By Sami Tamimi
Editor’s Note: Over the next several months, Mad in America’s Parent Resources section will publish selected chapters of Sami Tamimi’s new book, Insane Medicine. Dr. Timimi is a consultant in child and adolescent psychiatry at the UK’s Lincolnshire Partnership NHS Foundation Trust. His past works include Naughty Boys: Anti-Social Behaviour, ADHD and the Role of Culture and A Straight Talking Introduction to Children’s Mental Health Problems, among others.
Following is Chapter 3, Part 1. All chapters will be archived here.
What is Attention-Deficit/Hyperactivity Disorder (ADHD)? The conventional answer to this question is that it is hyperactivity, inattentiveness, and impulsivity that are caused by neurological dysfunction rooted primarily in genetics and abnormalities in the development of the brain. As a result, it is often referred to, alongside autism, as a “neurodevelopmental disorder.” This way of imagining the significance of such behaviours, firstly in children and then (with important modifications) in adults, started in North America and has been exported throughout the world.
Going hand in glove with this “neuro” paradigm are the pharmaceutical treatments using stimulants, such as Ritalin, Adderall, and Strattera, which have similarly dominated the treatment of children who get diagnosed with ADHD and played a major part in the construction of ADHD as having neurological origins.
Both the idea that there are some characteristic brain-based abnormalities or differences for those diagnosed with ADHD and that the medications used have specific properties that target a disease process—like a chemical imbalance—are false. Damagingly false.
Mainstream Construction of ADHD
The standard construction of ADHD in the psychiatric literature goes something like this:
ADHD is characterised by a pattern of behaviour, present in at least two settings (e.g., school and home) and that can result in performance issues in social, educational, or work settings. Symptoms can be divided into two categories of “inattention” and “hyperactivity and impulsivity” that include behaviours like failure to pay close attention to details, difficulty organising tasks and activities, excessive talking, fidgeting, or an inability to remain seated in appropriate situations.
According to the latest definitions, the individual’s ADHD symptoms must be present prior to the age of 12 years (until new definitions were printed in 2013, symptoms had to be present before 7 years old).
ADHD is described as a common psychiatric disorder that affects between 3% and 7% of children, mainly boys, and which many do not grow out of (i.e., it will be a lifelong disorder). ADHD has a primarily genetic basis that results in a “neurodevelopmental” abnormality that also causes a chemical imbalance in the brain. Treatment is usually a mixture of stimulant medication and behaviour therapy.
Let’s now examine these claims more carefully.
A Brief History
The behaviours that are said to make up the diagnosis of ADHD did not make up ADHD until it was imagined in that way. Literally: There was no ADHD until someone called it ADHD (or its precursor names). There has never been any basis in scientific discovery before ADHD was invented (or since) that has shown that what we call ADHD is the result of a known abnormality or difference sufficiently characteristic to think of it as a natural kind—a thing that occurs in an identifiable way in nature, just like pneumonia or diabetes.
Over-activity, poor concentration, and impulsivity in children were first conceptualised as possible medical phenomena over a century ago when a British paediatrician, Frederick Still, described a group of children who showed what he considered to be a poor capacity for sustained attention, restlessness, and fidgetiness, and went on to argue that these children had “abnormal defects of moral control,” although he generally assumed this was caused by pre-existing diseases affecting the brain such as cerebral tumours, meningitis, epilepsy, head injury, typhoid fever, or impairment of the intellect.
Although Still lists behaviours that could be considered more appropriate to the category of conduct disorder (such as cruelty, jealousy, lawlessness, dishonesty) than ADHD, ADHD enthusiasts often paint his 1902 article in The Lancet as an early example of the identification of the medical syndrome of ADHD.
The next important link in the developing ADHD narrative cited by the enthusiasts was a 1937 paper by Bradley describing the chance discovery, at an institution for neurologically impaired children, that stimulant treatment (with the stimulant Benzedrine) allegedly improved the behaviour, concentration, and school performance of a group of these children, at least in the short term. The children often presented with restlessness, personality changes, and learning difficulties, with many having previously suffered from encephalitis.
Neither Still’s nor Bradley’s papers received much attention at the time of their publication and would have disappeared like thousands of other ideas that come and go in the medical and scientific literature had ADHD precursors not started to gain traction in cultural and political circles decades later.
