Archive for the ‘brain’ Category
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
reading matters 11 – encephalitis lethargica. Will it return?
Asleep, by Molly C Crosby, 2010
Canto: This was one of the saddest books I’ve read in a long time. It’s about a disease that arose, and was recognised, at around the time of the ‘Spanish flu’ of 1918, though it was more sporadic and long-lasting, and rather more mysterious. It’s also a kind of cautionary tale for those among us who downplay the impact of diseases and their effects, which are so often long-term and horrifically devastating. It’s humbling to realise that we just don’t know all the answers to the pathogens that strike us down.
Jacinta: And could revisit us, in mutated and perhaps even more deadly form, some time in the future. This book is about encephalitis lethargica, a disease that was personal to the author, as it infected her grandmother, whose entire life, though she lived to a goodly age, was clearly stunted by it. She was struck down at the age of 16, and slept for 180 days, and though she lived almost 70 years afterwards, she was robbed by this brain-blasting illness of the life of the mind, the rising above ourselves and grasping of the world that we’re attempting in this blog. Through sheer bad luck.
Canto: And as Crosby points out, her grandmother was far from being the worst-affected victim of this disease. People died of course, but others were disastrously transformed.
Jacinta: So let’s go to a modern website, a department of the USA’s NIH, the National Institute of Neurological Disorders and Stroke, for a definition:
Encephalitis lethargica is a disease characterized by high fever, headache, double vision, delayed physical and mental response, and lethargy. In acute cases, patients may enter coma. Patients may also experience abnormal eye movements, upper body weakness, muscular pains, tremors, neck rigidity, and behavioral changes including psychosis. The cause of encephalitis lethargica is unknown. Between 1917 to 1928, an epidemic of encephalitis lethargica spread throughout the world, but no recurrence of the epidemic has since been reported. Postencephalitic Parkinson’s disease may develop after a bout of encephalitis-sometimes as long as a year after the illness.
Canto: Yes, and having read Crosby’s book and knowing about the worst symptoms and a few heart-rending cases, the sentence that most strikes me here is, ‘The cause.. is unknown’. Apparently Oliver Sacks’ book Awakenings, which we haven’t read, is all about patients who have ‘awakened’, permanently damaged, from this bizarre disease, and that’s a book we now must read, though of course it will provide us with no solutions.
Jacinta: And no arms against its future devastation, should it return – and why wouldn’t it? Crosby and others have suggested that ‘fairy stories’ like Sleeping Beauty and Rip van Winkle may have been inspired by outbreaks of the disease. Of course this is conjecture, and only if the disease returns will we be able to attack it with the technology we’ve developed in the intervening century. As the neurologist Robert Sapolsky points out in his mammoth book Behave, (so mammoth that I can’t find the quote), the number of papers published on the brain, its activity and functions, in the 21st century, has grown exponentially. We might just be ready to counteract the long term horrors of encephalitis lethargica next time round, if it comes around.
Canto: Crosby’s book is organised into case histories, featuring people who fell into this bizarre torpid state for long periods, and when aroused, often behaved in anti-social and self-destructive ways that in no way resembled depression, between bouts of a ‘normality’ that was never quite normal. And one of the saddest features of these case histories, richly described in the notes of famous figures in early neuropsychology, such as Constantin von Economo, Smith Ely Jellife and Frederick Tilney, is that the victims disappeared into the void once it became clear that no known treatment could save them.
Jacinta: Yes, some may have died soon afterward, others may have lived on in a limbo, locked-in state for decades. In fact the symptoms of this disease were bewilderingly varied -various tics, hiccupping, catatonia, salivation, schizoid episodes… Encephalitis literally means swelling of the brain, and it doesn’t take a medical degree to realise this could cause a variety of effects depending on which area of the most complex organism known to humanity is most affected.
Canto: Encephalitis is usually caused by viruses, and of course viruses hadn’t been fully conceptualised when von Economo wrote his 1917 paper on what was to become known as encephalitis lethargica, as the role of DNA and RNA was unknown. However, von Economo was the first to recognise the vital role of a tiny, almond-shaped section near the base of the brain, the hypothalamus, in the distorted sleep patterns of these patients. He also wondered if there was a connection between the so-called Spanish flu and this sleeping sickness.
Jacinta: Yes, and this brings to mind the current nightmare pandemic. People, including of course epidemiologists, are wondering about the long-term effects of this virus, especially in those who seem to have recovered from a serious infection. Crosby writes of the situation a hundred years ago:
The war had provided the first opportunity encephalitis lethargica had to crawl across the world with little notice from the medical community. And by 1918, the pandemic flu had given it the second opportunity, stealing worldwide attention, infecting and killing millions. Epidemic encephalitis moved with the flu, almost like a parasite to a host, often attacking many of the same victims, receiving very little notice at all.
Of course there has been no sign of a return of encephalitis lethargica – as yet – from a medical community that is somewhat forewarned, but it’s clear that inflammation can have very diverse effects, especially when it involves the brain.
Canto: But it’s like an undefeated enemy that has gone into hiding. We’ve defeated smallpox; tuberculosis and polio are in heavy retreat; leprosy seems as remote to us as the Bible, but this sleeping sickness, some of the victims of which have died within our lifetimes, has tantalised us with its bizarre and devastating effects, but has never really given us a chance to fight it.
Jacinta: Yes fighting is what it’s all about. The anti-vaxxers and the natural health crowd seem to want to leave everything to our immune system, to let diseases take their course, killing and maiming a substantial percentage of the herd to let the remainder grow stronger. If they were to read some of these case studies, to witness the lives of young Rosie, Adam and Ruth, they would surely think differently, if they had a modicum of humanity.
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
discussing mental health and illness
Canto: I’ve been told I’m on the autism spectrum, by someone who’s not on it, presumably, but who’s also not an expert on such things, but I’m not sure who is.
