Gilbert Ryle and the brain

During a recent Twitter conversation I was urged to read philosopher Gilbert Ryle’s book The Concept of Mind, written just after WW2.

The conversation was about the purpose of speech and evolved into a discussion of brain function. I enjoyed reading Ryle’s book – he thinks incisively, has a dry sense of humour and a strong sense of the absurd – and I think I grasped at least the key points of his argument.

On the mind

If I’ve understood him correctly, Ryle is saying:

1. When we talk about bodies and minds as if they are the same sort of thing, we make a ‘category error’. Even if we talk about bodies and minds as if they are the same sort of thing, we can’t infer that the mind exists in the same way as the body exists. A body is a publicly observable thing; we can see it, touch it, measure it, weigh it. We can’t do any of those things to minds; a surgeon couldn’t dissect out someone’s mind from their body. Ryle illustrates the point by comparing the clause ‘she came home in a flood of tears’ with ‘she came home in a sedan chair’; both clauses might be true, but they are true in different ways.

2. We use the term ‘mind’ to refer to a particular set of things that people do – thinking, feeling, knowing etc. But thinking, feeling and knowing are characteristics of people, in the same way as brittleness is a characteristic of glass. We might say ‘the glass broke because it was brittle’, but we don’t mean that the fact that the glass was brittle caused it to break; something else was the cause – like a stone striking the glass, or it being dropped.

3. Similarly, when we say “Jill stormed out of the room because she was angry” we don’t mean that Jill felt anger in her mind and the anger caused her to storm out of the room, we mean that something happened to make Jill feel angry and also to make her storm out of the room – someone was rude to her, perhaps. We don’t have to introduce a hypothetical construct like ‘mind’ in order to explain Jill’s feeling or her behaviour.

Having demonstrated that the concept of mind itself is flawed – it isn’t a thing inside human beings but a label that we attach to certain human activities, Ryle goes on to explore the far-reaching implications for the way we construe knowledge, will, emotion, sensation, intellect etc. I was with him up to this point.

On the brain

What was noticeable about The Concept of Mind is that Ryle hardly mentions the brain, except in respect of psychologists studying patients with brain damage. One could argue, with justification, that Ryle isn’t writing about the brain, he’s writing about the mind, or more accurately, the non-existence of the mind. Others have argued that the brain and the mind are the same thing, but that idea poses a problem if you don’t think the concept of ‘mind’ is necessary to explain thinking, feeling, knowing or behaving. So where does the brain come into all this?

Philosophers, brains and education

Philosophy isn’t my field, but I had come across Ryle previously. When my son started school, he was identified as having ‘special educational needs’. Years ago, when I was teaching, I’d taught kids like my son, and even more years ago had gone to school with kids like him, and I was puzzled as to why his not uncommon difficulties with literacy and numeracy seemed to be posing such a challenge for the education system. So I started reading up on the subject. One book I read was Deconstructing Special Education and Constructing Inclusion by Gary Thomas and Andrew Loxley, published in 2001. We were getting along swimmingly until chapter 4, ‘Thinking about learning failure, especially in reading’. Here, the authors questioned the existence of phonological awareness, a key concept in some models of learning to read, and they drew on the ideas of Ryle, Willard Van Orman Quine and Ludwig Wittgenstein, all philosophers of language, in support. Thomas and Loxley appeared to acknowledge the involvement of the brain in learning, but didn’t seem to know much about what happens in the brain during learning. They claimed, for example, that “When we learn to drive, we do just that: learn to drive – and we do so in a car, on a road” (p.69). From the perspective of a casual observer, maybe. But at the level of the brain, there’s a great deal of complex activity going on whilst learning to do something like drive a car. And of course some people don’t learn to drive however hard they try, and others can’t because of brain damage or physical disability.

Thomas and Loxley’s model of learning appears to be one in which the brain is an amorphous mass. For example, they cite Wittgenstein’s observation of seeds where he says;

“nothing in the seed corresponds to the plant which comes from it: so that it is impossible to infer the properties or structure of the plant from those of the seed … so an organism might come into being even out of something quite amorphous, as it were causelessly; and there is no reason why this should not really hold for our thoughts.” (p.69)

Wittgenstein made this observation in 1947, two years before Ryle wrote The Concept of Mind. He prefaced his comment by being quite explicit about brain function:

“No supposition seems to me more natural than that there is no process correlated with associating or thinking; so that it would be impossible to read off thought-processes from brain-processes. I mean this: If I talk or write there is, I assume, a system of impulses going out from my brain and correlated with my spoken or written thoughts. But why should the system continue further in the direction of the centre? Why should this order not proceed, so to speak out of chaos?” (Klagge p.98)

Thomas and Loxley also base their claim for the non-existence of phonological awareness on work by Karl Lashley and Antonio Damasio (p.70). In the 1950s Lashley had concluded that the ‘engrams’ he believed encoded memory were distributed evenly across the brain. Antonio Damasio’s work is much more recent, but the authors appear to have misunderstood it. They say “current knowledge of the brain provides a picture of indissoluble interconnections in which it is impossible to disaggregate, for example, the relationship of that which we call affect from that which we call reason” (p. 70). It’s certainly true that Damasio’s work showed that ‘affect’ and ‘reason’ aren’t clearly demarcated in the brain, but that’s as much to do with our constructs ‘affect’ and ‘reason’ as it is to do with the way the brain functions. You can’t deduce from that that the brain as a whole consists of ‘indissoluble interconnections in which it is impossible to disaggregate’ things the brain does.

Thomas and Loxley aren’t the only authors I’ve encountered who appear to have concluded that thinking, feeling and knowing aren’t an outcome of processes in the brain. I once ploughed through PMS Hacker’s Philosophical Foundations of Neuroscience (2003). What Hacker seemed to object to was neuroscientists referring to the brain as if it were an agent; as in ‘the brain detects…’ or ‘the brain responds by…’. I could see what he was getting at; one of the points Ryle makes about the mind is that if we have to construct it in order to explain what causes thinking, feeling and knowing etc., we then have to ask what causes the mind to cause thinking, feeling and knowing etc, and so on and so on in an infinite regression. I suspect Hacker sees the brain in the same way; that if we assume the brain causes thinking, feeling and knowing etc, we have to ask what causes the brain to cause these activities in another infinite regression. It makes more sense to construe thinking, feeling and knowing etc, as characteristics of people, as things people just do. But I think there are two problems with the arguments put forward by Hacker, Thomas and Loxley and Wittgenstein. The first is that they are making another category error and the second is that they have overlooked how the characteristics of things contribute to the causes of events.

Another category error

Ryle might not have been writing about the brain, but some of the people who are applying his reasoning to the brain are doing just that, and I think they are making exactly the same kind of category error that’s a key point in Ryle’s argument against the existence of the mind. Ryle, rightly, pointed out that even though we talk about the body and the mind as if they are the same type of thing, it doesn’t follow that they are the same type of thing. Indeed we know they’re not the same type of thing because bodies are publicly observable but minds aren’t. But bodies and brains are the same type of thing; brains might usually be hidden by the skull, but they can be dissected out, weighed, measured and made publicly observable. In other words, although there’s no evidence that the mind exists, the brain indisputably exists, is the same sort of thing as the body and is inextricably linked to it.

The characteristics of things

Ryle refers several times to the analogy of glass being brittle to show why we can’t argue that the mind must cause things to happen. He sees brittleness as being a ‘disposition’ of glass, something inherent in its nature that means it shatters rather than bends when certain causal events occur, such as it being hit by a stone. In the same way people have dispositional characteristics that result in them thinking, feeling or behaving in certain ways when certain causal events occur – they feel angry when people are rude to them, or sad when someone dies. Although I can see Ryle’s point, what he overlooks is the process that occurs when glass shatters.

Glass (mainly consisting of silicon dioxide) shatters rather than bends if hit by a stone, due to its molecular structure. And its molecular structure is an emergent property of the arrangement of the sub-atomic particles that make up silicon dioxide and that function according to the laws of physics. Biological organisms have structures that are much more complex than glass and they behave very differently to glass, but ultimately they are also made up of configurations of sub-atomic particles that conform to the laws of physics. It’s the configuration of the particles that makes glass behave like it behaves and allows human beings to behave as they behave; obviously because the configuration in humans is much more complex, we have constraints placed on us and affordances open to us that glass doesn’t have.

At one level, you could say that glass shatters if it’s hit by a stone because that’s just what glass is like; but at another level, being hit by a stone causes a reaction in the molecules of the glass that results in it not maintaining its structure and falling into fragments. Similarly, at one level you could say that people just get angry or feel sad when certain things happen, and you don’t need to invent some hypothetical thing called a ‘mind’ to explain it. At another level, that’s a cop-out, because it completely overlooks what happens in people’s bodies when they do get angry or feel sad in response to something happening.

Moving back to Bowlby

It was instructive to compare Ryle’s chapter on emotion with John Bowlby’s chapter on feeling and emotion in Attachment, published 20 years later. Bowlby applies Ryle’s line of reasoning to feelings. (He refers to ‘feelings’ rather than ‘affect’ or ‘emotion’ because ‘feelings’ encompasses the other two and is self-explanatory.) Bowlby doesn’t see feelings as having an independent existence but as characteristics of physiological processes, in exactly the same way as Ryle saw thinking, feeling and knowing as being ‘dispositions’ of people. Bowlby quotes philosopher Susanne Langer;

“When iron is heated to a critical degree it becomes red; yet its redness is not a new entity which must have gone somewhere else when it is no longer in the iron. It was a phase of the iron itself, at high temperature.

As soon as feeling is regarded as a phase of a physiological process instead of a product of it – namely a new entity physically different from it – the paradox of the physical and the psychical disappears.” (Bowlby p.108)

Like Ryle, Bowlby concludes that people’s feelings and dispositions aren’t things with an independent existence in the ‘mind’, nor are they what causes people to behave in certain ways. But what he does recognise is that physiological processes are involved in feelings, and Bowlby appears to know a good deal more about those physiological processes than Ryle, Thomas and Loxley, Hacker and Wittgenstein.

Why does any of this matter, anyway? Isn’t it all a storm in a philosophical teacup? It matters because Ryle’s reasoning is being applied, and applied wrongly, to child development and education.

Child development and education

Something that’s intrigued me in my recent exploration of the child development and education literatures is their focus on theoretical frameworks developed prior to the 1950s. Lev Vygotsky died in 1934, Sigmund Freud in 1939, Wittgenstein in 1951 and Lashley in 1958. The Concept of Mind was published in 1949. But the 1950s saw a sea-change in our understanding of both genetics and brain function. In 1953, James Watson and Francis Crick published their work on the structure of DNA and in 1959 David Hubel and Torsten Wiesel figured out the basic mechanism for sensory processing from their work on the visual cortex of the cat. These two discoveries alone essentially spawned the modern sciences of genetics, molecular biology and cognitive neuroscience that have transformed biology and medicine. But these discoveries have implications for child development and education of which people working in child development and education often seem blissfully unaware.

I suspect that lack of awareness is because of the increased specialisation that’s taken place alongside a rapid increase in human knowledge over the past century or so. People studying child development or education have their work cut out getting a good knowledge of their own field, never mind studying genetics, molecular biology and brain science as well. But you don’t need a vast knowledge of genes, molecules or neurons to understand the principles of how they function, and if our understanding of those principles has changed in the last sixty years, it’s important to know how it’s changed. It’s disastrous to carry on using models of child development and education devised before we knew how genes or brains functioned.