In the post-Second World War years, psychiatry became involved in the treatment of many traumatised men, women, and families and so began to expand its range of interests. The mental life of children—a group that had not drawn much interest from the psychiatric profession until then—became the focus of greater curiosity and interest. A number of doctors began to speculate that children who presented as hyperactive might have organic lesions in the brain that were causing their hyperactivity.
In 1947, Strauss and Lehtinen proposed a diagnosis of Minimal Brain Damage (MBD) to explain the occurrence of hyperactivity in the absence of overt evidence of brain injury. Arguing that children who experienced identifiable brain injuries (from, for example, encephalitis, birth trauma, and epilepsy) sometimes presented with hyperactivity, they suggested that those who presented with hyperactivity in the absence of readily identifiable brain injuries may have some as yet unidentified brain damage.
It was in the 1950s when a group of physicians, along with some educators, politicians, and parents, started to become more alarmed about children who had the behaviours that we now associate with ADHD and wondered whether such behaviours were the manifestations of an underlying pathology that warranted medical intervention.
As historian Matthew Smith found through searching medical databases, such concerns reached momentum during the late 1950s and, particularly, in 1957 when, amongst other events, a group of child psychiatrists at Emma Pendleton Bradley Home in Rhode Island, USA, coined the term “hyperkinetic impulse disorder” to describe a group of children. This was when what we now think of as ADHD was properly invented and a group of childhood behaviours, mainly displayed by (as any parent or teacher would tell you) boys, were brought under a medical gaze. There was to be no biological discovery either then or since to justify its entry into any system of knowledge as a “neuro”-based thing.
After 1957, the number of medical articles about children with the “symptoms” of ADHD escalated exponentially in the United States and later in other countries. In the previous half-century, medical literature, particularly that influenced by psychoanalytic ideas, was more concerned with withdrawn, shy, “neurotic” children. The late fifties, then, marked a turning point as interest transferred more to children who exhibited delinquent, violent, and other antisocial behaviours.
What was behind this shift? According to Matthew Smith, it may have been related to fear, following the Soviet launching of the Sputnik satellites in the autumn of 1957, that the US was falling behind the USSR in the race for scientific, technological, and military superiority. There was concern that if changes were not made to the American school system to redress the situation, they might lose the Cold War altogether. This caused a change in classroom structure, teaching methods, and expectations with regard pupil performance.
I am not entirely convinced by this and think that such events intersected with other changes taking place in the culture of the time, including (but not limited to) the growth of and fear of adolescent culture, changes in family structure and community rootedness, the growing size of an aspirational middle class, and greater concern about children both as perpetrators and victims.
The more important point here is recognising that ADHD emerges and gets popularised because there are cultural, not scientific, reasons for it becoming a sellable brand. Shifts in public and political concerns will shift interest, conversations, funding, service provision, and so on.
By the 1960s, the term MBD was being criticised and losing favour, as evidence for underlying organic lesions in children who displayed hyperactivity was not being found. In addition, higher rates of brain insults were found to be present across most psychiatric categories (rather than any specific one) and many who had evidence of brain damage did not show hyperactivity.
Instead, the Oxford International Study Group of Child Neurology suggested that MBD be redefined as Minimal Brain Dysfunction. The concept of Minimal Brain Dysfunction was wider and referred to children with learning or behavioural problems ranging from mild to severe, and presenting with “deviations” of perception, conceptualisation, language, memory, attention, impulse, or motor function.
As it was becoming recognised in the medical literature that the presence of hyperactivity couldn’t be thought of as evidence of some sort of brain damage, it began to be understood as being part of a behavioural syndrome that could arise from organic pathology, but could also occur in its absence. As a result, a movement away from causally based definitions towards behaviourally based ones occurred. Thus, in 1966, the North American-based Diagnostic and Statistical Manual of Mental Disorders, second edition (DSM-II) coined the label “Hyperkinetic reaction of childhood” to replace the diagnosis of MBD.
At the same time, growing interest from psychologists meant that psychological mechanisms were being hypothesised as the mediator between potential causal influences and subsequent behavioural manifestations. The role of attention came to the fore as a new theory proposed that problems in sustaining attention were the drivers of hyperactivity.
Thus, when the DSM-II was replaced in the early eighties by the third edition (DSM-III), the disorder was now termed Attention Deficit Disorder (ADD), reflecting this change in emphasis. This could be diagnosed with or without hyperactivity and was defined using three dimensions (three separate lists of symptoms): one for attention deficits, one for impulsivity, and one for hyperactivity. ADD now sets the scene for a revolution to take place in Western child psychiatric practice, as the drug Ritalin joins the growing popularity of using psycho-pharmaceuticals to deal with life’s challenges.
