Pérez-Álvarez, M. (2017) - The Four Causes of ADHD. Aristotle in The Classroom.
Pérez-Álvarez, M. (2017) - The Four Causes of ADHD. Aristotle in The Classroom.
The controversy cannot be resolved in empirical scientific labels” for abolition of the DSM/ICD, also on the basis of its lack
terms, on the plane of facts, as if the facts spoke for themselves, of validity (Timimi, 2014).
which is where it now stands. A metascientific, philosophical The DSM may have improved reliability with regard to
assessment is required, with an ontological scope asking what consistency among those who apply it, but validity is something
ADHD is, and epistemological scope asking how science itself else: its correctness and robustness for making a diagnosis.
knows and molds what has ended up as the actual “ADHD.” A Marcia Angell, ex-director of the New England Journal of
This approach is based on a critical position (not ingenuous) Medicine says about psychiatric diagnoses:
concerning the impressive neuroscientific evidence claimed
If nearly all physicians agreed that freckles were a sign of cancer,
as support for the established concept. Such an approach is
the diagnosis would be “reliable,” but not valid. The problem with
unthinkable for those who assume the standard concept, given the DSM is that in all of its editions, it has simply reflected the
their amazement that anyone would deny it. Without denying opinions of its writers (Angell, 2011).
their data, light will be shed on the rhetoric and metaphysics that
sustain it. If the rhetoric suggests more persuasive than truthful The diagnostic criteria are established by consensual opinion.
reasoning, metaphysics refers here to implicit assumptions about But the consensus reveals that there is no evidence. If there had
genetics and the brain which go beyond what genomics and been scientific evidence, a consensus would not be necessary.
brain connectomics really permit. The article has two parts. The What more can be said when many of the experts in the
first concentrates on revealing the rhetoric and metaphysics of consensus are plagued with conflicts of interest and a laboratory
ADHD neuroscience. The second develops the metascientific in the field funds the meetings (Kooij et al., 2010)? These
approach beyond the usual controversy – whether or not it statements of consensus are upheld by the superabundant
exists – attempting instead to understand what it is that exists bibliography on ADHD, like someone who grabs hold of a
and how it came to be that way. lamppost to keep standing up without using it to see by. One
consensus cites over 500 references (Barkley, 2002), like bulk
evidence by accumulation, without reviewing it to see if it really
RHETORIC AND METAPHYSICS OF THE is accumulated knowledge. Another uses 320 references to back
ADHD NEUROSCIENCE its validity (Kooij et al., 2010), without really being clear, firm
evidence. The statements of consensus assume a subtly deceitful
Instead of uncritically assuming the standard ADHD concept as if argument consisting of citing quantities of studies, without any of
scientific evidence required it, we review its consistency, focusing them being conclusive, which in the end are taken as convergent,
on the rhetoric and metaphysics on which it is largely based. promising support. A collection of promising support turns
Its three basic pillars, diagnosis, genetics, and neurobiology, are into evidence. For example, after recognizing the challenge of a
specifically reviewed. “diagnosis being based on reported symptoms alone; there are
no biological tests” (Thapar and Cooper, 2016, p. 1241), ADHD
How to Make a Diagnosis with Fallacious becomes in the conclusions a “robust and consistent across design
Reasoning (with Tautologies) type and sample. There are established assessment methods”
Everything begins and has its basis in the diagnostic criteria (Thapar and Cooper, 2016, p. 1247).
of the Diagnostic and Statistical Manual of Mental Disorders The truth is that the diagnosis of ADHD is established,
(DSM; American Psychiatric Association, 2013). For the case in but based on fallacious reasoning, typically two (Tait, 2009):
hand, it does not matter whether the International Classification the Affirming the Consequent Fallacy and Begging the Question
of Diseases (ICD; World Health Organization, 1992) is used. Fallacy. According to the affirming the consequent fallacy, if
It is the DSM/ICD diagnostic systems themselves which are the child “often fails to give close attention to details,” “often
questioned as a valid basis for making diagnoses. Suffice it to cite fidgets with or taps hands or squirms in seat”. . . (statements
in this respect the critical position of two international psychiatric in the DSM-5 criteria) then he has ADHD. According to the
organizations. The first is the statement by Thomas Insel on April begging the question fallacy it is already known that the child
29, 2013, as Director of the National Institute of Mental Health has ADHD because he/she “often fails to give close attention to
(NIMH), that the Institute was not going to use the DSM-5 details,” “often fidgets with or taps hands or squirms in seat,”
criteria at the point of being released, as in fact it was in May the and so on. The child does not pay attention and fidgets because
same year, due to its lack of validity. As Insel (2013) states: he/she has ADHD and he/she has ADHD because he does not
pay attention and fidgets. The symptoms are the guarantee of
The strength of each of the editions of DSM has been “reliability” – the diagnostic category, which in turn is invoked to explain
each edition has ensured that clinicians use the same terms in the symptoms in an endless loop (Brinkmann, 2014b, p. 128).
the same ways. The weakness is its lack of validity. Unlike our The diagnostic category is molded in the process of making the
definitions of ischemic heart disease, lymphoma, or AIDS, the
diagnosis of the case. In turn, the diagnosis of the case sustains
DSM diagnoses are based on a consensus about clusters of clinical
the clinical category without other independent tests or genetic
symptoms, not any objective laboratory measure.
evidence or neurobiology of diagnostic value as discussed below.
The Critical Psychiatry Network, an organization of critical The Non-Sequitur Fallacy, which assumes that if the medication
psychiatrists who focus on a biomedical approach in psychiatry, (typically stimulants) reduces hyperactivity, the hyperactivity is a
has promoted a campaign under the slogan, “No more psychiatric symptom and ADHD is a disorder, also commonly occurs. But
one does not follow the other, not logically and not empirically, The reviews show two things: the non-existence of real
since stimulants produce the same effect whether you have molecular genetic evidence and the persistence in their
ADHD or not. affirmation. We refer here to reviews by authors who are not
The diagnosis is based on fallacious reasoning, not on precisely critical of the genetic perspective, but as scientists are
clinical tests as would be expected in view of how sure the compelled to recognize what there is, not without their rhetoric.
affirmations are. Based on DSM/ICD diagnosis, a series of Thus Cortese, after reviewing the convergence of different
objective, complementary, and supposedly confirmatory tests approaches (none conclusive), refers to the future, “It is expected
are being studied. Among the most objective is the Test that future research will reveal similarly exciting convergent
of Variables of Attention (TOVA), a continuous performance findings” (Cortese, 2012, p. 430). Thapar and Cooper (2016,
test (CPT) (Fried et al., 2014; Rodríguez et al., 2016). The p. 1242) recognize that “ADHD-associated genomic variants are
TOVA presents a computerized task which evaluates omissions, non-specific.” A study by Thapar himself and others found that
commissions, reaction times, variability, and post-commission 14% of children diagnosed with ADHD had a rare chromosomic
response times. Apart from the scant ecological validity as a task difference known as “copy number variants” compared to 7% of
little representative of daily situations, the biggest problem with children not diagnosed with ADHD who also had it (Williams
the TOVA is its inadequate specificity, leading to false positives et al., 2010). Although the finding was magnified by emphasizing
and false negatives: children not ADHD who “fail” and ADHD double the chromosome rarity in ADHD (13.95% over 7.4%)
children who do well (Zelnik et al., 2012; Fried et al., 2014). and was even taken as “direct evidence that ADHD is a genetic
The problem of ecological validity can be reduced with virtual disorder” (Wellcome Trust, 2010), the truth is that 86% of
reality tests. However, up to now support is limited (Neguţ et al., children with ADHD did not have this rarity and 7% of those
2016). Virtual reality tests, even though they show sensitivity, also without ADHD did.
