We already know what is happening to the brain in autism

The following is a link to a lecture that I provided at Autism One 2014. The same is laden with some medical verbiage but it was meant to illustrate my way of thinking in regards to the causation of autism. I appreciate the kindness of the organizers in inviting me to offer a contrarian point of view to the antivaccine movement and to have published my lecture. (Note: Across the hall from my lecture Andrew Wakefield was delivering his presentations. When I directed members of the audience that believed in the mercury or MMR causation across the hall, it was meant to emphasize the fact that Mr. Wakefield and I hold polarizing views in regards to autism. Primarily, I emphasize hard science, not conspiracy theories).

The abstract for this lecture read as follows:

Autism is a developmental disorder caused by abnormal divisions of germinal cells. Evidence for this fact is based on the presence of malformations in the brains of autistic individuals. This mechanism of action appears to hold true for cases of autism of known (syndromic) or unknow (idiopathic) causation. Dr. Casanova’s specific area of focus recently has been the identification of risk factors that can propitiate germinal cell divisions during brain development in genetically susceptible individuals with autism. At present, one of the more intriguing factors appears to be the use of prenatal ultrasound. Dr. Casanova discusses the possibility that a triple hit in autism could explain the observed clinical heterogeneity of autism spectrum disorders. In this regard, variations in the severity of an exogenous factor(s) (one hit), timing during brain development (2nd hit), and genetic susceptibility of the individual (3rd hit) may account for clinical heterogeneity.

The video for the lecture (55 minutes long) is found at:


7 responses to “We already know what is happening to the brain in autism

  1. I am in complete agreement. I am a mother of fraternal twin boys whom both have autism. I had countless ultrasounds. I went into premature labor at 32 weeks. During my 2-3 day stay in the hospital to stop the labor I had at least 15 ultrasounds. That’s in about 2 days. I carried them to 37 weeks. Prior to delivery I was high risk and needed almost daily heart beat checks. It was hard to find both heart beats so they would get an ultrasound machine and check their location to find the heart. That was just laziness. I wish I knew more back then. They are 12 now. I’m sure I had over 25 ultrasounds throughout the pregnancy. I do have a 14 year old daughter that is fine. I had about 2 with her.


  2. Not so much a comment on the content of your lecture,but would you be willing to tell me why a serious researcher,like yourself,or like Dr. Frye,would speak at Autism One? Autism One has a questionable to poor reputation among many because of the doctors who speak there who believe vaccines cause autism,and advocate all sorts of pseudoscience to treat it.

    Do you believe that sharing the stage with such people harms the credibility of more serious researchers?


    • I believe you can spread good science regardless of the forum. Hopefully my own lectures have helped many individuals make correct decisions. I have not been invited again to AutismOne.


  3. A direct question: there are more than 100 genes linked to the disorder. They all convey within three functions in the brain. Which are these functions?


  4. There are possibly over a thousand risk genes identified in autism. For those where the genes have a strong penetrance and provide for syndromic forms the neuropathology shows evidence of abnormalities of germinal cell division, migrational abnormalities and cortical malformations.


  5. This may be what can cause autism, but neural migrations have been suspected to be responsible for schizophrenia, bipolar, adhd, and even epilepsy patients who are otherwise neurotypical. Two identical twins, neural migration error, but one gets autism and the other schizophrenia has been found. There is evidence of heavy genetic overlap for all these conditions. So if a neural migration error occurs, what decides who will get what? And there are patients with more than one of these disorders. But these are distinct conditions on their own, and while there is a lot of heterogenity in autism and the others, there is enough in common for them to be separate diagnosis. What stops a person from having a completely unique condition because of neural migration? Why do they cause specific disorders in particular? There may be enough differences in genes, timing, and the trigger for heterogenity and distinct conditions, but it seems not enough for it to be absolutely random what symptoms a persons displays. They gravitate towards definable diagnoses.

    Liked by 1 person

    • Also there are differences now being found in asperger syndrome, and possibly more subtypes of autism. The rule of thumb is the more severe and crippling the disorder is, the more enviromental and less genetic it is.
      Not all autistic people have been found to have gross abnormalities like abnormal brain masses like the severe end. What they have found is misplaced gene expression (which can result from migration abnormalities, the gene expression is misplaced but not enough has occured to cause dysplasias). Yet there are people with epilepsy with dysplasia and lesion who are not autistic. I think there is still much more to be found.

      Liked by 1 person

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