Archive for the ‘neurology’ Category
what’s on my mind, and in my brain?
The mind is certainly a very mysterious organ, I reflected,.. about which nothing whatever is known, though we depend upon it so completely.
Virginia Woolf, A room of one’s own, 1928
ah yes, it all makes sense now…
So there’s still plenty to learn about the mind, and maybe calling it the brain is only giving us a false sense of the matter (and I’m thinking of ye olde ‘what’s mind, it doesn’t matter, what’s matter, never mind’ jibe), though we’ve made great neurophysiological strides in recent decades. But having just read Virginia Woolf’s thoughts on the position of women almost a century ago, and being old enough to remember texts like ‘Women are from Venus, men are from Mars’, which sought to ‘explain’ and make the best of the pigeonholes the author presumably believed in, I’ve decided to have another quick look at the current expert views on the neurophysiological and hormonal differences between the sexes.
What I’ve found is that it’s still a contested issue. When I last reported on it, I found myself very happy to accept that there are statistical differences between male and female brains, but no categorical differences. That’s to say, both male and female brains vary widely, and it’s reasonable to say that the differences within each gender are as great as the differences between them. Another striking way to think about it is to say that, were you to hand a still living but completely disembodied human brain (just imagine!) to a trained and experienced neurologist, they’d be unable to say categorically that it was M or F.
Well, the first website I’ve come to disputes this claim. It’s from PNAS (often fondly vocalised as ‘penis’, which may or may not be relevant) and it’s a short essay with only one author, Marek Glezerman. My initial sense of it is that he misses the point, and seems disturbingly emphatic. To give an obvious example, the title of the piece is “Yes, there is a female and a male brain: Morphology versus functionality”. In his opening paragraph (but the essay only has two paragraphs), Glezerman summarises the conclusion he disagrees with, a conclusion I based my own essay on years ago:
The authors conclude that brains of women and men are not dimorphic and not categorically different, as are the genital systems of the two genders, but resemble more an overlapping mosaic of specific functional regions and therefore cannot be distinguished as male and female brains.
Reading this made me wonder, and I thought back to the night before – ahhh, the night before – when I spent time at a well-frequented pub full of individuals, male and female, well beyond the first flush of youth. It occurred to me that there wasn’t a single person there whose sex I would feel mistaken about. Many of the men, and none of the women, were balding, bearded and paunchy. Some did have breasts, I admit, that could’ve competed with the females, but I doubt if they’d have managed the same expression, so to speak. And though there was a lot of variety in the voices, it was easy enough to distinguish males from females in that characteristic. Of course there were also differences in dress, mannerisms and choice of drink, but those could be put down to ‘culture’ and dismissed. Even so there might be enough evidence on display to suggest a categorical difference – a morphological difference – traceable to the brain and hormones.
So, what did Glezerman mean, exactly, by ‘morphology versus functionality’? Well, here’s a long, but essential quote from his essay.
Whenever the terms “female brain” and “male brain” are used, the intention should be functional and not morphological, qualitative and not quantitative. Functionally, brains of women and men are indeed different. Not better, not worse, neither more nor less sophisticated, just different. The very brain cells differ chromosomally. The male brain is exposed to a completely different hormonal environment during intrauterine life than the female brain. The available scientific data as to the crucial effect of testosterone on the developing male brain is overwhelming.
Glezerman provides references for his claim about testosterone and its effects, a subject of great interest to me, but I’ll leave that for another essay. But one wonders if this isn’t a storm in a teacup. Going back to my pub reference, of course there were differences within the sexes – some males seemed more ‘feminine’ than others, whatever that may mean, and some women more ‘masculine’. This may again be a matter of hormone expression rather than personal choice, or a complex combination. I find it fascinating that male hormone levels (i.e testosterone) are dropping in the WEIRD world, a matter of concern to some, but not me…. oh, but that’s for that other essay, or did I already write that one?
PNAS has a reply to Glezerman’s essay, which I’ll now focus on. And I should note how polite and civilised these scientific disputes are: far from the world of social media. This response is even shorter that Glezerman’s little essay (I’ll bet that was by design!), so I’ll reflect on it here, passage by passage.
As Marek Glezerman (1) rightly points out, there are differences between females and males in brain and behavior. Glezerman overlooks, however, the fact that such differences may be different and even opposite under different environmental conditions. That is, what is typical under some conditions in a brain composed of cells with an XX chromosomal complement residing in a body with low levels of testosterone, may be typical under other conditions in a brain composed of cells with an XY chromosomal complement residing in a body with high levels of testosterone.
Being a person who spreads himself thinly over a wide variety of intellectual topics (i.e master of none), I had to look up XX and XY (remember mate, two kisses female, one kiss male – which is surely typical). What the response (which has three authors) appears to be saying is that what is typical for a low-testosterone female in some conditions, may also be typical for a high-testosterone male under quite different conditions, in spite of the fact that one set of brain cells carries an XY chromosomal complement, while the other carries XX. Not sure if this carries the day though. But to continue:
Such “reversals” of sex effects have also been reported when the manipulation of environmental conditions was done in utero (by manipulating the dam) and the offspring were tested in adulthood (reviewed in refs. 2 and 3). These observations led to the hypothesis that brains are composed of a “mosaic” of “male” and “female” features rather than of only “male” features or only “female” features, as expected of a “male brain” and a “female brain,” respectively (2, 3)
Wasn’t sure what ‘manipulating the dam’ meant, but a dam is a dam, something that reduces or stops flow, so I suppose this was done in non-human test species? Presumably if you’re able to change hormonal conditions in utero via such methods – or by changing environmental/social conditions, as bonobos appear to have done – you will change the mosaic of behaviour. Bonobos can be quite aggressive, but it appears to be more tilted towards the male of the species. Also, the drop in male testosterone is surely due to changed conditions and expectations for males over a relatively short period – for example in the mere century since A room of one’s own was written, but even more so in the past few decades of mechanisation and anti-machismo, at least in the WEIRD world.
