Archive for the ‘health’ Category
what is this thing called lymph? some more…
Canto: So we learned a lot about lymph recently, but strangely enough, it made us hungry for more. So, it has two functions, circulatory and immunological. I’d like get more detail on both those functions, and in particular I’d like to know more about lymphocytes, what they are, how they’re made and what they do.
Jacinta: Sounds like a plan. So first, lymph in the circulatory system. Here’s what I’ve gleaned from an online video. This system brings oxygen and nutrients to all our bodily tissues, as well as removing waste materials. Ultimately this feeding and removal process occurs in the smallest vessels, the capillaries, which penetrate into tissues and organs. Nutrient-rich blood plasma moves out of capillaries ‘at the arterial end of capillary beds, while tissue fluid containing wastes reabsorbs back in at the venous end’.
Canto: Okay, whoa. First, I have difficulty separating left from right, and east from west, what they call directional dyslexia. I also, in a probably related way, have problems with arteries and veins. One goes into the heart, the other goes out….
Jacinta: Haha, think arteries away (AA), and that’s all you need to know. I have the same problem, quelle surprise!
Canto: So I get that nutrient-rich ‘blood plasma’, presumably some kind of mixture of blood and plasma, moves out of arterial capillaries into tissues, to feed and energise and rejuvenate them and such, but I’ve never heard of capillary beds, and ’tissue fluid’ sounds a bit questionable…
Jacinta: These are all good issues to raise. Apparently there’s a whole capillary bed network. So, getting back to basics, our cardiovascular system is this super-complex network of veins, arteries and capillaries that move oxygen, nutrients, hormones and waste materials to and from our tissues and organs. It’s often analogised as something like a city road network, highways with off-ramps leading to main roads, side-roads and such. And capillary beds are the network of smaller vessels leading into and out of particular tissues. Anyway here’s a useful definition from a medical website:
Capillaries do not function independently. The capillary bed is an interwoven network of capillaries that supplies an organ. The more metabolically active the cells, the more capillaries required to supply nutrients and carry away waste products. A capillary bed can consist of two types of vessels: true capillaries, which branch mainly from arterioles and provide exchange between cells and the circulation, and vascular shunts, short vessels that directly connect arterioles and venules at opposite ends of the bed, allowing for bypass.
If all of the precapillary sphincters in a capillary bed are closed, blood will flow from the metarteriole directly into a thoroughfare channel and then into the venous circulation, bypassing the capillary bed entirely. This creates what is known as a vascular shunt.
And, since I know you’re wondering:
A metarteriole is a short microvessel in the microcirculation that links arterioles and capillaries. Instead of a continuous tunica media, they have individual smooth muscle cells placed a short distance apart, each forming a precapillary sphincter that encircles the entrance to that capillary bed.
And as for tunica media, I won’t quote, I’ll put it in my own words. Arteries and veins have three-layered linings called tunicae. The tunica media, as the name suggests, is the middle layer between the inner tunica intima and the outer tunica externa. The make-up and structure of this layer (and the others) varies in relation to the size of the artery. For example, there’s a lot more tissue in the layers of the aorta, the body’s largest artery.
Canto: Great, and yes, intrinsically interesting, but let’s return to lymph. So the lymphatic system is a ‘cleaning up’ and drainage system among other things. There are some 700 lymph nodes throughout the body – armpits, groin, throat, and in the intestines where they’re involved in the absorption of fat. A node in this context is a bean-like structure which filters the lymph passing through it. It contains lots of lymphocytes for combating/consuming pathogens. If the system fails to function properly, oedema or lymphoedema results (a swelling or puffiness). As well as these numerous tiny nodes, there’s the spleen, a multifunctional lymphatic organ located on the left side of our bodies next to the stomach. It produces a range of cells including many types of white blood cells such as murderous macrophages and of course lymphocytes. The spleen is divided into a ‘red pulp’ and a smaller ‘white pulp’ section, and I could go into greater detail about T cell zones and B cell zones and the various functions of these cells and their subdivisions.
Jacinta: Yes I think we have a general sense in that the lymphatic system of nodes and spleen improves circulation through removal and replacement, and immunity through renewal of ageing cells and production of lymphocytes and other antibody-type cells. All of this started with our attempt to get a handle on CFS or ME/CFS or CFIDS and its relation to the immune system. It’s been an interesting little journey into an unknown land for us, and my impression is that there’s still a lot to be learned even by researchers steeped in lymph, so to speak.
Canto: Yes, and it’s given us some little background into immunology and the amazing complexity of the animal body…
References
https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/lymphatic-system
https://en.wikipedia.org/wiki/Lymphatic_system
https://en.wikipedia.org/wiki/Metarteriole
exploring chronic fatigue syndrome, myalgic encephalomyelitis, etc
Canto: What do you know about chronic fatigue syndrome (CFS)?
Jacinta: Not much. I read somewhere recently that it’s a term not so much used now. Maybe because the term ‘syndrome’, I think, is a kind of ‘placeholder’, like a collection of symptoms – adding up to a regular feeling of fatigue for no clear reason, or without an established cause, or set of causes. And now maybe they’ve established some causes, and the ‘syndrome’ has been divided up into a few more clearly understood disorders.
Canto: Well, that may be so, but I know that, some twenty years ago or so, there seemed to be a spate of people coming down with what they called CFS – sports people, entertainers, people in the limelight for one reason or another – but I don’t hear so much about it now. So I’m wondering – can a person have this syndrome, or one of its instantiations, on and off for, say, 27 years?
Jacinta: I’ve no idea? Why do you ask?
Canto: Well, I know of someone who still attributes her aches and pains – at least some of them – to chronic fatigue, some twenty-odd years after getting that diagnosis, and it bothers me… I know that there’s an issue out there about women’s health, and women not being believed, particularly by male doctors, and I’m male…
Jacinta: Well recently what they call ‘long Covid’ has cropped up, and it seems to be similar. I know from experience that you can have a serious illness, I mean an infection, one that really puts you on your back and takes a long time to recover from, and it really changes your life in a ‘before and after’ sense. That’s to say, after that illness you never feel quite the same again, as if your immune system has been permanently compromised, damaged in some way. That seems to be happening with long Covid, and maybe it’s an issue for CFS. Maybe CFS starts with an infection that more or less compromises the immune system. Of course I’m no expert on matters medical…
Canto: So some research is required. As I recall, another name for CFS is myalgic encephalomyelitis (ME), which at least sounds like a right proper disease, one to scare the bejazus out of people – especially the ‘encephalo’ part. Clearly it eats your brain.
Jacinta: The ‘myalgic’ term has to do with muscles, tendons, ligaments and stuff. And muscle etc pain, or myalgia, can have an astronomical number of causes. The ‘encephalomyelitis’ term can be broken into two parts. The ‘myelitis’ part refers to myelin, the white-coloured material that sheaths our neural circuitry. ‘Encephalo’, as you say, refers to the brain in general. Encephalomyelitis is defined as ‘inflammation of the brain and spinal cord’, of which there are many types. For instance, Encephalomyelitis disseminata is another name for multiple sclerosis. So ME, if this is just another name for CFS, involves the muscles and associated tissue, and the nerves leading to and from them.
Canto: Okay, that’s all useful, but I’m just wondering whether, if you come down with CFS, or ME, it might be with you, like, forever.
Jacinta: It’s interesting that ME suggests there is evidence of damage to myelin in this condition. That needs to be explored further. I’ve accessed a book published in 1990 called The disease of a thousand names, by Dr David Bell, a pioneer in exploring this syndrome. The name he gives to it is Chronic Fatigue/Immune Dysfunction Syndrome (CFIDS), and on the cover he gives no less than 37 alternative names, some of them, such as Yuppie Flu and Yuppy plague, less serious, or more dismissive, than others. In the foreword he presents the hope that the book will be a starting point for further study, and makes his view of the disease/syndrome/condition clear:
I freely admit to bias in writing this book. I fully believe that CFIDS is a specific, organic illness, caused by a specific agent or agents. I make no claims to be impartial in the argument of whether the illness is real or not. It is interesting that of those researchers directly involved in epidemics of CFIDS, there is no discussion of this question. Personal experience has made the issue irrelevant and even insulting.
Canto: So that’s over 30 years ago, and now I’m watching a disturbing DW documentary from just under a year ago, telling the story of three German sufferers from this condition – and they’re suffering very badly, without a doubt. It also focuses on the doctors, neurologists and researchers trying to get a handle on it. One of them, Dr Carmen Scheibenbogen, an immunologist and oncologist, points out that still, after 30 years, we’ve made little progress, and that very few scientists are working on the disease (which for convenience, let’s call CFS), especially compared to the number of sufferers. They estimate that 17 to 24 million people have it worldwide, with women outnumbering men. They also estimate that only half of sufferers have been diagnosed – but whether that means they think the number may be as much as 50 million or that only 8 to 12 million have been diagnosed isn’t made clear.
Jacinta: Well Dr Bell’s intro ends optimistically:
It is my hope that by the time this book is published, much of the speculation presented here will have been confirmed. If so, the absurd argument of whether this illness is ‘real’ will have ended, an unnecessary argument that has caused so much pain and added so greatly to the burden of those ill with chronic fatigue/immune dysfunction syndrome.
I’d guess he’d be sadly disappointed if he’s still around today. As he notes in the first chapter, the number of names given to the illness is a testament to ignorance more than anything else. And the term CFS arguably downplays the seriousness and debilitating nature of the symptoms, and suggests nothing about damage to the immune system, for example.
Canto: Hearing the stories of the sufferers, and watching them actually and obviously suffering, is itself painful. They seem in a sense like the disappeared. Their illness causes them to disappear from the workplace, from civic or social activity, from any circle wider than immediate family. And all of them seem lost in the mystery of their condition. The term ME is suggestive of inflammation, but often there’s no detectable inflammation. The symptom most common to all sufferers according to Dr Scheibenbogen is a very low tolerance of exertion.
