Welcome to From the Spectrum Podcast. This is a podcast about autism. It is my goal to
explain what is autism. I plan to use a mixture of scientific literature, personal experience,
and opinion. With opinion, I will explain why. I fill the way I do and give examples.
I will provide links to various references for each episode. For each episode, we will discuss
various aspects of autism. For today's episode, we will explore eye tracking as an early biomarker
of autism. When I say early, the studies are on infants or toddlers. We've covered autism and
the embryo and we've covered two studies on six-week-olds, one from UC San Diego on brain
organoids and one from UCLA on the salience network connectivity. In addition, we've covered
autism and the salience network. All of these conversations are entangled. In addition,
a vital conversation is brain development from the eyes. Some regions of interest include vitamin A
or 11-cis retinol, opcins, especially melanopsin. Remember, melanopsin wasn't discovered until
1998. That does not mean it is new in our biology. It was just not discovered. Melanopsin predates
chore dates. All opcins and 11-cis retinol or the vitamin A have weak covalent bonds.
We've covered the most important item, light, both sunlight and artificial light. The spectra
and lux are everything here. Sunlight is 280 nanometer wavelength to 3100 nanometer wavelength.
And artificial light are specific or isolated wavelength. For example, most modern light
is blue light wavelength. 440 to 480 or so nanometer light. Remember, this isolated blue light
breaks that covalent bond of vitamin A and opcins and creates free radicals in the
aldehyde form. This is very damaging in the mitochondria.
What does this mean? Light is an electromagnetic field or EMF. Our mitochondria are driven by
light and specifically the electrons. Aldehyde in this form are toxic to the lipid rafts and
cell membranes. In other words, it complicates the electrons. And cytochrome 1 is electron transport
chain. Now just imagine the downstream processes of the other cytochromes
and cytochrome C oxidase where water is very crucial. How it destroys the membrane is by
demolishing human photoreceptors, which we have more than what you think. Also critical for the
eye tracking episode melanin, tryptophan, water, which is more mitochondria in that cytochrome
C oxidase and melanin. Most of this is mitochondria and melanin. Remember tryptophan is an aromatic
amino acid absorbing light 200 to 280 nanometer light. These components are crucial for development
and biological functioning. Before we get into the downstream topics, eye gaze, joint attention,
and so forth. Remember those are downstream. At the point we can notice, observe, and attempt to
connect some pieces of certain phenotypes. Then science can work towards understanding what it means.
We love to go here more so than going upstream with those biological processes I mentioned in the eye
for brain development. Other key points, the eyes are brain and the eyes and eye development is vital
for brain development and brain health. Remember you can get an OCT scan and it shows upstream
problems of brain and body diseases much earlier, years earlier in some cases of the disease phenotype.
In other words the symptoms or conditions that certain diseases create.
Melanopsin and retinal ganglion cells, especially at 3 and 6 o'clock, and the coroid plexus
are areas to target on an OCT. Things like dementia, obesity, and diabetes can be seen here.
The coroid plexus accounts for 85% of blood in the eye. The eye is very metabolically demanding
area for nutrients, oxygen, glucose, and so forth. Remember the layperson example. People that stand
up too fast or strain too hard can get lightheaded. Fuzzy vision. This is vasovagal. In other words,
those nutrients, the oxygen, and glucose didn't get to the coroid plexus fast enough.
This also considers cerebral spinal fluid or CSF.
Okay, lastly on the biology and it is important. I mentioned melanin. People think iris, skin,
and hair color, but there is so much more. The optimal way to charge separate water
is melanin. This creates free electrons, faster and more plentiful than any other process or
component. The powerhouse to the cell, this is in the mitochondria. Also remember melanopsin
has now been discovered all over the body and the brain, deep inside the brain, inside of tissues
and epithelial and inside of organs. This is everywhere. Nonlinear optics controls our biochemistry.
These components that we discussed is in charge of our biochemistry.
This is what we have been discussing so far in the episode. If and when the eye
isn't developed, the brain and body won't be developed, at least not optimal.
If and when the eye ages or becomes damaged, it breaks down, the brain and body becomes damaged.
