Autism Spectrum Disorder: REAL? (Literature Review)

There was another meta-analysis that found that parent implemented interventions were effective for pediatric patients with autism spectrum disorder. And this was true, this proved to be true in a variety of circumstances and environments.

These interventions by parents, trained parents, their interventions improved not only maladaptive behavior such as irritability, but also, for example, language and communication, positive behavior and social skills, and to some extent, adaptive behavior and life skills.

So, yes, the parents do have a role.

And it's the exact opposite of what we used to believe in the 1940s. They can help.

Okay, I promised you to discuss a few outliers.

I mentioned zinc.

What about omega-3 fatty acids?

There's been a few hints, a few wisps, a few speculations, but there is little evidence that supports the belief that the consumption of omega-3 fatty acids improve somehow autism spectrum disorder or even behaviors such as irritability.

So it seems that interventions with omega-3 fatty acids went nowhere.

However, I mentioned parent-parent intervention. And parental interventions include, for example, reading to the child. Reading to the autistic child improves phonological awareness.

But even so there's no evidence that reading to the child alone can manage irritability.

What about acupuncture?

So I'm discussing now the outliers, the speculative attempts to find ways to manage clinical features of autism that went nowhere, speculations that went nowhere.

And I mentioned fatty acids, I mentioned reading interventions.

Acupuncture.

There is very low quality, non-rigorous evidence that somehow attempted to link body acupuncture and modern acupuncture technology to the improvements in the social functioning of autistic children.

There's no evidence for skull acupuncture, acupuncture here on the head, but body acupuncture was linked somehow.

But the studies are beyond reprehensible. And I, having read them, I tend to feel comfortable and confident to say that acupuncture is definitely not effective in managing specific behavioral facets of autism such as irritability, maladaptive behaviors, that are not affected by acupuncture.

What about probiotics? Probiotic supplementation.

There's been some research on this and it compared daily probiotic supplementation and intranasal, so daily probiotic supplementation with intranasal oxytocin spray alone in combination and so on so forth.

What the study found is that patients receiving the combination treatment probiotics with oxytocin improved several indices, several indexes of autism. For example, they improve their autonomic indices.

Autonomic indices are bodily. So for example, heart rate variability is an autonomic index in autism spectrum disorder.

And a combination of probiotics and oxytocin allowed the subjects, allowed the patients with autism to control or to better manage some autonomic indices, for example, heart rate variability.

Other research indicated that probiotics alone might help relieve behavioral and gastrointestinal symptoms for patients with autism.

It was other work that suggested that intranasal oxytocin taken as monotherapyenhances neural sensitivity and improves results, overall results for people with autism.

So what I'm trying to say is that we are far from any conclusive evidence, but they're promising signs.

And also we're beginning to understand that the intestines, our guts, are as important as our brains in regulating mental health conditions.

And I have a video dedicated to the role of the gut or the role of the intestines in regulating and promoting mental health and in generating mental illness.

So clearly probiotics should have some impact. We're not yet sure what it is.

So these are the most recent developments in the study of autism spectrum disorder.

And now as promised the second half of the video, I will give you a general introduction to autism spectrum disorders.

We're starting with etiology.

Etiology is causation. What causes autism spectrum disorders?

In the 1940s, there was a series of papers which at the time were considered to be seminal. The papers were written by Leo Kanner, K-A-N-N-E-R. And Kanner suggested that autism spectrum disorders resulted from rejection of the infant by emotionally cold parents, especially the mother.

And he coined the phrase, refrigerator mother.

Bruno Bettelheim, a bit of a con artist in his own right, but a brilliant genius otherwise, in the 1950s and 1960s, popularized this idea and it became very, very influential.

So for three decades, the community of psychologists and psychiatrists and therapists and social workers believed firmly that it was the mother's fault if her children turned out to be autistic.

This was a gross injustice because it is absolutely not founded on any clinical data or experiment or study. It's an infuriating case of charlatanism.

Connor was a charlatan and so was Bettelheim in this particular case.

Since then there have been numerous studies, family studies, individual studies and so forth.

And this hypothesis, which has never been substantiated in any way, shape or form, this hypothesis has been utterly disproved and discredited.

The development of autism spectrum disorders in children has nothing to do with faulty bad parenting. It's a myth, a nonsensical myth, as nonsensical as the myth that autism is caused by vaccination or vaccines.

Now, of course, parents feel guilty when their children turn out to be defective somehow. And adding to that by saying that the parenting style of the mother has caused the autism really created a major mental health crisis among mothers and fathers of children with autism spectrum disorder.

