Tag Archives: Autoimmune Diseases

Autoimmune/inflammatory disease in children associated with COVID-19 has a new name

Dr Paul Kelly, Australia’s Deputy Chief Medical Officer has discussed this new and worrying paediatric syndrome at a press conference today. The new name is pediatric inflammatory multisystem syndrome temporally associated with SARSCoV2 pandemic or PIMS-TS for short. Catchy! He described it as an autoimmune disease. The world has a new autoimmune disease – just what we didn’t need. This is consistent with my prediction in an earlier post at this blog pointing out the similarities with complications of coronavirus infection in kids and teens and an adult autoimmune disease and its associated vascular disorders.

Dr Kelly stated that there has been no increase in Kawasaki syndrome in Australia, in an apparent rebuttal of my questioning whether Australia might have cases of P that have been misdiagnosed as the similar autoimmune disease with unidentified COVID-19 infection as an underlying cause. As far as I know, a lack of increase in the rate of Kawasaki disease diagnosis in Australia should not be reassuring, because it is my understanding that in Australia and globally there has been a general decline in people attending doctor’s clinics and hospitals during the covid crisis, so you’d expect to find a decline in Kawasaki disease, not a steady rate. I guess it also needs to be stated that statistical trends in small numers of data points can be hard to discern, so with small numbers of cases of a rare disease, we could be splitting hairs. But I like splitting hairs! It keeps my mind off the deadly pandemic menace.

Sad news from New York City, New York

The autoimmune/inflammatory Kawasaki-like disorder associated with covid-19 infection in children which I have written about in some previous blog posts, now named pediatric multisystem inflammatory syndrome (PMIS), has claimed a number of young lives in New York. Given that covid-19 has been allowed to run out of control in the USA, hitting the densely populated and in parts poverty-stricken New York hard, and the state of New York has a governor who doesn’t sugar-coat or cover-up the truth about covid, it makes sense that this is a place where the real and deadly character of covid-19 infection in children and adults has been identified and documented. The UK is another “advanced” country in which covid-19 has been allowed to run out of control, and a press report from last month hinted at a cover-up of child patient deaths from PMIS.

These documented covid/PMIS deaths in young children and at least one teen raises the question of how many kids in other countries, including Australia and the UK, are infected with covid-19 or are even sick with PMIS but haven’t been correctly diagnosed and are potentially infectious? It looks like this has been happening in Australia. Are children dying of covid-19 or its complications, in “advanced” countries, without ever being identified as covid-19 cases? It now appears that there is no established scientific consensus about whether or not kids are less infectious than adults due to a lower viral load of covid-19, so every case of covid-19 in a child should be assumed to have the potential to spark a cluster that could kill. There seems to be a false-negative problem with covid-19 tests in children, even in countries with supposedly advanced medical systems. So why are some Australian states allowing schools to open in the absence of widespread operating public covid-19 surveillance testing regimes of asymptomatic people of all ages, with covid-19 tests that reliably work in child cases? Will Australian politicians now stop saying that covid-19 in children is generally mild while dismissing spread of covid-19 in schools as “not a problem for students”? 

My observation that “covid toes” found in children is simlar to a group of related autoimmune diseases was sadly close to the mark

A few days ago I argued that there could be important similarities beween the potentially fatal illness caused by the new coronavirus and a group of related vascular and autoimmune diseases, based on reports of “covid toes” and hands observed in chidren, which was reported in medical and press reports as a painful but minor oddity. Now a much more concerning inflammatory-vascular syndrome in children has come to light, probably caused by covid19. The autoimmune Kawasaki disease and toxic shock rather than the other inflammatory/autoimmune diseases that I named in my previous post are the diseases that a dangerous new syndrome observed in children in the UK has been compared with. Nevertheless, I think it is interesting that “red fingers or toes”, pain and “a rash” are listed as symptoms of Kawasaki at the website of the famous NHS. Those are defining or major symptoms of some of the vascular and autoimmune-related diseases erythromelalgia and HGP which I mentioned in my previous post. 

While this new threat to children is probably rare, it flies in the face of Australian government assurances the children are safe to return to school classes and that covid19 is mild in children. It also demonstrates that this new virus is an unknown quantity, and new understandings are emerging all the time. We live in interesting times, for sure.