lack diagnostic specificity due to variability and overlapping of Tarver et al. (2014, p. 763) likewise acknowledge that
the measures (Areces et al., 2016; Neguţ et al., 2016). In fact, the “Genomic-wide searches have yet to identify a single candidate
TOVA, whether or not in virtual reality, is applied to children gene,” although they add that “This is probably due to insufficient
already differentiated by the DSM diagnostic criteria: children sample sizes to date.” However, as suggested by Sonuga-Barke
with ADHD or without ADHD, not as a diagnostic test itself. (2010, p. 113), “We are now using larger and larger samples of
These tests can be useful for evaluating attention skills, precision patients to demonstrate smaller and smaller molecular genetic
or reaction times, which may be relevant in themselves without main effects.” As Thapar et al. (2013) admit in their conclusions:
presupposing ADHD. They measure what they measure, but it
could not be said that the ADHD is measured. The genetic risks implicated in ADHD generally tend to have
On the basis of the self-interested consensus that may be small effect sizes or be rare and often increase risk of many
assumed from declared conflicts of interest and sponsorship of other types of psychopathology. Thus, they cannot be used for
commissioned work (Barkley, 2002; Kooij et al., 2010; Faraone prediction, genetic testing or diagnostic purposes beyond what is
et al., 2015), inconsistent conclusions (Thapar and Cooper, 2016) predicted by a family history” (Thapar et al., 2013, p. 3).
and fallacious reasoning (Tait, 2009), surprisingly, or perhaps
not, the sentence, as dogmatic as antiscientific, is that doubting Gallo and Posner (2016) also recognize the scant genetic
ADHD would be like “declaring the Earth flat, the laws of evidence, but not without inconsistent rhetoric between what
gravity debatable, and the periodic table in chemistry a fraud” they affirm and what they really find. They state that “ADHD is
(Barkley, 2002, p. 90). According to Timimi et al. (2004) in a highly heritable disorder” (Gallo and Posner, 2016, p. 558) to
his comment on this consensus, “It is regrettable that they continue by saying, “Despite substantial evidence for a genetic
wish to close down debate prematurely and in a way not origin of ADHD, specific genes or sets of genes causally linked
becoming of academics. The evidence shows that the debate to the disorder have yet to be discovered” (p. 559). This rhetoric
is far from over” (Timimi et al., 2004, p. 63). Even without of inconsistencies continues when they say, “Substantial progress
assuming intentionality due to conflicts of interest in establishing has been made in clarifying the complex genetic architecture of
a consensus, its unintentional influence through default brain- ADHD, yet the mismatch between the high heritability estimates
centered thinking cannot be discarded, as mentioned further and weak associations between ADHD and specific genetic
below. markers is puzzling” (p. 560). After all, they feel obliged to admit
that “Although candidate genes and neuro transmitter systems
have been implicated in ADHD, genome-wide associations
How to Make Genetics Seem Like between ADHD and individual genetic variants have yet to be
Evidence (with Ambiguities) found” (p. 563).
Beyond the diagnosis, one fundamental aspect of the ADHD The claimed heritability in ADHD is based on statistical data,
rhetoric is its consideration as a highly inheritable genetic not on genetic data as such. It often refers to ADHD running in
disorder (Tarver et al., 2014; Gallo and Posner, 2016; Thapar and the family and to the higher coincidence in monozygotic than in
Cooper, 2016). If the diagnosis is, as it is, based on a consensus dizygotic twins. Many things run in the family, such as an accent
dominated by conflicts of interest more than on tests, lacking in in language or religion without therefore being genetic. Identical
validity and more than anything else tautological, it is going to be twins share more environmental conditions than non-identical
hard for there to be specific genetic and neurobiological bases. twins so this and other “twin method” reasons do not enable the
genetic-environmental knot to be unraveled, much less talk about following a “program” or “code” for some behavioral trait?
percentages (Joseph, 2015). What specific interactions are in play if not even the ADHD
Attention-Deficit/Hyperactivity Disorder may be hereditary, phenotype is well-defined? Endophenotypes supposedly closer to
but not therefore genetic. Of the four ways of inheritance, genetic influences, such as reaction times, response inhibition
genetic, epigenetic, behavioral, and cultural (Jablonka and Lamb, or working memory, are also discussed. But research shows
2005), genetic is probably the least expectable in transmitting that endophenotypes lack specificity for the ADHD phenotype
ADHD-type behavioral traits. It is not among the functions itself (Gallo and Posner, 2016). Endophenotypes are expected
of genes to generate behavioral traits. The metaphors “code” to “increase statistical power to identify relevant associations
and “program” have seduced the imagination of scientists, between genes and neurobiological mechanisms,” but they
professionals and people in general so they sound like genes do remain “a promising route” (Gallo and Posner, 2016, p. 560); the
more than they really do. As development resources, more than new promise, not cold hard findings.
deterministic “programs,” everything related to genes depends The second argument says the gene–environment or biology-
on the context, from cellular, extracellular, embryonal, and culture dichotomy itself loses sense in genomic times (Keller,
intrauterine to perinatal and social, from womb to tomb. Recent 2012, 2014). It no longer makes sense to talk about interaction
research in epigenetic and genomic plasticity causes genes to as of two preexisting things that enter into interaction
be reconceived beyond their traditional conception as agents (gene–environment) and much less percentages of heritability.
instructing traits (González-Pardo and Pérez Álvarez, 2013). The
new conception means a change in genes to genome (including What research in genomics has shown is that biology itself is
constituted by those interactions, and is so constituted at every
non-codifying matter) and of action to reaction referred to
level, even at the level of genetics. Indeed, one might say that
genome reactivity as a dynamic system “exquisitely sensitive” to what makes a molecule—any molecule—biological is precisely
signals in both the organism’s immediate intracellular context its capacity to sense and react to its environment (Keller, 2012,
and external environment as a whole (Keller, 2014, p. 2428). The p. 139).
genome mediates adaptation and response to the environment;
it does not cause response and adaptive action. As Keller (2014, The reactivity inherent in biological systems enables
p. 2427) says: development to be understood as a set of cells with their multiple
molecules, functioning in mutual concert for a certain result, not
In addition to providing information required for building and
thereby executing a central program (Fisher et al., 2011, p. 74).
maintaining an organism, the genome also provides a vast
amount of information enabling it to adapt and respond to the
According to this conception of development, it is hard to argue
environment in which it finds itself. the conception of genes as “instructor agents” or “instructions” of
traits which some day, for example, at school age, or in adult life,
For lack of firm evidence, the defense of ADHD genetics will be “expressed” as ADHD behavior. What persistent genetic
at all costs is served by rhetoric, with two formulas, one research really underlines is the decisive role of environment in
consisting of saying that ADHD is a “heterogeneous,” the development of mental disorders (Sonuga-Barke, 2010). It
“multifactorial,” or “complex” disorder, and the other no longer makes sense to talk about percentages. Nature itself,
emphasizing “gene–environment interaction.” constituting organisms in their continuous interactions, places
Talking about “heterogeneous,” “multifactorial,” or “complex” us beyond typical topical percentages.
in psychiatry is synonymous today with lack of specific genetic The tangled nature of genetics and the environment, even in
evidence (Joseph, 2009, p. 72). These expressions sneakily suggest genetic conditions such as diabetes, keeps heritability from being
the genetic condition of a disorder by implying a complicated unpacked, or from there being any interest in doing so (Chaufan,
involvement of numerous genes, with no more evidence than thin 2008). To begin with, heritability in its technical sense is an
correlational associations. But an association is not causation. For attribute of a population, not of individual traits. Furthermore,
lack of precise and specific evidence, the genetic argument of organisms and phenotypes are non-additive products of genes, in
ADHD becomes a loop. As Pittelli (2002) says when commenting an historic sequence of development environments and chance
on a meta-analysis, “The argument that ADHD is “mediated by events, so their interdependence impedes any empirical or
many genes acting in concert” is rather circular in that it is based statistical quantification of the “ingredients” in this mixture.
primarily on the complete failure of molecular genetic studies Empirically, the genetic-environmental percentage could be
to find such genes and replicate those findings” (Pittelli, 2002). established in breeding animals and in agriculture, from which
ADHD is still “complex” even without thinking about genes. statistical techniques are derived, enabling quantification that
The commonly referred to gene–environment interaction also makes sense under controlled conditions. But statistical analyses
insinuates that there is more than there really is: supposed (typically analysis of variance) are not analyses of causes, and
genes interacting with the environment. The formula here is therefore do not permit understanding what caused a disorder
sibylline, as deceitful as it is hard to contradict. Nevertheless, two in an individual (Chaufan, 2008, pp. 21, 35). The problem of
arguments must be considered. heritability is not resolved with larger samples (Chaufan, 2008,
In the first place, if the ADHD genes are not identified, p. 37), as in the promise of the overused genetic perspective
and they are not, then it is going to be hard to talk sensibly (Thapar et al., 2013, p. 7; Tarver et al., 2014, p. 763; Gallo and
about their interaction. What are we talking about when we Posner, 2016, pp. 559–560). It has already seen in schizophrenia,
discuss interaction? Are the genes active agents able to interact a clinically well-established disorder (Pérez-Álvarez et al., 2016),
unlike ADHD, how larger samples of thousands of patients do 2012, p. 2) and in general, “findings from neurobiological
not lead to stronger genetic associations (Ross, 2016; Sekar et al., research do not have a direct application in daily clinical practice,”
2016). (Cortese, 2012, p. 9).
