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

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explain 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. For today's episode, we will explore eye tracking as an early biomarker

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of autism. When I say early, the studies are on infants or toddlers. We've covered autism and

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the embryo and we've covered two studies on six-week-olds, one from UC San Diego on brain

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organoids and one from UCLA on the salience network connectivity. In addition, we've covered

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autism and the salience network. All of these conversations are entangled. In addition,

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a vital conversation is brain development from the eyes. Some regions of interest include vitamin A

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or 11-cis retinol, opcins, especially melanopsin. Remember, melanopsin wasn't discovered until

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1998. That does not mean it is new in our biology. It was just not discovered. Melanopsin predates

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chore dates. All opcins and 11-cis retinol or the vitamin A have weak covalent bonds.

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We've covered the most important item, light, both sunlight and artificial light. The spectra

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and lux are everything here. Sunlight is 280 nanometer wavelength to 3100 nanometer wavelength.

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And artificial light are specific or isolated wavelength. For example, most modern light

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is blue light wavelength. 440 to 480 or so nanometer light. Remember, this isolated blue light

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breaks that covalent bond of vitamin A and opcins and creates free radicals in the

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aldehyde form. This is very damaging in the mitochondria.

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What does this mean? Light is an electromagnetic field or EMF. Our mitochondria are driven by

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light and specifically the electrons. Aldehyde in this form are toxic to the lipid rafts and

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cell membranes. In other words, it complicates the electrons. And cytochrome 1 is electron transport

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chain. Now just imagine the downstream processes of the other cytochromes

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and cytochrome C oxidase where water is very crucial. How it destroys the membrane is by

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demolishing human photoreceptors, which we have more than what you think. Also critical for the

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eye tracking episode melanin, tryptophan, water, which is more mitochondria in that cytochrome

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C oxidase and melanin. Most of this is mitochondria and melanin. Remember tryptophan is an aromatic

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amino acid absorbing light 200 to 280 nanometer light. These components are crucial for development

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and biological functioning. Before we get into the downstream topics, eye gaze, joint attention,

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and so forth. Remember those are downstream. At the point we can notice, observe, and attempt to

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connect some pieces of certain phenotypes. Then science can work towards understanding what it means.

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We love to go here more so than going upstream with those biological processes I mentioned in the eye

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for brain development. Other key points, the eyes are brain and the eyes and eye development is vital

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for brain development and brain health. Remember you can get an OCT scan and it shows upstream

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problems of brain and body diseases much earlier, years earlier in some cases of the disease phenotype.

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In other words the symptoms or conditions that certain diseases create.

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Melanopsin and retinal ganglion cells, especially at 3 and 6 o'clock, and the coroid plexus

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are areas to target on an OCT. Things like dementia, obesity, and diabetes can be seen here.

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The coroid plexus accounts for 85% of blood in the eye. The eye is very metabolically demanding

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area for nutrients, oxygen, glucose, and so forth. Remember the layperson example. People that stand

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up too fast or strain too hard can get lightheaded. Fuzzy vision. This is vasovagal. In other words,

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those nutrients, the oxygen, and glucose didn't get to the coroid plexus fast enough.

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This also considers cerebral spinal fluid or CSF.

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Okay, lastly on the biology and it is important. I mentioned melanin. People think iris, skin,

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and hair color, but there is so much more. The optimal way to charge separate water

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is melanin. This creates free electrons, faster and more plentiful than any other process or

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component. The powerhouse to the cell, this is in the mitochondria. Also remember melanopsin

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has now been discovered all over the body and the brain, deep inside the brain, inside of tissues

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and epithelial and inside of organs. This is everywhere. Nonlinear optics controls our biochemistry.

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These components that we discussed is in charge of our biochemistry.

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This is what we have been discussing so far in the episode. If and when the eye

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isn't developed, the brain and body won't be developed, at least not optimal.

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If and when the eye ages or becomes damaged, it breaks down, the brain and body becomes damaged.

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It's that simple. A lay public explanation or an example is if you have a fruit tree

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and you block the sun from the fruit tree, it could still produce fruit, but the amount of fruit

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and individual pieces of fruit will be damaged. It will drastically change the production

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of the fruit. However, if you give it full sunlight the way it has evolved to need,

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then you will have a better outcome, more optimal fruit production. This is similar to the how the

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human body is working. It's this simple eye tracking and autism as a biomarker. This is

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area of research I agree with. It is number two on my list of importance behind the cause of autism

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and above longitudinal studies of autistic adults. Remember the wonderful story of Jonathan Mitchell,

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now 69 years old, autistic. The purpose of eye tracking is having a biomarker.