Jacinta: I note that Dr Bell writes of the difficulty of defining a precise set of symptoms, which ‘has surrounded the illness for the past 20 years’, which dates the illness back to 1970 or before. He mentions recent recognition by the CDC, as ‘an illness characterised by months or years of severe pain and exhaustion nearly everywhere’. He also expresses his view, and hope, that ‘it is most likely caused by a single specific agent’. From my laywoman’s perspective, I’m very doubtful about that.
Canto: One of the subjects in the documentary, a teenager, contracted mononucleosis two years before, and hasn’t been the same since. Mononucleosis, often called the kissing disease, is carried by the Epstein-Barr virus (EBV), and so no doubt this virus and/or its relatives have been focused on as possible sources of the illness. Listening to her describing the problem as like a faulty battery which doesn’t recharge properly suddenly made me think of a far more horrific illness, encephalitis lethargica, which killed hundreds of thousands of Europeans from when it first appeared there in 1916. In their case, the battery often ceased to function, leaving them in a state something like total paralysis – but with some mental processes intact. In her book of the epidemic, Asleep, Molly Caldwell Crosby describes a very young woman struck down by the disease, visited by a physician, who rather unprofessionally told her family at the bedside that there was no hope. Her eyes welled with tears. She died shortly afterwards. The image it brings to life still haunts me. No cure or cause of the disease has ever been found.
Jacinta: So, as we explore this current ‘disease of a thousand names’ it does certainly seem that some manifestations can be lifelong. However, because they tend not to be life-threatening, and because causes can’t be found via biopsies, blood tests and the like, it’s generally seen as a ‘diagnosis by exclusion’. And of course it’s likely believed to be psychosomatic by many more than care to admit…
Canto: And yet the WHO recognised it as a neurological disease back in 1969. Perhaps that designation doesn’t help, because it’s often seen as a ‘mind’ disease, something like depression. But getting back to mononucleosis, which has been seen as a stepping-stone or trigger in some cases, it does seem likely that CFS starts with infection, particularly viral infection (SARS, enteroviruses), though again, not in all cases. It does seem to be a case of excessive immune reaction, which can perhaps also be triggered by injury or surgery. EBV is very common – more than 90% of humans catch it, usually in childhood, when it’s more often than not asymptomatic. But in can re-appear as mononucleosis later, usually in early adult life, according to the documentary, though it’s not clear whether that means reinfection, or a virus that lies dormant for a period. In any case, the symptoms are swollen lymph nodes, fatigue, sore throat and a high temperature.
Jacinta: I’ve heard of it, but I thought it was some exotic virus, nothing that I’d ever catch. Sounds like I’ve already been infected…
Canto: Perhaps, but not reinfected – and there can be much more serious, even life-threatening complications, such as spleen damage, low blood cell count and respiratory disease. And CFS.
Jacinta: Well it seems to me that the great mystery of encephalitis lethargica is an object lesson as to how little we know about the ailments and infections our bodies are prey to. It seems that they’re prone to over-reaction, as is the case with allergies, and the ‘cytokine storm’ in Covid-19. But the problem with CFS is that, quite often, no previous infection can be pinpointed.
Canto: Well, this may tell us something new about viruses, and about the immune system, as, to some extent, Covid-19 has. Mononucleosis, for example, is generally seen as a mild illness, but not always, and in some cases it can be life-threatening, or it can somehow stuff up the immune system, leaving sufferers prey to a range of ailments. Some of these are clearly described from symptoms rather than causative agents – for example post-exertional malaise (PEM). Without a clearly defined cause, one can only treat symptoms. And because the symptoms are mostly not life-threatening in any obvious way, it can easily be seen as ‘psychosomatic’, and it doesn’t attract funding. And even with encephalitis lethargica, a killing disease, no causative agent has been found. We just hope it has permanently disappeared, which isn’t very satisfactory. Also, with CFS there are generally no visible symptoms, so physicians must rely on reported symptoms, which actually takes the power out of the hands of the ‘expert’. So, the condition has this difficult status – difficult to attract funding, and virtually impossible to insure against.
Jacinta: Yes, so the hunt is really on for causal factors. It seems to be all about the immune system being ‘overactive and/or misdirected’ as Dr Scheibenbogen puts it. The argument some are putting forward is that it interferes with the autonomic nervous system, taking over much of its function. The autonomic nervous system controls our breathing, our heartbeat, our digestion, and our blood flow. Without effective blood flow, there will be muscle problems, dizziness, poor concentration and general feelings of weakness. Oxygenating the blood helps to energise our whole system. Key to all this is our beta 2 receptors. Here’s something about them from a NIH article:
Beta 2 receptors are predominantly present in airway smooth muscles. They also exist on cardiac muscles, uterine muscles, alveolar type II cells, mast cells, mucous glands, epithelial cells, vascular endothelium, eosinophils, lymphocytes, and skeletal muscles.
Canto: So, beta 2 receptors, something to be researched and kept in mind. The documentary presents a CFS sufferer whose autoimmune neurotransmitters are considerably elevated – whatever that means. They’re also described as ‘antibodies’. Dr Scheibenbogen suggests that CFS is disrupting their functionality. Muscles are not being properly supplied with blood, leading to pain and exhaustion. And all this has something to do with a dysfunctional immune system, and a possible problem with the normal dilation of the blood vessels, which carry oxygen to all the body’s muscles and organs. Which takes us back to the beta 2 receptors, located on the blood vessels in muscles. They’re controlled by adrenalin, released during exertion, and antibodies. These antibodies have been found to be dysfunctional in CFS sufferers, resulting in problems with oxygen supply. Dr Scheibenbogen describes one patient’s results:
We know the patient has antibodies against the beta 2 receptor. What we want to know is, which part of the receptor. We’ve divided up the beta 2 receptor into 15 small pieces and stuck each piece onto a different little bead. They glow in slightly different colours, and then we can see…We can compare these reactions to those of healthy subjects. This will help us understand the disruptive receptor pattern better. If there are distinct differences, a clear pattern, we could use this as a diagnostic test.
Samples from different patients are sent to the Julius Maximilians University in Wurzburg, where a team led by Dr Bhupesh Prusty, a microbiologist and virologist, are trying to find infectious agents that might be responsible for or contributory to the disease. Dr Prusty has been studying the role of viruses for many years and was the first to discover the link between EBV and CFS. Here’s what he had to say:
‘What we have found is that herpes viruses, particularly human herpes virus type 6 (HHV6), and Epstein-Barr virus, are the most interesting candidates which can contribute to the development of the disease. We have found that HHV6 produces a small RNA, and that this small RNA can directly target mitochondria to fragment, and it’s already known that in EBV infection mitochondria is also fragmented, so we believe that this virus-induced mitochondrial fragmentation is one of the most important steps in the development of CFS’.
So the documentary turns to mitochondria, the energy organelles in all our somatic cells.
Jacinta: So we turn to ATP and all that. Fragmented mitochondria aren’t going to bode well for our energy levels.
Canto: Dr Prusty’s team have injected antibodies from the blood of CFS patients into healthy cell cultures to see if a factor in the serum of those patients affects the healthy mitochondria. The experiment resulted in mitochondrial fragmentation, which would result in a weakened immune response in the event of future infections, and a generally slower metabolism. Tests of this kind could be used in the diagnosis of CFS – an enormous advance (I’m quoting or paraphrasing the documentary of course). Dr Prusty says the test works for seriously ill CFS patients, but much less so for milder cases. So it would be diagnostic in some cases and it also points towards something causal, though the precise mechanisms would have to be worked out. And there are funding problems hampering further research.
Jacinta: Dr Bell was writing about the lack of funding in his 1990 book, so nothing has changed. And as with the documentary, case histories are presented, of people cut down by this illness, unable to work, unable to obtain insurance or compensation, unable to find solutions, and suspicious or aware that health authorities, family members and others feel that they’re exaggerating or malingering. Often diagnoses cite depression, and of course depression does set in after a long period of incapacity.
Canto: The doco presents a graph that is, well, graphic, in comparing USA funding for multiple sclerosis and HIV compared to CFS (HIV outscores both of the others by a vast amount). Grassroots funding groups are struggling to make a difference, to amplify the issue and combat stigmatisation. Pharmaceutical companies have shown no interest, no doubt because the symptoms seem vague and lacking in ‘acuteness’, and there are no biological markers to provide focus for a cure or a clear form of relief. Meanwhile, the sufferers themselves feel a sense of being useless or having ‘disappeared’ from active social life. A possible drug for treating CFS, Rituximab, was recently trialed in Norway, based on the hypothesis that it is an auto-immune disease, ‘with a role for auto-antibodies and B-lymphocytes’, according to Dr Oystein Fluge, who led the trial. The documentary explains:
B cells are important immune cells in our body that produce antibodies that destroy viruses and bacteria. Unfortunately this process sometimes goes awry, and the B cells produce antibodies that don’t work properly, or actually attack the body itself. This occurs in many auto-immune diseases, like lupus or myasthenia gravis [a chronic autoimmune, neuromuscular disease that causes weakness in the skeletal muscles]. Scientists believe that ME/CFS is one such auto-immune disease. Rituximab is a medication which temporarily destroys B cells, preventing them from producing antibodies to attack a person’s own body.
