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Wednesday, 21 February 2018

The Scientism of Attention Deficit Hyperactivity Disorder (ADHD) by Professor Sami Timimi Courtesy of the MadinAmerica Website

The Scientism of Attention Deficit Hyperactivity Disorder (ADHD)

In my last blog I reviewed the scientific basis on which modern mainstream psychiatry rests and showed how a poor understanding of the basics of the scientific process was evident in mainstream academic and clinical frameworks that organise psychiatric research and practice. Modern psychiatry is built on scientism, not science. In this blog I start to illustrate how this scientism can be found in the literature on specific ‘conditions’.
As a practicing child psychiatrist, ADHD is one of the four common ‘diagnoses’ I encounter in my practice — the other three being autism, childhood depression, and generalised anxiety (diagnoses that are usually made by other doctors for patients I ‘inherit’). As mentioned in my last blog, it requires little intellectual effort to understand that calling ADHD a ‘diagnosis’ is not logical or accurate. In medicine, diagnoses are part of a system of classification based on explanation. What we are referring to as ‘diagnoses’ in psychiatry are descriptive classifications with no explanatory powers and therefore, strictly speaking, not a diagnosis. Calling ADHD a diagnosis, i.e., something with the capacity to explain the behaviours that it describes, is like saying the headache is causing the pain in my head or the inattention is caused by inattention.
My first ‘serious’ encounter with the phenomenon of ADHD was as a trainee in child psychiatry in the mid-1990s. ADHD was not being diagnosed in the UK at that time; in fact, child psychiatry was a largely systemically orientated profession that didn’t use diagnostic labels, and child psychiatrists rarely prescribed medications. We were aware of the growing medicalisation in the US and there were child psychiatrists in influential positions in the UK who were attracted by this. By the mid-1990s in the UK, their influence was beginning to tell. Thus one of my supervising consultants expressed an interest in carrying out a ‘project’ on ADHD and its relevance to the population we were serving in an ethnically diverse and deprived area of inner London. He asked me if I would like to join him. As an enthusiastic trainee eager to learn I jumped at the chance. My consultant hadn’t yet formulated a research question and so asked me to do a literature review summarising key data on ADHD (diagnosis, prevalence, causes, urban v rural etc.).
This proved to be an enlightening experience — just not in the way my supervisor imagined. I read studies and reviews but felt troubled by my inability to grasp what this concept was. The more I read the less certain I became. I couldn’t answer the basic question of “what is ADHD?” What is it, I kept thinking; surely it isn’t just ‘attention deficit’ and ‘hyperactivity’, just what it was called, followed by the word ‘disorder’. I found it incredibly frustrating that the literature I was reading wasn’t addressing this basic question. Instead there was an assumption that ADHD exists as a ‘thing’ and that this thing had a concrete reality that meant you could make authoritative statements about its features, implications, causes, prevalence, treatment and so on. I was astonished to realise that ADHD had been conjured into existence by a few people’s imaginations without evidential basis. The evidence then brought forward avoided the scientific methodology and ignored the ‘null hypothesis’ (the basic and starting assumption that ADHD does not represent a characteristic natural entity, which should be assumed until concrete evidence is presented that shows that this null hypothesis cannot be true). The papers I reviewed made me feel uneasy. How could this construct be taken at face value and treated as if it were a real entity? If the construct does not reflect a specific, measurable, identifiable, natural entity (as the null hypothesis presupposes), then all the data built using the idea that ADHD is a ‘thing’ is suspect. Castles built on sand.
This lack of foundational solidity has been confirmed for me in my subsequent years of examining various facets of the ADHD literature. As I will explain below, research in the name of showing ADHD to be a natural entity has provided convincing evidence of the opposite. Sadly, in an era in psychiatric thinking dominated by scientism, this is not the message that most people receive.
Instead, this is the sort of information you get from websites when you google “What is ADHD?”
ADHD stands for attention deficit hyperactivity disorder. It is a medical condition. A person with ADHD has differences in brain development and brain activity that affect attention, the ability to sit still, and self-control. ADHD can affect a child at school, at home, and in friendships.” (Kids health) Or “If you have attention deficit hyperactive disorder (ADHD), you may have lots of energy and find it difficult to concentrate. It can be hard to control your speech and actions. ADHD is the most common behavioural disorder in children. It usually starts at about 18 months old, but symptoms usually become noticeable between the ages of 3 and 7. We don’t know what causes ADHD but experts think it runs in families. It could also be caused by an imbalance in brain chemicals.” (Young Minds) Or “ADHD is characterised by periods of impulsiveness, hyperactivity and inattention, but it’s more than being a daydreamer or a fidget. ADHD affects about 2-5% of us, and it’s largely genetic – although environmental factors can make it worse.” (BBC advice).
