Tag Archives: Immune Hypothesis of Synesthesia

If we knew anything much about Sjogren’s syndrome, could that knowledge help us to understand the world-wrecking illness caused by COVID-19?

I’ve just stumbled across an article about another of the odd features of coronovirus illness. I thought it was quite interesting that the infection can cause a temporary loss of the sense of smell, which could happen in a number of different ways, but the covid infection feature that really fascinates me right now is “covid toes” This feature, which can also affect hands, has been identified as an atypical form of perniosis or chilblains that is not triggered by cold as is typical of perniosis/chilblains. These discomforts of the extremities fascinate me because they seem to have a lot in common with a cluster of inter-related medical conditions involving small blood vessels and typically affecting the hands and feet that are often associated with autoimmune diseases, including Sjogren’s syndrome, and Sjogren’s syndrome itself could be viewed as having many features in common with the coronovirus illness. 

Both Sjogren’s and COVID-19 infection can cause lung damage that creates “ground-glass” CT images, inflammation in the lungs and lung conditions that sound pneumonia-ey. One of the many lung diseases that can be caused by Sjogren’s is bronchiolitis, an inflammatory lung disease that “is almost always caused by a virus”, except when it is caused by Sjogren’s syndrome, of course. 

Sjogren’s can be associated with Raynaud’s phenomenon and erythromelagia; two related conditions of “dysfunctional vascular dynamics” reacting to temperature, affecting sensation and typically affecting the hands and feet. COVID-19 is associated with the “covid toe” phenomenon, affecting the hands and feet, resembling perniosis/chilblains which is normally triggered by cold temperature and “may be an abnormal blood vessel response” and can co-occur with Raynaud’s. The bluishly discoloured extremities shown in photos of covid toes and hands looks a lot like Raynaud’s. Covid toes can be painful and “have a hot burning sensation”, which sounds a lot like erythromelagia, the evil twin of Raynaud’s which hurts like a bitch and is worsened by heat and can sometimes be relieved by cooling. 

The “covid toes” phenomenon can involve a rash, which maybe isn’t surprising considering how common rashes are in bacterial and viral infections. Sjogren’s can also come with a rash, a rash that can last not just days or weeks, but decades. Like Raynaud’s and erythromelagia this autominnune rash involves stupid things happening to or inside blood vessels. It typically affects the feet and lower legs, and sometimes the hands and other parts of the body. This rash that can go on forever also has a name of impressive length; hypergammaglobulinemic purpura of Waldenström, or HGP for short.

Like the coronavirus illness, Sjogren’s affects the blood vessels, parts of the head, the lungs and sometimes the extremities, and typically causes tiredness or fatigue. Sjogren’s can affect the nose area, in addition to it’s more well-known autoimmune attacks on the tear and saliva glands in the face, and like the coronavirus illness, Sjogren’s can impair the sense of smell

As I’ve explained already, Sjogren’s can damage the lungs in the same way that a virus might. I think it is also quite interesting that one of the vascular diseases that can co-occur with Sjogrens, erythromelagia, was, according to one report, once caused by infection of humans with a virus that is typically found in small mammalian animals. Can you guess which country those humans and little animals lived in? Yes, China. 

I have not been able to find any evidence one way or the other as to whether the COVID-19 illness can directly damage the foetus of an infected pregnant woman. I’m interested in any research or observations about this possibility because if there are non-trivial commonalities between this illness and Sjogren’s some unusual and distinctive problems in babies born of infected mothers might occur. Antibodies characteristically found in Sjogren’s cases can cause congential heart block in the foetus in utero or “neonatal lupus”, a strange solid red rash around the baby’s eyes, but even among pregnancies of women with at least one of these antibodies, these rare conditions are found at a rate of only one or two percent. 

If it is true that there are non-trivial commonalities between COVID-19 illness and Sjogren’s syndrome, that might suggest a general explanation of the much-pondered question of why coronavirus kills more men than women. Sjogren’s syndrome, Raynaud’s phenomenon and erythromelagia are all more commonly found in women than in men. Maybe this indicates that the normal, healthy female body is generally more likely to manifest the kinds of immunological/vascular shenanigans that happen in these three related conditions. Maybe the normal male body rarely has these things happening, and has not adjusted to or accommodated these abnormal processes, so when male bodies encounter COVID-19, which apparently causes wierd vascular events to happen, the male body is less able to cope with these processes. Just a theory. Women have babies and men do not. Lots of interesting things happen during pregnancy to the vasular and blood systems that the male body will never have to deal with. Notice that I haven’t once mentioned the word “hormones” during this explanation? I so much hate it when boffins glibly explain differences in sex ratios for diseases and social problems as due to “hormones”. That is a non-explanation. That is inexcusably lame. 

