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A classification system to identify communication between brain regions brings us closer to predicting and diagnosing attention deficit hyperactivity disorder (ADHD) with better precision than ever before, according to a 

In this Q&A, we speak with lead author of the study, Chris McNorgan, PhD. Dr McNorgan is assistant professor, Department of Psychology at the University at Buffalo, State University of New York, and director of Computational Cognitive Neuroscience Laboratory, in the Department of Psychology at the University at Buffalo — SUNY.

Psychiatric Times (PT): You talk about task-based functional connectivity as a biomarker of ADHD. Can you tell us more about that?

 The challenge with using behavior to diagnose cognitive disorders is that behavior is extremely variable, even within individual patients. Behavioral indicators commonly used to identify ADHD might meet a subjective threshold on one day, but not during a follow-up test, leading to diagnostic instability.

 detects or confirms the presence of a condition of interest by virtue of covarying with the condition: If the biomarker is present, then so is the condition. ADHD is associated with atypical activity patterns, and because the brain does not rewire itself every day, we expected to find persistent differences between ADHD and controls in the connectivity that governs those activity patterns. 

Although a computer is required to represent the complex connectivity patterns that distinguished between controls and ADHD, the high classification accuracy for these machine-learning models establishes that these connectivity patterns provide sufficient evidence to reliably identify ADHD.

PT: What new information does the study provide?

 Ours was not the first study that assumed ADHD can be identified by characteristic functional connectivity. However, the substantial improvement in prediction accuracy over previous studies tells us a few things. First, that task-based functional connectivity within a brain network involved in a task that taxes inhibitory control appears to be more predictive of ADHD than resting state connectivity collected while individuals let their minds wander.

The second finding is more of an analytic innovation, explicitly tying diagnostic accuracy to performance on a relevant behavioral task. The 

 (IGT) was developed under a particular theory about the role of inhibitory processing in ADHD. However, just because it is theoretically tied to ADHD does not make it so. 

Because the classifiers had to identify both IGT performance and ADHD diagnosis from the same set of functional connections, it had to find which connections, if any, were predictive of both. Successfully solving the problem established that performance on the IGT is relevant to ADHD by virtue of the fact that the same functional connections predict both. The study provides a template for similarly linking other diagnostic measures to outcomes.

PT: What can you tell us about the future of machine learning in predicting ADHD with diagnostic accuracy?

 Although task-based connectivity was more diagnostic than resting-state, running an experimental task in an MRI scanner will not be a practical diagnostic tool anytime soon. However, by explicitly linking neuroimaging results to easily administered behavioral tasks, models like this might be used in the future. They may translate a particular behavioral performance profile into a likely connectivity profile confirmed by MRI if need be. These results might inform the choice of intervention. 

ADHD diagnoses have been described as unstable: The same individual may fall above or below threshold at different times. So the fact that childhood ADHD diagnoses were 

 in fMRI scans taken from young adults is remarkable, and I think points to the disorder as something that is deeply ingrained at the neurological level, although it may appear much more transitory at the behavioral level. We do not have information about severity in the participants at the time of the scan, but even if we assumed all of them were symptom-free, their brains are clearly doing something identifiably different.

Finally, these models are remarkably accurate because they make use of many different data points. The optimal precision was calculated based on 4 individual fMRI scans per participant. There may be different subtypes that could be identified by an extension of this paradigm using new tasks. All this points to the general idea that having more information on-hand leads to better evaluations, though the information required to achieve very high accuracy may take a computer to process it.

PT: Did you find anything in your research that was unexpected?

 In hindsight, finding subgroups seems obvious, but we were not looking for different connectivity profiles for high- and low-scorers on the IGT. This was purely for a proof-of-concept, and to make it easier to argue that the classifier had identified activity that was related to inhibitory control. This got us thinking about how this sort of approach might be useful for identifying subpopulations.

PT: Can you tell us about future directions in this research?

 There are a few interesting directions that immediately suggest themselves. Clinical endpoints may be based on subjective self-report. As a surrogate, the 

 must not only be correlated with the condition, but evidence of a causal link must be established between the condition and the biomarker. Research that examines whether and/or which interventions lead to related changes in functional connectivity and in clinical endpoints might establish functional connectivity as a surrogate endpoint. This would allow connectivity to provide additional context for interpreting subjective patient reports.

A second direction would be to link diagnostically predictive connectivity patterns to other commonly used behavioral indicators. We found different connectivity profiles for those with ADHD that scored uncharacteristically high on the IGT, which is commonly used in an experimental setting. This indicates that individuals with ADHD may be differentiated by different patterns of hyper- or hypo-connectivity, and these differences may inform choice of intervention, eg, a drug that targets the hypo-connected circuit. 

 to performance on other tasks more commonly used in a clinical setting may lead to more effective treatment of ADHD in patients who show atypical performance on 1 or more clinically relevant measures.

1. McNorgan C, Judson C, Handzlik, Holden JG. Linking ADHD and Behavioral Assessment Through Identification of Shared Diagnostic Task-Based Functional Connections. 

 2020;11:583005. Accessed April 13, 2021. 

https://www.frontiersin.org/articles/10.3389/fphys.2020.583005/full

New research brings us closer to linking diagnostically predictive connectivity patterns in patients with ADHD.

Advances in Predicting and Diagnosing ADHD

 and there is evidence that activation of the maternal immune system during pregnancy—whether by infection, chronic inflammation, or autoimmune disease—is associated with increased risk of neurodevelopmental disorders in the 

 In the case of the latter, maternal autoantibodies may cross the placenta and alter fetal development through epigenetic changes, brain microglial cell activation, and modulation of 

 Previous studies have focused on the association between maternal autoimmune disease and autism spectrum disorders, whereas attention-deficit/hyperactivity disorder (ADHD) has been less studied. Only 1 previous study examined the association between any maternal autoimmune disease and ADHD risk in 

Nielsen and colleagues aimed to investigate the association between any (and specific) maternal autoimmune disease and ADHD in children, and to incorporate those results into 

a systematic review and meta-analysis on this topic

 Using the New South Wales (NSW) Perinatal Data Collection, they identified all women with full-term, singleton live births from July 2000 to December 2010. Birth data were linked to all hospital admissions for both mother and child, and pharmaceutical data from the child for treatment of ADHD through registers. A child was considered to have ADHD if they had a stimulant prescription for ADHD and/or a hospital diagnosis of ADHD. Children linked to a first ADHD event before age 3 were excluded. Children were followed to death or at the end of follow-up in December 2014.

