I haven’t written a post about the Bear in a couple of months, so I figure that now is a good time for an update.
One of the things we’re interested in for the Bear is music therapy. I still don’t know much about it, but another parent at our IBI school told me of a program that her son was in, how much he enjoyed it, and how she thought that it was really beneficial. I have to admit that music therapy was not previously high on my ‘should do’ list, but she gave the program a good review. Momma Bear and I gave it a quick bit of thought and came to the conclusion that this might be a good option to try. So I gave the therapist a call, and while there was no space available, we did secure a spot at the top of the waiting list. We didn’t expect to start the program until the summer.
The Bear LOVES musical interaction. I’ve never noticed her exhibiting any particular attraction to songs on her videos, but whenever my wife or I sing to her she absolutely loves it. She constantly gestures for me to sing to her (I never said she had good taste ;-) ) and Momma Bear can get her to positively beam with delight when she sings. The Bear does not seem overly interested in making music herself, although she does occasionally enjoy playing with the piano at my outlaws’ house, and will sometimes play with a keyboard at home. She also has some toys that play songs, and sometimes will press the button to play a few repetitions of certain songs.
Last week I received a call from the music therapist telling me that one of her clients was out of town for three weeks, so there was an opening if we wanted to take it. I said I’d take the first one and we’d see how it went, with the expectation but not a firm commitment to take the other two. (I offered to pay for the other two if we bowed out, but she said there was no need.) So the Bear went to her first session on Saturday morning. I sat at the back of the room and watched.
What a great experience! The therapist allowed the Bear to get acclimatized, which she did by doing a quick exploration of the room, and then the therapist sat in front of the Bear and started playing guitar and singing. The Bear loved it, and was hooked. When the therapist put down the guitar and started singing and playing a shaker, the Bear crawled up into her lap to participate. Over the course of the 45 minute session the therapist played different instruments, banged on various drums, shook tambourines and bells, sang, played a keyboard, and physically interacted with the Bear to determine how to gain her interest. She also gave the Bear various instruments to play. She encouraged her to explore, to play, to imitate, and was even able to get her to play her bells as part of some of the songs. With the exception of a couple of trips over to Dad to get her ‘milk’ and a couple of quick sessions on a rocking chair (to which the therapist added some music), the Bear maintained her interest and focus on the session and the therapist for pretty much the entire time, and was smiling and grinning throughout.
At the end, the therapist asked if we would be returning for the other two sessions. Very definitely. What was also interesting to me was that the therapist said afterwards that she was surprised by the Bear’s level of exploration and interaction, especially for a first session. I had previously told her that the Bear was assessed as ‘autism at the severe end of the spectrum’. While she said that she was not a doctor and did not ‘do’ diagnoses, from her experience the Bear was much more interactive than she would have expected. That was very heartening to hear.
The Bear is also doing well at school. Among other programs, she’s mastering or mastered shape shorting, shape puzzles, matching 3D objects (and as an added surprise stacked blocks up to 5 high), 2D objects, matching on colour, and among other tasks is working on matching quantities (e.g. moving three objects to match the number 3) and matching object categories (e.g. matching different cars to a cars category, or different dogs to a dog category). Her fine motor skills are improving with various exercises. She also appears to know her primary colours. When as a lark I tested her one day with various colours in assorted combinations – e.g. “which one is the red ring” - she got the first ten correct before she became bored and stopped me. Until then I had no idea she knew her colours by name.
We also expose her a lot to numbers and the alphabet, not in any particularly structured way, but instead to familiarize her with them and see what at this point she can pick up implicitly. We’ve noticed that she prefers complicated over simple visuals (e.g. she prefers the back of her video cases to the front, will spend a lot of time analyzing detailed and complicated pictures, and loves to get hold of my Economists and flip through them), which suggests to me that she is potentially analyzing and interpreting the complexity that she sees.
She has also very recently learned to drink with a straw. I consider this a big deal, as we can now use this as part of OT. I’ve come across a couple of OT exercises that use sucking and blowing through straws to encourage mouth control and coordination, which the Bear may have issues with. The evil Dad that I am, I’m also trying to teach her to stick out her tongue (and greatly look forward to the day when she does so (in)appropriately). She tries to imitate me, but she either twists it or makes a U shape. Again, helping improve her ability to use her mouth effectively may also help her to produce more sounds and ultimately learn how to speak.
The Bear also dances with us. Nothing too fancy, but she will sway from side to side and foot to foot to follow our lead, usually alternating her focus between our faces and our feet while trying to match our sway. Her IBI program can also get her to spin while dancing, and I’ve been able to get her to do this myself at times.
So, overall I’m quite pleased with how things are going. Whether one wants to credit her progress to IBI, our efforts, or just natural development (my money is on a combination of the three), the fact is that she is progressing, and we are seeing learning and growth. I fully believe that she is more capable than we know, but what we can see suggests considerable and even accelerating gains.
I wrote the above not to boast, as obviously there are children who are progressing both faster, slower, and on alternate paths to the Bear. There are also things that are clearly a challenge to her that we feel she ultimately needs to learn and overcome. Instead, the point I’m trying to make is that there is learning, and there is progress. All too often autism is presented entirely negatively, and with a bleak prognosis. At least in our case, we can also see good reasons for optimism and hope.
Friday, February 23, 2007
Tuesday, February 20, 2007
Some Thoughts On Blogging
Phew, a narrow escape. I was worried that if I was hit by a bus and 'lost' that the previous post would have been left on my blog forever. Not that I regret the post. The way the comment that started it all was worded, it appeared that I was part of the 'mercury militia', so I felt the need to defend myself. Having said that, it was not my proudest moment. And FWIW, I accept Bazooka Joe’s overall explanation about what he meant (as opposed to what he originally wrote), even though I disagree that this blog is used by EoHers as evidence that an environmental trigger is responsible for autism. From my perspective there are no hard feelings.
Anyway, I’ve been thinking for a little bit now about why I’m blogging. Memory can sometimes be a bit self-serving, but I believe that I originally started for two reasons. First, as stated in my first post, I thought that in light of the increasing polarization of the ‘debate’, and as the “challenge to the more contentious bio-med practices is morphing into a more direct challenge against even mainstream accepted methods of investigating and potentially treating autism” that it was time for more moderates to join the debate. And second, I thought of the blog as a record of my thoughts and views for my daughter, the Bear. When she’s older she can read it, if she chooses, to understand the evolution of my thinking.
Very quickly, when I saw someone’s Demeaning Words I added a third reason – advocacy of understanding and (my view of) acceptance. I have intended to write a post specifically about ‘Acceptance’ for a while now, but I keep holding off. There is always one more post that I want to write first, to build my views upon. I don’t feel I can do the subject justice until I can point to what it is that I actually ‘accept’.
