34 COVID-19 questions

The new coronavirus pandemic is the topic dominating our lives at the moment, so I hope you won’t mind if I diverge from the usual neuroscience and psychology themes of this blog, to pose some questions (some a bit rhetorical) related to the virus.

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.

1. How many children, women and men will die or become victims of abuse as the result of increased domestic violence and opportunities to hide abuse and neglect under conditions of social distancing and online schooling?
2. Are there any aspects of the medical care of people infected by the virus or other measures to deal with it which could conceivably become the subject of a medical reversal in the future or be later regarded as negligent?
3. Is there any evidence that social distancing indoors and outdoors should be the same?
4. Would medical clinics or other places where people must share space be safer in terms of social distancing if they were conducted outdoors?
5. Are there documented cases of infection from the new coronavirus caught through the air in an outdoor place?
6. Are there any particular immune deficiency conditions or genetic immune system variations that are over-represented among people who have died from the new virus?
7. Have any researchers studied the vitamin D status of people infected with or killed by the new virus?
8. Vitamin D deficiency makes people more vulnerable to infection, and this deficiency related to limited sun exposure is surprisingly common, even in sunny nations like Australia, so could government prohibition of outdoor activities in which people often gain sun exposure, such as swimming and sunbaking at closed beaches, intended to prevent transmission of the virus, prove counter-productive by raising people’s vulnerability to the virus, if the virus is encountered?
9. Should saturation mass media messages from celebrities to “stay inside” be modified to a more nuanced message to prevent an epidemic of vitamin D deficiency and associated autoimmune diseases come the end of winter 2020?
10. Are any of the fatalities that followed after infection by the new coronovirus attributable to secondary infection by pneumonia-causing bacteria?
11. Is there a cohort of young Australians who have never been immunised against pneumococcal bacteria because they were born before it was scheduled as a standard childhood immunisation?
12. If the adult vaccination against pneumonia bacteria is safe and effective, and pneumonia is not a rare disease, why isn’t it recommended and funded in Australia for all adults, rather than recommended for a confusing collection of categories of adults?
13. Why is vaccination against influenza widely promoted as a good idea for everyone, especially within the context of the COVID-19 pandemic, while this does not appear to be the case in relation to immunisation against pneumonia bacteria?
14. Are social problems resulting from social distancing restrictions on recreational activities outside the home particularly acute in new suburbs in which tiny residential block sizes or large homes with tiny gardens have been compensated for by land developers with quality recreational facilities in public parks, which are now shut down or restricted?
15. Is it true that India has never been the site of origin of an infectious agent responsible for a major epidemic or pandemic, even though it is a large nation in terms of geography and massive in terms of human population? China is another massive nation, and it and surrounding nations have bred some troublesome infectious agents in recent years, including COVID-19. Does this show that the lacto-vegetarian/Hindu values of the Indian nation are safer and a benefit to all of humankind, because the lifestyle these values promote involves less human interference with and caging of wild animals? The WHO has recently thanked India for engaging the WHO’s national polio surveillance network to strengthen COVID-19 surveillance in India. Should India also be thanked for refraining from doing stupid and cruel things with disease-riddled bats and other wild animals?
16. Should wildlife carers be banned from caring for or touching bats?
17. In 2018 an estimated 1.5 million people died from tuberculosis. Why has the world stopped in its tracks to control covid-19, but has not solved the very long-standing global TB problem?   
18. The potential benefits of the BCG anti-TB vaccine on the immune system beyond TB protection have been known for many years, including potential to prevent allergy. Allergy has been described as a modern-day “epidemic” causing life-threatening medical problems for countless children and adults. Why has it taken the COVID-19 pandemic for Australian researchers to study the important possible benefits of the BCG vaccine? 
19. In the UK sniffer-dogs are being trained to sniff out cases of coronavirus. Already dogs, and even one British woman, have been used to sniff out medical conditions such as cancer and infectious and non-infectious diseases, and of course trained detection dogs have been used for a long time to sniff out drugs and explosives. Are there any disease-sniffer dogs in Australia?