Maternal autoimmune disease was determined based on the mother’s hospitalization records. Children whose mother had at least 1 hospitalization for autoimmune disease were considered exposed. Exposed and nonexposed mothers were propensity matched based on age, country of birth, socioeconomic status, place of residency, parity, smoking during pregnancy, and mental health diagnosis. Cox proportional hazard models were used to examine the association of maternal autoimmune disease and ADHD, adjusting for child sex. Analyses were performed for any maternal autoimmune disease and individual conditions with at least 15 cases of ADHD among exposed children.

The authors also performed a systematic search of MEDLINE, Embase, and Web of Science to identify studies on the association between maternal autoimmune disease and ADHD. Included studies were assessed for study quality using the Newcastle-Ottawa Quality Assessment Scale. Meta-analyses of any (and specific) maternal autoimmune disease with ADHD in the offspring were performed by calculating random-effects pooled hazard ratios (HRs) and inverse-variance weighting.

In the NSW Perinatal Data Collection, 831,718 mothers and children were including and 12,767 (1.5%) exposed to maternal autoimmune disease. Propensity score matching including a cohort of 12,610 exposed children and 50,440 controls. During follow-up, 1094 male (3.4%) and 332 female (1.1%) children were diagnosed with ADHD. After adjustment, any maternal autoimmune disease (HR = 1.30), type 1 diabetes mellitus (HR = 2.23), psoriasis (HR = 1.66), and rheumatic fever or carditis (HR = 1.75) were associated with increased risk of ADHD, and this association was not moderate by child sex. When considering mothers diagnosed before or within 180 days of birth (N = 9700), any maternal autoimmune disease (HR = 1.28) and type 1 diabetes mellitus (HR = 1.95) remained significantly associated with ADHD.

Five studies, including the present cohort, were included in the meta-analysis. Two studies estimated the association with any maternal autoimmune disease, and 11 specific conditions were investigated in 2 or more individual studies. In the meta-analyses, any maternal autoimmune disease (HR = 1.20), type 1 diabetes mellitus (HR = 1.53), hyperthyroidism (HR = 1.15), and psoriasis (HR = 1.31), were all associated with increased risk of ADHD.

The authors found an association between any maternal autoimmune disease, type 1 diabetes mellitus, and psoriasis in both the present study and meta-analysis, and an association with hyperthyroidism in the meta-analysis. They noted significant heterogeneity in findings across individual studies, and that non-immune factors such as glycemic control (in type 1 diabetes) and endocrine aspects of hyperthyroidism may also contribute to associations with ADHD.

Strengths of the present study include the hybrid design, including a large population-based cohort and meta-analysis. Limitations include the lack of outpatient/primary care records for identifying maternal autoimmune disease, absence of data on the clinical status of the mother’s autoimmune disease and associated medications, and absence of data on nonstimulant ADHD medications and severity of ADHD.

Maternal autoimmune disease is associated with increased risk of ADHD in offspring, adding evidence that adverse maternal immune function during pregnancy may alter fetal neurodevelopment. Children of affected mothers may benefit from additional follow-up and support for developmental issues.

is professor in the Department of Psychiatry and Health Behavior, Augusta University, Augusta, Georgia. He is on the Editorial Board and serves as the schizophrenia section chief for 

. The author reports that he receives research support from Augusta University, the National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Stanley Medical Research Institute.

1. Kipnis J. Multifaceted interactions between adaptive immunity and the central nervous system. 

2. Knuesel I, Chicha L, Britschgi M, et al. Maternal immune activation and abnormal brain development across CNS disorders. 

3. Estes ML, McAllister AK. Maternal immune activation: Implications for neuropsychiatric disorders. 

4. Gumusoglu SB, Stevens HE. Maternal inflammation and neurodevelopmental programming: a review of preclinical outcomes and implications for translational psychiatry. 

5. Nielsen PR, Benros ME, Dalsgaard S. Associations between autoimmune diseases and attention-deficit/hyperactivity disorder: a nationwide study. 

6. Nielsen TC, Nassar N, Shand AW, et al. Association of maternal autoimmune disease with attention-deficit/hyperactivity disorder in children. 

Activation of the maternal immune system during pregnancy is associated with increased risk of neurodevelopmental disorders in children. A recent review and meta-analysis examine the link in ADHD.

Maternal Autoimmune Disease and ADHD Risk in Children

An international group of experts analyzed findings from a large pool of select studies and developed an updated consensus statement with declarations about attention deficit hyperactivity disorder (ADHD). They curated a collection of validated statements, addressing questions on topics ranging from nutrition, neuropsychiatry, and nonpharmacologic treatments. The 

Lead author Stephen V. Faraone, PhD, joins us in this Q&A to talk about the study. Dr Faraone is Distinguished Professor in the Departments of Psychiatry and Neuroscience and Physiology, Psychiatry Research Division, SUNY Upstate Medical University, Syracuse, New York. He is President of the 

Psychiatric Times (PT): What prompted the consensus guidelines and why are they important now?

Despite a large scientific literature about ADHD, much misinformation about ADHD is spread by the internet and other media. This creates 

 and leads to treatment decisions that are not in the best interests of patients. Our consensus provides clinicians, patients, and family members evidence-based results they can use to make informed decisions.

I asked thought leaders from ADHD professional associations from around the world to nominate authors for the project.

PT: Since this is a worldwide consensus statement with 27 countries represented, what sort of differences did you find internationally? How does the United States

compare with other countries in terms of recognition and treatment?

The prevalence of ADHD, the symptoms of the disorder and its outcomes are essentially the same around the world, with some small exceptions. The main difference is in how often ADHD is appropriately diagnosed and treated. Diagnosis and treatment rate are better in countries with well-developed health care systems compared with other countries. The United States has higher rates of diagnosis compared with other high-income countries, although ADHD in adults is underdiagnosed in the United States and around the world.

