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Theory of mind and autism


Shawnus

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Hello, just a quick question, I am writing a little piece about theory of mind and I someone asked me something that should be obvious to answer but I feel a bit stumped. If theory of mind is such an excellent adaptation to our reproductive success, then why is the number of people diagnosed as autistic increasing?

 

 

My thoughts are.. diagnosis for autism has changed and this has increased the number of people labelled autistic?

 

Autism too generic a term to provide an accurate picture?

 

Potential environmental factors could be taken into consideration when looking at the number of people receiving this diagnosis?

 

Quite a rushed question, but a third persons opinion will help me focus my arguments a little better. Right now my brain feels mushy.

 

Thanks

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Your three arguments are exactly what I would use. They were my first thoughts when reading your question.

 

Also, you might add that theory of mind helps in reproduction because you can game the mind the potential mating partner better. Gaming someone else through a good understanding of what they're thinking or feeling to convince them to copulate with you has actually zero to do with how their genes will ultimately combine with yours when mating.

 

Basically, whether or not your prospective mate drops their pants (where theory of mind comes in) has zero to do with the probability of any offspring conceived during that session of coitus landing somewhere on the autism spectrum.

 

 

Beyond that, I agree that diagnoses have increased along with awareness, that the general term "autism" is a bit too broad to encompass the spectrum of issues we actually see, and that environmental factors could play a role.

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Hello, just a quick question, I am writing a little piece about theory of mind and I someone asked me something that should be obvious to answer but I feel a bit stumped. If theory of mind is such an excellent adaptation to our reproductive success, then why is the number of people diagnosed as autistic increasing?

 

 

If you look at the history of "treatment" for any mental abberations (or physical also) and the common prevalence of infanticide throughout history--until just the past several generations--you might wonder if many autists, aspies, or "idiot-savants" could ever survive to reproductive age... until just the past few generations.

 

The fact that these traits seem to be on a spectrum also lends support to the idea that, once allowed to reach reproductive age, some of those traits might increase in the general population. In fact, since it is just a few generations since this shift in treatment, we might not be surprised to expect a sort of "explosion" in phenotypes.

 

Also....

Many of the genes associated with "autism/Aspism" are located in a chromosomal hotspot currently undergoing increased rearrangement--associated with digestive genes in the same area. There is research on this; if you're interested, I could find that later.

What a surprise; evolution in our digestive genes....

 

Good luck,

~ :)

Edited by Essay
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Hi Shawnus - I am not 100% sure, but I believe Essay is referring to this research: http://www.scienceda...10917082721.htm

 

That is neat stuff and very recent! My stuff is up to 5 years old... but could only find this:

It is from an old posting and I should read/edit it first, but not now. Sorry if the links don't work or it is irrelevant, but hopefully it will suggest something fruitful.

~Cheers ;)

 

I don't know where I read about this "novel genetic architecture," but I know the video talks about it ...and there are some other sources....

http://www.researchc...D=572&rID=22219

The Changing Human Genome: Implications for Disease and Evolution (1 hr)...Now: http://www.uwtv.org/...spx?dwrid=22219 ??

 

I did jot down some quotes:...something about a unique (to only a few higher primates) gene "duplication architecture" especially as related to "hotspots that promote recurrent deletion events."

 

&...something about a new view of that ~1% difference between us and chimps--along the lines of "but some regions have changed extremely rapidly." ...referring to that 1% --that has "changed extremely rapidly." This unique "duplication architecture" allows for the original copy to function normally while the duplicate gene can mutate wildly (...who cares, as the original is still functioning normally, eh?)!

 

===>

or, Google: genetic hotspots novel architecture primates

 

http://www.plosgenet...al.pgen.1000840 Refinement of primate copy number variation hotspots identifies candidate genomic regions evolving under positive selection

 

http://genomebiology.com/2011/12/5/R52 Refinement of primate copy number variation hotspots identifies candidate genomic regions evolving under positive selection

 

http://www.nature.co...ll/nrg1895.html Primate segmental duplications: crucibles of evolution, diversity and disease Jeffrey A. Bailey & Evan E. Eichler Abstract: Compared with other mammals, the genomes of humans and other primates show an enrichment of large, interspersed segmental duplications (SDs) with high levels of sequence identity. Recent evidence has begun to shed light on the origin of primate SDs, pointing to a complex interplay of mechanisms and indicating that distinct waves of duplication took place during primate evolution. There is also evidence for a strong association between duplication, genomic instability and large-scale chromosomal rearrangements. Exciting new findings suggest that SDs have not only created novel primate gene families, but might have also influenced current human genic and phenotypic variation on a previously unappreciated scale.