As long-time readers of this blog might have noticed, I have quite a fascination for rare and autoimmune diseases. I was the original author in 2012, at this blog, of two hypotheses, one speculating that a rare form of dementia might be caused by high levels of a type of chemical that plays a part in both synaptic pruning and the immune system, and a twin hypothesis that the psychological/neurological developmental variation synaesthesia might be caused by low levels of one or more of the same group of immune chemicals. The latter novel hypothesis was later published in a peer-reviewed neuroscience journal, unfortunately without me listed as an author. Even though I’m pretty interested in a bit of amateur immunology (more than the average housewife), before tonight it had not occurred to me how much a cluster of inter-related autoimmune diseases could be similar to a virus.

So I guess the world-shaking, worth-a-million-bucks-to-someone-else, super-important question is whether established scientific knowledge about Sjogren’s syndrome and related autoimmune diseases could provide any useful insights into a vaccine or treatment or prevention of the COVID-19 illness. I think probably not, because I don’t think medical science knows terribly much about Sjogren’s or any of the other diseases that I’ve just wasted my time writing about here. It’s the same old story about rare diseases being the orphans of the world of disease research. Erythromelagia can be a horribly painful disease, once treated by amputation before doctors had any insight into how it works, and has been written about under a variety of names since 1878, but your GP has probably never heard of it. Like Raynaud’s phenomenon, there is apparently no blood/pathology test known to be useful for diagnosing erythromlagia. Has any researcher even bothered to search for pathology or autoimmune abnormalities in either of these diseases? If you Google Sjogren’s syndrome you will probably read that it is dry eyes and a dry mouth, then the details of symptomatic treatment. I guess that’s the level of interest and trivialisation that one might expect from the world of medical science for a mostly non-fatal disease affecting mostly middle-aged women. Outlines of Sjogren’s in medical literature and patient info might also give you the impression that Sjogren’s always coincides with rheumatoid joint problems, and the only pathology results associated with it are antinuclear antibodies, rheumatoid factors and SSA and SSB. None of this is true.

Does medicine understand how Sjogren’s syndrome works? No. Is there a unequivocally safe and effective treatment for it? Of course, no. Apparently “Hydroxychloroquine (Plaquenil), a drug designed to treat malaria, is often helpful in treating Sjogren’s syndrome.” I have no idea whether that is a useful insight in relation to COVID-19. So often prescription drugs are worse in the side effects than the disease, or don’t really work at all, but I guess in April 2020 we are all grasping at straws. I guess there’s one positive thing that might come out of my thoughts and speculations; maybe I’ve just discovered what triggers the development of Sjogren’s syndrome? A coronavirus? 

If medical science had taken diseases like Sjogren’s syndrome and associated vascular and autoimmune disorders seriously before now, would we now understand how COVID-19 kills and sickens people, and would science have already developed a safe and effective treatment for it? 

A note of warning – If you are thinking about copying or plagiarizing any of the text, original ideas or descriptions in this post or using it in your own work without giving me (C. Wright, author of the blog “Am I a Super-recognizer?”) the proper acknowledgement and citations, then think again. If you do that you will be found out and my objection will be well publicized. If you believe that you published any of these ideas before I did, please let me know the details in a comment on this article. If you want to make reference to this blog post or any of the ideas in it make sure that you state in your work exactly where you first read about these ideas. If you wish to quote any text from this post be sure to cite this post at this blog properly. There are many established citation methods. If you quote or make reference to material in this blog in your work, it would be a common courtesy to let me know about your work (I’m interested!) in a comment on any of the posts in this blog. Thank you.

Immune Hypothesis of Synaesthesia

The original place of publication (non-journal, non-academic, non-peer-reviewed) of the immune hypothesis of synesthesia or synaesthesia, by C. Wright, at this blog, in 2012, can be found at the link below.



So does this mean that folks with an immune deficiency in complement C3 have some kind of protection against Alzheimer’s?

You might have autoimmune diseases and chest infections that take forever to clear, but possibly also less of your brain disappearing with age, if research on mice is relevant to people.

Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice


Readers of this blog from back in 2011-2012 could have predicted this, because I pretty-much predicted this with my immune hypothesis of synaesthesia and my immune hypothesis of Benson’s syndrome (a variety of dementia). I wonder how many lives could have been saved and cases of dementia prevented if the world of science had bothered to read my blog and taken my theories seriously back then and set to work finding a therapy that reduces levels of C3? How hard could that be? It happens naturally, so how hard could it be to engineer a similar process? Instead all I got for my ideas and blogging was synaesthesia researchers plagiarizing my ideas shamelessly in a speculative paper about synaesthesia (a mere triviality in the world of neuroscience compared with the tragic and expensive problem of dementia). And all this time funding for dementia research has been counted in the hundreds of millions of dollars and has given the public virutally nothing in the way of effective therapies. How much of that research funding do I get? Not one single frickin’ red cent, because I’m not a scientist. I’m just a housewife with ideas, and a blog.


Surprising explanation for why face recognition matures unusually late in human development!

I didn’t expect to be reading this but I can recognize that this discovery seems to explain why face recognition is human cognitive ability that hits its peak surprisingly late in human development, and I’m now wondering how this fits into my theories about the relationship between my super-recognition and my synaesthesia, and that includes wondering how this discovery fits with my immune hypothesis of synaesthesia (which is all about pruning rather than proliferation), and of course I’m wondering how this fits in with what is known about super-recognizers. I guess I should just calm down and read the full text.

Coghlan, Andy Brain’s face recognition area grows much bigger as we get older. New Scientist. January 5th 2017.

Jesse Gomez, Michael A. Barnett, Vaidehi Natu, Aviv Mezer, Nicola Palomero-Gallagher, Kevin S. Weiner, Katrin Amunts, Karl Zilles, Kalanit Grill-Spector Microstructural proliferation in human cortex is coupled with the development of face processing. Science. January 6th 2017.



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.



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.



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.



Amazed, not in a good way

The 2013 journal paper that ripped-off my excellent and original idea linking synaesthesia with specific elements of the immune system (published in this blog in 2012) has been reprinted as a chapter in a book that was published just a few months ago. One of the book’s authors is also one of the two authors of that paper, and another one of the book’s authors was an editor of that paper. Have these people no shame?


The offending paper has also been cited in a 2015 paper by two of the book’s authors


Also not nice to know that recent work of those researchers was scheduled to be presented by one of them at the Eleventh Annual National Conference of the American Synesthesia Association at the University of Miami, Florida, held last month. This year’s conference was organized by the same academic who was the reviewer of the offending 2013 journal paper.



And one of those researchers will be the supervisor of a PhD studentship beginning January 2016


I’d like to invite those involved (so many of them) to individually or collectively go and dip their left eyes in hot cocky cack, to quote an Australian cinema classic




Wow, this is interesting

Scientists Find Vessels That Connect Immune System And Brain. June 3, 2015 | by Stephen Luntz. IFL Science.


Structural and functional features of central nervous system lymphatic vessels

Antoine Louveau, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Kevin S. Lee, Tajie H. Harris & Jonathan Kipnis
Nature (2015) doi:10.1038/nature14432
Received 30 October 2014 Accepted 20 March 2015 Published online 01 June 2015


I find this most interesting for a number of reasons. Firstly, the discovery showing that the human brain has functional lymphatic vessels connecting the brain with the immune system adds to a growing collection of evidence that the immune system plays important roles within the brain, which is an apparent partial violation of the long-held concept of the “blood-brain barrier” (as was described in a dated and inadequate chapter by Dr Karl in his 2013 pop science book Game of Knowns). In 2012 I was apparently the first person in the world, at this blog, to publish the ideas that high or low levels of the “component” immune chemicals at various points in development could be the cause of conditions of the brain such as developmental synaesthesia and Benson’s syndrome or PCA. My ideas were inspired by the very exciting research in areas such as microglia, complement, synaptic pruning and MHC1 molecules.

Another reason why this new discovery linking the central nervous system with the lymphatic and immune systems by researchers from the University of Virginia is so exciting is the fact that it is an unexpected discovery, as one might have thought that human anatomy would have already been thoroughly researched and discovered through the history of medical science to date, but then again, surprising new discoveries in human anatomy have not been unknown in recent years, with discoveries of new features in the human eye, knee and clitoris, the rediscovery last year of a major white matter tract (the vertical occipital fasciculus) at the rear of the brain that could play a central role in skills such as reading, and a new shape of neuron discovered in mouse brains. These new discoveries are exciting and also rather unsettling; exciting because it appears that important new discoveries in human neuroscience and anatomy are still possible, and unsettling because genuinely surprising new discoveries in science seem to indicate that science is not a steady accumulation of knowledge and a path of upward progress, as many believe. This may or may not be surprising to you, depending on which theory in the philosophy of science you favour. I think the discoveries of the VOF and the collection of discoveries about the roles and anatomy of the immune system in the human brain could be interpreted as evidence showing how incorrect ideas in science can become widely-accepted and widely-taught and could also have delayed the progress of new discoveries in neuroscience. How much further might we have come by now in our understanding of the human brain and mind if not for the popularity of the idea that the human brain is quarantined from the immune system? Which other influential ideas about the human brain are holding us back from a clearer understanding of the brain’s workings and diseases?

