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Human face recognition confirms the truth about a 62 year old mystery

Time to open our eyes to Chinese science?

I hope my readers will kindly tolerate another of my blog posts about the pandemic and science in general, not focused on the main topics of this blog, which have been superrecognition and synaesthesia.

When I began writing this post (August 26th 2020) I was watching a passionate and articulate address to the National Press Club of Australia in Canberra by Wang Xining, Deputy Ambassador of China in Australia, and I knew it was time to share observations and questions about Chinese science and the pandemic that I had been thinking about for a while. That address has been described as fascinating, and it is a big, big deal to Australians, as Australia’s economy is massively dependent on China. Their consumer goods flow here, our minerals, seafood, wine and agricultural products flow there and their university students formerly funded our higher education sector. There’s also the ever-present military threat of China, the world’s biggest nation in terms of population, with 55 times the population of Australia, and frequent news stories about cyber-espoinage with clear inferences that the Chinese government is behind these online attacks and hacks. The important economic and cultural relationship between our nations has been frought recently, following what appears to be a universal assumption that China created the coronavirus pandemic through their traditions of keeping live wild animals from all parts of the world for sale at markets, to be used as meat, pets and ingredients of traditional medicine. Australia’s Prime Minister apparently caused offence to China by calling for an inquiry into the origins of the pandemic virus, with some offensive commentary and a trade war from China in return. In early September China has continued their habit of placing unreasonable restrictions on Australian produce exported to China, and an Australian journalist has been detained in China.

Mr Xining spoke of the depth of sentiment felt by offended Chinese people in regard to our PM’s call for an inquiry into the origin of the pandemic. I think this is an important point, but I also reject Xining’s calls during his speech for Australia to mind our own business in regard to the way China run their country. There are too many terrible and large scale violations of basic human rights by the government of China going on for any decent person to ignore or excuse China’s government’s actions and policies. I’m certainly no fan of the Chinese governnment, but I do have questions about whether it has been fair of the world to have assumed the guilt of the Chinese nation, government and culture in regard to the origin of covid-19. It is common to hear the novel coronavirus referred to as “the Chinese virus” by the President of the USA, and similar angry and racist sentiments from my fellow Australians. It happens, and I believe these assumptions about the origin of the pandemic should be examined.

First, I’d like to offer my outline of Chinese science. As you’d expect from the world’s largest nation, it is huge. For a number of years China has ranked second behind the USA for the number of science papers published in English-language science journals. And as you’d expect from a nation that has a deep cultural history that has been largely insulated from the rest of the world, without the widespread use of a second language of a colonising nation (such as English or French), there is also a huge volume of research and scholarship from Chinese scientists published only in a Chinese language. This wealth of inaccessible scientific literature has been described as “…a kind of terra incognita of scholarship” (Chevassus-au-Louis, 2019, p. 67). What scientific insights from China is the rest of the world missing out on? I can only guess.

The unusual angle from which I have viewed the question of the origin of covid-19 is my interest in another vascular medical condition. Erythromelalgia is a supposedly rare and poorly-understood pain condition that can be caused by infection with a contagious pox virus similar to mousepox and also other infections, but also has many other causes and associations. There is a genetic primary form of the disorder and it can also be secondary to many other diseases, and can be “idiopathic”. As is the case with many rare medical conditions, Australian medicine does not do a great job of diagnosing and responding to erythromelalgia (EM). When a patient has any rare disease, Australian GPs seem to be too comfortable with making a “quick and dirty” diagnosis of a common disease that does not really fit the picture presented by the patient, then hastily write a script for an antibiotic or painkiller in the hope it will address the issue. There seems to be an assumption that the patient will keep coming back if the prescription doesn’t work. A good GP might investigate and search for a tricky but fitting explanation, or show the care and humility of making a referral to a medical specialist, but such doctors don’t grow on trees.

