Instant Genius - What we’re all getting wrong about ADHD

Episode Date: August 6, 2023

We’ve all heard of ADHD, or Attention Deficit Hyperactivity Disorder. But there’s actually a lot scientists don’t for sure know about the condition. From its causes, to what actually defines the disorder – or if it’s a disorder at all – is all hotly debated. To guide us through the latest ADHD research, we’re joined by one of the world’s biggest experts on the topic, Professor Edmund Sonuga-Barke. He’s professor of Developmental Psychology, Psychiatry and Neuroscience at King’s College London. Learn more about your ad choices. Visit podcastchoices.com/adchoices

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alongside French acoustic specialist, focal, combine handcrafted tradition with cutting-edge innovation and high-end materials, delivering digital precision with analogue warmth. So you can experience exceptional sound at home. Music just as the artist intended. Visit name audio.com to learn more. Hello and welcome to Instant Genius, the Bitesize masterclass in podcast form. I'm Thomas Ling, digital editor at BBC Science Focus magazine. Now, we've all heard of ADHD, attention definitely. hyperactivity disorder, but there's a lot of scientists don't know for sure about the condition. From ADHD's causes to what actually defines the disorder, or if it's a disorder at all,

it's all hotly debated. So to guide us through the new research of ADHD, today I'm joined by one of the world's biggest experts on the topic, Edmund Sunaga Park. He's professor of psychology, psychiatry and neuroscience at King's College London. Hello, Edmund. Welcome to the show. Hello, Thomas. Fantastic. Okay, so I'm going to start off with the big question, which is, what is ADHD? You know, is it a condition, a dysfunction or just a difference? Right. Yeah, thanks. So attention deficit, hyperactivity disorder, the clue is in the name,

is defined as a disorder generally. And it's classified. specifically as a neurodevelopmental disorder. So it sort of goes together with other neurodevelopmental disorders or conditions such as autism or developmental coordination disorder. So it's very much within that sort of that sort of grouping of conditions. ADHD is differentiated from them in terms of a number of defining features. Now, because at its core, there are three sort of related groups of behavioural characteristics. Inattention, such as having difficulty focusing or concentrating or avoiding distraction, impulsiveness or impulsivity, which is, for instance, acting too quickly without thinking

through the consequences, and hyperactivity sort of speaks for itself. So that's at the core, but the disorder itself requires a number of other characteristics or other criteria to be met. So it's not enough just to having attention, impulsivity and hyperactivity. This has to be excessive for age, particularly obviously when thinking about children. I mean, little kids, three year and four year olds are generally much more active than six and seven year olds. So obviously it's got to be age linked. It's got to be expressed in more than one situation. So they call it pervasiveness.

So it's got to be pervasive. And that's important because these behaviours shouldn't just be a function of being in a particular situation where say you feel uncomfortable. So maybe the classroom or, you know, with friends or whatever. It's got to span situation. So it's more of a characteristic of the individual, independent of the context. The next important one is it's got to have a childhood onset. That's still the case.

It's a neurodevelopmental condition. It should have a childhood onset. So that basically means that the symptoms manifest, according to current criteria, before the age of 12. So that's another important criteria for the diagnosis. And most crucially, and this applies to all, inverted commas disorders, it has to have an impact on your everyday functioning, a negative impact on your everyday functioning.

So that could be school functioning, that could be social relationships, that could be difficulties at home, etc, etc. So it's not enough to just have the behaviours to an excessive level. You have to have this sort of complex set of contextual criteria as well. So a lot of that seems to be covering sort of behaviours, but what about neurologically, sort of speaking? So how does the mind of somebody with ADHD be different from the quote unquote normal brain? Yeah, I mean, the mind and the brain, I mean, there's an interesting little confounding of terms there, Thomas. But let's focus on the brain because the mind is a bit more esoteric concept.

