Calling a spade a spade

In his comment on my previous post, Steve Flatt raised some interesting objections to my criticism of the way some philosophers construe brain function, citing Rom Harré and Daniel Dennett in support. I can’t comment on Harré’s and Dennett’s specific points because I haven’t read either of the texts Steve recommends, but I think I the objections Steve raises can be resolved by reframing them. I’m responding in a new post, because I need to explain the concepts involved.

Deconstructing a spade

Steve begins by pointing out that “Deconstruction is not necessarily the right thing to determine the purpose or “aboutness” of the brain”. He cites a colleague who used the analogy of a spade, arguing that if you were to systematically deconstruct a spade down to its component sub-atomic particles, “the further into the deconstruction we got the less apparent the purpose of the spade became”. That’s certainly true; but if you’re interested, not in the purpose of the spade, but how one could be made, deconstructing the spade becomes crucially important.

Human beings have not always been able to make spades as we know them today. Until we had tools that would cut and shape wood, and had figured out how to extract iron ore from rock, how to make it malleable and had the tools to shape it, even if we had wanted to dig holes in the ground we wouldn’t have been able to do it with a spade made of a steel blade and wooden handle. The first concept that I think would be useful in reframing deconstruction is the idea of levels of abstraction.

Levels of abstraction

Fields of knowledge that deal with complex systems are usually quite at home viewing a particular phenomenon as occurring simultaneously at different levels of abstraction; biologists, for example, can comfortably move between the molecular, cellular, tissue or whole organism levels when tracking a particular physiological pathway. What happens to molecules affects cells, what happens in cells affects tissues, and what happens in tissues affects the whole organism. If we apply this concept to the example of a spade, we find that a spade too can be construed at many different levels; the sub-atomic, atomic, molecular, compound, materials, parts, object and function levels. Each level of abstraction is dependent on the configuration of the level beneath it, so each level of abstraction is ultimately dependent on the configuration of the sub-atomic particles (for want of a better term) that make up the spade. A spade can be deconstructed as a series of levels of abstraction that have the following characteristics:

function level: digging (and multiple other functions)
object level: spade
parts level: blade, handle
materials level: steel, wood
compound level: steel, cellulose, lignin
molecular level: iron, carbon, glucose, monolignols
atomic level: Iron, carbon, hydrogen, oxygen
sub-atomic level: protons, electrons etc.

I agree with Steve that “Deconstruction is not necessarily the right thing to determine the purpose or “aboutness” of the brain”. But he then goes on to say “To assume that by taking it to pieces we will learn its functions seems highly unlikely to me.” In response I’d point out that most people studying the parts of brains aren’t doing that to determine its purpose, but to find out how it works, not the same thing at all.

I think levels of abstraction are what Harré is getting at when he refers to molecular, organism, person and soul ‘grammars’. Different levels of abstraction certainly have patterns of functioning that you could call ‘grammars’ if you wanted to. What concerns me is that Harré, like Wittgenstein and Ryle, appears to be making language his starting point for their analysis. To me this is starting from the wrong place. In terms of the levels of abstraction involved in human functioning, language is at a very high-level, and the patterns it forms will be influenced by what’s going on at the levels beneath it. It’s certainly true that language shapes the way we construe those lower levels, but it doesn’t shape the way they work, so applying patterns from language to other levels of abstraction isn’t necessarily helpful. Different levels of abstraction work in different ways, which where another concept comes in handy – constraints and affordances.

Constraints and affordances

Each level of abstraction has different constraints (things that can’t be done) and affordances (things that can be done). Random collections of sub-atomic particles can do things that atoms can’t, but atoms can do things that individual sub-atomic particles can’t. If you were to melt the blade of the spade, the puddle of molten steel that resulted would have constraints that the blade didn’t – you wouldn’t be able to dig with the molten steel or use it to build a sandcastle; but it would also have affordances that a blade didn’t – you’d be able to pour it into a cast or use it to start a fire. This brings us to a third useful concept, emergent properties.