20. Can anything be done about police informant drug dealers who fail to observe social distancing by hosting a steady parade of guests at their home? 
21. Does taking ACE inhibitor drugs make it more likely that you will die if you catch coronavirus?
22. Does coronavirus directly cause birth defects or other forms of harm to a child born to an infected mother? 
23. What is the evidence-base or group of published studies upon which Autralian governments’ policies of returning children to school in person has been based? 
24. How common among children infected by covid-19 is the development of the Kawasaki-like inflammatory/autoimmune disorder that has been reported recently?
25. Could there be unidentified deaths from or cases of the above disease in Australian children, as is possibly the case in the UK?
26. Why was the “Socialist medicine” NHS in the UK the first institution to alert the world to the new covid-19-associated Kawasaki-like inflammatory/autoimmune disorder affecting children, when it appears that evidence of the development of this new potentially serious disease in kids has been observed in Australia and other nations? 
27. Is it possible or likely that a thing to emerge from the covid-19 pandemic will be blocs or groupings of countries into a handful of categories: those nations with effective coronoavirus control, those without with current new infections, nations still to be affected by the virus, and nations with unreliable statistical reporting. If Australia and New Zealand might one day be able to have an arrangement to open borders, might this exclusive club one day widen to incorporate other nations that appear to be on top of covid-19, such as Hong Kong, Taiwan, South Korea, some Scandinavian countries, with trade, travel and tourism resuming between nations? Even though PNG and Indonesia are geographically closer to Australia than New Zealand, in the new post-covid world order New Zealand seems much closer to Australia, as on May 4th 2020 New Zealand Prime Minister Jacinda Ardern was invited to remotely attend an Australian National Cabinet meeting between Australian Prime Minister Scott Morrison and the state and territory heads.  Will Australia’s historically close social and trade ties with countries such as the USA, the UK and China be downgraded because these countries have done a poor job of controlling or honestly reporting about covid-19?
28. Is there any evidence or observations that people with autoimmune diseases are affected by covid-19 in a more or less serious way than the average person? 
29. Can people who have other diseases register a false positive in a covid-19 test, as is the case with the RPR Test for syphilis?
30. Can immunisation with existing vaccines cause a person to register a false positive in a covid-19 test, as is the case with the BCG TB immunisation that can cause a false positive result on a TB infection test? 
31. Given that there is still a lack of scientific consensus about whether children infected with covid have lower viral loads than infected adults, and thus might be just as infectious as adults, why are so many state and national governments in Australia and globally forcing parents to send their children to schools?
32. There appears to be a lot of uncertainty in reports of the emerging Kawasaki-like illness seen in children (now named pediatric multisystem inflammatory syndrome), and among recent cases of Kawasaki disease in children in Australia of an unexpected number, about whether or not all of these cases have had or do have covid infections. Is this evidence of a problem globally with identifying or testing covid-19 infection in children? Are children dying of covid-19 or its complications, in “advanced” countries, without ever being identified as covid-19 cases?
33. Given that pediatric multisymptom inflammatory syndrome clearly associated with covid-19 in kids killsbut has not reliably been identified or tested as being associated with covid-19 infection in cases seen in various parts of the world, including in Australia, pointing to the likelihood that covid-19 in kids “flies under the radar”, not reliably detected as the cause of illness by many doctors or by covid-19 testing, does Australia or the Australian states need to set up a reporting system in which doctors are compelled to report to a team of investigative medical specialists any adult or pediatric cases which could potentially be novel infectious diseases or novel presentations of known infectious diseases? 
34. Given that pediatric multisymptom inflammatory syndrome clearly associated with covid-19 in kids kills, with at least one press report suggesting a cover-up of PMIS deaths in the UK, and PMIS was not initially identified or tested as being associated with covid-19 infection in many cases seen in various parts of the world, including in Australia, pointing to the likelihood that covid-19 in kids “flies under the radar”, not reliably detected as an illness or by covid-19 testing, should schools in parts of the world where covid-19 is not close to eradicated and monitored by large-scale public random testing programs be open?