Three cheers for the criminally-neglected NHS!

https://www.theguardian.com/world/2020/apr/27/nhs-warns-of-rise-in-children-with-new-illness-that-may-be-linked-to-coronavirus

https://www.dailymail.co.uk/news/article-8260399/NHS-issues-doctors-urgent-alert-coronavirus-related-condition-children.html

 

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 erythromelalgia; 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 erythromelalgia, 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 erythromelalgia 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, erythromelalgia, 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 erythromelalgia 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. Erythromelalgia 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 erythromlalgia. 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.

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 Research59(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 Australia196(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 Scientist219(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

 

 

I want…

I want to organise a staring competition between Greta Thunberg and Tim Sebastian, I’d like to arrange a game of poker pitting Rudy Giuliani against Michaelia Cash, I think it would be amusing to place a vase of pure white flowers inside an unfashionably colourful home, I’m curious to try transfusing Lance Armstrong with blood from a hypergammaglobulinaemic and see how fast he could ride his bike then, and I’d also like to wish my readers, if there still are any, a very merry Christmas.

The spinster hypothesis of automimmune disease: another scientific idea of mine

Klein, Alice Semen reshapes immune system to boost chances of pregnancy. New Scientist. August 26th 2016.

https://www.newscientist.com/article/2102877-semen-reshapes-immune-system-to-boost-chances-of-pregnancy/

My first thought on reading the headline and blurb of this article of science news was that it explains the sex ratio and typical age of onset of the autoimmune disease lupus or Systemic Lupus Erythematosus (SLE) which typically affects women with typical ages of onset during the years between puberty and menopause, the childbearing years. There are also other autoimmune diseases that affect mainly women. Because of this pattern medicos have suspected a hormonal cause for SLE but as far as I know this theory has not gathered evidence. An alternative explanation would be that SLE is a harmful side-effect of a normal ramping up of the activity of a woman’s immune system during her reproductive years in anticipation of the immune-damping effects of heterosexual activity (not “safe sex” with condoms or barrier methods of contraception but sex as it was practiced in the times when the human immune system evolved). The normal lifestyle of early human female adults of reproductive ages would have included mostly years of pregnancy, breastfeeding and unprotected sexual activity. It is my understanding that pregnancy dampens the immune system to a degree, and it appears unprotected heterosexual activity also could do this for women. I have no idea about breastfeeding, but I know it alters the profile of reproductive hormones and can suppress ovulation. So it appears that the modern woman of reproductive years can be exposed to many years without the immune-suppressing activities that would have been a normal part of the lives of her distant ancestors, so it makes sense that this could elevate the risk of developing SLE or any of the huge range of other autoimmune diseases. Not all autoimmune diseases affect females preferentially, some affect males more, and these sex ratios are surely a clue to what causes them.

I apologize to any of my readers who might be jolted or offended by discussion of the above matters, but I think it is important to discuss scientific ideas about diseases that kill and harm many people. Please readers also remember, if my ideas expressed in this post or in my blog in general are original, or could be original, do not publish or re-use them as though they were your own original thoughts. I’ve had that done to me before by academics, and any such behaviour will be publicly highlighted and soundly criticized.

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.

 

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?

 

Have my ideas been plagiarized in a paper published in a neuroscience journal? I believe they have.

Top of C3 theory post

Middle of C3 theory post

End of C3 theory post

This post replaces a brief temporary posting which was previously published here, with the notice that it would be added to at a later date when I had more time. I’m a busy parent who gets paid nothing to write and I have struggled to find the time to give this important matter proper attention. Do not be surprised if you find this post edited or altered.

I’ll get to the point straight away. I believe that I am the victim of plagiarism. At the very least, I believe that I have scientific priority in regard to a group of related scientific ideas or hypotheses, and my priority in regard to two of those ideas has not been recognized, and as a result some ideas which I published at my blog in 2012 have been presented in a journal paper that was published this year as though those ideas were new. The two ideas which were re-published by others in 2013 as though they were their original ideas are the idea that synaesthesia could be caused by unusually low levels of complement (a group of immune system chemicals) and also the idea implied by that idea that synaesthesia could have as its origin some peculiarity in an element of the immune system which plays a dual role in the development of the brain. The complement chemicals are certainly not the only elements of the immune system which are thought to influence the brain. I am not alleging that plagiarism in the form of word-for-word copying of text has happened in regard to the documents cited below. I am alleging that plagiarism of ideas has happened, and even though this type of plagiarism is not easy to prove, I can prove that I published my blog article introducing my ideas over a year before the journal  paper by the others was even received as a manuscript by the journal which would eventually publish it.