Also, because of the tone of the ‘debate’, I expect to get ‘lawyered’, which - no disrespect intended to my friend in the legal profession - is a shorthand I use for being exposed to a rigorous and hostile cross-examination. I’ve gone through these before, and witnessed a lot of others facing them too (on both ‘sides’). I also notice that sometimes when people can’t find an opening in something that was said that they then proceed to attribute both statements and motives to people that happen to be non-existent. The best defence is to have material to which to link, to clearly substantiate one’s views.
Since then I’ve added another reason for blogging, which is to draw attention to some of the science in autism that I think is both important and interesting (and that I understand). At either end of the debate a lot of time is spent using science - and in some cases what loosely passes as 'science' - as a weapon, or to explain what ‘isn’t’. I’m trying to use it to explain hypotheses of ‘what may be’. So far I’ve focused on minicolumns, but there are also other subjects that I find of interest that I am also digging into. I also like to go after ToM, at this point anecdotally, to demonstrate where I think some of the accepted scientific beliefs – especially those that underestimate the Bear - may go a bit too far. I hope to back this up with more scientific evidence in the future. If nothing else, this aspect of the blog has been very educational for me, since I like to have a clue about what I’m writing about. In this regard, blogging is probably a good excuse for following my own perseverations. And on this note, I’ll point out that I’m very much looking forward to María Luján’s upcoming posts.
What I try to avoid is joining in some of the more vigorous causation debates. They already have enough participants. I do not see it as wrong to defend one’s POV in these debates, and I do support efforts to keep the discussions both scientifically honest and grounded in respect for those who are autistic. But I do believe that some (and by no means all) debaters can a) over-interpret some scientific evidence, b) support their positions using ‘bogus’ science, c) sometimes go beyond arguing the ‘science’ to arguing an agenda that is at this point still hypothetical, anecdotal, and/or unsupported, and d) have turned the debates into blood-sport and/or an opportunity to throw out gratuitous insults. There is an awful lot about autism that is still unknown at this point. Some argue as if all the evidence they need to support their opinion is already in. Maybe to them it is. Personally, I’m still waiting for some answers, and I don’t think that they will ultimately support either extreme. But that too is just an opinion.
Which brings me in a long-winded way to the final thought of this post. What I find more than a little sad is that last week’s post resulted in the highest readership that this blog has ever had. Not by a huge amount, but it was quite noticeable. I don't worry too much about readership stats, but I would have liked the Minicolumns, Genius, and Autism post to hold the top spot, because it - the subject, not the post - was about something potentially important to our understanding of autism. I’d like to think that this week's blip in readers occurred because over time a blog can build up a group of people who find it interesting, like to stop by to see what one has to say, and possibly to engage in some reasoned discussion of the material posted. Unfortunately, I don’t think that this is the case. I’m the one who is at fault here, as I am the one responsible for the blog’s content. But the post in question is not the direction in which I want this blog to go - I’m not interested in hosting one more autism battlefield. My next post will get back to more reasonable territory.
Okay, maybe I do regret my last post a little bit.
Anyway, I’ve been thinking for a little bit now about why I’m blogging. Memory can sometimes be a bit self-serving, but I believe that I originally started for two reasons. First, as stated in my first post, I thought that in light of the increasing polarization of the ‘debate’, and as the “challenge to the more contentious bio-med practices is morphing into a more direct challenge against even mainstream accepted methods of investigating and potentially treating autism” that it was time for more moderates to join the debate. And second, I thought of the blog as a record of my thoughts and views for my daughter, the Bear. When she’s older she can read it, if she chooses, to understand the evolution of my thinking.
Very quickly, when I saw someone’s Demeaning Words I added a third reason – advocacy of understanding and (my view of) acceptance. I have intended to write a post specifically about ‘Acceptance’ for a while now, but I keep holding off. There is always one more post that I want to write first, to build my views upon. I don’t feel I can do the subject justice until I can point to what it is that I actually ‘accept’.
Also, because of the tone of the ‘debate’, I expect to get ‘lawyered’, which - no disrespect intended to my friend in the legal profession - is a shorthand I use for being exposed to a rigorous and hostile cross-examination. I’ve gone through these before, and witnessed a lot of others facing them too (on both ‘sides’). I also notice that sometimes when people can’t find an opening in something that was said that they then proceed to attribute both statements and motives to people that happen to be non-existent. The best defence is to have material to which to link, to clearly substantiate one’s views.
Since then I’ve added another reason for blogging, which is to draw attention to some of the science in autism that I think is both important and interesting (and that I understand). At either end of the debate a lot of time is spent using science - and in some cases what loosely passes as 'science' - as a weapon, or to explain what ‘isn’t’. I’m trying to use it to explain hypotheses of ‘what may be’. So far I’ve focused on minicolumns, but there are also other subjects that I find of interest that I am also digging into. I also like to go after ToM, at this point anecdotally, to demonstrate where I think some of the accepted scientific beliefs – especially those that underestimate the Bear - may go a bit too far. I hope to back this up with more scientific evidence in the future. If nothing else, this aspect of the blog has been very educational for me, since I like to have a clue about what I’m writing about. In this regard, blogging is probably a good excuse for following my own perseverations. And on this note, I’ll point out that I’m very much looking forward to María Luján’s upcoming posts.
What I try to avoid is joining in some of the more vigorous causation debates. They already have enough participants. I do not see it as wrong to defend one’s POV in these debates, and I do support efforts to keep the discussions both scientifically honest and grounded in respect for those who are autistic. But I do believe that some (and by no means all) debaters can a) over-interpret some scientific evidence, b) support their positions using ‘bogus’ science, c) sometimes go beyond arguing the ‘science’ to arguing an agenda that is at this point still hypothetical, anecdotal, and/or unsupported, and d) have turned the debates into blood-sport and/or an opportunity to throw out gratuitous insults. There is an awful lot about autism that is still unknown at this point. Some argue as if all the evidence they need to support their opinion is already in. Maybe to them it is. Personally, I’m still waiting for some answers, and I don’t think that they will ultimately support either extreme. But that too is just an opinion.
Which brings me in a long-winded way to the final thought of this post. What I find more than a little sad is that last week’s post resulted in the highest readership that this blog has ever had. Not by a huge amount, but it was quite noticeable. I don't worry too much about readership stats, but I would have liked the Minicolumns, Genius, and Autism post to hold the top spot, because it - the subject, not the post - was about something potentially important to our understanding of autism. I’d like to think that this week's blip in readers occurred because over time a blog can build up a group of people who find it interesting, like to stop by to see what one has to say, and possibly to engage in some reasoned discussion of the material posted. Unfortunately, I don’t think that this is the case. I’m the one who is at fault here, as I am the one responsible for the blog’s content. But the post in question is not the direction in which I want this blog to go - I’m not interested in hosting one more autism battlefield. My next post will get back to more reasonable territory.