If you google “What causes ADHD?” you get things like:
ADHD tends to run in families and, in most cases, it’s thought the genes you inherit from your parents are a significant factor in developing the condition… Research has identified a number of possible differences in the brains of people with ADHD compared to those who don’t have the condition… Other studies have suggested that people with ADHD may have an imbalance in the level of neurotransmitters in the brain.” (NHS choices) Or “Scientific research has found there is a strong genetic link in ADHD. It is not a disorder that is learnt or passed on socially… Many of the genes that experts have identified as potentially contributing to the development of ADHD are genes that control certain types of neurotransmitter… Scientific studies have shown that in people with ADHD some important parts of the brain are developing more slowly and communicating less well.” (Netdoctor)
If you google “ADHD treatment” you get things like:
Treatments range from behavioral intervention to prescription medication. In many cases, medication alone is an effective treatment for ADHD.” (Healthline) Or “Treatment of attention deficit hyperactivity disorder (ADHD) relies on a combination of medicines and behavior therapy. Treatment with medicine depends on the age of your child. The first step is an accurate diagnosis of ADHD and an understanding of your child’s strengths and weaknesses. Learning about ADHD will help you and your child’s siblings better understand how to help your child.” (Webmd)
Thus you can see that the views you will likely encounter in most searches on the subject bring up lots of scientific-sounding stuff that tells you that ADHD is something that exists as an identifiable ‘thing’ and that this thing has something to do with your genes and brain (chemicals and structure), and can be treated by medication alongside some behaviour therapy. Scientism has turned ADHD from a vague, difficult to pin down concept into a fact of culture masquerading as a fact of nature.
As ADHD does not reach the required evidence base to be considered a ‘diagnosis’, it is not surprising that there has been a failure to find any specific and/or characteristic biological abnormality such as characteristic neuroanatomical, genetic or neurotransmitter abnormalities. Unlike the myths that have been spread to spur an ADHD industry on, the scientific reality is that we have a cupboard empty of confirming evidence and full instead of ‘junk’ scientism.
Scientism in ADHD genetics
The claim that ADHD is ‘genetic’ has been extrapolated from twin studies. In the twin method it is assumed that when a higher percentage of identical than non-identical twins are diagnosed with the same disorder, this is due to genetics rather than environmental factors. This is because identical twin pairs will share 100% of the genes whereas non-identical twins will have, on average, 50% of their genes the same. However, for identical twins to have a greater likelihood of having a disorder because of sharing the same genes, you have to assume that the psychosocial environment is the same for identical and non-identical twins. This is known as the Equal Environment Assumption or EEA for short. It has been long established that EEA doesn’t hold when comparing identical and non-identical twins. Identical twins are often treated similarly (e.g. dressed in same clothes) and experience a unique psychological environment (e.g. swapping roles to confuse others). Being one of a set of identical twins is a different experience to being a non-identical twin and so the psychosocial environment could (as well as genes) by itself be responsible for greater behavioural or emotional similarity in identical compared to non-identical twins. This means the twin study method cannot disentangle genetic from environmental factors for ‘psychiatric’ presentations, and so estimates of the genetic contribution to ADHD cannot be arrived at from this method.
The only way to reliably evidence a specific genetic contribution to ADHD is through molecular genetic studies. Since faster and cheaper whole genome scans have become available the molecular genetic evidence has been accumulating. This increasingly large volume of ADHD genetic research is not showing any particular genetic findings, whether in relation to abnormal genes or consistent genetic associations. Yet this has not stopped unscrupulous researchers from making claims to the contrary.
In 2010, a study was published in the medical journal The Lancet claiming to have found concrete molecular genetic evidence that ADHD is a genetic disorder. This study has been, and continues to be, referenced as the preeminent study that demonstrates the certainty with which we can call ADHD genetic. In the press release at the time, the research team lead, Professor Anita Thapar, left little room for doubt, saying: “Now we can say with confidence that ADHD is a genetic disease and that the brains of children with this condition develop differently to those of other children.” This is what they really found:
The study involved the comparison of whole genome scans of 366 children ‘with ADHD’ with those of 1047 ‘non-ADHD’ control children, looking for something called Copy Number Variants (CNVs). CNVs are abnormal bits of genetic code that are repeated where they shouldn’t be or deleted where they should. Researchers found 15.5% (57) of the children with ADHD had CNVs compared with 7.5% (78) of the non-ADHD controls. This leaves an excess of 8% in the ADHD group, hardly a significant figure. If we are to accept standard ‘mainstream’ quoted prevalence for ADHD, it also means that if you come across a young person who has CNVs they are more likely to not be diagnosable with ADHD than diagnosable with it.