Our study (4) is the first to empirically test whether brains are “male” or “female” by assessing internal consistency in the degree of “maleness-femaleness” of different elements within a single brain. We found that brains with both “female-end” and “male-end” characteristics were more prevalent than brains with only “female-end” or only “male-end” characteristics. This was true for both the volume of brain regions and the strength of connections between regions (assessed in a similar way to ref. 5), in contrast to Glezerman’s assumption that “Other imaging methods might have yielded different results.”
This is claiming evidence for mosaic traits in a majority of the brains under study, both for individual regions in isolation and for brain connectivity. All I can say is that this seems eminently plausible, indeed I would’ve expected such a finding. Not sure, of course, what ‘male-end’ and ‘female-end’ characteristics are exactly. There is a question here, though, about what Glezerman meant by ‘other imaging methods’.
To corroborate our analysis of different aspects of brain structure assessed using MRI, we also analyzed brain function, as revealed in people’s behaviors, personality characteristics, preferences, and attitudes. Also here there were many more people with both “feminine” (i.e., more common in females compared with males) and “masculine” (i.e., more common in males compared with females) characteristics than people with only feminine or only masculine characteristics (4).
Behaviour, over time, can affect brain function and brain regions mightily. An obvious case is language, spoken and written, which is a behaviour that has had considerably impact on the brain, as, for example Maryanne Wolf recounts in Proust and the squid. You’d hardly expect those brain regions that have been adapted/co-opted for language production/reception to have been much affected by gender. The same would go for other skills and practices, such as mathematics. As to the different physical characteristics of males and females (my pub observations), how connected are they to our brains? They certainly have much to do with hormones, of which we have at least fifty types, many of which are connected to/stimulated into action by the pituitary gland, which is in turn stimulated by the hypothalamus, but these regions account for a minuscule proportion of the brain.
There is no doubt that sex affects the structure and function of brain cells. However, the fact that sex can affect brain cells does not necessarily entail that the form and function of brain cells are either “male” or “female” nor that the brains comprised of these cells can be divided into two distinct categories. For such claims to be true it is necessary that the effects of sex are dimorphic, resulting in the formation of distinct “male” and “female” types, as well as internally consistent (2, 3, 6).
I think what’s being said here is that just because our brain cells, indeed all our somatic cells, have either an XX or XY chromosomal complement in their nuclei, this doesn’t dictate essential expressed traits – our intelligence, our humour, our physical skills, our bodily needs, and so forth. As this essay suggests, ‘manipulating the dam’ in utero is likely to have a far greater effect on human development than gender does, unless of course you’re born into a culture in which one gender is significantly undervalued. But let’s not go too near that hornet’s nest.
So to the last lines of the reply to Glezerman:
Hopefully, future studies looking at the relations between sex and other systems in which sex differences have been documented (e.g., the immune system, the cardiovascular system) will assess both internal consistency and degree of overlap, to reveal whether the relations between sex and other systems are more similar to the relations between sex and the brain (mosaicism) or to the relations between sex and the genitalia (dimorphism).
And no doubt there will be differences, especially in relation to hormonal levels associated with the reproductive system, but also in those associated with diabetes, the heart and the circulatory system and so forth, but these are not easily predictable based solely on gender. And there’s another problem with fixating on sex differences in a hard and fast way. It’s not exactly coincidental that male supremacists are all for favouring such differences. That’s why the bonobo example needs to be known and promoted far more than is currently the case.
References
https://www.pnas.org/doi/10.1073/pnas.1600791113#core-r2
What do we currently know about the differences between male and female brains in humans?
the male and female brain, revisited
dyslexia is not one thing 4: the left and the right
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
https://www.kenhub.com/en/library/anatomy/angular-gyrus
https://academic.oup.com/brain/article/126/9/2093/367492
dyslexia is not one thing 2: structural deficits
the human brain- a very very rough guide
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
https://www.kenhub.com/en/library/anatomy/angular-gyrus
adult ADHD – what’s the buzz?
Jacinta: So this is a commissioned piece, sort of, by someone who wants us to look into this disorder (attention deficit hyperactivity disorder, in full), for our sakes and of course for the sake of humanity.
Canto: Sounds like a first world issue to me.
Jacinta: Okay consider yourself lucky you don’t have to scrounge around rubbish heaps for a living, or travel miles on a half-dead donkey to see a medico, or dodge government bullets because you’re an outspoken female…
Canto: Okay okay. So we know that diagnoses of adult ADHD have risen substantially in recent years, in the WEIRD* world, along with autism spectrum disorder (ASD), bipolar disorder, major depressive disorder, PTSD, chronic fatigue syndrome, and others. A lot of work is being created for clinical psychologists, and the waiting lists are getting longer.
Jacinta: So we’ve started by watching a couple of videos, one from CNBC in the US, another from the ABC in Australia. And a few points here about research and reliable info. Avoid social media! And for the most part avoid commercial news and info networks, which are privately owned and often have a commercial-financial agenda. The most reliable sources in the WEIRD world are generally government subsidised and mandated sites (the ABC in Australia, the BBC in Britain, PBS and NPR in the USA, DW (Deutsche Welle) in Germany, France TV and Radio France, for example).
Canto: Well, we’ve broken that rule by starting with this video from CNBC, but it does give a good overview of the symptoms, via field professionals such as Dr Leonard Adler, director of an adult ADHD programme at NYU. The symptoms are divided into two types, those associated with inattentiveness and with hyperactivity, though there are obvious crossovers. Under each type heading, nine more or less connected symptoms are described. For example, symptoms of inattentiveness include ‘forgetfulness in daily activities’, ‘failure to finish tasks’ and ‘losing important things’, and under hyperactivity comes ‘interrupting others’ or ‘trouble with turn-taking’, and ‘being always ‘on the go”. Apparently you need at least five of the nine symptoms in either category to be diagnosed with ADHD, at least in the USA. Personally, I can relate to all of the symptoms some of the time. All of this, by the way, comes from the famous, or infamous, DSM-5, the 5th edition of the diagnostic and statistical manual of mental disorders.
