April 17, 2025

Why The New York Times’ Essay on ADHD Misses the Mark

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

Related posts

News Tuesday: Fidgeting and ADHD

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.

July 16, 2024

What is Evidenced-Based Medicine?

What is Evidenced-Based Medicine?

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:

  1. Mechanism-based reasoning.  For example, some data suggest that oxidative stress leads to ADHD, and we know that omega-3 fatty acids reduce oxidative stress. So there is a reasonable mechanism whereby omega-3 therapy might help ADHD people.
  2. Studies of one or a few people without a control group, or studies that compare treated patients to those that were not treated in the past.

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.  

  1. Non-randomized means that the comparison might be confounded by having placed different types of patients in the treatment and control groups.
  2. A single randomized trial.  This type of study is not confounded.
  3. Systematic review and meta-analysis of randomized trials. This means that many randomized trials have been completed and someone has combined them to reach a more accurate conclusion.

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.

April 23, 2021

ADHD Increases Risky Decision Making: Evidence from a Meta-Analysis

ADHD Increases Risky Decision Making: Evidence from a Meta-Analysis

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.

May 25, 2021

Beyond Dopamine: How Serotonin Influences ADHD Symptoms

ADHD is usually framed as a dopamine-and-norepinephrine condition, but recent studies have revealed that serotonin may also play a significant role. To delve deeper into this, we conducted a systematic literature review of studies looking at serotonin, its receptors, and the serotonin transporter (SERT) in relation to ADHD. The result: serotonin appears to be an important piece of the puzzle, but the overall picture is quite complex.

An ADHD & Serotonin Literature Review:

The authors searched the literature without time limits and screened thousands of records to end up with 95 relevant publications. Those included animal/basic-science work, neuroimaging, pharmacodynamics, a couple of large genetic/transcriptomic studies (GWAS and a cortico-striatal TWAS), and a few clinical reports. Each paper was graded for quality: 17 high, 59 medium, and 19 low.

The Results:
  • Most studies support a serotonergic role. About 81% (77/95) of the papers reported altered serotonin production, binding, transport, or degradation linked to ADHD or ADHD-like behaviors.

  • Multiple lines of evidence: animal models frequently show that changing serotonin levels or receptor activity alters hyperactivity and impulsivity; human imaging and clinical studies provide supportive but smaller and sometimes mixed signals; genetic/transcriptomic work points to serotonin-related pathways among many implicated systems.

  • Receptors and SERT matter: Multiple serotonin receptor subtypes (5-HT1A, 1B, 2A, 2C, 7) and SERT show associations with impulsivity, hyperactivity, attention, or brain activity patterns in ADHD models and some human studies.

  • Mixed and conflicting data: Central measures (brain, CSF) more often show serotonin deficits, while peripheral measures (platelets, plasma) sometimes show higher serotonin — methodological differences likely explain some contradictions.

  • Drugs used for ADHD can affect serotonin: Stimulants and non-stimulant drugs approved by FDA for treating ADHD (e.g., methylphenidate, atomoxetine, extended release viloxazine) or under investigation (centafafadine) have direct or indirect effects on serotonin systems, supporting the idea that monoamines interact rather than acting separately.  Because drugs that mainly affect serotonin are not useful for ADHD it seems likely that a pathway forward for ADHD drug development would be drugs that target multiple neurotransmitter systems.  A complex treatment for an etiologically complex disorder.

The Role of Serotonin in ADHD: What's The Take-Away?

As the study points out, the idea that serotonin may play a role in the neurobiology of ADHD is not new, but this literature review “identified multiple individual strands of evidence gathered over several decades and brought them into a more coherent focus”. It concludes that serotonergic neurotransmission is implicated in ADHD.  This doesn’t mean variations in serotonin levels cause ADHD, but that serotonin may be a plausible target for future treatments and research.

ADHD is polygenic and multi-systemic. For now, clinicians and patients should view serotonin as part of a complex network that may contribute to ADHD symptoms.  More research is needed before making treatment decisions based on these findings. 

Registry-based Cohort Study Finds No Association Between Maternal Diabetes and Offspring ADHD

Background:

A previous meta-analysis found that children born to mothers with diabetes had a 34% higher risk of developing ADHD compared to those born to non-diabetic mothers.  

However, previous studies suffered methodological limitations, such as small sample sizes, case-control or cross-sectional designs, and insufficient adjustment for key confounders such as maternal socio-economic status, mental health conditions, obesity, and substance use disorders.  

