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April 17, 2025
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This New York Times article, “5 Takeaways from New Research about ADHD”, earns a poor grade for accuracy. Let’s break down their (often misleading and frequently inaccurate) claims about ADHD.
The Claim: A.D.H.D. is hard to define/ No ADHD Biomarkers exist
The Reality: The claim that ADHD is hard to define “because scientists haven’t found a single biological marker” is misleading at best. While it is true that no biomarker exists, decades of rigorous research using structured clinical interviews and standardized rating scales show that ADHD is reliably diagnosed. Decades of validation research consistently show that ADHD is indeed a biologically-based disorder. One does not need a biomarker to draw that conclusion and recent research about ADHD has not changed that conclusion.
Additionally, research has in fact confirmed that genetics do play a role in the development of ADHD and several genes associated with ADHD have been identified.
The Claim: The efficacy of medication wanes over time
The Reality: The article’s statement that medications like Adderall or Ritalin only provide short-term benefits that fade over time is wrong. It relies almost entirely on one study—the Multimodal Treatment Study of ADHD (MTA). In the MTA study, the relative advantage of medication over behavioral treatments diminished after 36 months. This was largely because many patients who had not initially been given medication stopped taking it and many who had only been treated with behavior therapy suddenly began taking medication. The MTA shows that patients frequently switched treatments. It does not overturn other data documenting that these medications are highly effective. Moreover, many longitudinal studies clearly demonstrate sustained benefits of ADHD medications in reducing core symptoms, psychiatric comorbidity, substance abuse, and serious negative outcomes, including accidents, and school dropout rates. A study of nearly 150,000 people with ADHD in Sweden concluded “Among individuals diagnosed with ADHD, medication initiation was associated with significantly lower all-cause mortality, particularly for death due to unnatural causes”. The NY Times’ claim that medications lose their beneficial effects over time ignores compelling evidence to the contrary.
The Claim: Medications don’t help children with ADHD learn
The Reality: ADHD medications are proven to reliably improve attention, increase time spent on tasks, and reduce disruptive behavior, all critical factors directly linked to better academic performance.The article’s assertion that ADHD medications improve only classroom behavior and do not actually help students learn also oversimplifies and misunderstands the research evidence. While medication alone might not boost IQ or cognitive ability in a direct sense, extensive research confirms significant objective improvements in academic productivity and educational success—contrary to the claim made in the article that the medication’s effect is merely emotional or perceptual, rather than genuinely educational.
For example, a study of students with ADHD who were using medication intermittingly concluded “Individuals with ADHD had higher scores on the higher education entrance tests during periods they were taking ADHD medication vs non-medicated periods. These findings suggest that ADHD medications may help ameliorate educationally relevant outcomes in individuals with ADHD.”
The Claim: Changing a child’s environment can change his or her symptoms.
The Reality: The Times article asserts that ADHD symptoms are influenced by environmental fluctuations and thus might not have their roots in neurobiology. We have known for many years that the symptoms of ADHD fluctuate with environmental demands. The interpretation of this given by the NY Times is misleading because it confuses symptom variability with underlying causes. Many disorders with well-established biological origins are sensitive to environmental factors, yet their biology remains undisputed.
For example, hypertension is unquestionably a biologically based condition involving genetic and physiological factors. However, it is also well-known that environmental stressors, dietary
habits, and lifestyle factors can significantly worsen or improve hypertension. Similarly, asthma is biologically rooted in inflammation and airway hyper-reactivity, but environmental triggers such as allergens, pollution, or even emotional stress clearly impact symptom severity. Just as these environmental influences on hypertension or asthma do not negate their biological basis, the responsiveness of ADHD symptoms to environmental fluctuations (e.g., improvements in classroom structure, supportive home life) does not imply that ADHD lacks neurobiological roots. Rather, it underscores that ADHD, like many medical conditions, emerges from the interplay between underlying biological vulnerabilities and environmental influences.
Claim: There is no clear dividing line between those who have A.D.H.D. and those who don’t.