Jacinta: So you may be skeptical, but on the question posed throughout this video: ‘Is ADHD on the rise or is there simply a rise in diagnoses?’, my answer would be ‘yes there is a rise in diagnoses’, but not for the cynical reason you seem to favour – that it’s all about lining the pockets of psychiatrists. Remember we’ve been studying Freud and the post-Freudians, who pioneered the uncovering of disorders due to childhood trauma, sexual repression, unconscious guilt and the like, all in a groping, hit-and-miss sort of way, before anything much was known of neurology, endocrinology or genetics. Now in the 21st century, we can make connections between genetics, family and personal histories and brain processes in a more scientific way – at least slightly. There’s a long way to go. And this has led us to the reality of ongoing behavioural disorders, where previously people were just considered in vague terms as oddballs, eccentrics, psychos, losers or pains in the arse.
Canto: Steady on. I understand that it’s not about having some symptoms sometimes, which we all do, it’s about having a number of them to a degree that it becomes debilitating. And, as more than one expert has said, what’s frustrating to these sufferers is that sometimes, with certain specific tasks, or aspects of their professional lives, they perform perfectly well on a regular basis, while the rest of their lives are a mess of procrastination, disorganisation, impulsivity and the like. But the more I learn about the disorder, the more I wonder about treatment. These symptoms seem so multi-faceted, I can’t imagine how they can be dealt with though drugs. I can’t even begin to imagine the brain chemistry behind such varied behaviour. Surely there’s no medication that’s going to make you more organised or a better listener – never mind both at the same time.
Jacinta: Well, and yet it all has to be about brain chemistry and signalling. What else can it be? And patterns of behaviour – that’s to say, patterns of brain signalling, that have become habitual since childhood. In response to family dynamics and such. No free will, remember. Much that I’ve heard so far indicates that it runs in families. And of course there are prescription medications for the disorder. So we have to look at effectiveness (method of action), cost, availability and any side-effects or downsides. And then there are other treatments such as cognitive behavioural therapy.
Canto: Yeah I’ve heard that medications are expensive, and I doubt that therapy comes cheaply either. But let’s look at the brain of ADHD sufferers and what can be done medically, if anything, to alter it.
Jacinta: Well Britain’s National Health Service has this to say:
Research has identified a number of possible differences in the brains of people with ADHD from those without the condition, although the exact significance of these is not clear. For example, studies involving brain scans have suggested that certain areas of the brain may be smaller in people with ADHD, whereas other areas may be larger. Other studies have suggested that people with ADHD may have an imbalance in the level of neurotransmitters in the brain, or that these chemicals may not work properly.
Canto: Wow, that’s really informative. I like the bit about smaller or larger. Are they talking about brains or dicks? I mean, really…
Jacinta: Hmm. We need to look at research papers. And one thing I note is that researchers don’t readily distinguish ‘Adult ADHD’ because it’s understood to have emerged in childhood, though symptoms might have changed over time. In fact many children may ‘get over it’. Dr Judy Ho, in an interview on ADHD in the USA, quoted that childhood ADHD affects some 5% of the population but the adult version affects some 2.5%, which seems to make sense.
Canto: Well, having checked Google Scholar, I don’t see much in the way of recent research that jumps out. Sheeting home the various symptoms of the disorder to brain chemistry is really difficult…
Jacinta: Well since they do have medications on the market – the NHS describes 5 types- methylphenidate, lisdexamfetamine, dexamfetamine, atomoxetine and guanfacine – and these presumably work on brain chemistry, they must have some idea. ..
Canto: Well these are generally amfetamines, which act as stimulants, speeding up brain functions through the release of hormones and monoamine neurotransmitters such as dopamine and norepinephrine, and this kind of ‘upper’ activity would help with the disorder most associated with ADHD, which is depression, though there are definite downsides related to prolonged use or overuse. Combining, and possibly replacing, such medications with more behavioural-analytical treatments such as Cognitive Behavioural Therapy might be an idea, if there were enough decent therapists around, and if it was affordable, but it’s all a bit hit and miss.
Jacinta: You have to distinguish between proximal causes and ultimate causes. The proximal causes of most of these conditions is hormone levels and neurotransmitter activity, but that says nothing about why those levels are higher in some people than in others. If you don’t know the underlying causes, you’re just treating symptoms – drugging people to behave ‘normally’. But those underlying causes are generally fiendishly difficult to deal with – for example how can you cure an abused childhood, or damage done in the womb?
Canto: But many people with ADHD may just want to be ‘normalised’, to a degree. They know that what’s been done to them can’t be undone, but they just might want those symptoms reduced, to concentrate better, to be more organised, to calm down, whatever.
Jacinta: And given that we’re not that good at tolerating differences, why not give people drugs so they can all be the same, at least tolerably so….
*western ,educated,industrial,rich,democratic
References
ADD/ADHD – What is Attention Deficit Hyperactivity Disorder? (video)
https://www.nhs.uk/conditions/attention-deficit-hyperactivity-disorder-adhd/treatment/
https://www.cdc.gov/ncbddd/adhd/index.html
A bit about schizophrenia – a very bizarre ailment
Having, for a book group, read a strange novel written a little over 50 years ago, by Doris Lessing, Briefing for a descent into hell, the title of which may or may not be ironic, and being reasonably interested in the brain, its functions and dysfunctions, I’ve decided to use this post to update my tiny knowledge of schizophrenia, a disorder I’ve had some acquaintance with.