References / Links

Aranow C. (2011). Vitamin D and the immune system. Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 59(6), 881–886. https://doi.org/10.2310/JIM.0b013e31821b8755

Nowson, C. A., McGrath, J. J., Ebeling, P. R., Haikerwal, A., Daly, R. M., Sanders, K. M., … & Mason, R. S. (2012). Vitamin D and health in adults in Australia and New Zealand: a position statement. Medical journal of Australia, 196(11), 686-687. https://www.mja.com.au/journal/2012/196/11/vitamin-d-and-health-adults-australia-and-new-zealand-position-statement

Brooks, M. (2013). Small shot, big impact. New Scientist, 219(2930), 38-41. https://www.newscientist.com/article/dn24027-booster-shots-the-accidental-advantages-of-vaccines/

World Health Organisation. Tuberculosis. 24 March 2020. https://www.who.int/news-room/fact-sheets/detail/tuberculosis

Worldometer. Coronavirus. https://www.worldometers.info/coronavirus/

Quaggin, Lucy (2020) Coronavirus vaccine: West Australian hospital workers to take part in COVID-19 experiment. 7NEWS. Tuesday, 14 April 2020. https://7news.com.au/lifestyle/health-wellbeing/coronavirus-vaccine-west-australian-hospital-workers-to-take-part-in-covid-19-experiment-c-974237

Coronavirus: WHO thanks India for support, borrows polio-fighting strategy for COVID-19. business Today. April 16, 2020. https://www.businesstoday.in/current/economy-politics/coronavirus-who-thanks-india-for-support-borrows-polio-fighting-strategy-for-covid-19/story/401156.html

Dogs join fight against COVID-19 by learning how to detect the virus. Sandie Rinaldo. CTV National News. April 12, 2020. https://www.ctvnews.ca/health/coronavirus/dogs-join-fight-against-covid-19-by-learning-how-to-detect-the-virus-1.4893325

 

 

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.

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

 

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

http://stm.sciencemag.org/content/9/392/eaaf6295

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.

 

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/

 

Wow, this is interesting

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

http://www.iflscience.com/brain/vessels-found-connect-immune-system-and-brain

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

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14432.html

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?

Action-packed YouTube video clip

Immune cell in the brain swallows synapses to sculpt neurons during development.

Posted by NIHNINDS (National Institute of Neurological Disorders and Stroke) at YouTube on May 22, 2012.

http://youtu.be/wb8UAyf8Nhw

The green thing is a mouse’s microglial cell. The movie is “courtesy Dorothy Schafer, Ph.D. and Beth Stevens, Ph.D. at Boston Children’s Hospital.” At this blog I have speculated that the kind of process shown in this brief video clip possibly happens less often in the brains of some people because they have lower levels of some of the complement chemicals that are a part of the immune system, with the result being the development of, or the retaining of, childhood or developmental synaesthesia. Some of the complement chemicals mark out synapses for destruction, I believe.

There’s a back-story to my theory

I can show data dating back to the year 2000 that supports my theory that low levels of complement proteins, which are a part of the human immune system, specifically C3, C4 and most likely C1q, are the biological cause of the development of inherited synaesthesia (at least in some cases). Before I had thought of the idea of a link between the immune system and synaesthesia I had, at the blog, published a theory that synaesthesia is in some way the neurological opposite of a variety of dementia named Benson’s syndrome (aka PCA, posterior cortical atrophy), based on my observations and reading. I had speculated that there could be some “magical chemical” that regulated the brain in some way and that oppositely extreme levels of this magical chemical could be the biological basis of both synaesthesia and Benson’s syndrome. Back in 2012 I read a small article in New Scientist magazine that blew my mind, because it appeared that it gave me some major clues about what that magical chemical could be. The article was about the exciting work of Dr Beth Stevens on microglial pruning in the brain and the immune system’s complement proteins. The term “pruning” was familiar to me from all of my reading about synaesthesia, which is a fun heritable brain-based phenomenon which I share with some of my first-degree relatives, along with specific gifts in literacy skills. The term “complement” in the context of the immune system, and the individual names of complement proteins were also familiar to me.

Being a super-recognizer, I’m pretty good at recognizing patterns, and I recognized that all these elements of information fitted together into an important and original multi-faceted theory. I was so excited that I published a brief outline of my theory at this blog in 2012. In 2013 I was shocked to discover that a prominent synaesthesia researcher and her co-author had published a theoretical journal paper titled “The immune hypothesis of synesthesia” which even included speculation that the “complement system” could be the element of the immune system responsible for the development of synaesthesia. I found no credit given in that paper to me or my blog. As I had published my theory first I believe I should have been fully acknowledged. I never thought that this could have been a case of two separate parties thinking of the same idea independently. I read their paper through and I looked into the educational and research background of both authors and their previous publications and found no study or writing about the immune system and no indication or explanation of why they might have suddenly had their own insight linking synaesthesia with some of the many elements of the incredibly complex immune system that only an immunologist would find interesting. 