Here's the fact. The causes of autism spectrum disorder are unknown. I repeat, we do not know what causes autism spectrum disorder. End of story. Anyone who tells you otherwise is either ignorant or a con artist.

We don't know. There are as many hypotheses as I have socks and I have many socks.

So obstetric complications, infection, genetics, toxic exposure, none of these has been established as a definitive etiology.

No studies, no proof, no evidence.

There are many factors associated or correlated somehow with autism spectrum disorder, including, as I said, maternal and paternal ages, the difference between the ages of the mother and the father, Caucasian or Asian race of mother and father, college graduation of mother and father, and so on and so forth.

But these are tangential correlations. They are not really causative.

And because these are not randomized trials, but observational, they are not rigorous, and theyshould not be taken seriously.

Now, I review some of the more resounding hypothesis, the hypothesis that you can find in textbooks and so on so forth.

Starting with obstetric complications.

Many individuals with autism spectrum disorder and other neuro-related neurodevelopmental problems did experience problems in the prenatal and neonatal periods, and especially during delivery.

There is a high incidence of such problems in the etiology and the anamneses of patients with autism.

But it's not clear if there is causation. It's not clear whether the obstetric complication caused autism or whether the obstetric complications and the autism were caused by a third factor for example environmental problem of some kind drug consumption alcohol consumption and so on.

During the perinatal period, factors associated with the risk of autism are hypertension or diabetes in the mother, threatened abortion, antipartum hemorrhage, cesarean delivery, gestational age of under 36 weeks, parity of over four, spontaneous labor, induced labor, no labor, bridge presentation, preeclampsia, fetal distress, you name it.

During the postnatal period, factors associated with risk for autism include a low birth weight, postpartum hemorrhage, male gender and brain anomaly.

By the way, to the best of my knowledge, no one has studied the possible linkage between postpartum depression and autism spectrum disorder. But it's an interesting thing to explore.

In a very large Danish study published in Jama, the maternal use of valproate, which is a medicine used to treat epilepsy, migraines and bipolar disorder. It seems that the use of valproate during pregnancy was associated or is associated with a significantly increased risk for autism in the offspring.

So we are beginning to learn that certain medications consumed during pregnancy are correlated and sometimes strongly correlated like valproate to autism in the newborn, in the child.

Similarly, exposure of a mother to SSRI's antidepressants, particularly during the first semester, may increase the risk that her offspring will develop autism spectrum disorder.

Thyroid problems are also associated with the risk of having a child with autism. That was a pretty large study actually, more than 5,000 women and 4,000 children.

So there is no debate and there is no denying that problems with the mother's body, metabolism, exposure to substances, problems in the gestation, the pregnancy, problems in the environment within her body, problems in delivery, problems post-delivery, postnatal, are all definitely linked to the emergence of autism spectrum disorder.

We just don't know how and we don't know if there's a third cause something that causes both and we are not quite sure if these are critical factors or contributing factors sufficient or necessary conditions.

But autism spectrum disorders, as I said at the very beginning, are bodily, the body related.

So evidently, anything that affects the body might have an impact on the formation and the genesis of autism spectrum disorders, the pathogenesis of the disease, infection for example.

There have been a few, in the last few decades, there have been a few cases, a few scholars who suggested that there is an infectious basis for some cases of autism spectrum disorder.

A large number of children born with autism are born to women who contracted rubella during pregnancy, for example.

So the hypothesis that infections trigger some vulnerability to the development of autism in the fetus is not entirely crazy, not entirely lame, should be studied more deeply.

What about familial factors, genetic factors, hereditary factors?

If autism spectrum disorder is a body thing, and other body issues such as schizophrenia, such as borderline personality disorder, such as antisocial personality disorder, psychopathy, such as bipolar disorder, whenever the body is involved in the genesis or pathogenesis of mental illness, we find a hereditary, a pronounced hereditary genetic component.

Is autism the exception?

No, it is not.

Familial factors influence the risk for autism.

The rate of autism in children born into families that already have a child with autism spectrum disorder is as high as 19%. The risk is twice as high in children born to families with two or more children of autism. In other words, they have a 40% chance to develop autism. Girls born to a family that has a child with autism have 2.8 times the risk of having such a disorder, a neurodevelopmental disorder.

There's very, very strong evidence that autism spectrum disorders are hereditary.

