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Welcome to From the Spectrum podcast. This is a podcast about autism. It is my goal to explain

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what is autism. I plan to use a mixture of scientific literature, personal experience,

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and opinion. With opinion, I will explain why. I fill the way I do and give examples.

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I will provide links to various references for each episode. For each episode, we will discuss

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various aspects of autism. The From the Spectrum podcast will mostly avoid causes of autism.

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And I will try to avoid the increase of diagnoses of late. This is like playing tug-of-war with

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barbed wire. And I don't think I want to travel down that path. For today's episode, we will explore

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the roles of oxytocin and vasopressin with human development, human socialness, and the

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implications to autism. We will briefly do some time traveling to understand the phylogenetics

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of oxytocin and vasopressin. We will expand on some components of the excitation and inhibition

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balance. Discuss more serotonin, dopamine, and the line between socialness and anxiety,

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while connecting many brain regions and functions previously discussed. For today's episode,

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we have several objectives. 1. Introduce oxytocin and vasopressin. 2. Prepare to discuss vast

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differences found between female and male autistics in a future episode. 3. To prepare for the

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episode on autism and relationships. 4. To expand on the excitation and inhibition phenomena

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that is very worthy in autism. And finally, number 5. To learn more about what is autism.

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Oxytocin and vasopressin. Oxytocin is commonly known as a love hormone. And that's true.

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Both oxytocin and vasopressin are unique and dynamic parts of our biology. The phylogeny

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of oxytocin and vasopressin date back 700 million years ago and is found in many different

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species through evolution. Primarily back then there were lower vertebrates. Back before

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humans and more complex organisms were found on Earth. This hormone is vasotocin. You can

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see a combination of vasopressin and oxytocin. We could cover a lot here because of the amount

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of history, but we can't. We can't cover everything regarding our topic in modern humans,

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development and autism. However, the division of vasotocin into vasopressin and oxytocin

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appears to help create more complex organisms like humans. Oxytocin and vasopressin are

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both peptides and hormones and have three modes of transmission. They have three methods

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of getting around the body. One is endocrine, so a hormone. Hormones use the blood to transport

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and hormones are very slow acting, especially compared to cellular functions. Hormones act

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more to change us and build us based on experiences over time. The second mode is paracrine, released

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in dendrites and cell bodies and into cerebral spinal fluid or CSF. The CSF is a method to

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check levels of oxytocin or vasopressin in the body. This is a very challenging test.

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Not only the spinal tap is challenging, but finding accurate amounts of oxytocin and vasopressin

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can be a lab draw or blood draw, but it's hard to capture them because they have a short

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half life. They don't hang around in the body and you're likely only to see metabolites.

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It won't be a very accurate test. So a more accurate test is the spinal tap and that's

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not necessarily a feasible thing, something that people want to do. The third is subnaptic

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release, used for transporting to other brain regions. This is the neuropeptide or neurotransmitter

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type. Okay, so what are peptides? Peptides are a chain of protein collections. Oxytocin

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and vasopressin are very fascinating, whereby they are very similar and they have a smaller

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complex or smaller collection of proteins. Each oxytocin and vasopressin each contain

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nine proteins. These are very special types of proteins. Amino acids. We've discussed

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some amino acids like tryptophan and tyrosine. Those are aromatic amino acids. Remember serotonin

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comes from tryptophan and dopamine epinephrine or epinephrine and melanin comes from tyrosine.

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And remember our discussion on these special amino acids, the aromatic amino acids that

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need 280 nanometer wavelength light, which is UVB light to activate and think about how

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our light environment has changed. Let's say from modern day and all the different light

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sources to the 1930s, just the change between that time frame. When autism was first kind

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of observed, remember Leo Kanner and Hans Asperger. Now let's think about modern day

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to let's say 200 years ago when things like autism and Alzheimer's didn't even exist.

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This part of the environment and how our human biology is created with photoreceptors and

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such is going to be crucial. We will discuss serotonin and dopamine more in a little bit.

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Human biology loves these proteins. Oxytocin and vasopressin share seven of the nine proteins.

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So only two proteins make these two different. But remember the evolution. In complex organisms

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they separated, they divided, but still today in smaller or lower complex, less complex

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organisms, they still remain one. Okay, taking a brief step towards the upstream of the neuropath

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peptide. We're going to go just a little bit upstream. These neuropaths come from two cell

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types. Magnosecular and Parvocellular. I first learned about these while studying the eyes.

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Magnosecular provides information about large and fast objects. They are low spatial and

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high temporal, meaning low space, high time, fast time. And do not pick up color. They are

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color blind. Parvocellular provides information about small and slow objects and does see

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color. They are high spatial and low temporal. Magnosecular peptides release large quantities

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in the central and peripheral nervous system. This peripheral path will come into play later.