This Easter I’d like to pose the question; can Simner and Carmichael offer data dating back to the year 2000 as the basis of their published version of “the immune hypothesis of synesthesia”? I can, and I would be willing to share my data with serious medical researchers.

A while ago I was sorting through some piles of old papers that I had stowed away years ago without sorting through them. These things happen during a busy family life. These piles had been sitting around for years, some of it photocopies of articles from New Scientist magazine that had struck me as interesting but which I hadn’t always had the time to read through properly. I was amused to find that I had stowed away an article from the March 1st 2008 issue titled “Thought control” by Bijal Trivedi. It was all about exciting research by the likes of Carla Shatz, Ben Barres, Simon John, Staffan Cullheim, Eliezer Masliah, Robert Terry and Lisa Boulanger about synapse loss in dementia and the interesting things that elements of the immune system appeared to be doing in the brain, contrary to the received wisdom that there is a thing called the blood-brain barrier that keeps the immune system out of the brain. I’m not sure whether or not I had read the article back then, but I can understand why it had sparked my interest. Back then it wasn’t enough of a spark to give me the idea of a link between the immune system and synaesthesia, because back then I hadn’t even heard of the terms “super-recognizer” or “Benson’s syndrome”, in fact the concept and the term of “super-recognizer” hadn’t yet been published. Back then I had not the slightest inkling that I had better than average ability in face recognition, so I hadn’t started thinking about whether it was more than a coincidence that I was both a synaesthete and a super, and which parts of the brain might be atypical in both. I hadn’t read the human interest story in The West about a Perth citizen who had been diagnosed with Benson’s, and felt curious about how the description of that type of dementia sounded like the opposite of skills that were superior or associated with synaesthesia in myself and kin. I must have forgotten about the content of the 2008 New Scientist article, if I had ever read it at all, because it would have been the ribbon which I could have used to wrap up my package of ideas neatly. Curiosity can be rewarded, even if it takes a couple of coins before the penny drops.

 

Aussie Nobel Prize winner mentions citizen scientists on ABC’s Lateline

I very much enjoyed watching Professor Peter Doherty AC FRS, Australian immunologist and Nobel laureate being interviewed on Lateline tonight about cuts to science funding and the CSIRO. Professor Doherty did some very important research involving the MHC proteins, which I believe have also been the focus of researchers interested in the development of the mammalian and human brain.  I particularly liked Professor Doherty’s acknowledgement of the roles of citizen scientists in the science community, but I take issue a bit with his characterization of citizen scientists as generally people who have no training in science. There are plenty of people in the community who have academic achievements of various kinds in science or applied science who do not have paid jobs in science, for whatever reason. This doesn’t mean we aren’t educated or qualified or knowledgeable. Some voluntary roles in the community have more stringent training and screening processes than paid jobs, so the relationship between training and having a real job is also not absolute.

http://www.abc.net.au/lateline/content/2014/s3985479.htm

Thank you PubPeer

Thank you PubPeer for (after some fussing about) giving me a place on the internet that is recognized by scientists to publish my objection to some researchers publishing a highly original idea that I had thought of independently and had published at this blog over a year before their draft paper was received by their publisher. I’m certain that this is a case of plagiarism, but other people object to my use of that word, so the only place you will see the word plagiarism used in relation to that matter is here at this blog.

I have already published a very full account of my side of the story at this blog, but unfortunately this blog isn’t recognized as a part of the ecosystem of commentators attached to the world of science, the people and organizations in the league of science journalists, science magazine bloggers and internet services that are supposed to review the science literature but actually appear to be automatically-generated content. PubPeer isn’t like that; it appears to be run by people, but who they are is a mystery. I can completely understand why they wish to remain anonymous. Exposing the many ways in which peer review in science publishing is broken is a pastime that I am sure could be harmful to one’s career in science.

I believe that I can make a greater contribution to science as a blogger who has no job that is in any way connected to any university or any research institution, because I don’t have to deal with career-building and politics that goes with having that kind of career, and as a result I have more “mental bandwidth” free to devote to thinking about actual science. I am not expected to teach half-interested university students or organize conferences or write full-sized published papers or book chapters, and I’m not expected to know my proper place in the scheme of things. Very ordinary physical activities that I do in my everyday domesticated life automatically activate regions of my brain that deal with conceptual thinking and memory, and as a result I am often bombarded by novel ideas resulting from a boundless miscellany of concepts flashing onto the centre stage of my mind and colliding in a quite haphazard manner. I guarantee this kind of involuntary mental activity wouldn’t happen if I spent my days comfortably sedentary inside an airless office, staring at a wall or a dusty old painting. I’ve had jobs like that in the past, and years of study at an austere and ugly university which was also pretty much the staring at a wall lifestyle. I find it ironic that study at a university can offer an environment that has an effect on thought that must surely compare with a lobotomy.