I recognise that some people see brain science as the answer to everything – when it isn’t. We don’t need to know what’s happening in children’s brains to know whether a particular method of teaching reading or arithmetic has been effective, or to have to do a brain scan to demonstrate that maltreatment in infancy might have been harmful. But what happens in children’s brains is crucial to their development and learning, and the better we understand the processes, the better we will understand how to best support development and learning. If thinking, feeling, knowing and behaving are being construed, wrongly, as ‘just happening’ in children, and brain function and physiological processes are simply being overlooked, or worse, denied to be happening, we’re missing an important piece of the human jigsaw puzzle.

References
Bennett, MR & Hacker, PMS (2003) Philosophical Foundations of Neuroscience, Blackwell. Bowlby, J (1982) Attachment (2nd edition), Basic Books.
Klagge, J(2010) Wittgenstein in Exile, The MIT Press.
Ryle, G (1949) The Concept of Mind, Peregrine Books.
Thomas, G & Loxley A (2001) Deconstructing special education and constructing inclusion, Open University Press.

Acknowledgement: photograph of Ryle from Philosophy Pages http://www.philosophypages.com/ph/ryle.htm

the myth of the first three years

Reading John Bruer’s book The Myth of the First Three Years was like watching the past few months of my life flash before my eyes. That’s because, gratifyingly, Bruer comes to similar conclusions about the basis of child development theories currently influencing public policy. My one reservation about his book is its title and the repeated references to the ‘myth’ in the text. Technically Bruer is right to use this word for the cluster of popular ideas about the first three years because myths often have some basis in fact, but I think it’s a bit misleading because the word ‘myth’ is also widely used to mean something that has no basis in fact. The myth of the first three years conforms closely to the OECD definition of a ‘neuromyth’ – a “misconception generated by a misunderstanding, a misreading or a misquoting of facts scientifically established (by brain research) to make a case for the use of brain research in education and other contexts”. Other people have other reservations about Bruer’s work. One Amazon.com reviewer complained that the book jacket reveals he’s ‘not even a doctor!’ She obviously missed the significance of Bruer’s presidency of the James McConnell Foundation that awards grants for biomedical and educational research.

Bruer’s book deals with three aspects of what I’ll call the first three years model. He describes how the model migrated from research findings to public policy and the changes it underwent en route. He then explains what the research findings actually were, and what they mean for parents. Although the book was published over a decade ago, the first three years model has, as is traditional, taken a decade to cross the Atlantic, so is now very relevant to the coalition government’s social policy in the UK.

How the first three years model evolved

Bruer cites the developmental psychologist Jerome Kagan’s view that infant determinism – the idea that early experiences have a lasting effect on development – dates from a folk belief in 18th century Europe popularised by writers such as Rousseau. I think that the origins are more likely to be as old as parenthood. Like many of my contemporaries I was brought up on Biblical wisdom and was familiar with sayings such as; “Train up a child in the way he should go: and when he is old, he will not depart from it” (Proverbs 22:6). “He that spareth his rod hateth his son: but he that loveth him chasteneth him betimes” (Proverbs 13:24). The book of Proverbs dates from around 900 BC – the origins of the proverbs are likely to be much older.

Infant determinism was a theme explored by Freud and further developed by figures such as John Bowlby, Mary Ainsworth, Harry Harlow, Rene Spitz and Benjamin Bloom. During this period, as Bruer points out, the study of the brain and the study of behaviour, despite being seen as complementary in the late 19th century, have followed largely independent paths. It’s only since the implications of brain research for human behaviour have become clearer that the two paths have begun to cross more frequently. From the 1970s onwards, fields such as education and child development began to co-opt findings from neuroscience into their own theoretical models. Bruer traces the way neuroscience has been interwoven with child development theories from, for example, the Clinical Infant Development Project that began in the 1970s and developed into Zero to Three: The National Centre for Infants, Toddlers and Families. And from the 1979 book Education and the Brain, through to the I Am Your Child campaign that began in the mid-1990s, and on into public policy.

Research findings

Bruer identifies three key areas of neuroscience research that underpin the first three years model; neural connections, critical periods and the effects of enriched or complex environments. To illustrate how misconceptions about research have arisen, I’ll summarise the findings he discusses and what they might tell us about child development.

Neural connections Neurons are the cells in the brain that transmit information. They are formed – around 100 billion of them – by the second trimester of gestation, and soon after birth will have migrated to their final destinations in the brain. Neurons are nerve cells and in order to transmit information between each other, they need to be connected. The connections aren’t direct however, they are via synapses – points where the axon terminal of one neuron is close enough to the dendrite of another for chemical or electrical signals to pass from one to the other (see figure). In humans, synapse formation begins a couple of months before birth and peaks at 2-3 years after birth, when the number of synapses is many times greater than it is in adults.

At the same time, two other processes are going on – apoptosis and synaptic pruning. Apoptosis is cell death, and many neurons, like other cells in the body, do die off during normal development. During synaptic pruning the neurons don’t die, but the number of connections the neuron has with other neurons decreases. Between early childhood and puberty, the number of synapses in the brain gradually declines but remains above adult levels. Between puberty and adulthood, synaptic pruning increases rapidly.

Critical periods In early research into the functioning of the visual cortex of the cat, Torsten Hubel and David Wiesel found that if kittens were deprived of visual input from one eye during the first few weeks of life, they remained blind in that eye. It’s long been known that children with congenital cataracts usually develop normal vision if the cataract is removed within the first year after birth. If cataract removal is delayed, vision may never be normal. We know that children can learn to speak a second language like a native if they acquire that language before their teens – if not, the language can still be learned, but with a noticeable accent. So there are critical periods in child development when certain sensory input is necessary for typical development to take place.

Enriched or complex environments Charles Darwin had noted that animals reared in the wild tended to have larger brains than their domesticated offspring. Harlow’s famous experiments demonstrated that baby monkeys reared in isolation showed severe behavioural abnormalities. And experiments in the 1970s conducted by Greenough and colleagues showed that rats reared in complex environments had a greater density of synapses than those raised in solitary conditions. It was clear that the environment has a significant impact on brain development.

Applying the research findings to child development

The model of the first three years has arisen partly because research findings have been misunderstood. Several factors need to be borne in mind before applying the findings to children.

1. Many of the research findings relate to animals, notably rats and monkeys that are often used in research because they are small, easy to handle and have relatively short life-cycles. Rats and monkeys are also social, problem-solving mammals, which means they have a lot in common with humans. Although their brains are very likely to function in similar ways to human brains, there might be species-specific differences. One of the differences is that they develop at different rates; rats are sexually mature by about six weeks of age, and macaques at around five years, so extrapolating findings to humans relies on estimates for the ages at which children reach similar developmental stages.

2. Many of the research findings are estimations. It’s impossible to count the number of synapses or neurons in a brain, so proxy measures are used such as the density of synapses in a small portion of the cortex. But different techniques have been used to arrive at those measures; one group of scientists calculated density of synapses in whole human cortical tissue and found that density peaked at three years of age; others used a different method to calculate the synaptic density in monkeys and estimated that density would peak at seven months in humans. These differences were resolved, but demonstrate that research findings need to be interpreted carefully.

3. Many research findings apply to specific locations in the brain. Huttenlocher, for example, has reported the density of synapses in the human brain peaking at around three months after birth in the auditory cortex, at 8-12 months in the visual cortex but not until 3.5 years in the frontal area. Similarly, synaptic pruning in auditory and visual areas reduces synapse densities to adult levels by 11-12 years of age, but not in frontal areas until several years later.

4. It’s not always clear whether developmental changes in the brain are determined by biological factors, by environmental factors, or by both. Clearly biology would have more influence than environment on the migration of brain cells before birth, but work on synapse formation suggests it is triggered by novel learning experiences. Novel experiences tend to diminish as children get older, and familiar experiences are by definition experienced repeatedly, suggesting a cause for synaptic pruning. However, the increased rate of synaptic pruning after puberty implies that some biological control might be involved.

Common misunderstandings

It’s easy to see how the first three years model came into being. There are differences between the brains of toddlers, older children and adults. It’s tempting to assume that the rapid synapse formation and rapid learning that take place during the first three years of life offer a now-or-never window of developmental opportunity. Synaptic pruning, viewed from a ‘use it or lose it’ perspective, makes it look as if this opportunity soon runs out, despite clear evidence that older children, adolescents and adults can learn a great many things that toddlers can’t. This misconception underpins the current vogue for early interventions. The idea of critical periods has resulted in a tendency for governments (at least in the US and UK) to front-load the education system because of an assumption that the earlier learning takes place the better. What the evidence indicates is that critical periods tend to involve low-level processing of sensory information and that broader ‘sensitive periods’ (e.g. for language acquistion) are not clear-cut. With regard to enriched or complex environments, the enriched environment enjoyed by Greenough’s lab rats was probably a lot less stimulating than the environment experienced by wild rats. Lab rats, however well cared for, tend not to lead a very exciting existence. In other words, children would need to be pretty deprived to experience the kind of environment that resulted in a reduced synapse density.

Chinese whispers

The transformation of a tentative conclusion based on findings from rats or monkeys into public policy that lacks a sound evidence-base appears to have begun in one of two ways;

• Journalists have accurately summarised research findings but their reports have been misinterpreted by some readers
• Journalists have misunderstood research findings and have inadvertently misled readers.

Casual readers of newspapers or magazines can be forgiven for getting hold of the wrong end of the stick; they often don’t have the time or inclination to check the original data. Policy-makers, in my view, have no such excuse. Governments have enormous resources at their disposal, and academics, however busy, are usually only too keen to explain their findings to willing listeners. There is no good reason why public policy shouldn’t be based on sound evidence.

The first three years model fits easily into our pre-existing mental models. Infant determinism has been seen as the key to solving problems such as poor educational and health outcomes, addiction, anti-social behaviour and criminal activity that preoccupy policy makers – it’s simpler to blame parents for bringing up their children badly than to trace back the complex causes of ‘problem’ behaviours and address them all. The model has also played to the anxieties of parents who understandably want to do the best for their children. The acceptance of the first three years model by parents and policy-makers has resulted in a proliferation of early interventions. So what effect have they had?

The outcomes of early interventions

Evidence from the evaluation of early interventions cited by Bruer, and from studies tracking changes in people’s lives over time suggests that;

• the best predictor of a child’s school performance is mother’s IQ or educational attainment
• good quality childcare improves school performance for children from ‘deprived’ environments (but not from less deprived ones)
• early interventions that focus on verbal skills improve children’s school performance up to about the age of eight – enough to reduce the number of children who repeat the first few school years
• early interventions that focus on verbal skills result in a marginal improvement in school performance, in the length of time spent in education, and in slightly later parenthood
• people tend to settle down as they get older
• chance events play a big part in lifetime achievement.

The pattern that emerges from these evaluations – and this speculative because I don’t have access to raw data – appears to centre on two factors; children’s language skills when they start school, and the way schools educate children. I think these factors have two implications for early interventions.

Firstly, children who are behind their peers with verbal skills when they start school are clearly at a disadvantage, but only because schools use language as the primary medium for education. Language is one of the things that distinguishes homo sapiens from other species. Spoken and written language allow us to communicate vast amounts of information to each other, so it’s obviously desirable that as many children as possible develop good skills in spoken and written language. But being skilled in spoken and written language is not synonymous with learning; children can also learn through practical experience, watching plays or listening to stories. Language skills, although an important component of the school curriculum, shouldn’t be made an obstacle to learning.