Twin studies have demonstrated that there is a degree of genetic heritability for autism spectrum disorder, with the environment making a substantial contribution to the development of these conditions in the study subjects.

That's very intriguing.

It seems that autism, perhaps like narcissism, is a predisposition. It is genetic, it is inherited, but what is inherited is the predisposition.

And then somehow the environment triggers the predisposition, expresses, causes the genes to express. And the environment could be the mother's body during gestation. The environment could be postnatal events. The environment could be toxic chemicals.

Things in the environment somehow trigger the genes responsible for autism spectrum disorders, somehow cause them to express. It's nurture in nature in collaboration and I have a strong suspicion that this is precisely the case in pathological narcissism, by the way.

Multiple family studies suggested that there are genetic components in many cases of autism spectrum disorder.

So we know, for example, that asymptomatic first-degree relatives of some pro-bands with autism have abnormalities in serotonin and other chemicals similar to the probands.

And we have been trying very hard, especially in the past decade, to somehow locate the array of genes which would give rise to autism, finding the genetic base for autism.

Hitherto we have failed.

But it's a very interesting failure. It's a failure that contains the seeds of success.

So for example factor analysis of data sets from the autism genome project suggested some kind of linkage of a joint attention factor between some gene called 11 Q23 and a repetitive sensory motor behavior factor with another gene called 19Q13.

So what this means is that clinical features and elements of autism can be traced back to highly specific genes or to gene arrays which are somehow linked.

They work together. They are connected.

A third of monozygotic twins are concordant for autism spectrum disorder. Dizygotic twins are concordant for autism at the rates of 4 to 8% which is comparable to siblings.

So clearly monozygotic twins are much more susceptible to autism than dysegotic twins which are comparable to normal siblings.

Again, proof positive that genes have something to do with it.

A focused neurogenetic evaluation of children with autism yields a genetic disorder in two-fifth of the children.

It's huge, by the way. In most genetic studies, we get a much lower result.

Mutations in the gene Shank 3 are associated with autism very strongly.

And there is this story of the fragile X syndrome. It's a kind of autism spectrum disorder. It's a subtype and it can be identified through genetic testing.

Antagonists to metabotropic glutamate receptors can reverse the symptoms in mice at least with fragile X syndrome and there's another type of autism known as tuberous sclerosis it's a disorder with specific genetic mutations and there's a lot more.

This is not a seminar that's an introduction.

I've mentioned that I believe all the indications are that there is a predisposition to autism which is somehow triggered by the environment.

And among other things, I've mentioned toxins, toxic exposure. Exposure to toxins, chemicals, poisons and other substances. This has been hypothesized for a long time now as a cause for autism spectrum disorders.

Roberts and Sampson reported an association between exposure to the organochlorine pesticides and during the first trimester of pregnancy and subsequent development of autism spectrum disorder.

So it seems that pesticides or some types of pesticides induce autism to a level that a correlation can be safely established.

Potential mothers are advised to avoid, of course, these.

In parts of the world, exposure to specific toxins may influence local rates of autism spectrum disorder.

For example, there's a very high incidence of autism in areas of Japan.

And when we try to see what is different in these areas why the population of the cohorts in these areas are prone to autism we discovered that these areas and these areas only consume a highly specific fish with a toxin. This fish contains a toxin and they consume the toxin.

Now, toxins may play a role in the development of isolated cases of autism in Japan, but we have yet to prove that they are generally causative of autism in Japan or anywhere else.

Another possible explanation, for example, for this high rate of autism in Japan, is the excellent training of Japanese clinicians. They're among the best in the world in diagnosing autism.

Maybe low rates in other countries is because the clinicians there have limited abilities to diagnose autism spectrum disorders.

Now there are studies that connect or link autism spectrum disorders to air pollution.

In North Carolina, for example, there was a study that linked exposure to traffic-related air pollution, particularly during the third trimester, to the development of autism spectrum disorder in offspring.

And these results add to the evidence already provided by previous studies conducted in this case in California.

And there was a study of children living in counties in Pennsylvania. They found that children with autism were 1.4 to 2 times more likely to have been exposed to higher levels of air pollution, especially chromium and styrene and so on so forth, during pregnancy, and in the first two years of life.

So these children were twice as likely to have autism spectrum disorder.

Cyanide, methylene, chloride, methanol, and arsenic are also linked, or well linked in studies to autism spectrum disorder.

I mentioned parental age already. Epidemiological studies have shown that ASD risk in offspring increases when the age of either parent is 35 years or older or higher.

