National Institute for Health and Clinical Excellence
Attention Deficit Hyperactivity Disorder (ADHD)
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Pressures of time mean that this is a brief response that sets out some parameters that need thorough consideration in any NICE guideline on ADHD. This is a highly contested clinical area and the guidelines should attempt to encompass this rather than reaching for a homogonous meaningless ‘middle’ ground (where the middle ground lies of course changes over time and according to your particular perspective).
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Care in the NHS is a lottery. This has been aggravated by the unscientific nature of the ADHD construct and its categorisation as a ‘neurodevelopment’ disorder despite the lack of evidence to support this categorisation. The result has been that the majority of ADHD clinics that have been set up in the NHS are run by paediatricians, who have no training in assessment or treatment of broader psychosocial factors, resulting in ‘care’ revolving around drug treatment only, with little or no access for the vast majority of those diagnosed to other treatments.
There is a huge problem in the nature of the diagnostic process. There are no medical tests for ADHD. There are no specific brain functioning tests for ADHD. There are no specific psychological tests for ADHD. There are no specific observational tests for ADHD. A doctor, through that doctor’s assessment of a child’s history and reported behaviour problems, makes a diagnosis of ADHD. Rating scales, which the child’s parents or carers and teachers fill out about the child concerned, are frequently used to assist the doctor when they are assessing a child for ADHD. These rating scales are questionnaires in which adults looking after the child (most usually a separate questionnaire for a parent/carer and a separate questionnaire for a teacher) are asked to decide on the frequency with which hyperactive, inattentive or impulsive behaviours are occurring in the child. They are not a test for ADHD as all a rating questionnaire can measure is an adult’s opinion about a particular child’s behaviour at a particular moment in time and in a particular setting.
Common questions used in rating scales (which the person filling in the questionnaire has to rate for frequency or severity in the child) include:
Words such as "often", "seems", "difficulties", "reluctant", "easily", "quietly", and "excessively" that appear in these questionnaires are hard to define. For example the word "often" appears in every one of the above questions, but what does it mean? Does it mean that the child does those behaviours at least once a day or at least once a minute? These questionnaires can only rate a particular adult’s perception of a particular child at a particular moment in time and in a particular setting. In other words they are measures of the subjective perception of the adult filling in the rating scale. What they cannot be is an objective factual piece of ‘hard data’ about a child.
These days when making a diagnosis of ADHD, the doctor doing the evaluation does not need to observe the behaviours of hyperactivity, impulsivity or inattention in the child concerned during the assessment. Making the diagnosis is based on taking a history (to see if the behaviours, according to those giving the doctor the history, started early in a child’s life, and to exclude any other medical reason that may be causing the behavioural problems) and evaluating a couple of rating questionnaires. Ultimately the making of the diagnosis (or not) rests on the beliefs of the doctor and how they interpret the history and questionnaires. It’s an entirely subjective process.
Hyperactivity, impulsivity and limited attention span are behaviours that occur on a continuum. All children, particularly boys will present with such behaviour in some settings at some point. They are not behaviours that would be interpreted as abnormal whenever they occur. Contrast this to a hallucination (such as hearing voices that are not there) or a delusion which, in Western culture at least, are viewed as abnormal in most circumstances (However, even with these symptoms that are psychiatrically categorised as ‘psychotic’ symptoms, in other words symptoms of someone deemed to be out of touch with reality, it is not as straight forward as many believe. For example, it is now recognized that many otherwise healthy and socially well functioning people sometimes hear voices).
Without any medical tests to establish which individual has a physical problem causing the above behaviour problems, defining the cut off between normal and ADHD is arrived at by an arbitrary decision. Those who have argued that ADHD does not exist as a real disorder, start by pointing to the obvious uncertainty about its definition. Because of the uncertainty about definition it is hardly surprising that epidemiological studies (studies that measure how many have a disorder) have produced very different prevalence rates for ADHD or hyperkinetic disorders (ADHD’s equivalent in the International Classification of Diseases (ICD) system of diagnoses) ranging from about 0.5% of school age children to 26% of school age children (see below).
2. Validity and reliability of existing diagnostic criteria and criteria that can be used to determine circumstances in which the guideline should be used.
So what is the evidence for the existence of this disorder? Is there a medical test that will diagnose it? No. Are there any specific cognitive, metabolic or neurological markers for ADHD? No. Those who have argued that ADHD does not exist as a real disorder, start by pointing to the obvious uncertainty about its definition (McGuinness, 1989). Because of this uncertainty it is hardly surprising that epidemiological studies have produced very different prevalence rates for ADHD (in its various forms), ranging from about 0.5% of school age children to 26% of school age children (Taylor and Hemsley, 1995; Green et al, 1999).
There is a preponderance of boys over girls in ADHD symptomatology in the region of four (or more) to one (McGee et al, 1992). This is very similar to the gender distribution found in conduct disorder and other so-called externalising behavioural disorders in children. The meaning of this gender distribution is rarely questioned. What sort of biological variable are we attempting to categorise here if this is a biological abnormality? Is it that boys generally have bad genes compared to girls? Is it something to do with the normal biological differences between male and female genes? Is there an interaction between boy’s behaviour and changes in social expectations regarding children’s behaviour generally? Do social changes in family structure, lifestyles, teaching methods, classroom sizes, rates of violence, rates of substance misuse and so on have an effect on perceptions and beliefs about boy’s and girl’s behaviour, or even on their behaviour directly? Has life got harder for boys in some way? Has life got harder for parents trying to control normal boy behaviour? Are we still compelled to pay more attention to the externalised behaviour of boys than the internalised behaviour of girls, only now we medicalize this (after all adults in Western societies are usually more tolerant of hyperactivity in girls than in boys (Battle and Lacey, 1972))? Do changes in teaching methods have an effect on how we understand and deal with boys’ behaviour? These and other social/cultural questions need to be discussed.