But the brain, in terms of the brain, so the first thing to say is, that although sort of simplistic accounts, pop science accounts, do tend to talk about ADHD as a brain disorder of this or that brain regional process, there is no neurobiological brain-like signature that marks the brain of any individual with ADHD from any other person. Or in other words, you can't diagnose ADHD based on brain structure or function. I mean, that's increasingly clear. And if you've ever seen a picture that purports to show an ADHD brain and then a normal brain next to it, that is really, what do they call it? Fake news.

Disinformation, I would call it, because it's simply not the case. So obviously, the focus in neuroscience, including the work we've done, has rather been on examining statistical differences between groups of people, with ADHD and other groups of people. So these initial models, these initial sort of attempts to do that, going back, I suppose, 20 years now, you know, brain imaging has been kind of revolutionary in understanding the brains of people with ADHD. But they tended to focus on the notion that ADHD, was a single neurobiological entity and that the underlying problem in the most popular model

was this thing called executive dysfunction and that's the kind of failure of a set of brain higher order brain processes that help regulate your thought and your action so specific functions would be inhibitory control the ability to stop a response or a thought when needed or requested. And in some way, that's impaired in people with ADHD. And that that links to a particular brain system that connects sort of subcortical regions, particular striatum,

with prefrontal regions of the brain, very much that we know underpin these higher-order brain functions. So that was the model, and it was based on relatively small-scale studies and sort of, I would say, somewhat simplistic thinking, simplistic in terms of neuroscience and the way the brain is organized and structured. Bonjour, compadre. It's the Priceline negotiator.

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Visit focal powered by name.com for more information. That's incredibly interesting in itself. I think if there's no simple sort of neurological markers of ADHD, and I think some people would ask, well, what actually causes ADHD then? We can think about underlying genetic and environmental risks, and then be different for different people. I mean, obviously we know that, you know, ADHD is highly heritable,

runs in families, and we now know some of the work we've done, you know, consortia, big sort of genetic consortia, we know some of the genes that seem to be implicated. They don't account for an awful lot of the variants yet, but we're building it up. We're getting more predictive, more predictive power. But they're different for different people. So it's not just very variable in terms of the brains, it's very variable in terms of the underlying risks, the genetic risks, and the environmental risks.

So, for instance, we know that for some people having a very difficult pregnancy or delivery. So sort of pre and perinatal, we call it pre and perinatal risk can be important. So for instance, if you suffered hypoxia, you know, during delivery as a child, we know that. a risk factor. So it's this kind of complex interplay between multiple genetic and environmental risk factors that kind of create an underlying spectrum of neurobiological risk, but are very different for different people. And then that depending, and this is the way we think about it, and we're still studying and trying to put the links together, but those different genetic and environmental risks then manifest in different brain alterations, which then, quite amazingly,

if you think about it, lead to a common clinical outcome called ADHD. So it's like it's got a common final output, although that's itself very variable, obviously. But the causal pathways is a kind of multiple and interacting. So it's, I think the biggest thing we found, which is a bit disconcerting really. So 30 years ago, we all thought that our goal was probably an understanding ADHD, to the extent that we could actually improve treatments

was maybe 15 years, 15 years away. Now, what we've learned in those 15 years is that actually the goal is probably 100 years away because what we've learned is it's not a simple linear pathway or a single simple linear pathway. It's got multiple interacting factors that create these diverse pathways. And what do you do then clinically? you know, if you're trying to have a rational model for development of new interventions, they're going to help people with ADHD, based on science, you're going to be targeting these individual pathways in different ways.

So for instance, take the example of the subgroup of people that we think have executive function problems. Now they, and only they, are probably going to benefit from training in executive. function. If you don't have executive function problems, then that treatment approach is probably, well, from a rational point of view, shouldn't have any benefits, really. Certainly, it can't, it can't resolve the underlying problems because they're not there. So how can't ADHD be sort of treated and can it ever be, quote unquote, cured? So, so I mean, in terms of this, as I mentioned, this heterogeneity of processes and structures and brain, the different parts of the brain and the different brain networks are involved. We know we have an effective intervention,

at least in terms of controlling symptoms. And that's called psychostimilant medication. people will have heard of Ritalin, for instance, which is methylphenidate, it's a psychostimilant medication, and of, I think, I mean, I'm not a clinician, I'm a scientist, but as I, as my clinical colleagues tell me that compared with nearly every other medication for a neurodevelopmental or mental health problem, this is unbelievably affected. And this has been shown with, you know, enormous number of randomized controlled trials and so forth. So it suppresses symptoms. Do you know how it suppresses those symptoms?

