University of Groningen ADHD and the power of generalization te Meerman, Sanne

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ADHD and the power of generalization

te Meerman, Sanne

DOI:

10.33612/diss.84379221

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Publication date: 2019

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te Meerman, S. (2019). ADHD and the power of generalization: exploring the faces of reification. Rijksuniversiteit Groningen. https://doi.org/10.33612/diss.84379221

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531133-L-bw-Meerman 531133-L-bw-Meerman 531133-L-bw-Meerman 531133-L-bw-Meerman Processed on: 20-5-2019 Processed on: 20-5-2019 Processed on: 20-5-2019

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Exploring the faces of reification

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Processed on: 20-5-2019 PDF page: 2PDF page: 2PDF page: 2PDF page: 2 This artwork shows a figure that inflates when it is watched or approached by

someone until it reaches the restraints of the glass encasement it resides in. When I was writing my thesis, the way some scientists inflate their findings made me think of this artwork. The transparent, glass ‘container’ of the scientific enterprise hopefully stops the scientists from exaggerations. However, I remember the tension, when I saw the artwork for the first time. As the noisy motor (from a vacuum cleaner) pushed the figure against the glass, I wondered: is the glass box solid enough?

However, as I talked to Johnny about it, I Iearned he himself had associations with Sartre when he conceived the work: “The Other’s look fashions my body in its naked-ness, causes it to be born, sculptures it, produces it as it is, sees it as I shall never see it.” (Sartre, 1943, Being and Nothingness).

Johnny turned photographs from the artwork into a 3D picture that he remem-bered enjoying when he was a child. And when I showed it to others, they again had a completely different interpretation from Johnny’s or mine. There is not one true meaning ‘out there’ (or is there?). So, what do you think it means? Or, perhaps a better question would be, what does it mean to you?

Layout and design: Jesse Haaksman, persoonlijkproefschrift.nl Printed by: Ipskamp Printing, proefschriften.net

All rights reserved. No part of this thesis may be reproduced, stored or transmitted in any way or by any means without the prior permission of the author, artist, or when applicable, of the publishers of scientific papers.

ISBN: 978-94-034-1655-7

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Exploring the faces of reification

Proefschrift

ter verkrijging van de graad van doctor aan de Rijksuniversiteit Groningen

op gezag van de

rector magnificus prof. dr. E. Sterken en volgens besluit van het College voor Promoties.

De openbare verdediging zal plaatsvinden op Donderdag 20 juni 2019 om 14.30 uur

door

Sanne te Meerman

geboren op 21 maart 1975 te Nijmegen

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Copromotor Dr. L. Batstra Beoordelingscommissie Prof. dr. G. Timmerman Prof. dr. P. Verhaeghe Prof. dr. M. de Winter

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Chapter 1: General Introduction 8

Chapter 2: ADHD and the power of generalization 18

Chapter 3: Biomedical bias in academic textbooks 32

Chapter 4: Academic textbooks on ADHD genetics: balanced or biased 54 Chapter 5: ADHD: A critical Update For Educational Professionals 72

Chapter 6: ADHD and the faces of reification 84

Chapter 7: Discussion and Conclusion 108

References 129

Appendix A 149

English Summary 154

Samenvatting (in Dutch) 160

About the author 164

About the artist & artwork 165

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ADHD and the power of generalization

Exploring the faces of reification

General introduction

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“ADHD is kind of like a cancer disease but you’re not going to die from it.” Sylvia, US, on medication, age 11 (Singh, 2012, p. 20)

Introduction

In the VOICES study (Voices On Identity, Childhood, Ethics and Stimulants; (Singh, 2012) children classified with ADHD are asked about their perception of ADHD and, amongst others, their perception of the use of psycho-stimulants. In the above-men-tioned example, Sylvia’s account of ADHD is one of a physical and serious disease like cancer -although not lethal. A recent study reveals where children might pick up such a pathologizing view of unruly behavior: 10 of the most popular informational books on ADHD addressed at children in the Netherlands, mostly contain a medically-oriented view (Foget, Van Haeringen, Te Meerman, & Batstra, 2017) and many passages in those books suggest ADHD is a brain condition. However, this begs the question: where do the authors of such books base their information on? In this study we analyze academic textbooks and other sources of information that might advert a biomedical disease perspective on ADHD to (future) professionals. For our analysis, we focus on the four concepts included in the title of this dissertation: ADHD, reification, generalizations and power. We will introduce these concepts in relation to each other.

1. ADHD

ADHD is a concept that is defined, each time slightly different, in the subsequent edi-tions of the DSM; the Diagnostic and Statistical Manual of Mental Disorders. This psy-chiatric handbook is currently in its fifth edition and describes around 400 disorders. The acronym ADHD stands for “Attention Deficit/Hyperactivity Disorder”. Five sets of (mostly behavioral) criteria, A through E, are listed for ADHD in the DSM 5. A1 and A2 both list nine behaviors that describe attention problems and hyperactivity/impulsivity problems. When six out of nine of these criteria are met according to those who do the assessment, a child is eligible for an ADHD classification. However, some additional criteria must be met as well: the criteria B through E describe age of onset (before 12 years), setting (behaviors should occur in 2 or more settings), level of impairment (stipulating when the behavior should be considered as impairing) and considerations with regard to other classifications and which is the best applicable one (American Psychiatric Association, 2013, p. 59-61).

It should be clear that the behavioral criteria are unspecific and open to multiple interpretations, as they all contain the word “often”, and they are context-sensitive as well. For instance, the criterion “often leaves seat in situations when remaining seated is

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expected” is likely to be more annoying in a classroom setting with many as opposed to few children, and the presence of (other) children that behave unruly (Wienen, Batstra, Thoutenhoofd, Bos, & de Jonge, 2018). These ambiguous criteria reflect the “ontologi-cal vagueness that characterizes social science” (Hyde, 2008, p. 7). In the words of the authors of the DSM-IV-TR: “Nature did not choose to craft psychiatric disorders into neat little packages with clear boundaries”. More formally: “there is no assumption that each category of mental disorder is a completely discrete entity with absolute bounda-ries dividing it from other mental disorders or from no mental disorder” (Frances, First, & Pincus, 1995, p. 57).