The Reality: This is absolutely and resoundingly false. The article’s suggestion that ADHD diagnosis is arbitrary because ADHD symptoms exist on a continuum rather than as a clear-cut, binary condition is misleading. Although it is true that ADHD symptoms—like inattention, hyperactivity, and impulsivity—do vary continuously across the population, the existence of this continuum does not make the diagnosis arbitrary or invalidate the disorder’s biological basis. Many well-established medical conditions show the same pattern. For instance, hypertension (high blood pressure) and hypercholesterolemia (high cholesterol) both involve measures that are continuously distributed. Blood pressure and cholesterol levels exist along a continuum, yet clear diagnostic thresholds have been carefully established through decades of clinical research. Their continuous distribution does not lead clinicians to question whether these conditions have biological origins or whether diagnosing an individual with hypertension or hypercholesterolemia is arbitrary. Rather, it underscores that clinical decisions and diagnostic thresholds are established using evidence about what levels lead to meaningful impairment or increased risk of negative health outcomes. Similarly, the diagnosis of ADHD has been meticulously defined and refined over many decades using extensive empirical research, structured clinical interviews, and validated rating scales. The diagnostic criteria developed by experts carefully delineate the point at which symptoms become severe enough to cause significant impairment in an individual’s daily functioning. Far from being arbitrary, these thresholds reflect robust scientific evidence that individuals meeting these criteria face increased risks for the serious impairments in life including accidents, suicide and premature death.
The existence of milder forms of ADHD does not undermine the validity of the diagnosis; rather, it emphasizes the clinical reality that people experience varying degrees of symptom severity.
Moreover, acknowledging variability in severity has always been a core principle in medicine. Clinicians routinely adjust treatments to meet individual patient needs. Not everyone diagnosed with hypertension receives identical medication regimens, nor does everyone with elevated cholesterol get prescribed the same intervention. Similarly, people with ADHD receive personalized treatment plans tailored to the severity of their symptoms, their specific impairments, and their individual circumstances. This personalization is not evidence of arbitrariness; it is precisely how evidence-based medicine is practiced. In sum, the continuous nature of ADHD symptoms is fully compatible with a biologically-based diagnosis that has substantial evidence for validity, and acknowledging symptom variability does not render diagnosis arbitrary or diminish its clinical importance.
In sum, readers seeking a balanced, evidence-based understanding of ADHD deserve clearer, more careful reporting. By overstating diagnostic uncertainty, selectively interpreting research about medication efficacy, and inaccurately portraying the educational benefits of medication, this article presents an overly simplistic, misleading picture of ADHD.
Li L, Zhu N, Zhang L, et al. ADHD Pharmacotherapy and Mortality in Individuals With ADHD. JAMA. 2024;331(10):850–860. doi:10.1001/jama.2024.0851
Lu Y, Sjölander A, Cederlöf M, et al. Association Between Medication Use and Performance on Higher Education Entrance Tests in Individuals With Attention-Deficit/Hyperactivity Disorder. JAMA Psychiatry. 2017;74(8):815–822. doi:10.1001/jamapsychiatry.2017.1472
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A recent study delved into the connection between fidgeting and cognitive performance in adults with Attention-Deficit/Hyperactivity Disorder. Recognizing that hyperactivity often manifests as fidgeting, the researchers sought to understand its role in attention and performance during cognitively demanding tasks. They designed a framework to quantify meaningful fidgeting variables using actigraphy devices.
(Note: Actigraphy is a non-invasive method of monitoring human rest/activity cycles. It involves the use of a small, wearable device called an actigraph or actimetry sensor, typically worn on the wrist, similar to a watch. The actigraph records movement data over extended periods, often days to weeks, to track sleep patterns, activity levels, and circadian rhythms. In this study, actigraphy devices were used to measure fidgeting by recording the participants' movements continuously during the cognitive task. This data provided objective, quantitative measures of fidgeting, allowing the researchers to analyze its relationship with attention and task performance.)
The study involved 70 adult participants aged 18-50, all diagnosed with ADHD. Participants underwent a thorough screening process, including clinical interviews and ADHD symptom ratings. The analysis revealed that fidgeting increased during correct trials, particularly in participants with consistent reaction times, suggesting that fidgeting helps sustain attention. Interestingly, fidgeting patterns varied between early and later trials, further highlighting its role in maintaining focus over time.
Additionally, a correlation analysis validated the relevance of the newly defined fidget variables with ADHD symptom severity. This finding suggests that fidgeting may act as a compensatory mechanism for individuals with ADHD, aiding in their ability to maintain attention during tasks requiring cognitive control.
This study provides valuable insights into the role of fidgeting in adults with ADHD, suggesting that it may help sustain attention during challenging cognitive tasks. By introducing and validating new fidget variables, the researchers hope to standardize future quantitative research in this area. Understanding the compensatory role of fidgeting can lead to better management strategies for ADHD, emphasizing the potential benefits of movement for maintaining focus.