All those years of neuroimaging research on the brains of synaesthetes has found nothing of substance?

Hupé J and Dojat M (2015) A critical review of the neuroimaging literature on synesthesia. Frontiers in Human Neuroscience. 9:103.


“Our critical review therefore casts some doubts on whether any neural correlate of the synesthetic experience has been established yet”

That is a bit of a shock to read. This isn’t the first time that I’ve gotten a big shock after reading a paper in the journal Frontiers in Human Neuroscience. There was that little matter of some of my most amazing neuroscientific ideas published at this blog being ripped-off and used as the guts of an “opinion article” in that journal in 2013. I haven’t forgotten that episode. Who would have thought so much excitement is there to be found inside a science journal? I should make it clear that the researchers who did that thing in 2013 are NOT the authors of the above paper, but at the same time, I’ve got to wonder where Hupé and Dojat got this idea from

“…synesthesia could be reconsidered as a special kind of childhood memory, …”

Sure, they could have thought of that under their own steam, but I still want to point out that the central, seminal idea of this blog, right from the very first post in 2010, has been the idea that synaesthesia is linked in some meaningful way with face memory, in my case with super-recognizer ability in face memory, and there are many articles in this blog that show and hint that the heart of synaesthesia is memories created in childhood and many different types of synaesthesia operate in ways that are so much like memory that the differences are only quantitative. There was even one article published in 2013 at this blog in which I stated that

“…the Proust phenomenon is considered to be a type of memory and many of my observations at this blog have demonstrated that synaesthesia can involve memory, is an element of the “method of loci” memory technique and I would argue operates like memory. Yes, Yes, Yes, the Proust Phenomenon is a close relative of synaesthesia.”

Some ideas that I’d like to (explicitly) lay claim to (right now) in 2014

Radio show about Glenda Parkin living with dementia in suburb of Perth, Western Australia

Below are the details of a recent and very interesting radio interview on Perth public radio with Glenda and Bronte Parkin and Alzheimers WA CEO Rhonda Parker, focusing on Glenda’s experiences as a person who has a form of dementia that goes by a number of names including Benson’s syndrome, posterior cortical atrophy and PCA. This is not the first time that Glenda has shared her story with the media; she previously shared her story with Perth’s daily newspaper, the West Australian, in 2011 and she has recently been interviewed for the Community Newspaper Group.

I have unusual reasons to be grateful that Glenda has shared her story with the mass media. I happened upon her story in a copy of the West while I was enjoying coffee and one of those wonderfully greasy Sausage and Egg McMuffins in a McDonald’s restaurant in 2011, after dropping someone off to a selective school that offers students places based on high ability in the area of literacy and languages. I became intrigued by the fact that the particular type of dementia described in the article appeared to be a mirror-image of the pattern of intellectual gifts that appear to run in our family, associated with synaesthesia, a harmless, genetic, developmental and memory-enhancing condition that is caused by increased connectivity in the structure of the white matter of the brain. I wondered whether there could be an undiscovered developmental basis of Benson’s syndrome that works like the opposite of synesthesia, or could it be caused by some mature-age dysregulation of some chemical that regulates growth in the parts of the brain that seem to be hyper-developed in our family, and attacked, over-pruned or somehow damaged in Benson’s. I wrote about my ideas in this blog soon after. In 2012 my thinking on this theme took an important and exciting leap ahead when I happened across a brief article in New Scientist about research by Dr Beth Stevens on microglia, complement, synaptic pruning and elements of the immune system playing a central role in the development of the brain. I figured that one or maybe more of the complement chemicals could be the chemical that regulates growth or pruning in the parts of the brain that I had written about and attempted to identify in my 2011 blog post. I wrote a brief outline of these ideas at this blog in 2012 in an article that was archived by the Internet Archive Wayback Machine in 2012. In lat 2013 I got a big surprise when I saw my idea linking the immune system with synaesthesia as the main idea of a research paper published in a peer-reviewed neuroscience journal, and all without my permission! That’s another story….