Below are the details of my blog post published in June 2012 which contains the ideas which I believe have been plagiarized:

Wright, C. 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/

and permanently archived by the Internet Archive Wayback Machine on June 21st 2012: http://web.archive.org/web/20120621071430/https://superrecognizer.wordpress.com/

Below are the details of the published journal paper which includes what I believe is plagiarism of my ideas, or at the very least the re-publication of my ideas without any acknowledgement of me or my writing:

Carmichael, Duncan A. and Simner, Julia The immune hypothesis of synesthesia. Frontiers in Human Neuroscience. 2013; 7: 563.

Published online 2013 September 11. doi:  10.3389/fnhum.2013.00563

Received July 31, 2013; Accepted August 23, 2013.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769635/?report=classic

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769635/    (see the “article notes” at this version to view all the dates relevant to publication of this paper.)

http://www.frontiersin.org/human_neuroscience/10.3389/fnhum.2013.00563/full

https://pubpeer.com/publications/13259457EAEBF97186167E7BDFB6B3

Please note the dates cited relating to the process of getting this paper published. There is nothing in those dates that could serve as evidence that these authors independently thought of the ideas in the paper before I published my blog piece. I published my blog piece in June 2012 and the above paper was received by the above journal in July 2013. The authors could have been wildly plagiarizing during the thirteen months or so after I published my piece and before their paper reached the offices of the journal.

I think it is important to point out that I had no contact or communication with either of the authors of the above journal paper about my ideas about synaesthesia and the immune system during the period before their paper was published. I did not inform them about or discuss my ideas on this subject privately and I did not privately grant them permission to use or publish my ideas, and I am not one of the “anonymous reviewers” who made “helpful comments” on the manuscript of the above paper, who were mentioned in the acknowledgements section of the above paper. Shortly before I published my ideas about synaesthesia and the immune system I did have a short and one-sided email correspondence about some of my ideas with a microglia researcher and I also sent a non-specific email off to a local medical specialist. The authors of the above journal paper did not privately inform me about any ideas or theories linking the immune system with synaesthesia before the publication of my blog post on that subject. It is my sincere belief that my ideas in that post were new and original and had not previously been published. I also did not receive any information or “leaks” about the work of the authors of the journal paper from any third party.

If you take a careful look at the details of my blog post you might notice that one of my scientific hypotheses is presented within the internet address of that posting and also within the title of the posting, and the internet address also contains details of the date of publication. Like all of the internet addresses of the posts at this blog, it was automatically generated by WordPress when I published the post. The date of publication is also automatically added to the blog post during publication, as is the name of the author. Unfortunately, the date of blog posts can be altered post-publication, with this alteration reflected in the web address of the post and the situation of the post in the chronological sequence of the blog. While the blog can be altered, one cannot alter blog readers’ memories of my blog posts and any records that they might have kept of them, and this blog has a diverse and steady readership. In situations demanding proof of the date and also the content of a document published on the internet, one free resource on the internet is invaluable; the Internet Archive Wayback Machine. This internet archiving service archived my June 7th 2012 blog article on two different dates in two different forms. The earlier archived record was recorded on June the 21st 2012 with the blog post included in a record of the whole home page of my blog on that date.

http://web.archive.org/web/20120621071430/https://superrecognizer.wordpress.com/

This date was only a fortnight after the post was first published and over a year and a month before the others’ journal paper was received as a manuscript by the journal that would later publish it. This proves that my blog post was published on the internet at least before June 21st 2012, a long time before the journal paper was published online or in hardcopy, or was even received by the journal publisher. The content of my blog post as was published then is also documented and can be checked. The blog post was also archived in November 2013 within an archive of a month’s blog posts.