2. Reification

The authors of the DSM-IV attest to the usefulness of a categorical approach provided that sufficient consideration is given to its limitations. One of the problems is the human tendency to “reify categories” (Frances et al., 1995, p. 17). The act of giving names carries an inherent risk for such reification. This is probably why reification is often explained by quoting Philosopher John Stuart Mill: “The tendency has always been strong to believe that whatever received a name must be an entity or being, having an independent existence of its own” (for instance Hyman (2010); Turner & Edgley (1980)). Batstra et al. (Batstra, Nieweg, & Hadders-Algra, 2014, p. 696) define reification as “treating more or less abstract concepts as things, existing out there in the world”. However, “just as the category bachelor does not result in a man being single, the cat-egory ADHD does not result in hyperactivity and inattention” (Batstra et al., 2014, p. 697). Both Hyman and Batstra thereby exemplify reification with what is known as the “nominal fallacy”, confusing naming and explaining which is also related to circular reasoning (Boag, 2011).

Indeed, naming and explaining often seem to be confused in relation to ADHD and it is easy to find examples of this. For instance, Biederman and Faraone (Biederman & Faraone, 2005, p. 237) state in the Lancet: “ADHD affects 8–12% of children world-wide, and results in inattention, impulsivity, and hyperactivity”. This is a typical example of “behaviour that becomes the cause of behaviour” (Bandura, 1999, p. 168.). We have named these behaviors as ADHD, and now ADHD allegedly results in these behaviors.

3. Generalization

In my view, this nominal fallacy (Levy & Press, 2010), is merely one possible cause of reification. I argue that one of the most powerful fallacies involved with reification is “generalization”. For instance, when studies into brain-anatomy are conducted by

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comparing groups of children with an ADHD “diagnosis” with controls, small group differences are often presented as if every individual in the ADHD group is afflicted with an attribute like a smaller brain (part). This is reifying as it suggests the existence of a real physical identifiable attribute that sets those with an ADHD classification apart from “normal” people. A recent example is a study by Hoogman (Hoogman et al., 2017), the largest case-control study to date that found –on average- statistically significant smaller brains in those classified with ADHD. However, the effect size of the differ-ences was small. The highest effect size, a Cohen’s d of .19 was found for the nucleus accumbens, associated with reward processing. However, this implies an overlap of 95% between case and control groups. The chance of guessing if an individual belongs to either the case or control group based on the size of his accumbens is about 0.54 (Coe, 2002), which is slightly more than tossing a coin (Corrigan & Whitaker, 2017). Put differently, in many classified with ADHD this brain part was larger than average while at the same time in many without the classification this brain part was smaller.

The fuzzy boundaries of the DSM categories unfortunately further complicate this. The DSM-IV guidebook acknowledges that research designs may include only the more “prototypical” persons, while in other research designs a broader, more inclusive ap-proach may facilitate generalizability (Frances et al., 1995, p. 17). However, the common practice of using the more prototypical persons, often called “refined phenotypes” is problematic in light of the already problematic generalizations. The more rigorously screened research sample may not be a good representation of those classified with ADHD in everyday clinical practice. Suggesting that group findings in highly selected re-search samples apply to individuals in clinical practice thus becomes extra problematic.

4. Power

In politics, generalizations are a powerful tool to legitimate power. For instance, in his inauguration speech Donald Trump stated: “January 20th, 2017, will be remembered as the day the people became the rulers of this nation again”. Although he might have referred to many lower-income Americans who voted for him, generalizing by referring to them as “the people” was a convenient way to avoid the fact that most people in the United States actually chose Hillary Clinton, as she won the popular vote.

In politics, inflating the support base by means of generalizing can serve to legiti-mate power and influence. Likewise, scientists may inflate their knowledge base with similar generalizations for similar purposes. Suggesting that those with an ADHD diag-nosis all share a genetic make-up that “normal” people lack and all or most have smaller brains or lower levels of certain neurotransmitters, ascribes agency to bio-medically

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oriented researchers and practitioners. Generalizations and other means of reification might serve their interests, such as securing future funding of research and available resources for care. However, if such interests are sought after at the expense of other interests, such as those of the child and other orientations, this makes science more political than is ethically sound and may compromise the search for knowledge about etiology and treatment options.

Objectives of this study

There are several reasons why reification might occur. Self-interests versus broader considerations, career over cure (Miedema, 2014), could certainly be a motive for de-liberately reifying ADHD. To a degree, such boasting might be understandable con-sidering that positive findings tend to be published more often than studies that show that expected results are not found (Glasziou & Chalmers, 2017). However, beyond venturing into such individualistic motives, reification is ultimately a conflict-theoretical notion. Conflict-theory is a sociological paradigm that looks, for instance, at (scientific) subgroups that are in conflict over resources and influence. From this perspective reification might serve group interest. Furthermore, it is important to emphasize that reification does not have to occur intentionally but -like John Stuart Mill addressed- is inherent in the way language is used, for instance by naming difficult to define be-haviors. Finally, from a philosophical, historical perspective I aim to understand our tendency to name, classify and reify as part of a process of rationalization and a quest for concreteness gone awry.

However, before we touch upon these larger issues in the final chapter, this thesis first and foremost explores how, and how often, information shared in the scientific community tends to be reifying. The main research question is: how is ADHD reified in written discourse, and how often do such mechanisms of reification occur? By quanti-fying some of these mechanisms, as we do in chapter 3 and 4, we hope to alert readers to the widespread occurrence of reification. Our main goal, however, is to improve the discourse on ADHD by alerting authors and the general public on ways the ADHD-con-struct is reified and how to avoid this (all chapters).

Outline

We answer our main research question in the following chapters:

Chapter 2 centers on the Hoogman paper, published in 2017, the largest meta-study

on ADHD and brain anatomy to date. It is a prime example of the power of generalization.

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In this chapter, we discuss our response to this publication in the Lancet Psychiatry and the author’s reply.

Chapter 3 reflects on an empirical study of discourse in academic textbooks used

at Dutch universities to train future professionals. Generalizations on brain anatomy, similar to those found in the Hoogman paper, are analyzed.

Chapter 4 reflects on an empirical analysis that further explores the backgrounds of

popular beliefs about the genetic origins of ADHD. The analysis of textbooks shows how future professionals are led to believe that ADHD is mainly a genetic affliction.