Emergent properties

Different constraints and affordances emerge at each different level of abstraction, so each level of abstraction has different emergent properties. Individual atoms of iron, carbon, oxygen and hydrogen have different properties to a chunk of steel and a wooden pole, which in turn have different properties to a spade; even though the spade, chunk of steel and wooden pole are all made of atoms of iron, carbon, hydrogen and oxygen. The idea of emergent properties maps neatly on to Ryle’s concept of ‘disposition’ and Bowlby’s description of feelings as ‘phases’ of physiological processes. It also allows us to formulate answers to Dennett’s questions. I don’t know the context in which these questions were asked, but there is a response to the questions as they stand.

Dennett’s questions

First question; “Please tell me, Dr Physicist, just what colour is. Are there colours according to your theory?

‘Colour’ is the label we give to an emergent property of the interaction between our visual processing apparatus and a particular wavelength of light. Colour doesn’t exist in the same way as our visual processing apparatus or light exist, because it isn’t the same sort of thing as they are. Dennett’s questions are essentially meaningless (which I suspect is what he intended them to be) because colour can’t be reduced to sub-atomic particles, but without sub-atomic particles colour couldn’t be an emergent property of anything.

Then there’s; “Dr Chemist can you provide the chemical formula for a bargain?

Similarly, the question about the chemical formula for a bargain is meaningless because a bargain is an emergent property of a particular set of human interactions. It can’t be reduced to a chemical formula, but if chemical reactions weren’t involved, no bargains could ever be struck because there would be no one to strike them.

The third question Steve quoted; “Could you ever frame a clear concept of a bargain, or a mistake, or a promise…?

begs another question, which is; what do you mean by a ‘clear’ concept? Enormous amounts of time have been wasted by people trying to frame clear concepts of things that are far from clear and are never going to be. One clear concept that I think can resolve the problem is the idea of a fuzzy set.

Fuzzy sets

Category theory, derived from set theory, organizes entities in ways that derive from the features of the entities, rather than by forcing them into categories we prepared earlier. A fuzzy set is one whose elements have degrees of membership. Supporters of a political party would form a fuzzy set, because some people would be in total agreement with the party’s policies whereas others would agree to varying extents. (Members of a political party, by contrast, would form a crisp set, because someone is either a member or they’re not.)

A bargain (or a mistake or a promise) is a construct that applies to certain forms of human behavior. The category of things we call {bargain} has core (prototypical) features – that would include more than one party and an agreement – but its member bargains vary widely in their form and content. Because of those variations, it’s pointless trying to frame the concept ‘bargain’ clearly. It’s much more appropriate to frame it as a fuzzy category, with core distinguishing (prototypical) features but with degrees of membership and blurred boundaries.

Even though bargains (or mistakes or promises) might in general be fuzzy constructs it doesn’t follow that any particular bargain (or mistake or promise) is fuzzy in terms of what’s involved in specific cases. If I agree to pay my son £5 if he washes the car, some very concrete, clearly definable things are involved. The general concept ‘bargain’ isn’t the same sort of thing as; my son, a £5 note, water, shampoo or the car. A bargain is an emergent property of a particular configuration of those things, plus many others at lower levels of abstraction that it would take too long to list.

Epigenetics

Steve refers to epigenetics as a problem, but I’m not clear why. The discovery of epigenetic effects showed that the interaction between genetic expression and the environment is even more complex than was previously thought, but that doesn’t make genetic-environmental interaction intractably complex. Because of their emergent constraints and affordances, entities at each level of abstraction are bounded; they operate within limits and behave according to patterns determined by those constraints and affordances. So epigenetic factors don’t mean that human behavior and adaptability are infinitely variable; patterns will emerge from the variability.

Determinism

Steve also says “But the tool we can most effectively use to explore [the brain] is language and behaviour. While we may map these activities on to the brain in some form the sheer flexibility of processing means we can never be deterministic about what parts of the brain do what particular activity.”

I think Steve’s making two assumptions here. First, using language and behavior to explore the brain might be most useful to him in his work as a psychologist. But they might not be so useful to an occupational therapist working with a child with mobility problems or a brain surgeon trying to remove a tumour. Those people might find knowing how the brain’s primary motor cortex functions quite useful.

I think the second assumption is that looking at lower levels of abstraction to try and figure out how the brain works is deterministic. I don’t think it is. It’s just figuring out how the brain works at lower levels of abstraction. Higher levels of abstraction, such as language and behavior are to an extent determined by what happens at lower levels, but their constraints, affordances and emergent properties limit what goes on within different levels, rather than determine what goes on within them.


