Tag Archives: Clare Wilson

Does this explain that visual experience?

“OUR sight is sharpest at dawn and dusk – and now we may know why. It is not a result of changes within our eyes, but of how the brain processes visual signals.”

Clare Wilson Our eyesight is sharpest at twilight – and now we may know why. New Scientist. 10 April 2018.

https://www.newscientist.com/article/2165965-our-eyesight-is-sharpest-at-twilight-and-now-we-may-know-why/

This could be the solution to a mystery in sensory psychology that I’ve been wondering about for many years. I noticed a subtle effect in which my sense of sight without warning occassionally seems to improve, but not in any way that is obvious such as sharper focus or altered colour perception, resulting in a somewhat blissful effect that lasts a few seconds. I had noted that it seems to happen around the time of sunset, and I’d theorised that it is something to do with the visual system in my brain being able to readjust to a more optimal or fine-grained level of functioning as the result of a reduced level of light, similar to the effect of one’s eyes taking up to 20 minutes to adjust to the dark when one enters a dark cave during the day.

If synaesthesia is caused by low levels of complement, does that mean it is the opposite of schizophrenia?

The idea that schizophrenia is caused by brain dysfunction resulting from excessive synaptic pruning during the teenage years is certainly nothing new, I’ve been aware of it for many years and I think it is a winner, but the idea that this excessive pruning is triggered by higher than normal levels of complement appears to be new, although quite predictable in light of my immune hypothesis of synaesthesia which I published at this blog way back in 2012, even though, to be fair, at the time I was contrasting a variety of dementia (PCA or Benson’s syndrome) with synaesthesia, not schizophrenia. It is possibly worth noting though that schizophrenia was originally known as “dementia praecox” and might not be an entirely different thing to Bensons dementia in reality. I’ve written it before and I’ll repreat it again; I believe that Benson’s syndrome could be caused by excessive levels of complement, specifically C3 but I could be wrong in that specific suggestion. Regardless of the importance of the differences between Benson’s and schizophrenia, I’d still argue that this exciting theory about schizophrenia and high complement and over-pruning that is apparently supported by evidence is such a mirror-image of my theory about synaesthesia and low complement and under-pruning from 2012 that my theory could have been an influence on the schizophrenia researchers whose work has just been published in Nature, but I doubt that I got any credit.

It is exciting that progress is possibly being made into understanding and maybe even preventing schizophrenia, and it is about bloody time, (and how hard could it be to hinder the action of C4 or get rid of some of it, for heaven’s sake, to save some poor wretch’s brain and mind?) but now I’m left wondering what, if any, is the relationship between Benson’s syndrome and schizophrenia? My limited knowledge of Benson’s identifies only memory problems as a common feature of the two brain disorders, (and isn’t it interesting that I and more conventional synaesthesia researchers have linked synaesthesia with superiority in memory?) but I’m wondering if there is more in common between Sz and Benson’s than memory issues. I guess if I was really interested I’d turn to Google and PubMed to check whether someone has done a study of the immune system genetics of people who have Benson’s, but I have so many other less interesting things to do today. If no one has done such a study, then maybe they should, and then thank me for the tip.

 

Wilson, Clare Overactive brain pruning in teens could cause schizophrenia. New Scientist. January 27th 2016.

https://www.newscientist.com/article/2075495-overactive-brain-pruning-in-teens-could-cause-schizophrenia/

 

Aswin Sekar, Allison R. Bialas, Heather de Rivera, Avery Davis, Timothy R. Hammond et al. Schizophrenia risk from complex variation of complement component 4. Nature. January 27th 2016.

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16549.html

 

C. Wright Is synaesthesia caused by low levels of complement? Is Benson’s syndrome (PCA) caused by too much complement C3? Could synesthesia and posterior cortical atrophy be considered in some way opposites? Am I a super=recognizer? June 7, 2012.

https://superrecognizer.wordpress.com/2012/06/07/is-synaesthesia-caused-by-low-levels-of-complement-is-bensons-syndrome-caused-by-too-much-complement-c3/

 

Large twin study using the CFMT reportedly finds face recognition is heritable but largely independent of general intelligence and object recognition ability

http://www.pnas.org/content/early/2015/09/24/1421881112.full.pdf?with-ds=yes

https://www.newscientist.com/article/dn28258-our-knack-for-remembering-faces-is-a-highly-evolved-skill/

I wish I had the full scientific background to fully interpret this interesting new study, because the results have HUGE implications in psychology, but as far as I know are not particularly surprising or at odds with related research. The genetic and phenotypic independence of face recognition ability would smash to smithereens the long-debated idea of “g”, or one (mysterious) factor largely determining general mental ability. Face recognition or face memory appears to defy “g”, but all the same, I can’t help clinging to the idea that there’s a link between top ability in face recognition and at least some other cognitive gifts. Based on personal experience I find it hard to leave behind the idea of a link between elite reading and writing ability, synaesthesia and superior face recognition.

Placing the heritability of face recognition ability at 61%, as this study has done, kicks sand in the face of the long and bitterly debated idea that giftedness or talent is the result of long hours of focused training rather than innate ability, but I can think of one researcher who has championed the “trained not innate” position on talent or expertise for many years, who seems to lack an awareness of the entire body of face recognition research, instead focusing his attentions on elite performers in sport, music, memory and chess. Ignorance is bliss, they say.

I am a super-recognizer, and I have no memory of ever training my ability in recognizing or memorizing faces, and no one has coached, pressured nor trained me to this specific task. I defy those who argue that intelligence is “environment” not genetics to explain me and faces. Up until a few years ago I had no idea I was even above average with faces, so don’t ask me.

If dyslexia isn’t a visual problem, then what is it?

Forget colour overlays – dyslexia is not a vision problem. by Clare Wilson

New Scientist. 25 May 2015.

Do you want to know my theory about dyslexia? I think dyslexia is a lack of synaesthesia, for two very good reasons. Firstly, if you break the act of reading down into its most basic element (phonics or translating graphemes into phonemes), it is basically synaesthesia in which visual symbols as a visual stimuli evoke an experience of language sounds. Reading is basically hearing symbols, and that experience of language sounds further triggers the experience of concepts being triggered by language sounds. I know that things as complex as concepts can be synaesthesia concurrents because I myself experience a number of varieties of synaesthesia in which quite sophisticated concepts are the concurrents. I think the reason why some people are poor at reading or slower to pick up the skill is identical with the normal genetic variation in the degree which people are more or less syanesthete. There is debate about how much evidence has been found by researchers about brain structure and syanesthesia, but I still think it likely that syanesthesia is the result of a hyper-connected brain, and I think the opposite is true of dyslexics, and I believe the theory of dyslexia and hypoconnectivity is nothing new in dyslexia research.

The second reason why I think dyslexia can be regarded as the opposite of synaesthesia (even though I’m open to the possibility that there could be some individuals who have both conditions for reasons unknown) is that in my family of blood relatives we have a pedigree of generations who have a profession that primarily deals with the written word or have scored in academic selection tests in the highest levels of percentiles in reading, writing and general literacy skills, even though their results in other academic areas are above average but not exceptional, and most of these people appear to be grapheme-colour synaesthetes. I believe this association is not random, but such a relationship can only be proven by studies done by researchers on large numbers of people, and if any researcher would like to put my theory to the test and publish the results I would expect that I would be appropriately credited in their research paper.