a one-sided view (the left) of the parts of the brain involved in language and reading processing
Canto: So we’re still looking at automaticity, and it’s long been observed that dyslexic kids have trouble retrieving names of both letters and objects from age three, and then with time the problem with letters becomes more prominent. This means that there just might be a way of diagnosing dyslexia from early problems with object naming, which of course starts first.
Jacinta: And Wolf is saying that it may not be just slowness but the use of different neural pathways, which fMRI could reveal.
Canto: Well, Wolf suggests possibly the use of right-hemisphere circuitry. Anyway, here’s what she says re the future of this research:
It is my hope that future researchers will be able to image object naming before children ever learn to read, so that we can study whether the use of a particular set of structures in a circuit might be a cause or a consequence of not being able to adapt to the new task of literacy (Wolf, p181).
So that takes us to the next section: “An impediment in the circuit connections among the structures”.
Jacinta: Connections between. And if we’re talking about the two hemispheres, the corpus callosum could’ve provided a barrier, as it does with stroke victims…
Canto: Yes, connections within the overall reading circuit, which involves different parts of the brain, can be more important for reaching automaticity than the brain regions themselves, and a lot of neuroscientists are exploring this connectivity. Apparently, according to Wolf, three forms of disconnections are being focussed on by researchers. One is an apparent disconnection ‘between frontal and posterior language regions, based on underactivity in an expansive connecting area called the insula. This important region mediates between relatively distant brain regions and is critical for automatic processing’ (Wolf, p182). Another area of disconnection involves the occipital-temporal region, also known as Brodmann area 37, which is activated by reading in all languages. Normally, strong, automatic connections are created between this posterior region and frontal regions in the left hemisphere, but dyslexic people make connections between the left occipital-temporal area and the right-hemisphere frontal areas. It also seems to be the case that in dyslexics the left angular gyrus, accessed by good beginning readers, doesn’t effectively connect with other left-hemisphere language regions during reading and the processing of phonemes.
Jacinta: And it’s not just fMRI that’s used for neuro-imaging. There’s something called magnetoencephalography (a great word for dyslexics) – or MEG – that gives an ‘approximate’ account of the regions activated during reading, and using this tool a US research group found that children with dyslexia were using a completely different reading circuitry, which helps explain the underactivity in other regions observed by other researchers.
Canto: And leads to provocative suggestions of a differently arranged brain in some people. Which takes us to the last of the four principles: ‘a different circuit for reading’. In this section, Wolf begins by recounting the ideas of the neurologists Samuel T Orton and Anna Gillingham in the 1920s and 1930s. Orton rejected the term ‘dyslexia’, preferring ‘strephosymbolia’. Somehow it didn’t catch on, but essentially it means ‘twisted symbols’. He hypothesised that in the non-dyslexic, the left-hemisphere processes identify the correct orientation of letters and letter sequences, but in the dyslexic this identification was somehow hampered by a problem with left-right brain communication. And decades later, in the 70s this hypothesis appeared to be validated, in that tests on children in which they were given ‘dichotic tasks’ – to identify varied auditory signals presented to different ears – revealed that impaired readers didn’t use left-hemisphere auditory processes in the same way as average readers. Other research showed that dyslexic readers showed ‘right-hemisphere superiority’, by which I think is meant that they favoured the right hemisphere for tasks usually favoured by the left.
Jacinta: Yes, weakness in the left hemisphere for handling linguistic tasks. But a lot of this was dismissed, or questioned, for being overly simplistic. You know, the old left-brain right-brain dichotomy that was in vogue in popular psychology some 30 years ago. Here’s what Wolf, very much a leading expert in this field, has to say on the latest findings (well, circa 2010):
In ongoing studies of the neural of typical reading, the research group at Georgetown University [a private research university in Washington DC] found that over time there is ‘progressive disengagement’ of the right hemisphere’s larger visual recognition system in reading words, and an increasing engagement of left hemisphere’s frontal, temporal, and occipital-temporal regions. This supports Orton’s belief that during development the left hemisphere takes over the processing of words (Wolf, p185).
Canto: Yes, that’s ‘typical reading’. Children with dyslexia ‘used more frontal regions, and also showed much less activity in left posterior regions, particularly in the developmentally important left-hemisphere angular gyrus’. Basically, they used ‘auxiliary’ right-hemisphere regions to compensate for these apparently insufficiently functional left regions. It seems that they are using ‘memory’ strategies (from right-hemisphere structures) rather than analytic ones, and this causes highly predictable delays in processing.
Jacinta: A number of brain regions are named in this explanation/exploration of the problems/solutions for dyslexic learners, and these names mean very little to us, so let’s provide some – very basic – descriptions of their known functions, and their positions in the brain.
Canto: Right (or left):
The angular gyrus – which, like all other regions, is worth looking up on google images as to placement – is in a sense divided in two by the corpus callosum. Described as ‘horseshoe-shaped’, it’s in the parietal lobe, or more specifically ‘the posterior region of the inferior parietal lobe’. The parietal lobes are paired regions at the top and back of the brain, the superior sitting atop the inferior. The angular gyrus is the essential region for reading and writing, so it comes first.
The occipital-temporal zone presumably implies a combo of the occipital and temporal lobes. The occipital is the smallest of the four lobes (occipital, temporal, parietal, frontal), each of which is ‘sided’, left and right. The junction of these two lobes with the parietal (TPO junction) is heavily involved in language processing as well as many other high-order functions.
Jacinta: Okay, that’ll do. It’s those delays you mention, the inability to attain automaticity, which characterises the dyslexic, and it appears to be caused by the use of a different brain circuitry, circuitry of the right-hemisphere. Best to quote Wolf again:
The dyslexic brain consistently employs more right-hemisphere structures than left-hemisphere structures, beginning with visual association areas and the occipital-temporal zone, extending through the right angular gyrus, supramarginal gyrus, and temporal regions. There is bilateral use of pivotal frontal regions, but this frontal activation is delayed (Wolf, p186).
Canto: The supramarginal gyrus is located just in front of and connected to the angular gyrus (a gyrus is anatomically defined as ‘a ridge or fold between two clefts on the cerebral surface in the brain). These two gyri, as mentioned above, make up the inferior parietal lobe.
Jacinta: Wolf describes cumulative research from many parts of the world which tends towards a distinctive pattern in dyslexia, but also urges skepticism – the human brain’s complexity is almost too much for a mere human brain to comprehend. No two brains are precisely alike, and there’s unlikely to be a one-size-fits all cause or treatment, but explorations of this deficit are of course leading to a more detailed understanding of the brain’s processes involving particular types of object recognition, in visual and auditory terms.
Canto: It’s certainly a tantalising field, and we’ve barely touched on the surface, and we’ve certainly not covered any, or very much of the latest research. One of the obvious questions is why some brains resort to different pathways from the majority, and whether there are upsides to offset the downsides. Is there some clue in the achievements of people known or suspected to be have been dyslexic in the past? I feel rather jealous of those researchers who are trying to solve these riddles….