Reference

Harré, R & Moghaddam, FM (2012)’Psychoneurology:The Program’ in Psychology for the Third Millennium: Integrating Cultural and Neuroscience Perspectives,SAGE.

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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.

back to Bowlby, briefly

John Bowlby

Two names that keep cropping up in the child protection literature (apart from Bowlby) are those of Bruce Perry and Allan Schore. Perry is a recognised expert in child mental health and is especially interested in the effects of trauma. Schore has been described as ‘the American Bowlby’ and as ‘the world’s leading expert in neuropsychoanalysis’. I want to focus on one paper by each of them. I’ve chosen the Perry paper because it tackles the nature/nurture debate head-on and is the source of the brain photograph on the cover of Graham Allen’s report Early Intervention: the Next Steps. The Schore paper “Attachment and the regulation of the right brain” seeks to map Bowlby’s attachment theory onto recently acquired knowledge about how the brain develops, and a shortened version of it forms the foreword to a recent edition of Bowlby’s classic book Attachment. Attachment is the first of three volumes dealing with attachment; the others are entitled Separation and Loss.

The frequent mention of the same few names isn’t unusual in a specialist field, and what I expected to find when I read Perry’s and Schore’s work was the painstaking, step-by-step hypothesis testing typical of researchers working in a little-explored area. That wasn’t quite what I found. Before tackling either of the papers, I need to re-visit Bowlby’s attachment theory because Schore’s paper starts where Bowlby leaves off, and Perry’s paper opens with a discussion about the evolution of human behavioural characteristics – a topic central to Bowlby’s thesis.

The title of this post refers to a brief return to Bowlby’s theory, not to the length of the post. I’ve evaluated Bowlby’s ideas in some detail because later interpretations of his ideas are many and varied and sometimes haven’t taken into account Bowlby’s often meticulous reasoning.

Schore and Bowlby

Schore begins by summarising Bowlby’s view of the biological systems underpinning attachment, and then shows how recent findings about the development of regulator systems in the brain’s right hemisphere support Bowlby’s predictions. In the abstract to his paper Schore summarises Bowlby’s model of attachment like this:

“… 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”.

The first thing that struck me about Schore’s paper is that he doesn’t define terms such as attachment, instinct and emotion. Biologically speaking, none of these constructs is straightforward and Bowlby discusses their definitions at length. It’s a pity Schore doesn’t explore these terms, because re-reading Bowlby’s explanations half a century after publication (revisions in the second edition of the book in 1983 notwithstanding) suggests that there are some implicit assumptions in his thinking that are open to question. And anyone unfamiliar with either Bowlby or the animal behaviour literature might be unaware of the complexity of the issues involved.

Let’s start with some of the key concepts that underpin Bowlby’s theory of attachment – first, psychoanalysis.

Psychoanalysis

Bowlby opens Attachment with a chapter called “Point of View” in which he explains the basis for his model. He begins with a quote from Freud, and takes as his starting point an underlying principle of psychoanalysis; that personality, both healthy and pathological, is shaped by events that occur in childhood. But Bowlby differs from Freud on several key points;

Despite these differences, Bowlby assumes that personality (one construct that he doesn’t attempt to define) is shaped by childhood events and that pathologies of personality originate in traumatic experiences in childhood, observations suggesting that a significant trauma is separation from, or loss of, the mother. In the two later volumes of his Attachment trilogy Bowlby suggests that separation is an underlying cause of anxiety and that loss is a cause of sadness and depression. Bowlby points out that his model’s underlying mechanism involves biological processes rather than psychical energy. A central biological process is evolution.