PT: The article talks about stigma of both patients with ADHD and the health professionals who treat the disorder. Can you tell us more about that?

For patients diagnosed with ADHD, stigma leads to decreased self-esteem, less acceptance by peers, social isolation, and lower self-perceptions of confidence. When treatments are stigmatized, patients and parents are less likely to seek appropriate treatment. Moreover, clinicians are less likely to provide those treatments. This leads to unnecessary distress and disability and costs to society.

PT: The piece came up with 208 empirically supported statements about ADHD. Which ones were most impactful? What new information does the paper provide?

The degree of impact will vary with the reader. Learning about what treatments do and do not work for ADHD can be life changing for patients and families. Learning that ADHD costs societies billions of dollars each year will motivate policy makers to improve access to care. Learning about the medical conditions associated with ADHD will be of much interest to primary care clinicians.

By definition, strong evidence cannot be “new” because it arises from published scientific studies. But I expect that much of this information will be new to most nonprofessional readers and for those professionals that are new to 

PT: Of what clinical relevance is the consensus statement, and does it offer teaching points for readers?

In a nutshell, clinicians will learn that ADHD is a well-defined condition that can be diagnosed at any age; untreated ADHD has many, many serious consequences ranging from school failure in childhood to criminality in adulthood; and the medications for treating ADHD are much more effective than nonmedical treatments for relieving ADHD symptoms.

• ADHD is not an invention of modern society. The syndrome had been reported in medical writings in Europe as early as 1775.

• ADHD is rarely caused by a single genetic or environmental risk factor, but most cases of ADHD are caused by the combined effects of many genetic and environmental risks each having a very small effect.

• Neuroimaging studies find small differences in the structure and functioning of the brain between people with and without ADHD. These differences cannot be used to diagnose ADHD.

I was surprised to learn that ADHD puts people at increased risk for many medical disorders including obesity, asthma, allergies, diabetes mellitus, hypertension, sleep problems, psoriasis, epilepsy, sexually transmitted infections, abnormalities of the eye, immune disorders, and metabolic disorders.

Our next goal is to disseminate the International Consensus Statement as widely as possible. It has been translated into Spanish, French, and German and we also have a summary in Welsh. Colleagues are currently in the process of translating it into Mandarin, Turkish, Portuguese, Arabic, Hindi, Dutch, Japanese, and Italian. These translations will be available at the World Federation of ADHD website.

Readers can learn more about the Consensus Statement from Dr Faraone via Twitter: 

1. Faraone SV, Banaschewski T, Coghill D, et al. The World Federation of ADHD International Consensus Statement: 208 Evidence-based Conclusions about the Disorder. 

 2021;S0149-7634(21)00049-X. Accessed April 4, 2021. 

https://www.sciencedirect.com/science/article/pii/S014976342100049X#abs0010

A collection of validated statements addresses overarching topics ranging from nutrition, neuropsychiatry, and nonpharmacologic treatments.

Consensus Statement Revises Previous Assertions About ADHD

The US Food and Drug Administration (FDA) has approved Qelbree, viloxazine extended-release capsules created by Supernus Pharmaceuticals, for the treatment of attention-deficit/hyperactivity disorder (ADHD) in pediatric patients aged 6 to 17.

“Based on the efficacy demonstrated in the clinical program, we believe Qelbree offers a unique new alternative for the treatment of ADHD,” said Jack A. Khattar, President and Chief Executive Officer of Supernus Pharmaceuticals. “Qelbree provides prescribing physicians and patients living with ADHD a therapy that is not a controlled substance with proven efficacy and a tolerable safety profile. We are grateful to the patients, families and their care givers who participated in and supported our research.”

Qelbree is a once-daily, rapid and extended release, sprinkleable capsule. The approval of the medication is supported by data from 4 phase 3 clinical trials that studied more than 1000 pediatric patients whose ages ranged from 6 to 17 years.

“ADHD is one of the most common mental health issues in the US,” said Andrew J. Cutler, MD, clinical associate professor of psychiatry at SUNY Upstate Medical University, and Chief Medical Officer at the Neuroscience Education Institute. “The right treatment is key for children and adolescents, as they grow and navigate school and social relationships. This approval offers a novel once a day sprinkleable non-stimulant that can be a great option for children and adolescents with ADHD.”

Qelbree does carry the boxed warning of higher rates of suicidal thoughts and behaviors, which were observed in pediatric patients with ADHD during clinical trials. Qelbree-treated patients should be monitored for worsening or emergence of suicidal thoughts.

Supernus also announced positive results from a phase III trial in adult patients with ADHD in December 2020. They plan to submit a supplemental New Drug Application to the FDA for Qelbree in adults in the second half of 2021.

1. Supernus Pharmaceuticals. Supernus announces FDA approval of Qelbree™ (SPN-812) for the treatment of ADHD. News release. April 2, 2021. 

https://www.globenewswire.com/news-release/2021/04/02/2204030/0/en/Supernus-Announces-FDA-Approval-of-Qelbree-SPN-812-for-the-Treatment-of-ADHD.html

2. Supernus Pharmaceuticals. Highlights of prescribing information for Qelbree. 

https://www.supernus.com/sites/default/files/Qelbree-Prescribing-Info.pdf

This once-daily sprinkleable capsule may help patients aged 6 to 17 years with attention-deficit/hyperactivity disorder.

Pediatric ADHD Medication Gets FDA Green Light

Conversations in Critical Psychiatry is an interview series that explores critical and philosophical perspectives in psychiatry and engages with prominent commentators within and outside the profession who have made meaningful criticisms of the status quo.