Chapter 5 contains a critical review on ADHD in relation to both brain anatomy and

genetics but widens the scope by discussing additional vital topics that urge for caution in terms of validity and widespread use of the ADHD-construct and the prescription of psychostimulants. These issues are discussed in terms of what they mean for the power and agency of educational professionals in relation to biomedical healthcare professionals who are involved with children’s behavior.

Chapter 6 contains a critical review of mechanisms that can reify ADHD. Selective

writings on anatomy and genetics are included, but many more factors are identified, such as inappropriate word choice, logical fallacies, use of (deceptive) metaphors and the avoidance of information that places ADHD into perspective.

Chapter 7 contains conclusions and reflections upon the individual studies and aims

to provide suggestions on how to avoid reification. Furthermore, the motives for the tendency to reify ADHD are discussed in terms of power and contemporary cultural ideals about behavior.

Theoretical and methodological considerations

This section will reflect on the use of qualitative methodology in this thesis. Data selection

Academic textbooks are key-assets used to educate the new generation of social and medical academics. Our main source of data for this thesis is a selection of textbooks that are used in universities in the Netherlands. We have aimed to select all textbooks used in (pre) master’s programs that discuss ADHD. Of these books, the sections on ADHD are singled out.

Qualitative research

“Qualitative research exhibits a variety of approaches and continuously proliferates, leading to yet more methods and approaches” (Flick, 2014, p. 532). Although some

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experts in the field of qualitative research hold the position that: “too often researchers learn and embrace a handful of strategies and settle into comfortable methodologi-cal ruts” (Denzin & Lincoln, 2011, p. 595), it was difficult finding one methodologimethodologi-cal rut that matched well with the research question of this thesis. There is a plethora of approaches and different views, but unfortunately, there is often debate about what does and does not constitute a particular method.

Content analysis (qualitative/quantitative).

For example, according to some scholars, content analysis was by definition quantita-tive and other more qualitaquantita-tive approaches were mere forerunners and could not be considered as content analysis (George, 1959). According to Schreier (2012), however, quantitative content analysis was actually a forerunner of more qualitative approaches that emerged out of the perceived limitations of the quantitative approach.

This diversity in views and directions “keeps content analysis current-but also makes it difficult to standardize” (Krippendorff & Bock, 2009, p. ix). Nevertheless, it seemed that in the domain of content analysis the match with our research questions could be made. We –initially- had clear ideas about how certain information can be generalizing and used a strongly concept-driven/deductive approach which seemed to match best with this –quantitatively oriented- basic content analysis (Weber, 1990). Additionally, we focused only on manifest content features (without focusing on textual elements that were absent), which is characteristic of basic content analysis (Drisko & Maschi, 2016).

However, we soon discovered we needed to incorporate more context, so we ven-tured into more qualitative branches of content analysis that allowed for more flexibility to include data-driven elements (Schreier, 2012).

(Critical) Discourse Analysis

In the course of our research, we have also used elements from other approaches such as discourse analysis. One motive for doing so is that (critical) discourse analysis matches well with the ontological starting points of our study. These are strongly in-fluenced by Berger and Luckmann who state that “language provides the fundamental superimposition of logic on the objectivated social world. The edifice of legitimations is built upon language and uses language as its principal instrumentality” (Berger & Luckmann, 1966, p. 82).

This expresses our position well. Language does not (only) describe the social world, but (also) legitimates the social world as it is and suggests that it has a certain logic of

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itself. However, this logic is superimposed rather than inherent to this social world. So in short, language does not necessarily represent the (social) world but rather legitimiz-es the prlegitimiz-esumed logic of the status quo and even helps shape it. For example, Russel Barkley, a strong proponent of a realist view on ADHD, has a (video) presentation named: the neuro-anatomy of ADHD and thus how to treat it (Barkley, 2014). The title as well as the video itself suggests that there is one neuro-anatomy present in those that behave according to the behavioral criteria of the ADHD construct. We argue that this logic (questionable due to the generalization) is superimposed on the social world: it legitimizes for instance the institutionalized distribution of psycho-stimulants to alleged “patients” as Barkley names those classified with ADHD. However, there is no proof of a different neuro-anatomy (or any other brain attribute) shared by all or even many of those classified with ADHD as we will repeatedly argue in this thesis.

Discourse Analysis provides several tools to explain that (scientific) “knowledge” is less certain than some scientists make it appear. For instance, with the absence of

hedges, words that express caution (Swales, 1990), statements can portray more

cer-tainty than the underlying empirical data allow for.

Logic

The use of Berger and Luckmann’s (1966) statements also reveals my interest in logic surrounding ADHD. By exposing that the logic is flawed I hope to demonstrate that this “edifice of legitimations”, as Berger and Luckmann call it, is not a very solid one. Generalization -central in this thesis- is one example, but there are many others. For instance, Tait (2009) who analyses fallacious reasoning in relation to ADHD, claims the “false cause fallacy” (Tait, 2009, p. 245) is a common error in discourse on ADHD. He exemplifies this with the suggestion that because inmates often have attention problems their incarceration is caused by their disability ADHD (Hurley & Eme, 2004). This may merely be a spurious correlation, as both the attention problems and the in-carceration may be the result of adverse circumstances often seen in detainees (Hoeve et al., 2009; Jaffee, Caspi, Moffitt, Belsky, & Silva, 2001).

Finally, spurious correlations and other logical flaws such as the nominal fallacy also touch upon a larger subject this thesis aims to address. By using behavioral clas-sifications such as ADHD and by thinking they explain behavior, it may be tempting to overlook much broader societal issues. Many adverse circumstances such as divorce, child maltreatment, poverty, insufficient funding for education and large classrooms may lead to erratic behavior or may even cause normal responses to abnormal circum-stances to be seen as erratic.

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Based on:

Batstra, L., te Meerman, S., Conners, K., & Frances, A. (2017). Subcortical brain volume differences in participants with attention deficit

hyperac-tivity disorder in children and adults. The Lancet Psychiatry, 4(6), 439.