Evolution

Bowlby’s theory is rooted firmly in the Darwinian model of evolution. Darwin’s theory is based on two main concepts, inherited characteristics and natural selection. Neither of these concepts was new when Darwin proposed his theory. People had known for millennia that offspring inherit physical and behavioural characteristics from their parents and that plants and animals thrive in a particular environment only if their characteristics are well adapted to it. Farmers had been using artificial selection for centuries to breed characteristics into or out of plants and animals to suit a specific purpose or environment. What was new about Darwin’s theory was the idea that environmental factors acting on inherited characteristics could result in changes to a species, or in new species arising. What was missing from his theory was the mechanism by which characteristics were passed on to subsequent generations. Although DNA had been discovered in the mid-19th century, its structure and function were unknown and it wasn’t until the turn of the 20th century and the re-discovery of Gregor Mendel’s work showing that characteristics were inherited via discrete units of heritability, that the concept of genes was developed.

Genes

Bowlby sees ‘instinctive’ behaviours like attachment as emerging from the interaction between genetic endowment and environment, but essentially limits his comments on genes to the following paragraph:

The basic concept of the genetical theory of natural selection is that the unit central to the whole process is the individual gene and that all evolutionary change is due to the fact that certain genes increase in number over time whereas alternative genes decrease or die out. What this means in practice is that, through the process of differential breeding success, individuals that are carrying certain genes increase in numbers whilst individuals that are carrying others diminish. A corollary is that the adaptedness of any particular organism comes to be defined in terms of its ability to contribute more than the average number of genes to future generations. Not only, therefore, does it have to be designed so that it is capable of individual survival but so that it is capable also of promoting the survival of the genes it is carrying. This is commonly done through reproducing and promoting the survival of offspring.” (pp.55-56)

Although what Bowlby says is true at one level, his comments don’t give any indication of the complexity of genetic variation in a population. This is despite de novo (spontaneous) mutations having been discovered in fruit flies by the 1920s, and by the time Bowlby published Attachment in 1969 population genetics was a well-established field. The second edition of Attachment came out in 1983, only five years before the commencement of the Human Genome Project.

Bowlby is clear that a debate about whether development is primarily a matter of nature or nurture is meaningless because individual development is a product of an interaction between genes and the environment (pp.38, 296). Nonetheless Bowlby plays down the likelihood of genetic causes of behavioural anomalies in favour of environmental causes;

There are many reasons why, in the course of development, one or another feature of an animal’s diverse biological equipment may fail to develop satisfactorily… Though occasionally one or more genes are responsible for the failure, more often some anomaly of the embryo’s environment is the cause – a virus, a chemical, a mechanical trauma and so on. It is probably the same with failures in development of behavioural systems. Whilst genes may well account for some forms and cases of failure, anomalies of a juvenile’s environment beyond those to which behavioural equipment is adapted are likely to be the cause of most of them.” (pp. 129, my emphasis).

Bowlby couldn’t have known about the frequency of de novo mutations in humans and he was studying a behavioural interaction that’s highly susceptible to environmental factors, but his speculative ruling out of genetic causes is rather surprising. His emphasis leads to a detailed discussion of environments.

Environment

A central concept in Bowlby’s model is what he calls the environment of adaptedness. Although human beings occupy a wide range of environments, all those environments fall within limits outside which human beings can’t function efficiently. Bowlby argues that each biological system of each species has its own environment of adaptedness; the one to which it is evolutionarily adapted and the one in which it functions best. He points out that cardio-vascular systems work only within certain limits of oxygen and carbon dioxide, and that those limits vary for different species. So, he concludes, the behavioural systems responsible for maternal behaviour will work within certain limits of the physical and social environment, but not outside them. In short, the environment of adaptedness produced instinctive behaviour so instinctive behaviour will work effectively only within the environment of adaptedness.

Instinctive behaviour

Bowlby presents the traditional definition of instinctive behaviour as;

• species-typical
• a sequence of behaviours running a predictable course
• having obvious survival value for the individual and/or the species
• arising in the absence of opportunities for learning the behaviour.

During the heyday of research into instinctive behaviours there was considerable debate about whether they were innate (inborn) or acquired (learned). Bowlby thinks this is a pointless distinction, because all the characteristics of biological organisms are products of an interaction between genetic endowment and environment (p.38). He follows zoologist Robert Hinde in suggesting that instinctive behaviour forms a continuum ranging from characteristics that remain stable regardless of environment such as nest-building behaviour, to those that are labile and environmentally dependent, such as show jumping or piano playing. Although he wouldn’t include reflexes as instinctive behaviour, Bowlby’s continuum could be seen as extending from reflexes and simple stimulus-response reactions at the stable end, to complex chains or hierarchies of behaviour that include both innate and acquired behaviours, at the labile end. Although ‘instinctive’ might be a more useful concept than ‘innate’ or ‘acquired’ for researchers studying behaviour, for those investigating the biological mechanisms underpinning behaviour, a distinction between innate and acquired behaviours might be more useful than the umbrella term ‘instinctive’.