Jacinta: Well of course we’re all on the autism spectrum, it depends on your location on it, I suppose, if you need to worry. ‘You’re sick’ is one of the oldest lines of abuse, but I’m reminded of a passage in The moral landscape, which I’m currently rereading. He describes a funny-but-not-so-funny piece of research by one D L Rosenhan:
… in which he and seven confederates had themselves committed to psychiatric hospitals in five different states in an effort to determine whether mental health professionals could detect the presence of the sane among the mentally ill. In order to get committed, each researcher complained of hearing a voice repeating the words ’empty’, ‘hollow and ‘thud’. Beyond that, each behaved perfectly normally. Upon winning admission to the psychiatric ward, the pseudo-patients stopped complaining of their symptoms and immediately sought to convince the doctors, nurses and staff that they felt fine and were fit to be released. This proved surprisingly difficult. While these genuinely sane patients wanted to leave the hospital, repeatedly declared that they experienced no symptoms, and became ‘paragons of cooperation’, their average length of hospitalisation was 19 days (ranging from 7 to 52 days), during which they were bombarded with an astounding range of powerful drugs (which they discreetly deposited in the toilet. None were pronounced healthy. Each was ultimately discharged with a diagnosis of schizophrenia ‘in remission’ (with the exception of one who received a diagnosis of bipolar disorder). Interestingly, while the doctors, nurses and staff were apparently blind to the presence of normal people on the ward, actual mental patients frequently remarked on the obvious sanity of the researchers, saying things like ‘You’re not crazy – you’re a journalist’.
S. Harris, The moral landscape, p142
Canto: Well, that’s a fascinating story, but let’s get skeptical. Has that study been replicated? We know how rarely that happens. And there are quite a few other questions worth asking. Wouldn’t most of the staff etc have been primed to assume these patients had a genuine mental illness? And surely only a small percentage would have had the authority to make a decision either way. Who exactly had them committed, what was the process, and what was the relationship between those doing the diagnosis and those engaging in treatment and daily care? Was there any fudging on the part of the pseudo-patients (who were apparently also the researchers) in order to prove their point (which presumably was that mental illness can be easily shammed)? And wouldn’t you expect other patients, many of whom wouldn’t believe in their own mental problems, to be supportive of the sanity of those around them?
Jacinta: Okay, those are some valid points, but are you prepared to accept that a lot of these mental conditions, such as bipolar disorder, borderline personality disorder (the name speaks volumes), attention deficit disorder, narcissistic whatever disorder and so on, are a little flakey around the edges?
Canto: Maybe, but with solid centres I’m sure. Depression is probably the most common of those mental conditions, and too much skepticism on that count could obviously lead to disaster. Take the case of South Korea, which has one of the highest suicide rates in the world. There appears to be a nationwide skepticism about mental health issues there, which clashes with high stress levels to create a crisis of care. Professional help is rarely sought and isn’t widely available. It raises the question of the value of skepticism in some areas.
Jacinta: I wonder if the rapid advances in neurophysiology can help us here. Mental health is all about the brain. In the above quote, the pseudo-patients were mostly diagnosed with schizophrenia. That’s surprising. In my naïveté I would’ve thought there was a neurological test for schizophrenia by now.
Canto: Well, the experiment described in The moral landscape dates from the early seventies, but currently there’s still no diagnostic test for schizophrenia based on the brain itself, it’s all about such symptoms as specific delusions and hallucinations, which could still be shammed I suppose, if anyone wanted to. But what about borderline personality disorder – I was told recently that it’s very real, in spite of the name.
Jacinta: Well, there appears to be a mystery about the causes, and a general confusion about the symptoms, which seem to be rather wide-ranging – though I suppose if a patient displays several of them you can safely conclude that she’s stark staring bonkers.
Canto: Yes that’s a thing about mental illness, quite seriously. You don’t need to be an expert to notice when people are behaving in a way that’s detrimental to themselves and others, especially if it’s a sharp deviation from previous behaviour. And if it’s a slow descent, as quite often depression can be, it’s harder to pick from that person’s standard lugubrious personality, so to speak. And in the end, maybe the labelling isn’t so important as the help and the treatment. But then, people love a label – they want to know precisely what’s wrong with them.
Jacinta: I suppose the difficulty with mental illness and labelling, as opposed to labelling other more ‘physical’ illnesses or injuries, is the near-ineffable complexity of the brain. For example, I notice that among the symptoms of borderline personality disorder are apparent behaviours that don’t really cohere in any way. This site places the symptom of uncertainty and indecisiveness along with extreme risk-taking and impulsiveness, and then there is fear of abandonment, and other odd behaviours which seem to head in different directions, seeming to have one thing alone in common – being extreme or abnormal.
Canto: Yes, again, behaviour that tends to harm the self or others.
Jacinta: At the moment, I think there are still too few connections between neurology and psychiatry and the treatment of mental illness, though it’s a matter of enormous complexity. I had thought, for example, that the role of the neurotransmitter dopamine was essential to our understanding of schizophrenia, but more recent research has found that the neurochemistry of the condition involves many other factors, including glutamate, GABA, acetylcholine and serotonin. There’s so much more work to be done. But we also need to be very aware of the social and cultural conditions that tip people over the edge into mental illness. Changes in the way our brain is functioning might be seen as proximal causes of an increase in depression and suicide, but it’s more likely that the ultimate causes have to do with the stresses that particular organisations, societies and cultures impose upon us.
the self and its brain: free will encore
so long as, in certain regions, social asphyxia shall be possible – in other words, and from a yet more extended point of view, so long as ignorance and misery remain on earth, books like this cannot be useless.
Victor Hugo, author’s preface to Les Miserables
Listening to the Skeptics’ Guide podcast for the first time in a while, I was excited by the reporting on a discovery of great significance in North Dakota – a gigantic graveyard of prehistoric marine and other life forms precisely at the K-T boundary, some 3000 kms from where the asteroid struck. All indications are that the deaths of these creatures were instantaneous and synchronous, the first evidence of mass death at the K-T boundary. I felt I had to write about it, as a self-learning exercise if nothing else.
But then, as I listened to other reports and talking points in one of SGU’s most stimulating podcasts, I was hooked by something else, which I need to get out of the way first. It was a piece of research about the brain, or how people think about it, in particular when deciding court cases. When Steven Novella raised the ‘spectre’ of ‘my brain made me do it’ arguments, and the threat that this might pose to ‘free will’, I knew I had to respond, as this free will stuff keeps on bugging me. So the death of the dinosaurs will have to wait.