Lessing’s book may or may not be about schizophrenia, because it doesn’t concern itself with labeling any mental disorders, or with the science of brain dysfunction in any way. The focus is upon the imaginative world of an Oxbridge academic, a lecturer in classical mythology or some such, who, having been found wandering about in some Egdon Heath-type landscape, with no identification papers or money, and a lack of proper lucidity, is brought into a psychiatric facility for observation and treatment. The vast bulk of the book is told from this individuals’s perspective. Not that he tells the story of his illness, he simply tells stories – or Lessing tells stories on his behalf. Somehow the reader is allowed to to enter the main character’s inner landscape, which includes a voyage around the Pacific Ocean, another voyage around the solar system (conducted by classical deities) and harrowing, but fake, war-time experiences in the Balkans. Along the way we’re provided with the occasional dazzling piece of insight which I think we’re asked to consider as the upside, or mind-expanding nature, of ‘madness’ – somewhat in the spirit of Huxley’s Doors of Perception and Timothy Leary’s psychedelia. At the end of the book the professor is returned to ‘normality’ via electric shock treatment, and becomes, apparently, as uninteresting a character as most of the others in the book, especially the doctors responsible for his treatment, only known as X and Y.
So, there are problems here. First, Lessing’s apparent lack of interest in the science of the brain means that we’re at a loss to know what the academic is suffering from. Madness and insanity are not of course, legitimate terms for mental conditions, and Lessing avoids using them, but offers nothing more specific, so we’re reduced to trying to deduce the condition from what we know of the behaviour and ramblings of an entirely fictional character. I’ve come up with only two not very convincing possibilities – schizophrenia and brain tumour. A brain tumour is a useful literary device due to the multifaceted nature of our white and grey matter, which constitutes the most complex organ in the known universe, as many an expert has pointed out. A benign tumour – one that that doesn’t metastasise – may bring on a multiplicity of neurons or connections between them that increase the ability to confabulate – though I’ve never heard of such an outcome and it’s more likely that our ‘imagination’ is the product of multiple regions spread throughout the cortex. Schizophrenia only really occurs to me here because the professor was found wandering ‘lonely as a cloud’, far from home, having had his wallet presumably stolen, so that it took some time to identify him. This reminds me of a friend who has from this condition, and has suffered a similar experience more than once.
One of the symptoms of schizophrenia is called ‘loss of affect’, which means that the sufferer become relatively indifferent to the basics – food, clothing and shelter – so caught up is he in his mental ramblings, which he often voices aloud. It’s rare however, for schizophrenia to make its first appearance in middle-age, as appears to be the case here. Another reason, though, that my thoughts turned to schizophrenia was something I read online, in reference to Briefing for a descent into hell. I haven’t read any reviews of the book, and in fact I had no idea when the book was published, as I’d obtained a cheapie online version, which was undated. So in trying to ascertain the date – 1971, earlier than I’d expected, but in many ways illuminating – I happened to note a brief reference to a review written when the book came out, by the US essayist Joan Didion. She wrote that the book presented an ‘unconvincing description of mental illness’ and that the book displayed the influence of R D Laing. A double bullseye in my opinion.
I read a bit of R D Laing, the noted ‘anti-psychiatrist’ in the seventies, after which he went decidedly out of fashion. His focus was primarily on schizophrenia – as for example in his 1964 paper ‘Is schizophrenia a disease?’ – though he treated other psychoses in much the same way as ‘a perfectly rational response to an insane world’. This is doubtless an oversimplification of his views, but in any case he seems to have given scant regard to what is actually going on in the brain of schizophrenics.
Since the sixties and seventies, though, and especially since the nineties and the advent of PET scanning, MEG, fMRI and other technologies, the field of neurology has advanced exponentially, and the mental ailments we suffer from are being pinpointed a little more accurately vis-à-vis brain regions and processes. I’ve noted, though, that there’s still a certain romantic halo around the concept of ‘madness’, which after all human society has been ambivalent about since the beginning. The wise fool, the mad scientist and the like have long had their appeal, and it may even be that in extremis, insanity may be a ‘reasonable’ option. As for schizophrenia, maybe we can live with our ‘demons’, as was apparently the case for John Nash after years of struggle, but it’s surely worth trying to get to the bottom of this often crippling disorder, so that it can be managed or cured without resort to disabling or otherwise unhealthy or inconvenient dependence on medication.
Schizophrenia is certainly weird, and its causes are essentially unknown. There’s a genetic element – you’re more likely to suffer from it if it runs in the family – but it can also be brought on by stress and/or regular drug use, depending no doubt on the drug. It’s currently described as affecting a whopping one in a hundred people (with enormous regional variation, apparently), but perhaps if we’re able to learn more about the variety of symptoms we might be able to break it down into a group of affiliated disorders. There is no known cure as yet.
One feature of the ‘neurological revolution’ of the last few decades has been the focus on neurotransmission and electrochemical pathways in the brain, and dopamine, a neurotransmitter, was an early target for understanding and treating the disorder (and may others). And that’s still ongoing:
Current research suggests that schizophrenia is a neurodevelopmental disorder with an important dopamine component.
That’s from a very recent popular website, but research is of course growing, and pointing at other markers. A reading of the extensive Wikipedia article on schizophrenia has a near-paralysing effect on any attempt to define or describe it in a blog post like this. Glutamate, the brain’s ‘most abundant excitatory neurotransmitter’, has been a major recent focus, but it’s unlikely that we’ll get to the bottom of schizophrenia by examining brains in isolation from the lived experience of their owners. Genetics, epigenetics, stress, living conditions and associated disorders, inter alia, all appear to play a part. And due to its strangeness, its apparent hallucinatory nature, its modern associations of alienation and dystopia – think King Crimson’s ’21st century schizoid man’ and much of the oeuvre of Bowie (mostly his best work) – it’s hardly surprising that we feel something of an urge to venerate the schizoid personality, or at least to legitimate it.
Meanwhile, research will inevitably continue, as will the breaking down of intelligence and consciousness into neurotransmission pathways, hormone production, feedback loops, astrocytes etc etc, and ways of enhancing, re-routing, dampening and off-on switching neural signals via increasingly sophisticated and targeted medications… because a certain level of normality is optimal after all.
Meanwhile, I’m off to listen to some of that crazy music….