, is a consultant child and adolescent psychiatrist in the United Kingdom’s (UK) National Health Service and a visiting professor of Child Psychiatry and Mental Health Improvement at the University of Lincoln, UK. He writes from a critical psychiatry perspective on topics relating to mental health and childhood and has published over 130 articles and dozens of chapters on many subjects, including childhood, psychotherapy, and cross-cultural psychiatry. He has authored 6 books, co-authored 2 books, and co-edited 4 books, including 

Liberatory Psychiatry: Philosophy, Politics and Mental Health

 (co-edited with Carl Cohen, MD, Cambridge University Press, 2008), 

 (co-edited with Jonathan Leo, PhD, Macmillan Education UK, 2009), and 

 (co-written with Neil Gardner and Brian McCabe, Palgrave Macmillan, 2011). His latest book is 

Insane Medicine: How the Mental Health Industry Creates Damaging Treatment Traps and How You Can Escape Them

 (Kindle Direct Publishing, 2021), available in serialized form on 

Dr Timimi is among the fiercest critics of psychiatric diagnoses and the medical model in psychiatry (especially child psychiatry, his own area of specialization). He is a prominent voice of British critical psychiatry, and over the years he and his colleagues have argued that psychiatric conditions in their very nature reach beyond the brain to involve sociocultural dimensions and cannot be adequately understood through the epistemology of biomedicine (see article in the 

 Dr Timimi’s sweeping critique of and divergence from mainstream views is also illustrated in a 2018 debate with David Foreman, MD, in the 

 on the validity of attention-deficit/hyperactivity disorder (ADHD) as a diagnostic construct.

 This present interview with Dr Timimi is in the context of his new book 

: Your critique of current psychiatric thinking and practices is so broad and touches on so many conceptual and philosophical issues that I worry that it would be too easy for us in this interview to get mired in disagreements about more abstract questions regarding the nature and goals of psychiatric classification or the medical model. Perhaps a more fruitful way to start may be to do so with a focus on clinical practice. For instance, how would you approach the assessment and management of a child who is brought to your clinic by the family with a pervasive and persistent pattern of inattention and hyperactivity?

: First of all, many thanks for inviting me to be a part of your conversation series. It is so important for us to continue a discussion on the problems with, and alternatives to, dominant models, so I am glad that you are hosting these dialogues. I hear the concern in your first question, but do not think the conceptual and philosophical issues can be separated from clinical ones. How we imagine what we are dealing with, particularly if we are imbued with cultural meaning-making power, has a massive impact on what we show interest in clinically, what questions we ask, what interventions we make, and what impression our patients are given about what is happening in their lives.

This means the question you ask already sends us crashing against the shores of social construction. What do you (or this mythical family) mean by “pervasive,” “persistent,” “inattention,” and “hyperactivity” and why have these 2 bits of behavior been brought to the clinical foreground? If, like me, your clinical practice understands that what we do in psychiatry is essentially provide a new story about the stories our patients (or parents) might tell, then we cannot escape the interpretive nature of how we construct our story about them (after all, we have no recourse to independent of subjective opinion empirical evidence).

So, I would be more interested in knowing their broader narrative. What has happened in that child’s and family’s life? Like the vast majority of those who end up in my clinics, many children who present like this have had more than their fair share of adversity. What are the child’s strengths and existing skills? If there were a mythical perfect treatment, what would they like to see change (school, home, relationships)? Who is it (parents, teachers, child themselves) who most wants to see what sort of change? A 1-acronym formulation (such as ADHD) has powerful consequences. It acts as a hypnotic suggestion on those around the child and influences what they might view as important. It has the potential to obscure, or at least render as secondary, the things that might bolster the child’s esteem and the parent’s sense of empowerment.

I may choose an alternative label such as the child is “intense.” They engage with the world with an emotional intensity that provokes powerful emotions in those around them. We could see this as a gift that needs understanding, guidance, and nurturing, rather than using a label that views their behaviors as symptoms that need suppressing. With the cultural pressure to diagnose and medicate, this is not always easy, but maybe easier than we realize. In the last 5 years, I have started 1 child on stimulants, and although it helped ameliorate a dire situation in the short term, I do not think it has helped much in the long term. Much more common in my practice is to inherit young individuals on stimulants, where the perceived problems keep returning, but are now viewed through a medicalized lens leading down a one-way street of requests for increasing the dose or adding another medication in. Despite that, with time and patience, nearly every patient I inherit is off all stimulants by the time I discharge them at 18 years old, with their lives much improved.

: Yes, I do not think either conceptual and philosophical issues can be separated from clinical ones (something I strongly try to convey to my trainees as well as colleagues!). My hope was that by looking at how our clinical approach is informed by these issues, we may be better able to appreciate your views. And your response is very helpful in this regard. As you mention, you are not a fan of psychiatric diagnoses and you have criticized them extensively in your writings. From my perspective, one of the things psychiatric classifications do is to serve a sort of pragmatic function, which allows researchers to conduct studies about causes and treatments and allows clinicians to link the individual in front of them with the existing body of knowledge related to causes and treatments. For instance, the construct of ADHD allows clinicians to capitalize on the literature related to the use of stimulant medications. The short-term efficacy of stimulant medications for individuals who meet criteria for ADHD is so robust—and universally endorsed by practice guidelines—that it would be considered below the standard of care for a psychiatrist not to discuss them as a treatment option for individuals who could benefit from them. However, it is hard for me to imagine how we can determine who could benefit from stimulant medications if we were not making diagnostic distinctions, at least the very least in our head (for instance, differentiating between anxiety syndrome vs inattention-hyperactivity syndrome). This does not necessitate that we are forced to consider these diagnoses as natural kinds or as neurobiological disease entities; it only means that we recognize them, at minimum, as pragmatic constructs, more or less helpful given our goals. What is your view on how clinicians and researchers can carry out their pragmatic functions of research and treatment?

: These are great questions but need more than this interview to properly unpack; nevertheless, I will have a go. Firstly, there is an important difference between psychiatric diagnosis and a psychiatric classification. There are many different classification systems, with diagnosis being a particular system based on classification by cause (at least proximal cause). This is why your statement that diagnosis “allows clinicians to link the person in front of them with the existing body of knowledge related to causes and treatments” works when it is shedding light on cause and therefore the development of treatment technologies that address cause, but does not when the system of classification is unable to identify or even get close to identifying proximal causes. Worse than that, calling it diagnosis leads to (an understandable) assumption that cause and therefore evidence based useful treatments are known/knowable. Because what we call psychiatric diagnosis is not diagnosis (in that technical sense). Thinking that it is has led to practice that is skewed and patient expectations that are unrealistic.