The deceit doesn’t end there, however. The average recorded IQ of the children with ADHD was 86, 14 points below the general population average of 100. Furthermore, when 33 intellectually impaired (IQ lower than 70) ‘ADHD children’ were excluded from the ADHD group, only 11.4% of the remaining 333 had CNVs (now only 4% above the ‘non-ADHD’ control group). 39% (13) of the 33 children with ADHD and an intellectual impairment had CNVs. This evidence is more suggestive of a relationship between the presence of CNVs and intellectual disability (39%) than ADHD (11.4%). The authors of this study should therefore have controlled for IQ given its disproportionate impact on CNV levels, but chose not to. As mentioned above the average IQ in the ADHD group was significantly lower than the control group (whom we can assume would have a population average IQ of 100). The authors should have chosen a subgroup from their ADHD patients who had an average IQ of 100. This would then have made for a more legitimate comparison group to their control group. I can’t help wondering whether someone in the group did that, because I suspect they may have been left with no or a tiny 1% or so difference and so chose not to publicise this.
This sort of high-profile and media attention grabbing publication is worse than junk science, as the authors have misled the medical community and general public in their conclusions. With genetics then, the cupboard is empty and the null hypothesis stands: There is no characteristic identifiable genetic abnormality/profile associated with ADHD.
Scientism in ADHD brain imaging studies
As with genetics, ADHD brain imaging studies have not uncovered any specific or characteristic abnormality. The picture that emerges is of consistently inconsistent findings, which are statistical deviations (the brains would not be recognised by radiologists as being clinically abnormal), come from small sample size studies, don’t always accurately match for age (and you’ll see why this important when I comment on birthdate research below) and typically don’t control for IQ level, or for the possible effects of medication. One research team finds one bit of the brain smaller than ‘healthy’ controls and the next one doesn’t, or even finds that bit is a little larger.
But, as I have been explaining, the science should not get in the way of the dedicated scientismist! In 2017, The Lancet Psychiatry published a study that the authors claimed provided definitive evidence that young people with ADHD have different and smaller brains compared to their healthy peers. As with the genetics junk science, the lead researcher, Dr Hoogman, made bold claims that do not stand up to scrutiny. In a press release that was covered by mainstream media, he stated that “The results from our study confirm that people with ADHD have differences in their brain structure and therefore suggest that ADHD is a disorder of the brain.” In an excellent analysis by Michael Corrigan and Robert Whitaker for Mad in America, they show how the research reveals more about the desperation of the authors to find something than their ability to conduct a scientifically careful analysis of their findings.
The authors call their study a ‘mega-analysis’ as they took data from a large number of previous research projects and ‘number crunched’ all the different sites findings as if they were all just one big study. This process is sometimes illuminating, but can also make incidental findings look more significant than they are. In total, they had data from the brain scans of 1713 patients diagnosed with ADHD and 1529 individuals who did not have this diagnosis, gathered from 23 different sites around the world. They claim what amounts to tiny differences in some (not all) particular brain structures that become statistically significant when they add all the available recorded volumes for a particular structure in the ADHD and non-ADHD groups. Using certain measures of statistical variance enables them to make this claim on differences that are so tiny they are of no clinical relevance. This method enables them to hide the consistently inconsistent findings.
For example, the largest difference was found for a tiny brain structure called the nucleus accumbens. This mega-analysis thus makes the claim that children with ADHD have a smaller nucleus accumbens (NA). However, if you look at the data by site you find 10 sites that found an on average smaller NA in the ADHD group, 4 sites that found a larger NA in the ADHD group, and 6 sites that found no difference. This is the picture for the structure with the largest difference in the study. Staying with NA, you can also see that there are major technical issues with interpreting the scans. For example, individuals in Bergen Norway have an average NA volume of 758 mm3 v 805 mm3 (ADHD v control), whereas in Wuzberg, Germany they have an average NA volume of 462 mm3 v 449 mm3 (ADHD v control). Perhaps Norwegian children have amazing NAs compared to German children, whom by this standard must all have raging ADHD to contend with. However, given that the Norwegian group is one of the groups where the controls have larger volumes, whereas the ADHD group has larger volumes in the German centre, this huge variation which is larger between centres than within further biases the findings if (as is the case) those with larger total volumes lay more in the group that had differences in favour of controls having larger structures.