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When we discuss intranasal oxytocin as a treatment option. Whereas Parvocellular releases small

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quantities in the central nervous system. In large part, to support reward processes,

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low cognition and pair bonding. Downstream, Magnosecular is responsible for parental attachment,

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buffering, fear and anxiety, and emotional or affective empathy. Remember, we've discussed

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that and hypersensitivity. Parvocellular is responsible for various other types of attachment

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outside of the parental attachment, such as peer to peer. Now we're getting somewhere.

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And cognitive flexibility and social recognition memory. Cognitive empathy being able to understand

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others without knowing. Just by looking at them, that so called theory of mind and lack

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of social motivation. So that's Magnosecular and Parvocellular. Now these distinct pathways

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to a single molecule. The idea is the parallel paths for processing the social information

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allows a single molecule such as the oxytocin to encode multiple types of behaviors. And

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in my opinion, this is a huge finding. This was released in 2020. Furthermore, this idea

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of the Magnosecular and Parvocellular paths is new. Around 2015 or so, when this was really

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mentioned in the scientific literature. A keynote or to show appreciation. A researcher

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from John Hopkins does excellent work on this. Her last name is Dolan, I believe. Okay, back

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to oxytocin and vasopressin. Oxytocin is central to human reproduction and evolution. Transforming

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us into complex organisms. Especially their nervous system. Specifically, socialness and

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cognition. The peptides have connections with making us upright through evolution. Remember,

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our connections are one of the few or the only species completely upright. And oxytocin has

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a role with that. And developing our large cortex, the area of the brain. Above the imaginary

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line that we've previously discussed from the eyes to the back of the head. Remember,

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our heads extend up. Unlike any other species, it's fully developed. Also, connections with

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our curanium. This complex human brain then gives us social sensitivity, complex thinking

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capacities and language. Speech and language comes after song and dance. Correct. It was

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song and dance first, and then speech and language through our evolution. The pair bonding allows

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us to sustain our species. The connection of reproduction, birthing process and mother-child

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relationships. Lastly, it supports healing and is an antioxidant and anti-inflammatory.

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All crucial across the lifespan. Just a note. Veso in vasopressin means vessel. Vasopressin

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has many functions related to the circulatory system. A sidebar. If you have ever felt light-headed,

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maybe you stood up too fast or you're straining too much or too hard. That is vasovagal vessels

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and the vagus nerve. A major curanium nerve for regulating and acting on the parasympathetic

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side of the nervous system. The calming side. Vasopressin has vast roles in blood pressure,

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sodium regulation and interacting with water. Vasopressin is seen more in males than females

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and it does interact with that crude stress system and fear, anxiety and aggression. Anyway,

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oxytocin and vasopressin by the way of the magnosecular and parvocellular are released

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in the hypothalamus. Remember, we've discussed the hypothalamus at least a few times. Oxytocin

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and vasopressin are transported by dendrites and axons. Remember how cells connect and

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communicate to each other and remember the genetic and protein implications covered in

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episode 3. Oxytocin is distributed to sensory areas of the brain and large part for social

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relevant stimuli. Oxytocin mediates communication in the amygdala. Remember the amygdala mostly

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from autism and anxiety episode. Oxytocin mediates fear response and coping between two subdivisions

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in the amygdala. And oxytocin is used for synaptic transmission between the B and ST

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that bad nucleus of the striaterminalis and the hypothalamus. More from the autism and

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anxiety episode. Remember those two connections, the amygdala to the bad striaterminalis was

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consistent in those three dynamic structures and components that we covered in the autism

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and anxiety episode. Oxytocin also interacts closely to dopamine and serotonin. Those two

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neuro modulators previously discussed. Remember dopamine is one team and serotonin is having.

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Oxytocin also interacts with GABA. Remember the excitation is glutamate. The inubition

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is GABA. So this makes up that EI, that EI imbalance that is constant and consistent.

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Perhaps the most consistent thing in autism research about biology is this imbalance of

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excitation and inhibition. We will discuss more on GABA, the inhibition part. Also oxytocin

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increases trust. Remember that the root of that pair bonding and mother child development.