Secondly, although some early interventions have had positive outcomes, the effects have tended to be small. Politicians in favour of these programmes would doubtless argue that any positive outcomes are worth it, but given the importance of verbal skills, it might be more cost effective to improve access to speech and language therapy, especially since so many developmental disorders involve speech and language deficits.

What should parents do?

When I was expecting my first child, a friend gave me a book that advocated a ‘best odds’ approach to pregnancy – the author pointed out that nothing can guarantee that a baby will be completely healthy, but there are things that mothers can do that increase the odds in their baby’s favour. It’s a sensible and realistic approach. Bruer’s conclusion is that most parents are doing fine with their children and that we already know what children need and what’s bad for them. He advises parents to interact with their babies, fix known problems – especially visual, auditory and language ones – as soon as possible, and as neuroscientist Steve Petersen put it “Don’t raise your children in a closet, starve them or hit them in the head with a frying pan”.

References
Bruer, John T., (1999). The myth of the first three years, New York: The Free Press.

Green, E.J., Greenough, W.T. & Schlumpf, B.E. (1983). Effects of complex or isolated environments on cortical dendrites of middle-aged rats, Brain Research, 264,, 233–240.

Huttenlocher, P.R, de Courtena, C., Garey, L.J. & Van der Loosa, H. (1982). Synaptogenesis in human visual cortex — evidence for synapse elimination during normal development, Neuroscience Letters, 33, 247–252.

Organisation for Economic Co-operation and Development (2007) Understanding the brain: the birth of a learning science: The Birth of a New Learning Science: v. 2, OECD.

Image of synapses from Wikipedia.

Bruce Perry on nature, nurture and neglect

Bruce Perry is an internationally recognised authority on child trauma, and, like Allan Schore, is frequently cited in the child development and child protection literature. In this post, I look at Perry’s paper “Childhood Experience and the Expression of Genetic Potential: What Childhood Neglect Tells Us About Nature and Nurture”. I’ve chosen this paper because it tackles the nature/nurture issue head-on and also because it’s the source of the cover illustration for Graham Allen’s Early Intervention: The Next Steps. (The illustration also appears in a recent article in The Telegraph.)

On first reading, I found Perry’s paper slightly disconcerting due to its variable style. The opening section gets quite lyrical;

“Are we born evil – natural born killers or the most creative and compassionate of all animals? Are we both? Does our best and our worst come from our genes or from our learning? Nature or nurture?” (p.80)

and

“Humankind’s transient but magnificent rebellion against nature is allowed by the brain” (p.81).

That’s followed by a densely factual account of brain development and function, a brief review of historical studies of infant neglect, a detailed account of a study co-authored by Perry involving brain scans and finally a highly speculative section on socio-emotional growth derived from the concept of attachment. Stylistic issues aside, my first problem with this paper was that Perry frames human survival primarily in terms of social relationships.

Survival and instinctive behaviours

Although, oddly, Perry doesn’t actually mention Bowlby in this paper, he begins with what’s essentially an expansion on Bowlby’s environment of adaptedness ;

“Three key brain-mediated capabilities must be present for our species to survive: individual survival, procreation and the protection and nurturing of dependents. Failure in any of these three areas would lead to extinction of our species. The brain, therefore, has crucial neural systems dedicated to (1) the stress response and responding to threats – from internal and external sources; (2) the process of mate selection and reproduction and (3) protecting and nurturing dependents, primarily the young.” (p.81)

My reservation about this claim is that although Perry is right about the three capabilities, the first – individual survival – doesn’t map directly onto (1), a neural system dedicated to a stress response, because survival requires more than just a response to threat. It also requires the ability to find food and shelter, for example. I suppose the reflexes that underlie rooting, suckling, foraging, hunting and nest-building (used by many species for their sleeping arrangements) could at a stretch be classified as responses to threat (of starvation, predation or hypothermia), but these behaviours come into play in order to avert threat, rather than as a response to it. Not only are they not responses to stresses or direct threats, but stresses or threats usually disrupt them. In addition of course, the brain has ‘crucial neural systems’ dedicated to many functions other than the three listed.

Perry then goes on;

“The primary strategy we use to meet these objectives is to create relationships. Relationships which allow us to attach, affiliate, communicate and interact to promote survival, procreation and the protection of dependents. It is the brain that allows humans to form the relationships which connect us – one to another – creating the myriad groups – that have been the key to our success on this planet.” (p.81)

Creating relationships has certainly been an important factor in our ecological ‘success’ but whether it is the primary strategy is debatable. Our problem-solving capability and language have been also been crucial, demonstrated by the fact that human beings have been more successful, than say, chimpanzees, who are social primates par excellence.

So although I wouldn’t dispute Perry’s conclusion that

“… some of the most powerful and complex neural systems in the human are dedicated to social affiliation and communication.” (p.81),

I get the impression that he sees human ecological success in terms of social affiliation and communication, rather than social affiliation and communication being two factors that contribute to human ecological success. The nature of Perry’s model might explain the absence of a detailed discussion of the role of genetic factors in development.

Normal and abnormal: genetic variation

The next section of the paper consists of an excellent summary of brain development and function, listing eight key processes. My one reservation is about Perry’s conclusion. He says:

“The eight key neurodevelopmental processes described above are dependent
upon the genome and environmentally-determined microenvironmental cues …. Disruption of the pattern, timing or intensity of these cues can lead to abnormal neurodevelopment and profound dysfunction.” (p.85)

What bothered me was the implicit assumption that there is such a thing as ‘normal’ neurodevelopment. In a large population, the measures of many characteristics, such as height or weight, fall into a ‘normal’ distribution – when represented as a graph, they form a bell-shaped curve. The majority of individuals cluster around the middle of the curve – the 50th percentile. In the case of head circumference (the measure Perry uses in cases of neglect), as head size increases above or decreases below the 50th percentile, fewer and fewer individuals have those larger or smaller head sizes. With regard to measures used in medicine, approximately 95% of the population is generally considered to form the ‘normal range’. So around 2.5% of the population with the smallest head sizes and around 2.5% with the largest head sizes are considered to have ‘abnormal’ head sizes, but in a statistical sense only – it doesn’t mean there’s necessarily anything wrong with the individuals concerned.

normal distribution

The bell-shaped curve reflects the range of genetic and environmental factors that contribute to differences between individuals. I think Perry’s (and Bowlby’s and Schore’s) omission of a discussion about genetic variation between individuals is significant. It’s especially significant in Perry’s case, since his paper claims to be about genetic potential. Each of these authors appears to employ a model of genetic development similar to the one popular during the early days of genetic research – of an unfolding species-specific genetic blueprint. For example, Perry says;

“Sensitive periods are different for each brain area and neural system, and therefore, for different functions. The sequential development of the brain and the
sequential unfolding of the genetic map for development mean that the sensitive periods for neural system [sic] (and the functions they mediate) will be when that system is in the developmental ‘hot zone’ – when that area is most actively organizing.” (p.88, my emphasis)

which means that;

“The simple and unavoidable conclusion of these neurodevelopmental principles
is that the organizing, sensitive brain of an infant or young child is more malleable to experience than a mature brain. While experience may alter the behavior of an adult, experience literally provides the organizing framework for an infant and child. Because the brain is most plastic (receptive to environmental input) in early childhood, the child is most vulnerable to variance of experience during this time.” (p.88)

Although at one level Perry’s conclusion is correct, he doesn’t mention that individual variations in genetic endowment are also involved in neural development; I get the impression that he sees human genetic endowment as standard issue (any exceptions being immediately obvious), so that as a general rule experience alone provides the organizing framework for brain development. This isn’t the case, of course. Deletions, insertions and duplications of genetic material, both inherited and occurring spontaneously between generations, combined with epigenetic changes (the environment acting on genetic expression) that can also be inherited, result in each individual being genetically as well as environmentally unique. This means that the only way one can safely use the term ‘abnormal’ in relation to development is in a statistical sense – in terms of the normal range for any particular characteristic. But Perry’s paper isn’t about genetic endowment, it’s about genetic potential.

Genetic potential

Perry explains genetic potential like this;

“Genes are designed to work in an environment. Genes are expressed by microenvironmental cues, which, in turn, are influenced by the experiences of the individual. How an individual functions within an environment, then, is dependent upon the expression of a unique combination of genes available to the human species. We don’t have the genes to make wings. And what we become depends upon how experiences shape the expression – or not – of specific genes we do have. For thousands of years, the genetic potential to use “joysticks” was not expressed – nor that for written language or reading. Yet when experiences are provided in a structured, patterned and appropriately timed way, that potential can be expressed and neural systems which mediate all of those functions will develop.”(p.86; Perry’s emphasis)

There are several ambiguities in this paragraph; notably about genetic design and genetic expression and potential.

Firstly, as far as I’m aware, there’s no evidence that genes are designed to do anything. Genes are molecular units that behave in certain ways in the presence of other molecular units or in certain chemical and physical microenvironments. How an individual functions in response to those microenvironments is dependent not upon the expression of a unique combination of genes available to the human species, but to the individual human being. Genetic endowment alone, regardless of environment, can, for example, result in a failed conception, a miscarriage or an individual born with ‘profound dysfunction’.

Secondly, the term genetic expression usually refers to the chemical (in most cases a protein) that’s produced using information from a gene; using the term ‘genetic expression’ in relation to broader human potential is, I feel, a bit confusing. Being able to read, write or use joysticks aren’t abilities encoded in our genes, they are affordances– a range of things we have the potential to do as a consequence of genetic expression.

Normal and abnormal: environmental variation

Perry points out that animals raised in enriched environments have been found to have larger, more complex and functionally more flexible brains than those raised in more deprived environments, and that animals raised in the wild tend to have larger brains than their domesticated offspring. He concludes;

“It is plausible, however, that abnormal microenvironmental cues and atypical patterns of neural activity during sensitive periods in humans could result in malorganization and compromised function in a host of brain-mediated functions. Indeed, altered emotional, behavioral, cognitive, social and physical functioning has been demonstrated in humans following specific types of neglect.” (p.90)

I’m not convinced that Perry has fully thought through the implications of what he considers to be ‘normal’ and ‘abnormal’ microenvironmental cues. Perry clearly approves of the hunter-gatherer lifestyle – or at least the social aspects of it;

“The genetic potential for healthy socio-emotional functioning – to be empathic, to share, to invest in the welfare of the community – is better expressed in children living in hunter-gatherer bands or extended families or close-knit communities in comparison with our compartmentalized modern world.” (p.96)

And he disapproves of aspects of the modern developed world, questioning the size of households, the amount of television we watch and the way our children are segregated from adults in schools (p.96). What Perry fails to recognize, I feel, is that lifestyle isn’t necessarily based on free choice. Nor does he recognize that something that’s beneficial in some respects might be damaging in others.

