fabricated or induced illness

In November 1999, a solicitor named Sally Clark was found guilty of the murder of her two infant sons and sentenced to life imprisonment. Three years later, her conviction was overturned on her second appeal, but it was too late for Mrs Clark. She died of alcoholic poisoning in 2007, four years after her release. In response to this miscarriage of justice, the Attorney General ordered a review of similar cases, including those of Donna Anthony, Angela Cannings and Trupti Patel.

Two key factors in overturning Sally Clark’s conviction were that evidence of a bacterial infection had been known to the prosecution’s pathologist, but not disclosed to the defence, and the nature of the statistical evidence presented by an expert witness, Professor Sir Roy Meadow, a paediatrician and former Professor of Paediatrics. Meadow claimed that the chances of two children in a family like Clark’s dying of Sudden Infant Death Syndrome (SIDS) were 1 in 73 million. Meadow had calculated these odds by squaring the chances of one child dying (1 in 8,500). Statisticians have pointed out that since SIDS deaths are likely to have genetic and/or environmental factors in common, the probability of a second child in the same family dying of SIDS is increased, not decreased. They have also pointed out double murder is even less prevalent than double SIDS. After the case, the prosecution pathologist was found guilty of serious professional misconduct and Roy Meadow was struck off the medical register, only to be reinstated on appeal a year later.

Statistical anomalies aren’t Roy Meadow’s only claim to fame. He’s also responsible for describing Munchausen’s Syndrome by Proxy (MBP or MSbP). Munchausen’s Syndrome (that is, without the proxy) had first been described in 1951 by Richard Asher, an endocrinologist and haematologist (and the father of Peter, Jane and Clare Asher). It’s a supposed psychiatric disorder in which the patient fabricates the symptoms of an illness in order to get attention and/or sympathy. In MSbP (that is, with the proxy) a parent or carer exaggerates or fabricates symptoms in someone else – MsbP usually involving mothers fabricating symptoms in their children.

Those who have read my blog on autism will be familiar with the some of the theoretical problems involved in defining syndromes and psychiatric disorders. Syndromes often vary considerably between individuals and frequently it’s not clear whether or not a psychiatric disorder actually exists as a distinct disorder – in other words, patients might be experiencing similar symptoms, but it doesn’t follow that the same thing causes those symptoms in every case. Not surprisingly, the term Munchausen’s Syndrome by Proxy has largely been replaced in the UK by the concept of Fabricated or Induced Illness by carers (FII). In the USA, the term ‘factitious disorder by proxy’ is often used.

In order to explore the idea of FII I’ve focused on an NSPCC Research Briefing by Anne Lazenbatt, NSPCC Reader in Childhood Studies at Queen’s University, Belfast and Julie Taylor, Professor of Family Health at the University of Dundee, and also Head of Strategy and Development with the NSPCC. [The briefing no longer appears to be available on the NSPCC website but can be downloaded here.]§

What is FII?

The briefing describes FII like this;

FII occurs when a caregiver…misrepresents the child as ill either by fabricating, or much more rarely, producing symptoms and then presenting the child for medical care, disclaiming knowledge of the cause of the problem. (p.1)

The authors make it clear that there’s been a good deal of debate about the nature of FII, and they point out that it isn’t a clear-cut construct. FII is seen as a ‘spectrum’ (p.4) and The Royal College of Paediatrics and Child Health (RCPCH) introduced the term FII in 2001, and according to the briefing ‘helpfully offer five examples of behaviour across the FII spectrum’. They are (p.5);

1. Simple anxiety or over-interpretation of trivial symptoms.
2. Child’s symptoms are misperceived, perpetuated or reinforced.
3. Carer actively promotes sick role by exaggeration, fabrication or falsification.
4. Carer suffers from psychiatric illness.
5. Child has a genuine and unrecognised medical problem.

Note that according to the briefing, the RCPCH includes ‘simple anxiety or over-interpretation of trivial symptoms’ and ‘a genuine and unrecognised medical problem’ as part of the spectrum of FII. In fact the RCPCH Guide describes the spectrum as a ‘spectrum of cases where FII concerns may arise’ (p.8), which puts a rather different slant on things. The authors of the briefing do at least comment that ‘the extremes are useful to note and should be borne in mind throughout’. Indeed.