ADHD and the power of generalizations

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Abstract

This chapter discusses a meta-analysis of case-control studies into brain-anatomy of ADHD, comparing a group of people classified with ADHD to those without this classi-fication. The findings indicated that -on average- 5 brain parts were smaller in children classified with ADHD. The effect sizes of the findings were minor, which means that in many with an ADHD classification those brain parts were larger than than in many without a classification. At the same time, in many without a classification thoser brain parts are smaller than in those classified with ADHD. Furthermore, the average dif-ferences disappeared in adulthood. Nevertheless, the authors erroneously concluded that their findings mean that ADHD is a brain disorder and that this message could be given to individuals with an ADHD classification. The authors were criticized for their faulty group-to-individual generalization. However, they did not change their conclu-sion when confronted with the criticism. In this chapter, the authors’ response to the critique is analyzed.

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Introduction

According to a paper by Hoogman and colleagues clinicians can now tell patients and their parents that children with ADHD “have altered brains; therefore ADHD is a dis-order of the brain” (Hoogman et al., 2017b, p. 316). In this chapter, I will discuss our response to the Hoogman paper, the largest meta-study to date on brain anatomy and ADHD. The study compares the brain anatomy of 1713 individuals with an ADHD-clas-sification to 1529 controls. In the general introduction of this thesis, I posited that generalizations are probably the most important mechanism behind inflated research findings and reification of ADHD. I view the widely publicized and cited Hoogman paper as the epitome of the power of generalization and this chapter is therefore a good starting point for this thesis.

Many others also had serious objections to the Hoogman paper, including several scholars. A petition to withdraw the study on blogsite “Mad in America” has been signed 1800+ times and continues to be discussed online. Both Allen Frances, who is the former chair of the DSM-IV taskforce, and Keith Conners, who is considered the found-ing father of the ADHD-concept co-authored our letter to the publishers. Throughout the years, both have continuously voiced concerns about the overdiagnosis of ADHD. In 2013 Keith Conners said about the rate (15%) of children classified as having ADHD: “The numbers make it look like an epidemic. Well, it’s not. It’s preposterous,” (…) “This is a concoction to justify the giving out of medication at unprecedented and unjustifiable levels.” (Schwarz, 2013).

During the submission of our reply, Keith Conners was very ill and he passed away some two months after publication. To our knowledge, the letter is his last scientific output. We have reprinted our response to the Hoogman study and will discuss the authors’ reply to our criticism in detail. We will first demonstrate the logical flaws and the rhetorical devices they employ to deflect our arguments. Although we acknowledge the merits of the study, we criticize the authors for making far-reaching, misleading and harmful claims that are not supported by their data.

Reply to the Hoogman Study

The following is our full reply to the Hoogman paper:

“In their study on attention deficit hyperactivity disorder (ADHD) and brain volume, Martine Hoogman and colleagues concluded: “We confirm, with high-powered anal-ysis, that patients with ADHD have altered brains; therefore ADHD is a disorder of the brain. This message is clear for clinicians to convey to parents and patients,

“

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which can help to reduce the stigma of ADHD and improve understanding of the disorder” (Hoogman et al., 2017b, p. 440). Such a definitive statement, however, is not supported by their data. In our view, their statement is wildly speculative and dangerously misleading at a time when ADHD is already overdiagnosed and over-treated with medication in high-income and middle-income countries (Merten, Cwik, Margraf, & Schneider, 2017).

In their well-executed study, Hoogman and colleagues reanalysed data from 23 sites for brain volume differences in children and adults diagnosed with ADHD. On the basis of Cohen’s d values ranging from −0·19 to −0·10, the authors state that the volumes of the accumbens, amygdala, caudate, hippocampus, and putamen, and the intracranial volume, were smaller in individuals with ADHD than in healthy individuals. However, such small effect sizes mean that approximately 95% of the two groups overlap, and are usually interpreted as negligible or very small differences.

Even in studies with more compelling effect sizes than in this study, interpreta-tion of differences between ADHD-diagnosed and ADHD-undiagnosed groups is complicated. Within-group variation is always large and between-group differences are small and do not apply to many individuals diagnosed with ADHD. Furthermore, associations do not necessarily imply causality. When Hoogman and colleagues wrote that their study proves that ADHD is not “caused by incompetent parenting”, they do so without referring to the brain’s plasticity and the fact that environmental factors can change brain anatomy. Additionally, the behaviour we call ADHD is not caused by either brain defect or bad parenting, but is associated with many different factors, ranging from poverty (Pastor, Reuben, Duran, & Hawkins, 2015) to pesticide exposure (Yu et al., 2016).

Biological differences do not automatically imply abnormality or pathology. Ac-cording to Hoogman and colleagues, calling ADHD a brain disease can help to reduce the stigma of ADHD. This reduction of stigma does not, of course, justify labelling ADHD a brain disease if it is not, but more important, to label ADHD a brain disease is also simply wrong. Many people feel stigmatised and hopeless when told they have a brain disease (Reiner, 2011).

The fact that the message of this large-scale study now proving that ADHD is a brain disorder has already been widely echoed in the media is seriously concerning. This message risks misinforming the general public about the nature of ADHD, and could harm those diagnosed with the disorder. Furthermore, such simplification might easily increase the risk of sociological and other environmental factors relat-ed to (perceivrelat-ed) problematic behaviours being overlookrelat-ed. Yet the most important

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argument against the authors’ conclusion that “patients with ADHD have altered brains” is that it is not supported by their own findings.” (Batstra, te Meerman, Con-ners, & Frances, 2017, p. 439).

Reflection on author’s reply

The journal published four critical reactions to the Hoogman study, including ours. Hoogman et al. addressed the criticisms in these four letters in one, also published, response. We include the third paragraph of their reply. In this paragraph the authors partly address our issues and those of Dehue and colleagues and we will analyze every statement of it. Additionally, we focus on several statements made later in the authors’ reply in which they implicitly address other concerns we voiced.