While the concept of hereditability is confusing at least, for The variability and inconsistency of the findings may be
understanding the category, it lacks application to individuals. reflecting the heterogeneity and lack of entity of the so-called
Even if there were “ADHD genes,” predisposition does not imply “ADHD.” As Beare et al. (2016) say of their own findings:
availability of the phenotype, according to epigenetic chance
(González-Pardo and Pérez Álvarez, 2013; Dillon and Craven, Attention-Deficit/Hyperactivity Disorder is an extremely
heterogeneous disorder, with few common findings across
2014; Mukherjee, 2016).
studies. The variability in findings resulting from methodological
Quantification of heritability has little to offer for decisions in this study illustrates the caution that must be taken
understanding ADHD. According to Chaufan (2008), the in relating network differences to underlying neurobiology.
genetic emphasis may even be harmful to the extent that it
diverts public attention and research funding from the social Neurobiological research is moving from focusing on
determinants, which are decisive in the end, even in genetic brain areas toward dysfunctions in circuits distributed
conditions such as diabetes. There may be more science policy throughout the brain, leading to the new concept of
than science itself in pursuance of genetics, concerning interests “pathoconnectomics” (Cao et al., 2015). Pathoconnectomics
and status of the authors involved, beginning with the hegemony assumes that major psychiatric disorders (e.g., ADHD) involve
of the biomedical model. abnormalities of brain networks and that understanding
the aberrant organization of brain networks is critical for
understanding these brain disorders (Cao et al., 2015, p. 2802).
How to Make Causes Out of Correlations Connectomics combines the study of structural connectivity
and Correlates (by Calling Them between regions and functional connectivity consisting of
“Bases”) synchronies of remote neuronal activities (Cao et al., 2015).
A critical position must also be adopted regarding ADHD as A set of sophisticated mathematical techniques and functional
a disorder of neurodevelopment, as presented in its standard magnetic resonance imaging along with the more conventional
packaging, instead of simply assuming it without further electroencephalography/hemoencephalography and infrared
consideration. The literature in favor of the neurodevelopment spectroscopy, enable a new topology and cartography of the
approach is undeniably enormous and the amount of data brain (Rodríguez et al., 2011; Cao et al., 2015).
overwhelming. However, the data do not speak for themselves, Both regional and general wiring impairments have been
but by the perspective in which they are taken. In an uncritical found in ADHD. Among the regional impairments, are
neurodevelopment perspective which places the brain under volumetric reductions in the basal ganglia and abnormalities in
spotlights as if it were the place the keys to ADHD should be cortical thickness in frontal and parietotemporal brain regions
found, data providing feedback for this search are not lacking (Gallo and Posner, 2016, p. 556). In functional connectivity,
nor will they be. Things always happen in the brain related to the one “of the more commonly reported abnormalities is reduced
activities of organisms. It would be of concern if it were not. As connectivity within the default mode network (DMN)” (Gallo
more and more sensitive measurements of the brain’s functioning and Posner, 2016, p. 557). DMN is a set of areas in the brain
become available, neural correlates of the activities selected are described in 2001 which is associated with mental processes at
found more easily. Another thing is the relevance of the findings rest or wandering when one is not busy in some concrete external
and the meaning of the correlation: causal and in what direction, task (Raichle, 2015).
or artefactual due to third factors involved. The hypothesis is that persistent activity of the DMN can
A brain-centered approach like the one predominating interfere with the cognitive control network (CCN) involved
research and propagated for ADHD incurs easily in two biases: in executive functions. Another hypothesis is that individuals
a tunnel effect in which one looks in only one direction and with ADHD may have weaker connectivity in DMN when at
a zoom effect which magnifies what is seen. A new panoramic rest, suggesting immaturity and atypical development. The two
and even telescopic approach is necessary which puts the brain networks, DMN/CCN, seem to work in opposite directions in
in its place: in the body of a subject who behaves within a attentional tasks, “As attentional demands increase, activation
context and who sees from a distance what is known without of the CCN increases, whereas DMN activation decreases;
becoming “stuck” to the data. Without doubt, more and more conversely, during periods of internally focused cognitions,
is known about the brain due to the new technologies and activation in the CCN is reduced, and DMN activation increases”
concepts of its functioning, but not because of this is more (Gallo and Posner, 2016, p. 558). Interplay of correlative
known about ADHD, as it has been demonstrated that in spite transitions would mean normal, mature and typical development.
of everything, its status is still controversial. There is a mountain Four considerations must be made before or instead of taking
of data, that is, an enormous amount has been accumulated, but the neurodevelopment brain-centered perspective automatically,
it cannot be said that it is really the solid, accumulative scientific by default, as if there were no other option.
knowledge with which research progresses. After all, there are no In the first place, the neurodevelopment approach leads to
“diagnostic neurobiological markers” (Thapar and Cooper, 2016, establishing a dichotomy between typical, normal or mature
p. 1243), the “underlying mechanisms” are unknown (Cortese, development and atypical, abnormal or immature development
defining a psychiatric disorder (Cao et al., 2015). This dichotomy Beyond the ADHD cortex causal model assumed by
could be induced by the logic of the approach itself more than “structural equations” (Rodríguez et al., 2016), the real causation
anything else, with its tunnel and zoom effects, selecting and seems to be from the behaviors to the brain (Rodríguez et al.,
magnifying some things and leaving others out. If individuals 2011).
are selected for certain more or less conspicuous characteristics Convergent evidence, to use the rhetoric in vogue, is found
and taken to extremes with respect to others who do not have in the abundant literature showing that ADHD behavior can
them, more or less associated neuronal correlates could appear be modified by exercises and behavioral training, which is
depending on how well defined those characteristics are. Take hardly understandable if it has a neurological cause and genetic
the conditions of being a taxi driver or a non-taxi driver, or a origin. Furthermore, normalization of the brain, which is usually
musician or non-musician. As studies show, the brains of taxi referred to after medication with stimulants (Rubia et al., 2014,
drivers and musicians show alterations in specific areas and p. 529), could be due to its effect on behavior, and it would
connections associated with their activities compared to those really be the change in behavior that is promoting change in
who are not (Maguire et al., 2006; Hyde et al., 2009). Now it could the brain, something suggested by the authors themselves when
be said that taxi drivers and musicians develop an “atypical” brain they cite a study in which 4 weeks of training in juggling
compared to non-taxi drivers and non-musicians, who after all, induced relevant changes in the brain (Rubia et al., 2014,
make up the majority of the population, and would develop a p. 529).
“typical” brain. There might also be subtypes: Subtype pianist and A last consideration concerns how the neurodevelopment
subtype violinist and who knows whether subtypes of London, model reflects the problem of ADHD in real life in the brain
Bombay or small-town taxi drivers. space, both scientific related to its entity, and ethical referring
In fact, as a second consideration, the supposed “neuronal to the evaluation involved. Thus the reviews still warn of
bases” for ADHD do not consist of anything but correlations continuous ambiguities and inconsistencies, no matter how
and correlates. They are “associations,” which however, implicitly interested they are in finding accumulated knowledge (Rubia
suggest neuronal causes as “bases” (Rubia et al., 2014, p. 532), et al., 2014, p. 523; Gallo and Posner, 2016, pp. 558, 560). These
when not explicitly (Gallo and Posner, 2016; Rodríguez et al., neurobiological ambiguities and inconsistencies probably reflect
2016). Thus, Gallo and Posner (2016), after warning about the the very heterogeneity of “ADHD.”
