In chapter two, we examined the neuroscientific and (epi)genetic thought styles, attempting to summarise the current settlement within the ‘thought collective’. In this final chapter of Part I of the book, we consider how these work their way into a broader style of thinking, and programme of research, which aims at the reinterpretation of deviant behaviour as a disorder of the brain. We examine the ways in which biology has been brought to bear in understanding forms of behaviour variously known through the ages as madness, mental illness or developmental disorder. This has culminated in current preoccupations with finding the genetic markers and neurological traces for a variety of manifestations of the human condition, seen as deviant. Here we see how clinical researchers also follow well-trodden paths. We take a peek into how the primary science of the laboratory, discussed in the last chapter, makes its way into, in this case, psychiatric practice via its own form of journal science.

We begin with an overview of the ascendancy of biological psychiatry as the dominant explanatory narrative in the field of mental ‘illness’. This synopsis will include an extended general survey on the long history of research into the hereditability of mental disorder, and of the various methodologies which characterise this tradition. We then proceed to examine in depth two categories of mental disorder which are particularly pertinent in the context of child development. We first look at the state-of-the-art in autism research from a neuroscientific perspective, applying the Fleckian concepts we examined in chapter two. We then consider attention deficit hyperactivity disorder (ADHD), also of relatively recent origin, focusing on genetic research into its hereditability.

Statistical prelude: genesis of a (pseudo)scientific fact?

Before getting under way, the reader at this point is referred to appendix C. This takes the form of a thought experiment based on a real study (Hikida et al, 2007), the investigation of a gene (the disrupted-In-schizophrenia-1 gene, DISC1) which has been ‘implicated’ in the aetiology of schizophrenia.