Awareness of rare diseases is often lacking among doctors and patients alike, and information for the public about such conditions is often poor quality. EM can be treated cheaply and effectively without medical help with the application of cooling to the skin, but a good part of many popular English-language articles about EM warn patients to not immerse feet in cold water as it can damage skin, with no other reference to self-help measures. As if an EM patient suffering blazing pain would care about waterlogged feet! In contrast, there’s plenty of patient info on painkiller drugs to treat EM, despite the known serious  risks of such treatments.

Based on my experiences, I don’t believe there’s a lot of personal investment to be found among Australian doctors to identify cases of  rare diseases or novel infectious outbreaks. Within the Australian medical and pubic health system a lack of curiosity and an unwillingness to consider novel, speculative or rare diagnoses seems to be commonplace. There is also a common attitude that Australia is an island generally protected from interesting infectious diseases by geography, climate, vaccination and clean habits. This is why whenever we are required to answer disease screening questions the first question is “Have you travelled overseas recently?” This complacent Australian attitude that infectious diseases originate from somewhere else shows an ignorance of our history. The highly-dangerous zoonotic Hendra virus, named after a suburb in Queensland, has killed Australians in a number of outbreaks, and like the covid-19 virus it originated from bats and infects another mammal species (the horse in the case of Hendra) and infects humans. You don’t even need to go near a bat to catch Hendra; contact with an Australian horse living within the ever-expanding range of fruit bats is the way it is caught. Hendra is a disease that originates in Australia and was identified by Australians, but that’s not such a huge achievement of medical detective-work. Hendra is an obvious type of outbreak; it is high in morbidity and fatality, has shown no transmission between humans and its victims work with horses. If a less obvious infectious disease, such as the novel coronavirus, with its asymptomatic spread between humans and confusion with pneumonia, or epidemic erythromelalgia, with its main manifestation of pain that is easily dismissed or misdiagnosed and has no objective test,  jumped to humans from Australian bats or mice tomorrow, and started speading among people, would anyone notice? I doubt it.

My gripes about the Australian medical system are endless and might not be of interest, but I think the contrast with the way Chinese medical science has researched and written about erythromelalgia is revealing. The more I have read of the journal literature and research on the condition, the clearer it has become to me that Chinese doctors and scientists have made a massively greater contribution to the study of the condition as an epidemic disease than any other nation’s researchers. Even though erythromelalgia (EM) was first described in the 1800s, it appears that Chinese scientists are the only researchers who have documented the epidemic form of the syndrome. A Chinese scientist reported the first Chinese case study in 1945 and the first Chinese epidemic of EM in 1960 (Liu et al, 2015). According to Liu and colleagues (from universities in China and Australia) at least 100 studies of EM have come from Chinese authors, most of them about the epidemic form. Some of the leading pioneering researchers of epidemic EM were from the virus research institute in Wuhan. Liu and colleagues’ paper lists 12 epidemic EM events among Chinese school students, while another Chinese paper reports that dozens of EM outbreaks have been reported in China since the mid-20th century (Yuzhou et al, 2015). I think it is interesting to note that Liu et al write of schools reporting these events, which suggests to me that the Socialist social structure of China might mean that schools play a part in public health monitoring in a monolithic government network that would not exist in countries like Australia. I can’t imagine a high school principal in Australia being necessarily aware of or reporting a spate of pain-related illness among students (mostly teenage girls) to any government authority, especially not a principal of a private church-run school. In contrast, the Chinese are “right onto” EM as a public health problem. They have even researched the detection of EM outbreaks using a Chinese search engine for surveillance. Liu and colleagues suggest that EM outbreaks are common in China, but the language barrier prevents due recognition of this interesting phenomenon by international researchers. They have argued that the EM outbreaks are caused by temperature fluctuations, but they list other non-infectious epidemic causes theorised by other researchers. It is important to note that other Chinese researchers have noted pharyngitis associated with an EM outbreak, have taken throat swabs, and have isolated the erythromelelgia-related poxvirus (ERPV), and an American-funded team of researchers published their report of the sequence of the genome of ERPV in 2012, so there is strong evidence for the model of EM outbreaks as infectious disease, and most of this research work is from China.