Being a nobody to the world of science has many up-sides. I don’t feel a lot of need to consciously or unconsciously self-censor my ideas and publications to fit in with the beliefs and fashions of researcher peers (whether they make sense or not), and I don’t limit my thoughts to my job description, because I have no job description (and I also unfortunately have no salary, pay or financial benefit of any kind). Having no identity in the world of science means I also have no specialization or niche, leaving me free to see and write about a completely obvious connection between synaesthesia, an area of science typically researched by research psychologists and non-clinical neuroscience/psychiatry researchers, and the human immune system, an area of science that has I guess typically been researched by practicing medical doctors in the specialties of immunology or rheumatology. For sure there have been in the last ten years or so a group of pioneering and original researchers who have researched the incredibly complex ways in which the human immune system impacts on brain development, but I don’t think any of them have linked their work with synaesthesia or any particular type of dementia, as I have.  I’m guessing that they haven’t written about synaesthesia because they feel that it is too trivial a matter for them to bother with, which is probably a defensible point of view, as synaesthesia isn’t a disorder and I’ve never heard of a synaesthete who is looking for a cure. I feel free to write about concepts such as dementia, the complement immune chemicals and synaesthesia that are areas that are beyond my expertise, because I have no recognized area of scientific expertise or any recognized career in science. A lot of words have been written about the concept of intellectual freedom in academia, but I have found that being a non-entity outside of all that is a state that offers the most intellectual freedom. It’s a bit like being the invisible man; you can get up to all kinds of stuff but you can’t hope for recognition, because you have no face and no identity.

Being nobody is a state of freedom but it certainly has it’s frustrations, like having no income as reward for any of the work I put into this blog and the ideas published in it, and having no recognition, not even on the internet, but the most frustrating thing is the way that my most important idea has had no apparent impact in science. I’m not referring to my idea linking the immune system with synaesthesia, which was just an amusing step in my journey to the much more important idea that one particular type of dementia, known by the names Benson’s syndrome or posterior cortical atrophy or PCA, could be caused by an excess of one or more of the complement immune chemicals. Surely this is an idea that could be researched. Surely this is an idea that could lead to a number of different ideas for therapies if it turns out to have some value. Surely this is an idea worth at least checking, for if it reflects reality it surely has the potential to save minds and brains and lives. HELLO! Is anybody listening?

P.S. Late last month an Australian biotechnology company plunged on the stock market following the announcement of the failure of their drug aimed at treating Alzheimer’s dementia during a stage of a study. After years of hoopla and hype about drug companies finding a cure for Alzheimer’s or dementia, and anyone’s guess how much money spent on studies, all they can offer is symptomatic treatments. The story has been one failure after another. Benson’s syndrome is considered by some to be a variant of Alzheimer’s disease. Whether it is or not, maybe it is high time for researchers to stop obsessing about plaques in the brain and look at the immune system and the brain. My money is on C3 and C4 as concepts to focus on in a search for an understanding and cure for dementia. Would it kill you dementia researchers to accept some advice from a Perth blogger who is nobody in particular, and put my name on your research paper if my idea works out?

Some ideas that I’d like to (explicitly) lay claim to (right now) in 2014….2020…

New additions to this post added at the end.

A note of warning – If you are thinking about copying or plagiarizing any of the text, 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.

The idea that Benson’s syndrome or posterior cortical atrophy or PCA, a variety of dementia, is caused or develops in a way that can be seen as the opposite of the synaesthesia linked with exceptional visual memory and literacy skills that runs in my family (this idea has been explored previously in this blog).

The idea that the above cited states develop or are caused in a way that makes them seem like opposites because they both affect the same or similar areas of the brain, but in opposite ways.

The idea that the above described process happens because Benson’s syndrome and our variety of synaesthesia are both mediated by the same or similar natural chemical or cells or biological agent in the brain, one caused by high levels of the mystery substance and the other caused by low levels (a hypothesis that I briefly suggested in January 2011).