“limitations of correlational research” (p. 561) and “caution in The brain space also reflects ethical evaluation of ADHD,
imputing causality” (p. 563), in the end are thinking about describing the “findings” as volumetric or connectivity
mapping “causal pathways from genes to neural circuits to “reductions,” white matter “deficits,” “retarded” maturity,
symptoms” (p. 564). Rodríguez et al. (2016, p. 8), on the “abnormality” or “atypical” development. Transferring
other hand, argue for a “causal model” based on explicit normative values to the brain incurs in three problems.
assumptions required by the “structural equation modeling” First, components which are no more than normative values
which they use when they refer to the “direct effect” of cortex are neutralized as natural. Second, maturity is linked to
activation of variables measured by the TOVA as an ADHD age and environment in a disease. Finally, maturity itself is
index. misunderstood as an autonomous process independent of the
As a third consideration, in a discussion of causal directions, setting, ignoring that “maturation” is not merely a question of
it would be more coherent, both in conceptual terms based age, but also of what occurs during one’s life.
on brain plasticity and empirical terms related to correlations
and correlates found, to argue for the opposite hypothesis, Conclusion
that behaviors themselves are the causes of the correlates A critical review of the standard conception of ADHD
or neuron “alterations” found. It would be more coherent has underlined the tautological (rhetorical) reasoning and
to understand cerebral variations as “dependent variables” of assumptions implicit in the causal-explanatory role of the
the activities that organisms carry out in their environment genome and the brain (metaphysics) which impregnate it. It is
than as causal “independent variables.” The brain changes and understood that this conception cannot be taken uncritically as
adapts in line with an organism’s activities depending on the a starting point. Although this review may seem “demolishing,”
requirements of the environment. The neuron correlates or it is not everything. Up to here the criticism has been negative
brain “alterations” of the taxi drivers and musicians are not (“demolishing”), not reconstructive (explanatory) of what there
the cause of driving taxis or playing the piano or the violin. is. After all, ADHD does exist. It is real. Negationist critics
The explanation which Rodríguez et al. (2011) themselves offer must recognize that ADHD does exist, since we are even
in the case of measuring blood flow activated in the brain by discussing it, though it may be to argue and deny it. The
cognitive tasks and educational exercises is coherent with this question now is to see what it is that exists, the way it is
causal direction. After subjects are instructed to make mental real.
calculations, oxygenated hemoglobin in their blood increases. As In this respect, we recur to an ontological metascientific and
the authors say: metatheoretical approach, beyond the facts and terms of the
controversy itself. A new radical approach of this type related
This approach, combined with educational exercises as to the fundamental nature of something, and whole considering
brain-training, can maximize blood oxygenation directly in the different sides and dimensions of the problem, is found in
certain areas of the brain (Rodríguez et al., 2011, p. 66). Aristotle’s four causes.
METASCIENCE OF ADHD: ARISTOTLE’S efficient cause would consist, according to Killeen et al. (2012), of
FOUR CAUSES the symptom triggers. They refer to inadequate reinforcement,
processing demand overload (speed, duration, complexity),
Aristotle’s four causes do not refer to empirical or scientific inadequate control of context (chaotic, stressful, unpredictable),
causes. The terms Aristotle uses in his Physics and Metaphysics, boring environments and repetitive tasks. The ultimate efficient
in which he deals with causes are aition, in plural aitia, which is cause refers to the origins of the prenatal syndrome (maternal
where etiology comes from. Aition has a wider sense than cause in smoking, alcohol) and perinatal (head injury, malnutrition,
English or Spanish. Aristotle’s causes refer to explanatory factors stressful environment).
or principles that approach “why-questions” in order to explain The proximate material cause, according to Killeen et al.
why something exists the way it is (van Fraassen, 1980, p. 42). In (2012), would have to do with neurophysiological substrates,
any case, “cause” remains the best term to capture the meaning dynamic brain events and neuromodulatory systems. The
of Aristotle (Guthrie, 1981, p. 223). In the 21st century, we can ultimate material cause concerns genetic and epigenetic
still find refreshing thought in Aristotle for the problems of our conditions, static brain structure and differences in the brain.
times. In particular, the doctrine of the four causes is still useful The final proximate cause was found by Killeen et al. (2012) in
in the “sublunary world” of human things, so the process of negative reinforcement (escape from boredom and escape from
construction (workable materials, shapes, agents, purposes) is not mental fatigue) and positive reinforcement (approach novel
lost from sight and thus does not fall or remain in mechanicist stimuli, achieve goals more quickly, peer approval). The final
causes. The main Aristotelian causes of why, more than mere ultimate cause would be in evolutionary usefulness referring
empirical causes, enable us to think about how science itself to historical environmental consequences (new niches) and
works, from a metascientific perspective. adaptive advantages (exploitation of opportunities, escape from
Application of the four causes is not common in psychology, stressful environments).
but neither is it unheard of (Killeen, 2001, 2004; Pérez-Álvarez The application of Killeen et al. (2012) has several problems,
et al., 2008; Pérez-Álvarez, 2009; Ribes-Iñesta, 2015). In the clinic, beginning with the order of the causes: formal, efficient, material
the material cause asks what psychological disorders are made and final. The order is not indifferent, because it determines the
of, the formal cause asks what shape they take, why they are interplay and scope of the causes. The logical, chronological and
that way, the efficient cause asks who makes them that way, definitively, ontological would be material, formal, efficient and
and the final cause asks what purpose they have or what they final as usually expressed. The material and formal causes go first,
are for (Pérez-Álvarez et al., 2008). Even though the typical are interdependent on each other and imply the role of the others.
examples of Aristotle’s efficient cause are actors or individual Even when Aristotle gave the most importance to the formal
makers (sculptor, potter), here the possibility of collective actors cause as form, eidos, pattern, that which defines something as
or institutional agents (school, family, clinic) is also considered. what it is, whether a statue or a bowl, the material as amorphous,
The four causes have been specifically applied to ADHD unshaped raw material comes first, the marble in the statue or the
(Killeen et al., 2012). In spite of being systematic, documented, clay in the bowl.
and well-argued, the application by Killeen et al. (2012) failed in To begin with, the formal cause, which in ADHD, we could
important respects. To begin with, it fails by not fitting better to agree with Killeen et al. (2012) is the diagnosis made, means
Aristotle’s original concept, which would have made it of greater attributing the diagnosis entity in its own right, when the
interest. In the end, their application ends up being a mere diagnosis itself is in question. Without further questioning, the
reorganization of data from the official neurobiological concept, rest of the causes revolve around the diagnosis, with all its
and ignores that this concept itself is in question. assumptions, as if we were discussing a well-established clinical
The greatest contribution of the four causes might be in entity. Thus, the proximate efficient cause then becomes a mere
reconsidering the fundamental question of the way in which trigger of ADHD symptoms as if it were a natural entity. The
ADHD exists. In this article, the application by Killeen et al. distal efficient cause would be in the perinatal antecedents. But
(2012) will be briefly discussed first. In continuation, a new, the true Aristotelian sense of efficient cause refers to “actors”
more appropriately Aristotelian application is proposed to find (individuals or groups) not “factors” or “triggers.” The notion of
consequences that could reorient the controversy and eventually antecedent event does not capture the sense of efficient cause as
overcome it. the builder who builds.