Despite attempts at standardising criteria and assessment tools in cross-cultural studies, major and significant differences between raters from different countries continue to be apparent (Mann et al, 1992). There are also significant differences between raters when raters rate children from different ethnic minority backgrounds (Sonuga-Barke et al, 1993). One replicated finding is an apparently high rate of hyperactivity in China and Hong Kong (Shen et al, 1985; Luk and Leung, 1989). In these studies nearly three times as many Chinese as English children were rated as hyperactive. A more detailed assessment of these results suggested that most of the ‘hyperactive’ Chinese children would not have been rated as hyperactive by most English raters and were a good deal less hyperactive than English children rated as ‘hyperactive’ (Taylor, 1994). One suggestion for such a consistently large disparity in hyperactivity ratings between Chinese and English children is that it may be due to the great importance of school success in Chinese culture leading to an intolerance of much lesser degrees of disruptive behaviour (Taylor, 1994). Whatever the reason(s), it demonstrates that hyperactivity and disruptiveness in boys is a highly culturally constructed entity.
That ratings of hyperactivity, inattention and disruptiveness are culturally dependent is not surprising as inattention, impulsivity and motor restlessness are found in all children (and adults) to some degree. Diagnosis is based on an assessment of what is felt to be developmentally inappropriate intensity, frequency and duration of the behaviours, rather than on its mere presence. All the symptoms described in this disorder are of a subjective nature (e.g. ‘often does not seem to listen when spoken to’) and therefore highly influenced by the raters cultural beliefs and perceptions about such behaviours. After all how do you operationalize, define and understand non-specific words like ‘often’ and ‘excessive’, which are invariably found in ADHD rating questionnaires?
With regards co-morbidity numerous epidemiological and clinical studies demonstrate the high frequency with which supposedly separate child psychiatric disorders occur in individuals with ADHD (Caron and Rutter, 1991). In children with ADHD co-morbidity with other child psychiatric conditions is common no matter what definition is used (Beiderman et al, 1991). It is estimated that about half the children with ADHD also have a conduct disorder, about half also have an emotional disorder, about one third have an anxiety disorder and another third have depression (Barkley, 1994). Co-morbidity is so prevalent that at least three quarters of ADHD diagnosed children will have at least one other diagnosable child psychiatric condition (Hazell, 1997). The co-occurrence of the symptoms that make up oppositional/defiant and conduct disorders with those that make up hyperactivity and attention deficit disorders is so strong (Beiderman et al, 1991; Fergusson and Horwood, 1993) that many commentators have questioned the reality of the distinction between them. Psychiatrists have adopted co-morbidity as a way of trying to explain clinical reality when it does not appear to tally with research generated views of mental life. It’s a way of maintaining a fantasy that there is a natural, probably biological, boundary where no natural boundaries exist (Tyrer, 1996).
This lack of a coherent concept is reflected in the lack of consensus on the question of possible causal mechanisms. Thus the condition was initially viewed as being due to an underlying, excessive motor activity in the child (Schachar, 1991) and later as being due to an underlying central attention deficit (Douglas, 1972; 1983). Others have suggested that the central deficit is one of generalised intellectual impairment (Werry et al, 1987) or of motivation (Draeger et al, 1986). The conviction held by a number of influential researchers about the likely central deficit has had a big influence on the behavioural definitions of the disorder. For example, Douglas’s belief (1972) that attention, not hyperactivity, was the essential feature distinguishing these children from other difficult and disruptive children, led to the establishment of the ‘Attention Deficit Disorder (ADD)’ definition in DSM-III.
Claims have been made that neuroimaging studies confirm that ADHD is a brain disorder. Closer examination of the quoted studies not only reveals a more complex picture, it actually suggests the opposite, as the studies demonstrate that there is no characteristic neurophysiological or neuroanatomical pattern that can be found in children diagnosed as having ADHD. Brain scan studies have not uncovered a consistent deficit or abnormality, with a wide variety of brain structures being implicated, for example; Striatal, Orbital, Prefrontal, Fronto Posterior and Medial Orbital areas, Caudate Nucleus, Corpus Calosum and Parietal lobe (Rapport, 1995). The sample sizes in these studies have all been small and in no study have the brains of the ADHD diagnosed children been considered to be clinically abnormal (Hynd and Hooper, 1995), nor has any specific abnormality been convincingly demonstrated (Baumeister and Hawkins, 2001). Interestingly, after almost twenty five years and over thirty such studies, researchers have yet to do a simple comparison of unmedicated children diagnosed with ADHD with an age matched control group, the one large study that claimed to have done this (Castellanos et al, 2002) for reasons best known to themselves choosing a control group whose age was on average 2 years older (Leo and Cohen, 2003) and thereby all they scientifically managed to prove was that younger children had smaller brains than older ones! Most worryingly, animal studies suggest that any differences observed in these studies could well be due to the effects of medication that most children in these studies had taken (Breggin, 2001; Moll et al, 2001; Sproson et al., 2001).
As in the Castellanos et al. (2002) study, some of the ADHD subjects in the Sowell et al. (2003) study were apparently medication-naïve- ‘apparently’ because specific descriptions were not provided. The issue becomes considerably more muddled and confusing due to a brief discussion of the potential role of stimulant medication on their findings at the end of Sowell et al.’s (2003) paper. 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 medicated ADHD children with the unmedicated ADHD children. However, Sowell et al. consciously chose to not make that comparison. The authors further explain that this comparison, between unmedicated and medicated ADHD children, is not needed because the prior study by Castellanos et al. (2002) suggested that medications do not affect brain size! It is difficult to see why Sowell et al. would feel that they should not compare medicated and unmedicated ADHD subjects. Clearly, just as they acknowledged limitations to their main study results, Sowell et al. could obviously have reported the results of the more specific comparison with an acknowledgement of appropriate limitations. Sowell et al. cite Castellanos et al. to support the methodological choice of not comparing medicated and unmedicated ADHD subjects, but, Castellanos et al. made that very comparison regardless of medication history. Most importantly, Sowell et al.’s data appear directly relevant to either support or refute the conclusions that Castellanos et al. (2002) drew from their comparison. Such a tactic by the researchers raises the suspicion that the comparison of medicated with unmedicated ADHD subjects in Sowell et al.’s study might have produced results that would have diluted the findings that Sowell et al. chose to emphasize instead.
