why parents get the blame

Popular opinion about the right way to bring up children has, throughout history, varied between authoritarianism at one extreme and liberalism at the other. Child-rearing practices have typically been determined by expediency, experience or belief. Freud’s ideas about child-rearing caused a sea-change in thinking about the relationship between parents and children, because his ideas were based on an explicit theory involving the biological characteristics of human beings, rather than being derived from beliefs or pragmatic responses to circumstance.

Sigmund Freud

If I’ve understood Freudian psychodynamic theory correctly, it’s grounded in the Darwinian principles of inherited characteristics and natural selection. Freud proposed that the psychological forces that drive behaviour are passed on from generation to generation in the same way as physical characteristics are inherited. Over time, natural selection ensures that the physical characteristics and behavioural drives that maximise a species’ chances of survival are preserved. During a child’s development, all that’s required for these biologically provided physical and behavioural characteristics to ‘unfold’ naturally is a suitable environment. Physical development can be ‘disturbed’ by factors such as a poor diet or living conditions or by practices such as circumcision or foot-binding; behavioural development can be disturbed by parents or other adults being too controlling or imposing unnecessary social or religious taboos. In short, the model is one of each child having a species-specific genetic blueprint for development that, given appropriate conditions, will unfold naturally to produce a healthy adult human being. Two factors could disturb that unfolding process;

-a fault in the mechanism of inheritance (a chromosomal abnormality)
-external interference with the child’s natural course of development.

Two key points about the psychodynamic model

Firstly, the psychodynamic model assumes that potentially there is such a thing as a ‘normal’ human being – someone whose biologically provided development has been allowed to unfold naturally – even if in real life, the course of development is often disturbed, resulting in everybody having flaws of some kind.

The second point is that this theory puts parents squarely in the firing-line – developmental problems arise either because parents have passed on their faulty genes (even if they have no control over that) or because they are the most likely suspects when it comes to the child’s course of development being disrupted.

Psychodynamic theory had a huge impact on thinking about child development in the early part of the 20th century – it made people think about child development for a start. It also had beneficial outcomes for many children in terms of their health, education and psychological development. But there was a downside. Regardless of the personal views of psychodynamic theorists, psychodynamic theory is closely associated with eugenics. Although genocide, enforced sterilisation and limiting opportunities for certain sectors of the community have happened throughout history and would probably have happened in the early 20th century even if psychodynamics hadn’t been thought of, psychodynamic theory undoubtedly lent weight to these policies.

Logo from the Second International Eugenics Conference, 1921

Both Freud and Kanner were aware that knowledge about the biological process of inheritance was sketchy, and both expected subsequent research to shed light on their theories. Although some of Freud’s ideas have received support, there’s little evidence for the idea that social and sexual behaviour derives solely from unconscious drives. Although unconscious processes must affect social and sexual behaviour, the brain areas most involved during our interactions with others are higher-level rather than lower-level areas.

Despite 50 years of research into genetics and brain function bringing psychodynamic theory into question, the two explanations offered by psychodynamics for abnormal human behaviour have become deeply embedded in popular thinking in the developed world; either there’s a genetic/medical explanation or the parents must be responsible. Since WWII politicians and social scientists, not surprisingly, have been wary of genetic explanations for atypical or socially unacceptable behaviour, so causes are frequently framed only in environmental terms, often in terms of childhood experiences. In the absence of a medical diagnosis, the parent is often assumed to be responsible. But research suggests that the relationship between genes, environment and behaviour is much more complex than psychodynamic theory suggested.


The psychodynamic model saw genetic material as providing a blueprint – an engineering diagram – for development, based on Gregor Mendel’s ideas of independent segregation and assortment of genes. But later research has shown that DNA doesn’t work quite like that. DNA is a complex molecule, so when gametes (eggs or sperm) are formed, and when DNA from two parents combines during fertilisation, there’s plenty of scope for genetic variation. Indeed it’s the genetic variation in individuals that maximises a species’ chances of surviving environmental change. Because of the structure of the DNA molecule, some genetic variations are robust enough to be transmitted between generations and are inherited. Others might arise spontaneously. Some variations are common, others rare. As far as genetics is concerned, it’s meaningful to talk about ‘normal’ and ‘abnormal’ in descriptive terms (most people are like this but not like that) but not in normative terms (people should be like this but not like that).


Human beings are biochemical organisms so many environmental factors impact on our development. Some (epigenetic) factors can affect the expression of genes. Other factors, such as diet, toxins, allergens or infections can disrupt physiology and development. Other people’s behaviour affects children but parents aren’t the only people involved; other children, teachers, neighbours and wider community and societal issues can have a significant impact on a child’s development.

In short, what the last 50 years of research has shown is that inherited characteristics and parental behaviour are only two of many factors that interact in complex ways to influence a child’s development. But you wouldn’t know to that to look at current ideas regarding child health, education and social care. In fact, social policy relating to children often reflects the psychodynamic model rather than modern understandings about genetics and child development. I suggest this is largely because of the way we think.

The way we think; heuristics and biases

Human beings are capable of using logical, rational thought but as Herb Simon pointed out, we tend to do so only as a last resort. That’s because the ways of thinking that we’ve evolved as a default tend to be in the form of heuristics (rules of thumb) and biases (inbuilt tendencies) – rough and ready ways of responding to our environment. That’s because rough and ready ways of thinking that are due to the way our brains are wired up and that improve our chances of survival are more likely to get passed on to our offspring. These thinking strategies might maximise our chances of survival, but unfortunately they don’t lend themselves to figuring out solutions to complex problems or planning long-term strategies that will make everybody’s lives better.

For example, human beings have excellent pattern-matching skills. These enable us to recognise a tiger, a rattlesnake or our children, in an instant. They also result in pareidolia – seeing a pattern as significant when it isn’t. We’re good at spotting correlations; helpful when trying to figure out what causes what, but meaning we have a tendency to conflate correlation with causality. We like phenomena to have explanations; that improves our understanding of the world around us, but also results in us inventing concepts like ghosts or evil spirits. We’re also prone to looking for agents -assuming that if something happens someone must have made it happen – not that it could have happened by chance. Heuristics and biases have been investigated in some depth, notably by Daniel Kahnemann, Paul Slovic and Amos Tversky. You can find an extensive list of human biases here, though it’s likely that many of them are actually different facets of a few underlying cognitive phenomena.