Killeen et al. (2012) found the material cause in the
neurophysiological substrates (proximate cause) and in
Causes without Revelation or Rebellion: supposedly genetic proneness (distal cause). Nevertheless,
Aristotle for Nothing this material cause is neither justified by scientific evidence
Killeen et al. (2012) applied the four causes in the following (according to the discussion in the first part) nor is it
order: formal, efficient, material and final, distinguishing in homogeneous with regard to the formal cause. While the
turn, according to Aristotle, close or molecular (proximate) diagnostic form of ADHD is defined by behavior on a molar
and ultimate or molar (distal) causation. The proximate formal scale, the material refers here to neurophysiological substrates
cause of ADHD would be the formal DSM/ICD diagnosis itself. on a molecular scale, a leap of scale also taken with regard
The ultimate formal cause would be given by the explanatory to the efficient cause. While the efficient cause, according to
theories, typically in terms of executive functions. The proximate Aristotle is on the operatory scale due to agents, authors or
“actors” (not “factors” or “triggers”), the material cause of Killeen world. This does not refer to an organism or individual separate
et al. (2012) is on the physicochemical molecular scale. As they from a world they interact with, but a mutually constitutive
themselves admit, the problems met with are hyperactivity and relationship in which comportment, specifiable in behaviors for
inattention (behaviors), not with “ADHD” (Killeen et al., 2012, practical reasons, is the soul and incarnation of this relationship.
p. 415) or in this case, the neurophysiological substrates. The The structure of comportment constitutes a situated
sculptor and potter work with marble and clay as workable, functional corporal unit (Merleau-Ponty, 1942/1963; Thompson,
moldable materials, not their atomic molecular substrate, which 2007, p. 67). How we are situated is characterized by a
some may be. phenomenical structure (perceptive and operatory) from-toward,
Concerning the final cause, the sense of Killeen et al. (2012) as from what we pay attention to toward something and then we
positive and negative reinforcement may be assumed. However, operate on it. The human biophysical structure itself propels
the ADHD fabric has other actors in addition to the person both forward and outward, opening way on a horizon of time
diagnosed, involving a complex of final causes. and space. As sentient subjects and agents we are embodied,
In the end, the application of Killeen et al. (2012) simply embedded, and enacted subjects (Thompson, 2007; Fuchs, 2011).
reorganizes the data in a certain way, without suggesting their Belonging to the world in this way means that the essential way
ontological status, scientific epistemology, social practice or we relate to things is neither purely sensory and reflexive, nor
political ethics of a complex phenomenon with numerous actors cognitive and intellectual, but bodily and practical, articulated
and interests, not without reason controversial. The causes of by “motor intentionality.” This bodily motor intentionality-
Killeen et al. (2012) are causes which neither reveal nor rebel. environment loop constitutes what Merleau-Ponty calls the
Aristotle’s four causes duly applied could reveal the scientific- “intentional arch,” which subtends our relationship with the
practical tangle with which most convictions and best intentions world integrating sensitivity and motility, perception and action
sustain ADHD even though lacking in clinical entity and thus (Merleau-Ponty, 1945/1962, p. 136).
having grounds for a rebellion with cause. In this phenomenological, existential and behavioral
perspective, behaviors, including those defining ADHD, are
Rebellion with Causes: Unmasking the understood according to a circular causality or functional
ADHD Tangle cycles of perception and movement: interplay, feedback or
The four Aristotelian causes are related to each other in such reinforcement. Three cycles have been described (Fuchs, 2011):
a way that it is practically impossible to discuss one without cycles of organismic self-regulation engendering a basic bodily
assuming the others. However, for analytical and explanatory sense of self; cycles of sensorimotor coupling between organism
reasons, it is advisable to go one by one. Specifically, it is and environment, and cycles of intersubjective interaction. The
important to begin with the material cause. Not in vain, the problems come up when the functional cycles are somehow
material cause is the raw material from which something is made altered, but would not therefore be diseases of the brain (Fuchs,
(the marble in a statue or the clay in a bowl). 2011, 2012).
The behaviors by which ADHD is defined begin to
Material Cause attract attention and even become problematic because
The material cause of ADHD would be the behaviors by which, they alter functional cycles, starting with the intersubjective
in fact, it is defined. It refers to some behaviors of children with interaction cycles. A phenomenological study done with ADHD
problems in certain tasks and in certain school, family, and social adults highlighted a certain experience of time and rhythm
contexts. These behaviors, typically inattention, hyperactivity characterized by a desynchronized way of being-in-the-world
or impulsivity, become conspicuous and end up by defining (Nielsen, 2016). This desynchronization refers to an accelerated
a syndrome and the child itself, but in themselves are not rhythm in thinking, bodily discomfort and even anxiety in
problematic or pathological (“symptoms”), nor do they exhaust movement that is not in time with the rhythms of others, of
what the child is. Such behaviors attract attention and become things, of places or of events. An analysis of the different rhythms
problematic in terms of norms and values (Hawthorne, 2010; of daily life (Lefebvre, 2004) would probably explain many things
Brinkmann, 2016). But they are not symptoms of any disease, before pathologizing the different rhythms and styles.
such as a seizure in epilepsy, trembling hands in Parkinson’s or In brief, the material cause ADHD is made of would consist
the loss of memory in Alzheimer’s. They are part of a person’s of certain behaviors by which in fact it is diagnosed. Within this,
comportment which is not reduced to a few behaviors. it has been attempted to show that the behaviors forming part
A somewhat problematic distinction in the English language of functional cycles constitute the material itself of psychological
between comportment and behavior is introduced. In contrast problems (Pérez-Álvarez et al., 2008; Fuchs, 2012), including
to the term behavior that usually only captures discrete aspects so-called ADHD, in which the problem would be a certain
of the person, typically symptoms, as is the case in ADHD, desynchronized way of being in the world (Nielsen, 2016).
comportment refers to the whole Gestalt of being engaged with
the world. The concept of comportment introduced here captures Formal Cause
the “unifying structure of embodied affective (and cognitive) The formal cause of ADHD would be the formal diagnosis itself
engagement with the world, as the most general term to refer made by the diagnostic systems in use (DSM/ICD), in agreement
to all-encompassing changes,” (Jacobs et al., 2015, p. 90). with Killeen et al. (2012). It is no longer important that the
Comportment establishes our constitutive relationship with the diagnosis is more than anything tautological and lacking in
validity, as discussed above. The diagnosis ends up by becoming In short, the formal cause of ADHD would consist of
objectivized and obvious, through the process of selection, the diagnosis itself which provides it with entity in its own
definition and magnification of some behaviors over others, right. The diagnosis already functions as a “cultural idiom”
appropriately converted into “symptoms.” ADHD as it is in and counts on theoretical models which support it. It has
common use in school, family, and clinical contexts, as well as been attempted to show that the overused model based
in the media, functions as a model, form or “cultural idiom.” A on executive functions, far from explaining the supposed
cultural idiom is made up of value systems, ways of interpreting, breakdown, returns ADHD to its reconsideration in contextual
and epistemological assumptions, all of which structure the way affective terms rather than the abstract neurocognitive terms of
in which people experience, give meaning to, and react to the the model.
situations they face (Vanthuyne, 2003).
The formal cause includes the theoretical models proposed Efficient Cause
for explaining ADHD behaviors (Killeen et al., 2012). Among The efficient cause of ADHD would consist of social practices
the variety of models existing (Kofler et al., 2016) are (scientific, clinical, educational, and family) by which certain
those which postulate impaired executive functioning, such as behaviors of children or adults (material cause) take the form of
behavioral inhibition (Barkley, 1997) or monitoring attention a diagnostic category (formal cause). The efficient cause has to
(Brown, 2005). Within their different emphases, they coincide do rather with the actions of “actors” (Pérez-Álvarez et al., 2008),
in understanding the breakdown in executive functioning as than with risk “factors” as usually understood (Killeen et al.,
some type of disruption in the brain. The attractiveness of 2012). Although clinicians are the main “makers” of diagnoses,
an explanation in terms of executive functions may be in they are neither the only agents nor the first. ADHD agency begins
the apparent description of neurocognitive mechanisms which in school and family. But clinicians, parents and educators have
supposedly account for the behavior of individuals, something scientific institutions of reference, such as the National Institute of
doubtless very much in agreement with the individualist, Mental Health (NIMH) in the USA and the National Institute for
neuroscientific and biomedical view of our times. However, Health and Clinical Excellence (NICE) in the United Kingdom,
in spite of all their neuroscientific sophistication, the notion and associations such as Children and Adults with Attention-
of executive function is still a mechanicist, homunculist Deficit/Hyperactivity Disorder (CHADD) which support their
explanation, by personifying in an internal Cartesian scenario practices. These institutes and associations in turn are based on
what in fact individuals are doing in the real world scenario where scientific research. So it is really scientific research which molds
they execute their life. After all, neither the intentions are given ADHD (Hawthorne, 2014).