It's that simple. A lay public explanation or an example is if you have a fruit tree
and you block the sun from the fruit tree, it could still produce fruit, but the amount of fruit
and individual pieces of fruit will be damaged. It will drastically change the production
of the fruit. However, if you give it full sunlight the way it has evolved to need,
then you will have a better outcome, more optimal fruit production. This is similar to the how the
human body is working. It's this simple eye tracking and autism as a biomarker. This is
area of research I agree with. It is number two on my list of importance behind the cause of autism
and above longitudinal studies of autistic adults. Remember the wonderful story of Jonathan Mitchell,
now 69 years old, autistic. The purpose of eye tracking is having a biomarker.
As soon as possible to identify autism and begin interventions. It also, as we discussed earlier,
it informs research of what is autism. So with interventions, it is no surprise that earlier
the diagnosis and interventions are applied, the better the outcome. Here outcome to me is
being able to navigate society, not based off of social norms, but in a way that is manageable
for the autistic individual. We speak about neuroplasticity, how we become who we are as a
living and changing living organism. If we zoom in, this would include the ability to do certain
tasks, have certain preferences, enjoyments and dislikes, have intelligence, motor functions,
and these learning skills are all essentially infinite. Infinite to the point of the individual
living organism lives in its full potential. In reality, never does a living organism fulfill
its full potential. And we can make a counterpoint for neuroplasticity here as well. We experience
negative outcomes and we can be self debilitating. Humans think like no other creature. We have that
capacity for human thought and this takes us to wonderful places and it can severely hold us back.
No other species or living organism can put itself in harm like we do and it's not even close.
But know this, this does not determine valence or how we feel about life. It's wise to always
strive for higher goals to move our potential in an upwards trajectory. Now let's zoom out with an
example of neuroplasticity. This is easy. This is autism. Autism suddenly shows up in the first
part of the 1900s. Remember autism is a biological adaptation to the environmental change. Likely,
in my opinion, changes in light source and energy. Remember we ought to look at using the basic
concepts of human life and changing, altering one of those and then see what it creates. Not
adding something to the process like pesticides or toxins, neurotoxins or vaccines or BPA in plastics.
Those are all topics of interest but something not as demanding or debilitating in my opinion
and others opinion about what light can do. And to add, you can look around at society and everyone's
following this light. Everyone is involved in this change of light and this health complications are
out of control. If areas or regions of the world add artificial light and tech, more technology,
disease shortly follows. It's not that complicated. A layperson example is India and type 2 diabetes.
Okay, back to the eye tracking. There are a few items we will cover. Social attention,
gaze following and joint attention. Social attention are faces learning and remembering faces as an
infant. Much of what we see are faces. Everyone wants to see the baby and everyone wants to see
the baby smiling. So the other face typically laughs, smiles and alters its voice. A side note,
that altered voice is to adapt to early evolution of speech and language because that's the
trajectory or the placement of the baby. And remember song and dance predates speech and language.
Remember the roles of oxytocin and vasopressin in the autistic phenotype and the differences between
magnocellular and parvocellular paths and distinct characteristics with socialness.
For example, magnocellular is responsible for parental attention and emotional or sometimes
called affective empathy. Meaning once we are told what the other person is feeling,
then we respond. Then our empathy increases and we can share that. Parvocellular is responsible for
pair bonding, more peer-to-peer and cognitive empathy, sometimes called theory of mind,
when we can look at someone and understand what they're going through.
Remember cognitive empathy is more guessing, it's more gray area. We don't know, but emotional or
the affective empathy is conveyed directly to us with no guesswork, no gray area, it's very rigid.
Now hopefully you can understand why autistics are typically low in the guesswork empathy
and high in the conveyed direct empathy. Okay, autistics, it seems at all ages, prefers objects
over faces and objects over faces on joint and gaze attention. Likely, objects are less active,
less sensory processing and lower rates of information in the sensation and perception
processes, which also involves magnocellular and parvocellular and visual pathways of the lateral
geniculate nucleus of the thalamus. I have no doubt this is a region of interest or cause.
Gaze attention, around six months infants begin gaze following. This is explained in Autism and
Adaptive Responsive episode and other discussions around social cognition and building social skills.