&

http://www.aspiesfor...d.php?tid=11602 A Hot Spot of Genetic Instability in Autism

The genomic region identified by Weiss et al. corresponds to 1 of approximately 150 regions of the human genome that are predicted to be "hot spots" for recurrent deletion and duplication.11,12 The presence of large, highly similar duplications flanking the 16p11.2 region predisposes this particular portion of the chromosome to unequal crossing over during meiosis (Figure 1). Consequently, although the parental DNA is normal, the unique sequence between these duplicated sequences becomes microduplicated or microdeleted in offspring.13 The critical genomic segment described by Weiss et al. seems to be identical to a previously described de novo microdeletion in male monozygotic twins with mild mental retardation, aortic-valve abnormalities, and seizure disorder; no evidence of autism spectrum disorder was presented.14 As in other diseases associated with genomic disorders (e.g., the velocardiofacial syndrome and schizophrenia), it is likely that the effect of the 16p11.2 deletion or duplication extends beyond autism and that variability in clinical manifestations depends on differences in genetic background. This theory is consistent with an observation made by Weiss et al. in two families: affected children inherited the 16p11.2 duplication from unaffected parents.Figure 1. A Hot Spot of Genomic Instability Associated with Autism.Interspersed duplication blocks (12 and 13) on 16p11.2 promote unequal crossing over during meiosis (two of four chromosomes are shown). Gametes are produced that either lack or carry a double dose of the critical interval. Dosage-sensitive differences of genes in the critical interval (A, B, C) probably increase the susceptibility to disease. There are more than 25 genes or transcripts in the critical interval (e.g., DOC2A, QPRT, and TBX6), as well as rapidly evolving genes in the flanking duplications.The short arm of chromosome 16 is exceptional from an evolutionary perspective because it is populated by an excess of duplicated segments that emerged relatively recently during evolution (less than 15 million years ago).15 More than 16 blocks of segmental duplication are interspersed across the chromosome, and rearrangements among these blocks have been associated with various genomic disorders involving mental retardation, multiple congenital abnormalities, and autism. It is interesting that most of the duplicated sequences on chromosome 16 also carry copies of one of the most rapidly evolving gene families in the human species.16 Both the gene family and the genomic architecture are specific to apes and humans, which is consistent with other reports17 that from an evolutionary standpoint, autism may be a relatively "young" disease.RE:

 

http://www.nejm.org/...56/NEJMe0708756

This article (10.1056/NEJMe0708756) was published at www.nejm.org on January 9, 2008.New England Journal of Medicine

===Just think of how lactose tolerance has evolved, as well as... celiac disease/autism connection. There is something about kidney malformations too, along with many digestive conditions, that go along with certain brain developmental problems as a common association; which lends support to this overall idea....Of certain hotspots within the genome, which can change "extremely rapidly." So don't get too constrained by our relatively primitive definitions regarding how genetics might limit our (especially mental and social) evolution. ...and there are epigenetic effects too....

 

===> Hope that helps...

 

I'd like to add (but probably shouldn't):

The digestive system, termed “The Second Brain” in a book on the subject (though really the gut is the first brain and our brains are secondary…), develops early in embryology. Later during the stages where brain architecture is ongoing, those same genes are re-recruited to further brain development… so it seems.

 

 

~ :)

 

 

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That is fascinating. I was also reading this article:

https://sfari.org/news-and-opinion/news/2011/high-fetal-testosterone-triggers-autism-british-group-says

 

Obviously this is my homework thread :D And I am going off on a tangent and won't be able to include much of this in my essay..but damn you guys if you don't share interesting links that distract me.. smile.gif

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Obviously this is my homework thread :D And I am going off on a tangent and won't be able to include much of this in my essay..but damn you guys if you don't share interesting links that distract me..

Isn't that what we're here for? ;)

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