References
Maryanne Wolf, Proust and the squid: the story and science of the reading brain, 2010
Q Canto: So the next hypothesised basic source of dyslexia is ‘a failure to achieve automaticity’, that’s to say the sort of rapid, more or less unconscious processing of sounds into letters and vice versa, which probably means effective connection between brain regions or structures.
Jacinta: Perhaps because one of the structures is somehow internally dysfunctional.
Canto: wYes, and it often begins with vision. Researchers have found that many dyslexic individuals couldn’t separate two rapidly succeeding visual flickers as clearly as other individuals – an apparent processing problem. Similar research with dyslexic children found that, though they could identify stimuli initially as well as the non-dyslexic, they fell behind with added complexity and speed. This occurred more or less equally whether the stimuli were aural or visual. The connections just didn’t come ‘naturally’ to them.
Jacinta: So what about the connection between language – I mean speech, which is tens of thousands of years old – and reading and writing, a much newer development for our brains to deal with? Do dyslexic people have problems with processing good old speech? Are they slower to learn to talk?
Canto: Yes, a good question. Wolf describes research in which children with dyslexia in a number of languages, including English, ‘were less sensitive to the rhythm in natural speech, which is partly determined by how the sounds in words change through stress and ‘beat patterns’’ (Wolf, p177). Others have found breakdowns in processing in various motor tasks involving hearing and seeing. That’s to say, in the automaticity of such tasks. One psychologist who studies dyslexic children found an extensive range of problems with processing speed, especially a time gap or asynchrony between visual and auditory processing, and this observation has become commonplace.
Jacinta: But does this relate specifically to learning to speak? I’ve heard that Einstein was slow at that as a child.
Canto: Yes it’s said that he didn’t learn to speak full sentences before the age of five. But here we’re just talking about ‘naming speed’, and how it appears to use the same neurological structures as reading, as problems with one is predictive of problems with the other.
Jacinta: And the problem isn’t so much with naming per se, but the speed, the gap.
Canto: Yes, the lack of automaticity. Neurologists working in this field have developed ‘rapid automised naming’ (RAN) tasks which have become the most effective predictors of reading performance, regardless of language. Wolf herself has developed a refinement, rapid alternating stimulus (RAS), which, as the name suggests, gives more weight to attention-switching automaticity. Here’s an interesting quote from Wolf:
If you consider that the whole development of reading is directed toward the ability to decode so rapidly that the brain has time to think about incoming information, you will understand the deep significance of those naming speed findings. In many cases of dyslexia, the brain never reaches the highest stages of reading development, because it takes too long to connect the earliest parts of the process. Many children with dyslexia literally do not have time to think in the medium of print.
Jacinta: It makes me think of the unconscious, but not the Freudian one. A processing that you don’t have to think about. So that you can think about the info, not the form that encapsulates it.
Canto: Yes, and none of this explains why some have these problems with automaticity – which brings us back to neurology. Are dyslexic individuals using a different circuit from the rest of us, and does this explain their skills and abilities in other areas? Remember the names – Einstein, da Vinci, Gaudi, Picasso… not that dyslexia guarantees genius or anything…
Jacinta: Yes, far from it, I’d say, but it’s a fascinating conundrum.
Canto: So, neurology. And this takes us to how the ‘reading brain’, a very new phenomenon, evolutionarily speaking, came into being. fMRI images appear to confirm hypotheses that the brain ‘uses older object recognition pathways in the occipital-temporal zone (area 37) to name both letters and objects’ (Wolf, p179). It’s a process described as ‘neuronal recycling’. And it takes us to brain regions associated with particular tasks. For example, the left occipital-temporal area is apparently more associated with object naming, a much older task, evolutionarily speaking, than letter naming, and one that takes up more cortical space. The more streamlined, specialised use of this region for letters, and the development of automaticity for that purpose, is a prime example of our much-vaunted neuroplasticity.
Jacinta: What they’ve called RAN is always faster for letters than objects – that’s perhaps because letters are a small, even quite tiny subset of the near-infinite set of objects.
Canto: Yes, and here I’m going to quote a difficult passage by Wolf at some length, and then try, with your help, to make sense of it:
…culturally invented letters elicit more activation than objects in each of the other ‘older structures’ (especially temporal-parietal language areas) used for reading in the universal reading brain. This is why measures of naming speed like RAN and RAS predict reading across all known languages. It is also why, side-by-side, the brain images of the object- and letter-naming tasks are like comparative evolutionary photos of a pre-reading and post reading brain (Wolf, p181).
Jacinta: So this is a bit confusing. Culturally invented letters are new, evolutionarily speaking. And there are older language structures used for reading. Repurposed? Added onto? A bit of renovation? And what exactly is ‘the universal reading brain’?
Canto: Good question, and a quick internet research reveals much talk of a ‘universal reading network’. Here’s a fascinating abstract from a 2020 study, some ten years after the publication of Wolf’s book. It’s entitled “A universal reading network and its modulation by writing system and reading ability in French and Chinese children”:
Are the brain mechanisms of reading acquisition similar across writing systems? And do similar brain anomalies underlie reading difficulties in alphabetic and ideographic reading systems? In a cross-cultural paradigm, we measured the fMRI responses to words, faces, and houses in 96 Chinese and French 10-year-old children, half of whom were struggling with reading. We observed a reading circuit which was strikingly similar across languages and consisting of the left fusiform gyrus, superior temporal gyrus/sulcus, precentral and middle frontal gyri. Activations in some of these areas were modulated either by language or by reading ability, but without interaction between those factors. In various regions previously associated with dyslexia, reading difficulty affected activation similarly in Chinese and French readers, including the middle frontal gyrus, a region previously described as specifically altered in Chinese. Our analyses reveal a large degree of cross-cultural invariance in the neural correlates of reading acquisition and reading impairment.
So this research, like no doubt previous research, identifies various brain regions associated with reading ability and impairment, and finds that the same automacity, or lack thereof, is associated with the same regions, such as the middle frontal gyrus, in both alphabetic and ideographic reading systems. I think this is further confirmation of the research work Wolf is citing. Of course, I don’t know much about these brain regions. A course in neurology is required.
Jacinta: But what Wolf appears to be saying in that earlier quote is that you can get brain images (via fMRI) of object naming (older brain) tasks and put them side by side with images of letter naming tasks (younger brain), and it’s like seeing the results of evolution. Sounds a bit much to me. I suppose you can see a different pattern. Isn’t fMRI based on the magnetism of iron in the blood?