Emotion

Schore’s summary of the concept of attachment says ‘that emotional processes lie at the foundation of a model of instinctive behavior’. Bowlby devotes an entire chapter to emotion, which is well worth reading if you’re interested in behavioural theory. In it, he opts to use the term ‘feeling’ rather than ‘emotion’ because ‘feeling’ can be applied to a wide range of… well, feelings, but ‘emotion’ tends to have a more restricted use. (And one that’s proved notoriously difficult to define.) Essentially Bowlby sees feeling, not as a stand-alone biological phenomenon, but as having an important role in an organism’s appraisal of its internal and external state. The appraisal process involves;

• assigning a value (e.g. nice/nasty) to current sensory input
• comparing the current situation with previous ones
• selecting an appropriate behavioural response
• evaluating the behavioural response in terms of the organism’s goals

Bowlby shares the view of philosopher Susanne Langer that ‘being felt is a phase of the process itself’ (p.108). In other words, feelings are a phase of the process of appraisal.

He explores the role of feelings in communication – via facial expressions, for example, and whether feelings cause behaviours. Bowlby’s analysis is very thorough. So although feelings clearly play an important role in the interaction between mother and infant, I find it difficult to understand how Schore can conclude that Bowlby sees emotional processes as at the root of attachment, especially as Bowlby warns repeatedly about the danger of reifying feelings and emotions as if they can exist apart from the process of appraisal of the internal and external environment.

Strengths and weaknesses of Bowlby’s model

This is my understanding of Bowlby’s model of attachment;

Over time, human beings have evolved instinctive, biologically regulated behaviours that increase the likelihood of the survival of the individual and the species. Mating, parenting and attachment behaviours are critically important (p.179). Attachment involves infants seeking proximity to a primary caregiver, usually the mother. Separation from the attachment figure causes anxiety, and loss of the attachment figure causes depression.

Elsewhere I’ve been quite critical of attachment theory so it might be worth highlighting in more detail where I think Bowlby is wrong – and where he’s right.

There are some aspects of Bowlby’s model I wouldn’t question. It’s clear that childhood experiences affect development and adult behaviour. Some behaviour fits Bowlby’s definition of instinctive, and it’s valid to describe the proximity-seeking behaviour of young children toward a caregiver as ‘attachment’. Attachment behaviours would generally improve an infant’s chances of survival. And there’s no question that there’s usually an emotional bond between infants and their mothers and that separation from the mother can have lasting effects.

What I am questioning is some of Bowlby’s underlying assumptions about nature and nurture. I think there are four questionable assumptions – about genetic endowment, the environment of adaptedness, typical development and what causes developmental differences. Bowlby sees the nature/nurture debate as pointless because development – of the species and the individual – is the outcome of interactions between genetic endowment and environment. Yet he sees individual development as being influenced predominantly by environmental factors. How does he come to what appears to be a contradictory conclusion?

genetic endowment

As far as I can tell, the contradiction originates in his first implicit assumption about genetic endowment; that the human genome has already evolved and is unlikely to evolve further. In Bowlby’s model, instinctive behaviour has evolved once and for all in its environment of adaptedness. It’s as if human beings, like all other species, have ended up in a kind of evolutionary cul-de-sac. That’s true in the sense that past genetic changes limit future ones, but it doesn’t preclude the minute de novo changes in genetic material between generations that are now believed to be involved in many developmental disorders.