Sandin and his collaborators reported that after controlling for parental age, the adjusted relative risk for autism was 1.52 in the offspring of mothers aged 35 years or older compared to mothers age 25 to 29.

By the way, this applies equally well to mothers under the age of 20.

Haltmann and his collaborators found that after controlling for maternal age, offspring of men aged 50 years or older were 2.2 times more likely to have autism than offspring of men aged 29 or younger.

I mentioned vaccination at the outset of this video and now let's discuss the diagnosis of autism spectrum disorder.

Can we really diagnose such a fuzzy neurodevelopmental disorder? We don't know what causes it, we don't know what to link it to, we're not sure about anything. I mean, how can we safely diagnose it and how can we tell it apart from dozens of highly similar conditions, as we will see in a minute.

The criteria for diagnosing autism spectrum disorder are included in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, and then International Statistical Classification of Diseases and Related Health Problems, 11th Edition, ICD 11.

So the DSM and the ICD, both of them agree that there is such a neurodevelopmental disability called autism and that it is a spectrum and that there are multiple disorders related disorders in a kind of family.

But the criteria for autism differ in the DSM and the ICD. They're not the same.

The differences in the criteria for autism spectrum disorders and related conditions in the DSM-5 text revision and the ICD 11 and other nomenclatures is a major problem.

The criteria are presented in ways which render these disorders, arguable, if not incompatible.

Generally speaking, the description of autism spectrum disorders, and by the way, other childhood developmental and neurodevelopmental disorders and other child pathologies, psychopathologies, but especially autism spectrum disorders, in both the DSM and the ICD 11, DSM-5 and ICD 11, the description is very poor, ill-substantiated, speculative, and very problematic.

They do not fully describe, for example, the concepts incorporated in the criteria for autism and related conditions.

So an inexperienced clinician is likely to incorrectly apply the criteria for autism.

Because it's so fuzzy, so ill-defined, so vague.

The diagnosis of autism spectrum disorder and the DSM-5-TR text revision has two key criteria.

Number one, impairments in social communication and social interaction, vague as they come, and a restricted, repetitive range of interest, behaviors, and activities.

That's more specific, much more specific, but regrettably it's common to dozens, literally dozens of other disorders, some of them genetic, some of them neurodevelopmental, some of them mental, some as we will see.

Clinician experience therefore is supercritical because you cannot rely on the diagnostic text.

The diagnosis of autism and related conditions is very, very problematic and relies crucially on the personality, exposure and experience of the diagnostician, which is bad.

It means it's not a clinical entity. That's bad.

And everyone and his mother-in-law are diagnosing autism, pediatricians, clinicians, therapists, psychiatrists, social workers, you name it. They slap this label on children.

The same way they slap the label of ADHD, the same way people today slap the label of narcissism on everyone and his dog.

It's a problem. It's a problem because delayed diagnosis of autism and related conditions may hinder the chances of treatment if the diagnosis is delayed and treatment is not initiated early on the likelihood of a favorable prognosis, favorable outcome is much reduced.

And so we have what are the tools that we have except the clinicians experience, one in a hundred, what are the tools that we have?

Not much.

Start with screening tests.

There are procedures available for diagnostic screening, including what is known as the Checklist for Autism in Toddlers or Chat. And there's a modified chat, M-Chat, and quantitative chat, Q-Chat, the chat family.

The problem with chat is that quite a few of the items in this test are strongly culturally biased.

But I mean strongly. It's like a test written by white middle-class men in the West.

It can be applied probably in some parts of the United Kingdom, not all, and maybe some parts of the United States and Canada. I think that's about it.

There's a need to adapt chat, this tool, a need to adapt it to specific cultural settings, cross-cultural adaptation is crucial.

The three items of chat that are highly predictive of the development of autism spectrum disorder are proto-declarative pointing, gaze monitoring, and pretend play.

And even babies engage in these behaviors, in the presentation, the stage called presentation, which is essentially observing infants and toddlers, they engage in these behaviors.

And so this core of three behaviors, pointing, gaze monitoring and pretend play, they're faking as if they're playing, but actually they're not socially interacting. These are strong indications that autism spectrum disorders should be further investigated.

Motoric skills, self-care skills, clumsiness, sensory issues should all be observed as well.

But we need a standardized test to assess sensory processing difficulties.

And so, you knowthis is a problem. We don't have a really good sensory processing measure. We don't have anything that can cope aptly and amply with the short sensory profile of children with autism. And we cannot therefore construct a sensory profile for infants and toddlers in any meaningful or rigorous way.