“The critical letters by Dehue and colleagues and Batstra and colleagues claimed that we observed only small effect sizes and hence cannot conclude that individuals with ADHD have a brain disorder. ADHD is a disorder by all standards of psychiatric nosology, and our data support the idea that neuroanatomic brain abnormalities, although subtle, are associated with the disorder. The strength of our work comes from combining data collected worldwide. The observed brain abnormalities are heterogeneous and are likely to differ in individuals with ADHD (..). However, such heterogeneity at the individual level does not undermine the importance of effects at the group level. The criticisms of small effect sizes raised by these letters imply that we should only use the term brain disorder when everyone with the disorder shows the same pattern of brain abnormalities. By that definition, no psychiatric disorder would be a brain disorder. Our critics further ignore that our findings fit well with other features of ADHD, such as the link between emotional dysregulation and the amygdala, and the links between altered reward processing and striatum, to name just a few. Placing our findings within the broader scientific literature, as we did in our Article, provides the context for our conclusion.” (Hoogman et al., 2017a, p. 440)

Avoiding and misrepresenting our criticism

The authors first summarize our response: “The critical letters by Dehue and colleagues and Batstra and colleagues claimed that we observed only small effect sizes and hence cannot conclude that individuals with ADHD have a brain disorder” (Hoogman et al., 2017a, p. 440). On the surface, this covers our criticism correctly, although we empha-sized that the differences “do not apply to many individuals diagnosed with ADHD” (Batstra et al., 2017, p. 439). This is important, as this individualized message is exactly

”

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what group data with small effect sizes cannot convey, which is the core of our criti-cism. The authors ignore this and focus attention on the ADHD construct: “ADHD is a disorder by all standards of psychiatric nosology”. This is not something we questioned but is perhaps intended as a retort to Dehue and colleagues who –in line with Dehue’s earlier work- (Dehue, 2014) forwarded that people, and not brain scans can decide on what is a disorder (Dehue et al., 2017, p. 438). Although there is overlap between our response and that of Dehue et al., we did not raise this fundamental issue and we will not reflect on it here.

The authors add: “and our data support the idea that neuroanatomic brain abnor-malities, although subtle, are associated with the disorder” (Hoogman et al., 2017a, p. 440). We have not denied this and the statement is not untrue, however a (weak) association means that such brain “abnormalities” –or ‘differences’ as we prefer to call them- are far from unique to the ADHD group: they are not necessary nor sufficient for displaying such behaviors. Social adversity, such as lone parenthood and pover-ty are also –and more strongly- associated with ADHD-behaviors (Hjern, Weitoft, & Lindblad, 2010; Russell, Ford, Rosenberg, & Kelly, 2013), yet of course clinicians do not tell all those classified with ADHD and their parents that they are poor or divorced. The authors ignore the issue and continue with: “The strength of our work comes from combining data collected world wide” (Hoogman et al., 2017a, p. 440). This is a tenuous effort and one of the reasons we have praised them for their study, but it is not relevant to our criticism.

Then, the authors follow this up with a very relevant inaccuracy: “The observed brain abnormalities are heterogeneous and are likely to differ in individuals with ADHD” (Hoogman et al., 2017a). At first glance, this may seem to address our issue of heter-ogeneity in the research groups, but in fact it does not. Tindale calls such a strategy a “fallacy of diversion” (Tindale, 2007, p. 19) as it diverts attention from the issue we really address. In particular, this type of diversion is called a “Straw man”, which means a similar, but in fact different, argument is contested (Tait, 2009, p. 247). We posited that brain sizes in those with an ADHD classification differ, and –with low effect sizes- group differences do not apply to many with or without an ADHD classification. The authors avoid this issue and suggest that all those with ADHD have at least some type of abnormality while their data do not show this. On the contrary, many people in the ADHD group do not have any of the alleged brain “abnormalities”, while in the control group almost as many have these variations. In society at large, these variations are even expected to be far more common in “normal” people than in the ADHD-group.

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Then the authors add: “However, such heterogeneity at the individual level does not undermine the importance of effects at the group level”. This, again, is a diversion -another straw man- as it turns our argument around. We, nor Dehue et al. (2017), have stated that the individual heterogeneity undermines the importance of effects at the group level. We stated the opposite, that group level findings give little bearing for what we tell individuals and therefore contested their take home message that clinicians can tell all ADHD diagnosed individuals they have a disorder of the brain.

The authors continue with their false suggestion that those with an ADHD clas-sification have at least one abnormality: “The criticisms of small effect sizes raised by these letters imply that we should only use the term brain disorder when everyone with the disorder shows the same pattern of brain abnormalities”. We have not suggested nor implied the same pattern of brain abnormalities is a precondition for such a claim. However, if clinicians are told they can tell individual patients and parents that they have a disorder of the brain, we should at least be certain that those individuals have at least one outstanding difference from a typical brain. This is not what their own data show. Smaller brains are –again- not necessary or sufficient for an ADHD diagnosis, and similar “abnormalities” –by whatever standard- occur in those without an ADHD classification.

“Others are doing it too”: Ad-populum and authority appeals

The authors then state: “By that definition, no psychiatric disorder would be a brain dis-order”. However, we are discussing the authors’ conclusions and the empirical evidence in relation to ADHD and not other classifications of disorder. First, this seems to be a typical “Ad-Populum Fallacy”. Although it might be a popular habit to interpret brain associations as valid for concluding behavioral classifications are brain disorders, “truth is not simply a popularity poll” (Tait, 2009, p. 247). What other authors conclude about other psychiatric disorders and on what basis is not at stake. Second, if they would like to make comparisons to other psychiatric disorders, the taskforce of the DSM-5 une-quivocally stated: “it can be concluded that the field of psychiatry has thus far failed to identify a single neurobiological phenotypic marker or gene” (Kupfer, First, & Regier, 2002) and “not one laboratory marker has been found to be specific in identifying any of the DSM-defined syndromes” (Ibid, p. xviii). Blogsite Mad in America candidly retorted that with this, “Hoogman and colleagues themselves sum up the arguments of their critics nicely” (Simons, 2017). Indeed, there are no abnormalities unique –by whatever unclear standards a difference can be considered an abnormality- for those classified as having ADHD or any of the other DSM disorders.

