Editor’s Note: Over the next several months, Mad in America will publish a serialized version of Sami Timimi’s book, Insane Medicine. Part 1 of Chapter 3 was published last week. In Part 2, he discusses the lack of findings for a genetic basis or a neurobiological basis for ADHD, and explores the effect of stimulant drugs. Each Monday, a new section of the book will be published, and all chapters will be archived here.
Let me then look at the evidence supporting that ADHD is a “thing” that comes into being through genetics and brain problems.
ADHD genetics: Has the null hypothesis been disproven?
The claim that ADHD is genetic has been extrapolated mainly from twin studies, because identical twins are more often both diagnosed with ADHD than non-identical twins. 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 share, on average, 50% of their genes.
Researcher Jay Joseph has examined the question of heritability of psychiatric disorders (including ADHD) in great detail in his books and articles, and his critiques illustrate the problems with the evidence supporting ADHD being a disorder with high levels of genetic heritability.
For identical twins to have a greater likelihood of having a disorder because of sharing the same genes, you have to assume that the psychological and social 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 more similarly (e.g. dressed in same clothes) and experience a unique psychological environment (e.g. swapping roles to confuse others).
Being one of identical twins is a different experience from being one of non-identical twins, and so psychological and social factors could by themselves 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.
There are other methods used to estimate genetic heritability, such as family studies (looking at prevalence of ADHD symptoms in family trees) that also cannot disentangle environmental from genetic contributions. Another approach, which is more challenging logistically to carry out, is adoption studies. An ADHD adoption study would involve comparing rates of ADHD in adoptive parents’ families with rates in the biological families of children who have been adopted and subsequently diagnosed with ADHD.
There have been no true adoption studies in ADHD. Methodological problems have been numerous in adoption studies anyway, from the fact that most adoptees have already spent considerable time in biological families of origin or in foster care placements prior to adoption, to the differences parents of adoptees as a group may have from the average parent.
Adoption studies, like family studies, then are not capable of distinguishing environmental from genetic contributions, and so none of these methods used to estimate heritability can on their own or together disprove the null hypothesis that there is no characteristic genetic abnormality or difference associated with those who get an ADHD label.
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 findings, whether in relation to abnormal genes or consistent genetic associations. This has not stopped unscrupulous researchers 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 be.
Researchers found 15.6% (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 not to have an ADHD diagnosis than have it.
The deceit doesn’t end there, however. The average recorded IQ (a psychological measure of intelligence level used to assess level of learning, including level of learning difficulties) of the children with ADHD was 86, 14 points below the general population average of 100. Furthermore, when 33 intellectually impaired ADHD children (IQ lower than 70) were excluded from the ADHD group, only 11.4% of the remaining 333 children 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 CNVs and ADHD (11.4%). The authors of this study should therefore have controlled for IQ given its disproportionate impact on the likelihood of having CNVs, but chose not to.
As mentioned, 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 they did that, because I suspect they may have been left with no or a tiny 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.
Since then there has been an explosion in well-funded genetic research into ADHD. Thousands of those diagnosed with ADHD have had their entire genome scanned to detect what is known as “DNA variants”—bits of DNA that are different in persons with a condition compared to those without. These studies are called genome-wide association studies (GWAS).
In GWAS, each person gives a sample of DNA, from which the millions of genetic codes each person carries are read, looking for a gene that occurs more frequently in people with a condition than those without. If a gene is found more commonly in people with the condition, it is said to be associated with that condition. GWA studies investigate the entire genome, which makes them fundamentally different from methods that start with a hypothesis that a particular gene could be associated with (in this case) ADHD.
A hypothesis-based approach puts forward a theory that a particular gene or set of genes that code, for example, for the neurotransmitter dopamine or its receptors in nerve cells, is abnormal, and then compares these genes in people with a diagnosis and in non-ADHD controls. This latter type of study was the dominant way of investigating molecular genetic abnormalities or differences in ADHD, but drew a blank.