References
https://www.verywellmind.com/the-relationship-between-schizophrenia-and-dopamine-5219904
https://www.verywellmind.com/what-is-dopamine-5185621
more oxytocin fantasies: an interminable conversation 3
not sure if this measures a significant difference
Canto: So, as it turns out, the bonobo-oxytocin connection is all the rage on the internet. I mean, there are at least two articles on it. Here’s a quote from a PubMed article called ‘Divergent effects of oxytocin on eye contact in bonobos and chimpanzees’:
Previous studies have shown that bonobos and chimpanzees, humans’ two closest relatives, demonstrate considerable behavioral differences, including that bonobos look more at others’ eyes than chimpanzees. Oxytocin is known to increase attention to another’s eyes in many mammalian species (e.g. dogs, monkeys, and humans), yet this effect has not been tested in any nonhuman great ape species.
Jacinta: Hmm, so how do they know this? Presumably they’ve dosed subjects with oxytocin and measured their eye contact against controls?
Canto: No no, they know that bonobos have more eye contact than chimps, simply from observation. So they might infer from this that bonobos produce more oxytocin naturally than chimps…
Jacinta: So do women produce more oxytocin than men I wonder? I presume women make more eye contact than men.
Canto: Well in this study they dosed both bonobos and chimps with oxytocin, and the effect – more eye contact – was greater in bonobos than chimps. In fact, chimps even tended to avoid eye contact when shown images of conspecifics.
Jacinta: So, it’s a matter of interplay between this hormone/neurotransmitter and social conditioning?
Canto: Maybe, but you’d think that an increase in this supposedly touchy-feely hormone would act against social conditioning. Isn’t this the point of that drug, ecstacy? That it reduces social inhibitions… But presumably nothing is ever so simple. Being poor, I only have access to the abstract of this paper, but another abstract, which looks at the effects of oxytocin and vasopressin on chimps, describes them as neuropeptides, just to confuse matters. The abstract also refers to about a dozen brain regions, as well as specific oxytocin and vasopressin receptors, so it gets pretty complicated.
Jacinta: Okay, vasopressin… from Wikipedia:
Human vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP), or argipressin, is a hormone synthesised from the AVP gene as a peptide prohormone in neurons in the hypothalamus, and is converted to AVP. It then travels down the axon terminating in the posterior pituitary, and is released from vesicles into the circulation in response to extracellular hypertonicity (hyperosmolality). AVP has two major functions… etc etc
Canto: Okay thanks for that, let’s stick with oxytocin for now. It’s produced in the hypothalamus, a smallish region buried deep within the brain, just below the larger thalamus and above the even smaller amygdala. It releases and manages a variety of hormones. Brain signals are sent to the hypothalamus, exciting it to release oxytocin and other hormones, which are secreted into the bloodstream by the posterior pituitary gland….
Jacinta: Can you tell me what oxytocin is actually made of? Its structure? The term ‘hormone’ is just a black box to me.
Canto: Okay, here’s a diagram of oxytocin to try and make sense of:
It’s a polypeptide. A peptide is basically an amino acid chain. FYI:
An amino acid is an organic molecule that is made up of a basic amino group (−NH2), an acidic carboxyl group (−COOH), and an organic R group (or side chain) that is unique to each amino acid. The term amino acid is short for α-amino [alpha-amino] carboxylic acid.
Jacinta: So these are coded for, ultimately, by genes?
Canto: Yes, we’re heading backwards here, but each amino acid is encoded by a sequence of three of the four base pairs in our DNA. Anyway oxytocin, among other things is sometimes given to women while in labour. It helps with the contractions apparently. I’ve also heard that the recreational drug ‘ecstasy’, or MDMA, works essentially by releasing oxytocin.
Jacinta: It just so happens I’ve found an interesting 2014 paper published in Neuropsychopharmacology, my new favourite journal, called ‘Effects of MDMA and Intranasal Oxytocin on Social and Emotional Processing’, and here’s a quote from the abstract:
Oxytocin produced small but significant increases in feelings of sociability and enhanced recognition of sad facial expressions. Additionally, responses to oxytocin were related to responses to MDMA with subjects on two subjective measures of sociability. Thus, MDMA increased euphoria and feelings of sociability, perhaps by reducing sensitivity to subtle signs of negative emotions in others. The present findings provide only limited support for the idea that oxytocin produces the prosocial effects of MDMA.
Canto: That is interesting. If that finding can be replicated, I’d say forget the MDMA, dose people with oxytocin. A small but significant increase in feelings of sociability might just be enough to transform our human world.
Jacinta: Hmmm. Small but significant – that sounds a mite contradictory.
Canto: Not the same as significantly small. That slightly significant dose, administered to Messrs Pudding and Pingpong and their enablers, might’ve saved the lives of many Ukrainians, Uyghurs and advocates of multiculturalism, democracy, feminism and other wild and woolly notions. And it doesn’t really transform characters, it just softens their edges.
Jacinta: Yes it’s a nice fantasy – more productive than butchering the butchers, a fantasy I occasionally indulge in. But not workable really.
Canto: Why not? We dosed petrol with lead, and look at how that worked out. It certainly had an effect. In Japan they still use radium baths (at very low levels) for health purposes, even claiming it as a cure for cancer. I’m not sure if oxytocin baths can ever be a thing, but if so I’m sure there will be early adopters.
Jacinta: Well, it’s good to think positively. Oxytocin is often thought of as a bonding hormone between mother and child. The key would be to ensure it facilitates a more general bonding: to cause Mr Pingpong, for example, to see Uyghur, Tibetan, Yi, Limi, and all the other non-Han ethnicities in China as his sisters – or lovers even, revolting as that would be to those peoples.
Canto: Better than being their oppressors and exterminators.
Jacinta: Slightly. But I wonder, quite seriously, if, assuming such a dose of bonding could be effectuated, we could still function as the sometimes rational, problem-solving, highly creative species we indubitably are. Would there be a price to pay for all that oxytocin? And how would this affect all those other hormones and neurotransmitters and all their myriad effects? Humans are notorious for causing extra problems with their solutions, e.g lead, DDT, etc etc.