The Medeo Prefrontal Cortex and the Amygdala. This is crucial in the communication between
criteria B, the more innate, self-satisfied, restricted, fixated interest criteria,
and criteria A, the social communication and interaction. Joint attention, this is essentially
gaze attention to me, but this involves sustaining attention and sustained effort or ability to
stay with the other, singular, or others, plural. Joint attention also encompasses body language,
components towards the cue, the social cue, those items that have flexible meanings or said
differently or context dependent. An easy example is how long eye contact lasts. The length of eye
contact means different things. Great. Who determines this stuff? The social norms are hilarious,
but these are things across cultures, across the world. It's a wild component of the speech
and language dynamic. Through multiple cultures, they all have different meanings.
Some notes to mention. These are infants, so early diagnosis presents many challenges with
assessment and understanding specific phenotypes of the infant. A part of assessment is clinical
judgment. And eye tracking provides objective data that can remove certain weight of clinical judgment.
Always a good thing. At this age, instruments in the process, because the infant cannot do
too much and is very limited. But with the data on autism and the embryo and the neurological
studies at six weeks old, this is adding up as a crucial epoch for autism diagnosis.
Four scientific literatures to review. Four that I selected. These are not the only four.
You can go to PubMed or even a search engine to discover more.
One is Pierce et al from 2019. One is Keen et al from 2024.
Rudling et al from 2024 and Ween et al from 2022. All available in this show notes.
We've covered Pierce and UC San Diego with the embryo and the brain organoid predicting
profound autism at six weeks old. And a previous guest, Jonathan Mitchell,
participated in studies within this group.
Pierce et al.
Objective. Examine diagnostic stability of toddlers starting at 12 months old.
The study used data from January 1, 2006 to December 31, 2018, equaling 2,241 toddlers being
referred from the general population using a universal screening in primary care or community
service. Of the 2,241 toddlers, criteria as toddlers must have received a first evaluation between
12 and 36 months and have at least one subsequent eval using 12, 18, and 24 month wellness checkups.
So the final count of the study was 1,269 and 72% of these are male. So the ratio of what we see
across society is fairly accurate. During the eval, autism was not only consideration.
The phenotypes include autism spectrum disorder, autism features, developmental delay, language
delay, other typical sibling of an autism pro band and typical developed. Pro band is a starting
point in the first person in medicine or genetics. This study used what? They labeled experts,
which are doctoral level licensed psychologists, using diagnostic instruments, the ADOS,
remember Catherine Lord, the Mullen's scales of early learning, and the Venlon adaptive behavior
scales. Toddlers diagnosed younger than 36 months were diagnostically tested, again every 12 months,
until the age of 3. And the licensed psychologists were blinded of any previous diagnosis.
And after each session, the psychologist rated one of those seven phenotypes mentioned earlier.
The results included autism spectrum disorder, N equals 441,
autism features, N equals 78, developmental delay, N equals 89, language delay, N equals 80,
other N equals 91, typical sibling, N equals 51, and typical developed, N equals 439.
At age 12 months was the lowest specificity for diagnosis at 0.50. At 14 months, however,
accuracy jumps to 0.79. And at 16 months, it plateaued at 0.83. Considering the age,
the 0.8 or so accuracy is pretty wonderful. In addition to the diagnosis at 14 months,
autism out of all of those other phenotypes was more stable than developmental delay and
language delay as far as diagnostic accuracy. In the WAN study, which involves the same
University of Pierce, who is the lead contact now on this study, is essentially repeated
three different studies, including the first one we just reviewed, but use eye tracking devices
towards geometric images, whereby high fixation levels equal poor clinical profiles. So in other
words, the higher the infant fixated on a geometric image predicted the poor clinical profile.
In compared to other conditions, autistic toddlers have the highest levels of fixations.
This included N equals 1863, with N equals 725 autism spectrum disorder, N equals 103
103 autistic features. This is the largest eye tracking sample, at least at that time. I am
not sure if there has been one larger. However, the study resulted in 95% specificity. So this is
meaning few false positives. The researchers indicate the methodology used can accurately detect
autism before the second birthday. However, the researchers fail to recognize the harms of eye
tracking devices and nonlinear optics. This is devastating to a cell function.
Specifically, communication systems within the cells. Remember the first six or eight minutes
of this episode. This is harmful for all of those components of biological aspects we discussed.