Bettelheim’s philosophers

People have long been aware that we don’t get information directly from the world around us, but via the filter of our perceptions. Errors and biases in our perceptions result in theories like the sun moving round the earth or the earth being flat. It’s only when our observations don’t match up with how we think things work that we start using logical rational thought to figure out why. The problem of how to work round unreliable perceptions was what Bettelheim’s favourite philosophers were attempting to tackle. The reason they didn’t opt for the scientific method, which has developed as a way of counteracting unhelpful perceptive errors, was I suspect, because science also gets things wrong. A fundamental point to bear in mind is that science doesn’t deal in certainties, but in degrees of uncertainty. We have enough certainty about some phenomena to land probes on Mars, replace human organs and communicate instantly with someone on the other side of the world. We’re much less certain about the causes of other phenomena – human behaviour, for one. But science has a large toolbox of methods for systematically eliminating less likely explanations for phenomena and investigating explanations that are more likely, so even though our knowledge will always be subject to our perceptions and will always be limited, it is possible to have knowledge that’s reliable enough to be useful.

In my previous post, I highlighted two differences between Kanner and Bettelheim; their use of evidence and their level of relevant expertise. I suggest that these two factors are among the reasons why parents are often (wrongly) blamed for their children’s behaviour.

The use of evidence

Science evaluates evidence by comparing hypotheses about how things happen with observations of what happens. If a theory makes predictions and they turn out to be wrong, we modify the theory – evidence that conflicts with theory can be very informative. Other disciplines handle evidence differently. In disputes, for example, opposing parties marshal evidence that supports their argument, and in courts of law or formal debates an independent party evaluates the evidence from both sides and makes a decision about which is most likely to accurately map onto the real world. The difference between the use of evidence in science and in adversarial situations is that what’s most important to science is what’s actually happening in the real world, not who wins an argument about what’s happening. Obviously scientists do have arguments – and whoever wins influences which theories get investigated and which don’t, but that’s not what science is about.

Many people developing social policy in relation to children are from disciplines that don’t handle evidence in the way science does, so legislation is often derived from policy-based evidence rather than evidence-based policy.

Levels of relevant expertise

Some years ago, I carried out a short research project on men’s and women’s perceptions of the clothing that women wore to work. I employed a technique called card sorts which had previously been used to find out how experts categorised their knowledge. What I found was that men tended to see women’s workwear in either/or terms (e.g. either the woman is married or she isn’t) significantly more frequently than women did. Some people thought this demonstrated that men think in black-and-white terms whereas women think in shades of grey, but other work with card sorts shows that experts in a particular knowledge domain tend to use more complex categorisation than novices. This suggests that women are likely to be experts on the non-verbal signals conveyed by other women’s clothing, but men aren’t. There are implications for theories about how women dress, but that’s another story. Most of my male research participants were professionals, so for the purposes of this post, what my study demonstrated is that you can be an expert in one domain, but a novice in another.

I don’t dispute that GPs, teachers and social workers have expertise; whether they have expertise that enables them figure out who or what is to blame for a child’s abnormal behaviour is another matter. It would be unrealistic to expect everybody to know about everything, but it doesn’t seem unreasonable to expect professionals working with children to have a basic grasp of relevant factors from other domains. For example, I’ve had to explain to a local authority attendance officer why doctors don’t prescribe antibiotics for viral infections. I’ve disagreed with a GP about the ‘gold-standard’ nature of randomised controlled trials and NICE guidelines. And I didn’t even try to explain one of my son’s teachers why spelling isn’t simply reading in reverse, that is, why he might be a good reader but be incapable of spelling words of more than three letters. I’m not alone; recent reports from the UK have drawn attention to the lack of training in child development received by GPs, teachers and social workers.

In the next post, I want to examine three areas where use of evidence and levels of expertise have had a significant impact on social policy development and on the experience of children showing atypical behaviours; attachment theory, fabricated and induced illness and cyclical models of socio-economic deprivation.

Further reading

Kennedy, I (2010). Getting it right for children and young people: Overcoming cultural barriers in the NHS so as to meet their needs. HMSO.

Munro, E (2011). The Munro Review of Child Protection. Final Report: A Child-Centred System. HMSO.

Rugg, G. & McGeorge, P. (2005). The sorting techniques: a tutorial paper on card sorts, picture sorts and item sorts. Expert Systems,22, 94-107.

Teather, S. (2011). Support and Aspiration: A new approach to special educational needs and disability – a consultation. HMSO.

Photograph of Freud by Max Halberstadt, 1921. Image from the Google-hosted LIFE Photo Archive where it is available under the filename e45a47b1b422cca3.

refrigerator mothers

You could be forgiven for assuming that the ‘refrigerator mothers’ theory for the cause of autism has been consigned to the wastebasket of history. That might be true for children with a formal diagnosis of autistic disorder, but parents are still often under suspicion if their children have autistic characteristics but no diagnosis, or indeed any unusual behavioural characteristics but no diagnosis. Bruno Bettelheim is often credited with inventing the term ‘refrigerator mothers’, but Leo Kanner appears to have come up with the refrigerator analogy first.

Leo Kanner

Leo Kanner

In the comment section at the end of his 1943 paper, Kanner weighs up the evidence for the possible causes of autistic behaviour. The children have schizophrenic characteristics, but their condition differs from schizophrenia because it’s been present from birth – suggesting a biological origin. On the other hand “in the whole group, there are very few really warmhearted fathers and mothers” (p. 250), suggesting that development could have been disturbed by parental behaviour. In the end, Kanner concludes “The children’s aloneness from the beginning of life makes it difficult to attribute the whole picture exclusively to the type of the early parental relations with our patients. We must, then assume that these children have come into the world with innate inability to form the usual, biologically provided affective contact with people, just as other children come into the world with innate physical or intellectual handcaps [sic]” (p. 250).