any place in the brain (Schurger and Uithol, 2015), nor is the Clinicians epitomize the efficient cause as “official” providers
supposed breakdown in executive functioning found everywhere of the diagnosis. Typically, children referred to them by schools
(Brinkmann, 2016; Kofler et al., 2016). are taken to the doctor by their parents and are given the
The mechanisms which theoreticians and users of executive diagnosis and a prescription (Smith, 2013). What happened?
functions hypostasize as if they had a will of their own are The parents referred to the child’s problems which brought
only elements in a wider system in the sense of the structure them there. The clinician (DSM in hand or in mind) asked
of comportment mentioned above (Merleau-Ponty, 1942/1963) questions to confirm that the child had the “symptoms” in the
and its patterns of bodily interaction with the environment description. Other “complementary” tests may also have been
(Maiese, 2012). In its reconsideration of “central executive,” applied. Confirmed: the child did have ADHD. In fact, those
Michelle Maiese emphasizes the essential role of the affective behaviors really do exist and are observable. The child is from
framework in which “we interpret persons, objects, facts, states of now on observed and defined by ADHD behaviors. Everything
affairs, and situations in terms of embodied desiderative feelings.” else, other behavior, circumstances, contexts or history, remain
“Such framing typically occurs during essentially embodied, outside of the description. The clinician believes he has described
spontaneous subjective experience, prior to conceptual and an objective reality, but he has also created it this way by selecting
propositional information processing, and yields a pre-reflective, some behaviors in detriment to others and elevating them to the
non-conceptual, fine-grained contouring of that world, so that we category of “symptoms.”
immediately can target and focus our attention” (Maiese, 2012, There could be a sort of Charcot effect here (Pérez-Álvarez
p. 901). and García-Montes, 2007) by which the clinician “generates”
There may be different forms of bodily harmony with the the reality he describes to the extent that the subjects end up
surrounding world among individuals and situations and even by seeing themselves according to the diagnosis. This looping
within the same individual depending on what attracts their effect described by Ian Hacking consists of patients internalizing
attention and interests them. This would place the differences the biomedical view of their diagnosis (Hawthorne, 2014, pp.
among individuals and within the individual himself more 160–161). The confirmation the clinicians receive from their
within an affective framework than neurocognitive abstracts of patients should not be taken as proof of the objectivity of
a central executive function. In fact, those who are ADHD the diagnosis. There is nothing more objective in psychiatry
are not ADHD all of the time nor everywhere, any more than the grande hystérie (“major hysteria attack”) described
than by diagnostic prescription. Particular attunement to the by Charcot (Didi-Huberman, 2004) and which he himself was
environment, rather than a general breakdown, seems to be the really molding with his descriptions, drawings and photographs
problem of ADHD. (the “neuroimaging” of the time). Once the category has
been created, it works like an “a priori category” of the more refined studies, giving the impression of being on the
clinician’s understanding, who through his actions (interviews, right track. As Hawthorne (2014, p. 66) points out, “science
tests) reinfluences the patient’s understanding, adopting the builds on previous science; but it is also to say that previous
explanations and definitions offered. The creation of the category science constrains current science to some extent—novelty is
itself was already a process of “selection” of the most conspicuous not forbidden, just difficult—by imposing a structure of prior
and operative symptoms to which the problem and the individual formulation, categorization, and contexts—and tools, techniques,
(decontextualized from his history and circumstances) are and experimental models—of interest.” In scientific practice, a
reduced, as the Charcot effect suggests (Pérez-Álvarez and Charcot effect by which research studies what it generates itself
García-Montes, 2007). Now each case confirms the category and (hypotheses and so forth) in a sort of “collective hysteria” would
clinical conviction and at the same time is molded to it as the not be unthinkable.
patient adopts the clinicians point of view if in fact he does not Summarizing, the efficient cause of ADHD would be found
already have it as a “cultural idiom,” such as ADHD usually is. in scientific, clinical, educational, and family practices that make
Within a dynamic process, the looping effect reaffirms category it the way it is. Without denying that it is real, the efficient
and clinician and case and patient or user. cause shows how it becomes real. If it were a natural entity, as
The school itself professes the biomedical conception. As many medical illnesses are (epilepsy, Parkinson’s, Alzheimer’s), it
already occurred in the origins of ADHD starting at the end would make no sense to talk about the efficient cause. But neither
of the 1950s with the figure of the school counselor as the because it is not natural is it less real and easier to change. The
intermediary between the classroom and the clinic (Smith, 2013), genome and the brain may be more plastic than the scientific
the school staff still acts as a bridge. Textbooks used to train practices themselves with their institutionalization, patterns of
special education teachers show a strongly biomedical view reasoning and self-confirmatory methods.
(Freedman, 2016). Families also tend to see diverse problems even
without the ADHD diagnosis, canceling out other possibilities Final Cause
(Lewis-Morton et al., 2014). The influence, if not “pressure” from The final cause of ADHD refers to a series of functions which
the school, along with “information” from parents’ associations it meets for a variety of actors and institutions, beyond the
and associations of those affected, beginning with the CHADD, reinforcement of behaviors of those affected (Killeen et al.,
end up inculcating ADHD in the family, which the clinician only 2012). This variety of unintentional functions could explain its
confirms. expansion, as well as the conviction with which it is argued
If teachers, parents, and clinicians consult international against the “nay-sayers,” in spite of the persistent lack of firm
reference guidelines such as the NIMH and the NICE, they will evidence, as reviewed above. In fact, the success of ADHD may
have the impression of a consensus on the biomedical nature be due paradoxically to its imprecision: a case of the strength
of ADHD which really does not exist (Moncrieff and Timimi, of vague concepts (Löwy, 1992). As this author says, “Imprecise
2013; Erlandsson and Punzi, 2016; Erlandsson et al., 2016). All concepts may help to link professional domains and to create
in all, the ultimate or first efficient cause is how science molds alliances between professional groups.” ‘Fuzzy’ terms, continues
the ADHD which then feeds guidelines and their users. As the author, may last a lifetime and keep functioning (Löwy, 1992,
shown by Hawthorne (2014), science molds ADHD the way it p. 373). This is the case of ADHD.
is by certain patterns of reasoning (epistemology) and research The “trading zone,” which enables imprecise concepts (Löwy,
methods (methodology) which mutually reinforce each other in 1992), has its best expression in ADHD as a “semiotic mediator”
a continuous dynamic process. as defined by Svend Brinkmann. A semiotic mediator referring
Although there are a variety of approaches, levels of analysis to a diagnosis is a symbolic linguistic device with three
and sciences in the study of ADHD, all of them have two functions: an explanatory function with regard to the problems
things in common: the object and the method. The object is experienced, a self-affirming function in the sense that a variety
the DSM-defined ADHD and the method is some version of of phenomena appear as “symptoms” and a disclaiming function
the “scientific method” (Hawthorne, 2014, pp. 47–48). ADHD is related to responsibility (Brinkmann, 2014b). Semiotic mediation
assumed to be a natural, complex entity which must be objectively harmonizes the needs, interests and values that make up the
described and its mechanisms studied. The proper framework ADHD complex. According to Hawthorne (2010, 2014), the
implicitly involves the ADHD/no-ADHD dichotomy (it would solution is reinforced by a positive feedback loop.
