| 20 | CC | David Coghill | 1.1 | The document uses both the DSM-IV term of ADHD and ICD-10 hyperkinetic disorder. It also, however, uses ADHD as an umbrella term. The GDG should agree on a nomenclature and clarify this at the beginning of the document something along the lines of ‘we will use the terms ADHD (DSM-IV) and hyperkinetic disorder (ICD-10) when talking about the specific diagnostic categories, however when discussing the general disorder we will use ADHD as an umbrella term’ (others have chosen to use ‘AD/HKD’ as the umbrella. To this could be added the paragraph on ‘hyperactivity’ in the last paragraph in Section 1.2. | No reference suggested. | Comment addressed, see Section 5.2 ‘ADHD and hyperkinetic disorder’. |
| 78 | PR | Jonathan Leo | 1.1 | Just because we can diagnose a trait does not mean it is a disease. Your title could leave some people with the mistaken impression that if you can identify a trait and label it, that it can then be called a disease. The validity of the diagnosis – whether you can reliably identify it in some children – is an interesting question, but in this document it is simply a distraction from the main question. The essential question for the NICE committee should be: Is the disease concept of ADHD valid? With that in mind Section 1.4.1, 1.4.2, 1.4.2.1, and 1.4.2.2 have little relevance. The most important Section, which most of my comments address, is 1.4.6. | No reference suggested. | Comment addressed, see Sections 5.3 and 5.10. |
| 42 | PR | David Cottrell | 1.1 | This comment may be redundant as definitions may come earlier in the guide but reading this section in isolation I wanted to see a clearer definition of ADHD and HK disorder at the beginning of the chapter. | No reference suggested. | Comment addressed, see Section 5.2 ‘ADHD and hyperkinetic disorder’. |
| 21 | CC | David Coghill | 1.2 | Overall I feel this section needs considerable rewriting as it does not flow at all well. As such does not do justice to the rest of the document which is essentially well written and organised. I have made some suggestions in the text. | No reference suggested. | Comment addressed, see Sections 5.1 to 5.4. |
| 50 | PR | Stephen Faraone | 1.2 | You might note that the methodology used to create the Washington University Diagnostic Criteria has been widely accepted and that similar approaches have been used to validate categories for the Research Diagnostic Criteria, the DSM and the ICD criteria (when relevant validating data have been available). My point is that your choice of the WDC is far from arbitrary as there is some consensus as to what the ‘rules of evidence’ should be for asserting the validity of a psychiatric disorder. The intellectual foundation for all these criteria relies heavily on the concept of ‘construct validity’ so well articulated by Paul Meehl decades ago. | No reference suggested. | Comment addressed, see Section 5.4. |
| 22 | CC | David Coghill | 1.2 para 2 | ‘Furthermore, in keeping with other common behavioural disorders there is no clear distinction between the clinical condition and the normal variation in the general population’.
The meaning of this sentence is rather unclear. I think it is confusing (or maybe confounding?) symptoms and impairment and to do with the precise words used. There is a continuity of symptoms between those with the disorder and the population. However those with the clinical condition have both high levels of symptoms and impairment leading to a clearer ‘distinction’ between the two. Whilst this may seem trivial the actual sentence is contrary to the conclusions and will be picked up by those who wish to point out that NICE says ‘there is no clear distinction between the clinical condition and the normal variation in the general population’ without clarifying the context of the quotation. | No reference suggested. | Comment addressed, see Sections 5.3 (third paragraph) and 5.5.3. |
| 80 | PR | Jonathan Leo | 1.3 | I think that somehow you need to mention that your literature review was very selective and systematically ignored review articles that were critical of the ADHD diagnosis. As you are aware of both the controversy surrounding the diagnosis and those authors who have addressed the problem, I am assuming that it was a conscious decision to ignore one side of the debate. There is a large body of literature that sees forces other than biology as the source for the dramatic rise in the diagnosis of ADHD. This literature comes from wide and varied sources and is representative of a large segment of the mainstream media and academia. Since one reason that NICE is taking on this difficult task is because the ADHD diagnosis is controversial, it does not make sense to simply ignore critical publications. Just summarising the reviews from mainstream psychiatry journals does not give a balanced view, especially when one considers that it is extremely difficult to get anything published in a psychiatry journal or medical journal that is critical of the ADHD diagnosis. You even acknowledge in one section of the document that, because there was limited data ‘the systematic evidence was supplemented with expert opinion, drawing on evidence known to members of the GDG’.
By selectively choosing data in support of a particular point of view it suggests that your conclusions were made first, and the studies were then subsequently chosen to support your conclusion, and not the other way around, that a group of non-partisan academics analysed all the data and then came to a conclusion.
As just one example of how the debate is framed in academic journals, in 2002, a group of scientists published the International Consensus Statement on ADHD. The consensus statement had several surprising and remarkable declarations such as: ‘Numerous studies of twins demonstrate that family environment makes no significant separate contribution to these traits’ (which runs counter to the NICE document).
‘One gene has recently been reliably demonstrated to be associated with this disorder. . .’
‘Neuroimaging studies of groups with ADHD also demonstrate relatively smaller areas of brain matter.’
‘Most neurological studies find that as a group those with ADHD have less brain activity. . .’
When a group of academicians sent a letter to the editor of Child and Family Psychology Reviews about the Consensus Statement, the editor responded that the letter could be published, but only if Dr. Barkley, the lead author of the Consensus Statement, was given the courtesy of having the last chance to respond. However, this was not a courtesy initially granted to the academicians critical of the rising diagnosis of ADHD, who Barkley and his co-authors compared to members of the flat-earth society. Thus, the authors of the Consensus Statement were given a second chance to cite evidence in support of the biological basis of ADHD, yet rather than cite several specific articles; they instead mentioned that there were hundreds and hundreds of articles. However, good science is not determined by how high the papers can be stacked but by the quality of the papers. To paint those concerned about the rising use of stimulants as somehow on the fringe, shows how isolated academicians can become from the general public. For the GDG to not acknowledge anyone critical of the diagnosis in their own review puts the GDG in the same category as the Consensus authors. Does NICE want to be in the same category?
Nowhere in the GDG document is there a discussion about the ethics of giving a performance-enhancing drug to improve academic success in school - a major reason the drug is used in the first place. For instance, take the announcement about a recent survey, ‘Results of a survey of physicians suggest that parents often request a “behavioral drug”, such as Ritalin, with the goal of enhancing their child’s academic performance rather than treating an illness.’ (Gale, 2006, italics added). The headlines expressed surprise at this practice, yet the practice of prescribing stimulants to improve academic performance is exactly why these medications are prescribed in the first place, and it is fully sanctioned by the medical community. According to Joseph Biederman, ‘If a child is brilliant but is doing OK in school, that child may need treatment, which would result in performing brilliantly in school’ (Gale, 2006). In fact, no official organisation that supports the use of stimulants has ever said that using stimulants to improve academic performance is inappropriate. Even the GDG has not said this is inappropriate. Is it? | References suggested: Gale (2006) Ritalin requests often deemed inappropriate. Medscape.
Paper excluded: relevant to use of Ritalin, not validity of ADHD; not peer reviewed. | References included in the NICE guideline as evidence (found by systematic searches or identified by GDG members) have to meet quality assessment criteria. This is explained in Chapter 3, Methods.
Comments addressed, see Section 5.9 for limitations of references included and last two paragraphs for use of stimulants.
The use of drug treatment (recommendations) is addressed in Chapter 10, Pharmacological treatment. |
| 82 | PR | Jonathan Leo | 1.4 | In your framing of the question, you ask if environmental factors are associated with ADHD. You then address one review covering the evidence of prenatal exposure to drugs. Again you have systematically ignored a large body of evidence. Perhaps this section is the biggest flaw in your document. Any academic reading this discussion will have a hard time taking you seriously if you cannot think of a single environmental influence coming from the home or school environments that contributes to ADHD. Either you need to comment on this research or explain why you are ignoring it. For instance, a recent study showed that children from divorced families are twice as likely to be diagnosed with ADHD (Strohschein, 2007). And prior studies have shown that children from single family homes are more likely to be diagnosed with ADHD. For more information I have attached two tables and a discussion from Dr Nicky Hart at UCLA who addresses the differences in the ADHD diagnosis across the socioeconomic strata in England and Wales. The data will appear in a forthcoming book, ADHD and Health Inequality.
The statistical evidence generated by the British government as part of its policy making function runs against the impression that ADHD is best thought of as a bio-medical phenomenon. The social distribution of the disorder follows the contours of the class mortality gradient. In other words, it fits the classic profile of health inequality: low prevalence at the top, and high prevalence at the bottom of the social hierarchy. Children exhibiting the symptoms of emotional and conduct disorders, and those afflicted with the troubling symptoms of attention deficit and hyperactivity disorder are much more likely to be poor, to be raised by single and/or unemployed parents, to grow up in neighbourhoods scarred by the signs of under-privilege and to be exposed to stressful life events and social relationships in their early lives.
displays the class gradient of psychiatric morbidity as a whole in British children. The rate is around 4% among children in families where the main breadwinners are employed in higher professional occupations (for example, lawyers, doctors, professors). It is four times higher (16%) in families where parents are either chronically unemployed or have never worked at all.
This group includes single-parent families headed by young women with no labour market experience prior to becoming mothers. The rate of ADHD British style (hyperkinetic disorder) follows the same course. It increases from 0.5% in professional families to 2.6% in households with no attachment to the labour market, a five-fold increase. In between these two poles of social privilege and under-privilege, the risk of mental disorder is around 6% in other middle class strata before ‘jumping’ to more than 8% in the lower supervisory/technical occupations, from this point onwards, it rises steadily on each successive downward rung of the social hierarchy. If we take the lower supervisory occupational category in , as the division between the middle (white collar) and working class (blue collar) strata of British society (containing respectively 56 and 44% of the population), we can conclude that social class is strongly associated with children’s mental well-being. Working class kids face a much higher probability of experiencing the symptoms of mental disorder in all its forms than their peers in middle class homes, hyperkinetic disorder is no exception.
The occupational class gradient of ADHD can be translated to another variable representing the social and economic geography of health inequality. This variable is based on the ACORN classification which uses the census characteristics of the area where a child lives (the postal code) to summarise its salient social characteristics. , classifies the same sample of children by the quality of their living environment. In a literal sense this variable represents the social and economic environment of daily life and therefore the differential opportunities for physical and intellectual development in childhood.
Once again, we find the social gradient so typical in the health inequality research literature. The symptoms of childhood psychiatric morbidity in areas populated by wealthy families are only half the rate of areas where families with moderate means make their homes. The gap is even wider between the most advantaged and the least disadvantaged neighbourhoods and it apples to all mental disorders as well as hyperkinetic disorder. | References suggested:
Strohschein, L. A. (2007) Prevalence of methylphenidate use among Canadian children following parental divorce. CMAJ: Canadian Medical Association Journal 176, 1711–1714.
Paper included.
Hart, N. (in press) ADHD and Health Inequality. Macmillan.
Paper excluded: not peer-reviewed. | Comment addressed, see Section 5.8. |
| 23 | CC | David Coghill | 1.4 general | I do not think that the whole issue of impairment is dealt with well in this section. It makes a significant appearance in the discussion of the Consensus Conference and in the recommendations however it does not read as if it was critically appraised and considered by the GDG. I think this needs to be remedied within 1.4. | No references suggested. | Comment addressed, see Section 5.6. |
| 43 | PR | David Cottrell | 1.4.1 | First paragraph after subheading ‘Evidence’. I have a problem with the use of the word ‘symptom,’ in this chapter. The issue of the diagnostic validity is a contentious one as illustrated by the lengths the GDG have gone to in consulting widely. ‘Symptom’ implies an illness or disorder about which someone is complaining. Question A in 1.2, repeated at the start of 1.4, and question A1 at the start of 1.4.1 are careful in using the neutral term ‘phenomena’ to describe the behaviours of interest. This seems appropriate given that the whole point of this chapter is to reach conclusions about whether ADHD is or is not a useful construct. To then use the word ‘symptom’ seems to suggest that the issue is already decided. Its use may be appropriate when referring to clinical samples but the use at the end of this paragraph relates to a study where the sample is unclear.