The more I’ve thought about this matter, the more I’ve wondered how people – including my earlier self – could imagine that ‘free will’ is compatible with a determinist universe (leaving aside quantum indeterminacy, which I don’t think is relevant to this issue). The best argument for this compatibility, or at least the one I used to use, is that, yes, every act we perform is determined, but the determining factors are so mind-bogglingly complex that it’s ‘as if’ we have free will, and besides, we’re ‘conscious’, we know what we’re doing, we watch ourselves deciding between one act and another, and so of course we could have done otherwise.
Yet I was never quite comfortable about this, and it was in fact the arguments of compatibilists like Dennett that made me think again. They tended to be very cavalier about ‘criminals’ who might try to get away with their crimes by using a determinist argument – not so much ‘my brain made me do it’ as ‘my background of disadvantage and violence made me do it’. Dennett and other philosophers struck me as irritatingly dismissive of this sort of argument, though their own arguments, which usually boiled down to ‘you can always choose to do otherwise’ seemed a little too pat to me. Dennett, I assumed, was, like most academics, a middle-class silver-spoon type who would never have any difficulty resisting, say, getting involved in an armed robbery, or even stealing sweets from the local deli. Others, many others, including many kids I grew up with, were not exactly of that ilk. And as Robert Sapolsky points out in his book Behave, and as the Dunedin longitudinal study tends very much to confirm, the socio-economic environment of our earliest years is largely, though of course not entirely, determinative.
Let’s just run though some of this. Class is real, and in a general sense it makes a big difference. To simplify, and to recall how ancient the differences are, I’ll just name two classes, the patricians and the plebs (or think upper/lower, over/under, haves/have-nots).
Various studies have shown that, by age five, the more plebby you are (on average):
- the higher the basal glucocorticoid levels and/or the more reactive the glucocorticoid stress response
- the thinner the frontal cortex and the lower its metabolism
- the poorer the frontal function concerning working memory, emotion regulation , impulse control, and executive decision making.
All of this comes from Sapolsky, who cites all the research at the end of his book. I’ll do the same at the end of this post (which doesn’t mean I’ve analysed that research – I’m just a pleb after all. I’m happy to trust Sapolski). He goes on to say this:
moreover , to achieve equivalent frontal regulation, [plebeian] kids must activate more frontal cortex than do [patrician] kids. In addition, childhood poverty impairs maturation of the corpus collosum, a bundle of axonal fibres connecting the two hemispheres and integrating their function. This is so wrong – foolishly pick a poor family to be born into, and by kindergarten, the odds of your succeeding at life’s marshmallow tests are already stacked against you.
Behave, pp195-6
Of course, this is just the sort of ‘social asphyxia’ Victor Hugo was at pains to highlight in his great work. You don’t need to be a neurologist to realise all this, but the research helps to hammer it home.
These class differences are also reflected in parenting styles (and of course I’m always talking in general terms here). Pleb parents and ‘developing world’ parents are more concerned to keep their kids alive and protected from the world, while patrician and ‘developed world’ kids are encouraged to explore. The patrician parent is more a teacher and facilitator, the plebeian parent is more like a prison guard. Sapolsky cites research into parenting styles in ‘three tribes’: wealthy and privileged; poorish but honest (blue collar); poor and crime-ridden. The poor neighbourhood’s parents emphasised ‘hard defensive individualism’ – don’t let anyone push you around, be tough. Parenting was authoritarian, as was also the case in the blue-collar neighbourhood, though the style there was characterised as ‘hard offensive individualism’ – you can get ahead if you work hard enough, maybe even graduate into the middle class. Respect for family authority was pushed in both these neighbourhoods. I don’t think I need to elaborate too much on what the patrician parenting (soft individualism) was like – more choice, more stimulation, better health. And of course, ‘real life’ people don’t fit neatly into these categories, there are an infinity of variants, but they’re all determining.
And here’s another quote from Sapolsky on research into gene/environment interactions.
Heritability of various aspects of cognitive development is very high (e.g. around 70% for IQ) in kids from [patrician] families but is only around 10% in [plebeian] kids. Thus patrician-ness allows the full range of genetic influences on cognition to flourish, whereas plebeian settings restrict them. In other words, genes are nearly irrelevant to cognitive development if you’re growing up in awful poverty – poverty’s adverse affects trump the genetics.
Behave, p249
Another example of the huge impact of environment/class, too often underplayed by ivory tower philosophers and the silver-spoon judiciary.
Sapolsky makes some interesting points, always research-based of course, about the broader environment we inhabit. Is the country we live in more communal or more individualistic? Is there high or low income inequality? Generally, cultures with high income inequality have less ‘social capital’, meaning levels of trust, reciprocity and cooperation. Such cultures/countries generally vote less often and join fewer clubs and mutual societies. Research into game-playing, a beloved tool of psychological research, shows that individuals from high inequality/low social capital countries show high levels of bullying and of anti-social punishment (punishing ‘overly’ generous players because they make other players look bad) during economic games. They tend, in fact, to punish the too-generous more than they punish actual cheaters (think Trump).
So the determining factors into who we are and why we make the decisions we do range from the genetic and hormonal to the broadly cultural. A couple have two kids. One just happens to be conventionally good-looking, the other not so much. Many aspects of their lives will be profoundly affected by this simple difference. One screams and cries almost every night for her first twelve months or so, for some reason (and there are reasons), the other is relatively placid over the same period. Again, whatever caused this difference will likely profoundly affect their life trajectories. I could go on ad nauseam about these ‘little’ differences and their lifelong effects, as well as the greater differences of culture, environment, social capital and the like. Our sense of consciousness gives us a feeling of control which is largely illusory.
It’s strange to me that Dr Novella seems troubled by ‘my brain made me do it’, arguments, because in a sense that is the correct, if trivial, argument to ‘justify’ all our actions. Our brains ‘make us’ walk, talk, eat, think and breathe. Brains R Us. And not even brains – octopuses are newly-recognised as problem-solvers and tool-users without even having brains in the usual sense – they have more of a decentralised nervous system, with nine mini-brains somehow co-ordinating when needed. So ‘my brain made me do it’ essentially means ‘I made me do it’, which takes us nowhere. What makes us do things are the factors shaping our brain processes, and they have nothing to do with ‘free will’, this strange, inexplicable phenomenon which supposedly lies outside these complex but powerfully determining factors but is compatible with it. To say that we can do otherwise is just saying – it’s not a proof of anything.