Children raised in hunter-gatherer communities are essentially brought up in ‘the wild’. Animals and humans raised in the wild are at high risk of death from starvation, injury or disease, so we would expect their brains to reflect such an ‘enriched’ environment because of the constant need to be on the alert for risk factors. Domesticated animals (and humans) clearly don’t face the same challenges, so we’d expect their brains to reflect that difference. It doesn’t follow, of course, that an animal kept confined in a concrete pen, or a neglected child, is better off than a member of its species engaged in hunting and foraging. But hunter-gatherer communities have no choice about living in large groups, because nuclear family units wouldn’t have the resources to ensure a constant food supply or protection from attack. That doesn’t mean a high risk of starvation, injury or disease is a good thing, nor does it mean that people are necessarily happier when living in close proximity to large numbers of other people. One has only to read the Old Testament to learn some salutary lessons about how extended families can malfunction; I don’t think it’s any coincidence that when they’ve had the option, many families have chosen to live as nuclear units.

Perry clearly doesn’t think that a high risk of starvation, injury or disease is beneficial to children’s development, and despite his doubts about ‘electronic activities’ (p.97) believes that some modern technologies (reading, writing and joysticks) are benign. In short, he picks and chooses which aspects of modern life he considers to be damaging, but doesn’t provide a coherent explanation as to why. Suggesting that it’s because we’ve departed from a hunter-gatherer lifestyle doesn’t hold water, because there are aspects of hunter-gatherer lifestyles that Perry would object to. I think he needs to clarify what he means by ‘abnormal microenvironmental cues’, ‘atypical patterns of neural activity’ and ‘altered emotional, behavioral, cognitive, social and physical functioning’ – altered from what, exactly? What does he consider to be the norm and why?

Neglect

Following his discussion of neurodevelopment, Perry introduces the topic of neglect, which he defines as ‘the absence of critical organizing experiences at key times during development’(p.88). He then considers two forms of neglect, one involving sensory deprivation and the other affecting the development of socio-emotional potential.

“Two forms of “neglect” will be considered below: extreme multi-sensory
neglect in childhood and a more subtle, insidious decrease in our opportunities to
elaborate our socio-emotional potential caused by the sociocultural changes in how
we choose to live. The sensory deprivation neglect results in obvious alterations in
neurobiology and function while the second form has an almost invisible toxic
impact on the developing child – and ultimately, society.” (p.88)

Perry claims that neglect has – ironically – been neglected by researchers mainly because it’s difficult to “see”, citing specifically emotional neglect (p.88) and the importance of touch in early development and referring to Rene Spitz’ work with institutionalized infants (p.89). I wouldn’t dispute that emotional neglect is harmful, nor that tactile experience is important for the development of proprioceptive and motor function, but, as far as I recall, Spitz (and Harlow with his baby monkeys) made some assumptions about what was missing from the environment of the deprived infants. In addition to emotional engagement and tactile deprivation, there were clearly questions over the adequacy of nutrition – vitamin D levels, for example – and precisely what sensory stimuli were absent. Spitz’ children would have been very susceptible to viral infections, also difficult to “see”. For example, Spitz (1957) describes deprived children rotating their heads around the sagittal axis (i.e. from side to side) and interprets this movement as the children using a universal human signifier for ‘no’ – despite the fact that head-shaking isn’t a universal human signifier for ‘no’ and that it can result from middle ear infections (common in infants, especially if they are supine for long periods) or from impaired development of the cerebellum.

The outcomes of neglect

Perry then moves on to clinical findings in relation to neglect and presents the results from a study he co-authored comparing children subjected to different types of neglect. To summarise, institutionalized and neglected children tend to show low IQs, developmental delays and small head size. This developmental trend is reversed when children are placed in good foster homes or adopted, younger children making better progress than older ones. Perry’s investigation of head size leads him to conclude that neglect results in impaired brain development and he supports this conclusion by referring to evidence from brain scans.

Perry and Pollard (1997) investigated four groups of children;

“Global Neglect (GN; n = 40); Global Neglect with Prenatal Drug Exposure (GN+PND; n = 18); Chaotic Neglect (CN; n = 36); Chaotic Neglect with Prenatal Drug Exposure (CN+PND; n = 28). Measures of growth were compared across group [sic] and compared to standard norms developed and used in all major pediatric settings”. (p.92)

Global neglect is defined by “a history of relative sensory deprivation in more than one domain (e.g., minimal exposure to language, touch and social interactions)” and chaotic neglect as “far more common and was considered present if history was obtained that was consistent with physical, emotional, social or cognitive neglect.” (p.92)

Perry and Pollard found that for the global neglect group, the mean head circumference was below the 5th percentile, but such a dramatic variation from the norm wasn’t seen in the chaotic neglect group. For the global neglect group, 17 MRI or CT scans were available – 11 of them were judged ‘abnormal’ by neuroradiologists. 26 scans were available for the chaotic neglect group, but only 3 were judged ‘abnormal’.

Unanswered questions

The material on clinical and neurobiological findings raises many unanswered questions. Why were the children in institutions? Were their parents dead, ill or did they lack the resources or ability to care for their children? Were genetic or physiological causes for the children’s poor development ruled out? Why were children neglected at home? What specific factors necessary for healthy development were absent? Why were CT and MRI scans available? Had brain damage or a medical condition been previously suspected?

Until these questions are answered, all that Perry’s data can tell us is that specific groups of children, raised in specific conditions (characterized by unspecified inadequacies), showed delayed or abnormal development. All we have is a correlation between neglect and poor development. We don’t know if the neglect caused the poor development, or if it did, which elements of the neglect caused what developmental deficits.

But Perry doesn’t identify precisely which sensory domains were neglected or how, or what aspects of physical, emotional, social or cognitive input were missing. Specifying the components of neglect isn’t important if you’re interested only in the degree of neglect, but it becomes very important if you’re mapping neglect onto brain abnormalities or want to compensate for specific factors that might have been absent in early development.

Brain abnormalities

What Perry does tell us is that two particular brain anomalies were identified from the CT and MRI scans; enlarged ventricles or cortical atrophy. (You can see abnormalities of the ventricles and cortex in the right-hand image of Perry’s Figure 1, below.)

Perry’s Figure 1

The ventricles are spaces in the brain that join up with the central canal of the spinal cord and are filled with cerebro-spinal fluid. The lateral ventricles are visible in the centre of the CT scan images. Cortical atrophy means that the cortex of the brain has shrunk, usually due to the degeneration of cells.

It’s possible that the neglect experienced by the children resulted in these two brain anomalies; but there are other possible causes. Enlarged ventricles occur in around 1% of pregnancies for a variety of reasons, unlikely to be due to global or chaotic neglect as defined by Perry, but he doesn’t mention the possibility of enlarged ventricles occurring prenatally. Perry and Pollard’s data indicate that the globally neglected children also showed low height and weight, and the authors do mention that nutrition might be involved. Cortical atrophy can also have a variety of medical causes. In short, although neglect is a possible cause, it’s only one of several possibilities.

Support for the hypothesis that neglect rather than genetic make up or medical conditions caused the brain abnormalities comes from the finding that a year after neglected children were placed in foster care, head size had increased, the increase being inversely correlated with the child’s age (younger children showed greater increases). Even so, in the Perry and Pollard study the youngest children’s head size was still below the 30th percentile – we aren’t told whether the youngest children eventually ‘caught up’ with their non-neglected peers and we don’t know whether the children would have had small heads regardless of whether or not they were neglected. In addition, the head circumference data are presented as means – we aren’t told the range of measurements involved for each age range. It could be that the group mean is artificially high because one child’s head size increased significantly, or artificially low because one child’s head size remained small.

Although some parts of Perry’s paper are very useful – the sections on brain development and the summary of the history of child neglect research, for example – in general I found it frustrating, for three reasons. These are that Perry conflates correlation with causality, fails to take adequately take into account individual variations and doesn’t define neglect with sufficient accuracy.

Correlation and causality Running through this paper is an implicit assumption that if that neglect is associated with developmental and brain abnormalities, those abnormalities must be caused by neglect. This is a basic error of data analysis. Although it’s likely that neglect causes developmental problems – otherwise it wouldn’t be called ‘neglect’ – it’s impossible to tell from Perry’s data whether;

• neglect caused the brain abnormalities
• the brain abnormalities caused the neglect (if the brain abnormalities were also present in parents or neglect was a response to the children’s behaviour)
• there were other causes for the abnormalities, or
• which components of neglect were responsible for which brain abnormalities.

Individual variation Perry doesn’t seem to take individual variation into account; in his Figure 1 he compares a neglected brain on the 3rd percentile with a non-neglected one on the 50th percentile, when a comparison with a 3rd percentile non-neglected brain would probably have been more informative. And his graph of the increase in head-size when children of different ages are fostered, presents mean values for each age group rather than the range of head sizes for each group.

Defining neglect There’s no question that children need certain conditions for healthy development. A nutritious balanced diet, fresh air, exercise and sunlight, a stimulating environment and consistent, caring stable relationships suggest themselves. The absence of any of these factors can cause deficits in development – the child might not reach their genetic potential as Perry suggests. But apart from making a distinction between extreme (global) neglect and more common (chaotic) neglect, Perry doesn’t discriminate between the different components of neglect and their possible effects. It’s important that we know what components of neglect have what outcomes because if we don’t, whether or not a child has been ‘neglected’ ends up being a matter of personal judgement. In his closing section, for example, Perry suggests that living in small social units and watching several hours of television a day is detrimental. He’s entitled to his view of course, but provides no evidence to support his claim, apart from pointing out the decline in the number of people who vote in Presidential elections (p.97).

Why Perry’s paper worries me

What worries me about Perry’s paper is that, despite its weaknesses, because it’s relevant to a highly specialised domain, it’s unlikely to be read by the geneticists and the evolutionary, developmental and molecular biologists who are in a position to critique it. Perry’s work has been cited, uncritically, in a number of policy documents. His argument in this paper is superficially plausible because, like Bowlby, he constructs it by juxtaposing several indisputable ideas (e.g. human lifestyles have changed, children are developing, neglect can be harmful) but the definitions of underlying concepts and the causal links between them, by contrast, are rather tenuous. But a busy social worker, school nurse, health visitor or even doctor, is quite likely not to notice the weaknesses in the definitions or causal links. Perry’s paper is likely to be seen as providing evidence that neglect (sometimes seen by professionals as synonymous with parenting strategies of which they personally disapprove) causes abnormal brain development. Or worse, that abnormal brain development will be assumed to be caused by neglect, rather than by one or more of many possible causes.

References

Perry, B.D. and Pollard, D. (1997). “Altered brain development following global neglect in early childhood”. Society For Neuroscience: Proceedings from Annual Meeting, New Orleans.

Spitz, R.A. (1957). No and yes : on the genesis of human communication. New York : International Universities Press.

Normal distribution curve from: http://en.wikipedia.org/wiki/Percentile_rank

another post about nature and nurture: Allan Schore’s model

Allan Schore’s work is widely cited in the child development and child protection literatures – notably in documents relevant to public policy. In this post I look at Schore’s paper ‘Attachment and the regulation of the right brain’ because it deals directly with Bowlby’s theory of attachment. Schore seeks to map Bowlby’s model of attachment onto recently acquired knowledge about how the brain develops, and a shortened version of this paper forms the foreword to a reprint of Bowlby’s classic book Attachment.

Schore is described on his website as “the American Bowlby”, so I expected to see similarities between his model of attachment and Bowlby’s. There is indeed a resemblance, but Schore differs from Bowlby in the use of three terms; ‘emotion’, ‘imprinting’ and ‘environment of adaptedness’. These differences sound trivial, but in fact are quite important.