In addition to citing the archived old record of my blog post as evidence, there is other evidence that I can cite to show a long history of me expressing ideas such as those in my blog post, ideas that overlap with ideas presented in the journal paper, and many more novel, original and inter-related ideas besides. The origin and development of the ideas in my blog piece can be traced back a long way in time within my own writing at my blog. I theorized not only that synaesthesia could be caused by low levels of the immune chemical complement, I also theorized that a form of dementia, which to my knowledge has never by anyone else been linked to or contrasted with synaesthesia in scientific discussion, could be caused by excessively high levels of complement. I also theorized that this type of dementia, Benson’s syndrome or PCA, could be seen as the opposite of synaesthesia or at least the opposite of the cluster of unusual functional characteristics of my own brain. Implied within this theory is the idea that there is some kind of network within the brain of parts that are especially sensitive to some factor that influences growth or pruning or cell death, because the same mental functions appear to be boosted at least since early childhood in the brains of me and some of my first-degree relatives which decline in Benson’s syndrome. I have no reason to believe that the early specific cognitive enhancements are some unknown facet of Benson’s, because there is no particular history of dementia in my family. I still see the two conditions as opposites, potentially with one common factor (extreme levels of some influential chemical) unlocking the mystery of both. My post published in June 2102 was not the first place where I published my own ideas about Benson’s syndrome being the opposite of synaesthesia. I had first written about this apparently original and new idea in a blog post published in January 2011:

https://superrecognizer.wordpress.com/2011/01/04/the-opposite-of-bensons-syndrome/

This blog article was archived and recorded by the Internet Archive Wayback Machine in March of 2011:

http://web.archive.org/web/20120308215442/https://superrecognizer.wordpress.com/2011/01/04/the-opposite-of-bensons-syndrome/

It is clear that my ideas in my June 2012 blog post were a development of ideas that I had already published at this blog in January 2011, indeed I quoted from my earlier blog post in my latter blog post. My earlier blog post has been archived by a third party and stands with other related blog posts as a record of the direction and date of the development of my ideas, which are very congruent with the many ideas expressed in my June 2012 blog post. In contrast, it appears to me that that the authors of the journal paper which I believe is a plagiarism of ideas in my blog post cannot demonstrate any published and/or archived set of documents that show the development of their ideas towards any theory linking synaesthesia with any element of the immune system. I believe this because I have done a quick check of the lists of past publications of both authors. I have not been able to trace any development of theories about synaesthesia in their work or academic collaboration that might lead them to look at the immune system, and I was not able to find any hint or explanation in the journal paper itself about why these researchers arrived at a theory about the immune system. In my opinion, their theory linking synaesthesia with the immune system appeared “out of the blue” within the context of their own published research and published papers. If anyone can identify any dateable and/or archived document by either of the authors of the journal paper that shows an early development of the idea of linking synaesthesia with the immune system then I would be very interested to see that document, and I request that a comment detailing such document be left at this blog. The apparent absence of evidence of a theoretical progression or development towards “the immune hypothesis of synaesthesia” in the published work of the two authors of the journal paper is one reason why I cannot believe that they conceived of the immune hypothesis of synaesthesia independently as a team or as individuals.

The immune hypothesis of synaesthesia would not have been proposed had it not been for the work of researchers who investigate the dual roles of elements of the immune system which also play a role in brain development and neuroplasticity. The authors of the journal paper have primarily cited the work of Assistant Professor Lisa Boulanger who studies MHC Class 1 proteins, while in my blog post I concentrated on the work of Assistant Professor Beth Stevens who studies microglia and complement. It appears to me as though the authors of the journal paper have made a deliberate decision to anchor their theoretical ideas onto a different existing body of research in molecular biology than the body of research that inspired my theories. I believe they had the aim of distancing or differentiating the content of their paper from the content of my blog post. I first learned about the work of Beth Stevens from reading a June 2012 article in New Scientist magazine. Although the authors of the journal paper evidently at some point in time developed an interest in the work of Boulanger and consulted her during the writing of the paper, it is not clear why in 2013 they should be publishing a paper at least in part inspired by her work, because the papers of hers cited were published in the years 2004, 2009 and 2010, hardly the latest news in neuroscience. The most recent items in the journal paper’s references list relating to the immune system and the brain are a 2012 paper by Elmer and McAllister and a 2012 paper by Beth Stevens and two other authors. Boulanger does molecular biology at Princeton University in the United States while the authors of the journal paper do psychology and psychiatry at Edinburgh University in the UK, so it seems unlikely that the three by chance swapped ideas over lunch.

I have noticed an absence of mention of or enthusiasm for the immune hypothesis of synaesthesia in 2012 and 2013 media coverage and conference presentations featuring either of the authors of the journal paper, and I find this curious. It appears that they deliberately kept quiet about the hypothesis before it made it into publication. Why?

