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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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The Background:
Women with polycystic ovary syndrome (PCOS) themselves show higher rates of ADHD. Because ADHD is partly heritable (meaning genes contribute to the condition), some of the increased ADHD seen in children of mothers with PCOS could come from shared genetic factors. In other words, a mother’s and her child’s increased risk might sometimes reflect common genes rather than an effect of the pregnancy itself.
Beyond genetics, growing evidence points to maternal metabolic problems during pregnancy as another important risk factor for neurodevelopmental outcomes. PCOS is one of these conditions and is considered both potentially modifiable (treatable or manageable) and biologically plausible as a contributor to risk. PCOS affects an estimated 5–10% of women of reproductive age worldwide and is characterized by signs such as hyperandrogenism (higher-than-normal levels of “male” hormones), insulin resistance (poorer ability to use the hormone insulin, which can affect blood sugar and metabolism), and chronic low-grade inflammation.
However, studies to date have not all reached the same conclusions. Some research suggests the association between maternal PCOS and offspring ADHD is stronger for girls, while other studies did not analyze results by child sex. Methodological differences make it harder to draw clear conclusions.
The Study:
It’s important to note that the studies included in this meta-analysis were observational (cohort studies and case-control studies). Observational studies can identify associations (that two things occur together) but cannot prove that one causes the other. A cohort study follows people over time, and a case-control study compares people with a condition to similar people without it.
The pooled results came from six studies that together included almost 1.4 million mother–child pairs and that adjusted for confounders (other factors that might influence the result, such as maternal age or socioeconomic status). After statistical adjustment, children of mothers with PCOS had about 40% greater odds of ADHD than children of mothers without PCOS. The analysis reported no evidence of publication bias (no clear sign that only positive studies were published) and zero heterogeneity (the results were consistent across the studies).
There was no meaningful difference in results between cohort and case-control studies, and the meta-analysis did not find a significant difference in the association when comparing male and female offspring.
The Take-Away:
The research team concluded that this large-scale synthesis found an association between maternal PCOS and higher odds of ADHD and other neuropsychiatric conditions in children. They suggested that children born to mothers with PCOS may benefit from developmental monitoring to identify and address problems early, while emphasizing that causal relationships have not been established. They called for further studies to confirm these findings and to investigate the biological and environmental mechanisms that might explain the association. Indeed, because women with PCOS show higher rates of ADHD than other women, we need genetically informed research designs to see if the reported association is confounded.
The Background:
Food insecurity is a widespread public‑health problem. Food insecurity refers to limited or uncertain access to enough safe, nutritious food. This term is used to describe households that sometimes or often can’t afford enough food or can only buy cheaper, less‑healthy options.
In the United States, almost eleven million children and teens (14%) lived in food‑insecure households in 2019. By 2023, the share of households with food‑insecure children and adolescents was estimated to have risen to about 18%.
Food insecurity is linked to worse physical health in children, including conditions like anemia (low red‑blood‑cell count), asthma, and delays in physical or mental development. It is also associated with problems in thinking and conduct (for example, aggressive behavior, anxiety, depression, and trouble concentrating or sitting still).
Those thinking and behavior problems can look a lot like ADHD (persistent patterns of inattention, hyperactivity, and impulsivity. This can make it hard for clinicians to tell whether symptoms come from ADHD itself, from the stress of poverty and food insecurity, or a mix of both. That overlap can complicate diagnosis and sometimes lead to misdiagnosis.
Smaller recent studies have looked at mental‑health links and found higher odds of ADHD and other mental‑health conditions among food‑insecure children aged 5–11 years. In one set of findings, moderate food insecurity was associated with 50% greater odds of an ADHD diagnosis and severe food insecurity with about 67% greater odds relative to food‑secure children.
The Study:
Because many past studies looked at single risk factors or only measured symptom severity, fewer investigations have focused specifically on household food insecurity as it relates to actual ADHD diagnoses and how that might matter for care. To address that gap, researchers used multiple years (2016–2022) of data from the U.S. National Survey of Children’s Health (NSCH). This survey is designed to be nationally representative and asks parents about their child’s health, including whether a doctor or other clinician has diagnosed ADHD.
The study included 232,571 children and adolescents (ages 3–17) and used statistical methods to adjust for other factors that could affect ADHD risk. Those factors included the child’s sex and race/ethnicity; the mother’s age; family income expressed as a percentage of the federal poverty level (a government measure used to classify income groups); the highest level of parent education; adverse childhood experiences (such as exposure to abuse, household substance use, or parental separation); birthweight (for example, low birthweight); and not getting enough sleep. Adjusting for these variables helps isolate the association between food insecurity and ADHD, though it cannot prove cause and effect.
The Results:
In this large, nationally representative sample, the researchers found a clear dose–response relationship: as the level of household food insecurity increased, so did the odds of a child having a clinician‑diagnosed ADHD (as reported by parents). In other words, greater food insecurity was linked to a higher likelihood of ADHD.