This usage recurs in 1.4.1 and throughout the chapter. For example 1.4.3 has ‘phenomena’ in the title but then refers to ‘continuous distribution of symptoms in the population’ in paragraph 3. I will not list all examples here, and as stated above, ‘symptom’ may be appropriate for research on clinical samples but I think language could be used more carefully and would advocate a word search of the document and consideration on each occasion of the word ‘symptom’ whether it is in fact the best word available. | No references suggested. | Comment addressed, see Section 5.2 ‘Symptoms’. |
| 71 | CC | Sami Timimi | 1.4.1 | (A1) Do the phenomena of hyperactivity, inattention and impulsivity cluster together? The GDG conclude, ‘The number of factors varies between studies, with most finding two correlated factors for hyperactivity-impulsivity and inattention; others find that hyperactivity and impulsivity can be distinguished and a few find one combined factor of all three domains’ suggesting little consistency in the literature. | No references suggested. | Comment addressed, see Sections 5.5.1 and 5.10. |
| 24 | CC | David Coghill | 1.4.1 evidence section (should be 1.4.1.1?) | This section would be easier to read if it started with a comment along the lines of, ‘There was strong evidence for clustering of symptoms in both population and clinical samples. Evidence for one, two and three factor models was found with most evidence supporting a two factor model’. | No references suggested. | Comment addressed, see Section 5.5.1 ‘Summary’. |
| 25 | CC | David Coghill | 1.4.1 summary | The possibility of different patterns across different age ranges should be mentioned in the summary | No references suggested. | Comment addressed, see Section 5.5.1 ‘Summary’. |
| 44 | PR | David Cottrell | 1.4.2 | First paragraph, definitions again – it might be helpful to briefly define ‘oppositional defiant and conduct problems’, perhaps in a box? I confess to being unsure what these are myself. Are ‘conduct problems’ the same as conduct disorder? If so why not use a term with an agreed definition? If not we need a definition. The terms oppositional defiant problems, conduct problems, ODD (without ever being given in full), conduct disorder and ‘disruptive behavioural problems’ are all used in Section 1.4.2.1. | No references suggested. | Comment addressed, see Sections 5.2 ‘Oppositional defiant disorder and conduct disorder’. |
| 72 | CC | Sami Timimi | 1.4.2 | (A2) Are ADHD symptoms distinguishable from other conditions? It is noted that ‘Frouke and colleagues (2005) conducted a diagnostic study of 2,230 Dutch pre-adolescents from the general population. LCA revealed that ADHD symptoms clustered together with symptoms of oppositional-defiant disorder and conduct disorder. A further study from the Netherlands of disruptive behaviour in 636 7-year-old children (Pol et al., 2003) came to similar conclusions’ and ‘Multivariate twin modelling suggests that while the genetic influences on conduct disorder are largely shared with those that influence ADHD’ and ‘ADHD is reported to co-occur with personality disorder in young offenders (Young et al., 2003)’ and ‘Dysthymia, depression and anxiety symptoms and disorders are frequently associated with ADHD in adults.’ The GDG’s own evidence is suggesting high levels of comorbidity raising doubts about the specificity of ADHD symptoms. The GDG use a ‘get out of jail card’ by concluding that this is because ‘Longitudinal studies suggest that ADHD represents a separate condition that is a risk factor for the development of oppositional and conduct problems.’ However, only one reference is cited in support of this (and this was in a study in which the chair of the GDG is the lead author). | No references suggested. | Comment addressed, see Section 5.5.2 ‘Summary’ (third paragraph). |
| 62 | PR | Anita Thapar | 1.4.2.1 | ‘There are in addition environmental factors that influence the risk for conduct problems but not ADHD’. Suggest delete ‘but not ADHD’ Twin studies show important E contribution. | No references suggested. | Comment addressed, see Section 5.8.2. |
| 63 | PR | Anita Thapar | 1.4.2.1 | ‘The heritability of ADHD symptoms is also higher than that for ODD/CD symptoms in these studies’. Suggest delete that sentence.
It is not scientifically sensible to compare heritability estimates as they are population specific. Also some of the most genetic syndromes (for example, in general medicine) can show lower heritability estimates. | No references suggested. | Comment addressed, see Section 5.8.2. |
| 29 | CC | David Coghill | 1.4.2.1 and sumary for 1.4.2 | Pervasive developmental disorders are mentioned in the summary but not in the main body of the text. If there is info re. PDD it should be discussed, if there is not this also should be mentioned. | No references suggested. | Comment addressed, see Section 5.5.2 ‘Summary’. |
| 26 | CC | David Coghill | 1.4.2.1 para 2 | This paragraph should make it clearer that these studies disagree with those cited in para 1 by attaching a statement to that effect before giving the evidence (it is interesting that these are the only two studies in this Section with n reported). | No references suggested. | Comment addressed, see Section 5.5.2, ‘ADHD and oppositional defiant and conduct problems’. |
| 27 | CC | David Coghill | 1.4.2.1 para 2 | What is CP? | No references suggested. | Typing mistake, now reads ‘CD’ for conduct disorder. |
| 28 | CC | David Coghill | 1.4.2.1 para 4 | ‘However the two often occur independently of each other and only partially share aetiological factors’. Should read:
‘However the two often occurred independently of each other and only partially shared aetiological factors’, as it is citing the finding of the study not a general finding. | No references suggested. | Comment addressed, see Section 5.5.2 ‘Summary’. |
| 7 | PR | Margaret Alsop | 1.4.2.2 | Due to our involvement within many working and commissioning groups, it has been highlighted by Youth Offending Teams (YOTs), probation services, prisons, young offenders institutes, police, Youth Inclusion Support Programmes (YISPs) Connexions Services, Young People’s Supported Housing, Housing Advice, Young People leaving Care, drug advisory teams and the legal profession such as magistrates/judges that there is now a high percentage of individuals with ADHD or suspected ADHD reaching these services.
According to the Cambridgeshire study in 1995, 90% of recidivist juvenile offenders had a conduct disorder at age 7. Young offenders are now responsible for about a third of all the criminal convictions. A Youth Justice Board survey showed that the number of criminal offences committed by young people is probably far higher than the conviction rates suggest. | References suggested:
Cambridgeshire study (1995).
Asked reviewer for full reference; no response. | Comment taken into consideration, see Sections 5.5.2
‘ADHD and oppositional defiant and conduct problems’, ‘ADHD and other co-occurring conditions’ and 5.6 ‘Antisocial behaviour’. |
| 64 | PR | Anita Thapar | 1.4.2.2 | ‘Overlapping genetic influences on ADHD and conduct problems but the genetic influences estimated by twin studies are greater for ADHD than ODD/CD. . . .’
Delete part of sentence, ‘but the genetic influences estimated by twin studies are greater for ADHD than ODD/CD’. See above for reason. | No references suggested. | Comment addressed, see Section 5.5.2 ‘Summary’. |
| 30 | CC | David Coghill | 1.4.3 | I feel this section should precede the current 1.4.2 as it would seem logical to sat does adhd separate from normality and if so does it separate from other disorders. [sic] | No references suggested. | The sequence used follows the Washington University Diagnostic Criteria sequence. |
| 31 | CC | David Coghill | 1.4.3 | It should be made clearer that the factor approaches can only deal with the symptom level. It does not take into account the whole issue of impairment. Impairment is discussed in some depth in Section 1.7.1 but I feel that it should be discussed or at least better acknowledged in Section 1.4. Again a failure to do so will lead to misuse of isolated sections of the guidance out of context and could lead to misunderstandings. | No references suggested. | Comment addressed, see Section 5.5.3 ‘Summary’ (last paragraph). |
| 51 | PR | Stephen Faraone | 1.4.3 | I agree with the comments in this section. But one point is missing. I think that the studies which show ADHD to be an extreme of a quantitative trait have typically defined ADHD based on symptom criteria alone. Their results may have been different if impairment criteria were used to define disorder status. | No references suggested. | Comment addressed, see Section 5.5.3 ‘Summary’ (last paragraph). |
| 65 | PR | Anita Thapar | 1.4.3 | ‘. . .high ADHD symptom scores are the same as those that influence ADHD symptom levels. . .’
DF analysis can’t distinguish this – shows that the magnitude of the heritability estimate is the same for high as for ‘normal range’.
Suggest reword to ‘high ADHD symptoms scores are of the same magnitude as those that influence ADHD symptom levels. . .’ | No references suggested. | Comment addressed, see Section 5.5.3. |
| 73 | CC | Sami Timimi | 1.4.3 | (A3) Are the phenomena of hyperactivity, inattention and impulsivity distinguishable from the normal spectrum? It is stated that, ‘These studies show that children with ADHD appear to be at one extreme of a quantitative dimension and on this quantitative dimension there is no obvious bi-modality that separates children with ADHD from non-ADHD children.’ It is also noted that ‘there is no obvious threshold or cut-off between ADHD and the continuous distribution of symptoms in the population.’ In the introduction to the document it is stated that ‘in keeping with other common behavioural disorders there is no clear distinction between the clinical condition and the normal variation in the general population.’ The GDG conclude that, ‘Most analytic approaches are unable to make a clear distinction between the diagnosis of ADHD and the continuous distribution of ADHD symptoms in the general population’. In other words the answer to question 1.4.3 is, according to the evidence presented, ‘no’. | No references suggested. | Comment addressed, see Section 5.5.3 ‘Summary’. |
| 74 | CC | Sami Timimi | 1.4.4 | Is the cluster of symptoms that defines ADHD associated with significant clinical and psychosocial impairments? The GDG provides evidence that is consistent with ADHD being associated with significant impairment. However, what is not properly addressed is the nature of this association and direction of causality. For example, with regards academic difficulties it is noted that, ‘These impairments often lead to grade retention (Hinshaw, 2002), to a lower probability of completing schooling when compared with children who do not have ADHD (Mannuzza et al., 1993)’. This association could be mediated by a third factor, such as lowered self-esteem, boy-unfriendly school curricula, frustration, learning difficulties, and so on, that leads to both ADHD symptoms and poor school performance. In family difficulties it is mentioned that, ‘Follow-up studies indicate that mothers of children and adolescents with ADHD have more difficulty in child behaviour management practices and coping with their child’s behaviour (August et al., 1998), and display higher rates of conflict behaviours, such as negative comments, social irritability, hostility and maladaptive levels of communication and involvement (August et al., 1998; Fletcher et al., 1996). Family impairment also permeates the parent’s lives. Parents of children with ADHD report having less time to meet their own needs, fewer close friendships, greater peer rejection, less time for family activities, which might lead to less family cohesion and a significant effect on the parent’s emotional health (Bagwell et al., 2001).’ A vast repertoire of attachment studies also suggest that this association might well indicate important causal factors for ADHD symptoms (that is, these family difficulties cause rather than are caused by ADHD, or more likely interact in varying degrees and combinations depending on the family and individual). With regard to antisocial behaviour the GDG notes, ‘In a prospective follow-up of 103 males diagnosed with ADHD, the presence of an antisocial or conduct disorder almost completely accounted for the increased risk for criminal activities’ and ‘Lee and Hinshaw (2004) reported that the predictive power of ADHD status to adolescent delinquency diminishes when key indices of childhood externalising behaviour related to ADHD are taken into account’. Finally, discussion of long-term outcome is difficult to interpret given that no information is provided by the GDG on the relationship of outcome to other factors known to be associated with poorer outcome such as social class, IQ, comorbid diagnoses and so on. | References suggested: attachment studies.
Asked reviewer for full references, no response. | Comment addressed, see Sections 5.6 and 5.11. |
| 32 | CC | David Coghill | 1.4.4 and 1.4.5 | I think that the substance misuse issues should be considered in 1.4.4 rather than 1.4.5. This Section should also comment on the interactions between early treatment with stimulants and later occurring substance misuse and include nicotine as a drug of misuse that attenuates ADHD symptoms. | No references suggested. | Comment addressed, see Section 5.6. |
| 8 | PR | Margaret Alsop | 1.4.4.2 | Whilst we agree in principle, our own personal experiences and that of having worked with and supported many families for over a decade through the ADHD Support Group, there are clear indications that parents are still being subjected to accusations of ‘poor parenting’. As parents, not only are we dealing with the family members’ needs, and those of siblings but also with professional bodies such as health, education and social care in which to access an appropriate multi-agency, multi-disciplinary service for the ADHD family member, no one body taking responsibility in which to meet the needs of those with ADHD or those of family members.
