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March 12, 2021
You've heard all sorts of misinformation about Attention-Deficit/Hyperactivity Disorder(ADHD), whether from friends, the internet, or uninformed press articles:
"ADHD is not real."
"Pharmaceutical companies invented ADHD to make money."
"I'm just a little ADD."
"Natural solutions are the best for ADHD treatment."
ADHD symptoms were first described in the late 1700s, primarily among hyperactive boys. It was described variously over 200 years as "fidgeting," "defects of moral control," "hyperkinetic reaction," "minimal brain damage" and eventually ADD (Attention Deficit Disorder) in the 1980s and ADHD today.
Because the natural tendency toward hyperactivity decreased with age, ADHD was originally thought to be a developmental disorder that disappeared in mid-to-late adolescence. When medicines were developed and used in ADHD treatment for young boys, physicians stopped prescribing them around mid-adolescence, because it was presumed the condition had been remediated. They were wrong. We know now that ADHD persists into adulthood for about two-thirds of ADHD youth.
ADHD was not widely recognized in girls until the mid-1990s when it became clear that girls with ADHD were less disruptive than boys with ADHD and were not being appropriately diagnosed. Girls with ADHD show less of the physical hyperactivity of boys, but suffer from "dreaminess," "lack of focus" and "lack of follow-through."
It was also in the 1990s that ADHD' pervasive comorbidity with depression, anxiety, mood, and autism spectrum disorders was established. At the same time, researchers were beginning to describe deficits in executive functioning and emotional dysregulation that became targets of substantial research in the 21st century.
Even with the 1990s recognition that ADHD is a lifetime disorder, equally present (in different forms) in both men and women, medical schools and continuing medical education courses (required for realizing sure of health professionals) have only begun to teach the most up-to-date evidence-based knowledge to the medical community. There still is much misinformation and a lack of knowledge among primary care professionals and the public.
ADHD Throughout the Lifespan
Most cases of ADHD start in Otero before the child is born. As a fetus, the future ADHD person carries versions of genes that increase the risk for the disorder. At the same time, they are exposed to toxic environments. These genetic and environmental risks change the developing brain, setting the foundation for the future emergence of ADHD.
In preschool, early signs of ADHD are seen in emotional lability, hyperactivity, disinhibited behavior and speech, and language and coordination problems. The full-blown ADHD syndrome typically occurs in early childhood, but can be delayed until adolescence. In some cases, the future ADHD person is temporarily protected from the emergence of ADHD due to factors such as high intelligence or especially supportive family and/or school environments. But, as the challenges of life increase, this social, emotional, and intellectual scaffolding is no longer sufficient to control the emergence of disabling ADHD symptoms.
Throughout childhood and adolescence, the emergence and persistence of the disorder are regulated by additional environmental risk factors such as family chaos, as well as the age-dependent expression of risk genes that exert different effects at different stages of development. During adolescence, most cases of ADHD persist and by the teenage years, many youths with ADHD have onset with a mood, anxiety, or substance use disorder. Indeed, parents and clinicians need to monitor ADHD youth for early signs of these disorders. Prompt treatment can prevent years of distress and disability.
By adulthood, the number of comorbid conditions increases, including obesity, which likely impacts future medical outcomes. Emerging data shows people with ADHD to be at increased risk for hypertension and diabetes. ADHD adults tend to be very inattentive but show fewer symptoms of hyperactivity and impulsivity. They remain at risk for substance abuse, low self-esteem, injuries due to accidents, occupational failure, and social disability, especially if they are not treated for the disorder.
Seven Important Concepts About ADHD
There are approximately 10 million U.S. adults with ADHD, 9 million of whom are undiagnosed. But with diligent research by the medical profession, we have learned seven important concepts about ADHD:
1. ADHD has been documented worldwide in 5% of the population.
2. Sixty-seven percent of ADHD children grow into ADHD adults and seniors. ADHD is heritable, runs in families, and is impacted by the physical environment and familial lifestyle.
