off, turns systems or regions

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off, and this can be locally or distal.

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Inhibition quiets or stops things.

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So for today's episode, we will discuss a few known genetic factors associated with

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autism.

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We will discuss the implications to our biology that leads us to the deficits in social communication

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and interaction, the sensory processing problems, and the restricted and repetitive behaviors

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briefly discussed in the last two episodes.

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We will cover what is going on upstream.

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Now, I will have a moment when I touch on a significant region of interest of our environment

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that is a cause.

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This is rare, and I will not make it a habit.

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However, for this episode, we have two objectives.

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One, learn about the biological aspects, and two, prepare for the Excitation Inhibition

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episode.

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The first item is P10, which is short for Phosphate and Tensin.

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P10, P-T-E-N.

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P10 is a loss of neurons or cells, cause overgrowth and increase excitatory synapses,

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formation, and function.

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Synapses are how cells communicate, connect to each other.

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A major theme today involves the synapses and the synaptic cleft.

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There's small space in between the cells and how they communicate and connect.

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More on that in a moment.

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Further, P10 loss is involved with neuronal, hypertrophy, hyper-excitability, seizures,

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remember the closeness to focal epilepsy, and other autistic-like symptoms.

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P10 implicates soma size, migration, spine density, and dendritic overgrowth.

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A lot of biology here.

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For the soma, the soma is the cell body, cells and glia cells.

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The soma is the area dendrites branch off and give the cells multiple paths to communicate

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and travel.

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Migration is how cells form and develop.

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They migrate to common areas for better communication and forms spatial relationships.

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Staying of it as moving closer to friends and family.

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Moving closer to what brings you together, the common factors.

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Spine density helps communication within the cells and the destinations.

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Certain cells have and need specific amounts of spine.

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Finally, dendritic overgrowth.

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One idea is synapses strengthen dendrites and causes them to grow.

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Think of it as a big tree with many thick branches and then compare it to other less

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dense trees.

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Regardless, the nervous system and how we live and operate as a living organism needs

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proper sizes of these biological components that help cells operate.

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Dendritic growth essentially is how we organize and connect ourselves inside with the outside

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and vice versa.

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So really, we are talking about how cells act.

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How they act and function when called upon.

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Are they doing what they are supposed to be doing or not?

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P-tendis function is linked to inhibition abilities and glia cells and burst firing and

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action potentials.

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Again, are the cells acting like they should?

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And is their vehicle functioning and are their roads they travel down appropriate?

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This brings us to some glia cells and myelination.

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When cells fire, they need to fire efficiently and in the correct direction.

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Synapses is like turning a gravel road into a highway.

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The highway acts like to cells path traveling to the synapses.

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Into the cleft.

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Into the connecting synapses.

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Normally, the cleft, the space in between is 10 nanometers.

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You cannot imagine how small this is.

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There are 1000 nanometers and 1 micrometer, also called a micron.

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1000 nanometers for 1 micron.

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The thickness of a sheet of paper is about 80 microns.

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I wonder if the cleft is implicated with autism.

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Maybe in some parts, like those hyperconnected areas.

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Maybe they are smaller and larger.

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I don't know, I'm just thinking.

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I'm just thinking if this is something involved with autism.

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With P-tend, scientific literature offers hope.

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The hope is rapamycin.

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That's called mTOR, which means mammalian target of rapamycin.

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A side note, if you pull up research on aging or longevity, rapamycin is likely involved.

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Rapamycin and NAD are extremely popular regions of interest for aging and longevity.

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Okay, so what is it doing for autism?

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A complex of rapamycin, and don't worry about the specifics with each complex.

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Just a function of it.

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A complex of rapamycin, the data show prevention of increased soma-sies, proper migration and

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spine density, and dendritic growth.

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MTOR regulates cellular health whereby anabolic cell growth and catabolic cell death.

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This is why it is so crucial in the aging and longevity literature.

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Cinescence always wins.

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In other words, senescence, how we age and break down, is undefeated.

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Next is 16P11.2.

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Think of a deletion in our biology.

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Deletion and duplication are common with the genetic functioning.

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This is an implication to our serotonin.

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Serotonin comes from the RAFE.

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The RAFE is at the brain stem and responsible for the serotonergic release in the brain.

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The dorsal RAFE connects to the ventral striatum.

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They communicate.

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Remember the discussion on the striatum.

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A region of interest for us.

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Specifically in the ventral striatum is the nucleus accumbens.

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The nucleus accumbens is one of the most fascinating areas of the brain and body.