With the growth of the Internet, we are flooded with information about attention deficit hyperactivity disorder from many sources, most of which aim to provide useful and compelling "facts" about the disorder. But, for the cautious reader, separating fact from opinion can be difficult when writers have not spelled out how they have come to decide that the information they present is factual.
My blog has several guidelines to reassure readers that the information they read about ADHD is up-to-date and dependable. They are as follows:
Nearly all the information presented is based on peer-reviewed publications in the scientific literature about ADHD. "Peer-reviewed" means that other scientists read the article and made suggestions for changes and approved that it was of sufficient quality for publication. I say "nearly all" because in some cases I've used books or other information published by colleagues who have a reputation for high-quality science.
When expressing certainty about putative facts, I am guided by the principles of evidence-based medicine, which recognizes that the degree to which we can be certain about the truth of scientific statements depends on several features of the scientific papers used to justify the statements, such as the number of studies available and the quality of the individual studies. For example, compare these two types of studies. One study gives drug X to 10 ADHD patients and reported that 7 improved. Another gave drug Y to 100 patients and a placebo to 100 other patients and used statistics to show that the rate of improvement was significantly greater in the drug-treated group. The second study is much better and much larger, so we should be more confident in its conclusions. The rules of evidence are fairly complex and can be viewed at the Oxford Center for Evidenced Based Medicine (OCEBM;http://www.cebm.net/).
The evidenced-based approach incorporates two types of information: a) the quality of the evidence and b) the magnitude of the treatment effect. The OCEBM levels of evidence quality are defined as follows (higher numbers are better:
Non-randomized, controlled studies. In these studies, the treatment group is compared to a group that receives a placebo treatment, which is a fake treatment not expected to work.
It is possible to have high-quality evidence proving that a treatment works but the treatment might not work very well. So it is important to consider the magnitude of the treatment effect, also called the "effect size" by statisticians. For ADHD, it is easiest to think about ranking treatments on a ten-point scale. The stimulant medications have a quality rating of 5 and also have the strongest magnitude of effect, about 9 or 10.Omega-3 fatty acid supplementation 'works' with a quality rating of 5, but the score for the magnitude of the effect is only 2, so it doesn't work very well. We have to take into account patient or parent preferences, comorbid conditions, prior response to treatment, and other issues when choosing a treatment for a specific patient, but we can only use an evidence-based approach when deciding which treatments are well-supported as helpful for a disorder.
Adults with ADHD are more likely to have accidents, drive unsafely, have unsafe sex, and abuse substances. These 'real world' impairments suggest that people with ADHD may be predisposed to making risky decisions. Many studies have attempted to address this, but it is only recently that their results have been aggregated into a systematic review and meta-analysis. This paper by Dekkers and colleagues reports 37 laboratory studies of risky decision-making that studied a total of 1175 ADHD patients and 1222 controls. In these laboratory tasks, research participants are given a task to complete which requires that they make choices that have varying degrees of risk and reward. Using the results of such experiments, researchers can score the degree to which participants make risky decisions. When Dekkers and colleagues analyzed the 37 studies together, they found substantial evidence that ADHD people are more likely to make risky decisions than people without ADHD. The tendency to make risky decisions was greatest for those who, in addition to having ADHD, also had conduct or oppositional disorders, which both have features that indicate antisocial behavior and aggressiveness. We can not tell from these studies why ADHD patients make risky decisions. One explanation is that it is simply the impulsivity of ADHD people that leads to rash, unwise decisions. Another theory postulates that risky decisions reflect deficits in one's sensitivity to rewards and punishments. If we are very motivated by reward and not aware of or affected by the possibility of punishment, then risky decisions will be common. The studies analyzed in the meta-analysis were not designed to demonstrate a link between risky decision-making in the lab and the real world, risky decisions that lead to accidents, and other outcomes. It is reasonable to hypothesize such a link, which is why clinicians should consider risky decision-making when planning treatments. If you suspect deficits in this area, it will not change your approach to pharmacologic treatment but, given the potential adverse consequences of risky decisions, you should consider referring such patients to cognitive behavior therapy for adult ADHD as this talk therapy may be able to teach ADHD adults how to cope with their decision-making deficits.
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Language is powerful. The words we choose not only reflect our understanding of the world but also actively shape it. Recently, this truth has been at the center of a growing debate in the mental health field regarding how we talk about ADHD.