When the DSM-III was revised (and became DSM-III-R) in the late eighties, the symptoms were all combined into one list (one dimension) and ADD was now changed to Attention-Deficit/Hyperactivity Disorder (ADHD), with attention, hyperactivity, and impulsiveness now assumed to be part of one disorder with no distinctions, and thus the label ADHD was born.
When the fourth edition of the DSM (DSM-IV) was published in 1994, the criteria were again changed, this time in favour of a two-dimensional model with attention deficit being one subcategory and hyperactivity-impulsivity the other. With each revision, a larger number of children are found to be above the threshold for diagnosis. For example, changing from DSM-III to DSM-III-R more than doubled the number of children from the same population who could be diagnosed with the disorder. Changing from DSM-III-R to DSM-IV increased the prevalence by a further two-thirds, with the criteria now having the potential to diagnose the vast majority of children with academic or behavioural problems in a school setting.
In 2013, the fifth edition of DSM was published (DSM-5), with some key criteria having been broadened to allow more adolescents and adults to qualify for a diagnosis—for example, increasing the required age of onset for symptoms to age 12 or earlier, which had increased from age 7 or earlier in DSM-IV. The meteoric rise in numbers diagnosed with ADHD meant that by 2016 in the United States, an estimated 9.4% (6.1 million) of children aged 2-17 years had received an ADHD diagnosis.
The Biologisation of Childhood
The principal recommendation for treatment has long been that of prescribing stimulant medication—namely, the use of the amphetamine class of drugs (such as Ritalin and Dexedrine). The idea that ADHD has a specific medical treatment has acted as a powerful stimulant (pun intended) toward the popularisation of the concept, particularly in those countries that are dominated by a market-based economic value system where the perceived availability of a specific treatment has enabled commodification and commercialisation of the diagnosis.
The ideology that began gaining ground in the late 1950s for adults and early 1970s for children—that mental disorders are the result of chemical imbalances for which there are specific medications—had taken hold. The marketing of medications directly to physicians coincided with the US government becoming interested in the merits of using psychoactive medications to treat hyperactivity.
Furthermore, the expanding use of psychopharmaceuticals for hyperactivity happened at a time when “scientific” approaches to parenting became fashionable, reaching their zenith in the mid-to-late 20th century in the West. The ascendance of scientific ways of talking about children, child development, and parenting displaced more naturalistic approaches to childrearing characteristic of earlier eras, pushing the task of child-rearing further toward ownership by professional groups.
Previously in the United States, children were viewed as largely sturdy and resilient. An example of this can be found in the Fischers’ late fifties/early sixties New England town study. According to the study, families understood their children’s problematic behaviours as “stages” that most children could be expected to pass through. Viewing problems in this way meant that parents did not feel an obligation to seek professional help for them. In fact, to do so would run counter to another prevailing belief, which was that parents ought not to force children in case they damage their “potential.” Thus children’s “bad” behaviour was interpreted through a normative lens as expected and temporary.
These changing dynamics—moving childhood behaviour problems away from the parental “common sense” arena toward ownership by a professional class—together with the greater emphasis on using psychopharmaceuticals to control emotions and behaviours, contributed to diagnosis and prescription of medications for childhood mental disorders increasing steeply in the past few decades in most post-industrial countries (particularly in North America, Northern Europe, and Australasia).
While this fact is not disputed, it is subject to many different interpretations by scholars and professionals, depending on their divergent theoretical assumptions. Those who believe that scientific progress is behind this rapid change in practice argue that disorders such as ADHD were simply “under-recognised” in the past. According to this perspective, there have always been children suffering from such disorders, but only as a result of recent clinical and scientific advances have we discovered these to be symptoms of medical conditions that can cause abnormal development.
Critics of this view, like me, point to the lack of evidence to support the idea that there have been clinical or scientific discoveries that have led to progress.
By the beginning of this century, the concept of ADHD was migrating beyond that of a childhood developmental disorder to a lifelong disorder as the idea of adult ADHD took off, starting inevitably in the pharmaceutical marketing global capital, the United States. The emphasis in adult ADHD moves from observations of external behaviour to perceived failings of internal regulation, highlighting problems with “self-concept” and largely disregarding hyperactivity in its diagnostic framework.