The interaction between genes and environment can occur at a molecular level. A small genetic variation can result in changes to levels of a specific protein that can in turn trigger a cascade of developmental abnormalities, including abnormal social interaction, with variations between individuals resulting from interacting developmental and environmental factors interacting in different ways; this is what occurs in Williams syndrome, for example.

environment of adaptedness

The second assumption involves the environment of adaptedness – the environment that shaped the genetic endowment and the instinctive behaviour of a species. Bowlby says;

So long as the environment is kept within certain limits, it seems likely that much of the variation in the behaviour of different children is attributable to genetic differences. Once environmental variation is increased, however, the effects to which such variation gives rise are plain to see”. (p.296)

The problem with this view is that although the limits of the environment of adaptedness are clear for something like the cardiovascular system – if they are exceeded the system stops functioning and the organism dies – we don’t actually know for sure what those limits are for various behavioural systems. We can only speculate by observing the points at which behaviour begins to depart from typical patterns. And typical behaviour varies not only between individuals, but also within individuals – over time and in different environments. Although some behaviour patterns can be described as typical of a species, the typicality itself isn’t clear-cut; all we can say is that a species has a tendency to behave in particular ways in particular circumstances.

typical development

Although he doesn’t say so explicitly, Bowlby appears to be moving towards a normative view of child development. So a third assumption is that not only are some patterns of behaviour typical of human beings, those are also patterns that healthy human beings should be showing.

causes of developmental differences

The fourth assumption is that psychoanalysis is correct in locating the root of many pathologies in attachment patterns;

If the satisfactory development of attachment is as important for mental health as is claimed [by Freud], there is an urgent need to be able to distinguish favourable development from unfavourable and also to know what conditions promote one or the other.” (p.331)

Bowlby explains Freud’s view of separation anxiety as follows;

“… we try at times to withdraw or escape from a situation or object that we find alarming, and … we try to go towards or remain with some person or in some place that makes us feel secure. … So long as the required proximity to the attachment-figure can be maintained, no unpleasant feeling is experienced. When, however, proximity cannot be maintained … The consequent searching and striving are accompanied by a sense of disquiet … and the same is true when loss is threatened. In this disquiet at separation and at threat of separation Freud in his later work came to see ‘the key to an understanding of anxiety’.” (p.330)

Bowlby supports this thesis by referring to studies that show typical attachment patterns in infants. I think this is where his theory runs into problems because the studies also show a great deal of variation in behaviour in both babies and mothers. Despite this, Bowlby focuses on the correlation between infant and maternal behaviour and concludes;

Whatever the causes of a mother’s behaving in one way or another towards her infant, there is much evidence suggesting that whatever that way is plays a leading part in determining the pattern of attachment he ultimately develops.” (p.345)

At one level Bowlby understands the importance of the interaction between genetic endowment and environment in behaviour and that genetic endowment and environment can vary. But because of his underlying assumptions about the human genome, the environment in which it evolved, the nature of instinctive behaviours and a psychoanalytic model that locates the source of mental health in childhood experiences, it’s almost inevitable that Bowlby ends up placing a disproportionate emphasis on environmental factors – especially on the mother’s behaviour.

Does the nature/nurture debate really matter?

Despite child development theorists from Darwin onwards espousing the idea that behaviour develops from an interaction between genetic make up and environment, child development theory has throughout its history swung between an overemphasis on genes and an overemphasis on environment. An overemphasis one way or another isn’t just an obscure theoretical issue. Overemphasising the role of genes resulted in the eugenics movement that had catastrophic outcomes for minority groups worldwide. Overemphasising environmental factors (coupled with a misunderstanding of probability) led to the relatively recent imprisonment in the UK of several mothers wrongfully convicted of murdering their children – with tragic consequences.

Attachment theory has experienced something of a resurgence in recent years, but professionals using it don’t necessarily have sufficient biological knowledge to critique it. In the publications on child development referred to by the Munro review of child protection Bowlby’s ideas were generally presented as givens, with little discussion. In other words, there appears to be an assumption implicit in the child protection literature – and amongst politicians – that the most likely cause of abnormal behaviour in children is parental behaviour. The problem with an overemphasis on parental behaviour is that there’s a serious risk of genetic and medical disorders and alternative environmental factors being overlooked. I’ve lost count of the number of accounts I’ve read from parents who have been puzzled as to why their child refusing to go to school is attributed by teachers and social workers to a child having a problem with attachment (rather than a problem with school), or where problems with attachment have transformed into a diagnosis of autism or ADHD once practitioners who are specialists in those fields get involved.

