We no longer believe in inherited capacities, talent, temperament, mental constitution, and characteristics. Give me a dozen healthy infants, well-formed, and my own specified world to bring them up in and I’ll guarantee to take any one at random and train him to become any type of specialist I might select—doctor, lawyer, merchant-chief and yes, even beggar-man and thief, regardless of the talents, penchants, tendencies, abilities, vocations and race of his ancestors.
These famous and much quoted words of John B. Watson—often called the father of behaviorism—epitomize not just the movement’s belief in the overwhelming effectiveness of conditioning but also its complete repudiation of heredity and genetics. Such radical behaviorism is the philosophy of science that underpins applied behavior analysis (ABA) according to a quotation at the front of Genetic Syndromes and Applied Behaviour Analysis: A Handbook for ABA Practitioners just published by the world’s leading publisher on psychotherapy and related fields, Jessica Kingsley.
As the preface points out, this remarkable book is a unique integration of two fields of study: ABA and genetics. ABA is “the science of behavior change,” and to the extent that it is indeed based on radical behaviorism, stands at the opposite extreme to psychoanalysis on the diametric model’s continuum of mentalism, as I have pointed out before. Indeed, the fact that both Freudianism and behaviorism emphasized nurture and discounted nature—albeit in very different ways—probably explains much of the bio-phobia and denial of genetics that characterized later 20th century folk psychology (and still lingers on in sclerotic plaques of political dogma).
But with this landmark publication, ABA has revealed a remarkable readiness to embrace insights from genetics, and as such this book represents a complete reversal of the classical behaviorist denial of heredity and sets a striking precedent, not just for behaviorism, but also for psychology and psychiatry as a whole.
Syndromes covered in this book are Fragile X (the most common cause of cognitive disability), Down, Smith Magenis, Williams, Angelman, Prader Willi, Cri du Chat, Rubinstein Tabi, and Velocardiofacial/22q11.2 Deletion syndromes. In every case, the more or less exact genetic cause is known at the DNA level, and as the illustrative case histories make clear, far from stigmatizing or condemning individuals fatalistically to their afflictions, “syndrome identification helps us to understand the reality of the individual’s experience and provide invaluable information regarding how the person perceives and processes their experiences, thereby leading to both understanding and adaptation.” (p. 258) Specifically, positive genetic diagnosis is valuable because
- it give parents, teachers and therapists a clear definition of what is wrong, and why;
- it provides insights into signs and symptoms based on comparisons with other cases and related syndromes;
- it enables some measure of prediction and prognosis of likely developments and outcomes;
- it offers the prospect of rationally-designed and appropriately prescribed cognitive-behavioral therapy, medication, and ultimately perhaps, genetic therapy.
Of course, ABA could be said to have become interested in genetics simply because it had little else to go on, given its behaviorist rejection of mentalistic measures, and there is perhaps much truth in this. But the fact remains that even the most mentally disabled person still has a mind. Furthermore, if genetics gives such valuable insights into behavioral pathology, it can also give insights into much more mentalistic factors—and even into normality. Indeed, according to the imprinted brain theory, genetics explains not just why things go wrong, but also why—thankfully—they normally go more or less right.
And even if we limit ourselves to pathology, only the imprinted brain theory reveals the hidden pattern underlying the syndromes described in this book. Only the diametric model of mental illness can show how and why Angelman syndrome (AS) is the autistic corollary of Prader Willi syndrome (PWS) with its high risk of psychosis. The reason is that AS is caused by loss of maternal and gain of paternal gene expression in a run of critical genes on chromosome 15, while PWS is the result of loss of paternal and gain of maternal gene expression in the same region (below). Indeed, in the variant that goes with the highest of all known genetic risks of psychosis, PWS results from duplication of the maternal chromosome 15 and complete loss of the paternal one. And as I pointed out in a previous post, something of a similar pattern can be seen in Williams, Smith Magenis-Potocki Lupski, and Velocardiofacial/22q11.2 Deletion syndromes.
I suspect that this outstanding compendium is likely to go through many future editions, progressively adding more and more syndromes and—who knows?—perhaps eventually integrating them into the new imprinted brain paradigm underpinning not just ABA, but psychiatry and psychotherapy as a whole. At the very least, this timely publication marks the turn of the tide in behaviorist therapy, and where ABA leads, many others are likely to follow—perhaps even those at the opposite pole of the mentalistic continuum.
(With thanks to Marta Aubrey.)