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For a brain region, it is large.

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And it has two parts.

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A shell and a core.

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There are serotonergic receptors in both.

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The nucleus accumbens is related to motivation, emotional processing, learning.

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It has a significant amount of NMDA receptors that are crucial for learning.

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It is also involved in reward prediction error, pleasure, addiction, and analgesia or endogenous

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pain response.

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Now, essentially everything named here can be drawn back to autism.

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A crucial part of the nucleus accumbens is socialness.

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A future episode will dive into the roles of oxytocin and vasopressin and socialness.

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Specifically, autism versus non-autism, extroverts to introverts, and interesting.

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Female autistics and male autistics and reviewing some work by the Gendar Consortium.

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However, for the sake of today's discussion, the serotonin system from RAFE to NUCULUS

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ACCUMBENS and the implications to socialness is an interest.

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Likely, in the near future, cell-specific targets of serotonin and the NUCULUS ACCUMBENS

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could rescue social deficits.

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If decided by those with social implications caused by autism or any other social disorder

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or problem, if and when this becomes an option, you have to make that decision.

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See the links below from Stanford.

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I want to do a hard stop here, a very hard stop, because it needs to be conveyed.

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It needs to be known.

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I will not make a habit of this, but serotonin is synthesized from tryptophan.

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Tryptophan is an aromatic amino acid, which is a type of protein, a very special type

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of protein.

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This is critical and not well known information.

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Tryptophan makes serotonin and melatonin.

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Okay, so what's the big deal?

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The big deal is, as you know, autism came around starting in the late 1930s.

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Tryptophan, being an aromatic amino acid, activates for UVB light wavelength, specifically

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around 200 nanometer light.

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That's within the UVB spectra.

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Over the past 130 years or so, humans are responding to the shift in the light sources.

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This is true, and we are poorly responding to it.

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This is true too.

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Proteins and gene expression and various aspects of our biology responds differently and requires

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different types of light.

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This is true.

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For instance, do you know anything about melanopsin?

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Autism is a downstream cause of the shift from sunlight source to the artificial light

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environment that suffocates us today.

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And the circadian rhythm mismatch.

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We have the ability now to extend the day to see light after dark.

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Human biology has not evolved for that type of environment.

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You can look up any health trend and notice that we are trending in bad directions.

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Few, if any, of our health measurements are doing good.

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Many things are on the rise like chronic diseases, Alzheimer's, diabetes, autism, and so forth.

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All of these are new in the medical literature.

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Know this.

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Know this about light sources and our biology and the various functions of the photoreceptors

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across our body.

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The brain and skin are connected, extremely upstream, much farther upstream than the genetic

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implications that we are discussing here.

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The brain and skin are neuroectoderm.

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You won't hear that.

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You won't hear that any place else, essentially.

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Like amino acids, activate all three of them for UVB and fluorescent for UVA, roughly 353

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nanometers.

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You won't hear this on any other podcast about autism or any university or research

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center.

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Being involved with the centralized paradigm.

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But if you do, please reach out to me and give me their information.

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Discussions like this, we need those discussions so we can understand what is going on recently

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with our health.

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I will provide a link and a warning.

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This will offend your beliefs.

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So already we got you.

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Already that says something.

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Will you take a step towards that path of critical thinking and explore these subjects

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and topics that I just communicated to you?

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These things are somewhat obvious if you know the biological processes.

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Or will you simply take the easy path, the centralized path, and shut it down?

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Now back to the genetic discussion.

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With 16p112, there are implications with excitation and inhibition.

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That is an imbalance between the two types of cellular functions.

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Two cell types.

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All of this information today is a step up to properly cover the EI imbalance.

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16p11.2 implicates cortical development.

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Same as the artificial light mentioned previously.

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That has severe implications to our cortical development.

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Just like the light sources I mentioned earlier.

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And the myelination, brains in our biology aren't developing properly.

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16p11.2 implicates that cortical development.

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But what is not known is unknown.

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That is causing the complications with these things that we're discussing today.

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Remember the artificial light exposure.

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Remember that tech light exposure.

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Remember the protein that I mentioned with melanopsin.

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And remember the circadian mismatch.

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Humans, modern humans, are essentially the only species with a circadian mismatch.

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It's wild.

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And remember the lack of aromatic protein activation.

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Remember these modern world problems.

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Remember the development of electricity and that power grid.

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And remember autism came about as early as the late 1930s with Leo Kanner and Hans Asperger.

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Next is calling 3.

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Or call 3.

