The Big Idea: We have massive data showing the genetic or epigenetic basis of autism, together with a handful of environmental toxins.
What Does Cause Autism?
We now have data and information on more than one million children that show vaccines do not cause autism.
Instead, the brains of kids (and of course, ultimately, adults) with autism are structurally different.
Some children with an ASD seem to develop normally until around 18 to 24 months of age and then they stop gaining new skills, or they lose the skills they once had.
The first scientific article to use it came from Dr. Leo Kanner in a 1946 paper.
Children with ASD often have large heads.
The Piven group reported that brain volume overgrowth “was linked to the emergence and severity of autistic social deficits.”
Recently, additional evidence suggests that the changes in the brains of children with ASD begin even earlier than at 6 – 12 months old and actually start before birth — during prenatal development.
Possibly, we can now predict by 6 months of age whether a child will develop ASD, but the Courchesne findings suggest we might soon be able to predict autism at birth or even prenatally.
So what first triggers the alterations of the cortical layers in the prefrontal and temporal regions of the brain as described by Courchesne’s group? There is a lot of evidence pointing to altered genes — changes to the DNA either through point mutations or even deletions of entire regions of DNA.
“Our analysis identified a clear developmental pattern — a prenatal signal from the early, mid and late fetal stages — indicating that autism associated genetic changes affect the development of the fetal prefrontal, temporal and cerebellar cortex.”
Unfortunately, the yield for identifying alterations in autism genes is not high, because there may be almost 1,000 genes for autism and we have only identified about 65 of them.
An important influence is the role of epigenetics, a rapidly growing field of modern science, which refers to how genes are modified, especially in very early pregnancy, at or around the time of conception.
Epigenetics is likely to also have an important role in the events leading to ASD and autism. Again, we need significant investments in the science of autism epigenetics.
Possibly through epigenetic or as still yet undefined mechanisms, certain prenatal exposures or environmental factors, such as specific chemical toxins in the environment or even congenital infectious agents, may cause abnormal fetal development leading to ASD.
However, the Lipkin group has found that maternal fever, especially multiple fevers or fever in the second trimester of pregnancy, could be linked to ASD. Such findings provide further support for maternal infections during early pregnancy in promoting autism.
The Landrigan paper further identifies chemical toxins in the environment that could also lead to ASD.
They include drugs or chemicals such as valproic acid, a neuropsychiatric medicine that helps with mood stabilization, an organophosphate insecticide known as chlorpyrifos, thalidomide, and misoprostol, among others. In contrast, the Landrigan paper rules out vaccines.