Okay, maybe I do regret my last post a little bit.
Monday, February 12, 2007
Unmasked At Last
I knew it couldn’t last. No matter how hard I tried to disguise myself, someone would eventually discover that I’m part of the ‘Mercury Militia’. I tried all kinds of subterfuge to remain hidden, but alas, to no avail. A cunning sleuth has discovered my deception and 'outed' me.
(That was sarcasm, BTW)
The first comment on Prometheus’s post What You Want is What You Get was by Bazooka Joe (sorry, no link), who linked me and my blog to the ‘Mercury Militia’, and inferred a couple of other points. The comment has now been deleted from Prometheus’s blog, as has my reply below:
-----------------
Hi Prometheus,
Since you permitted Bazooka Joe’s comment, I hope that you will allow me the courtesy of a reply.
"They [linked to Generation Rescue et al, with the clear implication that ‘they’ refers to the ‘Mercury Militia’] have started blogs; here's a list:
…
Ian's blog, ashadeofgrey, has focused on reprinting Manny Cassanova's minicolumn research, including grant proposals and unpublished data.
…
So you see, it's no wonder that people like Kirby use the term, blogger, with derision. Effective blogging is not what the mercury militia do well."
The implication is that I am part of the mercury militia? Um, Bazooka Joe, can you show me any evidence where I’ve stated that mercury and/or thimerosal and/or vaccines cause autism? For the record, I’m Ian Parker, not the ‘Ian’ who sometimes comments on Kev’s blog (and maybe elsewhere), if that helps refine the search.
Regarding ‘reprinting’ Dr Casanova’s research, if you read his research you’ll find that I’ve added interpretations that go beyond what he has written, after first explaining his hypotheses from a body of work regarding minicolumns covering the period from 2002 to 2006. As for referencing the grant proposal (it sounds like you consider this pejorative), why not? I’d suggest that Dr Casanova’s reputation is as much on the line in his proposal (which has been widely distributed) as it is in his peer-reviewed published work. Besides, it included some cool illustrations.
As for ‘unpublished data’ (two papers), I know of other researchers (as in other than Dr C) who have also reviewed the same information, and the latter paper will be published shortly. FWIW, Dr Casanova forwarded me the papers because we correspond, and he knows of my high level of interest in such matters. I asked permission before I used them in my posts. The first paper is a hypothesis work, and fully referenced. The latter is now in review. The fact that some of this paper’s findings are now in circulation linked to his name (sans refutation) conveys a certain level of trust. When the paper is published, you are free to read it and compare it to my post to see how much original thought and interpretation, if any, that I have added.
I also write about subjects other than the three minicolumn posts, including some posts about ToM, autism and evolution (I waited for Prometheus to write this one, but…), and a variety of other subjects, including my daughter. If you’re interested (I somehow doubt it – if you were I doubt that I would be writing this) you can find them under ‘Blog Archive’ by clicking on the little triangular buttons on the right of the window and then following the links.
Regarding "Effective blogging is not what the mercury militia do well", while temporarily suspending disbelief that I’m part of the mercury militia, I’ll leave it to the people who read my blog to determine that. If they don’t like it then presumably they won’t come back.
As a final thought, I find it interesting that ‘we members of the mercury militia’ are often accused of ignoring peer-reviewed science, and yet my posting about peer-reviewed research is being used to indict me?
Curious.
-----------------
María Luján and Wade Rankin, were also mentioned - among others - in Bazooka Joe’s comment, and both tried to reply. Eventually Prometheus deleted both of our comments and added his own thoughts as follows:
"Bazooka Joe,
I think you and Ian Parker should take your discussion off this blog, since it seems to be related to your personal differences of opinion. You're both welcome to post comments here, but only if you stay a bit closer to the subject."
And following:
"Wade Rankin,
I realize now that approving Bazooka Joe's comment was a mistake, which is why I allowed Ian Parker to have a go. I do not intend to allow every aggrieved party a chance to vent their spleen at Bazooka Joe (or to allow him to reply to all of them in turn).
I have removed both Bazooka Joe's original comment and Ian Parker's reply. I suggest that anyone who feels a need for "satisfaction" find a more suitable venue (how about http://www.mudwrestling.blogspot.com ?)."
So, based on Prometheus’s comment, apparently Bazooka Joe seems to feel that this is unresolved. Meanwhile, I am curious as to why I was included in this ‘drive-by shooting’? I’ll leave aside the 'reprint' reference to my three of 23 posts that discuss the work of Dr Casanova, as I think I answered that sufficiently above, at least until someone takes another shot. As for the quality of my blog, as bad and/or ineffective as it is, if you're reading this then I've sucked you in one more time. And I'll resist the temptation to go pejorative and make comments about 'reading comprehension'.
Anyway, I’m presuming that being a member of the ‘Mercury Militia’ requires something more of me than walking upright and drawing breath (I do both, BTW). My assumption is that the term ‘Mercury Militia’ refers to those who believe that ‘thimerosal’ or ‘mercury’ injected during vaccinations has ‘caused’ their child’s autism. This definition could probably be extended to include the MMR causation hypothesis as well. I would suggest that a further qualification would be that one would not only believe the above but also be relatively active and adamant in discussing the matter, but for now let's take the more relaxed definition. If anyone wants to propose another definition, feel free.
I did a quick search on my blog, looking for some key words. I mention ‘mercury’ (excluding NotMercury, the blogger) in four posts. In the Respect Meme I indicated the following:
"A related issue is that some ‘wrap themselves in the flag’. On one side, some autistics view a disagreement with their ideas as a challenge or an attack on all of those who are autistic. "If you disagree with me then you don’t respect autistics". The mirror image on the 'all autism=mercury poisoning' side is "If you don’t agree with me then you are abusing children". Er, no, on both counts."
And
"Respect is very relevant to the autism discussion. I would suggest that from the point of view of the neurodiversity community, respect – and the perception (and in a lot of cases the reality) of the absence of respect - is one of the driving reasons behind their participation in the debate. I would suggest that the ‘autism = mercury’ parents also see the debate – in their case with the government and with many in the scientific community – as a respect issue, and also lack respect for the ND point of view as well as for many of its proponents. And for the majority of parents and caregivers, the respect issue revolves around government and support agencies not providing the amount of care and support that is required to improve the quality of life and accommodation of those touched by autism (i.e. not respecting what they see as the conditions required to respect the right to proper and adequate support)."