GWA studies are not hypothesis driven and are more data fishing exercises. They may lead to hypotheses that can be further investigated if they reveal regions that may be of interest and seem relevant to the condition being studied. But on their own, they tell you more about what’s not relevant than what is, particularly if the genes occurring more often than chance are spread across many different parts of the genome.
The numbers studied here are particularly important to understand. The initial GWA studies of ADHD did not discover any DNA variants that achieved genome-wide significance, even when most of these samples were combined in a meta-analysis including over three thousand patients with an ADHD diagnosis and/or their parents.
Later, using even larger samples going into tens of thousands, GWA studies showed ADHD to be associated with a large number of common variants, each having tiny effects, that are spread across the genome, cross over with other so-called psychiatric diagnoses (like autism, schizophrenia, bipolar disorder) and often with no control for the effects of learning difficulties.
What this means is that in order to pick up genes that occur very, very slightly more than chance in those with ADHD compared to healthy controls, you have to have a very large sample size (of at least ten thousand). Most of those with an ADHD diagnosis don’t have any of the individual genetic differences picked up in the massive GWAS samples, nor do we have any reasonable biological theory to test what is being picked up from these tiny, barely relevant findings.
Genetic aetiology enthusiasts have referred to the failure to find reliable molecular genetic abnormalities or differences as a conundrum they refer to as “the missing heritability.” Because they assume ADHD must be genetic, they imagine the genetic problems must be there somewhere; it’s just that we haven’t found it yet. The most likely reason for the “missing heritability” is, of course, that it was never there in the first place.
Scientifically speaking, we have to assume then that with regards to genetics, the cupboard is empty and the null hypothesis stands: There is no characteristic identifiable genetic abnormality/profile associated with ADHD.
ADHD brain imaging studies: Has the null hypothesis been disproven?
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 stating, in a press release that was covered by mainstream media, “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.” A careful analysis of their findings show how their research reveals more about the desperation of the authors to find something than their ability to conduct a proper scientific examination 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 research teams around the world. They claim that they found 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 when compared to 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 (NA). This mega-analysis thus makes the claim that children with ADHD have a smaller NA than non-ADHD children. However, if you look at the data by site you find 10 sites that found an average smaller NA in the ADHD group, 4 sites that found an average 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 the NA, you can also see that there are major technical issues with interpreting the scans, arising out of the different machinery and/or analytic algorithms the different research groups used. 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 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 NAs.
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 reanalysed their data, taking into account the 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 once 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.
ADHD caused by a chemical imbalance: Has the null hypothesis been disproven?
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 whether there was a lack of dopamine—or not—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 then a study comes along that challenges the accepted 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 by the brand name 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.
We should not be surprised by this finding. Stimulants like Ritalin act on the nervous system in almost identical ways to cocaine. Most stimulant medications are analogues of amphetamine and indeed some are amphetamine derivatives. Amphetamines are widely used illegally because they give you a kind of a tunnel vision, making you highly absorbed in what you are doing; thus, as well as taking them for their recreational effects, they are also used as exam study aids as they increase concentration and keep you awake. Like all other drugs we use in psychiatry, they have general effects on everybody. They do not correct any disease based “chemical imbalances.”
Here too then, the cupboard is also empty. The null hypothesis stands—there is no characteristic chemical imbalance associated with ADHD.
Children young for their class are more likely to “catch” ADHD
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 of the notion that relative immaturity to your peers is a significant risk factor for receiving this label (i.e. for adults noting and problematising a child’s ability to concentrate and their levels of activity—their “boisterousness”). Whether it’s over 6% of children (in the Icelandic study) who get prescribed stimulants or less than 1% (in the Finnish study), the pattern still holds. Whatever, the cultural norms for problematising 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 children who are older in the class might also be reflective of their relative slower developmental trajectory. Remember this is a diagnosis mainly given to boys, and males on average develop slower than females.
