Non-syndromic ASD is essentially nonverbal, nonresponsive ASD.
… There are many autistic people and kids who are not non-syndromic, an ASD diagnosis does not even require this kind of behavior.
Further, the proposed mechanism of action in using folinic acid to ‘treat’ autism is that it acts upon an abnormal level of folate blockers…
While it is true that ASD folks tend to have more of these folate blockers than non ASD folks…
Many of them do not.
Generally speaking, abnormal folate pathways… appear to be called Cerebral Folate Disorder (CFD) by this Dr. Frye who seems to be spearheading this line of research.
So… this would arguably be an identifiable subtype or subcomponent of ASD, that has an actual, physically identifiable (and seemingly potentially treatable) aspect to it, caused by a known cluster of genetic mutations, which themselves cause… basically, your neural pathways in your brain to just literally be different from those without the genetic mutation cluster.
Of course, epigenetics, to what extent and under what conditions genes actually express themselves is a complicating factor here.
Nurture can change how your Nature works, at a fundamental level.
More general commentary on the idea of Autism subtypes/conponents:
There is an emerging, but far from totally agreed on and fully explained… view, that, well, autistic brains, or at least certain potential subclasses of autistic brains… actually do have physically distinct brain chemistry and activity patterns than non autistic brains.
Basically, more and more actual genes and gene clusters are being identified, and at least some of those are being found to alter brain neurochemistry in measurable and mechanistically understood ways that nobody seems to have even known were possible before.
There could possibly thus be a propsensity toward an actually physically different reaction to many kinds of drugs from at least some autists.
But this is also fairly confusing because what is … currently being called ‘Autism Spectrum Disorder’ via psychological diagnosis… well, some autistic people have some of these mutations, some have all of them, some have none.
So… its far from fully understood, but it may be the case that in 5 or 10 years, Autism ends up being actually subclassed partially based on genetics and epigenetics, beyond just based on a description of behavioral patterns.
This paper is talking about using administered folinic acid to address a deficiency of folate transport within the brain, where that deficiency is caused by a known cluster of genetic mutations, in a person diagnosed with ASD.
This is not talking about causing autism via the mother taking something during pregnancy.
It is talking about how, for a subset of ASD people, who have this particular cluster of genetic mutations, that taking folinic acid can alleviate some of the symptoms associated with folate deficiency.
Nothing to do with folic or folinic acid taken by the mother during pregnancy causing autism.
Its talking about a potential subset of autism being potentially treateable, that subset being broadly in line with what the OP Nature article/paper here describes as ‘early diagnosis autism’, which has much more readily apparent and obviously recognizable behavior patterns than ‘late diagnosis autism’.
If you go into that paper, you will indeed see that they found that amongst people with ASD, but without the associated folate disorder connected mutations, giving them folinic acid doesn’t really make any noticeable difference…
… which arguably lends creedence to the idea that there are at least two different ‘kinds’ of actual things going on that, which are currently all being lumped together as ASD.
Copy pasting some sections of my own comments from similar discussions over the last month or so:
IRT Folinic Acid as a ‘treatment’ for Autism:
So… this would arguably be an identifiable subtype or subcomponent of ASD, that has an actual, physically identifiable (and seemingly potentially treatable) aspect to it, caused by a known cluster of genetic mutations, which themselves cause… basically, your neural pathways in your brain to just literally be different from those without the genetic mutation cluster.
Of course, epigenetics, to what extent and under what conditions genes actually express themselves is a complicating factor here.
Nurture can change how your Nature works, at a fundamental level.
More general commentary on the idea of Autism subtypes/conponents:
Folic Acid has been taken by pregnant women for over 40 years. Folic --> folinic
… ok?
This paper is talking about using administered folinic acid to address a deficiency of folate transport within the brain, where that deficiency is caused by a known cluster of genetic mutations, in a person diagnosed with ASD.
https://en.wikipedia.org/wiki/Cerebral_folate_deficiency
This is not talking about causing autism via the mother taking something during pregnancy.
It is talking about how, for a subset of ASD people, who have this particular cluster of genetic mutations, that taking folinic acid can alleviate some of the symptoms associated with folate deficiency.
Nothing to do with folic or folinic acid taken by the mother during pregnancy causing autism.
Its talking about a potential subset of autism being potentially treateable, that subset being broadly in line with what the OP Nature article/paper here describes as ‘early diagnosis autism’, which has much more readily apparent and obviously recognizable behavior patterns than ‘late diagnosis autism’.
If you go into that paper, you will indeed see that they found that amongst people with ASD, but without the associated folate disorder connected mutations, giving them folinic acid doesn’t really make any noticeable difference…
… which arguably lends creedence to the idea that there are at least two different ‘kinds’ of actual things going on that, which are currently all being lumped together as ASD.