Canto: Yes yes. This is complex, but of course it’s true that the neural networking required for reading and writing is much more recent than that for language – and remember that of the 7000 or so languages we know of, only about 300 have a written form, which suggests that the Aborigines, before whities arrived, and the Papua-New Guineans, who have about 700 different languages on their island, were unable to even be dyslexic, or were all dyslexic without knowing it, or giving a flying fuck about it, because they had no writing, and no wiring for reading it.
Jacinta: So it would be interesting, then, to scan the brains of those language users – and there are no humans who aren’t language users – who don’t have writing. Take for example the Australian Aborigines, who became swamped by white Christian missionaries determined to ‘civilise’ them, more or less overnight in evolutionary terms, through teaching them to read and write. And then would’ve been characterised as backward for not picking up those skills.
Canto: That’s an interesting point, but it’s the same even in ‘cradles of civilisation’ such as Britain, where the vast majority were illiterate, and encouraged to be so, 500 years ago. At that time the printing press was a new-fangled device, church services were mostly conducted in Latin, and it was convenient to keep the peasantry in ignorance and in line. And yet, when it became more convenient to have a literate population, the change appears to have been relatively seamless, dyslexia notwithstanding. So it seems that, from a neurological perspective, little change was required.
Jacinta: Yes, that’s a good point, and it points to brain plasticity. Curiouser and curiouser – so it’s not so much about evolution and genes, but relatively rapid neural developments…. to be continued…
Jacinta: So we’re going to look at earlier ideas about dyslexia, before the recent revolution in neurology, if that’s not being too hyperbolic. These ideas tended to focus on known systems, before there were well-identified or detailed neural correlates. ‘Word-blindness’ was an early term for dyslexia, highlighting the visual system. This was partly based on the 19th century case of a French businessman and musician who, after a stroke, could no longer read words or musical notes or name colours. A second stroke worsened the situation considerably, eventually causing his death.
Canto: An autopsy revealed that the first stroke had damaged the left visual area and part of the corpus callosum, which connects the two hemispheres. It appears that what the man was seeing with his right hemisphere was not able to be ‘backed up’ by the left visual area, and/or connected to the left language area. The second stroke struck mainly the angular gyrus, a complex and vital integrating and processing region towards the back of the brain.
Jacinta: Yes, and before we go on, what we’re doing here is looking in more detail at the four potential sources of dyslexia set down at the end of the previous post. So in this post we’re focusing on 1. a developmental, possibly genetic, flaw in the structures underlying language or vision.
Canto: Right, so there’ll be three more dyslexia posts after this. So this ‘Monsieur X’ case was one of ‘classic alexia’ or acquired dyslexia, and marked an important step forward in mapping regions in relation to the visual and processing aspects of language. Norman Geschwind described it as ‘disconnection syndrome’, when two brain regions essential to a function, in this case written language, are cut off from each other.
Jacinta: The auditory cortex became an important focus in the twentieth century, as researchers noted a problem with forming ‘auditory images’ – which sounds like a problem everyone would have! More specifically it means not being able to translate the images made by letters and phonemes into sounds.
Canto: Yes, so that a word like ‘come’ (which is actually quite complex – the hard ‘k’ followed by an ‘o’ which, orally, is neither the typically short nor long version, followed finally by the silent ‘e’ which has some quite strange effect on the previous vowel) would be quite a challenge. Perhaps the real surprise is that we have no trouble with it.
Jacinta: Yes, I prefer cum myself, but that’s a bit off-topic. Anyway, psycholinguistics, much derived from the work of Noam Chomsky, which came into prominence from the 1970s, tended to treat dyslexia more as specifically language-based rather than audio-visual. Taking this perspective, researchers found that ‘reading depended more on the linguistically demanding skills of phonological analysis and awareness than on sensory-based auditory perception of speech sounds’ (Wolf, p173). This was evidenced by the way impaired-reading children treated ‘visual reversal’ in letters (e.g p and q, b and d). They were able to draw the letters accurately, but had great trouble saying them (sounding them). This appears to be a spoken language problem, which carries over to writing.
Canto: Indeed, it highlighted a problem, which apparently had nothing to do with intelligence, or basic perception, but was more of a specific perception-within-language thing:
These children cannot readily delete a phoneme from the beginning or end of a word, much less from the middle, and then pronounce it; and their awareness of rhyme patterns (to decide whether two words like ‘fat’ and ’rat’ rhyme or not) develops much more slowly. More significantly, we now know that these children experience the most difficulties learning to read when they are expected to induce the rules of correspondence between letters and sounds on their own.
Phonological explanations of dyslexia have resulted in a lot of effective remedial work in recent decades, and a library of research in the field of reading deficits.
Jacinta: Yes, these are called structural hypotheses, noting deficits in awareness of phonemic structure, and phoneme-grapheme correspondences. And these deficits presumably have their home in specific neural regions and wiring. The executive processes of the frontal lobes may be at play, in terms of organised attention, the fixing of memory and the monitoring of comprehension, but also the more ‘basic’ processes of the cerebellum, involving timing and motor coordination. And co-ordination between these regions may also be an issue.
Canto: And, as Wolf points out, these structural hypotheses have sheeted home problems to so many brain regions – the frontal executive function region, the speech region close by, the central auditory region, the language and language/visual integration regions, the posterior visual cortex and the cerebellum – that it would be fair to say that ‘many of the collective hypothesised sources of dyslexia mirror the major component structures of the reading brain’ (Wolf, p176).
Jacinta: Which sounds pretty serious. Why is it happening? And why not for others…?
References
M Wolf, Proust and the squid: the story and science of the reading brain
Canto: So I’ve been reading Proust and the squid, by Maryanne Wolf, a book I bought back in 2010, when it was published, and apparently read at the time, though I remember very little about it. Did I really read it? I suspect I didn’t finish it. Anyway, it’s subtitled Science and the reading brain, and since we do a lot of reading, mostly still in the old-fashioned way (stuff written on paper), the subject is of obvious interest.
Jacinta: Yes, it’s interesting to reflect that though writing, of various types, came into being four to five thousand years ago, it’s only in the last few centuries that reading has become anything like universally adopted. And our brains have had to adapt to reading…
Canto: Yes, think of reading to ourselves, in a language that’s based on sound. Which not all languages are, if I’m not mistaken. So I imagine that non-phonological languages (is that a meaningful term?) use the brain in a different way…
Jacinta: It’s more complicated than that – for example, there’s a difference between phonetics and phonemics, in which the letter ‘t’ is sounded differently depending on its place within a word and what letters surround it, for example in ‘th’ words, and that phoneme is sounded differently, for example in ‘the’ and in ‘beneath’, if you listen carefully. We generally don’t notice these differences until they’re pointed out to us. And the English language is full of them. Phonemes can be divided into allophones, as they’re called. But getting back to dyslexia…
Canto: Well, first it needs to be made clear that dyslexia has nothing to do with lack of intelligence. Both Einstein and Leonardo da Vinci, the names most often trotted out as examples of genius, were likely dyslexic, or maybe I should say they suffered from some form of dyslexia – because it’s really really complex and multi-faceted, and seems to involve right-left brain differences. The last two chapters of Wolf’s book, ‘Dyslexia’s puzzle and the brain’s design’ and ‘Genes, gifts and dyslexia’, are fiendishly difficult for someone like me, with very little background in neurology, but fascinating, and I think it’ll take several posts to cover not only what’s in the book but the ongoing research since it was written.