In a recent paper published in The Lancet Psychiatry titled “The Power of Words: Respectful Language in ADHD Research,” French and colleagues advocated for a shift toward "neurodiversity-affirmative language”. Rooted in the social model of disability, their proposal encourages researchers to abandon traditional medical terminology, e.g., words like disorder and deficit, in favor of more neutral terms such as condition and challenge.
My colleague, Dr. Michael Miller, and I read this with great interest. We completely agree that revising language is essential to good science and that, both as researchers and as human beings, we are ethically bound to speak respectfully. However, we felt compelled to write a response. In our new paper, we argue that while language must evolve, it must do so scientifically.
The Two Prerequisites for Language Change
If we are going to fundamentally shift our scientific lexicon, two requirements must be met:
Currently, the proposal by French and colleagues meets neither requirement. While they claim consensus is accumulating that certain terms are disrespectful, they provide zero empirical evidence that this view is shared by the community of individuals living with ADHD. Even proponents of patient-centered language admit there is surprisingly little data supporting specific language changes.
More alarmingly, the recommended changes severely dilute the scientific accuracy of our field. Let’s look at two examples.
Why a "Deficit" is Not Just a “Challenge"
French and colleagues suggest replacing the term deficit with challenge. On the surface, challenge sounds softer and more affirming. But scientifically, these words are not interchangeable.
For decades, the term deficit has been defined by a specific performance metric that falls substantially below an expected level. It is a measurable reality. A challenge, on the other hand, refers to a new or difficult task that tests someone's ability.
Every single human being is "challenged" by complex neuropsychological tests, but only some individuals who face that challenge demonstrate scientifically significant deficits. If we relabel measurable deficits as universal challenges, we sacrifice the exactness required to communicate scientific findings and accurately measure the effects of life-changing treatments.
ADHD is a Disorder, Not Just a "Condition"
Another proposal is to replace the word disorder with condition.
In mainstream psychiatry, a disorder is a clinically significant disturbance that causes distress or disability. The word purposefully separates natural human variation from the suffering (pathos) that gives pathology its meaning.
Condition is a completely neutral term. Pregnancy is a condition. Being tall is a condition. Calling ADHD a condition distances the diagnosis from the profound suffering it can cause.
French et al. argue against framing ADHD as a disorder because it exists on a spectrum without a clear cutoff, its manifestation is context-dependent, and its definition evolves. But if we apply that logic across all of medicine, the concept of disease unravels:
The Real-World Danger of Imprecise Language
This is not merely an academic debate over semantics. The language we use has real-world implications. In the United States and across the globe, our healthcare, educational, and legal systems run on precise medical language. Terms like impairment, dysfunction, and disorder are legally and administratively required to justify support services, workplace accommodations, specialized educational therapies, and medications. The language of pathology in diagnostic manuals regulates the flow of these resources.
If we reclassify ADHD as a neutral condition characterized only by challenges, we risk erecting massive bureaucratic barriers. Imprecise language could easily be used by institutions or insurance companies to deny vital care to the people who need it most.
The Need for Lexical Discipline
Attempting to characterize a clinical disorder entirely through its strengths happens in a scientific vacuum. We cannot ignore the vast body of rigorous evidence confirming that ADHD meets the long-standing criteria used by mental health science to identify clinical disorders.
As professionals, our respect for the ADHD community demands a commitment to language that is clear, correct, and evidence-based. To build genuine consensus about how we talk about ADHD, we need meaningful, collaborative dialogue that integrates compelling empirical data and rigorous theory.
This standard of "lexical discipline" is not just a technical preference. It is a vital mechanism through which science and the mental health professions uphold their duty to society.
For many ADHD patients, getting properly diagnosed and starting meds is only half the battle. The next step is figuring out the exact right dose. Historically, clinical guidelines have provided scant guidance on this critical step. This lack of direction can inadvertently foster two extremes in clinical practice: therapeutic inertia (settling for a subtherapeutic dose that leaves symptoms undertreated) or uncritical escalation (driving doses higher and higher beyond licensed limits without meaningful benefit).
To clear up this pharmacological gray area, an international team of researchers published the first comprehensive dose-effect network meta-analysis of ADHD medications in The Lancet Psychiatry. By pulling together a massive vault of clinical trial data, they mapped out exactly how efficacy and tolerability shift as doses increase.
Traditional meta-analyses evaluate head-to-head, pairwise data, comparing one drug at a specific dose directly against a placebo. However, this study utilized an advanced Bayesian hierarchical network model using restricted cubic splines.