Canto: Well, there’s no need to worry about the fallout from this solution as yet. I just googled Putin and oxytocin together and came up empty. Obviously we’re way ahead of the curve.
Jacinta: Haha, it’s not a curve these days, it’s a pivot. Get with the program!
References
https://pubmed.ncbi.nlm.nih.gov/33388536/
https://www.yourhormones.info/hormones/oxytocin/
https://www.acs.org/content/acs/en/molecule-of-the-week/archive/o/oxytocin.html
https://www.britannica.com/science/amino-acid
https://www.wsj.com/articles/BL-JRTB-11551
still bitten by the bonobo bug…
Having written quite a few essays on a future bonoboesque world, I’ve found myself in possession of a whole book on our Pan paniscus relatives for the first time. All that I’ve gleaned about these fellow apes until now has been from the vasty depths of the internet, a gift that will doubtless keep on giving. My benefactor apologised for her gift to me, describing it as a coffee-table book, perhaps more pictorial than informative, but I’ve already learned much that’s new to me from the first few pages. For example, I knew from my basic research that bonobos were first identified as a distinct species in the late 1920s or early 1930s – I could never get the date straight, perhaps because I’d read conflicting accounts. De Waal presents a more comprehensive and interesting story, which involves, among other things, an ape called Mafuka, the most popular resident, or inmate, of Amsterdam Zoo between 2011 and 2016, later identified as a bonobo. The zoo now features a statue of Mafuka.
More important, though, for me, is that everything I’ve read so far reminds me of the purpose of my bonobo essays, but also makes me wonder if I haven’t focussed enough on one central feature of bonobo society, probably out of timidity. Here’s how De Waal puts it:
It is impossible to understand the social life of this ape without attention to its sex life: the two are inseparable. Whereas in most other species, sexual behaviour is a fairly distinct category, in the bonobo it has become an integral of social relationships, and not just between males and females. Bonobos engage in sex in virtually every partner combination: male-male, male-female, female-female, male-juvenile, female-juvenile, and so on. The frequency of sexual contact is also higher than among most other primates.
In our own society, definitely still male-dominated but also with a legacy of religious sexual conservatism, this kind of all-in, semi-masturbatory sexual contact is absolutely beyond the pale. I’m reminded of the Freudian concept of sublimation I learned about as a teen – the eros or sex drive is channelled into other passionate, creative activities, and, voila, human civilisation! And yet, we’re still obsessed with sex, which we’re expected to transmute into sexual fulfilment with a lifelong partner. Meanwhile, the popularity of porn, or what I prefer to call the sex video industry, as well as the world’s oldest profession, indicates that there’s much that’s not quite right about our sex lives.
This raises questions about monogamy, the nuclear family, and even the human concept of love. This is ancient, but nevertheless dangerous territory, so for now I’ll stick with bonobos. As with chimps, female bonobos often, though not always, move to other groups at sexual maturity, a practice known as philopatry. Interestingly, this practice has similarities to exogamous marriage practices, for example among some Australian Aboriginal groups. It’s interesting, then, that female-female bonds tend to be the strongest among bonobos, considering that there’s no kinship involved.
Needless to say, bonobos don’t live in nuclear families, and child-care is a more flexible arrangement than amongst humans, though the mother is naturally the principal carer. And it seems that bonobo mothers have a subtly closer relationship with their sons than their daughters:
the bond between mother and son is of particular significance in bonobo society where the son will maintain his connection with his mother for life and depend upon her for his social standing within the group. For example, the son of the society’s dominant female, the strong matriarch who maintains social order, will rise in the ranks of the group, presumably to ensure the establishment and perpetuation of unaggressive, non-competitive, cooperative male characteristics, both learnt and genetic, within the group.
Considering this point, it would be interesting to research mother-son relations among human single-parent families in the WEIRD world, a situation that has become more common in recent decades. Could it be that, given other support networks, rather than the disadvantages often associated with one-parent families in human societies, males from such backgrounds are of the type that command more respect than other males? Particularly, I would suspect, from females. Of course, it’s hard to generalise about human upbringing, but we might be able to derive lessons from bonobo methods. Bonobo mothers rarely behave punitively towards their sons, and those sons remain attached to their mothers throughout their lives. The sons of high-status females also attain high status within the male hierarchy.
Yet we are far from being able to emulate bonobo matriarchy, as we’re still a very patriarchal society. Research indicates that many women are still attracted to high-status, philandering men. That’s to say, they’ve been ‘trained’ to climb the success ladder through marriage or co-habitation than through personal achievement. They’ve also been trained into the idea of high-status males as dominating other males as well as females. It is of course changing, though too slowly, and with too many backward moves for the more impatient among us. Two macho thugocracies, Russia and China, are currently threatening the movement towards collaboration and inclusivity that we see in female-led democracies such as Taiwan, New Zealand and a number of Scandinavian countries. It may well be that in the aftermath of the massive destruction wrought by these thugocracies, there will come a reckoning, as occurred after the two ‘world wars’ with the creation of the UN and the growth of the human rights movement and international aid organisations, but it is frustrating to contemplate the suffering endured in the meantime, by those unlucky enough to be born in the wrong place at the wrong time.
Now of course all this might be seen as presenting a romanticised picture of bonobos (not to mention female humans), which De Waal and other experts warn us against. The difference in aggression between bonobos and chimps is more a matter of degree than of type, perhaps, and these differences can vary with habitat and the availability of resources. And yet we know from our studies of human societies that male-dominated societies are more violent. And male domination has nothing to do with simple numbers, it is rather about how a society is structured, and how that structure is reinforced. For example I’ve written recently about how the decidedly male god of the Abrahamic religions, originally written as YWH or Elohim, emerged from a patriarchal, polygamous society in the Sinai region, with its stories of Jacob and Abraham and their many wives, which was reinforced in its structure by origin myths in which woman was created out of a man’s rib and was principally responsible for the banishment from paradise. The WEIRD world is struggling to disentangle itself from these myths and attitudes, and modern science is its best tool for doing so.