What we end up with is speculative ‘biobabble’. Even if consistent differences in neuro-imaging studies were found, unidirectional cause and effect cannot be assumed. This is because neurophysiological measures may reflect different children’s different reaction to the same situation causing differences in brain chemistry rather than different brain chemistry causing different behaviour (Christie et al, 1995). Thus, differences in brain function have been demonstrated in normal healthy children who have different temperaments (Fox et al, 1995). At the turn of the century doctors used to measure the size and shape of the part of the skull housing the brain. They came up with all sorts of statistical differences and used these to justify a ‘scientific’ basis for amongst other things, the prevailing racist views of the time. This now discredited ‘science’, which lasted for over a hundred years before dying out early last century, was known as phrenology. It was believed that a skilled phrenologist could assess the moral and intellectual qualities of an individual by inspecting the skull and palpating its surface for characteristic bumps and protuberances. If we cannot stop ourselves from impulsively jumping to unwarranted conclusions about the reasons for differences found in brain scanning studies, we will create a modern version of phrenology.
Although ADHD-type behaviour may be familial in the sense that it ‘runs’ or clusters in families, we cannot determine whether this clustering is caused by the greater genetic resemblance of family members, since they also experience similar environmental factors. As Faraone and colleagues (2005, p. 1313) observed, "family studies cannot disentangle genetic from environmental sources . . ." In their opinion, "adoption and twin studies [are needed] to determine whether genes account for the familial transmission of a disorder."
All ADHD twin studies have used the ‘classical twin method,’ more commonly known as ‘the twin method.’ This research technique compares the concordance rates or correlations of reared-together MZ twins (also known as monozygotic or identical; who share a 100% genetic similarity), versus the same measures of reared-together same-sex DZ twins (also known as dizygotic or fraternal; who share a 50% genetic similarity). Based on the assumption that both types of twins experience the same kinds of environments, known as the ‘equal environment assumption’ or ‘EEA,’ twin researchers attribute a statistically significant greater resemblance of reared-together MZs versus reared-together DZs to genetic factors. There have been no studies of ‘reared-apart’ ADHD twins.
Although the twin method depends on additional assumptions, the equal environment assumption has been the main area of contention between twin researchers and their critics. However, the evidence clearly shows that MZ twins spend more time together, more often have the same friends, are treated more similarly by parents and others, and so forth (Joseph, 2004a). Moreover, MZs share a closer emotional bond than DZs, and more often view themselves as being two halves of the same whole (that is, they experience what some psychologists call identity confusion; see Ainslie, 1985; Jackson, 1960). The twin method—just like a family study—is unable to disentangle the potential influences of genetic and environmental factors. Instead, while belatedly recognizing that MZ twins do indeed experience more similar environments that DZs, some twin researchers attempted to rescue the twin method by redefining the equal environment assumption. Behaviour geneticists and others have renamed the EEA as the ‘equal trait-relevant environment assumption’ (Carey & DiLalla, 1994). Proponents of the trait-relevant EEA recognize that MZ twins experience more similar environments than DZs, but argue or imply that the burden of proof for demonstrating that MZ and DZ twins experience dissimilar trait-relevant environments falls not on twin researchers, but on critics of the twin method (examples of twin researchers reversing the burden of proof onto critics include Bouchard, 1993, 1997; Kendler, 1983; Lyons et al., 1991). However, it has been observed that "a basic tenet of science is that the burden of proof always falls squarely on the claimant, not the critic . . . Consequently, it is up to the proponents of these techniques to demonstrate that they work, not up to the critics of these techniques to demonstrate the converse" (Lilienfeld et al., 2003, p. 3). This means that the burden of proof falls on twin researchers to demonstrate that the greater environmental similarity of MZ versus DZ twins does not entirely explain their results.
Most twin researchers’ recognition that MZ twins experience more similar environments and treatments than DZs invalidates genetic interpretations of MZ-DZ comparisons, for the exact same reason that genetic interpretations of family studies are invalid. There is no reason, therefore, to accept that the twin method measures anything other than the more similar environments of MZ versus DZ twins (plus bias), and all conclusions in favour of genetic influences on psychiatric disorders (including ADHD) derived from the twin method must be disregarded.
Nevertheless, Barkley (1998, p. 68) has argued that twin studies furnish "the most conclusive evidence that genetics can contribute to ADHD." Twin research has found consistently that MZ twins are more concordant for ADHD, or correlate higher for ADHD-type behaviors, than same-sex DZ twins. To date, more than 20 ADHD twin studies have been published (for example, Cronk et al., 2002; Edelbrock et al., 1995; Gilger et al., 1992; Gillis et al., 1992; Hudziak et al., 2003; Saudino et al., 2005; Sherman et al., 1997; Thapar et al., 1995; Willcutt et al., 2000).
Although the EEA’s validity is an essential aspect of their conclusions in favour of genetics, few authors of the 20+ ADHD twin studies addressed the assumption’s merits or provided evidence or citations in support of the traditional or trait-relevant definitions of the EEA. To the extent that they discuss the EEA at all, most ADHD twin researchers adhere to the traditional EEA definition despite the fact that, in the words of twin researchers Scarr and Carter-Saltzman (1979, p. 528), "the evidence of greater environmental similarity for MZ than DZ twins is overwhelming."
Although most ADHD twin studies have found greater MZ versus DZ resemblance for ADHD or ADHD-type behaviors, the authors of only 3 of the last 18 published ADHD twin studies addressed the EEA (Joseph, 2006), and only Cronk et al. (2002) defined the EEA in the trait-relevant sense. Moreover, no ADHD twin researchers other than Cronk et al. cited previous research or publications supporting the validity of the EEA. Thus, implicitly or explicitly, all but one group of ADHD twin researchers based their conclusions on the traditional assumption that the environments of MZ and DZ twins are equal, yet only Gillis and associates (1992) argued that these environments are actually equal!
ADHD genetic researchers Hay, and Levy have written that identical twins "may well be treated more similarly than fraternal twins, but this is far more a consequence of their genetic similarity in behaviour (and of ensuing responses by parents and others) than a cause of such similarity" (Hay et al., 2001, p. 12). Like Kendler (1983) before them, Hay and associates failed to understand that the reason MZ twins experience more similar environments than DZs is not relevant in assessing the validity of the twin method. In order to invalidate genetic interpretations of ADHD twin data, critics need only show that MZ and DZ environments are different.
Thus, since the evidence overwhelmingly suggests that MZ twins are treated more alike, spend considerably more time together, and experience greater levels of identity confusion and closeness (Joseph, 2004), we would expect MZ twins—on purely environmental grounds—to correlate higher than same-sex DZs on ADHD-related measures. ADHD twin studies, therefore, are based on an unsupported theoretical assumption and, like family studies, are unable to disentangle the potential influences of genes and environment on ADHD-type behavior.