This mathematical framework allowed the researchers to combine both direct trial data and indirect evidence simultaneously across 113 double-blind randomized controlled trials (RCTs). In total, the study evaluated data from 14,138 children/adolescents and 11,016 adults. By standardizing various formulations into basic equivalents (e.g., converting amphetamines to dextroamphetamine equivalents), they created a clear, unified map of dose ranges.
The study yielded distinct dose-response curves depending on the patient's age and the specific medication class. Rather than a linear trend in which "more medicine equals more benefit," most treatments reach a clear statistical plateau or ceiling.
For Children and Adolescents (under 18)
In the pediatric population, medications hit clear peak efficacy boundaries:
For both amphetamines and guanfacine, escalating the dosage past these points resulted in U-shaped curves, meaning further dose hikes yielded diminishing group-level symptom reduction.
For Adults (18 and older)
Adult profiles showed slightly different trajectories:
The ultimate goal of this landmark analysis is to guide shared decision-making between clinicians, patients, and families. The results send a dual message to the medical community:
A medication's true efficacy hinges on its tolerability, typically measured by how often patients discontinue treatment due to severe side effects. For amphetamines, this dropout risk scales linearly with dosage, notably exceeding placebo in children above 25 mg/day and becoming prominent in adults past 50 mg/day. In contrast, methylphenidate shows no clear dose-dependent dropout risk in pediatric patients, whereas adults face a steep risk curve: increasing the dose from 60 mg/day to 90 mg/day raises the dropout risk from 7.3% to 10.0% for only modest symptom relief. Finally, youth taking guanfacine experience a sharp climb in discontinuation risks, reaching a 9.8% median risk at 4 mg/day before data limitations obscure further trends.
The authors strongly emphasize that these findings represent group averages. Because individual metabolism, genetics, and comorbidities vary widely, some specific patients may legitimately require and tolerate higher off-label doses. However, if an unusually high dose is needed, the study suggests it should prompt a careful clinical pause, either to reassess for co-occurring conditions (like anxiety, autism, or sleep disorders) or to manage realistic expectations regarding what the medication can achieve.
The persistent shortage of ADHD medications has been more than a simple annoyance for patients at the pharmacy; the inconsistent availability of these medications has had deep impacts on the daily lives of those struggling without them. While public discourse has pointed fingers at over-prescribing or at restrictive DEA quotas, a recent economic evaluation in JAMA Health Forum suggests we’ve been looking in the wrong direction for an answer to what is causing this.
The reality of the shortage is less about increased demand and more about a fragile, globalized supply chain that snapped at a critical link.
Debunking the "Quota Myth":
The prevailing narrative suggested that the Drug Enforcement Administration (DEA) was stifling production by refusing to raise quotas. However, the data tells a different story. In 2022, manufacturers collectively met only about 70% of their allotted production quotas.
So we know that the problem wasn't that this DEA quota ceiling was too low. In fact, most manufacturers couldn't even reach it. Even when accounting for exports and domestic retail, production remained significantly below the legal limit. Even if the DEA had doubled its quotas, these medications still likely wouldn't have magically appeared on pharmacy shelves.
The most striking finding in the study is the correlation between the shortage and a sharp decline in the import of raw Active Pharmaceutical Ingredients (APIs). For the past decade, Germany has accounted for over 85% of US amphetamine imports. In 2022, these imports dropped by approximately 36.7%. When the API doesn't arrive at the factory, production for medium and small manufacturers grinds to a halt. Unlike larger pharmaceutical giants, these smaller players often lack the inventory cushion or flexibility to quickly pivot to a new supplier.
When the primary supply of amphetamine-based stimulants (like Adderall) faltered, it triggered a secondary crisis. Patients and clinicians, seeking alternatives, shifted toward lisdexamfetamine (Vyvanse) and methylphenidate (Ritalin/Concerta).
If we view this shortage purely through a regulatory or clinical lens, we miss the underlying cause of the crisis. The pharmaceutical industry has become a victim of its reliance on "just-in-time manufacturing” and highly concentrated sourcing. Because over 30% of APIs for the US market are produced in just one or two facilities globally, the system isn't just inefficient; it’s brittle. We are, in a sense, trapped in a system that prioritizes cost-reduction over the resilience required for public health.
The researchers suggest several policy shifts to prevent a repeat of this supply chain failure:
The ADHD medication shortage wasn't a failure of clinical oversight or a sudden surge in "TikTok-driven diagnoses”, as many have suggested. It was a failure of logistics. It reminds us that the path from a lab in Germany to a patient's hand in the US is far more precarious than we realized.
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