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As soon as possible to identify autism and begin interventions. It also, as we discussed earlier,

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it informs research of what is autism. So with interventions, it is no surprise that earlier

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the diagnosis and interventions are applied, the better the outcome. Here outcome to me is

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being able to navigate society, not based off of social norms, but in a way that is manageable

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for the autistic individual. We speak about neuroplasticity, how we become who we are as a

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living and changing living organism. If we zoom in, this would include the ability to do certain

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tasks, have certain preferences, enjoyments and dislikes, have intelligence, motor functions,

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and these learning skills are all essentially infinite. Infinite to the point of the individual

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living organism lives in its full potential. In reality, never does a living organism fulfill

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its full potential. And we can make a counterpoint for neuroplasticity here as well. We experience

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negative outcomes and we can be self debilitating. Humans think like no other creature. We have that

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capacity for human thought and this takes us to wonderful places and it can severely hold us back.

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No other species or living organism can put itself in harm like we do and it's not even close.

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But know this, this does not determine valence or how we feel about life. It's wise to always

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strive for higher goals to move our potential in an upwards trajectory. Now let's zoom out with an

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example of neuroplasticity. This is easy. This is autism. Autism suddenly shows up in the first

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part of the 1900s. Remember autism is a biological adaptation to the environmental change. Likely,

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in my opinion, changes in light source and energy. Remember we ought to look at using the basic

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concepts of human life and changing, altering one of those and then see what it creates. Not

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adding something to the process like pesticides or toxins, neurotoxins or vaccines or BPA in plastics.

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Those are all topics of interest but something not as demanding or debilitating in my opinion

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and others opinion about what light can do. And to add, you can look around at society and everyone's

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following this light. Everyone is involved in this change of light and this health complications are

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out of control. If areas or regions of the world add artificial light and tech, more technology,

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disease shortly follows. It's not that complicated. A layperson example is India and type 2 diabetes.

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Okay, back to the eye tracking. There are a few items we will cover. Social attention,

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gaze following and joint attention. Social attention are faces learning and remembering faces as an

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infant. Much of what we see are faces. Everyone wants to see the baby and everyone wants to see

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the baby smiling. So the other face typically laughs, smiles and alters its voice. A side note,

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that altered voice is to adapt to early evolution of speech and language because that's the

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trajectory or the placement of the baby. And remember song and dance predates speech and language.

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Remember the roles of oxytocin and vasopressin in the autistic phenotype and the differences between

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magnocellular and parvocellular paths and distinct characteristics with socialness.

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For example, magnocellular is responsible for parental attention and emotional or sometimes

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called affective empathy. Meaning once we are told what the other person is feeling,

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then we respond. Then our empathy increases and we can share that. Parvocellular is responsible for

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pair bonding, more peer-to-peer and cognitive empathy, sometimes called theory of mind,

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when we can look at someone and understand what they're going through.

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Remember cognitive empathy is more guessing, it's more gray area. We don't know, but emotional or

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the affective empathy is conveyed directly to us with no guesswork, no gray area, it's very rigid.

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Now hopefully you can understand why autistics are typically low in the guesswork empathy

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and high in the conveyed direct empathy. Okay, autistics, it seems at all ages, prefers objects

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over faces and objects over faces on joint and gaze attention. Likely, objects are less active,

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less sensory processing and lower rates of information in the sensation and perception

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processes, which also involves magnocellular and parvocellular and visual pathways of the lateral

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geniculate nucleus of the thalamus. I have no doubt this is a region of interest or cause.

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Gaze attention, around six months infants begin gaze following. This is explained in Autism and

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Adaptive Responsive episode and other discussions around social cognition and building social skills.