Yeah. Yeah, we pretty much know the neurochemistry of the impact of methamphetamine. It increases, it basically increases the concentration of a neurotransmitter called dopamine within particular pathways and in particular, and especially the circuits, these frontistriatal circuits. but the crucial thing about it, which increases the signal, which helps you focus and concentrate. That's the sort of model.

But the kind of really fascinating thing about methylphenidate and the other psychostimulants, amphetamine and so forth that are used, is that it doesn't just target this system. It's a very non-specific drug. So it hits a lot of these systems that are implicated in the complex underlying causal pathways of ADHD. So that's kind of why it's effective, I think. That's my interpretation. It hits reward

networks. It hits, you know, increasing dopamine function in all those networks. What about the sort of the non-drug approaches? So does things like therapy or attention training, can that work? Yeah, but before get onto that, what I'd like to just say is that, and this this is really important caveat, is that we now know, of course, that medication isn't the full solution for people with ADHD. Absolutely not. It's good at controlling symptoms. In the short term, we know actually in the long term that it doesn't seem to lead to more beneficial outcomes. And that's got to be our real focus. I mean, obviously it's good to manage ADHD in the here and now

helps with learning, helps with developing social relationships and so forth. But in the long term, there's the very famous study called the multimodal treatment of ADHD study, the MTA study, and that's been kind of foundational

in many ways. And what they've done is they did a randomised control trial, medication, medication and psychosocial, non-farmar, like you say, psychological interventions. But then that,

was 14 months. And then after that, they followed these young people up and they followed them up into a young adulthood now. And what they've shown is that actually ADHD impairment persists in all the kids in the trial, independent or irrespective rather of whether they received medication in the trial or any medication they received since the trial. So it doesn't seem to be a relationship between long-term outcomes and medication exposure. This is hotly debating. but that seems to be the takeaway message from this famous study. So psychological treatments, you know, and as part of the European ADHD Guidelines Group,

I've led our analyses of psychological treatments. And we've looked at, for instance, parent training, where you obviously look to improve parenting skills. We've looked at cognitive training, like you mentioned, attention training, working memory training, We've looked at neurofeedback and so forth. And the bottom line is that none of these are effective in controlling core ADHD symptoms if you use the most rigorous evidence.

So they can't be used in the place of medication in terms of that short-term control. Now, of course, they may help in other ways, you know, in terms of improving functioning independent of these improvements in symptoms. So for instance, social skills training is pretty good at training social skills, which is just as well, because that's what it's developed to do. And this can be really helpful for people with ADHD. So for instance, parenting, parent training, as it's called, is developed to help parents manage challenging behavior. And it's very good at that with kids with ADHD. It doesn't get rid of their ADHD, but it helps the parents to restructure their approach to their child.

So that's a positive. So these can have additional benefits, even if they're not really treating the ADHD. So that's a really important message. But more generally in terms of treatment, I think if you move from the notion that ADHD is a disorder that needs treating to that it's a different way of thinking or being, then the focus becomes much more on trying to help people with ADHD thrive in the long term rather than just controlling their difficult behaviours if they're just a clinical problem or just a kind of a social cost.

And that's sometimes the way it's phrased. even, which is a little bit undermining, I think, for people with ADHD. So does ADHD exist on a sort of sliding scale? I mean, do we all have ADHD to some degree? So obviously the first thing to say is that the diagnosis is categorical. There have no sliding scale in the diagnosis. It either got it or you've not got it. And for a long time, we assume that that was actually reflecting reality. And now we know, like you say, that ADHD is actually a dementia. It's a continuous dimension, at least at the level of the symptom severity.