Such dealings may lead to conflict between parent carers and service providers, therefore having an impact on service delivery. A high percentage of parents and family members living with ADHD may be accessing mental health services for that of their own needs. | No references suggested. | Comment taken into consideration. |
| 45 | PR | David Cottrell | 1.4.4.2 | The other parts of 1.4.4 address the potential confounding influence of comorbid conduct disorder, this is not mentioned in this section on family difficulties. | No references suggested. | Comment addressed, see Section 5.6 ‘Family difficulties’. |
| 9 | PR | Margaret Alsop | 1.4.4.3 | Could it be that by the time the ADHD child is a teenager they may feel that they are somehow different from their friends, but may not understand why? To the ADHD adolescent, they often think that there is some kind of secret code going on between others. This ever widening void is being caused by their inability to learn the code of social cues–those nuances of physical expression and movement that carry half of any conversation and convey personal attitude, varying emotions and defence (or lack of it) between other conversing groups of people.
The ADHD adolescent may have a two-way body language problem involving interpreting others and giving the right signals in return. They may try and copy those around them, without being aware of the subtle complexities or of what is or is not socially acceptable.
‘Too many children fail to achieve their full potential and face involvement in crime, poor health, early unwanted pregnancies, substance misuse or under-achievement in education because services fail to spot the emerging risks or to intervene early enough to coordinate the support necessary. We know that factors such as poverty, failure at school, mental health, family problems or antisocial behaviour can each be possible indicators of future problems’. (Cross Cutting Review of Children at Risk for the 2002 Spending Review). | References suggested: Cross Cutting Review of Children at Risk (2002).
Paper excluded: Not specific to ADHD; not peer reviewed. | See Section 5.6. |
| 10 | PR | Margaret Alsop | 1.4.4.5 | Adults with ADHD we have found may have a criminal record of some sort, this highly impacting on their accessing appropriate adult educational programmes, many with no educational qualifications (under-achieving academically), poor record of school attendances or exclusions from education, all of which are contributing factors and play a major role in their employment or future employment status. Multi-agency working to include occupational therapists during transitional services would perhaps contribute towards meeting the needs of those with ADHD and working alongside future employers. | No references suggested. | Comment addressed, see Section 5.6 ‘Adolescent and adult problems’. |
| 52 | PR | Stephen Faraone | 1.4.4.5 | You might also mention the data showing ADHD patients to be at high risk for traffic citations and traffic accidents. You could also mention their increased healthcare utilisation. | References suggested:
Risk for traffic accidents.
Asked reviewer for full references, no response. | Comment addressed, see Section 5.6 ‘Adolescent and adult problems’. |
| 11 | PR | Margaret Alsop | 1.4.5 | Many children accessing CAMHS or paediatric services may do so until aged 16–17 years. A high percentage of this group may not be referred onto the adult community mental health teams, therefore a child who has received a multi-agency as well as a medicinal approach to treatments for ADHD may well end up in that ‘grey area’ of their not accessing the appropriate healthcare and treatments could all be contributing factors to the possibility of their self-medicating on other substances. | No references suggested. | Comment taken into consideration. For recommendations on this matter refer to the NICE guideline. |
| 46 | PR | David Cottrell | 1.4.5 | First paragraph after subheading ‘Summary’, line 10 – is ‘appropriate’ correct? Earlier you say the evidence is poor and that developmentally appropriate criteria have yet to be developed. I suspect this should be ‘inappropriate’. | No references suggested. | Comment addressed, see Section 5.7.2. |
| 53 | PR | Stephen Faraone | 1.4.5 | In the summary, the following sentence is not clear and should be re-worded: ‘The profile of symptoms may alter with a relative persistence of inattentive symptoms compared with hyperactive-impulsive symptoms, however the evidence base for this conclusion is poor, using developmentally appropriate measures of hyperactivity-impulsivity in adults.’ | No references suggested. | Comment addressed, see Section 5.7.2. |
| 54 | PR | Stephen Faraone | 1.4.5 | The summary states: ‘There was no evidence to warrant a different diagnostic concept in childhood and in adulthood.’ This seems a bit too strong. The DSM itself allows for a different diagnostic concept:
the category of in partial remission can be used for adults; a subjective feeling of restlessness can be diagnostic of motor hyperactivity.
Russ Barkley’s new book (and some of his prior work) suggests that the current ADHD symptoms are not developmentally sensitive and there have been some initiatives to re-write the ADHD rating scale (for example, work by Spencer and Adler) so that the questions are more relevant to adults. Also, I think that the greater reduction of hyperactive-impulsive versus inattentive symptoms is more strongly supported than you suggest. But these are all, for sure, debatable points. | References suggested:
Barkley’s book:
Paper excluded:
not peer-reviewed. | Comment addressed, see Section 5.7.2. |
| 55 | PR | Stephen Faraone | 1.4.5 | I don’t understand the statement, ‘there is a lack of data on the continuity of aetiological factors into adulthood.’ Given that many of the known risk factors for ADHD occur very early in development (for example, genes, fetal toxic exposures), why would we think their effects turn off during adult- hood? I think you mean that we know little about which risk factors modify the course of ADHD through adolescence into adulthood. Probably a re-wording is needed. | No references suggested. | Comment addressed, see Section 5.7.2. |
| 75 | CC | Sami Timimi | 1.4.5 | Is there evidence for a characteristic pattern of developmental changes, or outcomes associated with the symptoms, that define ADHD? It is noted that ‘Faraone and colleagues (2006) analysed data from 32 follow-up studies of children with ADHD into adulthood. Where full criteria for ADHD were used approximately 15% of children were still diagnosed with ADHD at age 25’. This is the only systematic review identified outside of point 1.4.6 (where seven were identified). This finding seems to suggest that ‘characteristic’ outcomes for those diagnosed with ADHD is far from established. Later the GDG speculates as to why rates of substance abuse are higher in those with ADHD symptoms (is this a ‘characteristic’ outcome?) stating: ‘The mechanisms involved can include one or more of the following: first, that individuals with ADHD may seek out highly stimulating or risky activities; second, that individuals with ADHD are exposed to higher levels of psychosocial risks for development of substance use disorders, resulting from educational and social impairments, social exclusion and antisocial behaviour associated with ADHD; third, that various substances, including cannabis, alcohol and stimulants can attenuate ADHD symptoms and are therefore sometimes used as a form of self-treatment.’ Whilst it is unclear why the GDG felt the need to speculate (without evidential references) on this issue, narrow linear biomedical paradigms seems to have allowed them to overlook fairly basic scientific issues. The relationship between ADHD and substance misuse that they are referring to is an association, and thus a third (or more) factor may be responsible for both the substance misuse and ADHD symptoms (such as low self-esteem, family conflict, learning difficulties, comorbid conditions, and so on) making the required criteria of ‘characteristic’ difficult to establish. | No references suggested. | Comment addressed, see Section 5.7.2. |
| 33 | CC | David Coghill | 1.4.5 summary | ‘Using child criteria, approximately 15% of children with ADHD retain the diagnosis by age 25 but a much larger proportion (65%) show persistence of symptoms with associated impairments.’
Could read: ‘Using child criteria, approximately 15% of children with ADHD retain the diagnosis by age 25 but a much larger proportion (65%) show some persistence of symptoms with significant associated impairments.’ | No references suggested. | Comment addressed, see Section 5.7.2. |
| 35 | CC | David Coghill | 1.4.6 | Also the whole issue of heterogeneity at all levels of analysis needs to be discussed as this is central to the whole issue of what is ADHD. I guess the current conclusion would be something like: here are a group of symptoms that hold together pretty well that can be distinguished from normal and other disorders that cause impairment but seem to be the end point (behavioural phenotypic expression) of a wide range of different causal pathways. This would assist the discussion of diversity in Section 1.6. | No references suggested. | Comment addressed, see Section 5.8. |
| 47 | PR | David Cottrell | 1.4.6 | Could/ should you define executive function for a lay readership? | No references suggested. | Comment addressed, see Section 5.8.1. |
| 56 | PR | Stephen Faraone | 1.4.6 | I suggest you include the following: Valera, E. M., Faraone, S. V., Murray, K. E., et al. (2007) Meta- analysis of structural imaging findings in attention- deficit/hyperactivity disorder. Biological Psychiatry, 61, 1361–1369. | References suggested: Valera, E. M., Faraone, S.V., Murray, K. E., et al. (2007) Meta-analysis of structural imaging findings in attention-deficit/ hyperactivity disorder. Biological Psychiatry, 61, 1361–1369. Paper included | Comment addressed, see Section 5.8.1 ‘Neuroimaging studies’ |
| 57 | PR | Stephen Faraone | 1.4.6 | A more thorough review of the molecular genetics literature would implicate other genes but that is not essential to make your point. If you’d like to improve the review of environmental risk factors, you could consult: Banerjee, T. D., Middleton, F. & Faraone, S. V. (2007) Environmental risk factors for attention-deficit hyperactivity disorder. Acta Paediatrica, 6, 1269–1274. | References suggested: Banerjee, T. D., Middleton, F. & Faraone, S. V. (2007) Environmental risk factors for attention-deficit hyperactivity disorder. Acta Paediatrica, 6, 1269–1274. Paper excluded: Review (no systematic search). | Comment taken into consideration. |
| 66 | PR | Anita Thapar | 1.4.6 | Li et al., 2006:
There have actually been a number of meta-analyses. Most but not all have found the same as Li et al. Might want to mention at least that there have been several. The point of contention is DAT, where most meta-analyses have found no association but some notably have, for example Weiss, S., Tzavara, E. T., Davis, R. J., et al. (2007) Functional alterations of nicotinic neurotransmission in dopamine transporter knock-out mice. Neuropharmacology, 52, 1496–508.
Epub 24 Feb 2007. | References suggested: Weiss, S., Tzavara, E. T., Davis, R. J., et al. (2007) Functional alterations of nicotinic neurotransmission in dopamine transporter knock-out mice. Neuropharmacology, 52, 1496–508. Paper excluded: Only studies on humans considered. | Comment taken into consideration. |
| 67 | PR | Anita Thapar | 1.4.6 | ‘..acting through gene-environment interactions’. Add ‘and gene-environment correlations ()’.
Jaffee, S. R. & Price, T. S. (2007) Gene-environment correlations: a review of the evidence and implications for prevention of mental illness. Molecular Psychiatry, 12, 432–442. Epub 16 Jan 2007. Review. | References suggested: Jaffee, S. R. & Price, T. S. (2007) Gene-environment correlations: a review of the evidence and implications for prevention of mental illness. Molecular Psychiatry, 12, 432–442. Paper excluded: Review (no systematic search). | Comment taken into consideration, see Section 5.13. |
| 68 | PR | Anita Thapar | 1.4.6 | Literature on prenatal stress? Few studies now on this and ADHD, even though not covered by Linnet study.
Talge, N. M., Neal, C. & Glover, V. (2007) Antenatal maternal stress and long-term effects on child neurodevelopment: how and why?
The Journal of Child Psychology and Psychiatry, 48, 245–61. Review. | References suggested: Talge, N. M., Neal, C. & Glover, V. (2007) Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? The Journal of Child Psychology and Psychiatry, 48, 245–61. Paper included. | Comment addressed, see Section 5.8.1, ‘Physical environ- mental risks’. |
| 76 | CC | Sami Timimi | 1.4.6 | Is there consistent evidence of genetic, environmental or neurobiological risk factors associated with ADHD? The GDG concludes, ‘Specific genetic variants that are associated with a small increase in the risk for ADHD have been identified in the dopamine D4 and close to the dopamine D5 receptor genes. Analysis of ADHD versus non-ADHD groups has identified consistent changes in brain function and performance on neurocognitive tests; however differences from controls are not universal, do not characterise all children and adults with a clinical diagnosis of ADHD, and do not usually establish causality in individual cases.’ [my italics] The GDG were provided with several papers providing a critical evaluation of research in this area. None were cited in this document.