Astonishingly and mysteriously, there are no records of any EM outbreak in “developed countries” (Yuzhou et al, 2015), and I have not found any report of any individual human ERPV infection outside of China. Why? I wouldn’t have thought that living conditions are hugely different between China and coutries like the US and the UK, and it’s not as though a viral infection can’t cross international borders. In 2020 we all know too well how a virus can span the globe. If EM epidemics really are caused by temperature fluctuations, why the heck wouldn’t they happen outside of mainland China? Could population density or diet be a factor in Chinese epidemic EM? EM outbreaks cannot be dismissed as some cultural psychological phenomenon or school-avoider’s malingering. One of the symptoms is red skin, and a virus has been isolated. Those things can’t be faked. Some research suggests that both the epidemic and non-epidemic forms of EM affect mostly females. Does a sexist bias prevent EM cases in developed countries being properly recognised and diagnosed? There are many reports of women in Anglophone countries afflicted with the painful condition of endometriosis being dismissed by doctors as “head-cases”. I guess it is possible that the Chinese have some kind of genetic vulnerability to EM that might explain why it is apparently rare outside of China but common within it, but if that is the case, I’ve got to wonder why the genetic form of EM seems to have been described by non-Chinese researchers, and I’ve found no suggestion of it being linked to race.

It seems to be not only the case that non-Chinese researchers haven’t studied epidemic EM, some of them also seem to be blissfully ignorant of its existence. I’ve found one outline of EM published by the American National Institutes of Health that fails to mention either the epidemic form of EM or EPRV, and claims that EM is “..extremely rare in children” but if it occurs in kids, is typically associated with serious outcomes. Such claims sit oddly with the fact that the many Chinese EM outbreaks mostly affected students in schools for the age range of 12 to 18.

I suspect that Chinese epidemiological research is somehow globally superior, able to identify new and obscure disease outbreaks, possibly due to access to data from a massive population and “surveillance state”. But what do I know? I’m only an over-educated housewife. I think it is possible that Chinese researchers have been studying in detail epidemics of EM within China while medical researchers outside of China have been blissfully ignorant of EM outbreaks happening in their own neighbourhoods. I think it is also possible that the same situation could have happened in relation to the covid-19 outbreak, first identified in December 2019 in Wuhan, China, with the first Chinese covid-19 case reportedly recorded on November 17th 2019. Were the Chinese merely the first to understand the existence of the deadly covid-19 virus in an epidemic form in their own (densely-populated) territory, without it having originated in their backyard? There have been hints and shreds of evidence that covid-19 existed outside of China before it should have, if you follow the popular narrative of coronavirus spreading out of China in 2020. There’s the possible French case from December 2019 (expert reaction here), a possible spate of early English cases, evidence of covid-19 in Spanish wastewater in March 2019, and a research paper by a Cambridge geneticist challenging the idea of an origin in Wuhan.

I think there’s something rather sad and strange going on when large numbers of people find it very suspicious that a new (mostly non-lethal and often asymptomatic) virual outbreak (the novel coronavirus) is identified in the same city that has a world-class institute for the study of viruses (Wuhan) and conclude that this coincidence must be the result of some foreign mad scientist’s mishap or misbehaviour. You can call me a Sinophile, you can call me a mug, but I think it is just possible that a city that includes world-class virologists might simply be better-placed to detect and report a new viral outbreak than a city without them. 


When I look at the dignified, rectangular face of the female candidate for Vice President of the United States of America, I see the face of a highly-respected Malaysian-born male Australian singer who was most popular in the 1960s-70s. Why? They have two thngs in common – similar names and Tamil genes. I never cease to be amazed at the talents of the Tamil people. I would love to see Kamala Harris running the USA!

This doco about identical strangers broadcast tonight on Nine TV network in Australia

Autism demystified.


Some of the more important posts in this blog’s history…

….are just a couple of clicks away…



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!


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.