As Western culture has heightened its focus on the individual, it has emphasised the fragility of their inner life, turned desires into commoditised needs, and taught people to measure their sense of self-worth through competitive achievements. Diagnoses, framed in ways that blame the problem on biochemical dysfunction, can appear to provide an avenue of relief from the struggles involved in keeping a positive sense of self in the absence of achievement or personal satisfaction.
The focus on “inner life” (such as with depression and anxiety) that dominates adult psychiatry (as opposed to the focus on behaviour that dominates child psychiatry), has led to women being the predominant “customers” for community psychiatric services. Not surprisingly perhaps, the shift in emphasis in definitions of adult ADHD from behavioural to internalised characteristics has been accompanied by an increase in the numbers of women being diagnosed with adult ADHD, and in many countries, women outnumber men for this label, despite the fact that the diagnosis of childhood ADHD is strongly associated with being male.
This attempted solution, however, remains fragile, as it also includes the notion of a permanent and biologically based disability, and thus that of “damaged goods,” creating a more long-term problem—with the diagnosed person invited into a potentially lifelong struggle to control and prevent their “ADHD” from ruining their life.
The pharmaceutical industry appears to have been instrumental in the rise of adult ADHD, especially over the last couple of decades. In 2004, for example, pharmaceutical marketing companies explicitly identified adult ADHD as an expanding and lucrative market for stimulants and related drugs.
Several companies have run direct-to-consumer advertising campaigns in the United States, which market the disorder by suggesting that common behaviours (such as forgetting car keys) may be symptoms. Company websites also contain screening questionnaires that encourage people to seek help if they think they have the diagnosis. Moreover, it has been revealed that some of the researchers who most vigorously promoted the concept of adult ADHD and conducted many of the drug trials failed to disclose millions of dollars of income they had received from pharmaceutical companies.
What we define as ADHD today is the product of these vested commercial, political, and institutional interests. Nowhere in the story of the emergence and popularisation of ADHD has there been any—and I mean any—significant scientific discovery.
Not Everywhere Sees ADHD
The drive to “discover” biomedical templates within which to place various children’s behaviours that are considered socially difficult has resulted in the exclusion of cultural meaning, the local significance of particular behaviours, and local beliefs and practices for dealing with such behaviours.
When we view childhood behaviours through the prism of local cultural beliefs, variations in practice can be found even within and between countries that recognise and have widespread availability of services for diagnosing and treating ADHD.
For example, in a context where self-control in response to aggression or provocation is highly valued, a lack of self-control is more likely to be interpreted as a disorder. Similarly, in contexts where school success is highly valued, poor school performance is more likely to be interpreted as being the result of a disorder.
Thus, a significant difference is found between the UK and the US in how ADHD is conceptualised in real-world practice. Both epidemiological and child/family interview studies have found considerable differences in the sort of problems likely to lead to a diagnosis of ADHD, and subsequent treatment, between these two countries.
In the UK, diagnosis and treatment is more likely to be given to children (mainly boys) from lower social classes and is associated with higher levels of behavioural problems, whereas in the US, middle-class children (again mainly boys), particularly in areas of lower academic achievement, are more likely to be diagnosed and treated.
Interviews with young people diagnosed with ADHD in the UK and US have found that their beliefs about ADHD mirror the epidemiological findings, with UK children much more likely to view ADHD as a disorder of self-control causing them to lose their temper and get into fights, whereas US children are more likely to believe that ADHD is a disorder that causes them to fail at school.
Cross-cultural ADHD studies find major and significant differences between assessors from different countries in what behaviours they rate as problematic. There are also significant differences between assessors when they assess children from different ethnic minority backgrounds. Some of the early studies found a surprisingly high rate of hyperactivity in children from China and Hong Kong. In these studies, nearly three times as many Chinese as English children were rated as hyperactive.
However, a closer look at the findings suggested that most of the “hyperactive” Chinese children would not have been rated as “hyperactive” by most English assessors and were in fact a good deal less hyperactive than English children rated as “hyperactive.” One suggestion for such a disparity in hyperactivity ratings between Chinese and English assessors and children is that it may be due to the greater importance of school success in Chinese culture, leading to an intolerance of lesser degrees of disruptive behaviour. Whatever the reason(s), it demonstrates that hyperactivity and disruptiveness are culturally constructed entities.
Another medical anthropology study, published in 2003, looked at a group of middle-class children at a Mexican school with over 200 pupils. Using standard questionnaires, the researchers concluded that about 8% of the children could be diagnosed as having ADHD, yet there was only one child in that school who had been given an ADHD diagnosis. Through interviews with parents and teachers of those more active children who were not diagnosed, the researchers discovered that these carers regarded ADHD-type behaviours as within the boundaries of behaviours viewed as normal and expected for these children, particularly boys, at those ages.