I mentioned culture. Culture is a problem.

When you evaluate children, cultural considerations are paramount.

For example, there are cultures and civilizations and societies where eye contact is forbidden. So gaze monitoring would fail in these cultures.

The way people play or avoid playing with each other, social interaction, pragmatic use of language, they're all culture-bound, they're all highly specific, sometimes within a region, not a country even, a region, a state, a county, a city.

So we need to take this into account, especially when the family's primary language is not English. And all the tools we have are in English.

We have serious problems in diagnosing autism spectrum disorders because the overlap of the clinical features of autism with other diseases is infinite, literally infinite. Differential diagnosis is near impossible.

So I can read to you a list of dozens of disorders that can be easily mistaken, even by experienced clinicians and diagnosticians, can be easily mistaken for autism spectrum disorders.

They include physical problems such as infantile hydrocephalus. They include genetic problems such as interstitial deletion of certain genes. They include language disorders. They include all kinds of diseases such as Minamata's disease or Mobius syndrome or non-ketotic hyperglycinemia. Epilepsy, they include disorders such as Tourette's syndrome, Trisomy 22, lead poisoning, I mean, it's mind-boggling.

The number of disorders we have to rule out before we reach a conclusion of autistic spectrum disorder is ginormous. And it includes very common problems such as anxiety disorder, obsessive compulsive disorder, attachment disorder, congenital rubella syndrome, down syndrome, failure to thrive, physical child abuse, Rett syndrome, William's syndrome, I can continue.

Someone has made a list of 100 conditions that we should rule out before we diagnose autistic spectrum disorder.

And who is doing this? No one.

There is a serious probability that the vast majority of children and people, adults, diagnosed with autism spectrum disorder, actually do not have autism spectrum disorder of any kind. They do not have a neurodevelopmental disorder. They have something else.

And that's a very sad and sorry state of affair.

Now, it's not that we are totally helpless. We do use some instruments developed to diagnose autism spectrum disorders.

We use these tools, if we know how to use them in a reliable and valid way, experience matters, as I mentioned, and experienced clinicians usually can immediately identify deficits, particular deficits in children with autism.

But we can't rely on a clinician's experience and intuition. This is not medicine. This is witchcraft. This is quackery. It's not serious.

And when we try to become serious, for example, there's been studies of metabolic abnormalities. And we identify some metabolic problems in people with autism spectrum disorder, but we couldn't find any biological markers. And so it went nowhere.

We tried neuroimaging. There's no clinical evidence to support the role of neuroimaging in the diagnostic evaluation of autism spectrum disorder. None.

Even when there are abnormalities in the brain, for example, megalencephaly or similar disorders, even then, neuroimaging is not very helpful. The results are inconsistent.

But we couldn't find a diagnostic. We couldn't come up with the diagnostic finding.

What about electroencephalography, EEG?

It's useful for ruling out, for example, seizure disorders, acquired aphasia with convulsive disorder, the Landau-Kleffner syndrome, biotin-responsive infantile encephalopathy, and so on so forth.

So EEG is used to rule out some, few of the hundred similar conditions but it cannot be used to diagnose autism.

So we are reduced to psychophysiologic assessment to observing the child or the infant or the toddler or the adults.

We observe. There's nothing else we can do. Nothing objective. Nothing quantifiable. We just observe.

How do people breathe? I'm kidding you not.

Response habituation in respiratory periods, electrical conductance or electrodional activity in the skin, vasoconstrictive peripheral pulse amplitudes, and so on so forth.

We're trying to isolate stimuli.

The very same technique is used in polygraph, in lie detectors. And that's why they're not admissible in court. They're not reliable.

We know, for example, the children with autism spectrum disorders, some children display auditory over-selectivity, but only some. Others don't.

What about polysomnography?

Most children with autism spectrum disorder, as I've mentioned, experience sleep disturbances. Early morning awakening, frequent arousals, fragmented sleep, and you name it. Poor kids.

So we could study this.

Children with autism display prolonged sleep onset and abnormal sleep architecture. Polysomnography can somehow be useful in identifying sleep disorders or even in demonstrating seizure discharges.

But can it tell us that someone with a sleep disorder also suffers from autism spectrum disorder?

No, of course it can't.

What about genetic testing?

General guidelines from the American Academy of Neurology and the Child Neurology Society recommend genetic tests. High resolution chromosome studies, DNA analysis, fragile X, chromosomes and so.

