ADHD diagnosis continues to fail the reliability and validity test

Written by Martin Whitely PhD

First published in the Australian and New Zealand Journal of Psychiatry in April 2015

Professor Florence Levy’s recent opinion piece[1] represents a shift in tone, but not core belief, from 2002 when she was one of 84 self-declared ‘leading scientists’ who signed the International Consensus Statement on ADHD. In the International Consensus Statement the evidence supporting the validity of ADHD was deemed to be equivalent to that supporting ‘the laws of gravity’ and the ‘periodic table’, and critics were dismissed as ‘flat earthers’.

In response ADHD critic, British psychiatrist Sami Timimi wrote; “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…The evidence shows that the debate is far from over.”[2]

Levy’s recent piece acknowledges the American Psychiatric Association’s DSM-IV Taskforce leader, Professor Alan Frances’, criticisms of the expanded DSM-5 definition of adult ADHD. However, she fails to address Frances’ concern that the ‘explosion’ in ADHD child prescribing that occurred prior to the publication of DSM-5 is a dangerous ‘fad’ that ‘requires taming’.[3] The closest Levy came is her recognition that the ‘DSM and ICD’ have only been moderately successful ‘in establishing diagnostic reliability.’[4]

This is a massive understatement. ADHD diagnoses are notoriously unreliable. As detailed below, a child’s chances of being prescribed ADHD drugs are significantly influenced by birthdate relative to classroom peers. Gender, postcode and clinician, teacher and parental attitudes, none of which have anything to do with a child’s neurology, are also significant factors.

Levy promotes the yet to be developed National Institute of Mental Health’s Research Domain Criteria (RDoC), which are to be based on ‘underlying neurobiological components, conceptualized as disorders in brain circuitry’, as ‘promising greater reliability of diagnosis’.[5] If, and it is a very big if, the RDoC develops hypothesised differences in ‘brain circuitry’ into a diagnostic tool, then ADHD may become a reliable diagnosis. However, that would not guarantee it was a valid diagnosis.

Nothing better demonstrates the invalidity of an ADHD diagnosis than an eleven year study of 938,000 Canadian children that confirmed the results of two earlier large scale American studies. The Canadian research found that children born in the last months of a school year are far more likely to be ‘medicated for ADHD’ (boys 41%. girls 77%) than their oldest classmates.[6]

The ‘Holy Grail’ for many proponents of ADHD is establishing its ‘genetic basis’, the logic being that this would validate it as a psychiatric disorder. In 2010, there was widespread international coverage of British psychiatric researcher Anita Thapar claim that ‘now we can say with confidence that ADHD is a genetic disease.’[7] The study that Thapar claimed established that ADHD as a ‘genetic disease’ involved the comparison of the genetic codes of 366 children ‘with ADHD’ with those of 1047 ‘non-ADHD’ control children. Researchers found 13.9 percent (51) of children with ADHD had short lengths of their genetic code that were either duplicated or missing. This compared with 7.4 percent (78) of the ‘control children’.[8]

The average recorded IQ of the 366 children ‘with ADHD’ was 86, 14 points below the general population average of 100. Whilst the IQ of the 1047 ‘non ADHD children’ was not specified, presumably they were as intelligent as the general population. Furthermore, when 33 intellectually impaired ‘ADHD children’ (IQ lower than 70) were excluded from the ADHD cohort, only 11 percent of the remaining 333 had the hypothesised ADHD genetic abnormality (Williams, Thapar, et al, 2010). Even with the intellectually impaired children removed, the average IQ (89) of the 333 remaining in the ADHD group was significantly lower than the general population mean of 100. This evidence is more suggestive of a relationship between the identified genetic abnormality and intellectual disadvantage rather than ADHD.

Ultimately, as defined in both the DSM and ICD, ADHD is a collection of behaviours, with children diagnosed as being less attentive and/or more impulsive/hyperactive than their peers. Finding a genetic basis for ADHD would therefore mean finding a genetic basis for inattentive and/or impulsive/hyperactive behavior. It is entirely reasonable to think behavior is a combination of nature and nurture. However conceding that ADHD may be in part a ‘genetic difference’ is vastly different from accepting it is a ’genetic disease’.

