I began seriously researching ADHD in 2010 with the purchase of Barkley’s Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. Positive reviews indicated that this would be a worthy source of information for my fourth-year psychology dissertation. At the end of Chapter 1, there was a copy of an International Consensus Statement on ADHD, which stated:
Occasional coverage of the disorder casts the story in the form with evenly matched competitors. The views of a handful of nonexpert doctors that ADHD does not exist are contrasted against mainstream scientific views that it does, as if both views have equal merit. Such attempts at balance give the public the impression that there is substantial disagreement over whether ADHD is a real medical condition. In fact, there is no such disagreement—at least no more so than there is over whether smoking causes cancer, for example, or whether a virus causes HIV/AIDS.
Somewhat cowed by the tone and the status of the 86 signatories, I continued with Barkley’s voluminous account of all things related to ADHD.
However, halfway through Chapter 2, Barkley once again criticised “nonexpert professionals”, before concluding:
Therefore, any claims that ADHD is a myth reflect either a stunning level of scientific illiteracy or outright attempts to misrepresent the science of ADHD so as to mislead the public with propaganda.
Throughout this section Barkley repeatedly referenced an article by Sami Timimi. Curious about what might constitute “scientific illiteracy”, I sourced the document to find Timimi was not the sole author; there were 33 co-endorsers, who were anything but “nonexpert”, judging by their qualifications, academic standing, and publications.1
(And they are far from the only experts who have critiqued the diagnosis of ADHD. In more recent years, Allen Frances—chair of the DSM-IV task force—has levied extensive critique against the diagnosis, as had Keith Conners—considered the “father of ADHD” and namesake of the Conners Comprehensive Behavior Rating Scale.)
Furthermore, Timimi’s article was a critique of the Consensus Statement, something Barkley did not acknowledge. Critique is a legitimate and important part of the scientific process. Additionally, Barkley’s use of the word myth was misleading, as it suggested Timimi et al. took the extreme position of stating ADHD did not exist. This was not the case.
The points they raised, and the manner in which these contrasted with Barkley et al.’s, were the impetus for my research. The focus of my PhD has been to identify the processes by which ADHD has come to be understood as a medical condition. My aim has been to establish whether these processes are sufficiently robust to withstand criticism without resorting to displays of hubris.
As publications about ADHD are now in their tens of thousands, finding a way to establish the veracity of Barkley et al.’s claims was somewhat problematic. However, the journal article with the highest citation count on the database Scopus is an article by Barkley called “Behavioral Inhibition, Sustained Attention, and Executive Functions: Constructing a Unifying Theory of ADHD.” (As of November 9, 2021 it has 4,772 citations with 263 added in 2021, by subject 2,749 are categorised as psychology, 2, 340 medicine, and 1,240 neuroscience).
As Barkley’s theory has had a strong influence on research into ADHD, evaluation of this theory has been a major part of my inquiry. What I found was that Barkley’s theory was akin to what Richard Feynman called “Cargo Cult Science,” only more misleading and dangerous.
Feynman, the famous physicist, used the term “Cargo Cult Science” in his 1974 commencement address to students at the California Institute of Technology (Caltech). He described how, in the South Seas during the Second World War, a group of unnamed islanders had watched planes land full of good materials. After the war ended, the islanders wanted the planes to return:
So they’ve arranged to make things like runways, to put fires along the sides of the runways, to make a wooden hut for a man to sit in, with two wooden pieces on his head like headphones and bars of bamboo sticking out like antennas—he’s the controller—and they wait for the airplanes to land. They are doing everything right. The form is perfect. It looks exactly the way it looked before. But it doesn’t work. No airplanes land. So I call these things Cargo Cult Science, because they follow all the apparent precepts and forms of scientific investigation, but they’re missing something essential, because the planes don’t land.
Feynman argued that Cargo Cult Science involves cherry-picking evidence to support an assumed conclusion, ignoring contradictory evidence, and giving the appearance of science while failing to actually follow the scientific method.
The explanation in Barkley’s highly-cited article was lengthy and confusing, especially when it led into a conceptual model of “executive, self-directed actions”. Key to the entire work was Barkley’s statement that “poor behavioral inhibition is specified as the central deficiency in ADHD”. He claimed this influences the “executive” actions, also referred to as “functions” in his model. However, Barkley did not give a precise definition for “behavioural inhibition.”
Based on the articles that Barkley cited to support his theory, I concluded that his hypothesised deficiency is what others refer to as impulsivity. Impulsivity is considered a major symptom of ADHD, but Barkley seemed to be saying that ADHD, including impulsivity, is caused by being impulsive—making his argument circular.
Following this, I evaluated the evidence Barkley provided for this proposal. This evidence relied almost entirely on experiments from the school of cognitive psychology—many of which attempted to ascertain the validity of ADHD by timing children’s responses to meaningless tasks within a laboratory setting.
The main authority Barkley cited in his argument that ADHD was due poor behavioural inhibition was a 1977 essay by the late Jacob Bronowski. Whilst Bronowski may well have been held in regard for his intellect, not least for his presentation of a British documentary series The Ascent of Man, this usage by Barkley is somewhat curious. All the more so, when the point of Bronowski’s essay was to explain the evolutionary differences between human language and animal communication. Bronowski admitted that he was writing as an amateur, but he hoped that what he had to say would throw light on his special interests “namely the language of science, and the language of poetry”.