Jacinta: Yes that reminds me of Sapolsky’s statement in Behave, that more neurological papers have been published in the 21st century than in all previous centuries combined – and that book was published five years ago.
Canto: Well, it’s not surprising, it’s a burgeoning area of research, looking for neural co-ordinates for various disabilities, proficiencies, tendencies… As well as genetic correlations. And epigenetic too, maybe. Anyway, to begin somewhere, Wolf describes a hypothesis that derives from the thinking of a famous and apparently prophetic 20th century neurologist, Norman Geschwind:
The genes that form the basis for a strengthened right hemisphere could have been highly productive in preliterate societies, but when these same genes are expressed within a literate society, they put structures in the right hemisphere in charge of the precise, time-based functions of reading. These functions would then be performed in the unique ways of the right hemisphere, rather than in the more precise, time-efficient ways of the left hemisphere. In the case of reading, that situation would lead inevitably to difficulties.
M Wolf, Proust & the squid: the story and science of the reading brain, pp205-6
Now, I had no idea that the left hemisphere was more precise and time-efficient than the right…
Jacinta: But this quote doesn’t quite make sense to me. We’re all descended from pre-literate societies after all, so with ‘highly productive right hemispheres’. And then, when literacy came along – what? The right hemisphere took on these ‘precise, time-based functions of reading’ in its ‘unique way’, when it would’ve been better to use the left hemisphere, which is better adapted for the purpose, apparently. Wouldn’t this make us all a bit dyslexic?
Canto: Yes, maybe that’s the point. But there’s also no doubt that the reading brain – which may one day become obsolete in the digital and post-digital world – has transformed our society more or less completely. So having serious reading/writing deficits can be a major problem, perhaps especially for highly intelligent people who might feel the disadvantage more.
So dyslexia, as the word suggests, is a broad and negative term which essentially covers all deficiencies in grasping and producing written text. Wolf presents, inter alia, the definition of The International Dyslexia Association:
Dyslexia is a specific learning disability that is neurological in origin. It is characterised by difficulties with accurate and/or fluent word recognition and by poor spelling and decoding abilities. These difficulties typically result from a deficit in the phonological component of language that is often unexpected in relation to other cognitive abilities and the provision of effective classroom instruction. Secondary consequences may include problems in reading comprehension and reduced reading experience that can impede growth of vocabulary and background knowledge.
Note that the only reference to causes here is that it’s ‘neurological in origin’.
Jacinta: Well mention has been made about right and left sides of the brain – does it get any more specific?
Canto: Of course – but as one researcher points out, dyslexia isn’t a reading disorder, as there are no reading centres in the brain. It’s rather a disorder in one or more regions of the brain that have been co-opted for reading and writing. Wolf describes a pyramid of nested connections regarding the disorder. First we observe a behavioural problem, in the act of getting words wrong in reading and writing, or an abnormal slowness and struggle in gaining proficiency in acquiring those skills. Next comes the observation of a pattern of disability, such as seeing/writing/speaking particular letters or phonemes incorrectly. Then there’s the connection between these deficits and neural structures. The next step is homing in on particular neurons and neural circuits, and finally taking this back to the level of particular genes.
Jacinta: But there aren’t any specific genes are there?
Canto: Well, not in the sense of genes for height or eye colour, or even language, which may go back to the earliest Homo sapiens. Literacy is a cultural invention. To quote Wolf:
Across all written languages, reading development involves: a rearrangement of older structures to make new learning circuits; a capacity for specialisation in working groups of neurons within these structures for representing information; and automaticity – the capacity of these neuronal groups and learning circuits to retrieve and connect this information at nearly automatic rates.
M Wolf, Proust and the squid, p 170
Genes aren’t specifically mentioned here – but neurologists are understandably asking whether this ‘rearrangement of older structures’, and possible failures in this rearrangement, have a genetic basis, just as the development of language itself presumably has (though this development too is shrouded in mystery). Wolf goes on to outline four ‘potential basic sources for dyslexia’. I’m going to set them down here because, frankly, I barely understand them. See what you make of them.
a developmental, possibly genetic, flaw in the structures underlying language or vision (e.g. a failure of working groups to learn to specialise within those structures)
a problem achieving automaticity – in retrieving representations within given specialised working groups, or in the connections among structures in the circuits, or both
an impediment in the circuit connections between and among these structures
the rearrangement of a different circuit altogether from the conventional ones used for a particular writing system
Jacinta: Hmmm. I don’t know what she means by ‘working groups’ – of neurons? The fourth one is the only one that I half comprehend. That some forms of dyslexia have harnessed a different circuit which isn’t quite as effective but gets there in the end? Or not?
Canto: Yes, on reflection I half-comprehend the others, and see them as rather connected. For example, failure to achieve automaticity sounds similar to having an impediment in the connections. With some it feels seamless – or doesn’t feel anything at all. I can’t remember ever learning to read or having problems with it, and loved school spelling bees, being very good at them. Anyway, Wolf elaborates on each of these four principles, and I think we should try to follow them in the next blog post. We’ll be better human beings for the process, I’m sure. Because, difficult though it is, I’ve found this to be one of the most intriguing and stimulating books I’ve read for some time.
Jacinta: Okay, let’s go for it.
References
Maryanne Wolf, Proust & the squid: the story and science of the reading brain, 2010
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, quellesurprise!
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.
Which, haha, introduces new terms, sorry. It never ends with his stuff.
Canto: You’re not kidding. The more metabolically active the cells? Okay, I sort of get that – major cellular activity requires more energy and creates more waste materials. Arterioles? No relation to arseholes, presumably?
Jacinta: Don’t know about the etymology, but arterioles are small blood vessels between arteries and capillaries. They control blood pressure to some degree by changing diameter, through some kind of muscular system.
Canto: Okay – I know we’re getting away from lymph a bit, but so many new terms – vascular shunts? venules?
Jacinta: Vascular shunts are explained above, sort of, and venules are like arterioles… Think a three-tiered system of traffic going towards the heart (capillaries to venules to veins) and coming from it (arteries to arterioles to capillaries). And vascular shunts… well, here’s another quote to confuse us:
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…
Canto: We’ve been watching US politics with a kind of painful obsessiveness, I suppose because it’s more colourful, but not in a particularly good way, than anything we experience in Australia. The Presidential system is largely a shocker, and should be best jettisoned altogether, IMHO, but that’ll never happen. The USA is exceptional only in its jingoism and its religiosity, as I’ve said many times and oft, and that is best seen in its attitude to its political system and its Dear Leader…
Jacinta: Well the thing is, before the advent of Trump we paid scant attention to the details of the US political system, but since the election of someone so obviously incapable of running a public toilet let alone a barely inhabited country, to the position of President of the most militarily and economically powerful nation on the planet, we’ve set ourselves on a steep learning curve.