One of the most interesting findings, then, from modern neurology, is that while there are no categorical differences between the male and the female brain in humans, there are significant statistical differences – which might make for a difference in human society as a whole. To explain further: no categorical difference means that, if you were a professional neurologist who had been studying the human brain for decades, and were presented with a completely disembodied but still functional human brain to analyse, you wouldn’t be able to assert categorically that this brain belonged to a male or a female. That’s because the differences among female brains, and among male brains, are substantial – a good reason for promoting gender fluidity. However, statistically, there are also substantial differences between male and female brains, with males having more ‘grey’ material (the neurons) and females having more ‘white’ material (the myelinated connections between neurons), and with males having slightly higher brain volume, in accord with general sexual dimorphism. In a 2017 British study involving some 5,000 subjects, researchers found that:
Adjusting for age, on average… women tended to have significantly thicker cortices than men. Thicker cortices have been associated with higher scores on a variety of cognitive and general intelligence tests.
This sounds promising, but it’s doubtful that anything too insightful can be made of it, any more than a study of bonobo neurophysiology would provide us with insights into their culture. But, you never know…
References
Frans De Waal & Frans Lanting, Bonobo: the forgotten ape, 1997.
https://www.humancondition.com/freedom-the-importance-of-nurturing-in-bonobo-society/
on the origin of the god called God, part 2: the first writings, the curse on women, the jealous god
a bonobo world? 11
another bitter-sweet reflection on capacities and failures
I was in a half-asleep state, and I don’t know how to describe it neurologically, but subjectively I was hearing or being subjected to a din in my head, a kind of babble, like in an echoing school canteen. Then I heard a knocking sound above the din, then in a transforming whoosh all the din stopped in my head, it became silent apart from the knocking, and then, as a kind of wakening crystallisation clarified things, another sound, of trickling water. I quickly realised this was the sound from the shower above me, and the knocking was of the pipes being affected by the rush of hot water. But what really interested me was what had just happened in my brain. The din, of thought, or inchoate thought, or of confusedly buzzing neural connections, was dampened down instantly when this new sound forced itself into my – consciousness? – at least into a place or a mini-network which commanded attention. It, the din, disappeared as if a door had been slammed on it.
I can’t describe what happened in my brain better than this, though I’m sure that this concentration of focus, or activity, in one area of my brain, and the concomitant dropping of all other foci or activity, to facilitate that concentration, was something essential to human, and of course other animal, neurology. Something observed but not controlled by ‘me’. Something evolved. I like the way this is shared by mice and men, women and wombats.
But of course there are big differences too. I’ve described the experience, whatever it is, in such a way that a neurologist, on reading or listening to me, would be able to explain my experience more fully, or, less likely, be inspired to examine it or experiment with its no-doubt miriad causal pathways. I suppose this experience, though more or less everyday and unthreatening, is associated with flight-or-fight. The oddity of the sound, its difference from the background din, or perhaps rather my awareness of its oddity, caused a kind of brain-flip, as all its forces, or most of them, became devoted to identifying it. Which caused me to awaken, to marshall a fuller consciousness. How essential this is, in a world of predators and home intruders, and how much fun it is, and how useful it is, to try for a fuller knowledge of what’s going on. And so we go, adding to our understanding, developing tools for further investigation, finding those tools might just have other uses in expanding other areas of our knowledge, and the world of our ape cousins is left further and further behind. For me, this is a matter of pride, and a worry. I’m torn. The fact that I think the way I do has to do with my reading and my reflections, the habits of a lifetime. Some have nerdiness, if that’s what it is, thrust upon them. I’m fascinated by the human adventure, in its beginnings and its future. Its beginnings are connected to other apes, to old world and new world monkeys, to tarsiers, to tree shrews and rodents and so on, all the way back to archaea and perhaps other forms yet to be discovered. We need to fully recognise this connectivity. Its future, what with our increasing dominance over other species and the earthly landscape, our obsession with growth, our throwaway mindset, but also our ingenious solutions, our capacity for compassion and for global cooperation, that future is and always will be a mystery, just outside of our manipulating grasp, with every new solution creating more problems requiring more solutions.
A few hundred years ago, indeed right up to the so-called Great War of 1914, human warfare was a much-celebrated way of life. And we still suffer a kind of hero-worship of military adventurism, and tell lies about it. In the USA, many times over the most powerful military nation on earth, the media are always extolling the sacrifice of those who fought to ‘keep America safe’. This is a hackneyed platitude, considering that, notwithstanding the highly anomalous September 11 2001 attack, the country has never had to defend its borders in any war. Military casualties are almost certain to occur in a foreign country, where the USA is seeking to preserve or promote its own interest, generally against the interests of that country. In this respect, the USA, it should be said, is no better or worse than any other powerful country throughout history. The myth of military might entailing moral superiority, which began with the dawn of civilisations, dies hard, as ‘American exceptionalism’ shows.
But globalism, international trade, travel, communication and co-operation, is making for a safer and less combative human society than ever before. So, as militarism as a way of life recedes, we need to focus on the problems of globalism and economic growth. As many have pointed out, the pursuit of growth and richesse is producing many victims, many ‘left-behind’. It’s dividing families and creating a culture of envy, resentment and often unmitigated hatred of the supposedly threatening ‘other’. The world of the bonobo – that tiny community of a few tens of thousands – tinier than any human nation – a gentle, fun-loving, struggling, sharing world – seems as distant to us as the world of the International Space Station, way out there. And yet…
reading matters 9
New Scientist – the collection: mysteries of the human brain. 2019
- content hints – history of neurology, Galen, Hippocrates, Descartes, Galvani, Thomas Willis, Emil Du Bois-Reymond, Santiago Ramon y Cajal, connectionism, plasticity, mind-maps, forebrain, midbrain, hindbrain, frontal, parietal and occipital lobes, basal ganglia, thalamus, hypothalamus, amygdala, hippocampus, cerebral cortex, substantia nigra, pons, cerebellum, medulla oblongata, connectome, action potentials, axons and dendritic spines, neurotransmitters, axon terminals, signalling, ion channels and receptors, deep brain stimulation, transcranial direct current stimulation, hyper-connected hubs, 170,000 kilometres of nerve fibres, trains of thought, unbidden thoughts, memory and imagination, the sleeping brain, unconscious activity, the role of dreams, brainwaves during sleep, sleep cycles, traumatic stress disorder, Parkinsons, ADHD, dementia, depression, epilepsy, anaesthesia, attention, working memory, first memories, rationality, consciousness, von Economo neurons, the sense of self…
the male and female brain, revisited
Culture does not make people. People make culture. If it is true that the full humanity of women is not our culture, then we can and must make it our culture.