Compared with children in households that “could always afford to eat good, nutritious meals” (the reference group), the study found the following increases in odds of ADHD: children in households that “could always afford enough to eat but not always the kinds of food we should eat” had about 30% greater odds; children in households that sometimes “could not afford enough to eat” had about 55% greater odds; and children in households that often “could not afford enough to eat” had about 80% greater odds. (Saying “30% greater odds,” etc., means the odds were 1.30, 1.55, and 1.80 times those of the reference group, respectively — this describes a relative increase, not the absolute percentage of children with ADHD.)
The Take-Away:
The authors conclude that household food insecurity was associated with higher odds of parent‑reported clinician‑diagnosed ADHD in a dose‑response pattern. They suggest that reducing food insecurity (for example, ,by improving access to nutritious food and combining nutritional supports with mental‑health care) may help lower ADHD risk or reduce symptoms in some children. Reducing food insecurity should be a priority for society, but it is premature to conclude it will reduce the risk for ADHD. We know that parents with ADHD are more likely to lose their jobs and have lower incomes compared to parents with ADHD. That might create food insecurity for their children who we know are at high risk for ADHD from genetic studies.
The Background:
Many studies have tried to determine whether exercise improves executive function in children and adolescents with ADHD, but their conclusions have not always agreed. To bring the evidence together more clearly, the research team re-analyzed the available randomized controlled trials using a statistical approach designed to handle the kinds of data common in this field.
Executive functions are skills that help us control attention and behavior. The three core components are inhibitory control (the ability to stop or override impulses), working memory (holding and manipulating information in mind), and cognitive flexibility (switching between tasks or perspectives). Because a single study often reports multiple tests that tap these different skills, one study can contribute several related results (called effect sizes). Traditional meta-analysis typically treats each effect size as independent; when they are actually correlated, that can bias the combined estimate or force reviewers to discard useful data.
To avoid those problems, the team used a three-level meta-analysis. In this model, variance in the data is separated into three sources:
(1) sampling variance: the random error in each measured effect
(2) within-study variance: differences between multiple effect sizes reported in the same study
(3) between-study variance: differences in effects from one study to another
Accounting for all three levels makes it possible to include every eligible effect size from each study, which preserves information and statistical power and reduces the risk that correlations among effect sizes will overstate results.
The Study:
The review focused on long-term exercise interventions and also tested whether certain factors might change (or moderate) the effects. These potential moderators included participant age, which executive-function subcomponent was measured, the type of exercise, how long each session lasted, the total length of the intervention, and how often sessions occurred.
To be included, studies had to be randomized controlled trials (RCTs) of children or adolescents aged 6–18 diagnosed with ADHD. RCTs randomly assign participants to an intervention or a comparison group and are considered a strong design for testing cause-and-effect. The exercise programs had to be structured and last at least six weeks. Comparison groups varied by study and could include usual care, medication, sedentary activities, health education, waiting lists, or everyday life without the specific exercise program. Fifteen studies including 658 participants met these criteria.
The Results:
The three-level meta-analysis showed that long-term exercise interventions were associated with moderate-to-strong improvements in overall executive function. When statistical outliers were removed, the result remained positive: 13 RCTs with 598 participants showed moderate improvements. In plain terms, this suggests improvements that are noticeable and meaningful on average, not just tiny changes that are unlikely to matter in daily life.
Those moderate gains appeared across all three executive-function domains (inhibitory control, working memory, and cognitive flexibility, meaning the benefits were not limited to a single cognitive skill. The authors also examined exercise type:
“Open-skill” activities, which require reacting to changing situations (for example, many team sports, martial arts sparring, or racket sports), produced moderate-to-large improvements.
“Closed-skill” activities, which are more predictable and repetitive (for example, running or stationary cycling), showed only small, non-significant improvements in this analysis.
The review also found dose-related patterns. Interventions lasting at least twelve weeks were about three times more effective than interventions of six to twelve weeks, and sessions longer than an hour were about twice as effective as shorter sessions. Benefits were largest among adolescents aged 13 and older.
These patterns suggest that longer, more intensive programs, and those that involve open-skill activities, may produce larger gains. However, the authors caution that the overall certainty of the evidence was low. “Low certainty” means that limitations in the available studies (for example, small sample sizes, variability in methods, or possible bias) make it difficult to be confident that the observed effects will hold up exactly the same way in future research. Some subgroup findings (age, intervention duration, and others) were based on only a small number of effect sizes, so those moderator results should be treated as exploratory rather than definitive.
The Take-Away:
In short, this three-level meta-analysis suggests that regular, structured exercise (particularly longer programs and open-skill activities) may help improve executive functions in children and adolescents with ADHD. The evidence is promising but not yet strong enough to be considered conclusive, and the authors recommend more, larger randomized trials to confirm specifically which types and doses of exercise are most effective. Moreover, neither this meta-analysis or others show that exercise can replace standard treatments for reducing the core symptoms of ADHD (inattention, hyperactivity, impulsivity).
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