The GDG after reviewing the evidence and mentioning that, ‘The quality of the evidence included in this review was variable and lacked any “gold standard” ’goes on to recommend that ADHD is valid and to make a diagnosis the following criteria should be met: ‘Symptoms of ADHD (DSM-IV) or hyperkinetic disorder (ICD-10) should be sufficient to reach a formal diagnosis in DSM-IV or ICD-10. ADHD should be considered in all age groups (children, adolescents and adults), with symptom criteria adjusted for age appropriate changes in behaviour. The level of impairment resulting from symptoms of hyperactivity and or inattention should be at least moderately clinically significant on the basis of interview and or direct observation in multiple settings, and pervasive (occur in all important settings) including social, familial educational and or occupational settings.’ This is essentially no different to current DSM-IV criteria and one wonders what the point of this expensive, time consuming exercise was if this is the best the GDG can come up with, particularly when the GDG provide little guidance as to how a clinician is to interpret words like ‘moderately’, and ‘significant’. Given that the chair of the group is well publicised for believing that ADHD is under-diagnosed in the UK, and that using DSM-IV criteria gives prevalence rates of between 3 and 7%, this guideline is likely to result in an increase of ADHD diagnosis. Given these potentially far reaching implications for children and adults in this country and the tenuous evidential support in the document, the basis for the GDG’s conclusions must be questioned.
The GDG states that, ‘It was recognised that defining psychiatric disorders is a difficult process due to the overlapping nature of behavioural and psychiatric syndromes, the complexity of the aetiological processes and the lack of a “gold standard” such as a biological test—in this regard ADHD is no different from other common psychiatric disorders.
Furthermore, in keeping with other common behavioural disorders there is no clear distinction between the clinical condition and the normal variation in the general population’. The phrase ‘two wrongs don’t make a right’ came to mind on reading this. A get-out clause that because other psychiatric diagnoses are problematic constructs (and there is a large literature that attests to this), it is acceptable for a lowering of standards and evidential basis with which to evaluate ADHD, is a circular argument to excuse poor science and insufficient rigour.
The GDG states that, ‘Furthermore, in keeping with other common behavioural disorders there is no clear distinction between the clinical condition and the normal variation in the general population (see Section A3). This is comparable to normal variation for medical traits such as hypertension and type II diabetes’. Such a spurious analogy reveals the extent to which the GDG has ignored one of the most important differences between physical states and psychiatric ones – meaning. 120/80 BP means the same whether it is measured in New York or New Delhi and reflects a physical state (universalism). Further, the pathophysiological processes resulting from high blood pressure are known and independent of the meaning any culture ascribes to symptoms (essentialism). This is not the case for behavioural presentations such as ADHD, which has varying interpretations and meanings, just as beliefs about what is a ‘normal childhood’ and ‘normal child development’ varies enormously over time and between cultures. It is of concern that the GDG seems unaware of the diverse literature (from disciplines such as transcultural psychiatry and psychology, philosophy, anthropology and sociology) criticising the inappropriate use of univeralist and essentialist models (drawn from the biomedical paradigm) in multicultural societies. This is considered a very basic error. Such an approach leads to institutional racism as it assumes that the beliefs and practices about children and childhood drawn from a narrow Western biomedical paradigm is the standard through which to judge those cultures who have differing beliefs and practices with regards their paradigms for understanding the nature of childhood, childhood problems and child care and rearing. This replicates the dynamics of colonialism and such attitudes being promoted for our institutional practices are simply unacceptable in modern multicultural Britain.
The most disappointing aspect of the document is the missed opportunity for a more erudite approach to the question of diagnosis. Given the poor quality of the document it is likely that the current GDG simply does not have the objectivity, knowledge, or sophistication to produce an evidence-based, ethical and progressive review and set of guidelines that could help curtail bad practice, but more importantly provide guidelines that take practice beyond current simplistic paradigms to make it fit for the realities of multi-cultural 21st century Britain. Psychiatry has been increasingly grasping the complexity that comes from a territory that sits at the meeting point of many disciplines’ discourses. Medicine too has increasingly grasped these cross-disciplinary perspectives leading to growth of practices such as narrative medicine and values-based medicine to try and encompass the subjective, cultural, social, political, economic and psychological influences on physical health and medical treatment. In this respect psychiatry should be providing a lead for the rest of medicine as we increasingly move away from redundant dualistic conceptualisations such as mind/body, nature/nurture and universal/relative and toward accepting multiplicity in a way that reflects the diverse nature of the client group we wish to assist. Engagement with these issues would lead to an ability to examine validity of ADHD from a number of angles, recognising that there are many different approaches to this question that reflect different values and aims. For example, in addition to scientific validity, there are considerations of pragmatics, utility, administrative, consistency, relevance, coherence, precision, fecundity, epistemic, ethical, onto-logical, and so on. Using these multiple positions would enable greater transparency and openness to the novel and more flexible guidelines that have greater likelihood of enabling more appropriate engagement with the diverse issues clients with ADHD symptoms present with. It is clear to this author at least, that the current GDG is simply not up to that task. | No specific references suggested. | Comment addressed, see Section 5.9. |
| 81 | PR | Jonathan Leo | 1.4.6 | Comments on D4, D5, DAT1.
Regarding your citation of specific genes involved in ADHD. The evidence is mixed at best. And further-more any connection would only be an association not a cause. Regarding D4 (DRD4) you state there is strong evidence for an association but this is not representative of the scientific literature. According to Willcutt (whom you cite earlier): ‘Similar to the results for DAT1, however, this result [DRD4] was not replicated in all samples and does not appear to be necessary or sufficient to cause ADHD. Moreover, the association with ADHD is much stronger in case-control comparisons than in family-based designs, suggesting that some significant results may be due to differences in gene frequencies in the populations from which the ADHD and comparison samples were drawn’ (Faraone et al., 2001).
In a detailed 2006 survey of the evidence in support of DRD4, DAT1, and other candidate genes, Waldman and Gizer (p. 421) concluded, ‘It should be clear. . .that for each [ADHD] candidate genes studied, there is a mixed picture of positive and negative findings.’ Or as Willcutt stated: ‘For 14 of the 27 candidate genes a significant association with ADHD has been reported in at least one study; however, virtually all of these results have been replicated inconsistently or await independent replication (Table 2). Moreover, each of these genes appears to account for a relatively small proportion of the variance in ADHD symptoms (for example., Faraone, Doyle, Mick, et al., 2001), suggesting that none are likely to be necessary or sufficient to cause ADHD.’ Or as Faraone has stated (2005, p. 1319) with regard to genome wide scans, ‘The handful of genome wide scans that have been conducted thus far show diver-gent findings and are, therefore, not conclusive.’ Regarding your summary of the genetic studies it would be more straightforward to say, ‘At this point in time no genes for ADHD have yet been identified.’
In advertisements for ADHD the supposed genetic basis for ADHD is often used to justify medical treatment. However, left unsaid in these same advertisements, is that a presumed genetic defect is in no way a necessary prerequisite to prescribe stimulants. As of now, the medical community finds it entirely acceptable to prescribe medication for psychological stress brought on by environmental stressors. One needs to look no further than foster care programmes which medicate an inordinate number of children. Presumably the common factor in these children is not their genetic makeup but their common environmental triggers. Although ADHD is considered a genetic defect, looking for a common gene in foster home children to explain their behaviour would seem to be a fruitless effort. Conversely, the results of a survey of environmental stressors in their lives would probably be very fruitful. The diagnosis and medication of children in foster homes is perhaps the best example of how, genes and biology aside, it is an acceptable practice to medicate children whose behaviour is explained by the environment. ‘Although some people question the assumption of the equal environment assumption for identical and non-identical twins this does not impact on the question of validity since the high twin correlations observed in these studies indicates that ADHD symptoms are highly familial.’
This is a very confusing sentence as it mixes up ‘familial’ with ‘genetic.’ It appears to be written by someone who does not understand the genetic studies. The claim that high MZ concordance shows that ADHD is ‘familial’ is erroneous. MZ concordance for speaking Italian is 100%, but does this mean speaking Italian is a genetic trait? The EEA does not just have an impact on estimates of genetic factors–if it is false then the twin method is deeply flawed.
‘There is consistent evidence of familial influences on ADHD symptoms in the general population.
Under the equal environment assumption these familial influences are thought to be largely genetic in origin.’
This is very problematic and should be reworded. The EEA pertains only to the twin method and not to family studies In addition, the document does not provide any citations that the EEA, which is counter intuitive, is correct.
The NICE document also makes the assumption that if it is genetic then it must be a disease. However, a host of other traits have also been investigated and these studies have determined that MZs have a higher concordance than DZs. For instance, twin studies have shown a heritability for loneliness (Boomsma et al. 2005), the frequency of orgasm in women (Daewood et al., 2005), the results of the United States 2004 presidential election (Alford et al., 2005), perfectionism (Tozzi et al., 2004), and breakfast eating patterns (Keski-Rahkonen et al., 2004) (cited in Joseph 2008). In 1990, Bouchard stated: ‘For almost every behavioural trait so far investigated, from reaction time to religiosity an important fraction of the variation among people turns out to be associated with genetic variation. This fact need no longer be subject to debate.’ Yet, if all our traits have a genetic basis then the genetic evidence of a trait does not automatically lead to ‘it’s a disease’ declarations. What many ADHD researchers seem to be saying is, that by implicating genetics in the behavioural trait of attention, this is somehow evidence of a disease. If Bouchard is correct, and all our traits have a strong basis in genetics, then can individuals exhibiting extremes of other traits also fall into the diseased category? The slippery-slope analogy seems almost too obvious to mention here, and might seem trite, however this appears to be exactly the trap that the child psychiatry profession has fallen into regarding other conditions, for instance child-onset bipolar disorder. The NICE statement on ADHD should not be seen with blinders on, as their statements about what constitutes a ‘disease’ will surely be revisited in the years ahead as they face other instances where traits can be classified as a disease in need of medication. NICE’s foray into ADHD is only the beginning.
1.4.6 Dickstein and colleagues completed a systematic meta-analysis of 16 neuroimaging studies that compared patterns of neuroactivity in children and adults with ADHD and controls. The GDG’s position would be stronger if indeed there was a biological marker for ADHD, however to cite the Dickstein paper will be seen as a desperate grasp for evidence. Like much of the ADHD neuroimaging research, on the surface the Dickstein paper might appear to make the case that there is a visible organic pathology in the brains of children diagnosed with ADHD, however a more in-depth view of the study reveals problems of experimental design that have plagued this entire body of research. The Dickstein paper is a meta-analysis of 16 ADHD imaging studies. Out of these 16 studies, four were used for a comparison of ADHD non-medicated to controls – the most important comparison. Interestingly, Dickstein et al. do not mention that two out of these four studies used the same ADHD subjects – the two studies were separate papers but came from the same research group. This is fairly obvious from reading the two studies, and was confirmed in an email to the lead author. Emails to the corresponding author of the Dickstein paper asking for clarification have gone unanswered. Double counting subjects is problematic for a meta-analysis, especially since Dickstein et al. did not mention it in their paper. Furthermore, even in the Dickstein analysis for the most important comparison in the study which was the non-medicated ADHD to controls the majority of the differences were for the most part not significant. It seems highly problematic for the NICE review to not mention this in their review.
Although positive findings on neuroimaging studies of psychiatric disorders, including ADHD, are usually given wide coverage in scientific publications and the mass media, the fact remains that this body of research has not provided support for a specific ‘biological basis’ of ADHD. This is well noted by Baumeister and Hawkins (2001) who report, ‘inconsistencies among studies raise questions about the reliability of the findings’ (p. 2). Writing, for instance, about the tendency for studies to find decreases in the size and activity of the frontal lobes, Baumeister and Hawkins summarise that:
‘Even in this instance, however, the data are not compelling. The number of independent replications is small, and the validity of reported effects is compromised by a lack of statistical rigor. For example, several of the major functional imaging studies failed to employ standard statistical controls for multiple comparisons. This means that many of the reported findings are almost certainly spurious. Moreover, considering the likely existence of bias toward reporting and publishing positive results, the literature probably overestimates the occurrence of significant differences between subjects with ADHD and control subjects’ (p. 8, references omitted).