For a while now, I have thought that the growth of pseudo-diagnoses like ADHD is 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 in modern culture.
ADHD treatment: Convincing parents their children need to take cocaine-like substances
In the 1970s, ‘80s, and ‘90s, ADHD as a concept had taken off, aided in large part by the growth in the use of amphetamine derivatives. This group of substances are referred to as “stimulants” as they increase the release of certain neurotransmitters (i.e. stimulate the nervous system), most notably dopamine. Ritalin was the most recognisable brand name of these drugs and became a best seller, making huge profits for Novartis Pharmaceuticals. Other companies soon realised the enormous potential that comes from medicalising children’s behaviours, particularly those that stress out parents and teachers, and so a variety of short- and long-acting preparations are now available.
Labelling children’s irritating, worrying, or distressing behaviours with a pseudo-medical label opens huge potential markets, so whilst the prescribing of dangerous and addictive stimulants to kids started out and stayed for a couple of decades as an almost solely US phenomena, it has since spread globally and numbers being medicated continue to rise.
This trend has not been without controversy. After all, amphetamines, like cocaine, are known to be highly addictive, with a marked potential for physical and psychological dependence and many serious health risks. As central nervous system stimulants, they elevate life functions, such as blood pressure, body temperature, and heart rate. Those using amphetamines will generally need less sleep, have less of an appetite, and have greater focus. How could we possibly justify giving to kids a substance we warn adults about taking because of the terrible long-term effects we know this can have on the body, brain, and so many aspects of a person’s everyday life?
This is where a chemical imbalance theory was needed. ADHD medication enthusiasts spun a myth, based not on evidence, but as a way of justifying what they were advocating. The argument was that those with ADHD react in a different way to stimulants than those without, because in ADHD there is a deficiency of dopamine—therefore, stimulants are just replacing what wasn’t there in the first place. This means it’s a corrective and not something that will lead to all the known terrible effects. Therefore, stimulants are dangerous if you don’t have ADHD, but safe and maybe vital for “normal” functioning if you do.
Or so the enthusiasts’ argument goes. As discussed earlier, the null hypothesis on a chemical imbalance in ADHD has yet to be disproved and therefore, that theory is unsupportable.
Like most medications used in psychiatry, its use was based on anecdote and had started before studies to show that they were safe and effective had been done. The assumption was that because stimulants appeared to calm these children down, it must be working in a different way to those who used it recreationally, who seemed more energised. When it was studied in the 1980s, though, it was found that actually it does have similar effects regardless of the diagnosis.
Its main effect in the doses prescribed is to create a kind of psychological tunnel vision, so you get absorbed in what you are doing. The apparent calming effect is related to this effect of increased focus. When you see your child sitting down, apparently concentrating on school work, and following instructions in a way they weren’t doing before, it can seem like this is a transformative treatment.
But this is a general short-term effect of a stimulant. It will do this for most children who take it, regardless of the label they have. The studies that supported the use of stimulants as a treatment were nearly all conducted by pharmaceutical companies, lasted for just a few weeks or months, and concentrated on rating ADHD “symptoms” rather than other quality of life measures. However, once children are prescribed a stimulant, the prescription isn’t for a few weeks or months, but usually for many years. This is where we need the evidence. What happens after several years?
Given that amphetamines are highly addictive, physical tolerance is likely to occur. Like many systems in the body the nerve synapses (the connections between nerve cells) have homeostatic properties. This means they like to keep their chemical messengers in a narrow range for optimal functioning. If there is more than the usual amount of dopamine (for example) being released as a result of taking an amphetamine regularly, the synapse will start switching off dopamine receptors to, in effect, reduce the overall amount of dopamine back to within its usual narrow range. This is why cocaine addicts who take a certain amount regularly find that in order to get the same hit, they have to take more cocaine—as the amount that used to give them that high is not doing so anymore.