Schore summarises Bowlby’s model of attachment as follows (page references are for Attachment unless otherwise indicated);

“…that attachment is instinctive behavior with a biological function, that emotional processes lie at the foundation of a model of instinctive behavior, and that a biological control system in the brain regulates affectively driven instinctive behavior.” (Schore p.24)

Emotion

A key departure from Bowlby is encapsulated in the phrase ‘emotional processes lie at the foundation of a model of instinctive behavior’. Schore’s reasoning goes as follows;

“Bowlby emphasizes the salience of ‘facial expression, posture, tone of voice, physiological changes, tempo of movement, and incipient action’ (p.120). The appraisal of this input is experienced ‘in terms of value, as pleasant or unpleasant’ (pp.111–112) and the movements ‘may be actively at work even when we are not aware of them’ (p.110); in this manner feeling provides a monitoring of both the behavioral and physiological state (p.121). Emotional processes thus, he says, lie at the foundation of a model of instinctive behavior.” (Schore pp.28-29)

Firstly, I think Schore differs from Bowlby over emotional processes lying at the foundation of anything. Bowlby’s reasons for avoiding using the term ‘emotion’ are pretty clear; he sees emotion as part of a range of ‘feelings’ and those feelings as being part of an organism’s appraisal of its environment; feelings would include hunger, thirst and discomfort – not usually classified as emotions. To clarify his point Bowlby quotes philosopher Susanne Langer’s analogy of the heating and cooling of iron:

“When iron is heated to a critical degree it becomes red; yet its redness is not a new entity which must have gone somewhere else when it is no longer in the iron. It was a phase of the iron itself, at high temperature.

As soon as feeling is regarded as a phase of a physiological process instead of a product of it – namely a new entity metaphysically different from it – the paradox of the pyschical and the physical disappears.” (p.108)

Certainly emotional processes (or more accurately ‘feelings’) are an important part of Bowlby’s model of attachment because the expression of feeling is the means of communication between infant and carer. But the phrase ‘emotional processes lie at the foundation of a model of instinctive behavior’ to me implies that in order to be foundational, emotional processes must have an existence independent of the process of appraisal – exactly the opposite of what Bowlby and Langer are saying.

The second point is that Schore doesn’t say that emotional processes lie at the foundation of a model of attachment, but at the foundation of a model of instinctive behaviour. I suspect many of the zoologists cited by Bowlby in his analysis of instinctive behaviour would disagree. Even according to Bowlby’s definition (which excludes reflexes) many behaviours he would consider instinctive don’t actively involve emotion as far as we can tell. He cites for example, imprinting (e.g. ducks and geese following the first object they see after they hatch) and nest-building as instinctive behaviours, but although these behaviours might be associated with emotion (difficult to assess in birds) there is as far as I’m aware no evidence that emotional processes are foundational to them. Of course it could be argued that Schore is referring exclusively to humans, in which case he would be departing from Bowlby’s model again, because Bowlby clearly sees human instinctive behaviour as on a continuum with instinctive behaviour across the animal kingdom.

Despite Bowlby explicitly choosing not to use the term ‘emotion’ Schore’s paper contains 69 mentions of it in 26 pages. Here are a couple of them;

“… Bowlby’s scientifically-informed curiosity…envisioned the center stage of human infancy, on which is played the first chapter of the human drama, to be a context in which a mother and her infant experience connections and disconnections of their vital emotional communications.” (Schore pp.23-24)

I’m not sure this Bowlby actually did this, since he saw emotional communications as only part of the complex interactions involved in attachment, he wasn’t happy with the use of the term ‘emotion’, and goes into some detail about why he doesn’t use it.

“… in his second volume Bowlby (1973) attempted to define more precisely the
set-goal of the attachment system as seeking not just proximity but access to
an attachment figure who is emotionally available and responsive.” (Schore p.26)

I haven’t read Bowlby’s two later volumes (Separation and Loss), but searching their text on-line shows Bowlby using the word ‘emotionally’ descriptively in case studies, but only one instance of him referring to the mother being “physically present but ‘emotionally’ absent” (Loss, p.43; the quotes around ‘emotionally’ are Bowlby’s). Again, he’s guarded about the use of this word and doesn’t seem to see emotion per se as central to the mother-child interaction.

Imprinting

‘Imprinting’ is a term that has several different meanings. In studies of development, it refers to an animal learning to recognise the features of a particular stimulus – regardless of what happens as a result. Konrad Lorenz’s famous experiments showed that goslings imprint on the first object they see, whether that object is their mother or Lorenz’s boots. But Schore doesn’t use ‘imprinting’ in quite the same way.

“Attachment theory, as first propounded in Bowlby’s (1969) definitional
volume, is fundamentally a regulatory theory. Attachment can thus be conceptualized
as the interactive regulation of synchrony between psychobiologically attuned organisms. This attachment dynamic, which operates at levels beneath awareness, underlies the dyadic regulation of emotion. Emotions are the highest order direct expression of bioregulation in complex organisms (Damasio, 1998). Imprinting, the learning process it accesses, is described by Petrovich and Gewirtz (1985) as synchrony between sequential infant maternal stimuli and behavior…” (Schore, p.34)

I think this paragraph simply lumps together attachment, emotion and imprinting and assumes they form a coherent whole. The first part of the paragraph – about attachment – makes sense in the light of Bowlby’s explanations. But no supporting evidence is offered for the claim that attachment underlies the dyadic regulation of emotion, and Damasio’s claim about emotions doesn’t necessarily have anything to do with dyadic interactions. And the final sentence is unclear about what ‘it’ refers to or why imprinting necessarily involves maternal stimuli or synchrony – young birds have been reported imprinting onto inanimate objects.

Emotion and imprinting are lumped together again here;

“Emotionally focused limbic learning underlies the unique and fast-acting processes of imprinting, the learning mechanism associated with attachment, as this dynamic evolves over the first and second years. Hinde (1990, p.162) points out that ‘the development of social behavior can be understood only in terms of a continuing dialectic between an active and changing organism and an active and changing environment.” (Schore pp.30-31)

Again, an unsupported claim is made about emotion and imprinting and Hinde’s comment about social behaviour being an interaction between an organism and its environment involves a dialectic much broader than that between an infant and primary caregiver.

Another anomaly in the use of the term ‘imprinting’ occurs here;

“… I offer evidence to show that attachment experiences, face-to-face transactions of affect synchrony between caregiver and infant, directly influence the imprinting, the circuit wiring of the orbital prefrontal cortex, a corticolimbic area that is known to begin a major maturational change at 10 to 12 months and to complete a critical period of growth from the middle to the end of the second year.” (Schore p.30)

‘Imprinting’ has a number of different meanings, including psychological imprinting (the way it’s usually used in studies of development), but it can also mean to impress or make a mark, so can be used in reference to neural circuits. It’s quite likely that imprinting in the behavioural sense is associated with imprinting in the neural sense, but to use the same term with different meanings without clarification is confusing.

Environment of adaptiveness

Bowlby frequently refers to what he calls the ‘environment of adaptedness’, the environment that shaped human instinctive behaviour. In other words, it’s an environment to which the behaviour is adapted (past tense). But Schore uses the term ‘environment of adaptiveness’ instead. I assumed he must explain elsewhere why he does this, until I noticed that he misquotes Bowlby;

“More specifically, it [the control system for instinctive behaviour] evolves in the infant’s interaction with an ‘environment of adaptiveness, and especially of his interaction with the principal figure in that environment, namely his mother’ (p.180).” (Schore p.28; Bowlby has ‘adaptedness’ in the original from which Schore quotes)

Schore also appears to use the term ‘environment of adaptiveness’ to mean something different to the ‘environment of adaptedness’;

“… Bowlby concludes that the mother–infant attachment relation is ‘accompanied by the strongest of feelings and emotions, happy or the reverse’ (p.242), that the infant’s ‘capacity to cope with stress’ is correlated with certain maternal behaviors (p.344), and that the instinctive behavior that emerges from the co-constructed environment of evolutionary adaptiveness has consequences that are ‘vital to the survival of the species’(p.137).” (Schore pp.28-29)

For Bowlby, the ‘environment of adaptedness’ was the evolutionary environment that interacted with genetic endowment to produce the instinctive behaviours typical of human beings. For healthy development to take place, a child needs to be raised within the limits of that environment. For Schore the ‘environment of adaptiveness’ is an environment co-constructed with the mother. In relation to attachment, the two would be very similar, but Bowlby’s environment is much broader than Schore’s. It includes, but isn’t limited to, the interaction with the mother. Schore not only narrows Bowlby’s concept considerably, he actually changes Bowlby’s terminology without – in this paper at least – explaining why.

Placing mother-child interactions centre-stage

I have three main problems with models like Freud’s, Bowlby’s and Schore’s, that make parental behaviour central to the development of child behaviour. The first is that making any factor central by definition marginalizes other factors. There’s a difference between saying “My theoretical model recognizes that there are n factors involved in the development of child behaviour and I’m going to focus on factor a” and saying “There are n factors involved in the development of child behaviour but only factor a is important, so it’s the only one I’ll include in my model”. Some factors are undoubtedly more important than others, and parental behaviour might be one of them, but that doesn’t mean we can assume it’s central to child development. Bowlby bases his assumption that it is, on the correlation found by psychoanalysts between pathologies of personality and childhood trauma. The problem with that correlation is that although childhood trauma might be the cause of a personality pathology it doesn’t mean it’s necessarily the cause or that it’s the only cause. There might be people with pathologies who didn’t have a traumatic childhood, or some who have had a traumatic childhood but haven’t developed pathologies. Psychoanalysts would be unlikely to see many patients in the latter group.

My second misgiving is that a link between childhood trauma and pathology is intuitively appealing. Most of us can recall childhood events involving our parents that we still find painful many years later and examples of other parents dealing with their children inappropriately readily spring to mind. But we don’t often hear people say “I reckon it’s due to a 7R variant of DRD4” or “I suspect serotonin levels, myself” or even, surprisingly since it affects up to 20% of some populations, “Have you considered lactose intolerance?” partly because all these possible causes of abnormal behaviour require more specialized rather than general knowledge and also because they are not obvious – they need to be tested for.

The third reason is related to the second – and it’s that the link between childhood trauma and pathology is superficially simple. Most people will know of examples that appear to confirm it. Fewer people are likely to be familiar with the complex physiological pathways triggered by genes that can affect brain chemistry, or the even more complex interactions between a constantly changing brain chemistry and a constantly changing environment, so fewer people are likely to opt for those explanations. However, when you look at Freud’s, Bowlby’s or Schore’s attempts to map out a possible biological mechanism for child-parent interactions, you realize that the apparent simplicity of the idea is deceptive.

Brains and behaviour

I haven’t yet discussed the second part of Schore’s paper, about the development of the orbitofrontal cortex and its links to the limbic system of the brain. That’s partly because I don’t have sufficient knowledge about brain development to question the accuracy of Schore’s account. It’s also because, although an overview of the development of the orbitofrontal cortex might be informative, I can’t see how it adds support to Bowlby’s theory. Schore asks;

“So the next question is, 30 years after the appearance of this volume [Attachment], at the end of the ‘decade of the brain’, how do Bowlby’s original chartings of the attachment domain hold up?” (Schore, p.29).