My fundamental problem with attachment theory is not that I think attachment behaviours don’t exist – they clearly do. It’s that Bowlby’s theory consists of a number of phenomena over which there’s little disagreement, held together by a series of assumptions. Those assumptions implicitly rule out a host of other possible causes for mothers and children behaving in the ways they do. In the next post, I’ll look at what Allan Schore makes of Bowlby’s model.

Edited for clarity 11/7/15.

Image of Bowlby from http://tinyfootprints.wikispaces.com/John+Bowlby

what’s wrong with attachment theory?

I’ve encountered enough examples of inadequate, chaotic, manipulative and abusive parenting to understand why people working with troubled children might view parents as prime suspects. However, there are many possible causes for children’s unusual behaviour and a focus only on parental behaviour means that other causal factors are likely to be overlooked.

In the next few posts, I want to explore three concepts – Attachment Theory, Fabricated or Induced Illness (FII) and the ‘cycle’ theories of deprivation and abuse – that attribute the cause of children’s abnormal behaviour primarily to parental behaviour. Although these concepts aren’t directly related to autism, parents of children with developmental issues and learning difficulties have reported these ideas being proposed as causes for their children’s behaviour despite evidence to the contrary.

Attachment theory

Attachment theory was an idea developed by John Bowlby, born in 1907, one of the six children of Sir Anthony Bowlby, surgeon to the King’s household, and his wife Maria. Like many children in well-to-do families of the period, Bowlby was brought up by a nanny and sent to boarding school at the age of seven. He later became a psychologist, psychiatrist and psychoanalyst who worked with maladjusted and delinquent children, studied the effects of maternal deprivation and after WWII became a mental health consultant to the World Health Organization. Bowlby’s work led him to the conclusion that ‘to thrive emotionally, children need a close and continuous caregiving relationship’ (Bretherton, 1992). He drew on new research in cybernetics, brain function and on Lorenz’s work on imprinting to develop his theory, and realized that a complete revision of Freudian ideas about child development was required. This he attempted to do in three books published under the title Attachment and Loss: Attachment (1969), Separation (1973) and Loss, Sadness and Depression (1980).

In 1950, a University of Toronto graduate called Mary Ainsworth had joined Bowlby’s research team. Three years later, having moved with her husband to Uganda, she carried out the first of several studies on infant-mother attachment. She then developed an assessment procedure for determining the nature of an infant’s attachment – the Strange Situation – and concluded that infants showed one of four distinct patterns of attachment to their mothers; secure, anxious-resistant insecure, anxious-avoidant insecure and disorganized/disoriented. The patterns of attachment developed with primary caregivers were seen as foundational for social interactions and mental health throughout later life – an insecure or disorganized attachment could lead to later problems.

It’s easy to see how attachment theory could be used to lay the blame for a child’s behavioural issues at the feet of parents, particularly mothers. Bowlby, however, doesn’t appear to have had any intention of blaming parents; his theory is firmly grounded in the idea of behaviour involving an interaction between genes and environment. But that doesn’t seem to be the way attachment theory is presented in texts that inform public policy. Before moving on to these texts I want to examine the ideas behind attachment theory in more detail because, like the concept of autism, it’s a theory constrained by the state of knowledge at the time of its inception.

Background to attachment theory

In the opening chapters of his first volume of the Attachment and Loss series – Attachment – Bowlby explains, systematically and in detail, the theoretical framework for his model. Bowlby brought together concepts from a number of different fields. Here’s a summary of his reasoning:

• Observations have shown that separation from the mother-figure can be extremely traumatic for children. There is evidence that this separation can result in problems with behaviour, personality and mental health in later life – e.g. stealing, depression and schizophrenia.

• Attachment theory is grounded in psychoanalytic theory because ‘despite limitations, psychoanalysis remains the most serviceable and most used of any present-day theory of psychopathology’ (p.xv).

• Data can be obtained by observing behaviour, as well as from introspective reports from participants.

• Freud drew attention to the importance of feedback in homeostatic biological systems; in behaviour, motivation is regulated by homeostasis in the same way.

• Instinctive behaviours can be complex and are the outcome of an interaction between ‘genetic endowment’ and environment – partly innate and partly acquired.