In addition, virtually all researchers in this field acknowledge that no brain scan can currently detect anomalies in any given individual diagnosed with a primary mental disorder, nor can it help clinicians to confirm such a diagnose. For example, in his authoritative Handbook of Brain Imaging, Bremmer (2005) states:
‘Unfortunately, we are not at a point where brain imaging can be used routinely for the diagnosis of psychiatric conditions. . . . We still do not understand the pathophysiology or mechanisms of response to treatment for most of these disorders. . .Most studies of psychiatric patients have found that even when a particular finding characterized a patient group, there remained as many as a third of patients who scored in the range of the control subjects’ (pp. 33–35).
Similarly, in the case of ADHD, Giedd and colleagues (2001) conclude unequivocally that: ‘If a child has no symptoms of ADHD but a brain scan consistent with what is found in groups of ADHD, treatment for ADHD is not indicated. Therefore, at the time of this writing, clinical history remains the gold standard of ADHD diagnosis’ (p. 45).
The Dickstein paper was funded by NIMH. Of interest to the NICE reviewers might be the 2003 paper by Sowell and colleagues also funded by NIMH. The Sowell study, involving 27 ADHD and 46 normal control subjects, reported that ADHD children had smaller frontal lobes compared to the control subjects, but overall the ADHD subjects had more cortical grey matter (Sowell et al., 2003). This study’s significance derives not necessarily from this result, but – as with several previous ADHD neuroimaging studies – from important comparisons that researchers could have made, but did not. One reason for bringing this study to your attention is because of your own acknowledgment in your previous reports about other conditions and treatments (the SSRIs for instance) that seeing the published data is not the same as seeing all the data, because the pharmaceutical companies do not publish all their studies. The same holds true for research into basic science topics, although in this case it is government-funded organisations that will not release data.
As in an earlier, similar paper by Castellanos and colleagues (2002), some of the ADHD subjects in the Sowell study were apparently medication-naïve. I say ‘apparently’ because specific descriptions were not provided: ‘15 of the 27 patients were taking stimulant medication at the time of imaging’ (p. 1705). It is unclear how to categorise the remaining 12 patients. Did they have a history of medication use prior to the start of the study, and then stop taking their medication for 48 hours, or some other arbitrary time period before imaging? It is surprising that a study published in The Lancet could be so vague about one of the most important variables in the study. Conclusions based on a comparison of normal control subjects to medication-naïve ADHD subjects would be very different from conclusions based on a comparison of control subjects to ADHD subjects with varying durations of medication exposure or undergoing abrupt withdrawal.
The issue becomes considerably more muddled and confusing due to a brief concluding discussion by Sowell and colleagues (2003) of the potential role of stimulant medication on their findings. The authors first appropriately acknowledged that, since 55% of their ADHD children were taking stimulants, ‘the effects of stimulant drugs could have confounded our findings of abnormal brain morphology in children with [ADHD]’ (p. 1705). The simplest way to properly evaluate this confounding effect would have been to compare the 15 medicated ADHD children with the 12 unmedicated ADHD children. However, Sowell and colleagues chose to not make that comparison: ‘We did not directly compare brain morphology across groups of patients on and off drugs because the sample size was considerably compromised when taking lifetime history of stimulant drugs into account’ (p.1705). The authors further explained that this comparison, between unmedicated and medicated, is not needed because a prior study by Castellanos and colleagues (2002) suggested that medications do not affect brain size.
Sowell and colleagues’ methodological choice, and its justification, is both unconvincing and puzzling. First, although one can sympathise with their judgement that ‘taking lifetime history of stimulant medication into account’ compromised their sample size, this judgement ignores that for 30 years ADHD neuroimaging researchers have deemed it perfectly acceptable to compare ADHD subjects and normal controls regardless of medication history. Indeed, virtually all the studies that Sowell and colleagues cite to contextualise their own study and interpret their results exemplify this practice. Thus it is difficult to see why Sowell and colleagues would feel that they should not compare medicated and unmedicated ADHD subjects. Clearly, just as they acknowledged limitations to their main study results, Sowell and colleagues could have reported the results of the more specific comparison with an acknowledgement of the appropriate limitations. Second, Sowell and colleagues cite Castellanos and colleagues to support the methodological choice of not comparing medicated and unmedicated ADHD subjects. But, third and most important, Sowell and colleagues’ data appear directly relevant to either support or refute the conclusions that Castellanos and colleagues (2002) drew from their comparison. In fact, the results of the Castellanos and colleagues’ comparison of brain volumes of medicated and unmedicated ADHD children were deemed worthy of a major press release by the NIMH concerning stimulant drugs’ effects on developing brains, yet the same comparison in the Sowell and colleagues study was considered insignificant and not even reportable.
Sowell and colleagues would not supply the information about the most important comparison in the study, and a subsequent Freedom of Information Act Request to NIMH to release the information was denied. This was in spite of the fact that on their own website NIMH encourages their grant recipients to share data. One could say that NIMH’s actions speak louder than their words. Given their own interest in the subject, possibly the NICE reviewers could request the data?
In June 2006, the American Journal of Psychiatry published three articles (Pliszka et al., 2006; Smith et al., 2006; Tamm et al., 2006) and an accompanying editorial about functional magnetic resonance imaging (Casey & Durston, 2006). The three studies conducted scans of children’s brains during a specified task, and, importantly, all three studies had a group of medication-naïve ADHD children. However, when considered together, the three studies implicated an inordinate number of different brain regions, with little replication of the regions between studies. In brief, Smith and colleagues (2006) implicated the frontal, parietal, and temporal lobes, along with the striatum. Pliszka and colleagues (2006) implicated the anterior cingulate cortex and the left ventrolateral prefrontal cortex. Tamm and colleagues (2006) implicated the parietal lobes, the right precuneus, and the thalamus. One could almost ask: What area of the brain is not implicated?
The accompanying editorial by Casey and Durston (2006) acknowledges these disparate findings, yet instead of looking at them as problematic for the ADHD neuroimaging field, Casey and Durston attempt to place the disparate findings within a theoretical construct that cognitive deficits in ADHD are due to a deficit in inhibitory control. They state: ‘Identification of core processes involved in a disorder can move a field from a disparate set of data-driven findings to a more theoretically coherent collection of studies’ (p. 957). Does Casey and Durston’s model provide a solid base for ADHD researchers to move forward, or is their explanation of these ‘disparate findings’ an attempt at salvaging a lack of reproducibility within the ADHD neuroimaging field? The model as proposed by Casey and Durston is that, ‘basic learning systems are important in signalling top-down systems to adjust behaviour when predicted outcomes are violated.’ This appears to be little more than a very general statement about learning. As a general statement it is hard to argue with it, because it is so broad and all-encompassing that it makes room for almost every conceivable finding. But it does little to explain how upwards of 10–15% of the population has a disease. One test for whether a theory is too broad, is to ask: What empirical findings would negate the theory? Casey and Durston have not proposed any findings that would negate their theory, and, indeed, it is hard to imagine any that would negate it. For instance, in Figure 16 of their article, Casey and Durston hypothesise the involvement of the prefrontal cortex, the basal ganglia, the parietal cortex, and the cerebellum in ADHD. Yet none of the three accompanying studies even suggested that the cerebellum was involved. Bringing the cerebellum into the picture without elaboration is also problematic because as Furman notes: ‘of the five studies that examined total cerebellar volume, four are listed as showing an association of ADHD with decreased volume, while three do not.’ And missing from Casey and Durston’s schematic is the thalamus, which one study did implicate.
Moreover, two of the studies were contradictory: Pliszka and colleagues found greater activity in ADHD subjects than controls in the inferior prefrontal cortex (p. 1059), while Smith and colleagues found less activity (underactiviation) in the mesial and front-parietal-temporal brain regions during the go/no go and switch tasks for the ADHD children. Yet, interestingly, while the imaging data for the ADHD children differed in these two studies, there was no difference in performance on the specified tasks between the ADHD children and controls. None of these issues are raised by Casey and Durston, and we are unsure how they could be fitted into the proposed model.
Perhaps the most significant aspect of putting forth such a highly theoretical model of ADHD is that Casey and Durston are implicitly acknowledging that the more practical aspect of developing an imaging scan as a diagnostic tool is becoming more and more unlikely.
A recent study by Volkow and colleagues (2007) utilised PET and compared dopamine transporter levels in 20 never medicated adults to 25 controls, and found that dopamine transporter levels were not positively correlated with the disease. In the NICE document, to your credit, you have few positive statements about this research, but on the other hand you do not come right out and acknowledge this. For instance, Volkow, in much more direct terms than NICE, has commented: ‘it should be noted that the imaging studies are still not definitive because of the discrepancies in the findings.’
The necessary and definitive test to confirm the suggestion that ADHD children have a neuroanatomic pathology consists of using an appropriate brain scan to detect a difference between a ‘typical’ unmedicated ADHD child as found in the classroom, and a ‘normal’ child. There is virtual unanimity that this cannot be accomplished at present. Experiments with highly selective patient and control groups are, at best, only preliminary studies, and the findings of these studies must be called into question. Ruling out the effects of psychotropic medication is merely one of the tasks confronting researchers conducting neuroimaging research with ADHD patients. Even if the field accomplishes this task, however, several other important tasks remain. One of these will involve trying to make sense of findings of brain abnormalities or differences among some individuals diagnosed with ADHD. In October 2005, for example, the New York Times published an article by Benedict Carey entitled ‘Can brain scans see depression?’ It contained interviews with prominent psychiatrists and child psychiatrists, many of whom have authored ADHD imaging papers. The Times article was notable for both its candour and frank assessment of the psychiatric neuroimaging field: ‘Yet, for a variety of reasons, the hopes and claims for brain imaging in psychiatry have far outpaced the science, experts say.’ And in the words of Paul Wolpe, a professor of psychiatry and sociology: ‘The thing for people to understand is that right now the only thing imaging can tell you is whether you have a brain tumor.’ A recent imaging study found a difference between the brains of conservatives and liberals. Does this difference equate to a disease? | References suggested: Waldman (2006)
Asked reviewer for full reference; no response.
Baumeister & Hawkins (2001)
Asked reviewer for full reference; no response.
Giedd (2001)
Asked reviewer for full reference; no response.
Sowell (2003)
Asked reviewer for full reference; no response.
Castellanos (2002)
Asked reviewer for full reference; no response.
Pliszka, S. R., Glahn, D. C., Semrud-Clikeman, M., et al. (2006) Neuroimaging of inhibitory control areas in children with attention deficit hyperactivity disorder who were treatment naive or in long-term treatment. American Journal of Psychiatry, 163, 1052–1060. Paper included.
Smith (2006)
Am J Psychiatry, 163, 1033–1043.
Paper to be included.
Tamm (2006)
Am J Psychiatry, 163, 1033–1043.
Paper to be included.
Casey & Durston (2006)
Am J Psychiatry, 163, 1033–1043. Paper excluded: not peer reviewed (editorial).
Volkow (2007)
Asked reviewer for full reference; no response.
Carey (2005) Can brain scans see depression? The New York Times. Paper excluded: not peer reviewed; opinion paper. | Comment addressed, see Appendix 17.1
‘Study characteristics – Diagnosis’ for information on funding of studies included, see Section 5.8
‘Neuroimaging studies’ for discussion of genetic studies. |
| 34 | CC | David Coghill | 1.4.6 evidence | I think this section would read better if it were reordered to deal with causal factors, that is genetic, environmental and then mediating factors. In addition to the mediating factors already discussed (functional imaging, neuropsychology) structural imaging and neurophysiology should be added).
The neuropsychology section stresses executive functions too strongly (although these are the most well studied other functions like delay aversion [Sonuga-Barke], timing [Tannock & Smith], non-executive memory [Rhodes & Coghill] and as noted variability also contribute – and may actually prove to be more important than executive functions).
On the other hand the statement, ‘Recently it has emerged that the strongest and most consistent association with ADHD is for intra-individual variability (Klein et al., 2006)’ is way too strong as it relies on only one study. A similar argument could be made for a range of different neuropsychological functions based on other comparative studies. | References suggested: Sonuga-Barke
Asked reviewer for full reference; no response.
Tannock & Smith Asked reviewer for full reference, no response.