But Kanner later changes his mind. In 1949 he describes his patients as in refrigerators which did not defrost.* In his 1956 paper with Leon Eisenberg he contrasts the low incidence of psychosis and neurosis in the children’s relatives (a sample of around 1000) with the much higher incidence in families of children with schizophrenia and concludes “Thus, if one limits his search for genetic factors to overt psychotic and neurotic episodes in family members, the results would appear to be negative” (p.8). After some discussion of parental characteristics, he decides; “The emotional frigidity in the typical autistic family suggests a dynamic experiential factor in the genesis of the disorder in the child” (p.8) and “These children were, in general, conceived less out of a positive desire than out an acceptance of childbearing as part of the marital contract” (p.10). But less than a decade later, when Bernard Rimland, in his book Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behaviour suggested that autism might have its origins in the brainstem, Kanner wrote the foreword. And in 1969, Kanner told the first annual meeting of the then National Society for Autistic children “I herewith especially acquit you people as parents” (Feinstein, 2010).

The discussion in the 1956 paper sheds light on what initially appears to be wavering on Kanner’s part about the cause of autism – now he’s blaming biology, now he’s blaming the parents. Kanner wasn’t so much undecided as aware that both factors could be involved. He goes into some detail about the interaction of biological and environmental factors in producing autistic characteristics and describes early infantile autism as ‘a total psychobiological disorder’ – in other words, it isn’t a case of its cause being either genetic or parental. As Michael Rutter observed; “What we have to differentiate is evidence of a broader phenotype. Kanner switched back and forward, which is a mark of his integrity” (Feinstein 2010).

Bruno Bettelheim

Bruno Bettelheim

For Bruno Bettelheim there was no uncertainty about the cause of autism. At first glance, Kanner and Bettelheim appear to have a good deal in common. They were both born into Jewish families in central Europe around the beginning of the 20th century. Both had their studies interrupted; Kanner by military service, Bettelheim by the death of his father. Both fled to the USA as ethnic refugees, both married and raised families there, and both became successful, respected figures in the field of child development. There the resemblance ends.

Bettelheim was born into a well-to-do Viennese family in 1903. As a teenager, he was fascinated by psychoanalysis and read all he could about it. He enrolled as a student of philosophy and history of art at the University of Vienna, but postponed his studies when his father died from syphilis and he had to take over the family lumber business. In 1930 Bruno married his first wife, Gina, who worked at a Montessori nursery. The couple took in a young American child, Patsy, whose mother had sent her to Vienna for therapy with Editha Sterba, a member of the Vienna Psychoanalytic Institute. Bruno was in therapy with Editha’s husband Richard for a while, and his connections with Patsy, the nursery and the Sterbas were to prove a turning point in his career.

Eventually, he was able to resume his studies and was awarded a doctorate in February 1938. Within a month, German troops had entered Austria and Gina had left for the USA with Patsy. Bruno remained in Vienna with his mother and sister. In June, he was arrested, jailed and then taken to Dachau. In September he was moved to Buchenwald and released the following April in an amnesty to mark Hitler’s 50th birthday. Patsy’s mother, Agnes, had managed to arrange a visa for him, and Bruno was reunited with Gina in the USA in May 1939. By then it was obvious that their marriage was over – both had had affairs – and Bruno settled down with Trude, a former girlfriend. His experience with psychoanalysis and child development also got him a job in the education department at the University of Chicago, which led to his appointment as director of the university’s Orthogenic School in 1944, where he was to remain until the early 1970s.

Most of these biographical details are from Richard Pollak’s fascinating biography of Bettelheim The Creation of Dr B. Pollak is aware that his account might be seen as biased. His younger brother, Stephen, had attended the Orthogenic School until his death in an accident whilst on holiday. Bettelheim’s disdain for the boys’ parents and his claim that Stephen had committed suicide despite Richard witnessing Stephen’s fall from a hayloft, and Bettelheim’s suicide in 1990, were what prompted Pollak to research Bettelheim’s life. Although Bettelheim probably had the children’s best interests at heart and certainly changed the Orthogenic School for the better, reactions to him were mixed to say the least. Comments from school staff, parents, children and his students are peppered with reports of admiration, intimidation and humiliation. There’s little doubt that he beat the children and there are some stories of sexual contact, although these accounts, if true, need to be set in context; corporal punishment was common at the time and the psychoanalytic theory embraced by Bettelheim saw sexual expression as natural. Some people hated him, but others felt that Bettelheim’s methods, even if frowned upon, were well-intentioned.

Refrigerator mothers

Probably more widespread harm was caused by Bettelheim’s view of parents, especially mothers. Bettelheim disapproved of children at his school going home for visits and viewed mothers as cold, uncaring and responsible for their children’s behavioural problems. Bettelheim set out his ideas in a series of books including The Empty Fortress: Infantile Autism and the Birth of the Self. Despite the popularity and influence of this book, it’s not clear how much experience of autistic children Bettelheim actually had. He claimed that two autistic children had lived at his home, although Patsy appears to have been the only one, and she wasn’t diagnosed as autistic. Visitors to the Orthogenic School commented on the fact that the children appeared to be normal, if troubled, kids. Bettelheim admitted only children with no physical or intellectual impairment, thus ruling out more severely autistic children. And the success of his techniques was called into question too. In the 1980s a study showed that during Bettelheim’s period as director Orthogenic School, of 220 children entering the school, only 13 were admitted with a diagnosis of autism (Bettelheim diagnosed many children himself) and not all the children had made the progress he claimed.

Aside from contrasts in their life experience, with regard to their contribution to autism research I want to highlight two key differences between Kanner and Bettelheim; the way they used evidence and their level of relevant expertise.