In Moderate Does Not Mean Neutral, I wrote:
"Having said that, I also oppose poorly conducted science, which I believe does not serve anyone well. Exploring a reasonable hypothesis that does not have mainstream support is not poor science. Exploring hypotheses without using the scientific method and without having the goal of arriving at replicable results that can withstand peer review is poor science. Some on the treatment side have conducted poor science, and I believe that the result has been an overstatement of results and a damaging loss of credibility that may slow the ultimate search for answers. I also think that the ‘all autism = mercury’ approach has hampered other research that may find other causes, and I disagree with those that take this one-size-fits-all approach to autism research."
(You may want to pay particular attention to that last sentence.)
And
"We do not chelate our child, and to be honest, the process scares me. For the record, my daughter has some potential heavy metal issues (not mercury) that showed up on a mainstream test (discovered by accident – we were testing for essential minerals and ticked the toxic panel as an afterthought). Our approach has been to monitor this and try to naturally rebuild the Bear's detox system rather than use chelation. But I do not oppose others using chelation as long as they have clearly dealt with other bio-medical issues first, have tested their child and found the presence of heavy metals, and are careful to conduct chelation under qualified and experienced supervision and with regular testing/monitoring performed by reputable labs to ensure that no harm is being done."
(I think this is one of only two spots where I mention chelation, BTW)
And
"There is a history of extremes targeting moderates to turn situations into a clear black vs. white, ‘us’ vs. ’them’ issues, eliminating any room for diversity of viewpoints or compromise. It is easy to caricature or ridicule an extremist opponent (e.g. ‘all autism = mercury’ is downright silly), but it is harder to ridicule a moderate interventionist approach backed by replicable medical tests and following a moderate educational approach based on what many would consider common sense."
In Demeaning Words I wrote:
"Second, it is not intended as a personal attack on JB Handley or his objectives. One may agree or disagree with his views (I personally do not agree with his view - if I perceive it correctly - that all autism is the result of mercury poisoning), but that is not the subject of this post."
And finally, in Autism – It’s Not Always A Natural Variation, I wrote:
"This logic does not support the conclusion that no autism is purely genetic (75% could still theoretically be purely genetic - or more if the 60% concordance rate is too low). In fact, it supports the conclusion that autism in a significant number of cases involves at a minimum a degree of genetic susceptibility. It does not prove or disprove that the 'second hit' is thimerosal or mercury. It does not argue for or against chelation. It does not suggest that autism originates either in the womb or after birth. It does not suggest or refute the possibility that autism is curable, or that a cure is or is not desirable."
This paragraph also contains my only reference to thimerosal.
Finally, I use vaccines once:
"But I also see a discussion that is increasingly polarizing, in which accepting that others have different views is giving way to an advocacy that rejects other viewpoints as unenlightened, wrong, or not yet at their level of "awakening". This used to be a hallmark of the more activist element within the anti-vaccine crowd, but is also becoming increasingly apparent in the "autism is natural variation" crowd too. It is one thing to oppose some of the more contentious attempts to cure autism, e.g. chelation, or lupron (which IMHO is just nuts), or to reject the concept of treatment for oneself. But as this challenge to the more contentious bio-med practices is morphing into a more direct challenge against even mainstream accepted methods of investigating and potentially treating autism, I think it is time for more moderates to join the debate."
(The other spot where 'chelation' is mentioned)
So, based on the above, what exactly is it again that marks me as being part of the Mercury Militia?
(That was sarcasm, BTW)
The first comment on Prometheus’s post What You Want is What You Get was by Bazooka Joe (sorry, no link), who linked me and my blog to the ‘Mercury Militia’, and inferred a couple of other points. The comment has now been deleted from Prometheus’s blog, as has my reply below:
-----------------
Hi Prometheus,
Since you permitted Bazooka Joe’s comment, I hope that you will allow me the courtesy of a reply.
"They [linked to Generation Rescue et al, with the clear implication that ‘they’ refers to the ‘Mercury Militia’] have started blogs; here's a list:
…
Ian's blog, ashadeofgrey, has focused on reprinting Manny Cassanova's minicolumn research, including grant proposals and unpublished data.
…
So you see, it's no wonder that people like Kirby use the term, blogger, with derision. Effective blogging is not what the mercury militia do well."
The implication is that I am part of the mercury militia? Um, Bazooka Joe, can you show me any evidence where I’ve stated that mercury and/or thimerosal and/or vaccines cause autism? For the record, I’m Ian Parker, not the ‘Ian’ who sometimes comments on Kev’s blog (and maybe elsewhere), if that helps refine the search.
Regarding ‘reprinting’ Dr Casanova’s research, if you read his research you’ll find that I’ve added interpretations that go beyond what he has written, after first explaining his hypotheses from a body of work regarding minicolumns covering the period from 2002 to 2006. As for referencing the grant proposal (it sounds like you consider this pejorative), why not? I’d suggest that Dr Casanova’s reputation is as much on the line in his proposal (which has been widely distributed) as it is in his peer-reviewed published work. Besides, it included some cool illustrations.
As for ‘unpublished data’ (two papers), I know of other researchers (as in other than Dr C) who have also reviewed the same information, and the latter paper will be published shortly. FWIW, Dr Casanova forwarded me the papers because we correspond, and he knows of my high level of interest in such matters. I asked permission before I used them in my posts. The first paper is a hypothesis work, and fully referenced. The latter is now in review. The fact that some of this paper’s findings are now in circulation linked to his name (sans refutation) conveys a certain level of trust. When the paper is published, you are free to read it and compare it to my post to see how much original thought and interpretation, if any, that I have added.
I also write about subjects other than the three minicolumn posts, including some posts about ToM, autism and evolution (I waited for Prometheus to write this one, but…), and a variety of other subjects, including my daughter. If you’re interested (I somehow doubt it – if you were I doubt that I would be writing this) you can find them under ‘Blog Archive’ by clicking on the little triangular buttons on the right of the window and then following the links.
Regarding "Effective blogging is not what the mercury militia do well", while temporarily suspending disbelief that I’m part of the mercury militia, I’ll leave it to the people who read my blog to determine that. If they don’t like it then presumably they won’t come back.
As a final thought, I find it interesting that ‘we members of the mercury militia’ are often accused of ignoring peer-reviewed science, and yet my posting about peer-reviewed research is being used to indict me?
Curious.
-----------------
María Luján and Wade Rankin, were also mentioned - among others - in Bazooka Joe’s comment, and both tried to reply. Eventually Prometheus deleted both of our comments and added his own thoughts as follows:
"Bazooka Joe,
I think you and Ian Parker should take your discussion off this blog, since it seems to be related to your personal differences of opinion. You're both welcome to post comments here, but only if you stay a bit closer to the subject."