Three small trials showed considerable promise, so a ‘phase 3’ randomised, double blind trial, involving 152 patients, was next conducted. One of the major hopes was that a diagnosis could be made based on defective antibodies, and ‘whether a marker could be found in the blood that could simplify the diagnosis’. Could they have been previously infected with EBV? There is apparently a diagnostic test for this, and this has been found in some CFS sufferers, but more proof, through larger-scale testing, is needed. Meanwhile, the SARS-Cov-2 pandemic has left many people with CFS-like symptoms, and while this is in one sense disastrous, it could be a wake-up call for trying to better understand auto-immune diseases – of which CFS is likely one. So far, we have associations rather than proven causes, but the association of a CFS-like illness such as ‘long Covid’ with a disease that clearly plays havoc with our immune system is, to say the least, extremely suggestive. As one researcher points out, being able to establish a cause will encourage people to seek treatment earlier, reducing the damage that time brings about.
Jacinta: Yes, people suffering from ‘long covid’, as it’s called, are of course making the connection with CFS and highlighting the lack of progress re this presumably auto-immune disease.
Canto: Yes, Dr Scheibenbogen is concerned that an after-effect of the pandemic will be a spike in long-term CFS sufferers, which we may already be seeing. The silver lining, though, may be an increased focus on, and increased funding for, solving its current mysteries. Dr Prusty is still of the view that latent herpes viruses are reactivated after covid and perhaps other autoimmune infections. It just isn’t known whether long covid and CFS are essentially the same condition. Meanwhile as Dr Uta Behrends, another frontline researcher in CFS, points out, sufferers need to have a diagnosis made as soon as possible so that they can be supported, so that they don’t feel isolated and become depressed, as so often happens.
Jacinta: Supported, but how can they be treated, when there’s no clear cause?
Canto: Indeed. The Norway trial returned a negative result. This may have been because the Rituximab dosage was low due to lack of funding. Still, the researchers have collected a sizeable bank of blood samples to test with other drugs or enhanced versions of Rituximab. There is also a problem with correct diagnosis of CFS, and perhaps a reluctance to diagnose such a condition in the absence of clear biomarkers. Meanwhile the suffering continues, and an untold number of people remain in limbo…
References
Dr David Bell, The disease of a thousand names, 1991
https://www.ncbi.nlm.nih.gov/books/NBK559069/
https://www.ninds.nih.gov/health-information/disorders/myasthenia-gravis
inspired by writers’ week, sort of – the internet, violence, testosterone and our future
Hmmm – needs further investigation. Vive les bonobos!
I spent some time at the Adelaide Writers’ Week tents yesterday, and heard a couple of remarks from speakers that exercised me in a negative way, so I thought I might air my grievances and expand on my thinking here. One was a quote taken, I think, from the historian and ‘public intellectual’ Bernard Lewis, on the influence of the internet on modern culture, and the other was a dismissal of the ‘better angels of our nature’ thesis of Steven Pinker.
I know Lewis only as a name, never having read any of his work, and I note that he died in 2018, just a few days shy of his 102nd birthday, so I can’t imagine him being an early adopter of the internet. I put his ‘public intellectual’ status in quotes largely out of jealousy, as I think I yearn to be a public intellectual myself, though I’m not sure. Anyway, from the little I heard of the quote, selected and spoken by Waleed Aly, Lewis was considering the double-edged sword of the internet in something like the manner of Marshall McLuhan in The Gutenberg Galaxy and The Medium is the Massage, only rather more negatively. I do recall dipping into McLuhan’s work decades ago, and finding it a bit over-hyped, and hyper. Anyway that’s enough of McLuhan. The concern being expressed about the internet was really mostly about social media and the ideological balkanisation it appears to foster. There’s some truth to this of course, which is why, without really thinking it through, I’ve been avoiding social media outlets more and more. Facebook lies dormant on my devices, and Twitter has come and gone.
But that is a minor part of the internet for me. Its advantages far outweigh the distractions of clickbait sites, and I personally consider it the greatest development in the dissemination of human knowledge at least since the invention of writing – and far more consequential than Gutenberg’s invention. For example, just in the past few months, without stepping outside my home, I’ve watched a lecture series from Yale University on the history of Russia, from the Kievan Rus to 1917 and the end of Tzardom; another lecture series – an Introduction to Neurology, from MIT, and a number of lengthy lectures from the Royal Institution, on palaeontology and on epigenetics, for example. I’ve subscribed to Brilliant.org and have completed 115 of their lessons on everyday science, and I’m boning up on the basics with Professor Dave’s Introduction to Mathematics series. Meanwhile, over the years I’ve observed Wikipedia growing in stature to become the first and best go-to site for learning about historical figures and events, as well as complex scientific subjects. And full scientific papers on just about every possible subject are becoming increasingly available online. I now have access to the greatest library in human history, which leaves me, at times, with a confused feeling – sometimes a dwarf, sometimes a titan. Bliss at this time it is to be alive, but to be young… I recall watching a video (online of course) about how a young African boy was able to build a wind turbine via online instructions, and so bring cheap electricity to his village. .. In short, the internet is an instrument – as is writing and the printing press. It can be used for a multiplicity of purposes, positive or negative. It’s up to us.
Second little irritant. I heard a brief segment of an onstage discussion between the philosopher and ethicist Peter Singer and a writer unknown to me, Samantha Rose Hill, author of a study on Hannah Arendt, about whether they viewed the future positively or negatively. Singer described himself as essentially an optimist, and spoke of his ‘expanding circle’ thesis. He also referred to Pinker’s The better angels of our nature, a book with which he was in broad agreement. The female writer, in her turn, said that she was definitely not in agreement with Pinker, after which I petulantly switched off.
I read The better angels of our nature, probably not long after it was published in 2011, and Pinker’s follow-up book, Enlightenment now, in 2018 or 2019. Right now I can say that I can’t recall a single sentence from either book, which is also the case for the hundreds of other books that have been consumed by the gaping maw of my mind. I might also say that I’ve written more than 800 pieces on this blog, and I’d be hard put to remember a line or two from any of them. In fact I’m sometimes moved to read an old blog piece – somebody has to – and find it amazing that I once knew so much on a topic about which I now know nothing.
But I digress. I don’t have to dig up my copy of Better angels to confirm my agreement with Pinker’s thesis. He wasn’t putting forward an argument that we’d become less violent as a species. He didn’t need to, because it was so obviously true, as anyone who reads a lot of history – as I do – knows full well. The real key to Pinker’s book lies in its sub-title, Why violence has declined. It seems to me that nobody in their right mind – or, I mean, nobody with an informed mind – would argue that the human world, a hundred years ago, 500 years ago, 1000 years ago, or, taking advantage of the knowledge provided to us from ancient DNA, 10,000 years ago, was more peaceful than it is today, on a per capita basis. The question is why.
Of course it’s impossible to keep track of the daily violent acts among a current global population of 8 billion, and to compare them to those of say, the year 1600, when the population has been estimated at about a half billion. And, yes, we’re now capable of, and have committed, acts of extreme, impersonal violence via nuclear weapons, but anybody who has read of the gruesome events of the Crusades, the Thirty Years War, the Scottish slaughters of England’s Edward I (a recent read for me), the centuries-long witch-hunts of Europe, and many other brutal engagements, as well as the public hangings, burnings, decapitations and tortures that were commonplace worldwide in earlier centuries, would surely not want to be transported back in a time machine without a cloak of invisibility or the support of a very powerful overlord – supernatural by preference.
Pinker’s book seeks to answer his own question with data and the possible/probable causal linkages, while recognising the complexity of isolating and independently weighing causes and correlations (he returns to this theme in his latest book Rationality, especially in the chapter entitled ‘Correlation and Causation’), including the spread of democracy, the growth of globalism and internationalism, the developing concepts of human rights, feminism, international monitoring agencies, and improved, less dangerous technologies re industry, medicine and transport, to name a few. Deaths can be no less violent, that’s to say violating, for being slow and accidental, after all.
Note that I snuck ‘feminism’ in there. Unsurprisingly, that’s the factor that most engages me. In the WEIRD world, thanks largely to Simone de Beauvoir (ok, a bit of flagrant heroine-worship there), feminism has been on the rise for several decades. During the same period, in the same regions of the world, male testosterone levels have been dropping. I would rest my case there, but I hear Mr Pinker tsk-tsking in the background. Seriously, the rise of feminism is surely one of a multiplicity of factors leading to a situation that medical researchers describe as ‘alarming’ – I’m not sure why.
Of course, testosterone is an important hormone, especially for men. On this medical website, Dr Kevin Pantalone, an endocrinologist, points out that, for males, testosterone helps maintain and develop:
- Sex organs, genitalia and reproductive function.
- A sense of well-being.
- Muscle mass.
- Bone health.
- Red blood cell count.
So, questions arise. Why are testosterone levels dropping (pace feminism), and is the drop significant enough to seriously compromise WEIRD men’s health? Well, according to the same website, different figures are given for what counts as a low testosterone level – 250 nanograms per deciliter (ng/dl), according to Dr Pantalone, and 300 ng/dl according to the American Urology Association. We’re not there yet, on average, but we’re inching closer, apparently.
So why the drop, apart from feminism? Some suggested factors include obesity (elevated BMI), reduced physical activity (however, endurance activities such as long-distance running and cycling have been shown to lower testosterone levels)., poor diet (but ‘several studies indicate that low-fat diets may lead to slightly lower testosterone levels‘), chronic and excessive alcohol consumption, lack of sleep (e.g. sleep apnea), and environmental toxins such as EDC (endocrine-disrupting chemicals – which sounds a bit vague).
That’s it. It all seems a bit thin to me – apart from the obesity bit. One factor they don’t mention, probably due to our overly polite society – or is it ‘wokeness?’ – is the serious drop in recent decades, and perhaps even centuries, of good old raping and pillaging. Nothing better for boosting ye olde testosterone, surely?
Seriously, would it be a terrible thing if male testosterone levels were reduced to those of females? And what about my darling bonobos?