Within any culture/society, ADHD shows different patterns of distribution that may be traced back to social and cultural dynamics. Thus, in the UK, the social distribution of ADHD diagnosis follows the contours of a class-based gradient. Children exhibiting the symptoms of any emotional or behavioural disorder, including those with symptoms of ADHD, are much more likely to be poor, to be raised by single and/or unemployed parents, to grow up in underprivileged neighbourhoods, and to be exposed to stressful life events in their early lives.
The highest excess of all is where a parent is in trouble with the law—a court appearance by a parent raises the risk of a diagnosis by almost 200%. This class gradient is not found in the US; the most economically advantaged children in the UK are much more protected against an ADHD diagnosis than their American counterparts.
Race and ethnicity is another area where within-country differences in diagnostic patterns can be found. In an ethnographic study of families with children diagnosed with ADHD in a metropolitan area of the northeastern United States, considerable differences between the beliefs and practices of “Euro-American” families and African-American families were found.
While Euro-American families voiced biomedical explanations and preferred to use a clinical lexicon of “disorders” and “conditions” or specific diagnostic categories to describe their children’s behaviour problems, African-American families resisted pathologising their children’s experience, which was reflected in using a more diffuse vocabulary of “issues,” “challenges,” and “difficulties” to describe problematic behaviours and feelings in their children. These African-American families displayed active questioning of, and scepticism toward, mental health interventions, whether these were medication or psychotherapeutic.
All these examples remind us that the gap between observations of a child’s behaviour and the meanings attached to them, including if and when ADHD is used as a label, is vast and cavernous. In that space, we construct our culturally biased interpretations with the consequences that then flow out of our choices.
So what has the actual science revealed about ADHD, its causes, and its treatments?
Science and Evidence-Based Medicine (EBM)
Science is generally regarded as the intellectual and practical activity encompassing the systematic study of the physical and natural world through observation and experimentation. Science is the use of a methodological approach involving hypothesis generation (suggesting a theory) and then testing that hypothesis through experimentation. The best scientists can live with and accept uncertainty as a prerequisite to being objective in the pursuit of knowledge.
In the natural sciences, which most of medicine relies on to develop a system of categorisation based on cause (diagnosis), knowledge develops and builds through carrying out a particular type of investigation, which is aimed at proving something called a “null hypothesis” can’t be true. The null hypothesis is a statement or default position that there is no relationship between certain measured phenomena. Rejecting or disproving the null hypothesis—and thus concluding that there are grounds for believing that there is a relationship and the actual hypothesis may be true—is a central task in the modern practice of science.
But before any finding can be accepted, you need other independent research teams to replicate results using the same or similar methods. This is because one team may have biases, inadequate sample sizes, technical issues with the accuracy of their equipment, or errors in analyses, and sometimes they may even have manipulated results.
The “replicability” crisis is a major problem in psychiatric and psychological research. One team announces it has found something (say an area of the brain that is smaller in ADHD patients compared with a healthy age-matched group), but the next two teams who carry out the same study come up with different findings.
A scientific approach requires starting with the assumption that your theory (hypothesis) is not true—the null hypothesis. Disproving the null hypothesis—meaning therefore that there is evidence that your theory may be true—must happen before you can then move to the next stage of allowing other research teams to do the same or similar experiments to see if they get the same findings as you.
If at any stage in this process your theory is not getting support, you must go back to the “null hypothesis” and assume your theory is not true. It is not scientific to ask someone to prove that the null hypothesis is true. You should always assume it’s true, until it has been proven through all the above steps that it can’t be true.
One of the major problems with the current concepts used in psychiatry can be understood by going back to these basic assumptions. In order to scientifically evaluate the proposition that there is a natural category of dysfunction/disorder called “Attention-Deficit/Hyperactivity Disorder” (ADHD) that is “neurodevelopmental,” we must start with the null hypothesis. That is, we must assume, until proven otherwise, that there is no characteristic relationship between what we are defining as ADHD and some identifiable measurable biological/neurological feature.
This is a foundational assumption behind the development of knowledge through the scientific method. Applying scientific methodology is the basis of EBM. Until we have demonstrated that this basic null hypothesis can’t be true, then scientifically, we cannot proceed with research that assumes that ADHD as a concept has any explanatory power for the behaviours it describes.