One of the authors, Duncan Carmichael, was interviewed for the British radio show The Naked Scientists on October 7th 2012, and his research on synaesthesia was the subject of the discussion:

http://www.thenakedscientists.com/HTML/content/interviews/interview/2269/

Even though this interview was conducted roughly nine months before Carmichael’s and Simner’s journal paper about synaesthesia was received by the journal as a manuscript, no evidence of a conception of the idea of an immune hypothesis of synaesthesia can be found within Carmichael’s answers in this interview. He spoke about a genetic study, but said not a thing about the immune system. I find it hard to believe that a researcher who gave such an ordinary account of the contemporary state of knowledge and research on synaesthesia was a member of the team who generated one of the most original ideas in synaesthesia research for a long time. Wouldn’t he have been barely able to contain his excitement about the novel scientific theory? I know that is how I felt about it when I thought of it.

This is a university web page outlining the work of Duncan Carmichael:

http://www.anc.ed.ac.uk/dtc/index.php?option=com_people&func=showall&userid=387

I cannot find evidence of a lot of originality in thinking or the development of ideas about the immune system in the work detailed at this page. It looks like some standard ideas about synaesthesia explored by a PhD student whose background in psychology and psychiatry is pretty standard for synaesthesia researchers.

An abstract of a conference presentation delivered and co-authored by Duncan Carmichael can be found at the below link and a link to what appears to be the slide images used in that talk can also be accessed at the below link:

http://www.synesthesia.info/recent.html

This conference was the Tenth Annual National Conference of the American Synesthesia Association held in Canada May 31 through June 2, 2013, roughly two months before the immune hypothesis of synaesthesia paper was received by the journal as a manuscript. I looked at the abstract and also the slide show and I found a spelling error and some questionable unexplained assumptions in the slide presentation but I found no hint of the development of the immune hypothesis of synaesthesia. I find it remarkable that Carmichael could have co-written and submitted a publishable a paper containing some highly original and paradigm-shifting ideas barely a couple of months after giving talks at a conference about the same general area of research which gave no clue about the intellectual development of the novel ideas. When I look at the highly conventional and ideas about synaesthesia in Carmichael’s written work, media appearance and May-June 2013 conference presentation I find it impossible to believe that he is a part of the team that theoretically wed synaesthesia with the immune system for the first time based on their own ideas. One could argue that Carmichael was deliberately keeping the new theory a secret, but what can account for the contrast between the conventionality of his other work and the originality of the immune theory?

Perhaps the originality of the novel idea was the contribution of the other author? I’ll happily admit that Dr Julia Simner’s work on synaesthesia has consistently been interesting and she has made important and fairly novel contributions, but I could likewise find nothing in her work or in her academic background to indicate a curiosity about or knowledge of the immune system. Dr Simner categorizes herself as a cognitive neuropsychologist, and her academic background is in “psychology, languages and linguistics”.

This is a link to her university web page in which Carmichael is listed as a student supervised by Simner:

http://www.ppls.ed.ac.uk/people/julia-simner

Two 2013 media appearances are listed at the above page. One was at the Guardian Edinburgh International Television Festival. These are pages related to an August 2013 talk by Dr Simner at that festival:

http://www.audionetwork.com/content/whats-new/events/geitf/julia-simner-q-and-a

http://www.audionetwork.com/blog/author/dr-julia-simner/2013/8/27/synaesthesia—a-merging-of-the-senses.aspx

http://www.audionetwork.com/show-article.aspx?id=386

Unfortunately a recording of that talk appears to be no longer available. The talk was presented while the immune theory paper was in the process of being published but I found no hint of the paper’s theme in the page about Dr Simner’s talk.

This is the page about an appearance that Dr Simner made at the Edinburgh International Science Festival on April 1st 2013:

http://www.sciencefestival.co.uk/whats-on/categories/activity/sensory-dining-1404

A PDF of the festival’s 2013 programme can be accessed here:

http://www.sciencefestival.co.uk/uploads/EventImages2013/Edinburgh%20Science%20Festival%202013%20brochure.pdf

There’s nothing related to the immune system to be found in info about that appearance.