Use of evidence

Kanner had a medical background, derived testable hypotheses from the best theory available at the time, and wasn’t afraid to change his conclusions if the evidence dictated. Bettelheim had trained in philosophy and appears to have made up his mind in advance about the cause of autism and then selected evidence to support his theory. Pollak refers to an essay Bettelheim wrote about the philosophers who shaped his thinking as a student. Significantly, the philosophers – Lessing, Lange and Vaihinger – all saw historical truth as a construct of the mind. Vaihinger argued in his book The Philosophy of “As If” that even though fictions should not be mistaken for true propositions, they can work As If true (Pollak, 1997; p.15). Bettelheim seems to have put Vaihinger’s ideas into practice; in a cv compiled in 1942 he exaggerated his credentials and frequently reported events in a way which conflicted with the recollection of other witnesses.

Level of relevant expertise

Kanner was aware that his theories about the cause of autistic characteristics were limited by the biological knowledge available at the time. Nonetheless, he clearly understood the complexity of child development and was careful to rule out a number of possible causes for autism before arriving at his conclusions. Without doubt, Bettelheim was also knowledgeable, about psychoanalysis and theories of child development that is; the reference section in The Empty Fortress is extensive. But he appears to have had little knowledge about biology and his explanations for the children’s behaviour are in terms of psychoanalytic concepts only. Indeed, he was actively opposed to biological theories for the causes of autism, attacking Kanner and Rimland in The Empty Fortress and telling Thomas Kemper that his brain studies must indicate a different kind of autism (Feinstein, 2010).

Bettelheim’s influence

What puzzles me is how Bettelheim’s book could become so influential amongst professionals with medical training, long after research into genetics and brain function had shown that psychoanalytic and psychodynamic theories of child development were lacking. Bettelheim was preoccupied by psychoanalytic symbolism. He saw the children’s interest in balls, balloons, light fittings and automobile headlamps as symbolic of their relationship with the breast. Their words had deep symbolic meaning – ‘breakfast’ meant ‘break breast’, ‘Connecticut’ meant ‘connect-I-cut’ and even an interest in the weather on the part of a non-verbal child symbolized her fear that she might be devoured (‘weather’ meant ‘we/eat/her’). This should have been enough to suggest that his theory might not have a solid grounding. Bettelheim’s use of symbolism extended to his lectures, resulting in the (in)famous knitting/masturbation story. Bettelheim is reported to have said to a female student, knitting during one of his lectures; “Don’t you realize your knitting is nothing but a sublimated form of masturbation? You’re sitting in front of the entire class masturbating.” The student is alleged to have replied; “Dr Bettelheim, when I knit, I knit! And when I masturbate, I masturbate!”

Despite the lack of evidence for his theories they were very influential. The Empty Fortress was the first book on autism translated into Spanish, Bettelheim’s lectures were shown on French national tv, in the 1980s most of the books on autism in Danish libraries were by Bettelheim, and it wasn’t until 1998 that the International Association for Child and Adolescent Psychiatry and Allied Professions decided that “parents have absolutely no responsibility for their children’s autism” (Feinstein 2010). As Judy Barron, the parent of an autistic child, observed when she read The Empty Fortress, “I wasn’t a scientific reader and I certainly wasn’t a researcher; I was a twenty-four-year-old mother; but I just didn’t see any evidence to support his pronouncements” (Pollak, 1997, p. 275).

The use of evidence and levels of expertise; two factors that I plan to explore further in the next post.


Bettelheim, B. (1967). The Empty Fortress: Infantile Autism and the Birth of the Self. The Free Press.
Eisenberg, L. & Kanner, L. (1958). Early infantile autism 1943-1955. In C. F. Reed, I. E. Alexander and S. S. Tomkins (eds.) Psychopathology: A Source Book, Harvard University Press.
Feinstein, A (2010). A History of Autism. Wiley Blackwell.
Kanner, L. (1943). Autistic disturbances of affective contact. Nervous Child, 2, 217-250.
*Kanner L (1949). Problems of nosology and psychodynamics in early childhood autism. American Journal of Orthopsychiatry, 19, 416–26.
Pollak, Richard (1997). The Creation of Dr B, Simon & Schuster

*Paper behind paywall – the citation is from various sources.

image of Bettelheim: Ottofroehlich under Creative Commons licence

social instinct

BlaiseLaPsy on Twitter, in response to what I said about the Freudian concept of social instinct, raised an important point about the work of John Bowlby and Harry Harlow that appeared to provide evidence for the existence of a social instinct. I have reservations about the conclusions drawn from Bowlby’s and Harlow’s findings, and about how the term ‘instinct’ is used. First, a brief round-up of Bowlby and Harlow’s research.

Bowlby, who graduated in medicine and qualified as a psychoanalyst in the UK in the 1930s, was interested in the development of children with behavioural problems and those who had been separated from their parents due to being orphaned or hospitalized. Influenced by René Spitz’s work on orphans, Bowlby became an authority on the effects of maternal deprivation and developed Attachment theory. He concluded that for normal social development, children need a secure relationship with a primary caregiver (usually the mother). Mary Ainsworth later found in her ‘strange situation’ experiments that children showed one of four patterns of attachment to their primary carer.

Harlow qualified at the same time as Bowlby but had a very different academic background. He was an American psychologist; his PhD supervisor was Lewis Terman, who developed the Stanford-Binet IQ test. Prompted by Bowlby’s work, Harlow studied maternal deprivation in rhesus monkeys and macaques. His most famous experiment showed that rhesus monkey infants raised with substitute ‘mothers’ consisting of a wire frame covered/not covered with a terry cloth, preferred the cloth ‘mother’ and clung to it when frightened, even if it was only the wire mother that provided milk. The baby macaques were raised for varying lengths of time in isolation; Harlow looked at the effect on their development, which was invariably abnormal.

What the work by Spitz, Bowlby, Ainsworth and Harlow appears to show is that human and/or primate infants have a social instinct and that instinct triggers a typical pattern of social development. If an infant’s relationship with their primary carer is disrupted by lengthy separation, abnormal social development results. My main problem with these conclusions is the concept of ‘instinct’. Instinct is one of those constructs like ‘love’ or ‘education’ that everybody thinks they understand until they try to find out how it works, or until they discover that their concept of it is different to someone else’s.