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The Medeo Prefrontal Cortex and the Amygdala. This is crucial in the communication between

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criteria B, the more innate, self-satisfied, restricted, fixated interest criteria,

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and criteria A, the social communication and interaction. Joint attention, this is essentially

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gaze attention to me, but this involves sustaining attention and sustained effort or ability to

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stay with the other, singular, or others, plural. Joint attention also encompasses body language,

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components towards the cue, the social cue, those items that have flexible meanings or said

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differently or context dependent. An easy example is how long eye contact lasts. The length of eye

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contact means different things. Great. Who determines this stuff? The social norms are hilarious,

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but these are things across cultures, across the world. It's a wild component of the speech

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and language dynamic. Through multiple cultures, they all have different meanings.

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Some notes to mention. These are infants, so early diagnosis presents many challenges with

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assessment and understanding specific phenotypes of the infant. A part of assessment is clinical

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judgment. And eye tracking provides objective data that can remove certain weight of clinical judgment.

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Always a good thing. At this age, instruments in the process, because the infant cannot do

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too much and is very limited. But with the data on autism and the embryo and the neurological

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studies at six weeks old, this is adding up as a crucial epoch for autism diagnosis.

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Four scientific literatures to review. Four that I selected. These are not the only four.

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You can go to PubMed or even a search engine to discover more.

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One is Pierce et al from 2019. One is Keen et al from 2024.

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Rudling et al from 2024 and Ween et al from 2022. All available in this show notes.

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We've covered Pierce and UC San Diego with the embryo and the brain organoid predicting

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profound autism at six weeks old. And a previous guest, Jonathan Mitchell,

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participated in studies within this group.

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Pierce et al.

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Objective. Examine diagnostic stability of toddlers starting at 12 months old.

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The study used data from January 1, 2006 to December 31, 2018, equaling 2,241 toddlers being

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referred from the general population using a universal screening in primary care or community

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service. Of the 2,241 toddlers, criteria as toddlers must have received a first evaluation between

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12 and 36 months and have at least one subsequent eval using 12, 18, and 24 month wellness checkups.

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So the final count of the study was 1,269 and 72% of these are male. So the ratio of what we see

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across society is fairly accurate. During the eval, autism was not only consideration.

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The phenotypes include autism spectrum disorder, autism features, developmental delay, language

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delay, other typical sibling of an autism pro band and typical developed. Pro band is a starting

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point in the first person in medicine or genetics. This study used what? They labeled experts,

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which are doctoral level licensed psychologists, using diagnostic instruments, the ADOS,

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remember Catherine Lord, the Mullen's scales of early learning, and the Venlon adaptive behavior

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scales. Toddlers diagnosed younger than 36 months were diagnostically tested, again every 12 months,

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until the age of 3. And the licensed psychologists were blinded of any previous diagnosis.

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And after each session, the psychologist rated one of those seven phenotypes mentioned earlier.

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The results included autism spectrum disorder, N equals 441,

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autism features, N equals 78, developmental delay, N equals 89, language delay, N equals 80,

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other N equals 91, typical sibling, N equals 51, and typical developed, N equals 439.

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At age 12 months was the lowest specificity for diagnosis at 0.50. At 14 months, however,

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accuracy jumps to 0.79. And at 16 months, it plateaued at 0.83. Considering the age,

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the 0.8 or so accuracy is pretty wonderful. In addition to the diagnosis at 14 months,

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autism out of all of those other phenotypes was more stable than developmental delay and

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language delay as far as diagnostic accuracy. In the WAN study, which involves the same

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University of Pierce, who is the lead contact now on this study, is essentially repeated

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three different studies, including the first one we just reviewed, but use eye tracking devices

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towards geometric images, whereby high fixation levels equal poor clinical profiles. So in other

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words, the higher the infant fixated on a geometric image predicted the poor clinical profile.

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In compared to other conditions, autistic toddlers have the highest levels of fixations.

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This included N equals 1863, with N equals 725 autism spectrum disorder, N equals 103

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103 autistic features. This is the largest eye tracking sample, at least at that time. I am

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not sure if there has been one larger. However, the study resulted in 95% specificity. So this is

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meaning few false positives. The researchers indicate the methodology used can accurately detect

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autism before the second birthday. However, the researchers fail to recognize the harms of eye

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tracking devices and nonlinear optics. This is devastating to a cell function.

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Specifically, communication systems within the cells. Remember the first six or eight minutes

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of this episode. This is harmful for all of those components of biological aspects we discussed.