A Word document of Dr Simner’s CV can be downloaded from Simner’s university page:

http://www.psy.ed.ac.uk/people/view.php?name=julia-simner

Simner’s CV includes a quite up-to-date list of the publications. I searched her CV and found only one mention of any word that I can think of that is related to the immune system, and it was in the title of the paper under dispute. I couldn’t even find one example of use of the words “synapse”, “synaptic”, “plasticity”, “pruning” or “neuronal” in Simner’s CV, which I take as an indication that Simner’s research on synaesthesia could hardly be described as “biomedical”, except for that one paper which stands out like dog’s balls within the contexts of the other work by Simner and by Carmichael. I invite you to check for yourself and let me know if I have missed something.

Here are some other links to information about Dr Simner:

http://www.biomedexperts.com/Profile.bme/1310901/Julia_Simner

http://www.research.ed.ac.uk/portal/en/persons/julia-simner(616de62b-07c6-430d-b217-d18880744549).html

http://ukcatalogue.oup.com/product/9780199603329.do

http://community.frontiersin.org/people/u/68706

I have argued that the originality of the immune hypothesis of synaesthesia stands in contrast with the conventionality of Carmichael’s other work and also stands in contrast with the lack of medical or molecular biology focus in Simner’s other work. I could also argue that the originality and the molecular biology of the immune hypothesis stands in contrast with synaesthesia research in general. Stale old models of synaesthesia proposing hyper-connectivity in the brain, inhibition of the process of neuronal pruning or disinhibited or hyper-excitable neurons have been doing the rounds forever. Researchers seem to be satisfied with explaining the biological basis of these theorized neurological peculiarities by suggesting that there are genes for these features, as though that is any explanation at all. The traditional models of synaesthesia seem to owe a lot to a layman’s understanding of simplistic models of psychiatric illnesses and neurodevelopmental disorders (endless guff about neurotransmitters and brain “wiring”) or owe a lot to a superficial resemblance between synaesthesia and hallucinogenic drugged states of mind. There have been genetic studies of synaesthesia and there have been brain scan studies as well, but I don’t think you will find a lot of molecular biology in pre-2013 synaesthesia research.

If the authors of a journal paper read my blog post and took my ideas in that post and used them in their journal paper without acknowledging me, could they have any possible excuse? It is perhaps worth noting that at my blog my name as the author of the posts (my blog is not a collaborative one and only has one author) is not shown on posts at the main page of the blog, but the author’s name in blog posts is displayed when individual posts are selected for viewing, along with any comments about the post. There is no information about me (the author) at the main page of my blog, so I guess it is not inconceivable that a reader might assume my blog is an anonymous publication. Nevertheless, if one wanted to properly cite any of the posts at my blog or the blog itself the title of the blog could be cited. It is a standard practice to cite the first few words in the title of a book or other type of document instead of the author’s name if the author is unknown, and if the author is known to be anonymous they should be cited as “Anonymous”. There is no technical or formal reason why any of the pieces of writing at my blog can’t or could not have been cited.

I can see one possible objection to my claim of having scientific priority regarding the idea of linking synaesthesia with complement and the immune system. It could be argued that my idea was never properly published as my idea, because it was published at a blog and was not published as my idea in a paper or some other document in a scientific journal. Such an objection would be based on the assumption that scientific publication can only happen within a select and specialized type of publication that is widely recognized as a scientific publication, and cannot legitimately be self-published or published in a print publication or internet web site which is not specifically devoted to the publication of scientific research and scientific theories. My answer to this objection is that it is snobbery and it is also at odds with the current realities of our online world. Such an idea seems to be based on the belief that science is an enterprise that legitimately operates like a closed society in which membership is only open to those who have particular credentials or those who have jobs in particular types of institutions (universities or research institutes for example) or those who have the resources and social connections to be able to successfully submit a full-length paper for publication in a peer-reviewed science journal. But the history of science is peppered with examples of scientists who done important work outside of universities, of amateur scientists and gentlemen scientists who have made very important contributions, and of scientists who have offered interesting and respected theories outside of the fields in which they are qualified. There are also plenty of examples of crackpots who present themselves as legitimate scientists and of researchers who have made laughable blunders while straying outside of their areas of specialization. There are also too many examples of scientists who have made serious blunders because they apparently did not know about important and relevant facts or knowledge from areas of science beyond their limited field or from beyond the world of academia. I can also think of some great examples of scientists who have only been able to make important discoveries once they have had the courage to question accepted scientific or medical knowledge. My point is that science is not a neat, closed and orderly enterprise. It can and it should be informed by non-scientists who have specialized expertise and amateur scientists. Science can be seriously failed by academics who are blinkered or who over-reach the limits of their knowledge or who engage in scientific misconduct. If science was a perfect and orderly enterprise we would call it The Church of Science and lecture theatres would be places of worship. Science belongs to everyone; everyone benefits from it and anyone who has good ideas and a respect for evidence can play a part, and should be given due credit.