• Behavioural systems are goal-directed (ie they evolve in order to fulfil a specific purpose) – analogous to engineering control systems.

As I understand it, at inception, the Freudian psychodynamic model of behaviour was a novel idea; it was developed from first principles derived from contemporary understanding of biological mechanisms. Bowlby’s model wasn’t novel; it was an extension of the psychodynamic model based on new knowledge about those mechanisms. This means that Freud and Bowlby based their theories on the same assumptions:

1. Species-specific patterns of behaviour are biologically ‘provided’ – although they can be affected by the environment.

2. Biologically provided behaviour patterns are normative. That means that in the ‘right’ environment they will unfold naturally, but could be disturbed if something goes ‘wrong’ with either the genetic endowment or the environment.

3. Biologically provided behaviour patterns are goal-directed – they have evolved to fulfil a specific purpose.

4. Behaviour is driven by the need to maintain emotional (feelings) homeostasis.

5. Relationships between parents and children are central to child development.

Attachment theory is clearly a theory of its time, since research in all these areas has since moved on. That doesn’t necessarily invalidate attachment theory, but does suggest there are some problems with it.

What’s wrong with attachment theory?

1. Freud saw social and sexual development as central to human behaviour because of their importance in sexual reproduction – the means by which inherited characteristics (including behavioural drives) are passed on to offspring. This is why a child’s relationship with his or her parents was seen as so important; it could disturb the natural unfolding of social and sexual drives. Subsequent research, by contrast, shows that social and sexual behaviour is influenced by complex array of factors that change over time. Despite revising Freud’s framework, Bowlby still viewed social and emotional factors as central to the development of human personality rather than being two factors amongst many.

2. Much of Bowlby’s research was carried out prior to the structure of DNA being discovered and the consequent development of molecular biology. Subsequent research suggests that rather than behaviour patterns being biologically provided, they emerge from interactions between genetic expression and environment. Similarities between individuals in both genetic material and environment result in species-specific behaviours but differences mean that species-specific behaviour patterns vary between individuals. Oppenheim et al. (2009) noted, for example, secure attachment patterns in autistic children that were different to the one that Ainsworth described.

3. Biological behaviour patterns can only be goal-directed if the genome and the environment remain stable – but they don’t. Genetic make-up is unique to an individual and the environment changes constantly; behaviour patterns emerge from a dynamic interaction between the two. Although there’s no doubt that children do exhibit patterns of behaviour towards their primary caregivers, and it’s likely that those patterns can be seen across different individuals, the patterns are descriptive, rather than normative. Even if the patterns provide a useful way of identifying problems in infant-parent relationships, they show how children interact, not how they should interact.

4. Some biological systems – those that regulate body temperature or the levels of oxygen and water in the body, for example – are maintained via homeostasis because the biochemical reactions necessary for survival can occur only within certain narrow limits. Emotions and behaviour aren’t so constrained and tend to be cyclical rather than stable.

5. There’s no doubt that a child’s relationship with his or her primary caregiver is important. But in focussing on a single relationship, attachment theory by definition marginalises the role of genetic, biological and other environmental factors – including other relationships – in a child’s social and emotional development.

This brings us back to the concept of reification that cropped up in a previous post about Kanner’s model of autism – although I didn’t call it that at the time. Reification literally means ‘making a thing’ – the implication being that a ‘thing’ is made that doesn’t necessarily exist in the real world. There’s no question that ‘attachment’ can be used as a descriptive label for certain kinds of behaviour, just as ‘autism’ can. It doesn’t follow that attachment must be a clear-cut psychological function, nor that autism must be a distinct medical disorder.

When I studied psychology as an undergraduate in the 1970s, attachment theory was already being viewed with some skepticism for the above reasons. I haven’t kept in touch with child development research so I was surprised to find that attachment theory is still alive, well and influencing social policy in the 21st century. That’s the subject of the next post.

References

Bowlby, J (1969). Attachment and Loss vol 1: Attachment. Revised 2nd edition, 1997, Pimlico.
Bretherton, I (1992). The origins of attachment theory:John Bowlby and Mary Ainsworth, Developmental Psychology, 28, 759-775.
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

Acknowledgements

I want to thank everyone who sent me links relevant to this and related posts. You know who you are!