You know, there's no point in the symptom severity range going from moderate, you know, low to moderate to high. There's no point at which you can say there's a non-arbitory cutoff. No, there's no point at which all of a sudden a different thing emerges. You know, and that's been tested in lots of different ways, but one of them, for instance, let's take genetic factors. So from studies of hereditary, we know that the, the, the, ADHD is equally heritable in the moderate range as in the severe range.

There are no difference. And in the low range, it's a continuous sort of factor underlying that. The key thing, I guess, to say is that it's a continuum. But every single mental health problem or every single neurodevelopmental condition is also a continuum. Schizophrenia is a continuum. Autism is a continuum. All that means is that around the threshold, it's very difficult to diagnose because it's small. But if you see a really ADHD person with severe ADHD and you compare them with a neurotypical person, it's not difficult at all to see the difference. It's around the thresholds that it becomes difficult clinically. And I would say

that around those thresholds is great work by research called Owens showing that actually diagnosing people in subclinical or, you know, around those thresholds can be a little bit damaging. It can lead to long-term difficulties for those people. So you need to be clear, kind of a clear manifestation, I would say, is really important before you make the diagnosis. Earlier you were saying that ADHD really have to sort of show symptoms in childhood. but there's been a lot of growth in talk around adult ADHD. You know, can somebody develop ADHD later in life, or is it a case of them being undiagnosed?

Yeah, that's a really hot topic. The, obviously, adult ADHD is not a new phenomenon. ADHD is a neurodevelopmental condition, and we've known for a long time that symptoms and impairment persist into adulthood. So, you know, prospective longitudinal studies, which have followed ADHD people from childhood to adulthood, have shown, yeah, many of them have still got ADHD, most of them have still probably got ADHD,

in one form or another. But that's not really the issue. The issue is ADHD that's first diagnosed in adulthood, as you say. Now, at the moment, you can only do that if you can show or you can prove to your clinician or convince your clinician that you did have a childhood onset. that's still part of the diagnostics for adult ADHD. The question is a twofold, really.

First of all, the information about your childhood is retrospective. And it's usually the person themselves that is giving the account. Although, you know, best clinical practice would have somebody else corroborating. But that's often not possible. And of course, that's very open to misremembering and also to, systematic bias. Your state of mind when you're giving that information may actually affect your recall of your childhood. So it's probably the case that quite a lot of people who are getting ADHD diagnoses, this is de novo. There wasn't really sufficient symptoms

or impairment in childhood to say they had a childhood form. The big question, I think, is what you said. So there's lots of evidence that people can meet the crisis. for ADHD and adulthood, even though they didn't have childhood difficulties. And, you know, the question is for that, you know, is that the same sort of thing as a childhood persistent type? And what it looks like, if you compare childhood onset ADHD that's persisted into adulthood and de novo adult ADHD, they do look rather different. So for instance, the genes that drive child or ADHD don't seem to drive adult onset ADHD. The patterns of psychological impairment seem rather different and cognitive impairment seem rather different.

So there are lots of ways it differs. There's also higher incidence, probably of substance abuse. There's a higher exposure to stress. So you can see it might have a totally different underlying set of causes. Does it mean we shouldn't treat it as ADHD? Well, I think the court is out on that. It all depends on whether interventions are effective in this group of people, I guess. And whether we need in the next diagnostic manual,

I think that's going to be called DSM6, whether we need an adult onset form of ADHD, or call it a completely different thing. I don't know. Is there any sort of concrete idea, ratio of the people who have ADHD? And is there any evidence that it's sort of undiagnosed in certain groups of people as well? That's a really great question. And so for in, so, the rates of ADHD in the population, that is nothing to do with diagnosis, you just go out

into the population and you give people an assessment. They're pretty constant over time. There's about five to six percent of people meet the diagnostic criteria. And fascinatingly, they're quite consistent across different nations and cultures, about five to six percent. Diagnosis is a totally different thing. And in some areas, diagnostic rates get up to 15 percent. Now, in some countries and some parts of countries, so the U.S. diagnostic rates are really high. And many people interpret that as over-diagnosis or really low-quality diagnostic procedures. And it's probably driven a bit by farmer advertising. It's probably driven a bit by school demands.