Schore’s answer is “In a word, they were indeed prescient.” My response would be a bit wordier; that since Bowlby’s theory (despite the fact that I think it’s flawed in some respects) was based on careful observations and thoroughly grounded in behavioural theories that Bowlby had worked through from first principles, it doesn’t actually need any evidence from brain research for it to ‘hold up’. The reason for this is that if a behaviour is occurring, we know that the part of the brain involved in that behaviour must be working, otherwise the behaviour wouldn’t happen. So if a child recognizes faces, it’s a pretty safe bet that the parts of the brain that deal with face-recognition are up and running. If a child can speak and understand language, we can be pretty sure that the language areas are functioning. If a baby cries when hungry and laughs when playing peek-a-boo, the control mechanism involved in the regulation of feelings is probably on track. It’s when there are deficits in face-recognition or language or sad/happy responses that we’d start to wonder about the pathways from the eyes to the fusiform facial area, from the ears to the fronto-temporal areas of the brain or in the limbic-orbitofrontal pathway.

The problem for Freud’s, Bowlby’s and Schore’s theories is that there are many factors in addition to maternal behaviour that can interfere with the typical development of the orbitofrontal cortex. A variation in a tiny section of genetic material can result in, say, the absence of an enzyme that regulates the way neurons connect to each other, or that changes levels of neurotransmitters. A genetic variation might result in a food intolerance in mother and/or baby, affecting the balance of nutrients available to the infant. These factors could affect the baby’s behaviour, impacting on the mother’s response, in turn influencing the baby’s behaviour, in a complex chain of interactions culminating in a unique pattern of attachment behaviours and in a unique brain structure in the infant.

In other words, if a child is behaving unusually, it’s highly likely that a brain scan would show ‘differences’ in brain structure and/or function. But that doesn’t tell you anything about the origins of the differences; they could be genetic, or environmental, or both. In order to draw useful conclusions about those origins, you’d need a DNA profile for mother and infant, a detailed history, some careful observations of the way they interact, and probably a long wait before the relevant gene-behaviour pathways were mapped out by researchers. Unfortunately, DNA profiling, brain scans, detailed histories and careful observation are expensive and require specialist expertise; it’s simpler and cheaper to attribute all behavioural anomalies to poor parenting.

The implications of Schore’s model

So if, as I claim, Bowlby’s model of child development is questionable and Schore’ model lacks Bowlby’s rigour, why take the time and trouble to critique what Schore has to say? The reason is that Schore’s work has had a significant impact. It’s frequently cited in policy documents and his emphasis on emotion is echoed in the child protection literature – Davies and Ward’s Safeguarding children across services: Messages from research mentions ‘emotional’ 261 times in 226 pages. Damasio was right to point out that research into emotion has been a neglected field of research, but as Bowlby explains, one of the reasons for that is because ’emotion’ is a construct that’s challenging to define. It would certainly be useful to find the mechanisms underlying specific emotions such as anger or sorrow, but the usefulness of ‘emotion’ as a general concept – despite its current popularity – is debatable.

I mentioned brain scans and behaviour; in my next post I’ll look at some of Bruce Perry’s work.

policy makers on the brain

Findings from neurobiology research are presented as ‘medical evidence’ by politicians Graham Allen and Iain Duncan Smith to support their proposals for early intervention programmes for children from deprived backgrounds. Before looking in detail at what they have to say about brain development, it might be helpful if I summarise my understanding of the process. It squares with the account cited by Munro here [1]; so I’m assuming I’m on the right track.

Brain development

Brain development is an outcome of the interaction between four factors [2];

• genetic
• epigenetic (the impact of the environment on gene expression)
• environmental (from nutrition to the behaviour of others)
• behavioural (the impact of the child’s own behaviour)

The relative impact of the different factors varies between individuals and at different stages of development.

The number, formation and location of brain cells (neurons) is almost entirely genetically determined, although it can be affected by environmental factors. A baby has a full complement of neurons at birth, although some neurogenesis occurs in some areas of the brain in adults.

Interconnections between neurons are formed by synapses.

diagram of synapse

The evidence suggests that the role of synapses in learning is essentially a three-stage process.

Novel patterns of sensory input result in new synapses being formed (synaptogenesis). The number of synapses in the brain increases dramatically in the first three years after birth, running into trillions – far more than are found in adult brains.

If the same patterns of sensory input are repeated, some neuronal connections are reinforced and others weakened by synapses dying off (synaptic pruning), resulting in the formation of efficient information-processing pathways.

A third stage, myelination, takes place when neuronal pathways that are used repeatedly develop a fatty myelin sheath that greatly increases the speed of transmission of electrical impulses along the neurons. This makes some processes very fast and they are experienced as ‘automatic’.

Learning also appears to be kick-started by genetically-controlled factors such as the underlying structure of the brain and reflex responses. Reflexes are automatic, unconscious motor responses to stimuli [3], ranging from tongue protrusion to the step-reflex that forms the basis for later walking [4].

When DNA divides during the formation of gametes (eggs and sperm), and then recombines at conception, it is susceptible to the deletion, duplication and transposition of genetic material. Because of these genetic variations, and the impact of epigenetic factors during development, each human being is genetically unique. This means that due to genes alone, one would expect to find a wide range in abilities, behaviours and personalities across a large population. This variation would increase through interaction with environmental factors.

The second chapters of the papers by Allen and Duncan Smith are about brain development and particularly about how maltreatment and neglect can affect it. Although I can see what these chapters are getting at, my impression is that they include a number of misunderstandings, over-simplifications, assumptions and statements that are simply incorrect. This is a long post – I’ve detailed several examples.

Early Intervention: Good Parents, Great Kids, Better Citizens

Graham Allen MP

Rt Hon Iain Duncan Smith MP

1. “Human infants arrive ready to be programmed by adults. From our first moments of life we are tuned into the facial expressions of those around us, as can be seen from the infant reflex to mimic.” (p.56)

Although there’s no doubt that children are influenced by adults, I think many parents and teachers would question whether they can be ‘programmed’; if that were the case, children with good parents would consistently display exemplary behaviour.

It’s not clear what is meant by a ‘reflex to mimic’. A reflex is an automatic response to a stimulus. Mimicry (in humans) involves copying an action made by someone else. Newborns do appear to mimic some facial movements such as mouth opening and tongue protrusion, although it’s not clear whether this is a reflex response (e.g. tongue protrusion occurring in response to objects moving toward the baby’s face [5]) or active mimicry. In addition, there is the question of which adult behaviours children mimic, since they clearly don’t mimic all of them, which suggests that mimicry isn’t a reflex. Newborns are indeed tuned in to facial expressions, but whether that’s because the infant visual system is good at pattern-matching and adult faces are a frequently encountered visual pattern, or whether infants have an inbuilt preference for faces is still unclear.

2. “The problem is that this wonderful advantage turns into a disadvantage when it is met by the longterm lack of positive expression on the nearest face, that of the primary caregiver. When this most basic need for a positive response is not met, and when a tiny child does not feel secure, attached and loved, the effect can be lifelong. Neuroscience can now explain why early conditions are so crucial: effectively, our brains are largely formed by what we experience in early life.” pp.(56-57)

This statement assumes that from the ‘first moments of life’ a baby recognizes a positive facial expression, is capable of feeling security, attachment and love, and that the absence of these feelings can have a lifelong effect. There’s no doubt that what a newborn experiences affects brain development, but no evidence is cited for a basic ‘need’ in newborns for any particular facial expression or affect state.

Neuroscience does not claim that ‘our brains are largely formed by what we experience in early life’. Quite the contrary; what it claims is that our brains are formed by the interaction between genetic expression and experience. In the first moments of life genetic factors are disproportionately predominant because the child has had very little experience.

3. “As synapses are also strengthened and reinforced by experience, early life defines which of them live and which die. Synapses become ‘hard-wired’, or protected, by repeated use, enabling very rapid learning via early life experience. Conversely, just as a memory will fade if it is hardly ever accessed, unused synapses wither away in what is called ‘pruning’. In computer terms what takes place is the software (programming by the caregiver) becomes the hardware (the child’s fully-grown brain). The whole process has the effect of making early learned behaviour resistant to change.” (p.57)

If this model were correct, adults would be unable to learn anything. They wouldn’t be able to correct early misconceptions because the relevant synapses would be ‘protected’, nor would they be able to develop new skills because the relevant synapses would have ‘withered away’ through early lack of use. The term ‘hard-wired’ is usually used to refer to biologically determined connections in the brain (those that don’t rely on information from the environment), not to neural pathways developed via experience. Training in the armed forces and emergency services demonstrates that well-established patterns of what’s normally considered instinctive behaviour (panic, aggression etc.) can be over-ridden, provided enough rehearsal of new behaviours takes place. And the Cambridge delinquency study shows that violent and aggressive behaviour in young males falls off rapidly as they get older indicating that behaviour patterns are not set in stone.

In addition, the passage allocates all experience to ‘programming by the caregiver’ as if children receive no other environmental input. This might be the case for a child kept in a sound-proofed, darkened room, but for most children, however deprived, the caregiver’s ‘programming’ forms only a part of the input from the environment.

4. “To summarise: scientific discoveries suggest it is nurture rather than nature that plays the lead role in creating the human personality.” (p.57)

What scientific discoveries actually suggest is that nature and nurture play an approximately equal role in influencing human behaviour and that their relative contributions vary throughout the lifespan. Much of the environmental variation is due to chance events in later life rather than early experience [6].

5. “The more positive stimuli a baby is given, the more brain cells and synapses it will be able to develop”. (p.57)

The number of brain cells is almost completely genetically determined; neurons are not formed in response to positive stimuli and the baby has a full complement at birth. What the research suggests is that connections between brain cells (synapses) are formed in response to novel sensory information (‘positive’ or otherwise) and are then pruned when those stimuli are repeated, to create robust pathways for processing information that is handled repeatedly. And that synaptic pruning is what is critical for making information processing efficient. People whose synapses are not pruned at the typical rate often have significant learning difficulties [7].

6. “Trauma also confuses the neurotransmitter signals that play key roles in directing the paths of growing neurons and therefore hinders brain development.” (p.60)

Some neurotransmitters are involved in neuronal migration but no evidence is presented as to how trauma confuses their signals or what deficits occur as a result. The primary role of neurotransmitters is to activate or inhibit neighbouring neurons across synapses.

7. “ To the best of current knowledge, the sensitive window for emotional sensitivity and empathy lies within the first 18 months of life, and these ‘skills’ are shaped by the prime caregiver”. (p.60)

This assertion appears to be based on work by Schore [8] although there is no attribution in this section. There’s a debate over sensitive or critical periods; they certainly exist for basic visual and auditory processing skills, but windows for other more complex skills are less clear-cut. If there is a sensitive window for emotional development within the first 18 months of life, how is the success of emotional literacy programmes explained and how could early interventions up to the age of 3 years be effective?

8. “Because the infant’s cortical and hippocampal emotional circuits require significant time and experience to mature, the child must regulate its inner world primarily through attachment relationships with primary caregivers. It accomplishes this through aligning its state of mind with that of the caregiver, by establishing a conduit of empathic attunement, functioning as an emotional umbilical chord.