Canto: Or we’re just watching like ghouls at a smouldering train wreck. By the way, I should point out that Russia has slightly more nuclear warheads than the USA (though as to the comparative cumulative power of those sets of warheads I’m not sure), though doubtless their non-nuclear materiel and personnel are far superior. And as for their economy, yes they have the world’s largest GDP, collectively (though I’m sure that’s an over-simplifying measure), but Ireland’s per capita GDP is quite a bit higher!
Jacinta: Yes I think per capita GDP is a better measure of economic success, but then you’d have to realise that’s just total GDP divided by population – doesn’t tell us about how the wealth is distributed. But it’s interesting to compare the USA with Australia, which has a similar land mass, especially if you exclude Alaska. The population of the USA is about 14 times that of Australia, and it’s not because the superiority of the USA’s ingenious people and political system has made it a magnet for immigrants. Most of Australia has infamously poor soil and climate for agriculture, as white colonists soon discovered, and it’s much further from Europe than the so-called New World is. We call ourselves ‘the lucky country’, dog knows why – presumably because every nation has to find or invent something positive to sing about itself, aka nationalism, but the fact is that Europeans found it very difficult to establish themselves here. We don’t have any records about the Aboriginal population that arrived here some 50,000 years ago, but my guess is that it was a slow, painstaking learning process, even if the climate was very different then.
Canto: So getting back to that steep learning curve, what the advent of Trump taught us was that, indeed, anyone can become the USA’s Dear Leader, even a tantrumming man-child who’s likely never read a book in his life and has spent the last fifty-odd years grifting, bullshitting and fucking people around. And what does that say about the USA?
Jacinta: And can it happen here? The reason that it’s unlikely to happen in Westminster-style countries like Australia, New Zealand, Canada and of course Britain is that a political leader first has to win his own local seat, then has to win over her political colleagues with her abilities – her understanding of policy, her articulacy, her charisma or je ne sais quoi, and so forth – which isn’t to say that a bunch of reasonably sophisticated pollies can’t be taken in by a pig-ignorant narcissist posing as one of their own – it’s just a lot less likely.
Canto: Yes, your point is that we don’t have a system where a wannabe demagogue can go straight to the people, bypassing parties, policies and local elections in an effort to be king for a few years. And we certainly don’t have a system which gives that demagogue/king massive pardoning powers, wholesale immunity, a White Palace to live in, and hand-picked courtiers in charge of foreign affairs, federal law, the treasury, the defence of the realm and dog knows what else.
Jacinta: And yet… with all the leeway given to Trump, I’m still amazed that someone so obviously a charlatan to us could have fooled so many into thinking he, of all people, would make a good leader, would somehow improve their lives, make their country ‘great’ in some vague way. Admittedly those people were never in the majority, he has never won an election on the numbers alone, but still a very substantial number were taken in by him. And still are.
Jacinta: There were probably some who thought him a useful idiot for their purposes – for example, libertarians who saw him as the sort of wrecker of government they were looking for – but their numbers wouldn’t have been that great. It’s a worry, but again it’s the US political system that’s largely at fault. As I said, the reason it’s unlikely to happen here isn’t because our population is smarter or less easily swayed by demagogues – it’s because of the checks and balances of our system. A Trump-like figure would have to persuade his political peers long before he tried to persuade the people. And if he couldn’t do that, he wouldn’t be in a position to go ‘to the people’. And of course we don’t do political rallies like United Staters do.
Canto: In any case, the Trump saga is becoming increasingly entertaining for us here in the peanut gallery, with a number of indictments converging upon him. Let me see – there’s the hush payments that Cohen was sentenced to three years’ jail for, and ‘individual one’, Trump, was regularly mentioned in the paperwork. It was obvious that Cohen only did it for Trump, so Trump should’ve gotten a much stiffer sentence than three years – at the time. Immunity for political leaders is total shite, and justice delayed is justice denied. I mean, duh!!!
Jacinta: Okay, calme-toi, better late than never. So that’s a biggie, and pretty much an open-and-shut case. Then there’s the classified docs case, which also looks straightforward, and looks even worse for him after recent revelations that he was personally involved in obstructing those trying to recover the documents. Again this is a jailable offence even without the obstruction, and Jack Smith, the DoJ’s Special Counsel, has himself handled lesser cases involving this crime, which have resulted in prison sentences. He’s also faced with a rape case brought against him by E Jean Carroll – in fact, now two cases involving rape and defamation, as the presiding judge refused to put them under one umbrella. You’ll be pleased to know that the defamation matter seems to hinge on whether the Dear Leader had immunity about what he said while holding office.
Canto: Yeah, despicable. So we’ve mentioned three, and there are at least two more – or no, three. There’s the investigation into Trump.org, which he can hardly be said to be innocent of. And then there’s the Fulton County case of election interference, which again looks open-and-shut, and of course the whole January 6 insurrection, resulting in well over 1000 people being charged thus far. And how involved was he in the fake electors scheme? It all makes me feel quite dizzy, in a pleasant way.
Jacinta: Meanwhile, there seems to be no appetite for diluting Presidential power or changing their system, or any realisation that it’s the screamingly obvious problem that outsiders see it as being.
Canto: And most of the current Republican leadership seem to be supporting Trump! How can that nation ever recover from this disaster? My view has long been that Biden (now 80 years old) should have declared himself a one-term President ages ago. They need renewal, to get over all this…
Jacinta: Yes, age limits might be a good idea. But I don’t want to be ageist – Biden has a lot of experience, and he’s surrounded himself with a very competent team, to be fair. Still, limiting all Presidential terms to four years would be an excellent reform, methinks.
Canto: The good thing, re Trump, is that they’re much more prepared now against his shenanigans. Let the court cases begin! The next year or so will be most memorable for Trumpworld.
Canto: So in the last post, lymph glands, or nodes or whatever, got a passing mention, and I realise I’ve lived a pretty full lifetime without having much of an idea of this substance – is it a solid, liquid or gas, or is it delightfully ethereal, like qi?
Jacinta: Okay, let’s explore. The Better Health Channel, an Australian website, manages to give a point by point summary of the lymphatic system without really explaining what lymph actually is. For example, here are a couple of points that come close, but not very….
The lymph nodes monitor the lymph flowing into them and produce cells and antibodies which protect our body from infection and disease.
It maintains fluid levels in our body tissues by removing all fluids that leak out of our blood vessels.