The idea that one of the many known or unknown elements of the immune system that impact brain development is the mystery substance referred to above (a hypothesis that I briefly outlined in 2012).

The (implied in above ideas) idea of the immune hypothesis of synaesthesia. (This idea was first published by me in 2012 in a blog post archived here, was I believe plagiarized in 2013 here, and was the subject of my plagiarism claim here.)

The idea that one or more of the complement immune chemicals is the  mystery substance referred to above.

The idea that the C3 complement immune chemical  is the  mystery substance referred to above.

The idea that synaesthesia is linked with one or maybe more immune diseases or conditions caused by low levels of complement.

The idea that genes for synaesthesia stay quite common in the gene pool because of some associated cognitive advantage (probably superior memory) that balances out any disadvantages caused by deficiencies in the immune system.

The idea that some or many people unintentionally experience a memory process that operates in a similar way to the method of loci memory technique in their everyday lives, unintentionally forming long-term associations between individual learned concepts and individual visual memories of scenes (I have named this phenomenon Involuntary Method of Loci Memorization or IMLM).

The idea that IMLM operates in such a similar way to synaesthesia that one could argue that it is a type of synaesthesia.

The idea that synaesthetes are more likely to experience IMLM than non-synaesthetes.

The (implied) idea that the method of loci memory technique is similar to or a type of synaesthesia.

The idea that synaesthetes might have a natural advantage in using the method of loci because the method of loci is similar to or is a type of  synaesthesia. This idea that seems likely in light of the case of “S” the Russian memory performer with many types of synaesthesia described by Luria. 

The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span.

The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span and can thus be used as an indicator of which synaesthetes are synaesthetes due to enhanced synaptic plasticity throughout the life span rather than other possible causes of synaesthesia. Support for this idea comes from the fact that IMLM appears to be a non-developmental variety of synaesthesia that can form new long-term associations in adolescence and adulthood.

The idea that IMLM is a phenomenon that is caused by the unusual possession of levels of synaptic plasticity typical of a young child, during adolescence or adulthood.

The idea that IMLM is caused or enhanced by some characteristic of the immune system that affects the functioning of the brain. Many different elements of the incredibly complex immune system are thought to affect the functioning or development of the brain, and could thus be involved in IMLM, including the complement system, microglia and the MHC class I molecules. Researchers such as Beth Stevens and Carla Shatz have investigated this exciting area of neuroscience. In 2012 I hypothesized at this blog that synaesthesia could be caused by low levels of complement, this idea implying that the immune system is directly involved in synaesthesia (or at least some cases of synaesthesia). I believe these ideas were plagiarized in a paper published in 2013.

The idea that IMLM is similar to the “Proust phenomenon” in that it is very similar to synaesthesia or is a type of synaesthesia and involves episodic or autobiographical memory as a concurrent.

The idea that phonics as a foundational reading skill is similar to or is arguably a type of synaesthesia in that it involves the involuntary association of individual speech sounds with individual printed letters or combinations of letters, as the result of learning in early to mid childhood.

The idea that at least one type of dyslexia is like a deficiency of synaesthesia.

The implied idea that if synaesthesia has as it’s basis hyperconnectivity in the white matter of the brain, dyslexia as an opposite of synaesthesia or a deficiency of synaesthesia is or could be caused by hypoconnectivity in the white matter of the brain (I suspect there might be existing research evidence that supports this idea).

The implied idea that in at least one cluster or grouping of cases synaesthesia is associated with superiority in literacy or reading skill.

The idea that synaesthesia can happen in different regions of the brain, and because of this the experience of various types of synaesthesia can vary in detectable ways because of the influence on the synaesthesia of the varied ways that different areas of the brain operate. This can mean that one synaesthete can experience different types of synaesthesia that operate in very different ways, for example, some types of synaesthesia more rare or spontaneous or intrusive than other types. (I am not completely sure of the originality or the novelty of all of this idea.)

The idea that there is an association between synaesthesia and super-recognition that is not merely coincidental.

The idea that synaesthesia is a type of memory or learning. (Not sure if I’m the first to note this obvious fact).

The idea that synaesthesia concurrents are re-experienced memories, or re-activated “learnings” of concepts, not perceptions. (Not sure if I’m the first to note this obvious fact). In support of this idea I can assert that synaesthesia is like face recognition in that both are visual memory-based phenomena which are subject to the Verbal Overshadowing Effect or something very similar. My assertion that synaesthesia is subject to the verbal overshadowing effect is based on my own observations (outlined elsewhere in this post).