And following:
"Wade Rankin,
I realize now that approving Bazooka Joe's comment was a mistake, which is why I allowed Ian Parker to have a go. I do not intend to allow every aggrieved party a chance to vent their spleen at Bazooka Joe (or to allow him to reply to all of them in turn).
I have removed both Bazooka Joe's original comment and Ian Parker's reply. I suggest that anyone who feels a need for "satisfaction" find a more suitable venue (how about http://www.mudwrestling.blogspot.com ?)."
So, based on Prometheus’s comment, apparently Bazooka Joe seems to feel that this is unresolved. Meanwhile, I am curious as to why I was included in this ‘drive-by shooting’? I’ll leave aside the 'reprint' reference to my three of 23 posts that discuss the work of Dr Casanova, as I think I answered that sufficiently above, at least until someone takes another shot. As for the quality of my blog, as bad and/or ineffective as it is, if you're reading this then I've sucked you in one more time. And I'll resist the temptation to go pejorative and make comments about 'reading comprehension'.
Anyway, I’m presuming that being a member of the ‘Mercury Militia’ requires something more of me than walking upright and drawing breath (I do both, BTW). My assumption is that the term ‘Mercury Militia’ refers to those who believe that ‘thimerosal’ or ‘mercury’ injected during vaccinations has ‘caused’ their child’s autism. This definition could probably be extended to include the MMR causation hypothesis as well. I would suggest that a further qualification would be that one would not only believe the above but also be relatively active and adamant in discussing the matter, but for now let's take the more relaxed definition. If anyone wants to propose another definition, feel free.
I did a quick search on my blog, looking for some key words. I mention ‘mercury’ (excluding NotMercury, the blogger) in four posts. In the Respect Meme I indicated the following:
"A related issue is that some ‘wrap themselves in the flag’. On one side, some autistics view a disagreement with their ideas as a challenge or an attack on all of those who are autistic. "If you disagree with me then you don’t respect autistics". The mirror image on the 'all autism=mercury poisoning' side is "If you don’t agree with me then you are abusing children". Er, no, on both counts."
And
"Respect is very relevant to the autism discussion. I would suggest that from the point of view of the neurodiversity community, respect – and the perception (and in a lot of cases the reality) of the absence of respect - is one of the driving reasons behind their participation in the debate. I would suggest that the ‘autism = mercury’ parents also see the debate – in their case with the government and with many in the scientific community – as a respect issue, and also lack respect for the ND point of view as well as for many of its proponents. And for the majority of parents and caregivers, the respect issue revolves around government and support agencies not providing the amount of care and support that is required to improve the quality of life and accommodation of those touched by autism (i.e. not respecting what they see as the conditions required to respect the right to proper and adequate support)."
In Moderate Does Not Mean Neutral, I wrote:
"Having said that, I also oppose poorly conducted science, which I believe does not serve anyone well. Exploring a reasonable hypothesis that does not have mainstream support is not poor science. Exploring hypotheses without using the scientific method and without having the goal of arriving at replicable results that can withstand peer review is poor science. Some on the treatment side have conducted poor science, and I believe that the result has been an overstatement of results and a damaging loss of credibility that may slow the ultimate search for answers. I also think that the ‘all autism = mercury’ approach has hampered other research that may find other causes, and I disagree with those that take this one-size-fits-all approach to autism research."
(You may want to pay particular attention to that last sentence.)
And
"We do not chelate our child, and to be honest, the process scares me. For the record, my daughter has some potential heavy metal issues (not mercury) that showed up on a mainstream test (discovered by accident – we were testing for essential minerals and ticked the toxic panel as an afterthought). Our approach has been to monitor this and try to naturally rebuild the Bear's detox system rather than use chelation. But I do not oppose others using chelation as long as they have clearly dealt with other bio-medical issues first, have tested their child and found the presence of heavy metals, and are careful to conduct chelation under qualified and experienced supervision and with regular testing/monitoring performed by reputable labs to ensure that no harm is being done."
(I think this is one of only two spots where I mention chelation, BTW)
And
"There is a history of extremes targeting moderates to turn situations into a clear black vs. white, ‘us’ vs. ’them’ issues, eliminating any room for diversity of viewpoints or compromise. It is easy to caricature or ridicule an extremist opponent (e.g. ‘all autism = mercury’ is downright silly), but it is harder to ridicule a moderate interventionist approach backed by replicable medical tests and following a moderate educational approach based on what many would consider common sense."
In Demeaning Words I wrote:
"Second, it is not intended as a personal attack on JB Handley or his objectives. One may agree or disagree with his views (I personally do not agree with his view - if I perceive it correctly - that all autism is the result of mercury poisoning), but that is not the subject of this post."
And finally, in Autism – It’s Not Always A Natural Variation, I wrote:
"This logic does not support the conclusion that no autism is purely genetic (75% could still theoretically be purely genetic - or more if the 60% concordance rate is too low). In fact, it supports the conclusion that autism in a significant number of cases involves at a minimum a degree of genetic susceptibility. It does not prove or disprove that the 'second hit' is thimerosal or mercury. It does not argue for or against chelation. It does not suggest that autism originates either in the womb or after birth. It does not suggest or refute the possibility that autism is curable, or that a cure is or is not desirable."
This paragraph also contains my only reference to thimerosal.
Finally, I use vaccines once:
"But I also see a discussion that is increasingly polarizing, in which accepting that others have different views is giving way to an advocacy that rejects other viewpoints as unenlightened, wrong, or not yet at their level of "awakening". This used to be a hallmark of the more activist element within the anti-vaccine crowd, but is also becoming increasingly apparent in the "autism is natural variation" crowd too. It is one thing to oppose some of the more contentious attempts to cure autism, e.g. chelation, or lupron (which IMHO is just nuts), or to reject the concept of treatment for oneself. But as this challenge to the more contentious bio-med practices is morphing into a more direct challenge against even mainstream accepted methods of investigating and potentially treating autism, I think it is time for more moderates to join the debate."
(The other spot where 'chelation' is mentioned)
So, based on the above, what exactly is it again that marks me as being part of the Mercury Militia?
Thursday, February 01, 2007
Minicolumns, Genius, and Autism
In earlier posts I wrote about Autism and Minicolumns and Autism and the Evolution of the Brain, based on research by Dr. Casanova et al. Minicolumns are the basic organizational unit of the cortex, and are vertical arrays of pyramidal cells (neurons). The underlying argument in these posts was that those with ASD have a higher number of minicolumns than average, but that those minicolumns are of a narrower than average width, with smaller neurons but the same average number of neurons per minicolumn. The net result is a brain structure that skews in favour of processing stimuli that require discrimination, potentially at the expense of generalizing the salience of a particular stimulus. Smaller and more densely packed minicolumns could also allow for more complex information processing.