Because of this homeostatic mechanism, after a while the problem behaviours start emerging in the child again as that increased focus effect the stimulant was having starts to wear off. This is what we call becoming “tolerant” to the dose of amphetamine. It means the synapses have switched off some of the dopamine receptors so you no longer get the same effect.
If you stop the amphetamine now however, you will get withdrawal effects, as the nerve cells will now get too little dopamine because of the reduced number of working receptors. The state of agitation that sudden or too-fast withdrawal of the stimulant can induce will look like the “ADHD” coming back with a vengeance, convincing all, including the doctors—few of whom seem to understand the above process—that the child really does need the amphetamine for more “normal” functioning.
Now, therefore, the dose will be increased and set in motion will be a process of increasing physical (in the child) and psychological (in parent and teacher) dependence that leads to gradual increases in the dose over time with temporary periods of improvement, which eventually wear off—leading to another dose increase—alongside a solidifying of the idea that the child has a brain-based condition called ADHD and that it requires amphetamines to keep it in control.
Interference with sleep often means that a sleeping aid will be added (like melatonin) and continuing behaviour difficulties often result, at some point, with the very heavy-end “antipsychotic” medication being added too. It’s not unusual, therefore, after several years to find ADHD-labelled young people who are taking several medications, often at high doses, and the problems keep coming back or never quite go away.
But what does the research evidence say about long-term outcomes?
In 1999 a famous American study of “treatment” for ADHD was published. By then, prescribing of stimulant medication in the US 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 the year 2000 and listening to the then-chair of the faculty explain to the audience of UK child psychiatrists that the implications of this study were that we would have to prescribe stimulants for anyone diagnosed with ADHD, and that probably (given resource limitations) prescribed stimulants alone would be sufficient for most.
So what did this famous study find? This study, referred to as the “MTA” study (Multimodal Treatment of Children with ADHD), was a 14-month multi-centre trial where young patients were randomised to 4 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 medication and behaviour therapy groups than the behavioural therapy only group, who in turn had better outcomes than the routine community care group.
As you might predict, there were considerable problems associated with the study that made 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 regular 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 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 14-month MTA study quickly became the most quoted study for ADHD treatments, regularly referred to in the treatment guidelines of many countries. Based on what is still quoted as best available evidence, you would have thought that the MTA study ended there and there was no more to say. But even if you accept the findings at face value, 14 months does not equate with the many years most end up being prescribed medication for. So the MTA study still couldn’t address the issue of what happens to those prescribed stimulants long term. Or could it?
The story of the MTA study doesn’t in fact end there. At a conference in Phoenix I attended in 2002, I ended up by chance sitting next to someone whom I discovered was a psychologist involved in the evaluations of the MTA trial at one of the centres. He told me that his team there had just completed analysing the data for the 3-year follow.
I remember him saying to me “Once these findings are published no one will want to have their child take medication anymore.” I was surprised by the clarity and certainty of his conclusion. He explained that in his centre, the children who stayed on medication had grown steadily worse and had lots of adverse effects, while those who had stayed off medication were now doing much better. He told me their results were similar to the other centres and it wouldn’t be too long before they were published.
I had to wait another 5 years before the 3-year follow up of the MTA was published in 2007. 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. After 14 months, the participants in the study had been free to choose their on-going treatments. It had, in effect, become a naturalistic study, similar to what happens in general outpatient settings.
The 3-year outcomes 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.
By 3 years then, those who continued to take stimulants were doing worse and experiencing more negative effects than those who didn’t. It confirmed my earlier hunch that placebo had played a major role in the 14-month findings. What the psychologist told me 5 years earlier was right. Who in their right mind reading this would want to continue giving any child stimulants?
But this (the end of prescribing stimulants to children) is not what happened. Science can’t trump marketing in a free market-driven economy. Prescriptions of stimulants hardly blinked after the publication of this follow-up study. The 14-month MTA kept being referred to and the 3-year follow-up ignored. The 3-year MTA follow-up study has similar findings to other long-term follow-up studies.
