Showing posts with label Autism Research Paradigm Shift. Show all posts

Autism Research Awakening: Environment Plays A Role In Causing Autism

“We have to look also at environmental factors, and from my point of view, the interaction between the genetic factors and the environmental factors ... It looks like some shared environmental factors play a role in autism, and the study really points toward factors that are early in life that affect the development of the child"

Joachim Hallmayer, MD,  associate professor of psychiatry at Stanford University in California

WebMD reports on a new study published in the Archives of General Psychiatry which  found that autism was surprisingly common in fraternal twins, despite the fact that they don’t share as many of the same genes as identical twins, suggesting that some common environmental factors might be playing as big a role in causing their autism disorders as genetics.  Dr. Hallmayer was one of the study researchers who were surprised with the result.  Is this an awakening in the autism research professions?

For some it probably is.  For others not so much.  Even this humble autism father/blogger reported an autism paradigm shift 4 years ago and I have followed it since then blogging on developments in the area of environmental causes of autism. But there are die-hards who will not be convinced, who will not change their minds no matter what. Academic careers and reputations as expert witnesses have been built promoting the view that autism is 100% genetic and that accordingly autism disorders are not actually increasing.  Reported increases of autism diagnoses are routinely dismissed as due entirely to diagnostic definition change and increased awareness.  Of course manufacturers of products from vaccines to children's toys have a vested interest in encouraging the "it's gotta be genetic" autism causation paradigm described over a decade ago by Teresa Binstock.  Many will never admit that autism could ever be caused by the interaction of environmental and genetic factors.  

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John Hopkins Study: Gene-Environment Interactions Influence Psychiatric Disorders


“Psychiatric diseases have genetic roots, but genes alone do not explain the entire disease ... When we study genes in conjunction with environmental challenges, we can better understand how diseases develop.” 

-  Mikhail V. Pletnikov, associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, Study: Gene-environment interactions influence psychiatric disorders, John Hopkins University Gazette

In a John Hopkins University study pregnant laboratory mice bred with a specific genetic variation known as mhDISC1 were given a drug to stimulate their immune systems at the end of the first trimester of  their pregnancies while other mice with the same genetic variation did not receive the drug. The genetic variation involved is believed to be associated with mental illnesses in humans. The mice receiving the drug produced behavioral abnormalities, elevated anxiety, depressionlike responses, an altered pattern of sociability and a weakened response to stress. These responses were not present in the mice who did not receive the drug which suggested that the conditions resulted from the gene-environment interaction not the genetic variation alone. The study reports  also indicate that the same genetic variation can give rise to different illnesses depending on interactions with environmental factors and can impact on the size of different brain parts incuding the amygdala and the hypothalamus areas found in the brains of humans with major depression and bipolar disorder.

The study results appear to be another significant example of  an emerging paradigm shift away from viewing psychiatric and mental disorders as purely genetically determined toward an understanding of such disorders, including autism disorders, as arising from gene-environment interaction.  Future studies are likely to reflect this paradigm shift:

"Previous studies have suggested that the prenatal immune response to a microbe—be it a major illness or just transient flulike symptoms barely noticed by the pregnant woman—may be responsible for the increased incidence of adult psychopathology in humans. But this hypothesis, Pletnikov said, has been difficult to prove. Using this mouse model, he suggested, is a valuable way to study the relationship between gene-environment interactions and mental illness, and should be replicated to find more of these interactions to gain a better understanding of these relationships.

Future studies, he said, will try to sort out whether different timing or stimulating different parts of the immune system might lead to specific types of mental illness, and will explore the consequences of other environmental adverse events such as stress or drug abuse."
 
The John Hopkins University Gazette article by Stephanie Desmon of John Hopkins Medicine lists several supporters of the study including Autism Speaks.

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