Prevalence of FII

The briefing then goes on to look at the prevalence of FII. Estimating the prevalence is challenging, given the width of the FII spectrum and the heated debate about its definition, or even whether it exists at all. In these circumstances, the authors’ comment that ‘epidemiological studies used to demonstrate prevalence rates are fraught with methodological difficulties’ is something of an understatement, but they have a go. Here are some of the estimates reported (pp.4-5):

• 0.5 per 100,000 children

• 2.8 cases per 100,000 children per year

• 89 per 100,000 children over two years

• 97 new cases of FII in two years

• 451 cases from many different countries

The definition of what constituted a ‘case’ varied widely.

Despite the huge variations in estimates, the briefing emphasizes the view of some professionals that FII is more common than might first appear. I thought it might be instructive to compare the prevalence of FII with that of disorders that might fall into the category of ‘genuine and unrecognised medical problem’.

• Ehlers-Danlos syndrome: (all types) 20 per 100,000*
• Fragile X: 25 per 100,000
• Coeliac disease: 1,000 per 100,000
• Autism: 1,000 per 100,000
• Lactose intolerance: (N. Europe) 5,000 per 100,000

In other words, even the highest estimates for FII are lower than for several medical conditions practitioners would have heard of, but which frequently go undiagnosed for years. But my search of the NHS Choices website could find no results for ‘under-diagnosed’ or terms similar to it, despite each of the conditions listed above being reported by researchers as likely to be under-diagnosed. The NSPCC briefing doesn’t expand on this issue, although it does warn that:

It is important to recognise that children may have genuine significant illnesses or medical conditions in addition to ones that are fabricated and/or induced. (p.10)

How is FII diagnosed?

So how is a clinician supposed to distinguish between a genuine and fabricated or induced illness? With difficulty, it seems. Here are examples of warning signs of FII (p.9):

• The child has repeated and unexplained illnesses or symptoms.

• The child has unexplained multiple illnesses or symptoms.

• The child’s supposed symptoms only occur when the mother is present.

• The mother appears to know a lot about medicine.

• Although the mother stays with the child all the time while he/she is in hospital and attends to him/her well, she may not appear as concerned about the child’s well being as the health care professionals who are providing treatment; in contrast she may appear overly concerned.

• The father is not involved in the care of the child, or his involvement is minimal. Note however that fathers are sometimes involved in FII.

One can understand why the NSPCC wants clinicians to be alert to the possibility that symptoms might be being fabricated or induced, and to protect children from further harm from unnecessary medical tests and procedures. On the other hand, it’s difficult to see how mothers who are single parents or whose partners are working, and whose children have genuine multiple, repeated, unexplained, intermittent symptoms are expected to approach health professionals without exhibiting the ‘warning signs’ of FII listed above.

And here are some words of advice for social workers:

It is not only health professionals who have a role in the detection of FII. Social workers play an important part and may struggle because they have little knowledge about FII, or when they suspect FII, they may not be able to convince the GP (Griffiths, 2010).

Of course that could also be because the GP has medical knowledge, which the social worker might also lack. Griffiths suggests specific points for social workers to bear in mind:

• Being honest about suspicions from the start may scare off the parent (making it difficult to gain evidence), attract undue media attention, or worse, can lead to an increase in harmful behaviour in an attempt to be more convincing.

• Consider motivation. For example, the family might be having financial trouble and fabricating or inducing an illness may entitle them to extra welfare benefits.

• Verify the personal histories of family members, as lies may have been told (for example, that one of the parents has a medical background).

• Remember that some parents may be extremely manipulative and convincing. They may be middle class and they will know how to invoke complaints procedures. (pp.10-11)

The last sentence is especially ironic. Interestingly, the Griffiths reference isn’t, as you might expect, to a research paper but to an article in Community Care magazine. I couldn’t find out who Julie Griffiths is, but she’s written a number of articles on the Community Care website. Her advice is summed up by the authors of the briefing as follows;

Although Griffiths offers cautionary advice, the point for social workers is ultimately the same as for health professionals: it is crucial to do the detective work. (p.11)

Yes it is, absolutely, but the detective work is required to find out the underlying cause of the child’s presenting symptoms, not to prove suspicions of FII correct.