Finally, here is yet another study that does not control for IQ differences. Associations between brain volume and IQ have been shown across a range of studies with adults and children. When the authors of this study published the correct IQ table (embarrassingly they had originally published an incorrect version), a separate group re-analysed their data, taking into account potential effects of IQ, and concluded that there was no significant difference between individuals with ADHD and those in the control group in any of the investigated areas of the brain when IQ difference is controlled for.
Here too then, as far as the science is concerned, the cupboard is also empty. No one has come near to finding a characteristic abnormality, and as a result there is no biological marker or brain scan used to diagnose ADHD. The null hypothesis stands — there is no characteristic brain abnormality associated with ADHD.
Scientism and ADHD as a chemical imbalance
There is no shortage of ‘experts’ prepared to claim that ADHD is related to a chemical lack or imbalance of the neurotransmitter ‘dopamine’. This idea is based solely on the perceived finding that drugs (like Ritalin) that act to stimulate the release of dopamine, and therefore increase its levels in brain synapses, appear to improve the ‘symptoms’ of ADHD (more on that later). Decades ago studies found that if you take stimulants, regardless of diagnosis, it improves your ability, in the short term at least, to maintain concentration on a task. However, as no one had yet demonstrated a lack or no lack of dopamine in individuals diagnosed with ADHD, the chemical imbalance theory was able to spread alongside aggressive marketing from manufacturers of drugs that increase the levels of these chemicals in the brain.
Every now and then a study comes along that challenges the received wisdom and so gets limited publicity. One such study was published in 2013. Its findings questioned “previous suggestions that attention deficit hyperactivity disorder (ADHD) is the result of fundamental abnormalities in dopamine transmission.” The researchers found that administering methylphenidate (more commonly known as Ritalin) to healthy adult volunteers as well as those who exhibit symptoms of ADHD led to similar increases of the chemical dopamine in their brain. Both groups also had equivalent levels of improvements as a result of the drug when tested on their ability to concentrate and pay attention.
Here too then the cupboard is also empty. The null hypothesis stands — there is no characteristic chemical imbalance associated with ADHD.
Scientism of ADHD revealed in diagnoses of young-for-class children
Several studies conducted in different countries have found that the youngest children in a class year have a significantly increased risk (compared to oldest children in a class year) of being diagnosed with ADHD and/or receiving medication for ADHD. These studies have found that whether you are in country that has high rates of diagnosing or prescribing (like USA) or low rates (like Finland), this pattern is still evident. Such a pattern of identifying ADHD is strongly suggestive that relative immaturity to your peers is a significant risk factor for receiving this label (i.e., for adults noting and problematizing the described behaviours associated with ADHD). Whether it’s over 6% of children (in Icelandic study) who get prescribed stimulants or less than 1% (in the Finnish study), the pattern still holds. Whatever the cultural norms for problematizing these behaviours are, relative immaturity in the class keeps emerging as a risk factor. Of course, children mature at different rates, raising an important question of whether a diagnosis of ADHD even for older-in-the-class children might also be reflective of their relative slower developmental trajectory. For a while now I have thought the growth of pseudo-diagnoses like ADHD to be a reflection of Western neoliberal intolerance of diversity amongst children, where from an early age children are given messages that they are valued for what they do (for their ‘performance’) rather than for just being. These findings lend further support to my concern that the prevalence of diagnoses like ADHD acts like a barometer of how intolerant of children and childishness we are.
Scientism in ADHD treatment
In 1999 a study of ‘treatment’ for ADHD was published. By then, prescribing of stimulant medication (the most famous name for a stimulant medication being ‘Ritalin’) was widespread. When this study was published it received extensive public and professional coverage. I remember attending our Faculty of Child and Adolescent Psychiatry (in the UK Royal College of Psychiatrists) annual conference in 2000, with the then chair of the faculty explaining to us that the implication of this study was that we would have to prescribe stimulants for anyone diagnosed with ADHD and probably (given resource limitations) that stimulants alone would be sufficient for most.