Despite over a century of research to establish possible causes using psychiatric diagnosis as the framing, the cupboard of positive findings remains astonishingly bare. No markers, no genes (apart from a significant portion of those with a learning disability), and no identifiable characteristic brain abnormalities (apart from dementias). Studies looking at outcome from treatment with either pharmaceutical or psychotherapeutic models matched to diagnosis have not shown outcomes improving over time. What has increased instead are the numbers of patients who get a psychiatric diagnosis, the amount of psychiatric medication prescribed, and the numbers who claim disability allowances for a psychiatric problem. If the classification system we use was on the way to becoming diagnostic then we should be seeing something very different in both the science and the outcomes.

What about making pragmatic decisions? I do not agree that the construct of ADHD allows clinicians to capitalize on the literature for stimulants (for example). It makes them imagine they can, which is far more dangerous. Thus, we end up with vested interests shaping guidelines, which then influence public perception, media reports, and distort doctors’ practice. The result has been catastrophic mass prescribing of stimulants to children and equally catastrophic convincing of children and their caregivers that they have a hardwired condition that makes them incapable of doing certain things and requires they ingest the same substance that we warn adults about its profound dangers.

The effect of stimulants has been known for a very long time and is no different whether you get the label of ADHD or not. 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. A 

concluded all the trials they included were considered poor quality with unblinding likely to be common (due to frequency of adverse effects), and so they could not conclude with any certainty that taking methylphenidate will improve the lives of children and adolescents with ADHD, even in the short term. The evidence is even worse for long term outcomes, where research without vested interest involvement finds that regardless of initial severity there is no evidence that long-term outcomes are any different whether or not a stimulant is prescribed, with some studies finding worse long-term outcomes (in physical, academic, or psychiatric measures) for those prescribed stimulants. So that is the danger of imagining these are pragmatic groupings: it embeds and reifies ideas, turning an imagined entity into an assumed concrete reality, which when done without realizing that this is what you are doing, has the potential for unhealthy consequences to individuals, the profession, and our culture more 

: You have talked about the “McDonaldization” of child development, where the difficulties of growing up are categorized neatly and then addressed with quick fixes. You have also talked about psychiatric diagnoses functioning as “brands” that are sold to the consumers and generate lucrative markets around them. Can you tell us more about what you mean by this?

: The “McDonaldization” of child development refers to the way the challenges and uncertainties connected with growing up are placed into neat categories of things wrong with individual children, which can then be fixed with simple, one-size-fits-all interventions. A market economy and culture preys on our desire for the here-and-now satisfaction of our cravings, provided in a fast timely manner that requires little engagement with the product beyond its consumption. Get your products and messaging right and you can entice your consumers when they are still young and then have them as potential customers for life. McDonaldization is just a more culturally familiar reference to the process of commodification; in other words, the process of turning something into an object of economic value. Commodification’s overriding value is making money. In this arena, you need to convince a population that all manner of experiences may lead to unpleasant and dangerous consequences if not identified and remedied with your products (a diagnosis, a book, a medication, a therapy, a course, a supplement, etc.). Furthermore, these products may also enhance your life.

Whatever else you may decide psychiatric diagnoses are or are not, in their public life they now operate as brands. As market brands, they have products like any other product in profit-driven consumer markets. They appeal to customers with the promise that if you purchase (literally and metaphorically) and identify with this or that brand, your life troubles will make sense and be improved in some way. Like most market consumables, they are objects of fantasy and desire; must-haves with a limited shelf life. For markets to keep growing, you must convince your customers they need your wares, and will continue to need them, hopefully with regular upgrades, to stay happy. Markets then develop around these psychiatric brands. Some brands develop huge markets worth billions from pharmaceutical products to services, from so-called “experts” to particular therapies, to research institutes, to courses, to trainings, to books, to other self-help materials, and more. Get your brand to cover an area of common public concern, and money and custom will flow. Like most consumables there is some immediate satisfaction, but the products ability sustain long-term satisfaction is limited, but hopefully (for the retailer), the consumer, once started down this avenue, will keep coming back for more.

Some psychiatric brands are more niche and harder to popularize (such as personality disorder and schizophrenia), but where the market can reach the professional classes in sufficient numbers to allow the brand to take root, then it can still, to some degree, influence public discourse too. However, brands that target mood, stress, and insecurities about the self in adults have enormous potential. Similarly, brands that target the behavior and development of children also have enormous potential (unless they are associated with blame for the care givers, the main group of customers). Thus, strong brands like bipolar disorder, depression, ADHD, and autism demonstrate their popularity by their rapid expansion in the absence of any scientifically tangible discovery that supports the existence of these constructs in an empirically identifiable form in the bodies of those labelled, and beyond the imaginations of those who label individuals with these brands.

: I think part of what you are describing is also captured by the notion of 

, so-called by Ian Hacking in the philosophical literature, the complex ways in which individuals interact with classifications, how classifications change them, and how they change classifications in turn, particularly when the classifications are imbued with sociocultural significance and these feedback interactions take place within a 

 The area where we may perhaps disagree is whether there is any reality to these brands beyond that of social construction. I am inclined to think of many psychological phenomena as being on the border of natural and social, as having characteristics of both. There are psychological patterns of behavior that are inevitably shaped by sociocultural influences, but they also have an existence that goes beyond such influences. Consider homosexuality. Many cultures in the past did not have the concept of sexual orientation that we do and did not think of individuals in terms of “heterosexuality” or “homosexuality,” so in a manner the concept is socially constructed, but the concept captures aspects of our psychological lives that are not, so to speak, made up. To the best of our knowledge, there is no gene for homosexuality or any identifiable neurobiological cause, yet being a homosexual is not like being a republican or a democrat. Setting aside the issue of disorder attribution, I think constructs such as autism have a similar sort of reality as homosexuality, in the sense that they capture patterns in our psychological lives that have a degree of stability and endurance, and which can neither be reduced to society nor biology. Both also have complex looping effects, as evident by their inclusion in current or past diagnostic manuals, and ongoing LGBTQ+ pride and neurodiversity movements. Your thoughts on this?