We all know what we mean by ‘instinct’ – an automatic, unconscious behaviour. We know what Bowlby, Harlow and others mean by ‘social instinct’ – it’s an automatic, unconscious, typical pattern of social behaviour that appears to develop in the same way in everyone unless something stops it. But Bowlby, Harlow and their contemporaries faced three problems when it came to instinct.

First, as Blaise points out, conceptual models are influenced by cultural worldviews. At the time Spitz, Bowlby, Ainsworth, Harlow and Kanner were researching, human social behaviour was generally assumed to be governed by instincts. Darwin’s work on natural selection implied that many characteristics peculiar to a given species – physical features, physiology and behaviour patterns – were inherited. All male blackbirds have similar songs. Bowerbirds build and decorate complex bowers to attract mates. Ants live in complex colonies, dogs run in packs, cats tend to be solitary. Because human beings tend to behave socially in similar ways across cultures, there was no reason to suppose human social behaviour wasn’t as instinctive as that of blackbirds, bowerbirds, ants, cats or dogs. The main alternative to the psychodynamic framework at the time was Watson and Skinner’s behaviourism, which proposed that complex behaviours such as social interaction were learned. But behaviourism was widely treated with suspicion because it was seen as reductionist. (How can you reduce something as nuanced and complex as social interaction to something as basic as a rat’s tendency to run through tunnels or a pigeon’s tendency to peck?)

Secondly, no one working in child development prior to the 1960s knew much about how the brain worked. They were all guessing. Their guesses were often extremely well informed, but they were guesses nonetheless. Spitz, Bowlby, Ainsworth, Harlow and Kanner all came down on the ‘instinct’ side; Watson and Skinner on the ‘learned’ side, but none of them knew about the biochemical mechanism of learning in the brain.

Thirdly, none of the child development researchers needed to figure out how social instinct worked because the idea of ‘instinct’ itself explained their findings. It was a ‘black box’ concept. They didn’t know what was inside it and didn’t need to know; what they were interested in was what happened when the social instinct was disrupted.

People who did need to figure out how instinct worked and what was inside the black box, were ethologists studying the development of animal behaviour. In the 1950s, researchers such as Lorenz and Tinbergen began to look more closely at the difference between instinctive and learned behaviour. Most people are familiar with the famous pictures of Lorenz being followed by a column of baby geese. Because goslings and ducklings follow their mother from the moment they hatch, it was assumed that this was an instinctive behaviour. What Lorenz discovered was that the tendency to follow something was instinctive, but that what the goslings followed was learned – they followed the first moving object they saw after hatching. It might be their mother, a chicken foster-mother, the farm dog, a pair of boots (didn’t matter who was wearing them) or Konrad Lorenz.

There was a debate about instinct amongst ethologists in the 1960s because it had become clear that different researchers were using the term in different ways and so definitions got tightened up. Unfortunately, apart from Bowlby, many practitioners working in medicine or psychiatry wouldn’t have read the ethology literature – they weren’t (and often still aren’t) interested in the behaviour of goslings or wild macaques even if they had time to keep up to date with it. That’s a pity, or a tragedy depending on how you look at it, as far as instinct is concerned because what has emerged from animal behaviour research is a picture of instinct as an umbrella term that can be applied to a range of different concepts. Essentially, instinct refers to behaviours that are genetically determined, biologically controlled, automatic and unconscious. But it isn’t quite as simple as that.

Levels of instinctive behaviour

Starting at the lowest level, human physiology is genetically determined, biologically controlled, automatic and unconscious; circulation, respiration, digestion, growth and sexual development occur without any awareness or intervention on our part although we are aware of what happens as a result of them. We know a lot about how these autonomic functions work and that they are very similar in everybody. But we wouldn’t usually call autonomic functions ‘instinctive’ because instinct is about how organisms behave rather than how they function.

The most simple form of instinctive behaviour is the reflex – a simple, automatic motor response to specific stimulus. Reflexes – such as the rooting, palmar grasp, startle, swimming and stepping reflexes – are present from birth. Some have obvious survival value; others, like the stepping reflex, form the foundation for behaviours that emerge later – in this case, walking. We know a lot about how reflexes work and that they are very similar in everybody. Most people would classify reflexes as instinctive, I think.

More complex species-specific behaviours, like birds learning songs or building nests, often vary between individuals. Songbirds develop their own unique songs, bowerbirds make their bowers out of whatever materials are available. Although all human beings, regardless of culture, show similarities in social behaviour, the evidence to support the existence of a social instinct is pretty flimsy. We’d expect organisms with similar autonomic functions and similar reflexes to behave in similar ways, but that’s about as far as the evidence takes us. How people interact and communicate with each other and how frequently they do so varies much more than their autonomic functions or reflexes. Some people choose to live in tightly-knit highly interdependent groups, others to live in isolation. Some are highly gregarious, others prefer the company of cats, dogs, horses, the landscape or machines.

I’m a fan of Monkey Life, the TV documentary series about Monkey World, the primate sanctuary in Dorset, UK. A few years ago, Monkey World took in 88 capuchin monkeys from a lab in Chile. Some of them had been born in captivity, others had been captured from the wild. During their rehabilitation, Alison Cronin the sanctuary director commented that the wild-born capuchins instinctively knew how to eat their natural food but the cage-born capuchins didn’t – they had to learn to do that. Alison’s comment introduces a slightly different use of the word ‘instinct’, meaning a behaviour that happens automatically and unconsciously, but isn’t genetically determined and biologically controlled. The documentary also showed that chimps and orang-utans born in captivity tend to be poor mothers. You could argue, as the psychodynamic theorists would have done, that the capuchins’ feeding instinct and the chimps’ and orang-utans’ maternal instincts had been disrupted by their captivity and so hadn’t been allowed to develop normally. That’s one theory. What’s also possible is that the cage-born primates, or those captured in infancy, simply hadn’t had the opportunity to learn how to forage, peel fruit or rear babies.

Human social behaviour varies widely. That variation could be because the normal social instinct is disrupted by events in childhood. But because we don’t know exactly what ‘normal’ human behaviour looks like, and we have no idea how the social instinct works (in contrast to what we know about autonomic functions and reflexes), a more likely explanation is that some aspects of human social interaction are instinctive and others aren’t. Social behaviour is hugely complex, so the question is which bits of social behaviour are instinctive and which aren’t?