From which we can deduce that it’s a fluid, since it flows.
Canto: The book we’ve been reading on CFS and its symptoms gives, en passant, this useful information on lymph nodes:
The lymph nodes are tender in multiple areas, such as in the front and back of the neck, armpits, elbows and groin…. One of the most characteristic symptoms is pain in the sub-auricular lymph nodes, the nodes located under the ear and behind the angle of the jaw.
Jacinta: Wow, they bin everywhere. And yes it does sound a bit like qi, some energy force that just needs to be needled at the nodes.
Canto: Time for some science. Lymph comes from Latin, lympha, ‘water’. So, very fluid. Here’s what Wikipedia says on its structure:
Lymph has a composition similar but not identical to that of blood plasma. Lymph that leaves a lymph node is richer in lymphocytes than blood plasma is. The lymph formed in the human digestive system called chyle is rich in triglycerides (fat), and looks milky white because of its lipid content.
Which sounds like the lymph nodes are where lymphocytes are produced. Lymphocytes are a type of leukocyte or white blood cell.
Jacinta: Well, here’s what I’ve come up with, to start things off.
The lymphatic system is the system of lymphoid channels and tissues that drains extracellular fluid from the periphery via the thoracic duct to the blood. It includes the lymph nodes, Peyer’s patches, and other organized lymphoid elements apart from the spleen, which communicates directly with the blood.
And what, you might ask, is the thoracic duct? Not to mention Peyer’s patches. The thorax, I think, is basically that part of the body covered by the rib cage, which includes the heart, the lungs and other organs, perhaps the spleen, perhaps the pancreas, the liver, the stomach, I’m very vague about it all. Anyway, the thoracic duct is an essential part of the lymphatic system, so here’s some more essential info about it:
The lymph from most of the body, except the head, neck, and right arm, is gathered in a large lymphatic vessel, the thoracic duct, which runs parallel to the aorta through the thorax and drains into the left subclavian vein. The thoracic duct thus returns the lymphatic fluid and lymphocytes back into the peripheral blood circulation.
So from this it’s clear that blood and lymph seem to circulate and work together in some respects.
Canto: It’s annoying that lymph is described as the ‘stuff of the lymphatic system’ or in the lymph nodes/vessels, etc etc. It reminds me of dormative virtue, somehow. Then again, it’s a bit like blood. What’s blood? It’s the stuff that comes out of us when we cut ourselves. Most people don’t know much beyond that – except for one key fact. It’s red, and it pools all over the floor in murder dramas. What colour is lymph? Have we ever seen a pool of it? Do we every lymph to death? Why can’t we turn lymph into a verb?
Jacinta: Okay, enough of the deepities. This really is a fascinating topic, and tracing the discovery of lymph, chyle, and the lymphatic system, starting with Hippocrates some 2400 years ago, would be the best, or at least the most interesting way to learn about the stuff, IMHO. I’ve found a recent series of pieces, The discovery of lymphatic system in the seventeenth century, which I’d love to read, but they’re behind a paywall, because we impoverished dilettantes need to be kept from accessing such things. They do give us access to the abstracts though. Here’s the abstract from part one:
The early history of lymphatic anatomy from Hippocrates (ca. 460–377 B.C.) to Eustachius (1510–1574). The presence of lymphatic vessels and lymph nodes was reported by ancient anatomists without any accurate knowledge of their true functions. Lymph nodes were described as spongy structures, spread over the whole body for the support of vulnerable body parts. Digestion was explained as being the resorption of clear chyle from digested food by the open endings of chyle vessels. The first insights into the place of lymphatic components within nutrition emanated from the medical school of Alexandria (fourth century B.C.) where vivisection was a common practice. Herophilus and Erasistratus described mesenteric veins [relating to the mesentery, a fold of membrane that attaches the intestine to the abdominal wall] full of clear liquid, air or milk. For Galen of Pergamum, (104–210) mesenteric lymph nodes also had a nutritional function. He described three different types of mesenteric vessels, namely, the arterial vessels, for the transport of spirituous blood to the intestines; the venous side branches of the portal vein, for the transport of nutritive blood from the liver to the intestines; and small vessels, from the intestines to the mesenteric lymph nodes (serous lymph vessels?). According to Galen, chyle was transported via the above-mentioned mesenteric venous vessels from the intestines to the portal vein and liver, where it was transformed into nutritive blood. This doctrine would be obliterated in the seventeenth century by the discovery of systemic circulation and of the drainage of chyle through a thoracic duct to the subclavian veins.
Canto: Hmmm. Chyle? Peritoneum? Subclavian?
Jacinta: Chyle’s a milky, fatty fluid (containing lymph), formed in the small intestine during digestion. It flows into those lymph vessels known as lacteals. These are special ‘lymph capillaries’ where the lipids ‘are colloidally suspended in chylomicrons’ My guess is that ‘chylomicrons’ are itty-bitty chyle bits. Colloidal suspension is ‘a stable phase showing little tendency to aggregate and separate from the aqueous phase’, according to ScienceDirect. The peritoneum is ‘the serous membrane that lines the abdominal cavity’. Other serous membranes are the pleura and the pericardium. They are two-layered membranes ‘lubricated by a fluid derived from serum’. The subclavian veins (and arteries) are those running from the neck down the left and right arms.
Canto: Serum?
Jacinta: Comes from the blood, and rich in proteins.
Canto: So it seems that lymph, or the lymphatic system, has a few functions. Three in particular are highlighted by a NIH website relating to cancer. First, it returns interstitial fluid – fluid that leaks from blood capillaries into the spaces between cells – to the venous blood. This is a sort of recycling process – a regular leakage and a regular return. The returned fluid is called lymph. The second function connects it to the digestive system. Fats and fat soluble vitamins are absorbed and transported to the venous circulation. This happens through those aforementioned lacteals. The small intestines are lined with villi, little finger-like projections, in the centre of which are blood capillaries, and lacteals, aka lymph capillaries. The blood and the lymph thus act together, with the blood capillaries absorbing most of the nutrients and the lymph capillaries absorbing the fatty stuff. And this high fat content lymph is called chyle. And the third function – the most well-known function according to my source – is immunological:
Lymph nodes and other lymphatic organs filter the lymph to remove microorganisms and other foreign particles. Lymphatic organs contain lymphocytes that destroy invading organisms.
Jacinta: A reasonably good dummies intro to lymph and the lymphatic system, IMHO, and it’s not really surprising that it took a while to work out what it was all about. We certainly don’t know ourselves, but we know a bit more than we did.
Canto: Yes, much more to learn, about lymphoid tissue, capillaries, vessels and that big thoracic duct. And since much of this info comes from the National Cancer Institute (in the US), the connection with cancer, positive or negative, might be worth exploring….