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Keen et al from Indiana University School of Medicine 2024. The question is, does an eye

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tracking battery reliably differentiate children with and without autism? The group used EAE,

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Early Autism Evaluation System from Primary Care Providers from June 7th, 2019 to September 23rd,

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2022, ages 14 to 48 months. The study investigated sensitivity and specificity

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and compared it to expert decisions. Experts here are three clinical psychologists. Then,

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they combined eye tracking and psychologist results. The average age of subjects was 2.6 years old.

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N equals 102 had standard assessment. So the psychologist only. N113 had eye tracking and

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a standard assessment. So both tools, the eye tracking device and study, and the assessment

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with the psychologist. The standard assessments only. So the N102 group received 77.5 percent

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sensitivity and 77.3 percent specificity for a 77 percent concordance.

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With eye tracking and assessment, the group received 90.7 percent sensitivity, 86.7 percent

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specificity for a 90 percent concordance. These are using 95 percent confidence intervals.

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This is exciting data from the first three studies. The eye tracking methods were modeled after the

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peer studies. Plural. Multiple studies are repeated here. So the reddling et al from autism

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in 2024 from Uppsala University in Sweden. Now remember, I just want to make a side note.

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I just want to make a side note. The latitude here is much higher. Much more

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implicated light. Even though the evolution of this group, people from Sweden, Norway, etc.,

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have evolved under this high latitude and cold temperatures. However, they did not evolve

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with this artificial light. So they have two factors here that are really implicating.

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The reddling study conflicts with other data. However, the methodology are slightly different.

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They used three groups. N equals 169 infants with 129 of them with high likelihood due to first

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degree relative of having autism diagnosis and 40 in 40 for typical likelihood. The high

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likelihood was broken into two groups. They had N equals 35 that already had a diagnosis of autism.

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So the three groups are one diagnosed autism N equals 35. A high likelihood, not yet or no

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diagnosis, N equals 94 and typical likelihood N equals 40. And the studies occurred at 10, 14,

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and 18 months old. This study suggests infants in all three groups responded to eye gaze

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essentially in the same manner. For validity, there was no consistency with how much nor

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how quickly the infants responded, differentiated within the three groups.

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The study notes infants in the high likelihood tended to look away quicker.

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The biggest takeaway for me, the study used a device again in destroying melanopsin and

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breaking those weak covalent bonds. However, the group suggests that the eye gaze is pretty similar

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across all three groups. Frankly, the last study does not seem to be as complex as the

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Pierce and the Keen study. However, maybe they would disagree with that.

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In psychological assessment, if you can get the sensitivity and specificity around 0.9 as we saw

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in some of the studies, this is phenomenal. Even 0.8 is pretty acceptable. Now we saw the

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psychologist only using the normal instruments in the normal assessment process was in the high 70s,

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77% or so. But when we add this extra test system, the sensitivity and the specificity increased

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quite a bit, which is optimal news for that early intervention at minimum to get the appearance

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ready and prepared for an active for the treatment or making sure the little individual

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with autism is prepared to meet the demanding social world. This is for most importance.

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We don't have to change the person with autism. Clearly stated, it is not right to

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change someone just so they can fit in. However, if society is more aware, if the child's, let's say,

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Pierce and other family members and school system is aware, then they can sort of accommodate,

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make changes so that the child can thrive in any system. The biology that gives us autism

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gives us the ability to be comfortable within ourselves. And this is our preference. This is

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the neuroplasticity. And there's ought to be nothing wrong with this because there's some great

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things that can come out of this. Now, however, I realize there's a range of autistic phenotypes

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and a range of different demands and challenges. This test or these studies, I should say,

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offers a solution, offers hope for those more severe cases, those profound

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individuals or the level two, level three area. And we can minimize the negative experience that

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they will have. Remember that neuroplasticity. This is why it's so crucial. This is why I always

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mentioned the neuroplasticity. We get ingrained and expect negative things. And then that human

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thought can kick in. And it's not a good equation. If you are listening to the podcast or listening

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to the episode, please feel free to leave a review or rating. In podcasting reviews, ratings,

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and downloads are huge. And I very much appreciate your feedback. You can contact me on X at RPS

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47586 for any topic and conversation with autism. You can email me at info.fromthespectrumatgmail.com.

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You can also check out the Hop website page that has links to all of my platforms and email address

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any way you want to contact me or listen. And lastly, thank you for listening to From the Spectrum

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podcast.