be stupid to divide the subjects of research repeatedly without A positive feedback loop incorporates values in concepts,
thinking that there are no differences among the groups), as methods and scientific conclusions. As the theme of interest
well as generalization from statistical means, reasoning linking chosen, research begins by establishing the division between
genetic, neural and behavioral levels, biological reductionism ADHD and non-ADHD (ADHD versus “controls,” “normal,”
(“mechanisms”) and the final reification of ADHD as an “healthy,” “typical development,” “unaffected”). Based on this
identifiable and treatable species (with its subtypes) (Hawthorne, dichotomy, an infinity of topics (“variables”) are chosen to
2014, p. 70). observe possible neurocognitive correlates and genetic and
The lack of firm evidence is supplemented with rhetoric behavioral associations. When a “difference” is found, as
as already shown above in order to make the reasoning Hawthorne says, “the observed difference is only relatively value-
convincing. Thus, “convergence” of a variety of data are discussed free, having been arrived at through several value-valenced
even when they are not significant and of the need for new choices. The slip from “difference” to “dysfunction,” which is an
ethical term, intensifies the valuation.” Positive results reinforce Third, the enquiry was carried out using Aristotle’s four causes.
the decisions and in any case, as they say, more studies are In addition to a clarifying view, this metascientific focus offers
necessary, strengthening the feedback loop (Hawthorne, 2014, an alternative to the understanding of “ADHD” beyond the
p. 136). “Overall, then, the social/scientific feedback loop is self- dominant biomedical model and its simple denial. According
reinforcing as long as science achieves results that society can to this analysis, the material of which ADHD is made would
take up and support. By this ongoing mutual influence, facts be some specific behaviors which can be problematic in certain
and values are jointly defined and reinforced” (Hawthorne, 2010, contexts and tasks. These behaviors are easily taken as the form of
p. 28). the “ADHD” diagnostic category according to diagnostic criteria
Attention-Deficit/Hyperactivity Disorder harmonizes a in use (typically the DSM). The efficient cause with regard to
variety of scientific, medical, educational and family interests what, or better, who makes ADHD the way it is may be found
besides pharmaceutical industry profits (the most openly on one hand in the clinicians who make the diagnosis and on
shameless and rightly denounced). The only party harmed seems the other in scientific research which has molded the established
to be the children, with the unintentional effect of “accidental concept. The final cause refers to a variety of functions which
intolerance” of the traits and ADHD-associated behaviors ADHD meets, not in spite of its scientific-clinical vagueness. On
(Hawthorne, 2014, p.142). the contrary, it would be precisely due to its imprecision which
Briefly, the final cause of ADHD would be in harmonizing makes it useful in a variety of contexts. The positive science-
the interests of a variety of actors and institutions, not just society feedback loop which surreptitiously combines facts and
the pharmaceutical industry. The particular feedback loop values as the reason for its success in harmonizing varied interests
between science and society in which normative values become has been shown.
naturalized and legitimated in research, which is valued and The metascientific perspective makes it possible to see and
supported by society, has been shown. Perhaps the children are go beyond the scientific controversy run aground on whether
the least benefited due to the resulting “accidental intolerance.” ADHD exists or not. According to this analysis, ADHD would
Individual differences become dysfunctions, disorder or mental not be sustainable as a clinical entity, although it is still real as
illness. a practical entity (Pérez-Álvarez et al., 2008). Far from being
a given natural kind, out there, ready for its research as a
scientific object, “ADHD” would be a practical kind, constructed
CONCLUSION on the scientific and clinical practices themselves, fulfilling a
variety of functions, who knows for whom or at what cost.
An argument has been developed in three steps. First, the Beyond the positivist science framework (typically neuroscience),
evidence claimed which sustains ADHD was reviewed. It was the “number one recommendation” would be to “establish a
shown that the diagnosis is based on fallacious reasoning pragmatist framework that carefully uses facts and values in all
(tautologies), for lack of clinical proof. At this point, the lack decisions and actions relevant to ADHD” (Hawthorne, 2014,
of specific genetic and neurobiological evidence should not be p. 176). As a scientifically and ethically coherent derivation, the
surprising, in spite of the enormous amount of literature pointing “ADHD”/non-“ADHD” dichotomy would have to be overcome,
in that direction. The fact that the science of ADHD seems to and instead of the essentialist conception in use, adopt a
be going on the right path is probably due more to the rhetoric pragmatic approach with regard to situations and concrete
and metaphysics of its literature than to accumulated scientific norms where the problem can be enacted according to a
findings. Rhetoric in use seems to convert ambiguous meager cultural, contextual, existential psychology (Brinkmann, 2016,
data into conclusions presented as “convergent evidence,” where p. 88).
the overused expressions “complex” or “heterogeneous” disorder Therefore, the problems to which “ADHD” refers should
really means that its causes are unknown, even if assumed to be never have left the family and school educational scope, making
genetic and neurobiological. Implicit metaphysical assumptions them pass through the clinical circuit and come back as “mental
are found for example, in correlates and correlations taken as disorder.” Any problems related to “attention,” “activity,” and
neural “causes” or “bases.” “impulsivity” are not outside learning as aspects of development
Second, a new metascientific approach to the science of of self-control. Some children may require additional “training”
ADHD was proposed, supposing that a mere critical review leaves (not treatment). More precisely, such “training” would be by
the controversy between “defenders” and “critics” the same as it parents and teachers with a view to promoting the skills children
was, in a dialog of the deaf. More so, criticism, as demolishing require. Training by parents using common games involving
as it is, still recognizes the sense, persuasion, and good faith, not attention and following rules (“Simon says,” “frozen dance”)
ignorance or simple interests, of the defenders. How are they as well as behavioral principles (availability of appropriate
not going to be convinced if the science they profess directs contexts, positive reinforcement), would “remove” children from
their path, sheds light on the subject and offers the method? (risk of receiving the diagnoses of) “ADHD” (Charach et al.,
The fact is that the science itself may have blind points and self- 2013; Laber-Warren, 2014). A study with a careful design
confirming methods, without even going down the right path. showed that behavioral training by parents and teachers was
The new metascientific approach proposed is Aristotle’s four more effective than medication (Pelham et al., 2016). These
causes, material, formal, efficient, and final, as an instrument of behavioral “interventions,” more than as an alternative to
enquiry. medication (which is no small thing), are referred to here as
an ontological argument demonstrating the practical behavioral (e.g., existential, moral, political)] with a hermeneutic interest in
nature (non-essentialist) of ADHD. It is already time to interpreting the person and her suffering in her life situation as it
overcome the “ADHD”/non-“ADHD” dichotomy without paying presents itself in its “facticity” (Brinkmann, 2014a, p. 645).
attention to the aspect of the problem when necessary without
pathologizing it. Since the diagnostic language is not inevitable,
only dominant, AUTHOR CONTRIBUTIONS
We must supplement the pragmatic interest in action possibilities The author himself conceived, wrote, reviewed and approved the
[afforded by different languages inherent in social practices article.
Kooij, S. J., Bejerot, S., Blackwell, A., Caci, H., Casas-Brugue, M., Carpentier, Ross, C. A. (2016). Extreme exaggeration of the results of genetic research
P. J., et al. (2010). European consensus statement on diagnosis and treatment on schizophrenia. Psychosis 8, 186–187. doi: 10.1080/17522439.2016.115
of adult ADHD: the European network adult ADHD. BMC Psychiatry 10:67. 3702
doi: 10.1186/1471-244X-10-67 Rubia, K., Alegria, A., and Brinson, H. (2014). Imaging the ADHD brain: disorder-
Laber-Warren, E. (2014). Concentrate. Sci. Am. Mind 25, 61–65. doi: 10.1038/ specificity, medication effects and clinical translation. Expert Rev. Neurother.
scientificamericanmind0314-61 14, 519–538. doi: 10.1586/14737175.2014.907526
Lefebvre, H. (2004). Rhythmanalysis: Space, Time and Everyday Life. London: Schurger, A., and Uithol, S. (2015). Nowhere and everywhere: the causal origin
Continuum. of voluntary action. Rev. Philos. Psychol. 6, 761–778. doi: 10.1007/s13164-014-
Lewis-Morton, R., Dallos, R., McClelland, L., and Clempson, R. (2014). “There is 0223-2
something not quite right with Brad ...”: The ways in which families construct Sekar, A., Bialas, A. R., de Rivera, H., Davis, A., Hammond, T. R., Kamitaki, N., et al.