Rhodes & Coghill Asked reviewer for full reference; no response. | Comment taken into consideration, see Section 5.8. |
| 36 | CC | David Coghill | 1.5 | Whilst there are not many child studies where healthy kids or kids with other disorders have been given methylphenidate or dexamfetamine there are many such adult studies. My understanding is that these support the notion that these stimulants in these doses work the same in healthy people as they do in those with problems. | No references suggested. | Comment addressed, see Section 5.9 (third paragraph). |
| 58 | PR | Stephen Faraone | 1.5 | You state: ‘When considering the Feighner criteria for validity of a psychiatric disorder, the question of whether there are specific responses to clinical, educational and other interventions for ADHD was excluded, since the data to answer this question was very limited.’ I don’t have the Feighner criteria in front of me but I thought that the idea was that the disorder showed a ‘characteristic’ response to treatment rather than a ‘specific’ response. For example, the fact the SSRIs treat depression, OCD and other anxiety disorders does not challenge the validity of any of these disorders. | No references suggested. | Comment addressed, see Section 5.8. |
| 84 | PR | Jonathan Leo | 1.5 | Limitations. When discussing the effect of stimulants on people not diagnosed with ADHD, regarding the Rapoport study, you state, ‘there were limited published data on the effects of stimulants in people who do not have ADHD.’
This is an incredible statement as it seems to be saying that we do not know the effect of stimulants on normal people. Underlying any discussion of ADHD (except for possibly the NICE document) and what every neuroscience researcher is aware of, is the understanding that the most straightforward experiment in all of neuroscience is the one seeking to determine if stimulant medication works, at least if one defines ‘works’ as a short-term improvement in attention span. Whether the subjects are male or female, whether they are pre-schoolers or geriatrics, whether they are diagnosed with ADHD or not, and whether the medication is provided by a doctor or a friend, it has been known for 75 years that stimulants improve anyone’s and everyone’s ability to pay attention.
The GDG sidesteps the issue of the fact that the stimulants such as methylphenidate (Ritalin) have a universal effect by stating that they are going to discuss the treatment of ADHD in a subsequent document. (However, even this is problematic because the document brings up the Rapoport study at one point.) Talking about treatment with stimulants in a future document is fine, but while it might be convenient this does not justify, in the current document, ignoring the universal effect of the stimulants on the CNS – as this does relate to the disease concept. Unfortunately much of the press still falls back on the so-called ‘paradoxical effect’ that sees stimulants only effecting ADHD children. Rapoport’s study shows this is false. Coffee drinkers also know this is false. Apparently one of the few organisations to not acknowledge this fact is the GDG.
Also regarding the Rapoport study, you state, ‘The very small numbers used in this study and lack of further similar studies means that considerable caution must be taken in drawing firm conclusions.’
Again, your double standard is evident. The NICE review suggests ‘considerable caution’ when drawing conclusions about a study looking at the effect of amphetamines on the normal brain. Yet, just one page before in the review, there seems to be no hesitation or ‘caution’ in your interpretation of the genetic studies, which have not discovered any ADHD genes, or the imaging studies, which are unable to distinguish ADHD children from controls. | No references suggested. | Comment addressed, see Section 5.9. |
| 13 | PR | Margaret Alsop | 1.6 | It is felt that the evidence submitted by parents, carers and others caring for an individual diagnosed as having ADHD is clear evidence on the validity of ADHD. There seems to be clear indication that the evidence submitted by professionals and those within the GDG echoes that of parents, carers and individuals themselves. | No references suggested. | Comment taken into consideration. |
| 37 | CC | David Coghill | 1.6 | The comment that, ‘In adults the profile of symptoms may alter with a relative persistence of inattentive symptoms compared to hyperactive-impulsive symptoms’ does not really match up with the evidence described in Section 1.4.5 where it is suggested that evidence for this is weak and that relative to controls levels of overactivity stay high. Here would be a good place to dispel this notion of a true reduction in overactivity problems as one of the ADHD myths. | No references suggested. | Comment taken into consideration. |
| 38 | CC | David Coghill | 1.6 | ‘There was no evidence of a need to apply a different concept of ADHD to children and adults. However age-related changes in the presentation are recognised.’ Could be expanded to add: ‘There was no evidence of a need to apply a different concept of ADHD to children and adults. However age-related changes in the presentation are recognised. These changes are not yet reflected within the various diagnostic criteria.’. | No references suggested. | Comment addressed, see Section 5.12. |
| 83 | PR | Jonathan Leo | 1.6 | Position Statement on the Validity of ADHD. ‘There is evidence of both genetic and environmental influences in the aetiology of ADHD. . . . .Contemporary research suggests that environmental risks are likely to interact with genetic factors. . . .’ Why is that whenever environmental influences are brought up that you feel the need to drop genetics into the discussion? When you say ‘contemporary research suggests that environmental risks are likely to interact with genetic factors’ what recent research are you referring to? You are making it sound like the ADHD genetic researchers have recently uncovered this startling fact. However, the fact that genes interact with the environment has been known for years.
According to Robert Sapolsky, ‘Genes influence behaviour, the environment influences behaviour, and genes and environment interact – this view is one of the great scientific clichés of the 20th century.’
Commenting on the usefulness of the ‘vulnerability – stress theory of mental disorders’ that any potential harmful environmental influences only operate on those with faulty genes, Mary Boyle points out that the theory is an important mechanism for managing the potential threat posed to biological psychiatrists whenever non-biological conditions are implicated in the aetiology of psychological stress. The usefulness of the hypothesis lies partly in its lack of specificity – since the nature of the claimed vulnerability has never been discovered, anything can count as an instance of it. Its usefulness also lies in its seeming reasonableness (who could deny that biological and psychological or social factors interact?) and its inclusiveness (it encompasses both the biological and social – surely better than focusing on only one?) while at the same time it firmly maintains the primacy of biology, not least through word order, and potentially de-emphasises the environment by making it look as if the ‘stress’ part of the vulnerability – stress model consists of ordinary stresses which most of us would cope with, but which over-whelm only ‘vulnerable’ people. We are thus excused from examining too closely either the events them-selves or their meaning to the ‘vulnerable’ person (Boyle, 2002).
Your document seems to be the perfect example of what Boyle is referring to. You maintain the primacy of biology with your wording, but as Boyle points out, the driving force behind your wording is not ‘contemporary research’ that has discovered an ADHD gene, but is the contrast between the genetic studies, that have failed to find a specific ADHD gene or even a gene of modest effect, and studies implicating environmental factors. If you had discovered a gene, then you would not be talking about the vulnerability-stress hypothesis. Again, take the example of foster care homes where an inordinate number of children are diagnosed with ADHD (and other conditions). Clearly this data points to environmental influences on ADHD, no matter what genes a child is born with.
As the data from Nicky Hart shows, there appears to be a strong role for socioeconomic strata. If we follow your logic, then the increased prevalence of children with smaller brains and less electrical activity (according to the current concept of ADHD) in the lower socioeconomic strata must be qualified with the statement that their smaller brains are due to faulty genes being influenced by the environment. | No references suggested. | Comment taken into consideration. |
| 88 | PR | Jonathan Leo | 1.6 | Position Statement on Validity of ADHD. ‘ADHD is distinguished from the normal range partly by the number and severity of symptoms and partly by the association with significant levels of impairment.’
Your statement points out why the diagnosis varies so much from one country to another, from one doctor’s practice to another, from one school to another, and from one household to another. Take the 2004 guidelines on the diagnosis of ADHD from the American Academy of Pediatricians. Take item 2 on their questionnaire as an example:
- 2)
Six (or more) of the following symptoms of hyperactivity-impulsivity have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:
Hyperactivity
Often fidgets with hands or feet or squirms in seat Often leaves seat in classroom or in other situations in which remaining seated is expected Often runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness) Often had difficulty playing or engaging in leisure activities quietly Is often ‘on the go’ or often acts as if ‘driven by a motor’ Often talks excessively
Note that every item on the list uses the term ‘often’, a very unscientific term. How does one quantify ‘often’. Since ‘often’ is in the eye of the beholder and can vary from one doctor’s office to the next it is easy to see how this document has little teeth to it.
Apparently as long as one adult decides that the child ‘often’ fidgets, then the child can be labelled and medicated. It is easy to see how a parent who does not get a diagnosis from one doctor can simply go to another doctor with different ideas about what ‘often’ means. As an example of how the general public sees through a document like this take this example provided by the late Kevin McCready (2002): ‘In an episode of The Sopranos, the popular and critically acclaimed HBO series about a New Jersey mobster and his family, the primary character, Tony Soprano, is called into a meeting with school officials, including the school psychologist. Tony is told that his son has been determined to “have” ADHD. He asks how this has been determined and is told there is a set of criteria, which the psychologist then begins to itemise. The third criterion on the list is “tends to fidget.” The poorly educated, psychologically unsophisticated, working class gangster looks at directly at the psychologist and asks simply in his earthy “Jersey” accent: “What constitutes a fidget?” There may be little to admire about a man who makes his living illegally, but at least he “gets it.”‘.
It is easy to see how guidelines that use the word ‘often’ mean very little. Is NICE going to develop more stringent guidelines? | No references suggested. | Comment taken into consideration. |
| 39 | CC | David Coghill | 1.7.1 | The term ‘medical treatment’ should be replaced by ‘pharmacological treatment’ or ‘drug treatment’. | No references suggested. | Comment addressed, see Section 5.12. |
| 59 | PR | Stephen Faraone | 1.7.1 | I don’t understand the following sentence: ‘The group concluded that treatment response should take into account the severity of the disorder in terms of clinical and functional impairments and evidence should be looked for on the impact of severity of the disorder on treatment response.’ | No references suggested. | Comment addressed, see Section 5.13.1. |
| 69 | PR | Anita Thapar | 1.7.1 | ‘The argument against genetic influences is not strong unless one questions the conventional interpretation of twin data’ and continuing paragraph. Contribution of genetic influences doesn’t rest purely on twin studies of ADHD. There have been five adoption studies all showing familial clustering due to genetic influences (refer to any review on ADHD genetics).
Thapar, A., Langley, K., Owen, M. J., et al. (2007) Advances in genetic findings on attention deficit hyperactivity disorder. Psychological Medicine, 17, 1–12.
Khan, S. A. & Faraone, S. V. (2006) The genetics of ADHD: a literature review of 2005. Current Psychiatry Reports, 8, 393–397. Review. | References suggested: Thapar, A., Langley, K., Owen, M. J., et al. (2007) Advances in genetic findings on attention deficit hyperactivity disorder. Psychological Medicine, 17, 1–12. Paper excluded: Review (no systematic search).
Khan, S. A. & Faraone, S. V. (2006) The genetics of ADHD: a literature review of 2005. Current Psychiatry Reports, 8, 393–397.
Paper excluded: Review (no systematic search).
References of individual studies were hand searched and those meeting the quality assessment criteria were included [Sprich et al., 2000]. | Comment addressed, see Section 5.8 and throughout the chapter. |
| 85 | PR | Jonathan Leo | 1.7.1 | ‘The level and types of behaviour that define the normal range remain a contentious issue.’
The current GDG believes that children with ADHD have an organic brain deficiency, resulting from a genetic defect that in the future, once the technology is available, will be detected by a brain scan. However nowhere in the document has NICE answered the controversial question: How many children have this defect? The obvious problem being that as the percentage of children taking Ritalin escalates, the harder it is to make the case that they have a disease. If, as in some school districts, upwards of 17% of the boys are prescribed Ritalin, this would suggest that the boundaries for normalcy have become narrower. As often happens after statistics documenting the increasing use of stimulants for younger and younger children make the headlines, many of the opinion leaders in the psychiatry community state that there is a problem with ‘over-prescribing’ or ‘misdiagnosis’, yet none of these leaders, or any of the major psychiatric organisations, has issued guidelines on how to identify this large group of ‘misdiagnosed’ children, nor have they clarified what they consider to be improper uses of prescribed stimulant medication (Johnson, 2006; Nakamura, 2002). No matter where NICE draws the line between normal and ADHD, whether it classifies 2%, 5% or 7% as having the disease, there will, by definition, be children who are inappropriately taking stimulant medication. Based on what criteria will NICE decide who these misdiagnosed children are? For instance, if according to NICE 7% of British children have ADHD then what if 10% are taking medication? How will doctors identify the 3% of misdiagnosed children?
