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Commentary on ‘ADHD diagnosis continues to fail the reliability and validity tests’ by Martin Whitely

Dr Whitely’s (2015) latest paper continues the emotive and sensationalist debate between those that promulgate a ‘core belief’ in attention deficit hyperactivity disorder (ADHD) as a valid and reliable diagnosis and those that do not. Furthermore, this latter group will not accept emerging systematic evidence proffered to support the robust psychometric properties of ADHD as a diagnosis. Dr Whitely incorporates small segments of specific discourses taken from rich, nuanced and varied narratives to build his rhetorical critique of Prof. Levy’s (2014) Commentary. For instance, Prof. Levy quotes First’s (2013) brief paper on the National Institute of Mental Health (NIMH) research domain criteria project found in Kendler’s and Parnas’ text Philosophical Issues In Psychiatry 2: Nosology, published by Oxford University Press. First outlines the success that the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Classification of Diseases (ICD) nosologies have had facilitating communication between clinicians, researchers and administrators while also noting their relatively moderate success establishing diagnostic reliability when applied by clinicians. Prof. Levy communicates no inferences about the wholly separate discourses of the diagnosis of ADHD in adulthood and ADHD prescription rates in children. Dr Whitely appears to present these inappropriate associations for rhetorical effect. Nevertheless, Prof. Levy and Dr Whitely’s papers articulate some important issues for clinicians, researchers and policy planners to consider. Dr Whitely draws our attention to the fundamental role of science in the ADHD field. This discourse is founded on a radical scepticism based on the null hypothesis and its systematic rejection to confirm significant associations between variables. Furthermore, the strength of association between such significantly associated variables can be quantified to determine their clinical importance. Such significant associations then form the foundation for further examination of related variables, and in this way, a scientific system of knowledge is built (Popper, 1962). It is not consistent within the spirit or methodology of scientific discourse to endlessly and continuously question significant associations unless simultaneously proffering a non-replication dataset with key confounding variables controlled. In addition, ethical and moral discourses are inherently recognised and managed within the extant scientific discourse: the central role of ethics committees attests to this point. Hence, any specific moral and/or ethical argument about some aspect of the ADHD field must first be well-grounded in the existing moral and/or ethical discourses and not syncretistically linked without reasoned and appropriate argument. Prof. Levy emphasises the replicated validity and reliability of the ADHD construct within the scientific discourse. Yet, the large number of greater than chance comorbid conditions encountered in young people with ADHD presents clinical and research dilemmas. Careful appraisal of each condition’s contribution to the impairments experienced by these young people in the classroom, playground and home environments is needed. Multi-informant reports over time, obtained through careful and thorough history taking, achieves this. But, the research domain criteria approach through improved reliability of objective measurement for specific neurobiological components will aid this complex process further, through linking conditions and their associated impairments to specific neurobiological component functions. Prof. Levy mounts a similar argument for the research domain criteria approach to help clarify variable treatment response, natural history and prognosis within the ADHD field. Both Dr Whitely and Prof Levy indirectly draw our attention to the current accepted model of ADHD internationally within an evidence-based framework (National Institute for Health and Clinical Excellence [NICE], 2009): ADHD is primarily driven by developmental delay biologically, psychologically and socially. Many genes of small effect interact with and are modulated by environmental factors, and vice versa. This cumulatively gives rise to ADHD in vulnerable people with or without vulnerable environments. There are many pathways into ADHD with varied biological through to psychosocial contributions: this is evidenced by socioeconomic status (especially poverty) not being clearly associated with ADHD occurrence. ADHD most commonly presents as one disorder in a setting of a number of comorbid disorders. Medication and psychosocial interventions for ADHD and these attendant disorders lead to the greatest decrease in functional impairment in classroom, school yard and home environments. A crucial future domain of research is the role of culture determining the evolution and maintenance of meaning and its dialogue with biological, psychological and social models of ADHD: e.g., adapting to ADHDlinked vulnerabilities, such as reduced working memory abilities, and understanding and complying with medication and psychosocial interventions are deeply modulated by cultural beliefs and standpoints. This is especially relevant in Australia given the urgent need for genuine dialogue between Aboriginal and nonAboriginal ways of addressing health.