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
Animals don’t ‘fall in love’, right? Only humans do that sort of thing. But wait on – humans are animals. Darwin told me so. Funny how we keep forgetting that. Or, if we’re members of particular religions, we insist it just isn’t so. Simone de Beauvoir, in a section near the end of her monumental work The Second Sex, titled ‘The woman in love’, describes this rather mythologised experience from the second sex’s perspective:
The supreme aim of human love, like mystical love, is identification with the loved one. The measure of values and the truth of the world are in his own consciousness; that is why serving him is still not enough. The woman tries to see with his eyes; she reads the books he reads, prefers the paintings and music he prefers, she is only interested in the landscapes she sees with him, in the ideas that come from him; she adopts his friends, his enemies and his opinions; when she questions herself, she endeavours to hear the answers he gives; she wants the air he has already breathed in her lungs; the fruit and flowers she has not received from his hands have neither fragrance nor taste; even her hodological space is upset: the centre of the world is no longer where she is but where the beloved is; all roads leave from and lead to his house. She uses his words, she repeats his gestures, adopts his manias and tics. ‘I am Heathcliff,’ says Catherine in Wuthering Heights; this is the cry of all women in love; she is another incarnation of the beloved, his reflection, his double: she is he. She lets her own world founder in contingence: she lives in his universe.
I can hear plenty of women I know roaring with laughter at this description. It might seem dated and extreme, but Beauvoir directly quotes women of her time and earlier who give expression to this type of mindset, and a whole sub-genre of romantic literature is still devoted to it. And after all, humans are essentially monogamous, unlike any of the other great apes.
But how essential is our monogamy, really?
Bonobos have been lightly referred to as the ‘make love not war’ apes, or our ‘hippy’ cousins. These are telling references, methinks. I have to say that when I was a young teen, and sometimes shell-shocked witness to a very unhappy parental marriage, I had high hopes that the hippy ‘love the one you’re with’ lifestyle (and revolution) was here to stay, and that marriage, the consecration of monogamy, was on its way out. I won’t say those hopes were entirely dashed, because over the past fifty years or so, with the introduction of no-fault divorce, the greater acceptance of same sex relations and non-marital partnerships, and the drop in religious belief, traditional marriage has certainly been tottering on its pedestal. But there are other barriers to our adopting a bonobo lifestyle of all-in, apparently indiscriminate frottage and sexual healing – including our ideas about ‘true love’.
One factor, surely, has ensured the continued supremacy of monogamy in our society – the production and maintenance of offspring. While it’s generally conservatives who maintain that ideally children need a father and a mother for a ‘balanced’ upbringing (in spite of many examples to the contrary), the idea, I’ve found, niggles at many a single parent I’ve encountered. My own mother – by far the dominant parent, the breadwinner, the rule-maker, the sometimes unnerving dictator – seemed obsessed that the weakness of my father was affecting my own masculinity. She sent information my way as I grew older, about a career in the military, or the police, and made the odd – indeed quite odd – remark about homosexuality as a disturbing and unhealthy condition. I wasn’t particularly inclined that way, though as a ten-year-old I definitely found some of the boys in my class as pretty (or ugly) as the girls. And later, my discovery of David Bowie, the most intense experience of my teenage life, had a clear sexual element.
The point here is that we’re plagued with traditional notions of masculinity, femininity and monogamy which will take time to break down. But changes are afoot, and the gradual fading of religion and the great work of pioneers like Beauvoir and many intellectual heroines before and after her are making for a much more female-friendly, not to say female dominant, political and social environment. Slowly slowly catchy monkey. Or in the case of bonobos, catchuppy monkey.
Bonobos don’t live in houses. They don’t have sex in bedrooms. And, like us, at least post-religion, they don’t have sex to produce offspring. It seems that, like dogs on their masters’ legs, they’ve learned about erogenous zones, but, being smarter than dogs, have taken that a step further in terms of bonding. Humans hide away to have sex, but consume ‘adult’ videos involving sex on beaches and other open air spaces, in bars, on stages, in public toilets, in palatial residences, in the best and worst of places. It’s as if we long to be open and brazen about our sexuality, but dare not.
I note that one of the biggest sex video industry in the world is in Japan, which is also, surely not coincidentally, the least religious country in the world. It’s also not exactly a haven of feminism, to be honest, and critics, including feminists, have often targeted the sex video world as, like prostitution, a haven of macho exploitation. I prefer to see it as, at least potentially, a haven of sex without love, but not without fellow-feeling. And certainly anyone familiar with the Japanese sex video industry would have to scoff at the characterisation I’ve heard, from conservative politicians among others, that a large proportion of the females employed in the industry, are entrapped and drug-addled (as is not infrequently the case, of course, with prostitution). Having said that, it’s still clearly an industry directed primarily at male consumers.
Feminists are generally divided about the industry, between those who want to kill it off and those who want, or hope, to transform it. In any case, one of the problems is that the industry compartmentalises sex. It becomes a product, most often accessed by men, alone, in their bedrooms, sometimes by couples or groups as an aid or an inspiration. It helps with fantasy and technique but has little if anything to do with fellow-feeling or – well, love.
And yet – what I note with Japanese sex videos is that they are more story-based than those of the Euro-American industry. Yes, the stories are often repetitive and predictable, and there’s too much ‘fake rape’, with the female invariably ending up ‘enjoying’ the experience, though it appears to be a fact that rape fantasies are common among women – an issue I feel way too squeamish to explore, at least for now. The point I’m trying to make is that many Japanese videos make the effort to place sex in a domestic or workplace context, to normalise it, even if in a somewhat ludicrous, and sometimes comical, way. I also note that sometimes they involve interviews with the performers before and after scenes, giving the impression of ‘happy families’, though there are definitely cases of coercion and the situation may be worsening. Again, more female empowerment is the key to changing this environment. The fact remains that both pornography and prostitution are signs of a culture that has never really come to terms with its sexual needs and its sexual nature. If we cannot accept that sex is healthy we will continue to pursue it in ways that are unhealthy – the drive will always be with us.
So what about love, again? And its relation to sex. As Beauvoir points out, the idea that two people will be able to satisfy each other sexually, exclusively, for decades, is ridiculous. Of course, many couples become increasingly comfortable with each other and co-dependent over the years – as do two dogs more or less forced to share the same home. This may be not so much a sign of love as of the standard living arrangements developed over the centuries in our civilised world – rows of few-bedroomed homes fit for maybe three to five people set out in grids of streets serviced with all the conveniences of modern life. We don’t build for anything like a bonobo world, understandably, and it’s hard to see beyond the reality that has shaped our whole lives. Still, I’m hearing a new term that might be worth clinging to – ‘ethical non-monogamy’. Something that might be worth considering once the hormones die down and the scales fall…
So that very bonoboesque idea I’ll endeavour to explore next time.
What kind of societies did our primate ancestors live in? Could they have been more egalitarian than the ones we have now?