These attributes come at a potential cost. The reduction in width is a result of a reduction in the minicolumn’s peripheral zone of inhibitory and disinhibitory activity. The inhibitory fibers act to keep stimuli within individual minicolumns, and the reduction in this space increases the chance of stimuli overflowing to adjacent minicolumns, providing an amplifier effect and potential hypersensitivity. Narrower minicolumns may also result in an increased number of minicolumns per macrocolumn, which can also result in an amplification of thalamic input, and as each minicolumn’s response to thalamic input is modulated by the activity of neighbouring columns, a reduction in GABAergic inhibitory activity could also result in a loss of inhibition and greater amplification. Stimuli ‘spill’ and greater amplification could result in the increased incidence of seizures in autistics.
An additional factor is the reduction in neuron size, which reduces the ability of neurons to sustain connections over distances. Smaller neurons result in a metabolic bias favouring shorter connections at the expense of both longer distance and inter-hemispheral connectivity. The result is that autistic brains have a bias towards local (intra-regional) over global (inter-regional) connectivity and processing. Short intra-regional processing functions include mathematical calculations and visual processing. Cognitive functions that require inter-regional processing would be less metabolically efficient, including language, face recognition, and joint attention (Casanova - Abnormalities Of Cortical Circuitry In The Brains Of Autistic Individuals). Given the high metabolic cost of the brain (2.5% of our body weight but 22% of our resting metabolism - Leonard and Robertson 1992, p 186), smaller neurons may be a response to resource constraints.
Of note, while reduced minicolumnar width appears to be a prerequisite for ASD, the reported minicolumn widths found within autistic brains are still within the normal distribution of minicolumnar width, albeit at the tail end (Casanova, 2006). In other words, people with narrow minicolumnar widths are not necessarily on the ASD spectrum.
Narrower Minicolumns Without ASD
Confirmation of this is suggested in "Comparison of the Minicolumnar Morphometry of Three Distinguished Neuroscientists and Controls", a new research paper by Dr. Casanova et al, currently in review. The research in question involved analyzing and comparing the minicolumns of three distinguished neuroscientists ("supernormals") and six normative controls. The ‘supernormals’ are described as:
"researchers of high distinction within the neurosciences. Although personal history and interviews with those who knew these neuroscientists emphasize their wide range of knowledge (polymaths) and divergent thinking no claim is made regarding their intelligence or creativity."
That being said, the descriptions of the three individuals in question clearly suggest that they were very intelligent, focused, productive, and intellectually self-assured.
The research found the following:
"Overall, there were significant differences (p < 0.001) between the comparison groups in both minicolumnar width (cw) and mean cell spacing (mcs). Although our supernormals did not exhibit deficits in communication or interpersonal skills the resultant minicolumnar phenotype bears similarity to that described for both autism and Asperger’s syndrome."
The findings in this paper are fascinating (at least to me) in that they clearly indicate both similarities and differences between the brains of autistics and those of the three neuroscientists, suggesting some answers and raising some interesting questions. The major reported similarity is the finding of narrow minicolumnar widths. As stated in the paper, "A minicolumnar phenotype that provides for discrimination and/or focused attention may help explain the savant abilities observed in the intellectually gifted." It is unknown at this point whether two other characteristics linked to narrower width minicolumns in autistics – i.e. smaller neurons and a higher number of minicolumns – also occurred in these neuroscientists’ brains, but it is a logical assumption that these characteristics were present too. Smaller neurons are hypothesized by Dr. Casanova to be a requirement for the existence of narrower width minicolumns, based on laws of conservation for brain grows and evolution (from personal correspondence, with permission).
Differences
There were also significant minicolumnar differences between the neuroscientist brains and ASD brains. First, the neuroscientists had a lower mean cell spacing (MCS) – i.e. a smaller average distance between neurons - than the controls. In other words, their neurons were closer together than in typical minicolumns with large mean cell spacing. Previously analyzed ASD brains had ‘normal’ or typical mean cell spacing. Unfortunately, no direct numerical comparisons of MCS between this research and previous analyses are possible due to the difference in age between the neuroscientists (58, 84, and 89) and the autistic patients (average age being 12 years).
Second, the neuroscientists differ from those with ASD in terms of the horizontal spacing between neurons (relative dispersion of cells). The neuroscientist minicolumns were similar to typical minicolumns in that they had a small relative dispersion, i.e. cells tended to be clustered closer to the axis of the column. Those with ASD have a large relative dispersion, with cells distributed more uniformly within the minicolumn core.
Figure 1 (below, based on Fig 2 from the research paper) is a hypothetical representation of both mean cell spacing and relative dispersion in minicolumns, (after disregarding both neuroscientist and ASD reduced minicolumnar width). The neuroscientist and typical minicolumns have a smaller relative dispersion than the ASD minicolumn (i.e. tighter clustering toward the column axis vs. more uniform distribution). The neuroscientist column also has a smaller mean cell spacing, with cells being closer to each other than in the other two minicolumnar types, regardless of their distribution around the minicolumn axis.
I would speculate that the differences between the neuroscientist and ASD minicolumns would have a significant - but incomplete - explanatory role in accounting for the differences between the two groups. In both groups, narrower width would increase the risk of ‘spill’ between minicolumns. But the reduced mean cell spacing in the neuroscientists would presumably result in greater integrity of processing within the column (as well as potentially an increase in speed), while the tighter grouping of neurons around the axis would increase the distance between the neurons and those in adjacent columns, maximizing the zone of interneuronal inhibitory activity between the adjacent vertical arrays of pyramidal cells. This is significant, in that this maximized inhibitory zone could at least partially compensate for any reductions due to the narrower column width.
In contrast, the higher ASD MCS could result in comparatively lower signal intensity and - along with a more uniform horizontal dispersion – result in a higher risk that neurons in adjacent columns might in fact be closer in distance than neurons within the same column, increasing the risk of ‘spill’. Plus, the more uniform horizontal dispersion would result in more neurons being found towards the outer periphery of the column, with an even smaller zone of inhibitory activity between these outer neurons and adjacent minicolumns.
More Questions
This still leaves some significant questions for further research regarding differences between the neuroscientist and ASD minicolumns. For one, as the paper suggests:
"the widespread morphometric changes in our scientists suggest that any brain-related ability they may have possessed (e.g., cross-discipline learning, abstracting, dimensional thinking) involved multiple cortical regions. In developing these abilities the various association cortices acted as nodes or epicenters, binding multimodal information, within a neural network (Mesulam 1994; 1998). Contrary to earlier formulations, modern observations suggest that higher cognitive processes are encoded in flexible distributed networks rather than rigid convergent ones (Mesulam, 1994; 1998)."