Chimamanda Ngozi Adichie
An article, ‘Do women and men have different brains?’, from Mysteries of the human brain, in the New Scientist ‘Collection’ series, has persuaded me to return to this issue – or perhaps non-issue. It convincingly argues, to me, that it’s largely a non-issue, and largely due to the problem of framing.
The above-mentioned article doesn’t go much into the neurology that I described in my piece written nearly 7 years ago, but it raises points that I largely neglected. For example, in noting differences in the amygdalae, and between white and grey matter, I failed to significantly emphasise that these were averages. The differences among women in these and other statistics is greater than the differences between women and men. Perhaps more importantly, we need to question, in these studies, who the female and male subjects were. Were they randomly selected, and what does that mean? What lives did they lead? We know more now about the plasticity of the brain, and it’s likely that our neurological activity and wiring has much more to do with our focus, and what we’ve been taught or encouraged to focus on from our earliest years, than our gender.
And this takes me back to framing. Studies designed to ‘seek out’ differences between male and female brains are in an important sense compromised from the start, as they tend to rule out the differences among men and among women due to a host of other variables. They also lead researchers to make too much of what might be quite minor statistical differences. To quote from the New Scientist article, written by Gina Rippon, author of the somewhat controversial book The gendered brain:
Revisiting the evidence suggests that women and men are more similar than they are different. In 2015, a review of more than 20,000 studies into behavioural differences, comprising data from over 12 million people, found that, overall, the differences between men and women on a wide range of characteristics such as impulsivity, cooperativeness and emotionality were vanishingly small.
What all the research seems more and more to be pointing to is that there’s no such thing as a male or a female brain, and that our brains are much more what we make of them than previously thought. Stereotyping, as the article points out, has led to ‘stereotype threat’ – the fact that we tend to conform to stereotypes if that’s what’s expected of us. And all this fuels my long-standing annoyance at the stereotyped advertising and sales directed at each gender, but especially girls and women, which, as some feminists have pointed out, has paradoxically become more crass and extreme since the advent of second-wave feminism.
And yet – there are ways of looking at ‘natural’ differences between males and females that might be enlightening. That is, are there informative neurological differences between male and female rats? Male and female wolves? Are there any such differences between male and female bonobos, and male and female chimps, that can inform us about why our two closest living relatives are so socially and behaviourally different from each other? These sorts of studies might help to isolate ‘real’, biological differences in the brains of male and female humans, as distinct from differences due to social and cultural stereotyping and reinforcement. Then again, biology is surely not destiny these days.
Not destiny, but not entirely to be discounted. In the same New Scientist collection there’s another article, ‘The real baby brain’, which looks at a so-called condition known as ‘mummy brain’ or ‘baby brain’, a supposed mild cognitive impairment due to pregnancy. I know of at least one woman who’s sure this is real (I don’t know many people), but up until recently it has been little more than an untested meme. There is, apparently, a slight, temporary shrinkage in the brain of a woman during pregnancy, but this hasn’t been found to correlate with any behavioural changes, and some think it has to do with streamlining. In fact, as one researcher, Craig Kinsley, explained, his skepticism about the claim was raised in watching his partner handling the many new tasks of motherhood with great efficiency while still maintaining a working life. So Kinsley and his team looked at rat behaviour to see what they could find:
In his years of studying the neurobiology underlying social behaviours in rats, his animals had never shown any evidence of baby brain. Quite the opposite, actually. Although rats in the final phase of their pregnancy show a slight dip in spacial ability, after their pups are born they surpass non-mothers at remembering the location of food in complex mazes. Mother rats are also much faster at catching prey. In one study in Kinsley’s lab the non-mothers took nearly 270 seconds on average to hunt down a cricket hidden in an enclosure, whereas the mothers took just over 50 seconds.
It’s true that human mothers don’t have to negotiate physical mazes or find tasty crickets (rat mothers, unlike humans, are solely responsible for raising offspring), but it’s also clear that they, like all mammalian mothers, have to be more alert than usual to any signs and dangers when they have someone very precious and fragile to nurture and attend to. In rats, this shows up in neurological and hormonal changes – lower levels of stress hormones in the blood, and less activity in brain regions such as the amygdalae, which regulate fear and anxiety. Other hormones, such as oestradiol and oxytocin, soar to multiple times more than normal levels, priming rapid responses to sensory stimuli from offspring. Many more connections between neurons are forged in late pregnancy and its immediate aftermath.
Okay, but we’re not rats – nothing like. But how about monkeys? Owl monkeys, like most humans, share the responsibilities of child-rearing, but research has found that mothers are better at finding and gaining access to stores of food than non-mothers. Different behaviours will be reflected in different neural connections.
So, while it’s certainly worth exploring how the female brain functions during an experience unique to females, most of the time women and men engage in the same activities – working, playing, studying, socialising and so forth. Our brain processes will reflect the particular patterns of our lives, often determined at an early age, as the famous Dunedin longitudinal study has shown. Gender, and how gender is treated in the culture in which we’re embedded, is just one of many factors that will affect those processes.
References
New Scientist – The Collection, Mysteries of the human brain, 2019
https://en.wikipedia.org/wiki/Dunedin_Multidisciplinary_Health_and_Development_Study