ADHD adoption studies have been published by Alberts-Corush et al. (1986), Cantwell (1975), Morrison and Stewart (1973), Safer (1973), Sprich et al. (2000), and van den Oord et al. (1994). The results of these studies are frequently cited in textbooks, review articles, and scientific papers as supporting genetic theories of ADHD.
The authors of the four Adoptive Parents studies (Alberts-Corush et al., 1986; Cantwell, 1975; Morrison & Stewart, 1973; Sprich et al., 2000) compared the ADHD rate among the relatives of different types of families, but had no information on their ADHD adoptees’ biological relatives. In fact, no ADHD adoption study has investigated the biological relatives of adopted-away children, meaning that their authors were unable to make direct comparisons between the biological and adoptive families of the same child. In contrast, Kety and colleagues’ (1994) schizophrenia adoption studies diagnosed adoptees’ adoptive and biological relatives. Unlike the schizophrenia adoption studies, the ADHD Adoptive Parents studies compared diagnoses in a group consisting of adopted-away ADHD children and their adoptive families (AH), versus a group consisting of the families of other ADHD children living with their biological parents.
Unfortunately, ADHD genetic researchers typically fail to discuss the severe limitations of the Adoptive Parents design. Too often, they fail to state clearly that researchers were unable to study adoptees’ biological relatives, often writing in potentially misleading ways about ADHD adoption research (Joseph, 2006). For example, Faraone and Biederman (2000, p. 57) wrote that a "testable psychosocial theory" must be able to explain "the elevated rates of ADHD and associated traits among the biological relatives of adopted away ADHD children," falsely implying that researchers obtained data on these biological relatives. And in a subsequent review article in which he discussed ADHD adoption research, Faraone (2004, pp. 305-306) wrote, "By examining both the adoptive and biological relatives of ill probands, one can disentangle genetic and environmental sources of familial transmission. " This was logic of Kety’s schizophrenia adoption studies. However, no ADHD adoption study has examined the "adoptive and biological relatives" of the same "ill" adoptees. Authoritative ADHD experts such as Barkley (2003, p. 117) then write for a larger audience in technically correct, yet potentially misleading ways: "Cantwell . . . and Morrison and Stewart . . . both reported higher rates of hyperactivity in the biological parents of hyperactive children than in the adoptive parents of such children."
Yet another issue in ADHD adoption research is evidence that adoptees as a population are more likely than non-adoptees to receive an ADHD diagnosis (Deutsch, 1989; Deutsch et al., 1982). If true, this casts further doubt on the already extremely shaky conclusions of the ADHD adoption studies. If adoptees and non-adoptees constitute different populations with respect to ADHD, it would be difficult to generalize findings of an ADHD adoption study to the non-adoptee population. Although adoption researchers usually do not address this, many adopted children are psychologically scarred on the basis of having been abandoned by their primary caregivers. Thus, a more evocative designation for adoption studies would be ‘the study of abandoned children’.
Jay Joseph has reviewed the individual ADHD adoption studies in detail (Joseph, 2000, 2002, 2006). His conclusions are that these studies are flawed on grounds that include, (1) their failure to study adoptees’ biological relatives; (2) researchers’ use of non-blinded diagnoses, which they sometimes made on the basis of relatives’ recollections; (3) inadequate definitions of ADHD; (4) researchers’ inability to control for environmental confounds; (5) researchers’ inability to control for the status of adoptive parents as a population screened for psychiatric disorders; (6) potential researcher bias; and (7) the use of late-separated adoptees.
The authors of textbooks and review articles usually report that the heritability of ADHD, as demonstrated by twin studies, is about 76% (Faraone et al., 2005), making it one of the "most heritable" disorders in child psychiatry. They arrive at this figure by doubling the MZ-DZ correlation difference. For example, if MZs correlate at .90, and DZs correlate at .50, twin researchers would estimate heritability at .80 (80%). In addition to the fact that these such estimates are based on the validity of the twin method’s untenable equal environment assumption, heritability estimates in psychiatry and psychology are inappropriate and misleading (Joseph, 2004).
The heritability statistic was developed in agriculture in order to predict the results of a selective breeding program (Joseph, 2004). However, as Hirsch (1997, 2004) has argued, a numerical heritability estimate (coefficient) is not a "nature/nurture ratio" of the relative contributions of genes and environment, and "highly heritable" single-gene disorders such as phenylketonuria (PKU) can be prevented by a dietary intervention. Thus, even if genes play a role in ADHD, we cannot determine "how much" of the "ADHD phenotype" variation is attributable to genes because, like PKU, a timely (and possibly simple) environmental intervention could prevent a condition with a stated heritability as high as 1.0.
Mainstream psychiatry sees ADHD as ‘multifactorial complex disorder’ meaning that there is ‘a complex interacting admixture of multiple genes and multiple environmental risk factors’ (Rutter, 2001, p. 227). Thus, molecular genetic researchers must assume that ADHD (1) is a valid entity that can be reliably diagnosed; (2) is caused by, among other factors, genetic variation (polymorphisms) or genetic mutations; and, (3) has corresponding biological defects in the brain. However, although ADHD is frequently referred to as a ‘complex genetic disorder,’ this is a theory, not a fact.
Psychiatric conditions such as ADHD are called ‘complex disorders’ because of the failure to find genes, while subsequent failures are explained on the basis of the ‘complex’ nature of the ‘disease’ leading to circular reasoning. In fact, the ‘lack of success’ in finding genes defines ‘complex diseases’ in psychiatry.
Moreover, even if a gene is necessary for ADHD to appear, it still doesn’t mean that it is a causative factor. As Ratner (2004, p. 30) pointed out, "The fact that something is a necessary foundation for something does not mean that it causes it." For example, all vehicles traveling over 60 miles per hour on the freeway have two or more tires. However, although tires are necessary for vehicles to move 60 miles per hour, tires do not cause vehicles to move forward; engines do. Ratner challenged claims that a defective gene causes language impairments. "Obviously, language requires a normal genetic substratum," he wrote, "and a defective genome undermines the ability to use language — just as it undermines the ability to play Monopoly." He concluded, however, "this does not mean that a gene causes or predisposes language, any more than it causes or predisposes me to play Monopoly."