As such, the neuroscientists had brains capable of exceptional thinking, combining deep focus and discrimination, but linked to distributed (global) processing. If the neuroscientist neurons were smaller, biasing against global connectivity, then was there a compensatory effect? Spindle neurons serve to connect more distant, non-neighbouring regions of the brain (Casanova - Big Brains Manuscript, in preparation for submission). From Wikipedia:
"Spindle cells appear to play a central role in the development of intelligent behavior and adaptive response to changing conditions and cognitive dissonance. They emerge postnatally [emphasis added] and eventually become widely connected with diverse parts of the brain, evidencing their essential contributions to the superior capacity of hominids to focus on difficult problems."
Spindle neurons are known to be found in reduced numbers in those with ASD. Perhaps they helped the neuroscientists compensate for – and even exploit the benefits of – the bias towards local processing inherent in reduced width minicolumns?
Another potential difference between the two groups might be found within their corpus callosi, the structure that connects the left and right cerebral hemispheres, which have consistently shown to be smaller in autistics. The research paper suggested that "the fact that the left hemisphere lags in development behind the right hemisphere may offer an alternate explanation to savant skills (Geschwind & Galaburda, 1986)." Examining the corpus callosi of the neuroscientists might also provide some insights regarding similarities and differences in connectivity between them and those with ASD.
Evolutionary Benefit and Risk
The neuroscientist finding also potentially answers some evolutionary questions. In my Autism, Genetics, and Evolution post, I suggested that the alleles that cause autism could have been with humanity for at least 40,000 years.
"Assuming 30 to 35 years per generation (which is conservative), there have been 1100 to 1300 generations since the two populations diverged. This presumably should have been enough time to eliminate the various alleles that cause autism from the gene pool, if they are in fact deleterious.
Obviously this has not occurred. This means that the individual alleles that in combination cause autism must individually or in lesser combinations have had a beneficial effect to compensate for the reduced reproductive rates of autistics."
As the neuroscientist paper indicates, the same narrower width minicolumnar structure found in ASD may be a competitive advantage in the case of the neuroscientists. If the same alleles that contribute to ASD can result in a competitive advantage in other circumstances through (intellectual) fitness, this would easily explain the continued existence of ASD over time. The research paper quotes T.G West from In the Mind’s Eye (1997):
"One of the most important lessons to be learned from the genetic study of many diseases in recent years has been that the paradoxically high frequency of certain conditions is explained by the fact that important advantages conferred on those who carry the predisposition to these conditions may outweigh the obvious dramatic disadvantages."
My Autism and Minicolumns post suggested that a) ASD has a minicolumnar underpinning, b) this underpinning is required (i.e. no narrow minicolumns means no ASD), c) it originates in the first 40 days of fetal development (i.e. it is not itself acquired post-natally), d) that this difference falls within the normal range (i.e. that having it does not ‘cause’ a diagnosis, although it may very well result in diversity of thought and cognition, i.e. neurodiversity), e) that something else is therefore required (with no significant speculation as to what that something else may be, other than to generically label it as a ‘second hit’), and f) that research needs to prove or exclude causality among the population of the vulnerable, i.e. proving that something does not cause ASD in those who are invulnerable does not prove that it does not cause ASD in those who are vulnerable.
I would suggest that the Neuroscientist research lends significant credence to the above, especially to point d, and suggests that the differences between the neuroscientists and those with ASD may point to the ‘something else required’ that follows.
These attributes come at a potential cost. The reduction in width is a result of a reduction in the minicolumn’s peripheral zone of inhibitory and disinhibitory activity. The inhibitory fibers act to keep stimuli within individual minicolumns, and the reduction in this space increases the chance of stimuli overflowing to adjacent minicolumns, providing an amplifier effect and potential hypersensitivity. Narrower minicolumns may also result in an increased number of minicolumns per macrocolumn, which can also result in an amplification of thalamic input, and as each minicolumn’s response to thalamic input is modulated by the activity of neighbouring columns, a reduction in GABAergic inhibitory activity could also result in a loss of inhibition and greater amplification. Stimuli ‘spill’ and greater amplification could result in the increased incidence of seizures in autistics.
An additional factor is the reduction in neuron size, which reduces the ability of neurons to sustain connections over distances. Smaller neurons result in a metabolic bias favouring shorter connections at the expense of both longer distance and inter-hemispheral connectivity. The result is that autistic brains have a bias towards local (intra-regional) over global (inter-regional) connectivity and processing. Short intra-regional processing functions include mathematical calculations and visual processing. Cognitive functions that require inter-regional processing would be less metabolically efficient, including language, face recognition, and joint attention (Casanova - Abnormalities Of Cortical Circuitry In The Brains Of Autistic Individuals). Given the high metabolic cost of the brain (2.5% of our body weight but 22% of our resting metabolism - Leonard and Robertson 1992, p 186), smaller neurons may be a response to resource constraints.
Of note, while reduced minicolumnar width appears to be a prerequisite for ASD, the reported minicolumn widths found within autistic brains are still within the normal distribution of minicolumnar width, albeit at the tail end (Casanova, 2006). In other words, people with narrow minicolumnar widths are not necessarily on the ASD spectrum.
Narrower Minicolumns Without ASD
Confirmation of this is suggested in "Comparison of the Minicolumnar Morphometry of Three Distinguished Neuroscientists and Controls", a new research paper by Dr. Casanova et al, currently in review. The research in question involved analyzing and comparing the minicolumns of three distinguished neuroscientists ("supernormals") and six normative controls. The ‘supernormals’ are described as:
"researchers of high distinction within the neurosciences. Although personal history and interviews with those who knew these neuroscientists emphasize their wide range of knowledge (polymaths) and divergent thinking no claim is made regarding their intelligence or creativity."
That being said, the descriptions of the three individuals in question clearly suggest that they were very intelligent, focused, productive, and intellectually self-assured.
The research found the following:
"Overall, there were significant differences (p < 0.001) between the comparison groups in both minicolumnar width (cw) and mean cell spacing (mcs). Although our supernormals did not exhibit deficits in communication or interpersonal skills the resultant minicolumnar phenotype bears similarity to that described for both autism and Asperger’s syndrome."
The findings in this paper are fascinating (at least to me) in that they clearly indicate both similarities and differences between the brains of autistics and those of the three neuroscientists, suggesting some answers and raising some interesting questions. The major reported similarity is the finding of narrow minicolumnar widths. As stated in the paper, "A minicolumnar phenotype that provides for discrimination and/or focused attention may help explain the savant abilities observed in the intellectually gifted." It is unknown at this point whether two other characteristics linked to narrower width minicolumns in autistics – i.e. smaller neurons and a higher number of minicolumns – also occurred in these neuroscientists’ brains, but it is a logical assumption that these characteristics were present too. Smaller neurons are hypothesized by Dr. Casanova to be a requirement for the existence of narrower width minicolumns, based on laws of conservation for brain grows and evolution (from personal correspondence, with permission).