As I pointed out in the post about the social instinct and Kanner’s syndrome, the areas of the brain dealing with social behaviour handle complex information from many areas of the brain. From an information-processing perspective, social behaviour, far from being instinctive, results from an interaction between the way the body works, environmental factors such as nutrition, and experience. Most researchers in all areas of child development are aware of the importance of interaction between factors in development, but by necessity, they are usually focusing on one factor only, and tend to overlook anything outside their field of expertise.

Social or sensory deprivation?

A final observation about Harlow’s work. There’s no question that Harlow’s baby primates were socially deprived. But they also suffered sensory deprivation as well, and I don’t know if Harlow controlled for that. Given his conclusions I don’t get the impression he did. Some of the infant macaques, for example, were kept in total darkness for months. Light is essential for entraining circadian rhythms, so absence of light alone would have seriously messed up their physiological functions. Coincidentally, I was listening to Crossing Continents yesterday on BBC Radio 4. A former inmate of Louisiana State Penitentiary, who’d been in solitary confinement for 30 years, was describing his experiences. He highlighted, not so much the social isolation, as the sensory deprivation. He’d had a long time to think about what it was he missed; it would be all too easy to assume in the same situation we’d miss other human beings, when what we might actually miss is the complex sensory input we get from interactions with other people. I’m not trying to reduce social contact to sensory stimuli – social contact is clearly more than the sum of its parts – I’m just saying that it’s very difficult to make a distinction between social interaction and the sensory input that comes with it.

The benefits of hindsight

I’ve been quite critical of psychodynamic theorists, but I’m very aware that they were working with the knowledge that was available at the time. I think what we need to be wary of is assuming that knowledge develops in a straight line; that Freud, Bowlby, Harlow and Kanner were basically right but we now know more than they did. With the benefit of hindsight we can see which aspects of earlier theories are supported by later research and which aren’t. I don’t think there’s much evidence to support the idea of social instinct. What the evidence does suggest is that although instinctive behaviours are quite likely involved in social interaction they are only part of the story.

turning Kanner’s model of autism upside-down

Kanner’s model of autism should be turned on its head.
The idea that Kanner’s syndrome was caused by a fundamental impairment in social interaction has prevented us discovering the causes of autism.
Those are quite bold claims. In the next couple of posts I’ll explain why I made them.

Previously, I suggested that Kanner was using two theoretical frameworks to analyse the behaviour of the 11 children with his unique syndrome; Kraepelin’s classification of mental disorders and psychodynamic theory. Kanner’s comments imply that he interpreted abnormalities in feeding, speech and movement in social and sexual terms because of the psychodynamic framework. I want to look more closely at psychodynamic theory and explain my claim that viewing Kanner’s syndrome as caused by a fundamental impairment in social interaction has proved an obstacle to research into the causes of autism.

How the brain works: the psychodynamic model

As I pointed out earlier, three of the founders of psychodynamic theory, Freud, Jung and Adler, had neurological experience and would have known a fair amount about brain anatomy and about the specific functions of different parts of the brain. What they also would have known about was the patterns of electrical activity that had been observed in the brain. What was little understood at the time was how the brain worked, so the psychodynamic theorists had to make an educated guess based on their observations of people’s behaviour.

What Freud came up with was the idea that human behaviour is driven by life instincts such as the will to survive, to eat, to seek pleasure and sexual gratification. He eventually grouped these instincts together into a primary life instinct or ‘drive’ (Eros) that created flows of energy through the brain. The life drive was the origin of all behaviours that increased the chance of survival, such as an awareness of one’s surroundings and the ability to interact and communicate with others. (Freud later added a death drive (Thanatos) to explain aggression and destructive behaviour). In the light of what we now know about how the brain works, it’s clear that some aspects of Freud’s model were very insightful but others weren’t.

How the brain works: the information-processing model

Fifteen years after Kanner first described his syndrome, David Hubel and Torsten Wiesel began publishing their work on the visual cortex of the cat. Hubel and Wiesel’s research was significant, not just because it told us a lot about how cat vision develops, but because it provided some important insights into how brains in general process information – the mechanism that the psychodynamic theorists were trying to figure out.

Hubel and Wiesel’s research, and the work that followed it, revealed some key principles about how the human brain processes information.

1. All information about the outside world enters the brain via the senses.

2. Sensory information is processed in a hierarchical way, from simple to complex – broadly speaking, from the back to the front of the brain.

3. Different parts of the sense organs respond to different aspects of sensory information and that information is then integrated increasingly as it’s transmitted through the brain.

Say, for example, that I am looking at a table. Different cells in my retina respond to different properties of the pattern of light reflected off the table and entering my eye; some cells respond to the boundaries between light and dark areas, others to light of different wavelengths (colour). This very basic information about the pattern of light from the table is then integrated as it passes through my brain; first it’s chunked up to form a pattern that represents the table I’m looking at. This representation is then linked with stored representations of other images, such as other tables and chairs, and is then integrated with information from other sensory modalities such as what the word ‘table’ sounds like, what the written word ‘table’ looks like, what tables feel like and so on. This information ends up in the frontal area of the brain, which has been described as having an ‘executive function’ – it integrates information from all over the brain and makes decisions on the basis of that information. Except that information doesn’t actually ‘end up’ anywhere, because the brain has a complex series of feedback loops that send information from higher-level areas back to lower-level ones.

What does the way sensory information is processed have to do with Kanner’s syndrome?

Kanner concluded that the ‘…fundamental disorder is the children’s inability to relate themselves in the ordinary way to people and situations’ because he was working within the psychodynamic framework. He saw the children’s abnormal behaviours essentially as caused by a disruption in ‘the usual biologically provided affective contact’ – an instinct that emerged from the life drive. Kanner doesn’t use the terms ‘instinct’ or ‘life drive’ – he doesn’t need to because all his readers would be familiar with that framework – but he makes it clear that he sees affective contact as an innate, biologically-based ability that the children didn’t have.