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C-U-L 3.

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Call 3 is a gene that makes a protein called callin 3.

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Call 3 is highly associated with autism and other neurodevelopmental disorders.

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Now you know how I feel about the word disorders.

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I don't really like it.

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In the critical stage of development when we're young, call 3 is a part of a pathway

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connecting 16p11.2 proteins to determine brain development.

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A call 3 deficiency in prefrontal area implicates social interaction and sensory gating.

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Or a way of determining sensations to perceptions.

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How we respond to physical phenomena in the environment.

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Remember with autism it is typically referred to as an abnormal response to our outside

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environment.

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Call 3 is associated with this.

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Also, call 3 deficiency causes low functioning in NMDA, that learning receptor I mentioned

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a little bit earlier.

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Call 3 deficiency also implicates stereotypic behaviors in the striatum.

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And lastly, neuronal excitability, that crucial EI relationship.

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The whole reason we are exploring this upstream components of our biology.

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Next is shank 3.

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Shank 3 is well studied in autism.

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Shank 3 is involved in tissues and brain.

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It involves synaptic connections or how cells connect and speak to each other.

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Shank 3 also involves the dendritic and spine formation.

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So more of that, specifically shank 3 encodes proteins for the excitatory synapses.

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Again, synapses are how cells connect and communicate.

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They move across the body or they move across the brain.

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Shank 3 will be involved in the sensory processing challenges of autism.

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In scientific literature, shank 3 knockout is shown to implicate neurotransmission in

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the striatum, whereby synaptic density were implicated.

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And behavior functioning shows repetitive behaviors, anxiety and deficits in social interaction

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and poor motor coordination.

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Does all of that sound familiar with autism?

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Something I have not mentioned yet is dyspraxia, which is seen in autism.

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It's basically poor motor coordination, especially at younger ages.

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In short, think about how cells talk to each other and areas of the brain connect.

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Synaptic is neurorexine and neurolegans or neuroligans.

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This is more synaptic development and functioning.

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Neurorexines are presynaptic.

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Neurolegans or ligands are post-synaptic.

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The synaptic cleft is remember 10 nanometers.

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That is the space in between each synaptic area.

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Neurolegans work alongside glia cells.

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Remember the Myelination part.

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A type of glia cell called astrocytes builds the myelin.

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It helps build the myelin.

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Myelination creates that highway of connection.

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It turns gravel roads into nicely paved highways.

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That's Myelination.

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Remember the explanation about B-movie.

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Remember how things just come fast.

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Remember how efficiency is a key characteristic of autism if you understand your superpowers.

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If you align with your ability, that becomes a superpower.

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It is my goal that more people with autism and others around them, especially others

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around them, understand autism is a collection of superpowers and super deficits.

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Let's worry about the super deficits.

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More focus on those awesome superpowers.

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Neurologan 3 mutations enhance repetitive behaviors.

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Neurologan 3 deletion impairs synaptic inhibition, some more EI imbalance, and those medium spiny

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neurons in this triadome.

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Remember the purpose of the spines.

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CNT-NAP2, our old friend, is a Neurorexin family member used in excitatory synapses

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formation.

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CNT-NAP2 impacts, highly impacts, metabolism in the medial prefrontal cortex.

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The medial prefrontal cortex has the highest resting metabolic rate.

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The medial prefrontal cortex is involved in decision making, memory integration, social

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cognition, understanding of the self, cognitive flexibility, excitatory and inhibition with

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medial prefrontal cortex transmission includes social behaviors and helps determine mood.

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As we wrap up today, I hope you understood a little bit about the genetic complications

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associated with autism.

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Further, what's more impressive is what these genetic mutations are causing.

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A lot with the synapses and cells, a lot with implications to our sensory processing and

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that balance.

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This balance is going to be crucial of excitation and inhibition.

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You want, you need that healthy balance.

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However, because there is an imbalance or potential imbalance, we will get into the

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superpowers and super deficits, the things that we can do and we can do well and the

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things we can't do or we struggle to do.

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So beyond the lookout for an episode about excitation and inhibition.

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Lastly, know and understand those implications with the light, light environment and our

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biology.

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If anything, you can improve your life by at least understanding this, at least making

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minor adjustments so your life can be better and healthier.

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If you would like to contact me, please do.

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Any types of questions, any types of comments, complaints, criticism, whatever the case,

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I will love to hear and have a conversation with you.

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You can email me at info.fromthespectrum at gmail.com.

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Lastly, thank you for listening to From the Spectrum podcast.