Babies who are healthily attached to their carer can regulate their emotions as they mature because the cortex, which exercises rational thought and control, has developed properly. However, when early conditions result in underdevelopment of the cortex, the child lacks an ‘emotional guardian’.”(pp.61-62)

I think what this passage is trying to say is that prior to the maturation of frontal cortex which plays a significant role in controlling behaviour, infants regulate their behaviour in response to what primary caregivers do. What the passage does say is open to question. It’s unclear what is meant by ‘emotional circuits’; there’s no mention of the significant role of the amygdala in emotional processing; no evidence is cited to support the idea that a child needs to ‘regulate its inner world’ as if through some form of emotional homeostasis, nor to support the idea that a child can do so only via an attachment relationship with a primary caregiver. What exactly is meant by a child ‘aligning its state of mind’ or ‘a conduit of empathetic attunement’ isn’t clear.

9. “Following a 10-year immersion in thousands of scientific papers on neurobiology, psychology and infant development, Alan Schore concluded:

‘The child’s first relationship, the one with the mother, acts as a template that permanently moulds the individual’s capacity to enter into all later emotional relationships’

We glimpse this in the way small children look to a parent’s facial expressions and other non-verbal signals to determine how to respond (and feel) in a strange or ambiguous situation.” (p.62)

Dr Schore has done some impressive work on brain development and emotion, but this statement doesn’t reflect the wide range of factors known to impact on emotional relationships. In fact, all the neurobiological findings cited in Early Intervention: Good Parents, Great Kids, Better Citizens appear to have been filtered through a psychodynamic model of child development, notably attachment theory. The paper also relies heavily on a small number of sources; Bruce Perry, for example, gets 17 mentions (and 11 in Early Intervention: The Next Steps). It’s difficult to avoid the impression that the paper started out with a thesis and then selected evidence to support it.

Now for;

Early Intervention: The Next Steps

10. The cover image

Cover image from “Early intervention: The next steps”

The caption for this image says the right hand scan is from a series of three children, but the original source (a paper by Bruce Perry) [9] says it’s from one child in a group of 40 identified as having suffered global neglect (defined as ‘relative sensory deprivation in more than one domain…e.g. minimal exposure to language, touch and social interactions’). MRI or CT scans were available for 17 of those children, of which 11 were deemed abnormal. It isn’t clear what variation there was within the group, or whether possible genetic causes or environmental causes other than sensory deprivation were investigated. Perry’s team found ‘dramatic differences’ from the average in head circumference. There was ‘some recovery of function and relative brain-size’ after a year in foster care. There were no marked differences between neglected and control groups in the much more common ‘chaotic neglect’ (physical, emotional, social or cognitive).

I don’t doubt that children with minimal exposure to language, touch and social interactions have brains that differ from the norm, nor that they improve in foster care. However, Perry’s analysis raises a number of questions. Healthy, non-neglected children don’t have identical brains (the healthy brain was on the 50th percentile), so why not compare the neglected brain with one at the lower end of the normal range? What type of neglect had the child suffered? Were genetic disorders taken into account? Or diet? Or disease? Does the rate of increase of head circumference change with age? Does it vary between individuals? Although striking, all this particular image actually tells us is that one child who suffered global neglect also had abnormal brain development.

11. “Our responses to situations are not pre-set at birth. The nature/nurture debate has moved on, as was demonstrated in ‘Early Intervention: Good Parents, Great Kids, Better Citizens’.” (p.13)

The nature/nurture debate has indeed moved on, but not quite in the way Good Parents, Great Kids, Better Citizens thinks. See point 3 above.

12. “ Children are born with an instinct to engage socially and emotionally, especially with their mothers. They communicate with the voice, face and hands. They express a curiosity about both the world and their need for comfort and security.” (p. 14)

See points 1 & 2 above.

13. “Recent research also shows insecure attachment is linked to a higher risk for a number of health conditions, including strokes, heart attacks and high blood pressure, and suffering pain, for example from headaches and arthritis. Secure attachment was not linked to any health problems that have been studied.” (p.15)

The validity of attachment theory appears to have been accepted without question. Like many constructs used in psychiatry, ‘attachment’ is loosely defined and difficult to operationalise. Not all children develop patterns of attachment that fit neatly into Ainsworth’s categories, nor are patterns of attachment solely determined by parental behaviour [10].

I’m also concerned about the conflation of correlation with causation. A correlation between insecure attachment and heart disease, smoking etc. does not mean that they are necessarily linked, or even if they are, it doesn’t follow that insecure attachment is the cause of heart disease, smoking or reckless driving. It could equally well be the case that inherited characteristics that predispose people to heart disease, addictions or risk-taking, via low dopamine levels for example [11], could also contribute to inadequate parenting.

14. “Although poor parenting practices can cause damage to children of all ages, the worst and deepest damage is done to children when their brains are being formed during their earliest months and years. The most serious damage takes place before birth and during the first 18 months of life when formation of the part of the brain governing emotional development has been identified to be taking place.” (p.15)

The second sentence appears on p.71 of the Munro Review of Child Protection: Final Report, and is attributed to a Royal Society publication Brain Waves Module 2: Neuroscience implications for education and lifelong learning (Munro reference 95) which contains no such statement. Munro’s reference 94 is to Early Intervention: The Next Steps, so the attribution is obviously a typo, but nonetheless the assertion that poor parenting causes ‘brain damage’ is presented here as a matter of fact without any supporting evidence.

15. “Different parts of the brain (governing, for example, sight, hearing, etc) develop in different sensitive windows of time. The estimated prime window for emotional development is up to 18 months, by which time the foundation of this has been shaped by the way in which the prime carer interacts with the child.” (p.16)

See point 7 above. Presumably this claim is based on the same source, but no sources are cited here.

16. “Infants of severely depressed mothers show reduced left lobe activity (associated with being happy, joyful and interested) and increased right lobe activity (associated with negative feelings)19” (p.16)

The Dawson et al. paper (reference 19) is behind a paywall so I couldn’t clarify what is meant by left and right ‘lobes’ and their supposed functions. Presumably this refers to work that suggests the left and right frontal lobes respectively have specialized functions, but this isn’t made clear. Nor is it clear whether the levels of activity in the ‘lobes’ is due to the mothers’ depression or whether mothers and babies share biologically inherited activity patterns.

17. “One result is significantly fewer synapses (or connections). Specialists viewing CAT scans of the key emotional areas in the brains of abused or neglected children have likened the experience to looking at a black hole. In extreme cases the brains of abused children are significantly smaller than the norm, and the limbic system (which governs the emotions) may be 20–30 per cent smaller and contain fewer synapses.” (p.16)

According to Sue Gerhardt in Why Love Matters: How Affection Shapes A Baby’s Brain (her presentation to the Quality of Childhood Group in the European Parliament in December 2009) the ‘black hole’ quote comes from Harry Chugani [12], and refers to the development of medial prefrontal cortex (MPC) in the brains of Romanian orphans. Here, Gerhardt is talking about the development of the ‘social brain’ (MPC):

“The less attention a baby receives, the less this part of the brain connects up. In the worst cases, like some of the most damaged Romanian orphans, this area of the brain was virtually a black hole according to one researcher, Harry Chugani.” (Gerhardt, p.89)

and illustrates the point using Perry’s image – the one that’s on the cover of the Allen report (Gerhardt, p.88). Although MPC is involved in emotional regulation, it is also involved in risk assessment and decision-making using information from many parts of the brain. It’s not clear whether MPC in the orphans was permanently or temporarily abnormal, or what had caused the abnormality. Genetic, nutritional or infective factors don’t appear to have been controlled for. And a small brain isn’t a bad thing per se; autistic children tend to have larger brains than average, for example. Chugani et al were investigating glucose metabolism in the brain, but Gerhardt doesn’t mention this, so it would be all too easy for people unfamiliar with the technical problems associated with interpreting brain scans to go away with the impression that neglect causes children to develop holes in their brains.

18. “Schore has spoken of ‘the child’s first relationship, the one with the mother, acts as a template … [that] permanently moulds the individual’s capacity to enter into all later emotional relationships’25. ”

“ To attune to a child means responding to their emotional needs, resulting in the child’s sense of being understood, cared for and valued. Empathy begins with the sense of oneness with the other created in this process of attunement. The quality of empathy – the ability to feel for and with another – is not only key to building sound emotional stability, it is also a key inhibitor of the development of a propensity to violence. Conversely, empathy fails to develop when prime carers fail to attune to infants in the first 18 months of life. Absence of such parental attunement, combined with harsh discipline, is a recipe for violent, antisocial offspring. Empathy is influenced very early in life by observed parental reactions to another’s suffering. Even in their first year, children already show signs of whether their reaction to the suffering of another is empathy, indifference or downright hostility.” (p.17)

The quotation from Schore also appears on page 62 of Early Intervention: Good Parents, Great Kids, Better Citizens and is widely cited on the internet, but I couldn’t locate the source; I couldn’t find it in note 25, Schore’s account of the right hemisphere’s role in emotion regulation. There is no question that a child’s early relationships are significant; but no evidence is provided that the relationship with the mother forms a template for all other relationships.

Conclusion

Both Allen and Allen & Duncan Smith papers are about Early Intervention Programmes – the brain development chapters are simply there to add weight to their arguments in favour of the programmes. I haven’t discussed the interventions themselves because I was primarily concerned about the material on brain development. There’s little question that many of the interventions will do some children some good; whether they will address the social problems they are meant to address is another matter. One of the difficulties with social problems is that they are often caused by complex interactions between many factors – so interventions aimed at one or two factors are likely to have only a small effect overall. For example, an evaluation of the Carolina Abecedarian project [13] shows that mean mental test scores for children improved by less than 10 percentage points and that early gains reduced markedly over time – there was little difference at age 21. Age at the birth of a first child was 19 in the treatment group compared to 17.5 yrs in controls. Differences in academic achievement were larger and were maintained – possibly due to the early language support in the programme leading to improved reading. In short, the programme had a beneficial effect, but whether it made significant inroads into ‘social problems’ is debatable.

What concerned me most about Early Intervention: Good Parents, Great Kids, Better Citizens and Early Intervention: The Next Steps is that neither is based on a systematic evaluation of neurobiological data, with the data themselves providing information about what could be done to reduce social problems. Instead, both papers start from a Freudian framework for child development, without questioning its fundamental assumptions; Allan Schore [8] is explicit about the direct descent of this framework from Freud via Bowlby’s attachment theory, and I’ve already drawn attention to the shortcomings of attachment theory.

Instead of drawing on our wide range of knowledge about child development as a whole, both papers focus on just one facet of it; emotional development. Furthermore, they focus on one facet of emotional development – attachment; and on one facet of attachment – the child’s relationship with the primary caregiver. The primary caregiver is often implicitly assumed to be the parent, and more specifically the child’s mother – even though fathers, grandparents and siblings are often primary carers and many children have more than one primary carer. This narrow model of child development is supported with often over-simplified and misunderstood neurobiological findings, selected, it appears, because they support the assumptions that the model makes. Findings that do not support these assumptions are simply omitted.

It could be argued, with good reason, that an in-depth analysis of the neurobiological evidence would be beyond the scope of policy papers like these. However, the omission of aspects of child development other than attachment to the primary caregiver is a serious one. It implies that interventions are being proposed on the basis of a belief that they will be effective, rather than on the basis of an evaluation of research evidence across all areas of child development. This introduces a significant risk of interventions failing to eliminate social problems and being abandoned despite some beneficial outcomes for the children involved. A better approach might have been to enlist the help of a developmental neurobiologist for the evaluation of neurobiological evidence, to identify all the reasons why young people fail to reach their potential and to look at interventions which address each reason, including taking a critical look at the efficacy of current healthcare, education and social support systems.