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So some overall trust. Some empathy. Remember we discussed the two types of empathy from

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magnosecular and parvocellular and eye contact. Oxytocin is related to eye contact, face memory

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and generosity. These peptides decreases activity of negative emotional experiences. And guess

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where? The amygdala, the anterior cingulate cortex and the insula. All areas from autism

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and adaptive responses episode. The peptides increase responses for automatic and effortful

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emotional regulation in the medial prefrontal cortex. Also the region of interest in autism

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and adaptive responses episode. The peptides targets motivational and rewarding regions

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by initiating and sustaining socialness by acting on the ventral tegmental area. Remember

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from autism and anxiety. The autism and anxiety episode. The VTA is the spot for providing

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valence or attaching how we feel in that moment, in that environment. Hopefully this is all

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coming together now. Oxytocin also targets three of the four areas in the striatum. The

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putamen and caudate, which is the dorsal part of the striatum. The putamen and caudate is

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responsible for stimulus response memories. Remember we've discussed stimulates responses.

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Those reflexive actions all humans do in response to something in the environment, the external

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stimuli. The stimulus response intends to return the individual back to homeostasis,

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back to the comfort that they prefer, that they've learned, that they've developed

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through neuroplasticity. Returning us as the living organism back to comfort. And remember

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one, because our nervous system mostly just responds based on who we are, based on our

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lifetime of neuroplasticity. And two, change is hard. Change is hard because the nervous

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system doesn't like to work. It likes to reflexively respond, pass things on to what

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it knows, how it knows, how it knows how to operate. Acting in a way it knows. See this

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is more than a discussion on autism. This is human life. We are who we are. A brief note,

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a brief review of this study comparing autistics and non-autistics. Reward processing is altered

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in large part at the cellular level with the autism group, the autistic groups, using two

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activities. The first one is monetary rewards found in the ventral striatum. Remember the

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ventral striatum in large part is the nucleus accumbens, our hotspot for rewards. And the

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ACC, which we discussed in depth in a previous episode, and the prefrontal cortex. And the

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second activity was reduced activity in the striatum during positive socialness. For instance,

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seeing smiling faces. And remember theory of mind, also called cognitive empathy, which

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we discussed earlier. This is a super deficit. But effective empathy is not. It is a possible

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superpower. We will discuss more on that in the future. So you can see from the study,

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the differences between autistics and non-autistics and how different brain regions are activated

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based on those two activities, receiving monetary rewards and experiencing positive socialness.

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This lack of reward attached to socialness prevents social learning opportunities. As

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far back as that critical period, and if you understand the social phenotypes of autism,

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they are very, how do I say they are behind or uneducated and poor. Things like loud and

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soft tone, porosity, when and how to join and in the conversation, speaking too much on a specific

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topic, despite obvious, well, to others, not so much for us, obvious this interest in the topic

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by the listener. In addition to these areas, there are hypo connectivity to downstream or

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connecting brain regions used in socialness, providing more proof and insight on what causes

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the autistic phenotypes, explaining what and who we are. This is giving you understanding

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to maybe calm any tendency of wanting to change someone with autism because they are different

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than you. I did not say you can't help them build social skills. I would not say that.

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However, if an autistic prefers being less active in socialness, the so called autistic

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aloneness. Remember the paper by Leo Kanner, that first paper on autism released in 1943.

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He highlighted this quite extensively. Be mindful, autism gives us the ability to be comfortable

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within ourselves. And this is a path for developing tremendous superpowers.

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In autism, data exists on lower levels of peripheral and central oxytocin,

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and deficient and altered expression of oxytocin receptors in both animal and human research.

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In addition, data also show the lower plasma oxytocin are present in children,

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and not so much adolescent or adult autistics. This is critical in the role of oxytocin in

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development. I think this is a good finding and correlation. A meta-analysis using 18 studies

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examined and determined this finding. And that was released in 2021. Oxytocin and serotonin.

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Oxytocin and serotonin appears to be the driving force and the role of supporting

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anxiety like features and supports socialness. The dorsal raffae, the raffae is the brain serotonin.

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Receives oxytocin fibers and the raffae has oxytocin receptors. This action causes a release

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of serotonin, specifically to frontal brain regions. And remember serotonin's role in active versus

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passive coping. In contrast, studies show genetically removing this connection after

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childbirth resulted in offspring loss. Remember the developmental roles. The impaired nursing

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increased aggression and behavior complications. When oxytocin and serotonin work in concert,

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it provides a perception of rewarding socialness occurring. In other words, when socialness is

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rewarding, coordinated activity of oxytocin and serotonin is required. And it goes to that ventral

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striatum area, the nucleus accumbens. Said differently, a lack of oxytocin prevents

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social enjoyment. And now, just a brief note. When we discuss female versus male autistics,

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the nucleus accumbens and oxytocin is going to be huge. This was a huge finding.