ADHD before receiving a diagnosis. Contemp. Fam. Ther. 36, 260–280. (2016). Schizophrenia risk from complex variation of complement component
doi: 10.1007/s10591-013-9288-9 4. Nature 530, 177–183. doi: 10.1038/nature16549
Löwy, I. (1992). The strength of loose concepts—Boundary concepts, federative Smith, M. (2013). Hyperactivity: The Controversial History of ADHD. London:
experimental strategies and disciplinary growth: the case of immunology. Hist. Reaction Books.
Sci. 30, 371–396. doi: 10.1177/007327539203000402 Sonuga-Barke, E. J. (2010). Editorial: ‘It’s the environment stupid!’ On epigenetics,
Maguire, E. A., Woollett, K., and Spiers, H. J. (2006). London taxi drivers and programming and plasticity in child mental health. J. Child Psychol. Psychiatry
bus drivers: a structural MRI and neuropsychological analysis. Hippocampus 51, 113–115. doi: 10.1111/j.1469-7610.2009.02213.x
16, 1091–1101. doi: 10.1002/hipo.20233 Tait, G. (2009). The logic of ADHD: a brief review of fallacious reasoning. Stud.
Maiese, M. (2012). Rethinking attention deficit hyperactivity disorder. Philos. Philos. Educ. 28, 239–254. doi: 10.1007/s11217-008-9114-2
Psychol. 25, 893–916. doi: 10.1080/09515089.2011.631998 Tarver, J., Daley, D., and Sayal, K. (2014). Attention-deficit hyperactivity disorder
Merleau-Ponty, M. (1942/1963). The Structure of Behavior, trans. A. L. Fisher. (ADHD): an updated review of the essential facts. Child Care Health Dev. 40,
Boston, MA: Beacon. 762–774. doi: 10.1111/cch.12139
Merleau-Ponty, M. (1945/1962). Phenomenology of Perception, trans. Colin Smith. Thapar, A., and Cooper, M. (2016). Attention deficit hyperactivity disorder. Lancet
London: Routledge. 387, 1240–1250. doi: 10.1016/S0140-6736(15)00238-X
Moncrieff, J., and Timimi, S. (2013). The social and cultural construction of Thapar, A., Cooper, M., Eyre, O., and Langley, K. (2013). What have we learnt about
psychiatric knowledge: an analysis of NICE guidelines on depression and the causes of ADHD? J. Child Psychol. Psychiatry 54, 3–16. doi: 10.1111/j.1469-
ADHD. Anthropol. Med. 20, 59–71. doi: 10.1080/13648470.2012.747591 7610.2012.02611.x
Mukherjee, S. (2016). The Gene: An Intimate History. New York, NY: Scribner Thompson, E. (2007). Mind in Life: Biology, Phenomenology, and the Sciences of
Macmillan. Mind. Cambridge, MA: Harvard University Press.
Neguţ, A., Jurma, A. M., and David, D. (2016). Virtual-reality-based attention Timimi, S. (2014). No more psychiatric labels: why formal psychiatric diagnostic
assessment of ADHD: ClinicaVR: classroom-CPT versus a traditional systems should be abolished. Int. J. Clin. Health Psychol. 14, 208–215. doi:
continuous performance test. Child Neuropsychol. doi: 10.1080/09297049.2016. 10.1016/j.ijchp.2014.03.004
1186617 Timimi, S., Moncrieff, J., Jureidini, J., Leo, J., Cohen, D., Whitfield, C., et al. (2004).
Nielsen, M. (2016). ADHD and temporality: a desynchronized way of being in the A critique of the international consensus statement on ADHD. A critique of the
world. Med. Anthropol. 36, 260–272. doi: 10.1080/01459740.2016.1274750 international consensus statement on ADHD. Clin. Child Fam. Psychol. Rev. 7,
Pelham, W. E., Fabiano, G. A., Waxmonsky, J. G., Greiner, A. R., Gnagy, 59–63. doi: 10.1023/B:CCFP.0000020192.49298.7a
E. M., Pelham, W. E. III, et al. (2016). Treatment sequencing for childhood van Fraassen, B. C. (1980). A re-examination of Aristotle’s philosophy of science.
ADHD: a multiple-randomization study of adptive medication and behavioral Dialogue 19, 20–45. doi: 10.1017/S0012217300024719
interventions. J. Clin. Child Adolesc. Psychol. 45, 396–415. doi: 10.1080/ Vanthuyne, K. (2003). Searching for the words to say it: the importance of cultural
15374416.2015.1105138 idioms in the articulation of the experience of mental illness. Ethos 31, 412–433.
Pérez-Álvarez, M. (2009). The four causes of behavior: Aristotle and Skinner. Int. doi: 10.1525/eth.2003.31.3.412
J. Psychol. Psychol. Ther. 9, 45–57. Wellcome Trust (2010). First Direct Evidence that ADHD is a Genetic
Pérez-Álvarez, M., and García-Montes, J. M. (2007). The Charcot effect: the Disorder: Children with ADHD more Likely to Have Missing or Duplicated
invention of mental illnesses. J. Constr. Psychol. 20, 309–336. doi: 10.1080/ Segments of DNA. ScienceDaily. Available at: www.sciencedaily.com/releases/
10720530701503843 2010/09/100929191312.htm [accessed December 20, 2016].
Pérez-Álvarez, M., García-Montes, J. M., Vallina-Fernández, O., and Perona- Williams, N. M., Zaharieva, I., Martin, A., Langley, K., Mantripragada, K.,
Garcelán, S. (2016). Rethinking schizophrenia in the context of the person and Fossdal, R., et al. (2010). Rare chromosomal deletions and duplications in
their circumstances: seven reasons. Front. Psychol. 7:1650. doi: 10.3389/fpsyg. attention-deficit hyperactivity disorder: a genome-wide analysis. Lancet 376,
2016.01650 1401–1408. doi: 10.1016/S0140-6736(10)61109-9
Pérez-Álvarez, M., Sass, L., and García Montes, J. M. (2008). More Aristotle, less World Health Organization (1992). International Classification of Diseases ICD-10,
DSM: the ontology of mental disorders in constructivist perspective. Philos. 10th Edn. Geneva: WHO.
Psychiatry Psychol. 15, 211–225. doi: 10.1353/ppp.0.0192 Zelnik, N., Bennett-Back, O., Miari, W., Goez, H. R., and Fattal-Valevski, A. (2012).
Pittelli, S. J. (2002). Meta-analysis and psychiatric genetics [letter to editor]. Am. J. Is the test of variables of attention reliable for the diagnosis of attention-deficit
Psychiatry 159, 496–497. doi: 10.1176/appi.ajp.159.3.496 hyperactivity disorder (ADHD)? J. Child Neurol. 27, 703–707. doi: 10.1177/
Raichle, M. D. (2015). The brain’s default mode network. Annu. Rev. Neurosci. 38, 0883073811423821
433–447. doi: 10.1146/annurev-neuro-071013-014030
Ribes-Iñesta, E. (2015). El desligamiento funcional y la causalidad Aristotélica: Conflict of Interest Statement: The author declares that the research was
un análisis teórico. [A functional detachment and Aristotelian causality: a conducted in the absence of any commercial or financial relationships that could
theoretical analysis]. Acta Comportamentalia 23, 5–15. be construed as a potential conflict of interest.
Rodríguez, C., González-Castro, P., Álvarez, L., Vicente, L., Núñez, J. C., González-
Pienda, J., et al. (2011). Nuevas técnicas de evaluación en el trastorno por déficit Copyright © 2017 Pérez-Álvarez. This is an open-access article distributed under the
de atención e hiperactividad (TDAH). Eur. J. Educ. Psychol. 4, 63–73. terms of the Creative Commons Attribution License (CC BY). The use, distribution or
Rodríguez, C., González-Castro, P., Cueli, M., Areces, D., and González-Pienda, reproduction in other forums is permitted, provided the original author(s) or licensor
J. A. (2016). Attention deficit/hyperactivity disorder (ADHD) diagnosis: an are credited and that the original publication in this journal is cited, in accordance
activation-executive model. Front. Psychol. 7:1406. doi: 10.3389/fpsyg.2016. with accepted academic practice. No use, distribution or reproduction is permitted
01406 which does not comply with these terms.