I am sure that many people listening to this radio interview would be fascinated with or even skeptical of Glenda’s account of being able to see but not perceive letters on the cover of a book. Her eyesight is not the problem, the problem lies in the visual processing areas of her brain and because of this a lady who in her impressive career has been an author of books can no longer read text or interpret symbols. Seeing is as much done in the brain as it is done in the eye and optic nerves, and a person who has no apparent problem with their eyes can lose visual perception as the result of dementia or injury or stroke.

“Simple things can be very frustrating” – Glenda and Bronte Parkin on dementia. Mornings with Geoff Hutchison. 720 ABC Perth.

Jarvis, Lucy Still making a contribution: retired educators share experience of living with dementia. Community Newspapers. 2015

Hiatt, Bethany Penrhos principal’s hardest battle.  West Australian. January 3, 2011. http://au.news.yahoo.com/thewest/a/-/mp/8588194/glenda-parkin/

Postscript March 10th 2015

The West Weekend liftout of the West Australian of February 14-15 2015 has a feature story about West Australians livng with dementia on pages 10-13. he story of Glenda and Bronte Parkin is included in that article and the content makes it clear that although Glenda Parkin has a diagnosis of Benson’s syndrome which has had a negative impact on her ability to recognize symbols, writing and objects, she can still somehow navigate her way in her neighbourhood. I find this interesting as some people who have prosopagnosia, which is an impairment in face memory, also have a similar impairment in visual memory of scenes or landscapes, and thus have serious problems with navigating their way through streets and neighbourhoods. I had thought that Benson’s syndrome, a type of dementia, and prosopagnosia, a developmental disability and also sometimes acquired from brain injury, must be in many ways similar in their manifestations, as they both feature disability in face recognition, but it appears that it is not safe to make assumptions and maybe each case of these two conditions should be considered unique. I do not recall reading about Glenda Parkin’s ability to recognize faces, so maybe I should assume it is still normal, along with her ability to recognize street-scapes and scenes.

Yeoman, William Open minds. West Weekend. p. 10-13 West Australian. February 14-15 2015.


Finding confirmation of my beliefs and ideas, as you do

A closely related family member of mine recently scored a perfect mark on an adult literacy test geared to normal adults (which was true to form) , and another closely related family member in mid-childhood recently explained that they perceive motor vehicles as having faces and they categorize cars, utes and 4WDs into genders, square old 4WDs being male. I can see how that makes sense, but all the same I’ve never been that much of a car personifier. Ever since I was a child I’ve personified numbers and alphabet letters in great detail, along with perceiving them as essentially associated with very specific colours, and the shapes and motions of cars often make me think of hunting animals in some deeply instinctive way, but unlike my young relative and the many Australians who decorate their own motor vehicles with oversized curly eyelashes or giant imitation testes, I don’t see motor vehicles as male or female.

On the surface most people seem pretty-much normal and average, but if you make the most superficial investigation by testing or speaking with people about their thoughts and perceptions, you might find that there is an interesting and sometimes significant range of differences in the way our minds work. Grapheme-colour synaesthesia, personifying synaesthesia and elite and precocious levels of ability in reading, spelling and general literacy are just some of the interesting things that run in my family and are also experienced by me, and I am also a super-recognizer. A super-recognizer is a person who has an elite level of ability in recognizing faces or face memory, and typically can achieve perfect or near-perfect scores on tests of face memory. I believe that this co-occurrence of synaesthesia and elite abilities in face memory and literacy are no coincidence. I believe all of these things are based on hyper-connectivity or hyper-development in the rear parts of the brain including the fusiform gyrus, and also in the right hemisphere of the brain. I believe the genetic basis of this development might be linked to genes that code for particular variations in the functioning of the immune system, possibly involving the complement chemicals, microglia and synaptic pruning. I’m fascinated by the possibility that research work that has been done in the last decade linking immunology and neuropsychology can inform us about the origins of synaesthesia and also specific gifts and deficits in memory and cognition, and maybe also inform us about some types of dementia. In 2012 at this blog I explicitly identified research on the immune system, complement, microglia and synaptic pruning done by Dr Beth Stevens as a possible explanation for the origins of developmental synaesthesia, an idea that was so good that some synaesthesia researchers made it the basis of a speculative paper that was published in a peer-reviewed journal last year (they forgot to acknowledge me as the first to publish this idea). Work done on MHC1 (part of the immune system) and the brain by Carla Shatz is another area of scientific research that I find tremendously exciting, and I believe that the general area of research on the relationships between brain structure and the immune system is of such originality and importance that it should attract one or more Nobel Prizes.