To be fair to Steve Novella and his band of rogues, they accept that this is an enormously complex issue, regarding individual responsibility, crime and punishment, culpability and the like. That’s why the free will issue isn’t just a philosophical game we’re playing. And lack of free will shouldn’t by any means be confused with fatalism. We can change or mitigate the factors that make us who we are in a huge variety of ways. More understanding of the factors that bring out the best in us, and fostering those factors, is what is urgently required.
Research articles and reading
Behave, Robert Sapolsky, Bodley Head, 2017
These are just a taster of the research articles and references used by Sapolsky re the above.
C Heim et al, ‘Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood’
R J Lee et al ‘CSF corticotrophin-releasing factor in personality disorder: relationship with self-reported parental care’
P McGowan et al, ‘Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse’
L Carpenter et al, ‘Cerebrospinal fluid corticotropin-releasing factor and perceived early life stress in depressed patients and healthy control subjects’
S Lupien et al, ‘Effects of stress throughout the lifespan on the brain, behaviour and cognition’
A Kusserow, ‘De-homogenising American individualism: socialising hard and soft individualism in Manhattan and Queens’
C Kobayashi et al ‘Cultural and linguistic influence on neural bases of ‘theory of mind”
S Kitayama & A Uskul, ‘Culture, mind and the brain: current evidence and future directions’.
etc etc etc
the amazing physiology of hummingbirds
The smallest bird on our planet is the bee hummingbird, of Cuba. The average adult weight ranges between 2 and 2.5 grams, with females being slightly larger than males. There are other tiny hummingbirds, including the bumblebee, from Mexico, and the calliope, of Canada and the US. Basically the adults of all these birds weigh little more than a couple of paper clips. Yet, as Jim Robbins reports in The wonder of birds, these featherlight birds are incredibly robust. Calliopes fly from the northern US down to Mexico every winter, often through powerful head-winds and raindrops as big as their ‘eads. They fly back north in spring, early arrivals, living on insects (their principal source of nutrients) until the flowers start blooming (providing nectar, their principal source of energy). It’s an annual journey of nearly 3000 kms.
It takes heart to undertake such a journey, and hummingbirds have plenty. The hummingbird heart is the largest of any known animal relative to its size, and its rate has been measured to reach over 1200 beats per minute (in the blue-throated hummingbird). There are some 350 species of hummingbird, all living in the Americas.
But it’s not just their long-distance flights that astonish, it’s their everyday manoeuvres. They can fly upside-down, change speed and direction smartly, and hover for long periods, even in strong winds, while collecting sweet nectar in vast quantities – as much as 12 times their body weight daily. Their wing-beat speed, which can reach 100 beats per second, is about ten times that of a pigeon, and they have the largest pectorals for their size of any bird. Birds’ pectorals, which power their flight, are always proportionally massive, taking up some 80% of their weight, but hummingbirds are clearly built for flight more than any other, which allows them to remain in the air more or less constantly. ‘It’s their default setting’, says Bret Tobalske of the University of Montana, who studies the mechanics of flight in birds, bats and insects. Tobalske has studied their flight using ultra high-speed cameras and atomised olive oil illuminated by lasers, so that the revealed air-flow around their wings can help in understanding the mechanical processes involved. He’s also used wind tunnel experiments to investigate how well the birds can withstand wind forces. In a 20mph headwind, they simply increase their wingbeat rate, and can remain hovering for up to an hour and a half.
Hummingbirds are very trainable and human-friendly, especially if you reward them with sugar water, their favourite energy hit, though the more food is laid on for them the less they’ll visit and pollinate flowers. Their beaks and long tongues are adapted to extracting nectar. The tongues themselves are an extraordinary adaptation. They’re forked at the tip, and when retracted they coil up inside their tiny heads like a garden hose. For years it was thought that the nectar was drawn out of the flowers by capillary action, like a blotter soaks up ink (showing my age), but Margaret Rubega of the University of Connecticut quickly recognised this was a crock, on first hearing of the hypothesis in the 1980s. Capillary action is a slow process, especially with more viscous liquids, but hummingbirds stick their tongues into flowers at a rate of up to 16 times a second. How their tongue works has been revealed by slow-motion photography, another example of technological advances leading to advances in knowledge – though the ingenuity of Rubega and her colleague Alejandro Rico-Guevara in working out the process played a large part. Ed Yong provides a good account here, and the more detailed original paper is also online. The hummingbird’s tongue appears to be a unique evolutionary invention, a bespoke tongue, so to speak. At its tip, where it forks, it curls up at the edges, creating two tubes. Here’s how it works, from Yong:
As the bird sticks its tongue out, it uses its beak to compress the two tubes at the tip, squeezing them flat. They momentarily stay compressed because the residual nectar inside them glues them in place. But when the tongue hits nectar, the liquid around it overwhelms whatever’s already inside. The tubes spring back to their original shape and nectar rushes into them.
The two tubes also separate from each other, giving the tongue a forked, snakelike appearance. And they unfurl, exposing a row of flaps along their long edges. It’s as if the entire tongue blooms open, like the very flowers from which it drinks.
When the bird retracts its tongue, all of these changes reverse. The tubes roll back up as their flaps curl inward, trapping nectar in the process. And because the flaps at the very tip are shorter than those further back, they curl into a shape that’s similar to an ice-cream cone; this seals the nectar in. The tongue is what Rubega calls a nectar trap. It opens up as it immerses, and closes on its way out, physically grabbing a mouthful in the process.
As Rubega and Rico-Guevara suggest in their abstract, such a unique fluid-trapping mechanism may well have biomimetic applications. As the researchers have shown, the tongue mechanism works even after the bird has died, showing that it’s in some sense independent of the bird itself, and requires none of the bird’s energy.
