American Professor Couple Identify Major Cause of Autism

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And I'll wait until this "amazing discovery" is replicated and verified by many other scientists.

Meanwhile, I’ve been carrying on with the diet and treatment protocol that works to treat ASD well enough for me to continue living the second life that I am. I’ve been working full time and having fun kiteboarding in the Summer, hanging out at the beach, going to a few major party weekends a year, and moving forward on various goals vs spinning my wheels in frustration waiting for someone else to tell me what to do. To each their own, though.

If I can persuade anyone local, or not, to analyze me and what I do in a clinical/lab enviro, I’d gladly participate in the name of science & sharing the wealth of this knowledge with the countless people it could help. But until then, all I have is my personal experience to share.

What diet?

Meanwhile, I’ve been carrying on with the diet and treatment protocol that works to treat ASD well enough for me to continue living the second life that I am. I’ve been working full time and having fun kiteboarding in the Summer, hanging out at the beach, going to a few major party weekends a year, and moving forward on various goals vs spinning my wheels in frustration waiting for someone else to tell me what to do. To each their own, though.

If I can persuade anyone local, or not, to analyze me and what I do in a clinical/lab enviro, I’d gladly participate in the name of science & sharing the wealth of this knowledge with the countless people it could help. But until then, all I have is my personal experience to share.

Probably a GFCF (Gluten free, casein free) diet or something like that.

And the article in question identifies the gut bacteria of the mother as a possible cause of autism. No mention of an individual's gut bacteria causing autism and then being cured via diet.

Also, I'd love to know how they diagnosed mice as "autistic."

As I posted about, here, in November of 2013. Science is slowly catching up to my experience, findings, and hypotheses. I’ve learned several things since but have yet to really write about them - some minor details, some significant experiences that confirmed a few things. Someday I’ll write an update.


Anyways; Link:
http://www.koreadailyus.com/korean-amer ... se-autism/

Apologies if it’s been posted. I did a quick search and didn’t find anything.

First off- Professors of what? Math? Economics? Doesn't say.

And I'll wait until this "amazing discovery" is replicated and verified by many other scientists.

"The researchers found out that certain bacteria in the mother’s digestive tract can develop immune cells that directly influence the baby’s brain cells development. When the researchers removed the bacteria with antibiotics, the mouse had a normal baby mouse."

Exp Neurol. 2017 Apr 25. pii: S0014-4886(17)30105-X. doi: 10.1016/j.expneurol.2017.04.010. [Epub ahead of print]
Maternal IL-17A in autism.
Wong H1, Hoeffer C2.
Prenatal exposure to maternal immune activation (MIA) has been implicated as an environmental risk factor for ASD.
...
Recent evidence points to a potential inflammation pathway linking MIA-associated ASD with the activity of T helper 17 (Th17) lymphocytes and their effector cytokine interleukin-17A (IL-17A). IL-17A has been implicated from human studies and elevated IL-17A levels in the blood have been found to correlate with phenotypic severity in a subset of ASD individuals. In MIA model mice, elevated IL-17A levels also have been observed. Additionally, antibody blockade to inhibit IL-17A signaling was found to prevent ASD-like behaviors in offspring exposed to MIA. Therefore, IL-17A dysregulation may play a causal role in the development of ASD. The source of increased IL-17A in the MIA mouse model was attributed to maternal Th17 cells because genetic removal of the transcription factor RORγt to selectively inhibit Th17 differentiation in pregnant mice was able to prevent ASD-like behaviors in the offspring.

Science. 2016 Feb 26;351(6276):933-9. doi: 10.1126/science.aad0314. Epub 2016 Jan 28.
The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring.
Choi GB1, Yim YS1, Wong H2, Kim S3, Kim H3, Kim SV4, Hoeffer CA5, Littman DR6, Huh JR7.
Author information
Abstract

Viral infection during pregnancy has been correlated with increased frequency of autism spectrum disorder (ASD) in offspring. This observation has been modeled in rodents subjected to maternal immune activation (MIA). The immune cell populations critical in the MIA model have not been identified. Using both genetic mutants and blocking antibodies in mice, we show that retinoic acid receptor-related orphan nuclear receptor gamma t (RORγt)-dependent effector T lymphocytes [for example, T helper 17 (TH17) cells] and the effector cytokine interleukin-17a (IL-17a) are required in mothers for MIA-induced behavioral abnormalities in offspring. We find that MIA induces an abnormal cortical phenotype, which is also dependent on maternal IL-17a, in the fetal brain. Our data suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD-like phenotypes.
Copyright © 2016, American Association for the Advancement of Science.
Comment in

Neuroimmunology: IL-17A mediates a path to autism. [Nat Rev Immunol. 2016]
IMMUNOLOGY. Maternal TH17 cells take a toll on baby's brain. [Science. 2016]

What a load of bollocks, honestly how can anyone give any credence to this rubbish. I would have thought that the researchers (lol) were in serious danger of committing professional suicide.

What a load of bollocks, honestly how can anyone give any credence to this rubbish. I would have thought that the researchers (lol) were in serious danger of committing professional suicide.