So, human males typically have testosterone levels ranging from 265 to 923 ng/dl, while females range from 15 to 70 ng/dl. That’s a big big difference. Which raises the question – if females have such low testosterone levels, what about their bone health, muscle mass and sense of well-being? I suppose this is where we get into the finer details of endocrinology and evolution, but my uneducated guess would be that, over time, the endocrine systems of male and female humans have diverged somewhat, perhaps in response to different activities between the sexes. One way of getting more information about this – and this rather excites me, I have to say – is to look at the endocrine systems of largely female-dominated bonobos and compare them to those of chimpanzees. So that’s what I’ll be looking at in my next post. I can’t wait.
References
Stephen Pinker, The better angels of our nature, 2011
Stephen Pinker,Enlightenment now, 2018
https://pubmed.ncbi.nlm.nih.gov/33741447/
exploring clogged ears
Canto: So we were going to have another go at Bayesian probability and reasoning. Even though I think I already understand it from last time…
Jacinta: Well actually the piece I wrote on this blog in August 2019 does a pretty good job of explaining it, but we easily forget…
Canto: So onto more pressing matters. I’ve developed a big hearing problem, as a result of a bacterial infection which cleared up soon enough with the help of antibiotics. These infections are a regular problem for me, as I have a chronic condition, bronchiectasis, which means my upper airways have a high bacterial load, and so I’m quite convinced that antibiotics have been a life-saver for me. But this time one of the symptoms was a blockage of some kind in my left ear, which appears to be behind the ear-drum. My regular doctor and an audiologist could find nothing visible – no build-up of wax for example. My doctor wrote something about glue ear, with a question mark, to the audiologist – so I need to research this condition. And there’s also a problem with my right ear – a perforated ear-drum, and quite a large one according to the audiologist. So the right ear problem has clearly been with me for a long time – I knew my hearing wasn’t the best – and is perhaps getting worse, but the sudden blockage to my left ear has caused something of a crisis. Just at the time this infection occurred I was asked to return to work at Eynesbury College, but I had to refuse, as my hearing was so bad. All of this happened in November, but I won’t be seeing the Otolaryngologist (a new term to me) until February 21st which is vraiment frustrant.
Jacinta: So we’re going to have a look at glue ear, common childhood complaint, and similar issues. By the way, otolaryngology is a shortened form of the term otorhinolaryngology (ear-nose-throatology), of course, and it’s the oto (Greek for ear) that we’re concerned about here:
Glue ear is caused by blockage of a small tube in the ear, called the Eustachian tube. When fluid is trapped inside this tube, fluid builds up in the middle ear cavity (called an effusion) and this can slowly get thicker. This often happens after a head cold. Glue ear can happen after repeated middle ear infections.
Canto: This sounds just like my problem, and I was worried precisely about this thickening, which is what I feel is happening, and I fully expect that, like glue, it’ll be much tougher to remove when it hardens. So why must I wait? Anyway, the blockage is the immediate problem, it makes my voice sound loudly in my ear, and if I’m eating something crunchy, the sound is like ice crashing down from Antarctic cliffs. When I’m talking one-on-one with someone I try to arrange it so they’re talking into my right ear, the one with the perforation.
Jacinta: Mmmm, well let’s learn more about the inner ear, the Eustachian tube and such. Glue ear is most often associated with children, but some one in three sufferers are adults. There are a variety of causes, and symptoms – it’s sometimes just referred to as a clogged ear. I can’t find much reference to your symptom of having an amplified voice….
Canto: I’m told sometimes to speak up, because apparently I’m lowering my voice because it sounds so loud in my head.
Jacinta: Yes, well here’s something:
Autophony is the unusually loud hearing of a person’s own voice. Possible causes are: The “occlusion effect”, caused by an object, such as an unvented hearing aid or a plug of ear wax, blocking the ear canal and reflecting sound vibration back towards the eardrum.
Canto: Autophony. Eureka! But none of those causes fit my situation.
Jacinta: Well, here’s something from another website that’ll be more helpful:
Autophony is the perception that your voice is too loud or echoing in your ears. Autophony also refers to the perception of all other sounds coming from your body, such as breathing or arterial noises. Typically, autophony results from a middle ear infection, such as tuba beante. Other causes may include eardrum occlusions, serous otitis media, open or patulous Eustachian tube, or Minor’s Syndrome.
Canto: Yes, that gives me plenty of material for research. So, first, a two-part YouTube piece taken from the over-slick US show The Doctors features someone who seems to have my problem intermittently, and worries whether she’ll be able to ‘go on’ if it becomes permanent like mine has – at least temporarily. She was finally diagnosed with patulous Eustachian tube dysfunction (I suspect this is not my problem though). Their resident otolaryngologist explains that the Eustachian tube starts at the back of the nasal cavity – though I tend to think of it from the other end, in the middle ear starting from behind the tympanum…
Jacinta: Patulous in the medical sense means wide open or distended. I’m not quite sure if I can picture this, does it mean that this airway – and it is an airway if you think of it as coming in through the nasal cavity – is distended just as your bronchial airways are distended due to your bronchiectasis?
Canto: Well, that’s a thought. Could it be an extension of my bronchiectasis? And not a problem of fluids at all? The otolaryngologist explained that this client’s Eustachian tube is ‘in open position more than normal, so all those sounds – chewing, breathing, etc, is going right into [her] Eustachian tube and is being transmitted in turn to the middle ear space’. So if this is my problem – another development of my bronchiectasis…
Jacinta: Don’t mean to scare you but bronchiectasis is described as a condition that can tend to worsen over time….
Canto: Yeah thanks. Our TV otolaryngologist describes helpful treatments that might close down this airway – drops (sounds unlikely) – oestrogen drops through the nose, and other preparations, or surgery to manipulate the opening, ‘injecting something to try to close it down’, all of which sounds eminently vague.
Jacinta: If it is fluid, and it’s thickening, I’m sure they have some means of thinning it down…
Canto: Well I’ve heard from someone – yes, a doctor friend – that they have a procedure which punctures or perforates the eardrum, drains the fluid (I’m not sure in my case) and then leaves a little plug to keep the drum open, but just a wee bitty.
Jacinta: Okay, on it…:
- Grommets are tiny ventilation tubes that are put inside the eardrum to prevent a build-up of fluid.
- They are needed if someone has a lot of ear infections that have caused ‘glue ear’.
- A person will need to go to a hospital to have grommets put in. They need minor surgery under general anaesthetic.
- Grommets usually fall out by themselves after 6 to 12 months.
Canto: Yeah that sounds like it. So we’ve dealt long enough with the left ear, how about the right one?
Jacinta: A large perforation, you say? Here’s the Mayo Clinic:
A hole in the tissue that separates the ear canal from the middle ear.A perforated eardrum may be caused by loud sounds, a foreign object in the ear, head trauma, a middle ear infection or rapid pressure changes, such as from air travel.Symptoms include sharp ear pain that subsides quickly, drainage, ringing in the ear (tinnitus) or hearing loss.The condition usually heals on its own within a few weeks. Antibiotics, an eardrum patch or surgery may be necessary.
References
https://www.otovent.co.uk/what-is-otovent-for/glue-ear-in-adults/
https://www.healthline.com/health/why-does-my-ear-feel-clogged#tube-blockage
https://www.amplifon.com/uk/ear-diseases-and-disorders/other-hearing-problems/autophony
https://www.cedars-sinai.org/health-library/diseases-and-conditions/b/bronchiectasis.html
https://www.healthdirect.gov.au/grommets
https://www.mayoclinic.org/diseases-conditions/ruptured-eardrum/symptoms-causes/syc-20351879
adult ADHD – what’s the buzz?
Jacinta: So this is a commissioned piece, sort of, by someone who wants us to look into this disorder (attention deficit hyperactivity disorder, in full), for our sakes and of course for the sake of humanity.
Canto: Sounds like a first world issue to me.
Jacinta: Okay consider yourself lucky you don’t have to scrounge around rubbish heaps for a living, or travel miles on a half-dead donkey to see a medico, or dodge government bullets because you’re an outspoken female…
Canto: Okay okay. So we know that diagnoses of adult ADHD have risen substantially in recent years, in the WEIRD* world, along with autism spectrum disorder (ASD), bipolar disorder, major depressive disorder, PTSD, chronic fatigue syndrome, and others. A lot of work is being created for clinical psychologists, and the waiting lists are getting longer.
Jacinta: So we’ve started by watching a couple of videos, one from CNBC in the US, another from the ABC in Australia. And a few points here about research and reliable info. Avoid social media! And for the most part avoid commercial news and info networks, which are privately owned and often have a commercial-financial agenda. The most reliable sources in the WEIRD world are generally government subsidised and mandated sites (the ABC in Australia, the BBC in Britain, PBS and NPR in the USA, DW (Deutsche Welle) in Germany, France TV and Radio France, for example).
Canto: Well, we’ve broken that rule by starting with this video from CNBC, but it does give a good overview of the symptoms, via field professionals such as Dr Leonard Adler, director of an adult ADHD programme at NYU. The symptoms are divided into two types, those associated with inattentiveness and with hyperactivity, though there are obvious crossovers. Under each type heading, nine more or less connected symptoms are described. For example, symptoms of inattentiveness include ‘forgetfulness in daily activities’, ‘failure to finish tasks’ and ‘losing important things’, and under hyperactivity comes ‘interrupting others’ or ‘trouble with turn-taking’, and ‘being always ‘on the go”. Apparently you need at least five of the nine symptoms in either category to be diagnosed with ADHD, at least in the USA. Personally, I can relate to all of the symptoms some of the time. All of this, by the way, comes from the famous, or infamous, DSM-5, the 5th edition of the diagnostic and statistical manual of mental disorders.