In its broadest form, EBM is an approach to improving healthcare that uses the application of the scientific method for decision-making. For much of its history, medicine relied more on the subjectivity of “clinical judgement,” and medical students learnt this or that professor’s favourite ideas. Practice developed more through anecdote and assumed authority of the “doctor” or “professor,” often with little supporting evidence.
The shift to greater use of scientific principles to inform practice occurred during the 1980s, with greater attention being paid to research on causes and treatments, alongside the development of international institutions such as the Cochrane Collaboration dedicated to systematically evaluating research evidence on important clinical questions. New analytic approaches (such as meta-analysis and systematic reviews) enabled researchers to pool results of a large number of studies contributing to the development of a comprehensive evidence base.
EBM was an important step forward in developing a more scientifically credible approach to healthcare. However, like all great ideas, it exists within a broader political framework. Scientific endeavour is ultimately a human activity and thus what counts as “science” and how we interpret it is shaped by broader cultural and political processes.
Pharmaceutical companies, to give one example, were able, through a variety of strategies, to bias the evidence base toward the products they made. EBM itself fell victim to these broader market-power political forces, leading to a corrupting collusion between profit-focused organisations and professional guilds. Marketing triumphed over science.
EBM too became susceptible to being afflicted with “scientism.” In Western culture, science has become a cosmology—that is, an ideology/faith that believes that science has an undeniable primacy over all other ways of seeing and understanding life and the world—making us vulnerable to being taken in by scientism. We want to believe there are easy explanations and simple ways to alleviate suffering. Marketing the promise of psychiatric diagnoses and medicinal treatments turned out to be relatively easy.
Even the Cochrane Collaboration—the institution most connected with the development of EBM—has fallen victim to prioritising marketing over science. Professor Peter Gøtzsche was expelled from Cochrane in September 2018. Gøtzsche has written a compelling account of what happened in his book on the subject, Death of a Whistleblower and Cochrane’s Moral Collapse. It’s a vivid account of how organisations become corrupted once they fall into the clutches of a hierarchy more concerned with finances and marketing than the reasons it was created.
Gøtzsche was one of the original co-founders of the Cochrane Collaboration and was key to developing it into a respected research network. He created many of the methodological tools used by Cochrane reviews and has never shied away from letting the data speak for itself, however unpopular the findings might be with some doctors, researchers, and in particular with pharmaceutical and other medical device manufacturers.
Gøtzsche’s brilliance and his fearless approach earned him many enemies. He is one of Denmark’s best-known researchers and is respected in research circles all over the world. But for years he had documented how many products promoted by the pharmaceutical industry and medical device manufacturers can cause more harms than benefits, with detailed analysis of how the research from these companies misleads, obfuscates, or sometimes straightforwardly lies in order to protect and promote their products.
His work on psychiatric drugs showing how poor they all are at delivering better lives for those who take them, at the same time as causing enormous harms to millions, has earned him the ire of the psychiatric establishment at large and was perhaps the most influential reason for Cochrane’s hierarchy deciding to expel him.
These days, what has happened to the idea of EBM is that it is quoted in a quasi-religious fashion. You often hear people repeat, like an incantation, phrases like, “we follow evidence-based guidelines,” “this is an evidence-based treatment,” “we are an evidence-based service” like a parody of earlier times when one might have said, “it says in the bible,” or “according to the bible” and then just say any shit that comes to mind.
We use this language as a social justification for what we practice, and the original assumptions and context around important null hypotheses just disappear behind the smoke and mirrors of puffed-up establishments and limelight-hungry professors.
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, 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, 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 versus rural, etc.).
This proved to be an enlightening experience—just not in the way my supervisor had 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 this crucial aspect of an evidential basis.
The articles I read avoided scientific methodology and ignored the null hypothesis. This 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 later in this chapter, research in the name of showing ADHD to be a natural entity has provided convincing evidence of the opposite. Sadly, in an era where psychiatric thinking is dominated by quasi-religious scientism, where you just repeat EBM-style phrases, 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 behavioural 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 behaviour 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)
Most of these websites are meant to be from reliable, bias-free, and pharmaceutical company influence-free information sites. You can see that the views you will likely encounter in most searches on the subject include lots of scientifically 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.
Next week, in Part 2 of this chapter, we will explore the actual scientific evidence on ADHD, including the genetics, brain imaging, and “chemical imbalance” theories of ADHD causality.
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.