Yet another problem is that, like twin and adoption studies, molecular genetic research depends on the acceptance of questionable theoretical assumptions. This is manifest not only in the investigators’ decision to perform this research, but also because they factor assumptions about genetics into mathematical models of familial transmission. According to McGuffin (2004, p. 179), "Unfortunately, conventional linkage requires several assumptions. These are that major gene effects (rather than just multiple small gene effects) exist, that there is some way of assuring genetic homogeneity, and that the mode of transmission of the disorder is known."
Thus, although ADHD molecular genetic researchers test multiple genetic models in computer analyses of their findings, all models assume that some type of genetic transmission is occurring. But what if no genetic transmission is occurring? The large number of false positive linkage findings in psychiatry in general, and ADHD in particular, may be another example of questionable assumptions leading researchers to the premature conclusion that genetic factors (or actual genes) exist. Their results may be influenced by plugging false assumptions about genetic transmission into their calculations.
Like other areas of psychiatry, we have seen many claims of ADHD gene findings. However, subsequent replication attempts fail to support these claims. Researchers currently focus on genes involved with the brain’s dopamine receptors, which they view as ‘candidate genes’ on the basis of an a priori hypothesis derived from neurochemical and neuropharmacological research (Asherson & Curran, 2001; Barr, 2001). The major areas of interest have been the DRD4 dopamine receptor gene, and the DAT1 dopamine transporter gene. Faraone and Biederman (2000, p. 573) claimed that "molecular genetic studies have implicated these two genes . . . in the etiology of ADHD." However, although the original claims have found some support, several subsequent studies have failed to replicate an association between ADHD and the DRD4 or DAT1 genes (e.g., Bakker et al., 2005; Langley et al., 2005; Mill et al., 2005; Ogdie et al., 2003; van der Meulen et al., 2005). Several complete genome scans have also failed to find consistent evidence in support of regions harboring suspected ADHD genes (Arcos-Burgos et al., 2004; Bakker et al., 2003; Fisher et al., 2002; Hebebrand et al., 2005; Ogdie et al., 2003). According to Faraone and colleagues, "The handful of genome-wide scans that have been conducted thus far show divergent findings and are, therefore, not conclusive" (Faraone et al., 2005, p. 1319). It is generous to state that these genome scan results are "not conclusive." It would be better to conclude that these studies have found no replicated evidence that genes have anything to do with ADHD.
ADHD genetic researchers have resorted to citing meta-analyses of studies finding negative and positive results in support of associations between ADHD and chromosomal regions (e.g., Faraone et al., 2001; Langley et al., 2004). As Pittelli (2004, p. 1134) wrote, however, "I find this trend of using meta-analysis to resurrect largely negative genetic linkage studies disturbing. It appears to be nothing more than a manipulation of data to obtain a desired result." It does indeed appear to be such a manipulation, yet readers relatively unsophisticated in genetic research and terminology may well conclude that yet another "ADHD gene" has been identified.
We have seen prominent genetic researchers such as Robert Plomin argue that, although genes for ADHD and other disorders have not been found, we "are on the cusp" of gene discoveries. What Plomin and other genetic researchers rarely consider in print, however, is the possibility that ADHD does not exist. Psychiatric geneticists and their supporters instead write optimistically about the great strides they have made, and how ADHD genes will soon be identified. They write as if they were searching for the cure of a deadly disease, or the virus causing an epidemic. But ADHD is simply a grouping of socially disapproved behaviours falsely passed off as a disease, and finding genes would do little if anything to "cure" these behaviours. Still, in the ADHD genetic literature we find many claims that gene discoveries are imminent, and that finding genes would be an important event.
Generally speaking, these investigators substitute language for real gene findings. Thus, when they scan the genome and find no ADHD genes, they can say that genes are "implicated," or that researchers are making "enormous advances," or that genes are "just beginning to be identified," or that studies "suggest" the finding of genes, and so on. Plomin wrote in 2005 (p. 1030) that, although genes in psychiatry and psychology remain to be discovered, this is "an exciting time for child psychology and psychiatry. The field will be transformed as we move from finding genes to using them as genetic risk indicators in our research and eventually in our clinics." And another researcher wrote in the same year, "Uncovering the genomic underpinnings of ADHD is proving to be one of the most exciting stories in psychiatric genetics" (McGough, 2005, p. 1371). Ultimately, however, optimistic statements cannot eliminate the necessity of finding actual genes.
3. Early identification of ADHD in children in primary care, and identification of factors that should lead to investigation of the possibility of ADHD.
Early intervention strategies are complicated by the potential impact of believing a child to have ADHD. This knowledge could, in itself, be a life-altering event, affecting how parents, classmates, teachers, and others treat a child. And even in the unlikely event that presumed ADHD genes are found in the future, society might still decide to concentrate on eliminating environmental factors contributing to ADHD-type behavior. These interventions would be aimed at all children in the same way that an anti-smoking campaign, which does not target its intended audience by genotype, can help reduce tobacco use.
4. Pathways to treatment.
Pathways have been adversely affected by categorisation of ADHD as a ‘neurodevelopment’ disorder despite the lack of evidence to support this categorisation. The result has been that the majority of ADHD clinics that have been set up in the NHS are run by paediatricians, who have no training in assessment or treatment of broader psychosocial factors, resulting in ‘care’ revolving around drug treatment only, with little or no access for the vast majority of those diagnosed to other treatments.
5. Identification and management of risk.
We need to be aware that the widespread diagnosis and use of stimulants creates many potential public health risks. Doctors may be unwittingly convincing children to control and manage themselves using medication, a pattern that could carry on into adulthood as the preferred or only way to cope with life’s stresses. Parents, teachers and others may lose interest in understanding the meaning behind an ADHD labelled child’s behaviour beyond that of an illness internal to the child that needs medication, thus contributing to a ‘de-skilling’ of parents’ and teachers’ ability to manage and deal with challenging behaviour.