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The merits of the study

Next, the authors comment: “Our critics further ignore that our findings fit well with other features of ADHD, such as the link between emotional dysregulation and the amygdala, and the links between altered reward processing and striatum, to name just a few” (Hoogman et al., 2017a, p. 440). We have not “ignored” those associations, but simply considered it irrelevant to the issue of unjust generalizations of small group findings to individuals we addressed. However, in case the authors feel we have insuf-ficiently acknowledged the value of their work, we do acknowledge that their study could indicate that the behavior of some individuals who are classified with ADHD could be related to maturational differences of brain parts associated with emotion regulation such as the amygdala. However, there are other theoretical possibilities as well: neuroplasticity, often seen in musicians (Hyde et al., 2009), indicates possible environmental influences on brain growth. Furthermore, prenatal alcohol exposure is also associated with inhibited brain growth (Archibald et al., 2001). This raises an important conceptual issue: should we include those prenatally exposed to alcohol when studying the brains of those classified with ADHD? Or should we in fact consider this a confounder that creates an artefact in group studies such as by Hoogman and colleagues? In other words, are we not diagnosing the wrong disorder in some cases and erroneously including those with affected brains due to prenatal exposure ADHD brain studies? For a discussion see for instance (Kable et al., 2016; Peadon & Elliott, 2010).

The authors end the third paragraph with: “Placing our findings within the broader scientific literature, as we did in our article, provides the context for our conclusion” (Hoogman et al., 2017a, p. 440). However, the broader scientific literature shows many statistical associations between ADHD behaviors and for instance divorce, poverty, parenting styles, lack of sleep, abuse, and much more (Richards, 2013; Russell, Ford, Rosenberg, & Kelly, 2013; te Meerman, Batstra, Grietens, & Frances, 2017; Thapar, Cooper, Eyre, & Langley, 2013). Hence, while we do acknowledge brain maturation is associated with the ADHD construct, we feel that the broader scientific context pro-vides no empirical ground whatsoever for dichotomizing the discussion by concluding that ADHD is a disorder of the brain.

Correlation and cause

In the fifth paragraph, the authors address our concerns about confusing correlation and causality. They write: “Although concluding that ADHD is a brain disorder, we did not claim that the neuroanatomic changes reported were causal. The cause of ADHD is complex, and genetic and environmental factors and their interplay will affect brain

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structure and function, which in turn will mediate effects on the clinical phenotype. As suggested, chronic altered patterns of behavior, such as persistent inattentiveness and hyperactivity impulsivity [sic], might also influence brain structure and function”. The authors acknowledge at least some of the etiological complexity of these behav-iors. And indeed, the authors have not explicitly claimed causality. However, we fear that just as influenza is called a viral infection, addressing the cause, the label “brain disorder” might be interpreted as implying causality. And again, as brain size is a mere weakly associated factor among many others, this is still a misleading suggestion just as a statement like “ADHD is a poverty disorder” would be.

Waiving responsibility

The authors end their paragraph as follows: “Finally, we cannot address concerns about press coverage; we discuss only the science reported in the paper and provide further rationale for our conclusions” (Hoogman et al., 2017a, p. 440). By this the authors evade responsibility for the fact that they generalized the group findings and also added this label of a “brain disorder” to their press release as Dehue et al., (2017) rightly assert. Furthermore, the main author emphasized the message that ADHD is just a brain dis-order and not related to, for instance, bad parenting- in an interview (Waterval, 2017). We fear that with this simplistic notion the authors facilitate others to overlook complex societal problems such as poverty, flaws in the educational system, divorce, intra-fa-milial violence, and social exclusion.

In the final paragraph, the authors also address the subject of stigma we brought up. “We wrote that understanding ADHD as a brain disorder might help reduce stigma, rather than increase it, a view shared by many others, including the US National Insti-tute of Mental Health and patient and service user advocacy groups”. The authors give no other argumentation than an ad-populum argument (Tait, 2009): “a view shared by many others” and an appeal to authority (Ruscio, 2006). In so far as one might indeed acknowledge that a mental health institute should have some authority in such matters, it must also be noted the NIMH does not have a particularly strong reputation as the US is often considered the “epicentre of the ’ADHD diagnosis’” (Erlandsson, Lundin, & Punzi, 2016, p. 3). The lack of control in the country with regard to market influences in healthcare, for instance by allowing direct to consumer advertising (Donohue, Cevasco, & Rosenthal, 2007), is notorious.

More importantly, it is unclear on which sources the authors base their claims about the presumed attitude of the NIMH. Hopefully, both the authors and the NIMH

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knowledge the wider scientific context that stresses the far from dichotomous relation between neuro-reductionism and stigma. There is empirical proof for bio-reductionistic explanations being a “mixed-blessing”. While they tend to alleviate guilt for problematic behaviour by suggesting lack of personal influence and responsibility, bio-reduction-istic explanations are likely to stigmatize in other areas. For instance, a meta-study of experimental research suggests bio-reductionistic explanations increase perceived dangerousness and prognostic pessimism (Kvaale, Gottdiener, & Haslam, 2013). A me-ta-study of correlational research found an additional likeliness for increased social distance (Kvaale, Haslam, & Gottdiener, 2013). For a recent meta-study, see Loughman & Haslam (2018).

The end justifies the means?

Finally, the authors seem to suggest that the end justifies the means: “We recognise that some disagree. However, we have no doubt that we all share the desire not to return to the relatively recent days when individuals with ADHD were dismissed as lazy, having bad parents, or being bad children. Understanding of ADHD as a brain disorder and clarifying the extent of its biological origins has helped direct focus away from moral judgments towards developing evidence-based treatment of the impairing symptoms of this disorder”. Of course, it is wrong to label children or their parents as being bad without knowing the reasons for the child’s behavior. However, as these ADHD-related behaviors are associated with many factors of which brain maturity is only one, the authors have simply jumped from one simplistic generalizing notion to another by suggesting these behaviors are caused by a brain disorder. Although this could theoretically explain attention problems and unruly behavior for a very small subgroup, it is simply wrong to tell this to individual children based on group data with small effect sizes.

Discussion

The suggestion that all those with an ADHD classification have “altered brains” as Hoogman et al. state, reifies ADHD and may lead to stigma. As the brain scans merely indicate very small group differences, the label of a brain disorder is likely to be mis-applied to many classified with ADHD. Although we and other authors have voiced concerns, the authors hardly acknowledge the critique. Their reply – like their original paper- contains several fallacies and additional rhetoric devices that deflect our argu-ments and those of other authors.

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It starts by avoiding the fact that group data are not applicable to many individuals with an ADHD classification, although the authors suggest they address this issue. However, the authors in fact only state that brain abnormalities differ across individuals diagnosed with ADHD, suggesting that all with an ADHD classification have at least some abnormalities. They conveniently avoid that such “abnormalities” occur almost just as often in the control group, and that far from everyone classified with ADHD has those alleged abnormalities. They then turn our argument around: they suggest we problematize the group level findings itself while in fact we problematize group level findings being applied to individuals.