They say in their guidelines that it could lead us to identify autism spectrum disorder in children.

But this is very misleading.

Only children who fulfill highly specific diagnostic features, only children with highly specific clinical features can be diagnosed with genetic testing.

For example, only children with an intellectual disability that cannot be excluded. Only children with a family history of fragile X or undiagnosed intellectual disability. Only children with dysmorphic features.

How many autistic children have all this? A fraction, a tiny fraction. It's useless. Genetic testing at this stage is useless.

What about neuroimaging? MRI?

MRI has been applied of course to patients with spectrum disorder, but the results were inconsistent and I'm being very charitable. Inconsistent.

There were typical findings, of course. There was enlargement of the total brain, the total brain tissue, and the lateral and fourth ventricles, along with reductions in the size of the midbrain, the medulla oblongata, the cerebral, the cerebellar hemispheres, and vermal lobules, six and seven.

Okay, so we found these features, these brain abnormalities in many children with autism spectrum disorder.

The problem is these features exist also in children with no autism, without autism, not autistic children.

For example, verbal hypoplasia is found in some individuals with ASD, and verbal hyperplasia is identified in others. The volume of gray matter is bilaterally decreased in the amygdala, the precuneus and the hypochampus of people with ASD.

Adolescents with ASD have shown greater decreases in the volume of the gray matter of the right pre-cuneus than adults. The volume of the gray matter in the middle inferior frontal gyrus has been found to be slightly decreased, I'm sorry, with people with autism.

So yes, there are all kinds of abnormalities, statistical abnormalities. By the way, increased decrease is a very relative term.

So imaging studies of people with, or patients with autism spectrum disorder, who, for example, exhibit head banging, show enlargement of the dipoleic space in the parietal and occipital bones, loss of gray matter, and with these bony changes.

But that's to be expected. Maybe it's nothing to do with the autism. It has to do with the headbang.

Okay. Same applies to diffusion tensor imaging, to computed tomography, to spec single photon emission CT scanning, and ironically, the oldest technology of all, EEG, is useful for ruling out several neurological and neurodevelopmental disorders and narrowing the field so that autism becomes much more likely.

But globally speaking, neuroimaging is not helpful. Simply not helpful.

And I mentioned already the genetics is not helpful, the neuroimaging is not helpful.

The dirty secret of autism spectrum disorder is that it depends, your diagnosis depends on the clinician. Your likelihood of receiving a diagnosis which is wrong is exceedingly high actually, unless you're willing to pay a fortune, not small fortune, to be investigated by the number one clinician in the field or number two, someone with vast experience.

So there are several research directions.

We're studying mutations. These mutations may explain the search and may explain the commonalities between several neurodevelopmental disorders.

We are studying metabolic abnormalities.

We try to find autism biomarkers through next generation sequencing, omics platforms, proteomics, metabolomics, maybe there's early age disease biomarkers, we don't know yet.

Beyond the brain, we're studying the role of other organ systems. So gastrointestinal system, quite a few studies taking place now.

Many individuals with autism spectrum disorder also report gastrointestinal dysfunction of some kind. It might be mediated psychologically. It might be some biological connection. We don't know yet.

Estimates of the prevalence of GI gastrointestinal disturbances within the autistic population vary among studies, but they range between 20 and a whopping 86%. Gastrointestinal dysfunction is more prevalent among individuals with autism than among non-autistic individuals. There's no debate about this.

The severity of gastrointestinal abnormalities is correlated with the severity of the autism.

There's a potential role for the gastrointestinal system. There's a modifier of ASD behavior and a factor in ASD ideology.

We're studying this abdominal pain, bloating, diarrhea, constipation, gastroesophageal reflux, we're studying all this, the connection to autism.

To summarize, more than 100 years after a Nazi Viennese doctor came up with Asperger's, we are still very, very, and I could add, another very, far, from knowing the first thing about autism spectrum disorder, to the point that there are scholars who doubt the very existence of autism spectrum disorders.

The same way other scholars doubt the existence of dissociative identity disorder or multiple personality disorder. It's a contested group of neurodevelopmental disorders.

And it's related so intimately and intricately to other kinds of diseases that, unless we find clear objective biomarkers, clear metabolic pathways, clear neurological pathways, a clear etiology, we're gonna continue with vague, equivocal, fuzzy, prone to speculation and conspiracy theories, discipline, which is the study of autistic spectrum disorders, as it is today.