what about attachment parenting?

During my excursion into the world of child development theory, I’ve been acutely aware of one important group I’ve so far overlooked; the advocates of attachment parenting (AP). Attachment parenting is an approach derived from John Bowlby’s theory, but includes practices like extended breastfeeding, ‘babywearing’ (carrying the baby close to the parent’s body), co-sleeping, and a high level of responsiveness to the baby’s needs. I must admit to being sympathetic to AP as an approach; I must also admit (like many other parents) to being something of an attachment parenting backslider. Both my children were in a buggy by the age of six weeks because I couldn’t find a sling that didn’t hurt my back, due to a series of complications I stopped breastfeeding my son at four months, and one child slept happily in bed with me whereas the other simply wouldn’t.

A significant influence in the AP movement is William (‘Dr Bill’) Sears, a paediatrician and author of a number of best-selling parenting books. Dr Sears’ wife Martha is a director of Attachment Parenting International (API), an organization founded in 1994 by Barbara Nicholson a learning disabilities specialist, and Lysa Parker, who also has a background in special education. Parker also worked with La Leche League International, as did four other of the API’s eight directors. (La Leche League was founded in Illinois in 1956 by a group of mothers who wanted to promote breastfeeding, a practice then rapidly dwindling in the USA.)

Dr Bill’s shoes have to an extent been filled by Gordon Neufeld, founder of the Neufeld Institute in Vancouver, Canada. Unsurprisingly, Neufeld’s approach is firmly grounded in attachment theory, with separation, for example, being seen as playing a key role in the ‘epidemic of anxiety’ that apparently afflicts our children. Neufeld’s ideas are very popular, but it’s instructive to read what a group of parents who have used the AP approach with their special needs children have to say here.

Why attachment parenting?

The predominant reasons given for the attachment parenting approach are that it involves ‘instinctive’ and ‘natural’ child-rearing practices that parents have used for thousands of years. In essence this is the same argument used by Bowlby and Bruce Perry in support of their models of child development. I think it’s flawed in two respects. One is that ‘instinctive’ behaviours have also led to the adoption of practices that attachment parenting advocates are unlikely to approve of, such as infanticide, cranial deformation and genital mutilation. You could argue, of course, that such practices might be instinctive but they’re not ‘natural’. Unfortunately, ‘nature’ isn’t always benign either.Throughout human history, infants in hunter-gatherer societies have been at high risk of death from predation, starvation, injury and infection. And if hunter-gatherer societies appear to be healthier than those in the developed world, it’s often because of the price paid by their ancestors and the weaker members of their community. Although AP proponents often advocate as natural a lifestyle as possible, few in the developed world would expect mothers and children to be self-sufficient, live in huts, cook over open fires or fail to take advantage of modern medical interventions if required.

Evidence or belief?

In other words, neither the ‘instinctive’ nor ‘natural’ justifications for attachment parenting provide sufficient evidence to support it. I suspect that rather than AP consisting of practices based on a careful evaluation of the evidence, AP is actually based on a set of beliefs. They’re not unreasonable beliefs; breastfeeding, carrying babies in a sling and being responsive to a child’s needs are highly likely to be of benefit because they optimize nutritional intake and reduce the risk of gastro-intestinal infection, keep the infant warm, comfortable and within the parent’s sight, and increase the likelihood of the child’s needs being responded to promptly. In other words, they are beneficial to the child for good, demonstrable reasons, not because they are ‘instinctive’ or ‘natural’. Other practices are less obviously beneficial; Attachment Parenting International has issued safety guidelines in respect of children sleeping in the parent’s bed, for example, and numerous parents have described attachment parenting resulting in outcomes such as a bad back and sleep deprivation.

Personally, I have no problem with parents basing their parenting approach on a set of beliefs; as long as children aren’t harmed, parents are free to bring up their children as they see fit. They are also entitled to share their beliefs with others and to try to persuade them that those beliefs are right. I don’t even have a problem with practitioners such as Sears or Neufeld advocating a particular approach to child-rearing, because parents and practitioners committed to an approach don’t generally claim to have carried out an exhaustive evaluation of the relevant evidence. It’s usually fairly obvious that they are propagating beliefs and are using evidence selectively to back up their views. What I do find worrying is researchers adopting the same approach. Even though their credentials suggest they are able to evaluate all the relevant evidence in a reasonably objective manner, some follow the same strategy as attachment parenting advocates and base their theoretical models on beliefs backed up with supporting evidence only. What’s also worrying is that an uncritical evaluation of the evidence appears to be acceptable to some peer-reviewed journals.

In a previous post I compared Leo Kanner’s and Bruno Bettelheim’s approaches to the early evidence relating to autism. Kanner’s initial model of autism was based on his evaluation of evidence in the light of contemporary child development theory. As time went by, he repeatedly revised his model as new evidence became available. Bettelheim, by contrast, not only based his model on a belief about the cause of autism (parental behaviour), but also used evidence selectively to support it, and his background in philosophy appears to have persuaded him that this was valid way of handling evidence. I don’t know if Bettelheim’s approach is embedded somehow in the world of child development research, but it keeps cropping up amongst child development researchers. Bowlby’s essential dismissal of genetics and unquestioning acceptance of the idea that the origins of psychiatric disorders are to be found in childhood experiences, contrasts starkly with his painstaking analysis of concepts such as instinctive behaviour and emotion. Allan Schore goes into considerable technical detail about the development of the orbitofrontal cortex, but doesn’t question Bowlby’s model of attachment, or the findings of researchers he uses to support his orbitofrontal model, despite Bowlby’s theory and the function of frontal areas of the brain being the subject of considerable debate. Perry’s discussion of the evolution of human socio-emotional behaviour is pretty speculative, and although on the face of it his brain scan findings are persuasive, digging a little deeper suggests that he hasn’t paid sufficient attention to defining concepts such as neglect, nor to the range of other possible causes of abnormal brain development.

Carrot or stick?

Another issue that’s concerned me is what the attachment model is used for. AP proponents tend to take a resoundingly positive approach to parenting – AP practices are recommended because they are seen as being good for babies and their families and ultimately, society at large. Parents are encouraged to use strategies flexibly and adapt them to their own lifestyles, even though some AP supporters might get a bit over-zealous and risk making parents feel needlessly guilty. When attachment theory filters through into public policy, however, a rather different picture emerges; one in which there’s a real risk of attachment theory being used as a stick with which to beat parents. Poor attachment is blamed for poor health, antisocial behaviour and psychiatric disorders, locating the source of those problems firmly within the family, particularly with parents and notably mothers.

Despite references being made in policy documents and textbooks to Bronfenbrenner’s ecological systems theory, his framework is rarely applied except in the sense of recommending interventions at the community, state or international level to prevent or compensate for the damage caused by poor parenting. So far, I’ve found little consideration given to the possibility that problems manifested by individuals could have causes at all levels, from genes through physiology, to economic, social and cultural pressures at the community, national or international level.

In my next post, I look at a book by a critic of current child development theories, John Bruer’s The Myth of the First Three Years.

Acknowledgement: with grateful thanks to Jennifer Skillen for information about the history of La Leche League.

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

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.