Other 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’s often with children on stimulants having worse outcomes than those not taking them: with physical (such as blood pressure), psychiatric (like mood “disorders”), and academic problems more common in those on long-term medication.
If these medications 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, stimulants that are being prescribed are amphetamine or amphetamine-like substances having near identical pharmacological properties to street drugs such as “speed” and cocaine that we regularly warn others of the 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. As there are 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.
If you search for information on the problems associated with stimulants when they are being categorised as drugs of abuse, you will get something like this:
“All stimulants share a set of side effects that can wreak havoc on a user’s system. Effects include increased heart rate, heightened blood pressure, heightened body temperature, muscle shakes or tremors, agitation. All of these effects are common. No matter how you cut it, stimulant abuse, even in the short term, can have disastrous consequences for the user, resulting in hyperthermia, cardiovascular abnormalities, and sudden death.
When a person abuses stimulants over a long period of time, however, they compound their risks of experiencing a number of other devastating physical and mental health issues, such as hallucinations, delusions, persistent anxiety, paranoia, depression, weight loss, reduced sexual functioning, gastrointestinal problems, muscle deterioration, cardiovascular damage, breathing problems, headaches, strokes, and seizures.
A chronic stimulant user is also at high risk of developing tolerance to, dependence on, and, eventually, addiction to stimulants. Furthermore, dependent individuals may experience a stimulant withdrawal syndrome when use of the drug stops or slows. Withdrawal from stimulant abuse is not a life-threatening process, but it can be uncomfortable. There are physical and psychological aspects of stimulant withdrawal that can be difficult to cope with. Common symptoms of withdrawal from stimulants include mental and physical exhaustion, insomnia, anhedonia (inability to feel pleasure), irritability, anxiety and agitation, excessive sleep, intense hunger. One of the biggest risks with stimulant withdrawal is depression with suicidal thoughts, and the severity can vary by substance. Sometimes, this depression can last beyond the acute withdrawal phase.”
There is no reason to believe that the above warnings aren’t just as relevant to legal prescription of stimulants as they are to illegal abuse of them.
The dangers of prescribed stimulants go beyond those described above, as patients may continue to take them for decades with all the potential consequences this has for messing up the chemicals in the brain. For example, in a study that did follow, for several decades, patients who were prescribed stimulants, the researchers found an over 8-fold increase in the likelihood that such patients developed neurological conditions such as Parkinson’s disease.
Parkinson’s is an illness that results from patients not having enough of the neurotransmitter dopamine in the nervous system. It’s highly likely that this finding relates to long term stimulant ingestion, given that stimulants mainly work by stimulating cells to release more than the usual amount of dopamine.
ADHD is not a diagnosis and cannot be supported as an evidence based construct
Whatever you might think are the perceived merits of constructing ADHD as a “diagnosis” that has biological origins and can be “treated” with medication, the scientific truth is that it cannot be thought of as a valid scientific entity and the current recommendation for its treatment that usually prioritises medication without time limits is not evidence based.
ADHD is an example of the way 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, including immaturity, learning difficulties, schooling issues, bullying, violence exposure, dietary, lifestyle, lack of family support, lack of confidence in parenting, and so on, that may be relevant.
It also blinds them to the ordinariness of childishness and the capacity of kids to irritate adults. ADHD is more of a commentary on the cultural intolerance we have for the diversities of the ways children grow up, and the pressure we put on them and their parents to perform to the narrow age-dependent standards we set.
As a practising child psychiatrist I have lived through the years of ADHD emerging from a rare condition of limited interest and usually constructed in systemic terms, to it proliferating into the most common childhood condition and constructed in largely biological terms. It reached saturation about 5 years ago when the new kid on the block was gaining unstoppable momentum—autism, the topic of my next chapter.