3. In youth, rates of ADHD are higher in males than females as males, but these rates even out by adulthood.
4. ADHD coexists and is often masked by several other disorders: anxiety, depression, spectrum bipolar and autism disorder, substance abuse, alcoholism, obesity, risky behaviors, disorganized lives, working memory deficits, and significant executive dysfunctions that affect personal, social, and work success.
5. ADHD medications(stimulants and non-stimulants) are the most effective treatments for ADHD symptoms. Psychological support/training designed for ADHD, and lifestyle modifications, are important adjuncts to medicine.
6. ADHD costs the U.S. economy more than $100 million annually in lost productivity, accidents, hospitalizations with comorbidities, and family and professional support for ADHD patients.
7. ADHD is diagnosable and safely treatable in trained primary care practices.
How do you know if you or someone you love has ADHD? Evaluate your life against the seven concepts above. Then get screened and diagnosed by a health care professional. The diagnosis of ADHD should be done only by a licensed clinician who has been trained in ADHD. That clinician should have one goal in mind: to plan a safe and effective course of evidence-based treatment.
When diagnosing adults, it is also useful to collect information from a significant other, which can be a parent for young adults or a spouse for older adults. But when such individuals are not available, diagnosing ADHD based on the patient's self-report is valid. Just remember that personal, work, and family lives are improved with treatment. Research and technology related to ADHD improve all the time.
ADHD in Adults is a great resource for anyone interested in learning more about ADHD, with evidence-based information and education for both healthcare professionals and the public. The website also features a new ADHD screener for predicting the presence of ADHD in adults.
Stephen V. Faraone, Ph.D., is a Distinguished Professor of Psychiatry and Neuroscience & Physiology at SUNY Update Medical University and a global expert on Adult ADHD.
Methylphenidate is an effective treatment for ADHD in adults who also have bipolar disorder (BD), but it carries a potential risk of triggering manic episodes. Current guidelines therefore recommend using it only alongside mood-stabilizing medication. A new study using French nationwide claims data sought to test and extend those recommendations with greater statistical power than previous research.
The study built on findings by Viktorin et al. (2017), who observed that adults with BD not taking mood stabilizers had more than a sixfold higher risk of manic events (defined as hospitalization for mania or a new antimanic prescription) within six months of starting methylphenidate. Patients on mood-stabilizing treatment, by contrast, showed nearly half the baseline risk in the first three months. Those findings were limited, however, by small event counts (fewer than 61 manic episodes) and an effect that did not persist beyond the initial three-month window.
To build on this, researchers drew on the French National Health Data System (which is a claims database covering more than 60 million people) spanning 2008 to 2024. The final sample included 6,022 adults with BD (56% women) who had started methylphenidate. Using a self-controlled design, the study compared each patient's rate of manic events in the six months before their first methylphenidate prescription with the rate in the six months after, effectively eliminating stable individual differences as a confound.
Patients were classified as receiving continuous mood-stabilizing treatment if they had been dispensed at least two courses of specific antipsychotics (aripiprazole, olanzapine, or quetiapine) or mood stabilizers (lithium or valproate) in the nine months before starting methylphenidate, including at least one dispensation in the final six months of that window.
The results largely confirmed the earlier findings. Among the 2,745 patients not on mood stabilizers, the rate of inpatient mania diagnosis was 5.1 times higher in the first three months after starting methylphenidate, though this elevation fell to a non-significant level over the subsequent three months. Patients receiving continuous mood-stabilizing treatment showed no statistically significant change in mania risk across the full six-month post-initiation period. A formulation-specific pattern also emerged: patients without mood-stabilizing treatment had a 2.5-fold higher risk associated with extended-release methylphenidate, while no significant risk increase was seen with the immediate-release formulation or in treated patients regardless of formulation.
The authors conclude that methylphenidate at doses below 30 mg does not appear to elevate manic relapse risk when prescribed alongside mood stabilizers. The elevated risk seen in untreated patients, particularly with extended-release formulations, must be interpreted cautiously, given limited statistical power and the likelihood that it partly reflects the natural fluctuation of manic relapse over time. The authors flag this as an inherent limitation of self-controlled survival analyses when studying drug-induced mania, where temporal trends in the underlying condition can be difficult to disentangle from treatment effects.
