MTT And Symptom Reduction In Autism

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Is the current hypothesis of autism being a biopsychosocial disease still valid? The study did not state if they considered the effect of increasing abundance of Bifidobacteria and Prevotella on neurotransmitter production. They mention the gut-brain axis but seem to skip over neurotransmitters. Bifidobacteria produce GABA.

Maybe it is related to early life diet via breastmilk or formula. Prevotella produces succinate which is involved with blood glucose regulation. Ref 1 states that Prevotella favor high monosaccharides and Bifidobacteria favors oligosaccharides (found in breast milk).

The study is good but there are many factors involved. Sure MTT can work (seems to be flavor, gross, of the month for many diseases) but note there was a study that indicated European children completely lack Bifidobacteria (or maybe Prevotella). Also, only n = 18 not sure about the statistical power of the experiment. So is it the diversity of gut microbiota or the fact that the gut microbiota helped digest/produce nutrients that an American diet is otherwise lacking compared to other parts of the world. The United States has one of the highest incidences of Autism compared to other similar countries.

Questions: Have there been studies that look at incidence in Autism for breastfed vs non-breastfed infants? Mother's diet during breastfeeding? History of GI/brain disorders in the mother corresponding to the incidence in Autism of their offspring?

Further Reading: 1 - The Gut Microbiome and the Brain
2 - Neurotransmitters: The critical modulators regulating gut-brain axis
 
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Is the current hypothesis of autism being a biopsychosocial disease still valid?

Not really sure what you mean by this. "Social" etiologies of ASD are largely discredited these days. The prevailing theory is that the cause of ASD is genetic and epigenetic.
 
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Not really sure what you mean by this. "Social" etiologies of ASD are largely discredited these days. The prevailing theory is that the cause of ASD is genetic and epigenetic.

That is true. Autism-linked genes are related to many other neuro diseases, a handful of which are nutrient and GI related. The social aspect (I would think, might be wrong) comes into play during the phase of development where environmental factors contribute to Austism. Again, it is a very multifaceted disease. Social determinants of health could be a large factor (teratogen exposure, maternity nutrition, epigenetic alterations, etc).

At least we can all agree that vaccines do not cause Autism.
 
That is true. Autism-linked genes are related to many other neuro diseases, a handful of which are nutrient and GI related. The social aspect (I would think, might be wrong) comes into play during the phase of development where environmental factors contribute to Austism. Again, it is a very multifaceted disease. Social determinants of health could be a large factor (teratogen exposure, maternity nutrition, epigenetic alterations, etc).

At least we can all agree that vaccines do not cause Autism.

By “social” factors I thought you were referring to, for example, the largely discounted “refrigerator mother” theory of ASD. I agree that environmental factors do affect epigenetics and could play a role in etiology or symptom severity. I would say that genetic factors are underestimated, as polygenic interactions are difficult to determine. Currently, approximately 25% of ASD can be attributed to a known genetic cause.
 
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I’m in an ASD research lab. From a neuropsych genetics standpoint (which is more of my area), ASD seems to primarily be related to ADHD and schizophrenia. However, many disorders and medical diseases are often comorbid (or run in the family) including autoimmune diseases and GI issues.

As far as I know, ASD is recognized by most researchers in the field to essentially be multiple disorders (hence the spectrum idea and combining of multiple diagnoses) with similar symptoms but multifactorial causes. For example, although PTEN is a gene associated with some cases of ASD, no one “ASD gene” has been found because there are different causes of different presentations.

As for the study, I actually attended a genetics of ASD lecture a few months ago and heard some similar findings. When someone asked why the “cause” of ASD is so hard to find and why there are conflicting research results, the presenter’s opinion was essentially what I mentioned earlier about there being different causes of different presentations of ASD (e.g., a kid macrocephaly and ID with no family history vs. one with above average intelligence, “quirkiness” regarding routines, and a family history of similar issues).
 
I’m in an ASD research lab. From a neuropsych genetics standpoint (which is more of my area), ASD seems to primarily be related to ADHD and schizophrenia. However, many disorders and medical diseases are often comorbid (or run in the family) including autoimmune diseases and GI issues.

As far as I know, ASD is recognized by most researchers in the field to essentially be multiple disorders (hence the spectrum idea and combining of multiple diagnoses) with similar symptoms but multifactorial causes. For example, although PTEN is a gene associated with some cases of ASD, no one “ASD gene” has been found because there are different causes of different presentations.

As for the study, I actually attended a genetics of ASD lecture a few months ago and heard some similar findings. When someone asked why the “cause” of ASD is so hard to find and why there are conflicting research results, the presenter’s opinion was essentially what I mentioned earlier about there being different causes of different presentations of ASD (e.g., a kid macrocephaly and ID with no family history vs. one with above average intelligence, “quirkiness” regarding routines, and a family history of similar issues).

You are largely correct. There is no one gene. There are hundreds of identified genes, each contributing to at most 1-2% of cases. But together, these highly penetrant mutations (FMR1, PTEN, SHANK3, CHD8, etc.) make up ~25% of ASD cases. The other 75% may be due to multiple “hits” (i.e polygenic or genetic susceptibility plus environmental factors).
 
You are largely correct. There is no one gene. There are hundreds of identified genes, each contributing to at most 1-2% of cases. But together, these highly penetrant mutations (FMR1, PTEN, SHANK3, CHD8, etc.) make up ~25% of ASD cases. The other 75% may be due to multiple “hits” (i.e polygenic or genetic susceptibility plus environmental factors).
Sorry if I wasn’t clear, but yes the other 75% is what I was referencing as being multifactorial. PTEN was just an example of one specific gene identified in some (the 25%) cases of ASD.
 
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