It shouldn’t be too much of a surprise to find that hummingbirds have the highest metabolism of any creature (excluding insects). Apart from their record heart rate, they take around 250 breaths a minute, even resting – which they rarely do. Their oxygen intake (per gram of muscle) during flight is ten times higher than that of the most elite human athletes, and they get almost all of their energy for this hyperactive life through ingested sugars – compared to a maximum of 30% for humans. They can utilise sugars for flight within 35 minutes of consumption, which requires a very rapid oxidation rate. Though it isn’t precisely known how this rapid oxidation occurs, it does explain how they can maintain flight while feeding – they’re essentially refuelling while in flight. This raises questions, though, about long-haul flights, for example across the Gulf of Mexico – a distance of 800 kms. It appears they’re able to store fat as a fuel reserve, like other migratory birds, thus almost doubling their weight before the big journey.
Hummingbird songs and calls are highly varied, and some are even ultrasonic – at a frequency above that of human hearing. These may be used to disturb the flight patterns of small edible insects. Most interestingly, neurological and genetic expression studies suggest that they are capable of vocal learning, something rare among birds as well as mammals. Research in this area is something I hope to explore more fully in future posts – it involves brain design, development and epigenetic factors.
A few other interesting points in closing. Hummingbirds do rest at night, and when there’s no available food – they can enter a state something like hibernation, when their metabolism slows almost to a full stop. They can lose about 10% of their body weight during these states. It’s also notable that they have surprisingly long life-spans for such hyperactive creatures. Average life-spans have been difficult to measure, but individuals of different species have been known to live for eleven or twelve years at least.
My growing interest in birds and other creatures, especially with regard to intelligence, has inevitably led me to the load of videos available online, displaying all sorts of amazing traits, as well as profound human-animal relations. There are too many to recommend, but I would strongly suggest to any reader that they sample some of them. Watching them is somehow uplifting, and inspires a sense of hope. Life is nothing if not ingenious, even if accidentally.
References
https://www.theatlantic.com/science/archive/2017/11/hummingbird-tongues/546992/
bird smarts and theory of mind
I like birds a lot – how could you not? I particularly like their brains, which considering their ‘beautiful plumage’, their grace in flight, their songs, their treatment of mates and offspring and their dinosaur history, is quite a big call. Not that I’ve ever seen or examined a bird’s brain, but I’ve seen and heard of some gobsmacking behaviour from some species, so I thought I might check out what’s known about their grey-white matter.
As with so many research fields, there’s been a surge in research into bird brains, and I’ve not heard the term bird-brain used as an insult in recent times. Still, when we think of bird intelligence, we tend to anthropomorphise, to compare them with us – do they play, do they use language or tools, do they recognise us individually, can they solve the same sorts of problems we can? That’s understandable enough, but in studying bird brains we should be just as thoughtful about the differences as the similarities.
The birds that have stood out for us so far are corvids – ravens, crows, jays and magpies, though many parrots such as the sadly endangered kea of New Zealand have also caught researchers’ attention. So how do these small-brained creatures manage to do the things that so impress us? Well for a start it may be more a matter of numbers than actual size (and it should be noted that birds have the largest brain to body ratio of any creature). Some research published in July 2016, which received a lot of media attention, found that bird brains pack neurons more densely than other animals. It was previously thought that neuron density didn’t vary much between species, but it’s now becoming clear this isn’t so, and actual brain size isn’t such a reliable guide to intelligence. But bird brains are really small compared to those of primates, so there must surely be other differences besides density.
But the 2016 research, which featured a revolutionary method for sampling brain tissue and making neuron counts, found that, in fact, a parrot brain contained as many neurons as some mid-sized primates. However, it’s also true that a bird’s brain is structurally different. Unsurprisingly, in the past, bird brains were thought of as primitive, and were classified as such, probably because they’re far removed from us on the evolutionary bush. Anthropomorphism again – understandably we used to feel that the only really intelligent creatures apart from us were those most closely related to us, but in recent decades we’ve learned that cetaceans, octopuses, elephants and birds, none of which are close to us evolutionarily, are highly intelligent creatures. And they’re not all mammals, and in the case of the octopus, not even vertebrates. This is quite exciting for our understanding of intelligent life forms – they can have a multitude of ‘brain plans’.
The first important bird brain anatomist was the 19th century German naturalist Ludwig Edinger, whose work was so influential that it provided the orthodox view until a few decades ago. Noting the very different structure of the bird brain, Edinger understandably assumed they couldn’t be as smart as mammals, and being one of the first to name brain structures in birds, he assigned names such as paleostriatum, suggesting a very basic region involving instinctual and motor activity. Basically, he assumed birds lacked a neocortex altogether. However, we now know that the bird brain evolved from the pallium rather than the striatum, and in 2005 it was agreed that an overhaul of bird brain nomenclature was required. All part of our more informed and respectful approach to these wondrous creatures.
National Geographic, in combination with other interested organisations, has declared 2018 the Year of the Bird, and has some fascinating pieces on bird behaviour on its website. That’s where I learned that, according to one researcher, birds’ brains are more distributed ‘like a pizza’, whereas the mammalian brain is more layered. However, the wiring that underlies long-term memory in birds (and they clearly have impressive long-term memory) and decision-making is similar to that in mammals.
Here are just a few of the extraordinary behaviours discovered. Green-rumped parrotlets of South America use calls as names for their chicks. Male palm cockatoos of New Guinea court females not only with calls but by drumming on hollow trees with twigs and seedpods – arguably a form of music. Goffin’s cockatoos, from Indonesia, make and use tools in captivity even though they’ve never been seen to do so in the wild. They’re also expert at opening locks. The National Geographic video ‘Beak and Brain: genius birds down under’ compares the kea of New Zealand’s South Island to the New Caledonian crow as problems solvers tasked with overcoming a variety of obstacles to obtain their favourite treats. It makes for riveting viewing. Other videos online show crows creating hooks on sticks and using them to pull food out of holes.
Another video, involving experiments with jackdaws by Princess Auguste of Bavaria (really), a behavioural scientist, shows that these birds are much influenced by the gaze of humans, and can be directed to act simply by the gaze of a human they have bonded with. They also appear to know when they’re not being watched, and can act more boldly in such circumstances. All of this raises obvious questions, voiced by Auguste in the video. How do jackdaws think? How is it similar to the way we think? Do they recognise intentions? Do they have a theory of mind?