The National Association for the Advancement of Coloured People in the United States has offered strong testimony stating their concern that young blacks could end up over represented in the ADHD category and over medicated and has been campaigning for black parents to reject such a diagnosis (British Psychological Society, 1996). The dynamics of Ritalin prescription in North America have changed in recent years however, with the majority of those who get the prescription coming from white middle class families (Olfson et al, 2002). In this context one dynamic appears to be middle class parent’s fears about their children’s education. The anxiety is that that if their children don’t get into college or university, they are ‘sunk’. Thus parents and the middle class teachers of their children are converting this anxiety into requests for the perceived performance enhancing properties of stimulants and with more children in classrooms taking stimulants many parents end up feeling their child is at a disadvantage if they don’t (Diller, 1998; 2002). This dynamic is reflected in the trend where stimulants are being prescribed to children without first making a diagnosis. This trend has now become so established that in some areas of the United States, less than half the children prescribed stimulants reach even the broad criteria for making a diagnosis of ADHD (Wasserman et al, 1999; Angold et al, 2000). In the UK anecdotal evidence suggests a different dynamic whereby stimulants are more likely to be used on children from poorer socioeconomic backgrounds thus effectively becoming a drug used for the social control of working class children (or more accurately boys).
Ritalin is a drug of abuse as it can be crushed and snorted to produce a high (Heyman, 1994). Surveys have shown that a significant proportion of adolescents in the United States self report using Ritalin for non-medical purposes (Robin and Barkley, 1998). Accounts of abuse of Ritalin and other stimulants are increasingly being reported in the lay press (Ravenel, 2002). A national survey in the United States found that 2.8% of high school seniors had used Ritalin without a physician’s prescription the previous year (Sannerud and Feussner, 2000). The neuro-chemical effects of Ritalin are very similar to that of Cocaine, which is one of the most addictive drugs. Cocaine users report that the effect of injected Ritalin is almost indistinguishable from that of Cocaine (Volkow et al, 1995). Advocates of the use of stimulants have claimed that the likelihood of substance misuse amongst those with a diagnosis of ADHD and treated with a stimulant, concluded that they were less likely to abuse substances when compared to those with ADHD who were not treated with stimulants. However, a larger, community based study (Lambert and Hartsough, 1998) which followed young people into their mid to late twenties (compared to the other studies which have followed young people on stimulants into their late teens) found a significant increase in cocaine and tobacco dependence amongst ADHD subjects taking stimulants when compared to controls, furthermore they discovered a linear relationship between the amount of stimulant treatment and the likelihood of either tobacco or cocaine dependence.
5. Appropriate use of pharmacological treatments.
Stimulants central nervous systems effects are not limited to those children who can be defined by the boundaries of this disorder. Thus stimulants have the same cognitive and behavioural effects on otherwise normal children, aggressive children regardless of diagnosis and children with co-morbid conduct disorder. This is not surprising. The pharmacological action of Ritalin on the brain is basically that of amphetamines (or its street name - speed) and cocaine which is known to have similar effects in most people who take it (see Timimi, 2005).
Research has focused almost exclusively on short-term outcomes. Outcome research in Ritalin treatment has been shown to have serious shortfalls in methodology such as small samples, inadequate description of randomisation or blinding and not accounting for withdrawals or drop outs (Zwi et al, 2000; Joughin and Zwi, 1999). The most recent meta-analysis of randomised controlled trials of methylphenidate found that the trials were of poor quality, there was strong evidence of publication bias, short term effects were inconsistent across different rating scales, side effects were frequent and problematic and long-term effects beyond 4 weeks of treatment were not demonstrated (Schachter et al, 2001).
The few long-term studies that have been conducted suggest that stimulants do not result in any long-term improvement in either behavioural or academic achievement (Weis et al, 1975; Rie et al, 1976; Charles and Schain, 1981; Gadow, 1983; Hetchman et al, 1984; Klein and Mannuzza, 1991). Despite the lack of evidence for any long -term effectiveness, Ritalin is most usually prescribed continuously for seven, eight or more years, with children as young as two being prescribed the drug in increasing numbers despite the manufacturers licence stating that it should not be prescribed to children under six (Zito et al, 2000; Baldwin and Anderson, 2000).
The idea that Ritalin is a safe drug with few harmful side effects couldn't be further from the truth. Troublesome and frequently reported side effects include poor appetite, weight loss, growth suppression, insomnia, depression, irritability, confusion, mood swings, obsessive compulsive behaviours, psychosis, explosive violent behaviour, personality change, a flattening of the emotions which, when observed, looks like a zombie-like state, stomach ache, headaches, staring, disinterest, tachycardia, pituitary dysfunction and dizziness. Ritalin is also associated with a lowered self-esteem and suppression of creativity in some children. Ritalin may also have long term adverse effects in as many as one third of those treated, including subtle cognitive effects such as perseveration (obsessive repetition of the same task), preoccupations, sombreness and deterioration in performance on complex cognitive tasks (see Timimi, 2005). Stimulants can also cause cardio-toxicity resulting in sudden death (see for example www.ritalindeath.com which documents that Between 1990 and 2000 there were 186 deaths from methylphenidate reported to the FDA MedWatch program). Recently Adderall XR, was withdrawn from use in Canada after a report found it was responsible for 20 sudden deaths and a dozen strokes. The lack of long-term studies into the effects of stimulants is a concern, as we do not really know what sort of effect giving an amphetamine like substance has on the developing brain.
Animal studies have found that taking stimulants can cause a long lasting change in the brain biochemistry of rats (Breggin, 1999; 2002; Moll et al, 2001; Sproson et al., 2001; Robinson and Kolb, 2001).Most recently a team at Harvard medical school, examined the effects of exposing rats to Ritalin during early development on behaviors later in life. They exposed normal rats to twice-daily doses of Ritalin during a period that is equivalent to approximately 4 to 12 years of age in humans. Examining the behavior during adulthood, the researchers found that the animals had a reduced ability to experience pleasure and reward. In addition, they found that the animals exposed to Ritalin during pre-adolescence were more prone to express despair-like behaviors in stressful situations (such as swim tests) as adults. Overall, the animals showed more evidence of dysfunctional brain reward systems and depressive-like behaviors in adulthood (press release available at http://www.mclean.harvard.edu/news/press/current.php?id=65).