American and Psychiatric Association. (1966) Diagnostic Statistical Manual of Mental Disorders, Second Edition (DSM-II). APA.
American and Psychiatric Association. (1980) Diagnostic Statistical Manual of Mental Disorders, Third Edition (DSM-III). APA.
American Psychiatric Association. (1987) Diagnostic and Statistical Manual of Mental Disorders, Third Edition Revised (DSM-III-R). APA.
American Psychiatric Association. (1994) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). APA.
American Psychiatric Association (APA). (2013) Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5). APA.
Bejerot, S., Nilsonne, G., Humble, M.B. (2017) Subcortical brain volume differences in participants with attention deficit hyperactivity disorder in children and adults. Lancet Psychiatry, 4, 437.
Bradley, C. (1937) The behaviour of children receiving Benzedrine. American Journal of Psychiatry, 94, 577-585.
Brewis, A., Schmidt, K. (2003) Gender variation in the identification of Mexican children’s psychiatric symptoms. Medical Anthropology Quarterly, 17, 376-393.
Carpenter-Song, E. (2008) Caught in the psychiatric net: Meanings and experiences of ADHD, pediatric bipolar disorder and mental health treatment among a diverse group of families in the United States. Culture Medicine and Psychiatry, 33, 61-85.
Conrad, P. (1975) The Discovery of Hyperkinesis: Notes on the Medicalization of Deviant Behavior. Social Problems, 23, 12–21.
Curtin, K., Fleckenstein, A.E., Keeshin, B.R., et al. (2018) Increased risk of diseases of the basal ganglia and cerebellum in patients with a history of attention-deficit/hyperactivity disorder. Neuropsychopharmacology, 43, 2548‐2555.
Danielson, M.L., Bitsko, R.H., Ghandour, R.M., Holbrook, J.R., Kogan, M.D., Blumberg, S.J. (2018) Prevalence of Parent-Reported ADHD Diagnosis and Associated Treatment Among U.S. Children and Adolescents, 2016. Journal of Clinical Child and Adolescent Psychology, 47, 199‐212.
De Campo, N., Fryer, T.D., Hong, Y.T., et al. (2013) A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment. Brain, 136, 3252-3270.
Faraone, S.V., Larsson, H. (2019) Genetics of attention deficit hyperactivity disorder. Molecular Psychiatry, 24, 562–575.
Fischer, J., Fischer, A. (1966) The New Englanders of Orchard Town. John Wiley and Sons.
Gøtzsche, P.C. (2019) Death of a Whistleblower and Cochrane’s Moral Collapse. People’s Press.
Hoogman, M., Bralten, J., Hibar, D.P., et al. (2017) Subcortical brain volume differences in participants with attention deficit hyperactivity disorder in children and adults: a cross-sectional mega-analysis. Lancet Psychiatry, 4, 310-319.
Jenkins, H. (ed.) (1998) The Children’s Culture Reader. New York University Press.
Jensen, P., Arnold, L., Swanson, J., et al. (2007) 3-year follow-up of the 248 NIMH MTA study. Journal of the American Academy of Child and Adolescent Psychiatry, 46, 989-1002.
Joseph, J. (2006) The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes. Algora Publishing.
Joseph, J. (2015) The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences. Routledge.
Luk, S.L., Leung, P.W. (1989) Connors teachers rating scale – a validity study in Hong Kong. Journal of Child Psychology and Psychiatry, 30, 785-794.
Mann, E.M., Ikeda, Y., Mueller, C.W., et al. (1992) Cross-cultural differences in rating hyperactive-disruptive behaviours in children. American Journal of Psychiatry, 149, 1539-1542.
Moncrieff, J., Timimi, S. (2010) Is ADHD a valid diagnosis in adults? No. British Medical Journal, 340, 736-737.
Moncrieff, J., Timimi, S. (2011) Critical analysis of the concept of adult attention deficit hyperactivity disorder. The Psychiatrist, 35, 334-338.