This theory of mind issue comes up with a lot of birds, and other animals. It refers to whether and to what extent a creature has the ability to attribute any or all of the variety of possible mental states to itself and/or others. The question of an avian theory of mind was explored in a study entitled ‘ravens attribute visual access to unseen competitors’. In describing their experiment, the authors highlight what they see – or what skeptics see – as a problem with much experimental work that tests for theory of mind in other species. This is the question – as I understand it – of whether the bird or animal actually ‘sees’ or reads what conspecifics are thinking, or is simply following particular observable cues. It was a complex experiment involving caching (hiding a store of food for later consumption, a common raven behaviour), peepholes that were either open or closed, and inference (by the researchers) from observed behaviour to either ‘minimal’ or ‘full-blown’ Theory of Mind. As a dilettante I found much of the discussion and analysis beyond me, but I found these remarks interesting:
In conclusion, the current experiment, together with the other recent studies on chimpanzees11,12, provides strong evidence against the skeptical hypothesis that the social cognition of nonhuman animals is limited to behaviour-reading. Peephole designs can allow researchers to overcome the confound of gaze cues, but further experimental work is needed to determine the specific limits of ravens and other animals—including humans—on such tasks.
In my general reading on these matters I’ve definitely found something like a rift between the skeptics on the behaviour of higher primates, dolphins and other ‘smart’ creatures, and those who have pushed, sometimes naively, other-life smarts with regard to ‘language’, memory and emotional intelligence. What I think needs to be kept clearly in mind is that in examining intelligence, or brain power or whatever, human intelligence may be only one of a possible infinity of gold standards. Is Theory of Mind itself an anthropomorphic concept, or one that lends itself too easily to anthropomorphic thinking?
Meanwhile, experimentation and investigation of the neurological underpinnings of bird behaviour will continue, and I’ll be watching for the results. Just about to embark on Jim Robbins’ book The wonder of birds, and I hope to learn more especially about bird neurology in the future, and how it relates to birdsong. That’s a whole other issue.
another look at free will, with thanks to Robert Sapolsky
Having recently had a brief conversation about free will, I’ve decided to look at the matter again. Fact is, it’s been playing on my mind. I know this is a very old chestnut in philosophy, renewed somewhat by neurologists recently, and I know that far more informed minds than mine have devoted oodles of time and energy to it, but my conversation was with someone with no philosophical or neurological background who simply found the idea of our having no free will, no autonomy, no ‘say’ whatever in our lives, frankly ludicrous. Free will, after all, was what made our lives worth living. It gives us our dignity, our self-respect, our pride in our achievements, our sense of shame or disappointment at having made bad or unworthy decisions. To deny us our free will would deny us…. far far too much.
My previous piece on the matter might be worth a look (having just reread it, it’s not bad), but it seems to me the conundrum can be made clear by thinking in two intuitively obvious but entirely contradictory ways. First, of course we have free will, which we demonstrate with a thousand voluntary decisions made every day – what to wear, what to eat, what to watch, what to read, whether to disagree or hold our tongue, whether to turn right or left in our daily walk, etc etc. Second, of course we don’t have free will – student A can’t learn English as quickly and effectively as student B, no matter how well you teach her; this student has a natural ability to excel at every sport, that one is eternally clumsy and uncoordinated; this girl is shy and withdrawn, that one’s a noisy show-off, etc etc.
The first way of thinking comes largely from self-observation, the second comes largely from observing others (if only others were as free to be like us as we are). And it seems to me that most relationship breakdowns come from 1) not allowing the other to be ‘free’ to be themselves, or 2) not recognising the other’s lack of freedom to change. Take your pick.
So I’ve just read Robert Sapolsky’s take on free will in his book Behave, and it strengthens me in my ‘free will is a myth’ conviction. Sapolsky somewhat mocks the free will advocates with the notion of an uncaused homunculus inside the brain that does the deciding with more or less good sense. The point is that ‘compatibilism’ can’t possibly make sense. How do you sensibly define ‘free will’ within a determinist framework? Is this compatibilism just a product of the eternal complexity of the human brain? We can’t tease out the chain of causal events, therefore free will? So if at some future date we were able to tease out those connections, free will would evaporate? As Sapolsky points out, we are much further along at understanding the parts of the prefrontal cortex and the neuronal pathways into and out of it, and research increases exponentially. Far enough along to realise how extraordinarily far we have to go.
One way of thinking of the absurdity of the self-deciding self is to wonder when this decider evolved. Is it in dogs? Is it in mosquitos? The probable response would be that dogs have a partial or diminished free will, mosquitos much less so, if at all. As if free will was an epiphenomen of complexity. But complexity is just complexity, there seems no point in adding free will to it.
But perhaps we should take a look at the best arguments we can find for compatibilism or any other position that advocates free will. Joachim Krueger presents five arguments on the Psychology Today website, though he’s not convinced by any of them. The second argument relates to consciousness (a fuzzy concept avoided by most neurologists I’ve read) and volition, a tricky concept that Krueger defines as ‘will’ but not free will. Yes, there are decisions we make, which we may weigh up in our minds, to take an overseas holiday or spend a day at the beach, and they are entirely voluntary, not externally coerced – at least to our minds. However, that doesn’t make them free, outside the causal chain. But presumably compatibilists will agree – they are wedded to determinism after all. So they must have to define freedom in a different way. I’ve yet to find any definition that works for the compatibilist.
There’s also a whiff of desperation in trying to connect free will with quantum indeterminacy, as some have done. Having read Life at the edge, by Jim Al-Khalili and Johnjoe McFadden, which examines the possibilities of quantum effects at the biological level, I’m certainly open to the science on this, but I can’t see how it would apply at the macro level of human decision-making. And this macro level is generally far more ‘unconscious’ than we have previously believed, which is another way of saying that, with the growth of neurology (and my previous mention of exponential growth in this field is no exaggeration), the mapping of neurological activity, the research into neurotransmission and general brain chemistry, the concept of ‘consciousness’ has largely been ignored, perhaps because it resembles too much the homunculus that Sapolsky mocks.