Moreover, many studies relied on self-reported maternal diabetes, and on non-clinical ADHD assessments, such as parental reports or screening tools, which are prone to bias and inaccuracies.  

Furthermore, the role of maternal antidiabetic medication use in relation to ADHD risk has rarely been examined. Antidiabetic medications are effective in controlling high blood sugar during pregnancy, but many can cross the placenta and the blood-brain barrier, raising concerns about potential effects on fetal brain development.  

Study:

To address these gaps, an Australian study team used a large cohort of linked health administrative data from New South Wales to investigate both the association between maternal diabetes and the risk of ADHD and the independent effect of prenatal exposure to antidiabetic medications. 

The study encompassed all mother-child pairs born from 2003 through 2005, with follow-up conducted through 2018 to monitor hospital admissions related to ADHD. That yielded a final cohort of almost 230,000 mother-child pairs. 

The team adjusted for potential confounders including maternal age, socioeconomic status, previous children, pregnancy-related hypertension, caesarean delivery, birth order and plurality, maternal anxiety, depression, schizophrenia, bipolar disorder, substance use (alcohol, tobacco, stimulants, opioids, cannabis), and child factors such as Apgar score, sex, prematurity, and low birth weight. 

Results:

For maternal diabetes overall, there was no significant association with offspring ADHD. That was also true when broken down into pre-existing maternal diabetes and gestational (pregnancy-induced) diabetes.  

In a subset of 11,668 mother-child pairs, including 3,210 involving exposure to antidiabetic medications, there was likewise no significant association with offspring ADHD

Conclusion:

The team concluded, “Our findings did not support the hypothesis that maternal diabetes increases the risk of ADHD in children. Additionally, maternal use of antidiabetic medication was not associated with ADHD.” 

This study highlights the importance of high-quality research. A previous meta-analysis linking ADHD and maternal diabetes did not appropriately adjust for confounders and cited many small studies that may have included biased self-report scales. This large, registry-based cohort study of nearly 230,000 mother–child pairs found no evidence that maternal diabetes—whether pre-existing or gestational—or prenatal exposure to antidiabetic medications was associated with subsequent offspring ADHD as measured by hospital-recorded ADHD outcomes. The study’s strengths include its population scale, prolonged follow-up, and extensive adjustment for maternal and perinatal confounders (including maternal mental health and substance-use disorders), which address many limitations of earlier, smaller studies that reported elevated risks.  

September 8, 2025

Population Study Finds Association Between COVID-19 Infection and ADHD

Background: 

The COVID-19 pandemic brought environmental changes that may have influenced ADHD symptoms and contributed to higher diagnosis rates. School closures, the transition to remote learning, and restrictions on outdoor activities led to increased screen time and isolation, both of which can affect attention and behavioral regulation. Children and adolescents, who usually depend on social interactions and structured routines, experienced significant disruptions during this period.  

Method:

South Korea has a nationwide single-payer health insurance system that keeps detailed health records on virtually its entire population. To explore the impact of COVID-19 on ADHD, a Korean research team used a database established by the Korean government that tracked all patients with COVID-19 between 2020 and 2023, nationwide COVID vaccination records, and insurance claims. They included all participants aged 6 through 29 years old. 

The onset of ADHD was determined by diagnosis combined with the prescription of ADHD medication. 

Altogether, the study encompassed almost 1.2 million Koreans, including over 150,000 children (6-12), more than 220,000 adolescents (13-19), and almost 800,000 young adults (20-29). 

The team adjusted for age, sex, income, Charlson Comorbidity Index, and medical visits. The Charlson Comorbidity Index predicts the mortality for a patient who may have a range of 17 concurrent conditions, such as heart disease, AIDS, or cancer. 

Results:

With these adjustments, young adults known to be infected with COVID-19 were about 40% more likely to be subsequently diagnosed with ADHD than their counterparts with no record of such infection

Adolescents known to be infected with COVID-19 were about twice as likely to be subsequently diagnosed with ADHD than their counterparts with no record of such infection. 

Children known to be infected with COVID-19 were 2.4 times as likely to be subsequently diagnosed with ADHD than their counterparts with no record of such infection

All these results were highly significant, and point to much greater impact on the youngest persons infected. 

Interpretation: 

The team concluded, “our nationwide study revealed that the COVID-19 pandemic significantly influenced ADHD incidence (raising incidence between 2020 and 2023), with SARS-CoV-2 infection identified as a critical risk factor,” and “In particular, early intervention and neurological evaluations are needed for children, adolescents, and young adults with a history of SARS-CoV-2 infection.”