The idea that super-recognizers should or could be trained and employed as expert consultants in the practice of medical genetics.

The idea that medical geneticists and all types of medical specialists need to have a super-recognizer level of face memory or face recognition ability, so that they can intuitively and quickly recognize medical facies.

The idea that there is no clear point of distinction between medical facies or faces associated with genetic syndromes and normal faces.

The idea that super-recognizers could be used to facially identify blood relatives of a person or persons.

The idea that super-recognizers could be used to facially identify the specific ethnicity of a person.

(below ideas added January 28th 2014)

The idea that super-recognition or being a super-recognizer could develop as the result of an unusual level of fascination with the visual appearance of landscapes or scenes, rather than from a fascination with faces, and thus be a side-effect hyper-development of a part of the brain that serves two similar functions.

The idea that super-recognition or being a super-recognizer could, at least  in some cases, develop as the result of a general hyper-development of the visual sense to compensate for problems in the auditory sense during childhood such as temporary deafness, recurrent ear infections, glue ear or poor auditory processing.

(below idea added February 1st 2014)

The idea that lexical-gustatory synaesthesia is an exaggerated form of some kind of evolutionary adaptation in the brain that biologically primes the mind to attend to or react to speech on the subject of food (this idea was discussed at this blog in a post dated January 27th 2011, with more consideration in a later post).

(below ideas added February 6th 2014)

The idea that creativity might be immediately enhanced during and only during the duration of physical or visual-spatial activity because the activity activates areas of the brain associated with movement and in turn these areas activate other areas of the brain including those that give rise to conceptual thinking, and the increased activation makes novel associations between diverse thoughts and concepts more likely, and that this process is like synaesthesia or is a type of synaesthesia, and the types of physical activity that are the most effective inducers of this effect might be highly specific, highly specific in effects, highly varied between individuals and highly idiosyncratic, as is typical of synaesthesia inducers and concurrents. Driving a car can act as an inducer of this effect. (I have gone some way to exploring this idea in past posts.)

The idea that mental flexibility might be immediately enhanced by the above effect, which I will name “movement – thought-flexibility synaesthesia”.

The idea that thinking might be immediately enhanced by the above effect.

The idea that memory might be immediately enhanced by the above effect.

The idea that the above effect is similar to embodied cognition or is a type of embodied cognition.

(below ideas added February 14th  and  February 20th 2014)

The idea that synaesthesia is like the process of face recognition (and vice versa), because they both

– are subject to the verbal overshadowing effect or something similar

– are automatic

– are involuntary

– have a sensory inducer, in face recognition always visual, in synaesthesia I think most frequently visual

– have or can have a concurrent that could be described as a memory, a concept or a personality (I’m comparing face recognition with personification synaesthesias and the synaesthesias that I have described at this blog which have visual memories of scenes as concurrents)

– are or can be visual in both the inducer and concurrent

– typically involve the fusiform gyrus

– involve set pairings of inducers and concurrents (same person’s face seen before then recognized later)

– involve set parings of highly specific inducers and concurrents (I recognize that an employee at my local supermarket has a sister who has just started working there too, as their faces and bodies and hair are near-identical, but for the extra acne and the more receding chin of the new employee. They are very similar in appearance but my discrimination is highly specific, just as I can recognize that the green wall on the lower floor of a public library is close to but not quite the same colour as Tuesday.)

– both can have, but do not always have an actual face as an inducer (we can recognize the faces of celebrities in photos, caricatures and art, even seeing Marilyn Monroe’s face in a pattern of brown coffee cups stuck to the wall at the coffee shop at the art gallery.)

(below idea added February 17th 2014)

“My particular interest in personification is my own theory that personification synaesthesia (as experienced by myself) or something like it gives rise to superiority in face memory (or being a super-recognizer) by naturally making the faces of unknown people more memorable and interesting”

The above is a quote from an article that was published at the blog in October 2013.

(below ideas added February 19th 2014)

The idea that the synaesthesia brain is the result of the developmental influence or shaping from, or the adaptation to, the behavioural phenomenon of “flow” as described by Mihaly Csikszentmihalyi.