Differences
There were also significant minicolumnar differences between the neuroscientist brains and ASD brains. First, the neuroscientists had a lower mean cell spacing (MCS) – i.e. a smaller average distance between neurons - than the controls. In other words, their neurons were closer together than in typical minicolumns with large mean cell spacing. Previously analyzed ASD brains had ‘normal’ or typical mean cell spacing. Unfortunately, no direct numerical comparisons of MCS between this research and previous analyses are possible due to the difference in age between the neuroscientists (58, 84, and 89) and the autistic patients (average age being 12 years).
Second, the neuroscientists differ from those with ASD in terms of the horizontal spacing between neurons (relative dispersion of cells). The neuroscientist minicolumns were similar to typical minicolumns in that they had a small relative dispersion, i.e. cells tended to be clustered closer to the axis of the column. Those with ASD have a large relative dispersion, with cells distributed more uniformly within the minicolumn core.
Figure 1 (below, based on Fig 2 from the research paper) is a hypothetical representation of both mean cell spacing and relative dispersion in minicolumns, (after disregarding both neuroscientist and ASD reduced minicolumnar width). The neuroscientist and typical minicolumns have a smaller relative dispersion than the ASD minicolumn (i.e. tighter clustering toward the column axis vs. more uniform distribution). The neuroscientist column also has a smaller mean cell spacing, with cells being closer to each other than in the other two minicolumnar types, regardless of their distribution around the minicolumn axis.
I would speculate that the differences between the neuroscientist and ASD minicolumns would have a significant - but incomplete - explanatory role in accounting for the differences between the two groups. In both groups, narrower width would increase the risk of ‘spill’ between minicolumns. But the reduced mean cell spacing in the neuroscientists would presumably result in greater integrity of processing within the column (as well as potentially an increase in speed), while the tighter grouping of neurons around the axis would increase the distance between the neurons and those in adjacent columns, maximizing the zone of interneuronal inhibitory activity between the adjacent vertical arrays of pyramidal cells. This is significant, in that this maximized inhibitory zone could at least partially compensate for any reductions due to the narrower column width.
In contrast, the higher ASD MCS could result in comparatively lower signal intensity and - along with a more uniform horizontal dispersion – result in a higher risk that neurons in adjacent columns might in fact be closer in distance than neurons within the same column, increasing the risk of ‘spill’. Plus, the more uniform horizontal dispersion would result in more neurons being found towards the outer periphery of the column, with an even smaller zone of inhibitory activity between these outer neurons and adjacent minicolumns.
More Questions
This still leaves some significant questions for further research regarding differences between the neuroscientist and ASD minicolumns. For one, as the paper suggests:
"the widespread morphometric changes in our scientists suggest that any brain-related ability they may have possessed (e.g., cross-discipline learning, abstracting, dimensional thinking) involved multiple cortical regions. In developing these abilities the various association cortices acted as nodes or epicenters, binding multimodal information, within a neural network (Mesulam 1994; 1998). Contrary to earlier formulations, modern observations suggest that higher cognitive processes are encoded in flexible distributed networks rather than rigid convergent ones (Mesulam, 1994; 1998)."
As such, the neuroscientists had brains capable of exceptional thinking, combining deep focus and discrimination, but linked to distributed (global) processing. If the neuroscientist neurons were smaller, biasing against global connectivity, then was there a compensatory effect? Spindle neurons serve to connect more distant, non-neighbouring regions of the brain (Casanova - Big Brains Manuscript, in preparation for submission). From Wikipedia:
"Spindle cells appear to play a central role in the development of intelligent behavior and adaptive response to changing conditions and cognitive dissonance. They emerge postnatally [emphasis added] and eventually become widely connected with diverse parts of the brain, evidencing their essential contributions to the superior capacity of hominids to focus on difficult problems."
Spindle neurons are known to be found in reduced numbers in those with ASD. Perhaps they helped the neuroscientists compensate for – and even exploit the benefits of – the bias towards local processing inherent in reduced width minicolumns?
Another potential difference between the two groups might be found within their corpus callosi, the structure that connects the left and right cerebral hemispheres, which have consistently shown to be smaller in autistics. The research paper suggested that "the fact that the left hemisphere lags in development behind the right hemisphere may offer an alternate explanation to savant skills (Geschwind & Galaburda, 1986)." Examining the corpus callosi of the neuroscientists might also provide some insights regarding similarities and differences in connectivity between them and those with ASD.
Evolutionary Benefit and Risk
The neuroscientist finding also potentially answers some evolutionary questions. In my Autism, Genetics, and Evolution post, I suggested that the alleles that cause autism could have been with humanity for at least 40,000 years.
"Assuming 30 to 35 years per generation (which is conservative), there have been 1100 to 1300 generations since the two populations diverged. This presumably should have been enough time to eliminate the various alleles that cause autism from the gene pool, if they are in fact deleterious.
Obviously this has not occurred. This means that the individual alleles that in combination cause autism must individually or in lesser combinations have had a beneficial effect to compensate for the reduced reproductive rates of autistics."
As the neuroscientist paper indicates, the same narrower width minicolumnar structure found in ASD may be a competitive advantage in the case of the neuroscientists. If the same alleles that contribute to ASD can result in a competitive advantage in other circumstances through (intellectual) fitness, this would easily explain the continued existence of ASD over time. The research paper quotes T.G West from In the Mind’s Eye (1997):
"One of the most important lessons to be learned from the genetic study of many diseases in recent years has been that the paradoxically high frequency of certain conditions is explained by the fact that important advantages conferred on those who carry the predisposition to these conditions may outweigh the obvious dramatic disadvantages."
My Autism and Minicolumns post suggested that a) ASD has a minicolumnar underpinning, b) this underpinning is required (i.e. no narrow minicolumns means no ASD), c) it originates in the first 40 days of fetal development (i.e. it is not itself acquired post-natally), d) that this difference falls within the normal range (i.e. that having it does not ‘cause’ a diagnosis, although it may very well result in diversity of thought and cognition, i.e. neurodiversity), e) that something else is therefore required (with no significant speculation as to what that something else may be, other than to generically label it as a ‘second hit’), and f) that research needs to prove or exclude causality among the population of the vulnerable, i.e. proving that something does not cause ASD in those who are invulnerable does not prove that it does not cause ASD in those who are vulnerable.
I would suggest that the Neuroscientist research lends significant credence to the above, especially to point d, and suggests that the differences between the neuroscientists and those with ASD may point to the ‘something else required’ that follows.
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