The authors seem well aware that their generalizing conclusion, that all those with a classification have at least some kind of abnormality, is flawed. After avoiding this and reframing our objections, they continue with a mixture of ad-populum arguments and appeal to authority: some other psychiatric disorders with similar statistical associa-tions relating to the brain are also called brain disorders and others, such as the NIMH, share their view on stigma.

The Hoogman study has received severe criticism by the Blogsite Mad in Ameri-ca, and more can be said about the article. For instance, an important point that has not been discussed in relation to this paper –to our knowledge- is the use of refined phenotypes and normal controls, a common practice that results in sample bias and places an extra burden on generalizing the findings and applying them on an individual level. Furthermore, theoretically it is even possible that most children with an ADHD classification have bigger brains than those without, despite the fact that –on aver-age- research and control groups might show on average ‘normals’ have bigger brains. Such counterintuitive relations between group versus individual findings are studied by the ergodic theorem. Researchers from this school warn for the limitations of group studies and state that “we may need to reconsider how we communicate statistical principles to students and researchers” in relation to such studies (Fisher, Medaglia, & Jeronimus, 2018, p. E6107).

However, we do feel that the study also has merits. It is a very large study and collecting and analyzing so much data is an admirable scientific effort. And, as the au-thors address in their reply, the statistical associations of the delayed growth of, for instance, the amygdala could be relevant. Indeed, for some with an ADHD classification, a maturational lag might partly explain their propensity to have a different emotional response than others.

Nevertheless, rather than suggesting these people have a brain disorder, this could also lead to a conclusion that is far more respectful to the individual. Given that children

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differ in their physical and psychological development, we could and perhaps should call into question society’s problems to accommodate to children’s idiosyncratic de-velopmental pathways.

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Chapter 3

Based on:

Te Meerman, S., Batstra, L., Hoekstra, R., Freedman, J., Grietens, H. (2018). Biomedical Bias in academic textbooks. Do authors report the limitations of brain-anatomical studies? (Submitted).

Biomedical bias in academic textbooks

When authors do not to mention the limitations of ADHD

brain-anatomical studies

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Abstract

Studies of brain size of those classified with ADHD appear to reveal smaller brains when compared to ‘normal’ children. Yet, what does this mean? Even with the use of rigorously screened subgroups, so-called ‘refined phenotypes’ and ’well-controls’, these studies show only group differences between children with and without an ADHD classification. Hence, many with ADHD do not have smaller brains while many without ADHD have relatively small brains. This study discusses academic textbooks used at universities in the Netherlands and reveals that textbook authors often generalize and rarely inform future professionals about the limitations of brain-anatomical studies into ADHD.

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Introduction

ADHD is one of 400+ disorders that are defined and described in the DSM-5, the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association 2013). According to the DSM-5, a ‘diagnosis’ is possible if a child meets six out of nine criteria for hyperactivity/impulsivity such as ‘often fidgets with or taps hands or feet’, ‘often leaves seat’, and/or six out of nine criteria for inattention, including ‘often loses things necessary for task or activities’. In addition, children have to meet additional criteria, such as exhibiting these behaviors before age 12 and for a duration of at least six months (American Psychiatric Association, 2013). Furthermore, the behaviors must interfere with social and academic functioning.

In the research agenda for the DSM-5, the authors clearly stated that ‘the field of psychiatry has thus far failed to indicate a single neurobiological cause for any of the mental disorders’ (Kupfer, First, & Regier, 2008, p. 33). After many years of expensive brain-studies, ADHD has proven to be no exception; ‘No single risk factor explains ADHD. Both inherited and non-inherited factors contribute and their effects are inter-dependent’ (Thapar, Cooper, Eyre and Langley 2013, p. 3). Despite several associated factors and despite the clear cultural underpinnings of what we perceive as (ab)normal behavior (Freedman & Honkasilta, 2017), the authors of the DSM-5 have decided to classify ADHD as a ‘neurodevelopmental disorder’.

Many scholars strengthen the image of ADHD as a discrete brain disorder with questionable claims. For example, Russel Barkley, in a 2.5 hour video addressing parents of children classified with ADHD, states that in those who have inherited the disorder (about 2/3 according to Barkley) several brain regions are slightly smaller (3-10%) and ‘cause’ the disorder. However, these differences are ‘not enough to use brain imaging to diagnose this disorder’ (Barkley, 2013, 56th minute). Barkley’s explanation is pecu-liar: how could they have discovered these differences other than by brain imaging? The differences are in fact not too small as one might assume from Barkley’s descrip-tion, but rather too inconsistent as the effect size between brain size and behavior is small – denoting the overlap between the case and the control groups. Such ‘lack of group-to-individual generalizability’ (Fisher et al., 2018) is the real reason that ‘no brain imaging technique (…) is of any value for diagnosis’ as Barkley states in the same video. In a similar vein, much is made from the largest ADHD case-control study to date by Hoogman et al. (Hoogman et al., 2017). The study indicated, on average, a small delayed growth in 5 subcortical brain areas, while one area also appeared to be slightly bigger in individuals diagnosed with ADHD. These mean differences disappeared in adulthood. However, far-reaching claims were made from the results of this study, such

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as: ‘the data from our highly powered analysis confirm that patients with ADHD do have altered brains and therefore that ADHD is a disorder of the brain. This message is clear for clinicians to convey to parents and patients’ (Hoogman et al. 2017, 316). Their con-clusion incited a storm of critique (Batstra, te Meerman, Conners, and Frances, 2017; Bejerot, Nilsonne and Humble, 2017; Dehue et al., 2017), and a petition to withdraw the study altogether was initiated by the blogsite Mad In America.