Tragically, there’s no doubt that some parents do harm their children and present the consequences of that harm as a medical condition. Controversial covert video surveillance at the Royal Brompton Hospital, carried out by another doctor with expertise in FII, Professor David Southall (also struck off the medical register and then reinstated) and numerous cases have made that clear. However, the content of the NSPCC research briefing implies that some serious questions need to be asked about how FII is being approached.

How valid is FII?

1. The Royal College of Paediatrics and Child Health’s definition of FII is so broad that accurate determination of the prevalence of FII is impossible.

2. Having said that, even the highest estimates for the prevalence of FII are much lower than the prevalence of genuine medical disorders that are frequently under-diagnosed. It might have been helpful for the research briefing to have provided a checklist of commonly under-diagnosed disorders for medical practitioners to rule out, prior to making a default assumption that FII is involved.

3. I don’t have figures for the prevalence of under-diagnosis of genuine medical conditions, although one study of coeliac disease showed an under-diagnosis rate in four European countries between 76% and 94%. Given the range of disorders involved and their estimated prevalence, it’s possible that children might be at significantly greater risk from undiagnosed medical conditions than from abuse or neglect from parents and carers. For obvious reasons the NSPCC sees its task as drawing attention to active abuse or neglect, but if our focus of concern is the health and wellbeing of children, systems neglect is an important issue that shouldn’t be overlooked.

4. The FII coin has two sides; one is the ability of carers to fabricate and induce illness in children without this being detected, and the other is the under-diagnosis of medical conditions. Both sides of the coin call into question the diagnostic capacity of health services. Clearly, it’s impossible for GPs to know about all illnesses, but rather than raise the profile of FII, it might make more sense to improve access to specialist medical knowledge, in order to rule out genuine medical conditions and increase detection of fabricated symptoms.

What’s FII got to do with child development theory?

FII is assumed to be both a medical disorder and a form of child abuse. However, the NSPCC briefing presents FII within a theoretical framework that will be familiar to readers of previous posts. Firstly, although there’s some discussion about its definitions and prevalence and the briefing does allude to FII being manifest at the systems level (p.1) the FII construct is framed in terms of individual carers’ behaviour towards individual children, even though children can come to harm in a variety of ways that don’t involve carers. Also, carers’ behaviour can be influenced by many factors, including economic policies and flaws in the design of the health, education and social care systems. In other words the FII model itself is framed in terms of the behaviour of individuals, rather than being set in the broader ecological context described, for example, by Uri Bronfenbrenner.

Secondly, even in cases where carers are guilty of abusing children, attempts to explain FII appear to have focused on psychoanalytic, attachment and ‘cycle of abuse’ models – an implicit assumption that the carers themselves might have been abused (p.7). What receives less attention is the possibility that the carers might have a neurological problem that results in delusions, lack of impulse control or fabrication that itself might require medical investigation. Alternatively, some carers might have a vested interest in harming their children – qualification for additional benefit payments is mentioned in the briefing. Although this motivation might be perverse, it isn’t necessarily the result of a delusional illness or of childhood abuse.

The briefing cites, uncritically, a definition of FII that includes over-anxiety and undiagnosed medical conditions, a list of warning signs for FII that include responses that would be common in non-abusive parents and carers, and frames FII predominantly in terms of a ‘cycle of abuse’ model involving only the behaviour of individuals. It overlooks systems factors such as the training of health professionals and the demise of the family doctor who would be familiar with a patients’ family history.

I contacted one of the authors of the briefing for her comments. It was clear from her response that the remit of the briefing and the limit on length made a complete analysis of FII impossible. In addition her area of expertise didn’t qualify her to comment on medical conditions that might be mistaken for FII and that the primary purpose of the briefing was to raise awareness of FII amongst health professionals. An analysis like the NSPCC one doesn’t provide an exhaustive overview of the FII research literature, obviously. However, this briefing is written for professionals and, because it’s endorsed by the NSPCC it is, worryingly, likely to be taken as authoritative despite its shortcomings.