: How do you know there is anything beyond social construction? Of course, there is in straightforward biological terms, as physiological mechanisms are at play all the time. But once we reach into what we construct as the mind (or the psyche if you want to sound scientific, or the soul if you prefer a religious frame) we have very few givens biologically. What we make of our embodied physiology relies on what paradigm we wish to superimpose on what we observe and experience. We have no scientific window on the mind; we can only measure (environmental) inputs and (functioning) outputs. We have no idea what goes on in between. Neither psychology nor neuroscience has been able to tell us anything particularly universal about that in-between bit. Understanding the mind requires a different epistemology to that of the natural sciences. In that sense I see psychology and psychiatry as ultimately branches of philosophy. We are always involved in making sense, so that one of the few universal characteristics of the mind is meaning-making. Our meaning-making frameworks (including the professional ones we use) are cultural models that provide us with meaning-making tools with consequences. Thus, I am more interested in the consequences of the cultural meaning-making framework we use, rather than whether such a framework can be thought of as providing a truth or something that can be viewed as stable and enduring.

You use the example of sexual orientation. This is a behavioral output, and as you state we do not know what causes that, nor should we particularly care. In relation to psychiatry, homosexuality is an interesting example, as it used to be viewed as a psychiatric illness but was narrowly voted out of DSM in 1973 (after a vigorous campaign). So, framework of interpretation mattered far more for consequences than the behavior/feeling state itself.

You are right to point out the powerful effects, at both a cultural and individual level, of looping effects. When we understand that all we really have are meaning-making tools with consequences, we can evaluate both the power of the interpretive frameworks we use and hopefully appreciate that, unlike kidney problems, what we say has an effect on the individual we say it to. Kidneys do not get delighted, anxious, offended, decide to stick with me, or desert me, if I read out the results of kidney function tests. However, if you tell me that a dangerous and paranoid state of mind caused me to write the above sentences, then the effects on my emotions, thoughts, and behaviors may be very different than if you told me that these sentences are a “breath of fresh air.” The effects will be more marked the more power the individual has (or I perceive them to have) over me.

As far as autism and the associated neurodiversity movement is concerned, where is the stable pattern? If there was, how did we go from having no idea of autism a century ago, to a prevalence of around 0.04% in the early epidemiological studies in the mid-1960s (nearly all of whom also had moderate to severe learning difficulties), to an estimated 1.6% now and growing (most of whom no longer have significant learning difficulties), without any scientific evidence at any point showing that this represents some universally recognizable pattern (no genes, brain differences, and massive heterogeneity of so-called symptoms)?

 How can a construct that at one end includes Einstein and many other geniuses (just google famous individuals with autism spectrum disorder [ASD]) and speechless residents of care facilities at the other be considered a recognizable typology? What are the potential unintended consequences of using a framework that imagines that when you label someone with an ASD, you are discovering something characteristically different or an abnormality in the way their nervous system works? The idea we can be divided into neurodiverse and neurotypical is oxymoronic. How can we not all be neurodiverse?

: Capitalism seems to have an endless capacity to commodify even resistance to the system (perhaps all human social systems do). In the mental health arena, even frameworks such as Open Dialogue and Power Threat Meaning Framework are being actively commodified, becoming brands, and developing markets around them. Perhaps a similar thing happened to dialectical behavior therapy (DBT). Marsha Linehan, PhD’s ideas were radical in many ways, but DBT was rapidly co-opted by the system, such that any revolutionary potential seems to have been lost. I wonder to what extent this dynamic is a consequence of the fact any revolutionary idea in its implementation will need to negotiate with other elements of the system (governments, insurance companies, law, etc.). I am reminded of the delightful phrase “all the élan of revolution with none of the drudge of responsible administration” (

). How confident do you feel your revolutionary proposals about health care will be able to survive “the drudge of responsible administration” if and when their time comes?

: Very insightful question. Mark Fisher wrote about the merciless commodification of everything in his book 

 and since our economic, political, and therefore much of our cultural value subsystem, is dominated by this neoliberal logic, the dominant way for ideas to gain purchase (quite literally) is for them to become branded. Still, some ideas are better than others and have greater potential to improve how mental health is understood and how services are then structured.

Is there any way to allow new models to develop without falling prey to a McDonaldized branding process that rips out a deeper more sustainable core by becoming a process-driven bureaucracy? Possibly not. Perhaps some of the worst commodification effects can at least be partly ameliorated by a commitment to the local: an understanding that a service needs to have a sense of ownership for the models it uses, an openness to ongoing evaluation of a range of outcomes, which are then used to adjust or change aspects of the service, and a commitment to broader politicization of mental health that sees the issues we deal with intertwined with local and national material realities and discourses. My hope would then be that a new generation of critics will come along and see holes and inconsistencies in these new systems that have developed and have some creative thoughts about how best to remedy them.

: You have argued the current system of mental health care alienates individuals from the meaning inherent in their own emotional difficulties, undermines their capacities for everyday resilience, and by doing so, perpetuates those very difficulties. Can you elaborate on how you think this process of alienation unfolds?

: The labelling of our experiences with medicalized language (diagnosis, symptoms, disorder, dysfunction, dysregulation, etc.) which has spread far and wide. My kids and their friends talk about feeling “depressed,” a medical word. It entrenches a fear of, and alienation from, an appreciation of the ordinariness and understandability of a panoply of human emotional experiences. When we place our emotional experiences in a problematizing framework, we extract the everyday meanings these have and become worried that there is something wrong in us beyond our (and our meaningful others’) capacity to comprehend. Mental health education campaigns have made this dynamic worse. Far from normalizing the diversity of our emotional experiences and helping create an awareness of the variety of reactions to all the things that happen in our life being ordinary and/or understandable, even in those more extreme states, we have instead made more individuals suspicious that their experiences are a signal that there is something deeply wrong in them.