As Sapolsky quite urgently points out, this question of free will and individual responsibility is far from being the fun and almost frolicsome philosophical conundrum that some have seemed to suggest. It has major implications for the law, and for crime and punishment. For example, there are legal discussions in the USA, one of the few ‘civilised’ nations that still execute people, as to the IQ level above which you’re smart enough to be executed, and how that IQ is to be measured. This legal and semi-neurological issue affects a significant percentage of those on death row. A significant percentage of the same people have been shown to have damage to the prefrontal cortex. How much damage? How did this affect the commission of the crime? Neurologists may not be able to answer this question today, but future neurologists might.
So, for me, the central issue in the free will debate is the term ‘free’. Let’s look at how Marvin Edwards describes it in his blog post ‘Free will skepticism: an incoherent notion’. I’ve had a bit of a to-and-fro with Marvin – check out the comments section on my previous post on the topic, referenced below. His definition is very basic. For a will, or perhaps I should say a decision, to be free it has to be void of ‘undue influences’. That’s it. And yet he’s an out and out determinist, agreeing that if we could account for all the ‘influences’, or causal operants, affecting a person’s decision, we could perfectly predict that decision in advance. So it is obvious to Marvin that free will and determinism are perfectly compatible.
That’s it, I say again. That’s the entire substance of the argument. It all hangs on this idea of ‘undue influence’, an idea apparently taken from standard philosophical definitions of free will. Presumably a ‘due influence’ is one that comes from ‘the self’ and so is ‘free’. But this is an incoherent notion, to borrow Marvin’s phrase. Again it runs up against Sapolsky’s homunculus, an uncaused decider living inside the brain, aka ‘the self’. Here’s what Sapolsky has to say about the kind of compatibilism Marvin is advocating for, which he (Sapolsky) calls ‘mitigated free will’, a term taken from his colleague Joshua Greene. It’s a long quote, but well worth transcribing, as it captures my own skepticism as exactly as anything I’ve read:
Here’s how I’ve always pictured mitigated free will:
There’s the brain – neurons, synapses, neurotransmitters, receptors, brain-specific transcription factors, epigenetic effects, gene transpositions during neurogenesis. Aspects of brain function can be influenced by someone’s prenatal environment, genes, and hormones, whether their parents were authoritarian or their culture egalitarian, whether they witnessed violence in childhood, when they had breakfast. It’s the whole shebang, all of this book.
And then, separate from that, in a concrete bunker tucked away in the brain, sits a little man (or woman, or agendered individual), a homunculus at a control panel. The homunculus is made of a mixture of nanochips, old vacuum tubes, crinkly ancient parchment, stalactites of your mother’s admonishing voice, streaks of brimstone, rivets made out of gumption. In other words, not squishy biological brain yuck.
And the homunculus sits there controlling behaviour. There are some things outside its purview – seizures blow the homunculus’s fuses, requiring it to reboot the system and check for damaged files. Same with alcohol, Alzheimer’s disease, a severed spinal cord, hypoglycaemic shock.
There are domains where the homunculus and that biology stuff have worked out a détente – for example, biology is usually automatically regulating your respiration, unless you must take a deep breath before singing an aria, in which case the homunculus briefly overrides the automatic pilot.
But other than that, the homunculus makes decisions. Sure, it takes careful note of all the inputs and information from the brain, checks your hormone levels, skims the neurobiology journals, takes it all under advisement, and then, after reflecting and deliberating, decides what you do. A homunculus in your brain, but not of it, operating independently of the material rules of the universe that constitute modern science.
This captures perfectly, to me, the dilemma of those sorts of compatibilists who insist on determinism but. They seem more than reluctant to recognise the implications of that determinist commitment. It’s an amusing description – I love the bit about the aria – But it seems to me just right. As to the implications for our cherished sense of freedom, we can at least reflect that it has ever been thus, and it hasn’t stopped us thriving in our selfish, selfless ways. But as to the implications for those of us less fortunate in the forces that have moved us since childhood and before, that’s another story.
References
https://ussromantics.com/2018/05/15/is-free-will-a-thing-apparently-not/
R Sapolsky, Behave: the biology of humans at our best and worst, Bodley Head 2017. Note especially Chapter 16, ‘Biology, the criminal justice system and free will’.
https://plato.stanford.edu/entries/compatibilism/#FreWil
https://www.psychologytoday.com/au/blog/one-among-many/201803/five-arguments-free-will
https://www.theatlantic.com/notes/2016/06/free-will-exists-and-is-measurable/486551/
What’s up with Trump’s frontal cortex? part 2
Before going on with my thoughts about little Donnie’s brain, I want to address two pieces of relevant reading I’ve done lately.
First, the short article by ‘Neuroskeptic’ entitled ‘Don’t blame Trump’s brain‘. Now, as anyone who’s read much of my blog knows, I consider myself a skeptic and a supporter of the skeptical community. However, I don’t entirely agree with Neuroskeptic here. First, describing people’s attempt to work out Trump’s psychology or neurology from his words and actions as ‘Trumphrenology’ is a silly put-down. In fact, all psychiatric conditions are diagnosed on the basis of observed words and acts – duh, what else? Unless there’s a brain injury or genetic abnormality. So the medical terms used to describe Trump and others do have some validity, though I agree that ‘medicalising’ the problem of Trump can be counter-productive, as it is with many ‘conditions’ which have appeared recently to describe the spectra of human behaviour. It’s more important, in my view, to recognise Trump as a career criminal than to put a psycho-neurological label on him. Then again, as someone who doesn’t believe in free will, the brain that makes Trump be Trump is of some interest to me. Second, Neuroskeptic describes the arguments of those who attribute medical conditions to people on the basis of behaviour as ‘circular’. This is false. Behaviour is more than s/he thinks it is. When we try to understand the brain, we look at how it behaves under particular conditions. According to Neuroskeptic ‘it’s rarely useful to try to understand a behaviour in neuroscientific terms’. If that’s true, then the monumental 700-page book Behave, by Robert Sapolsky, one of the world’s leading neurobiologists, was largely a waste of time. Third, Neuroskeptic questions the validity and ethics of Trump ‘diagnosis-at-a-distance’. This is absurd. Over the past two years alone, Americans have been subjected to several thousand tweets, hundreds of televised speeches and comments, and the day-to-day actions of the lad in the White House. Unless they make a real effort to switch off, most Americans can’t help knowing more about Trump than they do about just about anyone in their intimate circle. Where’s the distance?
