In a philosophically rigorous article published in Frontiers in Psychology, Spanish researcher Marino Pérez-Álvarez examines the logic of attention-deficit hyperactivity disorder (ADHD). The two-part analysis first deconstructs the rhetoric composing the diagnosis—including the symptoms and presumed causes of the “disorder.” Pérez-Álvarez then goes on to examine the philosophical bases of the diagnosis as it exists in society.

The researcher, from the University of Oviedo, Spain, has a background in logical theory, and provides specific examples of how the ADHD diagnosis violates the requirements for logically sound argument. His main point is that the reasoning is circular. As an example: If a child exhibits the behaviors that are agreed to constitute ADHD, then the child can be said to “have” ADHD, and by circular reasoning, therefore, the ADHD “causes” those behaviors. Pérez-Álvarez calls out this type of reasoning as illogical rhetoric.

However, he also asks: even if the reasoning is flawed, is there scientific evidence that the neurodevelopmental model is accurate?

His research finds that there is not. In fact, he writes that the general assumptions of genetic research on psychological health are flawed. The assumption that genetics can “cause” behaviors is not consistent with genetic theory. He writes, “The genome mediates adaptation and response to the environment; it does not cause response and adaptive action.” That is, behaviors are not “caused” by genetics. Behaviors are responses to the environment.

Pérez-Álvarez writes that this may help explain why psychiatric researchers include such caveats in their “conclusive” ADHD literature as:

Nonetheless, the same researchers who wrote these statements advocate the neurobiological model of ADHD, stating, for example, that there is “substantial evidence for a genetic origin of ADHD”—which Pérez-Álvarez argues is an illogical way of interpreting the conclusions above. In fact, that article is even titled “Moving toward causality in attention-deficit hyperactivity disorder” which is particularly misleading since the article reviews correlational evidence, not causal conclusions.

According to Pérez-Álvarez, the current direction in ADHD research—and in psychiatric research in general—is to use larger and larger samples in order to find smaller and smaller correlations. But he remarks that a tiny correlation that only shows up when you sample hundreds of thousands of people is not of any value to individual diagnosis.

He writes that researchers in psychiatry often work around the lack of evidence for their standpoint by arguing that “ADHD is a ‘heterogeneous,’ ‘multifactorial,’ or ‘complex’ disorder”—which may be true, but does not excuse researchers from the burden of showing data that can back up their claims.

Pérez-Álvarez also takes aim at the rhetoric of referring to brain-based findings as “bases” and “causes” rather than simple correlates. After all, “As studies show, the brains of taxi drivers and musicians show alterations in speciﬁc areas and connections associated with their activities compared to those who are not…” but those neural correlates are certainly not presumed to be the cause of driving taxis or playing the violin. Quite the opposite, in fact—those brain changes are understood to be results of those professions. So why do researchers assume that any brain differences detected when studying people that have been diagnosed are “causing” ADHD?

A key point made by Pérez-Álvarez is that although psychiatric diagnoses may be reliable—psychiatrists may agree on the criteria—there is no evidence that they are valid. Pérez-Álvarez quotes Thomas Insel (then Director of the National Institute of Mental Health) to make this point:

“The strength of each of the editions of DSM has been ‘reliability’—each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our deﬁnitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure.”

To further clarify the difference between reliability and validity, Pérez-Álvarez cites A. Marcia Angell, ex-director of the New England Journal of Medicine, who writes:

“If nearly all physicians agreed that freckles were a sign of cancer, the diagnosis would be ‘reliable,’ but not valid. The problem with the DSM is that in all of its editions, it has simply reﬂected the opinions of its writers.”

It is important to note that Pérez-Álvarez also argues that ADHD is “real” inasmuch as “the diagnosis already functions as a “cultural idiom.” The construct of ADHD serves to explain a way of being in relation to others that is culturally unacceptable—namely, being more active, more distractible, and more impulsive than other children.

He writes that the diagnosis of ADHD fits perfectly in a long tradition of psychiatry selecting ways of being that are considered culturally invalid, selecting and exaggerating behaviors as “symptoms,” and creating a category or label that can serve as a self-reinforcing a priori concept.

According to Pérez-Álvarez, “Any problems related to “attention,” “activity,” and “impulsivity” are not outside learning as aspects of the development of self-control. Some children may require additional “training” (not treatment).” That is, diagnosing these traits as a “brain disorder” and medicating children only serves to prevent children from learning skills of self-regulation and maintaining attention. Pérez-Álvarez advocates methods of teaching children these skills as part of the developmental process, rather than pathologizing children for acting impulsively and inattentively.

Pérez-Álvarez writes, “Attention-Deficit/Hyperactivity Disorder harmonizes a variety of scientific, medical, educational and family interests besides pharmaceutical industry profits (the most openly shameless and rightly denounced). The only party harmed seems to be the children.”

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Pérez-Álvarez, M. (2017). The four causes of ADHD: Aristotle in the classroom. Front. Psychol. 8(928). doi: 10.3389/fpsyg.2017.00928 (Link)