The study was not withdrawn nor were changes made to the conclusions, which were reported in many newspapers worldwide. Readers, and particularly laypersons, may have difficulty understanding the lack of group to individual generalizability. Many in the group of those classified with ADHD have a larger brain than average, and many in the control group have a smaller-than-average brain. Secondly, both case- and con-trol-groups often use rigorously screened individuals, called ‘refined-phenotypes’ (Holmes et al., 2000) and extremely ‘well controls’ (Horga, Kaur and Peterson, 2014), who hardly represent their respective populations (for a discussion see also te Meer-man, Batstra, Grietens and Frances (2017). Thirdly, brain maturation is a ‘moving de-velopmental target’ (Hyman, 2010) as children develop at their own rate. Mean differ-ences disappear because brain growth can catch up later in life (Hoogman et al., 2017; Shaw et al., 2007). Fourthly, a correlation between ADHD related behaviors and any (brain) measure does not necessarily imply causality. Neuroplasticity, or the fact that brain structure and function change as a result of interaction with the environment is a well-known phenomenon, seen in musicians for instance (Hyde et al., 2009; Münte, Altenmüller and Jäncke, 2002). On the downside, poverty (Noble et al., 2015) and maltreatment in children (Riem, Alink, Out, Van Ijzendoorn and Bakermans-Kranen-burg, 2015) are negatively associated with brain size. Lastly, even if differences would ever be found on the individual level, these would not necessarily imply a disorder. If a particular brain-characteristic will be discovered for homosexuality, does this mean we should add it to the DSM again after it was removed in the DSM-III? (Dehue, 2014). Brain scans might help studying behavior, but it is ultimately human beings that decide which behaviors are considered (in)appropriate (Dehue et al., 2017; Altermark, 2013).

Journalists (Gonon, Konsman, Cohen, Boraud and Boutron, 2012) and research-ers (Gonon, Bezard and Boraud, 2011) may have mutual benefits for simplifying and overstating findings. These benefits include standing out amidst the fierce competition for publications and readership amongst authors, scientific journals and newspapers? However, there is another, perhaps more daunting question: are academically trained healthcare professionals, researchers and journalists sufficiently aware of the compli-cated relation between individual and group?

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This study analyses how authors of academic textbooks disseminate critical infor-mation about case-control studies into brain anatomy of those classified with ADHD. We aim to answer the following two questions relating to group-to-individual and sam-ple-to-population generalizations: first: are group outcomes rightly presented as mere averages with little predictive value for individuals? And second, are students reading these textbooks presented with additional information regarding well-controls and refined phenotypes?

Method

Data Selection

The Netherlands has 18 public universities, ten of which have a wide academic orien-tation including medical and behavioral scientific bachelor’s and master’s programs. The latter are included in this study. The remaining universities are theological (4), (primarily) technical (2), and agricultural (1). (Source: Association of universities in the Netherlands http://www.vsnu.nl). Study guides of medical and behavioral science pro-grams were searched for the following subjects: psychopathology, (biological, cogni-tive, clinical, biological) psychology, psychiatry, psychiatric disorders, diagnostics and behavioral problems. The glossaries of the prescribed textbooks were then searched for the keywords ‘Attention Deficit Hyperactivity Disorder’ or ADHD. If the keyword was found, we checked if the book contained a (sub)section, paragraph or chapter on ADHD. Forty-three books were selected for analysis. We searched for the most recent versions up to January 2016. With this approach called purposeful sampling (Coyne, 1997), we selected the most up-to-date academic textbooks used by universities to educate future healthcare professionals.

Analytic framework and coding

Every section on ADHD was scanned, converted into text with optical character rec-ognition software (OCR) and imported to Atlas TI, an application for qualitative data analysis. Next, all claims relating to empirical research concerned with volumetric meas-ures of brains of subjects with ADHD were classified into five categories:

1. A non-generalizing claim, containing ‘hedged’ positions on the generalizations

Hedging can be considered as the ‘expression of tentativeness’ (Hyland, 1996, p. 433). Although hedges can bring unwanted ‘fuzziness’ (Crompton, 1997, p. 272), in the case of group-to-individual generalizations we argue hedges are necessary to avoid logical errors. A ‘classic’ way to hedge a generalization is by using ‘tend to’ (Black, Mecsnober,

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Thuss and Tommassen, 2015, p. 30), other possibilities are for instance ‘to contribute’ and ‘to cause’, the latter being more definite (Black et al., 2015). So-called ‘vague quan-tifiers’ (Bradburn and Miles, 1979), e.g. ‘a number of, a minority, a few, several, often’, etc. (Hamp-Lyons & Heasley, 2006, p. 65), are also considered as hedges. Research outcomes referred to as ‘group findings’ or ‘means/averages’ are seen as hedges as well. Other hedges we considered as relevant to generalizations are words used to express ‘a component of tentativeness or possibility’, for instance may, argue, believe, or hypothesis. Particularly words like hypothesis, or theory, express ‘epistemic modality’ (Varttala, 1999, p. 183) well in our view.

2. A generalizing claim, stating that all classified with ADHD share a certain anatomical feature without hedges to clarify this.

A neuro-anatomical finding without a hedge, was classified as generalizing. An example of this is: ‘several brain regions, including the prefrontal cortex, are smaller in children with ADHD than in children without the diagnosis’ (Bukatko and Daehler, 2012, p. 300). Note that these claims might contain hedges that do not relate to the generali-zation but to something else such as the number of researchers that allegedly support the claim. For instance: ‘All structural magnetic resonance imaging (MRI) studies that measured frontal regions reported reduced volume in PFC, and several studies re-ported volume reductions in the caudate nucleus of the basal ganglia, a structure with close connections to dorsolateral and ventrolateral PFC’ (Willcutt, 2010, p. 397). This sentence is classified as generalizing, and the reference to ‘all’, versus ‘several’ studies is not considered in this decision as it does not refer to brain-anatomy.

3. An ambiguous claim, in case of uncertainty about the claim being a generalization, or uncertainty about the claim referring to anatomy.

These aforementioned hedges and quantifiers served as ‘sensitizing concepts’, as it is ‘probably impossible to form an exhaustive taxonomy of potential lexical hedging devices in English’ (Varttala, 1999, p. 183). There are phrases in which no such words are used, yet the phrases still do not seem to be full out generalizations. For example: ‘volume of the frontal, striatal, and temporal lobe region has been found to be directly related

to inhibition’ (Wicks-Nelson, 2015, p. 232). ‘Directly related’ is considered ambiguous

because it seems to describe a stronger relation than the mere statistical association it actually refers to. Other phrases that we considered to be ambiguous are for in-stance those that are clearly generalizing, yet the authors do not make explicit whether brain-anatomy, -physiology or -chemistry, is implied.