The dilemma for medical professionals who want to go beyond simply talking about misdiagnosed children and to actually identifying these children is that, without an objective biological marker demarcating the line between the ‘correctly’ and ‘incorrectly’ diagnosed, the sole criterion for determining the appropriateness of stimulant treatment comes down to: Are the adults in the child’s life satisfied with the medication’s effect? Presumably there are not many parents unhappy with the medication’s effects, who still continue to medicate their children.
None of the medical professionals who talk about misdiagnosis has ever elaborated on how they plan to tell all these parents of misdiagnosed children that they should not be medicating their children, even though the medication is doing exactly what the medical community says it should be doing.
As an example of the forces at work in the diagnosis of an individual child with ADHD, take a case study in the journal Pediatrics. In 1999, the editors elicited commentaries from several prominent physicians about the case of a teenage boy who had been taking Ritalin for several years. The editors saw the boy’s scenario as an interesting case, worthy of commentary from a group of prominent child psychiatrists. But in an ironic twist of fate, they have unintentionally provided a much more interesting case study. From a sociological point of view the subject of the case was not the boy, but, instead, was the doctors and the editors. The case provides an excellent example of:
how a major determination in the diagnosis of ADHD is adult satisfaction, how the medical community fully supports the use of stimulant medication as a performance enhancing drug, how the same mindset that approves of using one psychotropic drug easily leads to the use of multiple medications and how the main stream medical journals have given little attention to the ethical implications of controlling and altering children to meet the demands of our contemporary educational/cultural system.
‘The 15-year-old boy announced to his parents and his pediatrician that he wanted to stop taking his medication: “I don’t need it. . .I’m fine. . .I don’t see why I should take it.” He purposefully did not take the medication for a few weeks and he said he could not tell the difference. . .. However, his parents observed that his test results, when off the medication, were below his standard scores. . .. They also noted that he was more distractible and less attentive when doing his homework during that time’ (Cohen & Leo, 2002).
As stated by the physicians, the most important variable in determining whether this boy should keep taking his medication was the parental satisfaction with the medication, and the subsequent commentaries all focused on how to convince the boy to continue taking his medication. The boy’s wishes were not something to be listened to, but rather something to be managed, whether through dialogue or with another medication. As an example of polypharmaceuticals for children one of the commentators even suggested that the boy’s reluctance to keep taking his Ritalin suggested this was a sign that he needed another medication. Thus the boy, who wants go off his one medication, would instead get two medications. None of the commentators in the Pediatrics article contemplated that the boy’s wishes might be legitimate, but more importantly, as a sign of how one-sided the issue has become in the medical community, the editors did not give space to a single commentator who questioned the ethics of giving a medication to improve grades.
As an example of who the experts in America are diagnosing with ADHD take this example from the Department of Psychiatry at New York University: ‘Sarah chooses to sit in the back of the classroom and much of the time she’s doodling in her notebook or staring out of the window. She seldom completes assignments and often forgets to bring the right book to class. Her desk is a mess and she generally can’t find what she is looking for. Then she gets weepy and says that nobody understands her.’ This 14-year-old girl is crying out ‘please understand me’. The New York University experts’ response is to label her with ADHD. Medication will surely follow. Examples like this and the others I have cited, which come from those who strongly believe that ADHD is biological, are just more examples of how little science is involved in the ADHD diagnosis. | References suggested:
Johnson (2006)
Study: ADHD drugs send thousands to ERs.
Paper excluded: not peer reviewed.
Nakamura (2002) Attention deficit/hyperactivity disorders: are children being overmedicated?
NIMH.
Paper excluded: not peer reviewed; opinion paper.
Case study & editor comments, Pediatrics (1999)
Asked reviewer for full reference; no response. | Comments taken into consideration. |
| 86 | PR | Jonathan Leo | 1.7.1 | ‘The GDG wish to stress that the role of important genetic influences does not exclude an important role for environmental influences since individual differences in genetic risk factors are likely to alter the sensitivity of an individual to environmental risks.’ This is confusing because earlier in the document the only environmental influences that you mentioned were prenatal exposure to drugs such as nicotine. What environmental influences are you referring to here? ‘Furthermore, the extent to which there are genetic influences has no direct bearing on the choice of treatment approaches since both medical and psychosocial interventions could be important in improving treatment outcomes.’ Let’s be honest here, the idea that ADHD is due to genetics is one of the most common reasons cited by the pharmaceutical companies and the psychiatric profession as evidence that ADHD is a biological disease, like diabetes. And diseases are treated with medications. Your statement is even going against much of modern day psychiatry. According to Nancy Andreasen, in The Broken Brain, the biological model of mental illness can be summed up as follows:
- 1.
The major psychiatric illnesses are diseases, - 2.
These diseases are caused principally by biological factors and most of these reside in the brain,. . .and - 4.
The treatment of these diseases emphasises the use of somatic therapies.’
As another example of this type of thinking, take the recent comments by Stephen Faraone in Science. In a discussion of ‘ADHD genes’ he stated: ‘My hope is that once we’ve discovered those genes, we’ll be able to do a prospective study of kids at high versus low genetic risk. That’s when you’ll see environmental factors at work.’ But certainly one can still see environmental factors at work in children without knowing their genotype. Yet, even more confusing is Faraone’s next comment. According to the reporter, ‘Eventually, he [Faraone] adds, environmental changes could play an important role in treating some ADHD patients’ (Brown, 2003, p. 160). Eventually? Why do we need to wait? Why not implement the changes right now? Changing the environment is exactly what many people opposed to stimulants have been saying for years. Faraone’s take on the aetiology of ADHD is strikingly similar to Thom Hartman’s view. Both believe that ADHD is a biological, hereditary trait (Hartmann, 1996). Where they differ is that Faraone, and other biological psychiatrists, see these children as dysfunctional, with a genetic defect in need of medication. The other group sees the children as having different genes, at one end of the spectrum, and that what is needed is a different environment (Hartmann, 1996). One purpose of the genetic studies, which the pharmaceutical companies, and the psychiatry profession, have propagated, is to imply that, because it’s genetic that drugs are needed. For instance, Faraone states: ‘Many parents are reluctant for their children to take psychotropic medication and others find it difficult to maintain the prescribed regimes. These problems are mitigated by discussing the genetic etiology of ADHD’ (Faraone, 1996, p. 598).
If you are going to acknowledge that knowing about genetics has nothing to do with treatment than you should be ready to answer the general public and politicians when they ask: Then why are you doing this research? If knowing about genetics has no benefit to the patient, then one possibility for this line of research is to justify current practices. If ADHD does not have a strong genetic influence then giving a medication would be seen as very problematic, and would call into question the entire practice of medicating children with stimulants. If I were you I would delete this line about genetics and treatment. | References suggested:
Andreasen (1984) The Broken Brain.
Paper excluded: book (not peer-reviewed).
Faraone, Science.
Asked reviewer for full reference; no response.
Brown (2003).
New attention to ADHD genes.
Science.
Paper excluded: not peer reviewed.
Hartmann (1996).
Asked reviewer for full reference; no response. | Comments taken into consideration. |
| 60 | PR | Stephen
Faraone | 1.8 | You state, ‘The quality of the evidence included in this review was variable and lacked any “gold standard” because no diagnostic tests for ADHD have been developed or tested.’ I suggest you be clear what you mean by ‘gold standard.’ I think you mean a laboratory test of some sort. Although I’m probably in the minority, I think that the DSM-IV diagnosis of ADHD as made by a competent health professional is a pretty good gold standard inasmuch as it is reproducible with high reliability and has clinical implications. The inter-rater reliability of the ADHD diagnosis is not much worse than, for example, many accepted ‘gold standard’ diagnoses made by radiologists. | No reference suggested. | Comment addressed, see Section 5.3. |
| 89 | PR | Jonathan Leo | 1.8 | Evidence Summary.
In your summary, after 22 pages of discussion about the evidence, you do not cite any direct evidence that ADHD results from a biological, hereditary defect. However, you do not come right out and acknowledge this lack of evidence. The 1998 National Institutes of Health conference was much more direct when it said, ‘there are no data to indicate that ADHD is due to a brain malfunction.’ | No references suggested. | Comment addressed, see Section 5.14. |
| 87 | PR | Jonathan Leo | 1.9 | ‘ADHD should be considered in all age groups (children adolescents, and adults), with symptom criteria adjusted for age appropriate changes in behaviour.’ And also in 1. 6, ‘There was no evidence of a need to apply a different concept of ADHD to children and adults.’ There is an important point to be mentioned here that the NICE document ignores. Allowing adults, who can make their own decisions, to take stimulants is one matter, however it is an entirely separate matter when it comes to children. The ethical questions surrounding the use of Ritalin are becoming more significant as once-medicated children are now reaching adulthood. According to a recent survey in the LA Times, a significant number of these adults are deciding to discontinue their medication (Healy, 2006b). The LA Times article quotes a 27-year-old girl who reflects back on the years she was medicated, ‘It was kind of weirdly amazing. . ..You get excited about monotonous work, honestly. Like, translating Spanish becomes totally fun . . .The thing is, it works. But why are we forcing people to be in that position that they should like something that they wouldn’t ordinarily’ (Healy, 2006). In just three short sentences this 27-year-old girl goes right to the heart of the ethical dilemma of stimulant medication: Is it right to medicate people so that they do well in school? How is it that a lay person can go right to the heart of the issue while a committee of physicians with years of training can produce a document that ignores this key point? Why are questions like this not raised by academicians in medical journals, or by the GDG? | Healy (2006) The Ritalin kids grow up: many of the ADD generation say no to meds.
LA Times.
Paper excluded: not peer reviewed; relevant to treatment not validity. | Comment taken into consideration. |
| 40 | CC | David Coghill | 1.9.1.1 | I felt that these were rather weakly described and a bit ‘fluffy’ for want of a better word. It is really saying you should use the diagnostic criteria, you should actually count the symptoms you should be clear about impairment and you should consider ADHD diagnosis in all ages. I think it just needs some re-wording to make it snappier.
Also it could benefit from starting off with a very clear and strong statement saying that the diagnostic categories of ADHD and hyperkinetic disorder are considered valid and should be used. This is a very important message to clinicians, the public, the government, the press, and so on. | No references suggested. | Comment addressed, see Sections 5.14 and 5.15. |
| 48 | PR | David Cottrell | 1.9.1.1 | Will you be able to operationally define ‘moderately clinically significant’ impairment? | No references suggested. | Comment addressed, see Section 5.15.2 (C) ‘How should impairment be judged?’ |
| 1 | CC | Edmund Sonuga-Barke | General | This seems a very accurate and sensible document. | No references suggested. | Comment taken into consideration. |
| 2 | CC | Russell Schachar | General | I read the document with great interest and think that it is a solid contribution to the ongoing debate about ADHD/HKD. Given that the document is based on a review of reviews, it is not altogether easy to judge how the summary statements were reached, but they look appropriate. | No references suggested. | Comment taken into consideration. |
| 3 | CC | Geoff Kewley | General | I felt the review was a reasonable summary of discussion and have nothing else to add. | No references suggested. | Comment taken into consideration. |
| 4 | PR | Margaret Alsop | General | We are concerned with processes preceding and following diagnosis rather than diagnosis. The concept of ADHD is multi-faceted, therefore no individual discipline is likely to be competent to identify, assess and intervene alone. As such diagnosis becomes a mechanical feature in a holistic process involving a range of professionals. A child psychiatrist or paediatrician should normally make the formal diagnosis. However, a diagnosis should only be considered valid if it is made on the basis of evidence that a particular agency is pertinent; that agency should be involved as appropriate. Medical practitioners also have a significant role to play in diagnosis and assessment in order to rule out physical factors which may lead to the symptoms similar to those of ADHD. | No references suggested. | Comment addressed, see Section 5.15. |
| 5 | PR | Margaret Alsop | General | If these guidelines are intended to be accessible to professionals and parents from a range of disciplines who might first identify, or have concerns about, problems that may or may not result in an ADHD diagnosis, their first efforts are likely to be of a broadly psychosocial nature (that is, behavioural/cognitive and educational interventions). Currently different professionals use different terminology to describe the phenomenon of ADHD (for example, hyperkinetic disorder, behavioural problems).
The use of different terms is not helpful to professionals, children, young people, adults or their families: therefore an attempt should be made in this document to be consistent in the use of terms that have been selected for their clarity and acceptability to a wide range of professionals.