MTA Co-operative Group. (1999) A 14 month randomized clinical trial of treatment strategies for attention deficit/hyperactivity disorder. Archives of General Psychiatry, 56, 1073-1086.
MTA Co-operative Group. (1999) Moderators and mediators of treatment response for children with attention deficit/hyperactivity disorder. Archives of General Psychiatry, 56, 1086-1096.
Rapoport, J.L., Buchsbaum, M.S., Zahn, T., Weingartner, H., Ludlow, C., Mickkelsen, E.J. (1978) Dextroamphetamine: cognitive and behavioural effects in normal prepubertal boys. Science, 199, 560-563.
Rapoport, J.L., Buchsbaum, M.S., Zahn, T., Weingarten, H., Ludlow, C., Mickkelsen, E.J. (1980) Dextroamphetamine: Its cognitive and behavioural effect in normal and hyperactive boys and normal men. Archives of General Psychiatry, 37, 933-943.
Singh, I. (2011) A disorder of anger and aggression: Children’s perspectives on attention deficit/hyperactivity disorder in the UK. Social Science and Medicine, 73, 889-896.
Storebø, O.J., Ramstad, E., Krogh, H.B., et al. (2015). Methylphenidate for children and adolescents with attention deficit hyperactivity disorder (ADHD). Cochrane Database of Systematic Reviews.
Smith, M. (2012) Hyperactive: The Controversial History of ADHD. Reaktion Books.
Still, G.F. (1902) Some abnormal psychiatric conditions in children. Lancet, I, 1008-1012, 1077-1082, 1163-1168.
Strauss, A., Lehtinen. L. (1947) Psychopathology and Education of the Brain Injured Child. Grune and Stratton.
Timimi, S. (2005) Naughty Boys: Anti-Social Behaviour, ADHD and the Role of Culture. Palgrave MacMillan.
Timimi, S. (2015) Attention deficit hyperactivity disorder is an example of bad Medicine. Australian and New Zealand Journal of Psychiatry, 49, 575-576.
Timimi, S. (2017) Non-diagnostic based approaches to helping children who could be labelled ADHD and their families. International Journal of Qualitative Studies on Health and Well-being 12, sup1.
Timimi, S. (2018) A critique of the concept of Attention Deficit Hyperactivity Disorder (ADHD). Irish Journal of Psychological Medicine, 35, 251-257.
Timimi, S. (2018) Rebuttal to Dr Foreman’s article on ‘ADHD: Progress and Controversy in Diagnosis and Treatment’. Irish Journal of Psychological Medicine, 35, 251-257.
Timimi, S. and 33 co-endorsers (2004) A critique of the international consensus statement on ADHD. Clinical Child and Family Psychology Review, 7, 59-63.
Timimi, S., Leo, J. (eds.) (2009) Rethinking ADHD: From Brain to Culture. Palgrave MacMillan.
Timimi, S., Taylor, E. (2004) In Debate: ADHD is best understood as a cultural construct. British Journal of Psychiatry, 184, 8-9.
Timimi, S., Timimi, L. (2015) The social construction of Attention Deficit Hyperactivity Disorder (ADHD). In, M. O’Reilly (ed.), The Palgrave Handbook of Child Mental Health. Palgrave MacMillan.
Whitaker, R., Cosgrove, L. (2015) Psychiatry Under the Influence: Institutional Corruption, Social Injury, and Prescriptions for Reform. Palgrave MacMillan.
Whitely, M., Raven, M., Timimi, S., et al. (2018) ADHD late birthdate effect common in both high and low prescribing international jurisdictions: Systematic review. Journal of Child Psychology and Psychiatry, 60, 380-391.
Williams, N. M., Zaharieva, I., Martin, A., et al. (2010) Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: a genome-wide analysis. The Lancet, 376, 1401-1408.
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.