We often forget that stimulants are powerful amphetamine like drugs with potentially addictive properties. Children can and do become tolerant to its effect resulting in gradually increasing doses being given to children as years on a stimulant clock up. The potential for tolerance and addiction is further demonstrated by withdrawal states (known as the rebound effect, which manifests in increased excitability, activity, talkativeness, irritability and insomnia) seen when the last dose of the day is wearing off or when the drug is withdrawn suddenly (Zahn et al, 1980). Stories of adults becoming addicted to prescribed stimulants are becoming more prevalent (e.g. Wurtzel, 2002).
In November 2004, an article was published with several interviews, which highlighted that questions about the scientific credibility of psychiatric drug research on children and adolescents in the field of child psychiatry (Hearn, 2004). Gene Haislip, the now retired director of the U.S. Drug Enforcement Agency (DEA), set production quotas for controlled substances like the federally restricted stimulant methylphenidate. During that time, he fought hard to raise public awareness about the over-prescribing of stimulants to children, about the drug’s high rate of non-prescription use/abuse, and about its long-term health impact on young patients. He notes that "When I was at the DEA, we created awareness about this issue. But the bottom line is we didn’t succeed in changing the situation because this – prescribing methylphenidate, for example – is spiraling." Adding "A few individuals in government expressing concern can’t equal the marketing power of large companies," (quoted in Hearn, 2004) Haislip suspects the dubious marketing tactics of big drug money have fueled the spiraled use of stimulants, specifically, a small group of prolific ADHD researchers whose work is funded by corporate producers of ADHD drugs. He also suspects that one or more ADHD patient advocacy groups that receive drug company donations have essentially become fronts to push the prescribing of stimulants to children.
William Pelham, a prominent ADHD researcher, and former member of the scientific advisory board for McNeil Pharmaceuticals was also interviewed (Hearn, 2004). Between 1997 and 1999, he was paid by McNeil to conduct one of three studies used to get Food and Drug Administration (FDA) approval for Concerta (a long acting slow release version of methylphenidate) and the company now uses these three studies to claim that 96 percent of children taking Concerta experience no problems in appetite, growth, or sleep. But Pelham says the studies were flawed and this claim is misleading because his study started with children who had already been taking Concerta and who had experienced no significant side effects—children who exhibited side effects weren’t included in the study to begin with. Pelham mentions that the company pressured him to delete a paragraph he wrote about the importance of behavioural therapy.
Pelham then discusses his experience in collaborating in a follow-up paper, in which the company did the data analysis and coordinated the writing of the paper. In Pelham’s words, "I insisted on seeing the analyses and having major inputs into the manuscript, and it was like pulling teeth to get wording and analyses changed. It was like a whitewash—a praise to Concerta." (quoted in Hearn, 2004).
In the world of ADHD advocacy, Children and Adults with Attention Deficit Hyperactivity Disorder (CHADD), a large American-based ‘parent support group’, engages in lobbying and claims to provide science-based, evidence-based information about ADHD to parents and the public. Critics point out that CHADD’s basic function has become that of promoting stimulant medications manufactured by its corporate donors. Pharmaceutical companies donated a total of $674,000 in the fiscal year 2002-2003. Pelham, listed by CHADD as a member of its professional advisory board, came face to face with what he says are the group’s glaring conflicts of interest. In 2002, after he received the CHADD Hall of Fame Award, he was subsequently interviewed for Attention!, the organization’s magazine. In the interview, Pelham said, among other things, that stimulant drugs have serious limitations particularly when employed alone and at high doses. He also pointed out that psychosocial treatments should be the treatment of first choice in ADHD, with adjunctive medication used only when necessary. Eight months later, Attention! published Pelham’s interview but with large swaths cut out, particularly his comments about the limitations of the stimulants. Commenting on this Pelham says "In recent years, I have come to believe that the individuals who advocate most strongly in favour of medication – both those from the professional community, including the National Institutes of Mental Health, and those from advocacy groups, including CHADD – have major and undisclosed conflicts of interest with the pharmaceutical companies that deal with ADHD products," (quoted in Hearn, 2004). Shire Pharmaceuticals, makers of the stimulant medication Adderall, buys 65,000 of the 100,000 copies each print run of Attention!. Shire sales representatives then place them in doctors’ offices (Hearn, 2004). In the UK, the main parent support ADDISS- Attention Deficit Disorder Information and Support Service- is also receiving significant funding from the pharmaceutical industry. For example a recent educational campaign ‘launched to support parents of children with ADHD’ includes a glossy booklet on ADHD called ‘Family Stress Points’ produced using an educational grant from Eily Lilly (ADDISS, 2005).
In a world run by those with the power to ‘buy’ media attention, it is not uncommon for single studies to become the basis on which practice develops. One such study was the large multi-centre trial in the United States, testing the efficacy of methylphenidate (MTA, 1999). It is notable that in the years since the publication and popularisation of this study there has been a sharp rise in the rates of stimulant prescription in the UK.
The study in question compared four groups of children who were given; medication only, intensive behavioural therapy only, combined behavioural therapy and medication, and standard community care. The study lasted 14 months and concluded that the medication only and combined behaviour therapy and medication groups had the best outcome, with the combined group having only a marginally better outcome than the medication only group. A closer look inevitably brings up important questions of methodology and the hidden question of conflict of interest (Breggin, 2000; Boyle & Jadad, 1999). The principle investigators were well known advocates of medication with long established financial ties to the pharmaceutical industry. Methodologically this was not a placebo controlled double blind clinical trial, and the parents and teachers who participated in the study were exposed to pro-drug propaganda at the start of the study thus putting them in a mindset of positive expectation for change in those children receiving medication. There are also many question marks with regard the selection and recruiting process, the behavioural interventions used, the lack of attention to the number of children experiencing side effects, and the dismissing of some reported side effects as probably being due to non medication factors (Breggin, 2000). In addition, two thirds of the community treated group were also receiving the same stimulant medication during the period of the study, yet were placed in the poorest outcome category.