The idea that synaesthesia, intellectual giftedness or high IQ and autism or Asperger syndrome seem to coincide more often than chance because gifted and autistic kids are more likely to experience “flow” and this in turn can influence the developing brain in a way that gives rise to synaesthesia.

(below ideas added February 20th 2014)

The idea that the genuine conscious awareness of synaesthesia is a threshold phenomenon that operates in conflict or competition with conscious thinking, meaning that consciously thinking about synaesthesia can inferfere with the perception of concurrents, and synaesthesia must reach a particular level of intensity before it interrupts the experience of consciousness and becomes itself the subject of conscious awareness. I think that the idea that thinking about synaesthesia can interfere with the perception of synaesthesia might be related to the “verbal overshadowing” effect which has been described and debated about by researchers. In fairness I should point out that Mark C. Price speculated in the recently published (2013) Oxford Handbook of Synesthesia that synaesthesia could be subject to the verbal overshadowing effect. My own ideas were arrived upon independently from Price’s writing or work.  I base the ideas of synaesthesia being a threshold phenomenon which can also be interfered with by conscious thinking on a number of my own observations. In direct contradiction to what I had expected to find, my scores for accuracy for individual letters and numbers in The Synesthesia Battery (a scientifically-validated online test of synaesthesia) were lower for the numbers and letters that have colours that I find beautiful and which I have thought about to some degree, while my best accuracy was for the numbers and letters that have the dull and ugly colours. It seems the less I think about the concurrents the more accurately I can percieve them when they are evoked. I have also noticed that most of the types of synaesthesia that I experience I was not consciously aware of before I started to think about and examine the idea of synaesthesia. I never realised that I had complete stability in the colours I associate with months and days of the week till I tested myself. While I had a dim awareness of colour colouring my thoughts, I’d not realised that this worked like synaesthesia till I went looking for a pattern using simple testing. My fine motor movement-visual memories of scenes synaesthesia evokes concurrents that are so fleetingly and subtly experienced that they just feel like random thoughts, and indeed I now believe it is possible that the random thoughts of many or even all people are in fact synaesthesia of various types. I have also observed that there are some very unsubtle and intrusive types of syn that I experience, and they are typically rarely experienced and are associated with people, emotions, faces, singing voices or music that I find striking or novel as inducers. Because of the circumstances of these examples of synaesthesia, I think some kind of threshold is being breached when these types of synaesthesia are experienced by me.

The idea that one of the established defining criteria for synaesthesia, that it gives rise to perceptions or concurrents which are “consistent and generic (i.e., simple rather than pictorial)”, is wrong, and specific categories of memories of complex visual images such as faces and scenes, which are processed in the fusiform gyrus, can also be experienced as genuine synaesthesia concurrents. I base this assertion on the fact that I often involuntarily experience synesthesia concurrents of this type, and I have written about such experiences right from the first post in this blog which was published in 2010. I have also named types of synesthesia that have complex visual memories as concurrents: the strange phenomenon, fine motor task – visual place memory synaesthesia, involuntary method of loci memorization, etc. There are also many accounts or scientific observations of synaesthesia with complex visual concurrents in the scientific literature on synaesthesia.

New additions 2020

Is the existence of hyperostosis frontalis interna or Morgagni-Stewart-Morel syndrome as a quite common but typically undiagnosed and untreated condition, and the common characterisation of it as a benign or inconsequential condition, evidence of the medical neglect of older women?

Could hypothalamic hamartoma be an underlying cause of hyperostosis frontalis interna? The hypothalamus, which is affected by HFI, plays a role in regulating calcium metabolism in rats, apparently. 

Are many cases of “autism” really undiagnosed cases of hypothalamic hamartoma? How many cases of “autism” could be cured or treated by surgical interventions for HH?

Does autism exist as a diagnosis because health and education professionals have always been unable or unmotivated to diagnose and treat the complexities of epileptic encephalopathy, rare genetic disorders and foetal alcohol syndrome?

Are more males than females diagnosed with autism because many cases of autism are caused by brain damage from a virus and the male immune system appears to be less able to fight at least one viral infection (as evident in the increased rate of male deaths from covid-19 and the greater numbers of females among asymptomatic carriers of covid-19)? Zika, rubella and cytomegalovirus are some viruses that can cause autism or brain damage in people who were exposed in-utero. Should all mothers of children diagnosed with autism be warned and medically-treated as though they were chronically and silently infected with an agent dangerous to a foetus before they plan another pregnancy?