References

1. National Research Council (2000), From Neurons to Neighborhoods: The Science of Early Childhood Development (Chapter 8), Washington D.C. (available online at http://www.nap.edu/openbook.php?isbn=0309069882)
2. Mareschal, D., Johnson, M., Sirois, S., Spratling, M., Thomas, M. & Westermann, G. (2007). Neuroconstructivism: How the Brain Constructs Cognition, vol. 1. Oxford: Oxford University Press.
3. See e.g. http://en.wikipedia.org/wiki/List_of_reflexes_%28alphabetical%29
4. Thelen, E. & Fisher, D. M. (1982). Newborn stepping: An explanation for a “disappearing” reflex. Developmental Psychology, 18, (5), 760-775.
5. Chen, X., Striano, T. & Rakoczy, H. (2004). Auditory–oral matching behavior in newborns, Developmental Science, 7, (1) 42–47.
6. Pinker, Steven (2002). The blank slate: The modern denial of human nature, Penguin.
7. Cohen, I.L. (2007). A neural network model of autism: implications for theory and treatment. In D. Mareschal, S. Sirois, G. Westermann & M. Johnson (2007). Neuroconstructivism: Perspectives and Prospects, vol. 2. Oxford: Oxford University Press.
8. Schore, A. (2000). Attachment and the regulation of the right brain, Attachment & Human Development, 2 (1), 23–47.
9. Perry, B. (2002). Childhood Experience and the Expression of Genetic Potential: What Childhood Neglect Tells Us About Nature and Nurture, Brain and Mind 3, 79–100.
10. Oppenheim, D., Koren-Karie, N., Dolev, S. and Yirmiya, N. (2009). Maternal insightfulness and resolution of the diagnosis are associated with secure attachment in preschoolers with autism spectrum disorders, Child Development, 80, 519–527.
11. Iversen, L. (2008). Speed, Ecstasy, Ritalin: The Science of Amphetamines, Oxford University Press.
12. Chugani, H.T., Behen, M.E., Muzik,O., Juhasz, C., Nagy, F. & Chugani, D.C. (2001). Local Brain Functional Activity Following Early Deprivation: A Study of Postinstitutionalized Romanian Orphans, NeuroImage 14, 1290–1301.
13. Early Learning, Later Success: The Abecedarian Study (1999). Highlights of the Age 21 Follow-up Study, Chapel Hill: University of North Carolina, FPG Child Development Center. Available at http://fpg.unc.edu/sites/fpg.unc.edu/files/resources/reports-and-policy-briefs/EarlyLearningLaterSuccess_1999.pdf

Image of synapses from Wikipedia.

brain development and social problems

Reading the final report of the Munro Review of child protection, my attention was caught by what turned out to be a minor typographical error. The last sentence of paragraph 5.8 appears to refer to reference 95, the Royal Society paper Brain Waves Module 2: Neuroscience: implications for education and lifelong learning, but in fact cites reference 94. Reference 94 is an independent report commissioned by the current UK coalition government, published in January 2011, written by Graham Allen, Labour MP for Nottingham North and entitled Early Intervention: The Next Steps.

Graham Allen MP

Early intervention is summed up as follows by the ‘Early Intervention Review Team’;

“Early Intervention is an approach which offers our country a real opportunity to make lasting improvements in the lives of our children, to forestall many persistent social problems and end their transmission from one generation to the next, and to make long-term savings in public spending….” (p.vi)

In 2008, Graham Allen had written another paper on early intervention, this one co-authored with Iain Duncan Smith and entitled Early Intervention: Good Parents, Great Kids, Better Citizens published jointly by the Centre for Social Justice (CSJ) and the Smith Institute. Iain Duncan Smith is a former leader of the Conservative Party and currently Secretary of State for Work and Pensions. In 2004, he founded the Centre for Social Justice, a centre-right think tank, just after his period of party leadership ended. The Smith Institute is a left-leaning think tank set up in 1996 in memory of the former Labour Party leader, John Smith. Ed Balls, later to become the Labour government’s Secretary of State for Children, Schools and Families, worked for the Institute between 2004 and 2005.

Rt Hon Iain Duncan Smith, Secretary of State for Work and Pensions

In previous posts I’ve complained (at some length) that the model of child development being used by children’s services pays little attention to recent biological research. It would be unfair to suggest that biology is entirely absent however. There are many references to physical development in this literature, Aldgate et al’s book contains a chapter on genetic and biological influences and the Munro report cites the National Research Council’s From Neurons to Neighbourhoods: The Science of Early Childhood Development – chapter 8 contains a comprehensive summary of brain development. The second chapter of each of the two documents written by Graham Allen is also dedicated to brain development. It’s these two chapters I want to concentrate on in this post.

I’m not entirely clear why it was deemed necessary to refer to brain development in papers about early interventions intended to forestall social problems. After all, few people would want to see evidence from brain scans before they could be persuaded that sanitation, a balanced diet or education have good outcomes for individuals and for the population as a whole. And given the technical problems with brain scanning and the interpretation of the resulting images, there are other more reliable ways of measuring the effectiveness of interventions. Allen and Duncan Smith’s Early Intervention: Good Parents, Great Kids, Better Citizens justifies the inclusion of material on brain development as follows;

“We make no apology for presenting, as laymen, a considerable body of medical evidence in this chapter. When economic resources are under intense pressure, and facing strong claims from well-established programmes and special interests, we believe that this medical evidence points overwhelmingly in favour of a shift to Early Intervention.” (Good Parents p.45)

What’s the evidence?

The first few pages of chapter 2 of Good Parents focus on results from three large-group, longitudinal studies purported to show that early adverse childhood experiences result in later health risks such as smoking, alcoholism, illicit drug use, obesity and high level promiscuity (Good Parents p.54). At first glance, the conclusions presented are persuasive, but when you look a little more carefully, the picture isn’t quite so clear-cut.

I’ve mentioned several other documents that in some cases refer to each other. To clarify how they are linked, I’ve mapped out the connections here:

Two of the studies, Farrington and West’s Cambridge Study in Delinquent Development, a Prospective Study of South London Males From Ages 8–32 and the Dunedin Multidisciplinary Health and Development Study are prospective – that is, they started with children and have periodically sampled their health, development and behaviour over many years.

According to Allen and Duncan Smith the Cambridge study showed that adult offending could be predicted in childhood (Good Parents p. 51). That’s not quite what the study records. The 2006 report, which tracked the participants up to the age of 48, found that there were predictive factors in childhood for adult offending. In other words, some factors were predictive of behaviour for a particular group, not for particular individuals. The highest correlation between childhood factors and persistent offending was for children having a convicted parent or sibling. What this means is that children with previous offenders in their families are more likely to offend, not that offending can reliably be predicted in individual children. A significant number of children from families with an offender didn’t commit crimes, whereas some children from non-offending families did.

The Dunedin study looked at the health and development of 1037 babies born in Dunedin, New Zealand, between 1972-73. Data from the Dunedin study has been used in over 1000 publications but I couldn’t find which one Allen and Duncan Smith were referring to. They claim that nurses’ assessments of which of a group of 3 year-olds were at risk, predicted criminal convictions, violent behaviour and domestic abuse at age 21. They conclude;

“the fact is that children who are likely to have poor outcomes, including adult criminality, can be identified at age three when they are still riding their tricycles.” (Good Parents p.52)

Not exactly. As Allen and Duncan Smith themselves point out, not all of the at-risk children offended, and some of the not-at-risk children did – 18% exhibiting violent behaviour and almost 10 % abusing their partners (Good Parents p.51).

The third study, the Adverse Childhood Experiences (ACE) Study, by contrast, is retrospective; it relies on self-reports about childhood maltreatment, family dysfunction and health status, and therefore on that notoriously unreliable data source, human memory. You can read the questions that were posed to participants in Preventing child maltreatment: a guide to taking action and generating evidence. It’s published jointly by the World Health Organization and ISPCAN, The International Society for the Prevention of Childhood Abuse and Neglect. My curiousity about Preventing child maltreatment: a guide to taking action and generating evidence was initially piqued by the title. I have no problem with taking action against child maltreatment, but do have concerns about ‘generating evidence’. Evidence is usually ‘gathered’ or ‘found’ – implying that it’s already out there, researchers just have to go and look for it. ‘Generating evidence’ suggests that, like Bettelheim, your case might not actually have strong evidence behind it so you need to create some.

I was also concerned by a reference in the Foreword to the idea that

“the traditional “privacy barrier” between the domestic and public spheres has inhibited the evolution of policies and legal instruments to prevent violence within the family and provide services for those affected by it.” (p.vi)

I’d predict that the prohibition of violence is as likely to be effective as the prohibition of alcohol consumption, but that violence might be lessened if its causes were to be addressed. Furthermore, the ‘traditional “privacy barrier”’ isn’t about “privacy” – a relatively recent development in human history – but about protecting the individual from the abuse of power by the state. I’m sure the author, who’s had extensive experience with the UN, is aware of that. But I digress.

I also had concerns about Box 1.1 (p.8). It’s entitled Child maltreatment and damage to the developing brain and is adapted from a pamphlet published in 2001 by the National Clearinghouse on Child Abuse and Neglect Information and the National Adoption Information Clearinghouse called In Focus: Understanding the Effects of Maltreatment on Early Brain Development. The pamphlet lists 31 references, 11 by Bruce Perry and one by Allen Schore. In 13 pages, Schore’s work is cited 17 times and Perry’s 40 times. These names crop up again in the papers by Allen and Duncan Smith.

My concerns about Box 1.1 and the In Focus pamphlet weren’t so much about what they said, as about their emphasis. Firstly, maltreatment and neglect of children is, by definition, harmful – that’s why they are called maltreatment and neglect. We already know that certain practices cause harm to children, at the time they happen, immediately afterwards, and, in some cases, throughout life. We don’t need evidence from brain scans to tell us that. But maltreatment and neglect are being presented as if pre-existing evidence of harm isn’t sufficient to persuade legislators that more stringent legislative measures are required to prevent maltreatment and neglect, so neurobiological findings are being recruited for this purpose. Secondly, although there is certainly evidence to suggest that maltreatment and neglect have a negative impact on brain development, they are only two of the factors that do so. In other words, you could predict with some confidence that maltreatment and neglect would result in ‘abnormal’ brain development, but you can’t assume that because someone’s brain has developed abnormally, that they were maltreated or neglected as a child. Thirdly, there’s an implicit assumption in the way the evidence is presented that maltreatment and neglect are the primary cause of ‘social problems’, when social scientists have been aware, for decades, that those causes are many, varied and have complex interactions.

In short, the evidence doesn’t appear to support the idea that the predominant cause of social problems is child maltreatment or neglect. Allen and Duncan Smith call for a study along the lines of the Dunedin study to be carried out in the UK “in order to provide definitive evidence on the benefits of Early Intervention” (Good Parents p.52). I can’t see why another study is necessary – the Cambridge study makes clear that the causes of antisocial behaviour are complex and that patterns of behaviour change significantly over the lifespan.

Update 13/12/16:  Thanks to @PaulWhiteleyPhD on Twitter for drawing attention to this article in Nature analysing the Dunedin study findings.

In the next post, I want to look at what Graham Allen and Iain Duncan Smith have to say about brain development.

Photographs of Graham Allen and Iain Duncan Smith from Early Intervention Early Intervention: Good Parents, Great Kids, Better Citizens.