These medicalized frames also undermine our natural resilience, sensitize us to an idea of our vulnerability, and encourage us to transfer our agency to practitioners who are assumed to have some special knowledge about our experiences that we cannot possess. A survey of 1000 young individuals in the UK in 2019 found that 68% thought they have had or have a mental health problem, and of those 62% thought “destigmatization” campaigns 

 It troubles me that by early adulthood nearly three-quarters of the population have fallen for the propaganda that leads them to suspect they have experienced a mental disorder, as opposed to ordinary/understandable human reactions. Identifying with an idea that your emotions emerge from a disorder within you invites you to a potential lifelong struggle to suppress/control this part of you.

Medical colonialism (of language and the concepts that flow from this) means we do not have any other strong culturally available model for emotions beyond banal mechanical ones. As a result, we fear (and are fascinated by) displays of emotions and easily slide into an idea that individuals need help to learn how to control and manage how they feel. One of the, to me, worst phrases to emerge in modernist mental health practice is the oxymoronic “emotionally dysregulated.” The aspired to neoliberal entrepreneurial individual has to learn how to nourish their ego and use their thoughts to control their emotions. There are too few resources in medicalized Western cultures for learning how to sit with, experience, withstand, and understand emotions as important forces for action and connection. We have little time or respect for the ordinariness and extra-ordinariness of our emotions. We have imbued our emotional life with a destructive power more than a liberatory one.

, “Psychiatry’s strength comes from the fact that it is different from the rest of medicine and involves an engagement with the nature of the human condition, suffering, and its wide roots in social, political, and cultural meanings and realities. This is what the rest of medicine needs help with and why psychiatry’s difference to the rest of medicine should be seen as valuable quality, not an embarrassment.”

 I am curious to hear more about your views on psychiatry’s medical identity and what medicine can learn from psychiatry. Setting aside the issues about medical model for now, I do not think it is particularly controversial to say that psychiatry is a branch of medicine in the sense that individuals who practice psychiatry are physicians by training and this training includes, among other things, expertise in the use of psychotropic medications in the treatment of psychiatric conditions. This means that in addition to the differences from medicine, there is also a certain continuity. You are a physician yourself. How do you understand your own medical identity?

: Medical practice originates in a care ethic devoted to eliminating suffering. In the distant past, the person of the doctor was more important in healing than any rudimentary technical knowhow. As great strides have been made in understanding our physiology and the accompanying ability to identify when and how this goes wrong, we developed a system of classification (which we refer to as diagnosis) largely based on etiology. This technical success sometimes leads us to forget that health care is a human social activity involving attending to individuals who are in distress. Yes, I would rather see a doctor with a lousy bedside manner but who knows how to treat my ruptured appendix, than a doctor with great empathy but lousy technical skills, but forgetting these social roots comes with costs, particularly at the system level.

We have had many scandals in our hospitals in the UK (as I am sure is common in many countries) where patients have been harmed and died due to staff neglecting the basics of looking after individuals, not just patients. Mesmerized by the miracles of science, medicine still has to find ways to deal with presentations that go well beyond the limits the science side of our profession can offer. Medicine is a craft informed by scientific principles performed by practitioners with some social power to shape how individuals understand their experiences. Medicalization is an issue that cuts across specialties leading to iatrogenic harms, as does commodification with profit-hungry pharmaceutical and medical device manufacturers. Chronic conditions and medically unexplained symptoms are widespread and require doctors to muddy their minds with meanings, adaptations, existential anxieties (involving loss and death), and the psychosocial milieu of their patients, without being overwhelmed or retreating to dehumanizing defenses. They have to encounter the patient, not just their diagnoses. My general practitioner friends regularly tell me that most of the work involves these psychosocial aspects. This surely is the territory where a more rigorous psychiatry, engaged with both the physical sciences and the humanities, would take the lead in collaborations that would help the rest of medicine wrestle with these pressing issues.

Instead, unnecessary identity insecurity coupled with (for some) the more profitable pretense that we are as technically advanced as other branches, has led psychiatry astray. On the lack of technical advances, we will be found out, but medicine would be a poorer profession if that also meant ejecting its need to engage with these deeper psychological, social, and political dimensions.

: Given that mental health is a multidisciplinary area, a professional space shared by psychiatrists, primary care physicians/general practitioners, psychologists, and social workers (among others), what are your thoughts on the relationship between these disciplines? How would you like this professional space to be reorganized? In what areas should psychiatry be at the forefront and in what areas should it take a backseat and let other professions take the lead?

: It is sad that psychiatrists have been pushed into being primarily viewed as the prescribers in mental health services. Our representative institutions and academics have been complicit in this. The flimsy appeal that our models and practices are biopsychosocial (apart from not really knowing what this looks like in practice) is a smokescreen to what much of practice as a psychiatrist has become.

I consider myself a traditional child psychiatrist. My first placement in child psychiatry in the early 1990s was in a children’s hospital in London. The lead consultant worked in collaboration with the other professionals and the team used primarily systemic models. We had access to 2 beds for in-patients and as well as outpatient work, we carried out consultation on cases requested by the pediatricians. In those 9 months, I only prescribed medication to 1 individual, and beyond broad formulations the idea of a diagnosis was nowhere. It all made sense to me and persuaded me that this was the career for me. I felt that child psychiatry’s gift to medicine was understanding that there was a context to individuals’ suffering (they existed in systems of support and meaning), and the idea of development (that life is dynamic and changes). As I undertook the 4-year training to become a consultant, I saw, with concern, the tide of medicalization sweeps across the Atlantic from the United States. It gradually colonized our curriculums.

Potentially, psychiatrists are the only mental health practitioners that can do it all, from prescribing to therapy. We also ought to be able to identify organic conditions that may cause psychological problems as well as the organic complications that arise from psychological challenges (such as eating issues). If we live up to our promise, we should be leaders in mental health services, helping bring other professions along, as well as not being afraid of becoming embroiled in the politics and politicization of services. Yet, it pains me to say that if I had a child, or other loved one that I was deeply concerned about, I would not take them to see a psychiatrist. They are more likely to be harmed in the long term than helped, because of the prevalence of the justifiable assumption that what a psychiatrist does is prescribe. If we do not seriously reform and reconnect with our wider roots as a profession (most psychotherapies were originally developed by doctors), which, for example, had historically strong relationships with disciplines such as anthropology, then there are plenty who would come and rightfully take our place. This would be a great loss to the task of humanizing medicine.