Some of the participants in the above study were followed up again after a further 10 months- in other words after a total of 24 months in the study- (MTA, 2004). These results are no longer looking so impressive. While the percentages of children with normalized symptom levels (in other words those who in the opinion of the researchers were no longer displaying any ADHD symptoms) were essentially unchanged for the behaviour therapy only and community care groups, they had declined substantially for the combined (from 68% to 47%) and medication only (from 56% to 37%) groups. The medication only group now had a similar percentage to the behaviour therapy only group. Furthermore, there was now no evidence of significant treatment group differences in social skills, reading achievement, and parents’ use of negative/ineffective discipline strategies, and those who were receiving medication were now significantly shorter than those who were not. Not surprisingly we have heard little about this potentially damaging (to stimulant sales) follow-up study which suggests that stimulants carry physical risks, may not work the long run and that behavioural modification approaches may serve just as well. According to Pelham, who is on the steering committee for the MTA studies, "No drug company in its literature mentions the fact that 40 years of research says there is no long-term benefit of medications. That is something parents need to know." (quoted in Hearn, 2004).
6. psychological interventions.
As with non-medical theories of causation, non-drug-based solutions to the problems children with ADHD type behaviours present have been marginalized by the more politically powerful, Drug Company supported medical and consumer bodies. A comprehensive set of therapeutic strategies and approaches needs to be able to tackle a whole set of diverse issues that children with ADHD type behaviours present with. The task should be that of broadening our understanding in a context rich manner rather than narrowing our understanding (and therefore interventions) into context depleted constructs like ADHD. Interventions should be framed to the particular needs of each individual circumstances from the adverse effects of labelling, therapy with the child concerned, right up to working with parents, schools and the local community. This does not mean doing all of these with all children referred but what it does mean is a wholesale shift in attitude away from that of labelling kids with a medical disorder, in the absence of any evidence that they are suffering from a physical defect.
In my opinion, the starting point for offering a holistic, integrated, multi-perspective model has to be the rejection of ADHD as label that offers anything meaningful or useful to clinical practice. Paradoxically, although the use of the ADHD diagnosis and stimulant medication may appear to offer a cheap, labour saving way of helping these children and their families, as with stimulants effectiveness it does the opposite. Although you may get quick results in the short term, in the long term you create a group of children who are dependent (on the drugs and the doctors who prescribe them) and need to carry on seeing their doctor for years (some say the rest of their lives), without ever having dealt with the original difficulties.
My experience is that if I see my basic role as that of empowering children, parents and schools to find their own solutions, then dependency on doctors doesn’t happen and my clients can be discharged from my clinics in a comparatively short time and with at least as good an outcome (particularly in terms of client’s satisfaction) than going down the more labour intensive (in the long term) diagnosis and medication route.
In terms of what might be considered ‘modernist’ (expert derived) interventions useful approaches include family and systemic therapy, such as interventions to improve communication and relationships in the family, address attachment issues, explore family and parental history, and consult with schools and other professionals (e.g. Alexander and Parsons, 1982, Alexander et al, 1988, Henggeller and Borduin, 1990, Oas, 2001); specific behaviour management strategies, such as those to enforce effective discipline (e.g. Stein, 2001, Breggin, 2000, Sells, 2001); addressing lifestyle issues, such as slowing down the pace of life, creating more family time, regular opportunities for exercise and looking at diet (e.g. De Grandpre, 1999, Armstrong, 1995, Jacobson and Schardt, 1999); and a discussion of the families value system as well as a questioning of my own cultural values and how this may effect my practice (see Timimi, 2005).
In terms of post-modern style interventions (privileging families existing knowledge), although little has been written specifically about ADHD, postmodern thinking has informed many useful therapeutic interventions including deconstructing traditional medical and psychological discourses (e.g. Law, 1997, Smith and Nylund, 1997); focusing on strengths and building solutions (e.g. Shazer, 1994); use of metaphor and stories (e.g. Rosen, 1982, Dwivedi, 1997), externalizing the problem (e.g. White and Epston, 1990, Smith and Nylund, 1997) and advocacy work on behalf of the family (Timimi, 2002, 2005). For the sake of convenience I have called the style of working that includes all these differing metaphors that we use in therapy to construct a (hopefully) meaningful and useful intervention a ‘multi-perspective’ approach (Timimi, 2002; 2005). Using this approach I have, in collaboration with their families, successfully weaned over 30 children off of stimulant medication in the past 2 years, without needing to start such a prescription for a single child, leaving me with no children on my current caseload that take a stimulant.
7. Other physical treatments including dietary elimination and supplementation.
8. Treatment approaches for adults with ADHD.
As childhood ADHD does not exist (as stated above the onus is on those who believe in it to provide proof of its existence, not on critics to prove it doesn’t) so there is no such thing as adult ADHD. As a culture there are grave public health as well as ethical concerns if we go down the route of medicalising common day-to-day problems for those living in fast paced modern life, such as disorganization and daydreaming.
9. Sensitivity to different beliefs and attitudes of different races and cultures, and issues of social exclusion.
Because of all the above lack of evidence on what component of ADHD is biologically and how to find the biological component, it must be viewed as a cultural construct. Within this construct will lay assumptions about what is ‘normal’ in terms of childhood behaviour and child rearing practices that is specific to the culture that invented it. Whatever part of conditions such as ADHD are biological (all behaviour ultimately derives from a biological substrate), how we construct meaning out of this is a cultural process. For example, Brewis and Schmidt (2003) carried out a study in a middle class, Mexican school of over 200 pupils. Using standard diagnostic criteria, they found that about 8% of the children could be diagnosed, as having ADHD, yet there was only one child in that school with the diagnosis. Through interviews with parents and teachers they found that these carers regarded ADHD-type behaviours as within the boundaries of behaviours viewed as normal for these children’s ages. Thus all diagnosis of ADHD are based on cultural assumption and any document that sets out guidelines on this diagnosis without acknowledging the cultural nature of the construct is institutionally racist, for it will project it’s own moral and ethical framework (rather than scientific one) using cultural assumptions that will necessarily (though unintentionally) place Western beliefs in a morally superior position to those of other cultures (Timimi, 2005).
10. The role of families and carers in the treatment and support of people with ADHD.
There is an opportunity for NICE to re-consider the basic assumptions behind the construct of ADHD. The only scientific conclusion if the null hypothesis is being observed is that ADHD is not a valid diagnosis (at the very least that it cannot be categorized as a ‘neurodevelopmental’ disorder). One major concern is that the members of the committee that will examine this will have too many vested interests to make for a scientifically objective examination of the evidence. If there is no representation from those who criticizes this construct then the guidelines will be flawed scientifically, ethically and this may lead to perpetuating practice that is dangerous to public health.
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