So what did this famous study find? This American study often referred to as the ‘MTA’ study (stands for Multimodal Treatment study of children with ADHD), was a 14 month multi-centre trial where young patients were randomised to four treatment groups: medication (stimulants) only, behaviour therapy only, combined medication and behaviour therapy, and routine community care. The authors concluded that after 14 months of treatment, there was more reduction of ADHD symptoms in the medication only and combined treatment groups than the behavioural therapy only group, who in turn had better outcomes than the routine community care group.
As you might predict by now, there were considerable problems associated with the study that make such a conclusion questionable. For example, two thirds of the routine community care group were also on the same medication as the medication arm of the study, yet had the poorest outcomes. Furthermore, the behavioural treatment arm consisted of an intensive 6 week course that was completed at any time during the 14 months, so that by the time of the 14 month evaluation, some of the families receiving the behavioural therapy intervention had completed it up to 9 months before the 14 month assessments, whilst the medication arm included appointments right up to 14 months. This raises the distinct possibility of a placebo response being the main reason for better outcomes in the medication and combined treatment arms at 14 months. At that time, conflict of interest statements were not mandatory in most journals. Predictably, when these were made known, many of the lead authors had long lists of pharmaceutical company connections.
The story of the MTA study doesn’t end there. By chance I ended up, at a conference in 2002, sitting next to a psychologist involved in the evaluations of the MTA trial. He told me they had just completed analysing the data for the 3 year follow up at his centre. I remember him saying to me “Once these findings are published no one will want to have their children take medication anymore.” I had to wait another 5 years before the 3 year follow up of the MTA was published. Unlike the original 1999 study, this publication, published 8 years later (allowing plenty of time for stimulant prescribing advocated by the 1999 paper to become the norm), had little accompanying press or professional coverage. The follow-up analysis of outcomes at 3 years of the MTA study patients could not find support for continuing superiority of medication regardless of initial severity of ADHD symptoms. Additionally, those who used more medication during the 3 years were more likely to experience a deterioration in ADHD symptoms, had higher rates of delinquency, and were significantly shorter (by an average of 4 cm) and lighter (by 3 kg) than those who had not taken medication.
This is typical of the findings in other long-term follow-up studies that are naturalistic rather than controlled trials (in other words, following people who attend usual services). These studies also fail to show that long-term use of stimulants is associated with any improved outcomes compared to those diagnosed with ADHD who don’t take them, and where there are differences it is often with children on stimulants having worse outcomes than those diagnosed with ADHD but not taking them (see for example the Western Australia and Canadian studies).
If these medications, which are used so widely now, had little evidence of harms associated with their use, perhaps we could tolerate the small initial improvement that is sometimes associated with their prescription, even if there is no evidence of improved longer term outcomes. However, the stimulants that are being prescribed have near identical pharmacological properties to street drugs such as ‘speed’ and ‘cocaine’ that we regularly warn others of the physical and mental dangers associated with their use. If these drugs were only prescribed to patients for a year or less it might be possible to put together evidence-based arguments for their use in this limited and controlled manner. Unfortunately, once started, a prescription is likely to continue being given for years. Given the considerable harms associated with the use of such powerful and addictive substances, you really need clear blue water in outcomes between those who receive such medications and those who don’t. I can’t think of a rational ethical argument (probably because there isn’t one) to justify the long-term prescribing of stimulants given the available evidence.
Conclusion: ADHD is an example of scientism
I hope I have convinced you that whatever the perceived merits of thinking of ADHD as a ‘diagnosis’ that has biological origins and can be ‘treated’ with medication, it cannot be thought of as a valid scientific entity, and the current recommendation for its treatment which usually prioritises medication without time limits is not evidence-based.
ADHD is an example of how academic psychiatry got infected with scientism that has likely led to untold harm. Imagining that ADHD is a diagnosis blinds children, parents, teachers, doctors and other practitioners to a whole variety of context-related factors such as immaturity, learning difficulties, exposure to violence, dietary factors, lifestyle, lack of family support, lack of confidence in parenting, and so on. It also blinds them to a whole variety of other approaches that may prove beneficial for such children. It’s time we stopped using ADHD as a label and scrapped any guideline attached to this scientism.

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Sami Timimi, MD
No More Psychiatric Labels: A child and adolescent psychiatrist, Sami Timimi writes about the Critical Psychiatry movement, an international network of doctors (primarily psychiatrists) who critique current mainstream practice in mental health and are hoping to reform it.

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