It may seem remarkable to produce a consensus statement (Barkley, 2002), which essentially says that ADHD is not primarily the result of environmental factors, without any references in the body of the document. Instead a long, non-specific list of supporting references for the statement is attached. It is as though the length of the list of references is supposed to provide weight to the argument. Surely there should be specific references to support the arguments that there are neurological and genetic contributions to the disorder, and that medication is effective, so that the strength of the evidence can be critically assessed.

In the same way the eminence of the signatories to the statement is meant to give it authority. However, critical theory seeks to analyse why and how people accept or consent to systems of collective beliefs that legitimate various power structures. Debate about whether this statement has the authority of consensus exemplifies the ideological nature of the issue.

To give the "consensus" statement its due, it does not make generally conclusive statements about aetiology. It merely recognises "the mounting evidence of neurological and genetic contributions to this disorder" and advocates the use of medication "combined with educational, family and other social accommodations". So where is the conflict that the consensus statement is supposed to combat?

It accuses critics of regarding ADHD as a "hoax". To make the case for more understanding of ADHD in the context of family and school life is not the same as viewing ADHD as a hoax (Double 2002a).

Nor is it correct to imply that biological factors are obviously primary. Findings are still provisional and anatomic differences on brain scans cannot contribute to diagnostic assessment (Overmeyer & Taylor, 2000). This is because neuroimaging studies are inconsistent and specific abnormalities have not yet been convincingly demonstrated (Baumeister & Hawkins, 2001).

Although claims are made that the genetic basis of ADHD is much better established than other disorders (Thapar & Thapar, 2003), the finding that ADHD is a familial disorder does not necessarily imply genetic transmission. Estimates of the extent to which traits are familial because of shared genes, shared environment or a combination of both, from twin and adoption studies are open to interpretation. In fact, twin studies confirm that environmental factors play a role as the risk for an identical twin is less than 100% (Faraone & Biederman, 2000). The available data do not permit integration of cognitive, neuroimaging and genetic studies (Tannock, 1998).

Despite the number of studies of effectiveness of medication, there is still a danger of misinterpreting bias in clinical trials as an indication of effectiveness (Double, 2002b). The placebo effect should not be underestimated.

In fact, the crux of the issue may not be about evidence as such. There may be a sense in which the consensus statement could never be proven. The nature of mental disorders, including ADHD, are such that their biological causation is inevitably hypothetical. Of course, constitutional factors and brain functioning are important, but the statement wishes to make claims about aetiology beyond the evidence.

The question is more about whether reducing people to objects that need their biology cured leads to appropriate interventions. The implication of the consensus statement is that it encourages an avoidance of understanding of the context of the presentation of ADHD. The last sentence of the statement makes clear that it is motivated to avoid blaming those who may suffer from ADHD or their parents and teachers. But can we really avoid looking at the reasons for human action? For example, parents may do dreadful things to their children, not always consciously. Developmental factors are crucial in the behaviour of children.

I can understand a wish to avoid blame. Indeed, it is not the primary motivation of critics that the consensus statement seeks to shut out of the debate. Statements about the causes of human behaviour can rarely demonstrate one-to-one correspondence. Blame does not necessarily arise as a consequence of environmental factors. Recent data on how experience moulds the brain holds out the possibility for mind-brain integration in the social construction of the brain (Eisenberg, 1995). Brain cytoarchitecture is itself fashioned by input from the social environment.

What the critical perspective seeks to establish is an understanding and social discourse about mental disorders such as ADHD. There is a consensus about ADHD being a cultural construct as much as there is a consensus for the so-called "scientific" worldview of ADHD (Timimi, 2002). People have devoted years, if not entire careers, to this cultural perspective, as much as the natural scientists who have signed the consensus statement. The implications for practice of taking the step of faith in believing the biomedical model of ADHD need to be acknowledged (Double, 2003).

Barkley, RA (2002) International consensus statement on ADHD. January 2002. Clin Child Fam Psychol Rev 5:89-111

Baumeister, AA & Hawkins, MF (2001) Incoherence of neuroimaging studies of attention deficit/hyperactivity disorder. Clin Neuropharmacol 24:2-10

Double, DB (2002a) Re: People with ADHD are not lazy, unmotivated and irresponsible. http://bmj.com/cgi/eletters/324/7352/1523#23222, 22 June 2002

Double DB (2002b) Misunderstanding ADHD: The reality of the efficacy of methlyphenidate. http://bmj.com/cgi/eletters/324/7352/1523#26823, 9 November 2002

Double, DB (2003) Can a biomedical approach to psychiatric practice be justified? J Child Fam Stud [in press]

Eisenberg, L. (1995) The social construction of the human brain. Am J Psychiatry, 152:1563-75

Faraone, SV & Biederman, J. (2000) Nature, nuture, and attention deficit hyperactivity disorder. Dev Rev 20:568-581.

Overmeyer, S & Taylor, E. (2000) Neuroimaging in hyperkinetic children and adults: an overview. Pediatr Rehabil 4:57-70

Tannock, R (1998) Attention deficit hyperactivity disorder: advances in cognitive, neurobiological, and gentic research. J Child Psychol Psychiatry 39:65-69

Thapar, AK & Thapar, A. (2003) Attention-deficit hyperactivity disorder. Br J Gen Pract 53:225-230

Timimi, S (2002) Pathological child psychiatry and the medicalisation of childhood. Brunner-Routledge