Jacinta: So you may be skeptical, but on the question posed throughout this video: ‘Is ADHD on the rise or is there simply a rise in diagnoses?’, my answer would be ‘yes there is a rise in diagnoses’, but not for the cynical reason you seem to favour – that it’s all about lining the pockets of psychiatrists. Remember we’ve been studying Freud and the post-Freudians, who pioneered the uncovering of disorders due to childhood trauma, sexual repression, unconscious guilt and the like, all in a groping, hit-and-miss sort of way, before anything much was known of neurology, endocrinology or genetics. Now in the 21st century, we can make connections between genetics, family and personal histories and brain processes in a more scientific way – at least slightly. There’s a long way to go. And this has led us to the reality of ongoing behavioural disorders, where previously people were just considered in vague terms as oddballs, eccentrics, psychos, losers or pains in the arse.
Canto: Steady on. I understand that it’s not about having some symptoms sometimes, which we all do, it’s about having a number of them to a degree that it becomes debilitating. And, as more than one expert has said, what’s frustrating to these sufferers is that sometimes, with certain specific tasks, or aspects of their professional lives, they perform perfectly well on a regular basis, while the rest of their lives are a mess of procrastination, disorganisation, impulsivity and the like. But the more I learn about the disorder, the more I wonder about treatment. These symptoms seem so multi-faceted, I can’t imagine how they can be dealt with though drugs. I can’t even begin to imagine the brain chemistry behind such varied behaviour. Surely there’s no medication that’s going to make you more organised or a better listener – never mind both at the same time.
Jacinta: Well, and yet it all has to be about brain chemistry and signalling. What else can it be? And patterns of behaviour – that’s to say, patterns of brain signalling, that have become habitual since childhood. In response to family dynamics and such. No free will, remember. Much that I’ve heard so far indicates that it runs in families. And of course there are prescription medications for the disorder. So we have to look at effectiveness (method of action), cost, availability and any side-effects or downsides. And then there are other treatments such as cognitive behavioural therapy.
Canto: Yeah I’ve heard that medications are expensive, and I doubt that therapy comes cheaply either. But let’s look at the brain of ADHD sufferers and what can be done medically, if anything, to alter it.
Jacinta: Well Britain’s National Health Service has this to say:
Research has identified a number of possible differences in the brains of people with ADHD from those without the condition, although the exact significance of these is not clear. For example, studies involving brain scans have suggested that certain areas of the brain may be smaller in people with ADHD, whereas other areas may be larger. Other studies have suggested that people with ADHD may have an imbalance in the level of neurotransmitters in the brain, or that these chemicals may not work properly.
Canto: Wow, that’s really informative. I like the bit about smaller or larger. Are they talking about brains or dicks? I mean, really…
Jacinta: Hmm. We need to look at research papers. And one thing I note is that researchers don’t readily distinguish ‘Adult ADHD’ because it’s understood to have emerged in childhood, though symptoms might have changed over time. In fact many children may ‘get over it’. Dr Judy Ho, in an interview on ADHD in the USA, quoted that childhood ADHD affects some 5% of the population but the adult version affects some 2.5%, which seems to make sense.
Canto: Well, having checked Google Scholar, I don’t see much in the way of recent research that jumps out. Sheeting home the various symptoms of the disorder to brain chemistry is really difficult…
Jacinta: Well since they do have medications on the market – the NHS describes 5 types- methylphenidate, lisdexamfetamine, dexamfetamine, atomoxetine and guanfacine – and these presumably work on brain chemistry, they must have some idea. ..
Canto: Well these are generally amfetamines, which act as stimulants, speeding up brain functions through the release of hormones and monoamine neurotransmitters such as dopamine and norepinephrine, and this kind of ‘upper’ activity would help with the disorder most associated with ADHD, which is depression, though there are definite downsides related to prolonged use or overuse. Combining, and possibly replacing, such medications with more behavioural-analytical treatments such as Cognitive Behavioural Therapy might be an idea, if there were enough decent therapists around, and if it was affordable, but it’s all a bit hit and miss.
Jacinta: You have to distinguish between proximal causes and ultimate causes. The proximal causes of most of these conditions is hormone levels and neurotransmitter activity, but that says nothing about why those levels are higher in some people than in others. If you don’t know the underlying causes, you’re just treating symptoms – drugging people to behave ‘normally’. But those underlying causes are generally fiendishly difficult to deal with – for example how can you cure an abused childhood, or damage done in the womb?
Canto: But many people with ADHD may just want to be ‘normalised’, to a degree. They know that what’s been done to them can’t be undone, but they just might want those symptoms reduced, to concentrate better, to be more organised, to calm down, whatever.
Jacinta: And given that we’re not that good at tolerating differences, why not give people drugs so they can all be the same, at least tolerably so….
*western ,educated,industrial,rich,democratic
References
ADD/ADHD – What is Attention Deficit Hyperactivity Disorder? (video)
https://www.nhs.uk/conditions/attention-deficit-hyperactivity-disorder-adhd/treatment/
https://www.cdc.gov/ncbddd/adhd/index.html
A bit about schizophrenia – a very bizarre ailment
Having, for a book group, read a strange novel written a little over 50 years ago, by Doris Lessing, Briefing for a descent into hell, the title of which may or may not be ironic, and being reasonably interested in the brain, its functions and dysfunctions, I’ve decided to use this post to update my tiny knowledge of schizophrenia, a disorder I’ve had some acquaintance with.
Lessing’s book may or may not be about schizophrenia, because it doesn’t concern itself with labeling any mental disorders, or with the science of brain dysfunction in any way. The focus is upon the imaginative world of an Oxbridge academic, a lecturer in classical mythology or some such, who, having been found wandering about in some Egdon Heath-type landscape, with no identification papers or money, and a lack of proper lucidity, is brought into a psychiatric facility for observation and treatment. The vast bulk of the book is told from this individuals’s perspective. Not that he tells the story of his illness, he simply tells stories – or Lessing tells stories on his behalf. Somehow the reader is allowed to to enter the main character’s inner landscape, which includes a voyage around the Pacific Ocean, another voyage around the solar system (conducted by classical deities) and harrowing, but fake, war-time experiences in the Balkans. Along the way we’re provided with the occasional dazzling piece of insight which I think we’re asked to consider as the upside, or mind-expanding nature, of ‘madness’ – somewhat in the spirit of Huxley’s Doors of Perception and Timothy Leary’s psychedelia. At the end of the book the professor is returned to ‘normality’ via electric shock treatment, and becomes, apparently, as uninteresting a character as most of the others in the book, especially the doctors responsible for his treatment, only known as X and Y.
So, there are problems here. First, Lessing’s apparent lack of interest in the science of the brain means that we’re at a loss to know what the academic is suffering from. Madness and insanity are not of course, legitimate terms for mental conditions, and Lessing avoids using them, but offers nothing more specific, so we’re reduced to trying to deduce the condition from what we know of the behaviour and ramblings of an entirely fictional character. I’ve come up with only two not very convincing possibilities – schizophrenia and brain tumour. A brain tumour is a useful literary device due to the multifaceted nature of our white and grey matter, which constitutes the most complex organ in the known universe, as many an expert has pointed out. A benign tumour – one that that doesn’t metastasise – may bring on a multiplicity of neurons or connections between them that increase the ability to confabulate – though I’ve never heard of such an outcome and it’s more likely that our ‘imagination’ is the product of multiple regions spread throughout the cortex. Schizophrenia only really occurs to me here because the professor was found wandering ‘lonely as a cloud’, far from home, having had his wallet presumably stolen, so that it took some time to identify him. This reminds me of a friend who has from this condition, and has suffered a similar experience more than once.
One of the symptoms of schizophrenia is called ‘loss of affect’, which means that the sufferer become relatively indifferent to the basics – food, clothing and shelter – so caught up is he in his mental ramblings, which he often voices aloud. It’s rare however, for schizophrenia to make its first appearance in middle-age, as appears to be the case here. Another reason, though, that my thoughts turned to schizophrenia was something I read online, in reference to Briefing for a descent into hell. I haven’t read any reviews of the book, and in fact I had no idea when the book was published, as I’d obtained a cheapie online version, which was undated. So in trying to ascertain the date – 1971, earlier than I’d expected, but in many ways illuminating – I happened to note a brief reference to a review written when the book came out, by the US essayist Joan Didion. She wrote that the book presented an ‘unconvincing description of mental illness’ and that the book displayed the influence of R D Laing. A double bullseye in my opinion.
I read a bit of R D Laing, the noted ‘anti-psychiatrist’ in the seventies, after which he went decidedly out of fashion. His focus was primarily on schizophrenia – as for example in his 1964 paper ‘Is schizophrenia a disease?’ – though he treated other psychoses in much the same way as ‘a perfectly rational response to an insane world’. This is doubtless an oversimplification of his views, but in any case he seems to have given scant regard to what is actually going on in the brain of schizophrenics.
Since the sixties and seventies, though, and especially since the nineties and the advent of PET scanning, MEG, fMRI and other technologies, the field of neurology has advanced exponentially, and the mental ailments we suffer from are being pinpointed a little more accurately vis-à-vis brain regions and processes. I’ve noted, though, that there’s still a certain romantic halo around the concept of ‘madness’, which after all human society has been ambivalent about since the beginning. The wise fool, the mad scientist and the like have long had their appeal, and it may even be that in extremis, insanity may be a ‘reasonable’ option. As for schizophrenia, maybe we can live with our ‘demons’, as was apparently the case for John Nash after years of struggle, but it’s surely worth trying to get to the bottom of this often crippling disorder, so that it can be managed or cured without resort to disabling or otherwise unhealthy or inconvenient dependence on medication.