The FDA has approved a new once-daily pill called centanafadine (trade name SIMTRIYO®). Approved for adults and kids aged 6 and older (weighing at least 44 lbs / 20 kg), centanafadine is a new category of ADHD treatment that aims to give fast results with fewer of the downsides of traditional stimulants.
To understand why centanafadine is unique among medications for ADHD, it helps to look at how ADHD brain chemistry works:
Stimulants like Ritalin and Adderall work mainly in the dopamine system. Nonstimulants like atomoxetine, viloxazine, clonidine and guanfacine work mainly on the norepinephrine system. Centanafadine is the first drug in a new class called NDSRIs (Norepinephrine, Dopamine, and Serotonin Reuptake Inhibitors). We can describe its effects as follows:
What Did Clinical Trials Show?
The FDA approved centanafadine based on studies involving thousands of adults, teens, and children. Here are the key findings:
Centanafadine showed some improvement in ADHD symptoms within the very first week of taking it although a full effect takes about six weeks.
In adult trials, taking 200 mg or 400 mg daily led to significant improvements in real-world skills:
In trials with children (ages 6–12) and teens (ages 13–17), centanafadine significantly reduced core ADHD symptoms like hyperactivity, impulsivity, and lack of focus compared to a placebo.
About 30% to 40% of adults with ADHD also suffer from anxiety. Traditional stimulants can make anxiety worse. In a trial specifically designed for adults dealing with both ADHD and anxiety, centanafadine effectively treated ADHD symptoms without firing up their anxiety, which might be due to its serotonin boost.
Does Centanafadine have Side Effects?
While Centanafadine was well-tolerated by most people in studies, like any prescription medication, it comes with important safety guidelines.
Prescribing Warnings:
Common Side Effects:
Other Warnings:
The Bottom Line
Overall, centanafadine is a new step forward in how we treat ADHD. Because it acts differently in the brain than traditional treatments, patients who struggle with stimulant-related anxiety or side effects may find it useful to explore with their doctor.
A landmark nationwide study from South Korea has uncovered a significant link between prenatal exposure to air pollution — specifically nitrogen dioxide (NO2) — and an increased risk of ADHD in children.
While researchers have long suspected that air pollutants interfere with fetal brain development through inflammation and oxidative stress, this study is one of the largest and most comprehensive of its kind, following nearly 1.5 million births for up to 13 years.
Why South Korea?
South Korea provided a unique countrywide “laboratory” for this research due to two key infrastructure strengths:
Key Findings: The “Smoking Gun” of NO2
While the study looked at several pollutants, nitrogen dioxide — a byproduct of fossil fuel combustion in cars and power plants — emerged as the primary concern.
Pollutant
Association with ADHD Risk
Nitrogen Dioxide (NO2)
Strongest Link: Every 1-ppb (part-per-billion) increase in exposure linked to a 22% rise in risk.
Sulfur Dioxide (SO2)
Minimal Link: Only a slight 4% increase per ppb.
Ozone (O3) carbon monoxide (CO), & particulates
No significant association was found.
The scale of the NO2 risk is particularly striking. Over the typical range of exposure levels found in the study (an interquartile range of 13 ppb), the data suggest a threefold increase in ADHD risk for children in the highest-exposure groups compared to the lowest.
Accounting for Other Factors
To ensure the results weren’t skewed by other variables, the researchers controlled for a wide range of confounders including:
The authors emphasized the strong association between maternal nitrogen dioxide exposure and ADHD, while also noting the small but significant association with sulfur dioxide.
The Take-Away: A New Frontier for Public Health
Historically, air quality laws have been designed to protect our lungs and hearts. However, this study adds to a growing body of evidence suggesting that the brain is likewise vulnerable.
In a commentary on the findings, expert George Ayoub argued that “neurodevelopment should be explicitly considered” when governments perform cost-benefit analyses on air quality regulation. My view is a bit different. The association is intriguing but the study does not establish cause and effect. Many statistically significant environmental risk associations for neurodevelopmental disorders have disappeared after controlling for maternal risk for ADHD. I hope this research team will do those analyses if feasible.
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