Bronowski proposed that “the central and formative feature in the evolution of human language” is “a delay between the arrival of the stimulus and the utterance of the message it has provoked”. Bronowski expanded on four consequences of this delay; these he named separation of affect, prolongation, internalization and reconstitution. But throughout, his main point was to explain “the difference between the way human beings can use language and the way animals do”.
Bronowski’s essay was published posthumously in its original form; it was neither edited nor peer reviewed, hence its accuracy was never debated. But Barkley’s idea of “deficient behavioural inhibition” is based on Bronowski’s hypothesised delay. Whereas Bronowski proposed this delay was the point in evolutionary history that humans and animals separated, in Barkley’s theory this is the point at which those with ADHD versus those without differ. Bronowski’s “consequences” led to different evolutionary pathways dating back possibly two million years.
For Barkley, the consequence of this delay was one which impacted executive functioning, a term Barkley attributed to Denckla, among others. Denckla stated that it was generally agreed that executive functions referred to “mental control processes”. Barkley used this notion to devise four categories, supposedly modelled on the four terms used by Bronowski. Barkley retained Bronowski’s term reconstitution but renamed the other categories as working memory, self-regulation of affect/motivation/arousal and internalization of speech. Then, under each heading, Barkley listed various behaviours, 22 in total, which he deemed could be improved or normalised by “amelioration of the inhibitory deficit”.
He didn’t suggest any specific form of intervention, but he later identified an unresolved issue worthy of future research: “the degree to which medications differently affect each of these domains of executive function”.
Although Barkley’s model bears little resemblance to Bronowski’s ideas, Barkley stated that “Bronowski attributed these four executive functions to the prefrontal lobes”. In fact, Bronowski made no mention of the functions being localised in the frontal lobes, or indeed anywhere in the brain. It appears the connection with the frontal lobe comes from Fuster’s theory of prefrontal function, which Barkley claimed to have “much in common” with Bronowski’s work. For this reason, he included Fuster’s theory of Neural Mechanisms Underlying Behavioral Structure in his executive function model.
Fuster’s theory first appeared in his book The Prefrontal Cortex: Anatomy, Physiology, and Neuropsychology of the Frontal Lobe. Barkley referred repeatedly to “behavioural structures”, but otherwise ignored the large portion of Fuster’s work that failed to support his approach. As to the commonality between the two sources, as noted, Bronowski did not mention the prefrontal cortex. Instead, he attributed his hypothesised delay to a “biochemical peculiarity”, one where humans lost the ability to make the enzyme uricase.
Furthermore, this delay was described by Bronowski as a “linguistic mechanism…an inherent delay in human response”. By contrast, Fuster stated that “automatic, or instinctual series of acts, however complex, does not qualify and is not within the purview of the prefrontal cortex”.
But most worryingly, this particular theory, based on flimsy cognitive psychology research, a curious use of Bronowski’s essay, and a bogus link to the prefrontal cortex, has been cited by some in the medical community in the context of validating ADHD as a condition relating to frontal cortex abnormalities—notably, Stephen Faraone and Joseph Biederman in their 1998 coining of the phrase “frontalsubcortical” abnormalities. In The Lancet, they claimed that the frontalsubcortical hypothesis had been confirmed.
Likewise, albeit without direct reference to Barkley, Faraone argued in 2005 that ADHD was a valid condition due to frontalsubcortical abnormalities. Not long afterwards, Halperin and Schulz noted that theories such as Barkley’s had led to numerous inconsistencies in the literature, to the extent that it was impossible to identify the precise nature of ADHD pathophysiology. But, rather than question the notion of abnormal neurological functioning, the authors proposed that a different brain area might be defective.
On this basis, “the largest dataset to date” was pooled by Hoogman et al., and supposedly found evidence of brain abnormalities. However, this research was criticized so roundly that Lancet Psychiatry devoted an entire issue to rebuttals by researchers as distinguished, again, as Allen Frances and Keith Conners, who all argued that Hoogman et al.’s own data did not support their claims.
In the Hoogman et al. study, the list of financial conflicts of interests tying the researchers, including Biederman and Faraone, to the pharmaceutical industry, is extensive. This is problematic because it has been found that researchers receiving money from industry biases the results; the greater the bias, the less likely research findings are to be true. John Ioannidis explained this in an article titled “Why Most Published Research Findings Are False”. He presented a formula to support his hypothesis, then outlined the many forms that bias can take.
Cosgrove and Wheeler specifically examined conflicts of interest in psychiatry, and concluded that organised psychiatry’s dependence on drug firm funding had distorted the science. In particular, they found that the evidence bases upon which “accurate diagnosis and sound treatment depend” had been corrupted.
This is not altogether surprising, since industry funds research with the expectation of financial gains. Biederman and Faraone made this commitment to Johnson and Johnson back in 2002 when they received funding for the Center for Pediatric Psychopathology at Massachusetts General Hospital, the largest teaching hospital of Harvard Medical School. Part of their brief was to “move forward the commercial goals of J&J”.