It's, you know, achievement-orientated culture or whatever. But in other countries, like the UK, it's been chronically underdiagnosed. And we're just starting to correct that now. So more people are getting the care that they need because more people are getting the diagnosis. So it varies an awful lot from country to country. Now in terms of underdiagnosed groups, yes, there are clear groups where, for very particular reasons where the diagnosis hasn't been given, and obviously the main one I would say is girls and young women.

The rates of diagnosis are much lower in girls than boys. some of this might be due to the fact that ADHD is just less prevalent, that's clearly true, but quite a lot of it may be due to the fact that we're kind of working on a phenotype or a clinical presentation that is very male-centric. Because don't forget, the diagnosis of ADHD, initial formulation came out of probably of, you know, chats between psychiatrists about patients that they'd seen, and those tended to be all boys. So, you know, we're doing research now with a PhD student of mine, Anna Maria, who are looking at kind of other aspects of female diagnosis that have been totally missed

in the clinical workup are the things that are particularly prominent in the female case compared to the male case that might equalize the rates a bit. What sort of factors are involved there? Yeah, well, we're looking at a number of things. One of the things, one of the things, one of the things we're looking at is this so-called camouflage or masking. And what girls are very good at doing, it seems, from our investigations, is covering over their most obvious aspects of ADHD. They kind of mask it, they kind of suppress it, particularly at school. At home, they let it go a little bit, but at school they tend to try and suppress. So they're not, because there's a sense, I think, that ADHD is like a male stereotype and girls still, you know, to them, to their mates and to the

probably to the teachers, they want to be considered as girls. And so they suppress this sort of these sort of behaviours, impulsive, hyperactive behaviours. So they're very good at that. I mean, it comes a point when that's not possible. And the costs of suppressing and masking, emotional costs are probably quite high. So by the time these girls get into adolescents, they've often developed all sorts of difficult mental health situate, like eating problems, eating disorders, self-harm, very low self-esteem. And it all sort of comes out and they start to get diagnosed with ADHD,

this underlying ADHD underlying a lot of these other problems. So that's one area. Earlier diagnosis for girls, I think, is something we need to really, really focus on. And that's certainly something we're trying to look at. What would you say to people listening who might think that this ADHD condition doesn't seem to be that well understood neurologically? And then the treatment is also quite limited as well. So is it that we actually don't understand quite a lot about ADHD?

I think we are becoming increasingly aware of how little we understand about ADHD. So, you know, I'm perhaps more than some of my colleagues. I'm not, I'm pessimistic, but I do recognize the field is somewhat in a state of crisis. You know, the idea that science will promote better care for people with ADHD for some reason hasn't really delivered. And I think it's because we've come into it thinking it's a relatively straightforward, problem to solve. These genes, this brain, this outcome, target the genes or the brain, be fine. But of course, life's much more complicated than that, as I've hopefully I've illustrated.

And it's a much more complex and heterogeneous problem. That's not even taking account of circumstances, which I've just talked about in terms of social deprivation or cultural stereotypes and so forth. So I think in a way, as we move to a more granular understanding of the particular risks, I think we will be able to add value. So I'm optimistic in that regard, but I think it's a much longer term program. But in a way, maybe that's not the main issue. The main issue is to focus on this arc of growth. And so we're not. going to treat it as if it's as if it's just a clinical problem or just a social burden, we're going to try and promote growth through focusing on environments and experiences of all

these young people. That was Edmund Sunaka Bark, Professor of Psychology, Psychiatry and neuroscience at King's College London. Thank you for listening to this episode of Instant Genius brought to you by the team behind BBC Science Focus magazine, which is you can find on sale now in supermarkets and newsagents as well as your preferred app store. You can, of course, also find us online at sciencefocus.com. This podcast is sponsored by Name, Audio and Focal. The texture and emotional depth of music can be lost through digital sources or poor signal. Name Audio believes you can have digital precision with analog warmth.

Alongside French acoustic specialist focal, name creates high, end audio systems combining innovation with craftsmanship so you can listen to music just as the artist intended discover more at name audio.com