Angela Saini
hormones follow social evolution?
So I wrote a piece a few months ago on this topic, and my most recent piece starts to revisit the issue. Human males, at least in the WEIRD world, are experiencing reduced testosterone levels, which in terms of general health, is apparently a bad thing. Females on the other hand, already have testosterone levels at between a tenth and a twentieth those of males. What does this mean, for their health, and their behaviour? And what about testosterone levels of male and female bonobos and chimps, our equally closest living relatives, whose behaviour is so strikingly different from each other, and from us? To paraphrase Sabine Hossenfelder, ‘that’s what I’m going to write about today’. Or maybe not!
First caveat – it’s far from being all about testosterone, as regards behaviour or physicality. And I’m interested in changes to behaviour, re humans, rather than changes to testosterone. So I’m looking for clues in bonobos for promoting more of the changes I already see occurring in male human behaviour, partly due to the increasing empowerment of women. It’s likely that testosterone levels, and endocrine changes generally, will follow changes in social behaviour, rather than vice versa. But I’m certainly no expert.
I mentioned in one of my previous pieces that bonobo sexual dimorphism is equal to that of chimps, and of humans. However, I’ve since read that the sexual dimorphism is a wee bit less in bonobos than in chimps and humans (and given that the split between bonobos and chimps is quite recent, in evolutionary terms, that difference might continue to diminish, and even reverse, if both species manage to survive…). Every little bit helps in the power struggle, though it’s likely that female bonding is the real key to bonobos’ female dominance. A key to our human future?
Having said that, let’s still consider testosterone, and its reduction, and what it means for men in the future. Carole Hooven says this in Testosterone:
The consensus of experts is that testosterone’s main job is to support the anatomy, physiology and behaviour that increases a male’s reproductive output – at least in nonhuman animals. And men are no exception – T helps them reproduce, and directs energy to be used in ways that support competition for mates.
So it’s probably true to say that the reduction in T among males, in ‘developed’ nations, over such a short period in evolutionary terms, is more disturbing than exciting. However, male aggression and violence has long been a problem, to say the least. Hooven again:
Men are much more likely than women to be sexually attracted to women, and they are far more physically aggressive than women in every pocket of the earth, at every age. For example, they are responsible for around 70 percent of all traffic fatalities and 98 percent of mass shootings in the United States, and worldwide commit over 95 percent of homicides and the overwhelming majority of violent acts of every kind, including sexual assault.
All of which is hardly new news (though I’ve encountered disbelieving males), and in most mammalian species males are the more aggressive sex, but there are exceptions. Hooven cites the naked mole rat, the meerkat and the spotted hyena as examples of high levels of female aggression, but the role of hormones in these animals’ behaviour is complex and not fully understood. In bonobos, female dominance isn’t achieved in anything like the way male dominance is achieved in chimps. They do it though female solidarity, most often achieved through ‘sexual closeness’, to speak euphemistically.
Surprisingly, while there’s a massive difference between male and female human testosterone levels, this is not the case for bonobos or chimps. Male chimps ‘have on average 397 ng/dl testosterone, which is below the human male average’,
On this basis,I’d like to do everything I can to support female-female bonding. One inspiring story I first heard about years ago is a coalition of Palestinian and Israeli women trying to find a way around the impasse that exists within Israeli-Palestinian lands, where both groups have an in-group approach to the cultural history of the region they share.
These women — both independently and part of nonprofits and organizations — are working to bridge the gap, break down the walls — both literally and metaphorically — and build a world where Israelis and Palestinians aren’t enemies but neighbors and friends.
I suspect that the walls they’re trying to break down are those of macho insistence on the rightness of their ‘ownership’ of the land they inhabit. This insistence, and resultant violence, has resulted in trauma on both sides. Considering this trauma (naturally felt more on the militarily weaker side than the other), and the fact that both sides in the conflict are dominated by belligerent males, women are often reluctant to speak out about the situation, particularly on the Palestinian side. Take this example, from an article linked below:
We struggled to find a Palestinian woman in Gaza to openly speak in fear of retribution from Hamas, the “Palestinian resistance group,” or fundamentalist, militant, and nationalist organization that controls the region.
The same article features Jewish women, brought to Israel as children from persecution in Middle Eastern or African countries, expressing mixed feelings of gratitude and shock on being exposed to apartheid-style conditions in their adopted country, and Palestinian Arab women, dedicated to education and a historical understanding of the complexities of belonging and loss experienced by both sides of the conflict in the region.
All of this has taken me far from what I earlier promised to talk about – the more speculative question of our ancestry. Were those ancestors less or more violent than we are now? Or – was the CHLCA (the last chimp-human common ancestor) more like chimps (and humans) or bonobos?
One of the features most notable in ape and monkey societies – and also in humans – is hierarchy. We don’t notice it so much in our vastly populous society, in which we might be born to ‘unskilled’ labourers, teachers, small business owners, billionaire entrepreneurs or royalty – the gradations are so numerous that it may take us quite a while to know where in the hierarchy we belong, if we ever do – and whether we’re failing or improving in terms of the rung on the ladder we started out on. And there’s no doubt that failure or success can be measured in a much greater variety of ways than ever before, by ourselves or by anyone who chooses to measure us. In any case, the fact that there are people we ‘look up to’ – artists, scientists, parents, activists, monarchs, whatever – is an indication that we strive to better ourselves in an essentially non-egalitarian cultural environment.
But there have been notable changes in that environment in the last 100 years or so – not only with respect to female empowerment, but major transformations due to science and technology, in transport, communications, medicine and industry. We’re living longer, educating ourselves more, and working less hard, in a physical sense. We’re having fewer children, and a greater diversity of sexual relations. Though there are still many who ‘fall through the gaps’, we’ve developed human welfare systems to reduce dire poverty and to enable the intellectually and physically disabled to experience better lives than was previously afforded them. We’ve become generally more sensitive to the web of life from which our species has emerged, and what we owe to it and to the planet whose environment has enabled all living things to survive and more or less thrive. Some of these developments have long roots, but most of their fruits have been recent, though of course far from universal in human societies and nations. Democracies and open societies have proved to be the most healthful and beneficial for their people, and the general tendency has been to grow those societal types, through migration or activism against repressive regimes.
We live in a world of growing prosperity, often compromised by the belligerence and repression of the odd authoritarian national leader. It might seem a mite ridiculous to compare this massive and complex human population with the tiny bonobo world in a small corner of a sadly benighted African country, but I see some utility in the comparison, precisely because I see signs that our best societies are heading in the bonobo direction. Not that we’re getting hairier or more arboreal, but that we’re gradually becoming more caring and socially responsible, less violent and more sexually tolerant and diverse. The circle has expanded, the better angels of our nature are managing to prevail, and like David Deutsch, though perhaps for slightly different reasons, I feel little cause to despair of the human species.