Even ADHD proponents acknowledge that many people without ADHD exhibit the eighteen behaviours at the core of a DSM or ICD diagnosis. What is supposed to distinguish ADHD sufferers from the rest of the population is their level of behavioural impairment or dysfunction. Specifically, ‘there must be clear evidence of clinically significant impairment in social, academic or occupational functioning’ and ‘some impairment from the symptoms…[must be] present in two or more settings (e.g. at school or work and at home)’.[9]

All eighteen behavioural diagnostic criteria include the word ‘often’. How often a child ‘fidgets or squirms in their seat’, or ‘interrupts’ or ‘avoids homework’ or ‘fails to remain seated when remaining seated is expected’ or ‘is distracted by external stimuli’ etc. so that they exhibit ‘some impairment’ is not defined in DSM-IV. The DSM-IV diagnostic criteria do not specify age-appropriate levels of attention or impulsivity control.

Furthermore, DSM-IV states: ‘Signs of the disorder may be minimal or absent when the person is receiving frequent rewards for appropriate behaviour, is under close supervision, is in a novel setting, is engaged in especially interesting activities, or is in a one-to-one situation (e.g., the clinician’s office.)’[10] Therefore, according to the DSM-IV, children with ADHD may behave appropriately and not display ADHD symptoms when they are rewarded, when people pay attention to them (close supervision) and when they are having interesting experiences. Conversely they will be easily distracted and display ADHD symptoms when their good behaviour goes unrewarded, no one pays any attention to them, or they are bored. Surely the nonsense of this proposition is self-evident?

As Levy identifies, the DSM-5 has broadened ADHD diagnostic criteria by raising the age from seven to twelve, before which ‘several inattentive or hyperactive/impulsive symptoms’ should be present and by reducing from six to five the number symptoms required for a diagnosis in those 17 or older. This is a well-established long term pattern with successive versions of the DSM expanding both the criteria and the markets for stimulants. Nonetheless Levy concludes her recent piece stating ‘while the RDoC approach promises the greater reliability of objective measurement, it will still be important to maintain careful phenomenological description… Ideally, DSM-5, ICD-11 and RDoC should enrich each other’.

In summary, Levy’s prediction of improved reliability comes twelve years after she and other signatories of the International Consensus Statement equated the science supporting the ADHD with the laws of gravity. In relation to the house of cards supporting the ever increasing ADHD prescribing rates, isn’t it time for the laws of gravity to prevail.


[1] Levy Florence, ‘DSM-5, ICD-11, RDoC, and ADHD Diagnosis’, Australian and New Zealand Journal of Psychiatry, Vol 48;12

[2] Timimi Sami, et al (2004), ‘A Critique of the International Consensus Statement on ADHD’, Clinical Child and Family Psychology Review, Vol. 7, No.1

[3] Frances Allen, ‘Taming the ADD Epidemic’, Huffington Post, 3 September 2012. Available

[4] Levy Florence, ‘DSM-5, ICD-11, RDoC, and ADHD Diagnosis’, Australian and New Zealand Journal of Psychiatry, Vol 48;12

[5] Levy Florence, ‘DSM-5, ICD-11, RDoC, and ADHD Diagnosis’, Australian and New Zealand Journal of Psychiatry, Vol 48;12

[6] Richard L. Morrow MA (et al), ‘Influence of relative age on diagnosis and treatment of attention-deficit/hyperactivity disorder in children’ CMAJ, March 5, 2012,

[7] ABC Online News, ‘Study finds genetic link to ADHD’, 30 September 2010. Available at

[8] Williams, Dr N.M. & Thapar, Prof. A., et al (2010), ‘Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: a genome-wide analysis’, The Lancet, Vol. 376:9750, pp.1401-1408. Available at (accessed 24 October 2012).

[9] American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, Washington DC: American Psychiatric Association.

[10] American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, Washington DC: American Psychiatric Association.

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