Schizophrenia is certainly weird, and its causes are essentially unknown. There’s a genetic element – you’re more likely to suffer from it if it runs in the family – but it can also be brought on by stress and/or regular drug use, depending no doubt on the drug. It’s currently described as affecting a whopping one in a hundred people (with enormous regional variation, apparently), but perhaps if we’re able to learn more about the variety of symptoms we might be able to break it down into a group of affiliated disorders. There is no known cure as yet.
One feature of the ‘neurological revolution’ of the last few decades has been the focus on neurotransmission and electrochemical pathways in the brain, and dopamine, a neurotransmitter, was an early target for understanding and treating the disorder (and may others). And that’s still ongoing:
Current research suggests that schizophrenia is a neurodevelopmental disorder with an important dopamine component.
That’s from a very recent popular website, but research is of course growing, and pointing at other markers. A reading of the extensive Wikipedia article on schizophrenia has a near-paralysing effect on any attempt to define or describe it in a blog post like this. Glutamate, the brain’s ‘most abundant excitatory neurotransmitter’, has been a major recent focus, but it’s unlikely that we’ll get to the bottom of schizophrenia by examining brains in isolation from the lived experience of their owners. Genetics, epigenetics, stress, living conditions and associated disorders, inter alia, all appear to play a part. And due to its strangeness, its apparent hallucinatory nature, its modern associations of alienation and dystopia – think King Crimson’s ’21st century schizoid man’ and much of the oeuvre of Bowie (mostly his best work) – it’s hardly surprising that we feel something of an urge to venerate the schizoid personality, or at least to legitimate it.
Meanwhile, research will inevitably continue, as will the breaking down of intelligence and consciousness into neurotransmission pathways, hormone production, feedback loops, astrocytes etc etc, and ways of enhancing, re-routing, dampening and off-on switching neural signals via increasingly sophisticated and targeted medications… because a certain level of normality is optimal after all.
Meanwhile, I’m off to listen to some of that crazy music….
References
https://www.verywellmind.com/the-relationship-between-schizophrenia-and-dopamine-5219904
https://www.verywellmind.com/what-is-dopamine-5185621
How Australia is faring on global indices
park yourself here?
Many Australians were greatly relieved at the change of Federal government from May 21 2022. Australia hadn’t been faring well on the international stage, especially with respect to the global warming crisis, but also regarding political governance and other issues. Of course the Labor government has only been in office for three months, so I don’t expect judgements to have turned around significantly at this point. The purpose of this piece is to describe Australia’s position on a number of international surveys, and then to return to those surveys in about twelve months’ time to see if and how the view of Australia internationally has changed.
I was motivated to write this by a passage in David Brophy’s book China Panic, in which he mentioned two such international surveys, the CIVICUS monitor, which apparently measures democratic credentials, and Transparency International’s Corruption Perception Index. I’d never heard of these surveys, which is hardly surprising for a dilettantish autodidact. Three surveys I have monitored are the Economist Intelligence Unit’s Democracy Index, the OECD’s Better Life Index and the UN’s Human Development Index. So now we have five, and counting. What follows is my attempt to summarise their most current findings.
The CIVICUS monitor. CIVICUS is, as far as I can tell, not an acronym. Based in Johannesburg, the organisation describes itself as:
a global alliance of civil society organisations and activists dedicated to strengthening citizen action and civil society throughout the world…. Our definition of civil society is broad and covers non-governmental organisations, activists, civil society coalitions and networks, protest and social movements, voluntary bodies, campaigning organisations, charities, faith-based groups, trade unions and philanthropic foundations. Our membership is diverse, spanning a wide range of issues, sizes and organisation types.
According to Brophy, the CIVICUS monitor downgraded Australia’a democratic status (in the broad sense described above) from ‘open’ to ‘narrowed’ in 2019. The latest findings, from 2021, are unchanged. To explain, the monitor divides the world’s nations into 5 levels, which, top to bottom, are open, narrowed, obstructed, repressed and closed. On further inspection, I’ve found that there’s a ‘live rating’, last updated for Australia on 25/5/22, a few days after the election. Hopefully things will have improved by 2023. To compare a few other countries – New Zealand, Canada, Ireland, Uruguay, Suriname, Taiwan, Portugal and most Northern European countries are classed as ‘open’. Other ‘narrowed’ countries include Namibia, Italy, France, the UK, Japan and Bulgaria. Obstructed countries include the USA, Brazil, South Africa, Ukraine, Poland, Indonesia and Morocco. A colour-coded map provides an at-a-glance reference to any country of interest. The repressed and closed countries can generally be guessed at. China, Vietnam and most Middle Eastern counties are classed as ‘closed’.
The Corruption Perceptions Index (CPI). The CPI is a product of Transparency International, which advertises itself thus:
Transparency International is a global movement working in over 100 countries to end the injustice of corruption. We focus on issues with the greatest impact on people’s lives and hold the powerful to account for the common good. Through our advocacy, campaigning and research, we work to expose the systems and networks that enable corruption to thrive, demanding greater transparency and integrity in all areas of public life.
First set up in 1993 by an ex-World Bank official, Peter Eigen and like-minded associates, first-hand witnesses of global corruption, the organisation was established in then recently re-unified Berlin.
An article in The Conversation, posted in late January 2022, points out that in 2012 Australia ranked level with Norway in 7th position as to ‘cleanness’. The 2021 index, to which The Conversation refers, sees Australia as having slipped to 18th while Norway has risen to 4th, out of 180 countries. Much of what Brophy writes in China Panic is an account of why the country I happen to have ended up in has fallen so far so fast. The Economist Intelligence Unit, which publishes the Democracy Index, is one of the sources for this index, along with Freedom House and the World Justice Project. The three equal top countries on this index are New Zealand, Denmark and Finland, and the bottom three are Somalia, Syria and South Sudan. Anyway, re Australia, this one will be worth watching over the next few years.
The Democracy Index. I’ve written about the Democracy Index, inter alia, in a previous piece. It’s produced by the Economist Intelligence Unit, associated with The Economist magazine in the UK. Here’s their raison d’être blurb:
The EIU Democracy Index provides a snapshot of the state of world democracy for 165 independent states and two territories. The Democracy Index is based on five categories: electoral process and pluralism, civil liberties, the functioning of government, political participation, and political culture. Based on their scores on 60 indicators within these categories, each country is then itself classified as one of four types of regime: full democracy, flawed democracy, hybrid regime or authoritarian regime
Australia ranks a fairly creditable 9th on the Democracy Index list for 2021, well below NewZealand (2nd) but also well above the country we’ve been showing so much allegiance to in recent decades, the USA, which ranks 26th and is considered a flawed democracy. According to the index’s ratings, the world is inching towards hell in a hand basket – 70% of the world’s nations have become less democratic in the last twelve months, and this downward trend has prevailed for some years. Australia, though, has been faring worse than most. I don’t have access to the previous rankings, but each nation is given an annual score out of ten. Australia’s 2021 score is 8.90, compared to 8.96 in 2020. The score has regularly dropped from a high of 9.22 in the years 2010-2012, the period of the Rudd-Gillard Labor Prime Ministerships.
The OECD Better Life Index. This measures the ‘life experience’ of an ‘elite’ group of about 40 of the world’s wealthiest countries, members of the Organisation for Economic Cooperation and Development, according to eleven different criteria, including education, environment, safety and health. When I first accessed the index, about 6 or 7 years ago, Australia was ranked number 2 across all criteria, behind the ever-triumphant Norway, and well ahead of the US in around 12th spot. Currently Australia is ranked 7th, and the USA 8th. Norway still ranks first.
On looking into Australia’s ranking for each criterion (the 11 criteria are housing, income, jobs, community, education, environment, civic engagement, health, life satisfaction, safety and work-life balance) I can’t help but scratch my head at some of the results. Australia ranks 1st for ‘civic engagement’, but 20th for ‘community’ (!!??). I would have thought that one entails the other. Also, Australia ranks 2nd for housing (but city rental has become unaffordable for most young people), and 2nd for education, which again surprises me from a general persecutive, though our post-grad sector definitely punches above its weight. At the other end of the spectrum, Australia ranks 30th for safety, another surprise. The OECD claims that the average homicide rate for member countries is 2.6 per 100,000 inhabitants. According to the Australian Institute of Criminology, Australia’s homicide rate for 2019-20 was 1.02 per 100,000, the highest in nearly ten years, but clearly well below the OECD average. Of course, homicide is only one measure, but I’ve not heard of Australia having a high crime rate in general. Strange. But the worst ranking is 33rd for work-life balance!? But having rarely worked a day in my life, I couldn’t possibly comment.
The UN Human Development Index (HDI). Here’s the blurb about this one:
The Human Development Index, or HDI, is a metric compiled by the United Nations and used to quantify a country’s “average achievement in three basic dimensions of human development: a long and healthy life, knowledge and a decent standard of living.” Human Development Index value is determined by combining a country’s scores in a vast and wide-ranging assortment of indicators including life expectancy, literacy rate, rural populations’ access to electricity, GDP per capita, exports and imports, homicide rate, multidimensional poverty index, income inequality, internet availability, and many more.
The HDI website only provides information from 2019 and places Australia in a tie with The Netherlands at 8th in the world, with a score of .944 on a scale from 0 to 1. Norway again gets top spot, just ahead of Ireland and Switzerland. Interestingly, Australia ranks higher than four countries it likes to compare itself with, the UK, New Zealand, Canada and the USA, but little explanation is given for the ranking, which appears to be have been stable for a few years.
So, to summarise, I don’t know what to make of all these indices, which I suspect subtly influence each other in their ratings. We appear to always make the top ten, but rarely the top 5. If we could take advantage of our climate and resources to be be a greater power in renewables, instead of lagging (except in domestic rooftop solar) as we have done over the last decade, we could really make the world pay more attention to us, for better or worse.