Keen et al from Indiana University School of Medicine 2024. The question is, does an eye
tracking battery reliably differentiate children with and without autism? The group used EAE,
Early Autism Evaluation System from Primary Care Providers from June 7th, 2019 to September 23rd,
2022, ages 14 to 48 months. The study investigated sensitivity and specificity
and compared it to expert decisions. Experts here are three clinical psychologists. Then,
they combined eye tracking and psychologist results. The average age of subjects was 2.6 years old.
N equals 102 had standard assessment. So the psychologist only. N113 had eye tracking and
a standard assessment. So both tools, the eye tracking device and study, and the assessment
with the psychologist. The standard assessments only. So the N102 group received 77.5 percent
sensitivity and 77.3 percent specificity for a 77 percent concordance.
With eye tracking and assessment, the group received 90.7 percent sensitivity, 86.7 percent
specificity for a 90 percent concordance. These are using 95 percent confidence intervals.
This is exciting data from the first three studies. The eye tracking methods were modeled after the
peer studies. Plural. Multiple studies are repeated here. So the reddling et al from autism
in 2024 from Uppsala University in Sweden. Now remember, I just want to make a side note.
I just want to make a side note. The latitude here is much higher. Much more
implicated light. Even though the evolution of this group, people from Sweden, Norway, etc.,
have evolved under this high latitude and cold temperatures. However, they did not evolve
with this artificial light. So they have two factors here that are really implicating.
The reddling study conflicts with other data. However, the methodology are slightly different.
They used three groups. N equals 169 infants with 129 of them with high likelihood due to first
degree relative of having autism diagnosis and 40 in 40 for typical likelihood. The high
likelihood was broken into two groups. They had N equals 35 that already had a diagnosis of autism.
So the three groups are one diagnosed autism N equals 35. A high likelihood, not yet or no
diagnosis, N equals 94 and typical likelihood N equals 40. And the studies occurred at 10, 14,
and 18 months old. This study suggests infants in all three groups responded to eye gaze
essentially in the same manner. For validity, there was no consistency with how much nor
how quickly the infants responded, differentiated within the three groups.
The study notes infants in the high likelihood tended to look away quicker.
The biggest takeaway for me, the study used a device again in destroying melanopsin and
breaking those weak covalent bonds. However, the group suggests that the eye gaze is pretty similar
across all three groups. Frankly, the last study does not seem to be as complex as the
Pierce and the Keen study. However, maybe they would disagree with that.
In psychological assessment, if you can get the sensitivity and specificity around 0.9 as we saw
in some of the studies, this is phenomenal. Even 0.8 is pretty acceptable. Now we saw the
psychologist only using the normal instruments in the normal assessment process was in the high 70s,
77% or so. But when we add this extra test system, the sensitivity and the specificity increased
quite a bit, which is optimal news for that early intervention at minimum to get the appearance
ready and prepared for an active for the treatment or making sure the little individual
with autism is prepared to meet the demanding social world. This is for most importance.
We don't have to change the person with autism. Clearly stated, it is not right to
change someone just so they can fit in. However, if society is more aware, if the child's, let's say,
Pierce and other family members and school system is aware, then they can sort of accommodate,
make changes so that the child can thrive in any system. The biology that gives us autism
gives us the ability to be comfortable within ourselves. And this is our preference. This is
the neuroplasticity. And there's ought to be nothing wrong with this because there's some great
things that can come out of this. Now, however, I realize there's a range of autistic phenotypes
and a range of different demands and challenges. This test or these studies, I should say,
offers a solution, offers hope for those more severe cases, those profound
individuals or the level two, level three area. And we can minimize the negative experience that
they will have. Remember that neuroplasticity. This is why it's so crucial. This is why I always
mentioned the neuroplasticity. We get ingrained and expect negative things. And then that human
thought can kick in. And it's not a good equation. If you are listening to the podcast or listening
to the episode, please feel free to leave a review or rating. In podcasting reviews, ratings,
and downloads are huge. And I very much appreciate your feedback. You can contact me on X at RPS
47586 for any topic and conversation with autism. You can email me at info.fromthespectrumatgmail.com.
You can also check out the Hop website page that has links to all of my platforms and email address
any way you want to contact me or listen. And lastly, thank you for listening to From the Spectrum
podcast.