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Anyway, data on various modeled organisms and humans show various oxytocin and serotonin

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connections, including in the prefrontal cortex, that area that makes us the superior species

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on earth and the amygdala, the striatal areas, and interesting, serotonin regulates the release

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of oxytocin in one of the areas of the hypothalamus. So, three things of interest here. One, the reward

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processing. Two, the fear response. And three, the social emotional processing.

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Oxytocin and dopamine. The roles in dopamine primarily stick to the main roles of dopamine.

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That is, connecting brain regions based on wanting, motivation, and craving.

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What you find rewarding and aspects of cognitive processing and sensory gating.

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This is a good one. Remember, dopamine is a neuromodulator and it conducts whole systems. It turns things on,

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turns certain brain regions on, or whole systems throughout the body. It activates them and it

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turns things off. Little brain regions or entire systems, biological systems, it inoculates them.

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And it regulates action through the nervous system. Dopamine has two receptor types.

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Dopamine has five total receptors broken down into two types. D1 is excitation,

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and that's dopamine receptor 1 and 5. And D2 is inhibition. These are dopamine receptors 2, 3, and 4.

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D2 type receptors are inhibition. So, now we will introduce GABA, which is inhibition.

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In autism, dysregulation of GABA receptors exist in the data. Remember one of those components or

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reasons that gives us the EI imbalance. Remember a critical role of GABA, which is inhibitory,

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turning things off or quieting the brain. One of GABA's main roles is regulating sensations

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via that thalamocortical path. These abnormal GABA receptors are also found in seizures.

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Remember the closeness to epilepsy and learning disabilities and our primary topic in social and

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cognitive dysfunctions. The excitation inhibition needs both oxytocin and GABA for a proper balance.

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For the developing brain, these components are critical for proper development. A study shows

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aberrations in these areas are a cause of autistic phenotypes. Also, abnormal GABA development in the

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dopaminergic areas of the brain is our region of interest. This expands on some dysfunction of the

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excitation and inhibition balance and offers a topic in recent research of pathophysiology of

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autism. In addition, neurogenesis, the development of neurons, remember cells divide and neurite growth

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and synapsis formation involve many factors. Nothing singular. These neuropeptides alongside GABA

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are critical for these roles. Okay, before we end, I just want to cover intranasal oxytocin as a

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therapeutic option for autism or for those autistic phenotypes. Intranasal oxytocin administration

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penetrates the brain. It crosses the blood-brain barrier with capillary beds and induces cognitive,

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emotional, and behavioral changes mostly related to socialness. To no surprise, for that reason,

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data exists on testing intranasal oxytocin for autism super deficits, social anxiety,

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increasing peer-to-peer capabilities, or said differently, acting on those roles oxytocin has

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in social functioning discussed earlier. The data on intranasal oxytocin is both inconsistent and

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low risk, meaning little to zero side effects. Criteria for the intranasal oxytocin include

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standardization of dosage, frequency, formulation, differences in sex, and devices used for

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administration. Two points to consider. There's an idea gender differences is a primary cause

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of the inconsistent data, and intranasal oxytocin is shown to improve socialness or more precisely

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shown to suppress anxiety and healthy participants. The reason we will explore this option is because

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there is proof and it is in the so-called low risk category as a helpful option for autism.

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There are several things to know here, several takeaways to consider. One, studies do show

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improvements and a few meta-analysis confirm this. Intranasal oxytocin, this approach,

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has been around for about 20 years now, I believe 2003. So some data has collected.

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The second thing to consider is it is low risk and this ought to be a tremendous factor. If it

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works, it works. If it doesn't, okay, it doesn't. Three, it is unknown if intranasal mimics the

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endogenous amounts released in the brain. The dosage has to really be pinpointed.

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Four, there is a chance intranasal oxytocin activates broad serotonin across the brain.

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In other words, it might lack specificity. And lastly, number five, and this is a big one,

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intranasal appears to target the magnosecular pathway, which is more peripheral. So it acts on

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hormones and it blunts stress responses in the hormonal systems such as cortisol. When in reality,

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the idea is acting on the central pathways that the area is responsible for the brain region,

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that cellular activity. You want more neuropeptide or neurotransmitter and less hormone. So it can

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target the nucleus accumbens. Remember, co-activating with serotonin and oxytocin to reach the

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nucleus accumbens, that is the primary target. And that works by the way of the parvocellular

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function or that parvocellular path and not the magnosecular. If you are listening and enjoy the

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episode or enjoy the podcast, feel free to leave a review or rating. And podcasting reviews, ratings,

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and downloads are huge. And I very much appreciate your feedback. You can email me at info.fromthespectrum.com.

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And thank you for listening to From the Spectrum podcast.