References
David Brophy, China Panic: Australia’s alternative to paranoia and pandering, 2021
https://en.wikipedia.org/wiki/Democracy_Index
https://www.oecdbetterlifeindex.org/#/11111111111
https://worldpopulationreview.com/country-rankings/hdi-by-country
a post to send you to sleep, or not
Häggström, Mikael (2014). “Medical gallery of Mikael Häggström
Canto: Anything interesting you’ve learned lately?
Jacinta: Well, there’s so much, it’s hard to keep track of it all, before it slides down the slippery slope into a past of fragmented memories.
Canto: A pasta of memories? That’s food for thought. I know you’ve been reading up on sleep, among all your other heavy reading. Tell me.
Jacinta: Yes, I’ve been reading up on feminism and misogyny as you know, which is mostly depressing, but this sciencey but very accessible book, Why we sleep by Matthew Walker, is not so much depressing as worrisome, for those of us whose sleep patterns are all over the place, like mine. He’s a big-time sleep researcher, and what he says about sleep deprivation is all bad – even for a wee bit of it.
Canto: So, those dreams of doing away with sleep, of zapping your brain for a few seconds to provide the instant reinvigoration that sleep takes eight hours of wasteful oblivion to achieve, allowing us that much more time to ruin the biosphere and all, or just to read more books and shit, those dreams are just a waste of sleep?
Jacinta: No zapping will ever replace the complexity of sleep, with all its REMness and non-REMness, let Mr Walker assure you. Sleep is a restorative and builder, which has complexly evolved with the complex evolution of our brains and bodies. And by ‘our’ I don’t just mean humans, but every complex or not-so complex evolved organism. They all sleep.
Canto: Well, there are many questions here. You’ve mentioned REM sleep, which I think has something to do with dreaming – your eyes, presumably under their lids, are rapidly moving about. Why? It doesn’t sound healthy.
Jacinta: They’re responding to brain signals, and it’s perfectly normal. More specifically, they seem to be responding to the brain’s changing visual representations while dreaming. They used electrodes in the brain to discover this – which sounds Frankensteinish but in this case they were patients with epilepsy preparing to have very invasive treatment to stop their seizures. They looked at activity in the medial temporal lobe, a region deep in the brain which includes the hippocampus and amygdala, and is involved in encoding and consolidating memories, and found fairly clear-cut connections between that activity and patients’ eye movements.
Canto: But how could they ‘see’ the eye movements?
Jacinta: Oh god, I don’t know, for now I’m more interested in sleep deprivation, which raises concerns for everything from diabetes to Alzheimer’s. And, although I haven’t measured anything carefully, my guess is that I average 6 to 7 hours’ sleep a night, and I need to amp that up.
Canto: And you’ve recently been diagnosed as pre-diabetic, so do you think more sleep can help with that? It’s usually pretty strongly correlated with diet isn’t it?
Jacinta: Less time sleeping, more time for eating, Walker writes. I’m certainly trying to lose weight, but only by eating less. I think my diet’s not too bad, less wine though. And I suppose if I slept more, which is easier said than done, I wouldn’t eat so much. I’ve found in the past that just reducing the quantity of food I ingest, without changing its make-up – in other words, being more disciplined – can take the weight off quite quickly. The key is to make it life-long.
Canto: More fibre is good, I think. For the microbiome.
Jacinta: So type 2 diabetes is generally about blood sugar levels and their regulation, or lack thereof. In a healthy person, eating a meal adds glucose to the blood, which triggers the hormone insulin, produced in the pancreas, to somehow bring about cellular absorption of the glucose as an energy source. In the case of diabetes, there’s usually a break-down in the cellular response to the insulin signal, I think, and so you become hyperglycaemic – not that this has ever happened to me, so far.
Canto: So how does this relate to lack of sleep, apart from giving you more time to guzzle sugar?
Jacinta: Walker describes a series of studies, independent from each other, in different continents, which found high rates of type 2 diabetes in people who reported sleeping for less than six hours a night on a regular basis. They controlled for other factors such as obesity, alcohol use, smoking etcetera. But of course correlation isn’t causation so they investigated further. They conducted experiments with a bunch of healthy people – no blood glucose problems or signs of diabetes. Firstly, they mildly tortured them – they permitted them only four hours of sleep per night over six straight nights. Then they tested their ability to absorb glucose, and found a 40% reduction in that ability. This would immediately classify them as pre-diabetic, and these studies, I’m assured, have been replicated numerous times.
Canto: That sounds incredible. And these guinea pigs quickly recovered? Or are they now full-blown diabetics? Doesn’t sound like mild torture to me. And do they know why a week’s sleep deprivation had such a dramatic effect?
Jacinta: Ha, well, Walker doesn’t mention the afterlife of the experimental subjects, but I’m assuming normality came bounding back after they recovered their sleep. As to the mechanism of action, Walker describes two options – sleep loss may have blocked the release of insulin by the pancreas, providing no signal for cell absorption to take place, or it may have interfered with the released insulin’s message to the cells. And though it seems that sleep loss probably had an effect on both, it was clear from biopsies taken from subjects that it was the latter, the cells’ lack of response to insulin, their ‘refusal’ to take up the blood glucose, that was the principal problem.
Canto: Just looking at the Sleep Foundation website, and they seem to get things the other way round, that diabetics are suffering from sleep loss. I must say, that, off the top of my head, I’d find being pre-diabetic easier to manage than my sleep behaviour. I mean, I can imagine changing my diet and exercise habits easily enough, but my sleep habits not so much. How do you turn off your brain?
Jacinta: Well, Mr Walker has some suggestions on that, which we’ll explore next time. And by the way, there seems to be tons of videos and websites providing knowledge and advice on the issue, which always makes me feel superfluous to requirements as a human being…
Canto: Well, try not to lose sleep over it.
References
Why we sleep, by Matthew Walker, 2017
https://www.sciencealert.com/scientists-have-worked-out-why-your-eyes-move-when-you-re-dreaming
https://en.wikipedia.org/wiki/Sleep_deprivation
https://www.sleepfoundation.org/physical-health/lack-of-sleep-and-diabetes
covid19 – the European CDC shows the way
poverty and crowding in Peru – BBC picture
Canto: The US response to the pandemic continues to be massively hampered by political muzzling of and interference with the science, especially at the federal level, but the Medcram updates continue to inform us, and to be, or pretend to be, indifferent to this political interference.
Jacinta: Yes, and update 109 has introduced us to the European CDC’s website, which provides us with a wealth of information, on the progress of the pandemic itself in European countries, but also in the political response to it, and how those two things interact.
Canto: The country overview page, and it’s currently updated to week 39 of the pandemic, is as data-rich as anyone can imagine, a statistician’s wet dream, but interpretation of the data needs to be handled carefully.
Jacinta: Dr Seheult does some interpretation of some of the data in his medcram update 109, but there’s so much more in there, and so much more to say. So let’s take a European country at random – Denmark – and look closely at the stats.
Canto: But before that, let’s look at some general European trends they report. It’s fascinating:
By the end of week 39 (27 September 2020), the 14-day case notification rate for the EU/EEA and the UK, based on data collected by ECDC from official national sources, was 113.6 (country range: 9.9–319.9) per 100 000 population. The rate has been increasing for 70 days.
So the EU is the European Union and the EEA is the European Economic Area. I’m not sure what is meant by ’14-day’ but I presume the case notification rate is simply the case rate, as far as they can ascertain from the data supplied to them – the cases they’ve been notified about. It’s good that they make that distinction, shifting the onus on the notifiers. So it’s 113.6 cases per 100,000 population over the whole region, and has been rising for over two months – a second wave.
Jacinta: I think ’14 day’ just means the rate over the previous 14 days. They report every seven days for the previous 14 days, so there’s a 7-day overlap. That data is not only dependent on the reliability of particular reporting countries, it’s also dependent on testing levels, obviously. So in the general trends they tell us which countries are doing the most testing. Highest is Denmark, followed by Luxembourg, Iceland, Malta and Cyprus. Small countries, unsurprisingly.
Canto: With all this, it’s interesting from Dr Seheult’s analysis of the data that the death rate isn’t mapping with the case rate, thankfully, and that the age of people contracting the virus in the second wave is much lower, which seems weird.
Jacinta: Probably explained by an increase in testing since the early days. Now they’re catching milder and asymptomatic cases. It suggests, of course, that the case rate was much higher during the first wave, when the testing regime was still being put together. So let’s look at Denmark, and now we have data for week 40. There are four graphs, and in the first we see the case notification rate experiencing a big bump peaking in April with the death notification rate mapping pretty closely with that bump. Then there’s a gradual falling away in both figures, until August when the case rate starts to rise again, but not the death rate. Then in September that case rate rises very sharply, rising well above the April bump, though in the last week it seems to have leveled off at this high level. But the death rate has stayed pretty well level and quite low. Now that raises questions that the other graphs might help to answer. The second graph looks at the testing rate – tests per 100,000. The testing rate was pretty flat and low from February into April, but after the April rise in cases the testing began to rise from late April into May. It flattened and even dipped a bit into June. It stayed fairly steady through the northern winter, but of course at a high level compared to the earliest period, then it started to rise in August, presumably in anticipation of a rise in cases as the colder weather arrived. That rise in testing peaked at a very high level in late September, but has dropped quite sharply in the the last week or so.
Canto: Interesting, so that does strongly suggest a sharp rise in mild cases being ‘caught’, and presumably dealt with, as the death rate hasn’t spiked at all.