Reference

Lazenbatt, A. & Taylor, J. (2011). Fabricated or induced illness in children: A rare form of child abuse?, NSPCC.
Royal College of Paediatrics and Child Health (2009). Fabricated or Induced Illness
by Carers (FII): A Practical Guide for Paediatricians.

Notes
*corrected 19.03.14
§ A set of slides on FII by the authors of the briefing is available online at http://www.baspcan.org.uk/files/Lazenbatt%20Ann%20F2.1%20Mon%2010.30.pdf
It highlights many of the problems with the FII concept.

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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 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 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. 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.

the big picture: do mothers cause social problems?

I’ve suggested Allen and Duncan Smith’s understanding of brain development and of data from large-scale studies isn’t as good as it might be. So what?

The role of evidence

It’s not clear why Allen and Duncan Smith feel compelled to use evidence from brain development to shore up their case for early intervention. We already know that maltreatment, neglect and poor attachment cause problems, often lasting ones; that’s why they’re called ‘maltreatment’, ‘neglect’ and ‘poor’ attachment. We’ve known for millennia that early intervention in children’s lives is more effective than late intervention. We can also demonstrate the effectiveness of an intervention without knowing how it works. The use of brain development as evidence is especially puzzling since Allen and Duncan Smith clearly don’t understand it well, and because people who understand it better suggest that the evidence linking maltreatment, neglect and attachment to abnormal brain development is still rather tenuous e.g. De Bellis (2005); Glaser (2000). Basing one’s case on unreliable evidence runs the risk of defeating one’s own aims.

Correlation and causality

Allen and Duncan Smith rely heavily on correlations to support their model. If I’ve understood it properly their model looks something like this:

Allen and Duncan Smith early intervention model

But all the causal connections implied in the model rely on correlations. Assuming that correlated variables must be causally linked – ie that one causes another – is a basic error in data analysis. It’s not the first time the Centre for Social Justice has made this mistake. Their paper on marriage published in December 2009, assumes that correlations between marriage and length of relationship, mental and physical health, violence and abuse and outcomes for children, mean that marriage itself results in more stable relationships, improved mental and physical health and a reduction in violence and abuse. Not that non-violent couples in stable relationships, with adequate parenting skills, who enjoy good mental and physical health might be more likely to get married and to stay together. As with the brain development data it’s clear that the error has been made by the authors of the reports, rather than in the research on which the reports are based. In order to change behaviour it’s essential to identify its causes accurately.

The causes of social problems

A name that keeps cropping up in the child development literature is that of Urie Bronfenbrenner, a psychologist renowned for his Ecological Systems Theory of child development, often depicted as a set of concentric circles representing nested systems as shown below.

external ecological systems affecting child development (after Bronfenbrenner)

The point made by Bronfenbrenner’s ecological systems model is that many external factors at different levels of complexity interact to influence a child’s development. The same point is made by Mareschal et al’s neuroconstructivist model, except that they include factors internal to the child (genetic, epigenetic and behavioural). In the diagram below I’ve integrated the neuroconstructivist framework with Bronfenbrenner’s and Allen’s and Duncan Smith’s models, taken a cross-section, and highlighted Allen and Duncan Smith’s causal pathway in red. Even though the diagram is sketchy (I’ve omitted many factors and their possible links to outcomes), it’s clear that Allen and Duncan Smith’s model of the links between poor attachment and social problems is a narrow one. Although there is little doubt that low levels of maternal ‘attunement’ and ‘empathy’ could result in the social problems referred to, there are clearly many other factors that could also cause them, not taken into account by Allen and Duncan Smith.

integrated outline of factors affecting child development

Of course there’s no reason why government shouldn’t focus on one particular cause of social problems. After all, water purification, sewage treatment, education, free healthcare and democracy have each resulted in major improvements to quality of life. The difference is that the evidence demonstrating the adverse effects from drinking polluted water, lack of access to sanitation, education, healthcare and living under an authoritarian regime, is robust. The evidence demonstrating a causal pathway between poor attachment, brain abnormalities and an array of ‘social problems’, isn’t.