Even if there were no plagiarism in the journal paper by Simner and Carmichael there are still plenty of things in that paper which I find objectionable. As a synaesthete I am personally offended by the frequent use of negative language in reference to synaesthesia in the paper. Here’s a list of words and phrases from the paper: “neurological condition”, “excess cortical connectivity”, “excess connectivity”, “excessive connectivity is indeed a feature of the synesthetic brain”, “failing to supress non-relevant activation”, “excessive activity of excitatory neurons”, “aberrant connectivity”, and ”misregulated feedback mechanisms”. This repeated use of terminology with negative connotations regarding synaesthesia is certainly not typical of scientific or popular literature on the subject. It is rather amusing when one reflects that these authors are being so negative about the type of mind which I believe provided them with the central idea of their journal paper. Talk about biting the hand that feeds! Even more offensive and stupid is the authors’ described quest to find a link between developmental synaesthesia and the degenerative nervous system disease multiple sclerosis (MS). They aren’t even being as bold as researching a link between diagnosed cases of MS and synaesthesia, they are only looking at “people with the radiological profile of multiple sclerosis”, whatever that means. Developmental synaesthesia is a generally stable inherited neuropsychological variation characterized by white matter in the brain that has been described as having greater volume, greater connectivity or being “more coherent”. It is not considered to be an illness or a disorder, and it appears to be associated with superiority in memory. Multiple sclerosis is an inflammatory disease typically with an onset in adulthood which damages the myelin covers of nerves in the brain and in the spinal cord. While there are some genetic risk factors it is not considered to be a hereditary disease. Vitamin D deficiency and infectious agents have been suggested as causes or triggers. MS causes a wide range of mental and physical problems and disability and substantially reduces life expectancy. It is not known whether is caused by an autoimmune process or a failure of the myelin-producing cells. The only apparent commonality between MS and synaesthesia appears to be that they both feature white matter that differs from the average state, but those differences could be characterized as opposite states, not similar. Simner and Carmichael’s idea that synaesthesia might be more common in those who look like MS cases strikes me as at best bizarre, but apparently they have submitted a paper on this subject. I think I know where that paper might belong.

To offend in so many ways certainly takes some doing, and I do acknowledge that there is a large difference between the amount of effort that went into the writing of my blog post and the amount of work that would have gone into writing and obtaining publication of the journal paper, but I believe that it is also true that the guts of that paper was an idea of mine, and I believe there would have been no paper to work on without my idea.

If I accept the proposition that this apparent case of plagiarism was really a case of two different parties reaching the same conclusion independently and within a year or so of each other, with the others being unaware of the existence of my prior publication, and then they innocently published their own paper as the first to introduce these ideas to the world, then I must ask why they were not aware of the existence of my blog post. Did they think they only had to search the traditional scientific literature to check whether their ideas were truly novel and original? I find that hard to believe, in this online, open-access world. Before I published these ideas at my blog I searched the internet and bibliographic databases to check whether my ideas were really as novel as I thought they were. I found nothing comparable. I am completely sure that my blog post would have been retrieved within the first page of a results display from a simple Google search on the terms “immune” and “synaesthesia” or “synaesthesia” performed in the months and year after I published my blog post. My blog has always done very well in Google searches.

I believe that the immune hypothesis of synaesthesia is the product of a synaesthete brain, my synaesthete brain. If anyone can show evidence that counters this, please let me know by leaving a comment. I have demonstrated that I was the first to publish the immune hypothesis of synaesthesia. I believe that I should have been acknowledged as the creator of this idea by the authors of the journal paper. I’m not pleased with what has happened. I do want my ideas which I have published at my blog to be read, considered and developed by other people. I am not a hoarder of ideas and I’m not out to make trouble. I just want to be contacted, asked and acknowledged, and properly acknowledged in print in the conventional manner if my original ideas are used or referred to in someone else’s work.  I don’t think that is too much to ask.