Jacinta: Yes, though we don’t know how well those cases have been dealt with – people are talking about ‘long covid’, people possibly having long-term issues. The two graphs don’t really give us granular detail – hospitalisation rates for example. So the third graph breaks the notified case numbers into age groups, and the results are fascinating. The first wave bump shows that most of the cases recorded were in the older age groups, particular those at 80 or over. There were cases in all age groups, but very few under 15. However, in the second wave, the cases found were predominantly in the young. In fact the 15-24 age group was way out in front, followed by the 25-49 group. Even the under 15s were well above the oldest age groups. So what does this mean? It seems to suggest that the older, and perhaps wiser, are recognising the dangers, especially to their age group, and taking fewer risks, and that the younger are still not very sick but can be carriers of the virus and more than ever a danger to the older generation.
Canto: I wonder is Denmark ‘typical’ in this regard?
Jacinta: There are variations of course, but the general trend is much the same. The fourth graph shows test positivity – the percentage of people who tested positive. There was a massive spike in positive test results in March, up to around 16 -17%, but this dropped as sharply at it rose, due presumably to the rapid rise in testing from that period. By May it was around 1% and it has remained much the same since, as the number of tests administered has never been higher, in spite of the recent drop I mentioned. It’s still much higher than it was pre-September.
Canto: But there are more than four graphs as we’ve found. We’ve looked at the data for notification rates and testing, there are other graphs which look at ICU and hospitalisation rates, public health response measures, and which break the nation down into specific regions.
Jacinta: Yes, it’s particularly important to look at public health measures – restrictions on mass gatherings, closures or partial closures of public spaces, workplaces and schools, the mandating or recommendations around face masks, and map them against notification rates, hospitalisations and so forth. The picture that emerges is generally pretty clear, though sadly some countries, such as the USA and Brazil, aren’t paying heed to the fact that public health measures save lives as well as a lot of suffering.
Canto: Well we should be talking about the governments rather than the countries, when we’re talking about public health measures. So I’ve assumed that the CDC in the USA has been hobbled by the Trump debacle, so I’ve gone to the Johns Hopkins site to see what detailed info they provide. Indeed they do have a lot of useful data both for the USA and other countries, though little on the effect of public health measures. An interesting graph they present on mortality shows that, in terms of deaths per 100,000 persons – and they show only the top 20 nations – Peru is on top, followed by Brazil, Ecuador, Spain, Mexico, the USA and the UK, in that order.
Jacinta: Well we know about the macho governments of Brazil, the UK and the USA – not that government is always entirely to blame, but it’s a key indicator – so what about the national governments of those other countries?
Canto: Well other key indicators would be the country’s wealth, or lack thereof, and its healthcare infrastructure, but as to government, Peru had a federal election in January this year – it’s a multi-multi-multi-party system with the most popular party getting only 10% of the vote. The result was that Martin Vizcarra retained the presidency. He appears to be a genuine reformist who has tried to implement stay-at-home orders, but widespread poverty and overcrowding are major problems there. Brazil we already know about. Ecuador’s current President is Lenin Moreno, a right-wing figure who has slashed government funding and seems obsessed with destroying political opponents. He has a popularity rating of 8%, according to an article in Open Democracy, and his mishandling of the pandemic has been extreme. Spain is a ‘parliamentary monarchy’, and its current Prime Minister is Pedro Sanchez, leader of a leftist coalition. Currently there’s a battle with right-wing local authorities, especially in Madrid, to enforce lockdowns as a second wave hits the country. So it’s the usual problem there of non-compliance, it seems. And Mexico is, as is I think well known, a country with a lot of poverty and a lot of problems. Its governmental system has long been a minefield – in fact I’d love to learn more about its chequered history. Currently the President is Andrés Manuel López Obrador, a veteran politician who has been a member of various parties and is essentially a political centrist. So again it’s about lack of political control, poverty, lack of services, overcrowding and so forth. As to the UK, years of conservative government have gutted the NIH, there has been a ton of mixed messaging from the top… I’m getting sick of all this. I want to go to Taiwan.
Jacinta: Hmm. How’s your Chinese? Things are pretty covid-safe here in South Australia. Here’s hoping a safe and effective vaccine is ready by next year, and some big improvements are made in certain countries, with a return to justice and human decency…
References
Coronavirus Pandemic Update 109: New Data From Europe As COVID 19 Infections Rise
https://www.ecdc.europa.eu/en/covid-19/country-overviews
https://coronavirus.jhu.edu/us-map
https://www.bbc.com/news/world-latin-america-53150808
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31955-3/fulltext
reading matters 11 – encephalitis lethargica. Will it return?
Asleep, by Molly C Crosby, 2010
Canto: This was one of the saddest books I’ve read in a long time. It’s about a disease that arose, and was recognised, at around the time of the ‘Spanish flu’ of 1918, though it was more sporadic and long-lasting, and rather more mysterious. It’s also a kind of cautionary tale for those among us who downplay the impact of diseases and their effects, which are so often long-term and horrifically devastating. It’s humbling to realise that we just don’t know all the answers to the pathogens that strike us down.
Jacinta: And could revisit us, in mutated and perhaps even more deadly form, some time in the future. This book is about encephalitis lethargica, a disease that was personal to the author, as it infected her grandmother, whose entire life, though she lived to a goodly age, was clearly stunted by it. She was struck down at the age of 16, and slept for 180 days, and though she lived almost 70 years afterwards, she was robbed by this brain-blasting illness of the life of the mind, the rising above ourselves and grasping of the world that we’re attempting in this blog. Through sheer bad luck.
Canto: And as Crosby points out, her grandmother was far from being the worst-affected victim of this disease. People died of course, but others were disastrously transformed.
Jacinta: So let’s go to a modern website, a department of the USA’s NIH, the National Institute of Neurological Disorders and Stroke, for a definition:
Encephalitis lethargica is a disease characterized by high fever, headache, double vision, delayed physical and mental response, and lethargy. In acute cases, patients may enter coma. Patients may also experience abnormal eye movements, upper body weakness, muscular pains, tremors, neck rigidity, and behavioral changes including psychosis. The cause of encephalitis lethargica is unknown. Between 1917 to 1928, an epidemic of encephalitis lethargica spread throughout the world, but no recurrence of the epidemic has since been reported. Postencephalitic Parkinson’s disease may develop after a bout of encephalitis-sometimes as long as a year after the illness.
Canto: Yes, and having read Crosby’s book and knowing about the worst symptoms and a few heart-rending cases, the sentence that most strikes me here is, ‘The cause.. is unknown’. Apparently Oliver Sacks’ book Awakenings, which we haven’t read, is all about patients who have ‘awakened’, permanently damaged, from this bizarre disease, and that’s a book we now must read, though of course it will provide us with no solutions.
Jacinta: And no arms against its future devastation, should it return – and why wouldn’t it? Crosby and others have suggested that ‘fairy stories’ like Sleeping Beauty and Rip van Winkle may have been inspired by outbreaks of the disease. Of course this is conjecture, and only if the disease returns will we be able to attack it with the technology we’ve developed in the intervening century. As the neurologist Robert Sapolsky points out in his mammoth book Behave, (so mammoth that I can’t find the quote), the number of papers published on the brain, its activity and functions, in the 21st century, has grown exponentially. We might just be ready to counteract the long term horrors of encephalitis lethargica next time round, if it comes around.
Canto: Crosby’s book is organised into case histories, featuring people who fell into this bizarre torpid state for long periods, and when aroused, often behaved in anti-social and self-destructive ways that in no way resembled depression, between bouts of a ‘normality’ that was never quite normal. And one of the saddest features of these case histories, richly described in the notes of famous figures in early neuropsychology, such as Constantin von Economo, Smith Ely Jellife and Frederick Tilney, is that the victims disappeared into the void once it became clear that no known treatment could save them.
Jacinta: Yes, some may have died soon afterward, others may have lived on in a limbo, locked-in state for decades. In fact the symptoms of this disease were bewilderingly varied -various tics, hiccupping, catatonia, salivation, schizoid episodes… Encephalitis literally means swelling of the brain, and it doesn’t take a medical degree to realise this could cause a variety of effects depending on which area of the most complex organism known to humanity is most affected.
Canto: Encephalitis is usually caused by viruses, and of course viruses hadn’t been fully conceptualised when von Economo wrote his 1917 paper on what was to become known as encephalitis lethargica, as the role of DNA and RNA was unknown. However, von Economo was the first to recognise the vital role of a tiny, almond-shaped section near the base of the brain, the hypothalamus, in the distorted sleep patterns of these patients. He also wondered if there was a connection between the so-called Spanish flu and this sleeping sickness.
Jacinta: Yes, and this brings to mind the current nightmare pandemic. People, including of course epidemiologists, are wondering about the long-term effects of this virus, especially in those who seem to have recovered from a serious infection. Crosby writes of the situation a hundred years ago:
The war had provided the first opportunity encephalitis lethargica had to crawl across the world with little notice from the medical community. And by 1918, the pandemic flu had given it the second opportunity, stealing worldwide attention, infecting and killing millions. Epidemic encephalitis moved with the flu, almost like a parasite to a host, often attacking many of the same victims, receiving very little notice at all.
Of course there has been no sign of a return of encephalitis lethargica – as yet – from a medical community that is somewhat forewarned, but it’s clear that inflammation can have very diverse effects, especially when it involves the brain.
Canto: But it’s like an undefeated enemy that has gone into hiding. We’ve defeated smallpox; tuberculosis and polio are in heavy retreat; leprosy seems as remote to us as the Bible, but this sleeping sickness, some of the victims of which have died within our lifetimes, has tantalised us with its bizarre and devastating effects, but has never really given us a chance to fight it.
Jacinta: Yes fighting is what it’s all about. The anti-vaxxers and the natural health crowd seem to want to leave everything to our immune system, to let diseases take their course, killing and maiming a substantial percentage of the herd to let the remainder grow stronger. If they were to read some of these case studies, to witness the lives of young Rosie, Adam and Ruth, they would surely think differently, if they had a modicum of humanity.