They also acknowledged that it was equally important to demonstrate the validity of childhood disorders as brain disorders. They stated that without data from genetic and brain imaging studies, “many clinicians question the wisdom of aggressively treating children with medications, especially those like neuroleptics, which expose children to potentially serious adverse events”.
Since their first citation of Barkley’s theory, with its false connection to prefrontal abnormalities, and with their continuing insistence that ADHD is a valid brain disorder, diagnoses and prescribing rates have sky-rocketed worldwide, and numerous new medications have entered the field.
But are we any the wiser, and are children diagnosed as “having” ADHD benefitting from current interventions? ADHD is now a worldwide phenomenon with large volumes of data available. Many of these are presented in a recent publication by Faraone et al. in what they claim to be an update of Barkley et al.’s International Consensus Statement. Space does not allow for a discussion of their “cataloguing of important scientific discoveries from the last twenty years”; but under the heading of “What we have learned from studying the brains of people with ADHD”, they reported that differences “are typically small and…are not useful for diagnosing the disorder”.
Meaning, as the researchers critiquing Hoogman et al. emphasized, there is no evidence of any structural abnormality, prefrontal or otherwise, in ADHD. The airplanes have not landed, nor are they likely to.
When Timimi et al. responded to the International Consensus Statesman on ADHD, they argued:
Not only is it completely counter to the spirit and practice of science to cease questioning the validity of ADHD as proposed by the consensus statement, there is an ethical and moral responsibility to do so. History teaches us again and again that one generation’s’ most cherished therapeutic ideas and practices, especially when applied on the powerless, are repudiated by the next, but not without leaving countless victims in their wake.
The data are now accruing to vindicate the stand taken by Timimi et al., including evidence on the poor long term efficacy of stimulants. A population-based cohort study by Fleming et al. analysed the health and educational data of 766,244 children attending Scottish primary, secondary, and special schools between 2009 and 2013. They concluded that:
The 7413 children receiving medication for attention-deficit/hyperactivity disorder had worse education outcomes (unauthorized absence, exclusion, special educational need, lower academic attainment, left school earlier, and higher unemployment) and health outcomes (hospitalizations overall and for injury).
Even the NIMH’s MTA study—the seminal study of stimulant use, whose 1999 short-term outcomes have been used to support stimulant prescribing for 20 years—has confirmed, in every long-term publication, that taking stimulant drugs leads to worse outcomes, not better. This includes the three-year follow-up, the six-to-eight year follow-up, and the 16-year follow-up.
These outcomes are all the more concerning when considering that the youngest kids in a classroom are far more likely to be given a diagnosis of “ADHD” and medicated (when it’s likely just an age/maturity gap)—a finding that has been corroborated over and over again in numerous countries.
Added to these concerns is the lack of knowledge about how the medications affect the developing brain. This was discussed in an article by Stern et al., where they proposed that early treatment with stimulants might actually worsen ADHD symptoms. They attributed this to “neuronal imprinting”—in which exposure to a drug can influence the functioning of the brain even when the drug is no longer present.
Stern et al. argued that neuronal imprinting altered behavior, including the way individuals responded to stimulation and to drugs. Based on evidence from animal and human studies, they proposed that, for some, stimulants might contribute to ADHD turning into a chronic lifetime disorder. Interestingly, although Barkley has proposed that the locale for his hypothesised defect is the prefrontal cortex, the word “neuron” only appears in his lengthy article once.
The point of Feynman’s address and his tale about “Cargo Cult Science” was that:
We’ve learned from experience that truth will out. Other experimenters will repeat your experiments and find out whether you were wrong or right. Nature’s phenomena will agree or they will disagree with your theory. And, although you may gain some temporary fame or excitement, you will not gain a reputation as a scientist if you haven’t tried to be very careful in this kind of work. And it’s this type of integrity, this kind of care not to fool yourself, that is missing to a large extent in much research into Cargo Cult Science.
Feynman was optimistic about the self-correcting processes of science, but he probably never envisioned a situation where the commercial interests of multiple pharmaceutical companies were prioritised to the extent they are now. Faraone et al. wrote that the worldwide economic burden of ADHD is in the hundreds of billions of dollars—a “burden” which largely goes to the pharmaceutical industry as “profit.”
Whilst key “experts” would have us believe this is due to some sort of frontalsubcortical abnormality, the alternative explanation is that the burden is due to the creation of a false narrative, intended to counteract those questioning what Biederman and Faraone called “the wisdom of aggressively treating children with medications, especially those like neuroleptics, which expose children to potentially serious adverse events”.
Acknowledgement: I would like to thank my supervisors, Professor Jon Jureidini and Dr. Melissa Raven, for feedback and assistance with this blog.
- In the interest of full disclosure, the principal supervisor of my PhD, Professor Jon Jureidini (University of Adelaide), was a signatory to the Timimi et al. (2004) critique. He kindly took over this role when my original supervisor, the late Professor Kevin Ronan (Central Queensland University) was diagnosed with motor neuron disease in 2018. ↩
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