I can understand where the psychodynamic idea of instincts came from. Most children develop skills like eating, walking, responding to the world around them, interacting with and communicating with other people, without any apparent effort on their part or any significant intervention from adults. Indeed, psychodynamic theorists felt that adult intervention often disrupted normal development. It made sense to assume that natural selection had ensured the ability to relate to people and situations developed instinctively – as automatically as growth or sexual development, or the way the heart, lungs and digestive system function.

I think Kanner’s conceptual model of his syndrome could be represented like this:

Kanner's conceptual model

But from what we now know about brain function, as far as the brain is concerned the ability to relate in the ordinary way to people and situations is exactly the opposite of a basic instinctive drive. There are areas of the brain that specialise in relating to people and situations; they are in the frontal lobes where information from many other brain areas is integrated. Relating to people and situations requires monitoring a constantly changing flow of complex information from a wide range of sources and constant feedback to other parts of the brain. The frontal lobes and their functions develop slowly and mature late – often not until early adulthood. Even after maturity, because of the plasticity of the brain, the frontal lobes continue to change in response to the environment.

Highly over-simplified schematic showing flow of sensory information to frontal lobes

We’re not usually aware of all this complex integration, monitoring and feedback of information; what we usually experience in ourselves, and observe in others, is that responses to the environment and to one another happen instinctively and automatically – that is, until something goes wrong. When we find we have too much or too little information, or that information is ambiguous, or we feel tired, hungry or anxious, then behaviours that most of the time feel and look instinctive and automatic, feel and look a bit less instinctive and automatic.

An impairment in processing any of the streams of information about people and situations would, to some extent, disrupt normal responses to people and situations. In the light of what we now know about the way the brain works, I propose that Kanner’s causal model should have looked more like this;

alternative model for Kanner's syndrome

What we now know about how the brain works suggests that Kanner’s conceptual model of his syndrome should actually be reversed; that relating to people and situations is the outcome of some very complex information-processing requiring input from many parts of the brain, rather than a basic, automatic instinct that drives other behaviours. The implication is that rather than a disturbance in affective contact causing problems with feeding, speech, body movements, social interaction and communication, what’s more likely is that problems with motor function, sensory processing, speech and language resulted in the children’s problems with relating to people and situations in the ordinary way; that Kanner’s model should be turned upside-down.

More on this later, but next I want to look again at Kraepelin’s classification system and find out what happened to Kanner’s syndrome after 1943.

a critical look at Kanner’s autism

In this post I want to take a close look at Leo Kanner’s ground-breaking paper ‘Autistic Disturbances of Affective Contact’ and explain why I consider Kanner’s analysis of the children featured in the paper to be critically flawed. I can understand why Kanner came to his conclusions; he was working in the light of knowledge that was available at the time. What concerns me is that his reasoning has been perpetuated in the diagnostic criteria for autism and in autism research. I suggest it’s because of this that 70 years later we are still scratching our heads about what causes autism.

In 1938, a five year-old boy named Don (later identified as Donald Triplett) was referred to Kanner’s clinic. Don’s was the first and most detailed of 11 case studies (eight boys and three girls) featured in Kanner’s paper published in the journal Nervous Child in 1943. Kanner claimed that he had identified a “unique ‘syndrome’, not heretofore reported” (p.242) consisting of “inborn autistic disturbances of affective contact” (p.250). He reviewed the children’s previous diagnoses and then outlined a list of “essential common characteristics” (p.242) that supported his hypothesis.

Previous diagnoses

Previous diagnoses included idiocy, imbecility, deafness or being hard of hearing, and schizophrenia. (At the time, ‘idiot’ and imbecile’ were technical terms; an imbecile was someone with an IQ score between 20 and 49, and an idiot had a score below 20. Anyone with an IQ between 50 and 69 was described as a ‘moron’). Kanner ruled out idiocy and imbecility because all the children had what he described as ‘good cognitive potentialities’ (p.247). He appears to have ruled out hearing difficulties on the grounds that another doctor had observed that one of the children (Virginia) “does not seem to be deaf from gross tests” (p.230). Kanner rejected the diagnosis of schizophrenia because the children had shown their unusual characteristics from birth.

The term ‘autism’ wasn’t invented by Kanner; it had been coined thirty years earlier by Eugen Bleuler, born near Zürich, and a contemporary of Kraepelin and Freud. Bleuler used ‘autism’ to describe the self-absorbed, withdrawn characteristics seen in schizophrenia, another label he came up with to replace Kraepelin’s ‘dementia praecox’. Bleuler’s book Dementia Praecox or the Group of Schizophrenias was published in 1911, ten years before Kanner graduated in Berlin and twenty years before Hans Asperger did so in Vienna, so both of them would have been familiar with the word they used to describe the children in their case studies.

Kanner’s syndrome

Kanner based his conclusion that he had identified a previously undiscovered syndrome on 20 “essential common characteristics” shared by the 11 children. Statistically, it’s highly unlikely that 11 children could show 20 common characteristics without having the same syndrome – until you take a closer look at the characteristics. Here’s the list (Kanner gives a short explanation for each of them);

•inability to relate themselves in the ordinary way to people and to situations from the beginning of life
•extreme autistic aloneness
•failure to assume at any time an anticipatory posture preparatory to being picked up
•ability to speak
•excellent rote memory
•personal pronouns are repeated just as heard
•loud noises and moving objects
•monotonously repetitious
•anxiously obsessive desire for sameness
•limitation in the variety of spontaneous activity
•good relation to objects
•masturbatory orgiastic gratification
•relation to people different to that of objects
•good cognitive potentialities
•anxious tenseness
•physically normal
•from highly intelligent families.

What’s interesting about the ‘common’ characteristics is that they are not common to all the children, nor do they all reflect what Kanner describes in his case studies. The second point applies to seven items on the list, which I’ll address in turn.