The opinions expressed in the interviews are those of the participants and do not necessarily reflect the opinions of 

is a psychiatrist in Cleveland, Ohio, and clinical assistant professor of Psychiatry at Case Western Reserve University. He is a member of the executive council of Association for the Advancement of Philosophy and Psychiatry and has been actively involved in initiatives to educate psychiatrists and trainees on the intersection of philosophy and psychiatry. He is also a member of the 

Dr Aftab and Dr Timimi have no relevant financial disclosures or conflicts of interest.

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Are current systems of mental health care alienating children and adults from the meaning inherent in their own emotional difficulties?   

Psychiatry and the Shores of Social Construction: Sami Timimi, MD

Four recent studies may have turned what we know about attention-deficit/hyperactivity disorder (ADHD) on its head. By following large cohorts from early childhood to adulthood, they claim to have discovered that ADHD can start in adults who did not have the disorder before the DSM-5 cutoff of 12 years. However, before we rewrite the DSM and start prescribing stimulants to every adult who cannot concentrate, it is important to take a closer look at this 

In 3 of the 4 papers, the adult-onset ADHD actually 

 Furthermore, many of these teenaged-onset cases (29% to 75%) had symptoms of ADHD in their childhood that were either below the threshold for the full diagnosis or were classified as part of a related disorder (eg, conduct disorder or oppositional-defiant disorder).

The fourth paper claimed to identify new-onset ADHD in middle-aged adults, and it made the biggest headlines.

 The study followed a group of more than 1000 residents of New Zealand from aged 3 to 38 years as part of a larger investigation on the effects of adverse birth experiences on health. Researchers gathered symptoms of ADHD at 3 time points: ages 5 to 7; 11 to 15; and finally at age 38. What they discovered surprised them. Most of the children with ADHD no longer had the full disorder as adults, and most of the adults who met criteria for ADHD in middle age did not have the full disorder in childhood. The problem with this surprise discovery is that they did not ask the participants when their ADHD symptoms began, so these may have been teenaged-onset cases like we saw in the other 3 studies.

Comorbid Confounders and Other Confusions

The New Zealand study counted 27 adults with ADHD who did not have the full disorder in their childhood. A quick breakdown of those cases suggests that other disorders could have caused the attention problems endorsed by these patients.

 Specifically, 10 patients had conduct disorder in childhood; 15 had substance use disorders as adults; and 15 sought treatment for major psychiatric disorders as adults.

Two other studies that looked at purported cases of adult-onset ADHD 

 that the majority (93% to 95%) of the cases were better explained by sleep disorders, substance use disorders, or another psychiatric disorder.

If adult-onset ADHD does exist, it may not be the same disorder as childhood-onset ADHD. Indeed, most cases of adult-onset ADHD can be better explained as true ADHD that was partially expressed in childhood; false positives in patients whose symptoms are due to another disorder; or false positives in healthy people who overendorsed their symptoms during the 

But what if there remains a small number of individuals whose ADHD genuinely begins in adulthood? These studies point to that possibility, but they do not tell us whether these cases share common biological markers, familial patterns, and treatment response with childhood-onset ADHD. The gender distribution, for example, was different, with more males in the childhood-onset cases.

When someone goes through the effort to see a psychiatrist, there is a good chance that they have a real psychiatric problem. Or, as Groucho Marx put it, “Anyone who goes to a psychiatrist ought to have their head examined.” With community samples, the working assumption is that the participants are “normal,” which is why this kind of research is so prone to false positives. The 

 in these community studies were further elevated by the reliance on self-report.

Although these studies attempted to rule out other causes of adult-onset ADHD, those exclusions are hampered by false-negative rates. For example, it is not unusual for patients to forget past episodes of mania or psychosis, and those episodes often cause long-standing cognitive problems that could be mistaken for ADHD. Some important causes, like autism spectrum or personality disorders, were not evaluated in these studies.

If nothing else, these studies are a good reminder to look for a cause before you reach for a stimulant. In practice, the first thing to do when a patient presents with adult-onset ADHD is to screen for other psychiatric disorders that might explain the symptoms. Medical and environmental factors, including age-related cognitive decline, sleep deprivation, sleep apnea, inflammation, obesity, air pollution, chemical exposure, and excessive use of digital media, can also 

 Patients who suffer from these problems might ask their doctor for a stimulant, but none of those syndromes require a psychopharmacologic approach.

is the Mood Disorders Section Editor for 

 and the director of the Mood Treatment Center. He has written several books on mood disorders, most recently 

The author does not accept honoraria from pharmaceutical companies but receives royalties from PESI for 

Discovery of Adult-Onset ADHD Raises Questions

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Investigating late-onset ADHD: a population cohort investigation

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4. Moffitt TE, Houts R, Asherson P, et al. Is adult ADHD a childhood-onset neurodevelopmental disorder? Evidence from a four-decade longitudinal cohort study. 

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Late-onset ADHD reconsidered with comprehensive repeated assessments between ages 10 and 25

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Can attention-deficit/hyperactivity disorder onset occur in adulthood? 

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Association of exposure to endocrine-disrupting chemicals during adolescence with attention-deficit/hyperactivity disorder-related behaviors

2020;3(8):e2015041. Published 2020 Aug 3.

Before starting to prescribe stimulants to every adult who cannot concentrate, it is important to take a closer look at the research.

ADHD

Advances in Predicting and Diagnosing ADHD

Maternal Autoimmune Disease and ADHD Risk in Children

Consensus Statement Revises Previous Assertions About ADHD

Pediatric ADHD Medication Gets FDA Green Light

Psychiatry and the Shores of Social Construction: Sami Timimi, MD

Adult-Onset ADHD Raises Questions

What to Expect When Your Patients With ADHD Are Expecting

How to Switch Stimulants: A Dosing Guide for ADHD

ADHD Treatment Gets the Green Light

New Deterrent Stimulants for ADHD