Second, on The dangerous case of Donald Trump, by 27 people working in the field of mental health. I’ve not read it, but I’ve read the ‘summary’, attributed to Bandy X Lee, the contributing editor of the full book, though I prefer to believe that Lee, a respected Yale professor of psychology, had no hand in writing this summary, which is, syntactically speaking, the worst piece of published writing I’ve ever read in my life (I say this as a language teacher). I prefer to believe it was written by an intellectually disabled computer. I’m sure the full book is far far better, but still I’m amused by the variety of conditions Trump may be suffering from – ADHD, malignant narcissism, borderline personality disorder, psychopathology, sociopathology, delusional disorder, generalised anxiety disorder etc (OK that last one is what most reasoning Americans are supposedly suffering from because of Trump). All of this is a bit of a turn-off, so I won’t be reading the book. I tend to agree with what Neuroskeptic seems to be inferring – that we don’t need a psychiatric diagnosis as an excuse to get rid of Trump – his obviously asinine remarks, his insouciant cruelty and his general incompetence are in full view. His criminality should have seen him in jail long ago, for a long time. Further, the idea that a diagnosis of mental instability could lead to invoking the 25th amendment is absurd on its face. Anyone who’s read the 25th amendment should see that. I don’t see any evidence that Trump’s condition is deteriorating – he’s been consistently deceitful and profoundly incurious throughout his life. That means he was elected as a fuckwitted dickhead. Don’t blame Trump, blame those who elected him. And blame the lack of checks and balances that should make it impossible for just anyone to become President. Democracy does have its flaws after all.
So what are the patterns of behaviour that might lead to a diagnosis, which then might be confirmed neurologically – if, for example we were to apply a tranquillising dart to this bull-in-a-china-shop’s voluminous rump, then tie him up and probe his frontal and pre-frontal regions and their connections, in response to questioning and other fun stimuli (I’d love to be in charge of that operation)?
I’ll first list some notable Trump behaviours and traits, recognised by the cognoscenti, without suggesting anything about their relation to frontal cortex disfunction.
- A tendency, or need, to take credit for everything positive that happens within his particular environment, and a concomitant tendency, or need, to blame anyone else for everything negative occurring in that environment
- a winner/loser mentality, in which losers are often members of ‘losing’ cultures, sub-groups or entities (blacks, latinos, women, the failing NYT) and winners are judged in terms of pure power and wealth (Putin, Kim, Manafort, Fred Trump)
- lack of focus in speeches and an inability to listen; generally a very limited attention span
- frequently cited temper tantrums
- lack of empathy and consideration for others, to quite an extreme degree, close to solipsism
- emphasis on compliance and deference from others, inability to deal with criticism
- extreme lack of curiosity
- lack of interest in or understanding of ethics
- lack of interest in or understanding of concepts of truth/falsehood
- extreme need to be the centre of attention
I think that’s a good start. As to how these traits map on to psychopathological states and then onto cortical development, I won’t be so psychopathological as to provide clear answers. Most people I’ve spoken to suggest malignant narcissism as a pretty good fit for his behaviour – perhaps due to its all-encompassing vagueness? Wikipedia describes it as ‘a hypothetical, experimental diagnostic category’, which doesn’t sound promising, and it isn’t recognised in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), though narcissistic personality disorder (NPD) is. I suppose that some people want to particularly emphasise Trump’s malignancy, but I think NPD is bad enough. Here’s the Wikipedia description, drawn from the latest DSM and other sources:
a personality disorder with a long-term pattern of abnormal behavior characterized by exaggerated feelings of self-importance, excessive need for admiration, and a lack of empathy. Those affected often spend a lot of time thinking about achieving power or success, or on their appearance. They often take advantage of the people around them. The behaviour typically begins by early adulthood, and occurs across a variety of social situations.
Now, I came up with the Trump behavioural traits before I read this description, I swear. I think the fit is pretty exact, but it’s clear that those responsible for diagnosing someone with NPD don’t do so on the basis of brain scans. I’ve explored enough neurology to fairly safely say that NPD, psychopathy and many other psychiatric conditions just can’t, as yet be reliably correlated with neurological connections or lack thereof. Even schizophrenia, one of the more treatable psychotic conditions, is rarely described in terms of brain function, and is diagnosed entirely through behaviour patterns.
Having said this, all of these conditions are entirely about brain function, and in Trump’s case, brain development since early childhood. We’ll never get to know what precisely is up with Trump’s frontal cortex, partly because we’ll never get that tranquilising dart to penetrate his fat arse and to then practise Nazi-like experimentation… sorry to dwell so lovingly on this. And partly because, in spite of the galloping advances we’re making in neurology, we’re not at the knowledge level, I suspect, of being able to pinpoint connections between the amygdalae, the hypothalamus, the hippocampus and the various regions of the frontal and prefrontal cortex. I plan to do more research and reading on this, and there may be another blog piece in the offing. However, one thing I can say – Trump probably isn’t a psychopath. Psychopaths tend not to have temper tantrums – their emotional responses are minimal, rather than being exacerbated by life’s slings and arrows, and their violence is instrumental rather than impassioned. Their amygdalae – the founts of aggression and anxiety – are correspondingly reduced. Doesn’t sound like Trump.
Again, though reflection on Trump’s curious psyche may be intrinsically interesting, it’s his crimes that should do him in. As I’ve said before, the fact that he’s not currently in custody is a disgrace to the American criminal and legal system. His fixer is facing a jail term, and in pleading guilty to two felony counts of campaign finance violations, has fingered Trump as the Mr Big of that operation. Those authorities who have not arrested him should themselves be facing legal action for such criminal negligence. And of course other crimes will be highlighted by the Mueller team in the near future, though such scams as Trump University should have seen him jailed long ago. Others have suffered lengthy prison terms for less. But that’s the USA, the greatest democracy in the greatest, free-est and fairest nation in the history of the multiverse. Maybe such overweening pride deserves this fall…