Blaming the parents

Decades of research have demonstrated that the causes of Allen and Duncan Smith’s ‘social problems’ are many, varied and often interact in complex ways. Identifying what interventions might be most successful in reducing social problems is a challenging task. And some potentially effective interventions, such as de-criminalising drug use or adopting alternatives to custodial sentences, are deeply unpopular politically. It’s much easier, and more intuitive, to allocate the blame for social problems to factors at Bronfenbrenner’s microsystems level than to tackle the complex, expensive and potentially embarrassing task of identifying possible causes at the economic, legislative or historical level. In locating the primary cause of social problems with parents – notably mothers – Allen and Duncan Smith are conveniently overlooking other possible causes at the level of the child (genetics, epigenetics, disease, diet, environmental toxins); the microsystems level (churches, schools, communities, quality of education, health and social care); the exosystems level (employment, economics, legislation, government policy); the macrosystems level (cultural assumptions, global trends) and the chronosystems level (constraints and affordances that have arisen historically). Again there is no doubt that bad mothering could cause abnormal brain development and could lead to social problems, but there is considerable doubt over whether it’s the main cause of either. In short, what Allen and Duncan Smith don’t say is as important as what they do say.

The real world is an uncompromising place

Concerned about the poor quality of evidence in the chapters on the brain in these two papers, I contacted Graham Allen. A member of his research team called me back. He assured me that the material on the brain in the Allen report had been approved prior to publication by a neuroscientist, Professor A. I contacted Professor A – who incidentally isn’t a neuroscientist. He said his role was to check the evidence on parenting programmes; the scientific advisor was Dr B. I contacted Dr B – also not a neuroscientist. No, he worked on the chapters on standards, what works and cost-benefit. Both Professor A and Dr B said they had questioned the use of the report’s cover image and had pointed out that it might be counterproductive.

This brings us back to the issues of expertise and use of evidence I highlighted in relation to Kanner and Bettelheim. The chapter on brain development in Allen’s Next Steps report doesn’t appear to have been written or checked by someone with expertise in the field – despite there being a number of high profile neuroscientists with excellent international reputations working in universities in the UK. It also raises questions about the role of ‘think tanks’. Despite inevitable shortcomings, universities have acquired a reputation for producing reasonably reliable, valid research findings; that is, research findings that reflect consistently and accurately the situation in the real world. Government policies based on a rigorous analysis of reliable, valid data are likely to be effective. Unfortunately politics tends to be not so much about the real world as about beliefs about the real world. Successful political campaigning involves persuading people that you are right and that those with opposing beliefs are wrong. It doesn’t matter, politically, if you haven’t understood the evidence or if you’ve misinterpreted the data, as long as you make a persuasive case for your policies. Of course for the people who benefit (or otherwise) from those policies, it’s quite important what evidence you are using, because if the evidence doesn’t reflect the situation in the real world, your policies won’t work. The adult social world might be open to manipulation and compromise, but as anyone who works with children, animals or materials will tell you, the real world is a pretty uncompromising place. The increasing reliance by politicians on material from think tanks founded by, or with strong links to politicians (as is the case with both the Centre for Social Justice and the Smith Institute who jointly published Early Intervention: Good Parents, Great Kids, Better Citizens) suggests we might see increasing amounts of policy-based evidence as distinct from evidence-based policy. It remains to be seen how the real world will respond.

References

De Bellis, M.D. (2005). The psychobiology of neglect, Child Maltreatment, 10, 150-172.
Glaser, D. (2000). Child abuse and neglect and the brain – a review, Journal of Child Psychology and Psychiatry, 41, 97-116.
Mareschal, D., Johnson, M., Sirois, S., Spratling, M.W., Thomas, M.S.C. & Westermann, G. (2007). Neuroconstructivism: How the brain constructs cognition, Oxford University Press.