Ability to speak, excellent rote memory, literalness and personal pronouns are repeated just as heard. Seven of the children had previously been considered deaf or hard of hearing because of their abnormal receptive and/or expressive speech. Three children (Richard, Herbert and Virginia) presented as mute. Richard had once been heard to whisper “good night” and pupils at Virginia’s school claimed she had said ‘chocolate’, ‘marshmallow’, ‘mama’ and ‘baby’ (p.231). There’s no record of Herbert saying anything. Despite speech or language impairments, other children in the group had clear enunciation, sophisticated vocabularies or good sentence structure, and some had specific problems with pronouns. Yet despite this range of differences, Kanner concludes “there is no fundamental difference between the eight speaking children and the three mute children” in terms of “the communicative functions of speech” (p.243).

Food. Six of the children had feeding difficulties as infants (one vomited repeatedly and another was tube-fed). But Kanner interprets these characteristics not as feeding difficulties per se, but in terms of “our patients…anxious to keep the outside world away, indicated this by the refusal of food” and contrasts their behaviour with those of “affect-hungry” children demanding excessive quantities of food when placed in foster-care (p.244).

Failure to assume at any time an anticipatory posture preparatory to being picked up. Kanner notes this in only two specific cases, but says that ‘almost [my emphasis] all the mothers …recalled their astonishment’ at the children’s failure to respond (p.242).

Masturbatory orgiastic gratification. Kanner’s evidence for this is the children’s preoccupation with spinning objects, jumping up and down with glee and rolling and rhythmic movements, despite his records indicating masturbation in only two cases.

Two questions

So, two questions: First, why did Kanner list as “essential common characteristics” characteristics that weren’t common to all the children? Second, why did he interpret some very somatic (bodily) characteristics (feeding, speech, jumping and rolling) in social and sexual terms rather than in terms of feeding, speech and motor movements? The answers, I suggest, lie in the theoretical frameworks that Kanner was using at the time – Kraepelin’s classification of mental disorders, and psychodynamic theory. (Kraepelin’s classification system and the psychodynamic model had both been in use for half a century, so were well-established. Adolf Meyer, who appointed Kanner to his post at Johns Hopkins, had been a keen advocate of both frameworks.)

Why weren’t Kanner’s ‘essential common characteristics’ common to all 11 children?

I mentioned earlier that Kraeplin’s classification system was based on syndromes – patterns of symptoms that tended to co-occur. Two observations about syndromes: First, syndromes are about correlation, not causality. It’s true that symptoms that tend to co-occur are more likely to be causally linked than symptoms that don’t, but all you can deduce from co-occurring symptoms is that the symptoms sometimes co-occur. You can only make deductions about how the symptoms might be causally linked once you know something about what causes them.

Second, although syndromes have consistent core symptoms (if they didn’t they wouldn’t be syndromes), the symptoms shown by individuals tend to vary. So everyone diagnosed with Syndrome Alpha, say, would show the core symptoms A, B and C, but together those people might also show symptoms D to T (making a total of 20 symptoms associated with Syndrome Alpha). Kanner couldn’t tell from a sample of 11 children which symptoms were core ones and which might have appeared by chance. He would no doubt have been interested to hear from clinicians who’d seen cases of any of the symptoms, so he wouldn’t have wanted to miss anything out. Hence he cast his net quite wide. In short, his “essential common characteristics” were characteristics of his proposed syndrome rather than of the individual children.

Why did Kanner interpret somatic abnormalities (feeding, speech and body movements) in social and sexual terms?

I noted in the previous post that psychodynamic theory recognised the link between behaviour and the brain. (Two of the founders of the psychodynamic school, Freud and Jung, had worked with renowned neurologists and Adler had begun his career as an ophthalmologist, so they would have been well aware of the brain-behaviour connection.) Because the brain was involved and the brain is an organ of the body, behavioural drives, like other bodily characteristics, could be inherited. Characteristics were inherited via sexual reproduction, so any characteristics that reduced the chances of sexual reproduction taking place, such as impairments in affect or communication, or atypical sexual behaviour, would be less likely to be passed on to the next generation, would not be ‘normal’ for the species and so could be considered pathological. Psychodynamic theory saw social and sexual behaviour as fundamentally important in normal child development, and impairments in social and sexual drives as being capable of causing problems with feeding, speech and motor control (Kanner cites David Levy and Hilde Bruch, both of whom used a psychodynamic approach, to support his argument). As Kanner says “the outstanding, “pathognomonic”, fundamental disorder is the children’s inability to related themselves in the ordinary way to people and situations…” (p. 242).

Why I see Kanner’s analysis as flawed

I see Kanner’s analysis as flawed because of three assumptions he made. First, that because the individual children’s characteristics overlapped, despite not all the children having all the symptoms, all the children had the same syndrome. Second, that the existence of a syndrome meant that the characteristics of the syndrome must be causally related. Third, the assumption that social and sexual drives are so fundamental that they must be the cause of problems with feeding, speech and motor movements. Although children certainly can refuse to eat or speak because of an underlying issue with affect, knowing what we now know about brain development, it’s highly unlikely that a babe-in-arms would not suckle or that an older child wouldn’t speak for years on end for that reason. Since motor function is implicated in all three behaviours it should at least be considered as a possible cause.

At the time, Kanner’s assumptions weren’t unreasonable, and at the end of his paper, he makes it clear that he’s making assumptions and that there’s uncertainty about how affect could result in the syndrome he proposes. At the time a good deal was known about brain structure and what brain areas controlled what types of behaviour, but brain function was still something of a mystery. In 1943 Karl Lashley was still attempting to find the location of memory, it would be a decade before Crick and Watson unveiled their model of DNA, and two decades before Hubel and Wiesel published their work on cat visual cortex.

In the light of current knowledge about brain function, Kanner’s conclusion that all the children’s unusual behaviors were attributable to an “inability to relate themselves in the ordinary way to people and situations” doesn’t hold water. Despite this, his assumptions have persisted in the diagnostic criteria for autism, and thus in autism research. I suggest the assumption that autism is caused by a fundamental impairment in social interaction has been the main reason why, half a century later, we are still trying to find the causes of autism. In my next post I propose that turning Kanner’s model on its head could break this log-jam.


Kanner, L. (1943). Autistic disturbances of affective contact. Nervous Child, 2, 217-250.
(pdf available on line)