There are significant differences, sometimes of an ideological nature between different professional groups (Cooper, 1997; Hughes, 1999; Maras & Redmayne, 1997). These differences can be exaggerated through training and practice and are often reflected in different professional perceptions and views of ADHD. Differences can sometimes result in confusion, misunderstandings and conflict and may have an adverse influence on the effectiveness of multi-disciplinary/agency working. However, there is also much common ground among professionals, especially in terms of sought after outcomes of intervention. ADHD by its very nature demands a multi- agency response and provides an opportunity for medical, educational, psychological, social care and other professionals to work together. | References suggested: Cooper (1997). Asked reviewer for full reference; no response.
Hughes (1999). Asked reviewer for full reference; no response.
Maras & Redmayne (1997). Asked reviewer for full reference; no response. | Comment taken into consideration. |
| 6 | PR | Margaret Alsop | General | We note that there is no reference made in relation to transition between CAMHS into the adult CMHT. There is clear evidence to indicate that a high percentage of those diagnosed with ADHD in child-hood will not have any appropriate transitional plan in place, therefore it is important that an appropriate multi-agency response for transitional arrangements are identified.
(Social Exclusion Unit – Transitions Young Adults with Complex Needs) | No references suggested. | Comment addressed, see NICE guideline ‘Transition to adult services’. |
| 12 | PR | Margaret Alsop | General | The following statistics provides an overview of the numbers of children facing particular risk factors out of a total population of children in England of 12 million:
In 2000, 2.7 million children lived in low income families. Up to 75,000 children may be missing from school rolls. Around ten per cent of children aged 5 to 15 have a mental disorder of sufficient severity to cause them distress or to have considerable effect on the way they live and 20% of children suffer from mental health problems. One in nine children run away from home for at least a night. One in ten families in England and Wales report incidences of domestic violence in a year. In 2000 there were 91,400 conceptions to girls aged under 20. At the end of September 2001 there were approximately 5,400 households with children in bed and breakfast accommodation. There are approximately 300,000 children with disabilities in England; 110,000 of these are severely disabled. 26,800 children and young people are on the child protection register. 58,900 children and young people are in public care. 11,000 young people aged 15–20 are in young offenders institutions.
Our concerns are, how many of these include those with ADHD or possible ADHD?
Figures released by the Children and Young People’s Unit on 6th September 2002, www.cypu.gov.uk | No references suggested. | Comment taken into consideration. |
| 14 | PR | Margaret Alsop | General | That the assessment, diagnosis and treatment for ADHD should be delivered throughout the lifespan, services delivery should be multi-agency, multi- model and incorporate professionals from many services such as: health, education, social care, behaviour support, parenting programmes, adult community mental health, community care, prison healthcare providers, housing, employment agencies and those within the criminal justice system. Our belief is that the term EBD (emotional and behavioural difficulties) should not be used in relation to service delivery for those already diagnosed as having ADHD. Within many services the term used for those with ADHD is described as having EBD, therefore access to a full multi-agency approach may not be forthcoming. We understand that this request may be out of the remit of the GDG and NICE but would still therefore like to request it for inclusion and consideration. | No references suggested. | Comment taken into consideration. |
| 15 | PR | Margaret Alsop | General | Not being qualified nor trained in medicine, I do not consider it appropriate for contributions from non- medically trained individuals to be included. I can only go on experiences as a parent-carer of a young adult (25 years old ) his having been un-medicated for the first 14 years of his life and as to how medications have now turned his life around and made him feel totally inclusive to society and not another statistic within our penal system or another fatality of drug abuse/overdose. | No references suggested. | Comment taken into consideration. |
| 16 | PR | Margaret Alsop | General | It is felt that the assessments for ADHD in children should be conducted through a ‘core diagnostic’ team, this way it is multi-agency, multi-model and will rule out/include any other underlying difficulties such as ASD, learning difficulties, dyslexia, and so on.
During my own experiences, those diagnosed with ADHD as children have received a dual diagnosis of ADHD and ASD in later adolescence or adulthood. | No references suggested. | Comment addressed, see Section 5.15. |
| 17 | CC | David Coghill | General | In general I very much agree with the way that the issues are addressed and the conclusions reached. Overall this is a well-structured document and reaches some clear conclusions. I think that the sample comment given above applies to this document and that, ‘The guideline highlights throughout the document where there are gaps in the evidence to support clinical practice. Although these areas are in the main text of the document, it would be helpful if there could be an additional section at the end of each chapter with areas where further research would be helpful. This would support the research agenda and maximise resources.’ | No references suggested. | Comment taken into consideration. |
| 18 | CC | David Coghill | General | Will the appendices detailing the literature be in tabular form showing sample size, and so on? As it would be very helpful to be able to see this information. | No references suggested. | Comment addressed, see Appendix 17.1 ‘Study characteristics – Diagnosis’. |
| 19 | CC | David Coghill | General | I have marked up minor comments on wording and so on in the document itself. | No references suggested. | Comments taken into consideration. |
| 41 | PR | David Cottrell | General | I found this to be a well written and coherent account of diagnostic validity issues. Given the potentially diverse readership of NICE guidelines and the complexity of the literature I thought the language clear and the research explained well.
The questions to be addressed and the methods used are set out clearly towards the end of Section 1.3 and in 1.3. The methods are appropriate for the questions asked. My comments are largely about the use of language and presentation. I have no substantive disagreement with the case that is presented. | No references suggested. | Comments taken into consideration. |
| 49 | PR | David Cottrell | General | 1.2. Third paragraph, line 8 – I think this should be ‘particularly’ but the whole sentence is clumsily worded and obscures meaning.
1.4.1. Second paragraph after subheading ‘Evidence’ – the final sentence is not grammatical and again obscures meaning.
1.4.3. First paragraph after subheading ‘evidence’, line 5 – presumably ‘that on this’ not ‘this on this’.
1.5. Second paragraph, line 7 – ‘who do not ADHD’ does not make sense
1.7.1. First sentence is ungrammatical.
There are other minor typos in the document but those above have the potential to distort the meaning of the text. | No references suggested. | Comment addressed, see Section 5.3. |
| 61 | PR | Stephen Faraone | General | The following article should be of interest to you: Faraone, S. V. (2005) The scientific foundation for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder. European Child and Adolescent Psychiatry, 14, 1–10. | References suggested: Faraone, S. V. (2005) The scientific foundation for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder. European Child and Adolescent Psychiatry, 14, 1–10. Paper excluded: opinion paper. | Comment taken into consideration. |
| 70 | CC | Sami Timimi | General | I wish to make the following points on the above document:
The document states in its introduction that, ‘The Guideline Development Group (GDG) acknowledged at the outset that the use of the diagnosis of ADHD has been the subject of considerable controversy and debate’ and ‘The relative lack of a validated reference standard (indicated by SIGN diagnostic study quality assessment, see Appendix A) means that the question of validity for the diagnosis of ADHD needs to draw on evidence from a wide range of sources’ [my italics]. Despite this the subsequent discussion of the evidence included no references drawn from authors who are critical of the concept of ADHD, despite the group being provided with a number of scientific reviews from such authors. The references included repeatedly cited research by a small number of researchers and research groups (including from the chair of the group) known to be supporters of the concept of ADHD. This suggests that the document lacks balance and is ideologically biased toward literature that confirms the majority of GDG members’ views.
Many members of the GDG have previously written papers or otherwise collaborated with the chair of this group. The fact that there is not one academic/practitioner who is able to represent the other side of this debate is reflected in the one-sided document the GDG has produced. It is my opinion that the conflict of interest in this group is to an extent that is unacceptable given the importance of their task.
It isn’t clear why the GDG decided to use the Washington University Diagnostic Criteria beyond the unexplained ‘ensure that a transparent, structured approach was taken’ nor is it evident whether any other systematic approach or framework was considered. However, even with these criteria, the interpretation of the GDG that the evidence they present is sufficient to support the validity of ADHD using these criteria is open to question. | No references suggested. | Comment addressed, see Sections 5.3 and 5.9. |
| 77 | CC | Sami Timimi | General | There is clear evidence in the document that the GDG has displayed unacceptable bias in its preferred paradigm for analysing the literature, in its selection of literature and in its interpretation of the literature they selected. The fact that most of the academic members of the GDG have previously published papers with the chair of the group and that the group does not include any members with a more critical stance, strengthens the impression that the levels of bias result from conflicts of interest that are seriously unethical. The conclusions are thus not valid and could lead to serious deficiencies in practice and provide poor protection for patients, possibly exposing many more children to significant harm. The document should not be accepted. The GDG should be dismantled, a new chair appointed and a new GDG convened with a more equitable balance of opinion reflected in its membership. | No references suggested. | Comment addressed, see Sections 5.3 and 5.9, as well as Chapter 3, Methods. |
| 79 | PR | Jonathan Leo | General | Take a trait – any trait, either physical or behavioural. Given normal biological variability, if the trait is measured and subsequently plotted on a graph there will be a spectrum. Some are tall and some are short, some have long legs and some have short legs, or some have a longer attention span than others. Variability of a trait is not proof of a disease.
Take a drug’s effect. There are certain drugs that have an effect on human traits. Alli, a new diet drug, will help people lose weight – no matter what their weight to begin with. There are also drugs that have an effect on an individual’s behaviour, no matter what their behaviour to begin with. Take the stimulants, for example: response to a drug with a universal effect, like the stimulants, is not proof of a disease. (See the GDG comments page 17 Section 1.5 limitations.) These are the two most common reasons cited as evidence for a biological basis of ADHD. The dilemma for NICE is to go beyond this. As it is stands now, NICE’s conclusion that the ADHD diagnosis is valid is primarily based on the flawed premise that variability of a trait is proof of a disease. Even your own ‘Evidence Summary’, basically says it is a trait, which in your opinion should be called a disease, at one end of the spectrum. In the summary you do not (or cannot) cite a single scientific study or even an area of study confirming that ADHD is primarily a problem of biology.
If traits can be called diseases then where does this stop? A recent Op-Ed article in the New York Times addresses the problem of pathologising traits: ‘It may seem baffling, even bizarre, that ordinary shyness could assume the dimension of a mental disease. But if a youngster is reserved, the odds are high that a psychiatrist will diagnose social anxiety disorder and recommend treatment. How much credence should we give the diagnosis? Shyness is so common among American children that 42 percent exhibit it. And, according to one major study, the trait increases with age. By the time they reach college, up to 51 percent of men and 43 percent of women describe themselves as shy or introverted. Among graduate students, half of men and 48 percent of women do. Psychiatrists say that at least one in eight of these people needs medical attention’ (Lane, 23 September, 2007).
In the future will NICE have a committee deciding if ‘Is shyness a valid diagnosis?’ According to the logic of the current document that identifying a trait is somehow proof of a disease the answer would appear to be ‘yes’. | No references suggested. | Comment taken into consideration. |
| 90 | PR | Jonathan Leo | General | Conclusion: The NICE document provides no new insight into the diagnosis of ADHD. It has systematically ignored one side of the debate and has simply summarised the views of those involved with the ongoing medication of children. The flaws are neither subtle nor minor, nor can they be rectified with editing. The entire approach of the panel is flawed. I am not privy to the make-up of the panel but it appears that the panel had no members with a broad societal view of the ADHD diagnosis – if it did, then they were ignored. In all your discussions you seem to have one standard for biology and one for the environment. Marginal imaging studies, that compared medicated ADHD children to controls, and genetic studies, which have not found an ADHD gene, are given credence, while you cannot even cite a study linking the environment to ADHD.
The other side of the debate, that variability of a trait, and the universal effect of stimulants, are not good evidence for justifying the belief that, upwards of 10 to 15% to of the world’s children have an organic brain defect, is simply not presented. Likewise the ethics surrounding the diagnosis are ignored in the NICE document. If the NICE statement on ADHD is approved no one should be surprised when 5 years from now more British children are being prescribed stimulants. In no way should the current NICE document be considered a fair and all encompassing view of the ADHD phenomena. On the surface, it is a document couched in the language of science, but when one looks deeper at the scientific studies there is little evidence to support the disease concept of ADHD. | No references suggested. | Comment taken into consideration. |
